By Douglas Starr When Jennifer Eberhardt appeared on The Daily Show with Trevor Noah in April 2019, she had a hard time keeping a straight face. But some of the laughs were painful. Discussing unconscious racial bias, which she has studied for years, the Stanford University psychologist mentioned the “other-race effect,” in which people have trouble recognizing faces of other racial groups. Criminals have learned to exploit the effect, she told Noah. In Oakland, California, a gang of black teenagers caused a mini–crime wave of purse snatchings among middle-aged women in Chinatown. When police asked the teens why they targeted that neighborhood, they said the Asian women, when faced with a lineup, “couldn’t tell the brothers apart.” “That is one of the most horrible, fantastic stories ever!” said Noah, a black South African. But it was true. Eberhardt has written that the phrase “they all look alike,” long the province of the bigot, “is actually a function of biology and exposure.” There’s no doubt plenty of overt bigotry exists, Eberhardt says; but she has found that most of us also harbor bias without knowing it. It stems from our brain’s tendency to categorize things—a useful function in a world of infinite stimuli, but one that can lead to discrimination, baseless assumptions, and worse, particularly in times of hurry or stress. Over the decades, Eberhardt and her Stanford team have explored the roots and ramifications of unconscious bias, from the level of the neuron to that of society. In cleverly designed experiments, she has shown how social conditions can interact with the workings of our brain to determine our responses to other people, especially in the context of race. Eberhardt’s studies are “strong methodologically and also super real-world relevant,” says Dolly Chugh of New York University’s Stern School of Business, a psychologist who studies decision-making. © 2020 American Association for the Advancement of Science.

Keyword: Attention; Emotions
Link ID: 27145 - Posted: 03.27.2020

By Adam Popescu Many people spend their nights now tossing and turning, struggling to unglue from the constant scroll of coronavirus news updates. But, while there is no body or life hack to make you impervious to the touch of disease, we do know that sleep is key to helping our bodies stay healthy. “Sleep is an essential part of protection from and response to any infection,” said Douglas B. Kirsch, a neurologist and former president of the American Academy of Sleep Medicine. But still, he hears you: “Sleep is hard when anxiety levels are high, such as in the case of a pandemic.” There are some answers as to what you can do now. You may not like them. Create and maintain a very consistent sleep practice and schedule that works for you. The more consistent your wake-up time, the more consistent your body functions. The National Sleep Foundation recommends sticking to a sleep schedule, and here’s a simple way to do it: Set a regular bedtime. Pair it with a set time to wake. (As many people aren’t currently commuting, this might be easier than normal.) Set yourself up for success by doing the little things: use blackout curtains if you’re sleeping while it’s bright, ditto to earplugs or a sleep mask (Wirecutter, a company owned by The New York Times that judges products, recommends this sleep mask, but even a light pillow or T-shirt works in a pinch). No matter what you do, make your bedroom very comfortable and very dark. Are you easily awakened? Use a fan or a repeated track on Spotify for white noise. Still, if you’re tired, get sleep while you can. “If you’re tired during the day, get your rest then,” said Janet Mullington, a professor in the department of neurology at Harvard Medical School. © 2020 The New York Times Company

