2019-nCoV: Just a Stop on the Zoonotic Highway – Medscape

Emerging viruses that spread to humans from an animal host are commonplace and represent some of the deadliest diseases known. Given the details of the Wuhan coronavirus (2019-nCoV) outbreak, including the genetic profile of the disease agent, the hypothesis of a snake origin was the first raised in the peer-reviewed literature.

Wuhan seafood market closed after the new coronavirus was detected there for the first time in 2020. SISTEMA 12/Wikimedia Commons/CC BY-SA 4.0

It is a highly controversial origin story, however, given that mammals have been the sources of all other such zoonotic coronaviruses, as well as a host of other zoonotic diseases.

An animal source for emerging infections such as the 2019-nCoV is the default hypothesis, because "around 60% of all infectious diseases in humans are zoonotic, as are 75% of all emerging infectious diseases," according to a United Nations report. The report goes on to say that, "on average, one new infectious disease emerges in humans every 4 months."

To appreciate the emergence and nature of 2019-nCoV, it is important to examine the history of zoonotic outbreaks of other such diseases, especially with regard to the "mixing-vessel" phenomenon, which has been noted in closely related coronaviruses, including SARS and MERS, as well as the widely disparate HIV, Ebola, and influenza viruses.

The mixing-vessel phenomenon is conceptually easy but molecularly complex. A single animal is coinfected with two related viruses; the virus genomes recombine together (virus "sex") in that animal to form a new variant of virus. Such new mutant viruses can be more or less infective, more or less deadly, and more or less able to jump the species or even genus barrier. An emerging viral zoonosis can occur when a human being is exposed to one of these new viruses (either from the origin species or another species intermediate) that is capable of also infecting a human cell. Such exposure can occur from close proximity to animal waste or body fluids, as in the farm environment, or from wildlife pets or the capturing and slaughtering of wildlife for food, as is proposed in the case of the Wuhan seafood market scenario. In fact, the scientists who postulated a snake intermediary as the potential mixing vessel also stated that 2019nCoV appears to be a recombinant virus between a bat coronavirus and an originunknown coronavirus.

Coronaviruses in particular have a history of moving from animal to human hosts (and even back again), and their detailed genetic pattern and taxonomy can reveal the animal origin of these diseases.

Bats, in particular, have been shown to be a reservoir species for both alphacoronaviruses and betacoronaviruses. Given their ecology and behavior, they have been found to play a key role in transmitting coronaviruses between species. A highly pertinent example of this is the SARS coronavirus , which was shown to have likely originated in Chinese horseshoe bats. The SARS virus, which is genetically closely related to the new Wuhan coronavirus, first infected humans in the Guangdong province of southern China in 2002.

Scientists speculate that the virus was then either transmitted directly to humans from bats, or passed through an intermediate host species, with SARS-like viruses isolated from Himalayan palm civets found in a live-animal market in Guangdong. The virus infection was also detected in other animals (including a raccoon dog, Nyctereutes procyonoides) and in humans working at the market.

The MERS coronavirus is a betacoronavirus that was first reported in Saudi Arabia in 2012. It turned out to be far more deadly than either SARS or the Wuhan virus (at least as far as current estimates of the new coronaviruss behavior). The MERS genotype was found to be closely related to MERS-like viruses in bats in Saudi Arabia, Africa, Europe, and Asia. Studies done on the cell receptor for MERS showed an apparently conserved viral receptor in both bats and humans. And an identical strain of MERS was found in bats in a nearby cave and near the workplace of the first known human patient.

However, in many of the other locations of the outbreak in the Middle East, there appeared to be limited contact between bats and humans, so scientists looked for another vector species, perhaps one that was acting as an intermediate. A high seroprevalence of MERS-CoV or a closely related virus was found in camels across the Arabian Peninsula and parts of eastern and northern Africa, while tests for MERS antibodies were negative in the most-likely other species of livestock or pet animals, including chickens, cows, goats, horses, and sheep.

In addition, the MERS-related CoV carried by camels was genetically highly similar to that detected in humans, as demonstrated in one particular outbreak on a farm in Qatar where the genetic sequences of MERS-CoV in the nasal swabs from 3 of 14 seropositive camels were similar to those of 2 human cases on the same farm. Similar genomic results were found in MERS-CoV from nasal swabs from camels in Saudi Arabia.

