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Neuroscience

How Stories Connect And Persuade Us: Unleashing The Brain Power Of Narrative – OPB News

When you listen to a story, your brain waves actually start to synchronize with those of the storyteller. And reading a narrative activates brain regions involved in deciphering or imagining a person's motives and perspective, research has found.

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When you listen to a story, whatever your age, youre transported mentally to another time and place and who couldnt use that rightnow?

We all know this delicious feeling of being swept into a story world, says Liz Neeley, who directs The Story Collider, a nonprofit production company that, in nonpandemic times, stages live events filled with personal stories about science. You forget about your surroundings, she says, and youre entirelyimmersed.

Depending on the story youre reading, watching or listening to, your palms may start to sweat, scientists find. Youll blink faster, and your heart might flutter or skip. Your facial expressions shift, and the muscles above your eyebrows will react to the words another sign that youreengaged.

A growing body of brain science offers even more insight into whats behind theseexperiences.

On functional MRI scans, many different areas of the brain light up when someone is listening to a narrative, Neeley says not only the networks involved in language processing, but other neural circuits, too. One study of listeners found that the brain networks that process emotions arising from sounds along with areas involved in movement were activated, especially during the emotional parts of thestory.

As you hear a story unfold, your brain waves actually start to synchronize with those of the storyteller, says Uri Hasson, professor of psychology and neuroscience at Princeton University. When he and his research team recorded the brain activity in two people as one person told a story and the other listened, they found that the greater the listeners comprehension, the more closely the brain wave patterns mirrored those of thestoryteller.

Brain regions that do complex information processing seem to be engaged, Hasson explains: Its as though, Im trying to make your brain similar to mine in areas that really capture the meaning, the situation, the schema the context of theworld.

Other scientists turned up interesting activity in the parts of the brain engaged in making predictions. When we read, brain networks involved in deciphering or imagining another persons motives, and the areas involved in guessing what will happen next are activated, Neeley says. Imagining what drives other people which feeds into our predictions helps us see a situation from different perspectives. It can even shift our core beliefs, Neeley says, when we come back out of the story world into regularlife.

Listeners, in turn, may keep thinking about the story and talk to others about it, she says, which reinforces the memory and, over time, can drive a broader change inattitudes.

Different formats of information lists of facts, say, or charts may be better suited to different situations, researchers say, but stories wield a particularly strong influence over our attitudes andbehavior.

In health care contexts, for example, people are more likely to change their lifestyles when they see a character they identify with making the same change, notes Melanie Green, a communication professor at the University at Buffalo who studies the power of narrative, including in doctor-patient communication. Anecdotes can make health advice personally important to a patient, she finds. When you hear or read about someone you identify with who has taken up meditation, for example, you might be more likely to stick with ityourself.

Stories can alter broader attitudes as well, Green says like our views on relationships, politics or the environment. Messages that feel like commands even good advice coming from a friend arent always received well. If you feel like youre being pushed into a corner, youre more likely to push back. But if someone tells you a story about the time they, too, had to end a painful relationship, for example, the information will likely come across less like a lecture and more like a personaltruth.

Neeley has been taking advantage of these effects to shift perceptions about science and scientists in her work with Story Collider. We try and take everybody all different people and perspectives put them onstage, and hear what a life in science is really like, shesays.

Solid information in any form is good, Green says. But thats not necessarily enough. A vivid, emotional story can give that extra push to make it feel more real or more important. If you look at the times somebodys beliefs have been changed, she says, its often because of a story that hits them in the heart.

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How Stories Connect And Persuade Us: Unleashing The Brain Power Of Narrative - OPB News

Neuroscience

Dealing With Coronavirus: It’s OK To Be Anxious – Duke Today

Right now, its OK not to feel OK.

In this unprecedented time of coronavirus-prompted social distancing, its unlikely that a person doesnt encounter some level of anxiety or stress.

But there are ways to approach it, according to three Duke experts who spoke to media Wednesday.

Here are excerpts:

ON BEING NORMAL

Timothy Strauman, professor of psychology and neuroscience:

If youre not feeling unsettled and worried and projecting into the future, then youre not paying attention. This is a momentous change in our lives that none of us anticipated. It has taken us by surprise. If youre not feeling distressed, to me, Id be wondering if youre just not admitting that to yourself.

Yan Li, director of counseling and psychological services, Duke Kunshan University

Dont judge yourself for feeling the way you are. Were human beings and were in a life-threatening situation. Accept it and be compassionate.

ON ONE WAY THIS ORDEAL IS GOOD FOR SOCIETY

Terrie Moffitt, professor of psychology

Some psychologists are comparing the attack of the coronavirus to the bombing attacks on London in World War II. The blitz and the COVID-19 are both scary and isolating. People have to stay home while being reminded constantly of uncontrollable death.

And its dragging along for weeks and weeks. But the other thing that the London Blitz and the COVID-19 have in common is fostering a sense of solidarity. Everyone is in this together. Theres quite a bit of historical evidence that this kind of ordeal can be good for society.

It can slow down our lives and give us a sense of shared purpose. It can provide an opportunity to practice helping others. All these things are good for our mental health.

In 1939 in Britain, ahead of the Blitz, Winston Churchill consulted psychologists and was told the air raids and bombings by Germany were going to cause such terror that millions would go insane. The psychiatric hospitals would be overwhelmed with patients. That turned not to be true then, and its not true now.

HOW LONELINESS AND ISOLATION DIFFER

Terrie Moffitt:

Social isolation and loneliness are very different things. Social isolation is a physical state -- having to be in a place by yourself. Loneliness is different, its a state of mind. Its possible to feel lonely in a room full of people. Its possible to feel lonely at your own birthday party.

