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Neuroscience

Athletics Roundup: Virtual Commencement for 72 USD Athletics in Class of 2020; Golf Wins Fall Tournament – University of San Diego Website

Tuesday, October 20, 2020 post has videoTOPICS: Alumni, Athletics, Changemaker, Academics, , Toreros Together

The University of San Diego and USD Athletics celebrated its 72 scholar-athlete graduates in the Class of 2020 with a virtual commencement ceremony in conjunction with the university's fully virtual commencement ceremony that took place on Oct. 17 during USD Homecoming and Family Week.

With special messages from Executive Director of Athletics Bill McGillisand each of the USD head coaches, the '20 Toreros were recognized and honored.

Among the 72 graduates, 12 were from football, nine from women's cross country, seven from women's soccer, five from men's soccer, softball, women's rowing and volleyball, four from baseball, and women's basketball, three from women's tennis and men's cross country, and two from golf, men's basketball, men's rowing, men's tennis, and swimming and diving.

Representing 14 states and 10 international countries, the Torero graduates earned degrees in 24 different majors. Of the 72, 61 completed their coursework in May 2020.

The 2020 graduating class featured two Academic All-Americans in Miguel Berry and Henry Lander of men's soccer and the Alcala Award winner, the highest honor from the University of San Diego for graduates, Clare Adams of women's rowing.

Class of 2020 University of San Diego Graduates

Softball: Madison Casiano (Visual Arts), Gabriela Grabowski (English), Delaney Heller (Business Administration), Savannah Shields (Biology), Sara Silveyra (English).Men's Soccer: Miguel Berry (Finance), Patric Krall (Finance & Real Estate), Henry Lander (Communication Studies), Freddy Polzer (Communication Studies & Psychology), Chase Van Wey (Anthropology).Women's Basketball: Patricia Brossmann (Communication Studies), Kat Olczak (Business Administration), Madison Pollock (Communication Studies), Ana Ramos (Business Administration).Volleyball: Thana Fayad (Communication Studies), Payton Douglass (Architecture), Megan Jacobsen (Business Administration), Anna Newsome (Communication Studies), Megan Priest (Biology).Men's Tennis: Joel Gamerov (Communication Studies), Guus Koevermans(Communication Studies).Women's Tennis: Nicole Anderson (Behavioral Neuroscience), Gemma Garcia (Communication Studies), Maria Paula Torres Draxl (Communication Studies).Swimming & Diving: Nicole Saladino (Behavioral Neuroscience), Sam Terranova (Industrial & Systems Engineering).Men's Cross Country: Patrick Bruce (Finance), Matt Sickman (Accountancy & Finance), Isaiah Quiambao (Psychology).Women's Soccer: Emma Barrow (Sociology), Kelley Carusa (Business Administration), Amber Michel (Marketing), Milan Moses (Anthropology), Angelica Sheils (Liberal Studies) Halle Walls (Biology), Julianne DeArmas (Marketing).Women's Cross Country: Erin Duncan (Accountancy), Cassidy Kuhn (Electrical Engineering), Madison Lambros (Accountancy), Cammy Manes (Biology), Hope McLaughlin (Environmental & Ocean Studies), Brianna Pertak (Psychology), Hailey Purtzer (Behavioral Neuroscience), Ally Roessling (Biochemistry), Beth Wade (Biochemistry).Baseball: Paul Kunst (Finance), Nicola Mislinski (Business Administration), Nathan Walker (Economics), Nigel Ward (Economics).Men's Basketball: Alex Floresca (Architecture), Jose Martinez(Psychology).Men's Rowing: Lucas Walbeck (Computer Science), Max O'Toole (Behavioral Neuroscience).Football: Michael Armstead (Communication Studies), JoJo Binda, Jr. (Sociology), Anthony Ellison (Business Administration), Alex Farina (Behavioral Neuroscience), Bryan Kelly (Biology), Tanner Kuljian (Marketing), Victor Lopez (Political Science), Zach Nelson (Marketing), Reid Sinnett (Finance), Daniel Tolbert (Business Administration), David Tolbert (Communication Studies), Marcus Vaivao (Mechanical Engineering).Golf: Kyle Bachelor (Finance), Yash Majmudar (Finance).Women's Rowing: Clare Adams (International Relations & Spanish), Sam Ahlman (Environmental & Ocean Studies), Kathryn Brady (Biochemistry), Roshni Pole (Psychology), Kadee Sylla (Psychology).

Golf

Toreros win Fall Tournament at La Purisima GC

San Diego golf earned its first tournament victory in more than six years on Oct. 20 as the Toreros were the only team to shoot below par at the two-day La Purisima College Invite at the La Purisima Golf Course (Par 72, 7,011 yards) in Lompoc, Calif.

