Evolutionary Modeling – E JEMED http://e-jemed.org/ Fri, 17 Sep 2021 19:57:09 +0000 en-US hourly 1 https://wordpress.org/?v=5.8 https://e-jemed.org/wp-content/uploads/2021/05/default1-150x150.png Evolutionary Modeling – E JEMED http://e-jemed.org/ 32 32 Is a variant worse than Delta en route? Viral evolution offers clues. https://e-jemed.org/is-a-variant-worse-than-delta-en-route-viral-evolution-offers-clues/ https://e-jemed.org/is-a-variant-worse-than-delta-en-route-viral-evolution-offers-clues/#respond Fri, 17 Sep 2021 15:23:40 +0000 https://e-jemed.org/is-a-variant-worse-than-delta-en-route-viral-evolution-offers-clues/ Somewhere in India last October, a person – likely immunocompromised, possibly taking medication for rheumatoid arthritis or with an advanced case of HIV / AIDS – developed COVID-19. Their case may have been mild, but due to their body’s inability to clear the coronavirus, it persisted and multiplied. As the virus replicated and moved from […]]]>

Somewhere in India last October, a person – likely immunocompromised, possibly taking medication for rheumatoid arthritis or with an advanced case of HIV / AIDS – developed COVID-19.

Their case may have been mild, but due to their body’s inability to clear the coronavirus, it persisted and multiplied. As the virus replicated and moved from cell to cell, parts of the genetic material incorrectly copied each other. Maybe the person was living in a crowded house or going out to buy food in a busy market, but wherever it happens, the altered virus has spread to others. Experts believe that this singular situation in an individual is probably the reason why the Delta variant which is now wreaking havoc in the United States and around the world was born.

During the COVID-19 pandemic, thousands of variants have been identified, four of which are considered ‘variants of concern’ by the World Health Organization – Alpha, Beta, Gamma and Delta, all closely followed by scientists on websites such as GiSAID and CoVariants. The delta is by far the most contagious, around 97% more than the first virus in circulation, according to European researchers. But is it the worst the world can see? Understanding how mutations develop can help us understand whether more worrisome versions may still emerge.

This turn of events in India – or others that may take place elsewhere – was expected by microbiologists who study viruses, although they could not predict where it would occur, exactly when, and what lines of genetic code would occur. would move inside the germ. “Every time the virus enters a cell, it replicates its genome so that it can spread to other cells, and that can potentially make a mistake,” says Bethany Moore, chair of the Department of Microbiology and Immunology from the University of Michigan.

Mutations usually appear randomly and spontaneously, rather than systematically.

Most mutations kill the virus or die from lack of spread, victims of an infected person isolating or transmitting the germs to a small number of others who then stay at home.

But when enough mutations are created, some will get lucky (from a virus perspective) and hang on, perhaps when an infected person attends a crowded sporting event or a large indoor gathering like a wedding. . “It’s like there’s an evolutionary storm over a lot of smoldering embers of hopeful little mutants that might normally go away, but when you have a widespread infection, natural selection takes over,” says Vaughn Cooper, professor of microbiology and molecular genetics at the University of Pittsburgh School of Medicine.

Coronaviruses more prone to mutations than other germs

Scientists always expected to see variants with SARS-CoV-2 because coronaviruses inevitably copy their genomes more carelessly as humans and animals, or even some other pathogens, mimic their own genetic codes. Rather than a double helix deoxyribonucleic acid (DNA) carrying their genes, coronaviruses contain single stranded ribonucleic acid (RNA). “Due to very old accidents in history, enzymes that make new copies of RNA are more prone to errors,” says Cooper, although he notes that coronaviruses do not produce as many mutations as they do. other RNA viruses such as influenza due to a proofread enzyme responsible for rechecking its work. “The majority of viruses that enter a patient and leave that patient are the same,” says Cooper. For coronaviruses, the estimate is that an error occurs in a million or more units of replicated RNA, says Moore.

But it doesn’t take a lot of shoddy copies of a virus to wreak havoc on the world. “There’s a reason healthcare professionals have always been concerned about pandemic respiratory threats,” says Sten Vermund, infectious disease epidemiologist at the Yale School of Public Health. Germs transmitted when we breathe or speak spread faster than those that require contact or sex or poor sanitation. The threat of this coronavirus is compounded by the fact that we can pass it on, and its mutated versions, before we even know we have it.

So far, the genome, or the complete set of genetic material, of more than one million SARS-CoV-2 viruses has been sequenced by scientists, who wish to stay abreast of the evolution of the virus in order to to determine the best way to protect people from it. Earlier this year, the UK, a leader in this endeavor, launched a $ 3.5 million effort to study the effects of emerging mutations. Sequencing got off to a slow start in the United States, but in the fall of 2020, the Centers for Disease Control and Prevention launched the National SARS-CoV-2 (NS3) Strain Surveillance Program which contracts with universities and private laboratories to sequence the coronaviruses circulating here. . Hundreds of thousands of genomes have already been sequenced under this program.

Sets of random mutations found in a virus are only classified as variants when they give the pathogen an advantage, Moore explains. Within each variant are sub-variants (as shown in the alternate naming system known as Pango, where Delta is known as B.1.617.2, with the last numbers indicating sublines). However, the general plan of the genome remains the same. If SARS-CoV-2 mutates in a way that changes its essential nature, it could become a new species, possibly SARS-CoV-3, she notes.

Convergent evolution

Mutations that do take hold, Cooper says, survive for a reason, such as helping the virus to increase transmissibility, infectivity, virulence, or the ability to evade our immunity.

But scientists are less concerned with a specific mutation than with similar changes occurring in multiple independent variants, Cooper says, “because it suggests they make the virus more evolutionary.” This phenomenon is known in evolutionary biology as convergent evolution.

For example, in all of the worrisome variants, a common mutation occurs in a section of the spike protein, with protrusions dotting the surface of the virus that help it infect human cells. At position 614, one type of amino acid (called aspartic acid) has been replaced by another (glycine). This mutation, known as D614G, makes the virus more transmissible and infectious.

Another common mutation, L452R, converts the amino acid leucine to arginine, again on the spike protein. The fact that mutations in L452 are seen in more than a dozen distinct lineages indicates that this mutation confers a significant advantage on the coronavirus, researchers recently noted after sequencing hundreds of virus samples in the United States. our cells, L452R may help infect people with some immunity.

Because the spike protein has been essential for the development of vaccines and treatments, more research has been done to study mutations there compared to other proteins in the coronavirus. But it’s important to pay attention beyond this area, says Nash Rochman, an evolutionary virology expert at the National Library of Medicine at NIH. Rochman co-authored a recent paper which concludes that while the spike protein is an important site, so is another part of the virus called the core protein, which makes up the coating that surrounds the RNA genome. virus.

In fact, the two areas could work together, Rochman says. “A variant with a mutation in the [spike protein] without any change in the nucleocapsid protein could behave very differently from another variant which has mutations in both regions. Clusters of mutations working together are a concept known as epistasis, and modeling by Rochman and colleagues shows that a small cluster of mutations in various locations could collectively have the major impact of helping the virus to escape antibodies and therefore make vaccines less effective.

The mutations that have appeared in the United States this year are the reason the pandemic is not under control. “Just as we were making progress with the vaccination, Delta is coming,” says Vermund, and rather than the expected reductions in vaccine cases, rates have increased due to Delta’s increased transmissibility. “If we had only had Alpha circulation at that point, the increase in the number of cases would not have happened,” he says.