Loneliness can be a state of mind and some people carry it with them to new situations. The reverse is also true. A lot of people who experience social isolation never experience loneliness.

Its important for the public to understand that social isolation doesnt automatically mean youll be lonely and depressed and anxious along with it.

ON THE IMPORTANCE OF KNOWING WHAT YOU CAN CONTROL - AND WHAT YOU CANT

Timothy Strauman:

What really is most important to me? What is still under my control? I may not be able to go to the office every day. I may be put into circumstances where my work is interrupted. I cant see the people I love. Its very easy for people to feel like theyre failing. Im letting other people down. That kind of thinking, in combination with this isolation and incredible disruption really does render people vulnerable.

The message Id like to get across is that its very important to stop and identify whats most important, what are the things that are and are not under your control. Are there novel ways, different ways that allow you to be the person you want to be and ride out this crisis?

ON SEEKING HELP

Yan Li:

If you have persistent sadness, anxiety, anger or hopelessness -- all the really vulnerable emotions -- and also lost interest in pleasurable activities and feeling overwhelmed, thats one of the criteria.

Another criteria is significant impairment or change in functions. If you cant sleep, or sleep is disrupted, or if you cant get out of bed, or lose appetite or lose concentration or youre not able to attend to daily hygiene. And also, if you notice impulsive or risky behavior . thoughts of death, dying or suicide. All those are signs that this is the time to seek professional help.

AND FINALLY, A SIMPLE THING YOU CAN DO TO HELP

Timothy Strauman:

Anytime we can focus on someone elses needs, it will take some of the pressure and stress off of us. Building that solidarity is absolutely essential. You really dont have to look very far to find people in dire circumstances. One of the best preventative measures is simply reaching out to somebody and saying, Im here for you.

MEET THE EXPERTS

Yan LiYan Li is associate dean of student affairs and director of Counseling and Psychological Services at Duke Kunshan University in China (she is currently in the United States). She is an expert on issues such as multicultural counseling (culture, gender, sexual orientation and other aspects of diversity), psychology of women and clinical supervision.yan.li3@duke.edu

Terrie MoffittTerrie Moffitt is a professor of psychology. Her expertise is in the areas of clinical mental health research, neuropsychology and genomics in behavioral science. She studies depression, psychosis, and addiction. Moffitt is also interested in the consequences of a lifetime of mental and behavioral disorder on processes of aging.terrie.moffitt@duke.edu

Timothy StraumanTimothy Strauman is a professor of psychology and neuroscience. His research focuses on the psychological and neurobiological processes that enable self-regulation, including the role of self-regulatory cognitive processes in vulnerability to depression and other disorders, and the impact of treatments for depression.tjstraum@duke.edu

Duke experts on a variety of other topics related the coronavirus pandemic can be found here.

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Neuroscience

Heres how video games boost visual attention of expert players – Hindustan Times

Long-term experience of action real-time strategy games such as World of Warcraft, Age of Empires, and Total War can cause long-term changes in the brain and leads to improvements in temporal visual selective attention, according to a study.

These games, which can be won through strategic planning, selective attention, sensorimotor skills, and teamwork place considerable demands on the brain.

Published in the journal, Frontiers in Human Neuroscience, the study shows that expert players of real-time strategy games have faster information processing, allocate more cognitive power to individual visual stimuli and allocate limited cognitive resources between successive stimuli more effectively through time.

Our aim was to evaluate the long-term effect of experience with action real-time strategy games on temporal visual selective attention, said study researcher Diankun Gong from University of Electronic Science and Technology of China.

In particular, we wanted to reveal the time course of cognitive processes during the attentional blink task, a typical task used by neuroscientists to study visual selective attention, Gong added.

To study the effect of gaming on temporal visual selective attention, the research team selected 38 volunteers, healthy young male students.

Half of the volunteers were expert players of the typical action real-time strategy game League of Legend, where teammates work together to destroy the towers of an opposing team.

They had played the game for at least two years and were masters, based on their ranking among the top seven per cent of players.

The others were beginners, with less than six months experience of the same game, and ranked among the bottom 30-45 per cent.

All volunteers were seated in front of a screen and tested in a blink task, with 480 trials over a period of approximately two hours.

The greater a volunteers tendency to blink targets, the less frequently he would press the correct button when one of the two targets appeared on the screen, and the worse he did overall in the task.

The volunteers also wore EEG electrodes on the parietal (i.e. sides and top) region of their scalp, allowing the researchers to measure and localise the brains activity throughout the experiment.

We found that expert League of Legend players outperformed beginners in the task. The experts were less prone to the blink effect, detecting targets more accurately and faster, and as shown by their stronger P3b (positive-going amplitude), gave more attentional cognitive resources to each target, said study co-author Weiyi Ma from the University of Arkansas in the US.

(This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed. )

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Heres how video games boost visual attention of expert players - Hindustan Times

Neuroscience

Watch and Learn: How the Brain Gains Knowledge Through Observation – SciTechDaily

Humans have a number of ways to learn how to do new things. One of those ways is through observation: watching another person perform a task, and then doing what they did. Think of a child that learns how to adult by observing their parents as they pay for groceries or make a phone call.

It has long been theorized that there are two types of observational learning: imitation and emulation. Imitation is when one person copies another persons behaviors to achieve the same goal. For example, if you watch the numbers a person dials to open a safe so that you, too, can open it. Emulation, on the other hand, occurs when someone watches another person achieve a goal, infers their goals, and then works to achieve those same goals without copying the other persons actions. In this case, you might watch the person open the safe, see there are valuables inside, and then later cut it open with a saw.