USD, which carried a 12-stroke lead going into the final round, gave fourth-year head coach Chris Riley his first career tournament victory. The Toreros have now posted five top-five finishes in their last nine tournaments dating back to last fall.

The win was the Toreros' first since September 2014 when they won the Saint Mary's College Invitational at the Bayonet & Blackhorse Golf Course in Seaside, Calif.

The Toreros finished atop the leaderboard with a four-stroke cushion with the help of freshman Andi Xu's 71 in the final round. He was only one of four players to shoot below par in Tuesday's final round, and he finished runner-up in the individual leaderboard with a 1-under 215 (71-73-71) for the tournament. He was six strokes back of medalist Blake Hathcoat of Saint Mary's.

Xu and Hathcoat were the only two golfers to finish below par over the two days.

Charlie Reiter, who entered the day in first, finished in the top-three after shooting 1-over 217 (69-70-78). Both Xu and Reiter have now finished top-10 in each of the fall's two tournaments. Donald Kay and Ryan Bisharat both scored for the Toreros on the final day. Kay, a redshirt junior, shot a 3-over 75 in the final round to finish tied for fifth while Bisharat was 2-over 74 on Tuesday to finish tied for ninth. Harrison Kingsley was the fourth and final scorer for the Toreros in the final round, shooting 4-over 76 and finishing in the top-10 with a 3-over 219 (67-76-76).

USD wraps up its fall slate Nov. 5-6 with the Rustic Collegiate Classic at the Rustic Canyon Golf Course in Moorpark, Calif.

For the latest USDAthletics news, scores and information, visit thewebsiteand follow the Toreros on social media platforms:Facebook,TwitterandInstagram.

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Athletics Roundup: Virtual Commencement for 72 USD Athletics in Class of 2020; Golf Wins Fall Tournament - University of San Diego Website

Neuroscience

New Research Claims That Consciousness Itself Is an Energy Field – Futurism

Making Waves

An unusual new idea in neuroscience suggests that our consciousness is derived from a field of electromagnetic waves given off by neurons as they fire.

The idea is that these waves of electrical activity get sent out by neurons and, as they propagate across swaths of the brain, orchestrate our entire conscious experience. The research, published last month in the journal Neuroscience of Consciousness, offers more theory than tangible evidence, but the author says it could pave the way for robots that genuinely think and feel.

That author is Johnjoe McFadden, a molecular geneticist and director of quantum biology at the University of Surrey, who points to flaws in other models of consciousness as the reason that we dont have sentient artificial intelligence or robots capable of achieving consciousness.

By recreating these electrical waves in machinery, McFadden suggests, engineers might be able to pull it off.

McFaddens hypothesis veers away from most neuroscientists, who generally see consciousness as a narrative that our brain constructs out of our senses, perceptions, and actions. Instead, McFadden returns to a more empirical version of dualism the idea that consciousness stems from something other than our brain matter in this case energy.

How brain matter becomes aware and manages to think is a mystery that has been pondered by philosophers, theologians, mystics and ordinary people for millennia, McFadden said in a press release. I believe this mystery has now been solved, and that consciousness is the experience of nerves plugging into the brains self-generated electromagnetic field to drive what we call free will and our voluntary actions.

READ MORE: Researcher proposes new theory of consciousness [University of Surrey]

More on consciousness: Artificial Consciousness: How To Give A Robot A Soul

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New Research Claims That Consciousness Itself Is an Energy Field - Futurism

Neuroscience

Testing the Fluorescent Proteins That Light Up the Brain – UConn Today

Neurons are cells in your brain. Shaped like little stars, they flicker and fire off signals to each other. The signals travel up and down the long tendrils, called dendrites, extending out from each point of a neurons star-shaped body. Chained into circuits like Christmas lights, neurons electrical firing forms the glimmers of our thoughts and actions.

But the process by which an individual neuron decides to fire is not completely understood. Every neuron can receive signals from other brain cells through its dendrites. Some of these excite the neuron, pushing it closer to firing, while others calm it down. A dendrite can add up all the signals it receives, both calming and exciting, and pass the sum on to the cell body of its neuron. The neuron then adds up all the signals from its dendrites and uses that sum to decide whether or not to fire. Thats the process that researchers still dont entirely understand. To research it, neuroscientists need methods for monitoring electrical signals in the thin dendritic branches. This video shows a new method using light to explore electrical signals in different compartments of a neuron simultaneously. The intensity of the light reveals the voltage in that section of the neuron:

The video shows three consecutive voltage waves (from three nerve impulses) spreading from a neurons cell body into its dendrites. The colors represent light intensity. The light intensity is proportional to the voltage on the surface of the neuron; black is the minimal intensity on this scale, and red is maximal intensity.

To track all those electrical signals, neuroscientists used to have to wire up tiny electrodes to thin dendritic branches. But that method is cumbersome and difficult.

