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Category Archives: Transhuman News

Study Unpicks What Drives the Need for Sleep at the Cellular Level – Genetic Engineering & Biotechnology News

Posted: November 21, 2021 at 9:15 pm

Why do humans spend a third of their lives sleeping? Why do animals sleep, even when there may be a continuous threat of predators? The question of how sleep benefits the brain and individual cells has remained a mystery, but studies in zebrafish, and in mice, by Bar-Ilan University researchers, have now provided a detailed description of the chain of events explaining sleep at the single-cell level. Their results indicated that a buildup of DNA damage in neurons during wakefulness increases sleep pressure. A protein called Parp1 senses this mounting DNA damage, signals when its time to sleep. During sleep efficient DNA repair occurs, which reduces the cellular homeostatic pressure that drives the need for sleep.

The team, led by Lior Appelbaum, PhD, a professor at Bar-Ilans Goodman Faculty of Life Sciences and Gonda (Goldschmied) Multidisciplinary Brain Research Center, suggests that the mechanism uncovered may explain the link between sleep disturbances, aging and neurodegenerative disorders such as Parkinsons disease and Alzheimers disease. Appelbaum believes that future research will help to apply this sleep function to other animals, ranging from lower invertebrates to eventually, humans.

The authors reported on their findings in Molecular Cell, in a paper titled, Parp1 promotes sleep, which enhances DNA repair in neurons, in which they concluded that their results demonstrate that DNA damage is a homeostatic driver for sleep, and Parp1 pathways sense this cellular pressure and facilitate sleep and repair activity.

Sleep, accompanied by reduced responsiveness to external stimuli, is a vulnerable behavioral state, the authors wrote. Yet throughout evolution sleep has remained universal and essential to all organisms with a nervous system, including invertebrates such as flies, worms, and even jellyfish.What is different between species is the amount of sleep required, the authors continued. Adult humans sleep approximately 78 h per day, whereas owl monkeys sleep for 17 h, and free-roaming wild elephants may sleep only 2 h. These diverse sleep requirements raise fundamental questions: what dictatesa species-specific sufficient amount of sleep, and what is the restorative neural process?

When we are awake, homeostatic sleep pressure (tiredness) builds up in the body. This pressure increases the longer we stay awake, and decreases during sleep, reaching a low after a full and good nights sleep. But what causes homeostatic pressure to increase to a point that we feel we must go to sleep, and what happens at night to reduce that pressure to such an extent that we are ready to start a new day, isnt clear. the cellular homeostatic mechanisms that drive sleep needs, as well as the identity of the homeostatic factors, are unclear, the researchers commented.

Studies have shown that during waking hours, DNA damage accumulates in neurons. Enriched wakefulness and neuronal activity induce DNA double-strand breaks (DSBs) in mice and flies, the team continued. This damage can be caused byvarious elements, includingUV light, neuronal activity, radiation, oxidative stress, and enzymatic errors.During sleep and waking hours, repair systems within each cell correct these DNA breaks. However, DNA damage in neurons continues to accumulate during wakefulness, and excessive DNA damage in the brain can reach dangerous levels that must be reduced.

A series of experiments by Appelbaum, together with postdoc researcher David Zada, PhD, and colleagues, sought to determine whether the buildup of DNA damage could be the driver for homeostatic pressure and the subsequent sleep state. The scientists turned first to zebrafish as a live vertebrate model that they could use to try to identify cellular sleep drivers and understand the role for sleep in restoring nuclear homeostasis, at the level of single neurons.

With their absolute transparency, nocturnal sleep, and a simple brain that is similar to humans, zebrafish are a perfect organism in which to study this phenomenon. The zebrafish is a well-established sleep model, and the structure and function of its brain, as well as the DNA damage and repair systems, are conserved with mammals, the scientists stated.

Using UV radiation, pharmacologic intervention and optogenetics, the researchers induced DNA damage in zebrafish to examine how it affects their sleep. Their results showed that as DNA damage was increased, the need for sleep also increased. The experiment suggested that at some point the accumulation of DNA damage reached a maximum threshold, and increased sleep (homeostatic) pressure to such an extent that the urge to sleep was triggered, and the fish went to sleep. The ensuing sleep facilitated DNA repair, which resulted in reduced DNA damage. Our causative experiments demonstrated that sleep increases the clustering of Rad52 and Ku80 repair proteins in neurons, which enables normalization of the levels of DNA damage.

