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5682 | dbpedia | 1 | 67 | https://www.airwarriors.com/community/threads/navy-facs-in-nam.46579/ | en | Navy FACs in 'Nam? | [
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] | 2019-05-27T17:56:12+00:00 | First post. I signed up here to ask this...
I'm a former USAF FAC with 300 combat missions in 'Nam. I'm currently helping a guy write a book based roughly... | en | Air Warriors | https://www.airwarriors.com/community/threads/navy-facs-in-nam.46579/ | First post. I signed up here to ask this...
I'm a former USAF FAC with 300 combat missions in 'Nam. I'm currently helping a guy write a book based roughly on the old JAG TV show. He needs to know if there were any Navy FACs in Vietnam, and if so where they trained, what type missions they flew, in what aircraft, and who they worked/controlled. I can't recall training with or working with any Navy FACs while in 'Nam. Nor can I recall any exchange program in which Navy pilots trained with us AF types.
But I'm hoping someone here can correct my memories with details. Thanks in advance.
My problem is that my own FAC role was so classified and compartmented that I know very little about what happened in the rest in the war. My lower left corner of the Big Picture was about one pixel in size. I'm familiar with some other Air Force FAC roles - but mostly from reading. Nothing else. This thread is the first I've ever heard of your HAL-3 Seawolves, for example. Posting here is the only way of "reaching out" I could conjure up. Besides talking to Pugs, that is.
Anyway, I'll stay tuned here in case some helpful jock turns up. I suspect, though, that my initial impressions are correct - there were no actual Navy FACs.
The US Navy had only one land based fixed wing attack squadron throughout the Vietnam War. The “Black Ponies” of Light Attack Squadron 4 (VAL
4) were technically a close air support squadron designed to protect brown water (riverine) forces and SEAL commando teams operating throughout the Mekong Delta. Even though CAS was their primary mission, the squadron assumed the mission of airborne forward air control soon after operations began in March of 1969, controlling CAS sorties and adjusting naval gunfire and artillery strikes from all services. They operated from two detachments located at Binh Thuy and Vung Tau.
The squadron was part of Zumwalt's “Sea Lords”, or South East Asia Lake, Oceans, River, and Delta Strategy, designed a broad campaign initiated in November 1968 to stop Vietcong infiltration into South Vietnam from the riverways leading out of Cambodia. US and ARVN forces needed the supply routes cut off if they were to regain the countryside from the Vietcong. VAL-4 and their brethren attack helicopter squadron HAL-3, were the primary naval air assets stood up to fill the gap of providing time critical CAS for U.S Navy, Army, and ARVN forces in the Delta.
Overall, the squadron had an interesting history. VAL-4 was commissioned on January 3, 1969 at Naval Air Station North Island, near San Diego, California, borrowing OV-10A Broncos from the Marine Corps. BUPERS believed they would have a hard time finding pilots for the unorthodox job. The assignment would take veteran aircrew from their own stable warfare (sound familiar?) communities into an unknown world not typical to the Navy. Most of the pilots came from the S-2 community with a healthy number of A-1 pilots signing on. Overall, the experiment was a moderate success especially when one considers the addition of HAL-3.
The deeper gold wing history is with the Marines of VMO-2 and HMM-362 (O-1 Bird Dogs, later Huey's and OV-10's) who flew the "Klondike Playboy" missions and the "Cat Killers" of the Army's 220th Reconnaissance Company who supported the Marines and Navy big-gun ships.
If we're talking the definition of a FAC being the directing of weapons from airborne in direct support of troops by other aircraft as a formalized role I suspect you are right - See my note on the other board. I will also reach out to Barrett Tillman and that crowd.
Good article here that indicates that UH-1 may have been used by the Marines but that would have certainly been out of necessity vice a formalized role. | |||||
5682 | dbpedia | 1 | 71 | https://www.pinterest.com/pin/vmo1-yazoo-1982-ov10a-model-etsy--155303887453517280/ | en | [] | [] | [] | [
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] | null | [] | 2021-07-25T18:47:29+00:00 | VMO-1 Yazoo 1982 OV-10a ModelFly with the VMO-1 Yazoo 1982 in this handcrafted OV-10a Model. Each piece is carved from wood and painted to provide a one of kind piece. Our pieces seek to recreate memories of these glorious aircraft.Length - 13.5 inchesMarine Observation Squadron 1 (VMO-1) was an observation squadron of… | en | Pinterest | https://www.pinterest.com/pin/vmo1-yazoo-1982-ov10a-model-etsy--155303887453517280/ | |||||||
5682 | dbpedia | 3 | 87 | https://www.catkillers.org/history-marine-ao-diary.html | en | 220th Aviation Company "Catkillers" History: A Marine Aerial Observer’s Diary | [
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A Marine AO Diary
by J. D. Richards, USMC AO, 1965–66
Lt. Col., Retired
Transcribed and edited for publication by Dennis D. Currie
Little did I know that my education at Franklin College in the heart of Indiana was going to lead me on a journey that would forever change my life. Attending Marine Corp Officers School in 1962, I finally found myself as a 1st Lieutenant attending Marine Aerial Observer School in the spring of 1964. Fate has a strange way of playing out our lives, and my activities with the Army’s 220th Aviation Company “Catkillers” unfolded. Beginning approximately 15 November 1965, and ending when my tour of duty was completed, approximately 30 May 1966, I went on the joy ride of my life.
The Marine AO’s had intially been attached to VMO–2, a marine reconnaissance unit located at Marble Mountain, outside of Da Nang, from May 1965 to October of 1965. Initially we flew in older model L–19’s; however, they were in such terrible condition and so unreliable that when VMO–2 acquired the new UH1E’s we were assigned left seat for our missions. In the summer of 1965, we moved from the south end of the Da Nang runway when Marble Mountain was completed. It was at that time we had adopted our squadron mascot, “Just N. Case”. I’m not sure what drew us to him at first, beside the fact that he was an incredibly cute monkey. However, we discovered very quickly that he would take out his pent up sexual tensions on just about anything that we would throw for him to chase down, including beer cans and the pictured football. It was our accumulated opinion that the attached photo, was indeed, the inspiration for that famous quotation that is used to describe every ridiculous situation that man finds themselves in, spinning their wheels, accomplishing absolutely nothing, while making an absolute fool of themselves!
On October 26, 1965, VC sappers conducted a very successful and devastating raid on our facilities, destroying approximately eighteen UH1E’s, including our Medevac helicopter on the tarmac and inflicting many casualties among our personnel. The only UH1E that survived was the commanding general’s UH1E, which was parked at the 3rd VMAR Division Command Post at Mainside.
First Lieutenant Dave Grinstead, the Officer–In–Charge of MMAF Security, had repeatedly asked in writing for additional concertina wire, land mines and night vision equipment to cover access from the beach at Da Nang. Repeatedly, he was advised by Command that his request for these security measures were unnecessary and that, “The VC would never come at us by the beach.” Lt. Grinstead had to do a “rug dance” in front of the CG; however, he produced his documentation for his requisitions and the letters denying his requests. The colonel responsible for the denials was relieved of duty and sent home, and Lt. Grinstead’s career was saved.
Since all of the UH1E’s were out of service, our AO Unit was assigned to ride left seat with a CH–34 Unit. Unfortunately, the passage of time does not allow me to recall the unit designation, however, the CH–34 was the Korean conflict work horse of the Marines, carrying troops and gear to landing zones. It was clear from the beginning that it was functionally unsuited for use as an observation aircraft. It was in a CH–34 that 1st Lt. Jon Schmid was killed in action, while conducting aerial observation southwest of Da Nang.
In the middle of November of 1965, an agreement between the Army and Marines resulted in the Marine AO’s being allowed to fly rear seat with the 2nd Platoon, 220th Aviation Company. What a difference, we were now flying in brand new, up–to–date, shiny L–19’s. Our unit could not have been more joyful, because by this time, in addition to Lt. Schmid, we had suffered the loss of Major Reilly a VMO pilot and another AO, Bobby Cole, who was wounded in action. This reassignment was a great day for our AO Unit and a morale booster that was sorely needed.
The professionalism of the 220th pilots, and the warmth of their welcome and assistance were well received by the AO’s as the first merger took place on the West End of the runway at Da Nang. Flight after flight occurred and the personalities, characters and camaraderie emerged as one happy family. Our friendships solidified and evolved at our favorite watering hole, a night club in downtown Da Nang, called the “China Night”. Our reserved room in the back for Pilots and AO’s was a welcomed relief where we shared our stories over a few bottles of 33 Beer.
The flights for me in the new L–19’s were such a pleasure after the experiences in the CH–34’s. One such mission flown with 1LT Jim Morris was covering the withdrawal of a battalion of Marines southwest of Da Nang, just west of a railroad and bridge. We were flying north and just east of the railroad and bridge when we observed three NVA crouched at the Southeast end of the bridge, watching the Marines retrograde movement. So intent on watching the Marines, they failed to see us. Jim circled to the right, and we began retracing our steps, flying in such a manner that when we saw them again they were still huddled close together watching the Marines. In–the–meantime, I possessed the new AR–15 assault rifle, and had it pointed out the window on the left side of the aircraft, set to full automatic. I need to mention that the AR–15 was such a pleasure to hold on target while firing full automatic, so while beside them, I let them have it with a healthy burst. One died where he sat, another slid down the railroad embankment headfirst on her back and the third enemy escaped into a small village nearby. Jim and I wanted to get a closer look at the KIA’s , so we made another pass to view the bodies. The soldier who slid down the embankment appeared to be female, with long hair and breasts. I was devastated. Our training was always towards enemy soldiers and not women. In our society, women were to be revered and loved, not abused and killed.
I was unsure, so I asked Jim to make another pass to see if my observation was as I initially saw it. Never in my experience or training was I told that personal combat, up close would include the killing of a female. Jim intuitively knew I was devastated, and understood that air strikes and artillery were not personal, however this was and he knew it bothered me. I credit Jim for saving my sanity and self worth as a human being through the questions he was to ask of me. I have thought about this for the past 46 years and will be forever grateful for the “rescue” questions he asked that day. “Let me ask you, are you married?”, I replied “yes”. “Do you have kids?”, I replied, “yes.”, “Is your wife happy that I was here?”, I replied, no”. “Would she be sad if you were killed?”, I replied, “yes”. “Would it make her feel any better to know that a woman killed you?”, I realized in that moment, as if I had hit a home run, that Jim’s point was made and that reality and sanity rules. Instantly, and from that point on, I was indebted to Jim for helping me to see what I should have known, a soldier is a soldier regardless of gender. Most importantly, I was at peace with myself and never again, when we were in these little firefights, did I fret about the “unconventional soldier”. To Jim, well done, well said and thanks!
Jim and I flew several missions together and among them that were notable was a reconnaissance mission south of Da Nang. We were making a pass over a possible VC village when we received a one round salute. We decided to make another low level pass over the same area, just to see. We violated the most basic of cardinal rules, “never make the same low pass over the same area”. As we flew low over the village, our lesson was to become evident, when the entire village opened up on us with automatic weapons fire and other weapon types as well. I was holding two red smoke grenades outside the window, with pins pulled, when the rounds hit our aircraft. Jim yelled, “ I’m hit!” I dropped the grenades and grabbed Jim’s harness to keep him from falling forward on the control stick. I recall talking to the 9th Marines, telling them I was leaving the area, the artillery unit/mission was cancelled. I also informed the DASC, (Direct Air Support Center), in charge of keeping track of the tactical aircraft in the area that we were covering.
Jim needed first aid, and he was bleeding from his left arm. He somehow moved his arm around to the back of his seat for me to apply first aid. While bandaging him, holding his harness, talking to all of these people on the ground, in addition to anticipating that I may have to fly this plane and land it, this was approaching an overwhelmingly busy time. We were just about five miles south of the Da Nang airfield when I contacted Da Nang tower, advising them that I needed a straight in approach with a wounded and bleeding pilot. As I recall this was the exchange with a Vietnamese air traffic controller. Vietnamese ATC, “Be advised C–123 on final. Go around.”
Jim had now recovered somewhat, and he said, “Request straight in, I’m wounded and bleeding!”
Vietnamese ATC, “C–123 on final, go around.”
Jim again, “Request straight in, I’m wounded and bleeding!”
Vietnamese ATC, “Go around C–123 on final.”
The C123 pilot cut in at that point responding, “We’ll pull off, Take her in—God speed, son.”
Finally an American ATC responded, “Bring it straight in, emergency equipment will meet you.”
As we bounced to a halt, I remember the medics taking Jim out and putting him into the ambulance. Reflecting back on this mission, despite the painful wounds, heavy bleeding and being in shock, Jim skillfully landed our aircraft. In retrospect, I should have put him in for an award; however, it didn’t occur to me at the time. Someone should have!
Later, after meeting with Captain (CPT) Chancellor, Ben Hartman and others, we tried counting the number of bullet holes in the fuselage. I don’t recall how many, only that there were a lot. There was one bullet hole that we discovered which entered through the bottom of the plane just in front of my seat. However, we could not find an exit hole anywhere above. The trajectory of the bullet was directly between my feet and if I had not been looking either right or left, the round would have conceivably caught me underneath my chin and through the top of my head, it was that close! The mystery remained, while neither the crew–chiefs, other pilots, or myself were able to determine where the round ended up. The mystery was solved a few weeks later when I noticed my flack jacket had a small tear in the bottom seam, on the left side of the zipper. Actually, it was a good sized hole that I hadn’t noticed until then. As I looked and prodded at the opening, suddenly a bullet fell out of the hole. To this day I am so happy that I was looking out the right hand window, instead of straight ahead! Somewhere, in my war souvenirs, I have this bullet as a reminder of that mission. Ben would fly me out to that same area, where we called in artillery, a “Fire–For–Effect’ (FFE) to eliminate future threats from that village.
Digressing a bit from the missions, I thought about the impact of our military training and having to multi–task several things while our drill instructors screamed at us at the top of their lungs. Trying to accomplish your lessons while under stress, threats and pain, was well worth it. While I was taking care of Jim, talking to the folks on the ground, thinking about getting back, and landing if Jim couldn’t, I never panicked or choked. I performed what I had to do, not to brag or extol myself, but to praise the value of realistic training. The harassment, and screams of the DI’s to get a weeks worth of work done in thirty seconds or less, worked for me and will continue to work for others. A special thanks you to Sgt. J.J. Winstanly, my DI, and other trainers. While Jim and I broke one of the cardinal rules of flight, we lived to make the experience a lesson for future pilots and AO’s, “Don’t do it.”
I remember Thanksgiving and Christmas with the 220th; poor CPT Chancellor succeeded in getting everyone to Christmas Dinner, scheduling around flights and duty officer, a job well done by our captain. However, the weather had begun to enter the monsoon season and we were grounded for several days. It was during Operation Harvest Moon that Tom Murray and I flew in support of a re–supply mission to the 9th Marine Battalion southwest of Da Nang. All went well during the first portion of this operation. The next morning, on the nose of a ridge running south to north, we found an AAA site on the south end of the ridge. The NVA had dug an elaborate AAA emplacement with supporting trenches going north, uphill into a forest. The AAA was playing havoc with the re–supply helicopters. There was a flight of A–4 Skyhawks on station, in case Tom and I located the gun. We saw the muzzle flash approximately a mile away, as we were way east of the nose of the ridge. I called the Skyhawks and told them we had found the AAA site and that we would mark it with red smoke. First of all, I had to make sure the Skyhawks had me in sight so that they could follow my path and see the red smoke drop. Tom put the L–19 into twisting, snakey turns as we descended in a shallow dive towards the nose of the ridge, allowing the Skyhawks to get us in their sight. At approximately 500 yards, the NVA gunner spotted us and was placing tracer rounds all around us. Tom kept the aircraft moving towards the ridge, diving below the fixed downward capability of the gun. At this point we were flying fast, well below the ridge line as we flew over the AAA site. I dropped the smoke within fifty feet of the gun, as we flew down the ridge and away from danger. The Skyhawk pilots saw the red smoke and confirmed the location. I told them to hit the smoke, since it was just fifty feet north of the AAA gun. The Skyhawk pilots had a ball strafing and bouncing 250–pound bombs and rockets on that target. The site was thoroughly destroyed, and we didn’t see any movement around that area for the next two days.
Tom was the master of the air that day. He was so calm and cool, maintaining a quiet and professional attitude that his peers and I appreciated. I wrote Tom up for a Bronze Star. My supervisor downgraded it to a Navy Commendation with a V–Device. His rationale was that Tom’s actions, diving into the muzzle of the AAA gun while maneuvering the aircraft into and out of the cone of fire, was not deserving of the Bronze Star. I believed he deserved the Bronze Star at minimum.
I’ll take a moment here to describe what was developing in this area of I–Corps during this time frame. Operation Harvest Moon had its beginnings in November 1965, when the 1st VC Regiment, with all three of its battalions, the 60th, 80th and 90th, overran Hiep Duc District Headquarters and the South Vietnamese reported 174 of the defenders missing and 315 weapons lost. By early December, three Marine battalions – the 2nd Battalion 1st Marines, the 3rd Battalion 3rd Marines, and the 2nd Battalion 7th Marines – were deployed to an area midway between Chu Lai and Da Nang to relieve the pressure on South Vietnamese forces that had been hit hard by the 70th Viet Cong Regiment. On the 18th, the 80th Viet Cong Battalion ambushed the 2nd Battalion 7th Marines, although the Viet Cong gained fire superiority in the beginning, the Marines turned viciously on the enemy. Harvest Moon was the last of the Marine's big battles in 1965. These large–scale efforts had become a regular feature of the war for the Marine forces. During the last half of its first calendar year in country, III MAF conducted fifteen operations of battalion size or larger. American intelligence agencies indicated that during 1966 the Marines would face even larger enemy forces as North Vietnamese troops entered South Vietnam to join their Vietcong comrades.
It was near the end of November and the close of Operation Harvest Moon that CPT Chancellor and I began covering the withdrawal of the 3rd Marines in their march out of the battle area, towards Highway 1. Prior to our going out on this mission, CPT Chancellor stated that there would be “no shooting out of the plane allowed. You’ll shoot my tires.” I thought, S**t! So we joined the exodus of the 3rd Marines, when all of a sudden they were receiving sniper fire and other sporadic rounds. CPT Chancellor and I spotted two VC/NVA in a ditch, one wearing a robin–egg blue shirt, while the other wore a tan shirt and shorts. I don’t believe they saw us; however, the next thing I heard was an order from CPT Chancellor, “JD, get that gun out the window and let’s get those guys! Don’t shoot my tires!” As we flew low, directly over them, CPT Chancellor put the plane into a slide, but we were too close for a good shot. I let a burst go, but missed all around them. They got up and ran into a large field surrounded by huge hedgerows. They were running approximately 100 feet apart and we were right behind them. CPT Chancellor then said, “I’ll put this in a side skid and you’ll have a better shot at both of them.” As CPT Chancellor put the plane in a skid, the VC were coming to the end of the field. At the end of the field was a small opening of about five to eight feet wide. They both entered the opening, close together, side by side and that’s where they died. I got them both with one burst. CPT Chancellor remarked, “JD, you got both of them, good shooting! Check my tires!” I thought, ‘Good flying Cap.’
One of my final missions at the 2nd Platoon in Da Nang was a day of routine stuff. The pilot was CPT Pepe, and we were west of Hoi An when we spotted two tan–shirted NVA running into a zigzag trench. I suggested the AR–15; however, CPT Pepe denied it. Instead we called in artillery on two people? Ok, so I contacted the artillery and got a mission and gave them the target, then I received an FFE. Splash, splash, wait, and I observed artillery rounds all over an acre of field. It appeared to me that it was a spread sheaf. I then requested a converged sheaf and here it came! Splash, splash, wait and on target. One round landed right on top of the two NVA, leaving nothing more than a very large hole in the trench where they had been. My KE28A camera was being repaired, so I was unable to take pictures of that action. Anyway, Merry Christmas, Nugyen!
On January 1, 1966, I was transferred to Phu Bai to support the 2nd Battalion, 1st Marine Division and fly with the 220th at Phu Bai International Airport. However, before checking out of the Da Nang area and the 2nd Platoon, I was given a run–down of the company area at Phu Bai. What stood out for me was a pilot whose name was Woodhurst. He was described as a super pilot who seemed to be always getting into scrapes, firefights and other skirmishes. A legend, from the standpoint that his skills in locating VC and rendering appropriate measures preceded him. It seemed to me that he had a personality of a “bullet magnet.” I thought at the time that this would be great, in that I had printed on my flack jacket, “Magnet Ass”. My assessment was that we would get along very well. The following photographs are included to frame the missions that I was to undertake with many of the pilots at Phu Bai. While I found Vietnam to be a deeply religious country, the enemy was not below using this to his advantage when taking up sniper positions.
I was billeted in the 2nd Battalion area, in a squad tent, with cots on the ground. My daily flights required transportation, everyday across Highway 1 to the Phu Bai airfield. I checked in with the 220th RAC late in the morning on January 2, 1966, at the personnel tent and was directed to Major Schmale’s office. Major Schmale knew I was coming from the 2nd Platoon in Da Nang, and he was very anxious to hook me up with CPT Charles Woodhurst. I was really needed, since I found out that I was the only school trained, experienced AO in northern I–Corps. CPT Woodhurst and I finally met and a great professional bond grew between us. It seemed that we both thrived on action, danger and close in combat, aimed at clearing the world of VC zombies. Neither one of us figured we would make it out of the Republic of Vietnam alive. The following narrative has remained with me for almost 50 years.
Woody and I departed in his O–1 and were told to look around the villages in the Co Be, Than Than area for NVA activity. This area had the reputation for a VC safe area and home to an NVA Regiment. In this one particular village there were more than a few green and tan uniforms that scattered upon our arrival. We flew low and fast and we were in and out before anyone knew we were coming. In the village there was a very large haystack sitting adjacent to an equally large square pit, approximately 10X10X10 feet in scale. In addition, there was a ladder leaning on the side, with an apparent tunnel leading under the haystack. What initially drew Woody’s and my attention in this particular pit was that there were two people inside the pit, one an NVA soldier with his weapon beside him on the ground, and his back towards the southwest corner of the pit. The other individual was an orange robed Buddhist monk, on his knees engaging in a sexual act with the NVA soldier, in violation of Article 125 of the UCMJ. In addition to the other military intelligence we procured that day, included in my report to the 4th Marine S2/S3, was this observation Woody and I had made regarding the Buddhist monk.
Little did I know that my reports were sent to G3, 3rd Marines Division in Da Nang, as well as to the Vietnamese general in charge of I–Corps, whose headquarters was in Dong Ha. Apparently, when the Vietnamese general read the report, he had to inquire as to what an Article 125 UCMJ was. When he was informed that it was sodomy, he went livid and had a temper tantrum. Based on what I had heard, he called the S2/S3 and wanted me arrested and confined for trial, with the intent to have me executed or imprisoned for insulting a revered representative of the Buddhist religious sect. He bitterly complained to the G2/G3, 3rd Marine Division . It was made clear to me that these Monks were revered and that their reputations were not going to be besmirched. I was informed that this report was developing into an international incident, and the G2/G3 advised S2/S3 to warn me to not venture into the cities of Hue or Dong Ha for any reason since I had a mark on my head. Now, I had to not only protect myself from the enemy, I had to watch out for friendly Vietnamese as well.
It appeared that things were quieting down after a couple of weeks as I had heard nothing further regarding this incident. However, I’m a believer in co–incidences, and while I have no proof, I strongly suspected that my next mission was staged for disaster. Prior to every mission I was always briefed by S2/S3 on where to go and what we would be doing. On this particular mission, I was told to check out specific coordinates for a specific NVA regiment , exactly at 1400 hours, not one minute before nor one minute after, but exactly 1400 hours. The rationale that required this precise timing was that the NVA communications would be monitored, triangulated and copied for further use. This area was just northwest of the City of Hue. I went to the airfield, picked up Woody where we were briefed on what the Army needed and we took off on our mission.
We tooled around the area west of Phu Bai and all of the while the term, “exactly 1400 hours”, rattled around in my head. “Exactly!” At approximately 1358, Woody and I headed for the coordinates and at 1359 hours, approximately one minute early, we flew over the coordinates at tree top level. There were people scurrying around as we flew overhead, and at the same time we were receiving voluminous automatic weapons fire. Given that we were flying so low and so fast, the gunners were unable to get a bead on us.
Because of the volume of AAA fire, I dropped two red smoke grenades to mark the area and give the NVA something to talk about. We continued West for approximately one–quarter mile and made a U–turn and began to parallel our original track. We were about four to five hundred yards south of the red smoke as it was beginning to rise above the treetops. Woody and I were looking at something on the right side of the aircraft away from the red smoke, when all of a sudden we heard terrific explosions as our aircraft rocked violently from the shock waves. Woody began screaming, “B–52’s! Arc Light! Arc Light!” As I looked out the left window I saw the explosions from the bombs engulfing the red smoke that I had just dropped no more than 30 seconds ago. I realized then that those bombs were on the way down when we had dropped the smoke.
Two things crossed my mind immediately at that point, one was funny, the other quite sinister. Had we been flying over the spot at exactly 1400 hours instead of 1359 hours we would have been in the center of the target area that was being destroyed. I firmly believe to this day, as circumstances strongly suggest, that I was intended to be over that target area at that precise time. 1400 hours—exactly—not early— not late, sending a single engine observation aircraft into the lions den wearing a pork chop overcoat was clearly intentional. Those planning this mission clearly knew that if the ground fire didn’t get us the Arc Light would, and we had to be exactly on time for the plan to succeed.
Can you imagine the surprise and shock of the NVA commanders, gunners and others who tried to shoot us down as almost immediately after firing on that little airplane who dropped the red smoke, that within 30 seconds the worst bombardment of their lives would occur? I can hear the NVA commanders now, “Don’t shoot at those little planes any more, they will bring a B–52 strike!” When this occurred I had thirty days left in country and I wondered, ‘What else, what next?’ I firmly believe that Charley and I, up to that time, were the closest Americans to a B–52 strike that survived.
In November of 1965, the Ashau Valley was the scene of some of the most intense fighting during the Vietnam War. By the spring of 1966 the Americans, ARVN and Nungs had abandoned the camp. However, Woody and I decided to take a trip to the Special Forces camp to see what remained. Our mission was to perform reconnaissance in the area and identify trucks, tanks, elephants or anything that would indicate NVA supply—or simply something to shoot at. West of Ashau we had spotted two, three–man patrols of NVA soldiers. Since Woody and I were always up for a fight, we got the first rounds off and killed everyone in both groups. We then flew parallel to the runway, the camp was totally wrecked , bombed out and abandoned, except for a few hundred NVA soldiers that Woody and I found. They were tightly packed under the camp runway. We observed them flying at between 100 to 150 feet altitude and about 100 yards south of the runway. There were hundreds of faces looking at us as we flew the entire length of the runway. “Hundreds!”
My first thought was, &lsquo"They are all in range, and I could get a lot of them.’ However, I then thought we were also in range and strongly outnumbered. I don’t know why they didn’t open up on us, since the odds were definitely not in our favor. We were basically sitting ducks, so we gained a little altitude, and I radioed the Direct Air Support Center (DASC) and was informed that there were no planes available. I further explained that I had several hundred NVA cornered in the open and received the same response that no planes were available to be scrambled to our target.
We then flew to Aloui, the next Special Forces camp in the Ashau Valley, were we spotted several AAA emplacements, camouflaged mortar pits, and dozens of NVA soldiers who were lounging about in the open. Once again, we were low, slow, sitting—duck targets, and still they held their fire and so did we. Since we were outgunned, out manned and an easy target we flew on to Tabat, the last Special Forces camp abandoned in the valley. Again, we spotted AAA pits, mortar pits and crews of NVA soldiers lounging around, who also held their fire. At this point, I rationalized that they had heard about our reputation as a scout for B–52 strikes and were terrified of what we could bring on them, if I dropped red smoke on their position. As we left the area, Woody and I developed a plan. The last group of NVA was in a small clearing next to a heavily forested woods. We would fly close to them, let them have it, and then disappear over the line of trees. It worked beautifully, at least four to six NVA soldiers fell as we made our pass. Did I mention that I love the AR–15? It stays steady on target on full auto.”
On our way back to Phu Bai we heard a “Mayday, Mayday” and saw an Air Force Skyraider circling around a descending orange and white parachute. They were a flight of two and had been working on a AAA emplacement on a ridge on the south edge of the Ashau Valley. Now, the circling Skyraider was strafing the NVA to keep the NVA off of his wingman. I informed Woody that I would handle this and answered the Mayday. The Skyraider was attempting to raise SAR but “no joy.” I explained to him that I had a helicopter squadron at Phu Bai and that I would attempt to get them. Woody at this time had to gain altitude to obtain line of sight to Phu Bai so that we could contact HMM–163.
They were monitoring their frequency, and I informed the operator that I had a Mayday, a downed American pilot and provided him with the coordinates. I continued to explain that I had the pilot in sight and his wingman was keeping the NVA at bay with strafing runs. I emphasized that we needed them here ASAP, or else “he’ll be killed or captured. Advise.” In a stunning reply the operator stated, “We won’t be able to take the mission.” Once again, I reinforced the issue and the situation the downed pilot was in and proceeded to say things unbecoming an officer and a gentleman. At that point, had I been an enlisted man, I would not have been eligible for a good conduct medal—nor would I have received a sportsmanship award for my outburst. However, there was silence, followed by a calm, collected and mature voice that I have remembered for the past 46 years. My call sign was Rosemont Golf, “Rosemont Golf, be advised that we are turning up now and will be there in fifteen minutes. “My God, the relief Woody and I felt!”
Prior to being shot down, HMM–163 had actually been flying at approximately 10,000 feet and had photographers photographing the Skyraiders bomb the AAA positions. However, as they returned to Phu Bai, Major Wyman Blakeman, the operations officer for HMM–163, gave the returning pilot the turn up sign and informed the pilot that one of the Skyraider pilots had been downed by AAA fire. After refueling, the H–34’s returned to Ashau, and I notified the Air Force wingman that help was fifteen away. At the same time the wingman was directing the downed pilot to move up hill while he held off the NVA. Woody and I joined the attack as we circled the pilot, picking off NVA as they tried to get to the top of the ridge to cut off the downed pilots escape route.
My concern with the Skyraider was that it was like a flying dump truck; however, the pilot assured us he had three to four hours of fuel left, plenty of ammunition, and a couple of bombs. We decided bombs were not advisable in this situation. It was at this point I heard a very welcome sound, “Rosemont Golf where are you? We are in the area.” I saw in the distance three H–34’s and immediately answered, “Make a left 45, then straight, I have you in sight.” The H–34’s saw our aircraft and entered the area. I then turned the rescue mission over to the Skyraider and HHM–163. What I observed, as an eternity, was described by the actual helicopter pilot in the following narrative:
“We flew back out at altitude, and contacted the O–1 Bird Dog pilot, who directed us to the downed pilot, I instructed my wingman to stay as high as he could, and try to keep us in sight. My co–pilot, 1st Lt. Joe Weiss, and I flew east, descended and approached the pick up point in defilade, keeping the hills between the AAA guns and us. I did a hover check and found we could not hover at that weight and altitude. I instructed the downed air force pilot on his survival radio to try and move down hill, while we flew off and burned off some fuel. About 45 minutes of flying in full rich mixture, at high power setting, plus throwing out the life raft, survival gear and toolbox, and anything else not fastened down finally did the job. We returned for the pickup, spotted his smoke flair, and came to a hover for an out–of–ground–effect, hoist pick–up. With Weiss on the throttle/collective, looking inside me, and with me on the cyclic and rudders, looking outside, with our wheels in the treetops, we made the pickup in the red paint on the 100 feet hoist cable. We got the pilot, Major Buzz Blaylock, USAF, and scooted out of there, with Blaylock hugging my feet from the cabin below. My wingman joined up, followed by the Skyraider wingman. I led the flight into a right echelon, left break over our camp at Phu Bai at 300 feet. The squadron, on stand down, alerted by Blakeman via the loudspeaker, welcomed us home.”
After watching the horse collar being lowered into the trees and then hearing “He’s in it!” has to rank as one of the most impressive events I’ve experienced in my lifetime. Since Woody and I were anxious to congratulate the rescued pilot, the rescuers, as well as the Skyraider pilot, we went directly to the officers club tent, where the celebration was in full swing. As Woody and I approached the air force pilots, we explained who we were, and we were greeted with the most vitriolic, rude and crude comments you would imagine. Given that it was a tough day for Woody and I, after all we had kicked up a lot of action for the day, we decided to leave and let the celebration prevail. This rescue still represents a high point in my career and I would still like to meet them now to shake their hands. I continue to hope that they successfully survived the remainder of the war.
Wednesday, April 6, 1966, the Stars & Stripes printed an article about Woody and me. The article titled, Pilots Pin Down VC With Pistols, Rifles documented our efforts on this mission. Unfortunately, they incorrectly stated that I was from Barkersville, Louisiana, instead of Barquesville, Indiana, as well reporting the body count incorrectly. However, on that day we were patrolling an area that was the beginning of the foothills of the mountains to the west of us. To the east lay flatlands of scrubs, short vegetation, bushes and swamps. We had flown over this area several times before and had noticed well used paths going from east to west. Woody was looking front and left and I had the right and rear, when Woody begins to scream several times, “VC!, VC!, beaucoup VC!, beaucoup VC!” I looked out the left window and saw approximately 100 to 200 VC tan and black uniforms carrying long bamboo poles with green camouflaged parachute cloth acting as a container, loaded with equipment and supplies. There were approximately five to seven of these poles with a VC on each end, heading east toward Dong Ha. Woody could not talk when he was excited, he simply yelled. The more he yelled, the higher pitched his voice became, and as he grew louder, he talked faster. Over time I became better and better at deciphering him as time went on.
As he made a U–turn, he switched on his rockets and began his dive, from what seemed like 100 feet, shooting into the middle of the pack. I began calling DASC for air support, and then they called for me to “stand by.” A few seconds later, DASC replied, “two flights of F–4’s are on the way.” A flight consists of two aircraft, with bombs, rockets and napalm. Also, a flight of two B–57 Canberra’s were dispatched, loaded with ten 500 pound bombs of napalm. I informed DASC of our location and requested that the F–4’s, call sign “Condol” contact me. I told Woody it was going to be a “hot time in the old town tonight.”
While waiting for air support to arrive, Woody and I, with my trusty AR–15, began picking off the VC attempting to hide and or flee. I had ten magazines and had used them all, trying to prevent the VC from retrieving their bundles. When I ran out of 223 ammunition for my AR, I resorted to my side arm, a S&W Highway Patrolman .357. Oh, did I fail to mention how much I loved my AR on full automatic, and that it holds steady and true on full auto? Well, I had 24 rounds in a pouch, so I did have a few reloads. I don’t recommend a revolver as an assault weapon, except of course when it’s a last resort—much too slow! Even with today’s speed loaders, the process takes too long. My idea is a fresh magazine, ready to go. I fired the remaining of my 357 rounds into the groups below and then proceeded to use Woody’s 45 with two extra magazines until that ammunition was exhausted. Finally, I resorted to my backup, which was a 1934 Beretta, .380 caliber with two extra seven round magazines. After using all but one of my magazines, I determined that no one was getting up and running and the bundles were still on the ground.
Suddenly, I heard, “Rosemont Golf, this is Condol 2 dash 2 with a flight of four F–4’s. “Your location?” I immediately dropped four smoke grenades using red and yellow to mark the length of the convoy. I then talked the F–4’s to a position directly over me, where they could see the smoke. I informed them that their target was large and to hit the red and yellow smoke on either side to about two to three hundred yards. The four F–4’s used up about 200 each 2.75 Zuni rockets all over the target area. In addition, they had ten napalm canisters each, which were used to incinerate the bundles on the ground, and completely destroying the area. When they finished, the B–57’s came in, and I had them hit the adjacent areas surrounding the site, anticipating that any survivors would be caught up in this strike. I was surprised to see as the Canberra’s began to work the target perimeter. How many VC had escaped the F–4’s? Unfortunately for them, they didn’t get far enough, as the Canberra’s uncovered and destroyed those remaining.
I’m not in the habit of bad mouthing our sister services, but showing up as the F–4’s were leaving, was a silver observation aircraft. As he entered the area directly in front of us, and very close I might add, the pilot informed us that he was now on station and that he was taking over and that we could depart the area. CPT Woodhurst advised him to go away and that we were not leaving. The air force pilot replied, “I told you to leave the area, I am a major, what is your rank?” It must have been a Canberra pilot that interjected, “Rosemont Golf is working with us, you leave the area. I’m a colonel!” He left—way to go colonel! As the Canberra aircraft finished their work and joined up to leave, the Canberra pilot told us that this was a very successful and fulfilling mission for them, having worked a target directly against the enemy. “Good job!” At that time the DOD was concerned heavily about body count and we tried to count bodies as best we could, and we came close to 60 KIA. The air force pilot did complain to the Army brass at Dong Ha that we wouldn’t let him control his own plane — wahhhh!!!
On many of our flights out west, I would see elephants. Not just any old elephant, but elephants which were orange in color, about the color of red Georgia clay. Sometimes I would see them loaded or pulling carts surrounded by their caretakers. In my reports to G–2, I wrote that I observed elephants that were orange in color and posed the question as to where they may have come from. Where would elephants bath themselves in orange clay, Vietnam, Cambodia, or Laos? I sent black and white photos to the 3rd Marine Division G–2 along with my reports. Unfortunately, my KE28A camera at the time did not have color film available. So, G–2 and others at Headquarters, despite verification by 220th pilots, thought I may have been drinking and flying. G–2 was concerned! The Bastards!
It came to a point that upon my return from a mission out west to debrief the S–2 Chief that a very stocky, M/Gy/Sgt Lucero would ask, “Did the Lieutenant see any orange elephants today?” To give this picture a little more life, Master Sergeant Lucero, was a power lifter, with a very out going, good natured and humorous disposition. As he asked the question, he would lower his voice so that all who were in the debriefing tent as well as those on either side of it could hear. “What was the Lieutenant drinking?”, “How can I see them?” Sgt. Lucero was so humorously disrespectful that he never offended me because we both knew what he was doing. However, after each question there was a deep, hearty “Har! Har! Har!” Good times were had by all.
During one mission out west, Jim Harris, an African–American pilot, and I were on a two aircraft mission, “way out west,” where we came upon what appeared to be elephants grazing on bales of hay. We surmised that it was their corral and several elephants were lined up and attached to carts and backpacks for an expedition. Jim and I determined that this was no time for them to re–supply, so Joe Hamm, flying the second aircraft, and Jim armed their rockets and rolled in on the lead bull elephant. Jim’s rocket hit the elephant squarely above the base of the tail, killing it instantly. It put the heels of his hind feet right behind his ears. Joe and Jim scattered the herds, leaving the carts, back packs and equipment scattered all over the target grid.
We continued our mission, returning with no further incidents. As we debriefed, the new 220th Aviation Company commanding officer [probably MAJ Estes], a very large native Cuban with a similar sense of humor, interjected himself as Sergeant Lucero, asked about the “elephant hunt.” As the officerturned to Jim, he said, “Lieutenant Harris, you have done well, expert marksmanship, one enemy elephant KIA and possibly more, but still I can’t call you a great white hunter!” Sergeant Lucero had a great time with that one. I have always felt sorry for the elephants; however, at that time they had become tools of war by the enemy and we had to destroy their means to wage it.
One day at the S2–S3 tent, the S2 major stated that G2 was sending an observer to verify what I was observing. I had been reporting:
Orange pack elephants
Truck tracks–vehicle uncertain
AAA emplacements in the trees on our side of the DMZ
This information was vigorously refuted, and I was called a fabricator or a liar. Also, to note, the pilots and I were accused of drinking. Reliable reconnaissance has been refuted since Braddocks defeat and death in the French and Indian Wars. The phrase, “There aren’t any Indians out there,” rang true in WWII when the American and British paratroopers jumped into an area surrounded by German tank divisions, dug in and ready. Photographs from the previous afternoon showed them there; however the brass stated the very next day when evidence was shown that, “The tanks really weren’t there now.” In addition, around Long Vei, reconnaissance and Special Forces reported seeing tank tracks and hearing tanks in their area. This information was communicated up the chain of command, and in a loud forceful denial a very high ranking officer stated with finality that there were no NVA tanks in South Vietnam. The General didn’t listen, he didn’t believe his troops, he knew it all. I hope he was sent home! In memory of the KIA’s, WIA’s and POW’s at Long Vei caused by a NVA tank.
A Major Judas (not his real name) from Da Nang, 3rd Marine Division, was sent to Phu Bai to fly along with me in another aircraft. He informed me that he was to verify everything that I had been reporting. We did not hit it off well, since he was a skinny fellow, with dark beady eyes that sat too close together and a large hook nose that looked like he could open cans with. He also displayed a haughty distrustful countenance, displaying feigned disgust and disbelief in everything I said and did.
I had a flight later on in the day, but the major wanted to be briefed by the S2. When I arrived at the airfield, I briefed Woody on the next days two–aircraft mission and Major Judas’s task. I loved the 220th for the support they gave me the next day! The commanding officer became angry when he heard of Major Judas’s mission and responded by saying that he would personally brief him in the morning. So when Woody and I returned from our mission, and were debriefed by S2 and Major Judas, Gunnery Sergeant Lucero was in rare form as he lit into me and placed Major Judas on guard. “Har, Har, Har, orange elephants, good booze and now a ‘truth detector!’” As he later stated, “Life is good at the front!” Har, Har, Har!
I briefed the major on the next day’s mission—two aircraft, west of Hue, Laos and Khe San, on our side of the DMZ. I explained that the major would be flying with Warrant Officer Joe Hamm, and Woody and I would be in the lead aircraft. When I arrived at the S2 tent in the morning, Major Judas was all decked out in an orange flight suit. I didn’t say anything, and we went to the airfield and arrived at the commanding officer’s office. Upon arriving, there was a new major that was only briefly talking to the CO and Woody. I introduced Major Judas to the CO and the major, whereupon the CO and major jumped his ass about the orange flight suit. In my opinion, he looked like a sissy cowboy at a dude ranch. It was clear he wasn’t going on this mission in any 220th aircraft dressed like that. The CO stated, “We will find you something else to wear.”
Major Judas, in defending himself, stated that he represented the 3rd Marine Division G2, and his job was to observe what I said, what I did and what I saw and reported. God love that 220th major, as he lit into Major Judas and told him that everything I saw and reported was true based upon verification of the 220th pilots. “If you and your G2 skulls are calling JD a liar, then you are calling my pilots liars!” Major Judas then stated that based upon his report, G2 would then decide whether I was replaced or not. At this time I was still the only trained USMC AO in northern I–Corps. The major then responded in a lengthy speech about my virtues, and his as well as the G2’s lack of intelligence. The final motivation for Major Judas tickled me so much when the major stated, “If I find that you have lied to your superiors and made JD and the 220th look bad, the entire U.S. Army Command in RVN, I–Corps, will be on your head and will prove you lying.” In addition, he said, “I will personally fly an L–19 up your ass!” The majors final comment, “JD has planned an interesting flight for you today, I hope you survive.” Major Judas was then handed a dirty green set of coveralls that would have been too large for PFC Castleberry. What a start to a glorious day!
We flew west of Hue, and the first thing I told Major Judas was that I had been seeding these trails with cashews to attract the elephants. At that time none were in sight, and when we spotted truck tracks I asked WO Hamm to take the low aircraft position to allow Major Judas get a good look. We then flew him to the VC rest areas, cleared over sides of hills with large openings into the hillside, with trails that resembled roads in rural America. They were much larger foot trails than those we saw as we started out. I had taken many of the first hand held photographs in the spring of 1966 of improvements that were being made on a daily basis.
As I had mentioned earlier, I usually had snacks with me, such as jellybeans, cashews, and peanuts to lunch on during our missions. As we returned to the area where I had salted the trail with cashews, I swear to my readers that there were elephants on that trail! I made sure that WO Hamm’s passenger got a good look at the orange elephants, making absolutely sure he answered me in the affirmative as seeing the same elephants I saw.
I had photographs of AAA emplacements on our side of the DMZ with reference points along the Ben Hai River that were difficult to refute. However, my photographs were called phony, doctored and borrowed from the Air Force, since the Air Force had a photo reconnaissance squadron at Phu Bai as well as a large photo development trailer. I routinely developed my KE28A film at this photo lab. As we flew to the DMZ, I made sure Major Judas saw those reference points. WO Hamm was the low plane on the edge of the trees under which the AAA emplacements were located, and had passed through the area before most of the gunners had a chance to get into their pits. Finally, one gunner did get off a few rounds at WO Hamm’s aircraft as he took evasive measures and “unassed the area”, a military term used to explain a retrograde movement to a place called elsewhere.
Upon returning to the airfield at Phu Bai, we went directly to the commanding officers tent for a debriefing. I’m sure Major Judas didn’t approve of the army debriefing, but he had no choice, either wait outside or join the discussion. We reported what we had seen, all that we had accomplished, as well as any other information that seemed relevant to our mission. Major Judas was asked, “ Do you agree with the reporting? This is the way we do it, do you have any comments?” “None,” was the reply. Master Gunnery Sergeant Lucero must have laid awake for several nights scheming on the borderline of humorous disrespect and ultimate humiliation. As we arrived at the S2 tent, Sergeant Lucero had been watching for us, as he asked Major Judas, “Did the major see orange elephants? “Har, Har!” When Major Judas admitted that he did indeed see the orange elephants, Sergeant Lucero laughed and asked, “What have you been drinking Major?” “You have been in the lieutenants booze locker!” “Good for you! Life is good! Har! Har!” Only Sergeant Lucero could have pulled this one off as he did.
There seemed to be a significant change in the Major Judas after being subjected to that day’s activities. All that he observed, he finally believed! He experienced the fear of hostile fire, and the possibility of escape and evasion through the jungle. He finally understood that we knew what we were doing and that this day was a typical day in the life of the 220th pilots and attached AO’s. I firmly believe he was humbled by his experience. Since I had an early flight the next day I returned to the 220th area. The next day after, returning from the flight, he had departed and I never heard from him or the G2 again.
After stewing about that situation and Major Judas for almost 50 years, I finally have let it go. It has been therapeutic to write it out. Now, as I look back, I hope that maybe G2 would have more confidence in other intelligence gatherers, both in the air and on the ground. Maybe the walrus–type senior staff officers will get sent home with all of their medals and make room for officers who could be relied on to be believed.
The tour at Phu Bai was great, as I was exposed to the finest pilots in the army. Time and time again, their skill, bravery and professionalism impressed me. I was always glad to fly with Bob Jordan, Jim Harris, Joe Hamm and others whose names I can not remember. Practically every day for the past 50 years I have thought of these men in one way or the other and the great memories we formed.
By June of 1966, I was applying for a 6th grade teaching position in the Indiana school system. While I loved the work, I was drawn towards a career in law enforcement, and by 1968 I had applied for a position with the Indiana State Police. By April of 1970, I was in training and finally assigned to Northeast Indiana as a patrolman. In July of 1972, my father passed away and I requested a transfer back to my hometown to help my mother. From the period of 1972 to my retirement from the state police in 1994, I was to also retire from the USMC Reserves achieving the rank of lieutenant colonel in 1988. However, after my military retirement I started training at the state police Tactical Intervention Platoon. Utilizing my military background, I realized that I could help improve the effectiveness of this operation and began redesigning the program. What developed was Indiana’s version of a SWAT Team, or as it was referred to, Emergency Response Team. We trained in tactics, and one notable skill I am proud to have transferred to this effort was the art of rappelling. Now this is not something that one naturally takes to, and I sensed a lack of will among my men. However, to motivate them I used my secret weapon— my ten years old daughter, Beth. She was fearless and could rappel with the best. All it took was for my men to see her rappel with ease, and they were on board. My proudest achievements, during my tenure in the state police, were the 110 missions, resulting in 105 apprehensions with no shots fired, when I retired in 1994.
My law enforcement career was hardly over, as I ran for sheriff of Johnson County in 1995. Once again opportunities abounded as I took over the helm and ultimately serving two terms as sheriff. My continuous improvement mentality resulted in the establishment of a new jail, upgraded computers and the implementation of a SCUBA program to our list of skills. However, for me, the highlight of my sheriff’s career occurred during the 2001 World Police and Fire Games. Of the over 3087 elected sheriff’s in the United States, I was the only one to enter as an athlete at the age of 62. I am proud to say that I won the silver medals in the Senior Division, in the 300–pound bench press event and the 450–pound dead lift event. Since I retired from the sheriff’s department in 2002, I continue to serve in a voluntary capacity through various Indiana state legislature activities.
While not my final chapter, I am fulfilling a journey that has certainly taken me onto a new path in life. It began quite innocently, as I was collecting eagle feathers for a Native American friend on a fishing trip. One thing led to another in our conversation, and I made what I thought was an offhand remark about having Native American ancestry in my past. I had never been able to prove this, one way or another, and probably decided that it was never true. However, throughout my life I had an insatiable interest in our native history. My friend quietly researched my family genealogy to discover that my great, great grandmother was full-blooded Shawnee.
Currently, an Indiana Shawnee Remnant Band of the Piqua Tribe, which is one of five major tribal divisions in the Shawnee Nation, is home to the Turtle Clan. So, with the news that I did in fact have Native American blood flowing through my veins, my family and I were given the opportunity to be adopted into the Turtle Clan. It was an honor to be received into the clan and receive our new family names. I became Blue Feather, my wife Wanda River Spirit, my daughter Beth became Silver Star, and finally my son Andy became Raven of Manitou.
The Piqua Tribe has the responsibility for religious and tribal rituals, governing rules and regulations and finally enforcing the treaties and keeping the peace. As I embraced my new found culture I had a Native American tattoo artist place the Turtle Clan totem on my left arm. The significance of the feather attached to the lower left of the turtle is the warrior feather for my service in Vietnam. Ultimately, I will be eligible for three other feathers, which will represent events spanning my law enforcement career. I speak of this to say that my background has provided me the opportunity to assume the role as the chief’s bodyguard when he travels around the nation, conducting Shawnee Nation business, as well as becoming the tribes firearms instructor. My fearless daughter Beth has also undergone the tattoo artist needle and has the Turtle Clan totem discretely applied to her body as well.
Now, with the discovery of the reunion, I’ll get to see the heroes of yesteryear and be in the Catkillers one more time. We all look back over the passage of time to see who we were, and finally who we have become. When I look in the mirror, I still see that 20–something marine, who despite all of his foolishness got me home and to where I am today.
I only wish that Woody and Ben could be here. “Semper Fi, Rosemont Golf Out!” | |||||||
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5682 | dbpedia | 2 | 73 | https://www.abcam.com/en-us/products/primary-antibodies/vmo1-antibody-ab126510 | en | Anti-VMO1 antibody (ab126510) | https://www.abcam.com/favicon.ico | https://www.abcam.com/favicon.ico | [
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""
] | null | [] | null | Rabbit Polyclonal VMO1 antibody. Suitable for IHC-P and reacts with Human samples. Immunogen corresponding to Recombinant Fragment Protein within Human VMO1 aa 1-150. | en | /favicon.ico | https://www.abcam.com/en-us/products/primary-antibodies/vmo1-antibody-ab126510 | New Lab Program
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5682 | dbpedia | 0 | 85 | https://whataday.info/e/1115402%3Fcloseby%3D1 | en | Everyday is Eventful | https://whataday.info/favicon.ico | https://whataday.info/favicon.ico | [] | [] | [] | [
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5682 | dbpedia | 2 | 53 | https://www.ptglab.com/products/VMO1-Antibody-21577-1-AP.htm | en | VMO1 antibody (21577-1-AP) | [
"https://www.ptglab.com/img/logos/Logo_Ptg_Main.png",
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"VMO1 Polyclonal antibody 21577-1-AP"
] | null | [] | 2024-08-09T05:15:28 | Proteintech's Rabbit Polyclonal VMO1 antibody is validated in WB, IF, IHC, ELISA and shows reactivity with human, mouse, rat samples. | en | https://www.ptglab.com/products/VMO1-Antibody-21577-1-AP.htm | Ã
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The Proteintech guarantee covers Proteintech antibodies in any species and any application, including those not listed on the datasheet. If the antibody doesnât perform, you can receive a hassle-free refund or credit note.
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WB Figures
WB analysis of HeLa using 21577-1-AP
HeLa cells were subjected to SDS PAGE followed by western blot with 21577-1-AP (VMO1 antibody) at dilution of 1:300 incubated at room temperature for 1.5 hours.
WB analysis of HeLa using 21577-1-AP
HeLa cells were subjected to SDS PAGE followed by western blot with 21577-1-AP (VMO1 antibody) at dilution of 1:500 incubated at room temperature for 1.5 hours.
WB analysis of HEK-293 using 21577-1-AP
HEK-293 cells were subjected to SDS PAGE followed by western blot with 21577-1-AP (VMO1 antibody) at dilution of 1:500 incubated at room temperature for 1.5 hours. | ||||||
5682 | dbpedia | 2 | 12 | https://en.wikipedia.org/wiki/Vitelline_membrane_outer_layer_protein_I_(VMO-I) | en | Vitelline membrane outer layer protein I (VMO | [
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] | null | [
"Contributors to Wikimedia projects"
] | 2012-07-18T12:23:12+00:00 | en | /static/apple-touch/wikipedia.png | https://en.wikipedia.org/wiki/Vitelline_membrane_outer_layer_protein_I_(VMO-I) | VOMIIdentifiersSymbolVOMIPfamPF03762InterProIPR005515SCOP21vmo / SCOPe / SUPFAM
Available protein structures:Pfam structures / ECOD PDBRCSB PDB; PDBe; PDBjPDBsumstructure summary
In molecular biology, this entry refers to a protein domain called, the Vitelline membrane outer layer protein I (VMO-I). It is a structure found on the outside of an egg, in the vitelline membrane.
Function
[edit]
The major role of the vitelline membrane is to prevent the mixing of the yolk and albumen and also act as an important anti-microbial barrier, as indicated by the high content of lysozyme in the outer layer [1] Vitelline membrane outer layer protein I (VMO-I) binds tightly to ovomucin fibrils, which construct the backbone of the outer layer membrane. VMO-I has considerable activity to synthesize N-acetylchito-oligosaccharide from N-acetylglucosamine hexasaccharides but no hydrolysis activity. VMO-I is composed of 163 aa[2]
Structure
[edit]
The structure[3] consists of three beta-sheets forming Greek key motifs, which are related by an internal pseudo three-fold symmetry. Furthermore, the structure of VOMI has strong similarity to the structure of the delta-endotoxin, as well as a carbohydrate-binding site in the top region of the common fold.[4] VMO-I revealed a unique structure of the P-prism fold, a new type of multi-sheet assembly.
References
[edit] | ||||||
5682 | dbpedia | 2 | 86 | https://www.alamy.com/stock-photo/vmo.html | en | res stock photography and images | [
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"Alamy Limited"
] | null | Find the perfect vmo stock photo, image, vector, illustration or 360 image. Available for both RF and RM licensing. | en | Alamy | https://www.alamy.com/stock-photo/vmo.html | Alamy and its logo are trademarks of Alamy Ltd. and are registered in certain countries. Copyright © 29/08/2024 Alamy Ltd. All rights reserved. | |||||
5682 | dbpedia | 3 | 72 | https://www.seaforces.org/usmcair/first.htm | en | US Marine Corps USMC aircraft units squadron wing group | [
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5682 | dbpedia | 2 | 28 | https://www.amazon.com/Observation-Squadron-VMO-1-Patch-Color/dp/B085Z74RZS | en | Amazon.com | [
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5682 | dbpedia | 3 | 64 | https://www.joebaugher.com/navy_serials/thirdseries17.html | en | US Navy and US Marine Corps BuNos | [
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] | null | [] | null | null | 140053/140077 North American T-28C Trojan MSN 226-1/25. North American Model NA-226, designated T-28C fitted with arrester gear for use in dummy deck approach and landing training 140053 (MSN 226-1) Assigned to Naval Air Test Center, NAS Patuxent River, VA [code FT-187] Assigned to VT-27, NAS Corpus Christi, TX [code D-709] To MASDC as 5T0059 3Aug76. SOC 16Aug77. Departed 19Jan78 Registered N51841 with Civil Defense, Laurel, MS 16Feb78; reregistered Registered N111TN 8Apr88; reregistered Registered N28TN 1Aug91; reregistered Registered N28GT 22Oct03; current [Dec15] 140054 (MSN 226-2) Assigned to VT-5, NAAS Saufley Field, FL. Crashed 17Aug60 140055 (MSN 226-3) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-714] Assigned to VT-2, NAS Whiting Field, FL. Crashed 28Nov61 140056 (MSN 226-4) Assigned to NAS Corpus Christi, TX. SOC 18Dec80 Allocated to National Museum of Naval Aviation, Pensacola, FL. On loan to NAS Corpus Christi, TX Preserved at NAS Corpus Christi, TX by 1982 140057 (MSN 226-5) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-700] [Mar63] Assigned to VT-6, NAS Whiting Field, FL. W/o 7Jun74 140058 (MSN 226-6) To MASDC as 5T0147 May 20, 1978, later as TA0185. SOC 1Apr82 Registered N303GB; current [Dec15] Registration N303GB reserved Jul 2002, taken up Nov 2002 140059 (MSN 226-7) Written off 5Aug59 140060 (MSN 226-8) To MASDC as 5T0136 May 9, 1978. SOC 30Apr79 Registration N28LD reserved Feb92; ntu, cancelled 26May11 Registered N28UH as a North American/Pride Aircraft T-28C with c/n C-008; reregistered On 15Apr99 the aircraft lost oil pressure and reported smoke in the cockpit. When the aircraft lost power, the pilot made an emergency landing on Old Creek Road, which is twenty miles northwest of Las Vegas, Nevada. The pilot, the only occupant, was not injured, and the aircraft did not sustain any damage. Registered N28KB; current [Dec15] 140061 (MSN 226-9) Assigned to Base Flight, NAS North Island, CA. Assigned to VT-2, NAS Whiting Field, FL. SOC 13Oct76 Registration N9036B reserved Feb87; cancelled 140062 (MSN 226-10) Assigned to NAS Corpus Christi, TX. SOC 26Nov80 Registered N9719G; reregistered Registered N121RH; reregistered Registered N9719G as a North American/Jones T-28C; cancelled 14Jun13 Crashed 2Jan88 whilst performing aerobatics at Woodstock, GA. A witness reported that the airplane first flew over the airport to the north at about 500 ft AGL, and subsequently performed a wingover at the north end of the airport. The airplane then made a high-speed pass over the runway to the south, at about 50 ft AGL. Upon reaching the south end of the runway, it entered into a climbing right turn. A few seconds later, the airplane performed another wingover; it subsequently disappeared into trees as it returned to a northerly heading, in a wings-level, slight nose- down attitude. Post-crash examination of the airplane and engine revealed no evidence of pre-existing mechanical malfunction or failure. 140063 (MSN 226-11) Transferred to US Marine Corps Assigned to SOES-12 [Station Operations and Engineer Squadron], MCAS Quantico, VA Assigned to Base Flight, NAS Pensacola, FL [code F-653]. SOC 18Jan78 Delivered 16Jan78 to Bradley Air Museum, Windsor Locks, CT; renamed as the New England Air Museum, Windsor Locks, CT, 1981-88 Registered N31431 27Oct92; current [Dec15] 140064 (MSN 226-12) Delivered to US Navy 16Feb56 Assigned to TW-5, NAS Whiting Field, FL [code E-464] To MASDC as 5T0127 May 5, 1978. SOC 25Jun80 Registration N55534 assigned 17Aug84; ntu, cancelled 26Apr11 To the Fred E. Weisbrod Aircraft Museum, Pueblo, CO, 1984 Preserved and on display at Pueblo Weisbrod Aircraft Museum, Pueblo Memorial Airport, CO, on loan from National Naval Aviation Museum. 140065 (MSN 226-13) Assigned to VT-2, NAS Whiting Field, FL. W/o 14Apr71 140066 (MSN 226-14) Assigned to VT-6, NAS Whiting Field, FL. W/o 13Sep72 140067 (MSN 226-15) Assigned to NAS Pensacola, FL. SOC 15Oct64 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise Sep64 as 067, code FA-067, later as FG-067 Crashed 13Dec68 during low level flying at Zongo Falls, DRC. [Congo was renamed Zaire 1971] 140068 (MSN 226-16) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-519] To MASDC as 5T0143 Feb 10, 1975. SOC 16Aug77. Bought at DoD sale 20May82 Registered N621JT 25Nov91; reregistered Registered N928C May99; current [Dec15], registered to Greatest Generation Naval Museum, Gillespie Field, CA 140069 (MSN 226-17) Active with VT-5 coded 2S-19 attached to the USS Lexington\ To VT-2 at NAS Whiting Field, FL. To MASDC as 5T0126 Dec 2, 1974. SOC 23Jan76. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N831VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140070 (MSN 226-18) to MASDC as 5T0130 May 9, 1978. Later as TA0186. SOC 1Apr82 140071 (MSN 226-19) To MASDC as 5T0152 May 26, 1978. SOC 1Apr82 Registered N28ZZ 17Apr89; current [Dec15] Noted at Rockford, IL Aug 9, 1996 as N28ZZ Damaged 6Aug11 during landing at Long Beach Airport, CA. As the nose wheel touched down, the lower section of the nose strut broke off and the nose of the aircraft settled down on the remaining section of strut. The propeller blades contacted the runway which in turn stopped the engine from rotating. The aircraft veered to the right of the runway center-line and came to a stop on the runway. 140072 (MSN 226-20) Written off 10Oct57 140073 (MSN 226-21) Written off Sep65 140074 (MSN 226-22) To MASDC as 5T0141 Feb 4, 1975. SOC 16Aug77. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registered N832VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140075 (MSN 226-23) Assigned to NAS Pensacola, FL. SOC 2Mar78 140076 (MSN 226-24) To MASDC as 5T0145 May 20, 1978. SOC 1Apr82. Registered N176RR; reregistered Registered N176RD; cancelled 12Jun13 On September 30, 2005 the aircraft impacted an earth berm during a forced landing in Arcadia, Florida. The airplane was destroyed. The flight originated from Arcadia Municipal Airport, Arcadia, Florida, earlier that day. The pilot stated that the annual inspection had recently been completed and he was flying the airplane to the North Perry Airport located in Pembroke Pines, Florida. At an altitude of 2,000 feet and after about 15 minutes en route, he noticed light colored smoke coming from and just above the right exhaust stack. He noticed the engine temperature rising shortly thereafter, followed by the engine oil metal chip detector light illuminating. The engine started producing unusual noises and a violent vibration followed. He looked for a suitable area to make a forced landing and elected to land on a gravel road with a canal running alongside it. About 150 feet into the landing roll, the right wing tip struck a high berm. The airplane snapped to the right as the nose of the airplane went partially into the canal. The aft section of the empennage partially separated and came to a stop, next to the left forward side of the airplane. Examination of the airplane's engine by a FAA inspector showed that the engine's oil system was contaminated with metal flakes. Pieces of silver and copper colored metal were observed in the oil filter. Metal chunks of approximately 1/8 to ¼ inches were found on the metal chip detector. The silver metal debris is consistent with material from the master rod bearing. 140077 (MSN 226-25) Assigned to NAS Pensacola, FL. W/o 4Feb70 140078/140102 Cessna OE-2 MSN 37000/37024. Cessna Model 321. USAF 54-1641/1665 transferred to US Marine Corps. Designation changed to O-1C in 1962. Transfer dates to MASDC from www.amarcexperience.com 140078 (MSN 37000) Accepted by USAF 5Aug55 as 54-1641. Delivered to US Marine Corps as 140078. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC. SOC 13Dec60 as damaged / salvaged. 140079 (MSN 37001) Accepted by USAF as 54-1642. Delivered to US Marine Corps as 140079. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. To VMO-2, Marine Aircraft Group 16, First Marine Aircraft Wing, Marble Mountain Air Facility, Da Nang Apr68. To VMO-6, Marine Aircraft Group 39, Quang Tri, Quang Tri Province, South Vietnam Jul68. Substantially damaged 13Apr69. SOC 1Mar70. To Military Assistance Program (MAP). To Republic of Korea Marine Corps 1Mar70 as 140079 for use in South Vietnam. 140080 (MSN 37002) Accepted by USAF 9Sep55 as 54-1643. Delivered to US Marine Corps as 140080. To VMO-6, Camp Pendleton, CA. SOC 21Nov62 as damaged / salvaged. 140081 (MSN 37003) Accepted by USAF as 54-1644. Delivered to US Marine Corps as 140081. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC 1955. Stored NAS Litchfield Park, AZ. Transferred to MASDC, Davis-Monthan AFB, Tucson, AZ for storage 13Sep65. Fleet Readiness Center East, MCAS Cherry Point, NC 12May66. H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. During a reconnaissance mission for potential helicopter landing sites in the Marble Mountain area, the aircraft struck some trees and crashed 8Dec66. Crew of 2 survived. SOC 8Dec66 as damaged / salvaged. 140082 (MSN 37004) Accepted by USAF as 54-1645. Delivered to US Marine Corps as 140082. To VMO-6, Camp Pendleton, CA. SOC 7Jan65 at NAS Litchfield Park, AZ. Transferred to USAF Auxiliary, Civil Air Patrol. Registered 1Apr66 as N16662; cancelled 22Jan71 as WFU and used as a ground instructional airframe. Registered Mar74 as N101GC; revoked 29Jan77, cancelled 16Jun11. Stored dismantled in poor condition at La Porte, TX. 140083 (MSN 37005) Accepted by USAF as 54-1646. Delivered to US Marine Corps as 140083. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. Damaged 17Mar67 [2WIA]. To VMO-2, Marine Aircraft Group 16, First Marine Aircraft Wing, Marble Mountain Air Facility, Da Nang Apr68. VMO-6, Marine Aircraft Group 39, Quang Tri, Quang Tri Province, South Vietnam Jul68. SOC 1Mar70. To Military Assistance Program (MAP). To Republic of Korea Marine Corps 1Mar70 as 140083 for use in South Vietnam. 140084 (MSN 37006) Accepted by USAF as 54-1647. Delivered to US Marine Corps as 140084. VMO-6, Camp Pendleton, CA. SOC 11Feb58 as damaged / salvaged. 140085 (MSN 37007) Accepted by USAF 22Sep55 as 54-1648. Delivered to US Marine Corps as 140085. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. To VMO-2, Marine Aircraft Group 16, First Marine Aircraft Wing, Marble Mountain Air Facility, Da Nang Apr68. To VMO-6, Marine Aircraft Group 39, Quang Tri, Quang Tri Province, South Vietnam Dec68. SOC 1Mar70. Military Assistance Program (MAP). To Republic of Korea Marine Corps 1Mar70 as 140085 for use in South Vietnam. 140086 (MSN 37008) Accepted by USAF as 54-1649. Delivered to US Marine Corps as 140086. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC. Last US Army report 28Feb65. SOC Sep65. 140087 (MSN 37009) Accepted by USAF 28Sep55 as 54-1650. Delivered to US Marine Corps as 140087. To VMO-6, Camp Pendleton, CA. Accident at Camp Pendleton, CA 17May56. SOC 17May56. 140088 (MSN 37010) Accepted by USAF as 54-1651. Delivered to US Marine Corps as 140088. To VMO-6, Camp Pendleton, CA. On the evening of 18Oct63, a Federal Aviation Agency radio station operator on Vulcan Mountain near Julian, California, heard a low-flying aircraft and took a compass azimuth of the plane's direction. After hearing that a VMO-6 plane was missing, he notified Camp Pendleton. Military aircraft had begun searching along the last known flight path of the missing airplane shortly after the OE became overdue, but low visibility restricted their flight operations. The next morning 1st Reconnaissance Battalion Marines searched the rugged mountains for the missing airplane. Under the guidance offered by the FAA operator, the search party finally located the wreckage and the body of the pilot. He had been killed when his plane crashed into a 3,000-foot ridge near Vulcan Peak during a mountain storm. SOC at Camp Pendleton 20Oct63. 140089 (MSN 37011) Accepted by USAF 7Dec55 as 54-1652. Delivered to US Marine Corps as 140089. To VMO-6, Camp Pendleton, CA. Accident at Camp Pendleton, CA 17Mar60. SOC 17Mar60 as damaged / salvaged. Exhibited at NAS Wildwood Aviation Museum, Cape May, NJ. 140090 (MSN 37012) Accepted by USAF as 54-1653. Delivered to US Marine Corps as 140090. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. To VMO-2, Marine Aircraft Group 16, First Marine Aircraft Wing, Marble Mountain Air Facility, Da Nang Apr68. To VMO-6, Marine Aircraft Group 39, Quang Tri, Quang Tri Province, South Vietnam Jul68. SOC 1Mar70. To Military Assistance Program (MAP). To Republic of Korea Marine Corps 1Mar70 as 140090 for use in South Vietnam. Note: reported to be the OE-2 at NAS Wildwood Aviation Museum painted as 140089, but that seems more likely to be the real 140089. 140091 (MSN 37013) Accepted by USAF 7Dec55 as 54-1654. Delivered to US Marine Corps as 140091. To VMO-6, Camp Pendleton, CA. SOC 13Oct59 as damaged / salvaged. 140092 (MSN 37014) Accepted by USAF as 54-1655. Delivered to US Marine Corps as 140092. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. To VMO-2, Marine Aircraft Group 16, First Marine Aircraft Wing, Marble Mountain Air Facility, Da Nang Apr68. To VMO-6, Marine Aircraft Group 39, Quang Tri, Quang Tri Province, South Vietnam Jul68. Substantially damaged 18Feb69. SOC 1Mar70. Military Assistance Program (MAP). Republic of Korea Marine Corps 1Mar70 as 140092 for use in South Vietnam. 140093 (MSN 37015) Accepted by USAF 6Dec55 as 54-1656. Delivered to US Marine Corps as 140093. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC. SOC 6May57 as damaged / salvaged. 140094 (MSN 37016) Accepted by USAF as 54-1657. Delivered to US Marine Corps as 140094. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. Destroyed 11May67. SOC 13May67 at Da Nang, South Vietnam. 140095 (MSN 37017) Accepted by USAF 6Dec55 as 54-1658. Delivered to US Marine Corps as 140095. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC. SOC 26Feb60 as damaged / salvaged. 140096 (MSN 37018) Accepted by USAF as 54-1659. Delivered to US Marine Corps as 140096. To NATC (Naval Air Test Center) RDT&E (Research, Development, Test and Evaluation), NAS Patuxent River, MD. Last US Army report 22Jun65. SOC by mid-1966. 140097 (MSN 37019) Accepted by USAF as 54-1660. Delivered to US Marine Corps as 140097. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC. To MASDC, Davis Monthan AFB, Tucson, AZ, 11Sep65. Naval Air Rework Facility, MCAS Cherry Point, NC 22Jun67. NAS Patuxent River, MD. Accident 25Oct67. SOC 1Nov67 at Patuxent River as damaged. 140098 (MSN 37020) Accepted by USAF as 54-1661. Delivered to US Marine Corps as 140098. Stored NAS Litchfield Park, AZ. Transferred to MASDC, Davis-Monthan AFB, Tucson, AZ for storage 20Sep65. To Fleet Readiness Center East, MCAS Cherry Point, NC 12May66. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. Crashed during a visual reconnaissance flight after engine failure near Marble Mountain 3Mar67. Pilot survived. Aircraft SOC 8Mar67 at Da Nang, South Vietnam. 140099 (MSN 37021) Accepted by USAF as 54-1662. Delivered to US Marine Corps as 140099. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. To VMO-2, Marine Aircraft Group 16, First Marine Aircraft Wing, Marble Mountain Air Facility, Da Nang Apr68. To VMO-6, Marine Aircraft Group 39, Quang Tri, Quang Tri Province, South Vietnam Jul68. SOC 1Mar70. Military Assistance Program (MAP). To Republic of Korea Marine Corps 1Mar70 as 140099 for use in South Vietnam. 140100 (MSN 37022) Accepted by USAF as 54-1663. Delivered to US Marine Corps as 140100. To US Marine Corps System Test Division, NAS Patuxent River, MD 1965. To H&MS-16, Marine Aircraft Group 16, Marble Mountain Air Facility, Da Nang, South Vietnam. Crashed after takeoff from Marble Mountain 12Aug67. SOC 12Aug67 at Da Nang, South Vietnam. 140101 (MSN 37023) Accepted by USAF 7Dec55 as 54-1664. Delivered to US Marine Corps as 140101. To VMO-6, Marine Aircraft Group 36, Camp Pendleton, CA. Crashed and burned at the mouth of Horno Canyon, CA 15Aug61 [2KIS]. A Kaman HOK-1 helicopter (BuNo 139973) had lost power and crashed at the location, and the OE-1, while attempting to render assistance, made a tight turn in the canyon, lost control and crashed. SOC 15Aug61. 140102 (MSN 37024) Accepted by USAF as 54-1665. Delivered to US Marine Corps as 140102. To VMO-1, Marine Aircraft Group 26, MCAS New River, Jacksonville, NC. SOC 4Aug63 as damaged / salvaged. 140103/140120 Grumman S2F-2 Tracker Cancelled contract. 140121/140139 Sikorsky HSS-1 Seabat Survivors redesignated SH-34G in 1962 (S for antisubmarine). 140121 (MSN 58-165) to Smithsonian. John Withers has this one as being in the Walter Soplata collection, Newbury, OH 140122 (MSN 58-166) to Vietnam. To MASDC as HD0019 Sep 23, 1969. To Moore Aviation. Cannibalized 1991. 140123 (MSN 58-167) to Vietnam. w/o Nov 6, 1967 140124 (MSN 58-168) 140125 (MSN 58-169) to Vietnam in 1967. To MASDC as HD021 Sep 24, 1969. to Allied Aircraft, presumably scrapped. 140126 (MSN 58-170) to Vietnam. W/o Mar 17, 1969, Tay Kontum. 140127 (MSN 58-171) 140128 (MSN 58-182) to Vietnam. W/o Nov 21, 1967. 140129 (MSN 58-183) 140130 (MSN 58-184) 140131 (MSN 58-185) to MASDC as HD0073 Aug 27, 1970. 140132 (MSN 58-186) 140133 (MSN 58-187). SOC Apr 14, 1967, NARF Pensacola. 140134 (MSN 58-188) to Vietnam AF. 140135 (MSN 58-189D) to MASDC as HD074 Aug 17, 1970. To Westair International as N8043V, then Solley Construction Co, Inc, then to State Helicopters, Inc. Renumbered N508. 140136 (MSN 58-190) to Vietnam in 1967. To MASDC as HD0010 Sep 15, 1969. seen at DMI Aviation, Tucson, 8/28/2000. Noted at Tennessee Museum of Aviation, Sevierville, TN in 2002. Still there Oct 2005. In SVNAF markings and is being restored. 140137 (MSN 58-191) to Vietnam. MIA Nov 15, 1969. 140138 (MSN 58-203) ditched at sea Jan 11, 1961 due to engine failure while on routine ferry flight to carrier underweight; engine shutdown at altitude; autorotate to surface; 2 pilots, 1 crewman, 1 passenger (Navy doctor) escaped; all rescued uninjuried. 140139 (MSN 58-204) 140140/140150 Martin P5M-2 Marlin 140144 (VP-45, coded LN-3 at NOB Bermuda) caught fire and crashed into sea 180 mi from Bermuda Sep 22, 1961. 3 survivors. 140145 assigned to VP-45, coded LN-10 at NOB Bermuda. Task Group "Delta" 140151/140160 Lockheed P2V-7 Neptune Redesignated P-2H in 1962. 140151 (MSN 726-7054) listed as P2V-7S from Jan 1960 but probably converted earlier. To MASDC Feb 7l, 1972, SOC Aug 19, 1977. 140152 (MSN 726-7055) listed as P2V-7S from Jan 1960 but probably converted earlier. To MASDC May 3, 1973, SOC Jul 19, 1974 140153 (MSN 726-7056) listed as P2V-7S from Jan 1960 but probably converted earlier. To MASDC Mar 25, 1973, SOC Jul 29, 1974. 140154 (MSN 726-7057) listed as P2V-7S from Jan 1960 but probably converted earlier. To MASDC May 30, 1973, SOC Jul 29, 1974. Later with Hawkins and Powers as N8056D in outside storage 140155 (MSN 726-7058) listed as P2V-7S from Jan 1960 but probably converted earlier. To MASDC Aug 2, 1973, SOC Jul 29, 1974. 140156 (MSN 726-7059) while searching for missing P2V-6 126535 flew into box canyon in Italian Alps and crashed with VP-23 near Bobio Pellice, Italy Jul 21, 1957, killing 9 out of 10 onboard. 140157 (MSN 726-7060) crashlanded at NAS Brunswick, ME or by Dec 29, 1959, but listed as being SOC Jan 28, 1959. 140158 (MSN 726-7061) listed as P2V-7S from Jan 1960 but probably converted earlier. Crashed with VP-9 onto reef about one mile short of runway at Johnston Island Nov 1/2, 1962 when starboard engine failed on final approach. Crew survived. SOC Nov 2, 1962. 140159 (MSN 726-7062) listed as P2V-7S from Jan 1960 but probably converted earlier. To MASDC Aug 21, 1972, SOC Aug 16, 1977. 140160 (MSN 726-7063) listed as P2V-7S from Jan 1960 but probably converted earlier. Crashed with VP-2 at or near NAS Whidbey Island, WA on or by Jan 3, 1969, SOC Jan 18, 1969. 140161/140310 Vought A2U-1 contract cancelled 140311/140313 Lockheed R7V-1 MSN 1049B-4167/4169. Model 1049B. Cargo/personnel transport version of 1049B Super Constellation. Transferred to USAF as C-121G 54-4077/4079 140314/140325 Sikorsky HR2S-1 Sikorsky Model 56. Redesignated CH-37C in 1962. 140316 assigned to FAA National Aviation Facilities Experimental Center (NAFEC), Atlantic City, NJ. Assigned to NASA, Langley Research Center, Langley Field, VA Jan 18, 1962 to Oct 30, 1963. Registered as N465 to US Department of the Navy, Atlantic City, NJ, Feb 13, 1962; cancelled Nov 14, 1963. On loan to FAA National Aviation Facilities Experimental Center (NAFEC-18) as N475 Feb 13, 1962. Cancelled Nov 14, 1963. Assigned to NAS Jacksonville, FL. 140326/140377 Douglas JD-1 Invader Surplus Army A-26Cs transferred to Navy. Survivors redesignated UB-26J in 1962. 140378 Convair R4Y-1Z Single CV-340 MSN 140 acquired by Navy as VIP transport. Designation changed to VC-131F in 1962. In accident at Atlantic City, NJ 2/23/1961. 140379/140413 Grumman F11F-1P Tiger Model G-98, photo reconnaissance. Contract cancelled 140414/140429 Bell HSL-1 Contract cancelled 140430/140433 Lockheed P2V-7 Neptune Redesignated P-2H in 1962. 140430 (MSN 726-7089Accepted as P2V-7 at Burbank 30 Apr 56. NARF Norfolk May 56 to Jun 56; VP-11 Brunswick Jun 56 to Sep 59; NARF Alameda Sep 59 to Jan 60; Lockheed Burbank Jan 60 to Jul 60 (P2V-7S conversion); VP-18 Jacksonville Jul 60 to Oct 62; VP-56 Norfolk Oct 62 to Apr 63; NARF Norfolk Apr 63 to Feb 64; VP-30 Jacksonville Feb 64 to Aug 68; NAS Los Alamitos Aug 68 to Nov 70; VP-65 Point Mugu Nov 70 to Apr 73 [code PG-5]; To storage at MASDC Davis-Monthan AFB 27 Apr 73; SOC 29 Jul 74. To Allied Aircraft, Tucson, AZ, 27Apr73 140431 (MSN 726-7090) Accepted as P2V-7 at Burbank 1 May 56. NARF Norfolk May 56 to Jun 56; VP-11 Brunswick Jun 56 to Sep 59; NARF Alameda Sep 59 to Jan 60; Lockheed Burbank Jan 60 to May 60 (P2V-7S conversion); VP-11 Brunswick May 60 to May 62; NARF Norfolk May 62 to Sep 62; VP-11 Brunswick Sep 62 to Jul 63; VP-30 Jacksonville Jul 63 to Nov 68; VP-23 Brunswick Nov 68 to Apr 69; VP-7 Jacksonville Apr 69 to Jun 69; NAS Los Alamitos Jun 69 to Mar 70 [code 7L-218]; To storage at MASDC Davis-Monthan AFB 27 Mar 70; SOC 19 Aug 77, 140432 (MSN 726-7091) Accepted as P2V-7 at Burbank 16 May 56, NARF Norfolk May 56 to Jun 56; VP-11 Brunswick Jun 56 to Oct 59; NARF Alameda Oct 59 to Apr 60 (P2V-7S conversion); Lockheed Burbank Apr 60 to Aug 60; VP-21 Brunswick Aug 60 to Dec 67; VP-7 Jacksonville Dec 67 to Jun 69; NARTU Washington Jun 69 to Jul 69; NAS Olathe Jul 69 to Jan 70; NARTU Memphis Jan 70 to Nov 70; VP-67 Memphis Nov 70 to May 73 [code PL-9]; To storage at MASDC Davis-Monthan AFB 9 May 73; SOC 29 Jul 74. To Allied Aircraft, Tucson, AZ, 16Dec86 140433 (MSN 726-7092) Accepted as P2V-7 at Burbank 6 Jun 56. NARF Norfolk Jun 56; FASRON-102 Norfolk Jun 56 to Sep 57; FASRON-108 Brunswick Sep 57 to Nov 57; VP-21 Brunswick Nov 57 to Feb 59; NARF Alameda Feb 59 to May 59; NARF Cherry Point May 59 to Jun 59, NARF Alameda Jun 59 to Jul 59; Lockheed Burbank Jul 59 to Nov 59; VP-24 Norfolk Nov 59 to Sep 60 (listed as P2V-7S from Jan 60); VP-30 Jacksonville Sep 60 to Mar 64; VP-11 Brunswick Mar 64 to Feb 67; VP-24 Norfolk Feb 67 to Jul 67; NARF Norfolk Jul 67 to Aug 68; NAS Seattle Aug 68 to Oct 69 Crashed at or near NAS Seattle, WA on/by Oct 17, 1969. 140434 Lockheed P2V-7LP Neptune MSN 726-7093. Accepted as P2V-7LP at Burbank 12 Jun 56 Lockheed Burbank Jun 56 to Nov 56; VX-6 Patuxent River Nov 56 to Feb 57: VX-6 Quonset Point Feb 57 to May 57: Lockheed Burbank May 57 to Aug 57; VX-6 Quonset Point Aug 57 to Mar 58; Lockheed Ontario Mar 58. Modified P2V-7 for ski landing aircraft for use in Operation Deep Freeze. Assigned to VX-6 at McMurdo Station, Antarctica. Named "George". Lost in a crash landing with VX-6 at Ontario, California Aug 11, 1958. While taking off for an acceptance check flight at Ontario, CA, a landing gear ski jammed and the aircraft was destroyed while attempting an emergency landing a few minutes later. No one was injured 140435 Lockheed P2V-7S Neptune MSN 726-7094) Accepted as P2V-7 at Burbank 5 Jul 56. Lockheed Burbank Jul 56-Dec 56; NADC Johnsville Dec 56-Apr 57; VX-1 Key West Apr 57-Jul 60 (not listed as P2V-7S until Mar 60 although this was actually the -7S prototype); NARF Alameda Jul 60-Feb 61; Lockheed Burbank Feb 61-Jul 61; VP-23 Brunswick Jul 61-Jul 64; VP-11 Brunswick Jul 64-Feb 67; NARF Norfolk Feb 67-May 67: VP-23 Brunswick May 67-Oct 68; NAS Glenview Oct 68-Jun 69; NARTU Memphis Jun 69; NAS Glenview Jun 69-Jul 70; NAS Dallas Jul 70; NAS South Weymouth Jul 70; NARTU Washington Jul 70-Aug 70, NAS South Weymouth Aug 70-Sep 70; NAS Glenview Sep 70-Nov 70; VP-60 Glenview Nov 70-Oct 73; VP-94 New Orleans Oct 73-Dec 74 [code LZ-10]; To MASDC Davis-Monthan AFB 11 Dec 74; SOC 16 Aug 77. Sold to Allied Aircraft Sales of Tucson, AZ Sep 23, 1986. 140436/140437 Lockheed P2V-7LP Neptune Redesignated LP-2J in 1962. Modified for polar exploration under Project Ski Jump. Armament removed, with ski landing gear and provision for JATO rockets. Fitted with early MAD gear for magnetic survey purposes. 140436 (MSN 726-7095) Accepted as P2V-7LP at Burbank 13 Jul 56 Lockheed Burbank Jul 56-Nov 56; FASRON-6 Jacksonville Nov 56; VX-6 Patuxent River Nov 56-Feb 57; VX-6 Quonset Point Feb 57-May 57; Lockheed Burbank May 57-Sep 57; VX-6 Quonset Point Sep 57-May 58; Lockheed Ontario May 58-Aug 58, VX-6 Quonset Point Aug 58-Feb 59; Assigned to VX-6 at McMurdo Station, Antarctica. Named "Candid Camera". NARF Alameda Feb 59-Jun 59; VX-6 Quonset Point Jun 59-Mar 61; NARF Alameda Mar 61-Jul 61; VX-6 Quonset Point Jul 61-Sep 63; NAS Litchfield Park Sep 63-Jul 65; to NAS Grosse lie 21 Jul 65; . SOC Jul 22, 1965. Now in the Walter Soplata collection, Newbury, OH 140437 (MSN 726-7096) Accepted as P2V-7LP at Burbank 30 Jul 56. Lockheed Burbank Jul 56-Nov 57; VX-6 Quonset Point Nov 57-Mar 58; Lockheed Ontario Mar 58-Aug 58; VX-6 Quonset Point Aug 5B-Nov 62; VX-6 McMurdo Station, Antarctica Nov 62-Sep 63, named "City of Auckland"; NAS Litchfield Park Sep 63-May 65; SOC May 21, 1965, eventually broken up 140438 Lockheed P2V-7U Neptune MSN 726-7097. Allocated to CIA on production line as P2V-7U and handed over (on paper only) to USAF as RB-69A 54-4038. To Taiwan. Crashed Jan 8, 1962 140439 Lockheed P2V-7LP Neptune MSN 726-7098. Accepted as P2V-7LP al Burbank 21 Aug 56. Lockheed Burbank Aug 56-Aug 57; VX-6 Quonset Point Aug 57-Mar 58: Lockheed Ontario Mar 58-Aug 58; VX-6 Quonset Point Aug 58-Nov 61; Assigned to VX-6 at McMurdo Station, Antarctica. Crashed on takeoff Nov 9, 1961, Wilkes Station, Antarctica. in support of Operation Deep Freeze 1962. While taking off from the skiway at Wilkes Station Antarctica the Neptune caught fire and crashed. Of the nine men on board, only four survived. An investigation of the crash reported the cause as a collision with the ground following an intense, uncontrollable fire in the landing gear - bomb bay fuel tank area. The previous landing had been so violently rough that it had broken loose the 400 gal internal tank in the bomb bay and the 4" filler pipe was spewing out raw fuel running down the bottom of the plane on take-off. At the ignition of the JATO on the t/o run, it acted like a Roman Candle. With the burning of the fiberglass tail cone, all of the acrid smoke was drawn right up to the cockpit and the pilots were blinded. They tried to return to the field and just couldn't make it. The pilot managed to level the wings before they hit and that saved some of the guys. 5 killed, 4 injured. 140440 Lockheed P2V-7U Neptune MSN 726-7099. Allocated to CIA on production line as P2V-7U and handed over (on paper only) to USAF as RB-69A 54-4039. To Taiwan. Shot down Liaodong, China Nov 6, 1961. 140441 Lockheed P2V-7 Neptune MSN 726-7100. Accepted as P2V-7 at Burbank 27 Sep 56. NARF Norfolk Oct 56; FASRON-102 Norfolk Oct 56-Mar 57; VP-23 Brunswick Mar 57-Feb 59; NARF Alameda Feb 59-Jul 59; Lockheed Burbank Jul 59-Nov 59; VP-23 Brunswick Nov 59-Jul 64 (listed as P2V-7S from Jan 60); VP-30 Jacksonville Jul 64-Nov 68; VP-23 Brunswick Nov 68-Mar 69; VP-7 Jacksonville Mar 69-Jun 69; NAS Atlanta Jun 69-Nov 70; VP-62 Det Atlanta Nov 70-Jun 72; VP-65 Point Mugu Jun 72-May 73 [code PG-10]; To MASDC Davis-Monthan AFB 4 May 73; SOC 29 Jul 74. To Hawkins and Powers, Greybulo, WY Jun 11, 1997 as N8908F being used as ground test aircraft with broken back. Cut up for scrap in 2006. 140442 Lockheed P2V-7U Neptune MSN 726-7101. Allocated to CIA on production line as P2V-7U, and handed over (on paper only) to USAF as RB-69A 54-4040. To Taiwan. Crashed Mar 25, 1969. 140443 Lockheed P2V-7 Neptune MSN 726-7102. Accepted as P2V-7 at Burbank 28 Sep 56. FASRON-108 Brunswick Oct 56-Apr 57; VP-23 Brunswick Apr 57-Mar 59; NARF Alameda Mar 59-Aug 59; Lockheed Burbank Aug 59-Dec 59; VP-24 Norfolk Dec 59-May 62 (listed as P2V-7S from Jan 60); VP-18 Jacksonville May 62-Nov 64; VP-18 Roosevelt Roads Nov 64-Sep 68; NARTU Washington Sep 68-Nov 70; VP-68 Washington Nov 70-May 71; VP-92 South Weymouth May 71-May 73. Redesignated P-2J in 1962. To MASDC May 9, 1973, SOC Jul 29, 1974. To N80635 Mar 23, 1989. To Hawkins and Powers Dec 1989 as N140HP flying as slurry bomber Tanker 140. Registration N445NA reserved Mar 20, 2006 with Neptune Aviation. Still current Is now located at the YANKEE AIR MUSEUM in Michigan. 