More recently, neuroscientists have begun creating fluorescent proteins that make the neuron light up when it receives an electrical signal. Thats whats being shown in the video. These Genetically Encoded Voltage Indicators (GEVIs), have potential to improve our ability to record voltages in neurons. This is what the glow looks like from many neurons fluorescing at the same time:

UConn School of Medicine neuroscientist Srdjan Antic and his colleagues noticed that many GEVIs have been invented, but few people use them. So they obtained as many GEVIs as possible and tested them in three separate ways, and reported the results in eNeuro on 08 September 2020.

First they tested the GEVIs in neurons cultured in a dish. They were able to detect single nerve impulses optically, but the cultured neurons were too variable to be used for systematic comparisons between the GEVIs.

So then they tested the GEVIs in non-neurons, cells called HEK293 cells. These cells are big, grow well in a dish, and were uniform enough to compare GEVIs:

Finally, the Antic lab expressed the GEVIs in animal brains and compared how various GEVIs did in groups of cells.

They found that all the GEVIs worked pretty well, and were easy to seein large populations of cells. The next step will be to test them in individual neurons, and perhaps even individual dendrites. Because when it comes to information processing in the brain,the most interesting things happen in dendrites, says Antic, associate professor of neuroscience at UConns medical school

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Testing the Fluorescent Proteins That Light Up the Brain - UConn Today

Neuroscience

The protein Klotho could extend the life of the brain. Is that a good thing? – Massive Science

Now's the time to live forever. Futurologists and transhumanists are poking themselves with what molecules they can, seeing what there is that might extend their lives or preserve their brains. One of the most intriguing molecules out there is called Klotho. Identified in 1997, it's named for the Fate of ancient Greek mythology who spun the thread the life. Mice that have a severely limited amount of Klotho in their body age rapidly and die prematurely. On the other hand, mice that carry more Klotho than normal live longer lives and appear to be resistant in some ways to aging.

Last April, an article appeared in the New York Times, titled "One Day There May Be a Drug to Turbocharge the Brain. Who Should Get it?" Massive contributor and neuroscientist Yewande Pearse and editor Dan Samorodnitsky sat down (in front of their computers) to talk about Klotho what it is, what it does, and whether prescribing a drug to supercharge the brain is a good idea.

Dan Samorodnitsky: Would it have to be prescribed by a doctor? Bought over the counter? Available at *chuckles to self* "Klotho shops"?

Yewande Pearse: This is a really interesting question because unlike a lot of other drugs, Klotho is a) a naturally occurring protein and b) has the potential to protect, treat and enhance the brain, therefore, the answer depends on the circumstances.

Mouse studies have revealed that Klotho plays an important role in the aging process. Mice with mutations in the Klotho gene have phenotypes which resemble different aspects of human aging, such as slowed growth, calcifying blood vessels, osteoporosis, and premature death. With respect to brain function, when mice with symptoms of age-related Alzheimer's disease are given Klotho, they are protected from cognitive decline. However, the exact biological function of Klotho and the way in which Klotho deficiency contributes to age-related diseases is not understood in mice, let alone humans.

Klotho has also has been shown to decrease with age in human blood serum samples, which may have something to do with cognitive decline in aging. Having said that, we all age, but we don't all develop Alzheimer's disease. Interestingly, people who carry a genetic variation of the Klotho gene that causes them to produce more Klotho, seem to not only be protected from Alzheimer's disease, but also perform better on cognitive tests like the Mini-Mental State Exam (MMSE)than people who produce average levels of Klotho.

Therefore, this becomes a question of dosage. To answer whether Klotho would have to be prescribed, we need to figure out the dose of Klotho required to prevent, treat, and enhance, and whether there are dose dependent risks. Perhaps a good starting point would be to calculate how much extra Klotho people with that gene variant produce compared to the average person versus how much less Klotho people who develop Alzheimer's disease have compared to those who do not of the same age.

It is also important to think about the structure and expression of Klotho when answering this question. Klotho is actually a transmembrane protein which means that it sits in the cell wall. Most of Klotho exists outside of the cell, but can be chopped off and released into the blood, urine, and cerebrospinal fluid. These different forms of Klotho all have different functions. Therefore, simply taking Klotho orally, is not as simple as it sounds, as it is unlikely that it will get it into its natural place in thebody, especially if we are trying to get it to the brain where it would have to cross the blood-brain-barrier, which prevents large molecules from passing through. To properly capture the full range of Klotho functions, we may be better off thinking about targeting the gene expression of Klotho itself something that may go beyond even a doctors prescription.

Multi-color whole brain image taken by fMRI

NIH via Flickr

But are naturally occurring levels of Klotho at the evolutionarily "correct" expression level?

Klotho is considered to be an aging-suppressor gene with multiple functions that protect organs. However, this protection doesn't last forever as Klotho declines with age.

