Val Sheffield, the Roy J. Carver Chair in Molecular Genetics at the University of Iowa Roy J. and Lucille A. Carver College of Medicine, has been elected tothe 2020 class of the American Academy of Arts and Sciences(AAAS).

Sheffield was recognized for playing a key role in constructing human genetic maps and developing efficient disease-gene discovery approaches. This paved the way for the completion of the human genome project and significantly contributed to genetic discoveries in blinding eye diseases, obesity, hypertension, and neurological disorders, potentially leading to noveltherapies.

The AAAS, founded in 1780 by John Adams and John Hancock, is both an honorary society that recognizes and celebrates the excellence of its members and an independent research center convening leaders from across disciplines, professions, and perspectives to address significant challenges. Elected members join with other experts in cross-disciplinary efforts to produce reflective, independent, and pragmatic studies that inform public policy and advance the publicgood.

This year, 276 new members were elected and include notable scientists, artists, scholars, and leaders in the public, nonprofit, and private sectors. Sheffield joins 58 other leaders in the medical sciences specialty. Academy members are nominated and elected by current members and chosen for excellence in their field and a record of continuedaccomplishment.

Sheffield is eager to contribute hisexpertise.

Genetic and genomic data are increasingly being integrated into the practice of medicine. With my expertise in human molecular and clinical genetics and genomics, Im hoping to be a useful resource to the academy, Sheffieldsays.

This is an incredible honor and well-deserved national recognition. We are extremely proud of Dr. Sheffield and his achievements, says Brooks Jackson, UI vice president for medical affairs and the Tyrone D. Artz Dean of the Carver College of Medicine.Given these turbulent times, it is especially gratifying to be able to celebrate hissuccess.

Sheffield joined the UI in in 1990 to perform research and practice clinical genetics in the Division of Medical Genetics for the UI Stead Family Department of Pediatrics. He has spent his entire career at Iowa, where he served as director of the Division of Medical Genetics for 22 years until stepping down in January 2020. He conducts scientific research related to human genetic diseases, however, he has recently converted a portion of his lab to join researchers across the world fighting the coronaviruspandemic.

Since the COVID-19 shutdown, I have switched some of my laboratory personnel to a COVID-19 project. We are trying to devise a simple method for collecting samples from patients for COVID-19 testing that doesnt require nasal swabs (in short supply) or use medical personnel to collect samples. The person being tested will self-collect the sample, thus saving on personnel and personal protective equipment. I am hoping to get FDA approval soon for this method so that it can be used to expand needed testing throughout Iowa, Sheffieldsays.

At the UI, Sheffield trains doctoral and medical students as a professor of pediatrics and a professor of ophthalmology and visual sciences. He also is an investigator for the UI Institute for Vision Research and practices medicine, caring for patients with human genetic disorders. He has co-authored more than 330 peer-reviewed scientific papers. He previously was an investigator for the Howard Hughes Medical Institute (HHMI), from 1998 to2016.

The members of the class of 2020 have excelled in laboratories and lecture halls, they have amazed on concert stages and in surgical suites, and they have led in board rooms and courtrooms, says academy President David W. Oxtoby. These new members are united by a place in history and by an opportunity to shape the future through the academys work to advance the publicgood.

Sheffield attended Brigham Young University, where he earned a bachelors degree in zoology and a masters degree in developmental biology. He received a doctoral degree in developmental biology and a medical degreewith honors from the University of Chicago. He was a resident in pediatrics and fellow in medical genetics at the University of California, SanFrancisco.

His research has been funded by the National Institutes of Health (NIH) for 29 consecutive years, as well as by the Roy J. Carver Charitable Trust. Sheffields honors include the E. Mead-Johnson Award for Pediatric Research and the Lewis Rudin Prize from the New York Academy of Science, and he is a member of the National Academy of Medicine. Sheffield is board certified by the American Board of Medical Genetics and Genomics in both clinical genetics and clinical moleculargenetics.

Sheffield joins the following UI faculty and administrators who havebeen elected members of the American Academy of Arts andSciences:

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Val Sheffield elected to the American Academy of Arts and Sciences - Iowa Now

The virus that has poked holes in the entire global infrastructure for the past few months is physically far smaller than the period at the end of this sentence.

That something so minuscule can act as one of the biggest threats currently imaginable to humanity is a testament to the ironically complex nature of viruses, which, without properly understanding, can make this disease even more baffling than it already is. Here, we break down the basics of COVID-19 to try to make sense of the way it infiltrates the body.

A coronavirus is defined as a single-stranded RNA virus that typically leads to an upper respiratory infection. Severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2, which was first reported in December in Wuhan, China, is of the same family of virus as the Middle East respiratory syndrome, the severe acute respiratory syndrome and even the common cold. Humans commonly fall ill at the hands of complications like bronchitis and pneumonia from less severe coronaviruses, and are able to recover.