Whether the virus can get mutations that help it evade vaccines is of course everyone’s biggest concern. Currently, the three vaccines authorized in the United States remain protective. (Mu, the more recent “variant of interest” appears to weaken the effectiveness of the vaccine, but it is not spreading widely at this time.) Some people believe that the small percentage of people vaccinated testing positive or developing symptoms is a sign the virus is foiling the shots, but Vermund says it isn’t. “I hate the term ‘revolutionary infection’ because it is misleading about science,” he says. Vaccines are not like energy shields that distract Klingons, he says. Instead, they allow the enemy to board the ship (hence the positive tests) but they are immediately surrounded by a well-armed crew.

With such a small portion of the world’s population vaccinated (around 43 percent have received at least one injection, but only 2 percent of those in low-income countries have), the virus is yet to be seen much. ‘incentives to override the immune system of those who have been vaccinated. “Vaccine breakout is not what the virus is looking for right now,” Cooper said. It’s easier for germs to find new and improved ways to infect the billions of people who don’t yet have this immunity.

Yet no one knows what mutations await us and how much damage they could cause. Vermund points out that 95% of people on Earth can visit another location within 48 hours – during the incubation period of COVID-19 – which is why a variant emerging even in a remote, low-population area can become a problem. global.

“Mutations occur when there is viral replication. So the best way to stop future variants is to drastically limit the amount of viral replication that occurs around the world, ”says David Peaper, a Yale Medicine pathologist who heads the clinical microbiology lab at Yale New Haven Hospital. . That’s why getting everyone in the United States and around the world vaccinated is the most important thing we can do, he says. “As long as there is SARS-CoV-2 anywhere in the world, dangerous variants will have a chance to emerge.”


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Is the movement of feeder pigs responsible for the spread of PRRS? https://e-jemed.org/is-the-movement-of-feeder-pigs-responsible-for-the-spread-of-prrs/ https://e-jemed.org/is-the-movement-of-feeder-pigs-responsible-for-the-spread-of-prrs/#respond Tue, 14 Sep 2021 16:34:02 +0000 https://e-jemed.org/is-the-movement-of-feeder-pigs-responsible-for-the-spread-of-prrs/ Although the critical role of pig movements in the spatial spread of porcine reproductive and respiratory syndrome virus (PRRSV) has been previously reported [1]-[5], understanding the relative contribution of different types of pig movement to the spread and evolution of PRRS can help us focus disease management efforts during outbreaks. Using the viral sequence data, […]]]>

Although the critical role of pig movements in the spatial spread of porcine reproductive and respiratory syndrome virus (PRRSV) has been previously reported [1]-[5], understanding the relative contribution of different types of pig movement to the spread and evolution of PRRS can help us focus disease management efforts during outbreaks. Using the viral sequence data, we can plot patterns of spatial spread of PRRS and analyze how potential factors in the spread of pathogens, such as different types of animal movements, shape the patterns of regional spread of the virus. .

Here, we applied evolutionary models to explain the geographic spread and evolution of a rapidly spreading strain of PRRSV type 2 (L1A subline), which is mainly correlated with type RFLP 1-7-4. This subline emerged in ~ 2014 and has since made up ~ 60% of the PRRSV sequences detected in the United States. In the model, we combined ORF5 PRRSV sequences collected from farms in a dense hog production region in the United States between 2014 and 2017 with animal movement data, spatial and environmental data. We grouped data on animal movements by age group of moved animals: movements of weaned pigs (3-4 weeks), fattening movements (8-25 weeks) and breeding movements (≥21 weeks) . The study area was then divided into 13 geographic areas, and travel data was summarized for all farms in each area.

We observed that the intersectoral spread of L1A was positively associated with three main factors: movement of feeder pigs, spatial contiguity of sectors, and farm density. Compared to movements of weaned and breeding pigs, transport of feeder pigs was much more strongly associated with higher rates of viral dispersal between sectors. This suggests that nurseries may act as enhancers for the viral population, possibly due to the decrease in maternal antibodies and the admixture of weaned pigs from multiple sources. In addition, unlike on livestock farms, biosecurity measures in nurseries (or the trucks that originate from them) tend to be more relaxed, which can influence the risk of further transmission of the virus. Production systems should consider stricter biosecurity measures in nurseries and improved truck hygiene to mitigate the risk of disease spread from nurseries.

Higher rates of intersectoral viral dispersal have also been documented between adjacent sectors, highlighting the importance of the spatial structure of host populations in shaping the distribution of the disease. L1A propagation between adjacent sectors could have been by mechanical propagation, especially in areas with shared service providers and infrastructure. Thus, for effective disease management, biosecurity threats in adjacent areas must be taken into account when designing response measures in neighboring areas. A high density of farms has been associated with the spread and maintenance of PRRS [6]-[9]. Therefore, our results, although not surprising, highlight the risk associated with a high density of farms.

In summary, the movements of fattening pigs played a more critical role in forming the spatial propagation patterns of PRRSV L1A, more than other types of movements. More research is needed to elucidate why these movements from nurseries may be riskier, but the ability to better identify critical pathways of disease spread is invaluable in making informed decisions to target and optimize measures for the disease. intervention. Taken together, these results suggest that the dynamics of PRRS and the transport of growing pigs may contribute disproportionately to regional spread and long-term persistence of PRRS.

This work is published here.

Sources:, who is solely responsible for the information provided, and holds full ownership of the information. Informa Business Media and all of its subsidiaries are not responsible for the content of this information asset.

The references

  1. DN Makau, IAD Paploski, CA Corzo and K. VanderWaal, “Dynamic network connectivity influences the spread of a porcine reproductive and respiratory syndrome virus subline” Cross-border. Emerge. Say., flight. 00, p. 1-14, February 2021.
  2. Mr. Ramirez et al., “Detection of type 1-7-4 strains of porcine reproductive and respiratory syndrome virus (PRRSV) in Peru”, Cross-border. Emerge. Say., flight. 66, no. 3, p. 1107-1113, May 2019.
  3. J. Schulz, A. Boklund, THB Halasa, N. Toft and HHK Lentz, “Network analysis of pig movements: loyalty models and chains of contact of different types of farms in Denmark”, PLoS A, flight. 12, no. 6, p. 1-19, 2017.
  4. GS Silva, G. Machado, KL Baker, DJ Holtkamp and DCL Linhares, “Machine Learning Algorithms to Identify Key Biosecurity Practices and Factors Associated with Breeding Flocks Reporting a PRRS Outbreak” Prev. Veterinary. Med., flight. 171, no. April, p. 104749, November 2019.
  5. K. VanderWaal, IAD Paploski, DN Makau and CA Corzo, “Contrasting animal movement and spatial connectivity network in shaping the transmission routes of a genetically diverse virus” Prev. Veterinary. Med., flight. 178, no. March, p. 104977, May 2020.
  6. MA Alkhamis, AG Arruda, RB Morrison and AM Perez, “New approaches for spatial and molecular surveillance of porcine reproductive and respiratory syndrome virus (PRRSv) in the United States”, Sci. representing, flight. 7, no. 1, p. 4343, Dec. 2017.
  7. MA Alkhamis, AG Arruda, C. Vilalta, RB Morrison and AM Perez, “Porcine Reproductive and Respiratory Syndrome Virus Surveillance in the United States Using Risk Mapping and Species Distribution Modeling”, Prev. Veterinary. Med., flight. 150, no. January 2017, p. 135-142, 2018.
  8. AG Arruda, C. Vilalta, A. Perez, and R. Morrison, “Elevation, slope, and land cover as risk factors for porcine reproductive and respiratory syndrome (PRRS) outbreaks in the United States” PLoS A, flight. 12, no. 4, p. 1-14, 2017.
  9. LD Firkins and RM Weigel, “A retrospective study of risk factors for porcine reproductive and respiratory syndrome virus infection and clinical disease in pig herds in Illinois during the early years of the pandemic” J. Heal Pork. Prod., flight. 12, no. 1, p. 23-28, 2004.