To answer this question, we need to address a different question first: How and why do we age? There is no unified theory to explain the overall transformation taking place in the body during aging, but several theories, such as random mutation of genes, accumulation of damage by free radicals and the degeneration of functions like immunity are all valid on a local level. The reduction in Klotho as we age, for example, might fall into the last category, helping to explain dementia in the aging brain.

The "why?" is about trying to understand aging in terms of its necessity for survival. That sounds like a contradiction but is important when considering whether or not we should be taking Klotho as a drug. In 1889, August Weismann proposed that aging is a natural process of wearing out. If this is the case, then it is tempting to argue that there is no evolutionarily "correct" expression level of Klotho beyond child-bearing age. Klotho protects us for long enough to pass on our genes, after which point evolution has no reason to select for prolonged lifespan. This is why we don't all carry the "extra Klotho" genetic variant. However, the fact that better health care has granted us longer life regardless means that having higher levels of Klotho to maintain cognition is certainly preferable, and we could also argue that naturally occurring levels of Klotho are inadequate and should be augmented. Does that make sense?

It does make sense. Should we be concerned about, I don't know how to put it, over-correction? It feels like a moving target to nail down a dosage of Klotho that works well with any individual's natural expression of Klotho, natural variants, mutations, the three different variants of Klotho, just the overall difficulty of nailing down medications aimed at the nervous system.

Definitely, I think that caution is certainly needed given the fact that some studies have shown that one variant is actually associated with increased dementia and schizophrenia, suggesting that positive effects of Klotho on cognition may actually be limited by time, sex, and other factors. Having said that, all drugs, many of which have saved and improved lives, face the same challenge.

I think that Klotho research should focus on preventing the development of Alzheimers in people at risk first. In other words, trying to better understand Klotho as a potential biomarker, not just a treatment. There are no human studies to show what happens when Klotho is given to those who already have dementia, so early intervention is probably key. For the rest of us, research should focus on how our natural expression level of Klotho might be impacted by diet, exercise, etc., rather than heading straight down the pharmaceutical rout. For example, studies show that exercise, carbs, activated charcoal, probiotics and even statins can all increase the production of Klotho.

Is there evidence of disease from lack of Klotho in the body (maybe similar to imbalances occurring in some mental illnesses)?

The first clues about the function of Klotho came from mouse studies in which, the Klotho gene was deliberately mutated so that they didn't produce the normal level of Klotho. These mice had shorter life-spans and interestingly, showed a rapid decline in cognitive function, but only after a certain age. With mouse studies continuing to support the idea that Klotho expression levels correlate with both body (Klotho is made in the kidney too!) and brain function, there is now a lot of interest in Klotho as an indicator of health and disease.

A lack of Klotho in the body has been shown to correlate with a number of psychological conditions from chronic stress, which can lead to other psychiatric illnesses, and bipolar disorder. Lower levels of Klotho have also been associated with disease severity in multiple sclerosis and epilepsy. Generally, Klotho levels are lower in older people, but in Alzheimer's disease, patients, especially female patients, have even less Klotho.

A cross-section of a mouse cerebellum

NIH via Flickr

Also, and I'm sorry to keep harping on this, there's this quote from the original New York Times article that started this conversation:

"Some people carry a genetic variation that causes them to produce higher levels of Klotho than average in their bodies. Dr. Dubal and her colleagues identified a group of healthy old people with the variant and tested their cognition.

They scored better than people who make an average level of Klotho. Its not like they didnt undergo cognitive decline, said Dr. Dubal. Its just that they started off higher.

Maybe I'm just confused about the difference between Klotho making people "smarter" and people having "higher cognition" or something?

This is the part of the article that really jumped out at me. This is an important distinction. In this study, they found that differences in cognition as measured by IQ scores were only apparent after the age of 60. This means that these individuals experienced a delay in cognitive decline compared to people of the same age with the normal level of Klotho. Before 60, IQ scores were comparable but then after 60, people with lower levels of Klotho experienced a drop in IQ. Klotho is all about anti-aging, so we need to thinking about cognitive decline as a feature of aging and Klotho as an anti-aging protein. Assuming that we have the same IQ and we don't have the Klotho variant, if you were to start taking Klotho now (pretend they've cracked the issues above) and I didn't, I don't think you'd suddenly get smarter, I just think that when we got older, I'd start experiencing cognitive decline before you.

Do you worry about the number of apparent medical functions Klotho has ascribed to it? Increases overall brain function (but doesn't make you smarter), increases lifespan, and protects against a bunch of different, un-related diseases like Alzheimer's, Parkinson's, and MS? Seems like a lot of effects for one protein.

I am fascinated by the fact that Klotho has so many effects! It's a bit of a super protein. I am not surprised though because although all these effects seem disparate, they share common pathways upon which Klotho acts. For example, Kotho has antioxidant effects that are important for multiple functions both in the brain and the kidneys.