Keyword: Sleep
Link ID: 27144 - Posted: 03.27.2020

Richard Masland The eye is something like a camera, but there is a whole lot more to vision than that. One profound difference is that our vision, like the rest of our senses, is malleable and modifiable by experience. Take the commonplace observation that people deprived of one sense may have a compensatory increase in others — for example, that blind people have heightened senses of hearing and touch. A skeptic could say that this was just a matter of attention, concentration and practice at the task, rather than a true sensory improvement. Indeed, experiments show that a person’s sensory acuity can achieve major improvement with practice. Yet with modern methodologies, neuroscientists have conclusively proved that the circuits of the brain neurons do physically change. Our senses are malleable because the sensory centers of the brain rewire themselves to strike a useful balance between the capacities of the available neural resources and the demands put on them by incoming sensory impressions. Studies of this phenomenon are revealing that some sensory areas have innate tendencies toward certain functions, but they show just as powerfully the plasticity of the developing brain. Take a rat that has been deprived of vision since birth — let’s say because of damage to both retinas. When the rat grows up, you train that rat to run a maze. Then you damage the visual cortex slightly. You ask the rat to run the maze again and compare its time before the operation and after. In principle, damaging the visual cortex should not do anything to the maze-running ability of that blind rat. But the classic experimental finding made decades ago by Karl Lashley of Yerkes Laboratories of Primate Biology and others is that the rat’s performance gets worse, suggesting that the visual cortex in the blind rat was contributing something, although we do not know what it was.­­ All Rights Reserved © 2020

Keyword: Vision; Development of the Brain
Link ID: 27143 - Posted: 03.25.2020

Eric Haseltine A recent bulletin from physicians in the UK described the loss of smell and taste in COVID-19 patients, suggesting that the virus might affect parts of the central nervous system, in addition to its well-known affinity for the respiratory system. Indeed, in an earlier outbreak of coronavirus in China, Hong Kong researcher Dr. K.K. Lau and co-workers found that some patients exhibited convulsions, delirium and restlessness, while Dr. Jun Xu, of the Guangzhou Institute of Respiratory Diseases estimated that 4-5% of all SARS coronavirus patients displayed central nervous system symptoms. Some SARS coronavirus patients have even exhibited marked brain damage on CAT scans. In the latest outbreak of coronavirus, evidence of central nervous system involvement is accumulating, such as a March 21st report by Dr. Asia Filatov of Charles E. Schmidt College of Medicine, that a COVID-19 patient exhibited encephalopathy (brain disease). And recent data from Wuhan, described in the March 12 edition of Neurology Today, indicate that neurological symptoms, such as "altered consciousness," occur in up to one third of COVID-19 cases. But could central nervous system action of COVID-19 directly contribute to the acute respiratory distress associated with the disease? The answer might be “yes” according to recent collaborative research from Drs. Y.C. LI and W.Z. Bai Dr. T. and Hashikawa in Japan. Writing in the Feb 27 edition of the Journal of Medical Virology, Li and colleagues, cite research on coronavirus showing that sometimes SARS-Cov infects brainstem centers that control respiration, making it difficult for infected patients to breathe spontaneously. © 2020 Sussex Publishers, LLC

Keyword: Miscellaneous
Link ID: 27142 - Posted: 03.25.2020

By Erin Garcia de Jesus Myriad microbes dwell on human tongues — and scientists have now gotten a glimpse at the neighborhoods that bacteria build for themselves. Bacteria grow in thick films, with different types of microbes clustered in patches around individual cells on the tongue’s surface, researchers report online March 24 in Cell Reports. This pattern suggests individual bacterial cells first attach to the tongue cell’s surface and then grow in layers as they form larger clusters — creating miniature environments the different species need to thrive. “It’s amazing, the complexity of the community that they build right there on your tongue,” says Jessica Mark Welch, a microbiologist at the Marine Biological Laboratory in Woods Hole, Mass. Methods to identify microbial communities typically hunt for genetic fingerprints from various types of bacteria (SN: 11/05/09). The techniques can reveal what lives on the tongue, but not how the bacterial community is organized in space, Mark Welch says. So she and her colleagues had people scrape the top of their tongues with plastic scrapers. Then the team tagged various types of bacteria in the tongue gunk with differently colored fluorescent markers to see how the microbial community was structured. Bacterial cells, largely grouped by type in a thick, densely packed biofilm, covered each tongue surface cell. While the overall patchwork appearance of the microbial community was consistent among cells from different samples and people, the specific composition of bacteria varied, Mark Welch says. © Society for Science & the Public 2000–2020.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27141 - Posted: 03.25.2020