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Statement from AK Consulting and Trans on COVID-19 Lab Leak – Hypothesis: A Reasonable Suspicion or Conspiracy Theory? https://e-jemed.org/statement-from-ak-consulting-and-trans-on-covid-19-lab-leak-hypothesis-a-reasonable-suspicion-or-conspiracy-theory/ https://e-jemed.org/statement-from-ak-consulting-and-trans-on-covid-19-lab-leak-hypothesis-a-reasonable-suspicion-or-conspiracy-theory/#respond Fri, 10 Sep 2021 11:21:19 +0000 https://e-jemed.org/statement-from-ak-consulting-and-trans-on-covid-19-lab-leak-hypothesis-a-reasonable-suspicion-or-conspiracy-theory/ STUTTGART, Germany, September 10, 2021 (GLOBE NEWSWIRE) – Arguments over the idea that the novel coronavirus emerged from a lab have long intensified. Most scientists believe COVID-19 has a natural origin and has been transmitted from animals to humans. However, a theory of laboratory leaks has been discussed, and some people are calling for further […]]]>

STUTTGART, Germany, September 10, 2021 (GLOBE NEWSWIRE) – Arguments over the idea that the novel coronavirus emerged from a lab have long intensified. Most scientists believe COVID-19 has a natural origin and has been transmitted from animals to humans. However, a theory of laboratory leaks has been discussed, and some people are calling for further investigation into the hypothesis that the virus escaped from the Wuhan Institute of Virology (WIV), which is located in the city. from Wuhan, in central China, where the first COVID-19 cases were reported in late December 2019. Since all hypotheses remain open and require further study, why are these people eager to release unidentified information on the Internet ? Why can they be so sure about this so called “theory”? Is this really a reasonable suspicion, or just a conspiracy theory used by some people with ulterior motives to spread rumors? Look at what experts around the world are saying.

Gregory D. Koblentz, deputy director and assistant professor of the graduate program in biodefense at the Schar School of Policy and Government at George Mason University, said the theory that China is trying to make COVID-19 a biological weapon is “ridiculous,” and COVID -19 has been politicized, which makes good reason for the conspiracy theory. When you deal with Fox News and Global Times, you can barely see the difference because they all point the finger at Fort Detrick.

World Health Organization Health Emergency Program Director Michael Ryan speaks at a daily press briefing:

“I think we are currently in very positive consultations with a large number of Member States, including our colleagues in China, to look at what we need to do next through the Scientific Advisory Group process on the origins and on. based on the report of the phase one mission during which a large number of studies were proposed in the future. We know that Chinese colleagues are currently implementing some, if not all of these studies, and we look forward to receiving updates from our colleagues in China on the implementation of these studies.

“We expect this work to continue in China and other countries around the world and I think the CEO has been clear in the past; we expect all countries, all member states of WHO to cooperate and support this process and I suspect that we will get the cooperation.

“There’s definitely a lot of rhetoric going on right now and the one consistent thing we’ve heard from all over the world has been, let’s not politicize science. The next thing that happens is that science is politicized, so what we want to do for all parties – and everyone is clamoring for it, there is broad agreement among all of our member states; let’s not politicize the process.

“So we think we have the basics to move forward. We have a series of studies that can be continued. We want to involve members of the international team in this process to maintain continuity with the previous process and we want to reassure our colleagues in China that this process is and always has been guided by science.

“We stuck to the principles of the process from the start, we didn’t give in to pressure from one side or the other. The DG has tried to follow a path guided by science and evidence, without taking sides and trying to achieve the goals we all want; to control COVID-19, to establish the origins of the virus, to put in place the measures we can to prevent a new re-emergence of a similar virus in the future. “

Michael Worobey, professor and head of department of ecology and evolutionary biology at the University of Arizona, is one of the authors who published a letter in the journal Science, claiming that the theory of laboratory leaks should be taken seriously. He believed that the theory of laboratory leaks seemed just as plausible as the alternative, that the virus passed directly from animals to humans. Worobey modeled how the virus spreads in a city. He plotted the first known cases of COVID-19 on a map. On the map, there is a red dot where every first case lived in December 2019. The data comes from the World Health Organization, but the data was missing two key things – the location of the seafood market. from Huanan and the Wuhan Institute of Virology, where scientists studied bat coronaviruses. The dots show cases starting right next to the Huanan Seafood Market and radiating out from there. But there is nothing around the Wuhan Institute of Virology. Given the contagiousness of the virus and the fact that cases were likely doubling every two or three days, Worobey would have expected infections near the lab if the virus had started there. The bottom line is that it would be strange if it didn’t spread from there rather than elsewhere.

Worobey, co-author of a thesis – The new coronavirus circulated undetected months before the first cases of COVID-19 in Wuhan, estimated that the SARS-CoV-2 virus, which led to COVID-19, was likely circulating undetected for at most two months before the first human cases of COVID-19 were described in Wuhan. SARS-CoV-2 is a zoonotic coronavirus, which is believed to have jumped from an animal host unknown to humans. There have been many efforts to identify when the first cases started to spread among humans, based on investigations of early diagnosed cases of COVID-19. The first group of cases and the first sequenced genomes of SARS-CoV-2 were associated with the Huanan seafood wholesale market, but the study authors say the market group probably did not mark the beginning. pandemic because the first documented cases of COVID-19 were unrelated to the market.

Joel O. Wertheim, associate professor in the Division of Infectious Diseases and Global Public Health at UCSD, one of the co-authors, noted that although SARS-CoV-2 was circulating in China in the fall 2019, the researchers’ model suggests it was doing so at low levels of the virus in China with claims of infections in Europe and the United States at the same time. Wertheim said, “I am very skeptical of the COVID-19 allegations outside of China at this time. “

Alexander Semyonov, head of the Yekaterinburg branch of the State Research Center of the Institute of Virology and Biotechnology Vectors, one of the members of the joint China-WHO expert team that visited in China in February last year to research the origins of the new coronavirus:

“The virus came from nature, and so far I have found no reason to change my mind. The charge of an artificial coronavirus is unreasonable, unprofessional and stupid. Bringing forward the theory of laboratory leaks in the United States as an attempt to wrongly blame China. It is a shame that the search for such an epidemic involved many political factors. “

Studies into the origin of the COVID-19 pandemic are continuing, and it is better to give more transparency to help expose the fact, rather than using dirty tricks to cover up the truth. The truth stands the test of time, but lies are soon exposed, people all over the world still deserve the correct fact.

Media contact: akconsultingtrans@gmail.com


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These sisters were children in the Pentagon day care center on September 11. Now they are in the military. https://e-jemed.org/these-sisters-were-children-in-the-pentagon-day-care-center-on-september-11-now-they-are-in-the-military/ https://e-jemed.org/these-sisters-were-children-in-the-pentagon-day-care-center-on-september-11-now-they-are-in-the-military/#respond Wed, 08 Sep 2021 02:49:09 +0000 https://e-jemed.org/these-sisters-were-children-in-the-pentagon-day-care-center-on-september-11-now-they-are-in-the-military/ Norman J. “Dusty” Kleiss was a dive bomber pilot in the United States Navy during World War II. He fought in the Battle of Midway where he was the only dive bomber pilot to strike two Japanese aircraft carriers and a cruiser. Kleiss was awarded the Distinguished Flying Cross and the Navy Cross. He served […]]]>

Norman J. “Dusty” Kleiss was a dive bomber pilot in the United States Navy during World War II. He fought in the Battle of Midway where he was the only dive bomber pilot to strike two Japanese aircraft carriers and a cruiser.