A new study conducted at Caltech has shown how the brain chooses between the two neural systems responsible for each of these kinds of learning. The study, which appears in the journal Neuron, reveals for the first time how the brain chooses which strategy to employ when faced with an observational learning task.

The research was led by Caroline Charpentier, a postdoctoral scholar in neuroscience who works in the lab of John ODoherty, professor of psychology in the Division of the Humanities and Social Sciences.

Depending on the context, sometimes imitation works best, and sometimes emulation is more reliable. Here we wanted to show whether and how the brain can keep track of both strategies in parallel and adaptively pick the best strategy in a given context, Charpentier says.

In the study, participants were placed in a functional magnetic resonance imaging (fMRI) machine so their brain activity could be monitored while they performed an observational learning task. Once in the machine, they were presented with virtual slot machines that would dispense three colors of tokens: red, green, or blue. Only one of those token colors had monetary value at a given time, but the participants were not told which color that was. The only information they were provided directly was the probability that a particular slot machine would dispense a token of a given color.

When emulation of another persons goals becomes too difficult, the brain resorts to imitative learning. Credit: Caltech

In most of the trials, the participants were asked to observe another person play the slot machines, and were told that this person had full knowledge of which color was valuable. By watching the other person pick which slot machine to play, they could gain information that would help improve their chances of receiving a valuable token when it was their turn to play.

However, because it was important for the researchers to discern which observational learning strategy the participants were using when they played the slot machine after watching the other people take a turn, the researchers created two different trial scenarios. In one scenario, the participant was permitted to play the same slot machine as the person they had been observing. Since they played the same machine, the participant could mimic the behavior of the other person and thus engaged in imitative observational learning. In the other scenario, the participant could not play the same machine, which prevented them from simply imitating the other players actions and forced them to use an emulation learning strategy.

Charpentier says the fMRI data showed that each of these strategies correlated with activity in specific parts of the brain.

Imitation tends to rely on regions that we refer to as the mirror system of the brain, which is active both when someone performs an action, such as grabbing an object off the table, or when they watch someone else perform that same action, she says. The emulation strategy mapped more to the mentalizing network, which is used for inferring another persons thoughts and goals, or basically putting yourself in someone elses shoes and trying to think what they would think.

Charpentier adds that once the research team had completed the participants brain scans, they were able to build a mathematical model of how participants learn from the observed player and chooses between the slot machines. The model suggests that the decision of which strategy to employ is determined by how reliable the emulation strategy is, and results show evidence for this reliability of emulation signal in several brain areas.

If emulation is reliable, these regions are more active and emulation is more likely to be used, while if emulation is not reliable or too uncertain these regions are less active and we prefer imitation, she says. In other words, our behavior is a mix of both strategies and the brain can weigh in on which one is best at any point in time.

Charpentier says that, going forward, she would like to investigate the interactions of the regions of the brain involved in observational learning, or their so-called functional connectivity. In addition, she would like to see if the brain follows a similar model for choosing between other types of learning: if, for example, a person has to choose between learning from experience or learning from observation.

Reference: A Neuro-computational Account of Arbitration between Choice Imitation and Goal Emulation during Human Observational Learning by Caroline C. Charpentier, Kiyohito Iigaya and John P. ODoherty, 17 March 2020, Neuron.DOI: 10.1016/j.neuron.2020.02.028bioRxiv: 10.1101/828723

The paper, titled, Neuro-computational account of arbitration between choice imitation and goal emulation during human observational learning, appears in the March 17 issue of Neuron. Charpentiers co-authors include Kiyohito Iiyaga and John ODoherty. Funding for the research was provided by the National Institute of Mental Health (Caltech Conte Center for the Neurobiology of Social Decision-Making).

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Watch and Learn: How the Brain Gains Knowledge Through Observation - SciTechDaily

Immunology

Here’s how your body gains immunity to coronavirus – The Guardian

As the daughter of an air force officer and a nurse, I am fascinated by defence systems. There is none more impressive than the human immune system, equipped as it is with a rich arsenal to defend against different types of pathogen. Viruses have evolved to trick, bypass and evade these defences. Our immune systems have, in turn, learned to recognise and deter these virus stealth tactics. In Covid-19, the enemy is a tiny piece of genetic material wearing a lipid coat and a protein crown.

So how is our immune system able to defend against viral infections, and how does this apply to Covid-19? The virus that causes Covid-19 is called severe acute respiratory syndrome coronavirus 2 (Sars-Cov-2), and was first detected in humans around five months ago. It is a coronavirus. Corona, in Latin, means crown. The virus is adorned with an outer layer of protein covered in spikes, like a crown. These spikes help the virus attach itself to target cells. The research community is fast learning about immunity to Covid-19, and we are also applying our knowledge of similar respiratory viruses to predict what to expect in this infection.

Importantly, Covid-19 cannot gain entry to our homes or bodies by itself we have to let it in

Think of a virus as a robot; it cannot reproduce so it needs a factory of materials proteins, lipids and nucleotides to build copies of itself. The coat allows the virus to attach itself to the target cells membrane. The virus then fuses with the cell and releases a shopping list of instructions on how to build and assemble new viruses. This shopping list, the virus genome, is written in nucleotides (RNA). The first job of a virus that enters our bodies is to invade target cells so that it can comfortably remove its coat and deploy its RNA.

Once inside, the virus commandeers the cell and borrows cellular machinery to build more viruses before immune cells detect the intruders and raise the alarm. Antibody proteins that are able to stick to the virus-spike proteins, and prevent attachment to the target cells, are called neutralising antibodies: generating them is often the goal of protective vaccination.