HIV, the viral cause of AIDS, provides an almost-textbook origin story of the rise of a zoonotic supervillain. The virus was genetically traced to have a chimpanzee-to-human origin, but it was found to be more complicated than that. The virus first emerged in the 1920s in Africa in what is now the Democratic Republic of the Congo, well before its rise to a global pandemic in the 1980s.

Researchers believe the chimpanzee virus is a hybrid of the simian immunodeficiency viruses (SIVs) naturally infecting two different monkey species: the red-capped mangabey (Cercocebus torquatus) and the greater spot-nosed monkey (Cercopithecus nictitans). Chimpanzees kill and eat monkeys, which is likely how they acquired the monkey viruses. The viruses hybridized in a chimpanzee; the hybrid virus then spread through the chimpanzee population and was later transmitted to humans who captured and slaughtered chimps for meat (becoming exposed to their blood). This was the most likely origin of HIV-1.

HIV-1 also shows one of the major risks of zoonotic infections. They can continue to mutate in its human host, increasing the risk of greater virulence, but also interfering with the production of a universally effective vaccine. Since its transmission to humans, for example, many subtypes of the HIV-1 strain have developed, with genetic differences even in the same subtypes found to be up to 20%.

Ebolavirus, first detected in 1976, is another case of bats being the potential culprit. Genetic analysis has shown that African fruit bats are likely involved in the spread of the virus and may be its reservoir host. Further evidence of this was found in the most recent human-infecting Bombali variant of the virus, which was identified in samples from bats collected from Sierra Leone.

It was also found that pigs can also become infected with Zaire ebolavirus, leading to the fear that pigs could serve as a mixing vessel for it and other filoviruses. Pigs have their own forms of Ebola-like disease viruses, which are not currently transmissible to humans, but could provide a potential mixing-vessel reservoir.

The Western world has been most affected by these highly mutable, multispecies zoonotic viruses. The 1957 and 1968 flu pandemics contained a mixture of gene segments from human and avian influenza viruses. "What is clear from genetic analysis of the viruses that caused these past pandemics is that reassortment (gene swapping) occurred to produce novel influenza viruses that caused the pandemics. In both of these cases, the new viruses that emerged showed major differences from the parent viruses," according to the Centers for Disease Control and Prevention.

Influenza is, however, a good example that all zoonoses are not the result of a mixing-vessel phenomenon, with evidence showing that the origin of the catastrophic 1918 virus pandemic likely resulted from a bird influenza virus directly infecting humans and pigs at about the same time without reassortment, according to the CDC.

The first 2 decades of the 21st century saw a huge increase in efforts to develop an infrastructure to monitor and potentially prevent the spread of new zoonoses. As part of a global effort led by the United Nations, the U.S. Agency for International AID developed the PREDICT program in 2009 "to strengthen global capacity for detection and discovery of zoonotic viruses with pandemic potential. Those include coronaviruses, the family to which SARS and MERS belong; paramyxoviruses, like Nipah virus; influenza viruses; and filoviruses, like the ebolavirus."

PREDICT funding to the EcoHealth Alliance led to discovery of the likely bat origins of the Zaire ebolavirus during the 2013-2016 outbreak. And throughout the existence of PREDICT, more than 145,000 animals and people were surveyed in areas of likely zoonotic outbreaks, leading to the detection of more than "1,100 unique viruses, including zoonotic diseases of public health concern such as Bombali ebolavirus, Zaire ebolavirus, Marburg virus, and MERS- and SARS-like coronaviruses," according to PREDICT partner, the University of California, Davis.

PREDICT-2 was launched in 2014 with the continuing goals of "identifying and better characterizing pathogens of known epidemic and unknown pandemic potential; recognizing animal reservoirs and amplification hosts of human-infectious viruses; and efficiently targeting intervention action at human behaviors which amplify disease transmission at critical animal-animal and animal-human interfaces in hotspots of viral evolution, spillover, amplification, and spread."

However, in October 2019, the Trump administration cut all funding to the PREDICT program, leading to its shutdown. In a New York Times interview, Peter Daszak, president of the EcoHealth Alliance, stated: "PREDICT was an approach to heading off pandemics, instead of sitting there waiting for them to emerge and then mobilizing."