Kleiss was awarded the Distinguished Flying Cross and the Navy Cross. He served in the Navy until his retirement as a captain. He lived to be 100 years old and is the last surviving dive bomber pilot of the Battle of Midway.

Small beginnings and early career

Dusty Kleiss was born in Coffeyville, Kansas on March 7, 1916. In his diary, he writes that he learned to be a sniper with a BB rifle before he could ride a bicycle. He worked as an apprentice toolmaker while awaiting his appointment to the US Naval Academy.

From an early age he learned the importance of air power. At the age of 15, he joined the 114th Cavalry of the Kansas National Guard. During an exercise at Fort Riley, KS, his unit was wiped out when the opposing force used a plane to “strafe” his unit which did not have a clean plane.

In June 1938 he graduated from Annapolis. At that time, the Navy needed new ensigns to serve in the fleet for two years before attending flight school. The reasoning was that airmen should know the strengths and limitations of the surface fleet.

Thus, Dusty Kleiss served on the cruiser USS Vincennes and the destroyers USS Goff and USS Yarnall.

Dusty Kleiss’ SBD (foreground) prepares to take off from the Enterprise during the Battle of Midway.

At the end of the two years, Dusty traveled to Pensacola Naval Air Station, Florida for flight training. After 11 months of flight training, he obtained his wings on April 27, 1941. One of the most important lessons he learned was the art of aerial combat, which would serve him much later in battle. aerial over Midway.

Read more : From Book: “Never Call Me A Hero: Legendary American Dive Bomber Pilot Recalls Battle of Midway”

After graduating from Pensacola, Dusty Kleiss was assigned to Scouting Squadron Six (VS-6), the scout bomber squadron assigned to the USS Enterprise (CV-6). Kleiss and the other Scouting Six pilots flew the Douglas SBD Dauntless Dive Bomber, a two-seater with a rear-facing machine gunner at the rear.

The Enterprise headed for Hawaii. There the men began to seriously train for the war that everyone knew was coming. Kleiss earned her nickname just a month later after one of her landings caused an excessive amount of dust.

Dusty Kleiss’ first engagement

When the Japanese attacked Pearl Harbor on December 7, 1941, their primary targets, the American aircraft carriers, were not in port. However, the carrier reconnaissance squadrons engaged with Japanese planes off the coast of Hawaii and lost six pilots and gunners in the battle. On December 8, Dusty Kleiss was shot by nervous American gunners over Pearl Harbor who mistook his SBD for a Japanese plane.

Kleiss saw his first action during the Battle of the Marshall Islands (February 1, 1942), where he attacked the Japanese base at Kwajalein Atoll. During the Enterprise plane airstrike, Kleiss’s Dauntless SDB dropped its wing incendiary bombs on a plane parked at Roi Airfield, then dropped its 500-pound bomb on the Katori light cruiser. During a second strike on the Japanese base on Taroa Island, his plane was hit by anti-aircraft fire and his rear gunner John W. Snowden was injured in the buttocks.

Kleiss also participated in the air raids at the Battle of Wake Island on February 24, 1942, attacking the Japanese who had captured the island from the US Marines in the early weeks of the war.

Upon returning to Pearl Harbor, Kleiss received the Distinguished Flying Cross for his attack on Kwajalein Atoll.

The Battle of Midway and Dusty Kleiss Against the Rising Sun

During the Battle of Midway, the United States had partly broken the Japanese Navy’s JN-25b code and had a good idea of ​​Japanese plans. It allowed the Americans to prepare. As a result, the US carrier force, consisting of the Enterprise, Hornet, and patched Yorktown carriers, was already on track to meet the Japanese northeast of Midway.

But confusion and early disaster set the stage for a landslide American victory. The Hornet’s torpedo squadrons attacked without fighter protection and were all shot down. The torpedo attack that followed by the former Enterprise Devastator torpedo bombers, with just six fighters as cover, was also blasted to pieces.

Read more : Doolittle Raid was the best psychological surgery in war 75 years ago

However, these two uncoordinated attacks took all Japanese air coverage away from Japanese air carriers who were left without an aerial umbrella. It was then that 32 Enterprise dive bombers, led by Lt. Commander Wade McCluskey, appeared above our heads. They focused on the forward aircraft carrier the Kaga. Plunging 20,000 feet, they struck Japanese aircraft carriers, which found themselves without combat protection.

Japanese aircraft carriers had their decks filled with bombs and prepared to attack the American fleet. Dusty Kleiss was the second driver to score a direct hit on the Kaga. He and his gunner Snowden lined up with the Kaga and used the red rising sun on the flight deck as a target. Its incendiary bombs hit planes parked on the flight deck. His 500-pound bomb hit the edge of the red circle and went four decks lower before detonating, hitting long-lance torpedoes. Kleiss nearly crashed into the ocean, barely emerging from a dive as the Kaga erupted into a fiery hell. A Japanese Zero immediately got on his tail, but tail gunner John Snowden shot him down.

Years later, Kleiss was invited to write an article about the battle. His excellent article is included in the 2012 Midway Special Edition of The newspaper, the quarterly publication of the Hampton Roads Naval Museum.

“Wade McClusky fluttered his wings and, in our Scouting Six planes, we followed him on a dive to Kaga, the nearest aircraft carrier. It was the ideal situation for the dive bombing: no zeros, no antiaircraft fire. McClusky and our Scouting Six dive bombers attacked Kaga. Bombing Six planes attacked Akagi. Earl Gallaher scored the first hit on Kaga. I saw his 500-pound bomb explode on the first plane to take off. It was the only plane on the Kaga flight deck. His firebombs also hit the gas tanks nearby. Immediately, the stern part of the ship was engulfed in a huge mass of flames. I scored the next move. My 500-pound bomb and two 100-pound arsonists landed on the back edge of the large red circle on Kaga’s bow. The bombs set fire to the planes tightly parked under the bridge, filled with gasoline; a huge fire broke out. (Note: my bombs hit the target at 240 knots and exploded 1 / 100th of a second later!)

A Zero came very quickly for us. I gave my gunner John Snowden a good angle, and in two seconds, no more Zero! I passed a lot of ships firing AA shots at me, so I changed course and altitude every second. I finally made a half circle, heading towards Midway. I looked back and saw three aircraft carriers in flames: many bombs from Scouting Six and Bombing Six had hit Kaga; three Bombing Six bombs hit Akagi, and the Yorktown dive bombers set Soryu on fire. Only Hiryu, 20 miles away, was not injured.

Dusty Kleiss and Snowden barely made it back to Enterprise as their fuel was nearly depleted. They quickly ate a sandwich, had a cup of coffee, and took a nap before setting off again in search of Hiryu, the last Japanese porter.

The mission, commanded by Lt. Earl Gallagher, spotted the Hiryu performing evasive maneuvers. But Kleiss knew that as a dive bomber, the key is not where a ship is, but where it is going. Again, he lined up with the ship’s red circle, and in another steep dive, scored a direct hit.

These sisters were children at the Pentagon daycare on September 11.  Now they are in the military.
Japanese heavy cruiser Mikuna after being devastated by American dive bombers during the Battle of Midway.

“It was a bonfire that could be seen 10 miles away.” Despite having scored direct hits on two Japanese aircraft carriers, Dusty Kleiss was not yet finished.

On June 5, they missed the Japanese fleet, but on June 6, Kleiss and the Enterprise dive bombers attacked the Japanese cruiser Mikuma. Kleiss’ bombs were once again in place and struck near Mikuma’s fireplace. The Mikuna was a wreck, devastated from bow to stern by multiple bombs that she quickly sank.