140444/140448 Vought F8U-1 Crusader Redesignated F-8A in 1962. Dispositions from www.forgottenjets.warbirdresourcegroup.org 140444 first flight Sep 30, 1955. Crashed north of Edwards AFB Feb 1, 1956. Test pilot Harry Brackett killed. 140445 1955-56: NATC 149446 Apr 4, 1956: Preformed first catapult shot of a Crusader. Put into storage at NAF Litchfield Park, AZ. Jan 7, 1965: Struck off charge 140447 converted to XF8U-2. Sep 9, 1963: Struck off charge at RDT&E Dallas, TX 140448 converted to XF8U-2. Converted to the YF-8C prototype. 1966: VF-703 Was on display at Pate Museum of Transportation, Borland, TX. This museum is now closed. Plane is now at McAuliffe-Shepard Discovery Center, Concord, NH 140449/140666 North American T-28C Trojan MSN 226-26/243. North American Model NA-226, designated T-28C fitted with arrester gear for use in dummy deck approach and landing training. Transfers to MASDC from www.amarcexperience.com 140449 (MSN 226-26) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140449 Assigned to 2nd Fighter Squadron [code A] Assigned to 516th Fighter Squadron To Royal Lao Air Force May64 as 54-140449/0-40449. W/o 12Apr66 140450 (MSN 226-27) Assigned to VT-5, NAS Saufley Field, FL. W/o 18Sep64 140451 (MSN 226-28) Assigned to NAS Whiting Field, FL [code E-451]. SOC 22Jan75 Preserved and on display as gate guard at Evergreen-Middleton Field, AL by 1994, on loan from National Naval Aviation Museum. 140452 (MSN 226-29) Assigned to NAS Pensacola, FL. SOC 25Sep75 Stored at Techatticup mine near Nelson, NV. Not reported Oct15 broken up for parts at Nelson, NV 140453 (MSN 226-30) Written off 27Jul60 140454 (MSN 226-31) Assigned to VT-27, NAS Corpus Christi, TX [code D-765]. SOC 28May80 Assigned to NAS South Weymouth, MA. Used for fire practice. Preserved and on display at Battleship Cove Naval Heritage Museum, Fall River, MA by 1986 Retrieved from fire dump at South Weymouth NAS, restored to static display condition and placed on show during 1986 at Marine Museum, Fall River, MA. 140455 (MSN 226-32) To MASDC as 5T0185 Nov 9, 1976. SOC 10Nov76. Bought at DoD sale 20May82. On civil registry as N328AK 140456 (MSN 226-33) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140456 Assigned to 2nd Fighter Squadron [code B] Assigned to 516th Fighter Squadron To Royal Lao Air Force May64 as 54-140456/0-40456. WFU 1Jul74 Assigned to Detachment 6, 4410th Combat Crew Training Squadron, 1st Air Commando Wing, Udorn RTAB, Thailand for Operation Water Pump. Used by Raven FAC under direction of the US Air Attaché in Laos To Philippine Air Force c1974 as 54-140456/140456, possibly for spares. Noted dismantled at Villamor AB 1980-88. Sold 14Mar89 Registered N2065J 12Sep89; sale reported 12Jun03, cancelled 13Aug12 Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140457 (MSN 226-34) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140457 Assigned to 2nd Fighter Squadron [code C] Assigned to 516th Fighter Squadron To Royal Lao Air Force [sic] May64 as 54-140457/0-40457. WFU 1Jul74 Used by Raven FAC under direction of the US Air Attaché in Laos To Philippine Air Force c1974 as 54-140457/140457, possibly for spares. Noted dismantled at Villamor AB 1980-88. Sold 14Mar89. Registered N2065R 12Sep89; current 140458 (MSN 226-35) Assigned to NAS Pensacola, FL. SOC 19Apr78 140459 (MSN 226-36) Assigned to VT-6, NAS Whiting Field, FL. SOC 14Oct76 140460 (MSN 226-37) Written off 8Jan59 140461 (MSN 226-38) to MASDC as 5T0114 Feb 28, 1978. SOC 29May78. To Historical Aviation Museum, Stone Mountain, GA Nov 22, 1978. Registered N9025T Nov78; reregistered. Registered N404DK Oct88; current [Dec15] On June 4, 2004 the aircraft was substantially damaged during a forced landing following a loss of engine power shortly after takeoff from the Manitowoc County Airport (MTW), Manitowoc, Wisconsin. The pilot stated that as he was reducing to climb power after takeoff, about 200 feet above ground level, he felt severe vibration and heard several "bangs." He reported that the engine "wound down". He made a slight left turn toward an open field adjacent to a barn to set up for a gear-up forced landing. He noted that the touchdown was smooth and the aircraft slid for approximately 335 feet. The aircraft yawed as it slid and came to a stop when the tail struck a ditch adjacent to a roadway. A post-accident examination determined that the #4 articulating rod had failed resulting in the engine failure. 140462 (MSN 226-39) To MASDC as 5T0023 Nov 22, 1974. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registered N834VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140463 (MSN 226-40) Assigned to VT-2, NAS Whiting Field, FL. W/o 14Jan63 140464 (MSN 226-41) Assigned to NAS Corpus Christi, TX. SOC 15Oct76 Registered N2800J; reregistered Registered N464SB 3Apr98; registered as a North American-Mark T-28C; Crashed 17Apr07 near Red Lodge, MT en-route to Billings, MT. The pilot said that he had just departed and had adjusted the engine controls for 36 inches of manifold pressure and 2,400 revolutions per minute for climb. He said that he turned to a north heading when the engine lost power. The pilot said that he attempted to land back at the airport, but ended up landing in an open field. He said the engine separated from the airframe and the empennage partially separated from the fuselage. The pilot said that the engine had been overhauled approximately 20 hours before the accident. The pilot reported that he fueled the airplane on March 14, 2007, with 63 gallons of fuel; he said, "both sides were topped off." He said that on March 21, 2007, he flew the airplane for approximately one hour, and on April 14, 2007, he flew the airplane again for approximately one hour. The reason for the loss of engine power was not determined. N464SB cancelled by FAA Aug 25, 2007 as w/o in forced landing at Red Lodge, MT Apr 17, 2007. 140465 (MSN 226-42) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0018 Oct 18, 1974. SOC 23Jan76. Transferred to USAF. Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82. Registration N835VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140466 (MSN 226-43) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0046 Feb 11, 1975. SOC 25Nov75. Transferred to USAF. Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] broken up for parts at Nelson, NV 140467 (MSN 226-44) Assigned to VT-5, NAS Saufley Field, FL. W/o 11May68 140468 (MSN 226-45) Assigned to VT-27, NAS Corpus Christi, TX. SOC 26Nov80 Preserved and on display as gate guard at NAS Corpus Christi, TX by 1982 [last reported 1996] 140469 (MSN 226-46) Written off 3Jun57 140470 (MSN 226-47) Assigned to VT-3, NAS Whiting Field, FL. W/o 11Jul69 140471 (MSN 226-48) Written off 28Sep56 140472 (MSN 226-49) Assigned to VT-5, NAS Saufley Field, FL. W/o 26Jul73 140473 (MSN 226-50) With TW-5 at NAS Whiting Field, FL. To MASDC as 5T0143 May 15, 1978. SOC 25Jun80 Registered N31425 13Mar92; reregistered. Registered N281TS 8Aug96; reregistered Registered N10NA 11Sep09; current [Dec15] 140474 (MSN 226-51) Assigned to VT-5, NAAS Saufley Field, FL. W/o 25Jul67 140475 (MSN 226-52) Assigned to VT-27, NAS Corpus Christi, TX [code 3G-714] To MASDC as 5T0037 21Dec74. Departed 22Nov78 to Georgia Historical Aviation Museum, Stone Mountain, GA Registered N9025Y Nov78; current [Dec15] 140476 (MSN 226-53) To NAS Pensacola, FL. SOC 10Mar65 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise Mar 10, 1965 as 476, code FA-476 Abandoned in mid-air 29May65 NW of Paulis after running out of fuel at night. The pilot bailed out safely 140477 (MSN 226-54) To NAS Pensacola, FL. SOC 25May64 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise May 25, 1964 as 477, code FA-477, later as FG-477 Delivered 27May64 by USAF C-133 to Leopoldville, Belgian Congo Crashed 9Jul65 during takeoff from Albertville and turned over into water. Pilot killed. Rebuild of aircraft abandoned c1968 140478 (MSN 226-55) Written off 15Aug59 140479 (MSN 226-56) Assigned to VT-5, NAS Saufley Field, FL. W/o 13Apr67 140480 (MSN 226-57) To NAS Pensacola, FL. SOC 2Mar78 Registration N2800N assigned 29Apr79; registered as a North American-Rivera T-28C; cancelled 25Sep14 To the Oklahoma Museum of Flying, Wiley Post Airport, Bethany, OK. Under restoration 140481 (MSN 226-58) to MASDC as 5T0027 Dec 12, 1974. SOC 25Nov75 To Pima Air and Space Museum, Tucson, AZ Mar 10, 1977, on loan from National Naval Aviation Museum. 140482 (MSN 226-59) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140482 Assigned to 2nd Fighter Squadron [code D]. Assigned to 516th Fighter Squadron To Royal Lao Air Force May/Jun64 as 54-140482/0-40482. W/o 6Apr66 Assigned to Detachment 6, 4410th Combat Crew Training Squadron, 1st Air Commando Wing, Udorn RTAB, Thailand for Operation Water Pump. 140483 (MSN 226-60) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140483 Assigned to 2nd Fighter Squadron [code E]. Assigned to 516th Fighter Squadron W/o sometime in 1963. 140484 (MSN 226-61) Assigned to VT-6, NAS Whiting Field, FL. W/o 13Sep74 140485 (MSN 226-62) To NAS Pensacola, FL. SOC 15Oct64 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise Sep64 as 485, code FA-485, later as FG-485 Captured by mutineers at Kisangani 5Jul67; blown up at Punia 2Aug67 140486 (MSN 226-63) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140486. Assigned to 2nd Fighter Squadron [code F] Assigned to 516th Fighter Squadron. W/o Oct 24, 1963. 140487 (MSN 226-64) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-733] Assigned to VT-27, NAS Corpus Christi, TX. SOC 18Dec80. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Stored at Techatticup mine near Nelson, NV. Not reported Oct15 Broken up for parts at Nelson, NV 140488 (MSN 226-65) with VA-122. To MASDC as 5T0099 Mar 3, 1977. SOC 16Aug77. Bought at DoD sale 20May82 Registered N28CX 6May91; current [Dec15] 140489 (MSN 226-66) Assigned to VT-27, NAS Corpus Christi, TX [code 3G-723] To MASDC as 5T0050 8Feb75. SOC 29May78. Departed 9Nov78 Registered N9019L Nov78; cancelled 17May13 To Civil Defence Council, Waynesboro, MS 1978 To Wayne Rescue Unit, Waynesboro, MS 20Sep91 140490 (MSN 226-67) To NAS Pensacola, FL. SOC 25May64 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise May 25, 1964 as 490, code FA-490 Delivered 27May64 by USAF C-133 to Leopoldville, Belgian Congo Crashed 17Dec64 into trees near Mahagi during a strafing run. Pilot killed 140491 (MSN 226-68) Assigned to VT-27, NAS Corpus Christi, TX [code 3G-717] To MASDC as 5T0032 16Dec74. SOC 16Aug77. Bought at DoD sale 20May82 Noted stored at Courtesy Aircraft, Rockford, IL Sep08 140492 (MSN 226-69) with TW-5 at NAS Whiting Field, FL To MASDC as 5T0139 May 9, 1978. SOC 30Apr79 To Indiana Museum of Military History, Indianapolis, IN 1988 Registered N4168H; cancelled on export to Canada Registered C-GTTF 29Jun92; cancelled 30Oct96 Registered N746SH Dec96; current [Dec15] 140493 (MSN 226-70) Written off 19Nov58 140494 (MSN 226-71) Written off 3Sep59 140495 (MSN 226-72) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 5Mar62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140495 Assigned to 2nd Fighter Squadron [code G] Assigned to 516th Fighter Squadron. W/o 13Jan62 or 13Jan63 at Nha Trang, RVN 140496 (MSN 226-73) Assigned to NAS Pensacola, FL. SOC 25May64 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise May 25, 1964 as 496, code FA-496, later as FG-563 Crash landed 17Feb65 near Sudanese border after running out of fuel. Pilot presumed killed by rebel forces. 140497 (MSN 226-74) Written off 16Dec58 140498 (MSN 226-75) Written off 25Sep58 140499 (MSN 226-76) Written off 14Oct58 140500 (MSN 226-77) Assigned to VA-122, NAS Lemoore, CA. W/o 17Nov72 140501 (MSN 226-78) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-745] Damaged in a hangar fire caused by a lightning strike To MASDC as 5T0131 May 9, 1978. SOC 30Apr79 Registered N9749N; reregistered. Registered N900BW Dec88; reregistered Registered N161JP 10Mar98; current [Dec15] 140502 (MSN 226-79) Assigned to NAS Pensacola, FL. SOC 16Nov78 140503 (MSN 226-80) Assigned to VT-5, NAS Saufley Field, FL. W/o 19Jul67 140504 (MSN 226-81) Written off 16Sep59 140505 (MSN 226-82) Assigned to VT-2, NAS Pensacola, FL. W/o 16Jun67 140506 (MSN 226-83) Assigned to VT-5, NAS Saufley Field, FL. SOC 2Nov64 140507 (MSN 226-84) Assigned to VT-3, NAS Whiting Field, FL. SOC 6Jul62 140508 (MSN 226-85) Written off 31Jan57 140509 (MSN 226-86) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0131 May 9, 1978. SOC 30Apr79 Registered N280BJ 22Oct91; reregistered. Registered N128BJ 13May96; cancelled 28Jun99 Crashed 4Feb99 15 miles NE of Palm Springs en-route Van Nuys to Thermal, CA. The aircraft was flying in the lead position in a two-aircraft formation with T-28 N128NJ [BuNo 140509]. The pilot of the lead aircraft received a pre-flight weather briefing that included an AIRMET for mountain obscuration throughout the intended area of flight. When the flight did not arrive at its destination, a search was initiated and the two airplanes were found on a mountain slope at 5,300 feet mean sea level (MSL). The lead aircraft impacted the slope about 250 feet below a ridgeline. The wingman impacted approximately 220 feet further up the same slope and offset 30 feet to the right. Park service rangers reported that weather near the accident site at the time consisted of overcast clouds with the tops of the mountains intermittently obscured in clouds, snow, and light rain. 140510 (MSN 226-87) Assigned to VT-6, NAS Whiting Field, FL. SOC 13Oct76 140511 (MSN 226-88) Assigned to VT-3, NAS Whiting Field, FL [code 2W-341] Assigned to VT-6, NAS Whiting Field, FL [code E-600] To NAS Pensacola, FL. SOC 29Oct74 Noted in external storage at the Naval Aviation Museum (Pensacola) Summer 1984 Registered N140NA Oct85; reregistered. Registered N140AG Sep89; current [Dec15]. 140512 (MSN 226-89) Assigned to VT-5, NAS Saufley Field, FL. W/o 14Jul66 140513 (MSN 226-90) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140513 Assigned to 2nd Fighter Squadron [code H] Assigned to 516th Fighter Squadron W/o sometime in 1963 140514 (MSN 226-91) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-744] Assigned to VA-122, NAS Lemoore, CA [code NJ-091] To MASDC as 5T0190 Mar 20, 1979. SOC 31Mar79 Registered N2141D; reregistered Damaged 7May83 when the pilot failed to lower the landing gear. Registered N28XC 31May01; current [Dec15] 140515 (MSN 226-92) With VT-3 at NAS Whiting Field, FL. To MASDC as 5T0044 Feb 10, 1975. SOC 25Nov75. Transferred to USAF. Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82. Stored at Techatticup mine near Nelson, NV [last reported Oct15] Broken up for parts at Nelson, NV 140516 (MSN 226-93) To NAS Pensacola, FL. SOC 25May64 Assigned to the Military Assistance Program [MAP] Delivered 27May64 by USAF C-133 to Leopoldville, Belgian Congo To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise May64 as 516, code FA-516, later as FG-516 Renamed Zaire Air Force / Force Aérienne Zairoise Oct71. WFU 29Sep75 Registered N99153 Nov77; current [Dec15] Ferry flight from Zaire to El Paso, TX (via Gabon, Nigeria, Togo, Abidjan, Monrovia, Freetown, Bissau, Dakar, Port Etienne, Villa Cisneros, Marrakech, Spain, France, London, Iceland, Greenland & Labrador) 1977; arrived Biggin Hill 16Dec77; departed Biggin Hill for USA 17Apr78. 140517 (MSN 226-94) Written off 14Oct58 140518 (MSN 226-95) Written off 27Sep56 140519 (MSN 226-96) Assigned to VT-5, NAAS Saufley Field, FL Assigned to NAS Whiting Field, FL. Assigned to NAAS Corry Field, FL Assigned to VT-27, NAS Corpus Christi, TX [code D-711] To MASDC as 5T0061 3Aug76. SOC 29May78. Departed 9Nov78. Registered N9019N Nov78; current [Dec15] To County Civil Defense, Jackson, MS Nov78 To Civil Defence Council, Waynesboro, MS 1984 Damaged 11Aug02 when the pilot experienced braking problems during the landing at Platte Valley airport (18V), and ran off the end of the runway. The aircraft nose gear and propeller was damaged. The aircraft was inspected and found some glazing on the brake rotor surface. The aircraft had been washed prior to this flight using a citric acid based degreaser and appeared to have coated the brakes causing them to fade during landing. 140520 (MSN 226-97) To MASDC. SOC 16Nov78 Registered N678MC 23Jun93; current [Dec15] Noted stored unrestored at Avra Valley, AZ 1993 140521 (MSN 226-98) To NAS Pensacola, FL. SOC 29Jun76 To National Museum of Naval Aviation, Pensacola, FL 1977 Preserved and on display at the National Museum of Naval Aviation, Pensacola, FL [last noted 1988] 140522 (MSN 226-99) Assigned to VT-2, NAS Whiting Field, FL. SOC 13Oct76 140523 (MSN 226-100) With TW-5 at NAS Whiting Field, FL. To MASDC as 5T0141 May 9, 1978, later as TA0192. SOC 30Apr79 Registered N470; cancelled 13May15 On October 21, 2006 the aircraft was destroyed when it impacted terrain following a loss of control while maneuvering near Georgetown, Louisiana. The flight originated from the St. Louis Downtown Airport, near Cahokia/St. Louis, Illinois and was destined for Lake Charles Regional Airport, near Lake Charles, Louisiana. Weather radar images indicated a level 5 storm cell west of the accident location. Pilot killed. 140524 (MSN 226-101) Assigned to VT-5, NAAS Saufley Field, FL Assigned to NAS Whiting Field, FL Assigned to NAS Barin Field, AL Assigned to VT-27, NAS Corpus Christi, TX. SOC 26Nov80. Sold as scrap 1986 140525 (MSN 226-102) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0081 Nov 8, 1976. SOC 9Nov76. Bought at DoD sale 20May82. Registered C-GTTE 5Dec91; cancelled 22Nov93 Crashed 17Jun93 at Delta Air Park, BC, Canada 140526 (MSN 226-103) Assigned to TW-5, NAS Whiting Field, FL To MASDC as 5T0104 6Jun77. SOC 29May78 Registration N7160B reserved 24May90; reregistered Registered N526D 9Nov91; current [Dec15]. Damaged in forced landing due to engine failure near Greenwood, MS Sep 23, 2016. 140527 (MSN 226-104) Assigned to NAS Pensacola, FL. SOC 25Sep75 140528 (MSN 226-105) Assigned to VT-5, NAAS Saufley Field, FL [code 2S-716] To MASDC as 5T0135 May 9, 1978, later as TA0194 . SOC 1Apr82 To National Museum of Naval Aviation, Pensacola, FL 1977 Preserved and on display at the National Museum of Naval Aviation, Pensacola, FL [last noted 1990] Registered N71546 Feb90; cancelled 26Sep13 Damaged 8Jun96 during landing at Waco Regional airport (ACT), Waco, Texas while the Waco air show was in progress. The gear down was selected and the gear extension appeared normal to the pilot. The pilot stated that all gears appeared down and locked. Several eye witnesses stated that the nose gear was not locked in the down position. Many of the witnesses called for the aircraft to go-around, but this call was received too late for the pilot to initiate this action. The nose gear locked in the down position after the propeller struck the runway seven times. During an inspection of the nose gear assembly the maintenance personnel discovered that the nose gear push pull rods were out of adjustment. This resulted in the nose gear not being able to fully extend. On February 21, 2002 the aircraft sustained substantial damage during a forced landing following a loss of engine power near Fredericksburg, Texas. The flight originated from Caldwell, Texas. The pilot reported that the airplane was topped with 155 gallons of fuel at Levelland, Texas. Subsequently, the airplane was flown cross-country for 1 hour 25 minutes to the destination of Caldwell, Texas. The airplane was not fueled at Caldwell, and the flight departed for Fredericksburg. During the descent to the Fredericksburg Gillespie County Airport, the engine lost total power. The pilot landed the airplane, gear retracted, in a rough field approximately 4 nautical miles east of the destination airport. Substantial damage occurred to the firewall, cowling, and fuselage. The engine and propeller were damaged. During inspection, approximately 12 ounces of fuel was drained from the airplane. The integrity of the fuel system was not compromised. 140529 (MSN 226-106) Assigned to NAS Pensacola, FL. SOC 19Apr78 140530 (MSN 226-107) Assigned to NAS Pensacola, FL. SOC 6May75 Crashed near Virginia International Raceway Sep 21, 2014. 2 killed. 140531 (MSN 226-108) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0108 Jul 25, 1977. SOC 29May78 To Indiana Museum of Military History, Indianapolis, IN 1987 Registered N91550 Nov87; reregistered. Registered N944SD 21Feb89; reregistered Damaged 22Oct94 when the pilot failed to extend the landing gear for landing. Registered N531KG 30Oct07; current [Dec15] On September 19, 2014 the aircraft was destroyed when it impacted a kudzu field, while performing aerobatics near Alton, Virginia. The flight departed Easton Airport (ESN), Easton, Maryland for the planned flight to Danville Regional Airport (DAN), Danville, Virginia. A witness, who was a friend of the pilot, was at a racing facility with a motorcycle racing team that the pilot owned. The accident airplane performed a low pass over the area, reversed direction, and initiated a barrel roll during the second pass. The witness stated that the airplane started to climb before the barrel roll, but it wasn't enough and he knew the airplane would not have enough altitude to complete the maneuver. The airplane subsequently collided with trees and terrain. The pilot and passenger [his mother] were killed. 140532 (MSN 226-109) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0025 Dec 2, 1974. SOC 23Jan76. Bought at DoD sale 20May82 Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] 140533 (MSN 226-110) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140533. Assigned to 2nd Fighter Squadron [code I] Assigned to 516th Fighter Squadron To Royal Lao Air Force May/Jun64 as 54-140533/0-40533. WFU 1Jul74 Assigned to Detachment 6, 4410th Combat Crew Training Squadron, 1st Air Commando Wing, Udorn RTAB, Thailand for Operation Water Pump. Used by Raven FAC under direction of the US Air Attaché in Laos To Philippine Air Force c1974 as 54-140533/140533. Preserved and on display at Philippine Air Force Museum, Villamor AB, Manila 140534 (MSN 226-111) with VT-6 at NAS Whiting Field, FL. To MASDC as 5t0047 Feb 11, 1975. SOC 25Nov75. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N836VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] Now reported to be at Philippine Air Force Museum, Manila painted as 109. 140535 (MSN 226-112) Assigned to NAS Quonset Point, RI. W/o 19Dec70 140536 (MSN 226-113) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0144 May 2, 1978. SOC 25Jun80 Registered N31428; current [Dec15] 140537 (MSN 226-114) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0146 May 21, 978, later TA0916 . SOC 1Apr82 Registration N7164Z reserved Jun90; reregistered. Registered N537Z Oct90; cancelled 3May13 On May 24, 2003 the aircraft collided with terrain following an in-flight loss of control after takeoff near Sherman Oaks, California. The accident site was about 4 miles southeast of the Van Nuys Airport (VNY), Van Nuys, California, and the flight's departure point. The pilot and one passenger were fatally injured; the airplane was destroyed. The flight departed en route to Thermal, California. The airplane came out of the clouds in a steep, nose down, inverted attitude and collided with terrain. Pilot killed. 140538 MSN 226-115) Assigned to VT-5, NAS Saufley Field, FL. W/o 17Apr63 140539 (MSN 226-116) Transferred to US Marines Corps Assigned to MCAS Yuma, AZ. To MASDC as 5T0110 Dec 3, 1977, SOC 29May78. Departed 18Dec78 to Texas Surplus Agency, Harlingen, TX. Registered N4993Y 22Sep78 to the Confederate Air Force, Harlingen, TX; reregistered Registered N28TN 26Jul85; reregistered. Registered N166ER 3May90 to Cinema Air; reregistered To Planes of Fame Grand Canyon, Valle, AZ; displayed Apr08 Registered N36NA 23Apr12; current [Dec15] 140540 (MSN 226-117) Assigned to VT-3, NAS Whiting Field, FL. W/o 8Sep75 140541 (MSN 226-118) Assigned to VT-3, NAS Whiting Field, FL. W/o 31Mar67 140542 (MSN 226-119) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0118 Apr 16, 1978. SOC 25Jun80 Registered N5321X Jan88; current [Dec15] 140543 (MSN 226-120) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0126 May 5, 1978. SOC 1Apr82 Registered N80269 26Jun89; current [Dec15] 140544 (MSN 226-121) with VT-278 at NAS Corpus Christi, TX. To MASDC as 5T0045 Feb 10, 1975. SOC 23Jan76 Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N837VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140545 (MSN 226-122) Assigned to NAS Corpus Christi, TX. SOC 26Nov80 Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] Broken up for parts at Nelson, NV 140546 (MSN 226-123) Assigned to NAS Pensacola, FL. SOC 2Mar78 140547 (MSN 226-124) Assigned to NAS Corpus Christi, TX. SOC 15Oct76 Registered N2800Q as a North American-Mark T-28C; cancelled 22Oct91 To the United Kingdom for air shows 23Jun86; operated by Scandinavian Historic Flight (based in Norway) 1986-91 Registered F-AZHN 2Apr92; current [Dec15] Noted as F-AZHN at Toussus-le-Noble, France July 2003 140548 (MSN 226-125) Assigned to BTU-2, NAAS Corry Field, NC [code SB-211] Assigned to Base Flight, MCAS Quantico, VA Assigned to NAS Pensacola, FL. SOC 29Jun76 Registered N548NA Oct85; current [Dec15] 140549 (MSN 226-126) Assigned to VT-5, NAS Saufley Field, FL [code 2S-745] To MASDC as 5T0107 Jun 24, 1977. SOC 29May78 Registered N34BJ; reregistered. Registered N128JC; current [Dec15] 140550 (MSN 226-127) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0132 May 9, 1978. SOC 30Apr79 Registered N990DB; cancelled 11Dec12. Registered N990DB 15Sep14; current [Dec15] 140551 (MSN 226-128) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0158 Jun 28, 1978. SOC 1Apr82 Registered N9748Y; current [Dec15] 140552 (MSN 226-129) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0020 Nov 8, 1974. SOC 25Nov75 Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N838VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140553 (MSN 226-130) Assigned to VT-3, NAS Whiting Field, FL [code 2W-355] Assigned to NAS Pensacola, FL. SOC 14Nov75 To the USAF Museum for preservation. Loaned to the Museum of Aviation, Robins AFB, Warner Robins, GA 1987-89 Registered N28941 4Mar98; current [Dec15] 140554 (MSN 226-131) Assigned to VT-3, NAS Whiting Field, FL. W/o 20Jun65 140555 (MSN 226-132) Assigned to VT-5, NAS Saufley Field, FL. W/o 18Jul63 140556 (MSN 226-133) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140556 Assigned to 2nd Fighter Squadron [code J]. Assigned to 516th Fighter Squadron W/o sometime in 1964. 140557 (MSN 226-134) Transferred to the US Marine Corps Assigned to MCAS Quantico, VA. SOC 27Feb75 To the US Marine Corps Aviation Museum, MCAS Quantico, VA 1988-94 Preserved and on display at the NAS Wildwood Aviation Museum, Cape May County Airport, Rio Grande, New Jersey 2007 140558 (MSN 226-135) Assigned to VA-122, NAS Lemoore, CA W/o 2Jul71 140559 (MSN 226-136) Written off 8Mar58 140560 (MSN 226-137) Written off 1Nov57 140561 (MSN 226-138) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0017 Oct 15, 1974. SOC 23Jan76. Bought at DoD sale 20May82. Registered N561WR 25Sep02; current [Dec15] 140562 (MSN 226-139) Written off 11Aug58 140563 (MSN 226-140) with VT-7 at NAS Whiting Field, FL. To MASDC as 5T0052 Feb 24, 1975. SOC 29May78 Registration N563GH assigned 24Apr89; ntu, cancelled 30Oct89 Registered ZK-JGS 28Nov89; current [Nov14] 140564 (MSN 226-141) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0089 Nov 19, 1976. SOC 20Nov76. Bought at DoD sale 20May82 Registered N40980; current [Dec15], registered to Hans O. Lauridsen, Buckeye, AZ Operated by the Lauridsen Aviation Museum, Buckeye, AZ Planned to be displayed in a proposed Glendale Aircraft Museum at Glendale APT, AZ, but in 2013 was still on civil registry. 140565 (MSN 226-142) Assigned to NAS Pensacola, FL. SOC 28Dec77 140566 (MSN 226-143) with TW-5 at NAS Whiting Field, FL. To MASDC May 9, 1978. SOC 25Jun80 Registered N556EB Dec85; current [Dec15]. Based at St. Ghislain, Belgium N556EB in 2020 reported based at la Ferte-Alais, France. 140567 (MSN 226-144) Assigned to VT-3, NAS Whiting Field, FL. SOC 13Oct76 140568 (MSN 226-145) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140568 Assigned to 2nd Fighter Squadron [code K]. Assigned to 516th Fighter Squadron Damaged sometime in 1964 140569 (MSN 226-146) Assigned to VT-3, NAS Whiting Field, FL. W/o 10Jul72 140570 (MSN 226-147) Assigned to TW-5, NAS Whiting Field, FL [code E-462] To MASDC as 5T0148 May 23, 1978. . SOC 1Apr82 Registered C-FNAA 18Jun93; cancelled 20Jun96 Registered N462NA 28Jun96; current [Dec15] 140571 (MSN 226-148) Assigned to VT-5, NAS Saufley Field, FL. W/o 14Nov60 140572 (MSN 226-149) Written off 16May58 140573 (MSN 226-150) Assigned to VT-3, NAS Whiting Field, FL. SOC 13Oct76 140574 (MSN 226-151) Assigned to VT-27, NAS Corpus Christi, TX. SOC 15Sep80 Registered N7066J 26Oct93 as a North American / Weber T-28C; current [Dec15] Damaged 4Jan09 when the aircraft ran off the runway at Baton Rouge, LA 140575 (MSN 226-152) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0124 May 1, 1978. SOC 25Jun80 Registered N575FL; current [Dec15] Stored unrestored at Specialized Aircraft Maintenance scrap yard, Tucson, AZ 1998-2007 140576 (MSN 226-153) Assigned to VT-5, NAS Saufley Field, FL [code 2S-153] Assigned to VT-3, NAS Whiting Field, FL. To NAS Pensacola, FL. SOC 15Oct64 Assigned to the Military Assistance Program [MAP] To Democratic Republic of the Congo Air Force / Force Aérienne Congolaise Sep 1964 as 576, code FA-576, later as FG-576 Renamed Zaire Air Force / Force Aérienne Zairoise Oct71. WFU 29Sep75 Sold by US Defense Sales Agency 29Sep75. Registered N99141 Nov77; reregistered Ferry flight from Zaire to El Paso, TX (via Gabon, Nigeria, Togo, Abidjan, Monrovia, Freetown, Bissau, Dakar, Port Etienne, Villa Cisneros, Marrakech, Spain, France, London, Iceland, Greenland & Labrador) 1977; arrived Biggin Hill 16Dec77; departed Biggin Hill for USA 17Apr78. Registered N289RD Jan79; current [Dec15] 140577 (MSN 226-154) ssigned to VT-2, NAS Whiting Field, FL. W/o 25Aug66 140578 (MSN 226-155) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0030 Dec 6, 1974. SOC 29May78 Registered N8039S; current [Dec15] 140579 (MSN 226-156) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140579 Assigned to 2nd Fighter Squadron [code L]. Assigned to 516th Fighter Squadron Modified with reconnaissance pack, designated RT-28C. Transferred to USAF Assigned to Detachment 2B, 4400th Combat Crew Training Squadron, code named "Farm Gate" To Royal Lao Air Force May 1964 as 54-140579/0-40579 Assigned to Detachment 6, 4410th Combat Crew Training Squadron, 1st Air Commando Wing, Udorn RTAB, Thailand for Operation Water Pump. Used by Raven FAC under direction of the US Air Attaché in Laos Assigned to Detachment 1, 56th Special Operations Wing, Nam Phong RTAFB, Thailand. Crashed 3Feb72 38km SW of Udorn, Thailand; 2 killed (both from 56th SOW, USAF) 140580 (MSN 226-157) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 1May62 Assigned to the Military Assistance Program [MAP] To South Vietnam Air Force Dec61 as 140580. Assigned to 2nd Fighter Squadron [code M]. Assigned to 516th Fighter Squadron To Royal Lao Air Force as 54-140580/0-40580. W/o Apr70 . 140581 (MSN 226-158) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0137 May 9, 1978. SOC 25Jun80 Registered N581JS 7Feb91; reregistered. Registered N666GR 9Sep02; reregistered Registered N688GR 12May10; expired 31Aug14 On September 17, 2011 the aircraft collided with terrain during a low altitude aerobatic maneuver at the Eastern WV Regional Airport/Shepherd Field (MRB), Martinsburg, West Virginia. The airplane sustained substantial damage, and the pilot, the sole occupant, was fatally injured. The purpose of the flight was a 15 minute performance of aerobatic and non-aerobatic maneuvers by 6 pilots of the Trojan Horsemen Demonstration Team (Trojan Horseman) for Thunder Over the Blue Ridge Open House and Air Show at MRB. The accident flight occurred during the single performance of the Trojan Horsemen that day. The pilot of the accident airplane was the No. 6 position for the Trojan Horsemen demonstration. As part of the flight, the Nos. 5 and 6 airplanes were to complete an opposing pass, crossing at show center at an altitude of 500 feet with smoke on, with an aileron roll immediately following the pass. After completion of the opposing pass, the accident pilot was to follow the formation with a four-point roll, and rejoin the formation behind the crowd. The accident occurred during the opposing pass maneuver. The pilot in the No. 5 position reported that he and the accident pilot were laterally displaced and flying towards each other. Their flight paths were to cross at 300 feet above ground level, and then both were to perform an aileron roll. The No. 5 position pilot was to roll to the right after crossing, while the pilot of the accident airplane was to roll to the left after crossing. Witnesses and recorded video indicated that after the two airplanes crossed, the accident pilot began an aileron roll to the left, which degraded into a barrel roll. After completing about 270 degrees of the roll, the airplane stopped rolling and continued in a right-wing-down, nose-low attitude until impact. Review of the video revealed no separation of airplane parts and no obvious attempt by the pilot to recover. Post accident examination of the airframe and flight controls and a cursory examination of the engine revealed no evidence of pre-impact failure or malfunction that would have precluded normal operation. According to the pilot's medical records, he developed early onset coronary artery disease and suffered a heart attack (myocardial infarction) at age 46, requiring urgent four-vessel coronary artery bypass graft (CABG) surgery in 2003. Contributing to the accident was the Federal Aviation Administration's willingness to allow an airman with well-documented, severe coronary artery disease to perform high-risk, low-altitude aerobatic maneuvers. 140582 (MSN 226-159) Written off Apr66 140583 (MSN 226-160) Assigned to NAS Pensacola, FL. W/o 18Feb77 140584 (MSN 226-161) Assigned to BAT-1, Aviation Officer Candidate School (AOCS), NAS Pensacola, FL Written off 28Mar57. Noted in external storage at the Naval Aviation Museum (Pensacola) Summer 1984 140585 (MSN 226-162) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0051q Feb 21, 1975. SOC 25Nov75, Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS. Bought at DoD sale 20May82 Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] Broken up for parts at Nelson, NV 140586 (MSN 226-163) Assigned to VT-27, NAS Corpus Christi, TX. SOC 15Oct76 Registered N2800R as a North American-Mark T-28C; reregistered Registered N128CT; sale reported 9Sep09 to Canada, cancelled 27Aug12 Stored dismantled & unrestored Victoria, BC, Canada 2007 140587 (MSN 226-164) Written off 14Apr59 140588 (MSN 226-165) Written off 10Jan59 140589 (MSN 226-166) Assigned to VT-27, NAS Corpus Christi, TX. SOC 18Dec80 To private user in Sheffield, UK Jun 28, 1962 and registered as G-USAF. Stored dismantled from 1982-1992. Cancelled Sep 2, 1991. To Canada and registered as C-FPTR Mar 23, 1992,cancelled Apr 28, 1993. To N280CR Jun 1, 1993, reregistered . To N280JM Feb 3, 1999, current Dec 2015. On December 8, 2012 the aircraft was substantially damaged when it impacted terrain during an off airport forced landing near Charping Airport (5TA1), Moody, Texas. The airplane had departed from Draughon-Miller Central Texas Regional Airport (TPL), Temple, Texas for the local flight. The pilot reported that he was on a base leg for a practice low approach to the 2,200 foot long turf runway at 5TA1, when there was a sudden complete loss of engine power. The pilot's brief efforts to restart the engine were unsuccessful and he executed an off-airport forced landing with the landing gear retracted and the speed brakes stowed. There was an immediate post impact fire in the engine compartment which was extinguished with handheld fire extinguishers brought by several witnesses who had responded quickly. A post accident examination showed the engine mount, lower forward fuselage, and wing spar sustained substantial damage. There was fire damage to the engine compartment and the upper engine cowling and smoke damage to the cockpit area. 140590 (MSN 226-167) Assigned to VT-3, NAS Whiting Field, FL. SOC 17Mar76 140591 (MSN 226-168) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0053 Feb 24, 1975. SOC 25Nov75. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS. Bought at DoD sale 20May82 Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] Broken up for parts at Nelson, NV 140592 (MSN 226-169) Assigned to VT-5, NAS Saufley Field, FL. W/o 14Jun72 140593 (MSN 226-170) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0040 Jan 16, 1975. SOC 29May78 Registered N9022Y Nov78; cancelled 9May91 To County Civil Defense, Jefferson City, MO Nov78 To Civil Defence Council, Greenwood, MO 1984 Forced landing 1Jan87 at Van Nuys, CA. The pilots were practicing landings and were on the 3rd flight after the engine had been overhauled. After takeoff from a tough-and-go, the instructor noticed that the oil temperature was high. Soon thereafter, the engine began to run rough, then it seized. Unable to get back to the runway, he landed in a plowed field. He said he intended to land with the gear retracted, but the aircraft touched down with the gear extended, then bounced and nosed over. The CFI believed that the student may have extended the gear just before landing. Investigation revealed that a catastrophic internal failure of the engine had occurred. There was evidence of an overspeed. A witness reported that due to improper installation of the carburettor throttle arm, the engine went to full power when it was started after overhaul. Reportedly, it stayed at full power for several minutes before it could be shut down. A teardown revealed the connecting rods had failed, the cylinder skirts were damaged, one piston was destroyed and others were damaged, several bearings were worn and overheated, metal chips/contamination found in the engine and oil system. The engine had been operated about 7 hrs since overhaul. 140594 (MSN 226-171) Written off 31May57 140595 (MSN 226-172) Assigned to VT-3, NAS Whiting Field, FL. W/o 21May73 140596 (MSN 226-173) Written off Aug65 140597 (MSN 226-174) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0049 Feb 13, 1975. SOC 25Nov75. Bought at DoD sale 20May82. To New Orleans, LA 140598 (MSN 226-175) Written off 21Apr58 140599 (MSN 226-176) Written off 30Sep59 140600 (MSN 226-177) Assigned to VT-2, NAS Whiting Field, FL. W/o 28Nov61 140601 (MSN 226-178) Assigned to Base Flight, NAS Saufley Field, FL Assigned to NAS Pensacola, FL. SOC 25Sep75 140602 (MSN 226-179) Assigned to NAS Saufley Field, FL. SOC 2Aug76 Transferred to the US Marine Corps To the US Marine Corps Aviation Museum, MCAS Quantico, VA Exchanged by USMC Aviation Museum for Lockheed PV-1 Bu34807 23Jun83 Registered N3948B 22Jun83; reregistered Registered N602JM Nov84; cancelled 23Mar15 140603 (MSN 226-180) Assigned to VT-2, NAS Whiting Field, FL. W/o 9Mar62 140604 (MSN 226-181) Assigned to VT-3, NAS Whiting Field, FL.. Crash landed and burned on NAS Pensacola golf course Oct 30, 1963. Pilot was rescued from the cockpit by another officer who was playing golf. 140605 (MSN 226-182) Written off 19Jun57 140606 (MSN 226-183) Written off 27Nov57 140607 (MSN 226-184) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0154 Jun 15, 1978. SOC 30Apr79. Registered N70447; cancelled 10Aug12. Seen at Richmond, VA airport in 2023, not airworthy. 140608 (MSN 226-185) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0054 Feb 26, 1975. SOC 25Nov75 Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N839VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140609 (MSN 226-186) Assigned to VT-3, NAS Whiting Field, FL. W/o 23Oct64 140610 (MSN 226-187) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0151 May 26, 1978. SOC 30Apr79 Registered N8084V; current [Dec15] 140611 (MSN 226-188) Assigned to VT-2, NAS Whiting Field, FL To MASDC as 5T0157 28Jun78. SOC 30Apr79 To Chesapeake College, MD Stored unrestored Rockford, IL 1996-2002 140612 (MSN 226-189) Written off 12Jun59 140613 (MSN 226-190) With VT-27 at NAS Corpus Christi, TX. To MASDC as 5T0060 Aug 3, 1976. SOC 16Aug77. Bought at DoD sale 20May82. Registered N28CZ Dec 23, 2004, current [Dec 2015] Cancelled as N28CZ on 14th April 2016 as exported to South Africa according to the FAA website, has turned up in Switzerland where it was registered as HB-RMW on 30th September 2022 140614 (MSN 226-191) assigned to VA-122, NAS Lemoore, CA [code NJ-092] To MASDC as 5T0100 Mar 4, 1977. SOC 5Mar77. Bought at DoD sale 20May82. To New Orleans, LA. Noted dismantled at McKinney, TX 2003 140615 (MSN 226-192) to MASDC as 5T0028 Dec 4, 1974. SOC 16Aug77. Bought at DoD sale 20May82 Registration N335JF reserved Oct 12, 2005, taken up Mar 14, 2006 140616 (MSN 226-193) assigned to NAS Pensacola, FL. SOC 19Apr78 140617 (MSN 226-194) assigned to NAS Pensacola, FL. SOC 25Sep75 140618 (MSN 226-195) assigned to VT-5, NAS Saufley Field, FL. W/o 30Mar61 140619 (MSN 226-196) with VT-27 at NAS Corpus Christi, TX. To MASDC as 5T0042 Feb 10, 1975. SOC 23Jan76. Bought at DoD sale 20May82. To New Orleans, LA. In September 2019 undergoing restoration at the Pacific Coast Air Museum, Santa Rosa, California. 140620 (MSN 226-197) with VT-3 at NAS Whiting Field, FL. To MASDC as 5T0056 May 28, 1975. SOC 25Nov75. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] 140621 (MSN 226-198) Assigned to VA-122, NAS Lemoore, CA. W/o 13Feb76 140622 (MSN 226-199) Assigned to NAS Pensacola, FL. SOC 29Nov68 140623 (MSN 226-200) Assigned to VT-5, NAS Saufley Field, FL. W/o 10Oct61 140624 (MSN 226-201) Written off 4Mar58 140625 (MSN 226-202) To MASDC as 5T0064 Oct 7, 1976. SOC 16Aug77. Bought at DoD sale 20May82 Registered N30625 11Jul90 as a North American / Germain T-28C; current [Dec15] 140626 (MSN 226-203) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0048 Feb 11, 1975. SOC 25Nov75. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N839VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] 140627 (MSN 226-204) Assigned to NAS Pensacola, FL. SOC 25Sep75 140628 (MSN 226-205) Written off 30Jun59 140629 (MSN 226-206) Assigned to VT-2, NAS Whiting Field, FL. W/o 29May61 140630 (MSN 226-207) Written off Jun66 140631 (MSN 226-208) Assigned to VT-5, NAS Saufley Field, FL [code 2S-714] Assigned to NAS Pensacola, FL. SOC 9Oct75 To the National Museum of Naval Aviation, Pensacola, FL. Noted stored at Chevalier Field 1977 Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] 140632 (MSN 226-209) Assigned to NAS Pensacola, FL. SOC 12Dec67 140633 (MSN 226-210) Written off 23Oct58 140634 (MSN 226-211) Assigned to VT-5, NAS Saufley Field, FL. W/o 5Feb63 140635 (MSN 226-212) Assigned to NAS Corpus Christi, TX. SOC 18Dec80 Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Stored dismantled at Techatticup mine near Nelson, NV [last reported Oct15] 140636 (MSN 226-213) with VT-2 at NAS Whiting Field, FL. To MASDC as 5T0116 Apr 12, 1978. SOC Apr 1, 1982. Stripped hulk dumped at Avra Valley, AZ 1993 140637 (MSN 226-214) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0105 Jun 20, 1977. SOC 29May78 Registered N65647; reregistered. Registered N28BZ Jul91; cancelled 29Mar05 Registration N637KB reserved Oct99; ntu On June 20, 2004 the aircraft made a forced landing to a field in the area of Deland, Florida. The pilot and one passenger were not injured, and the airplane incurred substantial damage. The flight had originated from New Smyrna Beach, Florida, a few minutes before the accident. The pilot stated that during a slow climb after takeoff, a lighted chip light in the airplane's cockpit illuminated. Shortly thereafter, he said he felt the first engine shudder/backfire, and he then made a "Mayday" call, and proceeded to the nearest airport to land. Along the way, the pilot said he increased power in an attempt to ensure he would reach the airport, and initially felt the airplane accelerate, but about 30 seconds later, in addition to the illuminated chip light and vibration associated with the engine, suddenly there was a severe rumble again, followed by the engine operating distinctively rough. He noted little puffs of black smoke, coming out of the stacks around the fuselage, and since there was a heavy forested area ahead, he said he turned the airplane toward a field, to affect a landing. The approach and landing flare/touchdown were uneventful, but during the landing rollout the airplane impacted a ditch, and incurred substantial damage. An engine master rod bearing had failed. 140638 (MSN 226-215) with NAF Washington at Andrews AFB, MD. To MASDC as 5T0095 Dec 14, 1976. SOC 16Aug77. Bought at DoD sale 20May82. To New Orleans, LA 140639 (MSN 226-216) with TW-5 at NAS Whiting Field, FL. To MASDC as 5T0140 May 9, 1978. SOC 25Jun80 Registered N775CH 1Oct86; cancelled 10Apr91 Crashed 10Mar89 at Titusville, FL. The aerobatic qualified pilot was practicing a Cuban 8 type of maneuver. According to a witness, the maneuver was performed in a reverse manner. When the pilot previously performed the maneuver, he allowed the aircraft to climb sufficiently before making a 180 deg roll and going down the back side of the maneuver. However, just before the accident, after completing the front side of the maneuver, the aircraft was immediately rolled 180 degrees without climbing sufficiently. Subsequently, during recovery from the descent on the back side of the maneuver, the aircraft mushed into the ground and crashed in a wings level attitude. 140640 (MSN 226-217) Assigned to VT-3, NAS Whiting Field, FL. W/o 7Aug63 140641 (MSN 226-218) Assigned to VT-2, NAS Whiting Field, FL. W/o 28Jun68 140642 (MSN 226-219) Assigned to NAS Pensacola, FL. SOC 17May66 140643 (MSN 226-220) Transferred to the US Marine Corps Assigned to MCAS Quantico, VA. W/o 4Dec74 140644 (MSN 226-221) Assigned to VT-2, NAS Whiting Field, FL. W/o 15Jul63 140645 (MSN 226-222) with NAF Andrews, MD To MASDC as 5T0094 Dec 2, 1976. SOC 29May78. Departed Nov 9, 1978 Registered N9016R; current [Dec15] To Delhi Richland Parish Civil Defense, Delhi, LA 1984. Sold 23Jun86 140646 (MSN 226-223) Written off Sep65 140647 (MSN 226-224) To MASDC as 5T0093 Dec 2, 1976. SOC 16Aug77. Bought at DoD sale 20May82 Registered N757K 30Sep94; current [Dec15] On civil registry as N757K with private owner at Santa Ynez, CA 140648 (MSN 226-225) Assigned to VT-2, NAS Whiting Field, FL. W/o 23Aug63 140649 (MSN 226-226) oAssigned to NAS Pensacola, FL. SOC 16Nov78 Registered N649JS 15Apr91; reregistered. Registration N28VW reserved Apr98; ntu Registration N649DF reserved Jun 278, 2005, taken up 3Aug05; current [Dec15] 140650 (MSN 226-227) with VT-27 at NAS Corpus Christi, TX. To MASDC as 5T0062 Aug 23, 1976. SOC 16Aug77 Registered N51928 to County Civil Defense, Laurel, MS 28Feb78. Sold 1988 Registration cancelled 30Jul13. Believe stored at Rockford, IL 2013 140651 (MSN 226-228) Assigned to VT-2, NAS Whiting Field, FL. W/o 21Nov69 140652 (MSN 226-229) Assigned to NAS North Island, CA To MASDC as 5T0192 May 23, 1979. SOC 1Apr82. Registered N652T; reregistered Registered N28LC 31Aug88; current [Dec15] 140653 (MSN 226-230) Assigned to BUWEPS FR, NAS Alameda, CA. SOC 14Feb77 Registered N10260; reregistered. Registered N653DB Apr87; current [Dec15] Stored unrestored at Avra Valley, AZ 1992-93 Stored Rockford, IL 1997-2002 To the Nevada Museum of Aviation & Military History, Las Vegas, NV 6Apr89. Sold Oct04 To N653MM on May 12, 2017 to Michael P. Marsicano, Hazle Township, Pennsylvania and cancelled on July 12, 2021. To Belgium on July 22, 2021 as OO-TTT 140654 (MSN 226-231) with VT-27 at NAS Corpus Christi, TX. To MASDC as 5T0035 Dec 18, 1974. SOC 16Aug77. Bought at DoD sale 20May82. Registered N75947 Sep91 as a North American / Bumgarner T-28C; current [Dec15] 140655 (MSN 226-232) Assigned to VT-2, NAS Whiting Field, FL. W/o 9Aug67 140656 (MSN 226-233) Written off 20Mar59 140657 (MSN 226-234) Assigned to Base Flight, NAS Quonset Point, RI To MASDC as 5T0021 Nov 19, 1974. SOC 16Aug77. Transferred to USAF Assigned to 3380th Maintenance and Supply Group, Keesler AFB, MS Bought at DoD sale 20May82 Registration N824VW reserved Oct 5, 2006 for Vintage Warbirds, taken up 6Dec06; current [Dec15] Stored at Techatticup mine near Nelson, NV [last reported Oct15] 140658 (MSN 226-235) Assigned to VT-2, NAS Whiting Field, FL Crashed 12Apr68 at the US Military Academy, West Point, NY [1 killed; 1 injured] Restored to flight. Registered N5094J Nov87; cancelled Jun99 Registered N78378 19Jun01; current [Dec15] 140659 (MSN 226-236) Assigned to NAS Pensacola, FL. SOC 1Dec77 Registered N75ES; cancelled To the Pate Transportation Museum, Cresson, Fort Worth, TX 1988-2003 To the Southern Museum of Flight, Birmingham, AL 2005 Seen in 2014 in fenced-off area at Birmingham IAP, AL 140660 (MSN 226-237) Assigned to VT-2, NAS Whiting Field, FL. W/o 18Apr62 140661 (MSN 226-238) Assigned to VT-27, NAS Corpus Christi, TX [code D-715] Assigned to NAS Pensacola, FL. SOC 16Jan81 Noted in external storage at the Naval Aviation Museum (Pensacola) Summer 1984 Registered N661NA Oct85; current [Dec15] 140662 (MSN 226-239) with TW-5 at NAS Whiting Field, FL. to MASDC as 5T0123 Apr 29, 1978, later to USAF as TA0199. SOC Apr 1, 1982. Registered N22134 26Mar90; reregistered Noted at Rockford, IL Aug 9, 1996 painted as NX22134. Registered N243DM 2Jun97; current [Dec15 Now airworthy at Prescott, AZ. 140663 (MSN 226-240) Assigned to VA-122, NAS Lemoore, CA. W/o 13Jan78 140664 (MSN 226-241) Written off 8Jan59 140665 (MSN 226-242) Assigned to VT-2, NAS Whiting Field, FL. . Crashed after takeoff due to engine failure at NOLF Evergreen, Alabama May 8, 1961. Aircraft was destroyed, no injuries. 140666 (MSN 226-243) with VT-6 at NAS Whiting Field, FL. To MASDC as 5T0031 Dec 13, 1974. SOC 29May78 Registered N9022N Nov 17, 1978; current [Dec15] To County Civil Defense, Jefferson City, MO 17Nov78 To Civil Defence Council, Greenwood, MO 1984 On April 11, 2008 the aircraft experienced a total loss of engine power while cruising about 5 miles east-southeast of the Kingman Airport, Kingman, Arizona. The pilot made a forced landing on open, rocky, desert terrain, and the airplane was substantially damaged. About 15 minutes after takeoff, during cruise flight, the pilot observed the engine oil pressure drop and the temperature increase, followed by a total loss of engine power. The pilot made an intentional gear-up forced landing on rough terrain. A partial tear down examination of the engine revealed ferrous and non-ferrous metal in the oil screens. The number 3 connecting rod was found bent, and the number 4 and number 5 cylinders were damaged. Numerous pieces of metal were observed in the crankcase that were associated with the number 4 and number 5 cylinders and pistons. The internal engine component that initially broke at the beginning of the sequence was not identified. 140667/140956 Beech T-34B Mentor MSN BG-1/BG-290 140784 and 140861 converted to YT-34C 140669 became N669MC. 140670 (MSN BG-4) to N100ZP 140675 (MSN BG-9) to N4028G 140676 to MASDC as 4T0089 Nov 1, 1970. Became N20684 140677 (MSN BG-11) to Honduras AF as FAH 1600. Sold to N171EA 140678 (MSN BG-12) to MASDC as 4T0161 Oct 30, 1976. To civil registry as N16116 140681 (MSN BG-15) to N2205C with North Island Navy Flying Club. 140684 to Uruguayan AF as FAU 666 140687 (MSN BG-21) to Honduras AF as FAH 1601 in 1977. Sold in 2001 to US user as N687HV 140688 to N2986F. In 2009 was at Flying Leatherneck Aviation Museum, MCAS Mirmar, CA, on loan from National Naval Aviation Museum. 140689 Seen at Memphis NATTC Oct 21, 1975. to N31362. To N2986F. At NAS North Island Flying Club Feb 2008. 140694 to Uruguayan AF as FAU 678 140697 to MASDC as TD0002 Mar 30, 1977 140698 (MSN BG-32) to MASDC as 4T0092 Nov 1, 1970 140699 with Planes of Fame Air Museum, Minnesota. 140701 (MSN BG-35) Seen at Memphis NATTC Oct 21, 1975. to civil registry as N31366. 140702 (MSN BG-36) registered to Blackwell Aviation as N7071X 140704 to Uruguayan AF as FAU 668 140706 became N32460 140707 (MSN BG-41) 1955: TOS USN. to MASDC as 4T0096 Mar 30, 1977, changed to TD0003. By 5/80: Registered N5359G. By 3/89: Registered N34VY (current) 140709 to MASDC as 4T0091 Nov 1, 1970 140712 to N96065 140714 to Uruguayan AF as FAU 673 140715 Accepted by the US Navy in 1955 as BUNO 140715. To the MCAS El Toro Flying Club, MCAS El Toro, CA in 1978 as N9663A. To Whidbey Island Navy Flying Club, Oak Harbor, WA in 1998 as N9663A. Grounded in 2004 for corrosion. Loaned to the Heritage Flight Museum at the Skagit Regional Airport, Burlington, WA in 2014. 140716 (MSN BG-50) 1955: TOS USN. By 5/70: Registered N3483F. 6/20/94: Bureau of Naval Personnel, Washington, DC. Noted in Feb 2015 stored with Parks Industries, Amarillo, Texas. Registered as N3483F 140717 (MSN BG-51) to Dominican Republic AF as 1602. US registration N173EA reserved Aug 2002. 140720 (MSN BG-54) to MASDC as 4T0104 Mar 30, 1977, later TD0004. 140721 (MSN BG-55) to MASDC as 4T0097 Mar 30, 1997. On civil registry as N5361G with Robert J. Barr of Logansport, IN 140725 (MSN BG-59) to MASDC as 4T0098 Mar 30, 1997, later TD0006. To civil registry as N424NM 140727 (MSN BG-61) to Honduras AF as FAH 1603 in 1977. WFU 1982 140731 (MSN BG-65) to MASDC as 4T0108 Mar 30, 1977, later TD0007. With Civil Air Patrol, Maxwell AFB, Alabama as N5656G in 1979. To civil registry as N143KC, Current since May 3, 2007 as N341MR 140732 to Uruguayan AF as 664 140733 (MSN BG-67) to MASDC as 4T0111 Mar 30, 1977, later TD0008. To civil registry as N2VY 140735 to Uruguayan AF as FAU 674 140739 became N20783. 140740 (MSN BG-74) to N14VY and on display at Southern Museum of Flight, Birmingham, Alabama 140741 (MSN BG-75) to Honduras AF as FAH 1604 in 1977. Sold to N341RH 140743 (MSN BG-77) to Honduras AF as FAH 1605. WFU May 1998, sold to N172EA. Current as N934RS. 140745 (MSN BG-79) 1955: TOS USN. 5/86: AMARC, Davis-Monthan AFB, AZ as 4T149. Jan 4, 1989: Registered N134TD. 1992: Restored. June 3, 1997: Based with Lima-Lima Squadron, Naper Aero Club Field, Naperville, IL. 140746 to N96081 140748 to Uruguayan AF as FAU 680 140749 to civil registry as N21729 140750 to Uruguayan AF as FAU 662 140751 with Forestry Service, NC. 140753 (MSN BG-87) to Colombian AF as FAC2306 and noted Feb 2015 with Parks Industries, Amarillo, Texas. 140754 to Uruguayan AF as FAU 660 140755 seen at Memphis NATTC Oct 21, 1975. To N31368 140756 to Uruguayan AF as FAU 683. Purchased from the Bolivian Air Force by Paul Pribble of Mentor Aviation, date of sale not listed 140758 )MSN BG-90) to civil registry as N85993. Airframe corroded & missing parts, for sale by GSA Auctions at NAS Pensacola, FL 15SEP21 140760 to Uruguayan AF as FAU 670 140761 to Uruguayan AF as FAU 661 140766 registered N20869 November 1993 140768 (MSN BG-102) to Kalamazoo Aviation History Museum. 140769 to Uruguayan AF as FAU 671 140773 (MSN BG-107) Current 2020 in US civil register as N51TT 140776 to N2177H 140781 to MASDC as 4T0113 Mar 30, 1977. Later TD0009 140784 (MSN BG-118) converted to YT-34C. By Aug 1998 had become N190AC 140790 to Uruguayan AF as FAU 671 140794 to N2179R 140795 registered N795FC November 1993. On display at San Diego Air and Space Museum, CA, on loan from National Naval Aviation Museum. 140796 (MSN BG-130) to Honduras AF as 1606. WFU May 1998, sold to N50699 140798 seen at Memphis NATTC Oct 21, 1975. To N31367. 140800 became N21793. 140802 (MSN BG-136) to Dominican Republic AF as 1607. Sold in 2001 as N802HV. Donated to Commemorative Air Force. 140804 to MASDC as 4T0112 Mar 30, 1977. Later TD0010 140805 became N87642. On display at Estrella Warbird Museum, Paso Robles, CA, on loan from National Naval Aviation Museum. 140806 to Uruguayan AF as FAU 684 140808 to Uruguayan AF as FAU 681 140810 (MSN BG-144) noted Sep 2003 at Linear Air Park, Dyess AFB, TX 140813 (MSN BG-147) 1/56: TOS USN. Unknown date: Navy Flying Club with c/r N7098U. 993: Last flight. 10/25/94: National Museum of Naval Aviation, NAS Pensacola, FL. Feb 4, 2013: C/r N7089U cancelled. 2021: Placed up for auction. 140814 (MSM BG-148) to N16166 of NAS Meridian Flying Club, Now N4986 with Danied Serrato of Eufala, AL 140815 to Uruguayan AF as FAU 679 140816 (MSN BG-150) noted on display at Naval Aviation Museum, NAS Pensacola, Florida Nov 1979 140818 (MSN BG-152) to civil registry as N27681. Noted Mar 2006 at National Museum of Naval Avaiation, Pensacola, FL 140819 (MSN BG-153) Purchased from NAS Pensacola as an AIRCRAFT CARCASS by Aircraft & Engine Enterprises on Jan 17, 197 140820 (MSN BG-154) to Spanish AF at E.17-21. To Uruguayan AF as 644 140824 (MSN BG-158) to Honduras AF as FAH 1608. Sold to N174EA 140830 became N1408N. On display at Naval Air Technical Training Center, Pensacola, FL, on loan from National Naval Aviation Museum. 140831 (MSN BG-165) to N134BD 140832 (MSN BG-166) 1956: TOS USN. By 1974: Training Squadron 5 (VT-5), NAS Pensacola, FL to Uruguayan AF as FAU 665. By 1983: Registered N24Z. Current 140833 (MSN BG-167) to civil registry as N9HX 140835 1956: TOS USN. 1964: US Agricultural Department, Forestry Division, San Francisco, CA with c/r N115Z. Lead plane for firefighting. Replaced 140841 which crashed. Feb 6, 1995: Registered N134DR, current. 140838 to N91153 of NAS Willog Grove Flying Club 140842 (MSN BG-176) was registered N1237, then N34RB, now to N816JB 140844 (MSN BF-178) Purchased from NAS Pensacola as an AIRCRAFT CARCASS by Aircraft & Engine Enterprises on Jan 17, 1973. Became N16636 on Jan 29, 1973. Later purchased by Paul Pribble of Mentor Aviation. 140845 to MASDC as 4T0168 Mar 26, 1987. 140846 became N54768 February 1994. 140847 to Uruguayan AF as FAU 667 140848 (MSN BG-182) became N10346, then CF-KCW. 140849 became N849MC. 140851 (MSN BG-185) noted Feb 2015 stored with Parks Industries, Amarillo, Texas. 140854 became N2188T 140855 (MSN BG-189) became N855MC. 140859 became N2191N 140860 became N2192K 140861 (MSN BG-195) On display at the 1975 Paris Air Show at Le Bourget. On display in preservation park at NAS Whiting Field, FL, on loan from National Naval Aviation Museum. 140863 became N21970 140864 (MSN BG-198) 1956: TOS USN. 1/15/62: US Navy, FPO, NY with c/r N4943C. Jul 7, 1970: C/r N4943C cancelled. 8/14/80: Registered N3CN. Still current. 140865 to MASDC as 4T0105 Aug 29, 1975 140868 (MSN BG-202) to civil registry as N45743. Noted Mar 2006 at National Museum of Naval Aviation, Pensacola, FL 140869 became N88796 April 1994. 140870 (MSN BG-204) 1956: TOS USN. Unknown date: Unknown owner with c/r N2198X. By 11/81 to current: Registered N20M. 11/13/81: Near Pontiac, MI, landed short of runway due to fuel exhuastion, incurring substantial damage. Owner not flying. 1983: Rebuilt as Beech-Parks conversion D45.. 140872 became N8764T. On display at San Diego Air and Space Museum, CA, on loan from National Naval Aviation Museum. 140873 became N2747F 140874 became N874MC. 140875 to N85995 140876 on tarmac behind National Naval Aviation Museum, Pensacola, FL. Allocsted N85684 with National Naval Aviation Museum 140878 to Uruguayan AF as FAU 663 140880 to MASDC as 4T0162 Oct 30, 1976 140886 (MSN BG-220) to Honduras AF as FAH 1609 in 1977. Crashed in 1986 140887 to MASDC as 4T0158 Oct 30, 1976, later TD0011. 140888 (MSN BG-222) to Uruguayan AF as FAU 675. In Mar 2015 on display at Museo Aeronautico, Montevideo, Uruguay 140889 to Uruguayan AF as FAU 676 140890 to Uruguayan AF as FAU 669 140891 to N81980 140892 to N37986. Fuselage seen 2010 sitting on a ramp on the south side of MKE airport, used for aircraft maintenance training at Milwaukee Area Technical College 140893 crashed at Boccadifalco/Palermo, Italy Jul 18, 1965 and DBR. Pilot was injured (the only one on board) 140900 (MSN BG-234) on civil register as N4945C 140901 (MSN BG-235) to MASDC as 4T0154 Mar 30, 1977, later TD0012. To civil registry as N45TB 140905 became N58743. 140907 became N84639 February 1994. 140908 is N34NV, registration N134Y reserved Dec 20, 2004, taken up Apr 11, 2005. 140909 to MASDC as 4T0160 Mar 30, 1977. LAter TD0013 140910 (MSN BG-244) to MASDC as 4T0107 Sep 25, 1975 140911 became N54641 February 1994. 140913 (MSN BG-247) to N54654. Noted in July 2019 with The American Flight Museum, Topeka, Kansas 140915 (MSN BG-249) to N6KM 140916 became N87964. 140920 (MSN BG-254) to civil registry as N74894. 140921 became N34PR. On display at NAS Patuxent River, MD, on loan from National Naval Aviation Museum. 140926 (MSN BG-260) became N8709S. Noted Mar 2006 at National Naval Aviation Museum, Pensacola, FL 140927 to N91370 140928 to N1870 140929 (MSN BG-263) 1/56: TOS USN. Unknown date: Navy Flying Club with c/r N7098C. 10/25/94: National Museum of Naval Aviation, NAS Pensacola. In storage. 9/21: Sold at GSA Auctions. Dec 11, 2012: C/r N7098C cancelled 140930 to N88994 140931 (MSN BG-265) noted Sep 11, 2003 at Ropkey Armor Museum, Indianapolis, IN 140932 to N46939 140935 to N10338 140936 on display at USS Lexington Museum, Corpus Christi, TX on loan from National Naval Aviation Museum 140937 to civil registry as N74563, later to civil registry as N34KT as Beech D45. Hit tree and crashed near Morrison, Florida Nov 5, 2011. 2 killed. 140938 became N9334B. In 2009 to Evergreen Aviation and Space Museum, McMinnville, OR, on loand from National Naval Aviation Museum. 140939 to N1008H 140940 to N91072 with NAS Norfolk Flying Club 140942 1/56: TOS USN. 1967: AMARC, Davis-Monthan AFB, AZ. By 7/86: Navy Flying Club, unknown location, with c/r N4028Y. Dec 12, 1993: United States Navy, Willow Grove, PA. Based at Aero Club, 111st Fighter Group (ANG), Warminster, PA. After 2008: National Museum of Naval Aviaiotn, NAS Pensacola, FL. 4/10: Loaned to Air Victory Museum, South Jersey Regional Airport, Lumberton, NJ. 1/18/18: C/r N4028Y cancelled. 140944 became N58687 February 1994. Now N341MN, owned by Monterey Navy Flying Club. 140945 to MASDC as 4T0086 Nov 1, 1970 140946 (MSN BG-280) to MASDC as 4T0167 Aug 9, 1977. To N4269A 140947 to N544E 140949 to MASDC as 4T0117 Jan 14, 1977, later TD0001. To N4944C 140950 to N96228. 140953 to N1410Z 140955 to N9131R 140956 to N6367T. ASN6367T, used in 1977 by US Navy Flying Club at NAS Rota, Spain 140957 Kellett KH-15 for ONR, test vehicle. 140958/140961 Sikorsky HRS-3 140958 (MSN 55678) transferred to US Navy from USAF 52-7559 May 25, 1954. Transferred to US Marine Corps Dec 20, 1954. Back to US Navy Jul 1958. W/o and SOC Sep 21, 1961. To N17756 Orlando Helicopter Airways Inc, Orlando, FL by 01JAN78. Registered N6020H to Whisper Jet Aug 5, 1993, current. 140959 (MSN 55679) transferred to US Navy from USAF 52-7560 May 25, 1954. Transferred to US Marine Corps Dec 20, 1954. Back to US Navy Jul 1958. W/o and SOC Sep 21, 1961. 140960 (MSN 55694) transferred to US Marine Corps from USAF 52-7565 May 25, 1954. Fitted with Rocket-On-Rotor system with small rocket nozzles on the rotor tips. W/o and SOC Jul 1959. 140961 (MSN 55698) transferred to US Navy from USAF 52-7569 May 25, 1954. 140962/140967 Lockheed P2V-7 Neptune Redesignated P-2H in 1962 140962 (MSN 726-7064) Accepted as P2V-7 at Burbank 13 Dec 55. Lockheed Burbank Dec 55-Feb 59; VP-23 Brunswick Feb 59-Nov 60 (listed as P2V-7S from Jan 60); VP-21 Brunswick Nov 60-Mar 62; VP-23 Brunswick Mar 62-Aug 63; VP-21 Brunswick Aug 63-Oct 68; NAS Los Alamitos Oct 68-May 69. Crashed just short of runway at NAS Los Alamitos, CA on May 4, 1969. Crew of 5 had nothing more than minor injuries. 140963 (MSN 726-7065) Accepted as P2V-7 at Burbank 14 Dec 55. NARF Jacksonville Dec 55-Jan 56; VP-11 Brunswick Jan 56-Feb 59; NARF Alameda Feb 59-Aug 59; Lockheed Burbank Aug 59-Jan 60; VP-11 Brunswick Jan 60-Mar 62 (listed as P2V-7S from Jan 60); NARF Norfolk Mar 62-Jun 62; VP-18 Jacksonville Jun 62-Nov 64; VP-18 Roosevelt Roads Nov 64-Sep 68; NAS Glenview Sep 68-Aug 69; NARTU Memphis Aug 69-Sep 69; NAS Glenview Sep 69-Nov 70; VP-60 Glenview Nov 70-Jan 74 [code LS-2]; To MASDC Davis-Monthan AFB 21Jan 74; SOC 29 Jul 74. To N142DP Apr 2, 1986, to N703AU Mar 1987. To N702AU Aug 1987, to N90YY Dec 1988. To Aero Union Corp Chico, CA in 1990 as N716AU, Tanker #16. Was "Firestar", which had jet engines taken off, the auxiliary fuel tanks, the oil expansion tanks removed and carried 2000 gallon of retardant on computer controlled constant flow doors. Slated to be destroyed, but registered to Bravo Airlines Oct 4, 2007. Cancelled Jun 12, 2013. 140964 (MSN 726-7066) Accepted as P2V-7 at Burbank 28 Dec 55. NARF Jacksonville Jan 56; VP-11 Brunswick Jan 56-Feb 59; NARF Alameda Feb 59-Jul 59; Lockheed Burbank Jul 59-Nov 59; NAS Alameda Nov 59-Dec 59; VP-17 Whidbey Island Dec 59-Jul 62 (listed as P2V-7S from Jan 60); VP-9 Alameda Jul 62-Jan 64; NARF Alameda Jan 64-Feb 64; VP-1 Whidbey Island Feb 64-Apr 67; VP-17 Whidbey Island Apr 67-Aug 67; NARF Alameda Aug 67-Dec 67; VP-1 Whidbey Island Dec 67-Mar 69. Crashed into Pacific Ocean 475 mi west of Guam on or by Mar 1, 1969. Crew rescued by liner "President Cleveland" 140965 (MSN 726-7067) ) Accepted as P2V-7 at Burbank 28 Dec 55. NARF Jacksonville Jan 56; VP-11 Brunswick Jan 56-Jut 58; NARF Alameda Jul 58-Dec 58; Lockheed Burbank Dec 58-Apr 59; VP-21 Brunswick Apr 59-Mar 61 (listed as P2V-7S from Jan 60); VP-56 Norfolk Mar 61-Aug. Crashed with VP-56 at or near NAS Norfolk, VA on or by Aug 28, 1961. 140966 (MSN 726-7068) Accepted as P2V-7 at Burbank 29 Dec 55. NARF Alameda Jan 56-Feb 56. VP-2 Whidbey Island Feb 56-May 58; \ VP-19 Alameda May 58-Jan 59; NARF Alameda Jan 59-Jun 59: Lockheed Burbank Jun 59-Oct 59; VP-9 Alameda Oct 59-Feb 63 (listed as P2V-7S from Jan 60. Port auxiliary jet engine caught fire shortly after takeoff from NAS Alameda Jan 7, 1963, attempted to return but became uncontrollable and ditched into San Francisco Bay. Crew rescued safely, plane SOC Feb 1, 1963. 140967 (MSN 726-7069) ) Accepted as P2V-7 at Burbank 30 Dec 55. NARF Alameda Jan 56-Feb 56; VP-2 Whidbey Island Feb 56-May 58; VP-19 Alameda May 58-Jan 59; NARF Alameda Jan 59-May 59; Lockheed Burbank May 59-Nov 59; VP-9 Alameda Nov 59-Dec 63 (listed as P2V-/S from Jan 60). NARF Alameda Dec 63-Feb 64; VP-1 Whidbey Island Feb 64-Apr 67; VP-17 Whidbey Island Apr 67-Nov 68; NAS Los Alamitos Nov 68-Nov 70; VP-65 Point Mugu Nov 70-May 73 [code PG-2]; To MASDC Davis-Monthan AFB 3 May 73: SOC 29 Jul 74. To Allied Aircraft, Tucson, AZ, 18Sep86. 140968 Lo | ||||||||
5682 | dbpedia | 0 | 66 | https://en-academic.com/dic.nsf/enwiki/4428001 | en | VMO | [
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] | null | [] | null | For the earlier VMO 1 which formed in MCB Quantico in 1937 see VMTB 151 Marine Observation Squadron 1 VMO 1 insignia Active July 27, 1943 – July 31, 1993 | en | https://en-academic.com/favicon.ico | Academic Dictionaries and Encyclopedias | https://en-academic.com/dic.nsf/enwiki/4428001 | For the earlier VMO-1 which formed in MCB Quantico in 1937 see VMTB-151
Marine Observation Squadron 1 (VMO-1) was an observation squadron of the United States Marine Corps which saw extensive action during World War II and supported numerous contingencies during the Cold War. They were based at Marine Corps Air Station New River, North Carolina and saw their final deployment in support of Operation Desert Storm in 1991. They were deactivated on July 31, 1993.
Contents
1 History
1.1 World War II
1.2 1946–1980s
1.3 1990s and deactivation
2 Awards
3 See also
4 Notes
5 References
History
World War II
Marine Observation Squadron 155 (VMO-155) was formed at Marine Corps Air Station Quantico, Virginia on July 27, 1943. In November of that year they moved out to San Diego, California and on January 1, 1944, they were redesignated Marine Observation Squadron 1 (VMO-1) and deployed to Espiritu Santo. In February 1944, they moved to Guadalcanal and in July they joined the III Amphibious Corps and participated in the Battle of Guam. In February and March 1945, the squadron also participated in the Battle of Iwo Jima.
1946–1980s
In January 1946, the squadron moved to Marine Corps Air Station Cherry Point. During the Korean War, they trained replacement pilots for the war and supported operation of the 2nd Marine Division. In 1952, they moved to Marine Corps Air Station New River and received their first helicopters. In 1958, the squadron was part of the U.S. 6th Fleet task force that intervened in Lebanon and in 1965 they participated in the U.S. intervention into the Dominican Republic.
In July 1968, VMO-1 became conversion to the OV-10 Bronco and by 1971 they were an all fixed-wing squadron. During the 1970s and 1980s, the squadron rotated through deployments to Japan and supported exercises throughout Asia, the Mediterranean, the Caribbean and Northern Europe.
1990s and deactivation
In December 1990, the squadron boarded the USS America and USS Theodore Roosevelt headed for Saudi Arabia to support Operation Desert Shield. When Operation Desert Storm began, the squadron flew over 1000 combat sorties with the loss of 1 aircraft and 1 pilot killed in action. Upon their return, the squadron was deactivated on July 31, 1993.
Awards
Navy Unit Commendation (with one bronze star)
Meritorious Unit Commendation
Asiatic-Pacific Campaign Medal
World War II Victory Medal
National Defense Service Medal (with two bronze stars)
Armed Forces Expeditionary Medal
Southwest Asia Service Medal (with two bronze stars)
See also
United States Marine Corps Aviation
List of active United States Marine Corps aircraft squadrons
List of inactive United States Marine Corps aircraft squadrons
Notes
References
Bibliography | ||||
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5682 | dbpedia | 2 | 23 | https://militaryuniformsupply.com/products/vmo-1-squadron-patch | en | VMO-1 "Can Do" - Marine Observation Squadron USMC Patch - CLEARANCE! | http://militaryuniformsupply.com/cdn/shop/files/vmo-1-can-do-squadron-patch-vietnam-sew-on.png?v=1691076832 | http://militaryuniformsupply.com/cdn/shop/files/vmo-1-can-do-squadron-patch-vietnam-sew-on.png?v=1691076832 | [
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Marine Observation Squadron 1 (VMO-1) was an observation squadron of the United States Marine Corps which saw extensive action during World War II and supported numerous contingencies during the Cold War. They were based at Marine Corps Air Station New River, North Carolina and saw their final deployment in support of Operation Desert Storm in 1991. They were deactivated on July 31, 1993. | |||||
5682 | dbpedia | 1 | 60 | http://www.aeroflight.co.uk/waf/usa/USMC/USMC-VMO151.htm | en | U.S. Marine Aviation | [
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] | null | [] | null | null | World Air Forces
Back to Marine Aviation Index Page
USA
Marine Aviation
Unit History
Marine Torpedo Bombing Squadron 151 (VMTB-151) "Ali Baba"
Role: Bomber. Tail Code: no
Marine Observation Squadron 1 (VMO-1) was commissioned in 1941 at MCAS Quantico. The unit was redesignated Marine Observation Squadron 151 (VMO-151) on July 1, 1941. The squadron left for San Diego, CA in December 1941 with the rest of the 1st Marine Aircraft Wing, but returned to MCB Quantico in January 1942. From January to April, they trained at NS Norfolk until departing for Samoa on April 9, 1942. They arrived a month later and remained for the next 13 months. On September 15, 1942, the squadron was re-designated again, this time as Marine Scout Bombing Squadron 151 (VMSB-151).
On June 10, 1943, the squadron moved to Uvea Island in the Wallis Group. The squadron remained there until February 29, 1944 when they arrived at Engebi. From March 9 - 12, the squadron covered Marine landings on Wotho Atoll, Ujae Atoll and Lae Atoll. During this time, they also made bombing runs against by-passed Japanese bases in the Marshall Islands until May 31, 1945. On June 9, 1945, the squadron boarded the USS Silverpeck for return to the United States.
Upon return to MCAS Mojave, they were assigned to Marine Air Support Group 51 and were redesignated Marine Torpedo Bombing Squadron 151 (VMTB-151) on June 30, 1945. The squadron was deactivated at MCAS Santa Barbara,CA on March 20, 1946.
Air Bases: Base Duration
MCAS Quantico/Triangle/VA
1941 - 12.1941
NAS San Diego/CA
12.1941 - 1.1942
MCAS Quantico/Triangle/VA
1.1942 - 4.1942
Tafuna Airfield/Samoa
4.1942 - 6.1943
Uvea Island/Wallis Group
6.1943 - 2.1944
Engebi
2.1944 - 6.1945
MCAS Majove/CA
6.1945 - 1946
MCAS Santa Barbara/CA
1946 - 1946
Aircraft Used: Type Qty Service Example Serials Curtiss SBC-4 Helldiver 12 1941 - 1943 n/a Douglas SBD Dauntless 12 1943 - 1946 n/a
Unit Insignia:
VMSB-151
References: | ||||||||
5682 | dbpedia | 3 | 79 | http://uscarrierhistory2.com/index_archivos/Page1068.htm | en | Home | [
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] | null | [] | null | null | VMO-1 began life as a fixed-wing squadron in World War 2, earning battle stars for service at Guam and Iwo Jima. After the war, VMO-1 was based at Cherry Point, and then New River. In 1952, the squadron received its first helicopters, Kaman HOK-1s. From this date, until 1971, the squadron would operate both fixed-wing and helos together. During this period, VMO-1 was the first squadron to operate the HO5S, HOK, UH-1E, UH-1N, and the AH-1J. During the Korean War, VMO-1 trained personnel headed for combat, as well as supporting the 2d Marine Division at home.
In March 1964, VMO-1 became the first USMC squadron to operate the turbine-powered UH-1E "Huey". Later that month two VMO-1 Hueys rescued a party of road engineers from hostile Indians in Peru. In 1965, VMO-1 supported the US intervention in the Dominican Republic. Later that year, the squadron transferred out all of its O-1C "Birdogs", and became an all-helicopter squadron.
In July 1968, VMO-1 began operating the OV-10A "Bronco". VMO-1 transferred all its helicopters in February 1971 and became a fixed-wing squadron again. During the late 1970s, the squadron began rotating detachments with VMO-2 to Okinawa to support Marines in the Far East. In 1980 the first OV-10D arrived, giving the squadron increased reconaissance capabilities. Throughout the 1980s VMO-1 continued to support exercises in the Caribbean, Northern Europe, and the Mediterranean. VMO-1 was awarded a Navy Unit Commendation during this period for supporting drug interdiction missions.
In December 1990, VMO-1 embarked its OV-10s aboard USS America and USS Theodore Roosevelt to deploy to Kuwait in support of Operation Desert Shield/Storm. The squadron flew over 1000 combat sorties, losing one crew to enemy action (1 KIA, 1 POW). VMO-1 was deactivated 28 July 1993 (Ref. Complete History at reference - http://hma1369.tripod.com/vmo1.html).
Marine Observation Squadron 1 (VMO-1) was an observation squadron of the United States Marine Corps which saw extensive action during World War II and supported numerous contingencies during the Cold War. They were based at Marine Corps Air Station New River, North Carolina and saw their final deployment in support of Operation Desert Storm in 1991. They were deactivated on July 31, 1993 (Ref. http://en.wikipedia.org/wiki/VMO-1).
(ASD)VMO-155
WW 2 1950s-60s OV-10s
VMO-2 was activated at Quantico, Virginia on 1 November 1943, with the designation (Artillery Spotting Division) VMO-251. After an initial training period with their OY "Grasshopper" aircraft, VMO-251 departed for San Diego, where it carried out more training. In January 1944 the squadron was redesignated VMO-2, and in February, moved to Hawaii. In Hawaii, VMO-2 trained with the 2d Marine Division. VMO-2 deployed to Saipan in June, flying in support of 2d Marine Division operations there, and at Tinian. During March and April 1945, VMO-2 flew spotting missions on Okinawa before being ordered back to Saipan. From September 1945 to January 1946, VMO-2 was attached to Marine Observation Group 1, and performed occupation duties in Japan. The squadron then relocated to Cherry Point*, and deactivated 26 August 1946.
VMO-2 was reactivated at Santa Ana, California, on 15 June 1951. Besides the OY-2 and OE-1 fixed-wing aircraft, the squadron also operated a mixture of light helicopters, including the HOK/OH-43D, HO5S-1, and HTL-4/5. In July 1953, VMO-2 deloyed to Camp Gifu, Japan. Three years later the squadron moved to Camp Sukiran, Okinawa. In October 1960 VMO-2 moved to new quarters at Futenma, Okinawa.
VMO-2 began operations in Vietnam with a small detachment of OE-1 (O-1B) "Birdogs" which were attached to Operation Shufly in 1962. In 1965, the entire squadron deployed to Vietnam. All its OH-43s and O-1s were left in Okinawa, and the squadron began to fly the UH-1E. In 1968, VMO-2 began operating the first OV-10A "Broncos" in Vietnam. In 1969 squadron capabilities were increased with the addition of the AH-1G "Cobra". All the squadron's helicopters were transferred out to other units in 1969, leaving only the OV-10s. VMO-2 remained in Vietnam until April 1971, when it relocated to MCALF Camp Pendleton.
VMO-2 was busy during the 1970s and 1980s, supporting the 1st Marine Division and 3d Marine Aircraft Wing at home, while rotating detachments to Okinawa to support MAG-36 operations there. In 1990, VMO-2 deployed to Kuwait in support of Operation Desert Shield/Storm. The squadron's OV-10As and Ds flew the entire distance From California to Kuwait. During the combat in Kuwait, VMO-2 lost one aircraft and crew (2 POW). Following its return to Camp Pendleton in 1991, the squadron began transferring all its OV-10As. In December 1992, VMO-2 finished its final Okinawa deployment. VMO-2 was deactivated 23 May 1993 at Camp Pendleton, ending nearly 50 years of service (Ref. Complete History at reference -
http://hma1369.tripod.com/vmo2.html).
Marine Observation Squadron 2 (VMO-2) was an observation squadron of the United States Marine Corps which saw extensive action during World War II and the Vietnam War. They were based at Marine Corps Air Station Futenma, Japan and Marine Corps Air Station Camp Pendleton, California and saw their final combat in support of Operation Desert Storm in 1991. They were deactivated on 23 May 1993 (Ref. http://en.wikipedia.org/wiki/VMO-2).
(ASD)VMO-251
No insignia VMO-2 WW 2 1953
OV-10 patches
"Angry Two" 1969
Marine Observation Squadron 3 was originally activated 1 December 1943, at Quantico, Virginia, as Marine Observation Squadron 351. It was to be the "eyes" for Marine Artillery units in the Pacific. The squadron was redesignated Marine Observation Squadron 3 in 1944. The squadron flew many hazardous spotting missions at Peleliu, and later, at Okinawa, earned the Presidential Unit Citation. After the war, VMO-3 served in Northern China, before relocating, first to Guam, and later to Cherry Point, North Carolina, where the squadron was deactivated in 1949.
In 1966, the Marine Corps received permission to activate two "temporary war-time only" VMOs. VMO-3 was reactivated at Camp Pendleton in August, and was on its way to Vietnam by December. VMO-3 flew its UH-1E Hueys from Hue/Phu Bai and MCAF Marble Mountain as part of 1st Marine Aircraft Wing. In 1968, with the addition of the OV-10A "Bronco" to the VMO inventory, the decision was made to remove the UH-1 from the VMOs and create three Light Helicopter Squadrons (HMLs). Instead of deactivation, VMO-3 and its sister squadron VMO-5 (UH-1 training squadron based at Camp Pendleton) were redesignated. VMO-3 became HML-367 (Ref. Complete History at reference - http://hma1369.tripod.com/vmo3.html).
These were assigned to VMOs to make up a shortage of aircraft while refitting.
**According to Navy listings, VMO-3 carried 1 SBD-5 on strength from Aug 1944 through mid-Apr 45.
Origins during WWII
HMLA-367 has a long and distinguished record in the United States Marine Corps. Its historical lineage can be traced back to December 1, 1943 when it was activated at Marine Corps Base Quantico, Virginia as Marine Observation Squadron 351 (VMO-351) which was assigned to the Artillery Spotting Division.
In January 1944, the squadron was re-designated as and deployed to Marine Aircraft Group 11 on the island of Espiritu Santo whereupon it took part in the campaigns on Peleliu and Okinawa. The squadron participated in the occupation of North China from October 1945 through June 1947 and was relocated in 1949 to MCAS Cherry Point, North Carolina and assigned to the 2nd Marine Aircraft Wing. The Squadron, having served honorably throughout the Pacific Theater, was deactivated on August 20, 1949.
As the United States increased its presence in the Republic of Vietnam, the Marine Corps reactivated VMO-3 at Marine Corps Air Station Camp Pendleton on August 1, 1966 and assigned it to Marine Aircraft Group 37. The squadron arrived in Vietnam in December 1966 and were now flying the UH-1E. VMO-3 became fully operational at Huế/Phu Bai on 16 January 1967 (Ref. http://en.wikipedia.org/wiki/HMLA-367).
(ASD)VMOVMO-3
WW 2 Alternate version - National Geographic 1944 Vietnam
VMO-4 was activated on 20 December 1943 at Quantico, VA. It initially carried the designation (ASD)VMO-951, but this was changed to VMO-4 on 15 January 1944. The squadron began initial VMO-training at Quantico, then moved to the West Coast for advanced training prior. Further training took place in Hawaii with the 4th Marine Division, then VMO-4 deployed with the Division and participated in the assault and capture of Saipan and Tinian.
After refitting in Hawaii, VMO-4 sailed for Guam in January 1945 in preparation for the Iwo Jima operation. VMO-4 flew missions over Iwo Jima from 26 February to 19 March 1945, then returned to Hawaii, where it remained through the end of the war. After the war's end, VMO-4 relocated to San Diego, and deactivated on 21 October 1945. The squadron had earned a Presidential Unit Citation (Saipan/Tinian operations) and a Navy Unit Commendation (Iwo Jima), in addition to the Asiatic-Pacific Campaign Streamer with two bronze stars, and the World War Two Victory Streamer.
On 1 September 1962, VMO-4 was reactivated at Grosse Ile, Michigan, as a squadron within the 4th Marine Aircraft Wing, Marine Air Reserve Training Command. The squadron was initially equipped with SH/UH-34Ds shared with the Navy Reserve squadrons at Grosse Ile, but later got it's own aircraft.
In 1972, the helos were replaced by OV-10A "Broncos". VMO-4 relocated to Detroit in 1973, then moved again in 1976 to Atlanta, Georgia.
During the first Gulf War (1990-91), VMO-4 was activated for possible deployment and attached to MAG-29, but ended up not deploying. On 1 March 1994, the last Marine Observation Squadron, VMO-4 was deactivated at Atlanta (Ref. Complete History at reference - http://hma1369.tripod.com/vmo4.html).
Marine Unmanned Aerial Vehicle Squadron 4 (VMU-4) is an unmanned aerial vehicle (UAV) squadron in the United States Marine Corps that operates the RQ-7B Shadow. It is the fourth UAV squadron in the Marine Corps and the first in the reserve component. The squadron, nicknamed the Evil Eyes, entered the force structure on July 1, 2010, when Marine Observation Squadron 4 (VMO-4) was reactivated and redesignated VMU-4.
The squadron inherited the history of VMO-4 which was an observation squadron that saw extensive action during World War II. They were last based at Naval Air Station Atlanta near Atlanta, Georgia and were deactivated on May 23, 1993 as part of the post-Cold War drawdown of forces. VMU-4 is a subordinate unit of Marine Air Control Group 48 and the 4th Marine Aircraft Wing (Ref. http://en.wikipedia.org/wiki/VMU-4).
VMO-951 VMO-4
WW2 1960s
via "Mule" Holmberg OV-10
VMO-5 was activated 15 February 1944 at Quantico, VA. The squadron trained for three months with their new OY "Grasshoppers" before leaving for the West Coast. Four months were spent training at Camp Pendleton, followed by another five months in Hawaii. In January 1945 VMO-5 divided into two groups and proceeded to Iwo Jima, staging through Guam and Saipan on the way. On 19 February the squadron arrived at Iwo Jima and by the 28th all its aircraft were ashore. In March, VMO-5 returned to Hawaii, where they saw the end of the war. Following a brief period of occupation duty at Sasebo, Japan, VMO-5 relocated to San Diego and was deactivated 31 January 1946.
On 15 December 1966, Sub Unit 1, H&MS-30, the UH-1E training unit based at Camp Pendleton, was redesignated VMO-5. During the next two years, VMO-5 continued to train new UH-1 pilots, as well as those transitioning from other types. Before deactivating, VMO-5 became the OV-10A training squadron as well. On 15 March 1968 VMO-5 was redesignated HML-267.
Activated 15 February 1944 at Quantico, VA, as Marine Observation Squadron 5, VMO-5, at Marine Corps Base Quantico, Virginia, Virginia on February 15, 1944 (Ref. Complete History at reference - http://hma1369.tripod.com/vmo5.html).
In August 1944 came its first deployment to Marine Corps Air Station Ewa, Hawaii under the 3rd Marine Aircraft Wing to participate in the Pacific theater. The squadron saw action during the Battle of Iwo Jima, and under the 2nd Marine Aircraft Wing participated in the occupation of Japan in Sasebo from September 1945 through January 1946, at which time the squadron returned to San Diego and was deactivated on January 31, 1946 (Ref. Complete History at reference - http://en.wikipedia.org/wiki/HMLA-267.
Deactivated 31 January 1946 at San Diego, CA. Sub Unit, Headquarters and Maintenance Squadron 30 activated at Camp Pendleton. Unit, Headquarters and Maintenance Squadron 30 redesignated 15 December 1966 as Marine Light Helicopter Squadron 267 and assigned to Marine Wing Service Group 37. Redesignated 15 March 1968 as Marine Light Helicopter Squadron 267 (Ref. Complete History at reference - http://hma1369.tripod.com/vmo5.html).
Marine Light Attack Helicopter Squadron 267 (HMLA-267) is a United States Marine Corps helicopter squadron consisting of AH-1Z Viper attack helicopters and UH-1Y Huey utility helicopters. The squadron is based at Marine Corps Base Camp Pendleton, California falls under the command of Marine Aircraft Group 39 (MAG-39) and the 3rd Marine Aircraft Wing (3rd MAW).
Vietnam
With the looming Vietnam War, the subunit of Headquarters and Maintenance Squadron 30 (H&MS-30) at Marine Corps Base Camp Pendleton was redesignated as VMO-5 on December 15, 1966 becoming a full fledged training squadron. They originally fell under the command of Marine Helicopter Training Group 30 under the 3rd Marine Aircraft Wing and were equipped with a complement of UH-1E "Huey"s and OV-10 "Bronco"s.[1] In March 1968, the squadron was redesignated HML-267 and remained at alert status and training replacement pilots and crew for the rest of the war. In 1971, reorganization left the squadron with only UH-1E helicopters, and by the end of 1976 only UH-1N aircraft were flown.
Every six months HML-267 rotated one-third of its assets to Marine Corps Air Station Futenma on Okinawa, Japan. The Hueys were joined by another aircraft in 1982 as the new AH-1J "Cobra"s were deployed. As part of the Unit Deployment Program (UDP) starting in 1983, HML-267 began a regular cycle of six months in Okinawa, 18 months on Camp Pendleton. During which the squadron participated in numerous training exercises including detachments to Korea, Guam, the Philippines, Hong Kong, Iwo Jima, and Australia. Redesignated HMLA-267 in 1987, the squadron received its first complement of AH-1 Cobra "SuperCobra"s. In 1988, the squadron split into three groups: A detachment on land in Okinawa, A detachment on a West Pac, and A detachment aboard the USS Dubuque (Ref. Complete History at reference - http://en.wikipedia.org/wiki/HMLA-267).
VMO-5
WW2 1966-68
Marine Observation Squadron 6 (VMO-6) traces it history to 1 December 1920, when Flight E, 3d Air Squadron was activated at Quantico, VA. Within the next seven years the squadron underwent a series of re-designations (Division 1, VF-1M; Division 1, VO-3M; Division 1, VO-6M) as new aircraft were assigned. VO-6M was assigned to the East Coast Expeditionary Force in 1927 and deployed to Nicaragua the following year. During 1928, VO-6M carried out counter-insurgency operations against the Sandinista forces until 1 September 1928, when the squadron was administratively relocated to Quantico (Squadron designation and colors only; personnel and aircraft remained in Nicaragua).
From 1930 to 1933, the squadron was engaged in training new pilots and mechanics, flying support for the Marine Corps schools at Quantico, and flying daily fire patrols for the Virginia Forest Service. In 1931, a flight demonstration team, the "Helldivers", was formed, and began performing at airshows as far away as Montreal and Cleveland.
In 1933, budget cuts led to a reduction in the number of Marine Corps aviation squadrons, and on 30 June 1933, VO-6M was deactivated.
World War Two saw the reactivation of Marine Observation Squadron 6. The "new" squadron was assigned to support the 6th Marine Division during the upcoming Okinawa operation. VMO-6 moved to San Diego, then to Hawaii, before embarking for Okinawa. From March through July 1945, VMO-6 participated in the Okinawa operation, flying from the Yontan airstrip. This would be the squadron's base until the end of the war.
In October 1945, VMO-6 deployed to Northern China to provide aerial reconaissance for Marine units operating there. VMO-6 relocated to Camp Pendleton in 1947.
With the start of the Korean War in 1950, VMO-6 was assigned to the 1st Provisional Brigade. Helicopters and crews were sent out from HMX-1 and joined the squadron. Over the next five years, VMO-6 performed numerous missions including artillery spotting, reconaissance, and search and rescue. VMO-6 helicopters performed countless medevac missions.
VMO-6 returned to Camp Pendleton in 1955. This would be its home for the next five years. In 1962, a detachment deployed in support of the Cuban Crisis operations; it was recalled before reaching the East Coast.
VMO-6 went to war again, deploying to South Vietnam in August 1965. At this time the squadron was operating UH-1E "Hueys"; in 1968, O-1C "Bird Dogs" were added, along with the OV-10A "Bronco". In 1967, Capt. Stephen W. Pless and his crew extracted four soldiers, under fire, from a beach where they were about to be overrun. For their heroism, Pless's crew were awarded the Navy Cross, while Pless was awarded the Medal of Honor.
In 1969, VMO-6 relocated to Okinawa as part of the drawdown of troops from Vietnam. The squadron supported the 9th Marine Amphibious Brigade and 1st Marine Aircraft Wing (Rear), and took part in numerous training exercises. The squadron rotated crews to Vietnam to fly with VMO-2, and in 1972, took custody of seven AH-1J "Sea Cobras" and trained replacement pilots for HMA-369.
VMO-6 was deactivated 1 January, 1977. It's personnel and aircraft were assigned to H&MS-36 (Ref. Complete History at reference - http://hma1369.tripod.com/vmo6.html).
· Activated 1 December 1920 at Marine Barracks, Quantico, Virginia, as Flight E, 3d Air Squadron.
· Redesignated 24 August 1924 as Division 1, Fighting Squadron 1, First Aviation Group, Quantico, Virginia.
· Redesignated 1 September 1925 as Division 1, Observation Squadron 3.
· Redesignated 1 July 1927 as Division 1, Observation Squadron 6, East Coast Expeditionary Force, Quantico, Virginia.
· Departed 27 January 1928 for expeditionary duty in Nicaragua.
· Assigned to Air Squadrons, 2d Brigade for counter-insurgency operations against the Sandinista rebels, 16 February - 1 September 1928.
· Administratively transferred from Air Squadrons, 2d Brigade to East Coast Expeditionary Force, Quantico, Virginia on 1 September 1928.
· Deactivated 30 June 1933.
· Reactivated 20 November 1944 at Quantico, Virginia, as Marine Observation Squadron 6.
· Deactivated 1 January 1977 (Ref. Complete History at reference - http://hma1369.tripod.com/vmo6.html).
Marine Observation Squadron 6 (VMO-6) was an observation squadron of the United States Marine Corps which saw extensive action during the Battle of Okinawa in World War II and the Korean War and Vietnam War. The squadron would become the first Marine Corps helicopter squadron to participate in combat operations when they participated in the Battle of Pusan Perimeter in August 1950.[1] They were deactivated on January 1, 1977.
In October 1969 VMO-6 departed South Vietnam for its new home at Marine Corps Air Station Futenma, Okinawa. From there they participated in exercises from such places as Cubi Point in the Philippines, Atsugi, Japan; Taegu, Korea; and the Republic of China. The squadron was deactivated on January 1, 1977 (Ref. Complete History at reference - http://en.wikipedia.org/wiki/VMO-6).
VO-6M VMO-6
WW2 1951 Korean War
"Sylvester - Viet Nam "Eyes of Death" | ||||||||
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Edited Oral History Transcript
Randy Brinkley
Interviewed by Rich Dinkel
Houston, TX – 15 January 1998
Dinkel: This is Rich Dinkel on 15 January 1998, for an interview with Randy Brinkley, the Space Station Program manager. We are just recently airborne out of Happy Valley, Goose Bay, Labrador, on our way to Keflavik, Iceland, on our way to Moscow for the FGB roll-out.
Mr. Brinkley, why don't we start with your birth and early years, family composition, high school, sports, things like that. Why don't you tell me about some of that.
Brinkley: I'll try to keep it short, Rich. I was born in western North Carolina in September of 1944. I grew up in western North Carolina, a very average kid. Played sports. My favorite sport was football. Graduated from high school, small town in western North Carolina. I went to the University of North Carolina, where I also played football and got a degree there from the University of North Carolina.
After I graduated at the University of North Carolina, which at the time the nation was involved in the Vietnam conflict, I had applied and been accepted for law school, and initially planned on attending law school, but received a draft notice. At that point in time I decided that, one, I didn't want to go to law school, and, two, I didn't want to be drafted into the Army.
As it turned out, a well-dressed Marine captain by the name of Carl Mundy, who later was the Commandant of the Marine Corps, came on campus, and I decided to join the United States Marine Corps, at least go to the Officer Candidate School. That was in 1965.
The reason, I guess, as a little side note, that I was interested in the Marine Corps, because in my time at the University of North Carolina we spent a lot of time on the beach in the spring and the summer. The one thing I always remembered is, if you happened to run across a Marine on the beach in an adversarial role, if you found yourself in an adversarial role with one Marine, you found yourself in an adversarial role with large numbers. I appreciated the fact that they stuck together. So that was probably one of the things that impressed me about the Marine Corps. I subsequently decided to join the Marine Corps and go to Officer Candidate School.
Dinkel: That's good, Randy. There was a couple of things in there that I didn't know, but I suspected all along. How about when you came in the Marine Corps? How did you get in? Tell me about your first days as an infantry officer.
Brinkley: Well, shortly after arriving in Quantico, Virginia, the first night in Officer Candidate School I asked myself, "What in the world have you done? How did you get yourself in this situation?"