Our infected cells make the ultimate sacrifice and invite their own destruction by displaying distress signals for T-cells, which swiftly detect and kill them. T-cells are cytotoxic powerful serial killers that can recognise peptide fragments of virus displayed on the infected cell surface. When they do, they release a payload of toxic enzymes that kill the infected cell in a kiss of death. This strategic martyrdom is organised by the immune system to deprive the virus of its replication factories and can lead to the reduction of viral load in the patient. It takes several days for antiviral T-cells to expand and antibodies to be generated. Heres the silver lining: memory cells ensure that if we encounter the same virus again, we can react immediately with pre-existing defences. Sars-Cov-2 is new to humanity so we have no protective immunological memory. Vaccines prepared using harmless parts of the virus can help us build protective memory.

The viruss enemy superpower is spreading. The virus achieves this through shedding from infected patients. Sars-Cov-2 is expert at hopping from person to person, and in some people, it achieves a stealthy existence with mild or no symptoms. Once many copies of the virus are made, it needs to jump to another host. It hitches a ride on droplets that can be coughed or sneezed to a distance of up to two metres. Droplets can survive on surfaces for several hours enabling pick-up by a new host, or they can be directly inhaled if another person is in close proximity. Studies are emerging into animal hosts so far the virus has been detected in a few ferrets, cats, tigers and dogs. No animal deaths have yet been reported, and we dont know if animals can transmit back to humans.

The age differential in fatalities for Covid-19 suggests, with some exceptions, that a healthy immune system is usually able to control infection. Meanwhile, an ageing or weakened immune system may struggle to deploy a protective arsenal. Importantly, Sars-Cov-2 cannot gain entry to our homes or bodies by itself we have to let it in. This is why official advice has centred around cleaning our hands and avoiding touching our faces.

We know that a healthy immune system is usually able to eliminate infection in a couple of weeks. However, we have no understanding of the components of our immune arsenal that contribute to this feat: some vaccines work by creating potent neutralising antibodies; other vaccines generate powerful memory T-cells. Antiviral antibodies emerge as early as three to four days after virus detection, but are they protective against future reinfection? We believe that antibodies to other coronaviruses (Sars, Mers) last from one to three years. Because this is a new virus, we dont yet know the answer to this question. Public Health England is recruiting 16,000 to 20,000 volunteers to monitor antibodies once a month for six to 12 months to confirm whether we can generate long-lasting antibody responses to Sars-Cov-2. Determining the quality of these antibodies will be important to understanding long-term protection.

What is our most potent immune weapon against Covid-19? Cytotoxic T-cells may play an important role. Immunologists and virologists are working together to discover the correlates of protection, to design vaccines that offer long-term defences against Covid-19. Years of investment in research means that we can use existing approaches to respond to this new threat, and early mobilisation of research funders, philanthropists and academics are diverting resources to bolster these efforts on an unprecedented scale. Experience has taught us that vaccines are able to eradicate infections from this planet (for instance, smallpox), and medicines against viruses that dont embed their genetic material to our own (for example, hepatitis C) can also achieve this.

Our secret weapon is research. Scientists are working hard on understanding Covid-19, and collaboration is key to this effort. But until a vaccine or treatment is available, we ought to work hard to protect ourselves and our families: isolate and prevent transmission by using physical distancing, face masks and sensible hygiene. If we all do our part, this little virus holding the world to ransom wont stand a chance.

Zania Stamataki is a senior lecturer and researcher in viral immunology at the University of Birmingham

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Immunology

UGA’s Landon Clark named 2020 Goldwater Scholar – University of Georgia

University of Georgia Honors student Landon Clark is among 396 undergraduates across the nation to be recognized as Barry Goldwater Scholars, earning the highest undergraduate award of its type for the fields of the natural sciences, mathematics and engineering.

Clark, from Leesburg, is a third-year CURO Honors Scholar who is triple majoring in biochemistry and molecular biology, genetics and biology.

Since 1995, 61 UGA students have received the Goldwater Scholarship, which recognizes exceptional sophomores and juniors across the United States.

The University of Georgia is proud of Landon and pleased that he is extending our record of success in this prestigious competition, said President Jere W. Morehead. Already as an undergraduate student, he is helping UGA fulfill our commitment to conduct research that helps people lead longer, healthier lives.

This year, recipients were selected from a field of more than 5,000 college sophomores and juniors who were nominated by 461 academic institutions nationwide. Each awardee will receive up to $7,500 toward the cost of tuition, fees, books, and room and board.

Of this years Goldwater Scholars, 50 are mathematics and computer science majors, 287 are majoring in the natural sciences and 59 are majoring in engineering.

I am thrilled for Landon, who is absolutely one of our very best students, said David S. Williams, associate provost and director of the Honors Program, who serves as the UGA campus faculty representative for the Goldwater Scholarship. As a CURO Honors Scholar, Landon was recruited to come to UGA because of his promise as a researcher. This Goldwater award and recognition proves that his hard work is paying off. I look forward to watching his career continue to blossom in the future.

Clarks long-term plans include pursuing an MD/PhD in immunology, performing translational research on immune diseases using gene and immunotherapy techniques, and teaching at a university. As a translational researcher specializing in immunology, he plans to use gene therapy techniques to treat and cure immune disorders in humans.

Since his first weeks as a UGA freshman in August 2017, Clark has conducted research in the lab of Michael Terns, Distinguished Research Professor of Biochemistry and Molecular Biology. He researches the complex processes of CRISPR-Cas immune systems through a model archaeal organism, Pyrococcus furiosus. Now a junior, he has collaborated on three different projects, co-authored a paper, and mentors other undergraduates in this field.