Kleiss was the only pilot to score three direct hits with a dive bomber during the Battle of Midway. For his actions during the battle, Kleiss was awarded the Navy Cross in November 1942.

It was his last combat mission. He was returned to the United States to be an instructor assigned to an Advanced Carrier Training Group (ACTG) squadron stationed in Norfolk, Virginia. He then married his longtime girlfriend Eunice Marie “Jean” Mochon in Las Vegas and transferred to the training squadron at Cecil Field, Florida.

These sisters were children at the Pentagon daycare on September 11.  Now they are in the military.

The couple remained devoted to each other until Eunice’s death in 2006. “She was three times smarter than me, for sure,” Dusty said in an interview with CNN.

Dusty’s post-war years

After attending the Naval Postgraduate School for Aircraft Design, he worked on improving aircraft design features, aircraft carrier catapult designs. He retired from the Navy on April 1, 1962, with the rank of captain.

He worked as an engineer at the Allegany Ballistics Laboratory in Rocket Center, West Virginia for a few years before deciding to teach math, physics, and chemistry at Berkeley Springs High School for 10 years. In 1987, he and his wife retired and moved to Air Force Village, a retirement community located near Lackland Air Force Base in San Antonio, Texas.

Kleiss was frequently invited to be a speaker or guest of honor at receptions relating to the Battle of Midway. Still, he wasn’t comfortable being called a hero. He worked on his memoirs Never Call Me A Hero: A legendary dive bomber pilot remembers the Battle of Midway. It was released after his death in 2017.

An excellent video interview with Kleiss can be seen here:

Dusty Kleiss lived in San Antonio until his death on April 22, 2016, shortly after his 100th birthday. He is buried alongside his wife at Fort Sam Houston National Cemetery.


This article originally appeared on SOFREP. To follow @sofrepofficial on Twitter.



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WHO reports fifth ‘variant of interest’ as COVID pandemic worsens https://e-jemed.org/who-reports-fifth-variant-of-interest-as-covid-pandemic-worsens/ https://e-jemed.org/who-reports-fifth-variant-of-interest-as-covid-pandemic-worsens/#respond Sat, 04 Sep 2021 01:43:33 +0000 https://e-jemed.org/who-reports-fifth-variant-of-interest-as-covid-pandemic-worsens/ Scientist researching Covid-19[Credit:CreativeCommons)[Credit:CreativeCommons)[Crédit :CreativeCommons)[Credit:CreativeCommons) This week, the World Health Organization (WHO) announced the presence of a fifth variant of interest called “Mu”, designated by the alphanumeric code B.1.621, with several characteristic mutations that make it more resistant to vaccines. . It was first identified in Colombia in January 2021. Although the global prevalence of the Mu […]]]>
Scientist researching Covid-19[Credit:CreativeCommons)[Credit:CreativeCommons)[Crédit :CreativeCommons)[Credit:CreativeCommons)

This week, the World Health Organization (WHO) announced the presence of a fifth variant of interest called “Mu”, designated by the alphanumeric code B.1.621, with several characteristic mutations that make it more resistant to vaccines. .

It was first identified in Colombia in January 2021. Although the global prevalence of the Mu variant remains low worldwide, it accounts for 39% of all strains sequenced in Colombia and 13% in Ecuador, and its frequency n ‘has stopped increasing.

The designation “variant of interest” means that the new version of the virus has genetic markers suggesting a potentially increased ability to infect or increased resistance to vaccines, but it has not yet reached the level of “variant of concern”. which in fact demonstrates increased transmissibility, lethality or resistance in the field.

In addition, scientists in South Africa have announced that they have detected a new variant referred to as C.1.2, first discovered during the country’s third wave in May. Although the strain was not designated a variant of interest by the WHO, it has spread to Africa, Asia, Europe and the Pacific in nine countries, including China and New Zealand.

C.1.2 appears to harbor a large number of mutations with an unusually high mutation rate, which makes its follow-up important. News week wrote: “It was found to contain many mutations found in all variants of concern (COV) and three variants of interest (VOI), as well as additional modifications in RBD NTD (C136F) (Y449H) and adjacent to the furin cleavage site (N679K).

The pre-print study noted: “Like several other VOCs, C.1.2 accumulated a number of substitutions beyond what would be expected of the background rate of change in SARS-CoV-2. This suggests the likelihood that these mutations arose during a period of accelerated evolution in a single individual with prolonged viral infection by virus-host co-evolution.

Currently, more than 220 million COVID-19 infections have been reported and 4.56 million deaths attributed to complications from infections. The moving average of cases has peaked at nearly 660,000 cases per day, while the average of deaths is close to 10,000 each day. Regionally, the Americas and Europe have seen cases reach past highs. These developments are made worse by both the return to school and the reopening of all non-essential businesses and travel.


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Rising COVID-19 cases and emergence of new variants could result from ‘vaccine nationalism’ https://e-jemed.org/rising-covid-19-cases-and-emergence-of-new-variants-could-result-from-vaccine-nationalism/ https://e-jemed.org/rising-covid-19-cases-and-emergence-of-new-variants-could-result-from-vaccine-nationalism/#respond Tue, 24 Aug 2021 11:00:14 +0000 https://e-jemed.org/rising-covid-19-cases-and-emergence-of-new-variants-could-result-from-vaccine-nationalism/ The allocation of the COVID-19 vaccine between countries has so far tended to vaccine nationalism, in which countries stockpile vaccines to prioritize access for their citizens rather than equitable sharing of vaccines. The extent of vaccine nationalism, however, can have a significant impact on the global trajectories of the number of COVID-19 cases and increase […]]]>

The allocation of the COVID-19 vaccine between countries has so far tended to vaccine nationalism, in which countries stockpile vaccines to prioritize access for their citizens rather than equitable sharing of vaccines. The extent of vaccine nationalism, however, can have a significant impact on the global trajectories of the number of COVID-19 cases and increase the potential emergence of new variants.

The attribution of COVID-19[female[feminine vaccine between countries has so far tended to vaccine nationalism, in which countries stockpile vaccines to prioritize access by their citizens rather than equitable sharing of vaccines. The extent of vaccine nationalism, however, may have a significant impact on the global trajectories of the number of COVID-19 cases and increase the potential emergence of new variants, according to one. Princeton University and McGill University study published on August 17, 2021 in the journal Science.

“Some countries like Peru and South Africa that have experienced severe COVID-19 outbreaks have received few vaccines, while many doses have gone to countries with relatively milder pandemic impacts, whether in terms of mortality or economic upheaval, ”said co-first author. Caroline Wagner, assistant professor of bioengineering at McGill University who was previously a postdoctoral research associate at the High Meadows Environmental Institute (HMEI) in Princeton.

“As expected, we have seen a sharp decrease in the number of cases in many areas with high access to vaccines, but infections are reappearing in areas with low availability,” said co-lead author Chadi Saad-Roy , Princeton graduate student in Ecology and Evolutionary Biology. and the Lewis-Sigler Institute for Integrative Genomics.

“Our goal was to explore the effects of different vaccine sharing programs on the global persistence of COVID-19 infections – as well as the possibility of evolving new variants – using mathematical models,” Saad said. -Roy.

Researchers projected the incidence of COVID-19 cases across a range of vaccine dosing regimens, vaccination rates, and hypotheses related to immune responses. They did this in two model regions: one with high access to vaccines – a high access region (HAR) – and a low access region (LAR). The models also made it possible to couple the regions either by importing cases or by developing a new variant in one of the regions.