By Joshua Sokol The city of Minamata, Japan, is dotted with monuments commemorating victims of an industrial mass poisoning decades ago. High in the hills, a small stone memorial honors other deaths—of cats sacrificed in secret to science. Now, after restudying the remains of one of those cats, a team of scientists is arguing, controversially, that the long-standing explanation for the tragedy is wrong. No one questions the root cause of the disaster, which at minimum poisoned more than 2000 people: mercury in a chemical factory’s wastewater that was dumped into Minamata Bay and taken up by seafood eaten by fishermen and their families. At first, the chemical form of the mercury, which ultimately killed many of its victims and left many babies with severe neurological disorders, was unknown. But in 1968, the Japanese government blamed methylmercury, a common byproduct of mercury pollution. Many studies supported that conclusion, finding methylmercury spikes in shellfish, bay sludge, and even hundreds of umbilical cords from babies delivered during the time. But methylmercury is not the culprit, says Ingrid Pickering, an x-ray spectroscopist at the University of Saskatchewan. “Our work is indicating that it’s something else”: an unusual mercury compound that may say little about the broader threat of mercury pollution. Minamata has long been a vivid case study of mercury’s dangers. The metal is toxic on its own, but it becomes far more dangerous when bacteria in natural environments convert it into methylmercury, an organic compound, readily absorbed by living tissues, that can be concentrated and passed up food chains. Since the 1990s, scientists have argued that the Chisso chemical factory in Minamata produced methylmercury and dumped it directly into the bay. © 2020 American Association for the Advancement of Science.

Keyword: Neurotoxins
Link ID: 27140 - Posted: 03.25.2020

Jordana Cepelewicz In the 1990s, an army of clones invaded Germany. Within a decade, they had spread to Italy, Croatia, Slovakia, Hungary, Sweden, France, Japan and Madagascar — wreaking havoc in rivers and lakes, rice paddies and swamps; in waters warm and cold, acidic and basic. The culprits: six-inch-long, lobster-like creatures called marbled crayfish. Scientists suspect that sometime around 1995, a genetic mutation allowed a pet crayfish to reproduce asexually, giving rise to a new, all-female species that could make clones of itself from its unfertilized eggs. Deliberately or accidentally, some of these mutants were released from aquariums into the wild, where they rapidly multiplied into the millions, threatening native waterways species and ecosystems. But their success is strange. “All marbled crayfish which exist today derive from a single animal,” said Günter Vogt, a biologist at Heidelberg University. “They are all genetically identical.” Ordinarily, the absence of genetic diversity makes a population exceedingly vulnerable to the vagaries of its environment. Yet the marbled crayfish have managed to thrive around the globe. A closer look reveals that the crayfishes’ uniformity is only genome-deep. According to studies conducted by Vogt and others in the mid-2000s, these aquatic clones actually vary quite a bit in their color, size, behavior and longevity. Which means that something other than their genes is inspiring that diversity. Common sense tells us that if it’s not nature, it’s nurture: environmental influences that interact with an animal’s genome to generate different outcomes for various traits. But that’s not the whole story. New research on crayfish and scores of other organisms is revealing an important role for a third, often-overlooked source of variation and diversity — a surprising foundation for what makes us unique that begins in the first days of an embryo’s development: random, intrinsic noise. All Rights Reserved © 2020

