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By Veronique Greenwood Human beings maintain the polite fiction that we’re not constantly smelling one another. Despite our efforts to the contrary, we all have our own odors, pleasant and less so, and if we are like other land mammals, our particular perfume might mean something to our fellow humans. Some of these, like the reek of someone who hasn’t bathed all month, or the distinctive whiff of a toddler who is pretending they didn’t just fill their diaper, are self-explanatory. But scientists who study human olfaction, or your sense of smell, wonder if the molecules wafting off our skin may be registering at some subconscious level in the noses and brains of people around us. Are they bearing messages that we use in decisions without realizing it? Might they even be shaping whom we do and don’t like to spend time around? Indeed, in a small study published Wednesday in the journal Science Advances, researchers investigating pairs of friends whose friendship “clicked” from the beginning found intriguing evidence that each person’s body odor was closer to their friend’s than expected by chance. And when the researchers got pairs of strangers to play a game together, their body odors predicted whether they felt they had a good connection. There are many factors that shape whom people become friends with, including how, when or where we meet a new person. But perhaps one thing we pick up on, the researchers suggest, is how they smell. Scientists who study friendship have found that friends have more in common than strangers — not just things like age and hobbies, but also genetics, patterns of brain activity and appearance. Inbal Ravreby, a graduate student in the lab of Noam Sobel, an olfaction researcher at the Weizmann Institute of Science in Israel, was curious whether particularly swift friendships, the kind that seem to form in an instant, had an olfactory component — whether people might be picking up on similarities in their smells. © 2022 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 28382 - Posted: 06.25.2022

By Lisa L. Lewis To any observers, the electrodes were the most visible sign that the Stanford Summer Sleep Camp was a bit out of the ordinary. Joe Oliveira, one of the original campers, recalls that right after check-in, four electrodes were glued to his hair, two taped next to his eyes, and several more by his chin. The electrodes remained in place the whole time. Long cords came out of them that were, “very small, like an iPhone charger,” he told me. During the day, the cords were often tied back and taped together into a compact bundle at the back of his head. The “trodes” (as the campers were called because of their electrode ponytails) attracted their fair share of weird looks on their outings around the university campus. And there was something else peculiar: Like clockwork, every two hours, they all returned to the dorm for “nap tests,” according to Mary Carskadon, who was pursuing her doctorate in neuro- and biobehavioral sciences at Stanford University. In their darkened dorm rooms, all the campers — a mix of kids and teens — would lie quietly for 20 minutes and attempt to fall asleep. Meanwhile, technicians in a nearby control room monitored their brainwaves, eye movements, and chin-muscle activity being transmitted from their electrodes via the cords, which had been plugged into a box near the headboard that had cables linked to a polysomnograph machine in the other room. There, a continuous paper trail issued forth mapping the campers’ data. When the time was up, the campers were roused and unplugged. The counselors recorded their vital signs, then plugged their wires into a second box closer to the dorm room desk and ran the campers through a short series of tests to measure their recall, attention span, and other aspects of alertness and cognitive functioning. Tom Harvey, who worked as a counselor/technician at the camp for several years, recalled a mix of “math tests and memory tests and ‘can you suffer through boredom’ tests.”

Keyword: Sleep; Development of the Brain
Link ID: 28381 - Posted: 06.25.2022

By Oliver Whang The sleep debt collectors are coming. They want you to know that there is no such thing as forgiveness, only a shifting expectation of how and when you’re going to pay them back. You think of them as you lie in bed at night. How much will they ask for? Are you solvent? You fall asleep, then wake up in a cold sweat an hour later. You fall asleep, then wake up, drifting in and out of consciousness until morning. As most every human has discovered, a couple nights of bad sleep is often followed by grogginess, difficulty concentrating, irritability, mood swings and sleepiness. For years, it was thought that these effects, accompanied by cognitive impairments like lousy performances on short-term memory tests, could be primarily attributed to a chemical called adenosine, a neurotransmitter that inhibits electrical impulses in the brain. Spikes of adenosine had been consistently observed in sleep-deprived rats and humans. Adenosine levels can be quickly righted after a few nights of good sleep, however. This gave rise to a scientific consensus that sleep debt could be forgiven with a couple of quality snoozes — as reflected in casual statements like “I’ll catch up on sleep” or “I’ll be more awake tomorrow.” But a review article published recently in the journal Trends in Neurosciences contends that the folk concept of sleep as something that can be saved up and paid off is bunk. The review, which canvassed the last couple of decades of research on long term neural effects of sleep deprivation in both animals and humans, points to mounting evidence that getting too little sleep most likely leads to long-lasting brain damage and increased risk of neurodegenerative disorders like Alzheimer’s disease. © 2022 The New York Times Company