Ultimately, in addition to its human cost, the current Wuhan coronavirus outbreak can be looked at an object lesson a test of the pandemic surveillance and control systems currently in place, and a practice run for the next and potentially more-deadly zoonotic outbreaks to come. Perhaps it is also a reminder that cutting resources to detect zoonoses at their source in their animal hosts before they enter the human chain is perhaps not the most prudent of ideas.

Mark Lesney is the managing editor of MDedge.com/IDPractioner. He has a PhD in plant virology and a PhD in the history of science, with a focus on the history of biotechnology and medicine. He has served as an adjunct assistant professor of the department of biochemistry and molecular & celluar biology at Georgetown University, Washington.

This article originally appeared on MDedge.com.

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2019-nCoV: Just a Stop on the Zoonotic Highway - Medscape

How to Reduce Bias in Hiring and Human Resource Decisions – Morningstar.com

Samantha Lamas

Most financial professionals know that investors suffer from behavioral biases when making financial decisions, and some may even catch themselves making the same mistakes from time to time. But when it comes to their job, professionals must also be on the lookout for other behavioral biases that can impact a companys greatest asset: their people.

Just like with investing, behavioral biases can lead peopleand companiesto underperform. For example, companies might fail to hire the best candidate for the job or lose a highly skilled employee to a competitor. Though everyone wants the best people on their team, many dont realize how the language in a job advertisement affects the candidate pool or how some diversity trainings have adverse effects.

Based on existing behavioral research, we created a guide and checklist that highlights techniques and lessons people can leverage to avoid behavioral bias in hiring and human resource decisions.

Behavioral research finds that human behavior is highly variable, and small details of presentation can have unexpected influence. For example, having too many job requirements can impact your candidate pool, especially since men are more likely to apply if they fit at least 60% of the requirements, whereas women are more likely to feel that they need to fill all of them before applying.

Mitigating bias in hiring starts with the job advertisement: how it looks, what it says, and where its placed. Here are a few quick tips to optimize your job advertisement:

Almost everyone has been guilty of this: talking to a job candidate in their interview, connecting about a random topic that has nothing to do with the job they applied for, and then, almost subconsciously, giving them a good review. This is just one way that biases make their way into peoples decisions when it comes to reviewing job candidates or current employees.

Everyone can be unintentionally swayed by a persons gender, ethnicity, age, or personality when evaluating an individual for a job or a raise. Plus, hiring professionals can be subject to their own environmentfor example, maybe its been a crazy week and making hiring decisions at 4 p.m. on a Friday is not a good idea.

To combat the impact of bias in hiring and compensation decisions, research has a identified a few techniques:

Even though we are all prone to behavioral biases, it doesnt mean we have to be subject to them. By implementing a few research-based techniques and processes, you can learn to make more logical decisions.

In the full paper, we discuss more ways in which biases can be problematic when making human resource decisions and how to avoid them. We also include a checklist to help professionals begin implementing behavioral techniques when it comes to finding, vetting, and hiring job candidates.

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How to Reduce Bias in Hiring and Human Resource Decisions - Morningstar.com

Jacobs School names chair of Physiology and Biophysics – UB Now: News and views for UB faculty and staff – University at Buffalo Reporter

Mikhail V. Pletnikov has been named professor and chair of the Department of Physiology and Biophysics in the Jacobs School of Medicine and Biomedical Sciences at UB.

The appointment was announced by Michael Cain, vice president for health sciences and dean of the Jacobs School.

Dr. Pletnikov rapidly emerged as our top candidate possessing the administrative, scientific, leadership and visionary skills needed to move the department forward and further align the department with the Jacobs Schools strategic plans, Cain said in a statement.

Pletnikov, a native of Moscow, Russia, will relocate to Buffalo and join UB on July 1. He will be accompanied by his wife, Olga Pletnikova.

I feel honored to be appointed to this position, Pletnikov said. I am grateful to the members of the search committee, the faculty of the department and personally to Dr. Cain for placing their trust in me to lead the department. I look forward to working with the faculty, staff and students to support and promote education and biomedical research in the department and the school.

On a personal note, Olga and I are excited to move to Buffalo, he said. As for its weather, I am sure we will appreciate all four seasons there as, after all, we used to live in Moscow.

Pletnikov will succeed Perry Hogan, who has served as department chair since 2015.

Pletnikovs research focuses on understanding how neurons and non-neuronal cells (glial cells) interact with one another to support critical brain functions, including emotion and cognition. He also studies the mechanisms whereby the brain regulates functions of different organs in the body and itself is influenced by peripheral systems, particularly the immune system and the gut.