What I am worried about though is the fact that little is actually known about the function of Klotho and how aging suppression might work. I think we should be very careful about altering something that does indeed have so many actions and effects. Once Klotho is secreted, it enters the blood stream and goes everywhere, but by taking Klotho orally, I am not sure how can we ensure Klotho is going to the right places in the right quantities in a way that is effective and safe.

Do you worry about the ethics of taking Klotho? Taking it as a replacement drug, like if someone has low Klotho, seems fine, but beyond that? Should neuroscience researchers worry about that?

Are you asking me whether I think it's unethical to want to live longer and better? I'm tempted to go off on a tangent about our human endeavor to live forever and what that is doing to the environment. But, if we are going to live longer, is it wrong to want a better quality of life as measured by staying sharper into out 70s, 80s and 90s? I don't think that desire is unethical.

However, if we are talking about the ethics of taking an enhancement drug that not everyone has access to then my answer would lean more towards no but I'd say the same about food equity and a hundred other things that influence our health and well-being. I guess that answer is more personal. As a neuroscience researcher, my priority is safety and the ethics around that. If we can ensure that taking "extra" Klotho is safe and effective then, I don't think we should be worried. I mean, I can't speak for neuroscientists everywhere, but if some of us are willing to research how zapping the brains of healthy adults to improve memory and potentially improve cognitive function, then relatively speaking, I don't think researching the additive effects of a naturally occurring protein is a concern.

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The protein Klotho could extend the life of the brain. Is that a good thing? - Massive Science

Neuroscience

Opinion: Scientists have failed to convey findings effectively – The Cincinnati Enquirer

Christin Godale, Opinion contributor Published 10:15 a.m. ET Oct. 19, 2020

(Photo: Getty Images)

In the depths of pursuing a Ph.D. in neuroscience, I spend most of my time in a dark, windowless room using a microscope to take pictures of brain cells. When I do emerge from behind my microscope, I rarely discuss my research with other people, frankly because, like many other early-career scientists, I have not been adequately trained in communicating my research with the public. The COVID-19 pandemic has dramatically changed this dynamic; however, scientists are now encouraged, expected, and even required to explain what is happening across the country.

The "new normal"that we live in poses quite a dilemma to the scientific community. Researchers, like myself, perform experiments and collect and analyze data within academic contexts. We are taught to acknowledge our experiments shortcomings and propose innovative approaches in our grants and peer-reviewed papers. As a result, scientists are open to change whether that is changing a predictive model because of new data or redesigning an experiment because they thought of a new and better approach. Now, scientists need to adapt to the changing conditions outside the lab and seek better ways to communicate science to the public and, as a scientist, I am no different.

Throughout my eight years of combined undergraduate and graduate education, public communication has never been part of the curriculum. Many rising early-career scientists, including myself, believe our field must learn to clearly and effectively communicate our research to the taxpayers that fund it. Yet, it is often challenging to translate complex scientific concepts filled with jargon into clear, concise terms and ideas that the public can thoughtfully digest.

Scientist looking at a digital rendering of a coronavirus(Photo: Getty Images)

But there is good news! Many scientists across the nation are trying to find ways to develop their science communication skills. Professional societies like the Society for Neuroscience, the American Association for the Advancement of Science, and The National Academies of Science have developed an extensive collection of tools and programs, like science communication courses and science policy fellowships to help scientists create the necessary skillset to communicate with you, the public. Locally, the University of Cincinnati offers science communication classes. I plan to enroll in one or two of these lectures because I owe it to you as a scientist and as a community member to improve my skills.

The scientific community should have learned lessons from the last pandemic in 1918 that science communication was critical to stifling misinformation. Instead, we are seeing the same missteps today as COVID-19 misinformation circulates on various websites and social media platforms. Much of this pandemic misinformation stems from focusing on single-study results without context; overemphasizing results, particularly treatment effects, without considering limitations; and communicating results that have not been peer-reviewed by the scientific community.

(Photo: Getty Images)

Still, there are a lot of trustworthy resources that you can use to learn about COVID-19s biology, transmission, symptoms, and how to protect yourself, your family, and your community from the coronavirus. I recommend using The Federation of American Scientists COVID-19 question resource (covid19.fas.org), which is designed to connect public members with scientists trained in science communication to answer any and every question you might have about COVID-19.

As scientists, our purpose is to stretch the bounds of human knowledge, but at times, we have failed to communicate our findings with the public effectively. Now we have to take a step back and acknowledge the gaps in our education and work to improve our science communication skills. Science is a powerful tool, but it is up to every individual scientist to become a communicator and ensure our work contributes to solving societal problems instead of making them worse.

Christin Godale is a Neuroscience Doctoral Candidate at the University of Cincinnati College of Medicine and the former Graduate Student Trustee on the University of Cincinnati Board of Trustees.