Having determined that accumulated DNA damage is the force that drives the sleep process, the researchers then wanted to see whether they could determine the minimum time that zebrafish need to sleep in order to reduce sleep pressure and DNA damage. Similarly to humans, zebrafish are sensitive to light interruption, and so the dark period was gradually decreased during the night.

These results suggested that six hours of sleep per night is sufficient to reduce DNA damage in the zebrafish. And, astoundingly, after less than six hours of sleep, DNA damage was not adequately reduced, and the zebrafish continued to sleep even during daylight. There was a strong positive correlation (R = 0.76) between levels of neuronal DNA damage and total sleep time, suggesting that the amount of DNA damage can predict the total sleep time required for repair, the team further noted.

During waking hours (top) the buildup of DNA damage in neurons increases tiredness. Acting as an antenna the PARP1 protein (yellow helmets) senses and marks DNA breaks in cells, drives sleep, and recruits repair systems (green and blue helmets, bottom). During sleep, the DNA repair systems repair the breaks enabling a fresh new start to the day. In red is the soma (cell body), blue the nucleolus, and green (DNA damage sites). [David Zada, PhD]Another question is what is the mechanism in the brain that tells us we need to sleep in order to facilitate efficient DNA repair? Sleep promotes the activity of the DNA damage repair (DDR) signaling pathway, which includes DNA damage sensors, signal transducers, and effector proteins required for repair, the team noted. we reasoned that activation of a DDR protein might signal the organism to sleep in order to increase chromosome dynamics and enable the efficient assembly of repair proteins.

The researchers focused on a protein called PARP1, which is part of the DNA damage repair system, and responds to single- and double-stranded DNA breaks. PARP1 marks DNA damage sites in cells, and recruits all relevant systems to clear out DNA damage. PARP-1 is a DNA damage detector, which is recruited to DNA repair response, they noted.

In accordance with DNA damage, the team found that clustering of PARP1 in DNA break sites increased during wakefulness and decreased during sleep. Through genetic and pharmacological manipulation, the overexpression and knockdown (KD) of PARP1 revealed that increasing PARP1 promoted sleep, and also increased sleep-dependent repair. Conversely, inhibition of PARP1 blocked the signal for DNA damage repair. As a result, the fish werent fully aware that they were tired, didnt go to sleep, and no DNA damage repair occurred. Inhibition of Parp1 activity abolished DNA damage-induced sleep, chromosome dynamics, and repair, even under strong sleep pressure, the investigators stated.

To strengthen the findings in zebrafish, the investigators teamed up with Yuval Nir, PhD, at Tel Aviv University, to further test the role of PARP1 in regulating sleep, mice, using EEG. These results showed that as theyd seen with zebrafish, the inhibition of PARP1 activity in mice reduced the duration and quality of non-rapid eye movement (NREM) sleep. These results extend those of zebrafish larvae along three separate dimensions, by (1) establishing them in mammals and (2) in adult animals, and (3) by showing that Parp1 affects sleep depth, beyond its effects on sleep duration, the team stated.

In a previous study, Appelbaum and team used 3D time-lapse imaging to determine that sleep increases chromosome dynamics. Adding the current piece to the puzzle, PARP1 increases sleep and chromosome dynamics, which facilitates efficient repair of DNA damage accumulated during waking hours. The DNA maintenance process may not be efficient enough during waking hours in neurons, and therefore requires an offline sleep period with reduced input to the brain in order to occur. Appelbaum noted, PARP1 pathways are capable of signaling the brain that it needs to sleep in order for DNA repair to occur.

The authors concluded, Here, imaging of cellular and nuclear markers, coupled with behavioral monitoring of zebrafish, showed that neuronal DNA damage can be a driver for sleep that promotes DNA repair activity our findings that sleep regulates the neuronal balance between DNA damage and repair and consequently the health of the cell provide the basis for future work focusing on the causative link between sleep, aging, and neurodegenerative diseases.