Hong Zhou, a professor in the Department of Microbiology, Immunology and Molecular Genetics as well as the director of the Electron Imaging Center for NanoMachines, explained how other coronaviruses function differently than the latest one.

The other coronaviruses are usually seasonal, Zhou said. We dont talk about them because they dont cause problems for humans.

The same cannot be said about the most recent coronavirus cousin. The thing that sets it apart is that human immune systems have no idea what to do with it.

Scientists often describe this phenomenon by referring to the virus as novel. Given SARS-CoV-2 originated in animals, it is a pathogen that is not just unfamiliar to anyones body but that is unbeknownst to the entirety of mankind, according to the Mayo Clinic.

It is believed that COVID-19 may have originated in a wet market in Wuhan, China, which was home to animals sold for consumption. Animals provide a vehicle for the virus to spread and it can exist within them without humans ever knowing. Moreover, an environment like a wet market can be conducive to the spread of viruses since many different species share a small space where bodily fluids can drop from one cage to another and eventually to human handlers.

[Related: Campus Queries: For how long does the novel coronavirus remain infectious on different surfaces?]

The microcosmic wet market ecosystem example goes to show the ease at which such viruses can spread among animals as well as people. However, when it comes to transmission, not all viruses are created equal. The 2019 coronavirus is extremely contagious in comparison to its predecessors: while all coronaviruses can spread through touch, it has become clear that COVID-19 may have a little bit more to it.

For starters, its important to note that viruses are entirely dependent on the cells they infect. These nonviral cells contain their own code for the government of healthy cellular mechanisms. Viruses, however, do not care about the health of the cells they infect. They invade, bringing with them their own instruction manual, and proceed to usurp cellular resources in order to make more of themselves. In comparison to the thousands of genes contained within healthy human cells, viruses bring with them two to 10 genes a gross oversimplification of whats required for health.

Picture a well-oiled democratic society with a complex system of checks and balances to keep everything running smoothly. Suddenly this society is overpowered by a ruler from another land who throws away the nuanced system and has the single goal of utilizing the resources of the city to help his people reproduce.

In their quest to hijack the human cell, viruses must first bind to it by means of some structure or protein. All coronaviruses use what is called a spike protein, but the proteins present in SARS-CoV-2 bind a lot more tightly. Then, the protein is activated by an enzyme called furin that is present in various human organs, essentially allowing the virus to attack the body from multiple different entry points causing potential failure in multiple different organs. Studies have shown the furin activation site discovered in SARS-CoV-2 is different than that of other coronaviruses, which likely influences the bodys violent reaction to it.

These are mechanisms that give COVID-19 a certain competitive edge against other coronaviruses. All viruses, however, attack with a certain brutality that is built into their very machinery and part of their danger comes with the mutations that arise every so often.

Just like anything in nature, viruses have to figure out a way to exist, Zhou said. To gain existence, the virus must adapt to the environment.

[Related: UCLA announces aim to offer remote instruction option for fall quarter]

Timothy Brewer, a professor of epidemiology in the Fielding School of Public Health, explained that many of the mutations that occur may be silent, thereby leaving a virus unchanged in a meaningful way.

And so the question is, will there be some meaningful mutation that either makes the virus more or less deadly, or more easy or less easy to transmit? he said. That certainly is possible, but we havent seen any real evidence for that yet.

As a result of the complicated nature of viral mechanisms, there is still no cure to target COVID-19. Scientists around the world are testing different contestants, but according to Brewer, the treatment plan will depend on the frequency of mutation.

Well have to see if it is more like influenza, (where) the mutation rate really isnt that important for treatment, and we can use one medicine, or if it is more like HIV, where we might need to use combinations of medicines because its mutating so rapidly, he said.

The timeline of such treatments for COVID-19 is still ambiguous. Zhou made clear that neither a treatment nor a vaccine will appear overnight. The polio vaccine, for example, was first widely used more than 60 years after the first epidemic began in the United States in 1894.

There is a process you have to follow for safety and efficacy, Zhou said. Many times it will not be successful and you have to repeat the process again.

As we await the approval of something more permanent, the best way to combat the tiny virus that has brought society to a standstill may just be to stop its spread by staying at home and washing our hands. Understanding how viral operations work is the first step in figuring out how to overcome them and get back to life as we know it.

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The Quad: Breaking down the science behind COVID-19 virus, looking into how it functions - Daily Bruin

Its hardly a secret that people everywhere are hurting from COVID-19.

From health care workers running out of proper medical supplies to students faced with quarantine boredom and isolation, the effects of COVID-19 are hitting everyone in ways we may not immediately think of.

Luckily, UCLA students and alumni are responding to this heightened need for support with their own leadership, time and effort. Heres the Quads look at what Bruins are doing to help out and provide hope in these difficult times.

Firstly, to financially help fellow Bruins in need, UCLAs Student Wellness Commission initiated two programs: the Basic Needs Subsidy and Student Relief Grant. The programs are open to all undergraduate students.