Last summer, he worked in the translational research lab of H. Trent Spencer, a professor of pediatrics and director of the gene and cell therapy program at Emorys Winship Cancer Institute. There, Clark researched immune diseases and potential gene therapy techniques. In 2017, he also conducted research on sociological variables influencing educational inequality with Dawn Robinson, a professor of sociology at UGA.

Clark is a Crane Leadership Scholar, director of academic outreach for the Student Government Association, director of internal communications for UGA Red Cross, an exam writer for UGA Science Olympiad Outreach, co-president of the Biochemistry Undergraduate Society, co-president of the Omicron Delta Kappa National Honor Society, and treasurer of the Honors Program Student Council. He also volunteers in the neuroscience and cardiology units at Piedmont Athens Regional Medical Center.

Clark has presented his research at 10 conferences. He also studied neurology and cancer biology through UGAs Studies Abroad Program in Cortona, located in Tuscany, Italy.

The scholarship honoring Sen. Barry Goldwater was created to encourage outstanding students to pursue careers in the fields of mathematics, natural sciences and engineering. Since its first award in 1989, the Barry Goldwater Scholarship and Excellence in Education Foundation has bestowed 8,628 scholarships worth more than $68 million.

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Immunology

These Are The Treatments And Cures Colorado Researchers Are Developing For Coronavirus – Colorado Public Radio

In Colorado, doctors and researchers are desperately looking for ways to treat patients with COVID-19.

Right now, there is no proven effective treatment, and it could be many months before a vaccine or a treatment to alleviate symptoms is tested and available for widespread use. Research into some drugs and treatments are farther along than others, and many show signs of promise.

Heres where things stand.

Weve eradicated smallpox and made diseases like the measles manageable through the use of vaccines. Those treatments are some of the biggest breakthroughs in public health, but they require time and money.

The World Health Organization announced in February that a vaccine for SARS-CoV-2, the virus that causes COVID-19, could be ready in 12-18 months, but some scientists argue that the timeline may be unrealistic. Typically, a vaccine can take 5-15 years to be developed, tested in clinical trials, and manufactured for distribution.

Around the country, several biotech companies have started human clinical trials of a vaccine, and its likely that multiple vaccines will be developed.

At Colorado State University, Gregg Dean, professor and head of the Department of Microbiology, Immunology, and Pathology, was working on a vaccine to treat a strain of coronavirus that cats contract when he shifted gears to address the strain thats now causing the pandemic.

Our experience with viruses in animals is quite valuable. This involves work by veterinarians and nonveterinarians to study these viruses in these nonhuman species, Dean said. When we think about the current pandemic, this virus has come out of an animal reservoir and it's jumped into the human population. Our understanding of those animals, the viruses they have and how these sort of emerging pathogens can come about is really critical.

Dean and his team are working on a vaccine made from the bacterium Lactobacillus acidophilus, a probiotic found in yogurt. This bacterium thrives in the mucous membrane the tissues of the nose, mouth, throat and lungs which is where the new coronavirus gains entry into the body.

The researchers engineered a form of the bacterium to block the virus from invading cells, exploiting the viruses Achilles heel.They're still developing the vaccine but hope to begin animal trials in the coming months to determine if it will be a good candidate for humans.

Over in Aurora, Greffex Inc., a Texas-based company, is developing an adenoviral vector-based vaccine. Scientists take an adenovirus, clear it of its disease-causing material and then introduce a part of the virus that causes COVID-19 into the viral shell. When injected into a person, the body will mount a response that results in immunity to the virus without having been exposed to a live or killed virus.

"The benefit is speed to get to the vaccine, cost, because ultimately when you get to production, you want to make a vaccine that's significantly cheaper for the population and safety," said John Price, CEO and president of Greffex Inc. "If you don't use a live virus or a killed virus, you're really not introducing anything that could be harmful to begin with."

Read more about that vaccine here.

Its likely that one of the first treatments well see in widespread use for COVID-19 will be one that uses an already-approved drug, like the antimalarial drugs chloroquine and hydroxychloroquine that President Donald Trump has pushed for.

Drugs that are already approved by the Food and Drug Administration have known side effects and manufacturers know how to produce them, but they arent likely to be the cure-all for COVID-19. These drugs are not likely to cure COVID-19, but they may alleviate the symptoms associated with the infection and keep them from becoming more severe.

Dr. Thomas Campbell, at the CU Anschutz Medical Campus, is working on a clinical trial of sarilumab, an anti-inflammatory drug used to treat rheumatoid arthritis. The trial was developed jointly by the pharmaceutical companies Regeneron and Sanofi. Hospitals all over the country will enroll hundreds of patients. In Colorado, Campbell has enrolled about 15 so far.

Sarilumab blocks the activity of a protein in the body that regulates inflammation. Many patients with severe COVID-19 develop hyperactive inflammation in their lungs. By targeting the inflammation mediator, patients may see improvements with this drug.

The idea is that if you can reduce that inflammation, interfere with that inflammation, then people will get better quicker, Campbell said. If they're not on a ventilator, they might not need to go on the ventilator, or if they're already on mechanical ventilation, they might come off of mechanical ventilation sooner than later.

When someone is exposed to COVID-19, the virus attacks the bodys cells and then starts to replicate itself. That replication process is what allows the virus to spread in the body and make us sick by damaging other cells or disrupting cell function.

Antiviral inhibitors prevent the virus from replicating, stopping or slowing the spread and allowing the body to catch up and recover. Campbell said UCHealth will start clinical trials of remdesivir, developed by the drug company Gilead Biosciences, in the coming weeks. One trial will focus on patients who have mild to moderate symptoms, and the second trial will focus on more severe patients.