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Study Unpicks What Drives the Need for Sleep at the Cellular Level - Genetic Engineering & Biotechnology News

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Was It a Lab Leak? The Mysterious Origin of COVID-19 – Reason

Posted: at 9:15 pm

Where did the virus that changed the world come from?

The prevailing theory for a long time was that wild animals sold as food at a wet market in Wuhan, China, had started the outbreak.

One of the first scientists to seriously question the official narrative was Botao Xiao, who in February 2020 published a pre-print paper arguing that "the killer coronavirus probably originated from a laboratory in Wuhan."

The author pointed out that there was no evidence that the vendors at the wet market in Wuhan sold bat meat. On the other hand, there were two research labs studying bat-borne coronaviruses located in Wuhan, where a virus could have accidentally infected workers, causing them to spread the disease to the general public. Xiao withdrew the paper two weeks later, after Chinese authorities declared that the lab-leak theory had no merit.

The Chinese government proceeded to clamp down on research into the virus's origins and ordered the closure of a lab that had shared the virus's genetic sequence with other scientists in January 2020. The government also forced the lab to destroy its viral samples.

To this day, the Chinese government won't allow outside researchers to test blood drawn from employees of the Wuhan Institute of Virology who, according to a U.S. intelligence report, were hospitalized for a flu-like illness in November 2019weeks before the first documented human-to-human transmission. Chinese authorities cited privacy concerns to the World Health Organization (WHO) team that requested the samples.

There's no direct proof that the virus originated from a lab. But there's also no such proof that humans first became infected by eating bats or through exposure to pangolins, theories that were treated as unimpeachable fact early in the pandemic.

In February 2020, a group of scientists signed a statement published in The Lancet denouncing speculation about potential nonnatural origins of the virus as "conspiracy theories."

Only following the publication of leaked emails did it become clear that the scientist who brought his colleagues together to co-sign the Lancet statement was Peter Daszak, head of EcoHealth Alliance, the nonprofit that secured U.S. government funding for controversial research on bat-borne coronaviruses at the Wuhan Institute of Virology. Daszak assured his co-signers that the EcoHealth logo wouldn't appear on the letter and wrote that he hoped "to avoid the appearance of a political statement."

Daszak also co-authored a June 2020 op-ed in The Guardian headlined"Ignore the Conspiracy Theories: Scientists Know COVID-19 Wasn't Created in a Lab" without disclosing a potential conflict of interest.

Media coverage following the publication of the Lancet letter overwhelmingly framed discussion of the lab-leak hypothesis as a "conspiracy theory," often tying it to former President Donald Trump after he and former Secretary of State Mike Pompeo made public statements promoting the lab-leak theory as the explanation.

"That episode does not reflect well on scientists," says science writer Matt Ridley, co-author of the new book Viral: The Search for the Origin of COVID-19.

Ridley says that White House COVID-19 adviser Anthony Fauci's emails, which were made public through a Freedom of Information Act request, show that behind the scenes scientists were taking the lab-leak theory seriously all along.

"A number of leading virologists were talking to each other and were saying to each other, 'we think this might look a bit like a virus that's been engineered in the laboratory,'" says Ridley, referencing a January 31, 2020, email in which researcher Kristian G. Andersen says that "one has to look really closely at all the sequences to see that some of the features (potentially) look engineered." Fauci replies a day later, "Thanks, Kristian. Talk soon on the call."

"And at the end of that phone call, they all did a very rapid volte-face, and started writing articles almost immediately," says Ridley, referring to an influential article Andersen and his colleagues published in Natureon March 17, 2020, stating that "our analyses clearly show that SARS-CoV-2 is not a laboratory construct or a purposefully manipulated virus." On March 6, Andersen emailed Fauci to tell him the paper had been accepted for publication, to which Fauci replied, "Nice job on the paper."

But Ridley says that it's Daszak's efforts to obscure his connections to the Wuhan Institute of Virology while publishing attacks on the lab-leak hypothesis that are most alarming.

"It does raise very serious concerns that Dr. Daszak needs to answer," says Ridley. "I've tried to correspond with him numerous times. I've never yet had a responseI never said anything rude about him, but he blocked me on Twitter. So I can't get answers out of him."

Daszak did not reply to Reason's interview request.