A growing number of studies suggest that abnormalities in these complex interactions lead to the development of disorders of the brain and peripheral organs, he said. Targeting cells, processes and pathways involved in the brain-periphery interplay is emerging as a new promising direction in treatment of complex brain disorders.

Pletnikovs research has been published in numerous journals. He lectures nationally and internationally, and serves on the editorial boards of leading scientific journals in his field, including Genes, Brains and Behavior; Biobehavioral Review; and Biological Psychiatry.

He received his doctorate in medicine from the I.M. Sechenov Moscow Medical Institute and his PhD in normal physiology from the PK Anokhin Institute of Normal Physiology in Moscow. He completed his postdoctoral training in behavioral neuroscience and neurovirology at Johns Hopkins University .

In 2000, Pletnikov joined the faculty at Johns Hopkins as an assistant professor and is currently a professor of psychiatry and behavioral sciences, neuroscience, and molecular and comparative pathology.

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Jacobs School names chair of Physiology and Biophysics - UB Now: News and views for UB faculty and staff - University at Buffalo Reporter

FEATURE PHOTO: Love and study abroad – The Daily Eastern News

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logan raschke | The Daily Eastern NewsHeather Vaupel (left), an Eastern graduate who majored in Spanish, Corinne Mausehund (middle), a biology senior, and Rolando Roly Monte de Oca (right), a biology and neuroscience double major, laugh and talk amongst themselves during the Study Abroad Fair in the University Ballroom of the Martin Luther King Jr. University Union Thursday afternoon. The trio went to Costa Rica and took their Spanish lessons at Vritas Universidad. Monte de Oca said studying abroad is literally life-changing; he proposed to Mausehund during the trip, and they got married just a month ago.

Logan Raschke

logan raschke | The Daily Eastern NewsHeather Vaupel (left), an Eastern graduate who majored in Spanish, Corinne Mausehund (middle), a biology senior, and Rolando Roly Monte de Oca (right), a biology and neuroscience double major, laugh and talk amongst themselves during the Study Abroad Fair in the University Ballroom of the Martin Luther King Jr. University Union Thursday afternoon. The trio went to Costa Rica and took their Spanish lessons at Vritas Universidad. Monte de Oca said studying abroad is literally life-changing; he proposed to Mausehund during the trip, and they got married just a month ago.

Logan Raschke

Logan Raschke

logan raschke | The Daily Eastern NewsHeather Vaupel (left), an Eastern graduate who majored in Spanish, Corinne Mausehund (middle), a biology senior, and Rolando Roly Monte de Oca (right), a biology and neuroscience double major, laugh and talk amongst themselves during the Study Abroad Fair in the University Ballroom of the Martin Luther King Jr. University Union Thursday afternoon. The trio went to Costa Rica and took their Spanish lessons at Vritas Universidad. Monte de Oca said studying abroad is literally life-changing; he proposed to Mausehund during the trip, and they got married just a month ago.

Heather Vaupel (left), an Eastern graduate who majored in Spanish, Corinne Mausehund (middle), a biology senior, and Rolando Roly Monte de Oca (right), a biology and neuroscience double major, laugh and talk amongst themselves during the Study Abroad Fair in the University Ballroom of the Martin Luther King Jr.

University Union Thursday afternoon. The trio went to Costa Rica and took their Spanish lessons at Vritas Universidad. Monte de Oca said studying abroad is literally life-changing; he proposed to Mausehund during the trip, and they got married just a month ago.

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FEATURE PHOTO: Love and study abroad - The Daily Eastern News

New light shed on neuronal circuits involved in behaviour, learning and dysfunction – UNSW Newsroom

Scientists at UNSW Sydneys Decision Neuroscience Lab have made a major discovery about the way brains influence behaviour which challenges theory that has stood for 30 years.

And the findings could one day have key implications for the way we treat brain related diseases such as Parkinsons or deal with conditions like Tourettes syndrome.

In a paper published today in the prestigious journal Science, the research team of Dr Miriam Matamales and Dr Jay Bertran-Gonzalez, together with Neuroscience Lab Director, Scientia Professor Bernard Balleine, wanted to determine the relationship between the two main types of neuron found in the striatum, a major area of the brain responsible for voluntary movement in animals and humans.