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27139 - Posted: 03.24.2020

By Eva Frederick They’re the undertakers of the bee world: a class of workers that scours hives for dead comrades, finding them in the dark in as little as 30 minutes, despite the fact that the deceased haven’t begun to give off the typical odors of decay. A new study may reveal how they do it. “The task of undertaking is fascinating” and the new work is “pretty cool,” says Jenny Jandt, a behavioral ecologist at the University of Otago, Dunedin, who was not involved with the study. Wen Ping, an ecologist at the Chinese Academy of Sciences’s Xishuangbanna Tropical Botanical Garden, wondered whether a specific type of scent molecule might help undertaker bees find their fallen hive mates. Ants, bees, and other insects are covered in compounds called cuticular hydrocarbons (CHCs), which compose part of the waxy coating on their cuticles (the shiny parts of their exoskeletons) and help prevent them from drying out. While the insects are alive, these molecules are continually released into the air and are used to recognize fellow hive members. Wen speculated that less of the pheromones were being released into the air after a bee died and its body temperature decreased. When he used chemical methods of detecting gases to test this hypothesis, he confirmed that cooled dead bees were indeed emitting fewer volatile CHCs than living bees. © 2020 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Animal Communication
Link ID: 27138 - Posted: 03.24.2020

By Matt McGrath Environment correspondent A new study that looks at lifespan in wild mammals shows that females live substantially longer than males. The research finds that, on average, females live 18.6% longer than males from the same species. This is much larger than the well-studied difference between men and women, which is around 8%. The scientists say the differences in these other mammals are due to a combination of sex-specific traits and local environmental factors. In every human population, women live longer than men, so much so that nine out of 10 people who live to be 110 years old are female. This pattern, researchers say, has been consistent since the first accurate birth records became available in the 18th Century. While the same assumption has been held about animal species, large-scale data on mammals in the wild has been lacking, Now, an international team of researchers has examined age-specific mortality estimates for a widely diverse group of 101 species. In 60% of the analysed populations, the scientists found that females outlived the males - on average, they had a lifespan that's 18.6% longer than males. "The magnitude of lifespan and ageing across species is probably an interaction between environmental conditions and sex-specific genetic variations," said lead author Dr Jean-Francois Lemaître, from the University of Lyon, France. He gives the example of bighorn sheep for which the researchers had access to good data on different populations. Where natural resources were consistently available there was little difference in lifespan. However, in one location where winters were particularly severe, the males lived much shorter lives. © 2020 BBC.

Keyword: Sexual Behavior; Evolution
Link ID: 27137 - Posted: 03.24.2020

By Alex Fox Deposits of a mineral found in tooth enamel at the back of the eye could be hastening the progression of age-related macular degeneration, the leading cause of deteriorating eyesight in people over 50. Now researchers have identified a protein called amelotin that experiments suggest is involved in producing the mineral deposits that are the hallmark of “dry” age-related macular degeneration, the most common of the two forms of the disease. Age-related macular degeneration, or AMD, affects about 3 million people in the United States. But the new finding, if confirmed, could change that. While the “wet” form of AMD, which comprises up to 30 percent of AMD cases, can be treated with injections, there are currently no treatments for dry AMD. “Finding amelotin in these deposits makes it a target to try to slow the progression of mineralization, which, if it’s borne out, could result in new therapies,” says Imre Lengyel, an ophthalmologist at Queen’s University Belfast in Scotland who was not involved in the research. These deposits, first documented in 2015, are made of a type of mineralized calcium called hydroxyapatite and appear beneath the retinal pigment epithelium — a layer of cells just outside the retina that keeps its light-sensing rods and cones happy and healthy. The deposits may worsen vision by blocking the flow of oxygen and nutrients needed to nourish those light-sensitive cells of the retina. By contrast, in wet AMD abnormal blood vessels intrude into the retina and often leak. Both types of AMD distort a person’s central vision — the focused, detailed sight needed for reading and recognizing faces — which can make independent living difficult. © Society for Science & the Public 2000–2020