As a little humor, my dad, who had been in the Army, suggested that if I got a haircut, which at that time I had very long hair, I would impress the drill instructors and they would probably be impressed and I wouldn't even have to get a haircut. Compared to looking like someone that had hair down to his back, I got what I considered to be an extreme haircut. It had no impact at Quantico and I found myself sixty seconds later with a shaved head, and that night in Quantico, actually in a state of shock, asking, "What in the world have I done?"
But having endured that and completing Officer Candidate School and being commissioned as second lieutenant, I went to The Basic School, at which [time] I applied for flight school and was accepted. I was convinced by my platoon commander that the only way you could really be a Marine was to be an infantry Marine, and that if you didn't have a bayonet in your teeth, then you weren't a Marine. So I tore my chit up and subsequently found myself in the infantry. As a footnote, a slow learner.
Then I ended up as a platoon commander on the East Coast and made a Mediterranean cruise. Then I was a general's aide. Then I got orders to Vietnam, like all of us did, after a very short period of time, and found myself at the ripe old age of twenty-two in Vietnam as a company commander along the demilitarized zone, participating in the battles of Con Thien and Khe Sanh and somehow surviving that.
I realized that I needed to adjust my career aspirations. I applied for flight school while I was in Vietnam, during the battle of Khe Sanh, and was subsequently approved for flight school, and left from Vietnam and went to flight school. At that time, the Marine Corps was killing pilots faster than the Navy could train them. As a result, I was one of the first Marines selected to go to the Air Force for flight training, which turned out to be somewhat of a shock for the Air Force and for me, because I arrived at Vance Air Force Base in Enid, Oklahoma, and found myself the senior student in class 7004. Much to the chagrin of the Air Force, I was made the class commander of that particular Air Force class.
It was an interesting time at Vance. Little did I ever realize that I would subsequently cross paths with and work with astronaut Joe Allen, who was the first mission specialist to undergo flight training as a civilian at Vance Air Force Base. He was two classes ahead of me. My next-door neighbor was Loren Shriver, who later was the shuttle commander and is now the Deputy…Director at KSC. I can remember one night, after a number of daiquiris, that Loren and I watched the landing on the moon, the first landing in 1969, while he and I were at Vance Air Force Base, he a plow-back instructor and myself as a student.
I finished after a year at Enid, Oklahoma, at Vance Air Force Base, received my Air Force wings, and I was subsequently returned to the Marine Corps to undergo follow-on transition training. After six months [at Marine Corps Air Station (MCAS)] Cherry Point, flying familiarization in the A-4, and then later in the F-4 syllabus, on completion of the F-4 syllabus at VMFAT 201, I received my Navy wings and was subsequently assigned to Marine Corps [Air] Station Beaufort, South Carolina, to MAG-32, in VMFA—that's 31 to a VMFAT Marine Fighter Attack Squadron 312.
That actually happened because the Maintenance Officer at VMFAT 201 was Major Jack Hammond, who had called a friend of his at the time, Major Jim Mead, and suggested that I might be a good candidate as a new pilot to come to his squadron. I suppose there's probably one little footnote there for Jack, because I didn't start out in very high esteem with Major Hammond, because one Saturday morning I was flying a syllabus hop, which was a supersonic flight. We had received a brand-new F-4 from McDonnell-Douglas. The RIO [Radar Intercept Officer] that was with me had never gone to…Mach 2, and this was a quiet Saturday morning. So he was determined that we would go Mach 2. So instead of going the normal supersonic, we went to Mach 2.15. I was very pleased that I was going to get my Mach 2 pin.
I can recall landing and being in the hot refueling pits at Cherry Point, when this—we called him Mini-Maj, Hammond, stormed out of maintenance, shaking his fist at me. I couldn't figure out what had happened until we pulled into the line and shut down, and realized that we had gone so fast that we had burnt the paint off the radome of this brand new F-4. But over a period of time, Major Hammond saw some redeeming characteristics [in] me, and subsequently thought that I would be a good candidate to join his friend's squadron in Beufort, South Carolina, VMFA-312.
Dinkel: That makes me think back [to] the Mini-Maj. The Mini-Maj thought the same thing about a lot of us, I think, as we went through at that time. But I won't tell my stories. Seems to me that I remember 312 being next door to the squadron I was on. I remember a story about arm-wrestling, its the first one that comes to mind. Do you recall anything about arm-wrestling at that time?
Brinkley: I guess you could say my arrival at Beufort into Marine fighter aviation was somewhat colorful and, on occasion, embarrassing for me. I guess my reputation had preceded me. In a previous life when I was a Second Lieutenant at [The] Basic School, I had the misfortune of wrestling an orangutan and coming up on the short end of that. So when I first arrived, the squadron suggested that I was going to represent their squadron and wrestle an orangutan at Beufort. I declined and said I would go back to the infantry before I was to get in the cage with another orangutan.
But shortly thereafter, the squadron offered me the opportunity to redeem myself, and that was to arm-wrestle the Executive Officer of our sister squadron, and that if I failed, I would embarrass the squadron and obviously be returned to the infantry. Fortunately for me, I was successful in not only beating the Executive Officer of our sister squadron, who had never been beaten before. Actually, I humiliated him. There's a saying that what goes around comes around. Because six months later I was transferred to that squadron and found myself standing in front of Major Wadsworth's desk, reporting aboard, after having humiliated him in front of his squadron and the rest of the squadrons in the Air Group. Fortunately, over a period of time, once again, like with Major Hammond, I was able to overcome my slow start and bad headwork.
Dinkel: I remember many portions of that, but I don't recall all the details. I think I remember, but I would like to hear from you, about exactly how the orangutan match turned out and how it transpired.
Brinkley: Well, we encountered a freak snowstorm in Quantico, Virginia, of such magnitude that they actually closed The Basic School. And as good Second Lieutenants with nothing to do, we headed to…[Washington, D.C.], found ourselves at Georgetown drinking beer and trying to impress a group of Georgetown law students who some of my friends had known and who had played sports, particularly football, in their undergraduate days. This group of individuals in the last few days had gone to a carnival there in Georgetown, in which for five dollars one could enter a cage with a muzzled orangutan, and if they were successful in staying in the cage with the orangutan for five minutes, they were paid $100. None of them were successful, and they were talking about this.
Of course, being Marine Second Lieutenants, there was no hill too tall or any obstacle that we couldn't overcome, so we felt obliged that we had to take on this challenge. After another several hours of strategy sessions and drinking beer in Old Town, we had devised a plan, and we launched off to encounter the orangutan.
Somewhere in the transit some changes were made, because, as I recall when we left, I was going to be number three on the sequence of events with the orangutan, but when we arrived, I found myself in the cage with the orangutan first. The orangutan looked docile enough, 110 pounds, long, skinny arms, who was sitting in the middle of this iron cage. I was pretty much full of myself and had already decided that I would wrestle this orangutan while two of my fellow Second Lieutenants were going to apply different strategies.
I approached the orangutan from the back side, and grabbed the orangutan in a half-nelson, and, much to my surprise and pleasure, I was offered no resistance. Encouraged by this situation, I made the mistake of lifting the orangutan off the ground. I can recall this big smile on my face as the Georgetown law students looked in awe and my fellow Second Lieutenants encouraged me on. This lasted probably for about fifteen seconds, and then I noticed that this long, skinny arm had reached up and had grabbed the iron bar over my head. I didn't pay much attention to it at the time, until about, oh, perhaps, ten seconds later I felt my feet leave the ground. I looked around and then just surmised that the orangutan, who weighed probably 100 pounds, and I weighed 230 at the time, had just done a one-arm pull-up with something like three times its body weight.
It was at this point in time that I realized that I was in deep and serious trouble, and this big grin on my face was changed to stark terror. I was no longer squeezing the orangutan, but actually holding on to the orangutan's back for fear of my life. Fortunately for me, this situation didn't last very long. The orangutan, while she held us in mid-air with one arm, reached around with this other long skinny arm and grabbed me from the back of my neck and slung me the length of the cage and, thank goodness, towards the door, [through] which I immediately took exit from the cage.
Now my fellow Marine Second Lieutenants first started laughing at me with my plight. But when I said, "All right. Now it's time for plan B and plan C," they indicated they had no intentions of executing plan B or C, or getting in the ring, or in this cage with the orangutan. I basically told them that I had been humiliated worse than at any time in my life, and there was nothing that they could do to me that the orangutan had not just done, and either they got in the cage or…we would have a physical confrontation [right there] on the spot.
Well, I'll try to summarize this. My follow-on, who was an All-American from [the] University of Texas, completely abandoned his well-thought-out approach, walked into the ring with the orangutan, and hit the orangutan between the eyes as hard as he could and then immediately retreated to the cage door. Fortunately for him, his one hit had stunned the orangutan, and he was able to, basically, with one hand on the door, stay the five minutes, and we won the $100.
We returned to Quantico the next day. I was the laughingstock of our company. He was the hero. So once again, my career, I figured, was over in the Marine Corps. This situation was somewhat eased though, several days later when our sister company had sent some of their…less intelligent and more physically endowed individuals to demonstrate that their company could equal or exceed our capability. Not realizing this, I had come down to The Basic School [dining hall] for breakfast, and I looked across and saw one of the lieutenants from our sister company, who I, at that time, felt, or thought, had encountered a terrible automobile wreck. The reason I did was because his nose was broken and plastered on one side of his face, both eyes were black, he was missing about six teeth, a number of stitches in his lips. I just commented at breakfast, I said, "My God, he must have been in a terrible accident."
I was sitting with one of my friends from OCS, who happened to be in his company, and he said, "Oh, no. He wasn't in an accident, not an automobile accident. He wrestled the orangutan last night."
As it turns out, this individual had represented the company, found out what was successful with my company, tried the same approach. Walked in, hit the orangutan as hard as he could, but this time it wasn't quite hard enough. The orangutan was knocked down, but then reached up with [her] long arms, grabbed this individual's hands, pulled them to his side, and then proceeded to walk up his chest and tap dance on his face with [her] heels until he passed out.
So even though I was somewhat of an embarrassment to the company, I was not nearly as embarrassed as the other individual, nor permanently scarred from the encounter with the orangutan.
Dinkel: Well, I have to admit, I shaded the truth prior to the listeners out there. I did know that story, but I just love hearing it.
After you left 312, you transferred next door, when 312 went north to Cherry Point to become an AV-8A squadron at that time. …I remember you coming to the squadron I was in, VMFA-251. Tell us approximately what year that was. I also remember an arm-wrestling incident in that squadron also, regarding a Navy individual at the Naval Station at Roosevelt Roads, Puerto Rico.
Brinkley: Well, as I mentioned to you, that what goes around, comes around. I found myself reporting in to the Executive Officer…Major Wadsworth, after I had humiliated him when I was the champion of 312. So, Major Wadsworth, [was] trying to seize the opportunity to recoup some of his money, because he enjoyed wagering on such events. We deployed to Roosevelt Roads Naval…Station for a missile deployment. While there, Major Wadsworth encountered a Navy SEAL, who indicated to him that he had never been beaten in arm-wrestling. So Major Wadsworth capitalized on the situation and told me that this was my opportunity to redeem myself, and that he was going to wager all the money that he had lost on his previous arm-wrestling match on me, and if I lost this match, it would be the end of my career in Marine aviation. Fortunately for me, I was able to win the arm-wrestling match and, after that, finally got out of the doghouse with Major Wadsworth.
Dinkel: Yes, I remember that. I think the part that you left out was, [it] was this great big Navy SEAL…that you wound up arm-wrestling. If I remember correctly, this guy's arms were as big as my thighs…
I also remember [a] cross-country, out of 251, when you headed west out into Texas. I'm a little vague on the details of that. I just remember something significant happening.
Brinkley: This was after our deployment. I had redeemed myself and Major Wadsworth decided that in addition to winning arm-wrestling matches, that I might be entrusted to go cross-country without someone as a flight lead. So we launched out on a cross-country on our way to the West Coast. Overhead Texas, I experienced a utility hydraulic failure. I had a brand-new radar interceptor operator in my back seat, who knew very little about the airplane. The difference between my knowledge and his was probably [not much, and] together you could put [all of it] in a thimble.
But we experienced a hydraulic failure. I followed our procedures, hoping that I could have my back-seater review the procedures for me. I found out that he had left his pocket checklist back at Beufort, South Carolina, so [he] was of no use to me at all.
But, at any rate, we set up for an approach and arrested landing to the north runway, and landed. For those of you who are not familiar with the F-4, with a utility failure you have no brakes, no nose wheel steering, or basically very little control on the ground. You have some pneumatic back-up air brakes. So you need to make [an] arrested landing and lower the arresting hook.
So we set up for a landing to the south with the arresting gear supposedly set up on the northern end of the runway, only to find out when we landed that they had set up the arrested landing on the south end of the runway. So we went flying down the runway with no brakes, no nose wheel steering, which then caused me to use the secondary emergency air brakes, which had no differential control. Being a young pilot, I promptly blew both tires, and found myself going sideways down this runway at 110 miles an hour.
Fortunately, with the luck and the grace of God, we somehow came to rest and didn't have to eject from the airplane. It was an experience that I later on was to repeat in my career in the F-4 again.
Dinkel: I find it ironic, as we reminisce about the old times, that we remember the spectacular things, but it's very difficult to remember those dull, boring training missions and the warning area at night doing radar intercepts to hone our proficiencies. But on that same line, I remember [that] VMFA-251 was back-to-back years Hanson Award winners, which is the finest fighter squadron in the Marine Corps. I remember General Leek coming down, who was the Commanding General of Fleet Marine Force Atlantic to give us an award at a mess night at Recruit Depot Parris Island. I remember that there were some events that I must admit I was peripherally involved in that occurred that night…[at the mess night at] Parris Island. Do you recall that night?
Brinkley: Yes, I recall, and I'm going to try to be diplomatic and not to embarrass the interviewer. But, yes, actually, we had a very lively competition with our sister squadrons. The time of year, we were in the softball season, and during that period of time Captain Dinkel, I think it was, Captain Dinkel, and a First Lieutenant, Ivan Zimmer, who was a defensive end or defensive tackle at Nebraska, had had some words. Our squadron commander at that time was Major Mead, and as the [senior] Captain, he called me aside and…referred to me as the Bull Captain, the Senior Captain. It was my responsibility to make sure that all the Junior Captains and First Lieutenants in the squadron were kept in line. He was particularly concerned about this adversarial relationship between Rich and this Ivan Zimmer. I was directed that during this mess night, to make sure that we did not have any incidents that would embarrass the squadron, and that my job was to stay between these two individuals and provide the adult supervision, at which I was successful for at least some portion of the evening, until we had had the traditional speeches and toasts.
We had been asked by the group commander, who was present at the mess, to join him at the bar, and we did. I found myself a few feet apart between some verbal confrontation between Rich Dinkel and this Ivan Zimmer, trying to execute my responsibilities as given to me by the squadron commander, Major Mead. Oh, yes, and [I forgot to mention] the fifty-pound differential, but that seemed to have little of importance to Rich Dinkel at the time.
I stepped between them and faced Ivan Zimmer and told him that this was an inappropriate situation, and I asked him to cease and desist. He looked at me, took a sip from his rum and Coke, which I can recall very vividly, and then spit it in my face. My response to that was to grab him by throat, slam him up against the wall and then to proceed to choke him, all in the guise of initially trying to preclude an embarrassing situation.
I remember someone trying to pull me off, to the point that my collar devices were penetrating my neck and blood was trickling down my neck, which at the time I was not interested in. There was only one thing I wanted to do, and that was to see that the purple color of Ivan Zimmer's face turned to stark white. But I finally was pulled off of First Lieutenant Zimmer and I found myself confronted by the group commander, who told me to leave his mess. So, obviously, my career was once again over. I'd embarrassed the squadron and the group in front of the three-star general. So my career in the Marine Corps was over, as far as I was concerned.
However, Major Mead immediately jumped to my support and said, "If Captain Brinkley leaves, my whole squadron leaves with him." So, now, not only is my career over, but so is my squadron commander's career and everybody in the squadron. So we all leave. I go home. Fortunately, for me, First Lieutenant Zimmer, who had a lot more to drink than anyone realized, for some strange reason went home, stripped down naked, and went running through the streets and was arrested by the military police. Then after it was said and done the next day— [Tape recorder turned off.]
Dinkel: This is Rich Dinkel back again. Side two of tape one for the Randy Brinkley interview. We had stopped abruptly on the last tape, because I was having too much fun listening to this story. But I think we left off where Ivan Zimmer was running naked through Laurel Bay housing.
Brinkley: Well, after being arrested, he was returned to his home and to his wife. Fortunately for me, after all the accounts of the evening were reviewed by the group commander, I was no longer in the doghouse with my squadron commander, and somehow I survived the evening, despite his personal embarrassment. I will point out that the group commander was not promoted to brigadier general. [Now] this incident or this evening may or may not have played into that.
It's funny because Lieutenant Colonel Rockie Plant, who pulled me off of Ivan, was subsequently my squadron commander a couple weeks later. So once again, just by sheer luck or divine intervention, I was able to overcome a very awkward situation.
Dinkel: Yes, I distinctly remember the event, and I apologize vociferously for causing the altercation. I also remember that General Leek, when afforded apologies for the situation, said that it was the greatest display of camaraderie he had seen in recent years. But you brought up another point of…temporary temporary Major Rockie Plant, who later became our squadron CO. I remember Rockie Plant as being quite a colorful individual myself, both in the air and on the ground. Rather than speak of his exploits in the air, I remember an event where we went to Rosie Roads on a deployment and worked with the OV-10 squadron, who spotted our hits and guided us…there…[as] forward air controllers. I remember inviting them down to Beufort and the entire VMO OV-10 squadron came down there. Events transpired at the Officers' Club that night that I think are worthy of mention. Do you remember the incidents of which I am speaking?
Brinkley: Yes, we had a very successful deployment and the OV-10s were doing the forward air control and tactical air control force, so as a result of that good relationship, we invited them down to Beaufort, South Carolina, the squadron, for a joint happy hour. Lieutenant Colonel Plant, whose nickname, call sign, was Rockie, because he was an All-Navy and All-Marine boxer, was there.
The commanding officer of the VMO squadron came down to this event. He had not been on the deployment with his detachment. In the ensuing activities there was a dice game at the Officers' Club, and some disagreement about the dice, in which there was a question as to who had rolled what, that ended up in the somewhat inebriated CO of the OV-10 squadron hitting Lieutenant Colonel Plant, who sort of just looked at him and then hit him back and knocked him out cold. Unfortunately for Lieutenant Colonel Plant, in doing so he broke his wrist, or his little finger on his right hand. Normally this would not be a problem, but after we had returned, Lieutenant Colonel Plant had been selected to go to [be] the CO of another squadron that was getting ready to carrier-qual for a Navy deployment. Now, the squadron commander could not carrier-qual because his right hand was in a cast from his elbow to the end of his little finger. Again, somewhat of an embarrassment with the General officers in our chain of command.
Dinkel: To the uninitiated, this might sound like we were a disciplineless rabble at the time, but of course, that was not the case. There just happened to be a war going on that we were training for.
After 251, Randy, I remember AWS, Amphibious Warfare School, and the training command, but I don't remember which order. Would you care to expand on that?
Brinkley: Well, after that, shortly thereafter, I received orders, along with a number of us, to go to the [Naval Air] Training Command as a flight instructor. For me, that was a very good thing, because most of the effort was in Vietnam, and we had poor maintenance and poor parts. So there was not a lot of flight time and experience to be derived in the squadrons in the States. So this was an opportunity for me, who had started, I had a late start in aviation, to build up some flight time.
So I went to the Navy Training Command as an instructor and went through instructor training in Pensacola and was assigned to Meridian, Mississippi, to VT-19. Again, because of my seniority, I ended up as the Assistant Director of Training for the squadron.
While I was there, after being checked out, and I was able to go on a cross-country and return to Key West, where one of the squadrons, VMFA-251, was on deployment, I offered to use our T-2 as a bogey for some of their intercepts. Rich Dinkel, once again, was still in the squadron, and so we had an interesting interface with my little T-2 acting as sort of the drone for the F-4 squadrons.
It was interesting. I had a young student with me and we would watch the F-4 come screaming by. At that time we had no forward [quarter] infrared capability on the Sidewinders in the F-4. With their turn radius, my young student in the back seat says, "Where did they go?"
I said, "They'll be back in about five minutes after they get turned around."
We did that until the F-4s ran out of gas, for a couple [of] flights, and then we returned.
After eighteen months in the Training Command, I had felt like I'd learned everything I needed to learn and it was time for me to get back into real airplanes, but the only way I could leave the Training Command early was to go to school in the Amphibious Warfare School at Quantico, Virginia. So I was selected for the last six-month course, before the Marine Corps found out how to take a three-month curriculum and spread into nine months.
So I went to Quantico and spent six months, and then, following that, was reassigned overseas, reassigned for F-4 training in Cherry Point. Then after completing two months of training, I was reassigned to VMFA-232, which at that time was in Nam Phong, Thailand, to join at this point in time, Lieutenant Colonel Jim Mead, my former squadron commander at [312], and Jack Hammond, the maintenance officer of 201, who was now the maintenance officer. That was my next iteration, having completed my academic studies, to return to flying Marine fighters.
Dinkel: [The] Rose Garden. I remember [the] Rose Garden well. …The CG of Task Force Delta at that time was Andy O'Donnell. If I remember correctly, Swede Bjorklin, later a Brigadier, was the group commander as a Colonel, isn't that right? If I remember also, you got there just after I had left. I was the unlucky guy that opened that place, and I think you were the lucky guy that closed that place. Isn't that correct?
Brinkley: Yes, it was an interesting iteration for me, arriving at the end of the war and having to retrograde or close the place. In typical fashion, when they deployed the other Marines didn't have very good records of who did what to whom. As we left there, Colonel Bjorklin was somewhat concerned, because they had a number of somewhat large numbers of items of major equipment that were unaccounted for, things like bulldozers and road scrapers and other things that somehow had disappeared.
[For] my first job in the squadron, Lieutenant Colonel Mead [had] told me that I was to do an investigation and find out, account for these items that had been missing, these large pieces of equipment that had been missing for a couple of years. I approached another friend, "Zippo," Carl Smith who had a law degree, sought his advice on how to deal with this investigation. After interviewing everyone that I could, and no one knew nothing, and recognizing that the squadron commander was not going to let me fly a combat mission until I had resolved this investigation, I concluded that it was somewhere between an act of God or an act of war.
My good friend Hugh Ronalds, who was very articulate with pen, was able to craft this investigation in such a way that somewhere in Southeast Asia today I'm sure there are road scrapers and bulldozers that are being productively employed, with the United States Marine Corps markings on them. But they have been accounted for in this investigation that I was able to complete.
After that, I was able to fly a few combat sorties in which we flew over to Laos and dropped bombs into the trees. Then we were able to, as the last Marine squadron in Southeast Asia, we left the war and returned to the Philippines, which is another saga that I won't go into here.
Dinkel: That's good, we didn't really want to hear that part. I just want you to know that those road graders and bulldozers were very great bargaining commodities when we first got there to Nam Phong at the Rose Garden. They weren't really Marine Corps after all. They really started off as Air Force, but they wound up with Marine Corps paint jobs and wound up on Marine Corps rolls.
Okay. Let's see, we're talking '73, '74 here. Then you rotated out of country. Where did you go? Refresh us on the year.
Brinkley: Well, 232 was a fine squadron and we were selected as Fighter Squadron of the Year. From there I was reassigned to the West Coast to the Third Marine Aircraft Wing and to VMFA-531. That was in 1973. I joined the squadron. Lieutenant Colonel Jack Gagan was the squadron commander. I was assigned as the Operations Officer of that squadron.
That was a very good squadron and a very good year. We subsequently won the Fighter Squadron of the Year, the Hanson Award. During that period of time, I came to know a young Navy Lieutenant flight surgeon by the name of Manley Lanier, Sonny Carter, who flew in my back seat on occasion. I can remember Sonny because every time he flew in my back seat he always got sick and threw up. I'm not sure it was because of my flying or his queasiness, but we became good friends.
After a year, that squadron was selected to transition the F-14s, and then I moved to a sister squadron, VMFA-323, as the Ops Officer, and as did Sonny Carter, and we subsequently won the Fighter Squadron of the Year again. We had a very good squadron. We had a great squadron commander, Mike Sullivan, the infamous Mike Sullivan, a wonderful squadron commander.
After a year in that squadron, I was selected to go to Marine Aviation Weapons and Training Unit, Pacific to head up the F-4 fighter training section there at El Toro.
Dinkel: Yes, that was when MAWTU Pac was at El Toro before the squadron…moved to Yuma, which we'll talk about later in your career.
The captain's making an announcement now. We're just going to speak over it.
If I remember correctly, also, that's when the MAWTU Pac conducted the first two Weapons Tactics Instructor courses. I remember an award during that same time. I'd like for you to talk about the WTI courses, the award, and your brother's award at the same time.
Brinkley: Well, because I had been fortunate enough to have been the Operations Officer of three Fighter Squadrons of the Year, 232 in the Pacific with Lieutenant Colonel Mead, and then, following that, with 531 and [Lieutenant Colonel] Jack Gagan at El Toro, then subsequently, 323 with Lieutenant Colonel Mike Sullivan, I had achieved a degree of notoriety, certainly not deserved, which resulted in me being selected to head up the very prestigious, at least in terms of the Marine fighter community, F-4 section of MAWTU Pac, and we proceeded to implement a combined and integrated training program, Weapons and Tactics Instructors' program, to train tactics instructions for all squadrons.
Dinkel: Why don't you say what…MAWTU Pac is.
Brinkley: MAWTU Pac is Marine Aviation Weapons and Training Unit. We had one on the East Coast and one on the West Coast.
We were able to put together an integrated training Weapons and Tactics Instructor program for graduate-level training of our instructors, each of which would go back to their squadrons and be responsible for training within that squadron. My job was basically to put together the curriculum for MAWTU Pac, which was subsequently adopted and led to the formation of a MAWTS-1, Marine Aviation Weapons and Tactics Squadron One.
Because of the previous success of the squadrons I had been [in], and the efforts in MAWTU Pac, I was selected for…the very prestigious Cunningham Award, which is the Marine Aviator of the Year, in honor of Alfred A. Cunningham, who was the first Marine aviator. That was a great honor for me, following such greats in Marine aviation as John Glenn. But like everything, there's good news and bad news, and as soon as I received this award, I was immediately reassigned to school and a non-flying follow-on staff billet.
At the time, or slightly thereafter, a few months later, my brother, Sam Brinkley, received the Leftwich Award, which was the award for outstanding leadership for the Marine ground officer, or infantry officer of the year, named after Colonel Leftwich.
I left El Toro and spent six months in Rome, Italy. It was interesting. I received orders to the NATO Defense College in Rome. My monitor called me and said, "You're going to Rome." I thought he meant Rome, Georgia, or Rome, New York. I had no idea he meant Rome, Italy, and I couldn't figure out what in the world the Marines were doing in either place.
But, at any rate, I left the West Coast and proceeded to Rome, Italy, for six months of school, subsequently spent a year and a half in Naples, Italy, on the NATO staff. I certainly, once I arrived in Naples, found myself in the company of friends that I had known in the past. Lieutenant Colonel Jack Hammond was there on the staff.
After a few months there, Sonny Carter arrived. Sonny had, after being sick in my back seat and others, had decided to go to flight school. But on his way to completing flight school, but before he was assigned to his first squadron, he was reassigned to the USS Forrestal as senior medical officer, and arrived at my doorstep one day in Naples, Italy. As a result of that, he became good friends with Jack Hammond and spent all his time in port when he was in Naples with me. As a result of that, when Lieutenant Colonel Hammond returned to Beaufort, South Carolina, as luck would have it, now Colonel Mead was the Air Group Commander. Lieutenant Colonel Hammond convinced him that we needed to have this young Navy Lieutenant Commander, Sonny Carter, join the air group as a young pilot.
Upon my completion of my staff tour in Naples, Italy, I, too, was reassigned to Beaufort, South Carolina, to join MAG-31, under the command of Jim Mead.
Dinkel: Yes, I remember all that. I have to correct Mr. Brinkley here, and I want to refer back to the Cunningham Award and the Leftwich Award, where Mr. Brinkley and his brother, Sam, receiving the fighter pilot and the finest ground officer award in the Marine Corps was an unequivocally one of a kind [event], only done once in…Marine Corps [history]. Never done before.
Sonny Carter's association with us from that time hence, would go down in our memory for a long time after he was subsequently selected for test pilot school and then to be an astronaut. That's another story on another tape. We'll come back to that.
Now, we want to talk about [you] as you came back to MAG-31 in Beaufort, South Carolina, again, you came back as the Commanding Officer of Marine Fighter Attack Squadron 312.
Brinkley: Well, it was kind of interesting. Not initially. I spent my year in purgatory as the Group Operations Officer for Colonel Mead. After he got his pound of blood out of me in a year, he allowed me to take over command of VMFA-312.
Now, in retrospect and during my days in Naples, Italy, with Lieutenant Colonel Jack Hammond and myself, we discussed which squadron we would like to have when we returned to flying and which squadron that we wouldn't like to have, because when we were in 232 in Southeast Asia, we competed with VMFA-115 for the Hanson Award, and we both very much disliked 115. Jack Hammond always said, "I would never want to be the CO of 115." As it turned out, after the war was over, 115 returned to MAG-31, was one of the squadrons that was in the air group.
In my case, my days in VMFA-312, I didn't particularly enjoy very much, because we didn't get to fly a great deal. So my response to that, "Well, I would never want to be the CO of VMFA-312," because it was such a poor squadron.
Everything that goes around, comes around. Lieutenant Colonel Hammond assumed command of the VMFA-115, and I assumed command of the VMFA-312, and Colonel Mead told us both it was time, [and] that we were responsible, for turning both of the squadrons around.
Dinkel: Okay. I think we'll stop here and take a break and change the tape, because I'm out of tape. [Tape recorder turned off.]
Okay. Now, this is a continuation of the interview with Randy Brinkley. The date is the same as it was before on the first tape and we're now about halfway between Goose Bay and Keflavik, Iceland.
We're going to continue…and pick up from the spot where we were talking about VMFA-312, where Randy was the Commanding Officer. Randy, who were some of the guys who were in the squadron at 312 at that time?
Brinkley: Well, one person in particular was, at that time First Lieutenant Andy Allen, who was a first-year aviator, and, as you know, subsequently went on to have a very prestigious career in the United States Marine Corps and has recently retired as an astronaut with NASA and Shuttle commander. But Andy was in the squadron as a first lieutenant, and during my tenure as commander, I made Andy the [squadron] maintenance officer…as a very young Captain.
We also had a very great group of young officers, highly talented aviators. Gil Butler, another very talented aviator. Jim Smee, who was later to serve with us in MAWTS-1, was also in the squadron. I had the squadron for about two years. We were on the unit deployment program from Beaufort, South Carolina, MAG-31. We trained. We were the first squadron to receive the F-4S, slated Ss, in the Marine Corps. We trained and took the squadron to the Pacific for six months.
During that deployment to the Pacific, I had a very lucky and unfortunate situation, a mid-air collision with an F-16, in which I lost half of my right wing. I was somehow able to continue to fly the F-4, and subsequently landed it, and it saved the airplane. The F-16 was cut basically in half, but the pilot was fortunate and ejected and landed in the only island in the North China Sea within 100 miles, in the middle of January. Otherwise, he would have not survived more than a couple of minutes.
But after finishing that tour with 312 and MAG-31, I was selected to go MAWTS-1, Marine Aviation Weapons and Tactics Squadron 1, in Yuma, Arizona, as the Executive Officer and selected for the follow-on command for MAWTS-1. MAWTS-1, as you may recall, was the follow-on to the MAWTU-2 Lant and Pac efforts that I had been involved in before I went on my staff tour and school in Europe.
I spent a year as the Executive Officer for that squadron for Major General Jake Vermilyea, at that time Lieutenant Colonel, and Colonel Jake Vermilyea. Then I assumed command of the squadron in a very challenging time. The squadron had undergone a series of unfortunate [ground] accidents and air crashes. Certainly, the task of the whole squadron, and particularly our Safety Officer, Rich Dinkel, was to eliminate the rash of accidents that we had experienced, and to further enhance the Weapons and Tactics…Instructor curriculum for the Marine Corps to incorporate night-vision goggles and the training for night vision and nap of the Earth, for the helicopter community, as well as low-altitude tactics training for the fixed-wing.
We also were able to incorporate a Senior Officers' Weapons and Tactics Instructors' Course during that time frame. The scope of activities—and this took place between 19[9]3 and '[9]6—also included aviation development and tactics evaluation, the development of Marine aviation requirements plan for all the Marine Corps. We had a very close relationship with the Department of Navy, and specifically John Lehman, the Secretary of the Navy. I'm proud to say that MAWTS-1 provided the prototype for the Navy Strike Warfare Center and integrated training that exists today in the Navy at Naval Air Station Fallon.
We also had a leadership role in the lessons learned in tactical exchange with the Israeli Air Force, as well as training with other foreign nationals, which included participation by those foreign nationals in the Weapons and Tactics Instructors' course that we conducted at Yuma, Arizona.
I spent a year and a half as Commanding Officer, following my tenure as the Executive Officer of MAWTS-1. Subsequently, I was selected by the Secretary of the Navy, or the [Commandant] of the Marine Corps, to participate on the Navy's Strategic Studies Group, a year-long fellowship in Newport, Rhode Island.
Dinkel: Let me interrupt just a second. I think you're being a little bashful [about] MAWTS-1. …MAWTS-1 was quite an organization. There's a couple of things I want to cover about MAWTS-1. …This is a very highly decorated organization. It's significant in that there was a lot of team-building going on down at MAWTS-1 at that time. There's a lot of names that [are] familiar with[in] NASA involved with the unit at that time. In addition to that, I'd like to talk about the scope of the tasking of the organization, and just how wide this scope was, and some of the things that came out of there. So let's talk about the awards and then we'll go the team-building portion of it.
Brinkley: Well, we were very, very fortunate. I think that the recognition that we received as a team was well deserved. We received the Navy Unit Commendation from the Secretary of the Navy for our achievements and integrated weapons and tactics training. We also received from the Marine Corps the Aviation and Efficiency Award as the most efficient organization in all of Marine aviation. We also received, for the first time in the history of MAWTS-1, an Aviation Safety Award for accident-free flying.
When you look at the type of flying that we did in that particular squadron, it's particularly impressive, because everything that we did was on the ragged edge in terms of the demands on the aircraft and the air crew, nap of the Earth, night-vision goggles, low-altitude tactics and training, large-scale strikes, coordinated efforts, day and night. The level of activities would include upwards of 100 flights a day.
If you look at the tempo of operations, it's particularly noteworthy, because the maintenance organization that supported this was a composite organization that came together in a matter of days for aircraft and personnel from all over the Navy, the Marine Corps, other services that were put together in a rapid integrated fashion that supported such a high tempo of operations.
So the fact that we were able to task-organize in such a rapid period of time, and be able to do so without any major aircraft accidents is certainly a noteworthy achievement. The lessons learned there ha[ve] been able to be incorporated into the Marine Corps' concept of rapid deployment and composite operations that exist today.
Dinkel: Let's talk about the familiar names to the NASA people that might have been involved down there. Why don't you just talk about that for just a quick second, and then talk about the association with Strike University.
Brinkley: I think the application of lessons learned from that particular effort was relevant, not only to the other services, particularly the United States Navy, with the development of Navy Strike Warfare Center and the incorporation of integrated training between Navy Fighter Weapons School and the Navy Strike Warfare Center, all consolidated at Fallon, but it's also had applicability in terms of integrated training in the space activities. I think it's particularly noteworthy today when we look at NASA and human space flight, operations and integrated training, that the pioneers of this effort have also been able to apply their skills and experience significantly and to the efforts of NASA and human space flight.
As an example, we look back at the Deputy Chief of Staff of Marine Aviation was Brigadier General Jack Dailey, now the Deputy Administrator of NASA. The head of the Aviation Development Tactics Evaluation [Department] of MAWTS-1 at that time was Major Mike Mott, who also is…[the] Associate [Deputy] Administrator for NASA. [If] we look more closely in terms of the Office of Space Flight and Human Space Flight Activities on the NASA side, Rich Dinkel, who led the efforts, provided the leadership, and [was] the catalyst for our safety efforts, and the recognition that we received, is now the Deputy for Safety, Reliability, and Quality Assurance for Johnson Space Center, the lead Center for all human space flight operations for NASA.
We also have the expertise of Major General Jake Vermilyea, who I had the opportunity to work for as his Executive Officer, who is the Vice President for Operations for United Space Alliance, [who are] responsible for [the] safe employment of the space shuttle. We also have Howard DeCastro, who is [the] Program Manager, and the first for the United Space Alliance [USA], for the Shuttle Program. Howard was the first Commanding Officer of MAWTS-1.
So we clearly have a strong relationship between the experience and lessons learned in MAWTS-1 that has been able to have been applied to safe and efficient and integrated operations for Space Shuttle and Station operations.
Dinkel: Well, that's good. I just wanted to cover some of that. Let's go back to this Strategic Studies Group. For the people out there listening, how about telling us where that is and what that Strategic Studies Group really does.
Brinkley: It is located at the Naval Warfare Center in Newport, Rhode Island. Each year a very fortunate selected group of individuals are brought together to work on specific projects as directed by the Chief of Naval Operations, and to make recommendations for the Department of the Navy and the Navy and the Marine Corps.
For me, I was very fortunate to participate in a very prestigious group of individuals, which included General Tony Zinni, who is now the Commander-in-Chief of CentCom, who [was] one of the three Marines on our group.
We also had Mike O'Brien, who is the Deputy Associate Administrator for International Affairs for NASA. We've been able to bring Mike's expertise from the Navy and the Strategic Studies Group to bear for NASA, and apply it particularly for the International Space Station, and our working in an international partnership in a cooperative effort for the Space Station. Skip Omen [phonetic], who's our nuclear submariner is now a four-star Admiral, as well as the other naval officers that are all two and three and four-star Admirals.
So it was a very great opportunity for us to interface with high-level flag officers and the highest levels within the State Department, and to learn from that, certainly something that has benefited me in my current position as a Program Manager of [the] International Space Station, understanding how to work in an international environment and understanding the intricacies of various partners.
Of particular note is our focus was studying the Russians, and I find myself spending a great deal of my time trying to incorporate the Russians into the International Space Station. I suppose you certainly learn a great deal in studying your enemies, because we have gone from enemies into partners. The time and effort that was spent studying the Russians has been well worthwhile in terms of learning how to bridge the gaps between the Russians and the Americans and define common ground and work together as a team.
Dinkel: That's good. That's really relevant to what we're doing right here, now, today, heading toward Moscow. It's also interesting to me, [in that] I never realized that all those important people were in the Strategic Studies Group at the same time.
Where did you go from there? If I remember correctly, you went back towards 2nd MAW.
Brinkley: From the Strategic Studies Group, I was selected to return to the Second Marine Aircraft Wing, assigned for a year as the Deputy Chief of Staff for Operations of the Second Marine Aircraft Wing, responsible for the operations of some 800 aircraft, [2nd MAW is] the largest organization within the Marine Corps.
I arrived at 2nd MAW as the Operations Officer, to find myself involved in the planning of operations in the Middle East, in the Persian Gulf. I spent a very busy year there trying to apply the lessons learned from MAWTS-1, in terms of integrated training not only within the Second Marine Aircraft Wing, but composite kind[s] of training and joint force training with the Navy and the Air Force units on the East Coast. That was a very beneficial experience for me.
But after a year there in that position, I was selected, or afforded the opportunity, to move back to Beaufort, South Carolina, for my third tour of duty, as the Commanding Officer of Marine Aircraft Group 31, the largest Marine Fighter…Group in the Marine Corps, commanding six F-18 squadrons.
I arrived there with a lot of the same faces, faces that even today that I still see. As an example, Major C. J. Sturckow, who we will join tomorrow [in Moscow], is the pilot on the first Space Station flight to assemble the International Space Station, was a young Captain in the Group. He and I went through aircraft tactics instructor refresher training together, or at least for me. C. J. was my instructor. I've been able to watch him grow and mature. Now he's certainly established himself as one of our finest pilots and potential commanders at NASA for the Shuttle. [Tape recorder turned off.]
I was disappointed not to be able to participate in the combat activities of the MAG-31 squadrons that were deployed to [Operation] Desert Storm, but I do take great pride and personal satisfaction that [because] of the training that we established for those squadrons and the fact that all the squadrons, all the F-18 squadrons in the Marine Corps, both deployed and returned safely back to the United States without loss of any of our aircraft, and, most importantly, any of our air crew. I attribute that to the applications of the lessons that we learned at MAWTS-1 and integrated training and composite and joint operations.
It's reassuring to hear from C. J. Sturckow that the things that I insisted on as a Group Commander, that the young officers didn't understand and thought were crazy, were exactly the things they had to do in Desert Storm, at least in C. J.'s view. [They] were the things that made them so successful. So, although personally I didn't get to participate, the fact that we did not lose any of our fine young Marines in that activity, and everyone came home safely, is probably the highlight of my Marine Corps career. | ||||||||
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5682 | dbpedia | 2 | 5 | https://militarygraphics.com/product/vmo-1-marine-observation-squadron-1-decal/ | en | 1 Marine Observation Squadron 1 Decal | [
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It is sticky on the back, meant to be placed on the outside of a window, or other non-porous smooth, hard surface (metal, painted wood, etc.) You may also clear coat it for extra durability, see our FAQ.
This VMO-1 Marine Observation Squadron 1 Decal is SATISFACTION GUARANTEED or it's FREE! Read our Veterans Guarantee. It also includes a ONE YEAR guarantee against peeling, cracking or fading.
Installation is a snap! Please read our simple Installation Instructions. If you do mess it up or something doesn't look right, please contact us, and we'll replace it!
Select from any of the sizes above or let us know of a custom size on the ORDER NOTES section of our checkout page, just select the next size above your desired size and we will downsize it for you.
Free Alignment - If you are purchasing several decals together and would like us to align them for you onto a single sheet for easy installation, please let us know the spacing requirements in the ORDER notes on the CHECKOUT page.
This VMO-1 Marine Observation Squadron 1 Decal is IN STOCK and will likely ship within 2 business days of your order (we are closed on Fridays) - any customizations will take 2 - 4 days longer.
Not computer savvy? - Call us at (928) 636-9580 during our business hours and we will be delighted to answer any questions and take your order over the phone.
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5682 | dbpedia | 2 | 97 | https://www.afgsci.com/product/mouse-vitelline-membrane-outer-layer-protein-1-homolog-vmo1-elisa-kit/ | en | Mouse Vitelline membrane outer layer protein 1 homolog (VMO1) Elisa Kit – AFG Scientific | [
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Sku Size Price Quantity EK731818 96 Wells $380
Mouse Vitelline membrane outer layer protein 1 homolog (VMO1) Elisa Kit quantity
MSDSDatasheet
Product Information
Components
Test Principal
Sample Collection
Reagent Preparation
Assay Procedure
Troubleshooting
SKU:EK731818Category: Elisa KitsSpecies:MouseAssay Principle:QuantitativeAssay Type:SandwichTarget Name:Vitelline membrane outer layer protein 1 homologSample Type:serum , plasma , urine , tissue homogenates , cell culture supernatesSensitivity:0.288 ng/mlStandard:13.5 ng/mlDetection Range:0.48 ng/ml - 12 ng/mlAssay Time:1 - 5 hSample Volume:50 - 100 ulDetection Wavelength:450 nmAbbreviation:VMO1
Components
Assay plate (12 × 8 coated Microwells) 1 Standard (Lyophilized) 1×0.5ml Standard Diluent 1×1.5ml HRP-Conjugate Reagent 1×6ml Sample Diluent 1×6ml Chromogen Solution A 1×6ml Chromogen Solution B 1×6ml Stop Solution 1×6ml Wash Solution 1×20ml×30 fold User manual 1 Adhesive Strip 1
Test Principle
This ELISA kit uses quantitative-ELISA as the method. The Micro-elisa strip plate provided in this kit has been pre-coated with an antibody specific to Vitelline membrane outer layer protein 1 homolog. Standards or samples are added to the appropriate Micro-elisa strip plate wells and combined to the specific antibody. Then a Horseradish Peroxidase (HRP)-conjugated antibody specific for Vitelline membrane outer layer protein 1 homolog is added to each Micro-elisa strip plate well and incubated. Free components are washed away. The TMB substrate solution is added to each well. Only those wells that contain Vitelline membrane outer layer protein 1 homolog and HRP conjugated Vitelline membrane outer layer protein 1 homolog antibody will appear blue in color and then turn yellow after the addition of the stop solution. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm. The OD value is proportional to the concentration of Vitelline membrane outer layer protein 1 homolog. You can calculate the concentration of Vitelline membrane outer layer protein 1 homolog in the samples by comparing the OD of the samples to the standard curve.
Sample Collection
Serum - Use a serum separator tube and allow samples to clot for two hours at room temperature or overnight at 4oC before centrifugation for 20 minutes at approximately 1,000×g. Assay freshly prepared serum immediately or store samples in aliquot at -20oC or -80oC for later use. Avoid repeated freeze/thaw cycles.
Plasma - Collect plasma using EDTA or heparin as an anticoagulant. Centrifuge samples for 15 minutes at 1,000×g at 2-8oC within 30 minutes of collection. Remove plasma and assay immediately or store samples in aliquot at -20oC or -80oC for later use. Avoid repeated freeze/thaw cycles.
Tissue homogenates - The preparation of tissue homogenates will vary depending upon tissue type.
Tissues were rinsed in ice-cold PBS to remove excess blood thoroughly and weighed before homogenization.
Minced the tissues to small pieces and homogenized them in fresh lysis buffer (Different lysis buffer needs to be chosen based on subcellular location of the target protein) (w:v = 1:20-1:50, e.g. 1mL lysis buffer is added in 20-50mg tissue sample) with a glass homogenizer on ice (Micro Tissue Grinders woks, too).
The resulting suspension was sonicated with an ultrasonic cell disrupter till the solution is clarified.
Then, the homogenates were centrifuged for 5 minutes at 10,000×g. Collect the supernates and assay immediately or aliquot and store at ≤-20°C.
Cell Lysates - Cells need to be lysed before assaying according to the following directions.
Adherent cells should be washed by cold PBS gently, and then detached with trypsin, and collected by centrifugation at 1,000×g for 5 minutes (suspension cells can be collected by centrifugation directly).
Wash cells three times in cold PBS
Resuspend cells in fresh lysis buffer with concentration of 107 cells/mL. If it is necessary, the cells could be subjected to ultrasonication till the solution is clarified.
Centrifuge at 1,500×g for 10 minutes at 2-8°C to remove cellular debris. Assay immediately or aliquot and store at $le -20°C.
Urine - Collect the first urine of the day (mid-stream) and discharge it directly into a sterile container. Centrifuge to remove particulate matter, assay immediately or aliquot and store at ≤ -20°C. Avoid repeated freeze-thaw cycles.
Saliva - Collect saliva using a collection device or equivalent. Centrifuge samples at 1000 × g at 2-8°Cfor15 minutes. Remove particulates and assay immediately or store samples in aliquot at ≤ -20°C. Avoid repeated freeze-thaw cycles.
Feces - Dry feces were collected as much as possible, weighing more than 50 mg. The feces were washed three times with PBS (w:v = 1:9, e.g. 900 µL lysis buffer is added in 100 mg feces), sonicated(or mashed)and centrifuged at 5000×g for 10 minutes, where the supernatant was collected for testing.
Cell culture supernates and other biological fluids - Centrifuge samples for 20 minutes at 1,000×g. Collect the supernates and assay immediately or store samples in aliquot at -20°C or -80°C for later use. Avoid repeated freeze/thaw cycles.
Note
Samples to be used within 5 days may be stored at 4°C, otherwise samples must be stored at -20°C (≤1 month) or -80°C (≤2 months) to avoid loss of bioactivity and contamination.
Sample hemolysis will influence the result, so hemolytic specimen should not be used.
When performing the assay, bring samples to room temperature.
It is highly recommended to use serum instead of plasma for the detection based on quantity of our in-house data.
Reagent Preparation
Prepare wash buffer
Combine 20 ml concentrated wash buffer (whole bottle) with 580 ml DI water
Standard Dilute the standard pipette 50 ul standard diluent in each tube. Pipette 100 ul standard in the fifth tube. And take out 100 ul from the fifth five tube into the fourth. Pipette 50 ul from the fourth tube to the third tube and produce dilution series as below. The undiluted Standard serves as the high standard. Sample Diluent serves as the zero standard blank well.
Tube 6 5 4 3 2 1 0 ng/ml 13.5 9 6 3 1.5 0.75 0
Assay Procedure
Prepare standards
Pipette 100 ul standard diluent into new microcentrifuge tubes (labeled 5-0)
Pipette 200 ul of standard into tube 5, vortex
Transfer 200 ul of tube 5 into tube 4,
Transfer 100 ul of tube 4 into tube 3 vortex repeat process to tube 1
Tube 0 will only be sample diluent
Add 50 ul of standards in duplicate to provided 96-well plate
Using a multichannel pipette, add 40 ul of sample diluent to all wells that will contain samples (NOT WELLS CONTAINING STANDARD)
Add 10 ul samples to wells in duplicate
Cover and incubate at 37°C for 40 minutes
Wash plate 5 times
Adding 300 ul wash solution/wash
Add 50 ul of HRP to all wells EXCEPT blank (standard tube 0)
Cover and incubate at 37°C for 40 minutes
Wash plate 5 times
Adding 300 ul wash solution/wash
Add 50 ul of Chromogen A to all wells followed by 50 ul of Chromogen B
Avoid light while preforming this step
Cover and incubate at 37°C for 20 minutes
Add 50 ul of Stop solution to each well
Read immediately at 450 nm
When analyzing the plate, subtract the reading of the blank well from all other absorbances
Additionally, a 5-fold dilution was done when samples were initially diluted so multiply concentration by 5 to get real concentration.
Troubleshoot Common Elisa Issues
Pipetting & Washing Color Signal High Background Poor Standard Curve Poor Replicate Data Assay Variable
Pipetting and washing techniques for ELISA
Pipetting technique
Use the correct pipette that is within the range suggested by manufacturer
Confirm tip is firmly seated on the pipette
Confirm there are no air bubbles while pipetting
Change tips between each standard, sample, or reagent
Use different reservoirs for each reagent
Pipette sample into the side of wells to avoid splashing
Always run samples/standards in replicate
Washing Procedure
Completely aspirate liquid from all wells by gently lowering an aspiration tip into the bottom of each well.
Note: Take care not to scratch the inside of the well.
Fill the wells with at least 500 µL of diluted wash buffer
Let soak for 25 to 30 seconds
Aspirate wash buffer from wells
Repeat as directed in protocol (usually 4-5 times)
After washing is complete, invert plate and tap (forcefully, if necessary) dry on absorbent tissue. Be sure to remove any residual liquid.
Alternatively, a squirt bottle or automated plate washer may be used. Be sure to follow the above.
Problem: No color plate
Possible Cause Solution Mixed use of component reagents Please read labels clearly when preparing or using In the process of plate washing and sample addition, the enzyme marker is contaminated and inactivated, and loses its ability to catalyze the color developing agent Confirm that the container holding the ELISA plate does not contain enzyme inhibitors (such as NaN3, etc.), and confirm that the container for preparing the Wash Solution has been washed. Missing a reagent or a step Review the manual in detail and strictly follow the operating steps.
Problem: Light Color
Possible Cause Solution The sample uses NaN3 preservative, which inhibits the reaction of the enzyme Samples cannot use NaN3 The sample to be tested may not contain strong positive samples, so the result may be normal In case of doubt, please test again. Wrong filter used for absorbance reading When TMB is used as the substrate, the absorbance should be read at 450 nm. Insufficient incubation time Make sure to follow recommended incubation times. Insufficient color reaction Usually 15 - 30 minutes The number of washings increases, and the dilution ratio of the concentrated lotion does not meet the requirements Reduce the impact of washing, dilute the concentrated lotion and washing time according to the manual, and accurately record the washing times and dosage. Distilled water quality problem The prepared lotion must be tested to see if the pH value is neutral. In the process of plate washing and sample addition, the enzyme marker is contaminated and inactivated, and loses its ability to catalyze the color developing agent. Confirm that the container holding the ELISA plate does not contain enzyme inhibitors (such as NaN3, etc.), confirm that the container for preparing the Washing Solution has been washed, and confirm that the purified water for preparing the Washing Solution meets the requirements and is not contaminated. The kit has expired or been improperly stored Please use it within the expiration and store it in accordance with the storage conditions recommended in the manual to avoid contamination. Reagents and samples are not equilibrated before use All reagents and samples should be equilibrated at room temperature for about 30 minutes. Insufficient suction volume of the pipette, too fast discharge of pipetting suction, too much liquid hanging on the inner wall of the tip or the inner wall is not clean. To calibrate the pipette, the tips should be matched, each time the tips should fit tightly, the pipetting should not be too fast, and the discharge should be complete. The inner wall of the tips should be clean, and it is best to use it once. Incubation temperature constant temperature effect is not good Keep the temperature constant to avoid the local temperature being too high or too low When adding liquid, too much remains on the medial wall of wells When adding liquid, the tip should try to add liquid along the bottom of the medial wall of wells without touching the bottom of the hole. Reuse of consumables The tips should be replaced when different reagents are drawn, and different storage vessels should be used when configuring different reagent components. The bottom of the microwell is scratched or there is dirt During incubations, cover assay plates with plate sealers. Use a fresh sealer each time the plate is opened. This will prevent wells from contaminating each other. Cross-contamination during sample addition Try to avoid cross-contamination when adding samples Cross-contamination from manual plate washing When washing the plates by hand, the first 3 injections of the lotion should be discarded immediately, and the soaking time should be set for the next few times to reduce cross-contamination. Cross-contamination when clapping Use a suitable absorbent paper towel when clapping the plate, do not pat irrelevant substances into the well of the plate, and try not to pat in the same position to avoid cross-contamination. The liquid filling head of the plate washer is blocked, resulting in unsatisfactory liquid addition or large residual amount of liquid suction, resulting in the color of plate is chaotic and irregular. Unblock the liquid addition head, so that each well is filled with washing liquid when washing the plate and the residual amount should be small when aspirating liquid. Incomplete centrifugation of the sample, resulting in coagulation in the reaction well or interference of sediment or residual cellular components Serum plasma should be fully centrifuged at 3000 rpm for more than 6 minutes The sample is stored for too long time, resulting in contamination. Samples should be kept fresh or stored at low temperature to prevent contamination Incorrect preparation of Washing Solution or direct misuse of concentrated Washing Solution Please configure according to the manual
Weak or no signal in ELISA
Possible Cause Solution Reagents not at room temperature at start of assay It is recommended that all reagents be at room temperature before starting the assay. Allow reagents to sit on bench for 15–20 minutes to reach room temperature. Incorrect storage of components Double check storage conditions on kit label. Most kits need to be stored at 2–8oC. Expired reagents Confirm expiration dates on all reagents. Do not use reagents that are past the expiration date. Reagents added/prepared incorrectly Check protocol, ensure reagents were added in the proper order and prepared to correct dilution. Incorrect dilutions prepared Check pipetting technique—see below—and double check calculations. Capture antibody didn’t bind to plate If using a ready-to-use kit: Manufactured kits come with plates pre-coated with capture antibody. If coating your own plate with an Antibody Pair Kit: Ensure that you are using an ELISA plate, not a tissue culture plate. Dilute antibody in PBS. Ensure correct preparation and incubation time for both coating and blocking steps. Wells scratched with pipette or washing tips Use caution when dispensing and aspirating into and out of wells. Automated plate washers may need to be calibrated so tips don’t touch bottom of wells. Plate read at incorrect wavelength Make sure to use recommended wavelength/filter.
Too much signal in ELISA
Possible Cause Solution Insufficient washing Use appropriate washing procedure—see below. At the end of each washing step, invert plate on absorbent tissue and allow to completely drain, tapping forcefully if necessary to remove any residual fluid. Plate sealers not used or reused During incubations, cover assay plates with plate sealers. Use a fresh sealer each time the plate is opened. This will prevent wells from contaminating each other. Incorrect dilutions prepared Check pipetting technique—see below—and double-check calculations. Longer incubation times thanrecommended Make sure to follow recommended incubation times.
Problem: High background in ELISA
Possible Cause Solution Insufficient washing Use appropriate washing procedure—see below. Increasing duration of soak steps may also help. Add 30 seconds each time you let wash buffer soak. At the end of each washing step, invert plate on absorbent tissue and allow to completely drain, tapping forcefully if necessary to remove any residual fluid. Substrateexposed to light prior to use Ensure substrate isnot exposed to light—store in a dark place. Limit exposure to light whilerunning assay. The yellowingof the whole plate may be caused by wrong addition of other reagents Check the componentsand lot numbers of the reagents before the experiment, and confirm that allcomponents belong to the corresponding kit. Reagents from differentkits or different lot numbers cannot be mixed. Streptavidin-HRP contaminates the tip and TMB container orpositive control contaminates the Pre-coated Microplate When absorbingdifferent reagents, the tips should be replaced. When configuring differentreagent components, different storage vessels should be used. Please use apipette during operation. BiotinylatedAntibody or Streptavidin-HRP concentration too high Checkwhether the concentration calculation is correct or use after furtherdilution. Color development time is too long Pleasestrictly follow the steps of the manual. Longerincubation times than recommended Make sure to followrecommended incubation times. Incorrectstandard curve dilutions prepared Check pipettingtechnique—see below—and double-check calculations. The wrongfilter was used when the absorbance value was read When TMB is used asthe substrate, the absorbance should be read at 450 nm.
Problem: High background in ELISA
Possible Cause Solution Incorrect standard curve dilutions prepared Check pipetting technique—see below—and double-check calculations. Capture antibody didn’t bind to plate Ensure that you are using an ELISA plate, not a tissue culture plate. Dilute antibody in PBS. Ensure correct preparation and incubation time for both coating and blocking steps.
Problem: Poor replicate data in ELISA
Possible Cause Solution Insufficient washing Use appropriate washing procedure—see below. Increasing duration of soak steps may also help. Add 30 seconds each time you let wash buffer soak. At the end of each washing step, invert plate on absorbent tissue and allow to completely drain, tapping forcefully if necessary to remove any residual fluid. Capture antibody didn’t bind to plate Ensure that you are using an ELISA plate, not a tissue culture plate. Dilute antibody in PBS. Ensure correct preparation and incubation time for both coating and blocking steps.
Problem: Inconsistent results assay-to-assay in ELISA
Possible Cause Solution Plate sealers not used or reused During incubations, cover assay plates with plate sealers. Use a fresh sealer each time the plate is opened. This will prevent wells from contaminating each other. Incorrect dilutions prepared Check pipetting technique—see below—and double-check calculations.
Product Information
SKU:EK731818Category: Elisa Kits
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] | 2024-07-29T22:27:06+00:00 | Marine Torpedo Bombing Squadron 151 (VMTB-151) was a dive bombing squadron in the United States Marine Corps. The squadron fought in World War II but was quickly deactivated after the war on March 20, 1946. Marine Observation Squadron 1 (VMO-1) was commissioned on July 1, 1937 at Marine Corps... | en | /skins-ucp/mw139/common/favicon.ico | Military Wiki | https://military-history.fandom.com/wiki/VMTB-151 | Marine Torpedo Bombing Squadron 151
VMSB-151 Insignia
Active July 1, 1937 – March 20, 1946Country United StatesBranch USMCType Fighter squadronRole Dive bombingPart of InactiveEngagements World War IIAircraft flownBomber Curtiss SBC Helldiver
Douglas SBD Dauntless
Curtiss SB2C Helldiver
Marine Torpedo Bombing Squadron 151 (VMTB-151) was a dive bombing squadron in the United States Marine Corps. The squadron fought in World War II but was quickly deactivated after the war on March 20, 1946.
History[]
Marine Observation Squadron 1 (VMO-1) was commissioned on July 1, 1937 at Marine Corps Base Quantico.[1] They were redesignated Marine Observation Squadron 151 (VMO-151) on July 1, 1941. The squadron left for San Diego, California in December 1941 with the rest of the 1st Marine Aircraft Wing, but returned to MCB Quantico in January 1942. From January to April, they trained at Naval Station Norfolk until departing for Tafuna Airfield in American Samoa on April 9, 1942. They arrived a month later and remained for the next 13 months. On September 15, 1942, the squadron was re-designated again, this time as Marine Scout Bombing Squadron 151 (VMSB-151).[2]
On June 10, 1943, the squadron moved to Uvea Island in the Wallis Group. The squadron remained there until February 29, 1944 when they arrived at Engebi.[2] From March 9–12, the squadron covered Marine landings on Wotho Atoll, Ujae Atoll and Lae Atoll. During this time, they also made bombing runs against by-passed Japanese bases in the Marshall Islands until May 31, 1945. On June 9, 1945, the squadron returned to the United States.
Upon return to Marine Corps Air Station Mojave, they were assigned to Marine Air Support Group 51 and were redesignated Marine Torpedo Bombing Squadron 151 (VMTB-151).[3] on June 30, 1945. The squadron was deactivated at Marine Corps Air Station Santa Barbara, California on March 20, 1946.[4]
See also[]
United States Marine Corps Aviation
List of inactive United States Marine Corps aircraft squadrons
List of United States Marine Corps aircraft squadrons
References[]
Notes
Bibliography | ||
5682 | dbpedia | 1 | 17 | https://military-history.fandom.com/wiki/List_of_inactive_United_States_Marine_Corps_aircraft_squadrons | en | List of inactive United States Marine Corps aircraft squadrons | https://static.wikia.nocookie.net/ucp-internal-test-starter-commons/images/a/aa/FandomFireLogo.png/revision/latest?cb=20210713142711 | https://static.wikia.nocookie.net/ucp-internal-test-starter-commons/images/a/aa/FandomFireLogo.png/revision/latest?cb=20210713142711 | [
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] | 2024-08-14T13:00:00+00:00 | While other nations have Marines who are aviators, only the United States Marine Corps has its own dedicated aviation arm.[1] Most squadrons have changed names and designations many times over the years so they are listed by their final designation. The basic tactical and administrative unit of... | en | /skins-ucp/mw139/common/favicon.ico | Military Wiki | https://military-history.fandom.com/wiki/List_of_inactive_United_States_Marine_Corps_aircraft_squadrons | While other nations have Marines who are aviators, only the United States Marine Corps has its own dedicated aviation arm.[1] Most squadrons have changed names and designations many times over the years so they are listed by their final designation.
Squadron designations[]
The basic tactical and administrative unit of United States Marine Corps aviation is the squadron. Fixed-wing aircraft squadrons (heavier than air) are denoted by the letter "V," which comes from the French verb "Voler" (to fly). Rotary wing (helicopter) squadrons use "H." Marine squadrons are always noted by the second letter "M." Squadron numbering is not linear as some were numbered in ascending order and others took numbers from the wing or the ship to which they were assigned. From 1920 to 1941, Marine flying squadrons were identified by one digit numbers. This changed on July 1, 1941 when all existing squadrons were redesignated to a three-digit system. The first two numbers were supposed to identify the squadrons parent group but with the rapid expansion during the war and frequent transfer of squadrons this system fell apart.[2]
Inactive squadrons[]
Squadrons are listed by their designation at the time they were decommissioned.
Pre–World War II squadrons[]
Following World War I, Marine aviation was significantly reduced. Many of the squadrons were renamed and redesignated numerous times and many still exist today with other designations. The squadrons listed below reflect those squadrons that were deactivated prior to World War II and were never reconstituted in any form.
Squadron Name Insignia Nickname Date Inactivated VP-3M
Marine Patrol Squadron 3 1931[3] VO-6M
Marine Observation Squadron 6
Hell Divers 1932[3] VO-10M
Marine Observation Squadron 10
April 1, 1931[3] VS-14M
Marine Scouting Squadron 14 July 1, 1933[3] VS-15M
Marine Scouting Squadron 15 July 1, 1933[3] ZK-1M
1st Marine Barrage Balloon Squadron December 1929[4]
Marine Reserve Scouting Squadrons[]
The Marine Aviation Reserve was inactive from 1918 through 1928.[5] When reconstituted the names and aircraft used by these squadrons changed frequently but their home duty stations remained constant. The aircraft for these squadrons were assigned to the reserve bases themselves and were shared with co-located Navy Reserve squadrons.[6] The squadrons were absorbed into the 1st and 2nd Marine Aircraft Wings and their identities lost when they were mobilized in December 1940.[3]
Squadron Name Insignia Nickname Location Date Inactivated VMS-1R Boston, Massachusetts December 1940[6] VMS-2R Brooklyn, New York December 1940[6] VMS-3R Anacostia, D.C. December 1940[6] VMS-4R Miami, Florida December 1940[6] VMS-5R Black Knights Grosse Ile, Michigan December 1940[7] VMS-6R Minneapolis, Minnesota December 1940[6] VMS-7R Long Beach, California December 1940[6] VMS-8R Oakland, California December 1940[6] VMS-9R Seattle, Washington December 1940[6] VMS-10R Kansas City, Kansas December 1940[6] VMS-11R Brooklyn, New York December 1940[6]
Marine Barrage Balloon Squadrons[]
Squadrons flying lighter than air vehicles (balloons), were indicated by the letter Z in naval squadron designation.[8] The first use of balloons by the Marine Corps was during World War I when they were used for artillery spotting.[9] After the outbreak of World War II, the Navy authorized the Marine Corps to create barrage balloon squadrons for the air defense of advanced naval bases.[10] Balloon training was cancelled in the summer of 1943 and the remaining units were deactivated by the end of the year.[11]
Squadron Name Insignia Nickname Date Inactivated ZMQ-1 December 15, 1943 ZMQ-2 August 21, 1942 ZMQ-3 December 9, 1943[12] ZMQ-4 February 20, 1943[13] ZMQ-5 December 5, 1943[13] ZMQ-6 December 8, 1943[13]
Marine Scout Bombing Squadrons[]
Scout bombing squadrons each had eighteen to twenty-four SBD Dauntless dive bombers and were tasked with conducting dive-bombing attacks and long range scouting and patrol missions. They also provided close air support, laid smoke screens and sprayed DDT around bases.[14] The majority of these squadrons were quickly deactivated following the end of World War II although three entered the Marine Air Reserve for a short period.
Marine Torpedo Bombing Squadrons[]
VMTBs were torpedo bomber squadrons that operated the TBF Avenger. They were in service with the Marine Corps during World War II and were deactivated shortly after the war. They were part of the Cactus Air Force on Guadalcanal, served on escort carriers during the campaign to retake the Philippines and provided close air support for Australian forces on Borneo and Marines during the Battle of Okinawa.[26]
Squadron Name Insignia Nickname Date Inactivated VMTB-151 Ali Baba March 20, 1946[27] VMTB-341 Torrid Turtles September 13, 1945[28] VMTB-454 Helldivers January 28, 1946[29] VMTB-621 March 10, 1945[29] VMTB-622 January 31, 1946[29] VMTB-623 March 20, 1946[29] VMTB-624 March 10, 1946[29]
Marine Fighting Squadrons[]
Marine Fighting Squadrons were multirole squadrons responsible for air-to-air combat, combat air patrols, attacking enemy shipping, escorting bombers and close air support.[30] By far the most numerous of any type of Marine Corps squadron, they first made their mark flying the F4F Wildcat as part of the Cactus Air Force on Guadalcanal and finished World War II flying the venerable F4U Corsair. Many VMF squadrons continued to operate after the war with most in the Marine Air Reserve; however, with the retirement of the F-8 Crusader the VMF squadrons either became VMFAs or were deactivated.
Marine Night Fighter Squadrons[]
After witnessing the Royal Air Force's success using radar directed fighters at night in 1941,[9] the Navy's Bureau of Aeronautics authorized eight Marine night fighter squadrons to be formed by 1945.[54] This timeline was brought forward considerably after the attack on Pearl Harbor and their need proven by the frustration of the Cactus Air Force's pilots not being able to engage Japanese bombers at night during the Battle of Guadalcanal. This led to the formation of the first VMF(N) in November 1942. After much deliberation the PV-1 Ventura was picked as the first choice of aircraft for these squadrons. The night fighting squadrons featured radar equipped aircraft, ground based radar and personnel that provided Ground-controlled interception (GCI). The VMF(N) designated squadrons were deactivated after the war as the night fighting mission was assumed by the fighter and attack communities.[55]
Squadron Name Insignia Nickname Date Inactivated VMF(N)-532 Night Fighters May 31, 1947[56] VMF(N)-534 May 31, 1947[56] VMF(N)-544 April 20, 1946[56]
Marine Bombing Squadrons[]
The Marine Bombing Squadrons were formed during World War II to fill the need for a long range, land based bomber that could be used against enemy shipping and submarines. In the Pacific Theater, the squadrons served ashore as a garrison air force to attack bypassed Japanese bases and other installations. The VMBs flew the PBJ-1, which was the naval version of the B-25 Mitchell. Sixteen of these squadrons were commissioned with seven serving in combat, four never able to leave the U.S. due to the war ending and four others converted to VMTB squadrons.[57] The seven PBJ squadrons that saw combat in the Pacific suffered the loss of 45 aircraft, 26 in combat and 19 in non-combat operations, and 173 crew, 62 officers and 111 enlisted men.[58]
Squadron Name Insignia Nickname Date Inactivated VMB-423 File:VMB-423insignia.jpg Seahorses November 30, 1945[59][60] VMB-433 Fork-Tailed Devils November 30, 1945[61] VMB-443 File:VMB-443 Insignia.jpg Wildcats November 30, 1945[62] VMB-453 March 20, 1946[57] VMB-473 March 20, 1946[57] VMB-483 March 15, 1945[57] VMB-611 File:Official VMB-611 Insignia.jpg Black Seahorse November 30, 1945[63] VMB-612 File:Vmb-612 Insignia.jpg Cram's Rams March 15, 1946[64] VMB-613 File:VMB-613 Insignia.PNG November 21, 1945[57] VMB-614 Ruptured Ducks December 28, 1945
Marine Operational Training Squadrons[]
All of these squadrons were activated at Marine Corps Air Station Cherry Point, North Carolina in February 1945 as medium bomber pilot training units. They instructed Marines learning to fly the PBJ-1. Following the end of the war they were quickly deactivated.[65]
Squadron Name Insignia Nickname Date Inactivated MOTS-811 September 10, 1945[66] MOTS-812 September 10, 1945[66] MOTS-813 November 1945[66] MOTS-814 November 1945[66]
Marine Photographic Squadrons[]
Marine photographic squadrons were first formed in 1942 and went through numerous name changes while they were active. VMDs/VMPs flew photographic modified versions of the SBD Dauntless, PB4Y-1 Liberator, PB4Y-2 Privateer and F7F Tigercat. The main mission of these squadrons was to conduct long range, very high-altitude photographic reconnaissance.[67]
Squadron Name Insignia Nickname Date Inactivated VMD-154 Pathfinders September 10, 1945[68] VMP-254 November 30, 1949[69] VMP-354 December 8, 1949[70] VMD-954 January 31, 1946[25]
Marine Glider Squadron[]
The Marine Corps established a glider program in April 1942. Eventually they set goals of having 10,800 Marines qualified as glider infantry, with 1,371 gliders and 3,436 pilots.[71] They originally operated from Page Field on MCRD Parris Island but later moved to Marine Corps Air Station Eagle Mountain Lake outside Dallas, Texas.[72] The program was disbanded in 1943 when it was determined that glider assaults into small, heavily fortified, jungle islands would be tactically unfeasible.[73]
Squadron Name Insignia Nickname Date Inactivated VML-711 May 24, 1943
Marine Transport Squadrons[]
Flying the R4D and the R5C-1, these squadrons were responsible for movings troops and cargo,aerial resupply, delivery of Paramarines and medical evacuation.The last of these squadrons was deactivated in 1949.[74]
Squadron Name Insignia Nickname Date Inactivated VMR-152 1950s[75] VMR-153 1949[75] VMR-353 February 15, 1946[76] VMR-952 May 31, 1947[77] VMR-953 Puss in Boots May 31, 1947[78]
Marine Scouting Squadrons[]
There were three Marine Scouting Squadrons prior to World War II; however, VMS-3 was the only squadron to retain the designation. The squadron served in Haiti from 1919 through 1934 and then spent its last ten years at St. Thomas, Virgin Islands. During World War II they were the only Marine Corps squadron to operate east of the United States. They began the war flying the Grumman J2F Duck, transitioned to the OS2N Kingfisher and at the time of deactivation were flying SBD Dauntless dive bombers.[67]
Squadron Name Insignia Nickname Date Inactivated VMS-3 Devilbirds May 20, 1944[79]
Marine Target Towing Detachments[]
Marine Target Towing detachments were first formed at Marine Corps Air Station Ewa in October 1944. They were responsible for towing targets for antiaircraft gunnery and radar tracking practice. They flew JM-1 Marauders and the R5C-1 Commandos. The last of these detachments was deactivated in March 1946.[74]
Squadron Name Insignia Nickname Date Inactivated VMJ-1 October, 1945 VMJ-2 March 6, 1946[80] VMJ-3 Red Asses October 21, 1945[79]
Marine Observation Squadrons[]
The Marine observation squadrons were formed during the latter stages of World War II with the primary mission of forward air control of strike aircraft for close air support and air interdiction.[81] They saw extensive service during the Vietnam War flying the OV-10 Bronco. The Marine Corps began decommissioning the VMO squadrons following their participation in Operation Desert Storm as propeller driven aircraft were seen as too dangerous to fly on the modern battlefield. Their mission has been assumed by the VMFA(AW) squadrons.
Squadron Name Insignia Nickname Date Inactivated VMO-1 July 31, 1993 VMO-2 Cherry Deuce May 20, 1993 VMO-4 Evil Eyes March 31, 1994 VMO-6 Tomcats January 1, 1976[82][83] VMO-7 November 16, 1945 VMO-8 July 1976
Marine Attack Squadrons[]
In 1951, the Marine Corps began fielding the AD-1 Skyraider ground attack aircraft which had as its main role close air support for the Marines on the ground. Thus many squadrons had their designation changed from VMF to VMA to reflect this ground attack role. 13 squadrons were equipped with the Skyraider until they were finally phased out in 1958.[84] Follow on VMA squadrons operated the A-4 Skyhawk during the Vietnam War through their retirement just after Operation Desert Storm. The VMA tradition is carried on today by squadrons flying the AV-8B Harrier II.
Squadron Name Insignia Nickname Date Inactivated VMA-124 Whistling Death 1996 VMA-131 Diamondbacks December 5, 1998[85] VMA-133 Dragons 1992 VMA-143 Rocket Raiders VMA-144 Hensagliska VMA-217 Max’s Wild Hares 1964 VMA-233 Flying Deadheads 1969 VMA-241 Sons of Satan VMA-322 Fighting Gamecocks June 27, 1992[86] VMA-324 Devildogs 29 August 1974[87] VMA-331 Bumblebeess October 1, 1992 VMA-543 Night Hawks April 1, 1974
Marine Reconnaissance Squadron[]
Marine Reconnaissance Squadron 4 was the only reserve photographic reconnaissance squadron in the Marine Corps. Initially based in Naval Air Station New Orleans, Louisiana they moved to Naval Air Station Olathe, Kansas May 1, 1967 and then again to Naval Air Station Dallas, Texas in 1970 when the reserves where reorganized. They flew RF-8A until 1969 when all the planes where replaced with the RF-8G.[47]
Squadron Name Insignia Nickname Date Inactivated VMJ-4 1973
Marine Composite Reconnaissance Squadrons[]
Following the Korean War Marine Composite Squadron 1 (VMC-1) and Marine Photographic Squadron 1 (VMJ-1) were combined to form VMCJ-1. The new squadron was responsible for both Photoreconnaissance and Electronic Warfare. In its early years it flew the RF-8A Crusader and EF-10B Skyknight but these were later replaced by the RF-4B Phantom II and the EA-6A Electric Intruder. The squadron was deactivated following the end of the Vietnam War and the reorganization of the Marine Corps' composite community in 1975.[88]
Squadron Name Insignia Nickname Date Inactivated VMCJ-1 Golden Hawks September 1975
Marine Tactical Reconnaissance Squadron[]
Upon the decommissioning of the Marine Composite Squadrons (VMCJs), VMFP-3 became the lone photographic reconnaissance squadron in the Marine Corps.[89] They flew the RF-4B Phantom II and operated from 1975 until being decommissioned in 1990. Their capability has since been replaced by various targeting pods used on Marine aircraft and the Advanced Tactical Airborne Reconnaissance System which is found in some of the F/A-18 Hornet squadrons.[90]
Squadron Name Insignia Nickname Date Inactivated VMFP-3 Eyes of the Corps September 3, 1990
Marine Fighter Attack Squadrons[]
The first Marine Corps squadron to be redesignated a VMFA was in June 1962 upon receipt of the first F-4 Phantom II aircraft. VMF and VMA squadrons were redesignated because the new Phantoms could be both fighter aircraft and ground attack aircraft.[91] These squadrons were heavily deployed during the Vietnam War. Most of these squadrons would eventually convert to the F/A-18 Hornet with the last F-4 Phantom leaving service in 1992.[92] The end of the Cold War saw the deactivation of some VMFA squadrons as part of the overall drawdown of the US Military[93]
Squadron Name Insignia Nickname Date Inactivated VMFA-134 Smoke April 1, 2007[94] VMFA-142 Gators July 2008[95] VMFA-212 Lancers March 11, 2008[96] VMFA-235 Death Angels June 14, 1996[97] VMFA-321 Hells Angels September 30, 2004[98] VMFA-333 File:Vmfa-333 patch.jpg Fighting Shamrocks March 31, 1992[99] VMFA-334 Falcons December 30, 1971[47] VMFA-351 1978[100] VMFA-531 Grey Ghosts April 27, 1992[101]
Marine All-Weather Fighter Attack Squadron[]
Squadron Name Insignia Nickname Date Inactivated VMFA(AW)-332 Moonlighters March 30, 2007[102]
Marine Heavy Helicopter Squadrons[]
Squadron Name Insignia Nickname Date Inactivated HMH-769 Titan August 2, 2008 HMH-777 Flying Armadillos 1980[103]
Marine Medium Helicopter Squadrons[]
The original Marine Medium Helicopter squadrons flew the UH-34D Sea Horse, which shortly after its inception saw extensive combat during the Vietnam War.[104] Beginning in 1966 they began to be replaced with the CH-46 Sea Knight which was faster, could carry more troops and is still in service today.[105] The decommissioned HMM squadrons reflect the UH-34D training squadron and various reserve squadrons.
Squadron Name Insignia Nickname Date Inactivated HMM-761 August 31, 1962 HMM-762 December 31, 1962[103] HMM-763 September 30, 1962 HMM-766 Beavers October 1, 1976 HMM-768 1976
Marine Light Helicopter Squadrons[]
Squadron Name Insignia Nickname Date Inactivated HML-765 June 30, 1976 HML-767 Nomads August 1, 1994 HML-770 1980/81 HML-771 Hummers August 1, 1994[106] HML-776 Gangsters July 1, 1994
Marine Light Attack Helicopter Squadrons[]
The Marine Corps’ light attack squadrons (HMLAs) are composite squadrons usually made up of 12 AH-1W Cobras and 6 UH-1N Hueys. The primary missions of the Cobra is close air support, forward air control, reconnaissance and armed escort,[107] while the Huey provided airborne command and control, utility support, supporting arms coordination and medical evacuation. These squadrons were first formed during the Vietnam War with the fielding of the AH-1 Cobra gunship and its being combined in the same squadron with the UH-1H Iroquois that initially belonged to the Marine Corps' VMO squadrons. The majority of these squadrons are still active today in the Opearting Forces today[108]
Squadron Name Insignia Nickname Date Inactivated HMLA-775 Coyotes September 6, 2008
Training squadrons[]
Squadron Name Insignia Nickname Date Inactivated VMAT-20
Marine Attack Training Squadron [109] VMAT-102
Marine Attack Training Squadron Skyhawks VMT-103
Marine Training Squadron Sky Chickens VMFAT-201
Marine Fighter Attack Training Squadron Hawks September 30, 1974[110] VMAT(AW)-202
Marine All-Weather Attack Training Squadron Double Eagles 1990[111] VMGRT-253
Marine Aerial Refueler Transport Training Squadron Titans September 14, 2006[112] HMT-301
Marine Helicopter Training Squadron
Windwalkers June 3, 2005[113] HMHT-401
Marine Heavy Helicopter Training Squadron May 1, 1972 HMMT-402
Marine Medium Helicopter Training Squadron May 1, 1972
See also[]
United States Marine Corps Aviation
List of United States Marine Corps battalions
List of United States Marine Corps aircraft wings
List of active United States Marine Corps aircraft squadrons
Notes[]
References[]
Bibliography | ||
5682 | dbpedia | 1 | 2 | https://militarygraphics.com/product/vmo-1-marine-observation-squadron-1-decal/ | en | 1 Marine Observation Squadron 1 Decal | [
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] | null | [] | 2023-07-03T16:17:25+00:00 | Text showing: Can Do | en | https://militarygraphics.com/wp-content/themes/military/images/favicon.ico | Military Graphics | https://militarygraphics.com/product/vmo-1-marine-observation-squadron-1-decal/ | This VMO-1 Marine Observation Squadron 1 Decal is a premium vinyl decal which is die cut and was hand drawn in great detail by Military Graphics' professional artists to look beautiful at any size. We use the highest quality vinyls and inks, so the VMO-1 Marine Observation Squadron 1 Decal is UV and water resistant and will last for many years.
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VMO1 INFORMATION Proteini
Full gene name according to HGNC.
Vitelline membrane outer layer 1 homolog Gene namei
Official gene symbol, which is typically a short form of the gene name, according to HGNC.
VMO1 Protein classi
Assigned HPA protein class(es) for the encoded protein(s).
Protein evidence Evidence at protein level (all genes) Number of transcriptsi
Number of protein-coding transcripts from the gene as defined by Ensembl.
4 Protein interactions No protein interactions
TISSUE RNA EXPRESSION Tissue specificityi
The RNA specificity category is based on normalized mRNA expression levels in the consensus dataset, calculated from the RNA expression levels in samples from HPA and GTEX. The categories include: tissue enriched, group enriched, tissue enhanced, low tissue specificity and not detected.
Tissue enhanced (lymphoid tissue, pituitary gland) Tissue expression clusteri
The RNA data was used to cluster genes according to their expression across tissues. Clusters contain genes that have similar expression patterns, and each cluster has been manually annotated to describe common features in terms of function and specificity.
Spleen - Immune response (mainly) Brain specificityi
The regional specificity category is based on mRNA expression levels in the analysed brain samples, grouped into 13 main brain regions and calculated for the three different species. All brain expression profiles are based on data from HPA. The specificity categories include: regionally enriched, group enriched, regionally enhanced, low regional specificity and not detected. The classification rules are the same used for the tissue specificity category
Low human brain regional specificity Brain expression clusteri
The RNA data was used to cluster genes according to their expression across tissues. Clusters contain genes that have similar expression patterns, and each cluster has been manually annotated to describe common features in terms of function and specificity.
Macrophages & Microglia - Immune response (mainly) Single cell type specificityi
The RNA specificity category is based on mRNA expression levels in the analyzed cell types based on scRNA-seq data from normal tissues. The categories include: cell type enriched, group enriched, cell type enhanced, low cell type specificity and not detected.
Cell type enhanced (Ionocytes, Club cells, monocytes, Basal respiratory cells, Langerhans cells) Single cell type
expression clusteri
The RNA data was used to cluster genes according to their expression across single cell types. Clusters contain genes that have similar expression patterns, and each cluster has been manually annotated to describe common features in terms of function and specificity.
Respiratory epithelial cells - Unknown function (mainly) Tissue cell type classificationi
Genes can have enriched specificity in different cell types in one or several tissues, or be enriched in a core cell type that appears in many different tissues.
Cell type enriched (Stomach - Fibroblasts)
IMMUNE CELLS Immune cell specificityi
The RNA specificity category is based on mRNA expression levels in the analyzed samples based on data from HPA. The categories include: cell type enriched, group enriched, cell type enhanced, low cell type specificity and not detected.
Immune cell enriched (non-classical monocyte) Immune cell
expression clusteri
The RNA data was used to cluster genes according to their expression across single cell types. Clusters contain genes that have similar expression patterns, and each cluster has been manually annotated to describe common features in terms of function and specificity.
Monocytes & Neutrophils - Innate immune response (mainly)
CANCER & CELL LINES Prognostic summary Prognostic marker in renal cancer (unfavorable) Renal cancer p<0.001 Cancer specificityi
Specificity of RNA expression in 17 cancer types is categorized as either cancer enriched, group enriched, cancer enhanced, low cancer specificity and not detected.
Low cancer specificity Cell line
expression clusteri
The RNA data was used to cluster genes according to their expression across cell lines. Clusters contain genes that have similar expression patterns, and each cluster has been manually annotated to describe common features in terms of function and specificity.
Sarcoma - Muscle contraction (mainly) Cell line specificityi
RNA specificity category based on RNA sequencing data from cancer cell lines in the Human Protein Atlas grouped according to type of cancer. Genes are classified into six different categories (enriched, group enriched, enhanced, low specificity and not detected) according to their RNA expression levels across the panel of cell lines.
Cancer enhanced (Bone cancer)
PROTEINS IN BLOOD Upregulated in diseasei
A gene is classified as upregulated in a disease if the average concentration of all samples of that disease is significantly higher (adj P-value<0.05) than the average concentration of samples of all diseases as measured by PEA . For gender specific diseases the analysis includes only samples corresponding to the same gender from the other diseases.
Myeloma, Acute myeloid leukemia Disease prediction modeli
The disease(s) the gene is associated with and able to predict according to glmnet prediction models. To be included the gene has to be upregulated according to differential expression analysis and have more than 50% overall importance as indicated by the prediction models.
No Secretome annotationi
All genes with at least one predicted secreted isoform have been annotated and classified with the aim to determine if the corresponding protein(s) are:
secreted into blood
locally secreted
or actually being attached to membrane or retained in intracellular locations like mitochondria, endoplasmatic reticulum (ER), Golgi apparatus or lysosomes.
Secreted to blood Detected in blood by
immunoassayi
The blood-based immunoassay category applies to actively secreted proteins and is based on plasma or serum protein concentrations established with enzyme-linked immunosorbent assays, compiled from a literature search. The categories include: detected and not detected, where detection refers to a concentration found in the literature search.
No Detected in blood by
mass spectrometryi
Detection or not of the gene in blood, based on spectral count estimations from a publicly available mass spectrometry-based plasma proteomics data set obtained from the PeptideAtlas.
Yes Detected in blood by
proximity extension assayi
Detection or not of the gene in blood, based on proximity extension assays (Olink) for a longitudinal wellness study covering 76 individuals with three visits during two years.
Yes | ||||||
5682 | dbpedia | 2 | 8 | https://popularpatch.com/vmo-1-us-marine-corps-observation-squadron-patch-can-do-eagle/ | en | VMO-1 US Marine Corps Observation Squadron Patch Can Do Eagle | [
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] | null | [] | null | VMO-1 US Marine Corps Observation Squadron One Military Patch CAN DO EAGLE | en | https://cdn11.bigcommerce.com/s-b3eudul5m7/product_images/favicon.ico?t=1547595107 | Popular Patch | https://popularpatch.com/vmo-1-us-marine-corps-observation-squadron-patch-can-do-eagle/ | VMO-2 US Marine Corps Observation Squadron Patch Devil
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5682 | dbpedia | 1 | 3 | https://en.wikipedia.org/wiki/List_of_active_United_States_Marine_Corps_aircraft_squadrons | en | List of active United States Marine Corps aircraft squadrons | https://en.wikipedia.org/static/favicon/wikipedia.ico | https://en.wikipedia.org/static/favicon/wikipedia.ico | [
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] | 2004-02-16T16:05:56+00:00 | en | /static/apple-touch/wikipedia.png | https://en.wikipedia.org/wiki/List_of_active_United_States_Marine_Corps_aircraft_squadrons | This is a list of all of the active squadrons that exist in the United States Marine Corps, sorted by type. Most squadrons have changed names and designations many times over the years, so they are listed by their current designation.
To see Marine Aviation units sorted by command hierarchy, see aviation combat element.
Squadron designations
[edit]
The basic tactical and administrative unit of United States Marine Corps aviation is the squadron. Fixed-wing aircraft squadrons (heavier than air) and tiltrotor squadrons are denoted by the letter "V", which comes from the Spanish verb "volar" (to fly). Rotary wing (helicopter) squadrons use "H." Marine squadrons are always noted by the second letter "M." Squadron numbering is not linear as some were numbered in ascending order and others took numbers from the wing or the ship to which they were assigned. From 1920 to 1941, Marine flying squadrons were identified by one digit numbers. This changed on 1 July 1941, when all existing squadrons were redesignated to a three-digit system. The first two numbers were supposed to identify the squadrons parent group but with the rapid expansion during World War II and frequent transfer of squadrons this system fell apart.[1]
Rotary-wing aircraft
[edit]
Marine Helicopter Squadron
[edit]
The squadron is responsible for the helicopter transportation of the president of the United States, vice president, Cabinet members and VIPs. In addition to its VIP transport role, it is also tasked with operational test and evaluation (OT&E) of new flight systems for Marine Corps helicopters.[2] The squadron flies the VH-3D Sea King the VH-60N Whitehawk, and the MV-22 Osprey. These were due to be replaced by the VH-71 Kestrel,[3] however that program was cancelled in April 2009.[4] HMX-1 is now preparing for the arrival of the VH-92A Patriot, which will replace the VH-3D that serves as Marine One. Lastly, HMX-1 provides support to training at The Basic School, providing aerial insertion for various training events, as well as MAGTF Air component orientation to the student officers.
Squadron Name Insignia Nickname Date Commissioned Senior Command Station HMX-1 Marine One 1 December 1947 Headquarters Marine Corps MCAF Quantico, VA[5]
Marine Heavy Helicopter Squadrons
[edit]
Heavy helicopter squadrons were first formed in 1966 when the Marine Corps began flying the heavy lift CH-53 Sea Stallion during the Vietnam War.[6] Each squadron is equipped with sixteen CH-53E Super Stallion helicopters. Their primary role is moving cargo and equipment with the secondary role of transferring troops ashore in an amphibious assault. The CH-53Es are the most powerful helicopter in the U.S. military inventory today.[7] As part of the current reorganization of the Corps, HMH-462 will be decommissioned by 2030.[8]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station HMH-361 Flying Tigers 25 February 1952 MAG-16, 3rd MAW MCAS Miramar, CA[9] HMH-461 Iron Horse 15 March 1944 MAG-29, 2nd MAW MCAS New River, NC[10] HMH-462 Heavy Haulers 15 April 1944 MAG-16, 3rd MAW MCAS Miramar, CA[11] HMH-464 Condors 5 April 1944 MAG-29, 2nd MAW MCAS New River, NC[12] HMH-465 Warhorse 1 December 1981 MAG-16, 3rd MAW MCAS Miramar, CA[13] HMH-466 Wolfpack 30 November 1984 MAG-16, 3rd MAW MCAS Miramar, CA[14] HMH-772 Hustler 15 April 1958 MAG-49, 4th MAW McGuire Air Force Base, NJ[15]
Marine Heavy Helicopter Training Squadron
[edit]
The squadron trains newly designated (i.e., winged) Naval Aviators, conversion pilots, refresher pilots, and enlisted aircrew on the CH-53E Super Stallion.[16]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station HMHT-302 Phoenix 1 November 1966 MAG-29, 2nd MAW MCAS New River, NC[16]
Marine Light Attack Helicopter Squadrons
[edit]
The Marine Corps’ light attack squadrons are composite squadrons made up of 18 AH-1Z Vipers and 9 UH-1Y Venoms.[17] The primary missions of the Viper is close air support, forward air control, reconnaissance and armed escort,[18] while the Huey provides airborne command and control, utility support, supporting arms coordination and medical evacuation.[19] The H-1 upgrade program will see both the AH-1 and UH-1 get greater power, improved avionics and an 85% commonality of parts.[20][21][22] The transition to the UH-1Y was completed in August 2014 when HMLA-773 flew the UH-1N for the last time. Due to the need for more light attack squadrons, the Marine Corps began adding new squadrons in 2008. HMLA-469 is the newest squadron. However, as part of the re-organization of the corps, HMLA-469 and HMLA-367 will be de-activated by 2030.[23]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station HMLA-167 Warriors 1 April 1968 MAG-29, 2nd MAW MCAS New River, NC[24] HMLA-169 Vipers 30 September 1971 MAG-39, 3rd MAW MCAS Camp Pendleton, CA[25] HMLA-267 Stingers 15 February 1944 MAG-39, 3rd MAW MCAS Camp Pendleton, CA[26] HMLA-269 The Gunrunners 22 February 1977 MAG-29, 2nd MAW MCAS New River, NC[27] HMLA-367 Scarface 1 December 1943 MAG-39, 3rd MAW MCAS Camp Pendleton, CA[28] HMLA-369 Gunfighters 1 April 1972 MAG-39, 3rd MAW MCAS Camp Pendleton, CA[29] HMLA-773 Red Dog June 1968 MAG-49, 4th MAW Joint Base McGuire–Dix–Lakehurst, NJ[30] HMLA-775 Coyote 1 October 2016 MAG-41, 4th MAW MCAS Camp Pendleton, CA[31]
Marine Light Attack Helicopter Training Squadron
[edit]
The squadron trains newly designated (i.e., winged) Naval Aviators, conversion pilots, refresher pilots, and enlisted aircrew on the UH-1Y Venom, and the AH-1Z Viper.[32]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station HMLAT-303 Atlas 30 April 1982 MAG-39, 3rd MAW MCAS Camp Pendleton, CA[32]
Tiltrotor Aircraft
[edit]
Marine Medium Tiltrotor Squadrons
[edit]
Marine tiltrotor squadrons are new units operating the MV-22 Osprey with their main mission being assault support. The Osprey offers twice the speed, five times the range, and can fly more than twice as high as the helicopters they are replacing.[33] As the Marine Corps’ number one aviation acquisition priority, the Osprey replaced the aging fleet of CH-46 Sea Knight helicopters and is a cornerstone of the capstone concept of Expeditionary maneuver warfare.[34] As of October 2017, the Marine Corps has 16 Fully Operationally Capable (FOC) MV-22 squadrons. VMM-268, VMM-364, and VMM-164 reached FOC in FY16. The two newest Osprey squadrons, VMM-362 and VMM-212, will stand up in FY18 and FY19 respectively, completing the Marine Corps' transition to 18 active component MV-22 squadrons. Each squadron operates 12 aircraft.
Squadron Name Insignia Nickname Date Commissioned Senior Command Station VMM-161 Greyhawks 15 January 1951 MAG-16, 3rd MAW MCAS Miramar, CA[35] VMM-162 Golden Eagles 30 June 1952 MAG-26, 2nd MAW MCAS New River, NC[36] VMM-163 Evil Eyes December 1951 MAG-16, 3rd MAW MCAS Miramar, CA[37] VMM-164 Knightriders 1 July 1962 MAG-39, 3rd MAW MCAS Camp Pendleton, CA VMM-165 White Knights 1 July 1965 MAG-16, 3rd MAW MCAS Miramar, CA[38] VMM-261 Raging Bulls 5 April 1951 MAG-26, 2nd MAW MCAS New River, NC[39] VMM-262 Flying Tigers September 1951 MAG-36, 1st MAW MCAS Futenma, Japan[40] VMM-263 Thunder Chickens 16 June 1952 MAG-26, 2nd MAW MCAS New River, NC[41] VMM-265 Dragons 1 October 1962 MAG-36, 1st MAW MCAS Futenma, Japan[42] VMM-266 Fighting Griffins 26 April 1983 MAG-26, 2nd MAW MCAS New River, NC[43] VMM-268 Red Dragons 26 April 1983 MAG-24, 1st MAW MCB Hawaii, HI[44] VMM-362 Ugly Angels 30 April 1952 MAG-16, 3rd MAW MCAS Miramar, CA[45] VMM-363 Red Lions 2 June 1952 MAG-24, 1st MAW MCB Hawaii, HI[46] VMM-364 Purple Foxes 1 September 1961 MAG-39, 3rd MAW MCAS Camp Pendleton, CA[47] VMM-365 Blue Knights 1 July 1963 MAG-26, 2nd MAW MCAS New River, NC[48] VMM-764 Moonlight 15 April 1958 MAG-41, 4th MAW MCAS Miramar, CA[49] VMM-774 Wild Goose 1969 MAG-49, 4th MAW MCAS New River, NC[50]
Marine Medium Tiltrotor Training Squadron
[edit]
The squadron provides new and conversion training to Marine Corps, Navy, and Air Force pilots and units in the use and maintenance of the Osprey tiltrotor aircraft.[51]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station VMMT-204 Raptors 1 May 1972 2nd MAW MCAS New River, NC
Fixed-Wing Aircraft
[edit]
Marine Attack Squadrons
[edit]
Marine attack squadrons fly the AV-8B Harrier II[52] and are tasked with providing close air support, air interdiction, surveillance and escort of helicopters. Because the STOVL Harrier can operate from amphibious assault ships, expeditionary airfields and tactical remote landing sites, it provides commanders with more flexibility in providing air support.[53] The Harrier is due to be replaced by the F-35B, the STOVL version of the F-35 Lightning II.[54] This transition began in 2016 when VMA-211 exchanged its Harriers for the F-35B and became VMFA-211.