Mihika Sridhar, a fourth-year microbiology, immunology and molecular genetics student, and the student wellness commissioner, said that as a programming commission, SWC largely relied on their physical location on campus to engage with students in person. This has become impossible in light of the global pandemic, she said.

We were thinking of what we could do in place of (our spring quarter events) that might be more effective given the current pandemic, Sridhar said. Because of how privileged we are to have this amount of money under purview, we decided that the right thing to do was to redistribute it to those in need like a student who doesnt have a roof over their head or doesnt know how theyre going to pay for their next meal.

[Related: Donations help Westwood businesses feed the frontline of health care workers]

The Basic Needs Subsidy is available on a first-come, first-served basis and provides students with upwards of $100 for necessities such as hygiene products, toiletries and medication.

The SWC is also offering the Student Relief Grant fund, a $500 need-based award to students facing financial hardships that are created or worsened by COVID-19. Approximately 200 grants are available, Sridhar said.

This pandemic is highlighting the inequities that exist at UCLA, the United States and the world, Sridhar said. Its necessary now for people to realize their privileges and thus also realize how their time, money and efforts could be spent helping others.

Many Bruin-led organizations have popped up to do just that one of them being Los Angeles COVID Volunteers, comprised of UCLA undergraduate and graduate student volunteers.

Haroon Rasheed and Hannah Hye Rhyn Chung, MD candidates at the David Geffen School of Medicine and the organizations co-directors of communication, said that their mission is to serve LA health care workers in need during the COVID-19 pandemic.

As a medical student early in training, there is little I can do to help on the front lines of this health pandemic, Chung said. But as students whose future will be in health care, my classmates and I felt called to relieve the burden on our health care system here in Los Angeles.

LA COVID Volunteers offers four main programs: PPE Management and Construction, Healthcare Worker Services, Food Corps and Community Partnerships. The organization works in collaboration with UCLA Engineering, the Anderson School of Business, local restaurants and volunteers to make this possible.

In the month since the organizations formation, LA COVID Volunteers has been focusing its service on UCLA Health organizations such as Ronald Reagan Medical Center, UCLA Mattel Childrens Hospital and Cedars-Sinai Medical Center, but they are looking to donate to smaller clinics in the future.

For those interested in getting involved, the organization is actively looking for volunteers in any of the four programs. Volunteers who can support weekday morning child care requests are most needed, Rasheed said.

COVID Transport Relief, commonly shortened to CTR, is an organization with a similar mission. Started by UCLA undergraduates who met during the 2019 Stanford Summer Community College Premedical Program, their mission is to coordinate the pick-up and delivery of essential supplies for health care workers in the Bay Area.

Rather than health care facilities at large, we aim to directly assist hospital employees and first responders to help minimize the added hurdles these essential workers face in trying to maintain personal safety, said Tasneem Sadok, a third-year neuroscience student and CTR co-founder.

Volunteer drivers are largely composed of CTR admin and their family and friends. CTR provides all drivers with a homemade mask and pair of gloves, and enforces pick-up and drop-off protocols based on CDC recommendations.

In the future, (we hope) to partner with larger and better-equipped organizations to facilitate bulk donation of supplies to local hospitals and clinics, Sadok said.

There are many different sectors of CTR that Bruins can get involved in, if interested. Donating spare supplies, contributing to the organizations GoFundMe or simply spreading the news through social media are some ways to help.

And for everyone struggling with quarantine boredom, do not fret: Concerts at the Kitchen Table seek to create a sense of community through virtual musical performances by fellow Bruins.

Concerts at the Kitchen Table was founded by third-year molecular cell and developmental biology student Akshay Anand, who was inspired by his own love for music at home and in college.

To source performers, Anand turned to friends, specifically those who, like him, were planning on participating in Spring Sing. As they watch these performances, audience members are given the opportunity to donate to World Central Kitchen, a nonprofit organization that is currently serving over 100,000 meals a day nationwide to those affected by COVID-19.

In order to create and strengthen the performer-audience relationship, Anand heavily relies on the power of social media, particularly Instagram. Here, he posts artist highlights that feature a picture of the performer, a short biography and the songs theyll be playing.

By doing this, it pushes people to be more invested in the performance because its not like, Oh, Im going on for 30 minutes today and I know no one whos playing except a few of my friends, Anand said. By putting them on Instagram, people know who these performers are and are more inclined to be into the performance. You feel proud of yourself for being part of this performance.

Concerts at the Kitchen Table, much like LA COVID Volunteers and COVID Transport Relief, is hoping to grow they are currently hoping to add dance performances to the mix. Likewise, for those interested in getting involved, simply message the organizations Instagram, Anand said.

Amid the uncertainty that the COVID-19 pandemic has left us with, its hard not to fall victim to the chaos. UCLA students and alumni are providing examples of how to turn this chaos into positivity, one medical-supply donation, hot meal and performance at a time.