Keyword: Vision
Link ID: 27136 - Posted: 03.24.2020

By Roni Caryn Rabin A mother who was infected with the coronavirus couldn’t smell her baby’s full diaper. Cooks who can usually name every spice in a restaurant dish can’t smell curry or garlic, and food tastes bland. Others say they can’t pick up the sweet scent of shampoo or the foul odor of kitty litter. Anosmia, the loss of sense of smell, and ageusia, an accompanying diminished sense of taste, have emerged as peculiar telltale signs of Covid-19, the disease caused by the coronavirus, and possible markers of infection. On Friday, British ear, nose and throat doctors, citing reports from colleagues around the world, called on adults who lose their senses of smell to isolate themselves for seven days, even if they have no other symptoms, to slow the disease’s spread. The published data is limited, but doctors are concerned enough to raise warnings. “We really want to raise awareness that this is a sign of infection and that anyone who develops loss of sense of smell should self-isolate,” Prof. Claire Hopkins, president of the British Rhinological Society, wrote in an email. “It could contribute to slowing transmission and save lives.” She and Nirmal Kumar, president of ENT UK, a group representing ear, nose and throat doctors in Britain, issued a joint statement urging health care workers to use personal protective equipment when treating any patients who have lost their senses of smell, and advised against performing nonessential sinus endoscopy procedures on anyone, because the virus replicates in the nose and the throat and an exam can prompt coughs or sneezes that expose the doctor to a high level of virus. Two ear, nose and throat specialists in Britain who have been infected with the coronavirus are in critical condition, Dr. Hopkins said. Earlier reports from Wuhan, China, where the coronavirus first emerged, had warned that ear, nose and throat specialists as well as eye doctors were infected and dying in large numbers, Dr. Hopkins said. © 2020 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27135 - Posted: 03.23.2020

By Amanda McCracken Over 30 years ago, Tom Johnson identified a gene that extended the very short life of a tiny roundworm, propelling him to the forefront of research on aging and raising the tantalizing possibility that aging could someday be slowed down in people, too. His work transformed the mind-set of scientists, launching a new field in the science of aging when he demonstrated that identifying and manipulating genes could lengthen life span. Although Johnson’s research has led to drug development to slow the effects of age-related diseases, he has yet to find the secret to stop aging. Now the soft-spoken redheaded scientist is running out of time as he confronts his own mortality. Five years ago, at age 66, work got confusing for Johnson, a professor in the Institute for Behavioral Genetics at the University of Colorado at Boulder. He found it impossible to keep track of his many projects. He began wondering whether he had Alzheimer’s like his newly diagnosed sister. He spoke to his wife, Vicki Simpson, about the little dogs he frequently saw running around the house (even though he knew they weren’t real). Simpson, a retired anesthesiologist, later learned such hallucinations are a trademark sign of Lewy body dementia. At first, she praised his imagination and then after several months suggested they visit a memory clinic. There he was diagnosed with probable Lewy body — a fatal disease with inescapable dementia that can be diagnosed with certainty only at death. Right now, there is no cure, only ways to ease symptoms.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27134 - Posted: 03.23.2020

Amy Schleunes Preti was a leading expert on human odors who sought to understand the chemistry of odor in the underarm and the behavior aspects of human scents, and an ambassador to patients suffering from rare metabolic diseases who provided communities worldwide with knowledge about their condition and how to cope with it. Preti was also dedicated to using odor biomarkers to detect cancer in its early stages, contributing both research and money to the cause, according to a Monell Center press release. Born on October 7, 1944 in Brooklyn, New York, Preti received a bachelor’s degree in chemistry from the Polytechnic Institute of Brooklyn in 1966. He then went on to MIT, where he earned a PhD in chemistry in 1971. His thesis was titled, “A Study of the Organic Compounds in the Lunar Crust and in Terrestrial Model Systems,” according to the Monell Center’s statement. Preti coauthored a paper published in Science on the same topic, and reportedly saved a vial of “moon dust” that he sometimes showed off to visitors to his lab. Upon completing his doctorate in 1971, he immediately accepted a postdoc at Monell and later become a member of the Monell Chemical Senses Center and an adjunct professor at the University of Pennsylvania School of Medicine. While Preti and his colleagues investigated a range of odors in different species—anal sac emissions from dogs, scent marks by marmoset monkeys, urine from guinea pigs and mice—Preti’s main focus was on the meaning of human odors. He studied the scents of human underarms and melanoma cells as well as the odors associated with generalized stress. Along with his collaborator, Charles Wysocki, Preti published papers on how human physiology and behavior are affected by body odor. Preti was skeptical of human pheromones and their associated hype, telling The Scientist in 2018, “I am not compelled by any studies that are out there that say there is an active steroid component from the underarm that causes [sexual attraction].” © 1986–2020 The Scientist