Squadron Name Insignia Nickname Date Commissioned Senior Command Station VMA-223 Bulldogs 1 May 1942 MAG-14, 2nd MAW MCAS Cherry Point, NC[55] VMA-231 Ace of Spades 8 February 1919 MAG-14, 2nd MAW MCAS Cherry Point, NC[56]
Marine Fighter Attack Squadrons
[edit]
The Marine Corps' VMFA squadrons fly the F/A-18 Hornet and F-35 Lightning II. Their primary mission is to attack and destroy surface targets, during both day and nighttime operations, under all weather conditions; conduct multi-sensor imagery reconnaissance; provide supporting arms coordination; and intercept and destroy enemy aircraft in all weather conditions. The current F/A-18s saw first deployments during Operation Desert Storm, after having replaced the A-6 Intruder. Each Hornet squadron operates 12 aircraft and each F-35 squadron operates 10 aircraft.[57][58]
Squadron Name Insignia Nickname Aircraft Date Commissioned Senior Command Station VMFA-112 Cowboys F/A-18C 1 March 1942 MAG-41, 4th MAW NASJRB Fort Worth, TX[59] VMFA-121 Green Knights F-35B 24 June 1941 MAG-12, 1st MAW MCAS Iwakuni, Japan[60] VMFA-122 Flying Leathernecks F-35B 1 March 1942 MAG-13, 3rd MAW MCAS Yuma, AZ[61] VMFA-211 Wake Island Avengers F-35B 1 January 1937 MAG-13, 3rd MAW MCAS Yuma, AZ[62] VMFA-214 Black Sheep F-35B 1 July 1942 MAG-13, 3rd MAW MCAS Yuma, AZ[63] VMFA(AW)-224 Fighting Bengals F/A-18D 1 May 1942 MAG-31, 2nd MAW MCAS Beaufort, SC[64] VMFA-225 Vikings F-35B 1 January 1943 MAG-13, 3rd MAW MCAS Yuma, AZ[65] VMFA-232 Red Devils F/A-18C 1 September 1925 MAG-11, 3rd MAW MCAS Miramar, CA[66] VMFA-242 Bats F-35B 1 July 1943 MAG-12, 1st MAW MCAS Iwakuni, Japan[67] VMFA-311 Tomcats F-35C 1 December 1942 MAG-11, 3rd MAW MCAS Miramar, CA[68] VMFA-312 Checkerboard F/A-18C 1 June 1943 MAG-31, 2nd MAW MCAS Beaufort, SC[69] VMFA-314 Black Knights F-35C 1 October 1943 MAG-11, 3rd MAW MCAS Miramar, CA[70] VMFA-323 Death Rattlers F/A-18C 1 August 1943 MAG-11, 3rd MAW MCAS Miramar, CA[71] VMFA-533 Hawks F-35B 1 October 1943 MAG-31, 2nd MAW MCAS Beaufort, SC[72] VMFA-542 Tigers F-35B 6 March 1944 MAG-14, 2nd MAW MCAS Cherry Point, NC[73]
Marine Fighter Attack Training Squadrons
[edit]
VMFAT squadrons train newly designated Naval Aviators to fly Marine Corps Aircraft.[74][75]
Squadron Name Insignia Nickname Aircraft Date Commissioned Senior Command Station VMFAT-501 Warlords F-35B 15 February 1944 MAG-31, 2nd MAW MCAS Beaufort, SC[76] VMFAT-502 Flying Nightmares F-35B 15 February 1944 MAG-11, 3rd MAW MCAS Miramar, CA
Marine Fighter Training Squadron
[edit]
VMFT-401 is the only aggressor squadron in the Marine Corps. It flies the F-5E Tiger II and provides instruction to active and reserve squadrons through dissimilar adversary combat tactics. The squadron is based at Marine Corps Air Station Yuma, AZ and is assigned to Marine Aircraft Group-41, 4th Marine Aircraft Wing, Marine Forces Reserve.
Squadron Name Insignia Nickname Date Commissioned Senior Command Station VMFT-401 Snipers 18 March 1986 MAG-41, 4th MAW MCAS Yuma, AZ
Marine Aerial Refueler Transport Squadrons
[edit]
VMGR squadrons operate the KC-130 Hercules tanker/transport. Their primary missions are aerial and rapid ground refueling, transportation of personnel and cargo to include MEDEVACs and parachute insertions, flying the airborne version of the Direct Air Support Center (DASC) and emergency resupply into unimproved landing zones.[77][78]
Squadron Name Insignia Nickname Aircraft Date Commissioned Senior Command Station VMGR-152 Sumos KC-130J 11 March 1942 MAG-12, 1st MAW MCAS Iwakuni, Japan[79] VMGR-153 Hercules KC-130J 1 March 1942 MAG-24, 1st MAW MCAS Kaneohe Bay, Hawaii VMGR-234 Rangers KC-130J 1 May 1942 MAG-41, 4th MAW NASJRB Fort Worth, TX[80] VMGR-252 Otis KC-130J 1 June 1928 MAG-14, 2nd MAW MCAS Cherry Point, NC[81] VMGR-352 Raiders KC-130J 1 April 1943 MAG-11, 3rd MAW MCAS Miramar, CA[82]
Marine Transport Squadron
[edit]
VMR squadrons provide search and rescue support as well as movement of key personnel and critical logistics support around the world. They also provide movement of high priority passengers and cargo during wartime in support of operations and other critical commitments.[83]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station VMR-1 Roadrunners January 1943 Marine Aircraft Group 41 Naval Air Station Joint Reserve Base Fort Worth, TX
Marine Operational Test and Evaluation Squadron
[edit]
The squadron is a Marine Corps test and development unit. Its mission is to conduct operational testing and evaluation of Marine Corps fixed, tiltrotor, and rotary-wing aircraft. The unit was re-designated to VMX-1 (from VMX-22) on 13 May 2016.[84]
Squadron Name Insignia Nickname Aircraft Date Commissioned Senior Command Station VMX-1 Flying Lions UH-1Y
AH-1Z
CH-53E/K
MV-22B
F-35B
RQ-21 28 August 2003 Operational Test and Evaluation Force MCAS Yuma, AZ
Unmanned Aerial Systems
[edit]
Marine Unmanned Aerial Vehicle Squadrons
[edit]
VMUs operate the RQ-21 Blackjack unmanned aerial system (UAS) which provides Marine ground forces with reconnaissance, surveillance, and target acquisition. They also provide artillery spotting and can assist in search and rescue operations. Due to the high operational tempo of the VMU squadrons in recent years, the Marine Corps stood up VMU-3 in 2008 and VMU-4, a reserve unit, was activated in 2010 with the lineage of VMO-4.[85]
Squadron Name Insignia Nickname Date Commissioned Senior Command Station VMU-1 Watchdogs 21 January 1987 MAG-13, 3rd MAW MCAS Yuma, AZ[86] VMU-2 Night Owls June 1984 MAG-14, 2nd MAW MCAS Cherry Point, NC[87] VMU-3 Phantoms 12 September 2008 MAG-24, 1st MAW MCAS Kaneohe Bay, HI VMU-4 Evil Eyes 20 December 1943 MAG-41, 4th MAW MCB Camp Pendleton, CA
See also
[edit]
United States Marine Corps Aviation
Aviation combat element
List of decommissioned United States Marine Corps aircraft squadrons
List of United States Navy aircraft squadrons
List of United States Marine Corps aircraft groups
List of United States Marine Corps aircraft wings
List of United States Marine Corps aviation support units
List of United States Marine Corps battalions | ||||
5682 | dbpedia | 2 | 55 | https://www.medchemexpress.com/recombinant-proteins/vmo1-protein-human-hek-293-his.html | en | VMO1 Protein, Human (HEK293, His) | [
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"VMO1 Protein",
"Human (HEK293",
"His) | Vitelline Membrane Outer Layer Protein 1 Homolog | VMO1"
] | null | [] | null | Vitelline membrane outer layer protein 1 homolog (VMO1) is first characterized in the outer layer of the vitelline membrane of hen鈥檚 eggs, where VMO1is present together with lysozyme, VMO2, and ovomucin. VMO1 is a secreted protein and exerts important functions in inner ear and tear film, VMO1 may also interact with glycosylated proteins. VMO1 Protein, Human (HEK293, His) is the recombinant human-derived VMO1 protein, expressed by HEK293, with C-6*His labeled tag. The total length of VMO1 Protein, Human (HEK293, His) is 178 a.a., with molecular weight of 18-22 kDa. MedChemExpress offers high purity VMO1 Protein, Human (HEK293, His) with excellent lot-to-lot consistency, superior biological activity and low endotoxin levels. | /favicon.ico | MedchemExpress.com | https://www.medchemexpress.com/recombinant-proteins/vmo1-protein-human-hek-293-his.html | Vitelline membrane outer layer protein 1 homolog (VMO1) is first characterized in the outer layer of the vitelline membrane of hen鈥檚 eggs, where VMO1is present together with lysozyme, VMO2, and ovomucin. VMO1 is a secreted protein and exerts important functions in inner ear and tear film, VMO1 may also interact with glycosylated proteins. VMO1 Protein, Human (HEK293, His) is the recombinant human-derived VMO1 protein, expressed by HEK293, with C-6*His labeled tag. The total length of VMO1 Protein, Human (HEK293, His) is 178 a.a., with molecular weight of 18-22 kDa.
Vitelline membrane outer layer protein 1 homolog (VMO1) is first characterized in the outer layer of the vitelline membrane of hen’s eggs, where VMO1is present together with lysozyme, VMO2, and ovomucin. Determination of the crystal structure of VMO1 revealed that VMO1 may interact with glycosylated proteins.VMO1 is a secreted protein and exerts important functions in inner ear and tear film[1].
QTDGRNGYTAVIEVTSGGPWGDWAWPEMCPDGFFASGFSLKVEPPQGIPGDDTALNGIRLHCARGNVLGNTHVVESQSGSWGEWSEPLWCRGGAYLVAFSLRVEAPTTLGDNTAANNVRFRCSDGEELQGPGLSWGDFGDWSDHCPKGACGLQTKIQGPRGLGDDTALNDARLFCCRS | |||||
5682 | dbpedia | 1 | 16 | https://squadronnostalgia.com/product/vmo-1-patch-plastic-backing/ | en | VMO-1 Patch – Plastic Backing | [
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] | null | [] | 2024-06-17T02:23:09+00:00 | 4.25"x3.75" VMO-1 Patch – Plastic Backing | en | Squadron Nostalgia | https://squadronnostalgia.com/product/vmo-1-patch-plastic-backing/ | Description
4.25″x3.75″ VMO-1 Patch – Plastic Backing
Marine Observation Squadron 1 (VMO-1) was an observation squadron of the United States Marine Corps which saw extensive action during World War II and supported numerous contingencies during the Cold War. They were based at Marine Corps Air Station New River, North Carolina and saw their final deployment in support of Operation Desert Storm in 1991. They were deactivated on July 31, 1993. | |||||
5682 | dbpedia | 2 | 38 | https://www.novusbio.com/primary-antibodies/vmo1 | en | VMO1 Antibodies | [
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5682 | dbpedia | 3 | 74 | https://www.defense.gov/News/Feature-Stories/Story/Article/2801382/tv-entertainer-ed-mcmahon-served-in-the-marine-corps-during-3-wars/ | en | TV Entertainer Ed McMahon Served in the Marine Corps During 3 Wars | [
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] | null | [] | null | Ed McMahon is best known as Johnny Carson's sidekick on TV's ''The Tonight Show Starring Johnny Carson,'' but he also had a career in the military, which began during World War II, continued during | en | /Portals/1/favicon.ico?ver=wSJzjXOlssZVvf5cay20vA%3d%3d | U.S. Department of Defense | https://www.defense.gov/https%3A%2F%2Fwww.defense.gov%2FNews%2FFeature-Stories%2FStory%2FArticle%2F2801382%2Ftv-entertainer-ed-mcmahon-served-in-the-marine-corps-during-3-wars%2F | You have accessed part of a historical collection on defense.gov. Some of the information contained within may be outdated and links may not function. Please contact the DOD Webmaster with any questions.
Ed McMahon is best known as Johnny Carson's sidekick on TV's "The Tonight Show Starring Johnny Carson," from 1962 to 1992. He always opened the show with his signature introduction: "Heeere's Johnny!"
McMahon also hosted the popular TV show "Star Search" from 1983 to 1995.
Less known to his legion of fans is that McMahon also had a career in the military, which began during World War II, continued during the Korean War and ended during the Vietnam War.
In 1944, he was commissioned in the Marine Corps and earned his pilot's wings. He became a Marine Corps test pilot and a flight instructor in F4U Corsair aircraft at Lee Field, in Green Cove Springs, Florida.
McMahon remained in the Marine Corps Reserve after the war and was recalled to active duty during the Korean War. He was awarded six Air Medals for flying 85 combat missions over North Korea in an OE-1 unarmed observation aircraft.
After the Korean War, McMahon remained in the Marine Corps Reserve and retired as a colonel in 1966.
In 1982, McMahon received a state commission as a brigadier general in the California Air National Guard, an honorary award to recognize his support for the National Guard and Reserve.
McMahon died June 23, 2009 in Los Angeles, California. He was 86.
Some other interesting facts about McMahon:
1
Before "The Tonight Show," McMahon worked with Carson as announcer and host on the ABC TV game show "Who Do You Trust," which aired from 1957 to 1962.
2
As a teenager, McMahon spent three years in Maine as a carnival barker and then a bingo caller. A carnival barker is a person who attracts patrons to entertainment events such as a circus or fair.
3
He authored two memoirs, "Here's Johnny!: My Memories of Johnny Carson, The Tonight Show, and 46 Years of Friendship" and "For Laughing Out Loud." | ||||
5682 | dbpedia | 3 | 1 | https://www.2ndmaw.marines.mil/Units/MAG-29/ | en | MAG | [
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] | null | [] | null | en | /Portals/7/favicon.ico?ver=ZQikU4c5sJtDJmXSFqyYKg%3d%3d | null | History
MAG-29 was commissioned 1 May 1972 at Marine Corps Air Station (Helicopter), New River, Jacksonville, North Carolina. MAG-29 was composed of Headquarters and Headquarters Support Squadron 29, Marine Air Base Squadron 29 and Marine Light Helicopter Squadron 268. The two squadrons were newly designated units awaiting assignment of personnel and material.
Four days after its activation, MAG-29 received its first aircraft, the UH-1N, directly from Bell Helicopter in Fort Worth, Texas. Eleven days later, the Group more than doubled in size with the addition of Marine Light Helicopter Squadron (HML) 167, Marine Attack Helicopter Squadron (HMA) 269 and Marine Observation Squadron (VMO) 1 from MAG-26. Less than one year after it was activated on 1 and 2 Feb 1973, MAG-29 was already conducting operations as HML 167 worked with the IRS to search for and destroy illegal stills throughout coastal North Carolina.
During 1982, the first phases of the MAG-29/MAG-26 reorganization were completed. UH-1N and AH-1T aircraft comprised HML-167 and HMA-269 and MAG-29 received its first Medium and Heavy Helicopter Squadrons. Marine Medium Helicopter Squadron (HMM) 162 and Marine Heavy Helicopter Squadron (HMH) 464 transferred to MAG-29 from MAG-26. During this period, HMH-464 demonstrated the capabilities of the new CH-53E as it was introduced into the Marine Corps inventory.
From the mid to late 1980s, MAG-29 supported multiple Marine Amphibious Unit deployments to the Mediterranean and deployments to Norway in support of Exercise BATTLE GRIFFIN. Throughout 1989 and 1990, MAG-29 participated in numerous exercises and operations which culminated with all MAG-29 units deployed in support of Operation DESERT SHIELD/STORM and Landing Force, Sixth Fleet commitments.
In 1993, MAG-29 units supported United Nations Operations RESTORE HOPE/CONTINUE HOPE in Somalia and DENY FLIGHT/PROVIDE PROMISE in the former Yugoslavia. In the summer of 1994, MAG-29 personnel and aircraft supported Operation RESTORE DEMOCRACY in Haiti.
On 7 June 1995, MAG-29’s continued support of Operations DENY FLIGHT/PROVIDE PROMISE was highlighted when HMM-263, with a detachment of Marines from HMH-464, escorted by AH-1W Cobra Helicopters from HML/A-269, successfully rescued downed U.S. Air Force pilot Captain Scott O'Grady.
During the early part of 2000, MAG-29 deployed HMM-263(REIN) to the Mediterranean and Adriatic for continued operations in Kosovo. The remaining squadrons deployed in support of ASCIET-00 and formed the newly activated SPMAGTF-8, which deployed to Vieques, Puerto Rico in support of Operation EASTERN ACCESS to clear protesters off the training area.
After the terrorist attacks on the United States on September 11, 2001, MAG-29 prepared for support operations in New York City and contingency operations overseas. HMM-365(REIN) was quickly deployed and ordered to be among the first troops into Afghanistan in support of Operation ENDURING FREEDOM. Two years later MAG-29(REIN) deployed in January 2003 to become the 3rd Rotary Wing Aircraft Group for 3d Marine Aircraft Wing (MAW) in support of Operation IRAQI FREEDOM (OIF).
In October 2003, MAG-29 deployed a CH-53E detachment to the Horn of Africa in support of Combined Joint Task Force Horn of Africa (CJTF HOA) as part of Operation ENDURING FREEDOM. Over the next three years, MAG-29’s enduring legacy was the ability to provide well-trained and equipped aviation units in support of world-wide combat operations.
From the Summer of 2005 to the Fall of 2006, MAG-29 oversaw the preparation and deployment of four MEU ACEs, four Marine Helicopter Light/Attack Squadron(HML/A) deployments to OIF, four CH-53E detachments in support of CJTF HOA for OEF missions and one Special Marine Air Ground Task Force(SPMAGTF) in support of relief operations after Hurricane Katrina.
In September 2005, MAG-29 formed a composite ACE of Marine Corps helicopters in support of SPMAGTF Katrina by using elements from five different squadrons to ensure commitments to the relief effort were completed. The six CH-53Es and two CH-46 aircraft provided assistance to over 4,000 people affected by what has been characterized as the most destructive natural disaster in U.S. history.
From February 2007 to February 2008 MAG-29(REIN) deployed to Al Asad Airbase, Iraq where it conducted combat operations as a Reinforced MAG, comprised of a Headquarters Squadron and 12 tactical squadrons from three different Marine Aircraft Wings and the U.S. Army. Throughout the year-long deployment the MAG provided exceptional support to Multi-National Forces-West (MNF-W) in the execution of OIF 06-08. During its combat deployment, MAG-29 (REIN) Squadrons flew in excess of 111,000 combat flight hours, supported the tactical movement of 187,000 passengers, and the aerial medical evacuation of 4,500 coalition and Iraqi force personnel. In February 2008, MAG-29 was replaced by MAG-16 and redeployed to MCAS New River.
"WAR EAGLES" PRINCIPLES
Use the following principles as guidelines in your daily activities: | ||||||
5682 | dbpedia | 0 | 60 | https://hma1369.tripod.com/vmo3.html | en | 351/VMO | [
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] | null | [] | null | null | MARINE OBSERVATION SQUADRON 3
VMO-3
"Scarface"
Marine Observation Squadron 3 was originally activated 1 December 1943, at Quantico, Virginia, as Marine Observation Squadron 351. It was to be the "eyes" for Marine Artillery units in the Pacific. The squadron was redesignated Marine Observation Squadron 3 in 1944. The squadron flew many hazardous spotting missions at Peleliu, and later, at Okinawa, earned the Presidential Unit Citation. After the war, VMO-3 served in Northern China, before relocating, first to Guam, and later to Cherry Point, North Carolina, where the squadron was deactivated in 1949.
In 1966, the Marine Corps received permission to activate two "temporary war-time only" VMOs. VMO-3 was reactivated at Camp Pendleton in August, and was on its way to Vietnam by December. VMO-3 flew its UH-1E Hueys from Hue/Phu Bai and MCAF Marble Mountain as part of 1st Marine Aircraft Wing. In 1968, with the addition of the OV-10A "Bronco" to the VMO inventory, the decision was made to remove the UH-1 from the VMOs and create three Light Helicopter Squadrons (HMLs). Instead of deactivation, VMO-3 and its sister squadron VMO-5 (UH-1 training squadron based at Camp Pendleton) were redesignated. VMO-3 became HML-367.
LINEAGE
1943 - 1949
Activated 1 December 1943 at Quantico, Virginia, as (Artillery Spotting Division) Marine Observation Squadron 351.
Redesignated 15 January 1944 as Marine Observation Squadron 3.
Deployed during January - March 1944 to Espiritu Santo and assigned to Marine Aircraft Group 11, Marine Air South Pacific.
Participated in the following World War II campaigns
PELELIU
OKINAWA
Redeployed during September - October 1945 to Tientsin, China and assigned to the 1st Marine Aircraft Wing.
Participated in the Occupation of North China, October 1945 - June 1947.
Redeployed during July 1947 to Orote, Guam, and reassigned to Marine Aircraft Group 24.
Redeployed during February 1949 to Agana, Guam.
Relocated during May 1949 to Cherry Point, North Carolina and reassigned to the 2nd Marine Aircraft Wing.
Deactivated 20 August 1949 at Cherry Point, North Carolina.
1966 -1968
Reactivated 1 August 1966 at Camp Pendleton, California, as Marine Observation Squadron 3 and assigned to Marine Wing Support Group 37, 3d Marine Aircraft Wing.
Deployed during December 1966 to Hue/Phu Bai and reassigned to Marine Aircraft Group 16, 1st Marine Aircraft Wing.
Participated in the war in Vietnam December 1966 to March 1968, operating from
Hue/Phu Bai
Marble Mountain
Redesignated 24 March 1968 as Marine Light Helicopter Squadron 367
HONORS
PRESIDENTIAL UNIT CITATION STREAMER with three bronze stars
World War II
Okinawa - 1945
Vietnam
1965 - 1967
1967
1968
NAVY UNIT COMMENDATION STREAMER
Vietnam
1968
ASIATIC-PACIFIC CAMPAIGN STREAMER with two bronze stars
WORLD WAR II VICTORY STREAMER
NAVY OCCUPATION SERVICE STREAMER with ASIA clasp
CHINA SERVICE STREAMER
NATIONAL DEFENSE SERVICE STREAMER
VIETNAM SERVICE STREAMER with three bronze stars
VIETNAM CROSS of GALLANTRY STREAMER with PALM
VIETNAM MERITORIOUS UNIT CITATION CIVIL ACTIONS STREAMER
These honors were inherited by HML-367.
Nicknames: "Scarface"
ID Code: AA 1946-47; AA 1947-49; VT 1966-68
Aircraft: OY-1 (WW2); AE-1*; SBD-5**; UH-1E
Squadron Web Pages:
* These were assigned to VMOs to make up a shortage of aircraft while refitting.
** According to Navy listings, VMO-3 carried 1 SBD-5 on strength from Aug 1944 through mid-Apr 45. | ||||||||
5682 | dbpedia | 2 | 79 | https://www.origene.com/catalog/cdna-clones/expression-plasmids/rn216021/vmo1-nm_001191823-rat-untagged-clone | en | Vmo1 (NM_001191823) Rat Untagged Clone – RN216021 | [
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] | null | Vmo1 (untagged) - Rat vitelline membrane outer layer 1 homolog (chicken) (Vmo1) | en | /img/icon-16px.png | https://www.origene.com/catalog/cdna-clones/expression-plasmids/rn216021/vmo1-nm_001191823-rat-untagged-clone | OTI Disclaimer Our molecular clone sequence data has been matched to the reference identifier above as a point of reference. Note that the complete sequence of our molecular clones may differ from the sequence published for this corresponding reference, e.g., by representing an alternative RNA splicing form or single nucleotide polymorphism (SNP). Reconstitution 1. Centrifuge at 5,000xg for 5min.
2. Carefully open the tube and add 100ul of sterile water to dissolve the DNA.
3. Close the tube and incubate for 10 minutes at room temperature.
4. Briefly vortex the tube and then do a quick spin (less than 5000xg) to concentrate the liquid at the bottom.
5. Store the suspended plasmid at -20°C. The DNA is stable for at least one year from date of shipping when stored at -20°C. | |||||
5682 | dbpedia | 3 | 42 | en | 1 on USS America (CV | [
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5682 | dbpedia | 2 | 4 | https://www.alliancegenome.org/gene/WB:WBGene00012631 | en | Alliance of Genome Resources | [] | [] | [] | [
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5682 | dbpedia | 2 | 59 | https://www.creative-biogene.com/human-VMO1-NM_001144941-lentivirus-particles-LV29610L-1398742-85.html | en | human VMO1 (NM_001144941) lentivirus particles (LV29610L) | [
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] | null | [] | null | Use human VMO1 (NM_001144941) lentivirus particles for functional genomics research and drug discovery study. | en | /images/favicon.png | https://www.creative-biogene.com/human-VMO1-NM_001144941-lentivirus-particles-LV29610L-1398742-85.html | DescriptionThe SureSilencing trade; shRNA Plasmids are designed to specifically knock down the expression of individual genes by RNA interference under either transient (with GFP) or stable transfection (for hygromycin, neomycin or puromycin-resistance) conditions after performance of the appropriate enrichment or selection procedures, respectively. Each vector contains the shRNA under control of the U1 promoter and either the GFP gene, for the enrichment of transiently transfected cells, or the neomycin or puromycin resistance genes, for the selection of stably transfected cells. DescriptionThe SureSilencing trade; shRNA Plasmids are designed to specifically knock down the expression of individual genes by RNA interference under either transient (with GFP) or stable transfection (for hygromycin, neomycin or puromycin-resistance) conditions after performance of the appropriate enrichment or selection procedures, respectively. Each vector contains the shRNA under control of the U1 promoter and either the GFP gene, for the enrichment of transiently transfected cells, or the neomycin or puromycin resistance genes, for the selection of stably transfected cells. DescriptionEach set contains 4 shRNA expression constructs. The hairpin consists of a 7 base loop and 19~29 base stem optimized for the specific gene sequence. The sequences of 19~29mer shRNAi will be delivered with shRNA clones. | |||||
5682 | dbpedia | 2 | 18 | https://www.acc.af.mil/News/Article/2492302/desert-storm-veteran-influences-daughters-call-to-service/ | en | Desert Storm veteran influences daughter's call to service | [
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] | null | [] | 2021-02-03T00:00:00 | As I sit in my freshly furnished apartment in Hampton, Virginia, I think back on my first year of being in the U.S. Air Force asking myself, why am I here? The 30th anniversary of Desert Storm was | en | /Portals/92/ACC_favicon.ico?ver=o_8rEHEETuufRUYNWraN9Q%3d%3d | Air Combat Command | https://www.acc.af.mil/https%3A%2F%2Fwww.acc.af.mil%2FNews%2FArticle-Display%2FArticle%2F2492302%2Fdesert-storm-veteran-influences-daughters-call-to-service%2F | As I sit in my freshly furnished apartment in Hampton, Virginia, I think back on my first year of being in the U.S. Air Force asking myself, why am I here?
The 30th anniversary of Desert Storm was Jan. 17, 2021, and I have come to the quick realization that my biggest motivation for joining the military in the first place was my father, former Staff Sgt. Larry Shanes of the U.S. Marines.
I always wondered what motivated and pushed him to join the military, but the one question I constantly ask myself is, “Who was Larry Shanes before he was ‘Dad’?”
He served in the early 1990s during the Gulf War, but more specifically Desert Storm. I realized I didn’t know much about what my father’s job.
My father was not adamantly driven to join the Marines, so he had to evaluate his options.
“I was talking to both Air Force and Marine recruiters at the same time, and the Marines could get me out of town sooner — he had a better job for me — the avionics guaranteed contract because of my ASVAB scores,” my father said. “The Air Force guy had me fixing helicopters, which I didn’t want to do, but it was the only job they could guarantee me. Plus, I was leaning towards the Marines anyway just because I wanted to be the best.”
He would go onto working in avionics, which was called Aviation Electronics — anything with a wire going to it on the OV10-Bronco as part of the Fixed Wing Marine Observation 1 (VMO-1) unit. Unbeknownst to him, his new unit would play an important role in Desert Storm
The forward-air-control plane was responsible for flying around the battlefield with a ground officer in the back, communicating with the troops and directing fire and troop movements.
While talking to him about his experiences and trying to put myself in his combat boots, it’s almost as if I can feel what he felt during that time. He said that he experienced similar feelings of realization while deployed.
“I think it was the ‘surrealness’ of us doing the exact job we had been trained to do back in the States,” my father said. “But now, we were in a combat situation to do it. They were slinging several scud missiles that flew over base; we had to go in bunkers. I know that was the real thing we had trained for. I mean that’s what you’re trained for in the military, right? Break stuff and do your job. But you don’t really realize you’re going to do it in combat until you’re standing there in the sand. So it’s not a scary feeling, just kind of an out-of-body type thing.”
Even though I’ve yet to see anything comparable to a warzone, I can relate to those feelings of realization during my time at basic military training (BMT) and technical school – since I went through training during the height of the COVID-19 pandemic. I can empathize with the constant feeling of not knowing what’s going on outside of a military base, not knowing if my friends and family are alright, not knowing when I’ll even get to see my family again.
Hearing my father talk about some of the missions he undertook chokes me up. Imagining a young, 20-year-old version of my dad in the middle of a combat zone is almost too much for me to handle. This was the early 1990s, too. There were no cell phones, no laptops, and none of the modern commodities we’re accustomed to now. My father had to wait to contact people in the outside world.
“The weird part was hearing about all the different nuances to the war when we got back because we didn’t watch TV or the news,” he continued. “And my mom, your grandma, was glued to the TV the whole time we were there. She was telling me about all these battles and all this stuff raging on.”
While my father began to open up about his time during Desert Storm, I wondered what kept him and his buddies going. I started to get a vague idea about what they all saw and felt.
“We were Marines,” he said simply. “It’s what we do. Not going isn’t an option. One of the good things about the training that I went through, was that it’s okay to break down and fall apart, but you do it after the mission. It’s just what it was. And plus, we had each other. That’s why we still meet up. Vince, Earl, Derek, Craig, and Eric – they were all there with me. We relied on each other to keep our spirits up. At the end of the day, we were just working and fixing a lot of planes.
“First and foremost, we were Marine riflemen,” he continued. “We weren’t directly in combat. No one was shooting at us while we were fixing the planes. So, we carried on and carried out the plan of the day. We got it done and were professional Marines.”
When I was younger, I just thought that my dad was out on the front lines. I had no idea the significance of his role during Desert Storm. He was, and continues to be, my hero, so he must have been everyone’s hero, right? Through this talk, I learned new insight on what my dad and his Marine family did during Desert Storm. He was able to become a better version of himself, and because of this, it led him to meet my mom, get married, and raise my brothers and me in a way that he can be proud of. | ||||
5682 | dbpedia | 0 | 6 | https://www.seaforces.org/usmcair/VMO-squadrons.htm | en | VMO Marine Observation Squadrons US Marine Corps USMC | [
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5682 | dbpedia | 1 | 61 | https://www.wikiwand.com/en/VMO-2 | en | Wikiwand | [
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] | null | [] | null | Marine Observation Squadron 2 (VMO-2) was an observation squadron of the United States Marine Corps which saw extensive action during World War II and the Vietnam War. They were based at Marine Corps Air Station Futenma, Japan and Marine Corps Air Station Camp Pendleton, California and saw their final combat in support of Operation Desert Storm in 1991. The squadron was decommissioned on 23 May 1993. | en | Wikiwand | https://www.wikiwand.com/en/VMO-2 | VMO-2
Former observation squadron of the US Marine Corps / From Wikipedia, the free encyclopedia
Dear Wikiwand AI, let's keep it short by simply answering these key questions:
Can you list the top facts and stats about VMO-2?
Summarize this article for a 10 year old
SHOW ALL QUESTIONS | |||||
5682 | dbpedia | 3 | 78 | http://www.korean-war.com/USMarines/us-marines.html | en | US Marines | [
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] | null | [] | null | null | When the Korean War began, the U.S. Marine Corps, like all services, was understrength and still equipped with World War Two equipment so when ordered to Korea, all that could be provided initially was a provisional brigade, designated the 1st Provisional Marine Brigade. The Brigade was formed from assets of the 1st Marine Division and 1st Marine Aircraft Wing at Camp Pendleton, CA. The Brigade was activated on 7 July 1950 and built around two units, the 5th Marines as a regimental combat team and Marine Aircraft Group 33 (MAG-33). The air component was consolidated under Forward Echelon, 1st Marine Aircraft Wing who's commander was double billeted as the deputy brigade commander. Troops were hurriedly reassigned to the Brigade from 1st Marine Division units as supplies and mothballed equipment were arriving. Some 6,800 troops were sent from the 2d Marine Division at Camp Lejeune, NC for both the Brigade and to begin the rebuilding of the 1st Marine Division. Much of the equipment and vehicles came from Marine Supply Depot, Barstow, CA and were recovered from Pacific islands and refurbish during Operation ROLL-UP in the late 1940s. Regardless, many units were still short men and equipment. The 5th Marines' three battalions had only two rifle companies apiece. While third rifle platoons were hastily formed for these six companies, they were still short some 50 men each. The three artillery batteries had only four 105mm howitzers instead of the normal six and the regimental Antitank Company lacked its organic tank platoon.
Load out of Task Group 53.7 at San Diego began soon after the Brigade was activated. The 266 officers and 4,503 enlisted men of the ground component sailed between 12-14 July on three troop transports, two attack cargo transports, and three landing ships dock. MAG-33 was embarked aboard two troop transports and an escort carrier. A total of 6,534 Brigade troops departed for Japan. The Brigade Advance Party with the commander, deputy commander, and part of their staffs departed by air on 16 July and arrived in Tokyo on the 19th. On 25 July, while en route to Japan, the Brigade's ground component was ordered to sail directly to Korea due to the deteriorating situation on the Pusan Perimeter. The Advance Party went on to Korea on the same day and situated itself at Taegu near the center of the Pusan Perimeter.
A significant combat capability exists within the Marine Corps that was not possessed by the Army. Marine ground combat units could have Marine aviation units placed in direct support to provide close air support, resupply, and medical evacuation. For the 1st Provisional Marine brigade this support was in the form of MAG-33. MAG-33 arrived at Kobe, Japan on 31 July. Marine Tactical Air Control Squadron 2 (MTACS-2) and the ground echelon of VMO-6 departed that same day by landing ship tank for Pusan arriving the next day. The 70 aircraft of the three fighting squadrons launched from the CVE and landed at Itami where they prepared for action. By 5 August VMF-214 and 323 were stationed aboard the USS Sicily(CVT-118) and USS Badoeng Strait (CVF-116), respectively, and VMF(N)-513 was split between them. The Brigade's ground component arrived at Pusan on 2 August and was attached to EUSAK, arriving just in time to blunt the North Korean offensive in the area along and west of the Naktong River. Although suffering heavy casualties in the fighting, the Brigade continued to stop North Korean attacks in its area until it was pulled from the Pusan Perimeter to join the 1st Marine Division at the Inchon Landings. It was deactivated as an independent brigade on 13 September 1950.
H&S Battalion, 1st Provisional Marine Brigade
* HQ Company, 1st Provisional Marine Brigade
* Detachment, Military Police Company, 1st Marine Division
* Detachment, Reconnaissance Company, 1st Marine Division
* Counter Intelligence Corps and Military Intelligence Special Detachment (USA)
Company A, 1st Engineer Battalion (Reinforced)
Company C, 1st Medical Battalion
Company A, 1st Motor Transport Battalion
Detachment, 1st Ordnance Battalion
Detachment, 1st Service Battalion
Company A, 1st Shore Party Battalion
Detachment, 1st Signal Battalion
Company A, 1st Tank Battalion
1st Amphibian Tractor Company
Detachment, 1st Combat Service Group
1st Platoon, 1st Amphibian Truck Company, FMF
5th Marines
* H&S Company
* 1st Battalion, 5th Marines (- Company C)
* 2d Battalion, 5th Marines (- Company F)
* 3d Battalion, 5th Marines (- Company I)
* 4.2-inch Mortar Company, 5th Marines
* Antitank Company, 5th Marines (-Tank Platoon) 1st Battalion, 11th Marines (-) (Reinforced)
Forward Echelon, 1st Marine Aircraft Wing Marine Aircraft Group 33
HQ Squadron, Marine Aircraft Group 33
Service Squadron, Marine Aircraft Group 33
Marine Fighter Squadron 214
Marine Fighter Squadron 323
Marine Fighter Squadron (Night) 513
Marine Observation Squadron 6* Marine Tactical Air Control Squadron 2
*(Under operational control of the 1st Provisional Marine Brigade.)
1st Marine Division (Reinforced)
This division was stationed at Camp Pendleton, CA having previously served as an occupation force in North China from September 1945 to June 1947. It was brought up to war strength mainly with reservists. The Division departed for Korea between 10-22 August 1950, minus 7th Marines, which departed on 3 September 1950. Lead elements of the 1st Marines and support units arrived in Japan in early September 1950. The bulk of the Division landed in Korea on 15 September and regained control of the former 1st Provisional Marine Brigade elements, which rejoined the Division by sailing directly from Pusan. It was joined by 7th Marines on 21 September 1950. The Division was relieved by 25th Infantry Division and returned to Camp Pendleton in April 1955. The associated 1st Marine Aircraft Wing redeployed to Japan at the same time.
Following the successful amphibious invasion at Inchon, the division fought its way in Seoul, South KoreaÂs capital. It was withdrawn and again loaded aboard ship to make another landing, this time at Wonsan on North KoreaÂs east coast. However, by the time the combat assault landing was scheduled to take place, North Korean forces had collapsed and Wonsan was already in the hands of South Korean forces advancing up the east coast highway so the division was landed and then trucked northward to the Hamhung-Hungnam area of North Korea. From there, the division advance up a narrow road leading to the Chinese-North Korean border via the towns of Koto-ri and Haga-ri. The division was north of Yudam-ni at the far north end of the Choshin Reservoir when Chinese Communist Forces attacked in November 1950, blocking the road to safety. What followed was days of hell as the division fought its way out the trap in sub-zero temperatures and down the narrow road to Hungnam. This battle is a classic the proud history of the United States Marine Corps.
The 1st Marine Division consisted of:
Division HQ and HQ Battalion
1st Marine Regiment
5th Marine Regiment
7th Marine Regiment
11th Marines (artillery)
1st Tank Battalion
1st Amphibian Tractor Battalion
1st Armored Amphibian Battalion
1st Engineer Battalion
1st Shore Party Battalion
1st Signal Battalion
1st Amphibious Reconnaissance Company
1st Military Police Company
1st Service Support Group *
1st Motor Transport Battalion
7th Motor Transport Battalion
1st Ordnance Battalion
1st Service Battalion
1st Medical Battalion
Battery C, 1st 4.5-inch Rocket Battalion
1st Air Delivery Platoon
1st Fumigation and Bath Platoon
Carrier Platoon, FMF
Attached units
1st Korean Marine Corps Regiment (initially 1st 63rd Battalions, later 5th Battalion)
1st Korean Marine Corps Artillery Battalion
1st Naval Construction Battalion ("Seabees")
Provisional Marine Units in Korea
The 1st Marine Division and FMF, Pacific formed several provisional units in 1952-53 to fulfill special requirements.
Kimpo Provisional Regiment
The Kimpo Provisional Regiment (KPR) was formed by the 1st Marine Division on 31 March 1952 to defend the Kimpo Peninsula, west of Seoul, on the Division's west flank. It was disbanded after the cease fire.
HHSC, Kimpo Provisional Regiment
1st Armored Amphibian Tractor Battalion (serving as supporting artillery)
2d Battalion, 7th Marines (this initial and subsequent battalions were rotated from the Division's reserve regiment)
5th Korean Marine Corps Battalion
13th ROK Security Battalion (-)
Company A, 1st Amphibian Tractor Battalion
Company B, 1st Shore Party Battalion (serving as engineers)
Company D, 1st Medical Battalion
Reconnaissance Company, 1st Marine Division
Detachment, Air and Naval Gunfire Liaison Company, 1st Signal Battalion
163d Military Intelligence Service Detachment (USA)
Detachment, 61st Engineer Searchlight Company (USA)
Detachment, 18 1st Counterintelligence Corps Unit (USA)
Other Provisional Marine Units
1st Provisional Casual Company, FMF Pac
1st Provisional Antiaircraft Artillery Automatic Weapons Battery (Apr 53)
1st Provisional Demilitarized Zone Military Police Company (Sep 53)
Non-Brigade/Division Marine and Navy Units
1st Marine Aircraft Wing (Sep 51)
* Marine Aircraft Groups 12 and 33
* 1st Antiaircraft Artillery Gun Battalion
Detachment, Navy Underwater Demolition Team 1 (Jul 50)
Detachment, Navy Underwater Demolition Team 3 (Sep 50)
Navy Underwater Demolition Team 5 (1951)
Marine Security Guard Detachment, US Embassy, Seoul
Back to US Units Page
Back to Korean War Homepage | ||||||||
5682 | dbpedia | 1 | 20 | https://military-history.fandom.com/wiki/VMTB-151 | en | VMTB-151 | https://static.wikia.nocookie.net/ucp-internal-test-starter-commons/images/a/aa/FandomFireLogo.png/revision/latest?cb=20210713142711 | https://static.wikia.nocookie.net/ucp-internal-test-starter-commons/images/a/aa/FandomFireLogo.png/revision/latest?cb=20210713142711 | [
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] | 2024-07-29T22:27:06+00:00 | Marine Torpedo Bombing Squadron 151 (VMTB-151) was a dive bombing squadron in the United States Marine Corps. The squadron fought in World War II but was quickly deactivated after the war on March 20, 1946. Marine Observation Squadron 1 (VMO-1) was commissioned on July 1, 1937 at Marine Corps... | en | /skins-ucp/mw139/common/favicon.ico | Military Wiki | https://military-history.fandom.com/wiki/VMTB-151 | Marine Torpedo Bombing Squadron 151
VMSB-151 Insignia
Active July 1, 1937 – March 20, 1946Country United StatesBranch USMCType Fighter squadronRole Dive bombingPart of InactiveEngagements World War IIAircraft flownBomber Curtiss SBC Helldiver
Douglas SBD Dauntless
Curtiss SB2C Helldiver
Marine Torpedo Bombing Squadron 151 (VMTB-151) was a dive bombing squadron in the United States Marine Corps. The squadron fought in World War II but was quickly deactivated after the war on March 20, 1946.
History[]
Marine Observation Squadron 1 (VMO-1) was commissioned on July 1, 1937 at Marine Corps Base Quantico.[1] They were redesignated Marine Observation Squadron 151 (VMO-151) on July 1, 1941. The squadron left for San Diego, California in December 1941 with the rest of the 1st Marine Aircraft Wing, but returned to MCB Quantico in January 1942. From January to April, they trained at Naval Station Norfolk until departing for Tafuna Airfield in American Samoa on April 9, 1942. They arrived a month later and remained for the next 13 months. On September 15, 1942, the squadron was re-designated again, this time as Marine Scout Bombing Squadron 151 (VMSB-151).[2]
On June 10, 1943, the squadron moved to Uvea Island in the Wallis Group. The squadron remained there until February 29, 1944 when they arrived at Engebi.[2] From March 9–12, the squadron covered Marine landings on Wotho Atoll, Ujae Atoll and Lae Atoll. During this time, they also made bombing runs against by-passed Japanese bases in the Marshall Islands until May 31, 1945. On June 9, 1945, the squadron returned to the United States.
Upon return to Marine Corps Air Station Mojave, they were assigned to Marine Air Support Group 51 and were redesignated Marine Torpedo Bombing Squadron 151 (VMTB-151).[3] on June 30, 1945. The squadron was deactivated at Marine Corps Air Station Santa Barbara, California on March 20, 1946.[4]
See also[]
United States Marine Corps Aviation
List of inactive United States Marine Corps aircraft squadrons
List of United States Marine Corps aircraft squadrons
References[]
Notes
Bibliography | ||
5682 | dbpedia | 3 | 39 | https://military-history.fandom.com/wiki/List_of_decommissioned_United_States_Marine_Corps_aircraft_squadrons | en | List of decommissioned United States Marine Corps aircraft squadrons | https://static.wikia.nocookie.net/ucp-internal-test-starter-commons/images/a/aa/FandomFireLogo.png/revision/latest?cb=20210713142711 | https://static.wikia.nocookie.net/ucp-internal-test-starter-commons/images/a/aa/FandomFireLogo.png/revision/latest?cb=20210713142711 | [
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] | 2024-07-29T22:27:06+00:00 | While other nations have Marines who are aviators, only the United States Marine Corps has its own dedicated aviation arm.[1] Most squadrons have changed names and designations many times over the years so they are listed by their final designation. The basic tactical and administrative unit of... | en | /skins-ucp/mw139/common/favicon.ico | Military Wiki | https://military-history.fandom.com/wiki/List_of_decommissioned_United_States_Marine_Corps_aircraft_squadrons | While other nations have Marines who are aviators, only the United States Marine Corps has its own dedicated aviation arm. Most squadrons have changed names and designations many times over the years so they are listed by their final designation.
Squadron designations[]
The basic tactical and administrative unit of United States Marine Corps Aviation is the squadron. Fixed-wing aircraft squadrons (heavier than air) are denoted by the letter "V," which comes from the French verb "Voler" (to fly). Rotary wing (helicopter) squadrons use "H." Marine squadrons are always noted by the second letter "M." Squadron numbering is not linear as some were numbered in ascending order and others took numbers from the wing or the ship to which they were assigned. From 1920 to 1941, Marine flying squadrons were identified by one digit numbers. This changed on July 1, 1941 when all existing squadrons were redesignated to a three-digit system. The first two numbers were supposed to identify the squadrons parent group but with the rapid expansion during the war and frequent transfer of squadrons this system fell apart.
Decommissioned squadrons[]
Squadrons are listed by their designation at the time they were decommissioned.
Pre–World War II squadrons[]
Following World War I, Marine aviation was significantly reduced from 8 to 3 squadrons. Many of the squadrons were renamed and re-designated numerous times and many still exist today with other designations. The squadrons listed below reflect those squadrons that were decommissioned prior to World War II and were never reconstituted in any form.
Squadron Name Insignia Nickname Date Decommissioned Sources VP-3M
Marine Patrol Squadron 3 1931 VO-6M
Marine Observation Squadron 6
Hell Divers 1932 VO-10M
Marine Observation Squadron 10
April 1, 1931 VS-14M
Marine Scouting Squadron 14 July 1, 1933 VS-15M
Marine Scouting Squadron 15 July 1, 1933 ZK-1M
1st Marine Barrage Balloon Squadron December 31, 1929
Marine Reserve Scouting Squadrons[]
The Marine Aviation Reserve was inactive from 1918 through 1928. When it was reconstituted, the names and aircraft used by these squadrons changed frequently but their home duty stations remained constant. The aircraft for these squadrons were assigned to the reserve bases themselves and were shared with co-located Navy Reserve squadrons.[6] The squadrons were absorbed into the 1st and 2nd Marine Aircraft Wings and their identities lost when they were mobilized in December 1940.
Squadron Name Insignia Nickname Location Date Decommissioned Source VMS-1R Boston, Massachusetts December 1940 [6] VMS-2R Brooklyn, New York December 1940 [6] VMS-3R Anacostia, D.C. December 1940 [6] VMS-4R Miami, Florida December 1940 [6] VMS-5R Black Knights Grosse Ile, Michigan December 1940 [7] VMS-6R Minneapolis, Minnesota December 1940 [6] VMS-7R Long Beach, California December 1940 [6] VMS-8R Oakland, California December 1940 [6] VMS-9R Seattle, Washington December 1940 [6] VMS-10R Kansas City, Kansas December 1940 [6] VMS-11R Brooklyn, New York December 1940 [6]
Marine Barrage Balloon Squadrons[]
Squadrons flying lighter than air vehicles (balloons), were indicated by the letter Z in naval squadron designation.[8] The first use of balloons by the Marine Corps was during World War I when they were used for artillery spotting. After the outbreak of World War II, the Navy authorized the Marine Corps to create barrage balloon squadrons for the air defense of advanced naval bases. Balloon training was cancelled in the summer of 1943 and the remaining units were decommissioned by the end of the year.
Squadron Name Insignia Nickname Date Decommissioned Source ZMQ-1 December 15, 1943 ZMQ-2 August 21, 1943 ZMQ-3 December 9, 1943 [13] ZMQ-4 February 20, 1943 ZMQ-5 December 5, 1943 ZMQ-6 December 8, 1943
Marine Balloon Observation Squadron[]
ZK-1M was formed in 1924 and disbanded in 1929.
Marine Scout Bombing Squadrons[]
Scout bombing squadrons each had eighteen to twenty-four Douglas SBD Dauntless dive bombers and were tasked with conducting dive-bombing attacks and long range scouting and patrol missions. They also provided close air support, laid smoke screens and sprayed DDT around bases.[14] The majority of these squadrons were quickly decommissioned following the end of World War II although three entered the Marine Air Reserve for a short period.
Marine Torpedo Bombing Squadrons[]
VMTBs were torpedo bomber squadrons that operated the Grumman TBF Avenger. They were in service with the Marine Corps during World War II and were decommissioned shortly after the war. They were part of the Cactus Air Force on Guadalcanal, served on escort carriers during the campaign to retake the Philippines and provided close air support for Australian forces on Borneo and Marines during the Battle of Okinawa.[27]
Squadron Name Insignia Nickname Date Decommissioned Source VMTB-151 Ali Baba March 20, 1946 [24] VMTB-341 Torrid Turtles September 13, 1945 VMTB-454 Helldivers January 28, 1946 VMTB-621 March 10, 1945 VMTB-622 January 31, 1946 VMTB-623 March 20, 1946 VMTB-624 March 10, 1946
Marine Fighting Squadrons[]
Marine Fighting Squadrons were multirole squadrons responsible for air-to-air combat, combat air patrols, attacking enemy shipping, escorting bombers and close air support. By far the most numerous of any type of Marine Corps squadron, they first made their mark flying the Grumman F4F Wildcat as part of the Cactus Air Force on Guadalcanal and finished World War II flying the venerable Vought F4U Corsair. Many VMF squadrons continued to operate after the war with most in the Marine Air Reserve; however, with the retirement of the Vought F-8 Crusader the VMF squadrons either became VMFAs or were decommissioned.
Marine Night Fighter Squadrons[]
After witnessing the Royal Air Force's success using radar directed fighters at night in 1941, the Navy's Bureau of Aeronautics authorized eight Marine night fighter squadrons to be formed by 1945. This timeline was brought forward considerably after the attack on Pearl Harbor and their need proven by the frustration of the Cactus Air Force's pilots not being able to engage Japanese bombers at night during the Battle of Guadalcanal. This led to the formation of VMF(N)-531 in November 1942. After much deliberation the Lockheed PV-1 Ventura was picked as the first choice of aircraft for these squadrons. The night fighting squadrons featured radar equipped aircraft, ground-based radar and personnel that provided Ground-controlled interception (GCI). The VMF(N) designated squadrons were decommissioned after the war, those that weren't were re-designated VMF(AW).[61]
Squadron Name Insignia Nickname Date Decommissioned Source VMF(N)-532 Night Fighters May 31, 1947 VMF(N)-534 May 31, 1947 VMF(N)-544 April 20, 1946
Marine Bombing Squadrons[]
The Marine Bombing Squadrons were formed during World War II to fill the need for a long range, land based bomber that could be used against enemy shipping and submarines. In the Pacific Theater, the squadrons served ashore as a garrison air force to attack bypassed Japanese bases and other installations. The VMBs flew the North American PBJ-1 Mitchell, which was the naval version of the U.S. Army Air Forces' B-25 Mitchell. Sixteen of these squadrons were commissioned with seven serving in combat, four never able to leave the U.S. due to the war ending and four others converted to VMTB squadrons.[62] The seven PBJ squadrons that saw combat in the Pacific suffered the loss of 45 aircraft, 26 in combat and 19 in non-combat operations, and 173 crew: 62 officers and 111 enlisted men.[63]
Squadron Name Insignia Nickname Date Decommissioned Source VMB-423 Seahorses November 30, 1945 VMB-433 Fork-Tailed Devils November 30, 1945 [65] VMB-443 Wildcats November 30, 1945 VMB-453 March 20, 1946 VMB-473 March 20, 1946 VMB-483 March 15, 1945 VMB-611 Black Seahorse November 30, 1945 VMB-612 Cram's Rams March 14, 1946 [24] VMB-613 November 21, 1945 VMB-614 Ruptured Ducks December 28, 1945
Marine Operational Training Squadrons[]
All of these squadrons were activated as Marine Training Squadrons (MTS) at Marine Corps Air Station Edenton, North Carolina in January 1944 and were redesignated as Marine Operational Training Squadrons (MOTS) and transferred to Marine Corps Air Station Cherry Point, North Carolina in February 1945 as medium bomber pilot training units. They instructed Marines learning to fly the North American PBJ-1 Mitchell. Following the end of the war they were quickly decommissioned.
Squadron Name Insignia Nickname Date Decommissioned Source MOTS-811 September 10, 1945 [24] MOTS-812 September 10, 1945 [24] MOTS-813 November 23, 1945 [24] MOTS-814 November 30, 1945 [24]
Marine Photographic Squadrons[]
Marine photographic squadrons were first formed in 1942 and went through numerous name changes while they were active. VMDs/VMPs flew photographic modified versions of the Douglas SBD Dauntless, Consolidated PB4Y-1 Liberator, Consolidated PB4Y-2 Privateer and Grumman F7F Tigercat. The main mission of these squadrons was to conduct long range, very high-altitude photographic reconnaissance.
Squadron Name Insignia Nickname Date Decommissioned Source VMD-154 Pathfinders September 10, 1945 [24] VMP-254 November 30, 1949 VMP-354 December 8, 1949 VMD-954 January 31, 1946 [24]
Marine Glider Squadron[]
The Marine Corps established a glider program in April 1942. Eventually they set goals of having 10,800 Marines qualified as glider infantry, with 1,371 gliders and 3,436 pilots.[73] They originally operated from Page Field on MCRD Parris Island but later moved to Marine Corps Air Station Eagle Mountain Lake outside Dallas, Texas.[74] The program was disbanded in 1943 when it was determined that glider assaults into small, heavily fortified, jungle islands would be tactically unfeasible.[75]
Squadron Name Insignia Nickname Date Decommissioned Source VML-711 May 24, 1943
Marine Transport Squadrons[]
Flying the Douglas R4D Skytrain and the Curtiss R5C-1 Commando, these squadrons were responsible for moving troops and cargo, aerial resupply, delivery of Paramarines, and medical evacuation. The last of these squadrons was decommissioned in 1949.
Squadron Name Insignia Nickname Date Decommissioned Source VMR-152 1950s VMR-153 Hermes 1959 [78] VMR-353 February 15, 1946 VMR-952 May 31, 1947 [80] VMR-953 Puss in Boots May 31, 1947
Marine Scouting Squadrons[]
There were three Marine Scouting Squadrons prior to World War II; however, VMS-3 was the only squadron to retain the designation. The squadron served in Haiti from 1919 through 1934 and then spent its last ten years at St. Thomas, Virgin Islands. During World War II they were the only Marine Corps squadron to operate east of the United States. They began the war flying the Grumman J2F Duck, transitioned to the Naval Aircraft Factory/Vought OS2N Kingfisher and at the time of deactivation were flying SBD Dauntless dive bombers.
Squadron Name Insignia Nickname Date Decommissioned Source VMS-3 Devilbirds May 20, 1944
Marine Target Towing Detachments[]
Marine Target Towing detachments were first formed at Marine Corps Air Station Ewa in October 1944. They were responsible for towing targets for antiaircraft gunnery and radar tracking practice. They flew Martin JM-1 Marauders and the Curtiss R5C-1 Commandos. The last of these detachments was decommissioned in March 1946.
Squadron Name Insignia Nickname Date Decommissioned Source VMJ-1 October 1945 VMJ-2 March 6, 1946 VMJ-3 Red Asses October 21, 1945
Marine Observation Squadrons[]
The Marine observation squadrons were formed during the latter stages of World War II with the primary mission of forward air control of strike aircraft for close air support and air interdiction.[83] They saw extensive service during the Vietnam War flying the North American OV-10 Bronco. The Marine Corps began decommissioning the VMO squadrons following their participation in Operation Desert Storm as turboprop-driven aircraft were being perceived in the wake of that conflict as being too vulnerable to surface-to-air missiles, especially shoulder-launched man-portable air defense systems (MANPADS), to fly over modern battlefields. Their mission has been assumed by the VMFA(AW) squadrons flying the F/A-18D Hornet.
Squadron Name Insignia Nickname Date Decommissioned Source VMO-1 July 31, 1993 VMO-2 Cherry Deuce May 20, 1993 VMO-4 Evil Eyes March 31, 1994 VMO-6 Tomcats January 1, 1976 [84][85] VMO-7 November 16, 1945 VMO-8 July 1976
Marine Attack Squadrons[]
In 1951, the Marine Corps began fielding the Douglas AD-1 Skyraider ground attack aircraft which had as its main role close air support for the Marines on the ground. Thus many squadrons had their designation changed from VMF to VMA to reflect this ground attack role. 13 squadrons were equipped with the Skyraider until they were finally phased out in 1958.[86] Follow on VMA squadrons operated the A-4 Skyhawk during the Vietnam War through their retirement just after Operation Desert Storm. The VMA tradition is carried on today by squadrons flying the AV-8B Harrier II.
Squadron Name Insignia Nickname Date Decommissioned Source VMA-131 Diamondbacks December 5, 1998 VMA-133 Dragons 30 September 1992 VMA-141 1 September 1969 VMA-143 Rocket Raiders VMA-144 Hensagliska October 31, 1965 [88] VMA-217 Max's Wild Hares 1964 VMA-233 Flying Deadheads 1969 VMA-241 Sons of Satan VMA-322 Fighting Gamecocks June 27, 1992 [89] VMA-324 Devildogs 29 August 1974 [90] VMA-331 Bumblebeess October 1, 1992 VMA-543 Night Hawks April 1, 1974
Marine Tactical Electronic Warfare Squadrons[]
VMAQ squadrons operated the EA-6B Prowler[91] and were tasked with providing electronic attack, electronic counter-countermeasures, radar jamming and suppression of enemy air defense using the AN/ALQ-99 jamming pod[92] and the AGM-88 HARM. Each of the four squadrons operated five aircraft and were land-based, although they were capable of landing on board U.S. Navy aircraft carriers.[93][94] VMAQ-2 decommissioned on March 8, 2019 marking the end of active service for the VMAQs and the EA-6B Prowler.
Squadron Name Insignia Nickname Date Decommissioned Source VMAQT-1 Banshees April 29, 2016 [95] VMAQ-2 Death Jesters March 8. 2019 [96] VMAQ-3 Moon Dogs May 11, 2018 [97] VMAQ-4 Seahawks June 2, 2017 [98]
Marine Reconnaissance Squadron[]
Marine Reconnaissance Squadron 4 was the only reserve photographic reconnaissance squadron in the Marine Corps. Initially based in Naval Air Station New Orleans, Louisiana they moved to Naval Air Station Olathe, Kansas May 1, 1967 and then again to Naval Air Station Dallas, Texas in 1970 when the reserves were reorganized. They flew Vought RF-8A Crusader until 1969 when all the planes were replaced with the Vought RF-8G Crusader.[99]
Squadron Name Insignia Nickname Date Decommissioned Source VMJ-4 1973
Marine Composite Reconnaissance Squadrons[]
Following the Korean War Marine Composite Squadron 1 (VMC-1) and Marine Photographic Squadron 1 (VMJ-1) were combined to form VMCJ-1. The new squadron was responsible for both Photoreconnaissance and Electronic Warfare. In its early years it flew the Vought RF-8A Crusader and Douglas EF-10B Skyknight but these were later replaced by the McDonnell-Douglas RF-4B Phantom II and the Grumman EA-6A Electric Intruder. The squadron was decommissioned following the end of the Vietnam War and the reorganization of the Marine Corps' composite community in 1975.[100]
Squadron Name Insignia Nickname Date Decommissioned Source VMCJ-1 Golden Hawks September 1, 1975 [101]
Marine Tactical Reconnaissance Squadron[]
Upon the decommissioning of the Marine Composite Squadrons (VMCJs), VMFP-3 became the lone photographic reconnaissance squadron in the Marine Corps.[102] They flew the McDonnell-Douglas RF-4B Phantom II and operated from 1975 until being decommissioned in 1990. Their capability has since been replaced by various targeting pods used on Marine aircraft and the Advanced Tactical Airborne Reconnaissance System which is found in some of the McDonnell-Douglas F/A-18 Hornet squadrons.[103]
Squadron Name Insignia Nickname Date Decommissioned Source VMFP-3 Eyes of the Corps September 3, 1990
Marine Fighter Attack Squadrons[]
The first Marine Corps squadron to be redesignated a VMFA was in June 1962 upon receipt of the first McDonnell-Douglas F-4 Phantom II aircraft. VMF and VMA squadrons were redesignated because the new Phantoms could be both fighter aircraft and ground attack aircraft.[104] These squadrons were heavily deployed during the Vietnam War. Most of these squadrons would eventually convert to the McDonnell-Douglas F/A-18 Hornet with the last F-4 Phantom leaving service in 1992.[105] The end of the Cold War saw the deactivation of some VMFA squadrons as part of the overall drawdown of the US Military[106]
Squadron Name Insignia Nickname Date Decommissioned Source VMFA-124 Whistling Death June 19, 1999 [107] VMFA-134 Smoke April 1, 2007 [108] VMFA-142 Gators July 2008 [109] VMFA-212 Lancers March 11, 2008 [110] VMFA-235 Death Angels June 14, 1996 VMFA-251 Thunderbolts April 23, 2020 [112] VMFA-321 Hells Angels September 30, 2004 [113] VMFA-333 Fighting Shamrocks March 31, 1992 VMFA-334 Falcons December 30, 1971 VMFA-351 1978 VMFA-531 Grey Ghosts April 27, 1992
Marine All-Weather Fighter Attack Squadron[]
Squadron Name Insignia Nickname Date Decommissioned Source VMFA(AW)-332 Moonlighters March 30, 2007 [118]
Marine Heavy Helicopter Squadrons[]
Squadron Name Insignia Nickname Date Decommissioned Source HMH-463 Pegasus April 22, 2022 [119] HMH-366 Hammerheads December 16, 2022 [120] HMH-769 Titan August 2, 2008 [121] HMH-777 Flying Armadillos 1980 [122]
Marine Medium Helicopter Squadrons[]
The original Marine Medium Helicopter squadrons flew the Sikorsky UH-34D Sea Horse, which shortly after its inception saw extensive combat during the Vietnam War.[123] Beginning in 1966 they began to be replaced with the CH-46 Sea Knight which was faster, could carry more troops and is still in service today.[124] The decommissioned HMM squadrons reflect the UH-34D training squadron and various reserve squadrons.
Squadron Name Insignia Nickname Date Decommissioned Source HMM-761 August 31, 1962 [125] HMM-762 December 31, 1962 [126] HMM-763 September 30, 1962 [127] HMM-766 Beavers October 1, 1976 [128] HMM-768 1976 [129]
Marine Light Helicopter Squadrons[]
Squadron Name Insignia Nickname Date Decommissioned ! !Source HML-765 June 30, 1976 [130] HML-767 Nomads August 1, 1994 [131] HMM-770 Stingers 1980 [132] HML-771 Hummers August 1, 1994 [131] HML-776 Gangsters July 1, 1994 [131]
Marine Light Attack Helicopter Squadrons[]
The Marine Corps’ light attack squadrons (HMLAs) are composite squadrons usually made up of 12 Bell AH-1Z Cobras and 6 Bell UH-1Y Hueys. The primary missions of the Cobra is close air support, forward air control, reconnaissance and armed escort, while the Huey provided airborne command and control, utility support, supporting arms coordination and medical evacuation. These squadrons were first formed during the Vietnam War with the fielding of the Bell AH-1 Cobra gunship and its being combined in the same squadron with the UH-1H Iroquois that initially belonged to the Marine Corps' VMO squadrons. The majority of these squadrons are still active in the Fleet Marine Force today.
Squadron Name Insignia Nickname Date Decommissioned Source HMLA-269 The Gunrunners December 9, 2022 [133] HMLA-467 Sabers June 16, 2016 [134] HMLA-469 Vengeance December 16, 2022 [135]
Marine Medium Tiltrotor Squadron[]
Marine tiltrotor squadrons operate the MV-22 Osprey with their main mission being assault support. The Osprey offers twice the speed, five times the range, and can fly more than twice as high as the CH-46 Sea Knight it replaced. The Marine Corps has 18 operational Osprey squadrons as of April 2018.
Squadron Name Insignia Nickname Date Decommissioned Source VMM-166 Sea Elk October 1, 2021 [136] VMM-264 Black Knights June 24, 2020 VMM-561 Pale Horses July 7, 2012
Training squadrons[]
Squadron Name Insignia Nickname Date Decommissioned Source VMAT-20
Marine Attack Training Squadron VMAT-102
Marine Attack Training Squadron Skyhawks October 1, 1987 VMT-103
Marine Training Squadron Sky Chickens June 1, 1972 [137] VMFAT-201
Marine Fighter Attack Training Squadron Hawks September 30, 1974 [138] VMAT(AW)-202
Marine All-Weather Attack Training Squadron Double Eagles 1990 VMAT-203
Marine Attack Training Squadron Hawks October 29, 2021 [139] VMGRT-253
Marine Aerial Refueler Transport Training Squadron Titans September 14, 2006 HMT-301
Marine Helicopter Training Squadron
Windwalkers June 3, 2005 [140] HMHT-401
Marine Heavy Helicopter Training Squadron May 1, 1972 [141] HMMT-402
Marine Medium Helicopter Training Squadron May 1, 1972 [141]
See also[]
United States Marine Corps Aviation
List of United States Marine Corps battalions
List of United States Marine Corps aircraft wings
List of active United States Marine Corps aircraft squadrons
Notes[]
References[]
Bibliography | ||
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Marine Observation Squadron
(VMO-251) History
Prologue: Although not the first observation squadron, VMO-251âs story is included because it was the first USMC squadron with a designated photo reconnaissance mission and the first to actually be assigned aircraft (F4F-3P, F4F-7P) modified with aerial camera systems. On 23 July 1942, by operational necessity, two ground photographers assigned to the squadron flew as operators of Navy supplied cameras installed in two USAAF B-17âs under inflight direction of Lcdr Quackenbush on a successful mission from their base in New Caledonia to take a set of pre-invasion photographs for the CG 1stMARDIV, perhaps the most critical photo mission of WWII!! (by Col H. Wayne Whitten USMC (ret), 2008)
VMO-251 was commissioned at NAS North Island on 1 December 1941. Ironically, the first CO (for 11 days) was Capt. Elliot Bard who subsequently was CO of VMD-154 during it deployment to the South Pacific combat zone in the Fall of 1942. Clearly, VMO-251 can lay claim as being the first USMC reconnaissance squadron although its first year of operations involved so many varied missions that the squadron patch depicted a war-like octopus! It wasnât until 1 May 1942 that a decision was made to transfer some Navy F4F-3 Hellcats to the squadron for conversion to the F4F-3P photo reconnaissance variant by the co-located support facility. The modification involved replacing the reserve fuel tank behind the pilot with two aerial cameras. This decision was quickly followed by a warning order to prepare to embark aboard transports for the South Pacific to support impending 1st MARDIV operations.
The advance party including most of the pilots, mechanics and photographers departed on 17 June under their CO Major John N. Hart with a few of the F4F-3Ps partially dismantled for shipment. Their ship arrived at Noumea, New Caledonia early in July and began to set up at Tontouta airfield about 35 miles away. The CO reported to COMAIRSOPAC (RADM McCain, the grandfather) who a couple of weeks later ordered him to begin training for air defense missions as their aircraft retained their guns and didnât as yet have extended range tanks. McCain no doubt was concerned about local air defense as on 15 July the Japanese hit Tontouta with a mini-Pearl Harbor like raid destroying or damaging 45 aircraft perhaps some of Hartâs F4F-3Ps which were being put together there. By coincidence, Lcdr Quackenbush, a classmate of Hart at Navy Photo School, had also just arrived and assigned as the Admirals photo officer with direction to get pre-invasion photos of Guadalcanal, albeit he had no photo aircraft! He commandeered 2 USAAF B-17s, modified them with Navy aerial cameras, and enlisted two of Hartâs photographers to accompany him on a crucial 27 July mission to get a mosaic of the landing areas and defenses of Guadalcanal, some 1000 miles to the North. Miraculously, they did so despite being attacked by Japanese float planes (they shot down several), and having to land on another island. The film was flown back to Noumea via PBYs, processed and then flown out to the Marinesâs flagship by a PBY flying boat.
When the Guadalcanal landing order was received a few days later the squadron was ordered to move North to the island of Espiritu Santo where it was to assume the primary air defense role and provide airbase support for the 11th Bombardment Groupâs B-17s supporting the invasion force, over 500 miles North. The advance party arrived on Espiritu Santo on 4 August, just 3 days before the landings, oddly enough on the same transport that had just arrived with the remainder of the squadron and its equipment. Luckily, the island was at the outer range of Japanese bombers as it was some time before a creditable air defense capability was established. From August through November, VMO-251 performed about every mission in the book, from full service air base support, ferrying combat aircraft back and forth to Guadalcanal and other bases, providing aircrews for observation missions on cruiser-based aircraft, and of course continuing to provide photographers for the USAAF B-17s. They also assisted Lcdr Quackenbush in setting up his photo lab on the island. On 10 August, the XO and a small detachment flew to Guadalcanal to lead the effort at Henderson field to prepare for MAG-23âs aircraft. MAG-23âs squadrons and others of the famous Cactus Air Force proved instrumental in staving off the relentless Japanese assaults against the Marines when the Navy aircraft carriers were forced to withdraw. Two of VMA-251âs TAD pilots were lost when their ships were sunk during the Japanese attacks on the night of 8 August. Many of VMO-251âs pilots were involved in combat action as they came and went over the first 3 months.
In early October, a newly arrived F4F-7P photo reconnaissance variant with extended range tanks but no armament was ferried into Guadalcanal and Capt Longley and a support team was sent TAD to fly it. This likely was the first dedicated USMC photo reconnaissance aircraft to enter combat as there is no mention of the squadrons F4F-3Ps making it to Guadalcanal before then, and VMD-154 didnât arrive with its B-24D/PBY4-1 dedicated photo reconnaissance aircraft until later at Espiritu Santo. In December, VMO-251 under a new CO was nearly completely reorganized as a fighter squadron and eventually in February 1943 moved to Guadalcanal presumably still with at least some of its photo variant aircraft.
VMO-251 departed the combat zone later in 1943 but was to return as a fighter squadron in 1944 although not being redesignated as VMF-251 until January 1945. VMO-251 received a Presidential Unit Citation for the period 7 August â 9 December 1942, and a citation from the USAAF 11th Bombardment Group for supporting its photo reconnaissance missions. | ||||||
wrong_mix_random_subsidiary_00131 | FactBench | 3 | 41 | https://medicine.wustl.edu/research/nobel-prize-winners/ | en | Nobel Prize Winners – Washington University School of Medicine in St. Louis | [
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] | null | [] | 2016-11-23T17:51:49+00:00 | Washington University and the School of Medicine have a long tradition of pursuing novel approaches and expanding the bounds of... MORE» | en | https://medicine.wustl.edu/wp-content/themes/medicine/_/img/favicon.ico | Washington University School of Medicine in St. Louis | https://medicine.wustl.edu/research/nobel-prize-winners/ | Nobel Prize Winners
Washington University and the School of Medicine have a long tradition of pursuing novel approaches and expanding the bounds of what is known.
At the School of Medicine, this tradition has roots in the vision of university board member Robert S. Brookings, who in 1909 was determined to transform the medical school into a model for American medical education and research. Among the first recruits to this “modern medical school” was Joseph Erlanger, who Brookings appointed head of the physiology department in 1910. Three decades later, Erlanger won a Nobel prize.
To date, 19 Nobel laureates have ties to the School of Medicine, and the tradition continues. With an ever-growing infrastructure that supports collaboration, innovation and entrepreneurship, we equip our outstanding faculty, students and trainees with the resources to pursue discoveries that may shape science and medicine for generations to come.
1927: Arthur H. Compton (1892 – 1962)
Physics
“For his discovery of the effect named after him”
Washington University affiliations:
Professor of Physics (1920 – 23); Chancellor (1945 – 53); Distinguished Service Professor of Natural Philosophy (1954 – 61)
Nobel biography »
1943: Edward A. Doisy (1893 – 1986)
Physiology or Medicine
“For his discovery of the chemical nature of vitamin K”
Washington University affiliations:
Instructor (1919 – 20), Associate (1920 – 22) and Associate Professor (1922 – 23) of Biological Chemistry
Nobel biography »
1944: Joseph Erlanger (1874 – 1965)
Physiology or Medicine
“For … discoveries relating to the highly differentiated functions of single nerve fibres”
Washington University affiliation:
Professor of Physiology (1910 – 46)
Nobel biography »
1944: Herbert S. Gasser (1888 – 1963)
Physiology or Medicine
“For … discoveries relating to the highly differentiated functions of single nerve fibres”
Washington University affiliations:
Instructor (1916 – 18), Associate (1918 – 20) and Associate Professor of Physiology (1920 – 21); Professor of Pharmacology (1921 – 31)
Nobel biography »
1947: Carl F. Cori (1896 – 1984)
Physiology or Medicine
“For … discovery of the course of the catalytic conversion of glycogen”
Washington University affiliations:
Professor of Pharmacology (1931 – 46); Professor of Biological Chemistry (1942 – 66)
Nobel biography »
1947: Gerty T. Cori (1896 – 1957)
Physiology or Medicine
“For … discovery of the course of the catalytic conversion of glycogen”
Washington University affiliations:
Fellow and Research Associate in Pharmacology (1931 – 44); Research Associate in Biological Chemistry (1943 – 44); Associate Professor of Pharmacology and Biological Chemistry (1944 – 47); Professor of Biological Chemistry (1947 – 57)
Nobel biography »
In the news: Cori Nobel Prize medals donated to Washington University
Watch the video »
1959: Arthur Kornberg (1918 – 2007)
Physiology or Medicine
“For … discovery of the mechanisms in the biological synthesis of ribonucleic acid and deoxiribonucleic acid”
Washington University affiliation:
Professor of Microbiology (1953 – 59)
Nobel biography »
1959: Severo Ochoa (1905 – 93)
Physiology or Medicine
“For … discovery of the mechanisms in the biological synthesis of ribonucleic acid and deoxiribonucleic acid”
Washington University affiliation:
Instructor and Research Associate in Pharmacology (1941 – 42)
Nobel biography »
1969: Alfred Hershey (1908 – 97)
Physiology or Medicine
“For … discoveries concerning the replication mechanism and the genetic structure of viruses”
Washington University affiliations:
Assistant (1934 – 36), Instructor (1936 – 39), Assistant Professor (1939 – 46) and Associate Professor (1946 – 50) of Bacteriology and Immunology
Nobel biography »
1971: Earl W. Sutherland, Jr.
(1915 – 74)
Physiology or Medicine
“For his discoveries concerning the mechanisms of the action of hormones”
Washington University affiliations:
Student Assistant (1940 – 43) and Instructor (1945 – 46) in Pharmacology; Instructor (1946 – 50), Assistant Professor (1950 – 51) and Associate Professor (1951 – 53) of Biological Chemistry
Nobel biography »
1978: Daniel Nathans (1928 – 99)
Physiology or Medicine
“For the discovery of restriction enzymes and their application to problems of molecular genetics”
Washington University affiliation:
Graduate of the School of Medicine (Class of 1954)
Nobel biography »
1980: Paul Berg (1926)
Chemistry
“For his fundamental studies of the biochemistry of nucleic acids, with particular regard to recombinant DNA”
Washington University affiliations:
Research Fellow and Instructor (1954); Assistant Professor (1955 – 57) and Associate Professor (1957 – 59) of Microbiology
Nobel biography »
1986: Stanley Cohen (1922 – 2020)
Physiology or Medicine
“For … discoveries of ‘Growth Factors'”
Washington University affiliations:
Research Fellow (1952 – 53) and Research Associate (1953 – 59) in Zoology
Nobel biography »
1986: Rita Levi-Montalcini (1909 – 2012)
Physiology or Medicine
“For … discoveries of ‘Growth Factors'”
Washington University affiliations:
Research Associate (1947 – 51), Associate Professor (1951 – 58) and Professor (1958 – 77) of Zoology
Nobel biography »
1992: Edwin G. Krebs (1918 – 2009)
Physiology or Medicine
“For … discoveries concerning reversible protein phosphorylation as a biological regulatory mechanism”
Washington University affiliations:
Graduate of the School of Medicine (Class of 1943); Intern and Resident at Barnes-Jewish Hospital (1944 – 46); Research Fellow in Biological Chemistry (1946 – 48)
Nobel biography »
1998: Robert F. Furchgott (1916 – 2009)
Physiology or Medicine
“For … discoveries concerning nitric oxide as a signalling molecule in the cardiovascular system”
Washington University affiliations:
Assistant Professor (1946 – 52) and Associate Professor (1952 – 56) of Pharmacology
Nobel biography »
2004: Aaron Ciechanover (1947)
Chemistry
“For the discovery of ubiquitin-mediated protein degradation”
Washington University affiliation:
Visiting Professor of Pediatrics (1987 – 2001)
Nobel biography »
2012: Brian K. Kobilka (1955)
Chemistry
“For studies of G-protein-coupled receptors”
Washington University affiliation:
Medical Resident at Barnes Hospital (1981 – 84)
Nobel biography »
2020: Charles M. Rice, PhD (1952)
Physiology or Medicine
“For the discovery of Hepatitis C virus”
Washington University affiliation:
Conducted his seminal work while on the faculty from 1986 to 2000 | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 0 | 14 | https://link.springer.com/content/pdf/10.1007/978-1-4684-4955-6.pdf | en | The Patient | [
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wrong_mix_random_subsidiary_00131 | FactBench | 1 | 19 | https://med.stanford.edu/news/all-news/2013/10/thomas-sudhof-wins-nobel-prize-in-physiology-or-medicine.html | en | Thomas Sudhof wins Nobel Prize in Physiology or Medicine | [
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] | 2013-10-07T00:00:00-07:00 | en | /etc/clientlibs/sm/images/SM-Shield-152x152.png | News Center | http://med.stanford.edu/news/all-news/2013/10/thomas-sudhof-wins-nobel-prize-in-physiology-or-medicine.html | Südhof noted that, although he hasn't directly worked with either of the other winners, their work was complementary and he called the Nobel committee "ingenious" in pairing the three of them. The researchers will share a prize that totals roughly $1.2 million, with about $413,600 going to each.
"Tom Südhof has done brilliant work that lays a molecular basis for neuroscience and brain chemistry," said Roger Kornberg, PhD, Stanford's Mrs. George A. Winzer Professor in Medicine. Kornberg was awarded the Nobel Prize in Chemistry in 2006. He is the son of Arthur Kornberg, in whose lab Schekman received his doctorate.
'Dazed and happy'
Robert Malenka, MD, Stanford's Nancy Friend Pritzker Professor in Psychiatry and Behavioral Sciences, is at the conference in Spain with Südhof, a close collaborator. "He's dazed, tired and happy," Malenka said by phone. "The only time I've seen him happier was when his children were born."
Südhof, the Avram Goldstein Professor in the School of Medicine, received the award for his work in exploring how neurons in the brain communicate with one another across gaps called synapses. Although his work has focused on the minutiae of how molecules interact on the cell membranes, the fundamental questions he's pursuing are large.
"The brain works by neurons communicating via synapses," Südhof said in a phone conversation this morning shortly after the announcement. "We'd like to understand how synapse communication leads to learning on a larger scale. How are the specific connections established? How do they form? And what happens in schizophrenia and autism when these connections are compromised?" In 2009, he published research describing how a gene implicated in autism and schizophrenia alters mice's synapses and produces behavioral changes in the mice, such as excessive grooming and impaired nest building, that are reminiscent of these human neuropsychiatric disorders.
Lloyd Minor, MD, dean of the School of Medicine, said, "Thomas Südhof is a consummate citizen of science. His unrelenting curiosity, his collaborative spirit, his drive to ascertain the minute details of cellular workings, and his skill to carefully uncover these truths — taken together it's truly awe-inspiring.
"He has patiently but relentlessly probed one of the fundamental questions of medical science — perhaps the fundamental question in neuroscience: How nerve cells communicate with each other. The answer is at the crux of human biology and of monumental importance to human health. Dr. Südhof's receipt of this prize is inordinately well-deserved, and I offer him my heartfelt congratulations. His accomplishment represents what Stanford Medicine and the biomedical revolution are all about."
Sweden calling
Robert Malenka
Thomas Sudhof pauses in Spain to celebrate winning a Nobel prize. Sudhof was on his way to the Sede Antonio Machado to deliver a lecture today about his work when he received the call from Sweden.
The Nobel committee called Südhof on his cell phone after trying his home in Menlo Park, Calif. His wife, Lu Chen, PhD, associate professor of neurosurgery and of psychiatry and behavioral sciences, then gave the committee his cell phone number to reach him in Spain.
"The phone rang three times before I decided to go downstairs and pick it up," Chen said. "I thought it was one of my Chinese relatives who couldn't figure out the time zone."
Chen and Südhof have two young children, and Südhof has four adult children from a previous marriage. "I was very surprised," Chen said, "but he's more concerned about how I'll get the kids up this morning in time for school."
"I was expecting a call from a colleague about the conference I'm here to attend, so I pulled off in a parking lot," said Südhof, who was driving from Madrid to Baeza at the time he received the announcement. "I hadn't slept at all the previous night, and I certainly wasn't expecting a call from the Nobel committee."
On the day he got that call, he was scheduled to give a talk at a conference, Membrane Traffic at the Synapse: The Cell Biology of Synaptic Plasticity, being held in Baeza in a 17th-century building that now serves as a conference center.
"Professor Sudhof's contributions to the understanding of how cells operate have been of enormous importance to medicine, and to his own work in understanding how connections form within the human brain," said Stanford President John Hennessy. "The recognition by the Nobel committee is a remarkable achievement."
Südhof, who is also a Howard Hughes Medical Institute investigator, has spent the past 30 years prying loose the secrets of the synapse, the all-important junction where information, in the form of chemical messengers called neurotransmitters, is passed from one neuron to another. The firing patterns of our synapses underwrite our consciousness, emotions and behavior. The simple act of taking a step forward, experiencing a fleeting twinge of regret, recalling an incident from the morning commute or tasting a doughnut requires millions of simultaneous and precise synaptic firing events throughout the brain and peripheral nervous system.
"We're thrilled to see years of curiosity and persistence pay off for Tom with this terrific recognition," said Erin O'Shea, PhD, vice president and chief scientific officer at HHMI. "You know, what culminates in a Nobel Prize usually begins 20 or 30 years earlier, with a good idea and the guts to pursue it. HHMI likes to say that it supports people, not projects, and we join Stanford in toasting Tom and his collaborators for showing us the promise of basic research, fulfilled."
Outnumbering the Milky Way
Thomas Sudhof
Even a moment's consideration of the total number of synapses in the typical human brain adds up to instant regard for that organ's complexity. Coupling neuroscientists' ballpark estimate of 200 billion neurons in a healthy adult brain with the fact that any single neuron may share synaptic contacts with as few as one or as many as 1 million other neurons (the median is somewhere in the vicinity of 10,000) suggests that your brain holds perhaps 2 quadrillion synapses — 10,000 times the number of stars in the Milky Way.
"The computing power of a human or animal brain is much, much higher than that of any computer," said Südhof. "A synapse is not just a relay station. It is not even like a computer chip, which is an immutable element. Every synapse is like a nanocomputer all by itself. The amount of neurotransmitter released, or even whether that release occurs at all, depends on that particular synapse's previous experience."
Much of a neuron can be visualized as a long, hollow cord whose outer surface conducts electrical impulses in one direction. At various points along this cordlike extension are bulbous nozzles known as presynaptic terminals, each one housing myriad tiny, balloon-like vesicles containing neurotransmitters and each one abutting a downstream (or postsynaptic) neuron.
When an electrical impulse traveling along a neuron reaches a presynaptic terminal, calcium from outside the neuron floods in through channels that open temporarily in the terminal. A portion of the neurotransmitter-containing vesicles fuse with the terminal's outer membrane and spill their contents into the narrow gap separating the presynaptic terminal from the postsynaptic neuron's receiving end.
Südhof, along with other researchers worldwide, has identified integral protein components critical to the membrane fusion process. Südhof purified key protein constituents sticking out of the surfaces of neurotransmitter-containing vesicles, protruding from nearby presynaptic-terminal membranes, or bridging them. Then, using biochemical, genetic and physiological techniques, he elucidated the ways in which the interactions among these proteins contribute to carefully orchestrated membrane fusion: As a result, synaptic transmission is today one of the best-understood phenomena in neuroscience.
Born in Germany
L.A. Cicero/Stanford News Service
(Right) Lu Chen, wife of Nobel prize winner Thomas Sudhof, gathers with Südhof's postdocs and grad students to celebrate the award today. The lab members ate pizza and toasted Sudhof, who is attending a conference in Spain.
Südhof, who was born in Germany in 1955, earned an MD in 1982 from Georg-August-Universität in Göttingen. He came to Stanford in 2008 after 25 years at the University of Texas Southwestern Medical Center at Dallas, where he first worked as a postdoctoral scholar in the laboratories of Michael Brown, MD, the director of the Eric Jonsson Center for Research in Molecular Genetics and Human Disease, and Joseph Goldstein, MD, chair of the Molecular Genetics Department. Brown and Goldstein were awarded the Nobel Prize in Physiology or Medicine in 1985 for their work in understanding the regulation of cholesterol metabolism. In 1986, Südhof established his own laboratory at the university.
"Thomas Südhof is a biomedical exceptionalist — like Babe Ruth was an exceptionalist in baseball, Leonard Bernstein in music, and Steve Jobs in computers," said Goldstein. "Having done his Nobel work at UT-Southwestern in Dallas, Thomas is our sixth faculty member to win a Nobel prize. This is quite a record for a relatively 'small' medical school."
Südhof became an HHMI investigator in 1986, and moved to Stanford as a professor in molecular and cellular physiology in 2008. With this award, Stanford's Department of Molecular and Cellular Physiology now includes three Nobel laureates: Südhof; Brian Kobilka, MD, who received the Nobel Prize in Chemistry in 2012; and Steven Chu, PhD, who received the Nobel Prize in Physics in 1997. (Chu recently joined the department. He is the William R. Kenan Jr. Professor of Physics and professor of molecular and cellular physiology at Stanford. Until April, he served as U.S. Secretary of Energy.)
"This is fantastic news and greatly deserved. I'm very happy for Tom, and we are all proud to have him as a colleague in our department," said Kobilka. "We've always been an amazing department; it's just that most of the academic world didn't know it."
"I'm really thrilled and proud that we have such outstanding and amazing research going on in our department," said Axel Brunger, PhD, professor and chair of molecular and cellular physiology, as well as professor of neurology and neurological sciences, who has been involved in a series of joint projects with Sudhof.
"Dr. Südhof's work has set the stage for a deep understanding of the complexities of neuronal communication."He's a great collaborator. We had really great interactions with him and his group. He's willing to help and to share data results."
The proteins Südhof and his lab have focused on for close to three decades are disciplined specialists. They recruit vesicles, bring them into "docked" positions near the terminals, herd calcium channels to the terminal membrane, and, cued by calcium, interweave like two sides of a zipper and force the vesicles into such close contact with terminal membranes that they fuse with them and release neurotransmitters into the synaptic gap. Although these specialists perform defined roles at the synapses, similar proteins, discovered later by Südhof and others, play comparable roles in other biological processes ranging from hormone secretion to fertilization of an egg during conception to immune cells' defense against foreign invaders.
"We've made so many major advances during the past 50 years in this field, but there's still much more to learn," said Südhof, who in a 2010 interview with The Lancet credited his bassoon instructor as his most influential teacher for helping him to learn the discipline to practice for hours on end. "Understanding how the brain works is one of the most fundamental problems in neuroscience."
He elaborated in the press call a few hours after the announcement. "There is a gap, a tremendous gap, between the need to understand diseases that affect the brain and the understanding that we have. Not because of lack of effort, but because the problem is so daunting. I do think that our work will contribute a little to the task, which is enormous. I am convinced that will eventually lead to therapies." In addition to schizophrenia and autism, Südhof cited the role of synapse dysfunction in Parkinson's disease and a rare but devastating childhood seizure disease called Ohtahara syndrome.
Südhof's accomplishments also earned him the 2013 Lasker Basic Medical Research Award. He is a member of the National Academy of Sciences, the Institute of Medicine and the American Academy of Arts & Sciences. He also is a recipient of the 2010 Kavli Prize in neuroscience.
The value of basic science
In the Lancet interview, Südhof defined basic research as an approach often neglected in the pursuit of medicine. "This 'solid descriptive science,' like neuroanatomy or biochemistry, [are] disciplines that cannot claim to immediately understand functions or provide cures, but which form the basis for everything we do."
"I think that in general the value of science is being heavily discussed in the U.S., and it worries me tremendously," said Südhof during the press call in response to a question about declining levels of funding for this type of research. "In my personal view, Western civilization is based in part on science; it is part of our Greco-Roman heritage, this search for truth. But it seems to me that there is a significant, increasingly vocal population that thinks we shouldn't go after truth, and that truth is not important. That worries the hell out of me."
Calling the value of unbiased information the "core of my personal beliefs," Südhof said he feels funding for his type of award-winning research is in danger. "Many people say, 'We've spent so much money on research, and we should get something out of it.'" Südhof argued that, in fact, there has been enormous progress, and enormous benefit, from research spending, the amount of which pales when compared to that spent on medical treatment.
"We need to make sure that research funding is awarded based on merit, and not based on location or political connections," said Südhof . "It should be based on what someone actually does."
Asked what advice he would give to a new college graduate, Südhof replied, "More than anything, follow your passions. What are you actually interested in? What work satisfies you? I have met so many unhappy rich people. I think that, in order for a person to reach his or her potential and to be happy is to work in an area that they enjoy, can support and feel good about. I have given the same advice to my adult children."
Südhof said this morning he is excited to speak with his family about the prize, although it may be too much for his youngest children, ages 3 and 4, to grasp. "I will try to explain it to them," he said. "It will be a wonderful occasion." He noted that he has already received congratulatory calls from two of his older children. For them, the news may have come as less of a surprise.
"The Nobel prize became an inevitable topic of conversation when Tom won the Lasker award," Chen said. "But the two of us share a feeling that one should never work for prizes." Asked if she was tempted to tell her husband herself, rather than letting the Nobel committee do the honors, Chen, who said her first two loves are "neuroscience and Tom," answered, "No, I wanted him to hear it from them because the thrill is different. I didn't want to deprive him of that."
"Everyone has pegged him as a potential Nobel prize winner for many years," said Malenka. "It was just a matter of time."
Although he plans to return to the United States later this week, Südhof has no plans to let the award slow his research — or even his plans for the day. He responded to an inquiry with a characteristically low-key reply. "Well, I think I'll go ahead and give my talk." | |||||
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] | null | [] | null | The Nobel Prize in Physiology or Medicine 2021 was awarded jointly to David Julius and Ardem Patapoutian "for their discoveries of receptors for temperature and touch" | en | NobelPrize.org | https://www.nobelprize.org/prizes/medicine/2021/advanced-information/ | Advanced information
Scientific background:
Discoveries of receptors for temperature and touch (pdf)
Scientific background
Discoveries of receptors for temperature and touch
The 2021 Nobel Prize in Physiology or Medicine is awarded to David Julius and Ardem Patapoutian for their discoveries of thermal and mechanical transducers. The question of how we sense the physical world through somatic sensation has fascinated humankind for millennia. During the first half of the 20th century, it became clear that temperature and pressure activate different types of nerves in the skin. However, the identity of the molecular transducers responsible for detecting and converting heat, cold and touch into nerve impulses in the sensory nervous system remained a mystery until the discoveries awarded with this year’s Nobel Prize. David Julius wished to identify the cellular target of capsaicin, the pungent ingredient of chili peppers, as he believed this could provide fundamental insights into mechanisms of pain. He used a cDNA library from sensory neurons in a functional screen to look for a gene that could confer capsaicin sensitivity to cells that were normally unresponsive. The screen identified a cDNA encoding a novel ion channel (now called TRPV1) belonging to the family of transient receptor potential ion channels. Importantly, TRPV1 was shown to be activated by temperatures perceived as painful. Following the discovery of TRPV1, David Julius and Ardem Patapoutian independently made another important advance with the discovery of TRPM8, a related cold-sensitive receptor. Several additional TRP-receptors were subsequently identified and shown to transduce thermal information in the somatosensory system. Thus, the seminal discovery of TRPV1 by David Julius opened the door to a molecular understanding of thermosensation. Ardem Patapoutian used a functional screen of candidate genes expressed in a mechanosensitive cell line to identify ion channels activated by mechanical stimuli. Two mechanically-activated ion channels, named PIEZO1 and PIEZO2, were identified and shown to represent an entirely novel class of ion channels functioning as mechanical sensors. Importantly, Patapoutian also demonstrated that PIEZO2 is the major mechanical transducer in somatic nerves and is required for our perception of touch and proprioception. In further work, he uncovered central roles of PIEZO1 and PIEZO2 for many additional physiological functions. The work by the two laureates has unlocked one of the secrets of nature by explaining the molecular basis for sensing heat, cold and mechanical force, which is fundamental for our ability to feel, interpret and interact with our internal and external environment.
From moving particles to nerve conduction
Somatic sensation has fascinated humankind for millennia. In an attempt to explain how we react to heat, the 17th century philosopher René Descartes depicted that particles of fire pulled a thread between the skin and brain [1]. In the 1880s, distinct sensory spots on the skin were shown to react to specific stimuli, such as touch, heat or cold, indicating that different stimuli activate different types of nerves [2, 3]. Three previous Nobel Prizes in Physiology or Medicine have significantly advanced our understanding of the somatic sensory nervous system. In 1906, Camillo Golgi and Santiago Ramón y Cajal received the Nobel Prize for their work on the structure of the nervous system, which included an anatomical description of the somatosensory system. Sir Charles Sherrington and Edgar Adrian received the Nobel Prize in 1932 for their discoveries regarding the function of neurons, including a description of somatosensory neurons. In 1944, Joseph Erlanger and Herbert Spencer Gasser received the Nobel Prize for their discoveries related to the differentiated functions of single somatosensory nerve fibers. These discoveries established important principles for the propagation of action potentials along skin and muscle sensory nerve fibers. The discovery of different nerve fiber types with distinct conduction velocities, activation thresholds and refractory periods, made it possible to link specific nerve fiber types to different somatosensory modalities, such as proprioception (the sense of our body’s movement and position in space), touch and temperature sensation. However, fundamental questions remained unsolved: What is the nature and molecular identity of the receptors that can sense temperature and touch and how can those sensors convert stimuli into action potentials within the somatosensory nerve fibers?