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The Quad: UCLA students, alumni band together to support those in need during global pandemic - Daily Bruin

The novel coronavirus pandemic has now resulted in more than 3 million confirmed cases globally and is pushing scientists to share ideas quickly and figure out the best ways to collaborate and contribute to solutions.

Recently, Duke researchers across the School of Medicine came together for an online symposium consisting of several short presentations to summarize the latest of what is known about the novel coronavirus, SARS-CoV-2.

This daylong event was organized by faculty in the Department of Molecular Genetics and Microbiology and researchers from different fields to share what they know about the virus and immunity to guide vaccine design. This conference highlighted the myriad new research pathways that Duke researchers are launching to better understand this pandemic virus.

One neat area of research is understanding viral processes within cells to identify steps at which antivirals may block the virus. Stacy Horners Laboratory studies how RNA viruses replicate inside human cells. By figuring out how viruses and cells interact at the molecular level, Horner can inform development of antivirals and strategies to block viral replication. Antivirals stop infections by preventing the virus from generating more of copies of itself and spreading to other cells. This controls damage to our cells and allows the immune system to catch up and clear the infection.

At the symposium, Horner explained how the SARS-CoV viral genome consists of 29,891 ribonucleotides, which are the building blocks of the RNA strand. The viral genome contains 14 areas where the RNA code can be transcribed into shorter RNA sequences for viral protein production. Though each RNA transcript generally contains the code for a single protein, this virus is intriguing in that it uses RNA tricks to code for up to 27 proteins. Horner highlighted two interesting ways that SARS-CoV packs in additional proteins to produce all the necessary components for its replication and assembly into new viral progeny.

The first way is through slippery sequences on the RNA genome of the virus. A ribosome is a machine inside the cell that runs along a string of RNA to translate its code into proteins that have various functions. Each set of 3 ribonucleotides forms one amino acid, a building block of proteins. In turn, a string of amino acids assembles into a distinct structure that gives rise to a functional protein.

One way that SARS-CoV-2 packs in additional proteins is with regions of its RNA genome that make the ribosome machinery slip back by one ribonucleotide. Once the ribosome gets offset it reads a new grouping of 3 ribonucleotides and creates a different amino acid for the same RNA sequence. In this way, SARS-CoV-2 makes multiple proteins from the same piece of RNA and maximizes space on its genome for additional viral proteins.

Secondly, the RNA genome of SARS-CoV-2 has regions where the single strand of RNA twists over itself and connects with another segment of RNA farther along the code to form a new protein. These folds create structures that look like diverse trees made of repetitive hairpin-like shapes. If the ribosome runs into a fold, it can hop from one spot in the RNA to another disjoint piece and attach a new string of amino acids instead of the ones directly ahead of it on the linear RNA sequence. This is another way the SARS-CoV-2 packs in extra proteins with the same piece of RNA.

Horner said a step-by-step understanding of what the virus needs to survive at each step of its replication cycle will allow us to design molecules that are able to block these crucial steps.

Indeed, shapes of molecules can determine their function inside the cell. Three Duke teams are pursuing detailed investigation of SARS-CoV-2 protein structures that might guide development of complementarily shaped molecules that can serve as drugs by interfering with viral processes inside cells.

For example the laboratory of Hashim Al-Hashimi, develops computational models to predict the diversity of structures produced by these tree-like RNA folds to identify possible targets for new therapeutics. Currently, the Laboratories of Nicholas Heaton and Claire Smith are teaming up to identify novel restriction factors inside cells that can stop SARS-CoV-2.

However, it is not just the structures of viral components expressed inside the cells that matter, but also those on the outside of a virus particle. In Latin, corona means a crown or garland, and coronaviruses have been named for their distinctive crown-like spikes that envelop each virus particle. The viral protein that forms this corona is aptly named the Spike protein.

This Spike protein on the viral surface connects with a human cell surface protein (Angiotensin-converting enzyme 2, abbreviated as ACE2) to allow the virus to enter our cells and cause an infection. Heaton proposed that molecules designed to block this contact, by blocking either the human cell surface protein or the viral Spike protein, should also be tested as possible therapies.

One promising type of molecule to block this interaction is an antibody. Antibodies are Y shaped molecules that are developed as part of the immune response in the body by the second week of coronavirus infection. These molecules can detect viral proteins, bind with them, and prevent viruses from entering cells. Unlike several other components on our immune defense, antibodies are shaped to specifically latch on to one type of virus. Teams of scientists at Duke led by Dr. Sallie Permar, Dr. Georgia Tomaras, and Dr. Genevieve Fouda are working to characterize this antibody response to SARS-CoV-2 infection and identify the types of antibodies that confer protection.

Infectious disease specialist Dr. Chris Woods is leading an effort to test whether plasma with antibodies from people who have recovered can prevent severe coronavirus disease in acutely infected patients.

Indeed, there are several intriguing research questions to resolve in the months ahead. Duke scientists are forging new plans for research and actively launching new projects to unravel the mysteries of SARS-CoV-2. With Duke laboratory scientists rolling up their sleeves and gowning up to conduct research on the novel coronavirus, there will be soon be many more vaccine and therapeutic interventions to test.