Jed Lampe, assistant professor in the Department of Pharmaceutical Sciences at the Anschutz Medical Campus, is working on an antiviral inhibitor used to treat HIV. He and his team are modifying the drugs ritonavir and lopinavir. Lampe said there is some clinical evidence that they may be useful against COVID-19.

What's nice about taking this approach where we're starting out using these old inhibitors that were very effective at treating the HIV virus to treat this virus is that we know that they are already safe and effective at least against that virus, Lampe said.

But for the inhibitors to be effective against the novel coronavirus, Lampe and his team are having to make changes to the shape of the inhibitor so that it better fits this virus. One problem with antiviral inhibitors is that as the virus mutates, the inhibitor becomes less effective. In treating HIV, doctors use a cocktail of drugs for this reason.

We hope that this iterative process that that'll lead to a library of compounds that we can use to treat the viruses that haven't even been identified yet, or mutant viruses in the future, he said.

Listen to Colorado Matters interview with Lampe.

When you get sick with a cold or the flu, or even when you have an allergic reaction, your body reacts and creates antibodies. Those antibodies are part of your immune response when youre exposed to that virus or allergen in the future. For COVID-19 patients, receiving the plasma from someone who has recovered from the virus can help their body to fight off the disease.

COVID-19 convalescent plasma has been used by doctors at UCHealth to treat severe cases, and its showing promise.

There is hope in this treatment, said Dr. Kyle Annen, medical director of the blood collection center at Childrens Hospital of Colorado. However, it's not a certainty. We don't know for sure that it is the best option or the only option. It may be a great option with other medications. There may be another medication that comes along that is identified to work better. But it's great that we have this one additional thing in our arsenal to try to fight COVID-19.

Theres anecdotal evidence that plasma was used to treat sick people during the 1918 Spanish Flu, and it was used successfully to treat H1N1 flu in 2009-2010, but in other cases, its not been effective. The Food and Drug Administration released its guidelines for giving convalescent plasma to COVID-19 patients, and has encouraged researchers to begin clinical trials to investigate its efficacy.

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These Are The Treatments And Cures Colorado Researchers Are Developing For Coronavirus - Colorado Public Radio

Immunology

When will we reopen the country? Antibody testing may help officials decide, experts say – USA TODAY

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As officials begin to discusswhen they can lift stay-at-home orders, companies are rushing to develop coronavirus antibody tests that could help them make those decisions without risking a second wave of infections.

Leading the fight against COVID-19, Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said Friday morning on CNN that antibody testing can show who has developed immunityto the coronavirus and can safely go back to work without getting reinfected.

As we get to the point of at least considering opening up the country, as it were, its very important to appreciate and understand how much this virus is penetrating this society, he said.

How would antibody tests factor into decisions to lift social distancing orders, and how reliable arethose tests? Here's everything you need to know about antibody testing.

Testing to see if people haveantibodies in their blood isnt the same as testing to see if they have been infected withthe coronavirus that causes COVID-19.

The antibody test can determine if someone was previously infectedand recovered, whereas the moleculartest shows whether that person was infected with the virus at the time the test was taken.

Antibodies are the bodys way of remembering how it responded to an infection so it can attack again if exposed to the same pathogen. If a person has antibodies in his blood, that means he hasimmune cells available to fight the virus, which lowers therisk of re-infection.

Antibody tests look for two antibodies in the blood, immunoglobulin M (IgM) and immunoglobulin G (IgG). IgM antibodies are the first line of defense, appearing within several days of infection. IgG antibodies come later, as the body is clearing up the infection.

IgM and IgG antibodies fight all kinds of infections. The blood tests for COVID-19 look for a protein particular to this coronavirus, which shows whether the body is producing antibodies to itand not, for example, the seasonal flu.

Marc Lipsitch, a professor of epidemiology at Harvard and an expert in public health interventions, told the USA TODAY Editorial Board on Wednesday that a significant portion of the population must be immune to the coronavirus before social distancing restrictions can be lifted. Widespread antibody testing can determine how many people carry the antibodies.

Antibody tests can reveal who is immune to a disease, but it can also determine how widely it has spread and how deadly it is.

Dr. Neeraj Sood, professor and vice dean of research and faculty at the University of Southern California Sol Price School of Public Policy, isleading a study in conjunction with the Los Angeles County Department of Public Health using antibody tests to answer that question.

There have been 223 deaths related to COVID-19in the county, according to the health department. If, based on the antibody study, researchers determine that about 2,500 people had been infected,it would be considered a deadly disease. But if more than 2 million people had been infected, it wouldn't be considered that dangerous.

If we find out COVID is far less deadly than the flu, we can open up the economy. You dont need to hit herd immunity to open it up. Sood said. But if you find out that COVID is 10 times deadlier than the flu, then you have to keep it closed.

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Antibody testing combined with the molecular coronavirus testcan determine if a person is immune and can transmit the disease, he said.This is crucial in deciding who can go back to work.

Those who are immune and cant transmit the disease can be on the front lines of the epidemic, keeping daily life afloatin grocery stores, hospitals and other essential businesses,Sood said.

Antibody tests can also identify people who had COVID-19 but didn't have any symptoms a group that may be much larger than we know.

Theres some data out there that 15% to 16% of kids have had asymptomatic infections. They could be the secret spreaders. But without tests, we dont know, said Mark Slifka, a professor of viral immunology at Oregon Health and Science University in Portland, Oregon.

Doing broad testing of even a portion of the population in the coming months could also give researchers a sense of how much of the U.S. populationwas infected this year. They could use that to predict who might be immune if the virus comes back again thisfall, said Slifka.