Sensing the environment
The ability to sense and adapt to the environment is essential for survival in all organisms. For example, bacteria adapt to changes in osmotic force through the activation of mechanosensitive ion channels enabling them to survive when trapped in rainwater [4, 5]. In humans and other animals, somatic sensation arises from the body surface or internal organs and endow us with the sense of touch, proprioception, pain and temperature. These are vital functions allowing organisms to continuously adapt to changes in the external and internal environment.
Somatic senses involve peripheral sensory pathways that detect and convert objective information about the physical properties of various stimuli (e.g. mechanical and thermal) into electrical signals that are conveyed to the central nervous system. The sense of touch, initiated by the detection of mechanical force, provides us with the recognition of texture, size and shape of objects as well as tactile and vibration sensitivity. This sense, for example, allows us to recognize the softness of a pillow, gentle caress of the skin or the feeling of a breeze. The capacity of discrimination of perceptual qualities arises from unique functions of a variety of sensory neurons involved in touch sensation. Thus, different stimuli, such as skin indentation, skin stretch, hair deflection or vibration, activate different types of sensory neurons [6]. The somatosensory system also conveys information on limb movement and position in space (i.e., proprioception), allowing us to sense when an arm or a leg is stretched or folded.
Another aspect of somatic sensation relates to pain induced by noxious stimuli that activate a class of polymodal nerve fibers (called nociceptors) in response to strong mechanical force and painful heat [7, 8]. These nociceptors transmit information on potentially harmful changes in our physical environment, e.g. when touching a hot stove or holding a hand in ice water. Accordingly, pain represents an essential protective mechanism that prevents tissue damage through reflex reactions.
Apart from providing conscious awareness about our body and its surroundings, the somatosensory system is also essential for tasks that we perform effortlessly and without much thought. For example, when drinking a glass of water, sensory neurons convey information about the weight, size, texture and temperature of the glass so that an appropriate grip strength can be applied and movements coordinated when taking a sip. Similarly, the seemingly simple task of walking also requires a continuous flow of sensory information to coordinate and correct limb move-ments and maintain balance.
Through their ground-breaking work the 2021 Nobel Prize laureates have identified the long sought molecular transducers for sensing temperature and mechanical force. Their discoveries have unlocked one of the remaining mysteries of how somatic sensation enables us to feel and interact with the physical world.
The discovery of thermosensitive ion channels for thermal sensation
A prelude
Capsaicin (8-methyl-N-vanillyl-6-nonenamide), the active component of chili peppers, gives the burning sensation when eating spicy food. Studies on the chemical provided important insights that opened for the discovery of the first heat-sensitive receptor. Studies in the 1950s showed that sweating of the head is induced when hot peppers are in contact with the mouth or lips, a phenomenon called gustatory sweating [9]. During the following decades, capsaicin was found to act on sensory nerves [10] and to induce ionic currents [11-14]. In parallel, it was also shown that noxious heat produced activation of ion channels in sensory neurons [15, 16]. However, it was not fully clear if the channel itself was the transducer of thermal energy.
The discovery of TRPV1 as a thermosensitive ion channel in sensory neurons
In the late 1990s, David Julius at the University of California, San Francisco, pursued a project to identify the receptor for capsaicin. He thought that understanding the action of capsaicin could provide insights into pain signaling. Together with a postdoctoral fellow, Michael J. Caterina, Julius decided to conduct an unbiased functional screen based on the assumption that a single gene can confer capsaicin sensitivity in cells that are normally insensitive to capsaicin. To find this putative gene, Julius and coworkers made a cDNA library from rodent dorsal root ganglia that contain the cell bodies of the capsaicin-activated sensory neurons. Capsaicin-insensitive cells were transfected with batches of these cDNAs and eventually a single cDNA clone was isolated that could confer responsiveness to capsaicin [17] (Figure 1A). The isolated gene was predicted to encode an integral membrane protein with six transmembrane domains and a homology search revealed that it belonged to the superfamily of transient receptor potential (TRP) cation channels [18, 19]. Julius continued to functionally characterize the TRPV1 receptor (at the time called vanilloid receptor 1, VR1) by ectopic expression in cells and found that the capsaicinevoked electrophysiological properties resembled those of channels found in native sensory neurons. He also noted that the transfected cells became sensitive to cytotoxic effects induced by capsaicin and that the capsaicin-evoked responses could be blocked with an antagonist. Further characterization showed that TRPV1 was expressed in nociceptive dorsal root ganglion neurons, thus providing an explanation for the selective actions of capsaicin on these cells (Figure 1B). While exploring the physiology of TRPV1, Julius examined its sensitivity to elevated temperature and found a pronounced activation by heat leading to cellular Ca2+ influx. Direct measurement of currents using patch-clamp recordings revealed a specific heat-evoked membrane current with properties similar to those of sensory neurons. Furthermore, TRPV1 had an activation threshold (above 40°C) close to the psychophysical threshold for thermal pain (Figure 1C).
Shortly after identifying TRPV1, Julius went on to show that heat directly activates this channel in the absence of other factors, and that it acts as a molecular integrator of painful heat stimuli and chemical stimuli [20]. TRPV1 was expressed in unmyelinated nociceptive neurons, but not in neurons involved in proprioception, touch and pressure sensation, consistent with its role as a transducer of noxious heat. The role of TRPV1 as the only receptor activated by capsaicin and its essential role for transducing the nociceptive, inflammatory and hyperthermic effects of capsaicin was subsequently established in mice. TRPV1 is also required for inflammatory heat hyperalgesia in mice [21, 22]. Recent clinical studies of selective TRPV1 antagonists confirms a major role for this ion channel for sensing noxious heat in humans [23, 24]. The seminal discovery of TRPV1 as the capsaicin- and heat-activated ion channel in 1997 opened the field and represented a landmark achievement in our quest to understand the molecular and neural basis for thermal sensing.
The overall transmembrane topology and subunit architecture of TRPV1 and other TRP channels is similar to voltage-gated sodium and potassium channels [25, 26]. The structure of TRPV1 has been determined by cryo-electron microscopy in a collaboration between the Julius and Yifan Cheng laboratories. TRPV1 seems to have two gates that form two prominent physical constrictions at either end of the cation-conducting pore [27, 28]. Capsaicin binds a pocket in TRPV1 located deep in the membrane close to the cytoplasmic side. A recent structural study showed that noxious heat produces two conformational gating transitions in capsaicin-bound TRPV1 channels [29]. The first transition primes the channel for opening, while the second leads to channel opening. The structural studies of TRPV1 channels have provided important insights into mechanisms for their ion permeation, ligand recognition and gating, but the mechanisms for their activation by heat are not fully understood at the structural level. sensation.
The sensation of noxious heat
Whereas TRPV1 was found to have a critical role for the increased sensitivity to heat during inflammation, it was evident that other heat sensitive receptors must exist because animals lacking Trpv1 showed only a minor loss of acute noxious heat sensation [21, 22, 30, 31]. In 2011, Voets’ group identified TRPM3 as a second sensor for noxious heat in Trpv1 knockout mice [32]. However, the inactivation of both Trpv1 and Trpm3 in mice blunted, but did not eliminate, reflex responses to noxious heat. The attention therefore turned to a third TRP channel, TRPA1, which had been discovered in 2004 as a transducer for pungent chemicals independently by Julius and Patapoutian laboratories [33, 34]. TRPA1 is involved in the detection of a wide variety of noxious external stimuli, such as active compounds in mustard oil, horseradish, cinnamon, garlic, cloves, and ginger, as well as lipid compounds, environmental irritants and other chemicals [33-38]. The TRPA1 ion channel is polymodal and can be activated by various chemical substances, as well as by cold and heat in a way that differ between mammalian species [39]. Because of this complexity, the role for TRPA1 as a thermosensor in mammalian sensory neurons was debated [36, 40-43]. The question of which ion channels contribute to noxious heat sensation in mice was resolved when Voets` group showed that it depends on a triad of ion channels, namely TRPV1, TRPM3 and TRPA1 [44].
The sensation of cold
Non-noxious cold sensation in humans and mice starts around 28°C and has a remarkable precision detecting changes as small as 0.5°C in skin temperature [43, 45, 46]. In 2002, the sensory transducer for cold was independently discovered by the Julius and Patapoutian laboratories [47, 48] in functional screens based on the assumption that menthol, a natural compound that elicits the sensation of innocuous coolness in humans, binds an ion channel that is activated by low temperature. Both groups identified TRPM8, yet another member of the TRP superfamily, and found that it is activated by low temperature in a heterologous expression system at a temperature range at which humans perceive innocuous cold [47, 48]. Consistent with these findings, Julius, Patapoutian and other groups independently found that deletion of Trpm8 in mice causes clear deficits in sensation of innocuous cold [49-51]. The discovery of TRPM8 as a cold sensor placed the TRP superfamily at the center stage of thermal somatosensation and paved the way to the identification of additional TRP channels responsible for thermal sensation.
The sensation of warmth
The detection of changes in skin temperature is very precise, with changes of warmth detected with perceptual thresholds of around 1°C in humans [45, 52]. Similar to humans, mice also detect subtle changes of temperature in the warm range and this remarkable sensitivity to changes in temperature relies on TRP channels. While TRPV1 was initially considered only as a receptor for noxious heat, subsequent studies unexpectedly found that TRPV1 also contributes to detection of innocuous warmth [43]. Furthermore, Peter McNaughton’s group identified another TRP channel, TRPM2, as a potential warmth sensor. Deletion of the gene for this channel in mice resulted in deficits in the sensation of innocuous warm temperatures in the range (33-38°C) [53]. Recently, it was found that discrimination between warm and cool temperatures depends on the simultaneous activation of warmth-sensing and inhibition of cold-sensing nerve fibers [54]. The emerging picture is that TRPV1, TRPA1, TRPM2 and TRPM3 ion channels collectively act as warm sensors, but that the warmth sensation is reliably signaled only when the activity in TRPM8 containing cold-sensing nerve fibers is simultaneously suppressed by warm temperatures [54].
In conclusion, the seminal discovery of TRPV1 initiated intense investigation that has now firmly established the critical role of TRP channels for thermal sensation (Figure 2). The findings show that several TRP channels gated at different temperature ranges act together to code for temperature and heat-induced pain in the somatosensory nervous system. At present, important roles for TRPV1, TRPA1, TRPM3, TRPM2 and TRPM8 in temperature sensing have been experimentally established. Future studies will likely provide additional insights in this active research field.
The discovery of a vertebrate mechanosensitive ion channel
A prelude
The existence of a vertebrate mechanosensitive ion channel was suggested more than 40 years ago based on data showing rapid membrane depolarizations following mechanical stimulation of cochlear hair cells in frogs [55]. However, the existence of mechanosensitive channels was not firmly established until the late 1980’s when Ching Kung and Boris Martinac identified and characterized such channels in Escherichia coli [5, 56, 57]. The identified channels act as force sensors for adaptation to environmental changes and have an essential role as even a mild change in osmolarity cause bacteria to lyse in the absence of mechanosensitive channels [58].
The finding of a mechanosensitive ion current in rat dorsal root ganglion neurons suggested that touch sensation in vertebrates also rely on activation of a mechanosensitive ion channel [59]. However, orthologs of candidate channels previously identified in Caenorhabditis elegans and Drosophila melanogaster did not seem to play key roles for touch sensation in vertebrates [60]. Furthermore, several potentially mechanosensitive channels identified in vertebrates were not confirmed as critical touch receptors in functional experiments [60-63]. The identity of the receptors for somatic mechanosensation in mammals thus remained an enigma.
The discovery of PIEZO2 as a mechanosensitive ion channel for touch and proprioception
Ardem Patapoutian at Scripps Research, California developed a novel screening approach to search for the elusive receptor for mechanosensation in mammals. Together with the postdoctoral fellow Bertrand Coste, he identified an intrinsically mechanosensitive cell line, called Neuro2A, by using brief and rapid indentation of the plasma membrane in combination with patchclamp recording to detect any possible current induced by the mechanical force (Figure 3A) [64]. Once the mechanosensitive Neuro2A cell line was identified, Patapoutian performed global expression analysis and identified 72 candidate genes predicted to encode proteins with at least two membrane-spanning domains, which included known ion channels and proteins of unknown function. The candidate genes were silenced oneby-one by RNA interference and the transfected cells were tested to determine whether the application of mechanical force resulted in a current that could be recorded using patch-clamp. Knockdown of the final gene on the list, previously known as FAM38A, eliminated the mechanicallyactivated current and the corresponding protein was named PIEZO1 from the Greek word “piesi” meaning pressure (Figure 3B, red data point). Patapoutian proceeded to show that ectopic expression of PIEZO1 made human embryonic kidney cells (HEK-293) mechanosensitive, as pressure applied to the plasma membrane induced a large current in these cells. A second mechanosensitive channel, named PIEZO2, was subsequently discovered by sequence homology. The newly identified PIEZO channels belonged to a previously unknown protein family present in vertebrates and many other eukaryotes. PIEZO2, but not PIEZO1, was found to be expressed in dorsal root ganglion sensory neurons (Figure 3C) and knockdown of PIEZO2 abolished the mechanosensitivity of these sensory neurons (Figure 3D).
Direct evidence that PIEZO2 is the sensor for light touch was established in 2014, when Patapoutian and other researchers demonstrated that Merkel cells display a PIEZO2-dependent current evoked by fast touch- and that this current is sufficient to sustain action potential firing in tactile sensory afferents [65-67]. However, consistent with a “tworeceptor-site hypothesis” [68], stating that both Merkel cells and innervating sensory neurons are mechanosensitive, major components of touch sensation remained in the absence of Merkel cell activity. In a later study in 2014, Patapoutian engineered mice that lack PIEZO2 in both Merkel cells and adult sensory neurons. These mice were profoundly deficient in light touch sensation without impairment of thermosensation [69]. Consistent with these findings, humans with lossof-function mutations in PIEZO2 also display profound deficits in touch sensation, including texture discrimination, hair deflection as well as tactile and vibration sensitivity [70-73].
The Patapoutian group also demonstrated that PIEZO2 is the principal transduction channel for proprioception in mice as its absence results in severely uncoordinated body movements and abnormal limb positions [74]. Similar observations were also made in humans lacking functional PIEZO2 [70, 72]. The groundbreaking discovery of PIEZO proteins as excitatory ion channels directly gated by mechanical force has revolutionized the field of neuroscience by providing a molecular basis for mechanosensation.
PIEZO proteins represent an entirely new class of vertebrate mechanosensitive channels without any resemblance to previously known ion channel families. They are the largest transmembrane ion channel subunits identified to date, composed of 2,500 amino acids and display a unique 38transmembrane helix topology. Work from Patapoutian and other laboratories has revealed the high resolution structure of PIEZO1 and PIEZO2 and has shown that these channels form homotrimeric structures with a central ionconducting pore and three peripheral large mechanosensing propeller-shaped blades [7578]. The three blades curve out and up creating a nano-bowl configuration in the surface of the cell membrane [77-79]. When a mechanical force is applied to the membrane, the curved blades flatten out and lead to the opening of the central pore. The propeller-like structure with curved blades generate a large in-plane membrane area expansion, which likely explain the exquisite mechanosensitivity of PIEZO channels [77, 80]. However, the exact mechanisms whereby mechanical force opens the central pore are still not completely understood. Through their mechanosensitivity, PIEZO channels serve as versatile mechanotransducers in many cell types and convert mechanical force into electrochemical signals (Figure 4).
PIEZOs as mechanosensors in internal organs
In 1938, the Nobel Prize in Physiology or Medicine was awarded to Corneille Heymans for discovering the sensory function of the vagus nerve in reflexes, including the respiratory reflex as described by Hering and Breuer. In a collaboration with other research groups, the Patapoutian lab showed that deletion of Piezo2 in visceral nodose (vagal) sensory ganglion neurons of adult mice led to impairment of the HeringBreuer reflex and increased the respiratory tidal volume. Furthermore, deletion of Piezo2 during development caused respiratory distress and death at birth [81]. Thus, these studies show that PIEZO2 channels present on pulmonary stretch receptors in the wall of bronchi and bronchioles are activated by large inspirations and initiate a reflex protecting the lung from over-inflation.
Studies of the glossopharyngeal and vagus nerves by Corneille Heymans also identified the baroreflex. Patapoutian and collaborators demonstrated that the arterial baroreflex, which continuously monitors and maintains blood pressure, relies on both PIEZO1 and PIEZO2 present in nodose (vagus) and petrosal (glossopharyngeal) sensory neuron ganglia. Mice lacking Piezo1 and Piezo2 display a labile hypertension and have increased blood pressure variability, similar to the finding in humans with baroreflex failure [82, 83].
PIEZO2 is also important in the gastrointestinal tract where the enterochromaffin cells are inherently mechanosensitive and release hormones and paracrine signaling molecules in response to mechanical stimulation by gastrointestinal luminal content [84, 85]. Furthermore, PIEZO2 is the mechanosensor in urothelial cells and bladder sensory neurons. Mice and humans lacking functional PIEZO2 therefore have impaired urinary bladder control [86].
PIEZO1 plays an important role as a sensor of mechanical forces in endothelial cells, red blood cells, and osteoblasts in mice. The sensing of shear-stress in endothelial cells is important for the formation of blood vessels during development, for angiogenesis in adult tissues as well as for the regulation of vascular tone [87-91]. In addition to its role in blood vessel integrity, PIEZO1 is also present in red blood cells where it is involved in cell volume homeostasis. Piezo1 deletion in mice leads to overhydration of red blood cells whereas a chemical compound called Yoda1 that activates PIEZO1 leads to dehydration of red blood cells [92]. Strain induced by mechanical forces is linked to skeletal remodeling, and in mice the mechanical load-dependent bone formation relies on PIEZO1 in osteoblasts, where it functions as a mechanotransducer [93-95].
Relevance for humans and medicine
Behavioral studies of animal models have been critical for our understanding of the molecular mechanisms underlying temperature and touch. However, it is impossible to fully recapitulate human somatic sensations in animals and we cannot truly know whether a rodent is sensing touch or proprioception by merely studying its reactions. Studies in human subjects with genetic mutations in TRP and PIEZO channels have therefore provided significant insights into the roles of these channels in transducing temperature, pain, touch, vibration and proprioception.
Human genetics and temperature sensing TRP channels
There are several genetic “TRP channelopathies” in humans. Among the temperature sensing TRP channels, an autosomal dominant TRPA1 channelopathy named Familial Episodic Pain Syndrome type 1 is caused by a point mutation in TRPA1 and manifested by episodes of debilitating upper body pain triggered by cold, fasting and physical stress [96]. Several studies have investigated the role of single nucleotide polymorphisms (SNPs) in TRP channel genes and identified an association of TRPA1 710G>A with neuropathic pain and a paradoxical heat sensation. In addition, TRPV1 1911A>G has been associated with cold hypoalgesia [97], while several other SNPs in TRPV1 alters the sensitivity to capsaicin.
Mutations in PIEZO2 profoundly impact the sense of touch, vibration and proprioception
Patapoutian and several other researchers have reported that mutations in the PIEZO2 gene underlie several genetic disorders manifested by altered sensations of touch, vibration and proprioception. Whereas mice lacking PIEZO2 die at birth due to respiratory distress, humans with biallelic loss-of-function mutations survive. Lossof-function mutations in the PIEZO2 gene result in an autosomal recessive condition named distal arthrogryposis (DA) with congenital contractions in multiple joints of fingers, feet and toes along with impaired proprioception and touch (DAIPT) [7072, 98]. As more families with DAIPT from different parts of the world have been reported and the phenotypic manifestations are better understood, the alternative name PIEZO2 deficiency syndrome has been coined. Patients with PIEZO2 deficiency syndrome exhibit greatly attenuated proprioception, sense of touch and vibration. This results in sensory ataxia, dysmetria, gait difficulties, muscle weakness and atrophy, scoliosis, hip dysplasia and progressive skeletal contractures. These patients also have deficiencies of interoceptive sensations from the lung leading to perinatal respiratory distress and the bladder causing impairments in urination [86]. These patients fail to develop sensitization and painful reactions to touch after skin inflammation, suggesting a critical role for PIEZO2 is tactile allodynia [99]. However, patients with PIEZO2 deficiency syndrome have intact sense of innocuous deep pressure [100] and noxious mechanical pain responses [70, 99, 101].
Gain-of-function mutations of PIEZO2 cause autosomal dominant DA type 5, a form with prominent oculomotor symptoms [102, 103]. Other autosomal dominant mutations cause DA type 3, also called Gordon syndrome [103, 104], which is distinguished from other distal arthrogryposes by the presence of short stature and cleft palate. PIEZO2 gain-of-function mutations have also been reported in Marden-Walker Syndrome, a DA form characterized by psychomotor retardation, micrognathia and kyphoscoliosis [103].
Mutations in PIEZO1 impair physiological functions of red blood cells and the development of the lymphatic system
Mice lacking PIEZO1 die embryonically, whereas humans with biallelic loss-of-function mutations survive. Patapoutian and several other researchers have shown that biallelic loss-offunction mutations or compound heterozygous mutations in PIEZO1 causes an autosomal recessive, unique form of generalized lymphatic dysplasia, known as lymphatic malformation 6 [105, 106]. It is characterized by general facial and limb lymphoedema and indicate that PIEZO1 is involved in the development of the corresponding lymphatic structures.
Gain-of-function mutations in PIEZO1 leads to an autosomal dominant hemolytic anemia named dehydrated hereditary stomatocytosis (DHS) or hereditary xerocytosis [107-109]. This anemia is characterized by macrocytosis, the presence of stomatocytes and dehydration of red blood cells. The dehydration is caused by a defect in cellular cation content and some patients have a pseudohyperkalemia. Point mutations underlying DHS have been found at highly conserved residues in the C-terminal half of the PIEZO1 protein.
Patapoutian has shown that a gain-of-function E756del PIEZO1 allele causes dehydration of red blood cells and decrease the risk for severe Plasmodium falciparum infection [110, 111]. This allele is highly prevalent and enriched in Africans, raising the possibility that it is under positive selection due to malaria. The E756del PIEZO1 allele is also linked to increased red blood cell turnover and elevated serum iron in African individuals [112].
Concluding remarks
The groundbreaking discoveries of the TRPV1, TRPM8 and PIEZO channels by this year’s Nobel Prize laureates have allowed us to understand how heat, cold and mechanical force are sensed and transformed into nervous impulses that enable us to perceive and adapt to the world around us. The TRP channels are central for our ability to perceive temperature. The PIEZO2 channel endows us with touch and proprioception. TRP and PIEZO channels also contribute to numerous additional physiological functions depending on sensing temperature or mechanical stimuli (Figure 5). Intensive ongoing research originating from this year’s Nobel Prize awarded discoveries are focused on elucidating the functions of these receptors in a variety of physiological processes and to develop treatments for a wide range of disease conditions, including chronic pain.
Patrik Ernfors, PhD, Professor at Karolinska Institutet
Member of the Nobel Committee
Abdel El Manira, PhD, Professor at Karolinska Institutet
Member of the Nobel Committee
Per Svenningsson, MD PhD, Professor at Karolinska Institutet
Member of the Nobel Committee
Illustrations: Mattias Karlén
The Nobel Assembly, consisting of 50 professors at Karolinska Institutet, awards the Nobel Prize in Physiology or Medicine. Its Nobel Committee evaluates the nominations. Since 1901 the Nobel Prize has been awarded to scientists who have made the most important discoveries for the benefit of humankind.
Nobel Prize® is the registered trademark of the Nobel Foundation
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Albuisson, J., S.E. Murthy, M. Bandell, B. Coste, H. Louis-Dit-Picard, J. Mathur, M. Fénéant- Thibault, G. Tertian, J.P. de Jaureguiberry, P.Y. Syfuss, S. Cahalan, L. Garçon, F. Toutain, P. Simon Rohrlich, J. Delaunay, V. Picard, X. Jeunemaitre, and A. Patapoutian, Dehydrated hereditary stomatocytosis linked to gain-of-function mutations in mechanically activated PIEZO1 ion channels. Nat Commun, 2013. 4: p. 1884.
Andolfo, I., S.L. Alper, L. De Franceschi, C. Auriemma, R. Russo, L. De Falco, F. Vallefuoco, M.R. Esposito, D.H. Vandorpe, B.E. Shmukler, R. Narayan, D. Montanaro, M. D’Armiento, A. Vetro, I. Limongelli, O. Zuffardi, B.E. Glader, S.L. Schrier, C. Brugnara, G.W. Stewart, J. Delaunay, and A. Iolascon, Multiple clinical forms of dehydrated hereditary stomatocytosis arise from mutations in PIEZO1. Blood, 2013. 121(19): p. 3925-35, s1-12.
Zarychanski, R., V.P. Schulz, B.L. Houston, Y. Maksimova, D.S. Houston, B. Smith, J. Rinehart, and P.G. Gallagher, Mutations in the mechanotransduction protein PIEZO1 are associated with hereditary xerocytosis. Blood, 2012. 120(9): p. 1908-15.
Ma, S., S. Cahalan, G. LaMonte, N.D. Grubaugh, W. Zeng, S.E. Murthy, E. Paytas, R. Gamini, V. Lukacs, T. Whitwam, M. Loud, R. Lohia, L. Berry, S.M. Khan, C.J. Janse, M. Bandell, C. Schmedt, K. Wengelnik, A.I. Su, E. Honore, E.A. Winzeler, K.G. Andersen, and A. Patapoutian, Common PIEZO1 Allele in African Populations Causes RBC Dehydration and Attenuates Plasmodium Infection. Cell, 2018. 173(2): p. 443-455.e12.
Nguetse, C.N., N. Purington, E.R. Ebel, B. Shakya, M. Tetard, P.G. Kremsner, T.P. Velavan, and E.S. Egan, A common polymorphism in the mechanosensitive ion channel PIEZO1 is associated with protection from severe malaria in humans. Proc Natl Acad Sci U S A, 2020. 117(16): p. 9074-9081.
Ma, S., A.E. Dubin, Y. Zhang, S.A.R. Mousavi, Y. Wang, A.M. Coombs, M. Loud, I. Andolfo, and A. Patapoutian, A role of PIEZO1 in iron metabolism in mice and humans. Cell, 2021. 184(4): p. 969-982.e13. | |||||
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] | 1965-12-31T00:00:00 | Share this: Events January–February January 14 – The Prime Minister of Northern Ireland and the Taoiseach of the Republic of Ireland meet for the first time in 43 years. January 20 Lyndon B. Johnson is sworn in for a full term as President of the United States. Indonesian President Sukarno announces the withdrawal of the Indonesian government from the United Nations. January 30 – The state funeral of Sir Winston Churchill takes place … | en | Smartencyclopedia | https://smartencyclopedia.org/1965/12/31/top-news-stories-of-1965/ | Events
January–February
January 14 – The Prime Minister of Northern Ireland and the Taoiseach of the Republic of Ireland meet for the first time in 43 years.
January 20
Lyndon B. Johnson is sworn in for a full term as President of the United States.
Indonesian President Sukarno announces the withdrawal of the Indonesian government from the United Nations.
January 30 – The state funeral of Sir Winston Churchill takes place in London with the largest assembly of dignitaries in the world until the 2005 funeral of Pope John Paul II.
February 4 – Trofim Lysenko is removed from his post as director of the Institute of Genetics at the Academy of Sciences in the Soviet Union. Lysenkoist theories are now treated as pseudoscience.
February 12
The African and Malagasy Common Organization (Organization Commune Africaine et Malgache; OCAM) is formed as successor to the Afro-Malagasy Union for Economic Cooperation (Union Africaine et Malgache de Cooperation Economique; UAMCE), formerly the African and Malagasy Union (Union Africaine et Malgache; UAM).
February 18 – The Gambia becomes independent from the United Kingdom.
February 20
Ranger 8 crashes into the Moon, after a successful mission of photographing possible landing sites for the Apollo program astronauts.
Suat Hayri Ürgüplü forms the new (interim) government of Turkey (29th government).
February 21 – Malcolm X is gunned down while giving a speech at the Audubon Ballroom in Harlem.
March–April
March 2 – Vietnam War: Operation Rolling Thunder – The United States Air Force 2nd Air Division, United States Navy and South Vietnamese air force begin a 31⁄2-year aerial bombardment campaign against North Vietnam.
March 7 – “Bloody Sunday”: Some 200 Alabama State Troopers attack 525 civil rights demonstrators in Selma, Alabama, as they attempt to march to the state capitol of Montgomery.
March 8 – Vietnam War: Some 3,500 United States Marines arrive in Da Nang, South Vietnam, becoming the first American ground combat troops in Vietnam.
March 9 – The “Turnaround Tuesday” march from Selma to Montgomery, Alabama, under the leadership of Martin Luther King Jr., stops at the site of “Bloody Sunday”, to hold a prayer service and return to Selma, in obedience to a court restraining order. On the same day, White supremacists attack three white ministers, leaving Unitarian Universalist minister James J. Reeb in a coma.
March 10 – An engagement is announced between Princess Margriet of the Netherlands and Pieter van Vollenhoven, who will become the first commoner and the first Dutchman to marry into the Dutch Royal Family.
March 18 – Cosmonaut Alexei Leonov leaves his Voskhod 2 spacecraft for 12 minutes, becoming the first person to walk in space.
March 20
“Poupée de cire, poupée de son”, sung by France Gall (music and lyrics by Serge Gainsbourg) wins the Eurovision Song Contest 1965 for Luxembourg.
The Indo-Pakistani War of 1965 begins.
March 23
Events of March 23, 1965: Large student demonstration in Morocco, joined by discontented masses, meets with violent police and military repression.
Gemini 3: NASA launches the United States’ first 2-person crew (Gus Grissom, John Young) into Earth orbit.
The first issue of The Vigilant is published from Khartoum.
March 25 – Martin Luther King Jr. and 25,000 civil rights activists successfully end the 4-day march from Selma, Alabama, to the capitol in Montgomery.
March 28 – At least 400 are killed or missing after an earthquake triggered a series of dam failures in La Ligua, Chile.[4]
March 30 – The second ODECA charter, signed by Central American states on December 12, 1962, becomes effective.
April 3 – The world’s first space nuclear power reactor, SNAP-10A, is launched by the United States from Vandenberg AFB, California. The reactor operates for 43 days and remains in low Earth orbit.
April 5 – At the 37th Academy Awards, My Fair Lady wins 8 Academy Awards, including Best Picture and Best Director. Rex Harrison wins an Oscar for Best Actor. Mary Poppins takes home 5 Oscars. Julie Andrews wins an Academy Award for Best Actress for her performance in the title role. Sherman Brothers receives 2 Oscars including Best Song, “Chim Chim Cher-ee”.
April 6 – The Intelsat I (“Early Bird”) communications satellite is launched. It becomes operational May 2 and is placed in commercial service in June.
April 9 – The West German parliament extends the statute of limitations on Nazi war crimes.
April 18 – Consecration of Saint Clement of Ohrid Macedonian Orthodox Cathedral in Toronto, Canada.
April 23 – The Pennine Way officially opens.
April 24
The 1965 Yerevan demonstrations start in Yerevan, demanding recognition of the Armenian genocide.
The bodies of Portuguese opposition politician Humberto Delgado and his secretary Arajaryr Moreira de Campos are found in a forest near Villanueva del Fresno, Spain (they were killed February 12).
In the Dominican Republic, officers and civilians loyal to deposed President Juan Bosch mutiny against the right-wing junta running the country, setting up a provisional government. Forces loyal to the deposed military-imposed government stage a countercoup the next day, and civil war breaks out, although the new government retains its hold on power.
April 26 – Rede Globo is founded in Rio de Janeiro, Brazil.
April 28
U.S. troops occupy the Dominican Republic.
Vietnam War: Prime Minister of Australia Robert Menzies announces that the country will substantially increase its number of troops in South Vietnam, supposedly at the request of the Saigon government (it is later revealed that Menzies had asked the leadership in Saigon to send the request at the behest of the Americans).
April 29 – Australia announces that it is sending an infantry battalion to support the South Vietnam government.
May–June
May 1
Bob Askin replaces Jack Renshaw as Premier of New South Wales.
The Battle of Dong-Yin occurs as a conflict between Taiwan and the People’s Republic of China.
May 9 – Pianist Vladimir Horowitz returns to the stage after a 12-year absence, performing a legendary concert in Carnegie Hall in New York.
May 12 –West Germany and Israel establish diplomatic relations.
May 25 – Muhammad Ali knocks out Sonny Liston in the first round of their championship rematch with the “Phantom Punch” at the Central Maine Civic Center in Lewiston.
May 27 – Internazionale beats Benfica 1–0 at the San Siro, Milan and wins the 1964-65 European Cup in Association football.
May 29 – A mining accident in Dhanbad, India, kills 274.
May 31 – Scottish racing driver Jim Clark wins the Indianapolis 500, later this year winning the Formula One world driving championship.
June 1 – A coal mine explosion in Fukuoka, Japan, kills 237.
June 2 – Vietnam War: The first contingent of Australian combat troops arrives in South Vietnam.
June 7 – Kakanj mine disaster: A mining accident in Kakanj, Bosnia and Herzegovina, results in 128 deaths.
June 10 – Vietnam War – Battle of Dong Xoai: About 1,500 Viet Cong mount a mortar attack on Đồng Xoài, overrunning its military headquarters and the adjoining militia compound.
June 19
Houari Boumediene’s Revolutionary Council ousts Ahmed Ben Bella, in a bloodless coup in Algeria.
Air Marshal Nguyen Cao Ky, head of the South Vietnamese Air Force, was appointed prime minister at the head of the military junta, with General Nguyễn Văn Thiệu becoming a figurehead president, ending two years of short-lived military juntas.
June 20 – Police in Algiers break up demonstrations by people who have taken to the streets chanting slogans in support of deposed President Ahmed Ben Bella.
June 22 – The Treaty on Basic Relations between Japan and the Republic of Korea is signed in Tokyo.
June 25 – A U.S. Air Force Boeing C-135 Stratolifter bound for Okinawa crashes just after takeoff at MCAS El Toro in Orange County, California, killing all 85 on board.
July–August
July – The Commonwealth secretariat is created.
July 14 – U.S. spacecraft Mariner 4 flies by Mars, becoming the first spacecraft to return images from the Red Planet.
July 15 – Greek Prime minister Georgios Papandreou and his government are dismissed by King Constantine II.
July 16 – The Mont Blanc Tunnel is inaugurated by presidents Giuseppe Saragat and Charles de Gaulle.
July 24 – Vietnam War: Four F-4C Phantoms escorting a bombing raid at Kang Chi are targeted by antiaircraft missiles, in the first such attack against American planes in the war. One is shot down and the other 3 sustain damage.
July 26 – The Maldives receive full independence from Great Britain.
July 27 – Edward Heath becomes Leader of the British Conservative Party.
July 28 – Vietnam War: U.S. President Lyndon B. Johnson announces his order to increase the number of United States troops in South Vietnam from 75,000 to 125,000, and to more than double the number of men drafted per month – from 17,000 to 35,000.
July 30 – War on Poverty: U.S. President Lyndon B. Johnson signs the Social Security Act of 1965 into law, establishing Medicare and Medicaid.
August 7 – Tunku Abdul Rahman, Prime Minister of Malaysia, recommends the expulsion of Singapore from the Federation of Malaysia following a deterioration of PAP–UMNO relations, negotiating its separation with Lee Kuan Yew, Prime Minister of Singapore.
August 9
Singapore is expelled from the Federation of Malaysia, which recognises it as a sovereign nation. Lee Kuan Yew announces Singapore’s independence and assumes the position of Prime Minister of the new island nation – a position he holds until 1990.
An explosion at an Arkansas missile plant kills 53.
Indonesian President Sukarno collapses in public.
August 18 – Vietnam War: Operation Starlite – 5,500 United States Marines destroy a Viet Cong stronghold on the Van Tuong peninsula in Quảng Ngãi Province, in the first major American ground battle of the war. The Marines were tipped off by a Viet Cong deserter who said that there was an attack planned against the U.S. base at Chu Lai.
August 19 – At the conclusion of the Frankfurt Auschwitz trials, 66 ex-SS personnel receive life sentences, 15 others shorter ones.
August 21 – NASA launches Gemini 5 (Gordon Cooper, Pete Conrad) on the first 1-week space flight, as well as the first test of fuel cells for electrical power on such a mission.
August 30 – An avalanche buries a dam construction site at Saas-Fee, Switzerland, killing 90 workers.
August 31 – U.S. President Johnson signs a law penalizing the burning of draft cards with up to 5 years in prison and a $1,000 fine.
September–October
September 2
Pakistani troops enter the Indian sector of Kashmir, while Indian troops try to invade Lahore.
The People’s Republic of China announces that it will reinforce its troops on the Indian border.
Vietnam War: In a follow-up to August’s Operation Starlite, United States Marines and South Vietnamese forces initiate Operation Piranha on the Batangan Peninsula, 23 miles (37 km) south of the Chu Lai Marine base.
September 8
India opens 2 additional fronts against Pakistan.
The Pakistan Navy destroys Indian Port of Dwarka. Operation Dwarka (Pakistan celebrates Victory Day annually).
September 9
U.N. Secretary General U Thant negotiates with Pakistan President Ayub Khan.
U Thant recommends China for United Nations membership.
September 14 – The fourth and final period of the Second Vatican Council opens.
September 16 – In Iraq, Prime Minister Arif Abd ar-Razzaq’s attempted coup fails.
September 17 – King Constantine II of Greece forms a new government with Prime Minister Stephanos Stephanopoulos, in an attempt to end a 2-year-old political crisis.
September 18
In Denmark, Palle Sørensen shoots 4 policemen in pursuit; he is apprehended the same day.
Comet Ikeya–Seki is first sighted by Japanese astronomers.
Soviet Premier Alexei Kosygin invites the leaders of India and Pakistan to meet in the Soviet Union to negotiate.
September 19 – Pakistani Forces achieve a decisive victory at the Battle of Chawinda, ultimately halting the Indian advance and successfully stabilizing the Sialkot Front.
September 20 – Vietnam War: An USAF F-104 Starfighter piloted by Captain Philip Eldon Smith is shot down by a Chinese MiG-19 Farmer. The pilot is held until March 15 1973.
September 21 – Gambia, Maldives and Singapore are admitted as members of the United Nations.
September 22 – Radio Peking announces that Indian troops have dismantled their equipment on the Chinese side of the border.
September 24
Fighting resumes between Indian and Pakistani troops.
The British governor of Aden cancels the constitution and takes direct control of the protectorate, due to the bad security situation.
September 27 – The largest tanker ship at this time, Tokyo Maru, is launched in Yokohama, Japan.
September 28
Fidel Castro announces that anyone who wants to can emigrate to the United States.
Taal Volcano in Luzon, Philippines, erupts, killing hundreds.
September 30
The Indonesian army, led by General Suharto, crushes an alleged communist coup attempt (see Transition to the New Order and 30 September Movement).
The classic family sci-fi show Thunderbirds debuts on ITV in the United Kingdom.
October 3 – Fidel Castro announces that Che Guevara has resigned and left Cuba.
October 4
At least 150 are killed when a commuter train derails at the outskirts of Durban, KwaZulu-Natal, South Africa.
Prime minister Ian Smith of Rhodesia and Arthur Bottomley of the Commonwealth of Nations begin negotiations in London.
Pope Paul VI visits the United States. He appears for a Mass in Yankee Stadium and makes a speech at the United Nations.
The University of California, Irvine opens its doors.
October 5 – Pakistan severs diplomatic relations with Malaysia because of their disagreement in the UN.
October 6 – Ian Brady, a 27-year-old stock clerk from Hyde in Cheshire, is arrested for allegedly hacking to death (with a hatchet) 17-year-old apprentice electrician Edward Evans at a house on the Hattersley housing estate.
October 7 – Seven Japanese fishing boats are sunk off Guam by super typhoon Carmen; 209 are killed.
October 8
Indonesian mass killings of 1965–1966: The Indonesian army instigates the arrest and execution of communists which last until next March.
The 7 Fundamental Principles of the Red Cross and Red Crescent are adopted at the XX International Conference in Vienna, Austria.
The International Olympic Committee admits East Germany as a member.
October 10 – The first group of Cuban refugees travels to the U.S.
October 12
Per Borten forms a government in Norway.
The U.N. General Council recommends that the United Kingdom try everything to stop a rebellion in Rhodesia.
October 13 – Congo President Joseph Kasavubu fires Prime Minister Moise Tshombe and forms a provisional government, with Évariste Kimba in a leading position.
October 15 – Vietnam War: The Catholic Worker Movement stages an anti-war protest in Manhattan. One draft card burner is arrested, the first under the new law.
October 17 – The New York World’s Fair at Flushing Meadows, closes. Due to financial losses, some of the projected site park improvements fail to materialize.
October 18 – The Indonesian government outlaws the Communist Party of Indonesia.
October 20 – Ludwig Erhard is re-elected Chancellor of West Germany (he had first been elected in 1963).
October 21
Comet Ikeya–Seki approaches perihelion, passing 450,000 kilometres (280,000 mi) from the sun.
The Organization of African Unity meets in Accra, Ghana.
October 22
African countries demand that the United Kingdom use force to prevent Rhodesia from declaring unilateral independence.
Colonel Christophe Soglo stages a second coup in Dahomey.
October 25 – The Soviet Union declares its support of African countries in case Rhodesia unilaterally declares independence.
October 27
Brazilian president Humberto de Alencar Castelo Branco removes power from parliament, legal courts and opposition parties.
Süleyman Demirel of AP forms the new government of Turkey (30th government).
October 28 – Pope Paul VI promulgates Nostra aetate, a “Declaration on the Relation of the (Roman Catholic) Church with Non-Christian Religions” by the Second Vatican Council which includes a statement that Jews are not collectively responsible for the death of Jesus (Jewish deicide).
October 29 – An 80-kiloton nuclear device is detonated at Amchitka Island, Alaska, as part of the Vela Uniform program, code-named Project Long Shot.
October 30 – Vietnam War: Near Da Nang, United States Marines repel an intense attack by Viet Cong forces, killing 56 guerrillas. A sketch of Marine positions is found on the dead body of a 13-year-old Vietnamese boy who sold drinks to the Marines the day before.
November–December
November 1 – A trolleybus plunges into the Nile at Cairo, Egypt, killing 74 passengers.
November 3 – French President Charles de Gaulle announces (just short of his 75th birthday) that he will stand for re-election.
November 5 – Martial law is announced in Rhodesia. The United Nations General Assembly accepts British intent to use force against Rhodesia if necessary by a vote of 82–9.
November 6 – Freedom Flights begin: Cuba and the United States formally agree to start an airlift for Cubans who want to go to the United States (by 1971, 250,000 Cubans take advantage of this program).
November 8 – Vietnam War – Operation Hump: The United States Army 173rd Airborne is ambushed by over 1,200 Viet Cong.
November 11
In Rhodesia (modern-day Zimbabwe), the white-minority government of Ian Smith unilaterally declares de facto independence (‘UDI’).
United Airlines Flight 227 crashes short of the runway and catches fire at Salt Lake City International Airport, killing 43 out of 91 passengers and crew.
November 12 – A UN Security Council resolution (voted 10–0) recommends that other countries not recognize independent Rhodesia.
November 13
The SS Yarmouth Castle burns and sinks 60 miles (97 km) off Nassau, Bahamas, with the loss of 90 lives.
British theatre critic Kenneth Tynan says “fuck” during a discussion on BBC satirical programme BBC-3 for what many believed was the first time on British television. The corporation later issues a public apology.
November 14 – Vietnam War – Battle of Ia Drang: In the Ia Drang Valley of the Central Highlands in Vietnam, the first major engagement of the war between regular United States and North Vietnamese forces begins.
November 15 – U.S. racer Craig Breedlove sets a new land speed record of 600.601 mph (966.574 km/h).
November 16 – Venera program: The Soviet Union launches the Venera 3 space probe from Baikonur, Kazakhstan toward Venus (on March 1, 1966, it becomes the first spacecraft to reach the surface of another planet).
November 20 – The United Nations Security Council recommends that all states stop trading with Rhodesia.
November 22 – The United Nations Development Programme (UNDP) is established as a specialized agency of the United Nations.
November 23 – Soviet general Mikhail Kazakov assumes command of the Warsaw Pact.
November 24 – Congolese lieutenant general Mobutu ousts Joseph Kasavubu and declares himself president.
November 26 – At the Hammaguir launch facility in the Sahara Desert, France launches a Diamant A rocket with its first satellite, Astérix-1 on board, becoming the third country to enter outer space.
November 27
Tens of thousands of Vietnam War protesters picket the White House, then march on the Washington Monument.
Vietnam War: The Pentagon tells U.S. President Lyndon B. Johnson that if planned major sweep operations to neutralize Viet Cong forces during the next year are to succeed, the number of American troops in Vietnam will have to be increased from 120,000 to 400,000.
November 28 – Vietnam War: In response to U.S. President Lyndon B. Johnson’s call for “more flags” in Vietnam, Philippines President-elect Ferdinand Marcos announces he will send troops to help fight in South Vietnam.
November 29 – The Canadian satellite Alouette 2 is launched.
December 5
Charles de Gaulle is re-elected as French president with 10,828,421 votes.
The “Glasnost Meeting” in Moscow becomes the first spontaneous political demonstration and the first demonstration for civil rights in the Soviet Union.
December 8
Rhodesian prime minister Ian Smith warns that Rhodesia will resist a trade embargo by neighboring countries with force.
The Race Relations Act becomes the first legislation to address racial discrimination in the UK.
The Second Vatican Council closes.
December 15
The Caribbean Free Trade Association (CARIFTA) is formed.
Gemini 6 and Gemini 7 perform the first controlled rendezvous in Earth orbit.
December 20 – The World Food Programme is made a permanent agency of the United Nations.
December 21
The Soviet Union announces that it has shipped rockets to North Vietnam.
In West Germany, Konrad Adenauer resigns as chairman of the Christian Democratic Party.
The United Nations adopts the International Convention on the Elimination of All Forms of Racial Discrimination.
A new 1-hour German-American production of the ballet The Nutcracker, with an international cast that includes Edward Villella in the title role, makes its U.S. television debut. It is repeated annually by CBS over the next 3 years but after that is virtually forgotten until issued on DVD in 2009 by Warner Archive.
December 22
A military coup is launched in Dahomey.
A 70 mph (110 km/h) speed limit is imposed on British roads.
David Lean’s film of Doctor Zhivago, starring Omar Sharif and Julie Christie, is released.
December 25 – The Yemeni Nasserist Unionist People’s Organisation is founded in Ta’izz.
December 30
President Kenneth Kaunda of Zambia announces that Zambia and the United Kingdom have agreed on a deadline before which the Rhodesian white government should be ousted.
Ferdinand Marcos becomes President of the Philippines.
December 31 – Bokassa takes power in the Central African Republic.
Tokyo officially becomes the largest city of the world, taking the lead from New York City.
Aborigines are given the vote in Queensland, Australia.
World population
World population 1965 1960 1970 World 3,334,874,000 3,021,475,000 313,399,000 3,692,492,000 357,618,000 Africa 313,744,000 277,398,000 36,346,000 357,283,000 43,539,000 Asia 1,899,424,000 1,701,336,000 198,088,000 2,143,118,000 243,694,000 Europe 634,026,000 604,401,000 29,625,000 655,855,000 21,829,000 Latin America 250,452,000 218,300,000 32,152,000 284,856,000 34,404,000 Northern America 219,570,000 204,152,000 15,418,000 231,937,000 12,367,000 Oceania 17,657,000 15,888,000 1,769,000 19,443,000 1,786,000
Births
January
January 4
Julia Ormond, British actress
Yvan Attal, Israeli-born French actor and director
January 5
Vinnie Jones, British footballer-turned-actor
Patrik Sjöberg, Swedish high jumper
January 9
Haddaway, German singer
Farah Khan, Indian choreographer, film director
Joely Richardson, British actress
January 10 – Butch Hartman, American animator and voice actor
January 12
Nikolai Borschevsky, Russian ice hockey player
Maybrit Illner, German television journalist and presenter
Rob Zombie, American musician
January 13 – Bill Bailey, British comedian, musician and actor
January 14
Shamil Basayev, Chechen terrorist (d. 2006)
Marc Delissen, Dutch field hockey player
Bob Essensa, Canadian ice hockey player
January 15
Adam Jones, American musician, guitarist of metal band Tool
James Nesbitt, Northern Irish actor
January 20 – Sophie, Duchess of Edinburgh, wife of Prince Edward, Duke of Edinburgh
January 21 – Jam Master Jay, American DJ, rapper and producer (d. 2002)
January 22
DJ Jazzy Jeff, American disc jockey
Diane Lane, American actress
January 23 – Catherine Guillouard, French businesswoman
January 24 – Porfirio Fisac, Spanish basketball coach
January 25
Esa Tikkanen, Finnish ice hockey player
Natalia Yurchenko, Soviet artistic gymnast
January 26 – Natalia Yurchenko, Soviet artistic gymnast
January 27
Alan Cumming, Scottish actor
Ignacio Noé, Argentine artist
January 29
Dominik Hašek, Czech hockey player
Jo Min-su, South Korean actress
February
February 1
Dave Callaghan, South African cricketer
Brandon Lee, Chinese-American actor (d. 1993)
Sherilyn Fenn, American actress
Princess Stéphanie of Monaco
February 3 – Maura Tierney, American actress
February 5 – Gheorghe Hagi, Romanian footballer, manager and club owner
February 6
Idania Martínez Grandales, Cuban broadcaster, journalist and professor
Jan Svěrák, Czech actor, director, and screenwriter
February 7 – Chris Rock, African-American actor, comedian, and film director
February 8 – Dicky Cheung, Hong Kong actor
February 9 – Keith Wickham, British actor
February 11 – Roberto Moya, Cuban athlete (d. 2020)
February 12 – Brett Kavanaugh, American attorney and Supreme Court Justice
February 15 – Héctor Beltrán Leyva, Mexican drug lord (d. 2018)
February 16 – Adama Barrow, Gambian politician, 3rd President of Gambia
February 17 – Michael Bay, American film director
February 18 – Dr. Dre, African-American rapper and music producer
February 23
Kristin Davis, American actress
Michael Dell, American computer manufacturer
Vincent Chalvon-Demersay, French producer
Helena Suková, Czech tennis player
February 25 – Sylvie Guillem, French ballerina
February 27 – Claudia Zobel, Filipina actress (d. 1984)
February 28 – Park Gok-ji, South Korean film editor
March
March 1
Mike Dean, Record producer
Stewart Elliott, Canadian jockey
Jack Tu, Taiwanese-Canadian cardiologist (d. 2018)
March 2 – Ami Bera, American politician
March 3
Tedros Adhanom, Director of the World Health Organization
Dragan Stojković, Serbian footballer and coach
March 4
Greg Alexander, Australian rugby league player
Paul W. S. Anderson, British filmmaker, producer and screenwriter
March 8
Mac Jack, South African educator and politician (d. 2020)
Caio Júnior, Brazilian football forward and manager (d. 2016)
March 9
Antonio Saca, 43rd President of El Salvador
Mike Pollock, American voice actor
March 11
Catherine Fulop, Venezuelan actress, model, beauty pageant contestant, and television presenter
Jesse Jackson Jr., African-American politician
Laurence Llewelyn-Bowen, British designer and television presenter
March 14 – Aamir Khan, Indian film director, producer, film and scriptwriter and actor
March 16
Utut Adianto, Indonesian chess grandmaster and politician
Mark Carney, Canadian-born economist and central banker
March 23 – Marti Pellow, Scottish singer (Wet Wet Wet)
March 24
Rob MacCachren, American racecar driver
The Undertaker, American professional wrestler
March 25
Stefka Kostadinova, Bulgarian high jumper and president of the Bulgarian Olympic Committee
Sarah Jessica Parker, American actress
March 26 – Prakash Raj, Indian actor, producer and director
March 27 – José Carlos Palma, Expert in international relations, such as foreign policy, international trade, domestic security, international security, developing nations, domestic security, intelligence, IT Consultant, world history, political consultant, and military analysis.
March 29 – Voula Patoulidou, Greek athlete
March 30 – Piers Morgan, British journalist and television personality
March 31 – Patty Fendick, American tennis player
April
April 1
Brian Marshall, Canadian retired track and field athlete
Bekir Bozdağ, Turkish theologian, lawyer, and politician
April 3 – Nazia Hassan, Pakistani pop singer-songwriter, lawyer and social activist (d. 2000)
April 4 – Robert Downey Jr., American actor, producer, and singer
April 6
Black Francis, American musician
Rica Reinisch, German swimmer
April 9 – Paulina Porizkova, Swedish-American model and actress
April 10 – Jure Robič, Slovenian cyclist (d. 2010)
April 11 – Eelco van Asperen, Dutch computer scientist
April 12 – Kim Bodnia, Danish actor and director
April 15 – Linda Perry, American musician
April 16 – Martin Lawrence, American actor, comedian, and producer
April 18 – Camille Coduri, English actress
April 18 – Steven Stayner, American kidnapping victim (d. 1989)
April 19 – Suge Knight, American record producer and convicted felon
April 20 – Jovy Marcelo, Filipino race car driver (d. 1992)
April 21
Tatul Krpeyan, Armenian commander (d. 1991)
Julio Robaina, Republican politician, Mayor of Hialeah, Florida
April 23 – Leni Robredo, 14th Vice President of the Philippines
April 24 – Michel Leclerc, French director and screenwriter
April 25 – Édouard Ferrand, French politician (d. 2018)
April 26 – Kevin James, American comedian and actor
April 27 – Edwin Poots, Irish politician
April 29 – David Shafer, American politician, Georgia
April 30 – Adrian Pasdar, Iranian-American actor and voice artist
May
May 2 – Myriam Hernández, Chilean singer
May 3
Gary Mitchell, Irish playwright
Rob Brydon, Welsh actor, comedian, impressionist and presenter
May 7
Owen Hart, Canadian professional wrestler (d. 1999)
Norman Whiteside, Northern Irish football player
May 9 – Steve Yzerman, Canadian hockey player
May 10 – Linda Evangelista, Canadian supermodel
May 11 – Monsour del Rosario, Filipino Olympic athlete and actor
May 12 – Renée Simonsen, Danish model and writer
May 13 – José Antonio Delgado, Venezuelan mountain climber (d. 2006)
May 14 – Eoin Colfer, Irish novelist
May 16 – Rodica Dunca, Romanian artistic gymnast
Krist Novoselic, American musician and activist (Nirvana)
May 17 – Trent Reznor, American rock musician (Nine Inch Nails)
May 19 – Philippe Dhondt, French singer
May 23
Manuel Sanchís Hontiyuelo, Spanish footballer
Melissa McBride, American actress (The Walking Dead)
May 24
Carlos Franco, Paraguayan golfer
John C. Reilly, American actor and comedian
Shinichirō Watanabe, Japanese anime director
May 25 – Yahya Jammeh, President of the Gambia
May 29 – Emilio Sánchez, Spanish tennis player
May 30 – Guadalupe Grande, Spanish poet (d. 2021)
May 31 – Brooke Shields, American actress and model
June
June 1
Larisa Lazutina, Russian cross-country skier
Nigel Short, English chess player
June 2 – Steve and Mark Waugh, Australian cricketers
June 4
Mick Doohan, Australian motorcycle racer
Andrea Jaeger, American tennis player
June 6
Cam Neely, Canadian ice hockey player
Megumi Ogata, Japanese voice actress and singer
June 7
Mick Foley, American professional wrestler
Damien Hirst, British artist
Christine Roque, French singer
June 8
Frank Grillo, American actor
Rob Pilatus, German model, dancer and singer (d. 1998)
June 10
Veronica Ferres, German actress
Elizabeth Hurley, English model and actress
June 11 – Manuel Uribe, morbidly obese Mexican (d. 2014)
June 12 – Carlos Luis Morales, Ecuadorian journalist (d. 2020)
June 13 – Infanta Cristina of Spain
June 15 – Bernard Hopkins, American boxer
June 16 – Andrea M. Ghez, American astronomer, recipient of the Nobel Prize in Physics
June 17
Dana Eskelson, American actress
Dan Jansen, American speedskater
Dara O’Kearney, Irish ultra runner and professional poker player
June 18
Kim Dickens, American actress
Hani Mohsin, Malaysian celebrity, actor and host (d. 2006)
June 21
Yang Liwei, Chinese major general, military pilot and China National Space Administration astronaut
Gabriella Selmeczi, Hungarian jurist and politician
Tim Lajcik, Czech American mixed martial artist, stuntman, actor and writer
June 22 – Anubhav Sinha, Indian film director
Gamal Abdul Nasir Zakaria, Indonesian writer and lecturer
June 23 – Paul Arthurs, English Musician (Oasis)
June 24 – Son Hyun-joo, South Korean actor
June 25 – Jean Castex, French politician
June 26 – Jana Hybášková, Czech politician and diplomat
June 27
Frédéric Lemoine, French businessman
S. Manikavasagam, Malaysian politician
June 28 – Belayneh Dinsamo, Ethiopian long-distance runner
June 29
Véronique Laury, French businesswoman
Dado Villa-Lobos, Brazilian musician
Matthew Weiner, American television writer, director and producer
June 30
Philippe Duquesne, French actor
Cho Jae-hyun, South Korean actor
Mitch Richmond, American basketball player
July
July 1
Teddy McCarthy, hurler and Gaelic footballer
Carl Fogarty, English motorcycle racer
Mohammed Abdul Hussein, Iraqi former footballer
July 2 – Fredrik Sejersted, Norwegian jurist
July 3
Komsan Pohkong, Thai lawyer
Shinya Hashimoto, Japanese professional wrestler (d. 2005)
Connie Nielsen, Danish actress
Tommy Flanagan, Scottish actor
July 4 – Tracy Letts, American actor, playwright and screenwriter
July 5
Kathryn Erbe, American actress
Eyran Katsenelenbogen, Israeli jazz pianist
July 7
Paula Devicq, Canadian actress
Jeremy Kyle, English radio and television presenter
July 10
Danny Boffin, Belgian footballer
Princess Alexia of Greece and Denmark
Alec Mapa, American comedian
July 11 – Ernesto Hoost, Dutch kickboxer
July 12 – Mama Kandeh, Gambian politician
July 13 – Akina Nakamori, Japanese singer and actress
July 14 – Lou Savarese, American boxer
July 15 – Dafna Rechter, Israeli actress and singer
July 17
Santiago Segura, Spanish actor, screenwriter, producer and director
Rosa Gumataotao Rios, 43rd Treasurer of the United States
Alex Winter, British actor
July 18 – Eva Ionesco, French actress, film director and screenwriter
July 19
Dame Evelyn Glennie, Scottish virtuoso percussionist
Hailemariam Desalegn, 15th Prime Minister of Ethiopia
July 21 – Guðni Bergsson, Icelandic footballer
July 22 – Shawn Michaels, American professional wrestler
July 23
Grace Mugabe, First Lady of Zimbabwe
Slash (Saul Hudson), American rock musician
July 25 – Illeana Douglas, American actress and producer
July 26
Vladimir Cruz, Cuban actor
Jeremy Piven, American actor
Jimmy Dore, American comedian and political commentator
July 27
José Luis Chilavert, Paraguayan footballer
Trifon Ivanov, Bulgarian footballer (d. 2016)
July 28 – Daniela Mercury, Brazilian singer, songwriter, dancer, producer, actress and television host
July 29 – Chang-Rae Lee, Korean-American novelist
July 31 – J. K. Rowling, English author
August
August 1 – Sam Mendes, English film director
August 2
Sandra Ng, Hong Kong actress
Hisanobu Watanabe, Japanese baseball player and coach
August 4
Terri Lyne Carrington, American jazz drummer
Dennis Lehane, American crime writer
Fredrik Reinfeldt, Swedish Prime Minister
August 5 – Monica Ward, Italian actress and voice actress
August 6 – David Robinson, American basketball player
August 10
Claudia Christian, American actress, writer, singer, musician, and director
Mike E. Smith, American jockey
John Starks, American basketball player
August 11 – Viola Davis, African-American actress
August 15 – Vincent Kok, Hong Kong director and actor
August 16 – Michael O’Gorman, American coxswain (d. 2018)
August 19
Kevin Dillon, American actor
Maria de Medeiros, Portuguese actress
Kyra Sedgwick, American actress
James Tomkins, Australian rower
August 22 – David Reimer, Canadian man, born male but reassigned female and raised as a girl after a botched circumcision (d. 2004)
August 24 – Reggie Miller, American basketball player and commentator
August 25 – Mia Zapata, American singer (d. 1993)
August 26 – Azela Robinson, Mexican actress
August 28
Satoshi Tajiri, Japanese video game designer and Pokémon creator
Amanda Tapping, Canadian actress
Shania Twain, Canadian country singer and songwriter
August 31 – Daniel Bernhardt, Swiss actor and martial artist
September
September 1 – Craig McLachlan, Australian actor and singer
September 2 – Lennox Lewis, British boxer
September 3
Costas Mandylor, Greek-Australian actor
Charlie Sheen, American actor and producer
September 5 – Derby Makinka, Zambian footballer (d. 1993)
September 6 – Gleisi Hoffmann, Brazilian lawyer and politician
September 7 – Jörg Pilawa, German television presenter
September 8
Tutilo Burger, German Benedictine monk and abbot
Darlene Zschech, Australian singer and worship leader
September 10 – Marco Pastors, Dutch politician
September 11
Bashar al-Assad, President of Syria
Moby, American musician
September 12
Einstein Kristiansen, Norwegian cartoonist, designer, and television host
September 14 – Dmitry Medvedev, former President of Russia
September 15 – Fernanda Torres, Brazilian actress
September 16 – Katy Kurtzman, American actress, director and producer
September 17
Kyle Chandler, American actor
Yuji Naka, Japanese video game programmer
September 19
Goldie, English record producer and DJ
Tim Scott, African-American politician and businessman
Tshering Tobgay, former Prime Minister of Bhutan
September 20 – Robert Rusler, American actor
September 21
Cheryl Hines, American actress
Johanna Vuoksenmaa, Finnish film director
David Wenham, Australian actor
Pramila Jayapal, American politician
September 23 – Mark Woodforde, Australian tennis player
September 25 – Scottie Pippen, American basketball player
September 26
Radisav Ćurčić, Serbian-Israeli basketball player
Alexei Mordashov, Russian businessman
Petro Poroshenko, former President of Ukraine
September 27 – Steve Kerr, American basketball player
October
October 1 – Andreas Keller, German field hockey player
October 2 – Gerardo Reyero, Mexican voice actor
October 3
Adriana Calcanhotto, Brazilian singer and composer
Jan-Ove Waldner, Swedish table tennis player
October 5
Mario Lemieux, Canadian ice hockey player
Patrick Roy, Canadian ice hockey player
October 6 – Steve Scalise, House Majority Whip and U.S. Representative of Louisiana’s 1st district
October 8
Matt Biondi, American swimmer
C. J. Ramone, American musician
October 9 – Dionicio Cerón, Mexican long-distance runner
October 10 – Chris Penn, American actor (d. 2006)
October 11
Julianne McNamara, American artistic gymnast
Lennie James, English actor, screenwriter, and playwright
October 13 – Kalpana, Indian film actress (d. 2016)
October 14
Steve Coogan, British comedian and actor
Jüri Jaanson, Estonian rower and politician
October 16 – Kang Kyung-ok, South Korean artist
October 17
Aravinda de Silva, Sri Lankan cricketer
Rhys Muldoon, Australian actor, writer, and director
October 18 – Zakir Naik, Indian doctor and Islamic activist
October 19
The Renegade, American professional wrestler (d. 1999)
Ty Pennington, American television presenter
Tracy Griffith, American actress, sushi chef, and painter
October 20
Amos Mansdorf, Israeli tennis player
Stefano Pioli, Italian football player and manager
October 26
Aaron Kwok, Hong Kong singer and actor
Kelly Rowan, Canadian actress
Kenneth Rutherford, New Zealand cricketer
October 29 – Christy Clark, Canadian politician
October 30 – Zaza Urushadze, Georgian film director, producer and screenwriter (d. 2019)
October 31 – Rob Rackstraw, British actor
November
November 2
Paweł Adamowicz, Polish politician and lawyer (d. 2019)
Shah Rukh Khan, Indian actor, film/television producer and television presenter
November 4 – Wayne Static, American singer and musician (Static-X) (d. 2014)
November 7 – Sigrun Wodars, German athlete
November 8 – Patricia Poleo, Venezuelan journalist
November 9 – Sir Bryn Terfel, Welsh baritone
November 10 – Eddie Irvine, Northern Irish racing driver
November 11 – Max Mutchnick, American television producer
November 12 – Ricard Zapata-Barrero, Spanish scholar of migration studies
November 13 – Rick Roberts, Canadian actor
November 19
Paulo Barreto, Brazilian cryptographer
Laurent Blanc, French football player and manager
November 20 – Yoshiki Hayashi, Japanese rock composer, pianist and drummer
November 21
Björk, Icelandic singer-songwriter and musician
Reggie Lewis, American basketball player (d. 1993)
Alexander Siddig, Sudanese-British actor
November 22 – Mads Mikkelsen, Danish actor
November 23 – Radion Gataullin, Uzbek-Russian pole-vaulter
November 24 – Shirley Henderson, Scottish actress
November 25 – Ana Paula Padrão, Brazilian journalist, chief editor, entrepreneur, writer and television presenter
November 26 – Scott Adsit, American actor
November 27 – Rachida Dati, French politician
November 29
Lauren Child, American author
Yutaka Ozaki, Japanese musician (d. 1992)
Raffaella Reggi, Italian tennis player
November 30
Ben Stiller, American actor, comedian and filmmaker
Tashi Tenzing, Indian mountaineer
December
December 3
Steve Harris, American actor
Katarina Witt, German figure skater
Andrew Stanton, American animator, storyboard artist, film director, and screenwriter
December 5 – Johnny Rzeznik, American rock singer and guitarist
December 7
Teruyuki Kagawa, Japanese actor
Jeffrey Wright, African-American actor
December 8 – David Harewood, English actor
December 9 – Brad Savage, American actor
December 10 – Stephanie Morgenstern, Canadian actress
December 15 – Luis Fabián Artime, Argentine footballer
December 16 – J. B. Smoove, African-American actor and comedian
December 18 – John Moshoeu, South African footballer (d. 2015)
December 19 – Jessica Steen, Canadian actress
December 21
Andy Dick, American actor and comedian
Anke Engelke, German comedian, actress and voice-over actress
December 23 – Andreas Kappes, German cyclist (d. 2018)
December 27 – Salman Khan, Indian actor, television presenter
December 30 – Valentina Legkostupova, Soviet and Russian pop singer, teacher and producer (d. 2020)
December 31
Nicholas Sparks, American author
Gong Li, Chinese actress
Yklymberdi Paromov, Turkmen politician
Marga Hoek, Dutch businesswoman
Deaths
January
January 4 – T. S. Eliot, American-British poet, Nobel Prize laureate (b. 1888)
January 10
Antonín Bečvář, Czechoslovak astronomer (b. 1901)
Frederick Fleet, British sailor and lookout aboard the RMS Titanic (b. 1887)
January 12 – Lorraine Hansberry, African-American playwright and writer (b. 1930)
January 14 – Jeanette MacDonald, American actress and singer (b. 1903)
January 15 – Pierre Ngendandumwe, 4th and 6th Prime Minister of Burundi (assassinated) (b. 1930)
January 20 – Alan Freed, American disc jockey (b. 1921)
January 24 – Sir Winston Churchill, British politician and statesman, twice Prime Minister of the United Kingdom, World War II leader, recipient of the Nobel Prize in Literature (b. 1874)
January 27 – Hassan Ali Mansur, Iranian politician, 69th Prime Minister of Iran (b. 1923)
January 28
Taimur bin Feisal, Sultan of Muscat and Oman (b. 1886)
Tich Freeman, English cricketer (b. 1888)
Maxime Weygand, French general (b. 1867)
January 31 – Konstantin Muraviev, 31st Prime Minister of Bulgaria (b. 1893)
February
February 5 – Irving Bacon, American actor (b. 1893)
February 6 – Frederick, Prince of Hohenzollern (b. 1891)
February 7 – Nance O’Neil, American stage and film actress (b. 1874)
February 9 – Khan Bahadur Ahsanullah, Indian educationist, philosopher, philanthropist, social reformer and spiritualist (b. 1874)
February 13
Humberto Delgado, Portuguese general and opposition politician (b. 1906)
William Heard Kilpatrick, American mathematician and philosopher (b. 1871)
February 14 – Désiré-Émile Inghelbrecht, French composer (b. 1880)
February 15 – Nat King Cole, American singer and musician (b. 1919)
February 19
Forrest Taylor, American actor (b. 1883)
Tom Wilson, American actor (b. 1880)
February 20 – Michał Waszyński, Polish film director and producer (b. 1904)
February 21 – Malcolm X, American civil rights activist (b. 1925)
February 22 – Felix Frankfurter, U.S. Supreme Court Justice (b. 1882)
February 23 – Stan Laurel, British actor (b. 1890)
February 24 – Takeo Itō, Japanese general (b. 1889)
February 28 – Adolf Schärf, Austrian politician, 6th President of Austria (b. 1890)
March
March 5 – Salvador Castaneda Castro, 31st President of El Salvador (b. 1888)
March 6 – Margaret Dumont, American actress (b. 1889)
March 7 – Louise Mountbatten, Queen of Sweden and second wife of King Gustaf VI Adolf (b. 1889)
March 13
Corrado Gini, Italian statistician (b. 1884)
Vittorio Jano, Italian automobile designer (b. 1891)
Fan Noli, Albanian bishop, poet and politician, 13th Prime Minister of Albania (b. 1882)
March 14 – Marion Jones Farquhar, American tennis champion (b. 1879)
March 17
Nancy Cunard, English writer, heiress, and political activist (b. 1896)
Amos Alonzo Stagg, American baseball, basketball and football player and coach (b. 1862)
March 18 – King Farouk of Egypt (b. 1920)
March 19 – Gheorghe Gheorghiu-Dej, Romanian communist leader, 47th Prime Minister of Romania (b. 1901)
March 22 – Fidel Dávila, Spanish general and minister (b. 1878)
March 23 – Mae Murray, American actress (b. 1885)
March 25
Giorgio Federico Ghedini, Italian composer (b. 1892)
Viola Liuzzo, American Unitarian Universalist and civil rights activist (b. 1925)
March 28
Mary, Princess Royal and Countess of Harewood (b. 1897)
Jack Hoxie, American actor, rodeo performer (b. 1885)
March 30 – Philip Showalter Hench, American physician, recipient of the Nobel Prize in Physiology or Medicine (b. 1896)
April
April 3 – Ray Enright, American film director (b. 1896)
April 10
Linda Darnell, American actress (b. 1923)
La Belle Otero, Spanish actress, dancer and courtesan (b. 1868)
April 14
Leonard Mudie, English actor (b. 1883)
Perry Smith (b. 1928) and Dick Hickock (b. 1931), American convicted murderers
April 16 – Sydney Chaplin, English actor (b. 1885)
April 18 – Guillermo González Camarena, Mexican inventor (b. 1917)
April 21 – Edward Victor Appleton, English physicist, Nobel Prize laureate (b. 1892)
April 23 – George Adamski, Polish-American UFO writer (b. 1891)
April 24 – Louise Dresser, American actress (b. 1878)
April 27 – Edward R. Murrow, American journalist (b. 1908)
April 30 – Helen Chandler, American actress (b. 1906)
May
May 1 – Spike Jones, American musician and bandleader (b. 1911)
May 6 – Oren E. Long, American politician, 10th Governor of Hawai’i (b. 1889)
May 7
Charles Sheeler, American photographer (b. 1883)
Alf Bjørnskau Bastiansen, Norwegian priest and politician (b. 1883)
May 9 – Leopold Figl, 14th Chancellor of Austria and acting President of Austria (b. 1902)
May 14 – Frances Perkins, first woman appointed as a United States Presidential cabinet member (Labor) (b. 1880)
May 15 – Yisrael Bar-Yehuda, Zionist activist and Israel politician (b. 1895)
May 16 – Maria Dąbrowska, Polish writer (b. 1886)
May 18 – Eli Cohen, Israeli spy (b. 1924)
May 21 – Sir Geoffrey de Havilland, British aviation pioneer and aircraft company founder (b. 1882)
May 23
Rosina Anselmi, Italian actress (b. 1880)
David Smith, American sculptor (b. 1906)
May 25 – Sonny Boy Williamson, American blues musician (b. 1899)
May 27 – John Rinehart Blue, American military officer, educator, businessperson, and politician (b. 1905)
June
June 1 – Curly Lambeau, American football player and coach (b. 1898)
June 5
Eleanor Farjeon, British author of children’s literature (b. 1881)
Prince Wilhelm, Duke of Södermanland (b. 1884)
June 7 – Judy Holliday, American actress, comedian, and singer (b. 1921)
June 11 – José Mendes Cabeçadas, Portuguese navy officer, 94th Prime Minister of Portugal and 9th President of Portugal (b. 1883)
June 13 – Martin Buber, Austrian-Israeli philosopher (b. 1878)
June 15 – Steve Cochran, American actor (b. 1917)
June 19 – James Collip, Canadian biochemist (b. 1892)
June 20 – Bernard Baruch, American financier and presidential adviser (b. 1870)
June 22 – David O. Selznick, American film producer (b. 1902)
June 23 – Mary Boland, American actress (b. 1882)
June 28 – Red Nichols, American jazz cornettist (b. 1905)
June 30 – Bessie Barriscale, American actress (b. 1884)
July
July 1 – Wally Hammond, English cricketer (b. 1903)
July 7 – Moshe Sharett, 2nd Prime Minister of Israel (b. 1894)
July 8 – T. S. Stribling, American novelist (b. 1881)
July 11 – Ray Collins, American actor (b. 1889)
July 13 – Laureano Gómez, 43rd President of Colombia (b. 1889)
July 14
Adlai Stevenson, American politician (b. 1900)
Max Woosnam, English sportsman (b. 1892)
July 19
Clyde Beatty, American animal trainer (b. 1903)
Ingrid Jonker, South African Afrikaans poet (b. 1933)
Syngman Rhee, Korean statesman, 1st President of South Korea (b. 1875)
July 24 – Constance Bennett, American actress (b. 1904)
July 28 – Rampo Edogawa, Japanese author and critic (b. 1894)
July 30
Pier Ruggero Piccio, Italian World War I fighter ace, air force general (b. 1880)
Jun’ichirō Tanizaki, Japanese writer (b. 1886)
August
August 1 – John Miller, American Olympic rower – Men’s eights (b. 1903)
August 6
Nancy Carroll, American actress (b. 1903)
Everett Sloane, American actor (b. 1909)
August 8 – Shirley Jackson, American author (b. 1916)
August 9 – Creighton Hale, American actor (b. 1882)
August 13 – Hayato Ikeda, Japanese politician, 38th Prime Minister of Japan (b. 1899)
August 25 – Johnny Hayes, American Olympic athlete (b. 1886)
August 27 – Le Corbusier, Swiss architect (b. 1887)
August 28
Rashid Ali al-Gaylani, Iraqi politician, 9th Prime Minister of Iraq (b. 1892)
Giulio Racah, Israeli physicist (b. 1909)
August 29 – Paul Waner, American baseball player (b. 1903)
September
September 4
Tommy Hampson, British Olympic athlete (b. 1907)
Albert Schweitzer, Alsatian physician and missionary, recipient of the Nobel Peace Prize (b. 1875)
September 8
Dorothy Dandridge, American actress (b. 1922)
Hermann Staudinger, German chemist, Nobel Prize laureate (b. 1881)
September 12 – Lucian Truscott, American general (b. 1895)
September 16 – Fred Quimby, American animated film producer (b. 1886)
September 17 – Alejandro Casona, Spanish poet and playwright (b. 1903)
September 22 – Othmar Ammann, Swiss-born American engineer (b. 1879)
September 27 – Clara Bow, American silent film actress (b. 1905)
October
October 1 – Anton Boisen, American founder of the clinical pastoral education movement (b. 1876)
October 3 – Zachary Scott, American actor (b. 1914)
October 6 – Edward Evans, English murder victim (b. 1948)
October 8 – Thomas B. Costain, Canadian author and journalist (b. 1885)
October 11
Dorothea Lange, American photographer (b. 1895)
Walther Stampfli, member of the Swiss Federal Council (b. 1884)
October 12 – Samir Al-Rifai, 6-time Prime Minister of Jordan (b. 1901)
October 13 – Paul Hermann Müller, Swiss chemist, recipient of the Nobel Prize in Physiology or Medicine (b. 1899)
October 14 – Randall Jarrell, American poet (b. 1914)
October 15 – Abraham Fraenkel, Israeli mathematician and recipient of the Israel Prize (b. 1891)
October 17 – Bart King, American cricketer (b. 1873)
October 18
Oscar Beregi, Hungarian actor (b. 1876)
Henry Travers, English actor (b. 1874)
October 21
Bill Black, American musician and bandleader (b. 1926)
Marie McDonald, American actress (b. 1923)
October 22 – Paul Tillich, German American Christian existentialist philosopher and theologian (b. 1886)
October 23 – Luis de la Puente Uceda, Peruvian guerrilla leader (b. 1926)
October 24 – Hans Meerwein, German chemist (b. 1879)
October 26 – Sylvia Likens, American murder victim (b. 1949)
October 29 – Miller Anderson, American Olympic diver (b. 1922)
October 30 – Arthur Schlesinger, Sr., American historian (b. 1888)
October 31 – Rita Johnson, American actress (b. 1913)
November
November 2
Félix Paiva, 28th President of Paraguay (b. 1877)
H.V. Evatt, Australian politician, judge (b. 1894)
November 6
Edgard Varèse, French-born American composer (b. 1883)
Clarence Williams, American musician (b. 1893)
November 7 – Mirza Basheer-ud-Din Mahmood Ahmad, 2nd Caliph of Ahmadiyya Muslim Community in Islam (b. 1889)
November 8
Dorothy Kilgallen, American newspaper columnist and television personality (b. 1913)
Emma Gramatica, Italian actress (b. 1874)
November 12 – Taher Saifuddin, Indian Bohra spiritual leader (b. 1888)
November 16
Harry Blackstone Sr., American magician and illusionist (b. 1885)
W. T. Cosgrave, Irish politician, president of the Provisional Government and the Executive Council of the Irish Free State (b. 1880)
November 18
Khalid al-Azm, 5-time Prime Minister of Syria and acting President of Syria (b. 1903)
Henry A. Wallace, 33rd Vice President of the United States (b. 1888)
November 24 – Abdullah III Al-Salim Al-Sabah, Emir of Kuwait (b. 1895)
November 25 – Dame Myra Hess, English pianist (b. 1890)
December
December 5 – Joseph Erlanger, American physiologist and academic, Nobel Prize laureate (b. 1874)
December 9 – Branch Rickey, American baseball executive (b. 1881)
December 10 – Henry Cowell, American composer (b. 1897)
December 11 – George Constantinescu, Romanian scientist (b. 1881)
December 15 – Joseph Bamina, 8th Prime Minister of Burundi (executed) (b. 1925)
December 16
W. Somerset Maugham, English writer (b. 1874)
Tito Schipa, Italian tenor (b. 1889)
December 24 – William M. Branham, American minister (b. 1909)
December 27 – Edgar Ende, German painter (b. 1901)
December 29 – Kosaku Yamada, Japanese composer, and conductor (b. 1886)
Nobel Prizes
Physics – Shin’ichirō Tomonaga, Julian Schwinger, Richard P. Feynman
Chemistry – Robert Burns Woodward
Physiology or Medicine – François Jacob, André Michel Lwoff, Jacques Monod
Literature – Mikhail Sholokhov
Peace – United Nation’s Children’s Fund (UNICEF)
BACK TO TOP NEWS STORIES | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 62 | https://medicine.yale.edu/news/yale-medicine-magazine/article/a-nobel-prize-for-studies-of-cell-trafficking | en | A Nobel Prize for studies of cell trafficking | https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/7653ce98-b7f6-4d6f-873e-a0b432ea0e16 | https://ysm-res.cloudinary.com/image/upload/c_limit,f_auto,h_630,q_auto,w_1200/v1/yms/prod/7653ce98-b7f6-4d6f-873e-a0b432ea0e16 | [] | [] | [] | [
""
] | null | [] | 2021-12-08T00:00:00 | As he neared the end of the day in October that began with an early-morning phone call from Sweden, James E. Rothman, Ph. | en | Yale School of Medicine | https://medicine.yale.edu/news/yale-medicine-magazine/article/a-nobel-prize-for-studies-of-cell-trafficking | As he neared the end of the day in October that began with an early-morning phone call from Sweden, James E. Rothman, Ph.D., recalled before a gathering of his colleagues, students, and university leaders what he described as an “out-of-body experience”—the news that he had shared in the 2013 Nobel Prize in physiology or medicine.
“I have gotten close to 1,000 e-mails,” said Rothman, the Fergus F. Wallace Professor of Biomedical Sciences and professor and chair of cell biology, speaking at a reception in the Beinecke Rare Book and Manuscript Library on the evening of October 7. “You hear from all kinds of people: someone who practiced medicine with my father, a third grade classmate.”
Earlier in the day at a press conference he said he was still absorbing the news. “It’s a little hard to believe all this is happening,” he said. Rothman noted his good fortune in having studied at Yale and learning “to appreciate science and intellectual activity at its highest, to have matured and started my career as a researcher when your idea was the only limit. Any risk could be taken, no matter how difficult. I was fortunate to have taken a few of those risks and today’s Nobel Prize recognizes the success that came out of that.”
The prize acknowledged his contributions to the understanding of membrane trafficking, the means by which proteins and other materials are transported within and between cells. Rothman, a 1971 Yale College graduate who previously shared in the Albert Lasker Award for Basic Medical Research, the Louise Gross Horwitz Prize of Columbia University, and the Kavli Prize in Neuroscience, is one of the world’s foremost experts on exocytosis, a form of trafficking in which cargo-bearing spheres called vesicles fuse with cell membranes to deliver their contents.
This process is essential to such processes as cell division and insulin secretion, for example, but also plays a crucial role in the nervous system. Vesicles carrying neurotransmitters fuse with cell membranes at synapses and pass on chemical messages that govern movement, perception, cognition, memory, and mood. For three decades, Rothman has performed experiments that have revealed the molecular machinery of membrane trafficking in fine detail. In much of his work Rothman sidestepped the complexities of working with complete cells by using a “cell-free” approach—isolating the intracellular components crucial to membrane trafficking.
Rothman and the two scientists who shared in the $1.2 million award—Randy W. Schekman, Ph.D., of the University of California−Berkeley, and Thomas Südhof, M.D., of Stanford University—all faced skepticism within the scientific community when they began their research. Each went on to solve a different piece of the puzzle.
While Rothman figured out the machinery under-lying membrane trafficking, Schekman discovered a set of genes essential for vesicle traffic, and Südhof determined how vesicles know when and where to release their cargo.
Rothman began his research career after receiving his Ph.D. from Harvard in 1976. From there he went on to the Massachusetts Institute of Technology, Stanford, Princeton, Memorial Sloan-Kettering, and Columbia before coming to Yale in 2008.
“When Jim started his career, a number of successful biochemists were recognizing the importance of studying molecular processes in cell-free systems, but no one imagined that you could study vesicle trafficking in a cell-free system,” said Robert J. Alpern, M.D., dean and Ensign Professor of Medicine, at the press conference. This bold approach revolutionized the field.”
“Yale is absolutely thrilled to have one of our most distinguished faculty—who is also one of our most distinguished alumni—receive this great honor,” said President Peter Salovey, Ph.D., the Chris Argyris Professor of Psychology. | |||
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] | null | [] | null | en | null | Charles Barkla (1877-1944) was awarded the Nobel Prize in Physics for research into X-rays and other emissions in 1917. Barkla was Professor of Physics at King's from 1909 to 1913.
Sir Owen Willans Richardson (1879-1959) was awarded the Nobel Prize in Physics in 1928 for his work on the thermionic phenomenon and especially for the discovery of the law named after him". Sir Owen was Wheatstone Professor of Physics at Kings from 1914-24.
Sir Frederick Gowland Hopkins (1861-1947), was awarded the Nobel Prize in Physiology or Medicine for discovery of essential nutrient factors—now known as vitamins—needed in animal diets to maintain health. Sir Frederick taught physiology and toxicology at Guy's Hospital from 1894 to 1898.
Sir Charles Scott Sherrington (1857-1952), was awarded the Nobel Prize in Physiology or Medicine in 1932 for his research on the nervous system. Sir Charles was Professor in Systematic Physiology at St Thomas' Hospital 1887-91.
Sir Edward Appleton (1892-1965), was awarded the Nobel Prize in Physics for exploration of the ionosophere in 1947. Sir Edward was Wheatstone Professor of Physics at King's from 1924-36.
Max Theiler (1899-1972) was awarded the Nobel Prize in Physiology or Medicine for developing a vaccine for yellow fever in 1951. He was the first African-born Nobel laureate. Dr Theiler studied at St. Thomas' Hospital. He also worked on the causes and immunology of Weil's disease, dengue fever, Japanese encephalitis and poliomyelitis.
Maurice Wilkins (1916–2004) was awarded the 1962 Nobel Prize in Physiology or Medicine for his work in using X-ray diffraction to take new images of a form of the DNA molecule. Maurice remained at King's for the rest of his career.
Archbishop Desmond Tutu (1931-2021) was awarded the Nobel Prize for Peace in 1984 in recognition of his work as Secretary-General of the South African Council of Churches.
Sir James Black (1924-2010) was awarded the Nobel Prize in Physiology or Medicine for the development of beta-blocker and anti-ulcer drugs in 1988. Sir James was Professor of Analytical Pharmacology at King's.
Mario Vargas Llosa was awarded the Nobel Prize in Literature in 2010 for "his cartography of structures of power and his trenchant images of the individual's resistance, revolt, and defeat". Llosa was a Lecturer in Spanish American Literature in the Department of Spanish & Spanish-American Studies at King's in 1969-70, before he became a full-time writer. He became a Fellow of King's in 2005.
Michael Levitt was awarded the Nobel Prize in Chemistry 2013 alongside Martin Karplus and Arieh Warshel, for ‘the development of multiscale models for complex chemical systems’, laying the foundation for the computer models now used to understand and predict chemical processes. He was awarded an honorary doctorate by King’s the following year.
Professor Peter Higgs was awarded the Nobel Prize in Physics in 2013. Among the many honours and awards Professor Higgs has received are the Fellowship of King's in 1998 and the university's Honorary Doctorate of Science in 2009.
Professor Sir Roger Penrose was awarded the 2020 Nobel Prize in Physics for the discovery which showed that the general theory of relativity leads to the formation of black holes. He spent two years as a research associate at King's between 1961 and 1963 and was awarded an honorary degree by King's in 2018. | |||||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 37 | https://www.rockefeller.edu/our-scientists/joshua-lederberg/2502-nobel-prize/ | en | Nobel Prize in Physiology or Medicine | [
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] | null | [] | 2017-03-06T16:43:48+00:00 | By the mid-20th century, science had established several crucial facts about the capabilities of bacteria, a seemingly primitive, unicellular organism first classified in 1676. Some bacteria, scientists understood, can cause life-threatening disease; some are resistant to even the strongest antibiotics; and some that are neither virulent nor resistant to begin with can gain both virulence […] | en | /img/favicon/apple-icon-57x57.png?v=8 | Our Scientists | https://www.rockefeller.edu/our-scientists/joshua-lederberg/2502-nobel-prize/ | By the mid-20th century, science had established several crucial facts about the capabilities of bacteria, a seemingly primitive, unicellular organism first classified in 1676. Some bacteria, scientists understood, can cause life-threatening disease; some are resistant to even the strongest antibiotics; and some that are neither virulent nor resistant to begin with can gain both virulence and resistance. The question of how bacteria accomplish such sleight of hand, which had been subject to decades of logical but inaccurate speculation, was resolved by a 22-year-old graduate student in 1947. Joshua Lederberg, Rockefeller University’s fifth president, won a share of the 1958 Nobel Prize in Physiology or Medicine for his discoveries of genetic transfer in bacteria.
Through the 1940s, scientific wisdom had it that bacteria do not have genetic mechanisms similar to those of higher organisms. The prevailing hypothesis, taught in Dr. Lederberg’s Columbia University medical school classes, classed bacteria with schizomycetes, organisms that reproduce by cloning. The 1944 discovery of Rockefeller scientists Oswald T. Avery, Maclyn McCarty and Colin MacLeod that deoxyribonucleic acid, or DNA, is the genetic material in Pneumococcus proved that bacteria have genes and thus drew an unexpected parallel between bacteria and higher organisms. But their discovery, unconnected to a method of proliferation, was met with widespread skepticism. Inspired by the new evidence, Dr. Lederberg interrupted medical school to pursue experimental genetics with Edward L. Tatum, the Yale University chemist with whom he would later share the Nobel Prize.
Initial experiments with the intestinal bacteria Escherichia coli led Dr. Lederberg to estimate that only one in 20 strains are fertile, and that if bacteria mate, they do so only during a particular phase of their life cycle. After crossing two strains of E. coli, each with different mutations for nutritional deficiencies, he found that some of the offspring of each strain had regained the ability to produce the nutrients its parent could not. When that ability continued to be inherited by successive generations, Dr. Lederberg had effectively proved the textbooks wrong. He named the bacterial mating process conjugation, received his Ph.D. for this research and officially left medical school to continue in bacterial genetics. We now understand that bacterial mating occurs only through cell-to-cell contact, when a bridge is formed between the two cells that transports genetic information from the donor cell to the recipient.
Dr. Lederberg’s experiments also identified E. coli as a haploid that carries only a single chromosome and suggested that conjugation is a form of unequal horizontal gene transfer: Rather than exchanging genes equally, the mating bacteria transfer partial genetic material from one parent to the other. He also developed a technique that allowed for the identification of antibiotic- or bacteriophage-resistant strains without exposing the bacteria to the phage or the drug, and proved that resistance is a genetic mutation rather than an adaptation.
Following his seminal research at Yale, Dr. Lederberg accepted a position to chair the newly founded department of genetics at the University of Wisconsin, Madison. With his graduate student Norton Zinder — later a colleague at Rockefeller University — Dr. Lederberg showed that bacteriophages can transfer genetic information between cells in Salmonella. The process, which they named transduction, was the first demonstration that it is possible to introduce new genes into an organism and in other ways manipulate its genetic material. The discovery explained how different species of bacteria can so quickly gain resistance to the same antibiotic.
The scientific contributions of Dr. Lederberg’s pathbreaking foray into bacterial genetics are legion. His work gave scientists an experimental model whose simplicity and rapid growth made it ideal for genetic studies. His description of bacterial conjugation led directly to the distinction denoted since 1962 by the terms prokaryotic and eukaryotic. His findings led to research that elucidated the mechanisms of bacteriophages and other viruses; explained how cell growth is interrupted; and clarified how cancer progresses. And his description of transduction led to the development of gene therapy and contributed to the boom in biotechnology and genetic engineering in the 1970s. Dr. Lederberg received half of the 1958 Nobel Prize “for his discoveries concerning genetic recombination and the organization of the genetic material of bacteria. Dr. Tatum and his colleague George Wells Beadle received the second half of the 1958 prize “for their discovery that genes act by regulating definite chemical events.”
CAREER
Born in 1925 and raised in New York City, Dr. Lederberg received his Ph.D. from Yale University in 1947 and then joined the University of Wisconsin, Madison, where he founded the department of medical genetics 10 years later. In 1959, he moved to Stanford University, where he was chair of the newly established department of genetics. There he also expanded his research into the fields of artificial intelligence and exobiology. In 1978, Dr. Lederberg became the fifth president of The Rockefeller University, a position he held until 1990, when he retired from the presidency and became University Professor and head of the Laboratory of Molecular Genetics and Informatics, where his research continued. Throughout his later research career, Dr. Lederberg was highly active in international science and human rights advocacy, serving as a public policy adviser to nine United States presidential administrations and authoring a weekly Washington Post column, “Science and Man,” for six years. He was a member of the National Academy of Sciences and a foreign member of The Royal Society. In addition to the Nobel Prize, he received the National Medal of Science and the Presidential Medal of Freedom. He died in New York in 2008. | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 74 | https://news.harvard.edu/gazette/story/2019/10/harvard-faculty-wins-nobel-in-physiology-or-medicine/ | en | Harvard faculty member wins Nobel in physiology or medicine | [
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] | 2019-10-07T09:46:37+00:00 | William G. Kaelin Jr., the Sidney Farber Professor of Medicine at Harvard Medical School and the Dana-Farber Cancer Institute, is one of three winners of the 2019 Nobel Prize in physiology or medicine for discovering how cells sense and adapt to changes in oxygen availability, a process critical for survival. | en | Harvard Gazette | https://news.harvard.edu/gazette/story/2019/10/harvard-faculty-wins-nobel-in-physiology-or-medicine/ | Every scientist starts out looking for one thing, but sometimes finds something else along the way.
On Monday, newly minted Nobel laureate William G. Kaelin described a decades-long scientific journey that was like that. It started as an exploration of a condition that can lead to kidney cancer but resulted in a prize-winning discovery about how cells recognize and regulate the oxygen needed to survive, a discovery whose most tangible fruit is a drug to treat anemia.
“I’m a cancer biologist and a cancer physician, but the first truly unique thing coming out of my lab was for anemia,” Kaelin said during a late-morning news conference at the Dana-Farber Cancer Institute in Boston.
The unexpected application shows the importance of basic research and curiosity-driven science — undervalued today in a culture that often wants to know what results to expect before the work is underway, and leaves little room to pursue the unknown, Kaelin said.
Kaelin, the Sidney Farber Professor of Medicine at Harvard Medical School and the Dana-Farber Cancer Institute, learned in a phone call from Stockholm at 4:50 a.m. that he had won the 2019 Nobel Prize in physiology or medicine. In a humorous and poignant telling, Kaelin recounted the story of his discovery, the science, and the importance of those around him, particularly his late wife, Carolyn, a breast cancer surgeon and an inspiration to him. She died of a brain tumor in 2015.
“I like to think she’s smiling and nodding, ‘I told you, I told you this was going to happen!’” said Kaelin, who is also a senior physician at Brigham and Women’s Hospital and an investigator at the Howard Hughes Medical Institute.
The Nobel committee recognized Kaelin, Sir Peter J. Ratcliffe of the Francis Crick Institute in London, and Gregg L. Semenza ’78 of Johns Hopkins University “for their discoveries of how cells sense and adapt to oxygen availability.” The work centers around two main molecules, called VHL — the focus of Kaelin’s work — and HIF. Together, they found that VHL works like a cellular garbage disposal, destroying HIF molecules when oxygen is plentiful in the cell. When oxygen levels drop, HIF builds up, signaling stress to the body and triggering a response that can include producing more red blood cells and growing new blood vessels. In 2001, Kaelin and Ratcliffe simultaneously found the missing link between the chemical reactions and oxygen levels, a process that, when oxygen is plentiful, chemically tags HIF for destruction.
In the years since, Kaelin said, similar pathways have been found in an array of animals, indicating it is evolutionarily conserved, a sign of its importance to survival.
Kaelin cut his scientific teeth in the lab of David Livingston, the Emil Frei III Distinguished Professor of Medicine at Dana-Farber. He arrived in 1987 after finishing medical school at Duke University and a residency at Johns Hopkins. Kaelin said Livingston mentored him during his postdoctoral fellowship and remains a mentor to this day. Livingston recalled Kaelin doing “spectacular work” in his lab, leaving him impressed with the clarity of the younger researcher’s scientific mind and his commitment to scientific rigor.
“I’m overjoyed — times 10 — but not surprised,” Livingston said of his friend’s good news. In the early 1990s, Livingston said, when Kaelin left the lab to start his own, it was an easy decision to keep him at Dana-Farber.
The heads of the three institutions with which Kaelin is affiliated had praise for the new laureate. Speaking at the morning news conference, Harvard Medical School Dean George Q. Daley said Kaelin’s story is an example of how clinical medicine can inform scientific discovery, describing him as the “finest medicine has to offer.”