Christin Godale(Photo: Provided)

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Opinion: Scientists have failed to convey findings effectively - The Cincinnati Enquirer

Neuroscience

Tim Chucks Cole, one half of The Correspondents, has died aged 35 – NME

Tim Cole, who performed as DJ Chucks in British electronic duo The Correspondents, died over the weekend, aged 35.

According to a Facebook post overnight from bandmate Ian Bruce (aka Mr Bruce), Cole passed away last Sunday (October 18). No cause of death was revealed.

He was a brilliant, complicated man who never fully appreciated the extent of his own talent. Hes the reason I bounced around like a lunatic for 13 years, Bruce said on Facebook.

And in a funny kind of way hes the reason the band lasted so long as he always chose integrity over hype, he was a facts not fads kinda guy.

I will miss his wit and cynicism. Him trying to explain neuroscience to me. I guess I will even miss having to sit through hours of cricket commentary on long car journeys to festivals.

Im devastated to inform you all that my band mate Tim Cole (aka Chucks) unexpectedly died last Sunday. We are all in

Posted by The Correspondents onTuesday, October 20, 2020

Cole and Bruce formed The Correspondents in 2007. Over the course of 13 years, the duo released two albums and a handful of EPs, and were on the lineups of Glastonbury, Bestival and WOMAD. Their last release was their 2019 EP, Who Knew.

Life on the road with endless gigs, airports, hotels and soundchecks took its toll, Bruce said, But the sense of achievement and satisfaction after each show was something palpable that we would always share and enjoy.

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Tim Chucks Cole, one half of The Correspondents, has died aged 35 - NME

Genetics

University is mapping the genetics of eating disorders to develop better treatments – yoursun.com

A new initiative at University of North Carolina at Chapel Hill is kicking off a genetic study of eating disorders that it says will be the largest of its kind.

If successful, the study, conducted by the Eating Disorders Genetic Initiative (EDGI), will be able to identify hundreds of genes that influence a person's likelihood of suffering from three prominent disorders: anorexia nervosa, bulimia nervosa and binge-eating disorder.

That knowledge could significantly improve the way those illnesses are treated, said Cynthia Bulik, a professor at the UNC School of Medicine and head of EDGI.

"It might help us with prediction and prevention in the future," Bulik said in a phone interview. "That is a direction we hope to go in help us identify those who are high risk."

Eating disorders affect a large number of people. About 9% of Americans, or 28.8 million, will have an eating disorder in their lifetime, according to the National Association of Anorexia Nervosa and Associated Disorders.

And that number could be increasing, as the coronavirus pandemic pushes the country into a mental health crisis as well. Bulik recently coauthored a study of individuals with eating disorders in the U.S. and the Netherlands that reported an increase in anxiety during the pandemic, which has disrupted the lives and routines of millions.

"We are clearly in the midst of a mental health pandemic," Bulik said. "The things (participants) talked about most was the lack of structure in their days ... (and) a lack of social support. Eating disorders thrive in isolation."

While there have been numerous psychiatric studies of eating disorders, the biologic underpinnings of the illness are still relatively unknown, and there are no medications to treat eating disorders

"Part of that is because we haven't understood the biology of eating disorders," she said.

EDGI is seeking 100,000 people across the world with a history of an eating disorder to volunteer as part of the genetic study. In the U.S., it is looking to reach 6,000 participants. In addition to genetics, EDGI will also survey participants from around the world to see how environmental factors influence the disorders.

Bulik said it will be important for EDGI to get a very diverse sample of volunteers. She hopes to complete the collection portion of the study by 2022.

The research is funded by the National Institute of Mental Health. The genetic samples will be collected via a saliva kit in the mail, and then be processed at a lab in Chapel Hill.

The study will build off a previous one that focused specifically on anorexia nervosa. Bulik said that study had transformational findings, identifying eight areas of the genome with significant associations with anorexia nervosa. Finding evidence for those associations, she said, helps reduce misunderstandings around the illness.

"These are serious illnesses with genetic bases, and we need to bust those myths about them being a choice," Bulik said. "One of the things that this research does is bust those myths. We can say with complete confidence that genes are involved."

That previous research only studied around 17,000 participants, and Bulik said the data would be much more reliable with a larger pool of volunteers.

By expanding the research to include other eating disorders, EDGI could determine if certain genetics predispose someone to multiple illnesses, or whether they all have unique causes.

"My gut says and preliminary information shows that there might be some shared genetic factors across all three disorders, but also unique genetic factors associated with them that decides the path (of treatment) you go down," she said. "There is not a clear demarcation between these disorders. People will toggle back and forth between anorexia and bulimia. They are not mutually exclusive."

EDGI is looking for participants who are 18 years or over and have, at any point in their lives, experienced anorexia nervosa, bulimia nervosa or binge-eating disorder. To volunteer or learn more, visit http://www.edgi.org.