Guest post by Tulika Singh, MPH, PhD Candidate in the Department of Molecular Genetics and Microbiology (T: @Singh_Tulika)

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Duke Scientists Studying the Shape of COVID Things to Come | Research Blog - Duke Today

Merck & Co. said today it will partner with the Institute for Systems Biology (ISB) to identify targets for medicines and vaccines against COVID-19 by investigating and defining the molecular mechanisms of the disease and specifically SARS-CoV-2 infection.

While the value of the collaboration was not disclosed in the announcement, Merck and ISB did say they will use a contract awarded to the pharma giant in 2016 by the Biomedical Advanced Research and Development Authority (BARDA). That contract (HHSO100201600031C) has a potential value of $78.5 million ($78,531,649), and was originally awarded August 29, 2016, to advance development of the vaccine candidate V920 against Ebola virus using a recombinant vesicular stomatitis virus vector, according to a contract summary published by GovTribe.

The contract has been extended from its scheduled end of May 31, 2020, through September 30, 2024.

In December, Merck announced FDA approval of the vaccine under the name ERVEBO (Ebola Zaire Vaccine, Live), indicated for the prevention of disease caused byZaire ebolavirusin individuals 18 years of age and older.

Merck said it had agreed to provide research funding and work with researchers at ISB to characterize targets for potential therapeutic intervention and vaccine development.

Through the collaboration with Merck, scientists from ISB, health workers from the Swedish Medical Center, and a consortium of research organizations and biomedical companies plan to analyze blood samples and nasal swabs from Swedish Medical Center patients with SARS-CoV-2 using samples from several time points that include initial presentation, acute illness and convalescence.

Merck and ISB said proteomic, metabolomic, transcriptomics and genetic techniques will be applied toward examining blood samples, with the aim of evaluating the impact of infection on different organs, and identifying potential biomarkers to predict the risk of severe disease.

In addition, samples will be analyzed to create a profile of the immune response, including quantitative changes in immune cells in patients following SARS CoV-2 infection and characterization of neutralizing antibodies in samples from convalescent patients. These insights can be used to inform vaccine design and antibody therapy, Merck and ISB reason.

The study will initially analyze samples from 200 patients with the potential to expand to 300, Merck and ISB said.

The announcement is Mercks first regarding development of a potential COVID-19 therapeutic. Last month, Merck announced donations of 500,000 personal protective masks to New York City Emergency Management and 300,000 masks to New Jerseys Office of Homeland Security and Preparedness, both toward urgent efforts to address COVID-19 emergency response.

This collaboration with Merck provides critical support for the recently launched scientific trial being co-led by ISB and Swedish Medical Center, both part of the Providence St. Joseph Health network. We launched this trial with the urgent need to improve our understanding of COVID-19, James R. Heath, PhD, president and professor at ISB, said in a statement. By applying the full power of our systems biology capabilities, we hope to gain important insights into the molecular basis for the dramatically contrasting outcomes observed for patients infected with SARS-CoV-2.

Heath and Jason D. Goldman, MD, at Swedish Medical Center, will be the studys principal investigators.

Initial funding support for the study came from the Wilke Family Foundation, M.J. Murdock Charitable Trust, Swedish Foundation, Parker Institute for Cancer Immunotherapy, and Washington State Andy Hill CARE Fund. Other research collaborators on the study include Stanford University, Adaptive Biotechnologies, Bloodworks Northwest, Isoplexis, Metabolon, Nanostring, Olink, Providence Molecular Genomics Laboratory, Scisco Genetics and 10x Genomics.

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Merck & Co. Partnering with ISB to Study Targets for COVID-19 Therapeutics - Genetic Engineering & Biotechnology News

As the COVID-19 pandemic continues, the question of where to turn for solid information has never been more important.

Many Duke experts are being approached now for their expertise and insight. But where do they turn for guidance and the latest information? In this ongoing series, Duke Today asks Duke experts to share their preferred sources.

Dr. Sallie Permar is a physician scientist who focuses on prevention and treatment of neonatal viral infections. A professor of immunology, pathology, pediatrics, molecular genetics and microbiology and associate dean for physician-scientist development, she recently wrote about the effect of the pandemic on medical research.

To stay abreast of how the infectious diseases field is responding to the novel coronavirus, she consults a mix of websites, podcasts and social media.

This Week in Virology, hosted by Vincent Racaniello and fellow virologists, has featured recent guest hosts who are stars of COVID-19 research, such as Drs. Daniel Griffin, Ralph Baric, Mark Denison, Stanley Perlman and Christian Drosten.

Immune, hosted by immunologists Cindy Leifer, Stephanie Langel, Vincent Racaniello, carried a recent two-part series on COVID-19 immunology with Dr. Brianne Barker that was especially compelling.