“He is the consummate physician-scientist,” Daley said. “He is fiercely dedicated to rigor and excellence in both the laboratory and in the clinic.”
Dana-Farber President Laurie Glimcher said because oxygen regulation is so important to so many biological processes, understanding and being able to manipulate the pathway discovered by Kaelin and co-laureates may be transformative in a host of diseases, including cancer, heart disease, anemia, and macular degeneration.
Kaelin said that popular media commonly falsely depicts scientists as loners jealously guarding research results, but it was a spirit of collaboration that boosted the Nobel-winning discoveries and, more broadly, made the Boston area’s medical-scientific community such fertile ground for discovery.
Though he didn’t collaborate directly with Semenza and Ratcliffe, they had a collegial relationship and would talk about the latest lab findings when they met at scientific gatherings, sharing work months before official scientific publication.
“I learned years ago that I learn fastest when surrounded by people smarter than me,” Kaelin said. “Science today is not done by an individual, but by an ecosystem.”
Kaelin has worked to create such an ecosystem in his lab, a series of rooms on the fourth floor of the Mayer Building. The rooms, containing laboratory benches crowded with equipment, host 10 to 15 postdoctoral fellows at a time working on related projects.
Hilary Nicholson, a fourth-year postdoctoral fellow whose work on a treatment for the most common kind of kidney cancer was recently on the cover of the journal Science Signaling, said Kaelin freely shares equipment with colleagues and selects people for his lab based not only on their interest in advancing science but also on their willingness to help others.
Nicholson said an important feature of their research is that it has potential applications that one day may help patients in the waiting rooms they pass each morning when they arrive at work.
“One of the great things about Bill’s discovery is that it’s been translatable, and it’s fundamental, and it’s stood up against the test of time. He always pursues the truth, very doggedly,” Nicholson said. “For me, it’s all about the patients waiting for you to come up with something amazing.” | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 23 | https://pci.upenn.edu/katalin-kariko-and-drew-weissman-named-co-recipients-of-the-2023-nobel-prize-for-medicine/ | en | Recipients of the 2023 Nobel Prize for Medicine | [
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] | 2023-10-10T18:00:00+00:00 | Penn’s Katalin Karikó, PhD, and Drew Weissman, MD, PhD, have been named winners of the 2023 Nobel Prize in Physiology or Medicine. | en | Penn Center for Innovation | https://pci.upenn.edu/katalin-kariko-and-drew-weissman-named-co-recipients-of-the-2023-nobel-prize-for-medicine/ | Penn’s Drew Weissman, MD, PhD, the Roberts Family Professor in Vaccine Research in Infectious Diseases and Katalin Karikó, PhD, adjunct professor of Neurosurgery, were jointly named winners of the 2023 Nobel Prize in Physiology or Medicine. Their groundbreaking and foundational research at Penn played a vital role in the development of modified mRNA-based COVID-19 vaccines that have been administered to billions of individuals globally, and helped to end the recent pandemic.
Karikó and Weissman first met at a copy machine at Penn during the late 1990s, while waiting to make copies of scientific journal articles. They quickly took an interest in each other’s research and agreed to work together to investigate the use of modified mRNA as a potentially new therapeutic modality. Their resultant collaborative research clearly established that mRNA could be precisely altered and then delivered in vivo without provoking deleterious effects from the body’s own immune system — an enormous advancement in the field of mRNA research that has opened up exciting new possibilities for vaccines and other types of therapeutic drug development.
When the COVID-19 pandemic struck, Karikó and Weissman’s foundational mRNA discoveries were instrumental in helping to make live-saving vaccines possible. Both Pfizer/BioNTech and Moderna utilized Karikó and Weissman’s technology as a key component of their highly effective vaccines to protect against severe illness and death from COVID-19.
In recognition of the remarkable impact of their technology, Nobel Foundation prize administrators reached out to Karikó and Weissman on the morning of October 02, 2023 to formally notify them of the news of their award. Since 1901, less than 1,000 people have received a Nobel Prize, and only 225 have been awarded a Nobel Prize in Physiology or Medicine. Further, Karikó is one of just 61 women to become a Nobel Laureate and only the 13th woman to be awarded the Nobel Prize in Physiology or Medicine. Penn and PCI are incredibly proud to congratulate Dr. Weissman and Dr. Karikó for their incredible achievements and well-deserved honor!
There is wide range of in-depth coverage by the Philadelphia Inquirer, which you can read here:
Philadelphia Inquirer, first article
Philadelphia Inqurier, editorial
Philadelphia Inquirer, vaccines and licensing revenue
Philadelphia Inquirer, Drew Weissman’s story
Philadelphia Inquirer, Katalin Karikó’s story, commentary
Philadelphia Inquirer, Katalin Karikó’s story, health
Philadelphia Inquirer, Susan Francia’s story (Karikó’s daughter)
Video content is available here:
Video of Drew Weissman telling his parents
Video of Drew Weissman’s first reaction
Video of Katalin Karikó’s first reaction
Additional articles published in global publications are available here: | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 0 | https://www.nobelprize.org/prizes/facts/facts-on-the-nobel-prize-in-physiology-or-medicine/ | en | Facts on the Nobel Prize in Physiology or Medicine | [
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] | null | [] | null | Facts on the Nobel Prize in Physiology or Medicine | en | NobelPrize.org | https://www.nobelprize.org/prizes/facts/facts-on-the-nobel-prize-in-physiology-or-medicine | On 27 November 1895, Alfred Nobel signed his last will and testament, giving the largest share of his fortune to a series of prizes, the Nobel Prizes. As described in Nobel’s will, one part was dedicated to “the person who shall have made the most important discovery within the domain of physiology or medicine”. Learn more about the Nobel Prize in Physiology or Medicine from 1901 to 2023.
Number of Nobel Prizes in Physiology or Medicine
114 Nobel Prizes in Physiology or Medicine have been awarded since 1901. It was not awarded on nine occasions: in 1915, 1916, 1917, 1918, 1921, 1925, 1940, 1941 and 1942.
Why were the medicine prizes not awarded in those years? In the statutes of the Nobel Foundation it says: “If none of the works under consideration is found to be of the importance indicated in the first paragraph, the prize money shall be reserved until the following year. If, even then, the prize cannot be awarded, the amount shall be added to the Foundation’s restricted funds.” During World War I and II, fewer Nobel Prizes were awarded.
Shared and unshared Nobel Prizes in Physiology or Medicine
40 medicine prizes have been given to one laureate only.
35 medicine prizes have been shared by two laureates.
39 medicine prizes have been shared between three laureates.
Why is that? In the statutes of the Nobel Foundation it says: A prize amount may be equally divided between two works, each of which is considered to merit a prize. If a work that is being rewarded has been produced by two or three persons, the prize shall be awarded to them jointly. In no case may a prize amount be divided between more than three persons.
Number of Nobel Prize laureates in physiology or medicine
227 individuals have been awarded 1901-2023.
List of all Nobel Prize laureates in physiology or medicinene
Youngest medicine laureate
To date, the youngest Nobel Prize laureate in physiology or medicine is Frederick G. Banting, who was 32 years old when he was awarded the medicine prize in 1923.
Oldest medicine laureate
The oldest Nobel Prize laureate in physiology or medicine to date is Peyton Rous, who was 87 years old when he was awarded the medicine prize in 1966.
Female Nobel Prize laureates in physiology or medicine
Of the 227 individuals awarded the Nobel Prize in Physiology or Medicine, 13 are women. Of these 13, Barabara McClintock is the only one who has received an unshared Nobel Prize.
List of all female Nobel Prize laureates
Multiple Nobel Prize laureates in physiology or medicine
No one has been awarded the Nobel Prize in Physiology or Medicine more than once. Yet …
List of multiple Nobel Prize laureates within other prize categories
Posthumous Nobel Prizes in Physiology or Medicine
There have been no posthumous Nobel Prizes in Chemistry. From 1974, the Statutes of the Nobel Foundation stipulate that a Nobel Prize cannot be awarded posthumously, unless death has occurred after the announcement of the Nobel Prize. Before 1974, the Nobel Prize has only been awarded posthumously twice: to Dag Hammarskjöld (Nobel Peace Prize 1961) and Erik Axel Karlfeldt (Nobel Prize in Literature 1931).
Following the 2011 announcement of the Nobel Prize in Physiology or Medicine, it was discovered that one of the medicine laureates, Ralph Steinman, had passed away three days earlier. The Board of the Nobel Foundation examined the statutes, and an interpretation of the purpose of the rule above lead to the conclusion that Ralph Steinman should to remain a Nobel Prize laureate, as the Nobel Assembly at Karolinska Institutet had announced the 2011 Nobel Prize laureates in physiology or medicine without knowing of his death.
Family Nobel Prize laureates in physiology or medicine
Married couples
Gerty Theresa Cori, née Radnitz
The Nobel Prize in Physiology or Medicine 1947 for their discovery of the course of the catalytic conversion of glycogen.
Carl Ferdinand Cori
The Nobel Prize in Physiology or Medicine 1947 for their discovery of the course of the catalytic conversion of glycogen.
May-Britt Moser
The Nobel Prize in Physiology or Medicine 2014 for their discoveries of cells that constitute a positioning system in the brain.
Edvard I. Moser
The Nobel Prize in Physiology or Medicine 2014 for their discoveries of cells that constitute a positioning system in the brain.
Father & son
Hans Karl August Simon von Euler-Chelpin
The Nobel Prize in Chemistry 1929 for their investigations on the fermentation of sugar and fermentative enzymes.
Ulf von Euler
The Nobel Prize in Physiology or Medicine 1970 for their discoveries concerning the humoral transmitters in the nerve terminals and the mechanism for their storage, release and inactivation.
Sune K. Bergström
The Nobel Prize in Physiology or Medicine 1982 for their discoveries concerning prostaglandins and related biologically active substances.
Svante Pääbo
The Nobel Prize in Physiology or Medicine 2022 for his discoveries concerning the genomes of extinct hominins and human evolution.
Brothers
Jan Tinbergen
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 1969 for having developed and applied dynamic models for the analysis of economic processes.
Nikolaas Tinbergen
The Nobel Prize in Physiology or Medicine 1973 for their discoveries concerning organization and elicitation of individual and social behaviour patterns.
Forced to decline the Nobel Prize
Two Nobel Prize laureates in chemistry have been forced by authorities to decline the Nobel Prize. Adolf Hitler forbade three German Nobel Prize laureates from receiving the Nobel Prize – two of whom were awarded the Nobel Prize in Chemistry, Richard Kuhn in 1938 and Adolf Butenandt in 1939. The third person, Gerhard Domagk was awarded the Nobel Prize in Physiology or Medicine in 1939. All of them could receive the Nobel Prize diploma and medal later, but not the prize amount.
Nobel Prize laureate partnerships in biomedical science
Many long scientific partnerships have resulted in Nobel Prizes:
List compiled in 2012, courtesy of Joseph L. Goldstein.
Nominations for the Nobel Prize in Physiology or Medicine
In the nomination database, you can find interesting nomination trivia, for example, that the Austrian neurologist and founder of psychoanalysis Sigmund Freud (1856-1939) was nominated 32 times for the Nobel Prize in Physiology or Medicine, but never awarded. In 1929, the Nobel Committee for Medicine engaged an expert who concluded that a further investigation in Freud was not necessary, since Freud’s work was of no proven scientific value. Freud was also nominated once for the 1936 Nobel Prize in Literature by Nobel Prize laureate Romain Rolland, an acquaintance of Freud.
The nominations for the Nobel Prizes are kept secret for 50 years.
Explore the nomination database for the Nobel Prizes
The Nobel Prize medal in physiology and medicine
The Nobel Prize medal in physiology and medicine was designed by Swedish sculptor and engraver Erik Lindberg and represents the Genius of Medicine holding an open book in her lap, collecting the water pouring out from a rock in order to quench a sick girl’s thirst.
Read more about Nobel medal in Physiology and Medicine
The Nobel Prize diplomas
Each Nobel Prize diploma is a unique work of art, created by foremost Swedish and Norwegian artists and calligraphers.
More about the Nobel Prize diplomas
The Nobel Prize amount
Alfred Nobel left most of his estate, more than SEK 31 million (today approximately SEK 1,702 million) to be converted into a fund and invested in “safe securities.” The income from the investments was to be “distributed annually in the form of prizes to those who during the preceding year have conferred the greatest benefit to humankind.”
The Nobel Prize amount for 2023 was set at Swedish kronor (SEK) 11 million per full Nobel Prize.
More about the Nobel Prize amount
Why are the individuals and organisations awarded a Nobel Prize called Nobel Prize laureates?
The word “laureate” refers to being signified by the laurel wreath. In Greek mythology, the god Apollo is represented wearing a laurel wreath on his head. A laurel wreath is a circular crown made of branches and leaves of the bay laurel (in Latin: Laurus nobilis). In Ancient Greece, laurel wreaths were awarded to victors as a sign of honour – both in athletic competitions and in poetic meets.
Links to more facts on the Nobel Prizes
Facts on the Nobel Prize in Physics
Facts on the Nobel Prize in Chemistry
Facts on the Nobel Prize in Physiology or Medicine
Facts on the Nobel Prize in Literature
Facts on the Nobel Peace Prize
Facts on the Prize in Economic Sciences
Facts on all Nobel Prizes
First published 5 October 2009. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 40 | https://archives.upenn.edu/exhibits/penn-people/notables/awards/nobel-prizes/ | en | Nobel Prizes • University Archives and Records Center | [
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] | null | [] | 2018-06-06T18:33:58+00:00 | en | University Archives and Records Center | https://archives.upenn.edu/exhibits/penn-people/notables/awards/nobel-prizes/ | Awards and Honors Nobel Prizes
Awarded annually since 1901 by the Nobel Foundation, Stockholm.
Katalin Karikó, 1955 –
Drew Weissman, 1959 –
Physiology or Medicine, 2023
Awarded “for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19.”
Karikó is an adjunct professor of Neurosurgery the Perelman School of Medicine and Weissman is the Roberts Family Professor of Vaccine Research in the Perelman School of Medicine.
Nobel Foundation information on this award.
Claudia Goldin, 1946 –
Economic Sciences, 2023
Awarded “for having advanced our understanding of women’s labour market outcomes.”
Goldin was a member of the University of Pennsylvania’s Department of Economics from 1979 to 1990, serving as Associate Professor, 1979–1985; Professor, 1985–1990; Chair of Graduate Group, 1983–1984.
Nobel Foundation information on this award.
Gregg L. Semenza, 1956 –
Physiology or Medicine, 2019
Awarded jointly to William G. Kaelin, Jr., and Sir Peter J. Ratcliffe “for their discoveries of how cells sense and adapt to oxygen availability.”
Penn Graduate: M.D. 1982; Ph.D. 1984
Nobel Foundation information on this award.
Robert J. Shiller, 1946 –
Economic Sciences, 2013
Awarded jointly to Robert J. Shiller, Eugene F. Fama, and Lars Peter Hansen “for their empirical analysis of asset prices.”
Shiller was on the University of Pennsylvania faculty from 1974 until 1982.
Nobel Foundation information on this award.
Thomas J. Sargent, 1943 –
Economic Sciences, 2011
Awarded jointly to Thomas J. Sargent and Christopher A. Sims “for their empirical research on cause and effect in the macroeconomy.”
Sargent was on the University of Pennsylvania faculty for three semesters, from January 1970 until June 1971.
Nobel Foundation information on this award.
Ei-ichi Negishi, 1935 – 2021
Chemistry, 2010
Awarded jointly to Richard F. Heck, Ei-ichi Negishi and Akira Suzuki “for palladium-catalyzed cross couplings in organic synthesis.”
Negishi earned his Ph.D. in Chemistry from the University of Pennsylvania, doing his dissertation work under Professor of Chemistry Allan Day.
Nobel Foundation information on this award.
Oliver E. Williamson, 1932 – 2020
Economics, 2009
Awarded “for his analysis of economic governance, especially the boundaries of the firm.”
Wilson was a member of the University of Pennsylvania’s Department of Economics from 1965 to 1983, serving as Associate Professor, 1965–1968; Professor, 1968–1983; Charles and William L. Day Professor of Economics and Social Science, 1977–1983.
Nobel Foundation information on this award.
George E. Smith, 1930 –
Physics, 2009
Awarded for the invention of an imaging semiconductor circuit – the CCD sensor. Charles K. Kao was the third recipient, for his work in fiber optics.
Penn Graduate: A.B. 1955
After earning his Ph.D. from the University of Chicago, Smith joined Bell Labs where he attained 31 patents, including one in 1969 for his work with Boyle on the CCD.
Nobel Foundation information on this award.
Harald zur Hausen, 1936 –
Physiology or Medicine, 2008
Awarded for for his discovery of human papilloma viruses causing cervical cancer. The other half of the prize was shared by Françoise Barré-Sinoussi and Luc Montagnier for their discovery of the immunodeficiency virus.
Assistant professor, 1968–1969, while working at the Virus Laboratories of Children’s Hospital.
Educated at the Universities of Bonn, Hamburg and Dusseldorf, zur Hausen returned to Germany in 1969 to continue his research and teaching. From 1983 to 2003 he served as professor of medicine at the University of Heidelberg and as a chair and member of the scientific advisory board of the German Cancer Research Center.
Nobel Foundation information on this award.
Edmund S. Phelps, 1933 –
Economics, 2006
Awarded for his analysis of intertemporal tradeoffs in macroeconomic policy.
Phelps was a professor in the Economics Department at the University of Pennsylvania from 1966 to 1971.
Nobel Foundation information on this award.
Edward C. Prescott, 1940 –
Economics, 2004
With Finn E. Kydland (Carnegie-Mellon University and the University of California Santa Barbara). Awarded for their contributions to dynamic macroeconomics: the time consistency of economic policy and the driving forces behind business cycles.
Prescott came to Penn in 1966 as a lecturer in the Economics Department. He was an assistant professor here from 1967 to 1971.
Nobel Foundation information on this award.
Irwin A. Rose, 1926 – 2015
Chemistry, 2004
With Aaron Ciechanover and Avram Hershko (Technion-Israel Institute of Technology, Haifa, Israel). Awarded for the discovery of ubiquitin-mediated protein degradation.
Rose joined Penn’s faculty during the 1970s. Rose was awarded a Guggenheim Fellowship in 1971 while he was Professor of Physical Biochemistry at Penn and a senior member of the Institute for Cancer Research in Philadelphia.
Nobel Foundation information on this award.
Raymond Davis, Jr., 1914 – 2006
Physics, 2002
With Masatoshi Koshiba (University of Tokyo, Japan) and Riccardo Giannoni (Associated Universities Inc.). Awarded in recognition of their groundbreaking research into the emission of neutrinos produced by nuclear fusion reactions in the center of the sun. The observation of these neutrinos demonstrated conclusively that the sun is powered by the fusion of hydrogen nuclei into helium nuclei.
Davis joined Penn’s faculty in 1985 after 37 years at Brookhaven Lab. Davis has also received the 2001 National Medal of Science from President George W. Bush.
Nobel Foundation information on this award.
Alan G. MacDiarmid, 1927 – 2007
Alan J. Heeger, 1936 –
Chemistry, 2000
With Hideki Shirakawa (University of Tsukuba, Japan); Awarded “for the discovery and development of conductive polymers.”
MacDiarmid joined the University of Pennsylvania faculty in 1955 and was named Blanchard Professor of Chemistry in 1988. Heeger was a member of Penn’s Physics faculty from 1962 to 1982 and was Director of the Laboratory for Research on the Structure of Matter from 1974 to 1980.
Nobel Foundation information on this award.
Ahmed Zewail, 1946 –
Chemistry, 1999
Awarded “for or his studies of the transition states of chemical reactions using femtosecond spectroscopy.”
Penn Graduate: Ph.D. 1974; Honorary Sc.D. 1997
Nobel Foundation information on this award
Almanac Article
Stanley B. Prusiner, 1942 –
Medicine, 1997
Awarded “for his discovery of Prions – a new biological principle of infection.” This new class of pathogen is now accepted as the infectious agent in “mad cow disease” and in human neurodegenerative diseases such as Creutzfeldt-Jakob disease.
Penn Graduate: A.B. 1964; M.D. 1968
Nobel Foundation information on this award
Almanac Article
Michael Stuart Brown, 1940 –
Medicine, 1985
and Joseph L. Goldstein; Awarded “for their discoveries concerning the regulation of cholesterol metabolism”
Penn Graduate: A.B. 1962; M.D. 1966; Honorary: Sc.D. 1986
Nobel Foundation information on this award
Lawrence Robert Klein, 1920 – 2013
Economics, 1980
Awarded “for the creation of econometric models and the application to the analysis of economic fluctuations and economic policies.” These models have been designed to forecast economic trends and shape policies to deal with them.
Professor of Economics, 1958 –
Nobel Foundation information on this award
Baruch Samuel Blumberg, 1925 – 2011
Medicine, 1976
with D. Carleton Gajdusek; Awarded “for their discoveries concerning new mechanisms for the origin and dissemination of infectious diseases.”
Professor of Medicine, 1964 – 1989; Honorary Degree: Sc.D. 1990
Nobel Foundation information on this award
John Robert Schrieffer, 1931 – 2019
Physics, 1972 (first faculty member to win)
with John Bardeen and Leon N. Cooper; Awarded “for their jointly developed theory of superconductivity, usually called the BCS-theory,” where electrical resistance in certain metals vanishes above absolute zero temperature.
Professor of Physics, 1962–1980; Honorary: Sc.D. 1973
Nobel Foundation information on this award
Gerald Maurice Edelman, 1929 – 2014
Medicine, 1972
with Rodney R. Porter (U.K.); Awarded “for their discoveries concerning the chemical structure of antibodies”
Penn Graduate: M.D. 1954; Honorary: Sc.D. 1973
Nobel Foundation information on this award
Christian Boehmer Anfinsen, 1916 – 1995
Chemistry, 1972
with Stanford Moore and William Howard Stein; Anfinsen’s award was “for his work on ribonuclease, especially concerning the connection between the amino acid sequence and the biologically active conformation”.
Penn Graduate: M.S. 1939; Honorary: Sc.D. 1973
Nobel Foundation information on this award
Simon Smith Kuznets, 1901 – 1985
Economics, 1971
Awarded “for his empirically founded interpretation of economic growth which has led to new and deepened insight into the economic and social structure and process of development.” This interpretation developed the concept of using a country’s gross national product to determine its economic growth.
Assistant Professor of Economic Statistics, 1930–1934; Associate Professor, 1934–1935; Professor, 1936–1954; Honorary Degrees: Sc.D. 1956, LL.D. 1976
Nobel Foundation information on this award
Haldan Keffer Hartline, 1903 – 1983
Medicine, 1967
with George Wald and Ragnar Granit; Awarded “for their discoveries concerning the primary physiological and chemical visual processes in the eye.”
Research Fellow in Biophysics, 1931–1936; Assistant Professor, 1936–1942; Associate Professor, 1943–1948; Professor, 1948–1949; Honorary Degree: Sc.D. 1971
Nobel Foundation information on this award
Ragnar Granit, 1900 – 1991
Medicine, 1967
with George Wald and Haldan K. Hartline; Awarded for work on the human eye.
Research Fellow, 1929–1931; Honorary Degree: Sc.D. 1971
Nobel Foundation information on this award
Robert Hofstadter, 1915 – 1990
Physics, 1961
with Rudolpf Mössbauer (Germany). Hofstadter’s award was “for his pioneering studies of electron scattering in atomic nuclei and for his thereby achieved discoveries concerning the structure of the nucleons.” Hofstadter was thus able to determine the shape and size of the atomic nucleus.
Research Fellow, 1939–1940; Physics Instructor, 1940–1941
Nobel Foundation information on this award
Vincent du Vigneaud, 1901 – 1978
Chemistry, 1955
Awarded “for his work on biochemically important sulphur compounds, especially for the first synthesis of a polypeptide hormone.”
Assistant in Biochemistry, Graduate School of Medicine, 1924–1925
Nobel Foundation information on this award
Otto F. Meyerhof, 1884 – 1951
Medicine, 1922 (awarded in 1923)
with Archibald V. Hill (England). Meyerhoff’s award was “for his discovery of the fixed relationship between the consumption of oxygen and the metabolism of lactic acid in the muscle.”
Research Professor in Physiological Chemistry, 1940–1951
Nobel Foundation information on this award
Otto F. Meyerhof Papers | ||||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 15 | https://news.temple.edu/news/2024-03-20/nobel-prize-winner-katalin-karik-lectures-campus | en | Nobel Prize-winner Katalin Karikó lectures on campus | [
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] | null | [] | 2024-03-20T00:00:00 | Katalin Karikó, recipient of the 2023 Nobel Prize in Medicine, served as a postdoctoral fellow in Temple University’s Department of Biochemistry. | https://news.temple.edu/sites/news/themes/tnr_fluid/favicon.ico | Temple Now | news.temple.edu | https://news.temple.edu/news/2024-03-20/nobel-prize-winner-katalin-karik-lectures-campus | Katalin Karikó is the 13th woman in history to win a Nobel Prize in Physiology or Medicine. The scientist, who did her postdoctoral work in Temple’s Department of Biochemistry, recently returned to campus to talk about the experience during the John von Neumann Series of Pure and Applied Sciences at Temple’s Charles Library on March 14.
Karikó, jointly with her research partner Drew Weissman, won the 2023 Nobel Laureate in Medicine for having developed effective mRNA vaccines that laid the groundwork for the COVID-19 vaccine. Their work together, published in seminal studies in 2005, 2008 and 2010, led to a paradigm change in our understanding of how dendritic cells respond to mRNA vaccines. The finding would later be used for the rapid development of the COVID-19 vaccine in 2020.
Both Karikó, and Weissman were guests of honor at the conference. During the conference, Kariko discussed the experience of receiving the Nobel Prize in Stockholm, showing personal photographs and sharing anecdotes of the various events and receptions held for laureates when they receive the prize. With humor, she described the experience of having a four-hour dinner in same room as the royal family of Sweden and a faux pas she made during the Nobel Prize award ceremony in the Stockholm Concert Hall.
She answered questions from the audience, describing the feeling of disbelief when making a breakthrough and outlining the major setbacks and obstacles she has overcome in her career.
She expressed gratitude to be back on Temple’s campus, where she spent three years doing a clinical trial using double-stranded RNA to treat patients with HIV, hematologic diseases and chronic fatigue syndrome. The work was considered groundbreaking for its time and was a precursor to her later work that would garner the world’s highest prize in science.
After leaving Temple, Karikó continued to do postdoctoral work at the University of Health Science, Bethesda. Following her postdoctoral research, she was appointed assistant professor at the University of Pennsylvania, where she remained until 2013, and then vice president at BioNTech RNA Pharmaceuticals. Since 2021, she has served as a professor at the Perelman School of Medicine at the University of Pennsylvania.
The John von Neumann Series of Pure and Applied Sciences invites people to explore the future challenges of scientific progress. The daylong conference, sponsored by the College of Science and Technology and the Office of the Vice President for Research, hosted more than 100 people from the Temple community and beyond to listen to lectures on scientific development by faculty from Temple and other universities and organizations. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 17 | https://www.physoc.org/about-us/excellence-in-physiology/nobel-prize-laureate-members-of-the-physiological-society/ | en | Nobel Prize Laureate Members | [
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] | null | [] | 2022-01-26T13:23:18+00:00 | What does The Physiological Society do? Find out how our aims and strategy help physiology flourish, and how our charitable activities benefit the public. | en | The Physiological Society | https://www.physoc.org/about-us/excellence-in-physiology/nobel-prize-laureate-members-of-the-physiological-society/ | Ivan Pavlov (1905)
Russian Ivan Pavlov (1849-1936) was awarded The Nobel Prize in Physiology or Medicine in 1904 in recognition of his work on the physiology of digestion, through which knowledge on vital aspects of the subject has been transformed and enlarged. He became the very first Nobel laureate non-Member to be elected to honorary membership in 1909.
Ramón y Cajal (1906)
Santiago Ramón y Cajal (1852-1934) was awarded The Nobel Prize in Physiology or Medicine jointly in 1906 alongside Camillo Golgi in recognition of their work on the structure of the nervous system. He was made an Honorary Member of The Society in 1931.
Paul Ehrlick (1908)
German Paul Ehrlich (1854-1915) was jointly awarded The Nobel Prize in Physiology or Medicine in 1908 alongside Ilya Ilyich Mechnikov in recognition of their work on immunity. He was elected as an Honorary Member to The Society in 1903, prior to receiving the award.
Charles Richet (1913)
Frenchman Charles Richet (1850-1935) established that by decreasing the sodium chloride in food, potassium bromide is rendered so effective for the treatment of epilepsy that the therapeutic dose falls from 10g to 2g. In 1913, he was awarded The Nobel Prize in Physiology or Medicine for his research on anaphylaxis. He was awarded Honorary membership to The Society in 1918.
August Krogh (1920)
August Krogh (1874-1949) from Denmark was awarded The Nobel Prize in Physiology or Medicine in 1920 “for his discovery of the capillary motor regulating mechanism.” During the 1939-40 Winter War between the Soviet Union and Finland, when the Danes began collecting money in support of Finland, August Krogh was urged to donate his Nobel medal, which was made of solid gold, for this purpose. He did so, but first he had his daughter Bodil Schmidt-Nielsen make a copy of the medal in silver, which was then gold-plated. Krogh became a Member in 1913 an Honorary Member in 1938.
Archibald Hill (1922)
The Society’s first British Laureate, Archibald Hill (1886-1977) was awarded a half share of The Nobel Prize in Physiology or Medicine in 1922 for his discovery relating to the production of heat in the muscle. He became a Member in 1912 and an Honorary Member in 1960.
Otto Meyerhof (1922)
German physician and biochemist Otto Meyerho (1884-1951) was awarded a half share of The Nobel Prize in Physiology or Medicine in 1922 for his discovery of the fixed relationship between the consumption of oxygen and the metabolism of lactic acid in the muscle. He became a Member of The Society in 1930.
John Macleod (1923)
Scottish physiologist John Macleod (1876-1935) shared the 1923 Nobel Prize in Physiology or Medicine with Frederick Banting for his help with the discovery of insulin. He became a Member in 1912.
Frederick Banting (1923)
Canadian Frederick Banting (1923) was jointly awarded The Nobel Prize in Physiology or Medicine in 1923 alongside John James Rickard Macleod for the discovery of insulin. He was elected a Member of The Society in 1924.
Willem Einthoven (1924)
Dutchman Willem Einthoven (1860-1927) was awarded The Nobel Prize in Physiology or Medicine in 1924 for his discovery of the mechanism of the electrocardiogram. He was made an Honorary Member of The Society the same year.
Federick Gowland Hopkins (1929) President of the Royal Society 1930-35
Federick Gowland Hopkins (1861-1947) was awarded a half share of The Nobel Prize in Physiology or Medicine in 1929 for his discovery of growth-stimulating vitamins. He became a Member in 1892.
Arthur Harden (1929)
Arthur Harden (1865-1940) was awarded a half share of the Nobel Prize in Chemistry in 1929 alongside Hans Karl August Simon von Euler-Chelpin for their investigations on the fermentation of sugar and fermentative enzymes. He became a Member in 1904.
Charles Sherrington (1932) President of the Royal Society 1920-25
Charles Sherrington (1857-1952) received a half share of the Nobel Prize in Physiology or Medicine 1932 alongside Edgar Douglas Adrian for their discoveries regarding the functions of neurons. Sherrington became a Member in 1885 and an Honorary Member in 1935.
Edgar Adrian (1932) President of the Royal Society 1950-55 (The Lord Adrian)
Edgar Adrian (1889-1977) received a half share of The Nobel Prize in Physiology or Medicine 1932 alongside Charles Sherrington for their discoveries regarding the functions of neurons. Adrian became a Member in 1917 and an Honorary Member in 1960.
Henry Dale (1936) President of the Royal Society 1940-1945
Sir Henry Hallett Dale (1875-1968) received a half share of The Nobel Prize in Physiology or Medicine in 1936 alongside Otto Loewi for their discoveries relating to chemical transmission of nerve impulses. Dale became a Member in 1900 and an Honorary Member in 1951.
Otto Loewi (1936)
German Otto Loewi (1873-1961) was awarded The Nobel Prize in Physiology or Medicine in 1936 alongside Sir Henry Dale for their discoveries relating to chemical transmission of nerve impulses. He was elected as an Honorary Member of The Society in 1934, prior to receiving the award.
Albert Szent-Gyorgyi (1937)
Hungarian Albert von Szent-Györgyi Nagyrápolt (1893-1986) was awarded The Nobel Prize in Physiology or Medicine in 1937 for his discoveries in connection with the biological combustion processes, with special reference to vitamin C and the catalysis of fumaric acid. He became a Member in 1929.
Corneille Heymans (1938)
Belgian Corneille Heymans (1892-1968) received The Nobel Prize in Physiology or Medicine in 1938 for the discovery of the role played by the sinus and aortic mechanisms in the regulation of respiration. He became a Member in 1931 and an Honorary Member in 1967.
Herbert Gasser (1944)
American physiologist Herbert Gasser (1888-1963) was jointly awarded The Nobel Prize in Physiology or Medicine in 1944 alongside Joseph Erlanger for their discoveries relating to the highly differentiated functions of single nerve fibres. He became a Member in 1924 and an Honorary Member in 1949.
Howard Florey (1945) President of the Royal Society 1960-65
Australian Howard Florey (1898-1968) shared The Nobel Prize in Physiology or Medicine in 1945 with Sir Ernst Chain and Sir Alexander Fleming for his role in the development of penicillin. Florey carried out the first ever clinical trials of penicillin in 1941 at the Radcliffe Infirmary in Oxford on the first patient, a police constable from Oxford. Florey’s discoveries are estimated to have saved over 200 million lives and he is esteemed as one of Australia’s greatest figures. Florey became a Member in 1925 and an Honorary Member in 1965.
Bernardo Houssay (1947)
Argentine physiologist Bernardo Houssay (1887-1972) was awarded half The Nobel Prize in Physiology or Medicine in 1947 for his discovery of the part played by the hormone of the anterior pituitary lobe in the metabolism of sugar. He was the first Argentine Nobel laureate in the sciences. He was elected as an Honorary Member of The Society in 1935, prior to his receiving the award.
John Boyd Orr (1949)
Scottish physician and biologist John Boyd Orr (1880-1971) was awarded The Nobel Peace Prize in 1949 for his scientific research into nutrition and his work as the first Director-General of the United Nations Food and Agriculture Organization. He emerged in the inter-war years as one of Britain’s leading experts on nutrition, maintaining that many Britons were malnourished because their incomes were too low. Orr became a Member in 1918.
Walter Hess (1949)
Swiss physiologist Walter Hess (1881-1973) won The Nobel Prize in Physiology or Medicine in 1949 for mapping the areas of the brain involved in the control of internal organs. He was elected an Honorary Member of The Society in 1936, prior to the award.
Hans Krebs (1953)
German-born, British-naturalised Hans Krebs (1900-1981) was awarded a half share of The Nobel Prize in Physiology or Medicine in 1953 for his discovery of the citric acid cycle. He became a Member in 1948.
Peter Medawar (1960)
Peter Medawar (1915-1987) was awarded the 1960 Nobel Prize in Physiology or Medicine jointly with Sir Macfarlane Burnet for their discovery of acquired immunological tolerance. Medawar’s interest in immunological tolerance grew directly out of his research in skin grafts begun during the Second World War. When a plane crashed near his Oxford home during the Battle of Britain, the doctors treating the severely burned pilot sought Medawar’s advice, hoping that his studies in cell development might provide some critical insight. He became a Member in 1941 and an Honorary Member in 1975.
Alan Hodgkin (1963) President of the Royal Society 1970-75
Alan Hodgkin (1914-1998) was awarded The Nobel Prize in Physiology or Medicine in 1963 jointly with Sir John Carew Eccles and Andrew Fielding Huxley for their discoveries concerning the ionic mechanisms involved in excitation and inhibition in the peripheral and central portions of the nerve cell membrane. He became a Member in 1938 and an Honorary Member in 1979.
Andrew Huxley (1963) President of the Royal Society 1980-85
Andrew Huxley (1917-2012) was awarded The Nobel Prize in Physiology or Medicine in 1963 jointly with Sir John Carew Eccles and Alan Lloyd Hodgkin for their discoveries concerning the ionic mechanisms involved in excitation and inhibition in the peripheral and central portions of the nerve cell membrane. He became a Member in 1942 and an Honorary Member in 1979.
John Eccles (1963)
Australian research physiologist John Eccles (1903-1997) shared The 1963 Nobel Prize in physiology or medicine with Alan Hodgkin and Andrew Huxley for their discoveries concerning the ionic mechanisms involved in excitation and inhibition in the peripheral and central portions of the nerve cell membrane. Eccles’ work profoundly influenced the medical treatment of nervous diseases and the research on kidney, heart, and brain function. His research on the fundamental transmission of nerve impulses is basic to the knowledge of how neurons interact with one another, especially in explaining integrated movements and their pathologic alterations, and to the eventual understanding of higher functions of the brain. Eccles became a Member in 1929 and an Honorary Member in 1982.
Peyton Rous (1966)
American Peyton Rous (1879-1970) was jointly awarded The Nobel Prize in Physiology or Medicine in 1966 for his discovery of tumour-inducing viruses. He was elected an Honorary Member of The Society in 1936, prior to receiving the award.
Ragnar Granit (1967)
Swede Ragnar Granit (1900-1991) was awarded the 1967 Nobel Prize in Physiology or Medicine for discoveries about chemical and physiological visual processes in the eye. He became a Member in 1932 and an Honorary Member in 1968.
Bernard Katz (1970)
German-born, British-naturalised Bernard Katz (1911-2003) was jointly awarded The Nobel Prize in Physiology or Medicine in 1970 alongside Ulf von Euler and Julius Axelrod for their discoveries concerning the humoral transmitters in the nerve terminals and the mechanism for their storage, release and inactivation. He became a Member in 1940 and an Honorary Member in 1979.
Ulf Von Euler (1970)
Swede Ulf Von Euler (1905-1983) was awarded The Nobel Prize in Physiology or Medicine in 1970 alongside Sir Bernard Katz and Julius Axelrod for their discoveries concerning the humoral transmitters in the nerve terminals and the mechanism for their storage, release and inactivation. He became a Member in 1937 and an Honorary Member in 1972.
David Hubel (1981)
Canadian American David Hubel (1926-2013) was jointly awarded half The Nobel Prize in Physiology or Medicine in 1981 alongside Torsten Wiesel for their discoveries concerning information processing in the visual system. He was made an Honorary Member in 1983.
Torsten Wiesel (1981)
Swedish neurophysiologist Torsten Wiesel (b.1924) was jointly awarded half The Nobel Prize in Physiology or Medicine in 1981 alongside David Hubel. He was made an Honorary Member in 1983.
John Vane (1982)
John Vane (1927-2004) was awarded The Nobel Prize in Physiology or Medicine for discovering how aspirin alongside with Sune Bergström and Bengt Samuelsson of Sweden. Vane’s research underpinned the finding that a daily low dose of aspirin prevents heart attacks and strokes, saving millions of lives each year, and the development of angiotensin converting enzyme (ACE) inhibitors for the treatment of hypertension. He made huge advances to our knowledge of inflammation. Vane became a Member in 1953 and an Honorary Member in 1988.
James Black (1988)
Scottish pharmacologist Sir James Black (1924-2010) was awarded The Nobel Prize for Physiology or Medicine in 1988 (alongside George Hitchings and Gertrude Elion) for his development of two important drugs, propranolol (a beta blocker used for the treatment of heart disease) and cimetidine (an H2 receptor antagonist, a drug used to treat stomach ulcers). He became a Member in 1962 and an Honorary Member in 1989.
Erwin Neher (1991)
German Erwin Neher (b.1944) was awarded The Nobel Prize in Physiology or Medicine in 1991 alongside Bert Sakmann for their discoveries concerning the function of single ion channels in cells. Neher became an Affiliate Member in 1981 and an Honorary Member in 1997.
Bert Sakmann (1991)
German Bert Sakmann (b.1942) was awarded The Nobel Prize in Physiology or Medicine in 1991 alongside Erwin Neher for their discoveries concerning the function of single ion channels in cells. He became an Affiliate Member in 1990 and an Honorary Member in 1997.
Eric Kandel (2000)
Austrian Eric R. Kandel (b.1929) was jointly awarded The Nobel Prize in Physiology or Medicine in 2000 alongside Arvid Carlsson and Paul Greengard for their discoveries concerning signal transduction in the nervous system. He was elected an Honorary Member to The Society in 2008.
Arvid Carlsson (2000)
Swede Arvid Carlsson (1923-2018) was jointly awarded The Nobel Prize in Physiology or Medicine in 2000 alongside Eric Kandel and Paul Greengard for their discoveries concerning signal transduction in the nervous system. He was elected an Honorary Member to The Society in 2009.
Paul Nurse (2001) President of the Royal Society (2010-15)
English geneticist Sir Paul Nurse (b.1949) was jointly awarded The Nobel Prize in Physiology or Medicine in 2001 along with Leland Hartwell and Tim Hunt for their research relating to the discovery of cell cycle regulatory molecules. He was elected as an Honorary Member of The Society in 2003.
Tim Hunt (2001)
British biochemist and molecular physiologist Sir Richard Timothy Hunt (b.1943) were jointly awarded The Nobel Prize in Physiology or Medicine in 2001 alongside Paul Nurse and Leland Hartwell for their discoveries of protein molecules that control the division of cells. He was elected as an Honorary Member of The Society in 2009.
John Sulston (2002)
British Biologist John E. Sulston (1942-2018) was jointly awarded The Nobel Prize in Physiology or Medicine in 2002 alongside Sydney Brenner and Robert Horvitz for their discoveries concerning genetic regulation of organ development and programmed cell death. Their research illustrated the entire sequence in which the daughters of a single cell divide and sometimes disappear as an embryo grows into an adult in the tiny roundworm Caenorhabditis elegans. He was better known for leading the British team working on the Human Genome Project (HGP) that sequenced a third of the human genome, and for the fierce integrity with which he successfully argued that all genomic data should be openly accessible to the scientific community without commercial involvement. Sulston was elected as an Honorary Member in 2003.
Sydney Brenner (2002)
South African Sydney Brenner (1927-2019) was jointly awarded The Nobel Prize in Physiology or Medicine in 2002 alongside John Sulston and Robert Horvitz for their discoveries concerning genetic regulation of organ development and programmed cell death. He was elected as an Honorary Member in 2003.
Peter Mansfield (2003)
English physicist Peter Mansfield (1933-2017) was jointly awarded The Nobel Prize in Physiology or Medicine in 2003 alongside Paul C. Lauterbur for their discoveries concerning magnetic resonance imaging. He was elected as an Honorary Member to The Society in 2004.
Paul Christian Lauterbur (2003)
American chemist Paul Christian Lauterbur (1929-2007) was jointly awarded The Nobel Prize in Physiology or Medicine in 2003 alongside Sir Peter Mansfield for their discoveries concerning magnetic resonance imaging. He was elected as an Honorary Member of The Society in 2004.
Richard Axel (2004)
American molecular biologist and university professor Richard Axel (b.1946) was jointly awarded The Nobel Prize in Physiology or Medicine in 2004 alongside Linda B. Buck for their discoveries of odorant receptors and the organization of the olfactory system. He was elected as an Honorary Member of The Society in 2012.
Linda Buck (2004)
American biologist Linda Buck (b.1947) was jointly awarded The Nobel Prize in Physiology or Medicine 2004 alongside Richard Axel for their discoveries of odorant receptors and the organization of the olfactory system. She was elected as an Honorary Member of The Society in 2012.
Martin Evans (2007)
British biologist Martin Evans (b.1941) was jointly awarded The Nobel Prize in Physiology or Medicine in 2007 alongside Mario R. Capecchi and Oliver Smithies for their discoveries of principles for introducing specific gene modifications in mice by the use of embryonic stem cells. He was elected as an Honorary Member of The Society in 2013.
Roger Tsien (2008)
American Roger Tsien (1952-2016) was awarded The Nobel Prize in Chemistry in 2008 for the discovery and development of the green fluorescent protein, GFP. Tsien demonstrated how GFP produces its shimmering light and succeeded in varying the colour, creating a rainbow of fluorescent proteins that could light up the dance of molecules within cells. This enabled different proteins and multiple, simultaneous biological processes to be tracked. Tsien became an Affiliate Member in 1974 and an Honorary Member in 2011.
John O’Keefe (2014)
American-British neuroscientist and psychologist John O’Keefe (b.1939) was jointly awarded The Nobel Prize in Physiology or Medicine in 2014 alongside May-Britt Moser and Edvard I. Moser for their discoveries of cells that constitute a positioning system in the brain. He was elected as an Honorary Member of The Society in 2015.
May-Britt Moser (2014)
Norwegian psychologist and neuroscientist May-Britt Moser (b. 1963) was jointly awarded The Nobel Prize in Physiology or Medicine 2014 alongside John O’Keefe and Edvard I. Moser for their discoveries of cells that constitute a positioning system in the brain. She was elected as an Honorary Member to The Society in 2015.
James Rothman (2013)
American biochemist James E. Rothman (b.1950) was jointly awarded The Nobel Prize in Physiology or Medicine in 2013 alongside Randy W. Schekman and Thomas C. Südhof for their discoveries of machinery regulating vesicle traffic, a major transport system in our cells. He was elected as an Honorary Member of The Society in 2014.
Randy Schekman (2013)
American cell biologist Randy Schekman (b.1948) was jointly awarded The Nobel Prize in Physiology or Medicine 2013 alongside James E. Rothman and Thomas C. Südhof for their discoveries of machinery regulating vesicle traffic, a major transport system in our cells. He was elected as an Honorary Member to The Society in 2014.
Edvard Ingjald Moser (2014)
Norwegian professor of psychology and neuroscience Edvard Ingjald Moser (b.1962) was jointly awarded The Nobel Prize in Physiology or Medicine 2014 alongside John O’Keefe and May-Britt Moser. He was elected as an Honorary Member to The Society in 2015.
Michael Warren Young (2017)
Michael Warren Young (b.1949) was awarded The Nobel Prize in Physiology or Medicine 2017 alongside Jeffrey C. Hall and Michael Rosbash for their discoveries of molecular mechanisms controlling the circadian rhythm. He was elected as an Honorary Member of The Society in 2018.
Tasuku Honjo (2018)
Tasuku Honjo (b.1942) was awarded The Nobel Prize in Physiology or Medicine in 2018 alongside James P. Allison for their discovery of cancer therapy by inhibition of negative immune regulation. He was elected as an Honorary Member to The Society in 2019.
Peter Ratcliffe (2019)
British physician-scientist Sir Peter J. Ratcliffe was awarded The Nobel Prize in Physiology or Medicine 2019 alongside William G. Kaelin Jr. and Gregg L. Semenza for their discoveries of how cells sense and adapt to oxygen availability. He was elected as an Honorary Member of The Society in 2020.
Harvey J. Alter, Michael Houghton and Charles M. Rice (2020)
Harvey J. Alter, Michael Houghton and Charles M. Rice were awarded the Nobel Prize in Physiology or Medicine for their contribution to the fight against blood-borne hepatitis, a major global health problem that causes cirrhosis and liver cancer in people around the world.
Professor David Julius and Professor Ardem Patapoutian (2021)
David Julius and Ardem Patapoutian won the 2021 Nobel Prize in Physiology or Medicine for their discoveries of receptors for temperature and touch.
Svante Pääbo (2022)
Nobel Prize in Physiology or Medicine “for his discoveries concerning the genomes of extinct hominins and human evolution.”
Katalin Karikó and Drew Weissman (2023)
Katalin Karikó and Drew Weissman were awarded the Nobel Prize in Physiology or Medicine for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19. | |||||
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] | null | [] | null | The Nobel Prize in Physiology or Medicine 2023 was awarded jointly to Katalin Karikó and Drew Weissman "for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19" | en | NobelPrize.org | https://www.nobelprize.org/prizes/medicine/2023/press-release/ | Press release
English
English (pdf)
Swedish
Swedish (pdf)
Press release
2023-10-02
The Nobel Assembly at Karolinska Institutet
has today decided to award
the 2023 Nobel Prize in Physiology or Medicine
jointly to
Katalin Karikó and Drew Weissman
for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19
The discoveries by the two Nobel Laureates were critical for developing effective mRNA vaccines against COVID-19 during the pandemic that began in early 2020. Through their groundbreaking findings, which have fundamentally changed our understanding of how mRNA interacts with our immune system, the laureates contributed to the unprecedented rate of vaccine development during one of the greatest threats to human health in modern times.
Vaccines before the pandemic
Vaccination stimulates the formation of an immune response to a particular pathogen. This gives the body a head start in the fight against disease in the event of a later exposure. Vaccines based on killed or weakened viruses have long been available, exemplified by the vaccines against polio, measles, and yellow fever. In 1951, Max Theiler was awarded the Nobel Prize in Physiology or Medicine for developing the yellow fever vaccine.
Thanks to the progress in molecular biology in recent decades, vaccines based on individual viral components, rather than whole viruses, have been developed. Parts of the viral genetic code, usually encoding proteins found on the virus surface, are used to make proteins that stimulate the formation of virus-blocking antibodies. Examples are the vaccines against the hepatitis B virus and human papillomavirus. Alternatively, parts of the viral genetic code can be moved to a harmless carrier virus, a “vector.” This method is used in vaccines against the Ebola virus. When vector vaccines are injected, the selected viral protein is produced in our cells, stimulating an immune response against the targeted virus.
Producing whole virus-, protein- and vector-based vaccines requires large-scale cell culture. This resource-intensive process limits the possibilities for rapid vaccine production in response to outbreaks and pandemics. Therefore, researchers have long attempted to develop vaccine technologies independent of cell culture, but this proved challenging.
mRNA vaccines: A promising idea
In our cells, genetic information encoded in DNA is transferred to messenger RNA (mRNA), which is used as a template for protein production. During the 1980s, efficient methods for producing mRNA without cell culture were introduced, called in vitro transcription. This decisive step accelerated the development of molecular biology applications in several fields. Ideas of using mRNA technologies for vaccine and therapeutic purposes also took off, but roadblocks lay ahead. In vitro transcribed mRNA was considered unstable and challenging to deliver, requiring the development of sophisticated carrier lipid systems to encapsulate the mRNA. Moreover, in vitro-produced mRNA gave rise to inflammatory reactions. Enthusiasm for developing the mRNA technology for clinical purposes was, therefore, initially limited.
These obstacles did not discourage the Hungarian biochemist Katalin Karikó, who was devoted to developing methods to use mRNA for therapy. During the early 1990s, when she was an assistant professor at the University of Pennsylvania, she remained true to her vision of realizing mRNA as a therapeutic despite encountering difficulties in convincing research funders of the significance of her project. A new colleague of Karikó at her university was the immunologist Drew Weissman. He was interested in dendritic cells, which have important functions in immune surveillance and the activation of vaccine-induced immune responses. Spurred by new ideas, a fruitful collaboration between the two soon began, focusing on how different RNA types interact with the immune system.
The breakthrough
Karikó and Weissman noticed that dendritic cells recognize in vitro transcribed mRNA as a foreign substance, which leads to their activation and the release of inflammatory signaling molecules. They wondered why the in vitro transcribed mRNA was recognized as foreign while mRNA from mammalian cells did not give rise to the same reaction. Karikó and Weissman realized that some critical properties must distinguish the different types of mRNA.
RNA contains four bases, abbreviated A, U, G, and C, corresponding to A, T, G, and C in DNA, the letters of the genetic code. Karikó and Weissman knew that bases in RNA from mammalian cells are frequently chemically modified, while in vitro transcribed mRNA is not. They wondered if the absence of altered bases in the in vitro transcribed RNA could explain the unwanted inflammatory reaction. To investigate this, they produced different variants of mRNA, each with unique chemical alterations in their bases, which they delivered to dendritic cells. The results were striking: The inflammatory response was almost abolished when base modifications were included in the mRNA. This was a paradigm change in our understanding of how cells recognize and respond to different forms of mRNA. Karikó and Weissman immediately understood that their discovery had profound significance for using mRNA as therapy. These seminal results were published in 2005, fifteen years before the COVID-19 pandemic.
In further studies published in 2008 and 2010, Karikó and Weissman showed that the delivery of mRNA generated with base modifications markedly increased protein production compared to unmodified mRNA. The effect was due to the reduced activation of an enzyme that regulates protein production. Through their discoveries that base modifications both reduced inflammatory responses and increased protein production, Karikó and Weissman had eliminated critical obstacles on the way to clinical applications of mRNA.
mRNA vaccines realized their potential
Interest in mRNA technology began to pick up, and in 2010, several companies were working on developing the method. Vaccines against Zika virus and MERS-CoV were pursued; the latter is closely related to SARS-CoV-2. After the outbreak of the COVID-19 pandemic, two base-modified mRNA vaccines encoding the SARS-CoV-2 surface protein were developed at record speed. Protective effects of around 95% were reported, and both vaccines were approved as early as December 2020.
The impressive flexibility and speed with which mRNA vaccines can be developed pave the way for using the new platform also for vaccines against other infectious diseases. In the future, the technology may also be used to deliver therapeutic proteins and treat some cancer types.
Several other vaccines against SARS-CoV-2, based on different methodologies, were also rapidly introduced, and together, more than 13 billion COVID-19 vaccine doses have been given globally. The vaccines have saved millions of lives and prevented severe disease in many more, allowing societies to open and return to normal conditions. Through their fundamental discoveries of the importance of base modifications in mRNA, this year’s Nobel laureates critically contributed to this transformative development during one of the biggest health crises of our time.
Key publications
Karikó, K., Buckstein, M., Ni, H. and Weissman, D. Suppression of RNA Recognition by Toll-like Receptors: The impact of nucleoside modification and the evolutionary origin of RNA. Immunity 23, 165–175 (2005).
Karikó, K., Muramatsu, H., Welsh, F.A., Ludwig, J., Kato, H., Akira, S. and Weissman, D. Incorporation of pseudouridine into mRNA yields superior nonimmunogenic vector with increased translational capacity and biological stability. Mol Ther 16, 1833–1840 (2008).
Anderson, B.R., Muramatsu, H., Nallagatla, S.R., Bevilacqua, P.C., Sansing, L.H., Weissman, D. and Karikó, K. Incorporation of pseudouridine into mRNA enhances translation by diminishing PKR activation. Nucleic Acids Res. 38, 5884–5892 (2010).
Read more about this year’s prize
Scientific background: Discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19
Katalin Karikó was born in 1955 in Szolnok, Hungary. She received her PhD from Szeged’s University in 1982 and performed postdoctoral research at the Hungarian Academy of Sciences in Szeged until 1985. She then conducted postdoctoral research at Temple University, Philadelphia, and the University of Health Science, Bethesda. In 1989, she was appointed Assistant Professor at the University of Pennsylvania, where she remained until 2013. After that, she became vice president and later senior vice president at BioNTech RNA Pharmaceuticals. Since 2021, she has been a Professor at Szeged University and an Adjunct Professor at Perelman School of Medicine at the University of Pennsylvania.
Drew Weissman was born in 1959 in Lexington, Massachusetts, USA. He received his MD, PhD degrees from Boston University in 1987. He did his clinical training at Beth Israel Deaconess Medical Center at Harvard Medical School and postdoctoral research at the National Institutes of Health. In 1997, Weissman established his research group at the Perelman School of Medicine at the University of Pennsylvania. He is the Roberts Family Professor in Vaccine Research and Director of the Penn Institute for RNA Innovations.
Illustrations: © The Nobel Committee for Physiology or Medicine. Illustrator: Mattias Karlén
The Nobel Assembly, consisting of 50 professors at Karolinska Institutet, awards the Nobel Prize in Physiology or Medicine. Its Nobel Committee evaluates the nominations. Since 1901 the Nobel Prize has been awarded to scientists who have made the most important discoveries for the benefit of humankind.
Nobel Prize® is the registered trademark of the Nobel Foundation | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 81 | https://telex.hu/english/2023/10/02/katalin-kariko-is-awarded-the-nobel-prize-in-physiology-and-medicine | en | Katalin Karikó is awarded the Nobel Prize in Physiology or Medicine | [
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"Bolcsó Dániel",
"István Dezsényi (translation)",
"bolcso-daniel",
"istvan-dezsenyi-translation"
] | 2023-10-02T00:00:00 | The discoveries made by Karikó and her research partner were critical for developing effective mRNA vaccines against COVID-19 during the pandemic. | hu | /apple-touch-icon.png | telex | https://telex.hu/english/2023/10/02/katalin-kariko-is-awarded-the-nobel-prize-in-physiology-and-medicine | Katalin Karikó and Drew Weissman have been awarded the Nobel Prize in Physiology or Medicine in Stockholm. According to the citation, the microbiologist born in Szolnok, Hungary, and her research partner played a key role in the development of new types of mRNA-based vaccines, in fighting the biggest pandemic in the past hundred years and in opening new paths for future medicine. This is the third time that a Hungarian citizen has been awarded the world's most prestigious prize: in 1937 Albert Szent-Györgyi received the Nobel Prize in Physiology or Medicine, and in 2002 Imre Kertész was awarded the Nobel Prize in Literature. They are now joined by Katalin Karikó, whose name has become known around the world in the past few years.
The Royal Swedish Academy's announcement of Karikó's prize can be watched here:
Nobel Committee Secretary Thomas Perlmann said he was able to speak to both researchers by phone before the announcement. Both Karikó and Weismann were overwhelmed with emotion and were very happy to receive the prize. During the conversation, Karikó recalled that she had also had some dramatic moments in her research career, one of which was when she relocated from the United States to Germany in 2013.
Rickard Sandberg, a member of the Nobel Prize's medical committee, said that more than 13 billion mRNA-based vaccines have been administered, saving the lives of millions of people or reducing the chances of serious diseases, which also kept societies functioning.
"This year's Nobel Prize is in recognition of their fundamental scientific discovery that has radically changed our understanding of the interaction between mRNA and the immune system," said Sandberg.
Many were already expecting Karikó's award
A few years ago, Karikó's name was unknown outside her narrow profession even in Hungary, but by 2021 she had become a global icon and has since been awarded a string of prestigious scientific prizes. Among them are a series of what are often referred to as the precursors to the Nobel Prize: the Horwitz Prize from Columbia University; the Albany Prize, the most prestigious US scientific award; the Breakthrough Prize, the prize with the largest prize money; and the Lasker Prize for clinical development.
Based on these, Katalin Karikó and her former research colleague Drew Weissman of the US were already mentioned among the contenders for two Nobel Prizes, in Physiology or Medicine as well as in Chemistry, in the year of the spread of mRNA-based coronavirus vaccines. However, there was some question as to whether the usually rather conservative Nobel committee would make an exception for them. Although Alfred Nobel's original idea was to recognise the greatest scientific achievements of the previous year, they actually tend to wait decades rather than award the greatest prize in science too quickly. It was not known whether an exception would be made, given the huge social impact made during the pandemic and the huge scientific prospects that opened up.
That didn't work out that year in the end, with the Prize in Physiology and Medicine going to David Julius and Ardem Patapoutian for their fundamental discoveries in skin sensation, and the Prize in Chemistry going to Benjamin List and David W.C. MacMillan for their work on asymmetric organocatalysis.
This year's top contenders for the Nobel Prize in Medicine were researchers in two fields. One was the study of sleep. Here the focus was on research into the relationship between narcolepsy and a neuropeptide called orexin.
Kevan Shokat was also shortlisted for his achievements in cancer research. The American biologist developed a method to block the KRAS gene, which is responsible for a third of cancers. Another type of cancer therapy, T-cell therapy, is another scientific work that could win a Nobel Prize, several researchers said in advance.
Not just because of the vaccine
The pandemic years were also an unprecedented challenge for the international scientific community, and the rapid development of vaccines against the coronavirus was an unprecedented success, even though it did not, of course, bring the epidemic to an end overnight. At stake – alongside such 'trivialities' as global health and the restoration of normal life – was the prestige of science in an age that is in many ways anti-science, and the world watched with bated breath as news of vaccines broke like probably no innovation before. Katalin Karikó's research laid the foundation for a new type of vaccine, which then brought the scientific breakthrough.
Although Karikó's award was clearly motivated by the COVID-19 vaccine, it was not solely for the vaccine that she was honoured, but for laying the foundations for the widespread pharmaceutical application of mRNA technology. Katalin Karikó herself, although she was awarded the Prize in Physiology or Medicine, considers herself primarily a chemist:
"Suddenly everyone is an epidemiologist now, but I'm not. I'm a biochemist who understands RNA."
– she said in an interview with Telex in May 2021.
Tamás Freund, President of the Hungarian Academy of Sciences, spoke to Telex ahead of the 2021 awards about what Katalin Karikó's Nobel Prize would mean for Hungary. As he said at the time, Karikó's "Nobel Prize, which many of us are hoping for, would put the international spotlight on the strength of Hungarian science and education, the creativity of the Hungarian scientific mind, and at the same time provide further convincing evidence to Hungarian policymakers of the importance of supporting basic research.
Katalin Karikó's Nobel Prize would also be a special joy because she would be the first female Nobel Prize winner from Hungary! Her success would draw attention to the outstanding achievements of Hungarian women researchers, who are among the international leaders, especially in fields related to Katalin Karikó's."
A long and hard road to the Nobel Prize
Karikó first heard about the medical use of mRNA in 1976, when she was a student at the University of Szeged. At the beginning of her studies, she was not particularly interested in microbiology, preferring plants, but under the guidance of Jenő Tomasz, an organic chemist, she soon found her future field of specialisation.
After graduation, she was employed in the Biological Research Centre in Szeged. She had to leave the research centre a few years later, at the age of 30, because of downsizing. She sought opportunities abroad and moved to America with her family in 1985. She first joined Temple University in Philadelphia, but after a few years there she fell out with her boss, who threatened to have her expelled from the United States. She transferred to another university in the city, the University of Pennsylvania, but they didn't really believe in her project.
Although the therapeutic application of messenger RNA, or simply mRNA, was considered one of the most promising areas of experimental medicine in the 1970s, its practical application seemed to many to be very distant or even hopeless, not worth the capital invested. It was only in 1961 that the mRNA molecule, which carries genetic information stored in DNA to the ribosomes that produce proteins, was discovered (it also earned a Nobel Prize at the time), and Katalin Karikó was one of those who hoped that it, or more precisely the use of artificial mRNA, would lead to a renewal of medicine. The idea was that by injecting the right RNA in nanoparticles into human cells, they could "teach" the immune system to recognise tumour cells or produce the right antibodies with a vaccine against viral infection.
By the 1990s, however, enthusiasm for mRNA in applied science had waned, mainly because it could not be stably delivered to the target organism. Karikó kept applying for grants, but her research wasn't bringing in much money for the university, and they began to see her efforts as a waste of time. She faced numerous unfairnesses, including being moved out of her lab and then being given a choice: either give up her research or take a pay cut. She chose the latter, continuing her decade-long quest, gradually becoming the only one in her environment who believed in it – for less than she would have gotten at a fast-food restaurant.
"I got about a dollar an hour, based on the time I spent in the lab and then worked at home, writing applications and articles"
– she recalled this period in an interview.
The way out was a chance meeting in the university photocopying room with Drew Weissman, now jointly Nobel laureate with Karikó, with whom they then worked on a solution that would not trigger an inflammatory immune response which made it impossible to deliver mRNA to the target organism. The solution was the replacement of one of the nucleosides that make up mRNA, which paved the way for practical applications. When the first mouse experiments were finally successful in 2005, hope awakened. "At that moment, we understood that this was a very important discovery that could be used in vaccines and therapies. We published a paper, filed a patent, and founded a company – and still nobody cared. Nobody invited us to talk about it, nothing happened," said the Hungarian researcher.
She and Weissman didn't give up, however, and within a few years, the revolutionary mRNA technology became exciting and less distant again in the field of medical research. In 2010, a company called Moderna was founded to apply modified mRNA to medicine, with the participation of several Harvard and MIT professors, and it was already building on Karikó and her colleague's research. The Hungarian researcher and Weissman also went their own way: they sold a licence based on their own development to BioNTech, a German company that was then counted as small. Today, the names of both companies are known practically all over the world. BioNTech created the first mRNA vaccine against the COVID-19, together with Pfizer, based on Karikó's decades of research, and this was followed shortly afterwards by Moderna's vaccine. (The latter has since sued the other two companies, accusing them of patent infringement.)
Many people would not have bet on that even a few years ago. In 2013, when Katalin Karikó tried to reapply for the Philadelphia professorship from which she had previously been removed, she was rejected and told she was not up to university standards. Then she announced that she was going to BioNTech and she was laughed at because the obscure company, run by Turkish immunologist Uğur Şahin from Germany, didn't even have a proper website.
"Recognition has been famously absent in my life, but it didn't bother me that much. I have done very well without my work being recognised as important. I was like Cassandra, I could see the future but I couldn't convince others of it. Even now, I don't feel like, ‘Oh well, I told you so’."
– said the Hungarian researcher in an interview with former classmate János Géczi last March.
The technology, based on the encoding of messenger RNA, has now reached a critical point, with many in a wide range of medical fields expecting much from it in the very near future. It took COVID-19 and the pandemic to show the potential for successful application on a global scale. The two new Nobel laureates, Katalin Karikó and Drew Weissman, were among the first to receive the vaccine together, based on their own development, and when tests on 8 November 2020 proved that the vaccine, which is a joint development with Pfizer, worked against the coronavirus, Karikó celebrated with a bag of chocolate peanuts.
The next mRNA vaccine will be against influenza, according to Katalin Karikó. It won't take long – she said in an interview with Telex in 2021 – for a universal vaccine to be developed against all coronaviruses, following the SARS-CoV-2 vaccine responsible for the current pandemic. But in addition to vaccine development, mRNA-based therapies are also expected to have a major impact on immunotherapy, cancer, cardiovascular and digestive diseases.
The Royal Swedish Academy of Sciences has now recognised Katalin Karikó and her fellow researcher, who were laughed at just a few years ago, for the latest revolution in medicine. Like the majority of Nobel Prize winners of Hungarian origin, the researcher from the small town of Kisújszállás spent half her life abroad – only at the lower rungs of the scientific hierarchy, and for a long time she was not only not rewarded, but her superiors sometimes tried to make her work impossible. As she said in an interview about moving, “If we had stayed, we would probably have been complaining, mediocre researchers. Perhaps we created more because we were in a constant struggle to survive, to succeed.”
Her message: Always focus on what you can change, don't worry about others
About half an hour after the Nobel Prize announcement, Karikó shared some of her thoughts with friends and journalists present in an online video chat.
The Nobel Prize-winning scientist was asked what message she would give to young researchers who are still at the beginning of their careers.
"The most important thing is to have physical and mental health, to learn to manage stress. The most important thing is that if they enjoy what they do, if they are happy doing it, they will get better and better," she said.
She then quoted another world-famous Hungarian scientist, János Selye, who laid the foundations for stress research. "We should always focus on what we can change, not on other people, because that's not the way forward."
When asked what her parents would say to her after she won the Nobel Prize, she became emotional and recalled her mother telling her repeatedly, "Maybe they will call your name, darling." Her mother was convinced that she would win a Nobel Prize one day, after all her hard work. Karikó used to explain to her that other researchers also work hard and that in itself is not enough for scientific recognition. | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 97 | https://www.history.com/news/who-were-the-first-women-to-win-nobel-prizes | en | Who Were the First Women to Win Nobel Prizes? | [
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"Nate Barksdale"
] | 2014-10-08T00:00:00+00:00 | Marie Curie was the first and most famous, but there were other early trailblazers. | en | HISTORY | https://www.history.com/news/who-were-the-first-women-to-win-nobel-prizes | When it comes to record-setting Nobel Prize recipients, there’s Marie Curie and there’s everyone else. The Polish-French scientist was the first woman to share a Nobel Prize (the 1903 physics award, with her husband Pierre and fellow French scientist Henri Becquerel, for their pioneering work on radioactivity) and was also the first woman to receive an unshared Nobel, the 1911 chemistry prize, for her discovery of the elements radium and polonium. That makes her the only person ever to win Nobel Prizes in two different sciences. As if that weren’t enough, four of her family members are also Nobel laureates. In addition to Pierre, her daughter and son-in-law shared the 1935 chemistry prize, while another son-in-law was the director of UNICEF when it won the 1965 peace prize.
The first woman to win the Nobel Peace Prize was Baroness Bertha Sophie Felicita von Suttner, née Countess Kinsky von Chinic und Tettau, who won in 1905. Von Sutter was the author of an influential anti-war novel and had a leading role in convincing dynamite magnate Alfred Nobel to include a peace prize in his bequest. The first female Nobel literature laureate was novelist Selma Lagerlöf, whose most popular book was about a boy who flies around Sweden on the back of a goose. The first woman to win the Nobel Prize for Physiology or Medicine was Gerty Theresa Cori, who shared the 1947 award for discovering how sugar-derived glycogen is used by the body as an energy source.
The last first woman to win the Nobel in her category was Elinor Ostrom, who shared the 2009 economics prize for her groundbreaking analysis of common property. The wait was so long for a woman economics laureate in part because that prize wasn’t established until 1969. In all, as of 2022, Nobel Prizes have been awarded to 60 women. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 96 | https://www.npr.org/2014/10/06/354124231/3-neuroscientists-to-share-nobel-prize-in-physiology-or-medicine | en | 3 Neuroscientists To Share Nobel Prize In Physiology Or Medicine | [
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"Rob Stein"
] | 2014-10-06T00:00:00 | The $1.1 million prize will be split between John O'Keefe of University College in London and a husband-and-wife team, May-Britt and Edvard Moser of the Norwegian University in Trondheim. | en | NPR | https://www.npr.org/2014/10/06/354124231/3-neuroscientists-to-share-nobel-prize-in-physiology-or-medicine | ROBERT SIEGEL, HOST:
The Nobel Prize in physiology or medicine was announced today. The 1.1 million-dollar prize will be split between John O'Keefe of University College London and a husband-and-wife team, May-Britt and Edvard Moser of the Norwegian University in Trondheim. NPR's Rob Stein explains why they won.
ROB STEIN, BYLINE: The three neuroscientists won for discovering what the Nobel committee calls our inner GPS.
(SOUNDBITE OF ARCHIVED RECORDING)
OLE KIEHN: An inner GPS that makes it possible to know where we are and find our way.
STEIN: That's Ole Kiehn, a professor of neuroscience who helped pick the winners.
(SOUNDBITE OF ARCHIVED RECORDING)
KIEHN: The abilities to know where we are and find our way are essential to our existence.
STEIN: How our brains do this has fascinated and puzzled philosophers and scientists for hundreds of years. Then John O'Keefe made a crucial discovery in 1971. He measured the activity of cells in a part of the brain called the hippocampus as rats moved around the room.
(SOUNDBITE OF ARCHIVED RECORDING)
KIEHN: And much to his surprise, he found in hippocampus nerve cells that were only active when a rat was in a certain position in the environment.
STEIN: And when the rats were in a different place, different cells became active. He called these place cells.
(SOUNDBITE OF ARCHIVED RECORDING)
KIEHN: The place cells in hippocampus generate many inner maps of the environment which gives us information about where we are and how we can recognize new environments.
STEIN: More than three decades later, the Mosers discovered another part of the brain's GPS system while studying connections between nerve cells.
(SOUNDBITE OF ARCHIVED RECORDING)
KIEHN: They discovered a complete new type of nerve cell activity.
STEIN: Nerve cell activity by cells they called grid cells because they create a kind of mental grid in the brain.
(SOUNDBITE OF ARCHIVED RECORDING)
KIEHN: Activity in many grid cells provide the brain with a coordinate system that allows to keep track on how far we are from a starting point and the turning point.
STEIN: And that's how we're able to figure out how to plan routes to get from one place to another. The committee says the discoveries have led to fundamental insights into how the brain produces all kinds of complicated thinking powers like memory and planning.
(SOUNDBITE OF ARCHIVED RECORDING)
KIEHN: The discoveries by the Nobel laureates provided a paradigm shift in our understanding of how groups of specialized nerve cells work together to execute our brain functions.
STEIN: The Nobel committee noted that one of the early signs of Alzheimer's disease is that people start getting lost and can't find their way home. So someday, this research might lead to ways to help people suffering from this devastating brain disease. May-Britt Moser described her reaction when she got a phone call from the Nobel committee.
MAY-BRITT MOSER: He said, you won the Nobel Prize. And I started to cry, and I said don't joke with me. (Laughter). I don't believe it. I think I'm dreaming. (Laughter).
STEIN: Rob Stein, NPR News.
Copyright © 2014 NPR. All rights reserved. Visit our website terms of use and permissions pages at www.npr.org for further information.
NPR transcripts are created on a rush deadline by an NPR contractor. This text may not be in its final form and may be updated or revised in the future. Accuracy and availability may vary. The authoritative record of NPR’s programming is the audio record. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 79 | https://www.nationalgeographic.com/science/article/151005-nobel-laureates-forget-racist-sexist-science | en | 10 Nobel Prize Winners Who Weren't Always Noble | [
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] | 2015-10-06T16:15:00+00:00 | Racists, frauds, and misogynists: Meet the rogues’ gallery of Nobel laureates. | en | Science | https://www.nationalgeographic.com/science/article/151005-nobel-laureates-forget-racist-sexist-science | Since the Nobel Prize's beginnings in 1901, fewer than 1,000 people have won the world's most prestigious award. As National Geographic has previously covered, many great discoveries have been incomprehensibly overlooked for the honor—and some Nobel Laureates could have done without.
Some failed to credit the female colleagues who had made their achievements possible. Others used their fame to promote junk science. And still others, under the guise of continuing their pursuit of knowledge, revealed their inner bigotry.
For convenience, we’ve divided these low points in Nobel history into categories:
White Supremacist
As a co-inventor of the transistor, William Shockley brought silicon to Silicon Valley. Unfortunately, he was also an unrepentant racist.
He won the Nobel Prize in Physics in 1956. But in later years, despite a complete lack of formal education in biology and genetics, Shockley tried to use these fields of study to support a set of racist ideas known as eugenics.
In particular, he warned of “retrogressive evolution” because he believed blacks were reproducing faster than what he considered to be intellectually superior whites. His proposed “solutions” included replacing the welfare system with financial incentives for “genetically disadvantaged” individuals to allow themselves to be sterilized.
Science Denial
Kary Mullis, the 1993 winner of the Nobel Prize in Chemistry, revels in his reputation as a "maverick." In his autobiography, Dancing Naked in the Mind Field, he extols the virtues of astrology, describes a possible encounter with aliens (which appeared to him in the form of a talking, glowing raccoon), and cheerfully admits his repeated use of LSD.
Unfortunately, Mullis’ maverick theories also include AIDS denialism. He has lent his Nobel Laureate star power to endorsing the theories of molecular biologist Peter Duesberg, who asserts—despite overwhelming evidence to the contrary—that the HIV virus is harmless and that AIDS is actually caused by recreational drug use and anti-HIV pharmaceuticals.
Agent of War
The 1918 Nobel Prize in Chemistry was awarded to Fritz Haber, who had developed a method for synthesizing ammonia from nitrogen and hydrogen for use as fertilizer. The discovery increased crop yields worldwide—and Haber was celebrated as the man who had made “bread out of air.”
But Haber would become known for another innovation: industrialized mass-killing. During the First World War, he initiated the program to develop and weaponize chlorine for use on the battlefield. On April 22, 1915, Haber personally oversaw the deployment of 6,000 cylinders of gas at Ypres, Belgium, killing 1,000 French and Algerian troops in less than ten minutes.
Least Qualified Winner
Nils Gustaf Dalén won the 1912 Nobel Prize for Physics to commemorate his groundbreaking research into… lighthouses. His invention, the Solventil, was a solar valve that regulated the operation of gaslight. It would shut down a beacon at sunrise and automatically relight it again at night—or during the day, if conditions became cloudy or foggy.
A nifty invention, to be sure, but not exactly paradigm-changing research—especially during an era when Max Planck and others were revolutionizing our understanding of physics.
“This remains the least impressive award in any science category,” writes Burton Feldman in his book, The Nobel Prize: A History of Genius, Controversy, and Prestige. “It seems to have happened because of the academy’s deadlock over far more impressive candidates such as Planck.”
It was later revealed that the academy originally had intended to offer a joint-prize to Nikola Tesla and Thomas Edison for their contributions to developing electricity. Tesla, however, refused to share the honor with Edison. Some historical accounts say Tesla remained bitter over a financial disagreement with Edison; others say that Tesla considered it an affront to share the award with a mere inventor.
And so, the prize instead went to a man who found a way to build a better lighthouse.
Clueless Sexists
Quite a few laureates deserve inclusion in this category—notably, those who denied their female colleagues the public acknowledgment they deserved for their research (see “Credit Stealers,” below).
Still, one name stands out for special recognition: Sir Tim Hunt, winner of the 2001 Nobel Prize in Physiology and Medicine.
The British biochemist created a social media tsunami in June 2015, when, during a luncheon for female journalists and scientists in Seoul, he remarked: “Let me tell you about my trouble with girls. Three things happen when they are in the lab: you fall in love with them, they fall in love with you, and when you criticize them they cry. Perhaps we should make separate labs for boys and girls?”
Hunt later issued a pseudo-apology, saying that he was sorry for causing offense and that his remarks were "intended as a light-hearted, ironic comment." But, he had also told a co-panelist that his comment was rooted in “honesty”—reflecting an apparent cluelessness about the vast underrepresentation of women working in STEM fields.
“Statements like this are indicators of an ingrained attitude that, yes, does make it harder for women to advance in the world of science,” wrote Pulitzer-Prize winning science writer Deborah Blum.
Credit Stealers
There is a long, not-so-proud history of Nobel Prizes awarded to men in place of their female colleagues. (Check out National Geographic’s story about women scientists snubbed by the Nobel committee).
Perhaps one of the most egregious is Joshua Lederberg, awarded the in 1958 Nobel Prize in Physiology or Medicine for research he conducted with his first wife, microbiologist Esther Lederberg.
Esther Lederberg discovered a virus that infects bacteria, and, with her husband, developed a way to transfer bacteria between petri dishes. Their first experiments used the powder puff from her compact to pick up and deposit bacteria in a lab dish. Today, scientists still use a similar technique to study antibiotic resistance.
For all of her contributions, she did not share the Nobel Prize with her husband, who mentioned her only once in his Nobel lecture.
Just Plain Wrong
Danish scientist Johannes Fibiger won the 1926 Nobel Prize in Physiology or Medicine for discovering what he thought was a cancer-causing parasite—a bold idea that turned out to be phenomenally wrong.
Fibiger studied wild rats with warty growths, which Fibiger believed was a form of cancer caused by parasitic worms. His Nobel Prize was awarded with the declaration that these findings were “the greatest contribution to experimental medicine in our generation.”
Only, it wasn’t. While it’s true that some infections can lead to cancer, his rats' disease wasn't caused by parasites. It wasn’t even cancer. The warty bumps in the rats’ stomachs were actually caused by a Vitamin A deficiency, exacerbated by the parasites.
Why the Nobel? “The dawn of the microbial age was at the end of the 19th century, and he was in the early 20th century,” says Stanford professor of epidemiology Julie Parsonnet. “People were very excited about this possibility that infections caused everything.” And it certainly didn’t hurt that Fibiger had friends on the Nobel committee.
Being James Watson
James Watson is a category unto himself. The co-discoverer of the structure of DNA doesn't miss an opportunity to offend.
During a lecture at Berkeley, he suggested there are biochemical links between sexual libido and skin color (“That’s why you have Latin lovers.”) and between body weight and ambition. He declared in an interview that “some anti-Semitism is justified.” He never gave credit to Rosalind Franklin, whose work with X-ray crystallography made his discovery possible—though he made it a point to criticize her appearance and taste in clothing.
Just when it seemed there were no more lines to cross, Watson declared himself “inherently gloomy about the prospect of Africa" because "all our social policies are based on the fact that their intelligence is the same as ours—whereas all the testing says not really.”
In a fit of pique and self-pity, Watson auctioned off his Nobel Prize medallion in 2014 for $4.1 million; he is the only laureate to have done so.
Editor's note: This story was last updated on September 29, 2017.
Follow Mark Strauss on Twitter. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 3 | 3 | https://en.wikipedia.org/wiki/Nobel_Prize_in_Physiology_or_Medicine | en | Nobel Prize in Physiology or Medicine | [
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For a list of laureates, see List of Nobel laureates in Physiology or Medicine.
Award
Nobel Prize in Physiology or MedicineAwarded forDiscoveries in physiology or medicine that led to benefit for humankindLocationStockholm, SwedenPresented byNobel Assembly at Karolinska InstitutetReward(s)11 million SEK (2023)[1]First awarded1901Currently held byKatalin Karikó and Drew Weissman (2023)Websitenobelprize .org /prizes /medicine
The Nobel Prize in Physiology or Medicine (Swedish: Nobelpriset i fysiologi eller medicin) is awarded yearly by the Nobel Assembly at the Karolinska Institute for outstanding discoveries in physiology or medicine. The Nobel Prize is not a single prize, but five separate prizes that, according to Alfred Nobel's 1895 will, are awarded "to those who, during the preceding year, have conferred the greatest benefit to humankind". Nobel Prizes are awarded in the fields of Physics, Medicine or Physiology, Chemistry, Literature, and Peace.
The Nobel Prize is presented annually on the anniversary of Alfred Nobel's death, 10 December. As of 2023, 115 Nobel Prizes in Physiology or Medicine have been awarded to 227 laureates, 214 men and 13 women. The first one was awarded in 1901 to the German physiologist, Emil von Behring, for his work on serum therapy and the development of a vaccine against diphtheria. The first woman to receive the Nobel Prize in Physiology or Medicine, Gerty Cori, received it in 1947 for her role in elucidating the metabolism of glucose, important in many aspects of medicine, including treatment of diabetes. The most recent Nobel prize was announced by the Karolinska Institute on 2 October 2023, and has been awarded to Hungarian-American Katalin Karikó and American Drew Weissman, for their discoveries leading to development of an effective COVID-19 vaccine.[2]
The prize consists of a medal along with a diploma and a certificate for the monetary award. The front side of the medal displays the same profile of Alfred Nobel depicted on the medals for Physics, Chemistry, and Literature; the reverse side is unique to this medal.
Some awards have been controversial. This includes one to António Egas Moniz in 1949 for the prefrontal lobotomy, bestowed despite protests from the medical establishment. Other controversies resulted from disagreements over who was included in the award. The 1952 prize to Selman Waksman was litigated in court, and half the patent rights were awarded to his co-discoverer Albert Schatz who was not recognised by the prize. Nobel prizes cannot be awarded posthumously. Also, no more than three recipients can receive a Nobel Prize in Physiology or Medicine, a limitation that is sometimes discussed because of an increasing trend for larger teams to conduct important scientific projects.
Alfred Nobel was born on 21 October 1833 in Stockholm, Sweden, into a family of engineers.[3] He was a chemist, engineer and inventor who amassed a fortune during his lifetime, most of it from his 355 inventions, of which dynamite is the most famous.[4] He was interested in experimental physiology and set up his own labs in France and Italy to conduct experiments in blood transfusions. Keeping abreast of scientific findings, he was generous in his donations to Ivan Pavlov's laboratory in Russia and was optimistic about the progress resulting from scientific discoveries made in laboratories.[5]
In 1888, Nobel was surprised to read his own obituary, titled "The merchant of death is dead", in a French newspaper. As it happened, it was Nobel's brother Ludvig who had died, but Nobel, unhappy with the content of the obituary and concerned that his legacy would reflect poorly on him, was inspired to change his will.[6] In his last will, Nobel requested that his money be used to create a series of prizes for those who confer the "greatest benefit on mankind" in physics, chemistry, peace, physiology or medicine, and literature.[7] Though Nobel wrote several wills during his lifetime, the last was written a little over a year before he died in 1896 at the age of 63.[8] Because his will was contested, it was not approved by the Storting (Norwegian Parliament) until 26 April 1897.[9]
After Nobel's death, the Nobel Foundation was set up to manage the assets of the bequest.[10] In 1900, the Nobel Foundation's newly created statutes were promulgated by Swedish King Oscar II.[11][12] According to Nobel's will, the Karolinska Institute in Sweden, a medical school and research centre, is responsible for the Prize in Physiology or Medicine.[13] Today, the prize is commonly referred to as the Nobel Prize in Medicine.[14]
It was important to Nobel that the prize be awarded for a "discovery" and that it be of "greatest benefit on mankind".[15] Per the provisions of the will, only select persons are eligible to nominate individuals for the award. These include members of academies around the world, professors of medicine in Sweden, Denmark, Norway, Iceland, and Finland, as well as professors of selected universities and research institutions in other countries. Past Nobel laureates may also nominate.[16] Until 1977, all professors of Karolinska Institute together decided on the Nobel Prize in Physiology or Medicine. That year, changes in Swedish law forced the institute to make public any documents pertaining to the Nobel Prize, and it was considered necessary to establish a legally independent body for the Prize work. Therefore, the Nobel Assembly was constituted, consisting of 50 professors at Karolinska Institute. It elects the Nobel Committee with five members who evaluate the nominees, the Secretary who is in charge of the organisation, and each year ten adjunct members to assist in the evaluation of candidates. In 1968, a provision was added that no more than three persons may share a Nobel prize.[17]
True to its mandate, the committee has chosen researchers working in the basic sciences over those who have made applied science contributions. Harvey Cushing, a pioneering American neurosurgeon who identified Cushing's syndrome, was not awarded the prize, nor was Sigmund Freud, as his psychoanalysis lacks hypotheses that can be experimentally confirmed.[18] The public expected Jonas Salk or Albert Sabin to receive the prize for their development of the polio vaccines, but instead the award went to John Enders, Thomas Weller, and Frederick Robbins whose basic discovery that the polio virus could reproduce in monkey cells in laboratory preparations made the vaccines possible.[19]
Through the 1930s, there were frequent prize laureates in classical physiology, but after that, the field began fragmenting into specialities. The last classical physiology laureates were John Eccles, Alan Hodgkin, and Andrew Huxley in 1963 for their findings regarding "unitary electrical events in the central and peripheral nervous system."[20]
A Medicine or Physiology Nobel Prize laureate earns a gold medal, a diploma bearing a citation, and a sum of money.[21] These are awarded during the prize ceremony at the Stockholm Concert Hall.
The Physiology and Medicine medal has a portrait of Alfred Nobel in left profile on the obverse.[22] The medal was designed by Erik Lindberg.[22] The reverse of the medal depicts the 'Genius of Medicine holding an open book in her lap, collecting the water pouring out from a rock in order to quench a sick girl's thirst'.[23] It is inscribed "Inventas vitam iuvat excoluisse per artes" ("It is beneficial to have improved (human) life through discovered arts") an adaptation of "inventas aut qui vitam excoluere per artes" from line 663 from book 6 of the Aeneid by the Roman poet Virgil.[23] A plate below the figures is inscribed with the name of the recipient. The text "REG. UNIVERSITAS MED. CHIR. CAROL." denoting the Karolinska Institute is also inscribed on the reverse.[23]
Between 1902 and 2010 the Nobel Prize medals were struck by the Myntverket, the Swedish royal mint, located in Eskilstuna. In 2011 the medals were made by the Det Norske Myntverket in Kongsberg. The medals have been made by Svenska Medalj in Eskilstuna since 2012.[22]
Nobel laureates receive a diploma directly from the King of Sweden. Each diploma is uniquely designed by the prize-awarding institutions for the laureate who receives it. In the case of the Nobel Prize in Physiology or Medicine, that is the Nobel Assembly at Karolinska Institute. Well-known artists and calligraphers from Sweden are commissioned to create it.[24] The diploma contains a picture and text which states the name of the laureate and a citation as to why they received the prize.[24]
At the awards ceremony, the laureate is given a document indicating the award sum. The amount of the cash award may differ from year to year, based on the funding available from the Nobel Foundation. For example, in 2009 the total cash awarded was 10 million SEK (US$1.4 million),[25] but in 2012, the amount was 8 million Swedish Krona, or US$1.1 million.[26] If there are two laureates in a particular category, the award grant is divided equally between the recipients, but if there are three, the awarding committee may opt to divide the grant equally, or award half to one recipient and a quarter to each of the two others.[27][28][29][30]
The awards are bestowed at a gala ceremony followed by a banquet.[31] The Nobel Banquet is an extravagant affair with the menu, planned months ahead of time, kept secret until the day of the event. The Nobel Foundation chooses the menu after tasting and testing selections submitted by selected chefs of international repute. Currently, it is a three-course dinner, although it was originally six courses in 1901. Each Nobel Prize laureate may bring up to 16 guests. Sweden's royal family attends, and typically the Prime Minister and other members of the government attend as well as representatives of the Nobel family.[32]
For a more comprehensive list, see List of Nobel laureates in Physiology or Medicine.
The first Nobel Prize in Physiology or Medicine was awarded in 1901 to the German physiologist Emil Adolf von Behring.[33] Behring's discovery of serum therapy in the development of the diphtheria and tetanus vaccines put "in the hands of the physician a victorious weapon against illness and deaths".[34][35] In 1902, the award went to Ronald Ross for his work on malaria, "by which he has shown how it enters the organism and thereby has laid the foundation for successful research on this disease and methods of combating it".[36] He identified the mosquito as the transmitter of malaria, and worked tirelessly on measures to prevent malaria worldwide.[37][38] The 1903 prize was awarded to Niels Ryberg Finsen, the first Faroese laureate, "in recognition of his contribution to the treatment of diseases, especially lupus vulgaris, with concentrated light radiation, whereby he has opened a new avenue for medical science".[39][40] He died within a year after receiving the prize at the age of 43.[41] Ivan Pavlov, whose work Nobel admired and supported, received the prize in 1904 for his work on the physiology of digestion.[42]
Subsequently, those selecting the recipients have exercised wide latitude in determining what falls under the umbrella of Physiology or Medicine. The awarding of the prize in 1973 to Nikolaas Tinbergen, Konrad Lorenz, and Karl von Frisch for their observations of animal behavioural patterns could be considered a prize in the behavioural sciences rather than medicine or physiology.[14] Tinbergen expressed surprise in his Nobel Prize acceptance speech at "the unconventional decision of the Nobel Foundation to award this year's prize 'for Physiology or Medicine' to three men who had until recently been regarded as 'mere animal watchers'".[44]
Laureates have been awarded the Nobel Prize in a wide range of fields that relate to physiology or medicine. As of 2010 , eight Prizes have been awarded for contributions in the field of signal transduction through G proteins and second messengers. 13 have been awarded for contributions in the field of neurobiology[45] and 13 have been awarded for contributions in Intermediary metabolism.[46] The 100 Nobel Prizes in Physiology or Medicine have been awarded to 195 individuals through 2009.[47][48]
Thirteen women have received the prize: Gerty Cori (1947), Rosalyn Yalow (1977), Barbara McClintock (1983), Rita Levi-Montalcini (1986), Gertrude B. Elion (1988), Christiane Nüsslein-Volhard (1995), Linda B. Buck (2004), Françoise Barré-Sinoussi (2008), Elizabeth H. Blackburn (2009), Carol W. Greider (2009), May-Britt Moser (2014), Youyou Tu (2015) and Katalin Karikó (2023).[49] Only one woman, Barbara McClintock, has received an unshared prize in this category, for the discovery of genetic transposition.[47][50]
Mario Capecchi, Martin Evans, and Oliver Smithies were awarded the prize in 2007 for the discovery of a gene targeting procedure (a type of genetic recombination) for introducing homologous recombination in mice, employing embryonic stem cells through the development of the knockout mouse.[51][52] In 2009, the Nobel Prize was awarded to Elizabeth Blackburn, Carol W. Greider and Jack W. Szostak of the United States for discovering the process by which chromosomes are protected by telomeres (regions of repetitive DNA at the ends of chromosomes) and the enzyme telomerase.[53]
Rita Levi-Montalcini, an Italian neurologist, who together with colleague Stanley Cohen, received the 1986 Nobel Prize in Physiology or Medicine for their discovery of Nerve growth factor (NGF), was the first Nobel laureate to reach the 100th birthday.[48]
There have been 38 times when the Nobel Prize in Physiology or Medicine was awarded to a single individual, 31 times when it was shared by two, and 33 times there were three laureates (the maximum allowed).
Because of the length of time that may pass before the significance of a discovery becomes apparent, some prizes are awarded many years after the initial discovery. Barbara McClintock made her discoveries in 1944, before the structure of the DNA molecule was known; she was not awarded the prize until 1983. Similarly, in 1916 Peyton Rous discovered the role of tumor viruses in chickens, but was not awarded the prize until 50 years later, in 1966.[54] Nobel laureate Carol Greider's research leading to the prize was conducted over 20 years before. She noted that the passage of time is an advantage in the medical sciences, as it may take many years for the significance of a discovery to become apparent.[55]
In 2011, Canadian immunologist Ralph M. Steinman was awarded the prize; however, unbeknownst to the committee, he had died three days before the announcement. The committee decided that since the prize was awarded "in good faith," it would be allowed to stand.
Main article: Nobel Prize controversies
Some of the awards have been controversial. The person who was deserving of the 1923 prize for the discovery of insulin as a central hormone for controlling diabetes (awarded only a year after its discovery)[56] has been heatedly debated. It was shared between Frederick Banting and John Macleod; this infuriated Banting who regarded Macleod's involvement as minimal. Macleod was the department head at the University of Toronto but otherwise was not directly involved in the findings. Banting thought his laboratory partner Charles Best, who had shared in the laboratory work of discovery, should have shared the prize with him as well. In fairness, he decided to give half of his prize money to Best. Macleod on his part felt the biochemist James Collip, who joined the laboratory team later, deserved to be included in the award and shared his prize money with him.[56] Some maintain that Nicolae Paulescu, a Romanian professor of physiology at the University of Medicine and Pharmacy in Bucharest, was the first to isolate insulin, in 1916, although his pancrein was an impure aqueous extract unfit for human treatment similar to the one used previously by Israel Kleiner.[57][58][59] When Banting published the paper that brought him the Nobel,[60] Paulescu already held a patent for his discovery (10 April 1922, patent no. 6254 (8322) "Pancreina şi procedeul fabricaţiei ei"/"Pancrein and the process of making it", from the Romanian Ministry of Industry and Trade).[61][62][63]
The Spanish neurophysiologist Fernando de Castro (1896–1967) was the first to describe arterial chemoreceptors and circumscribe them to the carotid body for the respiratory reflexes in 1926–1928. For many experts, this direct disciple of Santiago Ramón y Cajal deserved to share the Nobel Prize 1938 with the awarded Corneille Heymans, but at that time Spain was immersed in the Spanish Civil War and it seems that the Nobel Board even doubted if he was alive or not, being at the front since almost the beginning of the conflict. Heymans himself recognised the merits of De Castro for the Nobel Prize in different occasions, including a famous talk in Montevideo (Uruguay).[64]
In 1949, despite protests from the medical establishment, the Portuguese neurologist António Egas Moniz received the Physiology or Medicine Prize for his development of the prefrontal leucotomy, which he promoted by declaring the procedure's success just 10 days postoperative. Due largely to the publicity surrounding the award, it was prescribed without regard for modern medical ethics. Favourable results were reported by such publications as The New York Times. It is estimated that around 40,000 lobotomies were performed in the United States before the procedure's popularity faded.[65] Rosemary Kennedy, the sister of John F. Kennedy, was subjected to the procedure by their father; it incapacitated her to the extent that she needed to be institutionalised for the rest of her life.[66][67]
The 1952 prize, awarded solely to Selman Waksman for his discovery of streptomycin, omitted the recognition some felt due to his co-discoverer Albert Schatz.[68][69] There was litigation brought by Schatz against Waksman over the details and credit of the streptomycin discovery; Schatz was awarded a substantial settlement, and, together with Waksman, Schatz was to be officially recognised as a co-discoverer of streptomycin as concerned patent rights. He is not a Nobel Prize laureate.[68]
The 1962 Prize awarded to James D. Watson, Francis Crick, and Maurice Wilkins—for their work on DNA structure and properties—did not recognise contributing work from others, such as Alec Stokes and Herbert Wilson. In addition, Erwin Chargaff, Oswald Avery, and Rosalind Franklin (whose key DNA x-ray crystallography work was the most detailed yet least acknowledged among the three)[70][page needed] contributed directly to the ability of Watson and Crick to solve the structure of the DNA molecule. Avery died in 1955, Franklin died in 1958 and posthumous nominations for the Nobel Prize are not permitted. Files of Nobel Prize nominations show Franklin was not nominated when she was alive.[71] As a result of Watson's misrepresentations of Franklin and her role in the discovery of the double helix in his book The Double Helix, Franklin has come to be portrayed as a classic victim of sexism in science.[72][73] Chargaff, for his part, was not quiet about his exclusion from the prize, bitterly writing to other scientists about his disillusionment regarding the field of molecular biology.[74]
The 2008 award went to Harald zur Hausen in recognition of his discovery that human papillomavirus (HPV) can cause cervical cancer, and to Françoise Barré-Sinoussi and Luc Montagnier for discovering the human immunodeficiency virus (HIV).[75] Whether Robert Gallo or Luc Montagnier deserved more credit for the discovery of the virus that causes AIDS has been a matter of considerable controversy. As it was, Gallo was left out and not awarded a prize.[76][77] Additionally, there was a scandal when it was learned that Harald zur Hausen was being investigated for having a financial interest in vaccines for the cervical cancer that HPV can cause. AstraZeneca, which had a stake in two lucrative HPV vaccines could benefit financially from the prize, had agreed to sponsor Nobel Media and Nobel Web. According to Times Online, two senior figures in the selection process that chose zur Hausen also had strong links with AstraZeneca.[78]
The provision that restricts the maximum number of nominees to three for any one prize, introduced in 1968, has caused considerable controversy.[17][79] From the 1950s onward, there has been an increasing trend to award the Nobel Prize in Physiology or Medicine to more than one person. There were 59 people who received the prize in the first 50 years of the last century, while 113 individuals received it between 1951 and 2000. This increase could be attributed to the rise of the international scientific community after World War II, resulting in more persons being responsible for the discovery, and nominated for, a particular prize. Also, current biomedical research is more often carried out by teams rather than by scientists working alone, making it unlikely that any one scientist, or even a few, is primarily responsible for a discovery;[19] this has meant that a prize nomination that would have to include more than three contributors is automatically excluded from consideration.[54] Also, deserving contributors may not be nominated at all because the restriction results in a cut-off point of three nominees per prize, leading to controversial exclusions.[15]
There have been nine years in which the Nobel Prize in Physiology or Medicine was not awarded (1915–1918, 1921, 1925, 1940–1942). Most of these occurred during either World War I (1914–1918) or World War II (1939–1945).[48] In 1939, Nazi Germany forbade Gerhard Domagk from accepting his prize.[80] He was later able to receive the diploma and medal but not the money.[48][81]
List of medicine awards
List of Nobel laureates in Physiology or Medicine
Doherty, Peter (2008). The Beginner's Guide to Winning the Nobel Prize: Advice for Young Scientists. Columbia University Press. ISBN 978-0-231-13897-0.