They set up experiments to observe mice while they learned new actions that led to a reward of food, then examined the activity of these neurons in large areas of the striatum. They looked specifically at the activity of the two classes of neuron in this area those expressing D1 or D2 types of dopamine receptors.

For the last three decades, these D1- and D2-neurons were thought to have an independent influence on voluntary action, respectively initiating and inhibiting reward-seeking behaviour. While studying how these two types of neuron became active during learning, the team began to find an unexpectedly high degree of interaction between them which happened locally, within the striatum itself.

Lightbulb moment

For an example of behaviour where these neurons would be active, Dr Matamales suggests a simple, but common scenario of walking into a room and flicking on a light switch to find the light doesnt work.

So you walk into a room, flick the switch without even thinking about it, and theres no light, she says. You learn something has changed and so the behavioural response has to be modified by that learning. What were interested in is what changes in the brain are necessary to update that learning to realise oh, the bulbs blown, I should stop flicking the switch expecting the light to go on. Although this may seem trivial at one level, this kind of plasticity in decision making processes is going on all the time. Updating learning to control our actions is a critical aspect of brain function acquired through evolution, to stop us wasting valuable energy by repeating a task for no reward.

Professor Balleine explains that what is happening is that prior learning about behaviour tied to one outcome is put on hold while an updated version relevant to the change in the environment is rewritten.

This regulation of voluntary action is not about getting rid of or replacing the knowledge or behaviour, its about being more efficient in stopping actions that use energy for no reward, he says. Youve got a neuron, the D1-neuron, thats involved in acquiring and maintaining ongoing behaviour and another, the D2-neuron, thats engaged in updating that behaviour when there are changes in the environment. And what is game changing is that this critical interaction is going on in the striatum, not further downstream in more distant motor output structures of the brain as was thought previously.

Rethinking brain health

Professor Balleine says this new understanding of the D1 and D2 neurons intermingling in the striatum during learning could have important implications for medicine and even our concept of how voluntary actions are acquired and altered.

Our research suggests that the whole theory of basal ganglia function that people have been working with in order to try and treat diseases of various kinds, is seriously incomplete, he says.

Diseases that are associated with basal ganglia function include Parkinsons and Huntingtons disease, dementia, dystonia, Tourette syndrome and obsessive-compulsive disorder.

Dr Bertran-Gonzalez suggests that a clue to understanding at least some of these conditions could be found in the learning-related functions of the striatum.

Most basal ganglia dysfunction appears later in life and takes years to settle, he says. Some conditions are expressed by aberrant behaviour, where movements or whole actions that should be inhibited are not inhibited, perhaps because they never learned to be inhibited in the striatum, or because that learning was deficient. In such cases, in addition to simply attempting to counter uncontrolled motor movements, we should perhaps explore more progressive therapy that tries to correct this early learning. I think that we should add a learning perspective to virtually all treatments of basal ganglia dysfunction. After all, most of our current behaviour is no more than learnings work in progress.

Targeted medicine

Professor Balleine notes that with health conditions related to the basal ganglia, the striatum could be the new target area for medical intervention.

We believe these findings have the potential to re-target treatments of basal ganglia disorders to the striatum, Professor Balleine says. One of the most exciting parts of this research is that it speaks to particular connections between particular neurons within a particular structure. So it really gives great targeting information for treatment, and gives us new ways to think about these problems.

Dr Matamales says while the research raises hopes for new ways to treat health problems relating to brain function, there is still plenty of research ahead before the observations in mice are replicated in humans.

It is exciting to think that our new understanding could one day be used to target problems in the brain with more depth, she says. But the important thing you can say about this work right now is that we are providing more evidence to relate these neurons in the striatum with learning and cognition rather than simply motor output.

Hopefully this will lead to further breakthroughs that help us understand how the brain learns and how we adapt our behaviour to our environment.

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New light shed on neuronal circuits involved in behaviour, learning and dysfunction - UNSW Newsroom

Brain Organoids are Farther From Consciousness Than You Might Think – Discover Magazine

Cerebral organoids, or so-called brains in a dish, have taken the world of neuroscience by storm. These balls of neurons and brain tissue, grown in a petri dish, are supposed to mimic early brain development in humans.