“In this way, we could assess the dependence of our epidemiological projections on different immunological parameters, regional characteristics such as population size and local transmission rate, and our assumptions related to vaccine allocation,” said Wagner.

Overall, the study found that increased vaccine sharing resulted in a reduction in the number of cases in ARL. “Because vaccines appear to be very effective in reducing the clinical severity of infections, the public health implications of these reductions are very significant,” said co-author Michael Mina, assistant professor at Harvard TH Chan School of Public Health.

Lead author C. Jessica E. Metcalf, associate professor of ecology and evolutionary biology and public affairs at Princeton and associate professor at HMEI, added: Highly vaccinated populations.

The authors also drew on a framework developed in their previous work to begin trying to quantify the potential for viral evolution in different vaccine sharing programs. In their model, repeated infections in individuals with partial immunity – either from a previous infection or from a vaccine – may result in the development of new variants.

“Overall, the models predict that a high number of cases in ARL with limited vaccine availability will lead to a high potential for viral progression,” said lead author Bryan Grenfell, professor of ecology and science. Evolutionary Biology and Public Affairs of Princeton Kathryn Briger and Sarah Fenton. a faculty member associated with HMEI.

“As with our previous work, this study strongly underscores how important the rapid and equitable global distribution of vaccines is,” said Grenfell. “In a plausible scenario where secondary infections in individuals who have previously been infected strongly contribute to viral progression, uneven allocation of vaccines appears particularly problematic. “

As the pandemic progresses, viral evolution may play an increasingly important role in sustaining transmission, said senior author Simon Levin, distinguished professor at Princeton’s James S. McDonnell University in ecology. and evolutionary biology and associate faculty member of HMEI. “In particular, the antigenically new variants have the potential to threaten vaccination efforts around the world through several mechanisms,” he said, “including higher transmissibility, reduced vaccine efficacy or immune evasion. “

Saad-Roy added, “In this way, global vaccine coverage will reduce the clinical burden of new variants, while also decreasing the likelihood that these variants will emerge. “

There are additional considerations for vaccine equity beyond epidemiological and evolutionary considerations, said co-author Ezekiel Emanuel, University professor Diane vS Levy and Robert M. Levy and co-director of the Healthcare Transformation Institute of the ‘University of Pennsylvania.

“Ethics are also against countries stocking vaccines or allocating doses for boosters,” Emanuel said. “This study strongly supports this ethical position showing that storage will harm global health.”

Co-author Jeremy Farrar, director of the Wellcome Trust, UK, said the timing of vaccines being shared is also likely to be critical: “In particular, parallel sharing is what matters most. impact, not in sequence. “

Reference: “Vaccine nationalism and the dynamics and control of SARS-CoV-2By Caroline E. Wagner, Chadi M. Saad-Roy, Sinead E. Morris, Rachel E. Baker, Michael J. Mina, Jeremy Farrar, Edward C. Holmes, Oliver G. Pybus, Andrea L. Graham, Ezekiel J. Emanuel, Simon A. Levin, C. Jessica E. Metcalf and Bryan T. Grenfell, August 17, 2021, Science.
DOI: 10.1126 / science.abj7364

Other co-authors of the study include Sinead Morris, postdoctoral researcher at Columbia university who obtained his doctorate. in Ecology and Evolutionary Biology from Princeton; Rachel Baker, Associate Researcher at HMEI; Andrea Graham, Professor of Ecology and Evolutionary Biology at Princeton and Associate HMEI Faculty; Edward Holmes, Australian ARC laureate and professor at the University of Sydney; and Oliver Pybus, professor of evolution and infectious diseases at the Oxford University.

The article, “Vaccine nationalism and the dynamics and control of SARS-CoV-2,” was published online August 17 by Science. The work was supported by funds from the Natural Sciences and Engineering Research Council of Canada, the Cooperative Institute for Modeling the Earth System at Princeton University, the James S. McDonnell Foundation, the C3.ai Digital Transformation Institute and Microsoft Corporation, Google, National Science Foundation, US Centers for Disease Control and Prevention, and Flu Lab.


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New University of Maine research center to focus on potato virus Y https://e-jemed.org/new-university-of-maine-research-center-to-focus-on-potato-virus-y/ https://e-jemed.org/new-university-of-maine-research-center-to-focus-on-potato-virus-y/#respond Sun, 22 Aug 2021 12:00:00 +0000 https://e-jemed.org/new-university-of-maine-research-center-to-focus-on-potato-virus-y/ A better understanding of the biology of one of the most destructive plant viruses for potato crops will be the focus of a research hub at the University of Maine which is part of a new 6.1 institute. million dollars focused on virology and host-virus dynamics. The National Science Foundation awarded the grant to the […]]]>
A better understanding of the biology of one of the most destructive plant viruses for potato crops will be the focus of a research hub at the University of Maine which is part of a new 6.1 institute. million dollars focused on virology and host-virus dynamics.

The National Science Foundation awarded the grant to the University of Arkansas to establish the Host-Virus Evolutionary Dynamics Institute. The central sites will be located at the University of Maine, the University of Arkansas at Pine Bluff, the Baptist University of Ouachita and the Universidad Interamericana in Puerto Rico.

Scientists will study several viral systems in all areas of life: bacteria, archaea and eukaryas. The aim is to establish basic “rules of life” or laws of virology, which apply to all viruses – or at least to large sets of viral systems.

The institute will be headed by Ruben Michael Ceballos, assistant professor in the Department of Biological Sciences at the University of Arkansas, working with an interdisciplinary team of geneticists, virologists, ecologists and mathematicians. The UMaine hub will be headed by E. Han Tan, assistant professor of plant genetics.

UMaine will receive more than $ 446,800 to fund research led by Tan and Peter Nelson, director of forest ecology at the Schoodic Institute in Acadia National Park. Their research team will use hyperspectral methods to study potato virus Y (PVY), whose strains in Maine and elsewhere cause severe crop yield losses.

Researchers will also use genomic tools at UMaine’s Maine Center for Genetics in the Environment to study PVY in potatoes.

E. Han Tan, Assistant Professor of Plant Genetics:

“Not only will our research test a new method for detecting the PVY-infected potato, which costs the potato industry substantial sums of money for laboratory testing each year, but we hope to better understand the race for armaments between PVY and potato which will be integrated with other viral systems being studied in this institute. “

Tan is a co-principal investigator of the NSF Grant, along with other leaders: Anissa Buckner, professor and chair of the Department of Biology at the University of Arkansas at Pine Bluff; Nathan Reyna, associate professor at the Baptist University of Ouachita; and Elizabeth Padilla, assistant professor at La Universidad Interamericana.

Researchers at the Host-Virus Evolutionary Dynamics Institute will study disparate virus systems in areas of life, the University of Arkansas noted in its press release announcing the NSF award. While viruses are ubiquitous in all areas of life, the diversity of the virosphere presents a challenge in establishing universal laws to which all viruses adhere.

Using a common experimental approach, data from studies of all viral systems will be compared and integrated to generate rules of life that determine variables such as species skipping, virus port status, changes in transmission rate and emergence of highly virulent viral strains.

Rules of Life is one of the National Science Foundation’s 10 Big Ideas for pioneering research that will serve the nation’s future.

Peter Nelson, Director of Forest Ecology at the Schoodic Institute:

“By studying viruses in potatoes using statistical modeling of reflectance analyzes, we can potentially provide a way to quickly and easily detect and manage viral outbreaks.”