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Immunity to viruses can last from months to a lifetime.William Schaffner, a professor of preventive medicine and infectious disease at Vanderbilt University, expects that contracting the coronavirus once would likely give someone pretty solid protection for a year. But he cautioned predictions for a newly emerged virus are difficult to make.

We dont know that this new coronavirus has read the textbook and knows what its supposed to do, he said.

On the TODAY show Thursday, Fauci said a large number of antibody tests should be available in a matter of days or weeks, according to the companies developing them.

Dr. Elitza Theel, directorof theInfectious Diseases Serology Laboratory at the Mayo Clinic, said laboratories throughout the country have been working to validate and select antibody tests.

She expects they will be widely available in about one to three weeks.

Cellex Inc. of Research Triangle Park in North Carolina was the first company to receive emergency use authorization of its test by the U.S. Food and Drug Administration last week.

Over50 commercial manufacturers are seeking FDA approval forantibody tests, Theel said.

ButDr. Raed Dweik, chairman of the Respiratory Institute at the Cleveland Clinic, saidsome of the tests he's seen aren't accurateenough to determine if someone is truly immune to the coronavirus.

This is becauseantibodies for the coronavirus that causes COVID-19 look very similar to antibodies that respond to coronaviruses that cause other illnesses, such as the common cold.

Tests could mistakenly identify antibodies as being for the coronavirus that causes COVID-19, producing a false positive. Dweik said it will take more time to develop a test that can accurately detect the right antibodies.

"The timing is tricky," he said. "Developing this test has been fraught with problems."

In addition, scientists don't know a lot about the protective value of coronavirus antibodies, said Dr. Carlos del Rio, an infectious disease expert and executive associate dean at Emory University.The test to identify HIV, for example, is an antibody test. "Having those antibodies doesn't necessarily mean immunity," he said.

Few of the coronavirus antibody tests have been vetted to determinetheir clinical accuracy, Theel said. No test is 100 percent accurate, she said, and it's up to the clinical laboratories to decidewhich ones are best for their patients.

"It's one of the biggest concerns right now because there's so many tests out there and we dont know how the vast majority of them work," she said.

Contributing: Letitia Stein andElizabeth Weise, USA TODAY.Follow Adrianna Rodriguez on Twitter: @AdriannaUSAT.

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When will we reopen the country? Antibody testing may help officials decide, experts say - USA TODAY

Neuroscience

Researchers Have Demonstrated the Ability to Implant Ultrathin, Flexible Neural Interface Into the Brain – Technology Networks

Researchers have demonstrated the ability to implant an ultrathin, flexible neural interface with thousands of electrodes into the brain with a projected lifetime of more than six years. Protected from the ravaging environment of internal biological processes by less than a micrometer of material, the achievement is an important step toward creating high-resolution neural interfaces that can persist within a human body for an entire lifetime.

The results, appearing online April 8 in the journal Science Translational Medicine, were published by a team of researchers led by Jonathan Viventi, assistant professor of biomedical engineering at Duke University; John Rogers, the Louis Simpson and Kimberly Querrey Professor of Materials Science and Engineering, Biomedical Engineering and Neurological Surgery at Northwestern University; and Bijan Pesaran, professor of neural science at New York University.

Trying to get these sensors to work in the brain is like tossing your foldable, flexible smartphone in the ocean and expecting it to work for 70 years, said Viventi. Except were making devices that are much thinner and much more flexible than the phones currently on the market. Thats the challenge.

The human body is an unforgiving place to live if youre an uninvited guest especially if youre made of polymers or metal. Besides attacks from the surrounding tissues and immune system, foreign objects must be able to stand up to a corrosive, salty environment.

Engineering electrical devices that can withstand this assault is an even more daunting prospect. Current long-term implantable devices are almost universally hermetically sealed within a laser-welded titanium casing. Think of a pacemaker, for example.

Building water-tight, bulk enclosures for such types of implants represents one level of engineering challenge, Rogers said. Were reporting here the successful development of materials that provide similar levels of isolation, but with thin, flexible membranes that are one hundred times thinner than a sheet of paper.

But when it comes to the human brain, space and flexibility is of the essence. There is no room for rigid devices with millimeter-thick walls. These challenges mean that existing neural interfaces can sample only about a hundred sites, which pales in comparison to the tens of billions of neurons that make up the human brain. Any attempt to make these devices larger invariably runs into the hurdle of wiring logisticsbecause each sensor requires its own wire, size constraints quickly become an issue.

Viventi and his colleagues have been working on a different approach.

You need to move the electronics to the sensors themselves and develop local intelligence that can handle multiple incoming signals, said Viventi. This is how digital cameras work. You can have tens of millions of pixels without tens of millions of wires because many pixels share the same data channels.

Through their work, the researchers have already demonstrated flexible neural devices just 25 micrometers thick with 360 electrodes. But previous attempts to keep them safe from harm inside the body have failed, as even the tiniest defect can thwart the entire effort.

We tried a bunch of strategies before. Depositing polymers as thin as is required resulted in defects that caused them to fail, and thicker polymers didnt have the flexibility that was required, said Viventi. But we finally found a strategy that outlasts them all and have now made it work in the brain.

All it took was perfection.

In the new paper, Viventi, Rogers, Pesaran and their colleagues demonstrate that a thermally grown layer of silicon dioxide less than a micrometer thick can ward off the hostile environment within the brain, degrading at a rate of only 0.46 nanometers per day. And because this form of glass is biocompatible, any trace amount that dissolves into the body should not create any problems of its own.

They also show that, even though the glass encapsulation is not conductive, the devices electrodes can detect neural activity through capacitive sensing. This is the same sort of technology that can detect the movements of a finger on a smartphones touchscreen. They implanted a 64-electrode neural interface into a rat for over a year and a 1,008-electrode neural interface into the motor cortex of a monkey reaching to a touchscreen.