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27133 - Posted: 03.23.2020

Peter Hess The coronavirus pandemic has shuttered universities and institutes, leaving scientists scrambling to continue their research. Hundreds of colleges and universities in the United States have dispatched students home and are aiming to transition to remote learning. Scientific organizations are canceling conferences or moving them online. And scientists have had to put research projects and clinical trials on hold. These decisions—all done with the intention of slowing the pandemic—may stall and stymie research, with long-term consequences for the field. It may also hurt career prospects for graduate students who rely on conference presentations to gain exposure. “From everything that we’re seeing, this isn’t like a two-week hiatus,” says Helen Egger, chair of the child and adolescent psychiatry department at NYU Langone Health in New York City. “We’re in the middle of the hurricane, and there’s no indication how much worse it’s going to get or when it will end.” One long-term benefit is that the crisis may give universities and professional organizations a crash course in embracing technology. “These types of experiences—as long as we are having them, unfortunately—are giving autism [researchers] and other researchers more skills to be able to have online conferences and online teaching as needed,” says Steven Kapp, lecturer in psychology at the University of Portsmouth in the United Kingdom. Backup plans: Some labs were prepared to meet the challenge, and they quickly put their emergency plans into place when news of the pandemic intensified. But, illustrating how rapidly the situation is changing, some of their plans derailed over the weekend. © 1986–2020 The Scientist

Keyword: Autism
Link ID: 27132 - Posted: 03.21.2020

By Monica Schoch-Spana The novel coronavirus has touched off another stealthy and growing public health crisis that calls for an equally matched emergency response. Like other pandemics and emerging disease outbreaks, COVID-19 is creating immense psychosocial disturbances. The disease involves an unfamiliar threat that is difficult to detect and challenging to distinguish from more benign illnesses. Protracted and dynamic pandemic conditions will draw out the anxiety. Things will get worse before they get better. Absent a vaccine, nonpharmaceutical interventions are the only way to prevent infections, and they dramatically upset everyday bodily habits, social interactions and economic exchanges. Recent grocery store runs are a sign of concern in the community. Personal actions to avoid infection such as stockpiling hand sanitizer also confer a sense of control over an uncertain danger. Improvements to current risk communication can alleviate widespread distress. Top elected officials and health authorities should empathize with people’s fear, normalize stress reactions, provide clear guidance on recommended health behaviors, instruct in concrete protections including those for mental health and share solidarity and resilience messages. Advertisement However, more interventions are essential because specific groups are at a higher risk of both acute and lingering emotional distress. Health care workers on the epidemic front lines face compounding stressors: the prospect of more and longer shifts, the need to improvise childcare coverage, finite supplies of personal protective equipment, fear of bringing infection home, witnessing co-workers becoming ill, and making tough allocation decisions about scarce, lifesaving resources like mechanical ventilators. © 2020 Scientific American