Ridley's writing partner on the new book is the Broad Institute of MIT and Harvard's Alina Chan, one of the earliest and most outspoken public skeptics of the natural-origin hypothesis. She says that when she and her colleagues published a pre-print paper questioning the consensus, she hadn't been aware of the Lancet letter organized by Daszak. She says she believes it could've had a major chilling effect on the scientific discussion in those early days.

"They were saying that anyone saying that this virus didn't come from nature is a conspiracy theorist," says Chan. "Other people, when they read this letter, they might have thought, 'I'm not going to put my neck out to say that this may have come from a lab.'"

Chan, a molecular biologist, argued in the paper that because SARS-CoV-2 was so well adapted to humans, there was reason to be skeptical that it had recently come from an animal. If it had recently come from bats or pangolins, she would've expected the virus to have been rapidly mutating in the early days of the pandemic to become better adapted to human tissue.

Chan partially credits this insight to her experience in the severe acute respiratory syndrome (SARS) outbreak of 2003, which she lived through in Singapore.

"In that situation and that outbreak, the virus had rapidly picked up dozens of mutations in the early three months," says Chan. "By comparison, for SARS-CoV-2, that had very few of these mutations. So it's suggested to me that this virus had really picked up many useful mutations for infecting and transmitting amongst humans prior to its detection in December 2019."

Another major difference is that during the 2003 outbreak, authorities discovered previous SARS infections among animals being sold at markets in south China within a couple of months. That's not the case with SARS-CoV-2, despite initial suspicions that a wet market was to blame.

"Even though the first class of cases identified was at the seafood market, they never found any signs of animals that were infected by this virus," says Chan. "So up until today, there's no sign of an animal [in Wuhan] that was ever infected by SARS-CoV-2 and then gave it to humans."

When the WHO sent a team to investigate the virus's origins in January 2021, Daszak was the only American member included. The team dismissed the lab-leak hypothesis before WHO leadership later backtracked.

Daszak granted an interview to 60 Minutes following that trip to Wuhan and suggested that farm animals were the likely culprit.

"Now what we've gotta do is go to those farms and investigate. Talk to the farmers. Talk to their relatives. Test them. See if there were spikes in virus there first," Daszak told 60 Minutes.But no farm animals have been identified as the hosts yet.

There's a detail that emerged after the 60 Minutes report that Ridley would like Daszak to explain: Recently-leaked documents show that EcoHealth Alliance applied for a research grant related to inserting what's called a furin cleavage site into SARS-like coronaviruses. This very furin cleavage site may be what makes SARS-CoV-2 so infectious, and it's what distinguishes it from any SARS-like coronaviruses as yet found in the wild. The grant request was rejected. But did the Wuhan laboratory engage in this research even without funding from that grant? Daszak may be able to help answer that question.

"The fact that that is probably the feature that makes the virus sufficiently infectious to start a pandemic means that it is a highly important thing," says Ridley. "So you would think that a scientist who knew that he had put in a grant application in 2018 to put furin cleavage sites into SARS-like viruseswould volunteer that information early in the pandemic."

Ridley and Chan also find it suspicious that when China's premier bat coronavirus expertand Daszak's collaborator in Wuhanpublished her complete analysis of the SARS-CoV-2 genome, she neglected to mention this highly unusual furin cleavage site.

After the 60 Minutes interview, more leaked documents showed that EcoHealth Alliance worked with the Wuhan Institute of Virology to make several bat-borne SARS-like coronavirusesand even Middle East respiratory syndrome (MERS)more infectious to human cells.

Chan and Ridley say that when they started writing the book they didn't have a strong view about which theory was correct, but these recent revelations have shifted their thinking in favor of the lab-leak theory.

"In light of grant proposals and reports released in the past 2 months," Chan wrote on Twitter, "we know novel SARS-like viruses were being synthesized and engineered at unprecedented scale."

"That changed my mind completely, knowing that there actually was a plan, a pipeline, a protocol for doing this work in 2018. So now for me, genetic engineering is very much on the table," says Chan. "If it came from a lab, [the likelihood is] close to a 5050 chance that [genetic engineering] happened."

This question was at the center of a heated exchange between Fauci and Sen. Rand Paul (RKy.) over possible National Institutes of Health (NIH) funding of so-called gain of function research, which involves purposely making a virus more infectious to humans.