I also listen to COVID-19: Commonsense Conversations on the Coronavirus Pandemic, with host Dr. Ted OConnell, a family physician and writer.

For the latest on numbers by region, I check Johns Hopkins Universitys COVID-19 map.

COVID-19 guidelines can be found on the Centers for Disease Control website.

For the latest on viral sequence dynamics, I check gisaid.org.

For recent COVID-19 research reports, I consult bioxiv.org and medrxiv.org. The Twitter sources below provide real-time critical reviews of the newly posted manuscripts.

For the latest on epidemiology and case series reports, I consult: - the CDC Morbidity and Mortality Weekly Report and - World Health Organization situation reports.

And for compilations of the latest research I check: - Duke Pharmacist Elizabeth Dodds-Ashleys Daily Digest. - The American Association of Medical Colleges Novel Coronavirus Update by chief scientific officer and former Duke faculty member Dr. Ross McKinney. - Publons compilation of latest research manuscripts, which includes some crowd-sourced reviews.

Finally, great sources to follow on Twitter include:@NIAIDNews; @CEPIvaccines;NIH Vaccine Research Center scientist Kizzmekia Corbett (@KizzyPhD);The laboratory of UNC-Chapel Hills Dr. Ralph Baric (@Baric_Lab);The laboratory of Vanderbilt Universitys Dr. Mark Denison (@Denisonlab);Florian Krammer, an immunologist who is developing antibody assays (@florian_krammer); Virologists Dr. Benhur Lee (@VirusWhisperer) and Angela Rasmussen (@angie_rasmussen);COVID-19 drug developer Timothy Sheahan (@timothysheahan);David Martinez, a former Ph.D. student who is now testing vaccine and therapeutic antibodies in the lab of Ralph Baric (@David_RMartinez).

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Sallie Permar: Who Are Your Trusted Sources on COVID-19? - Duke Today

Welcome back to My Favorite Things.

We're isolated from each other, trying to survivea global pandemic. Each day bringsmore uncertainty and terrifyingnews, as wetake shelterfrom an invisible global scourge. A single cough can send your mind to a dark place. Life is paused. Sports are on hold. This sucks.

PREVIOUSLY ON MY FAVORITE THINGS:Episode 5: Meltdown

My Favorite Things is an escape from all of that. The philosophyis simple:

When I'm feeling sadI simply remember my favorite thingsAnd then I don't feel so bad

So let's do that. Today, we're back in Ohio Stadium on Nov 23, 2002. There's one second on the game clock.

After closing the first full century of college football on a 32-yeardry spell, Ohio State picked up a BCS championship in 2002. It claimed the first CFP title a dozen seasons later.

The Buckeyes donotlive for free in the national spotlight these days. They overpaid for this era.

Their fresh championship - which still feels impossible five years later -was delivered by a third-string quarterback whose first career start came that December. The one right after the century turned came courtesy of a molecular genetics major andtrue freshman enigma. Far greater and more imposing Buckeye teams (the parts, not the sum) failed to achieve what they did.

That 2002 season ended with Craig Krenzel and Maurice Clarett ending a 34-year drought, along with the defending champs' 34-game winning streak. When it began, the word luckeyes quite literally did not exist. And why would it?

Four seasons beforethe Luckeyes went 14-0, the Buckeyes went 11-1 with four All-America players, a Butkus winner, the Thorpe winner and the Silver Football winner. They beat every team they faced by double-digits...except the four-touchdown underdog they lost to at home.

In one impossibly unluckyhalf against Michigan State, the best team in the countryand arguably the most talentedOhio State team of that century did the following to itself:

We could repeat this exercise for 1997, when the Buckeyes held the eventual national champions to 42 yards rushing on 42 carries in their own stadium - and still lost. Do you remember which play was far bigger for the outcome than Charles Woodson's punt return touchdown, which is how Michigan memorializes that game?

The decisive points, which were an absolute gift. Ohio State wins otherwise.

You cannotremember any gifts the Buckeyes got against the Wolverines during the 1990s forclassic 404 FILE NOT FOUND reasons. This century, Michigan has been quite generous just about every season,but we're wading through an era where the termluckeyeswas never uttered. It would been viewed as gibberish by everyone, especially Ohio State fans.

In 1996 the Buckeyesallowed a fatal case of the yips cancel their national title hopes in a game where they could not catch a break. In 1995, four All America players - the Heisman and Biletnikoff winners, pros all over the place and shattered school records in their wake - manufactured a way to lose by letting an unremarkable running back look like Jim Brown in his prime.

The slightest bit of luck cancelsthat nightmare. All of the breaks went to the winged helmets.

Ohio State was good enough to win it all numerous times. Every title team is talented, well-coached, a bit magical - and catches a break here or there. Those enormously talented title contenders just couldn't ever seem to catch one. Ever.

After decades of FACE-PLANTINGin shit EVERY SEASON,Ohio State suddenly had a horseshoe jammed up its ass.