Keyword: Emotions
Link ID: 27131 - Posted: 03.21.2020

May-Britt Moser & Edvard Moser There was something of the Viking about Per Andersen. The intrepid and steadfast Norwegian was renowned for his attacks on the deepest puzzle of the brain: how its wiring and electrical activity give rise to behaviour and experience. When he was a student in the 1950s, most neuroscientists studied accessible parts of the mammalian nervous system — the junctions between nerves and muscles, say. Andersen worked on the cerebral cortex, which processes higher-level functions: perception, voluntary movement, planning and abstract thinking. His pioneering recordings of electrical activity in the hippocampus — a part of the cortex involved in memory — launched a new era in physiological understanding of the brain and laid the foundations of modern systems neuroscience. He died on 17 February, aged 90. In 1949, it was predicted that learning might depend on repeated activity strengthening the connections — synapses — in networks of neurons. Andersen saw that this was the case in the hippocampus. As the effect was too fleeting to account directly for memory storage, he encouraged his student Terje Lømo to investigate. In 1973, in one of the greatest discoveries of twentieth-century neuroscience, Lømo and British visiting scholar Tim Bliss reported from Andersen’s laboratory that many bursts of electrical stimulation at certain frequencies enhanced connectivity for hours or days. This phenomenon — long-term potentiation (LTP) — remains the main explanation for how we form and store memories (T. V. P. Bliss and T. Lømo J. Physiol. 232, 331–356; 1973). We met Andersen as students, in the late 1980s. Our work with him on LTP and animal learning found differences in function between regions of the hippocampus and demonstrated changes in connectivity related to behaviour. His hunch that we should record activity from single cells led to our discovery of specialized neurons in the cortex that support the sense of where the body is in space. The work was a direct result of his insight. © 2020 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 27130 - Posted: 03.21.2020

By Inés Gutiérrez, Rodrigo Pérez Ortega Earlier this month, Mexico’s leading university, the National Autonomous University of Mexico (UNAM), announced that renowned neuroscientist Ranulfo Romo Trujillo would leave his position after being disciplined for an unspecified offense. According to a 4 March press release from UNAM, Romo Trujillo voluntarily asked to be separated from his job at UNAM’s University City campus in Mexico City. Sources close to the case say he had been temporarily suspended because a female worker made a formal complaint of sexual harassment against him following an incident in January. But current and former UNAM students and staff say that reports of inappropriate behavior by Romo Trujillo had circulated for years before his departure. Romo Trujillo, who works at UNAM’s Institute of Cellular Physiology (IFC), did not respond to repeated requests for comment. He is arguably the most famous neuroscientist in Mexico, studying perception, working memory, and decision-making. He has more than 150 publications, including in top journals such as Science and Nature; is on the editorial board of Neuron and other journals; and is one of 11 Mexican members of the U.S. National Academy of Sciences. IFC physiologist Marcia Hiriart Urdanivia acknowledged in an email to Science that, while director of IFC from 2009 to 2017, she received multiple accounts of sexual harassment or inappropriate conduct by Romo Trujillo. Hiriart Urdanivia says she warned Romo Trujillo that “his career was endangered by such actions.” But the women involved did not choose to file official complaints, she says. As a result, “I had no authority to do anything else.” © 2020 American Association for the Advancement of Science.

Keyword: Sexual Behavior
Link ID: 27129 - Posted: 03.21.2020

By Scott Barry Kaufman Who are you and how did you become interested in free will? I am an Assistant Professor of Philosophy at Iona College where I also serve as a faculty member for the Iona Neuroscience program. I have previously worked in the Scientific and Philosophical Studies of Mind program at Franklin and Marshall College as well as previous appointments as a Lecturer at King’s College London and University of Alabama. My recent and forthcoming publications focus on issues of autonomy in terms of philosophical accounts of free will as well as how it intersects with neuroscience and psychiatry. One of the main questions I investigate is what neuroscience can tell us about meaningful agency (see here for my recent review of the topic as part of an extended review of research on agency, freedom, and responsibility for the John Templeton Foundation). I became interested in free will via an interdisciplinary route. As an undergraduate at Grinnell College, I majored in psychology with a strong emphasis on experimental psychology and clinical psychology. During my senior year at Grinnell I realized that I was fascinated by the theoretical issues operating in the background of the psychological studies that we read and conducted, especially issues of how the mind is related to the brain, prospects for the scientific study of consciousness, and how humans as agents fit into a natural picture of the world. So I followed these interests to the study of philosophy of psychology and eventually found my way to the perfect fusion of these topics: the neuroscience of free will. What is free will? Free will seems to be a familiar feature of our everyday lives — most of us believe that (at least at times) what we do is up to us to some extent. For instance, that I freely decided to take my job or that I am acting freely when I decide to go for a run this afternoon. Free will is not just that I move about in the world to achieve a goal, but that I exercise meaningful control over what I decide to do. My decisions and actions are up to me in the sense that they are mine — a product of my values, desires, beliefs, and intentions. I decided to take this job because I valued the institution’s mission or I believed that this job would be enriching or a good fit for me. Correspondingly, it seems to me that at least at times I could have decided to and done something else than what I did. I decided to go for a run this afternoon, but no one made me and I wasn’t subject to any compulsion; I could have gone for a coffee instead, at least it seems to me. Philosophers take these starting points and work to construct plausible accounts of free will. Broadly speaking, there is a lot of disagreement as to the right view of free will, but most philosophers believe that a person has free will if they have the ability to act freely, and that this kind of control is linked to whether it would be appropriate to hold that person responsible (e.g., blame or praise them) for what they do. For instance, we don’t typically hold people responsible for what they do if they were acting under severe threat or inner compulsion. © 2020 Scientific American