Leroy, Francis (2003). A century of Nobel Prizes recipients: chemistry, physics, and medicine. CRC Press. ISBN 978-0-8247-0876-4.
Rifkind, David; Freeman, Geraldine L. (2005). The Nobel Prize winning discoveries in infectious diseases. Academic Press. ISBN 978-0-12-369353-2. | ||||||
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] | 2019-10-07T00:00:00 | William G. Kaelin Jr., MD, a physician-scientist at the Brigham, has been awarded the 2019 Nobel Prize in Physiology or Medicine. | en | Brigham Bulletin | http://bwhbulletin.org/2019/10/07/kaelin-wins-2019-nobel-prize/ | Early Monday morning, William G. Kaelin Jr., MD, a senior physician-scientist at the Brigham, received one of the most thrilling calls a scientist can get. The call from Stockholm revealed that Kaelin had been awarded the 2019 Nobel Prize in Physiology or Medicine.
“Like most scientists, I did occasionally dream that maybe one day this would happen,” said Kaelin. “I try to ignore that most days, but when I was younger, my late wife and I would have fun together talking about what would that be like. I’m accepting this prize partly on behalf of my late wife, Carolyn Kaelin. I like to think she’s smiling down and nodding.”
Kaelin, who is the Sidney Farber Professor of Medicine at Dana-Farber and Harvard Medical School, and a Howard Hughes Medical Institute Investigator, joined the Brigham in 1991 and currently has a research staff appointment in the Division of Medical Oncology in the Department of Medicine.
Kaelin is being honored jointly with Sir Peter J. Ratcliffe, MD, of the University of Oxford, and Gregg L. Semenza, MD, PhD, of Johns Hopkins University for their discoveries of how cells sense and adapt to oxygen availability. Their contributions and insights have paved the way for new strategies to treat diseases such as heart disease, anemia and cancer.
“As part of the Dana-Farber/Brigham and Women’s Cancer Center, we have great pride in the scientific research, discovery and innovation that occur at the Dana-Farber Cancer Institute. That pride extends to taking those basic discoveries and translating them into new advances for patients to improve their lives on a daily basis,” said Betsy Nabel, MD, president of Brigham Health. “There are broad applications for this oxygen sensing mechanism across many fields — heart and vascular disease, pulmonary disease, kidney disease and many other organ systems. Bill’s advances extend to cancer and far beyond, and for that, we are enormously grateful.”
The Path to Discovery
In his laboratory based at Dana-Farber, Kaelin’s work focuses on how mutations in genes known as tumor suppressors can lead to cancer. When Kaelin first established his lab, he read about the identification of a mutation in a tumor suppressor gene that leads to von Hippel-Lindau (VHL) disease. Patients with this rare, hereditary syndrome are at heightened risk for developing tumors in the kidneys, adrenal glands or pancreas.
Kaelin’s lab found that the VHL protein prevents the onset of cancer and helps control responses to low oxygen levels by regulating another protein that can trigger or suppress the production of red blood cells and the formation of new blood vessels. Cancer cells with VHL mutations can take advantage of this mechanism to surround themselves with new blood vessels that can fuel their growth. This process is known as angiogenesis and has become a target for combating many diseases, including cancer.
Oxygen sensing is essential for many different functions, including fetal development, metabolism, immune response, and exercise. When oxygen sensing goes amiss, it can lead to many diseases, including anemia, cancer, stroke, infection, heart attacks and more. Kaelin’s contributions to the fundamental understanding of how cells sense and respond to oxygen have led to the development of new drugs that can manipulate oxygen-sensing machinery to treat various diseases. Kaelin said he is continuing to search for new, promising targets.
“My mentor David Livingston, MD, taught me to think, ‘The most important thing you’re ever going to discover lies ahead of you,’” said Kaelin. “I still try to adhere to David’s advice.” | |||
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NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 82 | https://news.cornell.edu/content/nobel-laureates-affiliated-cornell-university | en | Nobel Laureates Affiliated with Cornell University | https://news.cornell.edu/favicon.ico | https://news.cornell.edu/favicon.ico | [] | [] | [] | [
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] | null | [] | null | Fifty Nobel Prize winners have been affiliated with Cornell University as alumni or faculty members. Current Faculty Members Roald Hoffmann, the Frank H.T. Rhodes Professor in Humane Letters, Emeritus, 1981 Prize in Chemistry David M. Lee, professor emeritus of physics, 1996 Prize in Physics Harold Varmus, the Lewis Thomas University Professor of Medicine at Weill Cornell Medical College, 1989 Prize in Physiology or Medicine Alumni | en | /favicon.ico | https://news.cornell.edu/content/nobel-laureates-affiliated-cornell-university | Fifty Nobel Prize winners have been affiliated with Cornell University as alumni or faculty members.
Current Faculty Members
Roald Hoffmann, the Frank H.T. Rhodes Professor in Humane Letters, Emeritus, 1981 Prize in Chemistry
David M. Lee, professor emeritus of physics, 1996 Prize in Physics
Harold Varmus, the Lewis Thomas University Professor of Medicine at Weill Cornell Medical College, 1989 Prize in Physiology or Medicine
Alumni
Arthur Ashkin, '52 Ph.D. Physics, 2018 Prize in Physics
George W. Beadle, '31 Ph.D. Genetics, 1958 Prize in Physiology or Medicine (also was professor of agriculture)
Eric Betzig, M.S. ’85, Ph.D. ’88, 2014 Prize in Chemistry
Pearl Buck, '25 M.A., 1938 Prize in Literature
Robert F. Engle III, '66 M.S., '69 Ph.D., 2003 Prize in Economic Sciences
Robert W. Fogel, '48 A.B. Economics, 1993 Prize in Economic Sciences
Sheldon Glashow, '54 B.S. Physics, 1979 Prize in Physics
Claudia Goldin, '67 B.A. Economics, 2023 Prize in Economic Sciences
Barbara McClintock, '23 B.S. Botany, '25 M.A., '27 Ph.D. Plant Genetics, 1983 Prize in Physiology or Medicine
William Moerner, M.S. ’78, Ph.D. ’82, 2014 Prize in Chemistry
Toni Morrison, '55 M.A. English, 1993 Prize in Literature
John R. Mott, Class of 1888, B.S. Philosophy, 1946 Peace Prize
Hermann J. Muller, graduate study 1911-12, 1946 Prize for Physiology or Medicine
Douglas Osheroff, '73 Ph.D., 1996 Prize in Physics
Isidor Isaac Rabi, '19 B.S. Chemistry and graduate study, 1944 Prize in Physics
Jack Szostak, Ph.D. '77 Biochemistry, 2009 Prize in Physiology or Medicine
David J. Thouless, '58 Ph.D., 2016 Prize in Physics
Steven Weinberg, '54 B.S. Physics, 1979 Prize in Physics
Former Cornell Faculty Members
Hannes Alfven, Distinguished Visiting Professor in Engineering, 1970 Prize in Physics
James P. Allison, professor of immunology in medicine at Weill Cornell Medicine (2005-06), 2018 Prize in Physiology or Medicine
Hans Bethe, the John Wendell Anderson Professor of Physics (1935-2005), 1967 Prize in Physics
Norman E. Borlaug, A.D. White Professor-at-Large (1982-88), 1970 Peace Prize
Peter J.W. Debye, Professor and Chairman (1940-50) of Chemistry, 1936 Prize in Chemistry
Pierre-Gilles de Gennes, A.D. White Professor-at-Large (1977-83) and Bethe Lecturer in Physics (1989-90), 1991 Prize in Physics
Vincent du Vigneaud, Professor at Cornell Medical College, 1955 Prize in Chemistry
Manfried Eigen, A.D. White Professor-at-Large, 1967 Prize in Chemistry
François Englert, assistant professor (1960-61) and research associate (1959-60), 2013 Prize in Physics
Richard Ernst, A.D. White Professor-at-Large (1998), 1991 Prize in Chemistry
Richard P. Feynman, Physics faculty (1945-50), 1965 Prize in Physics
Paul J. Flory, Chemistry faculty (1948-57), 1974 Prize in Chemistry
Robert F. Furchgott, Cornell Medical College (1941-1949: research associate in medicine, instructor in physiology and biophysics, assistant professor of biochemistry in medicine), 1998 Prize in Physiology or Medicine
Herbert S. Gasser, Cornell Medical College (1931-34), 1944 Prize in Physiology or Medicine
Paul Greengard, A.D. White Professor-at-Large (1981-87), 2000 Prize in Physiology or Medicine
Haldan Hartline, Associate Professor, Cornell Medical College (1940-41), 1967 Prize in Physiology or Medicine
Robert W. Holley, '47 Ph.D., Professor and Department Chair in Biochemistry (1948-64), 1968 Prize in Physiology or Medicine
H. Gobind Khorana, A.D. White Professor-at-Large (1974-80), 1968 Prize in Physiology or Medicine
Fritz Lipmann, Research Associate, Cornell Medical College (1939-1941), 1953 Prize in Physiology or Medicine
Peter B. Medawar, A.D. White Professor-at-Large, 1960 Prize in Physiology or Medicine
Octavio Paz, A.D. White Professor-at-Large (1972-74), 1990 Prize in Literature
Robert C. Richardson, the Floyd R. Newman Professor of Physics, 1996 Prize in Physics
J. Robert Schrieffer, A.D. White Professor-at-Large (1969-75), 1972 Prize in Physics
Amartya K. Sen, A.D. White Professor-at-Large (1978-84), 1998 Prize in Economic Sciences
Wole Soyinka, Senior Fellow, Society for the Humanities (1985), 1986 Prize in Literature
James B. Sumner, Professor (1929-55) and Professor Emeritus of Biochemistry/Nutrition, 1946 Prize in Chemistry
Henry Taube, Assistant Professor (1944-46), 1983 Prize in Chemistry
Richard H. Thaler, the Henrietta Johnson Louis Professor of Economics (1978-95), 2017 Prize in Economic Sciences
Kip Thorne, A.D. White Professor-at-Large (1986-92) and Visiting Senior Research Associate (1977), 2017 Prize in Physics
Kenneth Wilson, Professor of Physics and Nuclear Studies, Director of the Cornell Theory Center (1963-1988), 1982 Prize in Physics
Updated: June 26, 2024, Compiled by Cornell Chronicle | |||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 16 | https://www.harvard.edu/about/history/nobel-laureates/medicine/ | en | Nobel Laureates in Medicine | [
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] | 2021-02-04T19:57:56+00:00 | Harvard faculty honored with the Nobel Prize acknowledging outstanding contributions to the field of medicine. | en | Harvard University | https://www.harvard.edu/about/history/nobel-laureates/medicine/ | William Kaelin, the Sidney Farber Professor of Medicine at Harvard Medical School and a professor of medicine at Dana-Farber Cancer Institute, is one of three winners of the 2019 Nobel Prize in physiology or medicine. He shares the award with Sir Peter J. Ratcliffe of the University of Oxford and the Francis Crick Institute, and Gregg L. Semenza of Johns Hopkins University School of Medicine. The three were cited jointly for the discovery of the pathway by which cells from humans and most animals sense and adapt to changes in oxygen availability, a process essential for survival.
What began as a simple question regarding yeast cells, has broadened the scientific community’s understanding of aging and death on the cellular level, and quite possibly, our bodies as a whole. Described as a “scientist’s scientist,” Szostak has been studying the ends of chromosomes and a special enzyme, called telomerase, which helps hold the ends of chromosomes together and protect them from deterioration. In his research, he discovered that some cells whose telomeres do not activate normally have a way of evading destruction – enter cancer cells – and this finding has brought forth a flood of larger questions surrounding cancer research and the aging process. British born, Jack Szostak is a Professor of Genetics at Harvard Medical School and the affiliated Massachusetts General Hospital. Since his award-winning reaching on telomeres, Szostak has shifted his intellectual curiosity from the death of cells, to the genesis of life itself as co-director of the Origins of Life Initiate at Harvard University.
Buck received the Nobel Prize for work relating to the sense of smell, which the Nobel committee noted had “long remained the most enigmatic of our senses. The basic principles for recognizing and remembering about 10,000 different odours were not understood.” Buck and Richard Axel, with whom she shared the prize, published the fundamental paper describing odorant receptors in 1991. That year Buck became an assistant professor at Harvard Medical School. “The discoveries on the organization of the olfactory system that were cited by the Nobel Foundation were made over a period of 10 years, during which I was a faculty member at Harvard,” she said. Since 2002, Buck has been at the Fred Hutchison Cancer Research Center in Seattle.
The ambidextrous Murray, who performed the first successful human kidney transplant, is one of the few surgeon-scientists to win the Nobel. Although committed to his lab work, Murray’s first concern has always been the patient. During World War II, doing reparative surgery, particularly with burns patients, Murray became intrigued by the dynamics of tissue rejection and acceptance, leading him to his interest in transplant surgery.
When told he’d been awarded the Nobel Prize, Wiesel said, “Oh, no, I was afraid of that! I better go and hide.” For Wiesel, what really counts is the research and its results, like improvements in the treatment of congenital cataracts and other blinding conditions found in children. Wiesel is President Emeritus of The Rockefeller University.
In a partnership spanning decades, Hubel and Torsten Wiesel have provided the basis for our understanding of how the brain analyzes visual information. The pair describe their work as a 50-50 effort. Says Hubel, “It’s been a real Gilbert and Sullivan sort of thing. Not that we would compare ourselves to those celestial people, but they did do different things and you wouldn’t say one did more than the other.” Hubel is John Franklin Enders University Professor of Neurobiology and Senior Fellow of the Society of Fellows.
Benacerraf’s discovery has several dramatic applications, helping us to understand: 1) the body’s ability to repel microbial invasions, 2) the mechanism by which the body accepts or rejects skin grafts or organ transplants, and 3) the growth of tumors, invaders that outwit or fool the body’s defense system. Benacerraf is the George Fabyan Professor of Comparative Pathology Emeritus.
Wald contributed greatly to our knowledge of the human eye, particularly the visual pigments and how light affects them. He was on the forefront of the revolution that changed biology from a cellular to a molecular science. An early and outspoken opponent of the Vietnam War, Wald was always a lively, engaged, and formidable figure in the political arena.
Bloch’s painstaking research helped cap the half-century dubbed the “Golden Age of Biochemistry.” Determined to communicate with the intelligent layperson outside of the scientific community, the emeritus professor in (1994) published a book of lively pieces titled Blondes in Venetian Paintings, The Nine-Banded Armadillo, and other Essays in Biochemistry, which demonstrates (among other things) that many Renaissance portraits featured “bottle blondes.”
In 1953, at the tender age of 25, the enfant terrible Watson, with British scientist Francis Crick, presented a model for DNA, beating Linus Pauling in a neck-and-neck race to one of the most significant scientific discoveries of the 20th century. His controversial book, The Double Helix, “has been called,” says The New York Times, “the most honest book ever written about scientific research.” Watson is currently president of the Cold Spring Harbor Laboratory on Long Island, N.Y.
This engineer, who in his youth was intrigued by the high-pitched Gypsy music of his native Hungary, has been lauded for “fathoming the enigmas and disclosing the elegance of the auditory system.” His delicate engineering feats included the design of special scissors, whose blades were a few thousandths of an inch long, to manipulate the cochlea, a minute structure in the inner ear.
In addition to his work on the polio virus, Weller made significant contributions to the study of human parasites and the viruses that cause rubella (German measles) and chicken pox. Later in his career, Weller distinguished himself as an administrator, serving as director of the Center for Prevention of Infectious Diseases at Harvard’s School of Public Health, where he significantly advanced the School’s international reputation. Weller is the Richard Pearson Strong Professor of Tropical Public Health Emeritus.
At Harvard Medical School in the late 1930s, Robbins studied with John Enders and roomed with Thomas Weller. After earning his M.D., he served in North Africa and Italy during the war, investigating bacterial diseases. He was awarded a Bronze Star. By 1950, he was back with his old college colleagues, Enders and Weller, doing the experiments which led to their Nobel Prize — and a vaccine for polio.
Without Enders’ subtle triumph of learning how to grow a virus, the more celebrated Jonas Salk would have been unable to bring his own work to its powerful conclusion. In addition to his many achievements in human biology, “The Chief,” as Enders was called, was esteemed for his impeccable standards of personal and scientific honesty.
A slow starter and a self-admitted failure at academic politics, Lipmann wandered early in his career from laboratory to laboratory as a researcher. His wife remembers that he “had no position, no prospects, and it did not seem to trouble him.” This lack of obsessive focus is, perhaps, related to his famed ability to see the wider picture, a trait which eventually led to pivotal discoveries about how living organisms function.
The scion of a Boston Brahmin family, the at-first unambitious Minot eventually became a pioneer in the field of hematology, the study of blood. While researching the deadly blood disease known as pernicious anemia, Minot himself was stricken by diabetes. It was the discovery of insulin in 1921 that allowed him to continue his research, which ultimately led to his own discovery of the cure for pernicious anemia. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 14 | https://www.theguardian.com/science/2014/oct/06/nobel-prize-physiology-medicine-brain-navigation | en | Nobel prize in physiology or medicine for finding brain’s ‘you are here’ cells | [
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] | 2014-10-06T00:00:00 | Winning research answered question that stumped philosophers for hundreds of years: how do we know our place in the world?<br> | en | the Guardian | https://www.theguardian.com/science/2014/oct/06/nobel-prize-physiology-medicine-brain-navigation | Three neuroscientists, including a married couple from Norway, have won the 2014 Nobel prize in physiology or medicine for their discovery of the brain’s internal GPS.
Their work, which collectively spans four decades, revealed the existence of nerve cells that build up a map of the space around us and then track our progress as we move around.
The groundbreaking research transformed neuroscientists’ understanding of the brain’s ability to navigate and answered a question that had stumped scientists and philosophers for hundreds of years: how do we know our place in the world?
John O’Keefe, 75, a US-British citizen at University College London, received half of the award and takes a share of 8m Swedish kronor (£690,000) for his pioneering work in 1971 that identified “place cells” in the brain that map the environment. Born in New York to Irish immigrant parents, he is a keen basketball player and claims never to have given up his dream of playing in the NBA.
On hearing that he had won the prize O’Keefe said yesterday: I’m delighted and thrilled. I’m still in a state of shock. It is the highest accolade you can get.” He said in the past he had given prize money to charity and put some into science-related funds. “Prize money should be spent on the common good.” He also praised the funding system in Britain, adding: “I don’t know how I would have fared in the American system.”
John Stein, professor of physiology at Oxford University, said: “This is great news and well deserved. I remember how great was the scoffing in the early 1970s when John first described place cells. ‘Bound to be an artifact’, ‘he clearly underestimates rats’ sense of smell’ were typical reactions. Now, like so many ideas that were at first highly controversial, people say: ‘Well that’s obvious.’”
The remaining half of the prize was shared by May-Britt Moser, 51, and her husband, Edvard, 52, who work at the Norwegian University of Science and Technology in Trondheim. The two met in the 1990s as postdocs in O’Keefe’s lab, where they learned how to record signals from rats’ brains.
May-Britt Moser is only the 11th woman to have won the medicine prize since it was first awarded in 1901. But rarer still are Nobel laureate couples: the Mosers are only the fifth to have won the Nobel prize. The Curie family had a phenomenal record, with Marie and her husband Pierre sharing the physics prize in 1903, and their daughter Irene and her husband Frédéric Joliot sharing the chemistry prize in 1935.
May-Britt Moser was in a meeting when she heard she had won the prize. But her husband was on a plane to Munich and could not be reached. Staff at the Nobel Foundation hoped to have the news announced by the pilot mid-flight. Speaking moments after the award became public, May-Britt said: “I was crying. I was in shock and I’m still in shock. This is so great.”
The couple’s secret, she said, was sharing the same vision. “We love to understand and we do that by talking to each other, talking to other people, and trying to address the questions we are interested in in the best way we can. To be able to discuss this, when you get an idea on the spot instead of planning a meeting in one or two or three weeks, makes a huge difference,” she said.
In the late 1960s, O’Keefe became fascinated with how the brain controls behaviour. He set out to record signals from individual nerve cells in rats’ brains as the animals moved around a room. He discovered that certain nerve cells in the hippocampus fired when the animals reached a specific place in the room. These “place cells”, he showed later, helped the rat build up inner maps of its environment.
More than 30 years later, May-Britt and Edvard Moser, who trained under O’Keefe, were recording brain signals from rats as they moved around. They noticed an extraordinary pattern of activity in a neighbouring part of the brain called the entorhinal cortex. Specific nerve cells sprang into action when the rats passed through different locations. These “grid cells” provided the brain with the equivalent of latitude and longitude, and together with place cells formed an inner GPS in the brain.
Humans are thought to have similar cells in their own brains, and damage to these areas may explain symptoms of dementia and other brain diseases. The early stages of Alzheimer’s can affect the hippocampus and entorhinal cortex, causing people to lose their way and forget their surroundings.
“All three scientists awarded the prize have dramatically changed how we understand the brain’s navigation and memory systems,” said Hugo Spiers, head of the spatial cognition group at UCL. “Grid cells and place cells offer one of the few bridges neuroscientists have linking the cellular level to the cognitive level, as they help explain how individual brain cells help us navigate, remember the past and imagine the future.” | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 41 | https://www.vanderbilt.edu/about/nobel/ | en | Nobel Laureates | [
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] | 2021-07-08T00:00:00 | Six Nobel laureates are affiliated with Vanderbilt University and Vanderbilt University Medical Center. | en | Vanderbilt University | https://www.vanderbilt.edu/about/nobel/ | Al Gore
Former U.S. Vice President Al Gore, along with the Intergovernmental Panel on Climate Change, was awarded the Nobel Peace Prize in 2007 for "efforts to build up and disseminate greater knowledge about man-made climate change, and to lay the foundations for the measures that are needed to counteract such change."
Gore took classes at the Vanderbilt Divinity School and at Vanderbilt Law School in the 1970s.
During his childhood, Gore divided his time between Washington D.C. for school and his familyâs farm in Carthage, Tenn., for summer breaks. Upon the completion of high school, Gore attended Harvard University where he earned a degree in government in June 1969 after writing a senior thesis titled "The Impact of Television on the Conduct of the Presidency, 1947-1969."
Gore opposed the Vietnam War, but said that his sense of civic duty compelled him to enlist in the U.S. Army in August 1969. After basic training, Gore was assigned as a military journalist writing for The Army Flier, the base newspaper at Fort Rucker. With only seven months left in his enlistment, Gore was shipped to Vietnam, arriving in January 1971. He served with the 20th Engineer Brigade in Bien Hoa and at the Army Engineer Command in Long Binh.
When he returned to the States in 1971, he worked as a reporter at the Tennessean. When he was later moved to the city politics beat, Gore uncovered political and bribery cases that led to convictions. While at the Tennessean, Gore, a Baptist, also studied philosophy and phenomenology at Vanderbilt University. In 1974, he enrolled in Vanderbilt's law school.
Gore quit law school in March 1976 to run for the U.S. House from Tennessee. He was elected four times: in 1976, 1978, 1980 and 1982 and the U.S. Senate in 1984 and 1990. He was inaugurated as the forty-fifth vice president of the United States on January 20, 1993, and served eight years.
He is the author of the bestsellers Earth in the Balance and An Inconvenient Truth and is the subject of an Oscar-winning documentary.
Muhammad Yunus
Muhammad Yunus and Grameen Bank were awarded the Nobel Peace Prize in 2006 for "for their efforts to create economic and social development from below."
Yunus received his Ph.D. in economics from Vanderbilt in 1969.
Yunus established the Grameen Bank in Bangladesh in 1983, fueled by the belief that credit is a fundamental human right. His objective was to help poor people escape from poverty by providing loans on terms suitable to them and by teaching them a few sound financial principles so they could help themselves.
From Yunus' personal loan of small amounts of money to destitute basketweavers in Bangladesh in the mid-70s, the Grameen Bank advanced to the forefront of a burgeoning world movement toward eradicating poverty through microlending. Spinoffs of the Grameen Bank model operate in more than 100 countries worldwide.
Born in 1940 in the seaport city of Chittagong, Yunus studied at Dhaka University in Bangladesh, then received a Fulbright scholarship to study economics at Vanderbilt. After earning his Ph.D. in economics from Vanderbilt in 1969, he became an assistant professor of economics at Middle Tennessee State University. He later returned to Bangladesh, where he headed the economics department at Chittagong University.
From 1993 to 1995, Professor Yunus was a member of the International Advisory Group for the Fourth World Conference on Women, a post to which he was appointed by the secretary general of the United Nations. He has served on the Global Commission of Women's Health, the Advisory Council for Sustainable Economic Development and the UN Expert Group on Women and Finance.
In 2007, Yunus returned to Vanderbilt to receive the Nichols-Chancellor's Medal and gave the Senior Day commencement address.
Stanley Cohen
Stanley Cohen and Rita Levi-Montalcini were awarded the Nobel Prize in Physiology or Medicine in 1986 for their discovery of growth factors.
Cohen joined the Vanderbilt University School of Medicine faculty in 1959 and holds the title of Distinguished Professor of Biochemistry, Emeritus.
Cohen was born in Brooklyn, New York in 1922. Both his mother and father were Russian-Jewish emigrants who came to America in the early 1900s. His father was a tailor and his mother a homemaker. Though of limited education themselves, Dr. Cohen wrote in his biography that his parents "instilled in me the values of intellectual achievement and the use of whatever talents I possessed." He was educated in the Brooklyn public school system, but earned a full scholarship to Brooklyn College, where he received his bachelor's degree in 1943 with a double major in chemistry and zoology. After working as a bacteriologist at a milk processing plant to earn money, he received his M.A. in zoology from Oberlin College in 1945. He earned a Ph.D. from the department of biochemistry at the University of Michigan in 1948.
After a short stint at the University of Colorado, he went to Washington University in 1952 to work with Martin Kamen in the Department of Radiology as a postdoctoral fellow of the American Cancer Society. He learned isotope methodology while studying carbon dioxide fixation in frog eggs and embryos. In 1953, he became associated with the Department of Zoology under the leadership of Viktor Hamburger at Washington University and joined Rita Levi-Montalcini to isolate a Nerve Growth Factor (NGF) that she had discovered in certain mouse tumors and to become educated in the field of experimental embryology. Cohen isolated nerve growth factor and then went on to discover epidermal growth factor. He continued his research on cellular growth factors after moving to Vanderbilt University in 1959 as an assistant professor in the Biochemistry Department, exploring the chemistry and biology of epidermal growth factor (EGF). His research on cellular growth factors has proven fundamental to understanding the development of cancer and designing anti-cancer drugs.
Stanford Moore
Stanford Moore, along with Christian Anfinsen and William H. Stein, was awarded the Nobel Prize for Chemistry in 1972 for "contribution to the understanding of the connection between chemical structure and catalytic activity of the active center of the ribonuclease molecule."
Stanford Moore, a Vanderbilt alumnus, spent his life in the Vanderbilt community. During his childhood, his father was a member of the faculty of the Law School and was later a student at the university.
Moore graduated from Vanderbilt (B.A. 1935, summa cum laude ) with a major in chemistry. The faculty recommended him for a Wisconsin Alumni Research Foundation Fellowship, and he earned his Ph.D. in organic chemistry from the University of Wisconsin in 1938.
His thesis research was in biochemistry in the laboratory of Karl Paul Link. Karl Paul Link was a friend of Max Bergmann, who had recently arrived from Germany to lead a laboratory at the Rockefeller Institute for Medical Research in New York.
Through that friendship, Moore was encouraged to join the Bergmann Laboratory in 1939, which was an internationally renowned center of research on the chemistry of proteins and enzymes. During Emil Fischer's last years, Max Bergmann had been his senior research associate, and Bergmann had attracted to Rockefeller a group of versatile chemists, including his future research partner William H. Stein. The advent of World War II drew Moore out of the laboratory to serve as a junior administrative officer in Washington for academic and industrial chemical projects administered by the Office of Scientific Research Development.
After the war, Moore returned to Rockefeller, beginning a collaboration with Stein that led to the development of quantitative chromatographic methods for amino acid analysis that the pair summarized in their Nobel address.
In 1968, Moore returned to Vanderbilt as a visiting professor of health sciences.
Earl W. Sutherland Jr.
Earl Wilbur Sutherland Jr. was awarded the Nobel Prize in Physiology or Medicine in 1971 "for his discoveries concerning the mechanisms of the action of hormones."
Sutherland was born in 1915 in Burlingame, Kansas. Sutherland received his bachelor's degree in chemistry in 1937 from Washburn University (Topeka, Kan.) and earned his medical degree in 1942 from Washington University School of Medicine in St. Louis. After serving as a doctor in World War II, he returned to Washington University as a researcher in the pharmacology laboratory of Nobel laureate Carl Ferdinand Cori.
In 1953, he became director of the department of pharmacology at Western Reserve University (now Case Western Reserve University) in Cleveland, Ohio, where, in 1956, he discovered the role of cyclic AMP in mediating the action of certain hormones.
Sutherland's further research demonstrated the ubiquitous nature and prime importance of this chemical and its associated compounds, notably adenyl cyclase, in all living things. As the result of Sutherland's work and that of those who followed his lead, it became known that hormones are not the sole regulatory substances in the chemistry of living organisms, as had previously been believed. In many cases, necessary cellular reactions are triggered by cyclic AMP, the almost universal "second messenger," responding to the hormonal signal. Sutherland's work on hormones opened up new paths of research into diabetes, cancer, and cholera.
Sutherland was a professor of physiology at Vanderbilt University Medical Center from 1963 to 1973.
He was elected to the National Academy of Sciences in 1966. In addition to the Nobel Prize, Sutherland won the Albert Lasker Award for basic medical research in 1970 and received the National Medal of Science in 1973. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 1 | https://www.nobelprize.org/prizes/lists/nobel-prize-awarded-women/ | en | Nobel Prize awarded women | [
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] | null | [] | null | Nobel Prize awarded women | en | NobelPrize.org | https://www.nobelprize.org/prizes/lists/nobel-prize-awarded-women | The Nobel Prize and the Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel have been awarded to women 65 times between 1901 and 2023. Only one woman, Marie Curie, has been honoured twice, with the Nobel Prize in Physics 1903 and the Nobel Prize in Chemistry 1911. This means that 64 women in total have been awarded the Nobel Prize between 1901 and 2023.
The Nobel Prize in Physics
The Nobel Prize in Physics 2023
“for experimental methods that generate attosecond pulses of light for the study of electron dynamics in matter”
The Nobel Prize in Physics 2020
“for the discovery of a supermassive compact object at the centre of our galaxy”
The Nobel Prize in Physics 2018
“for groundbreaking inventions in the field of laser physics”
“for their method of generating high-intensity, ultra-short optical pulses”
The Nobel Prize in Physics 1963
“for their discoveries concerning nuclear shell structure”
The Nobel Prize in Physics 1903
“in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel”
The Nobel Prize in Chemistry
The Nobel Prize in Chemistry 2022
“for the development of click chemistry and bioorthogonal chemistry”
The Nobel Prize in Chemistry 2020
“for the development of a method for genome editing”
“for the development of a method for genome editing”
The Nobel Prize in Chemistry 2018
“for the directed evolution of enzymes”
The Nobel Prize in Chemistry 2009
“for studies of the structure and function of the ribosome”
The Nobel Prize in Chemistry 1964
“for her determinations by X-ray techniques of the structures of important biochemical substances”
The Nobel Prize in Chemistry 1935
“in recognition of their synthesis of new radioactive elements”
The Nobel Prize in Chemistry 1911
“in recognition of her services to the advancement of chemistry by the discovery of the elements radium and polonium, by the isolation of radium and the study of the nature and compounds of this remarkable element”
The Nobel Prize in Physiology or Medicine
The Nobel Prize in Physiology or Medicine 2023
“for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19”
The Nobel Prize in Physiology or Medicine 2015
“for her discoveries concerning a novel therapy against Malaria”
The Nobel Prize in Physiology or Medicine 2014
“for their discoveries of cells that constitute a positioning system in the brain”
The Nobel Prize in Physiology or Medicine 2009
“for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase”
“for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase”
The Nobel Prize in Physiology or Medicine 2008
“for their discovery of human immunodeficiency virus”
The Nobel Prize in Physiology or Medicine 2004
“for their discoveries of odorant receptors and the organization of the olfactory system”
The Nobel Prize in Physiology or Medicine 1995
“for their discoveries concerning the genetic control of early embryonic development”
The Nobel Prize in Physiology or Medicine 1988
“for their discoveries of important principles for drug treatment”
The Nobel Prize in Physiology or Medicine 1986
“for their discoveries of growth factors”
The Nobel Prize in Physiology or Medicine 1983
“for her discovery of mobile genetic elements”
The Nobel Prize in Physiology or Medicine 1977
“for the development of radioimmunoassays of peptide hormones”
The Nobel Prize in Physiology or Medicine 1947
“for their discovery of the course of the catalytic conversion of glycogen”
The Nobel Prize in Literature
The Nobel Prize in Literature 2022
“for the courage and clinical acuity with which she uncovers the roots, estrangements and collective restraints of personal memory”
The Nobel Prize in Literature 2020
“for her unmistakable poetic voice that with austere beauty makes individual existence universal”
The Nobel Prize in Literature 2018
“for a narrative imagination that with encyclopedic passion represents the crossing of boundaries as a form of life”
The Nobel Prize in Literature 2015
“for her polyphonic writings, a monument to suffering and courage in our time”
The Nobel Prize in Literature 2013
“master of the contemporary short story”
The Nobel Prize in Literature 2009
“who, with the concentration of poetry and the frankness of prose, depicts the landscape of the dispossessed”
The Nobel Prize in Literature 2007
“that epicist of the female experience, who with scepticism, fire and visionary power has subjected a divided civilisation to scrutiny”
The Nobel Prize in Literature 2004
“for her musical flow of voices and counter-voices in novels and plays that with extraordinary linguistic zeal reveal the absurdity of society's clichés and their subjugating power”
The Nobel Prize in Literature 1996
“for poetry that with ironic precision allows the historical and biological context to come to light in fragments of human reality”
The Nobel Prize in Literature 1993
“who in novels characterized by visionary force and poetic import, gives life to an essential aspect of American reality”
The Nobel Prize in Literature 1991
“who through her magnificent epic writing has - in the words of Alfred Nobel - been of very great benefit to humanity”
The Nobel Prize in Literature 1966
“for her outstanding lyrical and dramatic writing, which interprets Israel's destiny with touching strength”
The Nobel Prize in Literature 1945
“for her lyric poetry which, inspired by powerful emotions, has made her name a symbol of the idealistic aspirations of the entire Latin American world”
The Nobel Prize in Literature 1938
“for her rich and truly epic descriptions of peasant life in China and for her biographical masterpieces”
The Nobel Prize in Literature 1928
“principally for her powerful descriptions of Northern life during the Middle Ages”
The Nobel Prize in Literature 1926
“for her idealistically inspired writings which with plastic clarity picture the life on her native island and with depth and sympathy deal with human problems in general”
The Nobel Prize in Literature 1909
“in appreciation of the lofty idealism, vivid imagination and spiritual perception that characterize her writings”
The Nobel Peace Prize
The Nobel Peace Prize 2023
“for her fight against the oppression of women in Iran and her fight to promote human rights and freedom for all”
The Nobel Peace Prize 2021
“for their efforts to safeguard freedom of expression, which is a precondition for democracy and lasting peace”
The Nobel Peace Prize 2018
“for their efforts to end the use of sexual violence as a weapon of war and armed conflict”
The Nobel Peace Prize 2014
“for their struggle against the suppression of children and young people and for the right of all children to education”
The Nobel Peace Prize 2011
“for their non-violent struggle for the safety of women and for women's rights to full participation in peace-building work”
“for their non-violent struggle for the safety of women and for women's rights to full participation in peace-building work”
“for their non-violent struggle for the safety of women and for women's rights to full participation in peace-building work”
The Nobel Peace Prize 2004
“for her contribution to sustainable development, democracy and peace”
The Nobel Peace Prize 2003
“for her efforts for democracy and human rights. She has focused especially on the struggle for the rights of women and children”
The Nobel Peace Prize 1997
“for their work for the banning and clearing of anti-personnel mines”
The Nobel Peace Prize 1992
“for her struggle for social justice and ethno-cultural reconciliation based on respect for the rights of indigenous peoples”
The Nobel Peace Prize 1991
“for her non-violent struggle for democracy and human rights”
The Nobel Peace Prize 1982
“for their work for disarmament and nuclear and weapon-free zones”
The Nobel Peace Prize 1979
“for her work for bringing help to suffering humanity”
The Nobel Peace Prize 1976
“for the courageous efforts in founding a movement to put an end to the violent conflict in Northern Ireland”
“for the courageous efforts in founding a movement to put an end to the violent conflict in Northern Ireland”
The Nobel Peace Prize 1946
“for her lifelong work for the cause of peace”
The Nobel Peace Prize 1931
“for their assiduous effort to revive the ideal of peace and to rekindle the spirit of peace in their own nation and in the whole of mankind”
The Nobel Peace Prize 1905
“for her audacity to oppose the horrors of war”
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 2023
“for having advanced our understanding of women’s labour market outcomes”
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 2019
“for their experimental approach to alleviating global poverty”
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 2009
“for her analysis of economic governance, especially the commons”
To cite this section
MLA style: Nobel Prize awarded women. NobelPrize.org. Nobel Prize Outreach AB 2024. Wed. 24 Jul 2024. <https://www.nobelprize.org/prizes/lists/nobel-prize-awarded-women> | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 0 | 19 | https://colonelunthanksnorwich.com/tag/the-forum-norwich/ | en | COLONEL UNTHANK'S NORWICH | https://secure.gravatar.com/blavatar/4046253e5d67e381c1e8c72f309e6292733647442fd04e4b3ce113332d4a644a?s=200&ts=1721830772 | https://secure.gravatar.com/blavatar/4046253e5d67e381c1e8c72f309e6292733647442fd04e4b3ce113332d4a644a?s=200&ts=1721830772 | [
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] | null | Posts about The Forum Norwich written by reggie unthank | en | https://secure.gravatar.com/blavatar/4046253e5d67e381c1e8c72f309e6292733647442fd04e4b3ce113332d4a644a?s=32 | COLONEL UNTHANK'S NORWICH | https://colonelunthanksnorwich.com/tag/the-forum-norwich/ | The confrontation between the Classical Revival (based on Greco-Roman principles of symmetry and proportion) and the Gothic Revival (based on the pointed arches and pinnacles of English medieval cathedral-building) dominated this country’s architecture in the nineteenth century. There is very little Victorian Gothic in Norwich but the Classical influence endured well into the twentieth century as the preferred style for temples of commerce. It took World War II and the post-war clearances before the modern took hold.
At the beginning of the century, George Skipper designed his masterwork for Norwich Union: “Without any doubt … one of the most convinced Edwardian office buildings [1].
In 1926, FCR Palmer and WFC Holden designed a ‘splendid’ building for the National Westminster Bank in London Street. Pevsner and Wilson wrote that it was modelled on a Wren city church: “One would assign a much earlier date to it [1].”
And as late as 1929 “a kind of Renaissance [1]” style was employed for the large Barclays Bank on Bank Plain that replaced the C18 bank of Gurney & Co, formed as an amalgamation of Quaker banking interests.
Below, the Stuart Court apartments in Recorder Road show that the Arts and Crafts Movement also survived into the C20. These were built in the manner of almshouses by ET Boardman; he had married into the Colman family and designed the Dutch-gabled houses in memory of his brother-in-law James Stuart who had been concerned about the poor quality of housing for the elderly. The Dutch gables are a perfect example of vernacular revival in a city whose population at one time contained one third or more religious refugees from the Spanish Netherlands.
Behind the traditional facade the Stuart apartments were built around reinforced concrete but this material, and metal framework, had been used in the Boardman practice for decades. In fact a more forward-looking kind of architecture – neither Gothic nor Classical but proto-modern in the suppression of detail – had been introduced to the city by Boardman Senior with his factory buildings nearly half a century earlier.
In 1912, Bunting’s Drapers and General Warehousemen of St Stephen’s Street was constructed by Norwich-based architect AF Scott using non-traditional techniques. Here, an internal steel support was clad with stone curtain-walling but there was still a diffidence in giving it a more modern external appearance. Instead, the building was decorated in a genteel Classical Revival style, the stone panels beneath the windows carved with ‘Adam’ swags.
The structure was topped by a cupola of the kind that George Skipper had used as a signature on his buildings around 1900 [3].
After WWI the city’s priority was to build, in Lloyd George’s words, “homes fit for heroes”. This involved massive slum clearance followed by a programme of local authority house-building that led to 40% of the population living in council houses by the end of the 1950s [1]. The most notable of the municipal estates was at Mile Cross, north of the city centre (1918-20). This was the council’s first foray into large estate building, for which they engaged Stanley Adshead, the first Professor of Town Planning at University College London, who laid out the estate on Garden City principles [4].
Variety was achieved by modifying standard house plans. Local architects such as George Skipper (a long way from his ‘fireworks’ of the turn of the century) and AF Scott (better known for his work on Methodist chapels) adapted these to reflect early C19 Norwich neo-Georgian housing; others incorporated Arts and Crafts details, such as pin tiles on the first floor elevation that seem more reminiscent of Kent and Sussex than Norfolk [4].
While social housing was adhering to the traditional, a revolutionary new international movement was evolving. In 1927 the Bauhaus, founded in Germany by Walter Gropius, began teaching a new kind of architecture in which reinforced concrete was used to produce sweeping layers, its minimalist horizontal lines emphasised by long runs of ribbon window.
It would be some years before the International style took hold in Norwich. Diffident nods towards Modernism were provided by the rounded steel windows of the Streamline Moderne version of Art Deco: first at the former Abbey National Building Society offices in London Street …
… and in the Pottergate Tavern.
Pevsner and Wilson [1] presumed the pub to have been designed by J Owen Bond, a protégé of George Skipper, possibly because of the much larger building he is known to have designed with similar Streamline Moderne influences. J Owen, third son of Robert Bond, designed this replacement for his father, whose department store was damaged by bombing in WWII. A follower on Twitter said that her neighbour could see the flames from Arminghall, to the south of the city.
By sticking with its medieval Guildhall throughout the C19, Norwich missed out on the grandiose Victorian town halls erected by its competitors in the industrial north. In the late 1930s Norwich did build a new city hall and Pevsner and Wilson [1] wrote that it “must go down in history as the foremost English public building of between the wars.”
The essentially plain style was borrowed from the Swedish Classical of Stockholm’s City Hall with the colonnaded portico of that city’s Concert Hall. But, because of these backward-looking references, architectural historian Stefan Muthesius felt that the term ‘modern’ didn’t quite apply to Norwich City Hall [5].
Instead, Muthesius awarded the accolade for the city’s first real International Modern-style to David Percival’s City Library, opposite the City Hall. Percival had come from Coventry in 1954, “then the hot-bed of civic-minded modernism”; as Norwich’s new City Architect he designed the new library, which was completed in 1962 and burned down in 1994.
Percival was responsible for introducing mainstream Modernism into Norwich’s postwar public buildings though he strove to soften its hard edges with regional references, especially on domestic-scale projects. By tempering Modernism with the local spirit, Percival is credited with pioneering the Vernacular Revival style [6]. The impact of massed concrete panels on the library, for example, was moderated by pre-cast panels of split-flint cladding (although a glance at the nearby Guildhall shows just how far this was from vernacular techniques).
Perhaps the most famous example of Vernacular Revival in Norwich’s public housing is the Camp Grove scheme off Kett’s Hill. Here, Tayler and Green’s signature decorative brickwork and patterned bargeboards – combined with changes in roof pitch, four different pantiles and 16 types of brick and flint – provide an unexpected degree of variation [7].
In contrast to the City Hall, Norfolk County Hall – built in 1966 in the International Modern style – never attracted much praise. Pevsner and Wilson dismissed it as “an ordinary steel-framed office tower.”
Other forays into the International Style, such as the eight-storey block to the right of Skipper’s building for Norwich Union in Surrey Street, were also poorly received. Never one for mincing his words, Ian Nairn thought it “a completely anonymous slab” [8]. Evidently not a style for an ancient county town.
The 1945 City Plan envisaged a post-war Norwich in which the car played a major part [9]. In 1971 the inner ring road split Norwich-over-the-Water: the two halves were to receive different treatments. The northern half was to be the site of the Anglia Square development with a large cinema, offices, multi-storey parking plus that symbol of the new age – a pedestrian shopping precinct. Her Majesty’s Stationery Office at Sovereign House was a key part of the scheme and it was this New Brutalist building that marked the rise and fall of the site as a whole – the HMSO pulling out well short of its 40-year lease, leaving the building derelict by the new millennium.
Currently, we await the outcome of a planning application to redevelop the entire Anglia Square site with 12-storey blocks and a 20-storey tower. The scale of the proposal shows that no lessons have been learned from the brief history of Anglia Square in which an ‘out of scale’ [10] development was imposed upon a historic site. For an appreciation of the Gildencroft area see [11].
There was no such grand project on the city side of the inner ring road and this part of Norwich-over-the Water fared better.
In this snapshot from the evolution of office building, the 1960s curtain-walling of St Mary’s House on the far side of the St Crispin’s roundabout was succeeded by the 1970s layers of concrete and glass in St Crispin’s House, built for HMSO when permission was denied for an extension to Sovereign House at Anglia Square. A starker contrast was between the Brutalist concrete of St Crispin’s House juxtaposed against the red brickwork of 1990s Cavell House. This was part of what has been recognised as a “welcome softening of approach since the late 1980s” [1] for, as part of the Postmodern credo, Cavell House reacted against Modernism by providing local context missing from Anglia Square. Here, the windows on the upper floor referenced the long through-light weavers’ windows once common in this, the heart of the city’s textile trade. The flat arches heading the lower windows were borrowed from Sherwyn House, an old brush factory (now renovated apartments by Feilden & Mawson) further down St George’s Street. (See [12] for more about this district).
There was no such confrontation between new and old at the University of East Anglia where Denys Lasdun in the 1960s (replaced by Bernard Feilden in 1969), and Rick Mather in the 1980s, were able to build on a green-field site without planning constraints [1]. A Teaching Wall snaked through the original scheme, separated from the residential blocks by a first-floor walkway. Lasdun’s residences consisted of a cascade of study/bedrooms forming the ziggurats that have become emblematic of the UEA.
As part of the second-phase of the masterplan, Rick Mather’s Constable Terrace echoed the serpentine form of Lasdun’s original layout but its smooth white rendering was a deliberate break from the hardline grayness of the earlier student housing.
Facing Constable terrace is the Sainsbury Centre for the Visual Arts (1974-8). Designed by Norman Foster and Wendy Cheeseman, the tubular steel exoskeleton represents what is probably this country’s first use of High-Tech industrial architecture applied to a museum or gallery. The superstructure encloses a magnificent open space, some 130 metres long, that accommodates Sir Robert and Lady Sainsbury’s art collection, along with university teaching areas.
Just squeaking in at the close of the twentieth century The Forum, funded by the Millennium Commission, was begun in 1999. Designed by Hopkins and Associates the Forum replaced David Percival’s flint-clad Central Library of the 1960s, destroyed by fire. This ‘Son of High Tech’ building [2] houses BBC studios, a restaurant, a café and what has become the most popular library in the country. The jaws of the horseshoe-shaped plan are closed by a glazed wall that – in a display of good manners – withdraws from, rather than confronts, the glorious St Peter Mancroft opposite.
©Reggie Unthank 2020
Sources
Nikolaus Wilson and Bill Wilson (1997). The Buildings of England. Norfolk 1: Norwich and the North-East. Pub: Yale University Press.
Vic Nierop-Reading (2013). Twentieth-century Norwich in a nutshell. Norfolk Historic Buildings Group Newsletter No.25 pp 14-15.
https://colonelunthanksnorwich.com/2017/02/15/the-flamboyant-mr-skipper/
Mary Ash and Paul Burall (2019). Norwich leading the Way: Social Housing. Pub: The Norwich Society.
Stefan Muthesius (2004). Architecture since 1800. In, ‘Norwich since 1550’ by Carole Rawcliffe and Richard Wilson pp 323-342. Pub: Hambledon and London.
John Boughton (2018). Municipal Dreams: The Rise and Fall of Council Housing. Pub: Verso.
Elain Harwood and Alan Powers (1998). Tayler and Green, Architects 1938-1973: The Spirit of Place in Modern Housing. Pub: The Prince of Wales’s Institute of Architecture.
Ian Nairn (1967). Norwich: Regional Capital. Reprinted, with an introduction by Owen Hatherley, in Nairn’s Towns (2013). Pub: Notting Hill Editions.
CH James and SR Pierce (1945). City Plan of Norwich 1945. Pub: Norwich Corporation.
Charles McKean (1982). Architectural Guide to Cambridge and East Anglia since 1920. Pub: ERA Publication Board.
https://colonelunthanksnorwich.com/2017/10/15/gildencroft-and-psychogeography/
https://colonelunthanksnorwich.com/2017/11/15/reggie-through-the-underpass/ | ||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 22 | https://www.cnn.com/2023/10/02/europe/nobel-prize-medicine-mrna-covid-vaccines-2023-intl-scn/index.html | en | Nobel Prize in medicine won by two scientists for ‘groundbreaking findings’ on mRNA Covid-19 vaccines | [
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] | 2023-10-02T00:00:00 | This year’s Nobel Prize in physiology or medicine has been awarded to Katalin Karikó and Drew Weissman for their work on mRNA vaccines, a crucial tool in curtailing the spread of Covid-19. | en | /media/sites/cnn/apple-touch-icon.png | CNN | https://www.cnn.com/2023/10/02/europe/nobel-prize-medicine-mrna-covid-vaccines-2023-intl-scn/index.html | Editor’s Note: Sign up for CNN’s Wonder Theory science newsletter. Explore the universe with news on fascinating discoveries, scientific advancements and more.
This year’s Nobel Prize in physiology or medicine has been awarded to Katalin Karikó and Drew Weissman for their work on mRNA vaccines, a crucial tool in curtailing the spread of Covid-19.
The Nobel Prize committee announced the prestigious honor, seen as the pinnacle of scientific achievement, in Sweden on Monday.
It praised the scientists’ “groundbreaking findings,” which the committee said “fundamentally changed our understanding of how mRNA interacts with our immune system.”
Karikó and Weissman published their results in a 2005 paper that received little attention at the time, it said, but later laid the foundation for critically important developments that served humanity during the coronavirus pandemic.
“The laureates contributed to the unprecedented rate of vaccine development during one of the greatest threats to human health in modern times,” the committee added in a statement.
Rickard Sandberg, a member of the Nobel Prize in medicine committee, said, “mRNA vaccines together with other Covid-19 vaccines have been administered over 13 billion times. Together they have saved millions of lives, prevented severe Covid-19, reduced the overall disease burden and enabled societies to open up again.”
Karikó, a Hungarian-American biochemist, and Weissman, an American physician, are both professors at the University of Pennsylvania. Their work became the foundation for Pfizer and its Germany-based partner BioNTech, as well as Moderna, to use a new approach to produce vaccines that use messenger RNA or mRNA.
The revolutionary technology has opened a new chapter of medicine. It can potentially be harnessed to develop vaccines against other diseases like malaria, RSV and HIV. It also offers a new approach to infectious disease like cancer, with the prospect of personalized vaccines.
Messenger RNA
Researchers often compare DNA to a massive recipe book with all the instructions for life. Messenger RNA is a temporary single strand of the genetic code that cells can “read” and use to make a protein – a bit like a handwritten copy of a recipe in the cookbook analogy.
In the case of mRNA vaccines, the temporary genetic code is used to tell cells to make what looks like a piece of virus, so the body produces antibodies and special immune system cells in response. Unlike other vaccines, a live or attenuated virus is not injected or required at any point.
All that is needed is the genetic sequence. Vaccine makers don’t even need the virus itself – just the sequence.
“The impressive flexibility and speed with which mRNA vaccines can be developed pave the way for using the new platform also for vaccines against other infectious diseases,” the Nobel committee said, adding that the technology “may also be used to deliver therapeutic proteins and treat some cancer types.”
J. Larry Jameson, executive vice president of UPenn’s School of Medicine, praised the scientists’ work which he said “changed the world.”
“During the biggest public health crisis of our lifetimes, vaccine developers relied upon the discoveries by Dr. Weissman and Dr. Karikó, which saved innumerable lives and paved a path out of the pandemic,” Jameson said in a statement. “More than 15 years after their visionary laboratory partnership, Kati and Drew have made an everlasting imprint on medicine.”
The Nobel Prize announcements began in Sweden Monday and will continue throughout this week and into next, with awards in physics, chemistry, literature and economics set to be announced in the coming days. The Nobel Peace Prize will be announced in Norway on Friday.
The road to the Nobel
Karikó, 68, began her career in her native Hungary in the 1970s, when mRNA research was new. She, her husband and young daughter left for the United States after she received an invitation from Temple University in Philadelphia. They sold their car, Karikó told The Guardian, and stuffed the money – an equivalent of about $1,200 – in their daughter’s teddy bear for safekeeping.
“We had just moved into our new apartment, our daughter was 2 years old, everything was so good, we were happy,” Karikó told the Hungarian news site G7 of her family’s departure. “But we had to go.”
She continued her research at Temple, before joining the UPenn’s School of Medicine in 19xx. But by then, the initial excitement surrounding mRNA research had started to fizz out. Hope turned to skepticism: Karikó’s idea that it could be used to fight disease was deemed too radical – and too financially risky to fund.
She applied to grant after grant, but a string of rejections meant that in 1995, she was demoted from her position at UPenn. She was also diagnosed with cancer at the same time.
“It was difficult because people did not believe that messenger RNA can be a therapy,” Karikó told CNN, in an interview during the pandemic in December 2020.
But she stuck at it. “Together with my colleague, Drew Weissman, at the University of Pennsylvania, we developed this method where we changed one component in the RNA which made it less immunogenic. It is possible to use it for different kinds of therapies, Karikó said.
Karikó and Weissman met by chance in the late 1990s while photocopying research papers. In 2005, they published their key discovery: mRNA could be altered and delivered effectively into the body to activate the body’s protective immune system.
Weissman told CNN that their technology is much more efficient than traditional methods of producing vaccines.
“When the Chinese released the sequence of the SARS-CoV-2 virus, we started the process of making RNA the next day. A couple weeks later, we were injecting animals with the vaccine,” he said.
At the time Karikó said she was not at all surprised by the successful results of the trials conducted by Pfizer and Moderna. “I expected that it would work, because we already had enough experiments,” she said.
She celebrated the successful trial results with a bag of Goobers, chocolate-covered peanuts, her favorite candy. “I’m not an exuberant person,” Karikó told CNN at the time. | ||||
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] | 1999-11-05T00:00:00+00:00 | Nobel Prize - Medicine, Research, Discovery: The table provides a chronological list of recipients of the Nobel Prize for Physiology or Medicine. | en | /favicon.png | Encyclopedia Britannica | https://www.britannica.com/topic/Nobel-Prize/Physiology-or-Medicine | 1901 Emil von Behring Germany work on serum therapy 1902 Sir Ronald Ross U.K. discovery of how malaria enters an organism 1903 Niels Ryberg Finsen Denmark treatment of skin diseases with light 1904 Ivan Pavlov Russia work on the physiology of digestion 1905 Robert Koch Germany tuberculosis research 1906 Camillo Golgi Italy work on the structure of the nervous system Santiago Ramón y Cajal Spain work on the structure of the nervous system 1907 Alphonse Laveran France discovery of the role of protozoans in diseases 1908 Paul Ehrlich Germany work on immunity Élie Metchnikoff Russia work on immunity 1909 Emil Theodor Kocher Switzerland physiology, pathology, and surgery of the thyroid gland 1910 Albrecht Kossel Germany researches in cellular chemistry 1911 Allvar Gullstrand Sweden work on dioptrics of the eye 1912 Alexis Carrel France work on vascular suture; transplantation of organs 1913 Charles Richet France work on anaphylaxis 1914 Robert Bárány Austria-Hungary work on vestibular apparatus 1919 Jules Bordet Belgium work on immunity factors in blood serum 1920 August Krogh Denmark discovery of the capillary motor-regulating mechanism 1922 A.V. Hill U.K. discoveries concerning heat production in muscles Otto Meyerhof Germany work on metabolism of lactic acid in muscles 1923 Sir Frederick Grant Banting Canada discovery of insulin J.J.R. Macleod U.K. discovery of insulin 1924 Willem Einthoven Netherlands discovery of electrocardiogram mechanism 1926 Johannes Fibiger Denmark contributions to cancer research 1927 Julius Wagner-Jauregg Austria work on malaria inoculation in dementia paralytica 1928 Charles-Jules-Henri Nicolle France work on typhus 1929 Christiaan Eijkman Netherlands discovery of the antineuritic vitamin Sir Frederick Gowland Hopkins U.K. discovery of growth-stimulating vitamins 1930 Karl Landsteiner U.S. discovery of human blood groups 1931 Otto Warburg Germany discovery of the nature and action of the respiratory enzyme 1932 Edgar Douglas Adrian, 1st Baron Adrian U.K. discoveries regarding function of neurons Sir Charles Scott Sherrington U.K. discoveries regarding function of neurons 1933 Thomas Hunt Morgan U.S. heredity transmission functions of chromosomes 1934 George Richards Minot U.S. discoveries concerning liver treatment for anemia William P. Murphy U.S. discoveries concerning liver treatment for anemia George H. Whipple U.S. discoveries concerning liver treatment for anemia 1935 Hans Spemann Germany organizer effect in embryos 1936 Sir Henry Dale U.K. work on chemical transmission of nerve impulses Otto Loewi Germany work on chemical transmission of nerve impulses 1937 Albert Szent-Györgyi Hungary work on biological combustion 1938 Corneille Heymans Belgium discovery of the role of sinus and aortic mechanisms in respiration regulation 1939 Gerhard Domagk (declined) Germany antibacterial effect of Prontosil 1943 Henrik Dam Denmark discovery of vitamin K Edward Adelbert Doisy U.S. discovery of the chemical nature of vitamin K 1944 Joseph Erlanger U.S. researches on differentiated functions of nerve fibres Herbert Spencer Gasser U.S. researches on differentiated functions of nerve fibres 1945 Sir Ernst Boris Chain U.K. discovery of penicillin and its curative value Sir Alexander Fleming U.K. discovery of penicillin and its curative value Howard Walter Florey, Baron Florey Australia discovery of penicillin and its curative value 1946 Hermann Joseph Muller U.S. production of mutations by X-radiation 1947 Carl and Gerty Cori U.S. discovery of how glycogen is catalytically converted Bernardo Alberto Houssay Argentina pituitary hormone function in sugar metabolism 1948 Paul Hermann Müller Switzerland properties of DDT 1949 António Egas Moniz Portugal therapeutic value of leucotomy in psychoses Walter Rudolf Hess Switzerland discovery of functions of the interbrain 1950 Philip Showalter Hench U.S. research on adrenal cortex hormones, their structure and biological effects Edward Calvin Kendall U.S. research on adrenal cortex hormones, their structure and biological effects Tadeus Reichstein Switzerland research on adrenal cortex hormones, their structure and biological effects 1951 Max Theiler South Africa yellow fever discoveries 1952 Selman Abraham Waksman U.S. discovery of streptomycin 1953 Sir Hans Adolf Krebs U.K. discovery of the citric acid cycle in metabolism of carbohydrates Fritz Albert Lipmann U.S. discovery of coenzyme A in metabolism of carbohydrates 1954 John Franklin Enders U.S. cultivation of the poliomyelitis virus in tissue cultures Frederick Chapman Robbins U.S. cultivation of the poliomyelitis virus in tissue cultures Thomas H. Weller U.S. cultivation of the poliomyelitis virus in tissue cultures 1955 Axel Hugo Teodor Theorell Sweden nature and mode of action of oxidation enzymes 1956 André F. Cournand U.S. discoveries concerning heart catheterization and circulatory changes Werner Forssmann West Germany discoveries concerning heart catheterization and circulatory changes Dickinson Woodruff Richards U.S. discoveries concerning heart catheterization and circulatory changes 1957 Daniel Bovet Italy production of synthetic curare 1958 George Wells Beadle U.S. genetic regulation of chemical processes Joshua Lederberg U.S. genetic recombination Edward L. Tatum U.S. genetic regulation of chemical processes 1959 Arthur Kornberg U.S. work on producing nucleic acids artificially Severo Ochoa U.S. work on producing nucleic acids artificially 1960 Sir Macfarlane Burnet Australia acquired immunity to tissue transplants Sir Peter B. Medawar U.K. acquired immunity to tissue transplants 1961 Georg von Békésy U.S. functions of the inner ear 1962 Francis Harry Compton Crick U.K. discoveries concerning the molecular structure of DNA James Dewey Watson U.S. discoveries concerning the molecular structure of DNA Maurice Wilkins U.K. discoveries concerning the molecular structure of DNA 1963 Sir John Carew Eccles Australia study of the transmission of impulses along a nerve fibre Sir Alan Hodgkin U.K. study of the transmission of impulses along a nerve fibre Sir Andrew Fielding Huxley U.K. study of the transmission of impulses along a nerve fibre 1964 Konrad Bloch U.S. discoveries concerning cholesterol and fatty acid metabolism Feodor Lynen West Germany discoveries concerning cholesterol and fatty acid metabolism 1965 François Jacob France discoveries concerning regulatory activities of body cells André Lwoff France discoveries concerning regulatory activities of body cells Jacques Monod France discoveries concerning regulatory activities of body cells 1966 Charles B. Huggins U.S. research on causes and treatment of cancer Peyton Rous U.S. research on causes and treatment of cancer 1967 Ragnar Arthur Granit Sweden discoveries about chemical and physiological visual processes in the eye Haldan Keffer Hartline U.S. discoveries about chemical and physiological visual processes in the eye George Wald U.S. discoveries about chemical and physiological visual processes in the eye 1968 Robert William Holley U.S. deciphering the genetic code Har Gobind Khorana U.S. deciphering the genetic code Marshall Warren Nirenberg U.S. deciphering the genetic code 1969 Max Delbrück U.S. research and discoveries concerning viruses and viral diseases A.D. Hershey U.S. research and discoveries concerning viruses and viral diseases Salvador Luria U.S. research and discoveries concerning viruses and viral diseases 1970 Julius Axelrod U.S. discoveries concerning the chemistry of nerve impulse transmission Ulf von Euler Sweden discoveries concerning the chemistry of nerve impulse transmission Sir Bernard Katz U.K. discoveries concerning the chemistry of nerve impulse transmission 1971 Earl W. Sutherland, Jr. U.S. action of hormones 1972 Gerald Maurice Edelman U.S. research on the chemical structure of antibodies Rodney Robert Porter U.K. research on the chemical structure of antibodies 1973 Karl von Frisch Austria discoveries in animal behaviour patterns Konrad Lorenz Austria discoveries in animal behaviour patterns Nikolaas Tinbergen U.K. discoveries in animal behaviour patterns 1974 Albert Claude U.S. research on structural and functional organization of cells Christian René de Duve Belgium research on structural and functional organization of cells George E. Palade U.S. research on structural and functional organization of cells 1975 David Baltimore U.S. interaction between tumour viruses and the genetic material of the cell Renato Dulbecco U.S. interaction between tumour viruses and the genetic material of the cell Howard Martin Temin U.S. interaction between tumour viruses and the genetic material of the cell 1976 Baruch S. Blumberg U.S. studies of the origin and spread of infectious diseases D. Carleton Gajdusek U.S. studies of the origin and spread of infectious diseases 1977 Roger Charles Louis Guillemin U.S. research on pituitary hormones Andrew Victor Schally U.S. research on pituitary hormones Rosalyn S. Yalow U.S. development of radioimmunoassay 1978 Werner Arber Switzerland discovery and application of enzymes that fragment DNA Daniel Nathans U.S. discovery and application of enzymes that fragment DNA Hamilton Othanel Smith U.S. discovery and application of enzymes that fragment DNA 1979 Allan MacLeod Cormack U.S. development of the CAT scan Sir Godfrey Newbold Hounsfield U.K. development of the CAT scan 1980 Baruj Benacerraf U.S. investigations of genetic control of the response of the immune system to foreign substances Jean-Baptiste-Gabriel-Joachim Dausset France investigations of genetic control of the response of the immune system to foreign substances George Davis Snell U.S. investigations of genetic control of the response of the immune system to foreign substances 1981 David Hunter Hubel U.S. processing of visual information by the brain Roger Wolcott Sperry U.S. functions of the cerebral hemispheres Torsten Nils Wiesel Sweden processing of visual information by the brain 1982 Sune K. Bergström Sweden biochemistry and physiology of prostaglandins Bengt Ingemar Samuelsson Sweden biochemistry and physiology of prostaglandins John Robert Vane U.K. biochemistry and physiology of prostaglandins 1983 Barbara McClintock U.S. discovery of mobile plant genes that affect heredity 1984 Niels K. Jerne U.K.-Denmark theory and development of a technique for producing monoclonal antibodies Georges J.F. Köhler West Germany theory and development of a technique for producing monoclonal antibodies César Milstein Argentina theory and development of a technique for producing monoclonal antibodies 1985 Michael S. Brown U.S. discovery of cell receptors relating to cholesterol metabolism Joseph L. Goldstein U.S. discovery of cell receptors relating to cholesterol metabolism 1986 Stanley Cohen U.S. discovery of chemical agents that help regulate the growth of cells Rita Levi-Montalcini Italy discovery of chemical agents that help regulate the growth of cells 1987 Tonegawa Susumu Japan study of genetic aspects of antibodies 1988 Sir James Black U.K. development of new classes of drugs for combating disease Gertrude Belle Elion U.S. development of new classes of drugs for combating disease George Herbert Hitchings U.S. development of new classes of drugs for combating disease 1989 J. Michael Bishop U.S. study of cancer-causing genes (oncogenes) Harold Varmus U.S. study of cancer-causing genes (oncogenes) 1990 Joseph E. Murray U.S. development of kidney and bone marrow transplants E. Donnall Thomas U.S. development of kidney and bone marrow transplants 1991 Erwin Neher Germany discovery of how cells communicate, as related to diseases Bert Sakmann Germany discovery of how cells communicate, as related to diseases 1992 Edmond H. Fischer U.S. discovery of the class of enzymes called protein kinases Edwin Gerhard Krebs U.S. discovery of the class of enzymes called protein kinases 1993 Richard J. Roberts U.K. discovery of "split," or interrupted, genetic structure Phillip A. Sharp U.S. discovery of "split," or interrupted, genetic structure 1994 Alfred G. Gilman U.S. discovery of cell signalers called G-proteins Martin Rodbell U.S. discovery of cell signalers called G-proteins 1995 Edward B. Lewis U.S. identification of genes that control the body's early structural development Christiane Nüsslein-Volhard Germany identification of genes that control the body's early structural development Eric F. Wieschaus U.S. identification of genes that control the body's early structural development 1996 Peter C. Doherty Australia discovery of how the immune system recognizes virus-infected cells Rolf M. Zinkernagel Switzerland discovery of how the immune system recognizes virus-infected cells 1997 Stanley B. Prusiner U.S. discovery of the prion, a type of disease-causing protein 1998 Robert F. Furchgott U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system Louis J. Ignarro U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system Ferid Murad U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system 1999 Günter Blobel U.S. discovery that proteins have signals governing cellular organization 2000 Arvid Carlsson Sweden discovery of how signals are transmitted between nerve cells in the brain Paul Greengard U.S. discovery of how signals are transmitted between nerve cells in the brain Eric Kandel U.S. discovery of how signals are transmitted between nerve cells in the brain 2001 Leland H. Hartwell U.S. discovery of key regulators of the cell cycle R. Timothy Hunt U.K. discovery of key regulators of the cell cycle Sir Paul M. Nurse U.K. discovery of key regulators of the cell cycle 2002 Sydney Brenner U.K. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) H. Robert Horvitz U.S. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) John E. Sulston U.K. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) 2003 Paul Lauterbur U.S. development of magnetic resonance imaging (MRI) Sir Peter Mansfield U.K. development of magnetic resonance imaging (MRI) 2004 Richard Axel U.S. discovery of odorant receptors and the organization of the olfactory system Linda B. Buck U.S. discovery of odorant receptors and the organization of the olfactory system 2005 Barry J. Marshall Australia discovery of bacteria's role in peptic ulcer disease J. Robin Warren Australia discovery of bacteria's role in peptic ulcer disease 2006 Andrew Z. Fire U.S. discovery of RNA interference—gene silencing by double-stranded RNA Craig C. Mello U.S. discovery of RNA interference—gene silencing by double-stranded RNA 2007 Mario R. Capecchi U.S. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells Sir Martin J. Evans U.K. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells Oliver Smithies U.S. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells 2008 Françoise Barré-Sinoussi France discovery of human immunodeficiency virus Luc Montagnier France discovery of human immunodeficiency virus Harald zur Hausen Germany discovery of human papilloma viruses causing cervical cancer 2009 Elizabeth H. Blackburn U.S. discovery of how chromosomes are protected by telomeres and the enzyme telomerase Carol W. Greider U.S. discovery of how chromosomes are protected by telomeres and the enzyme telomerase 2010 Robert Edwards U.K. development of in vitro fertilization 2012 Sir John Bertrand Gurdon U.K. discovery that mature cells can be reprogrammed to become pluripotent Shinya Yamanaka Japan discovery that mature cells can be reprogrammed to become pluripotent 2013 James E. Rothman U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells Randy W. Schekman U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells Thomas C. Südhof Germany/U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells 2014 Edvard I. Moser Norway discoveries of cells that constitute a positioning system in the brain May-Britt Moser Norway discoveries of cells that constitute a positioning system in the brain John O'Keefe U.S./U.K. discoveries of cells that constitute a positioning system in the brain 2015 William C. Campbell Ireland discoveries concerning a novel therapy against infections caused by roundworm parasites Ōmura Satoshi Japan discoveries concerning a novel therapy against infections caused by roundworm parasites Tu Youyou China discoveries concerning a novel therapy against malaria 2016 Yoshinori Ohsumi Japan discoveries of mechanisms for autophagy 2017 Jeffrey C. Hall U.S. discoveries of molecular mechanisms controlling the circadian rhythm Michael Rosbash U.S. discoveries of molecular mechanisms controlling the circadian rhythm Michael W. Young U.S. discoveries of molecular mechanisms controlling the circadian rhythm 2018 James P. Allison U.S. discovery of cancer therapy by inhibition of negative immune regulation Honjo Tasuku Japan discovery of cancer therapy by inhibition of negative immune regulation 2019 William G. Kaelin, Jr. U.S. discoveries of how cells sense and adapt to oxygen availability Peter J. Ratcliffe U.K. discoveries of how cells sense and adapt to oxygen availability Gregg L. Semenza U.S. discoveries of how cells sense and adapt to oxygen availability 2020 Harvey J. Alter U.S. discovery of hepatitis C virus Michael Houghton U.K. discovery of hepatitis C virus Charles M. Rice U.S. discovery of hepatitis C virus 2021 David Julius U.S. discoveries of receptors for temperature and touch Ardem Patapoutian Leb./U.S. discoveries of receptors for temperature and touch 2022 Svante Pääbo Sweden discoveries concerning the genomes of extinct hominins and human evolution 2023 Katalin Karikó Hungary/U.S. discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19 | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 75 | https://www.acs.org/education/whatischemistry/women-scientists/rosalyn-sussman-yalow.html | en | American Chemical Society | [
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] | null | [] | null | In 1977, Rosalyn Yalow became the second woman to win a Nobel prize in medicine for co-developing radio-immunoassay (RIA). | en | https://assetscloud.acs.org/v2.0/acs-bootstrap/images/favicon.ico | American Chemical Society | https://www.acs.org/education/whatischemistry/women-scientists/rosalyn-sussman-yalow.html | In 1977, Rosalyn Yalow became the second woman to win a Nobel prize in medicine for co-developing radio-immunoassay (RIA), a groundbreaking technique that uses radioactive isotopes to quickly and precisely measure concentrations of hormones, vitamins, viruses, enzymes, drugs, and hundreds more substances. The technique is so sensitive that it can detect a teaspoonful of sugar in a body of water 62 miles long.
As a result of Yalow’s work, many diseases and conditions can be diagnosed, treated, or tested. Children with dwarfism can be treated with human growth hormones; fetuses are checked for serious deformities; newborns are tested to prevent retardation; blood banks are screened for diseases; and athletes are tested for drug abuse.
Born in Bronx, NY, Yalow’s interest in chemistry began at Walton High School. By the time she got to Hunter College, an all-women’s school in New York (now part of the City University of New York), two professors managed to pique her interest in physics, influencing her decision to switch majors.
Yalow received her master’s degree in 1942 and Ph.D. in 1945. After a few jobs in electrical engineering and teaching, she decided to devote her career to full-time research. In 1950, Yalow began working with physician Solomon Berson with whom she gained clinical expertise while strengthening her physics, math, and chemistry. Together they discovered new ways to use radioactive isotopes to measure blood, study iodine metabolism, and diagnose thyroid diseases.
Later they decided to apply their methods to hormones, one of the most important classes of small peptides. Because insulin was the most readily-available hormone in a highly-purified form, the scientists began investigating the adult onset of diabetes. Yalow also had a personal interest in this area because her husband, Aaron, was diabetic. Among the endocrine gland disorders, diabetes affects the greatest number of people, making insulin uniquely important. Death is unavoidable without insulin and its ability to lower blood sugar.
Using radioisotopes, Yalow and Berson discovered the need to detect insulin antibodies at low concentrations to measure circulating insulin. Upon discovering that globulins (serum proteins) bound radioactive insulin in the blood of insulin-treated diabetics, they concluded that insulin injections immunized patients so that they develop insulin-binding antibodies, which keeps the insulin molecules in the bloodstream.
This was the first evidence that very small proteins could stimulate an immunologic response, and demonstrated how remarkably sensitive the radioisotopic technique is in measuring incredibly low concentrations of substances. In 1959, Yalow and Berson published their proof of studying the primary reaction of antigen with antibody using the radioisotopic method, which they labeled radioimmunoassay (RIA).
Before this revolutionary breakthrough, scientists could only analyze reactions between antigens and antibodies and those that produced visible precipitation or other evidence, such as the clumping of red blood cells. The RIA method revolutionized endocrinology—the study of ductless glands and hormones—and the treatment of disorders like diabetes. For the first time, doctors could diagnose conditions caused by minute changes in hormones and treat conditions with hormones.
In 1968, Yalow became a research professor at Mt. Sinai School of Medicine and chief of Nuclear Medicine Service at the Veterans Administration Hospital. For her work, she was recognized with the Albert Lasker Prize for Basic Medical Research and the following year she was awarded the Nobel Prize with Andrew V. Schally and Roger Guillemin for their work on radioimmunoassay. Berson was not recognized, because he died before the award was announced.
See more Notable Women Scientists in History | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 63 | https://www.mcgill.ca/oss/article/medical-contributors/dr-ralph-steinman-nobel-prize-winning-scientist-who-became-own-patient | en | The Nobel Prize Winning Scientist Who Became His Own Patient | [
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] | null | [] | 2024-02-09T16:39:48-05:00 | For over 100 years the Nobel foundation has recognized outstanding individuals for contributions to their respective fields; however, the rules stipulate that prizes cannot be awarded posthumously. But in October 2011 an exception was made for an exceptional individual: Dr. Ralph Steinman was awarded the joint Nobel Prize in Physiology or Medicine three days after he died of pancreatic cancer. At the time of the announcement, the news of his death had not yet reached the Nobel committee. So they decided that his wife and children would be able to accept his prize on his behalf. But the story doesn’t end there; Steinman had been battling pancreatic cancer for over 4 years and was treating himself using exactly what the Nobel committee was awarding him for – his 40-year career in researching a previously unknown immune system component he called ‘dendritic cells’. Steinman, a Montreal native and McGill alumnus, was jointly credited with the discovery of dendritic cells in 1973 and spent the rest of his career researching how these special cells might be used to fight difficult diseases like HIV and cancer. Dendritic cells, so named because of their tree-like shape, mediate communication between harmful antigens (molecules that stimulate the immune system) and lymphatic T-cells (white blood cells that activate molecules to fight off these antigens). Steinman showed that these dendritic cells are able to capture invaders, like the common cold virus, and signal specific lymphocytes to destroy them. However, cancer is not like the common cold. Tumor antigens released from cancer cells evade the immune system by either eliminating or hiding from our defensive T-cells. A common way they do this is by activating checkpoint pathways, which tell the body to “turn off” active white blood cells, preventing them from destroying the invading cancer cells. Our greatest weapon against them, chemotherapy, works like a bomb: it blasts through the entire body directly destroying cancerous cells, but is not very selective and many healthy cells are destroyed as well. But thanks to research like Steinman’s, cancer immunotherapy treatments can harness the selective abilities of our natural immune system, and fight back with extreme precision. Immunotherapy vaccinations would manipulate dendritic cells to capture tumor antigens and present them to cancer-specific lymphocytes thereby improving the ability of the body to find and destroy tricky cancer cells with much better accuracy than chemotherapy. However, unlike chemotherapy, which works relatively quickly, immunotherapy builds the body’s immune system over time, time that patients often do not have, especially if the treatment should fail. Furthermore, it appears that not all patients respond in the same way. It has been estimated that currently about 10% of cancer patients can benefit from immunotherapy treatments. But this number is expected to grow as more research unveils how these mechanisms work. Thus in 2007 when Steinman received his cancer diagnosis with an estimated 6 months to live, he set to work right away, sending samples of his golf-ball sized tumor across the globe to several colleagues in immunotherapy labs. Even at the time Steinman knew he was perhaps a decade or two too early for this kind of treatment; we now know there are dozens of kinds of dendritic cells which target different antigens, whereas back then they were essentially taking shots in the dark. Even so, he put his faith behind his research and in his last experiment he became his own patient. In total, he was treated with 8 different FDA-approved cancer vaccines in addition to several rounds of chemotherapy. He managed to prolong his life three and a half years longer than predicted and maintained good physical health for most of it. But without another patient to compare, and with the hasty time taken in between treatments, it’s very difficult to tell what exactly was keeping Ralph Steinman alive. Eventually the cancer stopped responding to the vaccines he was given and the disease spread throughout his whole body. He passed away on September 30, 2011, just three days shy of knowing that he had been awarded the most prestigious mark of scientific achievement. Now he stands as the only deceased recipient of a Nobel prize who actually became a patient of his own research. I’d say that’s well worth the exception. @CassandraLee | en | Office for Science and Society | https://www.mcgill.ca/oss/article/medical-contributors/dr-ralph-steinman-nobel-prize-winning-scientist-who-became-own-patient | For over 100 years the Nobel foundation has recognized outstanding individuals for contributions to their respective fields; however, the rules stipulate that prizes cannot be awarded posthumously. But in October 2011 an exception was made for an exceptional individual: Dr. Ralph Steinman was awarded the joint Nobel Prize in Physiology or Medicine three days after he died of pancreatic cancer. At the time of the announcement, the news of his death had not yet reached the Nobel committee. So they decided that his wife and children would be able to accept his prize on his behalf. But the story doesn’t end there; Steinman had been battling pancreatic cancer for over 4 years and was treating himself using exactly what the Nobel committee was awarding him for – his 40-year career in researching a previously unknown immune system component he called ‘dendritic cells’.
Steinman, a Montreal native and McGill alumnus, was jointly credited with the discovery of dendritic cells in 1973 and spent the rest of his career researching how these special cells might be used to fight difficult diseases like HIV and cancer. Dendritic cells, so named because of their tree-like shape, mediate communication between harmful antigens (molecules that stimulate the immune system) and lymphatic T-cells (white blood cells that activate molecules to fight off these antigens). Steinman showed that these dendritic cells are able to capture invaders, like the common cold virus, and signal specific lymphocytes to destroy them.
However, cancer is not like the common cold. Tumor antigens released from cancer cells evade the immune system by either eliminating or hiding from our defensive T-cells. A common way they do this is by activating checkpoint pathways, which tell the body to “turn off” active white blood cells, preventing them from destroying the invading cancer cells. Our greatest weapon against them, chemotherapy, works like a bomb: it blasts through the entire body directly destroying cancerous cells, but is not very selective and many healthy cells are destroyed as well.
But thanks to research like Steinman’s, cancer immunotherapy treatments can harness the selective abilities of our natural immune system, and fight back with extreme precision. Immunotherapy vaccinations would manipulate dendritic cells to capture tumor antigens and present them to cancer-specific lymphocytes thereby improving the ability of the body to find and destroy tricky cancer cells with much better accuracy than chemotherapy. However, unlike chemotherapy, which works relatively quickly, immunotherapy builds the body’s immune system over time, time that patients often do not have, especially if the treatment should fail. Furthermore, it appears that not all patients respond in the same way. It has been estimated that currently about 10% of cancer patients can benefit from immunotherapy treatments. But this number is expected to grow as more research unveils how these mechanisms work.
Thus in 2007 when Steinman received his cancer diagnosis with an estimated 6 months to live, he set to work right away, sending samples of his golf-ball sized tumor across the globe to several colleagues in immunotherapy labs. Even at the time Steinman knew he was perhaps a decade or two too early for this kind of treatment; we now know there are dozens of kinds of dendritic cells which target different antigens, whereas back then they were essentially taking shots in the dark. Even so, he put his faith behind his research and in his last experiment he became his own patient. In total, he was treated with 8 different FDA-approved cancer vaccines in addition to several rounds of chemotherapy. He managed to prolong his life three and a half years longer than predicted and maintained good physical health for most of it. But without another patient to compare, and with the hasty time taken in between treatments, it’s very difficult to tell what exactly was keeping Ralph Steinman alive. Eventually the cancer stopped responding to the vaccines he was given and the disease spread throughout his whole body. He passed away on September 30, 2011, just three days shy of knowing that he had been awarded the most prestigious mark of scientific achievement. Now he stands as the only deceased recipient of a Nobel prize who actually became a patient of his own research. I’d say that’s well worth the exception. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 3 | 95 | https://www.ucsf.edu/about/achievements | en | Achievements at UCSF | [
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Identified receptors in cells of the peripheral nervous system that play key roles in the body’s ability to sense heat and cold, providing major insights into how the body experiences pain – findings that are valuable for development of pain therapeutics. (David Julius, PhD, 2002 and 1997)
Determined that chronic pain is a medical condition and not just a symptom, leading to improved strategies of management. (Christine Miaskowski, RN, PhD, 2001)
Discovered genes that can double the lifespan of the roundworm C. elegans. These genes encode components of a conserved hormone signaling pathway, and have now been linked to exceptional longevity in flies and mammals, including humans. (Cynthia Kenyon, PhD, 1993)
Discovered the regulatory machinery of the "unfolded protein response," a signaling pathway that controls protein folding in the cell. Improper protein folding is the biological basis for numerous diseases, including cancer, diabetes and neurodegenerative disorders. (Peter Walter, PhD, 1993)
Identified oral lesions as one of the first signs of AIDS, leading to major research breakthroughs in the oral aspects of AIDS and the role of viruses in oral lesions. (John Greenspan, BDS, PhD; and Deborah Greenspan, BDS, DSc, 1984)
Co-discovered the AIDS virus – known as HIV, human immunodeficiency virus – originally calling it AIDS-related retrovirus (Jay Levy, MD, 1983), and discovered that the virus could be transmitted through blood transfusions, leading to new methods of screening donors. (Arthur Ammann, MD; Diane Wara, MD; and Morton Cowan, MD, 1982)
Co-discovered embryonic stem cells in mice and coined the term embryonic stem cells, laying the groundwork for worldwide research on human embryonic stem cells to treat disease. (Gail Martin, PhD, 1981)
Reported for the first time that elevated blood sugar caused abnormal structures in cells, helping to pioneer the intensive glucose control strategies now used throughout the world for managing diabetes. (John Karam, MD, and Gerold Grodsky, PhD, 1980)
Isolated the gene for insulin, leading to the mass production of genetically engineered insulin to treat diabetes. This was recognized as the first major triumph using recombinant DNA technology. Later, discovered the recombinant DNA techniques that led to the creation of the hepatitis B vaccine. (William Rutter, PhD, 1978, 1981)
Discovered that a missing protein called surfactant is the culprit in the deaths of newborns with respiratory distress syndrome. This led to development of a synthetic substitute for surfactant, reducing infant death rates significantly. (John Clements, MD; William Tooley, MD; and Roderic Phibbs, MD, 1961 – 1980)
Created the first recombinant organism through DNA splicing, an achievement that spawned the entire biotechnology industry and has led to development of numerous lifesaving treatments. (Herbert Boyer, PhD, with colleague Stanley Cohen of Stanford University, 1973)
First to link obesity to type 2 diabetes, a finding that resulted in revolutionary changes in diabetes treatment and prevention. (John Karam, MD; and Gerold Grodsky, PhD, 1963)
Discovered vitamin E. (Herbert Evans, MD, during the period when the basic science departments were based at UC Berkeley, 1923)
Conducted initial studies on liver metabolism and the relationship between the liver and blood components, leading to successful treatment of pernicious anemia, a usually fatal form of the disease. (George Whipple, MD, who left UC in 1921, later received the 1934 Nobel Prize in Physiology or Medicine for this body of research)
Led the world’s first clinical trial using blood stem cells transplanted prior to birth, leading to the live birth of an infant with a normally fatal fetal condition called alpha thalassemia. (Tippi Mackenzie, MD, 2018)
Conducted first-ever genome editing inside a human body, aiming to treat a severe inherited disease called mucopolysaccharidosis type II (MPS II), also known as Hunter syndrome. (Paul Harmatz, MD, 2018)
Led a National Academy of Sciences Committee that recommended the creation of an extensive data network to revolutionize medical discovery, diagnosis and treatment, and coined the term “precision medicine.” (Susan Desmond-Hellmann, MD, MPH, and Keith Yamamoto, PhD, 2011)
Pioneered techniques in brain mapping to safely remove tumors without harming language and other pathways of the brain. (Mitchel Berger, MD, mid-1990s - 2008)
Developed the ViroChip, a microarray that contains DNA from every known virus and a valuable diagnostic tool for identifying previously unknown viruses in both humans and animals. The tool was first used in 2003 to confirm the identity of the virus that caused severe acute respiratory syndrome, known as SARS. (Joseph DeRisi, PhD, and Don Ganem, MD, 2002)
Established the Legacy Tobacco Documents Library to house and maintain tobacco industry internal corporate documents produced during litigation between 46 states and the seven major tobacco industry organizations. Today, the library has more than 80 million pages. (Stanton Glantz, PhD, 2002)
Created two of the first human embryonic stem cell lines in the world, enabling scientists to study how stem cells might be used to treat such diseases and disorders as cancer, heart disease, diabetes and birth defects. (Roger Pedersen, PhD, 2001)
First to use the X-ray structure of HIV protease to identify an inhibitor that effectively blocks the enzyme's activity, the same method used today to design protease inhibitor drugs. (Charles Craik, PhD, 1990)
Produced clear, dramatic images of the soft tissues of the body, using nuclear magnetic resonance (now known as MRI). UCSF researchers went on to direct some of the first clinical placements in the country of devices that provided the images. (Leon Kaufman, PhD, and Larry Crooks, PhD, 1983)
Established the first special care units for AIDS patients in 1983 at San Francisco General Hospital, which led to the “San Francisco Model” that is now used worldwide.
Performed the first successful fetal surgery, which involves correcting a life-threatening birth defect on a still in the mother's womb. (Michael Harrison, MD; Mitchell Golbus, MD; and Roy Filly, MD, 1981)
Conducted groundbreaking studies on the importance of gender-based health care research that was instrumental in shaping the field of women's health. (Virginia Olesen, PhD, 1981)
Developed a cochlear implant device that enables the deaf to hear. (Michael Merzenich, PhD; Robert Schindler, MD; and Robin Michelson, MD, 1979)
Developed the first prenatal tests for inherited blood diseases such as sickle-cell anemia and thalassemia. (Y.W. Kan, MD, DSc, 1976)
Pioneered the field of “clinical pharmacy” that positioned pharmacists as active members of the health care team, working side by side with physicians and nurses, and trained as drug therapy specialists rather than simply drug dispensers. (Jere Goyan, PharmD; Eric Owyang, PharmD; Sidney Riegelman, PharmD; and Donald Sorby, PhD, 1966)
First university west of the Mississippi to offer a doctoral degree in nursing.