You can do this going back to 1979, when the undefeated Big Ten champs left too many opportunities on the field in Pasadena and lost by a single point. Luckeyes?Man, that nickname would have sounded dumb as hell in September 2002.Luck?What fucking luck?

In 2002 Krenzel took over for Steve Bellisari while true freshman Clarett beat out Lydell Ross, Maurice Hall, JaJa Riley and Jesse Kline to start at tailback. It was Jim Tressel's sophomore season, and while he had already installed a hinge in the rivalry- that 2001 team also finished with five losses. A little luckwould have turned those closeWisconsin, Penn State and South Carolina Ls into close Ws.

They roared out of the gate in 2002, dissecting Texas Tech, Kent State and No.10 Washington State with relative ease - but September footballhas been hot in Columbus since Woody Hayes was singing Sigma Chi drinking songs in Licking County. September is seductive.This is the month we get Charlie Brown'd - we're here every season.

A trip to Cincinnati proved to be a little trickier than it was supposed to be. The Buckeyes stumbled for most of the 1st half against an in-state ambush, and - as you might expect during that era - they got a nice thing that was immediately taken away.

Chris Gamble didn't need holdingto run away from all of those Bearcats. That penalty (keep your eyes on UC's Chick-fil-A logo at midfield) was barely holding anyway! But luck was still a myth, and it was beginning to look like a special kind of nightmare in Paul Brown Stadium. Fast-forward to late in the 4th quarter and Cincinnati was engineering a legendary drive.

Got a perfect matchup against a freshman corner. Ah shoot, that's a dropped game-winner.

Opposite field, the next play. Got a linebacker on a fade route this time. Right through his hands.

Thisbrought up 4th down, and we'll come back to what happened there shortly.

The Buckeyes would win agame they had every reason to lose because a) their opponent gagged on the opportunity andb) their luck ran out. Losing like that had been Ohio State's music for decades, but nowit was blaring on the other sideline. Luckeyes Escape Queen City Unscathed would have been have been passable usage for that term. But it was just one game.

But then the Buckeyes escaped Evanston despite a comedy of errors. Then they snatched victory from the jaws of defeat inMadison. They beat Penn State without scoring an offensive touchdown. Then they went to West Lafayette - and there's a reason history has chosen to remember onlyone play from that game.

Because the Purdue trip blended with all of the sluggish angina games that preceded it.

One week after Holy Buckeye, Ohio State needed overtime to take down a 5-7 Illinois team. That put the Buckeyes - who were cheating death every week - at 12-0 on the year. Do you know how many times in program history Ohio State had won 12 game in a single season prior to 2002?

Don't look it up. The answer is nonetimes. Zero. All of the luck the teams that preceded this one failed to receive was showering the 2002 Buckeyes, and we were now basking in the first 12th win in Ohio State history. Half of them are in this chart (warning: NSFW)

That's every road game - on aschedule that had no byes. Ohio State's starters were playing 60 minutes each week, even against their lousy opponents. They had no business being 12-0.

The Buckeyes were equal parts lucky and good-enough heading into Game 13, which a) is an unlucky number and b) involved Michigan, a team Ohio State had beaten in Columbus twice in seven tries. And the home teamwas undefeated, again. This was a Nineties flashback nobody was excited about, because - as we knew very well by 2002 - Charlie Brown is forged in September.

That 2002 Michigan game played out as a composite of the 12 games that preceded it, where Ohio State battled, fumbled, prevailed and stumbled as minutes slipped off the clock. This was their identity now;ateam that had somehow engineered resilience, bouts of competence, plodding efficiency and raw, uncut pharmaceutical-grade luck into the game plan each week.

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So of course the Wolverines had the ball inside the Ohio State 30 with one second remaining on the clock and a five-point deficit. The Buckeyes were out of timeouts and weren't given the luxury of overthinking what to do next.

As crushing as 1988, 1990, 1992 (the tie, which they win with the slightest bit of luck) 1993, 1995, 1996, 1997, 1999 and 2000 had been - losing like this would have been more devastating. And the clock operator who allowed one second to remain for that play would have woken up Sunday in the Franklin County morgue.

Here's what 0:00 on the clock and John Navarre winding up looked like. Oh...oh god.

Something supernaturally shitty was boundto happen here. This universe demanded it.

Shawn Springs had fallen down on a slant routein 1996, which gave Tai Streets and Michigan all of the life they needed to escape from a gamethey had no business winning. Someone in a red jersey was going to sliphere, on account of a slick grass patch or a gust of wind. It's amazing how many thoughts can race through your head in one second when you're paralyzed in C-Deck with 100,000 other Saturday prisoners.

A well-timed screen pass had deflated Ohio Stadium in every Michigan game since Earle Bruce was calling in superfecta betson a rotary phone during halftime. Two Buckeye defenders were boundcollide on this play, allowing a Wolverine to snatch the game winner out of the sky and then dance in the south endzone for the ensuing few seconds in reality - and forever in our nightmares.