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How a poisonous snake got its fangs https://e-jemed.org/how-a-poisonous-snake-got-its-fangs/ https://e-jemed.org/how-a-poisonous-snake-got-its-fangs/#respond Wed, 11 Aug 2021 01:21:08 +0000 https://e-jemed.org/how-a-poisonous-snake-got-its-fangs/ Poisonous snakes use poisonous fangs to inject a cocktail of toxins – a special tooth with grooves and channels that guide the poison to the bites. Unique among animals, grooved tubular teeth have repeatedly evolved with snakes. Our new study announced today in the Bulletin of the Royal Society BR reveals that this was likely […]]]>

Poisonous snakes use poisonous fangs to inject a cocktail of toxins – a special tooth with grooves and channels that guide the poison to the bites. Unique among animals, grooved tubular teeth have repeatedly evolved with snakes.

Our new study announced today in the Bulletin of the Royal Society BR reveals that this was likely caused by a change in the tooth structure that helped attach the snake’s teeth to the socket. In some species, these structures have evolved into grooves that run the length of the tooth and act as convenient conduits for transporting poison.

of nearly 4,000 species About 600 of the snakes are considered “medically important”. That is, it can give bites that require hospital treatment, but most snakes have small tusks and are mildly poisonous. NS Appearance of a light poison It is believed to have occurred before the appearance of the poisonous fangs of the snake.

Poisonous fangs are primarily placed in one of three ways. It is attached behind the mouth, like a crab-eating water snake, cat’s eye snake, twig snake, or boomslang. Like cobras, coral snakes, multi-banded kraits, taipans, and sea snakes, they are attached in front of the mouth. Or in front of your mouth, you can bend it back or sideways, like vipers, vipers, rattlesnakes, sword snakes.

Repeated story of fangs

Looking at the evolutionary snake tree, it can be inferred that the last common ancestor of all tusk snakes was probably fangless. It seems to be much more likely than the other methods. Fangs were acquired once and then lost independently in dozens of different snake strains.

read more: How Snake Fangs Evolve to Perfectly Adapt to Food

So how did the serpent repeatedly evolve syringe-shaped teeth from the simpler tapered teeth of its ancestors?

To answer this question, we looked at snake teeth and their development. We examined 19 species of snakes, including poisonous and non-poisonous snakes and early fossil morphology. We used traditional and advanced methods, such as studying slides under a microscope. microCT scan When biomechanical modeling ..

Snake Tooth Tips: Dental Origami

The roots of almost all snake teeth, with or without poison, were found to be firmly bent and wrinkled in cross section (red wrinkles in the figure below).

These folds and wrinkles occur in a layer of teeth called dentin and are known as “presidentin” from “prica” ​​which means “fold” in Latin. Plicidentine has been found in many extinct animals and a few living species of fish and lizards. The function of these folds is unclear, but one theory is to reduce the chances of your teeth breaking or bending when you chew.

However, when I tested this idea using a computer simulation with a digital tooth model with and without these folds, I found out that it was not.

Snakes, like sharks, change teeth throughout their lives and there are no deep holes in their teeth. Therefore, Folds believe that increasing the mounting area can improve the initial set-up of new teeth in shallow indentations.

What is really interesting, whatever the original function of the teeth of the bent snake, is that in a poisonous snake, one of these folds is much larger than the other, and the teeth are stretched out to form a furrow, or poisonous furrow. Is to generate.

read more: Why are some snakes so poisonous?

These long, simple grooves are sometimes found on the teeth of other species, such as poisonous teeth. Monster of Gila, Each tooth has a groove associated with the folds of the preferred pewter. It is important to note that the grooved teeth of the Gila monster can appear in the mouth far from the poison gland, meaning a cut in between. We have also found that some poisonous snakes have grooves in their teeth other than their poisonous snakes. These teeth are not connected to the venom gland.

Therefore, it was found that grooved teeth can appear throughout the mouth, even if they are far away from the venom gland and its duct, and that there is a clear relationship between the presence of prefercidentin and the groove of venom. This hypothesized that the original condition of the poisonous snake, independent of the poisonous snake, may have been a random representation of grooves in the teeth due to simply enlarged folds of the preferred dentin. I did.

Next, we investigated how the grooved tusks and poison glands of the poisonous snake together evolved into an efficient structure for delivering venom.

Among the ancestors of today’s poisonous species, the presence of poison glands (or their precursors, the modified salivary glands called Dubernoy’s glands) was an important prerequisite for purifying grooved teeth into enlarged poisonous fangs.

Natural selection appears to have favored an increase in size and efficiency, as a grooved tooth appeared near the exit of the venom gland, which was more efficient at injecting the venom.

This sophisticated evolutionary process ultimately produces the large syringe-shaped fangs found today in snakes such as cobras and vipers, where the ends of the grooves merge to form a needle-like tubular structure.

This discovery alters simple ancestral characteristics such as dentin preference (wrinkles at the base of the tooth that are likely associated with tooth adhesion) and reuses them for a whole new function (groove for poison injection). Displays the method. And that may help explain why snakes, which are unique among all animals, have developed poisonous fangs so often.

Author: AlessandroPalci-Postdoctoral Fellow in Evolutionary Biology, Flinders University | Aaron Leblanc-Postdoctoral Fellow in Paleontology, Royal University of London | Olga Panagiotopoulou-Keynote speaker, Monash University


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The SMC protein complex ensures the dynamics of holocentromers https://e-jemed.org/the-smc-protein-complex-ensures-the-dynamics-of-holocentromers/ https://e-jemed.org/the-smc-protein-complex-ensures-the-dynamics-of-holocentromers/#respond Fri, 06 Aug 2021 14:16:41 +0000 https://e-jemed.org/the-smc-protein-complex-ensures-the-dynamics-of-holocentromers/ The SMC protein complex ensures the dynamics of holocentromers. Credit: IPK Monocentromers are typical of the chromosomes of most animals and plants. The centromere is necessary for the transport of chromosomes and represents the point of connection between chromatids. This is how the classic X-shape of the chromosome is formed. However, in about 350,000 species, […]]]>

The SMC protein complex ensures the dynamics of holocentromers. Credit: IPK

Monocentromers are typical of the chromosomes of most animals and plants. The centromere is necessary for the transport of chromosomes and represents the point of connection between chromatids. This is how the classic X-shape of the chromosome is formed. However, in about 350,000 species, including butterflies, nematodes, and some plants, centromeres are distributed throughout the length of the chromosome. For this reason, they are called holocentromers.

A research team from the IPK Leibniz Institute has now used modeling to study how the centromere changes dynamically during cell division in these species. The results are now published in the journal Nucleic Acid Research.

Holocentric plant species such as Cyperus papyrus were already of great importance to the ancient Egyptians. “This fiber factory was used to make one of the first papers at the time,” explains Professor Andreas Houben, head of the chromosome structure and function research group at the IPK Leibniz Institute. What all of these species have in common is an evolutionary advantage. If a piece of the chromosome breaks due to mutagenesis, the corresponding fragment is lost in monocentric species. “This does not happen in holocentric species, because there the centromere extends over the entire chromosome,” explains the IPK scientist.

However, the research team now wanted to know how the cell division process takes place in these species. First, the fibers of the spindle attach to the centromere, then separate the two chromatids. “It works like a rubber band,” explains Professor Dr Andreas Houben. In what is called the interphase, the holocentromer breaks up and countless centromeric units are formed, which are evenly distributed throughout the cell nucleus. In the next mitosis, the chromosome condenses and the centromere units gradually form a linear centromere along the chromatids.

Using modeling, IPK junior scientist Dr Amanda Câmara of the Domestication Genomics research group led by Dr Martin Mascher was able to prove that a protein complex called SMC plays a decisive role in this process. .