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University is mapping the genetics of eating disorders to develop better treatments - yoursun.com

Genetics

ICR Discovery Club gives members a virtual glimpse into the cancer genetics lab – The Institute of Cancer Research

Image: Dr Zsofia Kote-Jorai, who is a Senior Staff Scientist in Profesor Ros Eeles' lab explains to the Discovery Club how they perform genetic sequencing on tumour samples from men with prostate cancer

Members of the ICRs Discovery Clubwere given an exclusive insight into how researchers sample, process and analyse tumour cells in the lab, as part of the ICRs first virtual event for our donors.

Professor Ros Eeles, who leads the ICRs Oncogenetics Teamand is a world-leading expert in the genetics of prostate cancer, explained during a video event how she and her team analyse the DNA from thousands of men with and without prostate cancer to find genetic clues about the disease.

The ICR's Discovery Club offers a regular series of events for our donors to hear from some of our leading scientists and clinicians about their work. The event took place online for the first time instead of in person due to the coronavirus pandemic.

A video featuring members of Professor Eeles team showed how they are continuing their important work and making progress in studying cancer geneticsdespite the impact of coronavirus on research.

The virtual event was a chance for ICR researchers to share examples of cutting-edge research into the genetic causes of cancer with Discovery Club members from the comfort of their own home.

Professor Eeles explained that there are three billion letters that make up the human genome, our entire DNA structure in every cell, which was first read by scientists nearly 20 years ago.

This medical revolution means scientists can now identify genetic markers in our DNA linked to diseases like prostate cancer heralding a new era of personalised healthcare.

Finding the genetic markers for prostate canceris important because many men will never develop aggressive disease, so genetic screening can prevent unnecessary biopsies and scans in those that are likely to stay healthy, and pick up the disease sooner in men who need urgent treatment.

Discovery Club members watched a video showing Professor Eeles team preparing tumour samples in the lab, and explaining the steps needed to read their DNA.

This incredibly complex task requires sophisticated equipment and know-how, but ICR scientists are making great strides in uncovering genetic risk markers for prostate cancer.

Professor Ros Eeles has been has been instrumental in ensuring new discoveries in cancer genetics, immediately benefit patients. Learn about the work of Professor Eeles and the Oncogenetics Team.

Find out more

By comparing tiny changes across thousands of DNA sequences, scientists can pick out common variations in men that indicate an increased risk of prostate cancer.

Researchers like Professor Eeles and her team have identified 256 changes in DNA which increase the risk of men developing the disease, accounting for nearly half of all the inherited genetic risks for prostate cancer.

Professor Eeles is also identifying rare mutations that can lead to the most aggressive forms of prostate cancer.

Her team has found that men with BRCA2 mutations, a genetic fault also linked with breast cancer in women, were much more likely to develop prostate cancer than men without the mutation.

Professor Eeles is leading clinical trialslooking into whether regular DNA screening of men with mutations like BRCA2, could help diagnose prostate cancer earlier.

DNA screening could also give men more insight into their own health, helping them make decisions that could influence not only their cancer diagnosis, but their treatment too and which ultimately, could help them live longer and better lives.

We've lost many vital research hours to the coronavirus crisis but the need for our work continues to grow. Please help uskick-startour research to make up for lost time in discovering smarter, kinder and more effective cancer treatments, andto ensure cancer patients don't get left behind.

Support our work

ICR Chief Executive Professor Paul Workmansaid: It was great to hear from Professor Eeles today, whose research into cancer genetics is truly world leading. Her work is helping us to identify those people who have increased risk of prostate cancer, in order that we can detect and treat the disease sooner, and even potentially prevent men from developing prostate cancer in the first place. We know that cancer has not been self-isolating during this time, and we continue to publish major discoveries that will help us to make the discoveries that defeat cancer.

There is going to be an even greater need for cancer treatments and interventions as a result of Covid-19, and the support of our donors and their messages of encouragement is absolutely vital and appreciated. I cant thank you enough for your continued help and commitment to support us through these difficult times.

The Discovery Club is our high-value giving club whose members help us to drive forward our scientific strategy through philanthropic investment in key organisational priorities.

The events are an opportunity for members to hear from leading ICR scientists and clinicians about their work, and the ways that their support is making a difference.

It takes multidisciplinary teams of researchers and sophisticated data analysis to uncover the genetic causes of cancer, and we couldnt do it without your generous donations.

Your continued support helps push forward our vital research, ensuring that new discoveries in cancer genetics are brought rapidly into the clinic to benefit patients. If you would like to find out more,please contact Hannah Joyce, Deputy Director of Philanthropy.