But much of the blame for the devastating scope of the pandemic, says Ridley, rests on Chinese authorities, who punished whistleblowers like ophthalmologist Li Wenliang, who tried to get the word out about the emergence of a new SARS-like virus to his colleagues. The government successfully kept human-to-human transmission of the disease under wraps for weeks and maybe longer.

"Communist regimes tend to be secretive," says Ridley. "There tends to be an assumption that you don't talk about things unless you're allowed to, rather than the other way around. But [Chinese President] Xi Jinping, being a much more dictatorial and authoritarian ruler than his immediate predecessors, by 2019 it was more and more the case that scientists in laboratories and doctors in hospitals were under orders not to communicate with theoutside world about things that the regime might not want them toDid that play a part in the epidemic escaping and getting to the rest of the world and turning into a pandemic? You bet it did."

The Wuhan Institute of Virology houses samples of RaTG13, a bat virus that is one of the closest known genetic matches to SARS-CoV-2. But to this day, information about other coronaviruses in the Wuhan lab hasn't been released, so we don't know if the lab was working with a virus that's even more closely related to SARS-CoV-2.

The lab's public database of viral samples could hold some answers, but it was taken offline in February and had been modified in December, which we know because of work by the Dedicated Research and Scientific Team Investigating COVID-19 (DRASTIC), a decentralized group of volunteers who compile and analyze open-source material and leaked documents to investigate the origins of COVID-19.

"Once I realized [the lab-leak hypothesis] was being discredited without any evidence, I just couldn't stay silent," says Yuri Deigin, a biotech entrepreneur and one of the founding members of DRASTIC.

A key revelation uncovered by the group was that the Wuhan Institute of Virology database was first taken down in September 2019, three months before the pandemic became publicly known. A description of the database was modified on December 30, 2019, the day Shi Zhenglitold Chinese state television that her lab first obtained samples of the virus in Wuhan.

Wuhan scientists accessed the database a few times before it was permanently removed in February 2020 for alleged "security concerns."

"For them to take it down is very suspicious. And of course, Shi's explanation that she took it down to prevent hackers from attacking is complete bullshit because it was a public database to begin with," says Deigin.

A member of the DRASTIC team also discovered that the Wuhan team had collected key samplesincluding one of the virus's closest known genetic matchesfrom a mine where some workers had fallen sick and died after clearing out bat droppings. Chinese authorities have denied outsiders any access to examine the mine.

Though there's mounting circumstantial evidence to support the lab-leak theory, government officials maintain that the natural-origin hypothesis is more likely. A U.S. intelligence report declassified on October 29, 2020, said four intel agencies had low confidence that the virus most likely emerged in nature; one agency had moderate confidence that it leaked from a lab; and analysts at three agencies remained "unable to coalesce around either explanation without additional information." The report did conclude that SARS-CoV-2 was unlikely to be a biological weapon.

NIH Director Francis Collins, who didn't reply to Reason's interview request, told computer scientist and podcast host Lex Fridman in early November that he's open to the lab-leak hypothesis but still believes strongly that the virus is of natural origin.

Between July 2020 and January 2021, an international team of scientists captured bats in Laos carrying a newly discovered coronavirus that's the closest known genetic match to SARS-CoV-2even closer than the virus held in the Wuhan lab, which some say supports the natural-origin theory. But Ridley, Chan, and Deigin point out that it lacks the crucial furin cleavage site, which they suspect scientists inserted in a lab.

Supporters of the natural-origin theory point out that no "smoking gun" virus has yet been found in the version of the Wuhan database uncovered by DRASTIC. But Chan points out that this version of the database is years out of date because the Wuhan researchers generally don't enter new viruses until they've had a chance to sequence and publish studies about them.

"So we have barely any concept of what viruses and sequences they might have found after 2016 in the years leading up to COVID-19," says Chan. "So without access to the informationitbecomes very difficult for us to guess whether or not they finally found the precursor of SARS-CoV-2 in the labs and were working with it."

Ridley says that he doesn't want a fear of biotechnology, which he credits for alleviating human suffering, to hamper scientific progress because of what may have happened in Wuhan. But he thinks scientists should convene an international forum to set stricter ethical guidelines prohibiting dangerous types of research, such as harvesting bat viruses from faraway caves and bringing them to large urban centers to run experiments that make them more infectious to human cells. One China-produced documentary released in December 2019 showcases researchers doing this work, some of them without proper protective gear.