“When the protein complex approaches a centromeric unit, it attaches to the chromatin thread,” explains Dr. Amanda Câmara. As a result, several loops are formed, the chromosome is thus condensed and a centromeric line is formed, which ultimately gives rise to the new holocentromer. “This makes the SMC complex quite essential for the dynamics of holocentromers. This possible function of SMC discovered through modeling was previously unknown,” explains the IPK scientist.

In the next step, IPK researchers will try to experimentally confirm the results of the modeling.


Unique centromere type found in European dodder


More information:
Amanda Souza Câmara et al, A Simple Model Explains the Cell Cycle Dependent Assembly of Centromeric Nucleosomes in Holocentric Species, Nucleic Acid Research (2021). DOI: 10.1093 / nar / gkab648

Provided by the Leibniz Institute of Plant Genetics and Crop Plant Research

Quote: SMC protein complex demonstrated to support holocentromeric dynamics (2021, August 6) retrieved August 6, 2021 from https://phys.org/news/2021-08-protein-complex-smc-shown-dynamics.html

This document is subject to copyright. Other than fair use for private study or research purposes, no part may be reproduced without written permission. The content is provided for information only.


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AlphaFold 2, open source AI for protein structure prediction – Technology https://e-jemed.org/alphafold-2-open-source-ai-for-protein-structure-prediction-technology/ https://e-jemed.org/alphafold-2-open-source-ai-for-protein-structure-prediction-technology/#respond Tue, 03 Aug 2021 17:42:55 +0000 https://e-jemed.org/alphafold-2-open-source-ai-for-protein-structure-prediction-technology/ To print this article, simply register or connect to Mondaq.com. On July 15, a team of scientists released a Nature article titled “Highly Accurate Protein Structure Prediction with AlphaFold”.1 The article describes how the neural network model developed by Google’s DeepMind can predict protein structures “with atomic precision even when no similar structure is known.”2 […]]]>

To print this article, simply register or connect to Mondaq.com.

On July 15, a team of scientists released a
Nature article titled “Highly Accurate Protein Structure Prediction with AlphaFold”.1 The article describes how the neural network model developed by Google’s DeepMind can predict protein structures “with atomic precision even when no similar structure is known.”2 Additionally, DeepMind has now opened the code for AlphaFold 2, enabling new collaborations for even more accurate prediction of protein structure.

A protein can have a very complex 3D structure through a process called protein folding, and the task of predicting structure is “a major research problem open for over 50 years.”3 Last year, DeepMind entered the CASP14 (14th Critical Appraisal of Protein Structure Prediction) research competition, won the competition, and redesigned AlphaFold to create AlphaFold 2 in December 2020. The CASP competitions, considered ” the protein folding Olympics “,4 have taken place every two years since 1994, and after the development of AlphaFold 2, some believe that the protein folding problem has essentially been solved. DeepMind has successfully improved the accuracy of prediction “by incorporating new neural network architectures and training procedures based on the evolutionary, physical and geometric constraints of protein structure”.5

AlphaFold inspired further research efforts, which led to the publication of another article on July 15, “Accurate Prediction of Protein Structures and Interactions Using a Three-Track Neural Network”.6 The article by university researchers describes how their RoseTTAFold model predicted protein structures to a level of accuracy close to that of AlphaFold. The model comprises a three-track network where “the information at the level of the 1D sequence, at the level of the 2D distance map and at the level of the 3D coordinates are successively transformed and integrated”. With such technology, “RoseTTAFold solves difficult X-ray crystallography and cryo-EM modeling problems, provides insight into protein function in the absence of experimentally determined structures, and rapidly generates accurate models of protein complexes. -protein.”

The misfolding of proteins could lead to various diseases and disorders, and therefore the availability of computer tools that provide insight into protein folding is important for drug discovery and development. Prediction models, along with experimental techniques, should help to better understand the causes of diseases and to design compounds that could effectively treat diseases.

In terms of patent protection, London-based DeepMind filed three PCT international applications with the same title “Machine Learning for Determining Protein Structures” on September 16, 2019, claiming priority from the same three US provisional applications filed in September and November. 2018.

Provisional claims in the United States:

N ° 62/734 757 filed on September 21, 2018

N ° 62/734 773 filed on September 21, 2018

N ° 62/770 490 filed on November 21, 2018

WO2020 / 058174 includes claims on a prediction method, system and computer storage media. Claim 1 is as follows.

A method performed by one or more data processing apparatuses to determine a final predicted structure of a given protein, wherein the given protein comprises an amino acid sequence, wherein a predicted structure of the given protein is defined by values ​​of a plurality of structure parameters, the method comprising:

generating a plurality of predicted structures of the given protein, wherein generating a predicted structure of the given protein comprises:

obtaining initial values ​​of the plurality of structure parameters defining the predicted structure;

updating the initial values ​​of the plurality of structure parameters, comprising, on each of a plurality of update iterations:

determining a quality score characterizing a predicted quality of the structure defined by the current values ​​of the structure parameters, in which the quality score is based on the respective outputs of one or more scores

neural networks which are each configured to process: (i) current values ​​of structural parameters, (ii) a representation of the amino acid sequence of the given protein, or (iii) both; and

for one or more of the plurality of structure parameters:

determining a gradient of the quality score with respect to the current value of the structure parameter; and

updating the current value of the structure parameter using the gradient of the quality score relative to the current value of the structure parameter; and determining the predicted structure of the given protein to be defined by the current values ​​of the plurality of structure parameters after a final update iteration of the plurality of update iterations; and

selecting a particular predicted structure of the given protein as the final predicted structure of the given protein.

The prediction method of claim 1 generates multiple predicted structures of a given protein, performs certain calculations and, upon completion, selects a particular predicted structure of the given protein as the final predicted structure. The calculations consist of obtaining initial values ​​of structural parameters defining the predicted structure and updating the values. The update process includes the following determination process using neural networks (emphasis added):

“determining a quality score characterizing a predicted quality of the structure defined by the current values ​​of the structure parameters, in which the quality score is based on the respective outputs of one or more scoring neural networks which are each configured to process: (i) current values ​​of structural parameters, (ii) a representation of the amino acid sequence of the given protein, or (iii) both

Claim 1 therefore sets out the general functions of neural networks, but does not cite any specific architecture of neural networks. So, like Ed Garlepp’s discussion of unique disclosure issues with AI, the neural network is treated more as a ‘black box’ in the claim, although DeepMind was presumably working to develop new ones. network architectures. This claim is a good example of the balance patent practitioners need when drafting claims involving a neural network.

We note that the PCT application was filed long before DeepMind conducted further studies in CASP14, faced with the challenge of modeling various structures of unknown proteins provided in May-August 2020. During the pandemic, the team worked on the prediction of the structure of SARS-CoV-2 Orf8, one of the proteins of the coronavirus. Given the serious circumstances, DeepMind shared the findings and published the results as they were obtained. The patent strategy at DeepMind may have evolved into an open strategy as a result of such work, resulting in the recent release of details of their technology, with the source code being made available under an open source license.

We look forward to following the continuation of this patent as well as the general evolution of this technology.

Footnotes

1 Jumper, J. et al. Highly accurate prediction of protein structure with AlphaFold. Nature https://doi.org/10.1038/s41586-021-03819-2 (2021).

2 Identifier., Abstract.

3 Identifier.

4 DeepMind (2020). AlphaFold: the achievement of a scientific breakthrough [Video]. Youtube. https://www.youtube.com/watch?v=gg7WjuFs8F4

5 Jumper, J. et al. Highly accurate prediction of protein structure with AlphaFold. Nature https://doi.org/10.1038/s41586-021-03819-2 (2021).

6 Mr. Baek et al., Science 10.1126 / science.abj8754 (2021).

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