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ICR Discovery Club gives members a virtual glimpse into the cancer genetics lab - The Institute of Cancer Research

Genetics

Breast Cancer Predictive Genetic Testing Market Industry Development, Growth Opportunities and Demand Analysis : Roche, Thermo Fisher Scientific -…

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Breast Cancer Predictive Genetic Testing Market Industry Development, Growth Opportunities and Demand Analysis : Roche, Thermo Fisher Scientific -...

Genetics

Hunt on for future Covid mutations that cause treatments to lose potency – The Guardian

Scientists are to increase surveillance for new coronavirus mutations amid concerns that future strains of the virus could develop at least partial resistance to antibody treatments and Covid-19 vaccines.

There is no evidence that the mutations seen so far could help the virus evade vaccines or treatments now in development, but genetic analysis of circulating strains suggests that partially-resistant variants can emerge and spread among humans.

1 September 2020

Boris Johnson

Not only are we getting the pandemic under control, with deaths down and hospital admissions way, way down, but we will continue to tackle it, with local lockdowns and with our superlative test-and-trace system.

9 September 2020

Boris Johnson

NHS Test and Trace is doing a heroic job, and today most people get an in-person test result within 24 hours, and the median journey is under 10 miles if someone has to take a journey to get one [To Keir Starmer] We make the tough calls all he does is sit on the sidelines and carp.

9 September 2020

Boris Johnson

[On the moonshot proposal for mass, near-instant testing:] We are hopeful this approach will be widespread by the spring and, if everything comes together, it may be possible even for challenging sectors like theatres to have life much closer to normal before Christmas.

16 September 2020

Boris Johnson

We dont have enough testing capacity now because, in an ideal world, I would like to test absolutely everybody that wants a test immediately Yes, theres a long way to go, and we will work night and day to ensure that we get there.

17 September 2020

Matt Hancock

Of course there is a challenge in testing We have sent tests to all schools to make sure that they have tests available. But of course I also recognise the challenges in getting hold of tests Tests are available, even though it is a challenge to get hold of them.

In a paper drawn up for the governments Sage committee of experts, the UK Covid genomics consortium (Cog-UK) reports that a number of mutations have cropped up in the crucial spike protein which covers the virus like pins in a pin cushion and allows the pathogen to invade human cells.

Because many vaccines use the spike protein to generate immunity against the virus, mutations that subsequently change the spike can affect how well that immunity works.

Anything that affects the spike protein can potentially change how either natural immunity or vaccine-induced immunity responds to the virus, said Jeffrey Barrett, a geneticist and member of the consortium at the Sanger Institute near Cambridge.

The coronavirus that causes Covid-19 is genetically fairly stable, but it still acquires mutations, creating a multitude of lineages that geneticists can use to track the virus around the world and from outbreak to outbreak. By chance, some lineages will pick up mutations in the spike protein, a process called antigenic change. Many of these are likely to make the virus worse at spreading, but others may be neutral or even improve the viruss ability to infect.

The potential risk comes if the virus accumulates mutations in the spike protein that change it enough for antibody treatments and vaccines to lose their potency. This could be most problematic for so-called monoclonal antibody treatments, of the type given to Donald Trump, where patients are infused with a mixture of two different types of antibodies. Vaccines tend to induce a greater variety of antibodies, so even if some are ineffective, the rest should still target the virus.

The scientists describe how in the spring more than 500 people in Scotland contracted coronavirus with a spike mutation known as N439K. The mutant version vanished during lockdown, but later re-emerged in Romania, Norway, Switzerland, Ireland, Belgium, Germany, and is now circulating in the UK. The mutation, and at least half a dozen others, show that the spike protein can change without destroying the viruss ability to spread.

Scientists have shown already that coronavirus with the N439K mutation is resistant to at least one type of antibody that infected people can produce. The aim of the surveillance is to watch for future mutations that might, with time, make the virus resistant to a greater variety of antibodies.

The genetics consortium is setting up a group to monitor new and existing mutations to ensure that signs of potential resistance are spotted early. It is particularly important that surveillance of antigenic change is established in the lead up to the roll out of a vaccination program in the UK, since many of the vaccines under development target the spike protein, the paper states.

Paul Bieniasz, a virologist at Rockefeller University in New York, said it was important to monitor genetic variation in the viruss spike protein in order to anticipate potential problems ahead, rather than because there is any immediate threat from currently circulating variants.

The sporadic emergence of antibody resistance mutations, such as N439K, is one reason most antibody therapies rely on a cocktail of two antibodies. But Bieniasz said that depending on how widely those treatments are used, it will be important to monitor resistance to them in the same way that we monitor bacterial resistance to antibiotics, or HIV resistance to antiviral drugs.

A single mutation would be unlikely to render a Covid-19 vaccine impotent, he added, but as the virus evolves over the coming years, pharmaceutical firms might need to reformulate vaccines to take account of genetic changes that arise in the virus.

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Hunt on for future Covid mutations that cause treatments to lose potency - The Guardian