Keyword: Consciousness
Link ID: 27128 - Posted: 03.17.2020

Jonathan Kanter and Adam Kuczynski To fight the spread of coronavirus, government officials have asked Americans to swallow a hard pill: Stay away from each other. In times of societal stress, such a demand runs counter to what evolution has hard-wired people to do: Seek out and support each other as families, friends and communities. We yearn to huddle together. The warmth of our breath and bodies, of holding hands and hugging, of talking and listening, is a primary source of soothing. These connections are pivotal for responding to and maximizing our survival in times of stress. Priority number one is to follow the recommended social distancing guidelines to control the virus. The cure is definitely not worse than the disease – experts’ projections of disease spread and mortality without strong intervention make this clear. But as with any pill, there are side effects. As psychological scientists at the University of Washington’s Center for the Science of Social Connection, our lab studies social connectedness, why it is important and how to maximize its benefits. Our clinical and research experiences help us understand the side effects of social distancing and suggest strategies for addressing them. In times of stress and illness, being deprived of social connection can create more stress and illness. People who are lonely have higher levels of the hormone cortisol, an indicator of stress; show weaker immune responses to pathogens; and are at increased risk for premature death. Isolation can lead to depression, suicidal thoughts and other clinical conditions. © 2010–2020, The Conversation US, Inc.

Keyword: Stress
Link ID: 27127 - Posted: 03.17.2020

By Maria Temming When it comes to identifying scents, a “neuromorphic” artificial intelligence beats other AI by more than a nose. The new AI learns to recognize smells more efficiently and reliably than other algorithms. And unlike other AI, this system can keep learning new aromas without forgetting others, researchers report online March 16 in Nature Machine Intelligence. The key to the program’s success is its neuromorphic structure, which resembles the neural circuitry in mammalian brains more than other AI designs. This kind of algorithm, which excels at detecting faint signals amidst background noise and continually learning on the job, could someday be used for air quality monitoring, toxic waste detection or medical diagnoses. The new AI is an artificial neural network, composed of many computing elements that mimic nerve cells to process scent information (SN: 5/2/19). The AI “sniffs” by taking in electrical voltage readouts from chemical sensors in a wind tunnel that were exposed to plumes of different scents, such as methane or ammonia. When the AI whiffs a new smell, that triggers a cascade of electrical activity among its nerve cells, or neurons, which the system remembers and can recognize in the future. Like the olfactory system in the mammal brain, some of the AI’s neurons are designed to react to chemical sensor inputs by emitting differently timed pulses. Other neurons learn to recognize patterns in those blips that make up the odor’s electrical signature. © Society for Science & the Public 2000–2020

Keyword: Chemical Senses (Smell & Taste); Robotics
Link ID: 27126 - Posted: 03.17.2020