Recent studies have touted swift progress, including lab-grown brains that are capable of forming neural circuits and producing brain waves similar to a developing embryo. But a new paper in Nature this week offers another take, suggesting that lab-grown brain models are far from humanlike.

In this new work, a team of scientists at the University of California, San Francisco, compared samples of real developing brains to organoids and say the lab-grown versions show patterns of abnormal development. As such, the organoids are unlikely to form the complex circuitry needed to study brain diseases.

Given these shortcomings, the odds that organoids will develop cognition or consciousness are still pretty far off, the researchers note.

Our brains rely on intricate networks of neurons to function. In real brains, neuronal cells form identities which determines their characteristics and role in the brain based on genetic instructions.

But in organoids, scientists observed that neurons appeared confused about their identities and failed to mature. This would prevent an organoid from organizing and functioning like an actual human brain, and impede the formation of specific brain circuits important for understanding diseases.

These abnormalities were not only present in the organoids created in the UCSF lab; a data analysis found them in organoid models used by other labs.

But the good news is that scientists think these abnormalities can be corrected.Signs of excess environmental stress, such as a lack of oxygen, showed up in many of the organoids' cells. Placing them in an environment resembling conditions that actual human brains encounter eased the stress and allowed the cells to develop normally.

We found that if we transplanted stressed organoid cells into the developing mouse brain, we could relieve the stress, said co-author Arnold Kriegstein, a neuroscientist at UCSF, in an email to Discover. When stress was relieved, the gene identity improved. This finding suggests that the stress induces the gene identity issues, and that both are reversible.

In light of the problems the UCSF team uncovered, Kriegstein is skeptical of some recently reported breakthroughs in organoid research and thinks the public should be, too.

There are overstated conclusions in some published papers concerning organoids, and overblown hype in the reporting about organoids, Kriegstein said. Organoids are already proving to be important models of human disease, but they are still extremely rudimentary compared to even fragments of the actual human brain. They are not brains in a dish.

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Brain Organoids are Farther From Consciousness Than You Might Think - Discover Magazine

Fresh Tri Wins CDC Multi-Year Contract to Build Habit Practice into the Diabetes Prevention Program – PR Web

"This collaboration with CDCs Lifestyle Change Program has the potential to scale and impact millions of underserved people affected by prediabetes," said Kyra Bobinet, MD, MPH, CEO and Founder of Fresh Tri.

SILICON VALLEY, Calif. (PRWEB) January 30, 2020

The United States Centers for Disease Control and Prevention (CDC) has awarded Fresh Tri, a fast-growth neuroscience-based digital health company, a multi-year contract to leverage its mindset- and habit-formation technology to improve the success of the National Diabetes Prevention Program Lifestyle Change Program (LCP).

In collaboration with CDC and certain LCP partner sites, Fresh Tri will adapt its weight-loss-focused mobile app, also called Fresh Tri, and apply its neuroscience-based methodology to create a companion app for DPP LCP participants, particularly focused on better engaging underserved populations. The app will guide participants in turning the food and fitness behaviors promoted by the LCP curriculum into sustainable habits. The new version of Fresh Tri will also help LCP lifestyle coaches monitor and support LCP participants daily to further improve outcomes.

CDC selected the Fresh Tri app for adaptation based on the mobile apps demonstrated ability to help users form healthy habits. Fresh Tri does this by training users in the Iterative Mindset a practice-and-modify approach to habit change.

The scientific definition of a habit is a repeated behavior that requires no thought. In contrast, conventional goal-setting and tracking requires immense thought and can backfire by triggering the habenula, a brain area that perceives failure and then suppresses ones motivation to try again. As a result, people quit trying.

Fresh Tris research on thousands of underserved people found that adopting the Iterative Mindset enabled them to persist in their efforts and maintain motivation while they found and adjusted the right new habits to fit their lives.

Using this approach in a recent study conducted with Walmart associates, Fresh Tri demonstrated statistically-significant (p < 0.001) weight loss, habit formation, and improvements in mindset, persistence, and resilience. Fresh Tri is customizable for other healthcare organizations to target patient behavior change, as well as for employers seeking to improve various types of health habits for their employees.

This collaboration with CDCs Lifestyle Change Program has the potential to scale and impact millions of underserved people affected by prediabetes, said Kyra Bobinet, MD, MPH, CEO and Founder of Fresh Tri. We are honored by this opportunity to spread this more natural, science-based approach to sustainable behavior change and to replace the outdated model of using goals and tracking that backfires for so many people.