Successfully deploying the device in monkeys doing human-like tasks is a huge leap forward, said Perasan. Now we can refine our technology to help people suffering brain disorders.

Based on these results and experiments to heat the devices to simulate longer periods of time, the researchers believe their devices could withstand implantation for more than six years.

While these results are enormous steps forward in comparison to current state-of-the-art devices, theyre not anywhere near the level of the researchers aspirations. Viventis student is currently working to scale the prototype up from 1,000 electrodes to more than 65,000. And they expect that by using commercial foundries to make the electrodes, which are far superior to their own capabilities, that the performance of their neural interface will increase greatly both in terms of signal quality and surviving within the human body.

One of our goals is to create a new type of visual prosthetic that interacts directly with the brain that can restore at least some sight capacity for people with damaged optic nerves, said Viventi. But we can also use these types of devices to control other types of prosthetics or in a wide range of neuroscience research projects.

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Researchers Have Demonstrated the Ability to Implant Ultrathin, Flexible Neural Interface Into the Brain - Technology Networks

Neuroscience

Mount Sinai researchers discover a novel role for dopamine that impacts gene expression related to cocaine abuse – Science Codex

Scientists at the Icahn School of Medicine at Mount Sinai have discovered a new role for the brain chemical dopamine that is independent of classic neurotransmission. The new role appears to be critical to changes in gene expression related to chronic exposure to, or abuse of, cocaine, according to a study published Friday, April 10, in the journal Science.

"Our study provides the first evidence of how dopamine can directly impact drug-induced gene expression abnormalities and subsequent relapse behavior," says Ian Maze, PhD, Associate Professor of Neuroscience, and Pharmacological Sciences, at the Icahn School of Medicine at Mount Sinai, and lead author of the study. "Beyond transmission of signals between neurons in the brain, we have found that dopamine can be chemically attached to histone proteins, which causes cells to switch different genes on and off, affecting regions of the brain that are involved in motivation and reward behavior. This biochemical process significantly affects cocaine vulnerability and relapse when perturbed by drugs of abuse."

The study revolves around DNA and how it works to form each person's individual biological map. Each cell in the body contains two meters of DNA, the blueprint for all functions of all cells in the body. This DNA is wound around spools of histone proteins (proteins that package DNA in the nucleus of cells, and are heavily prone to chemical modifications that aid in the regulation of gene expression) into structures referred to as nucleosomes. When DNA encoding a specific gene is wound tightly within the spool, that gene is less likely to be expressed. When the gene is not wound as tightly, it is more likely to be expressed. This can affect many functions of a given cell.

Dopamine, known as the feel-good neurotransmitter, is a chemical that ferries information between neurons. The brain releases it when we eat food that we crave or while we have sex, contributing to feelings of pleasure and satisfaction as part of the natural reward system. This important neurochemical boosts mood, motivation, and attention, and helps regulate movement, learning, and emotional responses. Dopamine also enables us not only to see rewards but to take action to move toward them.

Vulnerability to relapse during periods of cocaine withdrawal is believed to result from functional rewiring of the brain's reward circuitry, particularly within mid-brain regions, such as the ventral tegmental area (VTA). The research team discovered that a protein called transglutaminase 2 can directly attach dopamine molecules to histone proteins (a process called histone dopaminylation or H3Q5dop) which, in turn, affects the histone-DNA spool to enable environmentally regulated alterations in gene expression. They found that histone dopaminylation plays a critical role in fueling heightened vulnerability to relapse over a prolonged period of time. Specifically, accumulation of H3Q5dop in the VTA can, in effect, hijack the reward circuitry, making it difficult to distinguish between good and maladaptive behavior. The study found, however, that reducing H3Q5dop in rats programmed to undergo withdrawal from cocaine significantly reversed cocaine-mediated gene expression changes and reduced cocaine-seeking behavior.

"The question that has always challenged neuroscientists is, what are the underlying molecular phenomena that drive increased vulnerability to drug relapse in people," says Ashley Lepack, PhD, a researcher in the Department of Neuroscience, The Friedman Brain Institute, in Dr. Maze's lab at Mount Sinai, and first author of the study. "Our research is shedding valuable light on this area by identifying histone dopaminylation as a new, neurotransmission-independent role for dopamine that hasn't been implicated before in brain pathology."

"We believe these findings represent a paradigm shift in how we think of dopamine, not just in the context of drug abuse, but also potentially in other reward-related behaviors and disorders, as well as in neurodegenerative diseases like Parkinson's, where dopamine neurons are dying," says Dr. Maze. "In this case, the question becomes, 'could this neuronal death be due, in part, to aberrant dopaminylation of histone proteins?' "

In a study published last year, Dr. Maze and his team found that another neurotransmitter, serotonin, a chemical involved in the regulation of mood, acts in a similar way as dopamine on gene expression inside brain cells.

"When we observed this unique signaling mechanism with serotonin, we decided to look at other neurotransmitters, particularly dopamine, and found that it could also undergo this type of chemical modification on the same histone protein," explains Dr. Maze.

Early-stage work with human post-mortem tissues has demonstrated to Dr. Maze that strong parallels may well exist, but that basic questions around biochemical function still remain before human trials can begin. "From a therapeutic standpoint, we've started to identify from rodent models the mechanisms that can actually reverse aberrant and addictive behaviors," says Dr. Maze, "and that knowledge could be vital to moving this novel research into the clinic."

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Mount Sinai researchers discover a novel role for dopamine that impacts gene expression related to cocaine abuse - Science Codex