"Going out and harvesting viruses in wild places with pandemic potential and bringing them back to cities to work on them, probably isn't very sensible," says Ridley. "If we could get the U.S., the U.K., Australia, Japan, other major countries to sign a treaty saying, 'When there's an outbreak in our country, we promise to open up as far as possible and tell you everything we know,' then the very fact that some countries won't sign that treaty will itself put pressure on them."

He points to the emergence of the International Atomic Energy Agency as a model for nations to follow in terms of preventing future lab leaks of potentially pandemic-causing pathogens.

And Ridley says that despite the months of obfuscation by Chinese authorities, virologists, and even some U.S. media outlets, he's optimistic that the truth will emerge in time.

"It may take a long time," says Ridley. "The fall of the Soviet Union did lead to significant revelations about biological accidents thereI think therefore it may take a change of regime in Beijing before we find out more. But I think there are people who know what happened, whatever happened, even if it's just what happened in a marketThere are plenty of people who say it's too late; we've lost the chance to find out. I'm not one of them, at least not yet."

Produced by Zach Weissmueller; graphic intro and timeline graphics by Tomasz Kaye; additional graphics by Calvin Tran

Images: He Huan / Xinhua News Agency/Newscom; Yin Gang / Xinhua News Agency/Newscom; Imagine China/Newscom; Kyodo/Newscom; Hitoshi Katanoda/Polaris/Newscom; Dickson Lee/SCMP/Newscom; DESIGN CELLS/SCIENCE PHOTO LIBRARY/Newscom; Wang Bingyu/EyePress / EyePress/Newscom; EyePress / EyePress/Newscom; Edwin Remsberg / VWPics/Newscom; SHEPHERD ZHOU/FEATURECHINA/Newscom; Xie Huanchi / Xinhua News Agency/Newscom; Li Xueren / Xinhua News Agency/Newscom; Wang Ye / Xinhua News Agency/Newscom; Imagine China/Newscom; CHINE NOUVELLE/SIPA/Newscom; CHINE NOUVELLE/SIPA/Newscom; CHINE NOUVELLE/SIPA/Newscom; SHI ZHI/FEATURECHINA/Newscom; Xiao Yijiu / Xinhua News Agency/Newscom; Christophe Gateau/dpa/picture-alliance/Newscom; Yin Gang / Xinhua News Agency/Newscom; Andre Malerba/ZUMAPRESS/Newscom; u Peng / Xinhua News Agency/Newscom

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Was It a Lab Leak? The Mysterious Origin of COVID-19 - Reason

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Biologist Sarah Kocher receives Packard Foundation fellowship for early-career scientists for her ‘social brain’ research with bees – Princeton…

Posted: at 9:15 pm

The David and Lucile Packard Foundation announced that Princeton's Sarah Kocher is one of 20 early-career researchers to be awarded a 2021 Packard Fellowship for Science and Engineering. Each fellow will each receive $875,000 over five years to pursue their research.

Kocher, an assistant professor of ecology and evolutionary biology and the Lewis-Sigler Institute for Integrative Genomics, investigates the genetic and neurobiological mechanisms behind social living. Herresearch takes advantage of naturally occurring variation in sweat bees, where some species live alone while others build social units like their better-known cousins the honeybees.

Photo by

Denise Applewhite, Office of Communications

"Through this comparative lens, we can examine the genetic factors that shape variation in social behavior within and among species and link these genetic changes with neurobiological and behavioral traits," Kocher said. "My work traverses different levels of biological complexity, from genes to brains to behavior, to gain a comprehensive understanding of the factors that shape the evolution of the social brain.'"

The Packard Fellowships in Science and Engineering are among the nations largest nongovernmental fellowships, designed to allow maximum flexibility in how the funding is used. Since 1988, this program has supported the blue-sky thinking of scientists and engineers whose research over time has led to new discoveries that improve peoples lives and enhance our understanding of the universe.