Developed basic sterilization and hygiene procedures for the U.S. canning industry to prevent botulism, thereby safeguarding consumers and saving the industry. (Karl F. Meyer, DVM, PhD, 1920s) | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 18 | https://www.ucsf.edu/news/2021-nobel-prize-physiology-or-medicine-david-julius | en | 2021 Nobel Prize in Physiology or Medicine | [
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"The Editors of Encyclopaedia Britannica"
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Hill U.K. discoveries concerning heat production in muscles Otto Meyerhof Germany work on metabolism of lactic acid in muscles 1923 Sir Frederick Grant Banting Canada discovery of insulin J.J.R. Macleod U.K. discovery of insulin 1924 Willem Einthoven Netherlands discovery of electrocardiogram mechanism 1926 Johannes Fibiger Denmark contributions to cancer research 1927 Julius Wagner-Jauregg Austria work on malaria inoculation in dementia paralytica 1928 Charles-Jules-Henri Nicolle France work on typhus 1929 Christiaan Eijkman Netherlands discovery of the antineuritic vitamin Sir Frederick Gowland Hopkins U.K. discovery of growth-stimulating vitamins 1930 Karl Landsteiner U.S. discovery of human blood groups 1931 Otto Warburg Germany discovery of the nature and action of the respiratory enzyme 1932 Edgar Douglas Adrian, 1st Baron Adrian U.K. discoveries regarding function of neurons Sir Charles Scott Sherrington U.K. discoveries regarding function of neurons 1933 Thomas Hunt Morgan U.S. heredity transmission functions of chromosomes 1934 George Richards Minot U.S. discoveries concerning liver treatment for anemia William P. Murphy U.S. discoveries concerning liver treatment for anemia George H. Whipple U.S. discoveries concerning liver treatment for anemia 1935 Hans Spemann Germany organizer effect in embryos 1936 Sir Henry Dale U.K. work on chemical transmission of nerve impulses Otto Loewi Germany work on chemical transmission of nerve impulses 1937 Albert Szent-Györgyi Hungary work on biological combustion 1938 Corneille Heymans Belgium discovery of the role of sinus and aortic mechanisms in respiration regulation 1939 Gerhard Domagk (declined) Germany antibacterial effect of Prontosil 1943 Henrik Dam Denmark discovery of vitamin K Edward Adelbert Doisy U.S. discovery of the chemical nature of vitamin K 1944 Joseph Erlanger U.S. researches on differentiated functions of nerve fibres Herbert Spencer Gasser U.S. researches on differentiated functions of nerve fibres 1945 Sir Ernst Boris Chain U.K. discovery of penicillin and its curative value Sir Alexander Fleming U.K. discovery of penicillin and its curative value Howard Walter Florey, Baron Florey Australia discovery of penicillin and its curative value 1946 Hermann Joseph Muller U.S. production of mutations by X-radiation 1947 Carl and Gerty Cori U.S. discovery of how glycogen is catalytically converted Bernardo Alberto Houssay Argentina pituitary hormone function in sugar metabolism 1948 Paul Hermann Müller Switzerland properties of DDT 1949 António Egas Moniz Portugal therapeutic value of leucotomy in psychoses Walter Rudolf Hess Switzerland discovery of functions of the interbrain 1950 Philip Showalter Hench U.S. research on adrenal cortex hormones, their structure and biological effects Edward Calvin Kendall U.S. research on adrenal cortex hormones, their structure and biological effects Tadeus Reichstein Switzerland research on adrenal cortex hormones, their structure and biological effects 1951 Max Theiler South Africa yellow fever discoveries 1952 Selman Abraham Waksman U.S. discovery of streptomycin 1953 Sir Hans Adolf Krebs U.K. discovery of the citric acid cycle in metabolism of carbohydrates Fritz Albert Lipmann U.S. discovery of coenzyme A in metabolism of carbohydrates 1954 John Franklin Enders U.S. cultivation of the poliomyelitis virus in tissue cultures Frederick Chapman Robbins U.S. cultivation of the poliomyelitis virus in tissue cultures Thomas H. Weller U.S. cultivation of the poliomyelitis virus in tissue cultures 1955 Axel Hugo Teodor Theorell Sweden nature and mode of action of oxidation enzymes 1956 André F. Cournand U.S. discoveries concerning heart catheterization and circulatory changes Werner Forssmann West Germany discoveries concerning heart catheterization and circulatory changes Dickinson Woodruff Richards U.S. discoveries concerning heart catheterization and circulatory changes 1957 Daniel Bovet Italy production of synthetic curare 1958 George Wells Beadle U.S. genetic regulation of chemical processes Joshua Lederberg U.S. genetic recombination Edward L. Tatum U.S. genetic regulation of chemical processes 1959 Arthur Kornberg U.S. work on producing nucleic acids artificially Severo Ochoa U.S. work on producing nucleic acids artificially 1960 Sir Macfarlane Burnet Australia acquired immunity to tissue transplants Sir Peter B. Medawar U.K. acquired immunity to tissue transplants 1961 Georg von Békésy U.S. functions of the inner ear 1962 Francis Harry Compton Crick U.K. discoveries concerning the molecular structure of DNA James Dewey Watson U.S. discoveries concerning the molecular structure of DNA Maurice Wilkins U.K. discoveries concerning the molecular structure of DNA 1963 Sir John Carew Eccles Australia study of the transmission of impulses along a nerve fibre Sir Alan Hodgkin U.K. study of the transmission of impulses along a nerve fibre Sir Andrew Fielding Huxley U.K. study of the transmission of impulses along a nerve fibre 1964 Konrad Bloch U.S. discoveries concerning cholesterol and fatty acid metabolism Feodor Lynen West Germany discoveries concerning cholesterol and fatty acid metabolism 1965 François Jacob France discoveries concerning regulatory activities of body cells André Lwoff France discoveries concerning regulatory activities of body cells Jacques Monod France discoveries concerning regulatory activities of body cells 1966 Charles B. Huggins U.S. research on causes and treatment of cancer Peyton Rous U.S. research on causes and treatment of cancer 1967 Ragnar Arthur Granit Sweden discoveries about chemical and physiological visual processes in the eye Haldan Keffer Hartline U.S. discoveries about chemical and physiological visual processes in the eye George Wald U.S. discoveries about chemical and physiological visual processes in the eye 1968 Robert William Holley U.S. deciphering the genetic code Har Gobind Khorana U.S. deciphering the genetic code Marshall Warren Nirenberg U.S. deciphering the genetic code 1969 Max Delbrück U.S. research and discoveries concerning viruses and viral diseases A.D. Hershey U.S. research and discoveries concerning viruses and viral diseases Salvador Luria U.S. research and discoveries concerning viruses and viral diseases 1970 Julius Axelrod U.S. discoveries concerning the chemistry of nerve impulse transmission Ulf von Euler Sweden discoveries concerning the chemistry of nerve impulse transmission Sir Bernard Katz U.K. discoveries concerning the chemistry of nerve impulse transmission 1971 Earl W. Sutherland, Jr. U.S. action of hormones 1972 Gerald Maurice Edelman U.S. research on the chemical structure of antibodies Rodney Robert Porter U.K. research on the chemical structure of antibodies 1973 Karl von Frisch Austria discoveries in animal behaviour patterns Konrad Lorenz Austria discoveries in animal behaviour patterns Nikolaas Tinbergen U.K. discoveries in animal behaviour patterns 1974 Albert Claude U.S. research on structural and functional organization of cells Christian René de Duve Belgium research on structural and functional organization of cells George E. Palade U.S. research on structural and functional organization of cells 1975 David Baltimore U.S. interaction between tumour viruses and the genetic material of the cell Renato Dulbecco U.S. interaction between tumour viruses and the genetic material of the cell Howard Martin Temin U.S. interaction between tumour viruses and the genetic material of the cell 1976 Baruch S. Blumberg U.S. studies of the origin and spread of infectious diseases D. Carleton Gajdusek U.S. studies of the origin and spread of infectious diseases 1977 Roger Charles Louis Guillemin U.S. research on pituitary hormones Andrew Victor Schally U.S. research on pituitary hormones Rosalyn S. Yalow U.S. development of radioimmunoassay 1978 Werner Arber Switzerland discovery and application of enzymes that fragment DNA Daniel Nathans U.S. discovery and application of enzymes that fragment DNA Hamilton Othanel Smith U.S. discovery and application of enzymes that fragment DNA 1979 Allan MacLeod Cormack U.S. development of the CAT scan Sir Godfrey Newbold Hounsfield U.K. development of the CAT scan 1980 Baruj Benacerraf U.S. investigations of genetic control of the response of the immune system to foreign substances Jean-Baptiste-Gabriel-Joachim Dausset France investigations of genetic control of the response of the immune system to foreign substances George Davis Snell U.S. investigations of genetic control of the response of the immune system to foreign substances 1981 David Hunter Hubel U.S. processing of visual information by the brain Roger Wolcott Sperry U.S. functions of the cerebral hemispheres Torsten Nils Wiesel Sweden processing of visual information by the brain 1982 Sune K. Bergström Sweden biochemistry and physiology of prostaglandins Bengt Ingemar Samuelsson Sweden biochemistry and physiology of prostaglandins John Robert Vane U.K. biochemistry and physiology of prostaglandins 1983 Barbara McClintock U.S. discovery of mobile plant genes that affect heredity 1984 Niels K. Jerne U.K.-Denmark theory and development of a technique for producing monoclonal antibodies Georges J.F. Köhler West Germany theory and development of a technique for producing monoclonal antibodies César Milstein Argentina theory and development of a technique for producing monoclonal antibodies 1985 Michael S. Brown U.S. discovery of cell receptors relating to cholesterol metabolism Joseph L. Goldstein U.S. discovery of cell receptors relating to cholesterol metabolism 1986 Stanley Cohen U.S. discovery of chemical agents that help regulate the growth of cells Rita Levi-Montalcini Italy discovery of chemical agents that help regulate the growth of cells 1987 Tonegawa Susumu Japan study of genetic aspects of antibodies 1988 Sir James Black U.K. development of new classes of drugs for combating disease Gertrude Belle Elion U.S. development of new classes of drugs for combating disease George Herbert Hitchings U.S. development of new classes of drugs for combating disease 1989 J. Michael Bishop U.S. study of cancer-causing genes (oncogenes) Harold Varmus U.S. study of cancer-causing genes (oncogenes) 1990 Joseph E. Murray U.S. development of kidney and bone marrow transplants E. Donnall Thomas U.S. development of kidney and bone marrow transplants 1991 Erwin Neher Germany discovery of how cells communicate, as related to diseases Bert Sakmann Germany discovery of how cells communicate, as related to diseases 1992 Edmond H. Fischer U.S. discovery of the class of enzymes called protein kinases Edwin Gerhard Krebs U.S. discovery of the class of enzymes called protein kinases 1993 Richard J. Roberts U.K. discovery of "split," or interrupted, genetic structure Phillip A. Sharp U.S. discovery of "split," or interrupted, genetic structure 1994 Alfred G. Gilman U.S. discovery of cell signalers called G-proteins Martin Rodbell U.S. discovery of cell signalers called G-proteins 1995 Edward B. Lewis U.S. identification of genes that control the body's early structural development Christiane Nüsslein-Volhard Germany identification of genes that control the body's early structural development Eric F. Wieschaus U.S. identification of genes that control the body's early structural development 1996 Peter C. Doherty Australia discovery of how the immune system recognizes virus-infected cells Rolf M. Zinkernagel Switzerland discovery of how the immune system recognizes virus-infected cells 1997 Stanley B. Prusiner U.S. discovery of the prion, a type of disease-causing protein 1998 Robert F. Furchgott U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system Louis J. Ignarro U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system Ferid Murad U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system 1999 Günter Blobel U.S. discovery that proteins have signals governing cellular organization 2000 Arvid Carlsson Sweden discovery of how signals are transmitted between nerve cells in the brain Paul Greengard U.S. discovery of how signals are transmitted between nerve cells in the brain Eric Kandel U.S. discovery of how signals are transmitted between nerve cells in the brain 2001 Leland H. Hartwell U.S. discovery of key regulators of the cell cycle R. Timothy Hunt U.K. discovery of key regulators of the cell cycle Sir Paul M. Nurse U.K. discovery of key regulators of the cell cycle 2002 Sydney Brenner U.K. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) H. Robert Horvitz U.S. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) John E. Sulston U.K. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) 2003 Paul Lauterbur U.S. development of magnetic resonance imaging (MRI) Sir Peter Mansfield U.K. development of magnetic resonance imaging (MRI) 2004 Richard Axel U.S. discovery of odorant receptors and the organization of the olfactory system Linda B. Buck U.S. discovery of odorant receptors and the organization of the olfactory system 2005 Barry J. Marshall Australia discovery of bacteria's role in peptic ulcer disease J. Robin Warren Australia discovery of bacteria's role in peptic ulcer disease 2006 Andrew Z. Fire U.S. discovery of RNA interference—gene silencing by double-stranded RNA Craig C. Mello U.S. discovery of RNA interference—gene silencing by double-stranded RNA 2007 Mario R. Capecchi U.S. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells Sir Martin J. Evans U.K. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells Oliver Smithies U.S. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells 2008 Françoise Barré-Sinoussi France discovery of human immunodeficiency virus Luc Montagnier France discovery of human immunodeficiency virus Harald zur Hausen Germany discovery of human papilloma viruses causing cervical cancer 2009 Elizabeth H. Blackburn U.S. discovery of how chromosomes are protected by telomeres and the enzyme telomerase Carol W. Greider U.S. discovery of how chromosomes are protected by telomeres and the enzyme telomerase 2010 Robert Edwards U.K. development of in vitro fertilization 2012 Sir John Bertrand Gurdon U.K. discovery that mature cells can be reprogrammed to become pluripotent Shinya Yamanaka Japan discovery that mature cells can be reprogrammed to become pluripotent 2013 James E. Rothman U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells Randy W. Schekman U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells Thomas C. Südhof Germany/U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells 2014 Edvard I. Moser Norway discoveries of cells that constitute a positioning system in the brain May-Britt Moser Norway discoveries of cells that constitute a positioning system in the brain John O'Keefe U.S./U.K. discoveries of cells that constitute a positioning system in the brain 2015 William C. Campbell Ireland discoveries concerning a novel therapy against infections caused by roundworm parasites Ōmura Satoshi Japan discoveries concerning a novel therapy against infections caused by roundworm parasites Tu Youyou China discoveries concerning a novel therapy against malaria 2016 Yoshinori Ohsumi Japan discoveries of mechanisms for autophagy 2017 Jeffrey C. Hall U.S. discoveries of molecular mechanisms controlling the circadian rhythm Michael Rosbash U.S. discoveries of molecular mechanisms controlling the circadian rhythm Michael W. Young U.S. discoveries of molecular mechanisms controlling the circadian rhythm 2018 James P. Allison U.S. discovery of cancer therapy by inhibition of negative immune regulation Honjo Tasuku Japan discovery of cancer therapy by inhibition of negative immune regulation 2019 William G. Kaelin, Jr. U.S. discoveries of how cells sense and adapt to oxygen availability Peter J. Ratcliffe U.K. discoveries of how cells sense and adapt to oxygen availability Gregg L. Semenza U.S. discoveries of how cells sense and adapt to oxygen availability 2020 Harvey J. Alter U.S. discovery of hepatitis C virus Michael Houghton U.K. discovery of hepatitis C virus Charles M. Rice U.S. discovery of hepatitis C virus 2021 David Julius U.S. discoveries of receptors for temperature and touch Ardem Patapoutian Leb./U.S. discoveries of receptors for temperature and touch 2022 Svante Pääbo Sweden discoveries concerning the genomes of extinct hominins and human evolution 2023 Katalin Karikó Hungary/U.S. discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19 | ||||
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"The Editors of Encyclopaedia Britannica"
] | 2012-06-25T00:00:00+00:00 | The Nobel Prize for Physiology or Medicine is awarded, according to the will of Swedish inventor and industrialist Alfred Bernhard Nobel, “to those who, during the preceding year, shall have conferred the greatest benefit on mankind” in the fields of physiology or medicine. It is conferred by the | en | /favicon.png | Encyclopedia Britannica | https://www.britannica.com/topic/Winners-of-the-Nobel-Prize-for-Physiology-or-Medicine-1856944 | 1901 Emil von Behring Germany work on serum therapy 1902 Sir Ronald Ross U.K. discovery of how malaria enters an organism 1903 Niels Ryberg Finsen Denmark treatment of skin diseases with light 1904 Ivan Pavlov Russia work on the physiology of digestion 1905 Robert Koch Germany tuberculosis research 1906 Camillo Golgi Italy work on the structure of the nervous system Santiago Ramón y Cajal Spain work on the structure of the nervous system 1907 Alphonse Laveran France discovery of the role of protozoans in diseases 1908 Paul Ehrlich Germany work on immunity Élie Metchnikoff Russia work on immunity 1909 Emil Theodor Kocher Switzerland physiology, pathology, and surgery of the thyroid gland 1910 Albrecht Kossel Germany researches in cellular chemistry 1911 Allvar Gullstrand Sweden work on dioptrics of the eye 1912 Alexis Carrel France work on vascular suture; transplantation of organs 1913 Charles Richet France work on anaphylaxis 1914 Robert Bárány Austria-Hungary work on vestibular apparatus 1919 Jules Bordet Belgium work on immunity factors in blood serum 1920 August Krogh Denmark discovery of the capillary motor-regulating mechanism 1922 A.V. Hill U.K. discoveries concerning heat production in muscles Otto Meyerhof Germany work on metabolism of lactic acid in muscles 1923 Sir Frederick Grant Banting Canada discovery of insulin J.J.R. Macleod U.K. discovery of insulin 1924 Willem Einthoven Netherlands discovery of electrocardiogram mechanism 1926 Johannes Fibiger Denmark contributions to cancer research 1927 Julius Wagner-Jauregg Austria work on malaria inoculation in dementia paralytica 1928 Charles-Jules-Henri Nicolle France work on typhus 1929 Christiaan Eijkman Netherlands discovery of the antineuritic vitamin Sir Frederick Gowland Hopkins U.K. discovery of growth-stimulating vitamins 1930 Karl Landsteiner U.S. discovery of human blood groups 1931 Otto Warburg Germany discovery of the nature and action of the respiratory enzyme 1932 Edgar Douglas Adrian, 1st Baron Adrian U.K. discoveries regarding function of neurons Sir Charles Scott Sherrington U.K. discoveries regarding function of neurons 1933 Thomas Hunt Morgan U.S. heredity transmission functions of chromosomes 1934 George Richards Minot U.S. discoveries concerning liver treatment for anemia William P. Murphy U.S. discoveries concerning liver treatment for anemia George H. Whipple U.S. discoveries concerning liver treatment for anemia 1935 Hans Spemann Germany organizer effect in embryos 1936 Sir Henry Dale U.K. work on chemical transmission of nerve impulses Otto Loewi Germany work on chemical transmission of nerve impulses 1937 Albert Szent-Györgyi Hungary work on biological combustion 1938 Corneille Heymans Belgium discovery of the role of sinus and aortic mechanisms in respiration regulation 1939 Gerhard Domagk (declined) Germany antibacterial effect of Prontosil 1943 Henrik Dam Denmark discovery of vitamin K Edward Adelbert Doisy U.S. discovery of the chemical nature of vitamin K 1944 Joseph Erlanger U.S. researches on differentiated functions of nerve fibres Herbert Spencer Gasser U.S. researches on differentiated functions of nerve fibres 1945 Sir Ernst Boris Chain U.K. discovery of penicillin and its curative value Sir Alexander Fleming U.K. discovery of penicillin and its curative value Howard Walter Florey, Baron Florey Australia discovery of penicillin and its curative value 1946 Hermann Joseph Muller U.S. production of mutations by X-radiation 1947 Carl and Gerty Cori U.S. discovery of how glycogen is catalytically converted Bernardo Alberto Houssay Argentina pituitary hormone function in sugar metabolism 1948 Paul Hermann Müller Switzerland properties of DDT 1949 António Egas Moniz Portugal therapeutic value of leucotomy in psychoses Walter Rudolf Hess Switzerland discovery of functions of the interbrain 1950 Philip Showalter Hench U.S. research on adrenal cortex hormones, their structure and biological effects Edward Calvin Kendall U.S. research on adrenal cortex hormones, their structure and biological effects Tadeus Reichstein Switzerland research on adrenal cortex hormones, their structure and biological effects 1951 Max Theiler South Africa yellow fever discoveries 1952 Selman Abraham Waksman U.S. discovery of streptomycin 1953 Sir Hans Adolf Krebs U.K. discovery of the citric acid cycle in metabolism of carbohydrates Fritz Albert Lipmann U.S. discovery of coenzyme A in metabolism of carbohydrates 1954 John Franklin Enders U.S. cultivation of the poliomyelitis virus in tissue cultures Frederick Chapman Robbins U.S. cultivation of the poliomyelitis virus in tissue cultures Thomas H. Weller U.S. cultivation of the poliomyelitis virus in tissue cultures 1955 Axel Hugo Teodor Theorell Sweden nature and mode of action of oxidation enzymes 1956 André F. Cournand U.S. discoveries concerning heart catheterization and circulatory changes Werner Forssmann West Germany discoveries concerning heart catheterization and circulatory changes Dickinson Woodruff Richards U.S. discoveries concerning heart catheterization and circulatory changes 1957 Daniel Bovet Italy production of synthetic curare 1958 George Wells Beadle U.S. genetic regulation of chemical processes Joshua Lederberg U.S. genetic recombination Edward L. Tatum U.S. genetic regulation of chemical processes 1959 Arthur Kornberg U.S. work on producing nucleic acids artificially Severo Ochoa U.S. work on producing nucleic acids artificially 1960 Sir Macfarlane Burnet Australia acquired immunity to tissue transplants Sir Peter B. Medawar U.K. acquired immunity to tissue transplants 1961 Georg von Békésy U.S. functions of the inner ear 1962 Francis Harry Compton Crick U.K. discoveries concerning the molecular structure of DNA James Dewey Watson U.S. discoveries concerning the molecular structure of DNA Maurice Wilkins U.K. discoveries concerning the molecular structure of DNA 1963 Sir John Carew Eccles Australia study of the transmission of impulses along a nerve fibre Sir Alan Hodgkin U.K. study of the transmission of impulses along a nerve fibre Sir Andrew Fielding Huxley U.K. study of the transmission of impulses along a nerve fibre 1964 Konrad Bloch U.S. discoveries concerning cholesterol and fatty acid metabolism Feodor Lynen West Germany discoveries concerning cholesterol and fatty acid metabolism 1965 François Jacob France discoveries concerning regulatory activities of body cells André Lwoff France discoveries concerning regulatory activities of body cells Jacques Monod France discoveries concerning regulatory activities of body cells 1966 Charles B. Huggins U.S. research on causes and treatment of cancer Peyton Rous U.S. research on causes and treatment of cancer 1967 Ragnar Arthur Granit Sweden discoveries about chemical and physiological visual processes in the eye Haldan Keffer Hartline U.S. discoveries about chemical and physiological visual processes in the eye George Wald U.S. discoveries about chemical and physiological visual processes in the eye 1968 Robert William Holley U.S. deciphering the genetic code Har Gobind Khorana U.S. deciphering the genetic code Marshall Warren Nirenberg U.S. deciphering the genetic code 1969 Max Delbrück U.S. research and discoveries concerning viruses and viral diseases A.D. Hershey U.S. research and discoveries concerning viruses and viral diseases Salvador Luria U.S. research and discoveries concerning viruses and viral diseases 1970 Julius Axelrod U.S. discoveries concerning the chemistry of nerve impulse transmission Ulf von Euler Sweden discoveries concerning the chemistry of nerve impulse transmission Sir Bernard Katz U.K. discoveries concerning the chemistry of nerve impulse transmission 1971 Earl W. Sutherland, Jr. U.S. action of hormones 1972 Gerald Maurice Edelman U.S. research on the chemical structure of antibodies Rodney Robert Porter U.K. research on the chemical structure of antibodies 1973 Karl von Frisch Austria discoveries in animal behaviour patterns Konrad Lorenz Austria discoveries in animal behaviour patterns Nikolaas Tinbergen U.K. discoveries in animal behaviour patterns 1974 Albert Claude U.S. research on structural and functional organization of cells Christian René de Duve Belgium research on structural and functional organization of cells George E. Palade U.S. research on structural and functional organization of cells 1975 David Baltimore U.S. interaction between tumour viruses and the genetic material of the cell Renato Dulbecco U.S. interaction between tumour viruses and the genetic material of the cell Howard Martin Temin U.S. interaction between tumour viruses and the genetic material of the cell 1976 Baruch S. Blumberg U.S. studies of the origin and spread of infectious diseases D. Carleton Gajdusek U.S. studies of the origin and spread of infectious diseases 1977 Roger Charles Louis Guillemin U.S. research on pituitary hormones Andrew Victor Schally U.S. research on pituitary hormones Rosalyn S. Yalow U.S. development of radioimmunoassay 1978 Werner Arber Switzerland discovery and application of enzymes that fragment DNA Daniel Nathans U.S. discovery and application of enzymes that fragment DNA Hamilton Othanel Smith U.S. discovery and application of enzymes that fragment DNA 1979 Allan MacLeod Cormack U.S. development of the CAT scan Sir Godfrey Newbold Hounsfield U.K. development of the CAT scan 1980 Baruj Benacerraf U.S. investigations of genetic control of the response of the immune system to foreign substances Jean-Baptiste-Gabriel-Joachim Dausset France investigations of genetic control of the response of the immune system to foreign substances George Davis Snell U.S. investigations of genetic control of the response of the immune system to foreign substances 1981 David Hunter Hubel U.S. processing of visual information by the brain Roger Wolcott Sperry U.S. functions of the cerebral hemispheres Torsten Nils Wiesel Sweden processing of visual information by the brain 1982 Sune K. Bergström Sweden biochemistry and physiology of prostaglandins Bengt Ingemar Samuelsson Sweden biochemistry and physiology of prostaglandins John Robert Vane U.K. biochemistry and physiology of prostaglandins 1983 Barbara McClintock U.S. discovery of mobile plant genes that affect heredity 1984 Niels K. Jerne U.K.-Denmark theory and development of a technique for producing monoclonal antibodies Georges J.F. Köhler West Germany theory and development of a technique for producing monoclonal antibodies César Milstein Argentina theory and development of a technique for producing monoclonal antibodies 1985 Michael S. Brown U.S. discovery of cell receptors relating to cholesterol metabolism Joseph L. Goldstein U.S. discovery of cell receptors relating to cholesterol metabolism 1986 Stanley Cohen U.S. discovery of chemical agents that help regulate the growth of cells Rita Levi-Montalcini Italy discovery of chemical agents that help regulate the growth of cells 1987 Tonegawa Susumu Japan study of genetic aspects of antibodies 1988 Sir James Black U.K. development of new classes of drugs for combating disease Gertrude Belle Elion U.S. development of new classes of drugs for combating disease George Herbert Hitchings U.S. development of new classes of drugs for combating disease 1989 J. Michael Bishop U.S. study of cancer-causing genes (oncogenes) Harold Varmus U.S. study of cancer-causing genes (oncogenes) 1990 Joseph E. Murray U.S. development of kidney and bone marrow transplants E. Donnall Thomas U.S. development of kidney and bone marrow transplants 1991 Erwin Neher Germany discovery of how cells communicate, as related to diseases Bert Sakmann Germany discovery of how cells communicate, as related to diseases 1992 Edmond H. Fischer U.S. discovery of the class of enzymes called protein kinases Edwin Gerhard Krebs U.S. discovery of the class of enzymes called protein kinases 1993 Richard J. Roberts U.K. discovery of "split," or interrupted, genetic structure Phillip A. Sharp U.S. discovery of "split," or interrupted, genetic structure 1994 Alfred G. Gilman U.S. discovery of cell signalers called G-proteins Martin Rodbell U.S. discovery of cell signalers called G-proteins 1995 Edward B. Lewis U.S. identification of genes that control the body's early structural development Christiane Nüsslein-Volhard Germany identification of genes that control the body's early structural development Eric F. Wieschaus U.S. identification of genes that control the body's early structural development 1996 Peter C. Doherty Australia discovery of how the immune system recognizes virus-infected cells Rolf M. Zinkernagel Switzerland discovery of how the immune system recognizes virus-infected cells 1997 Stanley B. Prusiner U.S. discovery of the prion, a type of disease-causing protein 1998 Robert F. Furchgott U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system Louis J. Ignarro U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system Ferid Murad U.S. discovery that nitric oxide (NO) acts as a signaling molecule in the cardiovascular system 1999 Günter Blobel U.S. discovery that proteins have signals governing cellular organization 2000 Arvid Carlsson Sweden discovery of how signals are transmitted between nerve cells in the brain Paul Greengard U.S. discovery of how signals are transmitted between nerve cells in the brain Eric Kandel U.S. discovery of how signals are transmitted between nerve cells in the brain 2001 Leland H. Hartwell U.S. discovery of key regulators of the cell cycle R. Timothy Hunt U.K. discovery of key regulators of the cell cycle Sir Paul M. Nurse U.K. discovery of key regulators of the cell cycle 2002 Sydney Brenner U.K. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) H. Robert Horvitz U.S. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) John E. Sulston U.K. discoveries concerning genetic regulation of organ development and programmed cell death (apoptosis) 2003 Paul Lauterbur U.S. development of magnetic resonance imaging (MRI) Sir Peter Mansfield U.K. development of magnetic resonance imaging (MRI) 2004 Richard Axel U.S. discovery of odorant receptors and the organization of the olfactory system Linda B. Buck U.S. discovery of odorant receptors and the organization of the olfactory system 2005 Barry J. Marshall Australia discovery of bacteria's role in peptic ulcer disease J. Robin Warren Australia discovery of bacteria's role in peptic ulcer disease 2006 Andrew Z. Fire U.S. discovery of RNA interference—gene silencing by double-stranded RNA Craig C. Mello U.S. discovery of RNA interference—gene silencing by double-stranded RNA 2007 Mario R. Capecchi U.S. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells Sir Martin J. Evans U.K. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells Oliver Smithies U.S. discovery of principles for introducing specific gene modifications in mice by the use of embryonic stem cells 2008 Françoise Barré-Sinoussi France discovery of human immunodeficiency virus Luc Montagnier France discovery of human immunodeficiency virus Harald zur Hausen Germany discovery of human papilloma viruses causing cervical cancer 2009 Elizabeth H. Blackburn U.S. discovery of how chromosomes are protected by telomeres and the enzyme telomerase 2010 Robert Edwards U.K. development of in vitro fertilization Ralph M. Steinman Canada discovery of the dendritic cell and its role in adaptive immunity 2012 Sir John Bertrand Gurdon U.K. discovery that mature cells can be reprogrammed to become pluripotent Shinya Yamanaka Japan discovery that mature cells can be reprogrammed to become pluripotent 2013 James E. Rothman U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells Randy W. Schekman U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells Thomas C. Südhof Germany/U.S. discoveries of machinery regulating vesicle traffic, a major transport system in cells 2014 Edvard I. Moser Norway discoveries of cells that constitute a positioning system in the brain May-Britt Moser Norway discoveries of cells that constitute a positioning system in the brain John O'Keefe U.S./U.K. discoveries of cells that constitute a positioning system in the brain 2015 William C. Campbell Ireland discoveries concerning a novel therapy against infections caused by roundworm parasites Ōmura Satoshi Japan discoveries concerning a novel therapy against infections caused by roundworm parasites Tu Youyou China discoveries concerning a novel therapy against malaria 2016 Yoshinori Ohsumi Japan discoveries of mechanisms for autophagy 2017 Jeffrey C. Hall U.S. discoveries of molecular mechanisms controlling the circadian rhythm Michael Rosbash U.S. discoveries of molecular mechanisms controlling the circadian rhythm Michael W. Young U.S. discoveries of molecular mechanisms controlling the circadian rhythm 2018 James P. Allison U.S. discovery of cancer therapy by inhibition of negative immune regulation Honjo Tasuku Japan discovery of cancer therapy by inhibition of negative immune regulation 2019 William G. Kaelin, Jr. U.S. discoveries of how cells sense and adapt to oxygen availability Peter J. Ratcliffe U.K. discoveries of how cells sense and adapt to oxygen availability Gregg L. Semenza U.S. discoveries of how cells sense and adapt to oxygen availability 2020 Harvey J. Alter U.S. discovery of hepatitis C virus Michael Houghton U.K. discovery of hepatitis C virus Charles M. Rice U.S. discovery of hepatitis C virus 2021 David Julius U.S. discoveries of receptors for temperature and touch Ardem Patapoutian Leb./U.S. discoveries of receptors for temperature and touch 2022 Svante Pääbo Sweden discoveries concerning the genomes of extinct hominins and human evolution 2023 Katalin Karikó Hungary/U.S. discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19 | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 3 | 40 | https://www.washington.edu/research/or/honors-and-awards/nobel-prize/ | en | Nobel Prize | http://s3-us-west-2.amazonaws.com/uw-s3-cdn/wp-content/uploads/sites/10/2019/06/21094817/Univ-of-Washington_Memorial-Way.jpg | http://s3-us-west-2.amazonaws.com/uw-s3-cdn/wp-content/uploads/sites/10/2019/06/21094817/Univ-of-Washington_Memorial-Way.jpg | [] | [] | [] | [
""
] | null | [] | 2016-12-13T18:36:14+00:00 | The Nobel Prize is an annual award for outstanding contributions to chemistry, physics, physiology and medicine, literature, economics, and peace, and is widely regarded as the... | en | UW Research | https://www.washington.edu/research/or/honors-and-awards/nobel-prize/ | The Nobel Prize is an annual award for outstanding contributions to chemistry, physics, physiology and medicine, literature, economics, and peace, and is widely regarded as the most prestigious award one can receive in those fields. | |||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 6 | https://www.aljazeera.com/news/2023/10/2/katalin-kariko-drew-weissman-win-nobel-prize-in-medicine | en | Katalin Kariko, Drew Weissman win Nobel Prize in medicine for mRNA vaccines | [
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"Al Jazeera"
] | 2023-10-02T00:00:00 | The duo win the prestigious prize for the research that led directly to the first mRNA vaccines to fight COVID-19. | en | /favicon_aje.ico | Al Jazeera | https://www.aljazeera.com/news/2023/10/2/katalin-kariko-drew-weissman-win-nobel-prize-in-medicine | Hungarian-born Katalin Kariko and Drew Weissman of the US have won the 2023 Nobel Prize in Physiology or Medicine for their research that led directly to the first mRNA vaccines to fight COVID-19, made by Pfizer and Moderna, according to the awarding body.
“The laureates contributed to the unprecedented rate of vaccine development during one of the greatest threats to human health in modern times,” the jury said in Sweden’s capital Stockholm on Monday.
Katalin Kariko is a professor at Sagan’s University in Hungary and an adjunct professor at the University of Pennsylvania. Drew Weissman conducted his prizewinning research together with Kariko at the University of Pennsylvania.
The pair will receive their prize, consisting of a diploma, a gold medal and a $1m cheque, from King Carl XVI Gustaf at a formal ceremony in Stockholm on December 10, the anniversary of the 1896 death of scientist Alfred Nobel who created the prizes in his last will and testament.
The frontrunners for this year’s award in medicine included Kevan Shokat, an American biologist who figured out how to block the KRAS cancer gene behind a third of cancers, including challenging-to-treat lung, colon, and pancreatic tumours.
Two American biologists, Stanislas Leibler and Michael Elowitz, were also in the run for their work on synthetic gene circuits which established the field of synthetic biology.
It enables scientists to redesign organisms by engineering them to have new abilities.
The Nobel Prize in physiology or medicine was won last year by Swedish scientist Svante Paabo for discoveries in human evolution that unlocked secrets of Neanderthal DNA which provided key insights into our immune system, including our vulnerability to severe COVID-19.
The physics prize will be announced on Tuesday, chemistry on Wednesday and literature on Thursday. The Nobel Peace Prize will be announced on Friday and the economics award on October 9. | ||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 50 | https://www.wum.edu.pl/en/our-experts-comment-on-this-years-nobel-prize-in-physiology-or-medicine | en | Our experts comment on this year’s Nobel Prize in Physiology or Medicine | https://www.wum.edu.pl/sites/www.wum.edu.pl/files/favicon.ico | https://www.wum.edu.pl/sites/www.wum.edu.pl/files/favicon.ico | [
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] | null | [] | null | The Novel Assembly published its decision on October 2. The explanatory memorandum stated that the practical implementation of the Nobel Laureates’ findings has saved millions of lives and prevented severe disease in many more. | en | /sites/www.wum.edu.pl/files/favicon.ico | https://www.wum.edu.pl/en/our-experts-comment-on-this-years-nobel-prize-in-physiology-or-medicine | The Novel Assembly published its decision on October 2. The explanatory memorandum stated that the practical implementation of the Nobel Laureates’ findings has saved millions of lives and prevented severe disease in many more.
Who are the Laureates
Katalin Kariko is a Hungarian biochemist working in the United States, and Drew Weissman is a U.S. immunologist. They met in 1997 at The University of Pennsylvania. They started their research on mRNA technology by the end of the 1990s and made their breakthrough discovery in 2005. It had never happened before that a new technology would be awarded by the Nobel Assembly in such a short time after development.
Meeting of experts
The award of the Nobel Prize in Physiology or Medicine was an opportunity for a meeting of experts who commented on the decision of the Nobel Assembly in the course of the Nobel Week. Our University was represented by prof. Rafał Płoski, head of the Medical Genetics Department at the Faculty of Medicine, and prof. Paweł Włodarski, head of the Research Methodology Department of the Faculty of Medicine.
The Warsaw University was represented by prof. Maria Anna Ciemerych-Litwinienko of the Institute of Development Biology and Biomedical Sciences, Faculty of Biology, and prof. Katarzyna Tońska of the Institute of Genetics and Biotechnology, Faculty of Biology.
The essence of the discovery
The experts explained this years Nobel Laureates’ discovery.
– mRNA, and RNA in general are relatively unstable molecules – prof. Tońska said – and therefore it would be difficult to produce such a quantity of protein on their basis that would be capable of triggering an immune reaction in the body. This year’s Nobel Prize was awarded, among other things, for successfully stabilizing that molecule, applying it to the body and making it generate a response, for example by immunizing us to some kind of virus - the Warsaw University expert explained.
Prof. Rafał Płoski noted that the Nobel Laureates’ findings appeared concurrently with technological advancements that allow for fast, inexpensive and good sequencing of mRNA. Otherwise, the discovery would be harder to use in practice. – I think we are now facing the process of vaccine printing – the professor said – meaning that just a few days or weeks will pass from the point at which a hazard, such as a virus, is identified to actual vaccine production. This is a real breakthrough.
Possible applications
Prof. Włodarski noted that this year’s Nobel Prize was not awarded for the vaccine but for the mRNA modification technology used in the production of vaccines. – Among the numerous possible applications of this technology, there is cancer treatment, too. At our University, prof. Jakub Gołąb, in collaboration with prof. Jacek Jemielity from the Warsaw University, are working right now on the applications of a similarly modified RNA in oncology.
The experts’ Nobel Week discussion took place at the Warsaw University, with Jacek Sztolcman as facilitator. | |||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 46 | https://www.livescience.com/16342-nobel-prize-medicine-history-list.html | en | Nobel Prize in Medicine: 1901-Present | [
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"Live Science Staff"
] | 2022-10-03T14:19:50+00:00 | Here's a look at past winners of the Nobel Prize in Medicine, including the three immune researchers who took home the 2011 award.. | en | livescience.com | https://www.livescience.com/16342-nobel-prize-medicine-history-list.html | Physiology or medicine was the third prize area Alfred Nobel mentioned in his will laying out his wishes for the Nobel Prize. In 2023, the Nobel Prize came with an award of 11 Swedish kronor, or nearly $1 million dollars, which is split between each winner.
Here are the winners from 1901 to today:
2023: Katalin Karikó and Drew Weissman, "for their discoveries concerning nucleoside base modifications that enabled the development of effective mRNA vaccines against COVID-19," according to the Nobel Prize organization.
2022: Svante Pääbo, "for his discoveries concerning the genomes of extinct hominins and human evolution", according to the Nobel Prize organization.
2021: David Julius and Ardem Patapoutian, "for their discoveries of receptors for temperature and touch," according to the Nobel Prize organization.
2020: Harvey J. Alter, Michael Houghton and Charles M. Rice, "for the discovery of Hepatitis C virus," according to the Nobel Prize organization.
2019: William G. Kaelin Jr., Sir Peter J. Ratcliffe and Gregg L. Semenza, jointly "for their discoveries of how cells sense and adapt to oxygen availability," according to the Nobel Prize organization.
2018: James P. Allison and Tasuku Honjo, jointly, "for their discovery of cancer therapy by inhibition of negative immune regulation," according to the Nobel Prize organization. Their discoveries involved two different proteins that put the brakes on a person's immune system. By figuring out how to release these brakes, the researchers were able to harness a person's own immune system to fight various types of cancer.
2017: Jeffrey C. Hall, Michael Rosbash and Michael W. Young "for their discoveries of molecular mechanisms controlling the circadian rhythm," according to NobelPrize.org.
2016: Yoshinori Ohsumi for his discoveries of autophagy, or "self-eating," in yeast cells, revealing that human cells also partake in this odd cellular process, which has also been linked to diseases.
2015: William C. Campbell and Satoshi Ōmura were jointly for discovering a new treatment for infections caused by roundworm parasites. Youyou Tu was awarded the other half of the Nobel for discovering a drug to fight malaria. [Read more on the 2015 Nobel Prize in Medicine]
2014: John O'Keefe, May-Britt Moser and her husband Edvard I. Moser, "for their discoveries of cells that constitute a positioning system in the brain."
2013: James Rothman, Randy Schekman and Thomas Südhof, for their work in revealing how cells control the delivery and release of molecules — such as hormones, proteins and neurotransmitters.
2012: Sir John B. Gurdon and Shinya Yamanaka, for their groundbreaking work on stem cells.
2011: Bruce A. Beutler of the United States, Jules A. Hoffmann, born in Luxembourg, and Dr. Ralph M. Steinman, of Canada, won the prize of $1.5 million (10 million kronor). Steinman was awarded half the prize and Beutler and Hoffmann shared the other half. [Read: Immune System Researchers Win Nobel Prize in Medicine]
2010: Robert G. Edwards, "for the development of in vitro fertilization."
2009: Elizabeth H. Blackburn, Carol W. Greider, Jack W. Szostak, "for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase."
2008: Harald zur Hausen, "for his discovery of human papilloma viruses causing cervical cancer" and Françoise Barré-Sinoussi and Luc Montagnier, "for their discovery of human immunodeficiency virus."
2007: Mario R. Capecchi, Sir Martin J. Evans, Oliver Smithies, "for their discoveries of principles for introducing specific gene modifications in mice by the use of embryonic stem cells."
2006: Andrew Z. Fire, Craig C. Mello, "for their discovery of RNA interference - gene silencing by double-stranded RNA."
2005: Barry J. Marshall, J. Robin Warren, "for their discovery of the bacterium Helicobacter pylori and its role in gastritis and peptic ulcer disease."
2004: Richard Axel, Linda B. Buck, "for their discoveries of odorant receptors and the organization of the olfactory system."
2003: Paul C. Lauterbur, Sir Peter Mansfield, "for their discoveries concerning magnetic resonance imaging."
2002: Sydney Brenner, H. Robert Horvitz, John E. Sulston, "for their discoveries concerning 'genetic regulation of organ development and programmed cell death."
2001: Leland H. Hartwell, Tim Hunt, Sir Paul M. Nurse, "for their discoveries of key regulators of the cell cycle."
2000: Arvid Carlsson, Paul Greengard, Eric R. Kandel, "for their discoveries concerning signal transduction in the nervous system."
1999: Günter Blobel, "for the discovery that proteins have intrinsic signals that govern their transport and localization in the cell."
1998: Robert F. Furchgott, Louis J. Ignarro, Ferid Murad, "for their discoveries concerning nitric oxide as a signaling molecule in the cardiovascular system."
1997: Stanley B. Prusiner, "for his discovery of Prions - a new biological principle of infection."
1996: Peter C. Doherty, Rolf M. Zinkernagel, "for their discoveries concerning the specificity of the cell mediated immune defense."
1995: Edward B. Lewis, Christiane Nüsslein-Volhard, Eric F. Wieschaus, "for their discoveries concerning the genetic control of early embryonic development."
1994: Alfred G. Gilman, Martin Rodbell, "for their discovery of G-proteins and the role of these proteins in signal transduction in cells."
1993: Richard J. Roberts, Phillip A. Sharp, "for their discoveries of split genes."
1992: Edmond H. Fischer, Edwin G. Krebs, "for their discoveries concerning reversible protein phosphorylation as a biological regulatory mechanism."
1991: Erwin Neher, Bert Sakmann, "for their discoveries concerning the function of single ion channels in cells."
1990: Joseph E. Murray, E. Donnall Thomas, "for their discoveries concerning organ and cell transplantation in the treatment of human disease."
1989: J. Michael Bishop, Harold E. Varmus, "for their discovery of the cellular origin of retroviral oncogenes."
1988: Sir James W. Black, Gertrude B. Elion, George H. Hitchings, "for their discoveries of important principles for drug treatment."
1987: Susumu Tonegawa, "for his discovery of the genetic principle for generation of antibody diversity."
1986: Stanley Cohen, Rita Levi-Montalcini, "for their discoveries of growth factors."
1985: Michael S. Brown, Joseph L. Goldstein, "for their discoveries concerning the regulation of cholesterol metabolism."
1984: Niels K. Jerne, Georges J.F. Köhler, César Milstein, "for theories concerning the specificity in development and control of the immune system and the discovery of the principle for production of monoclonal antibodies."
1983: Barbara McClintock, "for her discovery of mobile genetic elements."
1982: Sune K. Bergström, Bengt I. Samuelsson, John R. Vane, "for their discoveries concerning prostaglandins and related biologically active substances."
1981: Roger W. Sperry, "for his discoveries concerning the functional specialization of the cerebral hemispheres" and David H. Hubel and Torsten N. Wiesel, "for their discoveries concerning information processing in the visual system."
1980: Baruj Benacerraf, Jean Dausset, George D. Snell, "for their discoveries concerning genetically determined structures on the cell surface that regulate immunological reactions."
1979: Allan M. Cormack, Godfrey N. Hounsfield, "for the development of computer assisted tomography."
1978: Werner Arber, Daniel Nathans, Hamilton O. Smith, "for the discovery of restriction enzymes and their application to problems of molecular genetics."
1977: Roger Guillemin and Andrew V. Schally, "for their discoveries concerning the peptide hormone production of the brain" and Rosalyn Yalow, "for the development of radioimmunoassays of peptide hormones."
1976: Baruch S. Blumberg, D. Carleton Gajdusek, "for their discoveries concerning new mechanisms for the origin and dissemination of infectious diseases."
1975: David Baltimore, Renato Dulbecco, Howard Martin Temin, "for their discoveries concerning the interaction between tumour viruses and the genetic material of the cell."
1974: Albert Claude, Christian de Duve, George E. Palade, "for their discoveries concerning the structural and functional organization of the cell."
1973: Karl von Frisch, Konrad Lorenz, Nikolaas Tinbergen, "for their discoveries concerning organization and elicitation of individual and social behaviour patterns."
1972: Gerald M. Edelman, Rodney R. Porter, "for their discoveries concerning the chemical structure of antibodies."
1971: Earl W. Sutherland, Jr., "for his discoveries concerning the mechanisms of the action of hormones."
1970: Sir Bernard Katz, Ulf von Euler, Julius Axelrod, "for their discoveries concerning the humoral transmittors in the nerve terminals and the mechanism for their storage, release and inactivation."
1969: Max Delbrück, Alfred D. Hershey, Salvador E. Luria, "for their discoveries concerning the replication mechanism and the genetic structure of viruses."
1968: Robert W. Holley, Har Gobind Khorana, Marshall W. Nirenberg, "for their interpretation of the genetic code and its function in protein synthesis."
1967: Ragnar Granit, Haldan Keffer Hartline, George Wald, "for their discoveries concerning the primary physiological and chemical visual processes in the eye."
1966: Peyton Rous, "for his discovery of tumour-inducing viruses" and Charles Brenton Huggins, "for his discoveries concerning hormonal treatment of prostatic cancer."
1965: François Jacob, André Lwoff, Jacques Monod, "for their discoveries concerning genetic control of enzyme and virus synthesis."
1964: Konrad Bloch, Feodor Lynen, "for their discoveries concerning the mechanism and regulation of the cholesterol and fatty acid metabolism."
1963: Sir John Carew Eccles, Alan Lloyd Hodgkin, Andrew Fielding Huxley, "for their discoveries concerning the ionic mechanisms involved in excitation and inhibition in the peripheral and central portions of the nerve cell membrane."
1962: Francis Harry Compton Crick, James Dewey Watson, Maurice Hugh Frederick Wilkins, "for their discoveries concerning the molecular structure of nucleic acids and its significance for information transfer in living material."
1961: Georg von Békésy, "for his discoveries of the physical mechanism of stimulation within the cochlea."
1960: Sir Frank Macfarlane Burnet, Peter Brian Medawar, "for discovery of acquired immunological tolerance."
1959: Severo Ochoa, Arthur Kornberg, "for their discovery of the mechanisms in the biological synthesis of ribonucleic acid and deoxyribonucleic acid."
1958: George Wells Beadle and Edward Lawrie Tatum, "for their discovery that genes act by regulating definite chemical events" and Joshua Lederberg, "for his discoveries concerning genetic recombination and the organization of the genetic material of bacteria."
1957: Daniel Bovet, "for his discoveries relating to synthetic compounds that inhibit the action of certain body substances, and especially their action on the vascular system and the skeletal muscles."
1956: André Frédéric Cournand, Werner Forssmann, Dickinson W. Richards, "for their discoveries concerning heart catheterization and pathological changes in the circulatory system."
1955: Axel Hugo Theodor Theorell, "for his discoveries concerning the nature and mode of action of oxidation enzymes."
1954: John Franklin Enders, Thomas Huckle Weller, Frederick Chapman Robbins, "for their discovery of the ability of poliomyelitis viruses to grow in cultures of various types of tissue."
1953: Hans Adolf Krebs, "for his discovery of the citric acid cycle" and Fritz Albert Lipmann "for his discovery of co-enzyme A and its importance for intermediary metabolism."
1952: Selman Abraham Waksman, "for his discovery of streptomycin, the first antibiotic effective against tuberculosis."
1951: Max Theiler, "for his discoveries concerning yellow fever and how to combat it."
1950: Edward Calvin Kendall, Tadeus Reichstein, Philip Showalter Hench, "for their discoveries relating to the hormones of the adrenal cortex, their structure and biological effects."
1949: Walter Rudolf Hess, "for his discovery of the functional organization of the interbrain as a coordinator of the activities of the internal organs" and Antonio Caetano de Abreu Freire Egas Moniz, "for his discovery of the therapeutic value of leucotomy in certain psychoses."
1948: Paul Hermann Müller, "for his discovery of the high efficiency of DDT as a contact poison against several arthropods."
1947: Carl Ferdinand Cori and Gerty Theresa Cori, née Radnitz, "for their discovery of the course of the catalytic conversion of glycogen" and Bernardo Alberto Houssay, "for his discovery of the part played by the hormone of the anterior pituitary lobe in the metabolism of sugar."
1946: Hermann Joseph Muller, "for the discovery of the production of mutations by means of X-ray irradiation."
1945: Sir Alexander Fleming, Ernst Boris Chain, Sir Howard Walter Florey, "for the discovery of penicillin and its curative effect in various infectious diseases."
1944: Joseph Erlanger, Herbert Spencer Gasser, "for their discoveries relating to the highly differentiated functions of single nerve fibers."
1943: Henrik Carl Peter Dam, Edward Adelbert Doisy, "for his discovery of vitamin K" and Edward Adelbert Doisy"for his discovery of the chemical nature of vitamin K."
1942: No Nobel Prize awarded
1941: No Nobel Prize awarded
1940: No Nobel Prize awarded
1939: Gerhard Domagk, "for the discovery of the antibacterial effects of prontosil."
1938: Corneille Jean François Heymans, "for the discovery of the role played by the sinus and aortic mechanisms in the regulation of respiration."
1937: Albert von Szent-Györgyi Nagyrápolt, "for his discoveries in connection with the biological combustion processes, with special reference to vitamin C and the catalysis of fumaric acid."
1936: Sir Henry Hallett Dale, Otto Loewi, "for their discoveries relating to chemical transmission of nerve impulses."
1935: Hans Spemann, "for his discovery of the organizer effect in embryonic development."
1934: George Hoyt Whipple, George Richards Minot, William Parry Murphy, "for their discoveries concerning liver therapy in cases of anemia."
1933: Thomas Hunt Morgan, "for his discoveries concerning the role played by the chromosome in heredity."
1932: Sir Charles Scott Sherrington, Edgar Douglas Adrian, "for their discoveries regarding the functions of neurons."
1931: Otto Heinrich Warburg, "for his discovery of the nature and mode of action of the respiratory enzyme."
1930: Karl Landsteiner, "for his discovery of human blood groups."
1929: Christiaan Eijkman, "for his discovery of the antineuritic vitamin" and Sir Frederick Gowland Hopkins, "for his discovery of the growth-stimulating vitamins."
1928: Charles Jules Henri Nicolle, "for his work on typhus."
1927: Julius Wagner-Jauregg, "for his discovery of the therapeutic value of malaria inoculation in the treatment of dementia paralytica."
1926: Johannes Andreas Grib Fibiger, "for his discovery of the Spiroptera carcinoma."
1925: No Nobel Prize awarded
1924: Willem Einthoven, "for his discovery of the mechanism of the electrocardiogram."
1923: Frederick Grant Banting, John James Rickard Macleod, "for the discovery of insulin."
1922: Archibald Vivian Hill, "for his discovery relating to the production of heat in the muscle" and Otto Fritz Meyerhof, "for his discovery of the fixed relationship between the consumption of oxygen and the metabolism of lactic acid in the muscle."
1921: No Nobel Prize awarded
1920: Schack August Steenberg Krogh, "for his discovery of the capillary motor regulating mechanism."
1919: Jules Bordet, "for his discoveries relating to immunity."
1918: No Nobel Prize awarded
1917: No Nobel Prize awarded
1916: No Nobel Prize awarded
1915: No Nobel Prize awarded
1914: Robert Bárány, "for his work on the physiology and pathology of the vestibular apparatus."
1913: Charles Robert Richet, "in recognition of his work on anaphylaxis."
1912: Alexis Carrel, "in recognition of his work on vascular suture and the transplantation of blood vessels and organs."
1911: Allvar Gullstrand, "for his work on the dioptrics of the eye."
1910: Albrecht Kossel, "in recognition of the contributions to our knowledge of cell chemistry made through his work on proteins, including the nucleic substances."
1909: Emil Theodor Kocher, "for his work on the physiology, pathology and surgery of the thyroid gland."
1908: Ilya Ilyich Mechnikov, Paul Ehrlich, "in recognition of their work on immunity."
1907: Charles Louis Alphonse Laveran, "in recognition of his work on the role played by protozoa in causing diseases."
1906: Camillo Golgi, Santiago Ramón y Cajal, "in recognition of their work on the structure of the nervous system."
1905: Robert Koch, "for his investigations and discoveries in relation to tuberculosis."
1904: Ivan Petrovich Pavlov, "in recognition of his work on the physiology of digestion, through which knowledge on vital aspects of the subject has been transformed and enlarged."
1903: Niels Ryberg Finsen, "in recognition of his contribution to the treatment of diseases, especially lupus vulgaris, with concentrated light radiation, whereby he has opened a new avenue for medical science."
1902: Ronald Ross, "for his work on malaria, by which he has shown how it enters the organism and thereby has laid the foundation for successful research on this disease and methods of combating it." | |||||
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] | null | [] | null | Nobel Prize facts | en | NobelPrize.org | https://www.nobelprize.org/prizes/facts/nobel-prize-facts | On 27 November 1895, Alfred Nobel signed his last will and testament, giving the largest share of his fortune to a series of prizes in physics, chemistry, physiology or medicine, literature and peace – the Nobel Prizes. In 1968, Sveriges Riksbank (Sweden’s central bank) established The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel. Learn more about the Nobel Prize laureates here.
621 Nobel Prizes
In the statutes of the Nobel Foundation it says: “A prize amount may be equally divided between two works, each of which is considered to merit a prize. If a work that is being rewarded has been produced by two or three persons, the prize shall be awarded to them jointly. In no case may a prize amount be divided between more than three persons.”
All Nobel Prize laureates
Between 1901 and 2023, the Nobel Prizes and the Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel were awarded 621 times to 1000 people and organisations. With some receiving the Nobel Prize more than once, this makes a total of 965 individuals and 27 organisations. See Multiple Nobel Prize laureates.
List of all Nobel Prize laureates
List of Nobel Prize awarded organisations
Lists of all Nobel Prize laureates in
| Physics | Chemistry | Physiology or medicine | Literature | Peace | Economic sciences |
Years without Nobel Prizes
Since the start, in 1901, there are some years when the Nobel Prizes have not been awarded. The total number of times are 49. Most of them during World War I (1914-1918) and II (1939-1945). In the statutes of the Nobel Foundation it says: “If none of the works under consideration is found to be of the importance indicated in the first paragraph, the prize money shall be reserved until the following year. If, even then, the prize cannot be awarded, the amount shall be added to the Foundation’s restricted funds.”.
Physics: 1916, 1931, 1934, 1940, 1941, 1942
Chemistry: 1916, 1917, 1919, 1924, 1933, 1940, 1941, 1942
Physiology or medicine: 1915, 1916, 1917, 1918, 1921, 1925, 1940, 1941, 1942
Literature: 1914, 1918, 1935, 1940, 1941, 1942, 1943
Peace: 1914, 1915, 1916, 1918, 1923, 1924, 1928, 1932, 1939, 1940, 1941, 1942, 1943, 1948, 1955, 1956, 1966, 1967, 1972
Economic sciences: –
Nobel Prize laureates and affiliation
Here you can find out which universities, research institutions or companies Nobel Prize laureates were affiliated with at the time of the Nobel Prize announcement.
Nobel Prize laureates listedby affiliation
The youngest Nobel Prize laureates
Physics
Chemistry
Physiology or medicine
Literature
Peace
Economic sciences
The oldest Nobel Prize laureates
Physics
Chemistry
Physiology or medicine
Literature
Peace
Economic sciences
65 Nobel Prizes to women
Between 1901 and 2023 the Nobel Prize and prize in economic sciences have been awarded 65 times to women.
List of all female Nobel Prize laureates
Two Nobel Prize laureates declined the prize
Jean-Paul Sartre, awarded the 1964 Nobel Prize in Literature, declined the prize because he had consistently declined all official honours.
Le DucTho, awarded the 1973 Nobel Peace Prize jointly with US Secretary of State Henry Kissinger. They were awarded the prize for negotiating the Vietnam peace accord. Le Duc Tho said that he was not in a position to accept the Nobel Peace Prize, citing the situation in Vietnam as his reason.
Forced to decline the Nobel Prize
Four Nobel Prize laureates have been forced by authorities to decline the Nobel Prize. Adolf Hitler forbade three German Nobel Prize laureates, Richard Kuhn, Adolf Butenandt and Gerhard Domagk, from accepting the Nobel Prize. All of them could later receive the Nobel Prize diploma and medal, but not the prize amount.
Boris Pasternak, the 1958 Nobel Laureate in Literature, initially accepted the Nobel Prize but was later coerced by the authorities of the Soviet Union, his native country, to decline the Nobel Prize.
Nobel Prize laureates under arrest at the time of the award
Five Nobel Prize laureates were under arrest at the time of the award of the Nobel Prize, all of them Nobel Peace Prize laureates:
German pacifist and journalist Carl von Ossietzky
Burmese politician Aung San Suu Kyi
Chinese human rights activist Liu Xiaobo
Belarus human rights advocate Ales Bialiatski
Iranian human rights advocate and freedom fighter Narges Mohammadi
Carl von Ossietzky
The Nobel Peace Prize 1935 for his burning love for freedom of thought and expression and his valuable contribution to the cause of peace.
Aung San Suu Kyi
The Nobel Peace Prize 1991 for her non-violent struggle for democracy and human rights.
Liu Xiaobo
The Nobel Peace Prize 2010 for his long and non-violent struggle for fundamental human rights in China.
Ales Bialiatski
The Nobel Peace Prize 2022 The Peace Prize laureates represent civil society in their home countries. They have for many years promoted the right to criticise power and protect the fundamental rights of citizens. They have made an outstanding effort to document war crimes, human right abuses and the abuse of power. Together they demonstrate the significance of civil society for peace and democracy.
Narges Mohammadi
The Nobel Peace Prize 2023 for her fight against the oppression of women in Iran and her fight to promote human rights and freedom for all.
Multiple Nobel Prize laureates
The work of the International Committee of the Red Cross (ICRC) has been honoured by a Nobel Peace Prize three times. Besides, the founder of the ICRC, Henry Dunant, was awarded the first Nobel Peace Prize in 1901.
Linus Pauling is the only person to have been awarded two unshared Nobel Prizes – the 1954 Nobel Prize in Chemistry and the 1962 Nobel Peace Prize.
John Bardeen
The Nobel Prize in Physics 1972 for their jointly developed theory of superconductivity, usually called the BCS-theory.
The Nobel Prize in Physics 1956 for their researches on semiconductors and their discovery of the transistor effect.
Marie Curie, née Skłodowska
The Nobel Prize in Chemistry 1911 in recognition of her services to the advancement of chemistry by the discovery of the elements radium and polonium, by the isolation of radium and the study of the nature and compounds of this remarkable element.
The Nobel Prize in Physics 1903 in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel.
Linus Carl Pauling
The Nobel Peace Prize 1962 for his fight against the nuclear arms race between East and West.
The Nobel Prize in Chemistry 1954 for his research into the nature of the chemical bond and its application to the elucidation of the structure of complex substances.
Frederick Sanger
The Nobel Prize in Chemistry 1980 for their contributions concerning the determination of base sequences in nucleic acids.
The Nobel Prize in Chemistry 1958 for his work on the structure of proteins, especially that of insulin.
K. Barry Sharpless
The Nobel Prize in Chemistry 2022 for the development of click chemistry and bioorthogonal chemistry.
The Nobel Prize in Chemistry 2001 for his work on chirally catalysed oxidation reactions.
Comité international de la Croix Rouge (International Committee of the Red Cross)
The Nobel Peace Prize 1963 for promoting the principles of the Geneva Convention and cooperation with the UN.
The Nobel Peace Prize 1944 for the great work it has performed during the war on behalf of humanity.
The Nobel Peace Prize 1917 for the efforts to take care of wounded soldiers and prisoners of war and their families.
Office of the United Nations High Commissioner for Refugees (UNHCR)
The Nobel Peace Prize 1981 for promoting the fundamental rights of refugees.
The Nobel Peace Prize 1954 for its efforts to heal the wounds of war by providing help and protection to refugees all over the world.
Posthumous Nobel Prizes
From 1974, the Statutes of the Nobel Foundation stipulate that a prize cannot be awarded posthumously, unless death has occurred after the announcement of the Nobel Prize. Before 1974, the Nobel Prize has only been awarded posthumously twice: to Dag Hammarskjöld (Nobel Peace Prize 1961) and Erik Axel Karlfeldt (Nobel Prize in Literature 1931).
Following the 2011 announcement of the Nobel Prize in Physiology or Medicine, it was discovered that one of the medicine laureates, Ralph Steinman, had passed away three days earlier. The Board of the Nobel Foundation examined the statutes, and an interpretation of the purpose of the rule above led to the conclusion that Ralph Steinman should continue to remain a Nobel Prize laureate, as the Nobel Assembly at Karolinska Institutet had announced the 2011 Nobel Prize laureates in physiology or medicine without knowing of his death.
“Family Nobel Prize laureates”
The Curies were a very successful ‘Nobel Prize family’. Marie Curie herself was awarded two Nobel Prizes.
Read more about Marie and Pierre Curie and the discovery of polonium and radium
More about Nobel Prize awarded couples
Married couples (at the time of the award)
Marie Curie, née Skłodowska
The Nobel Prize in Chemistry 1911 in recognition of her services to the advancement of chemistry by the discovery of the elements radium and polonium, by the isolation of radium and the study of the nature and compounds of this remarkable element.
The Nobel Prize in Physics 1903 in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel.
Pierre Curie
The Nobel Prize in Physics 1903 in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel.
Irène Joliot-Curie
The Nobel Prize in Chemistry 1935 in recognition of their synthesis of new radioactive elements.
Frédéric Joliot
The Nobel Prize in Chemistry 1935 in recognition of their synthesis of new radioactive elements.
Gerty Theresa Cori, née Radnitz
The Nobel Prize in Physiology or Medicine 1947 for their discovery of the course of the catalytic conversion of glycogen.
Carl Ferdinand Cori
The Nobel Prize in Physiology or Medicine 1947 for their discovery of the course of the catalytic conversion of glycogen.
Gunnar Myrdal
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 1974 for their pioneering work in the theory of money and economic fluctuations and for their penetrating analysis of the interdependence of economic, social and institutional phenomena.
Alva Myrdal
The Nobel Peace Prize 1982 for their work for disarmament and nuclear and weapon-free zones.
May-Britt Moser
The Nobel Prize in Physiology or Medicine 2014 for their discoveries of cells that constitute a positioning system in the brain.
Edvard I. Moser
The Nobel Prize in Physiology or Medicine 2014 for their discoveries of cells that constitute a positioning system in the brain.
Esther Duflo
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 2019 for their experimental approach to alleviating global poverty.
Abhijit Banerjee
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 2019 for their experimental approach to alleviating global poverty.
Mother & daughter
Marie Curie, née Skłodowska
The Nobel Prize in Chemistry 1911 in recognition of her services to the advancement of chemistry by the discovery of the elements radium and polonium, by the isolation of radium and the study of the nature and compounds of this remarkable element.
The Nobel Prize in Physics 1903 in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel.
Irène Joliot-Curie
The Nobel Prize in Chemistry 1935 in recognition of their synthesis of new radioactive elements.
Father & daughter
Pierre Curie
The Nobel Prize in Physics 1903 in recognition of the extraordinary services they have rendered by their joint researches on the radiation phenomena discovered by Professor Henri Becquerel.
Irène Joliot-Curie
The Nobel Prize in Chemistry 1935 in recognition of their synthesis of new radioactive elements.
Father & son
Sir William Henry Bragg
The Nobel Prize in Physics 1915 for their services in the analysis of crystal structure by means of X-rays.
William Lawrence Bragg
The Nobel Prize in Physics 1915 for their services in the analysis of crystal structure by means of X-rays.
Niels Henrik David Bohr
The Nobel Prize in Physics 1922 for his services in the investigation of the structure of atoms and of the radiation emanating from them.
Aage Niels Bohr
The Nobel Prize in Physics 1975 for the discovery of the connection between collective motion and particle motion in atomic nuclei and the development of the theory of the structure of the atomic nucleus based on this connection.
Hans Karl August Simon von Euler-Chelpin
The Nobel Prize in Chemistry 1929 for their investigations on the fermentation of sugar and fermentative enzymes.
Ulf von Euler
The Nobel Prize in Physiology or Medicine 1970 for their discoveries concerning the humoral transmitters in the nerve terminals and the mechanism for their storage, release and inactivation.
Arthur Kornberg
The Nobel Prize in Physiology or Medicine 1959 for their discovery of the mechanisms in the biological synthesis of ribonucleic acid and deoxyribonucleic acid.
Roger D. Kornberg
The Nobel Prize in Chemistry 2006 for his studies of the molecular basis of eukaryotic transcription.
Karl Manne Georg Siegbahn
The Nobel Prize in Physics 1924 for his discoveries and research in the field of X-ray spectroscopy.
Kai M. Siegbahn
The Nobel Prize in Physics 1981 for his contribution to the development of high-resolution electron spectroscopy.
Joseph John Thomson
The Nobel Prize in Physics 1906 in recognition of the great merits of his theoretical and experimental investigations on the conduction of electricity by gases.
George Paget Thomson
The Nobel Prize in Physics 1937 for their experimental discovery of the diffraction of electrons by crystals.
Sune K. Bergström
The Nobel Prize in Physiology or Medicine 1982 for their discoveries concerning prostaglandins and related biologically active substances.
Svante Pääbo
The Nobel Prize in Physiology or Medicine 2022 for his discoveries concerning the genomes of extinct hominins and human evolution.
Brothers
Jan Tinbergen
The Sveriges Riksbank Prize in Economic Sciences in Memory of Alfred Nobel 1969 for having developed and applied dynamic models for the analysis of economic processes.
Nikolaas Tinbergen
The Nobel Prize in Physiology or Medicine 1973 for their discoveries concerning organization and elicitation of individual and social behaviour patterns.
The Nobel Prize award ceremonies
On December 10, 1901, the Nobel Prizes were awarded for the first time in Stockholm and in Christiania (now Oslo) respectively.
The Nobel Prize award ceremony in Stockholm took place at the Old Royal Academy of Music during the years 1901-1925. Since 1926, the ceremony has taken place at the Stockholm Concert Hall with few exceptions: 1971 in the Philadelphia Church; 1972 in the St. Erik International Fair (known today as Stockholm International Fairs) in Älvsjö, 1975 in the St. Erik International Fair and in 1991 at the Stockholm Globe Arena. The King of Sweden hands over the prize to the laureate/s.
In Norway, during the years 1901-1904 the decision on the peace prize was announced at a meeting of the Storting on 10 December, after which the recipients were informed in writing. During 1905-1946 the Nobel Peace Prize award ceremonies were held at the Nobel Institute building, during 1947-1989 in the auditorium of the University of Oslo and since 1990 at the Oslo City Hall. The King of Norway is present, but it is the Chairman of the Nobel Committee who hands over the prize to the laureate/s.
Ceremonies archive
The Nobel Prize insignias
At the Nobel Prize award ceremonies on 10 December the Nobel Prize laureates receive three things: a Nobel Prize diploma, a Nobel Prize medal and a document confirming the Nobel Prize amount. Each Nobel Prize diploma is a unique work of art, created by foremost Swedish and Norwegian artists and calligraphers. The Nobel Prize medals are handmade with careful precision and in 18 carat recycled gold.
The Nobel Prize medals in physics, chemistry, physiology or medicine and literature are identical on the face: it shows the image of Alfred Nobel and the years of his birth and death (1833-1896). Nobel’s portrait also appears on the Nobel Peace Prize medal and the medal for the prize in economic sciences, but with a slightly different design. The image on the reverse varies according to the institution awarding the prize.
More about the Nobel Prize medals
The Nobel Prize diplomas
Each Nobel Prize diploma is a unique work of art, created by foremost Swedish and Norwegian artists and calligraphers.
More about the Nobel Prize diplomas
The Nobel Prize amount
Alfred Nobel left most of his estate, more than SEK 31 million (today approximately SEK 1,702 million) to be converted into a fund and invested in “safe securities.” The income from the investments was to be “distributed annually in the form of prizes to those who during the preceding year have conferred the greatest benefit to mankind.”
The Nobel Prize amount for 2023 was set at Swedish kronor (SEK) 11.0 million per full Nobel Prize.
More about the Nobel Prize amount
* Why are the individuals and organisations awarded a Nobel Prize called Nobel Prize laureates?
The word “laureate” refers to being signified by the laurel wreath. In Greek mythology, the god Apollo is represented wearing a laurel wreath on his head. A laurel wreath is a circular crown made of branches and leaves of the bay laurel (in Latin: Laurus nobilis). In Ancient Greece, laurel wreaths were awarded to victors as a sign of honour – both in athletic competitions and in poetic meets.
More facts on the Nobel Prizes | |||||
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] | null | [] | null | In the first week of October each year, the recipients of the Nobel Prizes in Physiology or Medicine, Physics, Chemistry, Literature and Peace are announced, as Alfred Nobel stated in his will. First out is the Nobel Prize in Physiology or Medicine — and it is the Nobel Assembly at Karolinska Institutet that selects the recipients since 1901. | en | /themes/custom/theorell/images/favicon/apple-touch-icon.png | https://ki.se/en/about-ki/prizes-and-ceremonies/prizes-and-awards/the-nobel-prize-in-physiology-or-medicine | Few prizes attract the same attention worldwide and have such a rigorous selection process as the Nobel Prize. Thomas Perlmann is the one who makes that life-changing phone call the first Monday of every October. But it's actually not his favourite part of the job. Find out what thrills the secretary of KI's Nobel Assembly and Committee the most.
Most researchers will never come close to winning a Nobel Prize. But some are fortunate enough to work with one of the 200 or so living Nobel legends of the research world. Meet three of the lucky ones.
During Nobel Week, the world's eyes are directed towards Stockholm and ground-breaking research. For KI's researchers, it is a chance to focus on research that deserves more attention. Organize your event during the week and get traction in marketing via Nobel Calling Stockholm.
In 2022, research on the importance of Neanderthals to modern humans was rewarded. Or rather, how we carry their genes, which have been shown to be associated with both sensitivity to pain and the risk of developing severe covid-19, to name a few examples.
Svante Pääbo's Nobel Prize-winning research has also presented Denisovans, a previously unknown human species that has also contributed to the DNA of living humans.
The 2021 prize is about how people can feel temperature and touch. The discoveries explain basic functions in our lives and have opened doors to new treatments for pain, for example. We take for granted the fact that we can feel an icy wind or a hot plate, but how this actually works was discovered by the Nobel Laureates.
The 2020 prize awarded the discovery of the hepatitis C virus. Thanks to the work of the laureates, it is now possible to detect the virus in blood and to provide an effective treatment for the infection. It has saved the lives of millions of people. The prize also focuses on the importance of research into viruses.
The 2019 prize went to three laureates that explained a vital ability – how cells adapt to the availability of oxygen. These discoveries have opened the door to new strategies for combating anaemia, cancer and many other diseases and are now being investigated further at institutions like Karolinska Institutet.
The Royal Swedish Academy of Sciences awarded the 2022 Nobel Prize in Chemistry to K. Barry Sharpless, Morten Meldal and Carolyn R. Bertozzi for the development of click chemistry, a quick and efficient way to build molecules. Several KI researchers use the “Lego-like” technique in their daily research and one has co-authored a study with one of this year's prize winners.
The 2021 Nobel Prize in Chemistry rewarded Benjamin List and David MacMillan for a new and ingenious tool for building molecules, asymmetric organocatalysis, which has contributed to more environmentally friendly chemical and pharmaceutical manufacturing. KI researcher Per I Arvidsson was one of those who introduced organocatalysis in Sweden and says that the prize was expected.
The Royal Swedish Academy of Sciences awarded the 2020 Nobel Prize in Chemistry to Emmanuelle Charpentier and Jennifer A. Doudna for the development of a method for genome editing. Several KI researchers use the method in their own research. “It’s the best tool to study gene function at the molecular level,” says KI Professor Galina Selivanova who has met one of the laureates. | |||||
wrong_mix_random_subsidiary_00131 | FactBench | 2 | 85 | https://www.lindau-nobel.org/blog-nobel-prize-in-physiology-medicine-2023-a-new-way-of-looking-at-vaccines/ | en | Nobel Prize in Physiology/Medicine 2023: A New Way of Looking at Vaccines | [
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"Hanna Kurlanda-Witek"
] | 2023-12-07T12:37:48+00:00 | The Nobel Prize in Physiology or Medicine 2023 is awarded to Katalin Karikó and Drew Weissman who laid the basis for inventing mRNA vaccines. Their research made it possible to develop COVID-19-vaccines quickly. | en | Lindau Nobel Laureate Meetings | https://www.lindau-nobel.org/blog-nobel-prize-in-physiology-medicine-2023-a-new-way-of-looking-at-vaccines/ | Just three years ago, in December 2020, the first COVID-19 vaccine was given to a person outside of a clinical trial. Ninety-year-old Margaret Keenan received the vaccine at a hospital in Coventry, UK, and news of the event spread far and wide. At the time, many people were facing strict restrictions for the upcoming holidays, the Alpha, Beta, and Delta variants of the SARS-CoV-2 virus were identified as variants of concern, and an estimated 1.5 million people worldwide had died from the disease. That vaccination marked a turning point for many throughout the long months of quarantines, lockdowns and COVID-19 waves, particularly for healthcare workers. It also spurred the fastest vaccine rollout in history.
The first COVID-19 vaccine brought to market was based on the use of messenger RNA (mRNA) to induce an immune response to a pathogen, a different approach to developing vaccines, as opposed to using weakened or inactivated viruses, or viral vectors. It took many years to overcome the technical obstacles to enable mRNA vaccines to work, and for these efforts, the Nobel Prize in Physiology or Medicine 2023 was awarded to Katalin Karikó and Drew Weissman.
A Recipe for a Protein
mRNA is a single strand of genetic material that serves as a copy of one gene from a cell’s DNA. Once the information is copied onto mRNA, the molecule can travel from the cell’s nucleus, where the DNA is stored, to the cytoplasm, where the information is translated into a protein molecule. mRNA was discovered in 1961 and the concept of using it as a potential vaccine was envisioned in the late 1980s after in vitro transcription made it possible to synthesise RNA without a cell culture. But the problem was that mRNA induced inflammation in the organism. And even without that significant obstacle, mRNA was considered an unstable molecule, one that would be quickly degraded by the organism before it could perform its function.
Biochemistry and Immunology
In the early 1990s the development of mRNA into therapeutics became a central theme in Katalin Karikó’s research. The biochemist had recently emigrated to the U.S. from Hungary and for years faced many difficulties in getting grants. In 1997, she met the immunologist Drew Weissman, who had just been hired by the University of Pennsylvania, where Karikó had worked since 1989 and had recently been demoted. Weissmann was interested in dendritic cells, which can control adaptive immune responses. They began to work together to figure out how mRNA can be administered safely, without triggering a strong inflammatory response.
Success came in 2005, when Karikó and Weissman found that by modifying uridine, one of the four nucleosides of RNA, into pseudouridine, it was possible to suppress the capacity of mRNA to activate dendritic cells. Yet the time still wasn’t ripe for the scientific community to appreciate these findings. Despite many efforts and continued research, Karikó was refused a faculty position by the University of Pennsylvania in 2013 and for the next nine years commuted to Germany, where she was Senior Vice President of BioNTech. She had no idea that an mRNA vaccine would soon be one of the most sought-after therapeutics on the planet.
The Value of Perseverance
The story behind this year’s Nobel Prize in Physiology or Medicine isn’t only about excellence in scientific research, it’s also a story of remarkable resilience, fuelled by determination and a love of science. “Nothing distracts me from my work,” Weissman told Nobel Media’s Adam Smith soon after learning he had won the prize. Career trajectories can go awry even after reaching important milestones. Karikó was mostly dependent on the support and encouragement of her family to keep going, and remained optimistic by echoing the words of Hans Selye, the Hungarian-Canadian endocrinologist, “You have to focus on the things you can change.”
Recent studies have shown that mRNA-based vaccines against COVID-19 have the highest total efficacy and effectiveness compared to other vaccines. But the hurdles are still there in convincing people that the technology is safe. “As important as the vaccine is, if you don’t take it, it won’t work,” said Weissman. This is crucial for potential future applications of mRNA-based therapeutics, which aim to treat a wide range of illnesses, from genetic diseases to cancer.
A pandemic unexpectedly brought mRNA technology to the forefront of medical research, but as a knock-on effect, effective science communication became more important than ever. The a bundance of Q&As, graphics and videos on how mRNA vaccines work is a good example for science communication with a comprehensive approach. | |||||
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wrong_mix_random_subsidiary_00131 | FactBench | 1 | 87 | https://www.binghamton.edu/news/story/2424/the-nobel-journey-of-m-stanley-whittingham | en | The Nobel journey of M. Stanley Whittingham | [
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"Rachel Coker"
] | null | Distinguished professor earns chemistry prize for lithium-ion battery development | en | /favicon.ico | News - Binghamton University | https://www.binghamton.edu/news/story/2424/the-nobel-journey-of-m-stanley-whittingham | M. Stanley Whittingham was attending a scientific conference in Germany when the news reached him: You are a Nobel laureate.
The Binghamton University chemist had delivered the keynote address that morning. During a break in the meeting, one of the conference organizers told him someone was trying to reach him. She said they were going to call her phone and she’d hand it to him.
The call was from two members of the Nobel committee. And they had life-changing news for Whittingham: He and two other pioneers in the development of the lithium-ion battery — Akira Yoshino and John B. Goodenough — would share in the 2019 Nobel Prize for Chemistry.
“A number of things clicked,” says Whittingham, whose colleague later asked why he didn’t seem more jubilant. “I was probably in shock, and I smiled later.”
Next Whittingham tried calling home. It was Oct. 9 and his wife, who’s Jewish, had turned off her phone for Yom Kippur observances. He sent texts to his son and daughter after that. It turned out that one of his four grandkids had already heard the news.
It was the beginning of an adventure more than 40 years in the making.
Whittingham, now 78, invented the first rechargeable lithium-ion battery in 1977 at Exxon Research and Engineering Co. Although he worked alongside Nobel winners there, he didn’t consider the possibility he’d one day join their ranks.
“When you’re 30 years old,” he says, “you don’t really think about Nobel prizes.”
Decades later, however, the prize was very much on the minds of many at Binghamton University. In 2015, Thomson Reuters named Whittingham to a list of likely future laureates, noting the significance of his work on the lithium-ion battery.
That fall, the campus communications office was on alert during the Nobel announcements. But when years passed without a prize for Whittingham, that sense of anticipation lessened. By 2019, the news caught Binghamton by surprise.
***
In December, Whittingham traveled to Sweden for a week of events that included the presentation of the Nobel prizes. He was joined by his wife, their children and grandchildren, other relatives and a small number of Binghamton colleagues. President Harvey Stenger, university photographer Jonathan Cohen and Whittingham’s longtime assistant, Elaine Schmitz, were on hand for some of the festivities.
Stenger was struck by the way Whittingham was received during a program at the home of Judith Gough, the British ambassador to Sweden. The event honored Whittingham and Sir Peter J. Ratcliffe, a British physician-scientist who shared in the 2019 Nobel Prize in Physiology or Medicine. Gough had two electric vehicles — a Jaguar and a London city taxicab — on hand for the occasion.
“Stan was introduced by the British ambassador,” Stenger says. “She just gushed over him. She was so excited about his work.”
Whittingham was one of three laureates chosen to speak via satellite with astronauts on the International Space Station. Lithium-ion batteries had been installed on the station within the past month, so they had a lot to talk about, he says.
He also enjoyed talking to a couple of the Swedish princesses during some of the formal meals that were held in honor of the laureates.
The week was packed with activities and receptions, but Whittingham did do a little bit of sight-seeing. He went to Abba The Museum (No. 4 on TripAdvisor’s list of things to do in Stockholm) as well as to the Vasa Museum nearby (No. 1). The Vasa, a warship that sank on her maiden voyage in the 17th century, was salvaged some 300 years later.
“The experience that I had with him in Stockholm was probably one of the highlights of my life,” Stenger says. “It was fun. It was exciting. The different ceremonies were impressive.”
The award ceremony itself was quite staid and scripted, with men in tuxedos and women in gowns. All of the participants — except Swedish King Carl XVI Gustaf, who has been presenting the prizes since 1973 — rehearsed their roles in advance.
Carl-Henrik Heldin, chairman of the Board of Directors of the Nobel Foundation, opened the ceremony with remarks in English about the value of science and scientific progress, including a quote from Carl Sagan: “There are many hypotheses in science which are wrong. That’s perfectly all right: it’s the aperture to finding out what’s right. Science is a self-correcting process.”
Afterward, some 1,300 people, including the king and queen of Sweden, attended a formal banquet at city hall for a three-course meal.
Stenger, who has attended his fair share of fancy occasions as a university president, described the scene as “unbelievable.” The menu featured caviar, stuffed duck and several desserts. “I can’t imagine anything being more elaborate than this banquet,” Stenger says. He heard there were 50 chefs and 350 waiters on hand for the occasion.
Whittingham and his wife were seated at the king and queen’s table. One person representing each prize gets to speak, and Whittingham represented his colleagues.
He took the opportunity to celebrate innovation across the world: “This prize also reinforces that science is truly an international endeavor involving most of the countries in this world,” he remarked. “I am an Englishman in America. John Goodenough, an American, made his inventions in England. Akira Yoshino was in Japan. Science knows no geographical boundaries.”
Stenger says Whittingham was the only speaker who addressed the human dimension of his work, not just the research itself. “He was so humble,” Stenger says. “It was a great speech with just a perfect message.”
Whittingham, who sometimes used to wonder if his research was “too applied” to attract the notice of the Nobel committee, now says he thinks the invention fits Alfred Nobel’s original plan for the prizes quite well. Nobel specified in his will that the bulk of his fortune should be used for prizes in physics, chemistry, physiology or medicine, literature and peace to those who “have conferred the greatest benefit to humankind.”
Everyone can relate to batteries, Whittingham says, and maybe even understand them a little. After all, these days almost everyone is walking around with lithium-ion batteries in their cellphones and laptops.
Now he says he prefers to describe his work as “focused” research. “There’s some goal in mind; it’s not just research for its own sake,” Whittingham says. “I like to feel it makes a difference.”
While Whittingham was in Sweden, the BBC broadcast a program called “Nobel Minds Debate.” He represented the chemistry laureates for the discussion. When moderator Zeinab Badawi described the invention of the lithium-ion battery, she didn’t hold back: “This provided stable, lightweight, renewable energy storage, helping to create the right conditions for a wireless world free of fossil fuels. The world’s most powerful battery.”
***
Whittingham was born in Nottingham, England, and attended school in Lincolnshire before going to New College, Oxford, where he did his undergraduate and graduate work in chemistry.
Whittingham’s father, a civil engineer, was the first in his family to go to college. Since then, relatives have embraced the sciences: Whittingham’s brother is also a chemist, and a niece earned her doctorate in materials science from Cambridge.
When he completed his degree at Oxford, Whittingham came to the United States for a postdoctoral fellowship at Stanford University.
“I wanted to see the world,” he recalls. “I wanted to see the sunshine. There was an opportunity in California, and I grabbed it!”
Several scientists from his former group at Oxford have gone on to do work at Stanford in the decades since. “It’s not a bad pedigree,” Whittingham says with a small smile.
After he completed his postdoctoral studies, Whittingham went to work at Exxon. This was before the oil crisis, he notes, and Exxon aspired to be the best energy company in the world, with investments in research related to renewable energy as well as oil.
The battery Whittingham and his team developed at Exxon was smaller than other rechargeable batteries of the day (lead-acid cells like the ones still found in many cars) and unlike smaller, disposable batteries (the kind you probably still use in your TV remote), it could be recharged.
The critical discovery? As Exxon explains: That when lithium ions were held between plates of titanium sulfide, the ions could move back and forth between the positive and negative contacts, creating electricity. Whittingham was the first to find a way to use lithium to store energy at room temperature and without the risk of explosion.
Later, Goodenough built on Whittingham’s work to use metal oxides and higher, 4-volt materials. Yoshino expanded on that work, providing a safe carbon anode to replace lithium metal and developing the first commercial lithium-ion battery.
The key word in describing this chemistry is “intercalation,” Whittingham says. The word used to refer to putting Feb. 29 into the calendar every fourth year and taking it back out. In chemical terms, it means putting lithium ions into a structure without changing the structure itself.
Think of it like adding a layer of jam between two pieces of bread. “The lithium is the jam in the sandwich,” Whittingham says, and the bread isn’t changed.
***
Several years later, Whittingham — by then at Schlumberger-Doll Research — decided he was going to leave industry.
The opportunity to be a mentor and to work with scientists at all different stages of their careers appealed to him. “In companies, you all age together,” he says. “In a university, you get a new group of 18-year-olds in each year. It keeps you younger.”
He spoke to people at several schools, including campuses that were looking for department chairs. “What’s special at Binghamton is that there are no barriers between the departments,” he says. “You can interact with geologists, physicists, engineers with no issues. At many major schools, you have fiefdoms.”
Another big plus? Greater Binghamton’s reasonable commute times. Whittingham wanted to be able to live in the country and drive to work in five or 10 minutes.
At Binghamton, Whittingham has continued to thrive. He helped to establish the Materials Science and Engineering Program, built international collaborations and published about 200 journal articles. His work has been supported with more than $20 million in federal funding.
Whittingham has no plans to rest on his new laurels. He thinks it’s possible to double the energy density in today’s batteries within the next decade — moving from 250 watt-hours per kilogram to perhaps 500 — but his real goal is to cut down the price.
He is motivated by a desire to tackle climate change, and he’s not shy about saying so. In Sweden, he checked to see if people would object to him speaking about the crisis, and instead the idea was met with encouragement. “There’s no issue in Europe about global warming,” he says. “There’s no issue in this country among sensible people.”
Batteries should make it possible to store energy produced by large-scale solar facilities and wind farms, he notes. “Lithium batteries can play a big role,” Whittingham says. “They will enable the shutting down of the dirtiest coal plants.”
Stenger says Whittingham is eager to translate the Nobel into support for research and manufacturing in Greater Binghamton. If that means attending the governor’s State of the State address or appearing at a large alumni dinner, Whittingham’s game.
“He wants to use this to get even more research done, and more applied research done,” Stenger notes. “He’s trying to leverage his Nobel into more research and more work. He also is being very generous with his time.”
Stenger describes Whittingham as “the consummate absent-minded professor,” a modest man who sometimes forgets to get his hair cut for a while and doesn’t care much about his clothes.
That may be, but these days Whittingham can’t go to Wegmans for groceries without being recognized. And he can no longer respond to all of his email the day it arrives. He keeps the Nobel Prize in a safe at the bank, though he’s been known to pull one of the duplicates he ordered — gold plated instead of solid gold — from his pocket during a speech.
He poses for lots of photos, though he stopped signing so many autographs after his wife noticed some of them popping up on eBay for more than $100 apiece.
Whittingham has received invitations to speak all over the world, but a couple of honors stand out among the rest. His birthday — Dec. 22 — was listed in The Times of London. And he was named an honorary Fellow of his college at Oxford. (It may be called New College, but it was founded in 1379.)
“The biggest perk is I’m allowed to park my car inside the college,” he says with a laugh.
For now, Whittingham has no plans to leave the research that has been his life’s work.
“My doctor says don’t retire,” he says. “As long as I’m happy and I like what I’m doing, I’ll be around.” | ||||
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Nobel Peace Prize 2014
Already at eleven years of age Malala Yousafzai fought for girls’ right to education. After having suffered an attack on her life by Taliban gunmen in 2012, she has continued her struggle and become a leading advocate of girls’ rights.
In memoriam
Bengt Samuelsson passed away on 5 July 2024, age 90. He was awarded the 1982 Nobel Prize in Physiology or Medicine for discoveries concerning prostaglandins and related biologically active substances.
Biography
Canadian author Alice Munro passed away on 15 May 2024. She was awarded the Nobel Prize in Literature 2013 with the motivation “master of the contemporary short story”.
Biography
Roger Guillemin passade away on 21 February, age 100. He was awarded the Nobel Prize in Physiology or Medicine 1977 for discoveries concerning the peptide hormone production of the brain.
Biography
Physicist Peter Higgs passed away on 8 April 2024, age 94. He was awarded the Nobel Prize in Physics 2013 for the theory of how particles acquire mass.
Biography | ||||||
wrong_mix_random_subsidiary_00131 | FactBench | 1 | 68 | https://apnews.com/article/nobel-prize-medicine-71306bd18785477f3a85a69caa6e09c9 | en | Karikó and Weissman win Nobel Prize in medicine for work that enabled mRNA vaccines against COVID-19 | https://dims.apnews.com/dims4/default/23b35d1/2147483647/strip/true/crop/5616x3159+0+293/resize/1440x810!/quality/90/?url=https%3A%2F%2Fassets.apnews.com%2F9d%2Fe7%2F65325a43429fbe0ab6543d6e691b%2F7adfba2ec17d4608b4b75943af5da56d | https://dims.apnews.com/dims4/default/23b35d1/2147483647/strip/true/crop/5616x3159+0+293/resize/1440x810!/quality/90/?url=https%3A%2F%2Fassets.apnews.com%2F9d%2Fe7%2F65325a43429fbe0ab6543d6e691b%2F7adfba2ec17d4608b4b75943af5da56d | [
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] | 2023-10-02T07:06:22+00:00 | The Nobel Prize in medicine went to Katalin Karikó and Drew Weissman for discoveries that enabled the development of mRNA vaccines against COVID-19. | en | /apple-touch-icon.png | AP News | https://apnews.com/article/nobel-prize-medicine-71306bd18785477f3a85a69caa6e09c9 | STOCKHOLM (AP) — Two scientists won the Nobel Prize in medicine on Monday for discoveries that enabled the creation of mRNA vaccines against COVID-19 that were critical in slowing the pandemic — technology that’s also being studied to fight cancer and other diseases.
Hungarian-American Katalin Karikó and American Drew Weissman were cited for contributing “to the unprecedented rate of vaccine development during one of the greatest threats to human health,” according to the panel that awarded the prize in Stockholm.
The panel said the pair’s “groundbreaking findings ... fundamentally changed our understanding of how mRNA interacts with our immune system.”
WHAT IS THE NOBEL PRIZE FOR?
Traditionally, making vaccines required growing viruses or pieces of viruses and then purifying them before next steps. The messenger RNA approach starts with a snippet of genetic code carrying instructions for making proteins. Pick the right virus protein to target, and the body turns into a mini vaccine factory.
In early experiments with animals, simply injecting lab-grown mRNA triggered a reaction that usually destroyed it. Those early challenges caused many to lose faith in the approach: “Pretty much everybody gave up on it,” Weissman said.
But Karikó, a professor at Szeged University in Hungary and an adjunct professor at the University of Pennsylvania, and Weissman, of the University of Pennsylvania, figured out a tiny modification to the building blocks of RNA that made it stealthy enough to slip past immune defenses.
Karikó, 68, is the 13th woman to win the Nobel Prize in medicine. She was a senior vice president at BioNTech, which partnered with Pfizer to make one of the COVID-19 vaccines. Karikó and Weissman, 64, met by chance in the 1990s while photocopying research papers, Karikó told The Associated Press.
WHY DO MRNA VACCINES MATTER?
Dr. Paul Hunter, a professor of medicine at Britain’s University of East Anglia, described the mRNA vaccines made by BioNTech-Pfizer and Moderna Inc. as a “game changer” in shutting down the coronavirus pandemic, crediting the shots with saving millions of lives.
“We would likely only now be coming out of the depths of COVID without the mRNA vaccines,” Hunter said.
John Tregoning, of Imperial College London, called Karikó “one of the most inspirational scientists I have met.” Her work together with Weissman “shows the importance of basic, fundamental research in the path to solutions to the most pressing societal needs,” he said.
The duo’s pivotal mRNA research was combined with two other earlier scientific discoveries to create the COVID-19 vaccines. Researchers in Canada had developed a fatty coating to help mRNA get inside cells to do its work. And studies with prior vaccines at the U.S. National Institutes of Health showed how to stabilize the coronavirus spike protein that the new mRNA shots needed to deliver.
Dr. Bharat Pankhania, an infectious diseases expert at Exeter University, predicted the technology used in the vaccines could be used to refine vaccines for other diseases like Ebola, malaria and dengue, and might also be used to create shots that immunize people against certain types of cancer or auto-immune diseases including lupus.
HOW DID KATALIN KARIKÓ AND DREW WEISSMAN REACT?
“The future is just so incredible,” Weissman said. “We’ve been thinking for years about everything that we could do with RNA, and now it’s here.”
Karikó said her husband was the first to pick up the early morning call, handing it to her to hear the news. And Karikó was the one to break the news to Weissman, since she got in touch before the Nobel committee could reach him.
Both scientists thought it was a prank at first, until they watched the official announcement.
“I was very much surprised,” Karikó said. “But I am very happy.”
The two have collaborated for decades, with Karikó focusing on the RNA side and Weissman handling the immunology: “We educated each other,” she said.
Before COVID-19, mRNA vaccines were already being tested for diseases like Zika, influenza and rabies — but the pandemic brought more attention to this approach, Karikó said. Now, scientists are trying out mRNA approaches for cancer, allergies and other gene therapies, Weissman said.
“It’s already been going on for many years, but this has just given RNA the recognition,” Weissman said.
Karikó's family is no stranger to high honors. Her daughter, Susan Francia, is a double Olympic gold medalist in rowing, competing for the United States.
The prize carries a cash award of 11 million Swedish kronor ($1 million) from a bequest left by the prize’s creator, Swedish inventor Alfred Nobel. The laureates are invited to receive their awards at ceremonies on Dec. 10, the anniversary of Nobel’s death.
Nobel announcements continue with the physics prize on Tuesday, chemistry on Wednesday and literature on Thursday. The Nobel Peace Prize will be announced Friday and the economics award on Oct. 9.
___
This story has been updated to correct that Karikó is a professor at Szeged University, not Sagan’s University.
___
Corder reported from The Hague, Netherlands. Burakoff reported from New York. Associated Press writers Maria Cheng in London and Lauran Neergaard in Washington contributed.
___
The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institute’s Science and Educational Media Group. The AP is solely responsible for all content.
___ | ||
wrong_mix_random_subsidiary_00131 | FactBench | 3 | 67 | https://www.lakeforest.edu/news/the-nobel-prize-in-physiology-or-medicine-a-century-of-winners | en | The Nobel Prize in Physiology or Medicine: A Century of Winners | [
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] | null | [] | null | Amber Craghead Department of Biology Lake Forest College Lake Forest, Illinois 60045 Download PDF | en | /Content/assets/img/favicon.ico | null | Thomas Morgan received the Nobel Prize in 1933 for his discoveries involving chromosomes and heredity [1]. Morgan was the first to propose that genes are linear despite the conclusion made by Castle that they were not (Morgan et al., 1920). Using Drosophila as his model organism, Morgan was also able to determine that some genes were sex-linked and were limited to the sex chromosomes (Morgan, 1910). Morgan’s work on genetics using Drosophila provided the ground work for Hermann Joseph Muller’s 1946 Nobel Prize for his discovery that x-ray irradiation can produce mutations [1]. At the time that Morgan and Muller were performing their genetics research, Barbara McClintock was also investigating genetics and heredity using corn as her model. Through studying the pigmentation of corn kernels, McClintock was able to discover mobile genetic elements for which she did not win the Nobel Prize until 1983 [1].
In 1929, Sir Alexander Fleming noticed that a contaminating Penicillium mold was inhibiting the growth of Staphylococcus colonies and was causing them to undergo lysis (Fleming, 1929). From this “by chance” observation, he had discovered penicillin, one of the most effective antibiotics. For this discovery, he received the Nobel Prize in 1945 along with Ernst Boris Chain and Sir Howard Walter Florey [1]. The discovery of penicillin had dramatic effects worldwide as it was able to treat a wide range of bacterial infections by inhibiting bacterial cell wall formation. Fleming’s work played a role in Selman Waksman’s discovery of streptomycin, which won him the Nobel Prize in 1952 [1].
The 1962 Nobel Prize in Physiology or Medicine went to James Watson, Francis Crick and Maurice Wilkins for their discovery of the molecular structure of DNA (the double helix) [1]. During the 1950s, the race was on to determine the structure of DNA and prominent scientists, including Linus Pauling, were actively searching for it. X-ray crystallographer Rosalind Franklin successfully produced images of DNA that clearly showed a helical pattern but without her permission, Watson and Crick used these images to propose the double helix structure in their 1953 paper “Molecular structure of nucleic acids: a structure for deoxyribose nucleic acid”. While we know now that Watson and Crick were correct, one of the most important parts of their paper comes in one of the last sentences in which they suggest that this structure may play a role in the copying of genetic information, which we also now know to be true.
The concept of the DNA double helix seems so basic to us today, but 60 years ago it was completely unknown. Another concept of biology that seems elementary to us, the organelles of the cell, was also not completely nailed down until recently. In 1974, George Palade received the Nobel Prize for discoveries regarding the structure and organization of the cell [1]. More notably, Palade discovered the ribosome; he noticed a “small granule” that was present in multiple cell types that seemed to concentrate around the endoplasmic reticulum, while a small minority could be found floating freely around the cell (Palade, 1955). Because of Palade’s discovery, we now understand the process of protein synthesis via translation within the cytoplasm of the cell.
In the 1980s, two very important Nobel Prizes were awarded in the fields of cholesterol metabolism and neuroembryology. In 1985, Michael Brown and Joseph Goldstein won the Prize for their discoveries involving cholesterol metabolism. Through studying a man with familial hypercholesterolemia, they were able to determine the mechanism of LDL binding in cells, the importance of coated pits on the cell surface, and how FH forms as a result of failure of the cells to uptake LDL (Anderson, Goldstein, & Brown, 1977). The following year, Rita Levi-Montalcini won the Prize for her discovery of growth factors. Using chicken embryos as her model organism, she exposed the embryos to mouse sarcomas and snake venom and noticed a dramatic increase in sensory ganglia growth (Levi-Montalcini & Cohen, 1956). From her experiments, she was able to determine that an agent secreted from the sarcomas and snake venom was causing the increase in nerve cell growth and today, this knowledge has been applied to cancer research. |