To request a demo, please contact Jonathan Har-Even at jhareven@freshtri.com.

###

About FreshTri Fresh Tri is a behavior-change technology company with offerings focusing on mindset, practice and iteration that invite users to test-drive healthy habits, removing the guesswork and feelings of failure that can often accompany lifestyle changes. Fresh Tri uses a simple, positive approach based on the brain science of habit formation. In a recent study, use of the Fresh Tri app, in combination with mindset training, led to statistically significant weight loss and habit formation, as well as improvements in positive psychology metrics highly associated with overall health and well-being. Find out more about Fresh Tri: freshtri.com, Instagram, Facebook

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This week: Coronavirus, vaping and drugs of abuse – WRVO Public Media

China is dealing with the outbreak of a respiratory illness caused by a new coronavirus. Thousands of people have been infected; some have died. And more cases are being diagnosed in people all over the world, including a relatively small number in the United States.

Providing perspective on this outbreak is Stephen Thomas, MD, a professor of medicine and microbiology and immunology at Upstate and its chief of infectious disease.

Also on "HealthLink on Air" this week, toxicologist Christine Stork from the Upstate New York Poison Center talks about vaping dangers and the most common drugs of abuse. Tune in this Sunday, February 2 at 6 a.m. and 9 p.m. for "HealthLink on Air."

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This week: Coronavirus, vaping and drugs of abuse - WRVO Public Media

Coronavirus outbreak in US may depend on this: ‘We just don’t know yet’ says infectious disease doc – Home – WSFX

A top infectious disease doctor warned that the likelihood of preventing a U.S. outbreak of the coronavirus dependson whether the virusis transmitted by peoplewho are not exhibiting symptoms.And that information, he warned, is something that world health experts do not know yet.

You could be carrying it and not know so you wouldnt have the symptoms. Doesnt that make it extremely dangerous? Wall Street Journal columnist Mary Anastasia OGradyasked a panel of doctors on Fox NationsDeep Dive.

The Chinese Ministry of Health has said that they believe this is possible, that people can be spreading it before they show symptoms, said Dr. Stephen Morse, who is a professor of epidemiologyat the Columbia University Medical Center.

But thats why were doing a lot of screening at the airports based largely on geography, he continued. But once it spreads further, its going to be hard to be that targeted.

I agree that we have heard that from the Chinese, but we havent seen the evidence thats behind that, saidDr. Mark Mulligan, whois a senior professor in the NYU Langone Department of Medicine anddirector of both NYU Langone Vaccine Center and theDivision of Infectious Diseases and Immunology.

We do know you can have asymptomatic infection, he went on. There are reports of people that were shown to be infected but we dont know that those people can transmit.

The World Health Organization on Thursday declared the newcoronavirus outbreaka global emergency, as38 new deaths and 1,737 new infected cases have been reported in the last 24 hours.

In general, the transmission occurs when an ill person is coughing a lot. When youre sicker, you have more virus around. It may be that older people get more illness and transmit more. Younger people, less illness, maybe transmit less. But we dont know everything yet., Dr. Mulliganwarned.

Roughly 99 percent of all cases of the virus have appeared in China but it has spread to at least 18 countries.

The American officials are all saying, Dont panic, dont panic. But you can be carrying the disease without showing the symptoms, you have all this air travel going on, its already gotten out of China. How reasonable is it to think that were not going to have a serious outbreak here? asked OGrady.

I dont think we should panic, saidDr. Janette Nesheiwat,the medical director at CityMD,an urgent care practice in New York City. But we should remain on alert and be vigilant because it can take up to two weeks for symptoms to appear.

We know that the usual sort of shoe leather, public healthsteps of isolationof cases, contact tracing, quarantining of them works, notedMulligan. So I think if those things also work for this novel coronavirus, that we do have the opportunity to contain it.

However, Mulligan cautioned if it is shown that individuals can carry and transmit the virus without exhibiting symptoms that would be a troubling discovery.

We think that we have a real opportunity [to contain coronavirus], assuming there arent any curves like this thing about asymptomatic individuals transmitting. If that were true, that would change things, he concluded.

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Fox News Vandana Rambaran contributed to this report.

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Coronavirus outbreak in US may depend on this: 'We just don't know yet' says infectious disease doc - Home - WSFX