What was Ohio State's 12-0 recipe again?

Engineered resilience, bouts of competence, plodding efficiency and raw, uncut pharmaceutical-grade luck

Ah, right. Here's that recipe in GIF form.

Gamble and Mike Doss collided, because of course they did.

A little more air under the ball might have resulted in the worst kind of celebration, but the air wasn't there;Will Allen was. He shoveled dirt all over Michigan's corpse and the Buckeyes escaped victorious yetagain.

But it wasn't the first time Allen played gravedigger. BACK TO CINCINNATI:

The UC receiver Doss bodiesat the goal line on that 4th down play would have been in optimal position to compete with Allen forthe deflection - had he, you know, not been lying on the grass. Allen briefly celebrates his game-clincher before remembering he's a live target and takes a knee (if you're wondering why Allen immediately went fetal position after picking off Navarre, please refer to how the UC game ended).

Pass interference committed against an ancillary receiver while the ball is already in flight and the back judge is focused on it, the intended receiver and the guy covering him? That flag happens approximately zero times, unless the defending team is unlucky, which we now know the Buckeyes were not.

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After decades of face-planting in shit every season,Ohio State suddenly had a horseshoe jammed up its ass. This upset a lot of people.

The Buckeyes - a northern program, a slow program, a reliable choking program, a supposed-to-lose-to-Michigan program - would now be playing for the BCS title. This infuriatedthosewho had grown accustomed to Ohio State's tradition of never catching any breaks. The Luckeyes had arrived in 2002, and this change went down like shards of glass for non-fans of the program.

Ohio State arrived in Tempe has 13-point underdogs to Miami - rightfully; that team was obnoxiously loaded and hadn't lost a game in years - and left Arizona with the Canes' belt. The Buckeyes brought their engineered resilience, bouts of competence, plodding efficiency and raw, uncut pharmaceutical-grade luck into a 14th game - and it worked for the14th time.

And you'll have to forgive Ohio State fans for not wanting to hear about benefiting from officiating in the first overtime, since the Fiesta Bowl should have ended in regulation after Gamble converted this game-clinching 3rd down, which was ruled incomplete.

Luck only matters in football if you're in position to win.

Getting lucky down 42 points produces gallows humor. Catching a break that flips momentum or changes an outcome is living the kind ofcharmed life that eluded Ohio State football for decades. The Buckeyes, in spite of how their most recent trip to Arizona transpired, are charmed. They overpaid to gain admission intotheir current era.

The 2002 Buckeyes are routinely cited as the weakest national champion of the current century, no doubt in part to the negative optics of getting lucky for so many reasons against so many opponents. Entering that season, Ohio State fans were still whining about how their beloved 1998 team needed a break just once- and was denied.

Meanwhile, eventual champion Tennessee stayed perfect because of a no-touch fumble by Arkansaswhile it was trying to end the game. Yeah, must be nice.

Luck seemed to be everywhere but Columbus. That changed in 2002, and it was both long overdue and deserved. Getting lucky diminishes nothing. The ring is just as shiny and the memories are just as rosy. Do youknow what the term is forleast-deserving, most mediocre, impossibly resilient and luckiest title winner of the current century?

It's champions. They're called champions.

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SALT LAKE CITY, April 28, 2020 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN), a leader in molecular diagnostics and precision medicine, announced that it will hold its fiscal third-quarter 2020 sales and earnings conference call with investors and analysts at 4:30 p.m. EDT on Tuesday, May 5, 2020. During the call, R. Bryan Riggsbee, interim president and CEO and chief financial officer, and Scott Gleason, senior vice president of Investor Relations and Corporate Strategy, will provide an overview of Myriads financial performance for the fiscal third-quarter and provide a business update.

To listen to the earnings call, interested parties in the United States may dial 1-800-272-6255 or +1-303-223-4384 for international callers. All callers will be asked to reference reservation number 21960364. The conference call also will be available through a live webcast and a slide presentation pertaining to the earnings call also will be available under the investor section of our website at http://www.myriad.com. A replay of the call will be available two hours after the end of the call for seven days and may be accessed by dialing 800-633-8284 within the United States or +1 402-977-9140 for international callers and entering reservation number 21960364.

About Myriad GeneticsMyriad Genetics, Inc. is a leading molecular diagnostic and precision medicine company dedicated to being a trusted advisor transforming patient lives worldwide with pioneering molecular diagnostics. Myriad discovers and commercializes molecular diagnostic tests that determine the risk of developing disease, accurately diagnose disease, assess the risk of disease progression, and guide treatment decisions across six major medical specialties where molecular diagnostics can significantly improve patient care and lower healthcare costs. Myriad is focused on three strategic imperatives: transitioning and expanding its hereditary cancer testing markets, diversifying its product portfolio through the introduction of new products and increasing the revenue contribution from international markets. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com.

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Myriad to Announce Fiscal Third-Quarter 2020 Financial Results on May 5, 2020 - Yahoo Finance