What a moment for celebration, saidNancy Lindborg, the president and CEO of the Packard Foundation.At a time when we are confronting so many difficult, intertwined challenges, including climate change, a global pandemic and racial injustice, I am buoyed by the determination and energy of these 20 scientists and engineers. Through their research, creativity and mentorship to their students and in their labs, these young leaders have the potential to help equip us all to better understand and address the challenges we face.

The fellowships program was inspired by David Packards commitment to strengthen university-based science and engineering programs in the United States. He recognized that the success of the Hewlett-Packard Company, which he cofounded, was derived in large measure from research and development in university laboratories. Since 1988, the Packard Foundation has awarded $464 million to 657 scientists and engineers from 54 national universities.

The fellowship will be paid over five years, beginning in November 2021. Kocher will join other fellows at an annual conference held online this year and last yearto discuss their research and possibly spark interdisciplinary collaborations. Next years meeting is scheduled for Sept. 7-10 in Monterey, California.

Other Princetonians who have been named Packard Fellows include quantum chemist Leslie Schoop in 2020, mathematicianAleksander Logunov in 2019, biologist Mary "Cassie" Stoddard in 2018, mathematician John Pardon in 2017, physicist Waseem Bakr in 2016, biologist Sabine Petry in 2014, computer scientist Mark Braverman in 2013, astrophysicist Gspr Bakos in 2012, physicist William Jones in 2010, chemical engineer Celeste Nelson and physicist Jason Petta in 2008 and mathematicianManjul Bhargava in 2004.

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Biologist Sarah Kocher receives Packard Foundation fellowship for early-career scientists for her 'social brain' research with bees - Princeton...

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Investigating pathogens and their life cycles, for the benefit of society – MIT News

Posted: at 9:15 pm

Desmond Edwards was a little kid when first learned about typhoid fever. Fortunately, he didnt have the disease. He was looking at a cartoon public health announcement. The cartoon, produced by the Pan American Health Organization, was designed to educate people in his home country of Jamaica about the importance of immunizations for diseases like typhoid. The typhoid character in the cartoon was so unpleasant it gave him nightmares.

Edwards did have his fair share of hospital visits throughout his childhood. But, his own struggles with infection and illness, and those typhoid cartoon nightmares, became his inspiration for pursuing a career studying human disease. At age 6, Edwards was running impromptu baking soda experiments in repurposed glitter containers in his kitchen. Today, he is a senior at MIT, majoring in biology and biological engineering, thanks to a team of dedicated mentors and an insatiable curiosity about how the human body works or, more accurately, how diseases stop it from working.

Finding a way into research

Edwards knew he wanted to do research but says he assumed that that was something you did after you got your degree. Imagine his surprise, then, upon arriving at MIT in 2018 and meeting classmates who not only had done research, but already had publications. Realizing that he could get a jump-start on his career, he sought out research opportunities and enrolled in the biology class 7.102 (Introduction to Molecular Biology Techniques) for his first-year Independent Activities Period. The class was specifically geared toward first-year students like him with no lab experience.

It was a great first look at how research is done, Edwards says of the class. Students took water samples from the Charles River and were expected to identify the strains of bacteria found in those samples using various biological techniques. They looked at the bacteria under a microscope. They examined how the samples metabolized different sources of carbon and determined if they could be stained by different dyes. They even got to try out basic genetic sequencing. We knew where we were starting. And we knew the end goal, says Edwards. The in-between was up to them.

Class 7.102 is taught by Mandana Sassanfar, a lecturer in biology and the departments director of diversity and science outreach. For Sassanfar, the class is also an opportunity to find lab placements for students. In Edwards case, she literally led him to the lab of Assistant Professor Becky Lamason, walking up with him one evening to meet a postdoc, Jon McGinn, to talk about the lab and opportunities there. After Edwards expressed his interest to Lamason, she responded within 30 minutes. McGinn even followed up to answer any lingering questions.

I think that was really what pushed it over the edge, he says of his decision to take a position in the Lamason lab. I saw that they were interested not only in having me as someone to help them do research, but also interested in my personal development.

At the edges of cells and disciplines

The Lamason lab researches the life cycle of two different pathogens, trying to understand how the bacteria move between cells. Edwards has focused on Rickettsia parkeri, a tick-borne pathogen thats responsible for causing spotted fever. This type of Rickettsia is what biologists call an obligate intracellular pathogen, meaning that it resides within cells and can only survive when its in a host. I like to call it a glorified virus, Edwards jokes.

Edwards gets excited describing the various ways in which R. parkeri can outsmart its infected host. Its evolved to escape the phagosome of the cell, the small liquid sac that forms from the cell membrane and engulfs organisms like bacteria that pose a threat. Once it gets past the phagosome and enters the cell, it takes over cellular machinery, just like a virus. At this point of the life cycle, a bacterium will typically replicate so many times that the infected cell will burst, and the pathogen will spread widely. R. parkeri, though, can also spread to uninfected cells directly through the membrane where two cells touch. By not causing a cell to burst, the bacterium can spread without alerting the host to its presence.

From a disease standpoint, thats extremely interesting, says Edwards. If youre not leaving the cell or being detected, you dont see antibodies. You dont see immune cells. Its very hard to get that standard immune response.

In his time in the lab, Edwards has worked on various projects related to Rickettsia, including developing genetic tools to study the pathogen and examining the potential genes that might be important in its life cycle. His projects sit at the intersection of biology and biological engineering.

For me, I kind of live in between those spaces, Edwards explains. I am extremely interested in understanding the mechanisms that underlie all of biology. But I dont only want to understand those systems. I also want to engineer them and apply them in ways that can be beneficial to society.

Science for society

Last year, Edwards won the Whitehead Prize from the Department of Biology, recognizing students with outstanding promise for a career in biological research. But his extracurricular activities have been driven more by his desire to apply science for tangible social benefits.

How do you take the science that youve done in the lab, in different research contexts, and translate that in a way that the public will actually benefit from it? he asks.

Science education is particularly important for Edwards, given the educational opportunities he was given to help get to MIT. As a high schooler, Edwards participated in a Caribbean Science Foundation initiative called the Student Programme for Innovation in Science and Engineering. SPISE, as its known, is designed to encourage and support Caribbean students interested in careers in STEM fields. The program is modeled on the Minority Introduction to Engineering and Science program (MITES) at MIT. Cardinal Warde, a professor of electrical engineering, is himself from the Caribbean and serves as the faculty director for both MITES and SPISE.

That experience not only kind of opened my eyes a bit more to what was available, what was in the realm of possibilities, but also provided support to get to MIT, Edwards says of SPISE. For example, the program helped with college applications and worked with him to secure an internship at a biotech company when he first moved to the United States.

If education falters, then you dont replenish the field of science, Edwards argues. You dont get younger generations excited, and the public wont care.

Edwards has also taken a leadership role in the MIT Biotechnology Group, a campus-wide student group meant to build connections between the MIT community and thought leaders in industry, business, and academia. For Edwards, the biotech and pharmaceutical industries play a clear role in disease treatment, and he knew he wanted to join the group before he even arrived at MIT. In 2019, he became co-director of the Biotech Groups Industry Initiative, a program focused on preparing members for industry careers. In 2020, he became undergraduate president, and this year hes co-president of the entire organization. Edwards speaks proudly of what the Biotech Group has accomplished during his tenure on the executive board, highlighting that they not only have the largest cohort ever this year, but its also the first time the group has been majority undergraduate.

Somehow, in between his research and outreach work, Edwards finds time to minor in French, play for the Quidditch team, and serve as co-president on the Course 20 Undergraduate Board, among other activities. Its a balancing act that Edwards has mastered over his time at MIT because of his genuine excitement and interest in everything that he does.

I dont like not understanding things, he jokes. That applies to science, but it also extends to people.

Excerpt from:
Investigating pathogens and their life cycles, for the benefit of society - MIT News

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Has a new race for the moon started? ; A quantum computer reveals the secrets of protons and neutrons for the first time – Tech News Inc

Posted: at 9:14 pm

NASA / JSC

Exobiology: Pseudo-fossils could mislead the search for life forms on Mars; Gravitational waves would have made the Big Bang turbulent spacetime. The Moon contains enough oxygen to allow 8 billion people to breathe for 100,000 years

The United States, Europe, China, Russia, brutal missiles, the Moon. Add a touch of geopolitical tensions to it and weve got the perfect cocktail for a new space race. Are we right to believe this? And if so, who could be the winner?