Keyword: Sleep
Link ID: 28380 - Posted: 06.25.2022

Killian Fox Born in Aldershot in 1959, Russell Foster is a professor of circadian neuroscience at Oxford and the director of the Nuffield Laboratory of Ophthalmology. For his discovery of non-rod, non-cone ocular photoreceptors he received numerous awards including the Zoological Society scientific medal. His latest book – the first he has written without a co-author – is Life Time: The New Science of the Body Clock, and How It Can Revolutionize Your Sleep and Health. What is circadian neuroscience? It’s the fundamental understanding of how our biology ticks on a 24-hour basis. But also it’s bigger than that – it’s an understanding of how different structures interact within the brain and how different genes and their protein products generate a complex behaviour. And that is then embedded throughout our entire biology. Is it an exciting field? What’s happened over the past 25 years has been a move into understanding how these internal 24-hour oscillations are generated and I think it’s one of the amazing success stories in biomedicine. One of the great aims of neuroscience is identifying different bits of the brain with different functions and here we’ve got one: the suprachiasmatic nucleus (SCN), with 50,000 cells, is the master circadian pacemaker. If you don’t have that, then all of our 24-hour rhythms just disappear. How did you first get interested in circadian research? It was largely through photoreceptors. During my second year as an undergraduate – I did zoology at Bristol – I was reading the extraordinary The Life of Vertebrates by JZ Young and I came across a bit about lampreys. They have a parietal third eye, which mammals don’t have; we only have ocular photoreceptors, whereas fish, reptiles, birds, all have multiple photoreceptors. And I just thought: wow, this is so cool. For my PhD, I was trying to understand how light is detected and measured to regulate the seasonal biology of birds. Then I started to address what seemed a simple question: how are the clocks of mammals regulated? We don’t have weird photoreceptors, we have visual cells that grab light in a fraction of a second and then forget it. So how can that light sensory system also be used to gather light information over long periods of time – dawn-dusk detectors? Way back in the early 1990s, we suggested that there was [an undiscovered photoreceptor] in the eye and there was a huge outcry. © 2022 Guardian News & Media Limited

Keyword: Biological Rhythms; Sleep
Link ID: 28379 - Posted: 06.25.2022

By Rachel Yehuda Rachel Yehuda is a professor of psychiatry and neuroscience and director of the Center for Psychedelic Psychotherapy and Trauma Research at the Icahn School of Medicine at Mount Sinai. She is also director of mental health at the James J. Peters Veterans Affairs Medical Center. Credit: Nick Higgins After the twin towers of the World Trade Center collapsed on September 11, 2001, in a haze of horror and smoke, clinicians at the Icahn School of Medicine at Mount Sinai in Manhattan offered to check anyone who'd been in the area for exposure to toxins. Among those who came in for evaluation were 187 pregnant women. Many were in shock, and a colleague asked if I could help diagnose and monitor them. They were at risk of developing post-traumatic stress disorder, or PTSD—experiencing flashbacks, nightmares, emotional numbness or other psychiatric symptoms for years afterward. And were the fetuses at risk? My trauma research team quickly trained health professionals to evaluate and, if needed, treat the women. We monitored them through their pregnancies and beyond. When the babies were born, they were smaller than usual—the first sign that the trauma of the World Trade Center attack had reached the womb. Nine months later we examined 38 women and their infants when they came in for a wellness visit. Psychological evaluations revealed that many of the mothers had developed PTSD. And those with PTSD had unusually low levels of the stress-related hormone cortisol, a feature that researchers were coming to associate with the disorder. Surprisingly and disturbingly, the saliva of the nine-month-old babies of the women with PTSD also showed low cortisol. The effect was most prominent in babies whose mothers had been in their third trimester on that fateful day. Just a year earlier a team I led had reported low cortisol levels in adult children of Holocaust survivors, but we'd assumed that it had something to do with being raised by parents who were suffering from the long-term emotional consequences of severe trauma. Now it looked like trauma leaves a trace in offspring even before they are born. © 2022 Scientific American

Keyword: Epigenetics; Stress
Link ID: 28378 - Posted: 06.25.2022

By Christina Jewett and Andrew Jacobs The Food and Drug Administration is planning to require tobacco companies to slash the amount of nicotine in traditional cigarettes to make them less addictive and reduce the toll of smoking that claims 480,000 lives each year. The proposal, which could take years to go into effect, would put the United States at the forefront of global antismoking efforts. Only one other nation, New Zealand, has advanced such a plan. The headwinds are fierce. Tobacco companies have already indicated that any plan with significant reductions in nicotine would violate the law. And some conservative lawmakers might consider such a policy another example of government overreach, ammunition that could spill over into the midterm elections. Few specifics were released on Tuesday, but according to a notice published on a U.S. government website, a proposed rule would be issued in May 2023 seeking public comment on establishing a maximum nicotine level in cigarettes and other products. “Because tobacco-related harms primarily result from addiction to products that repeatedly expose users to toxins, F.D.A. would take this action to reduce addictiveness to certain tobacco products, thus giving addicted users a greater ability to quit,” the notice said. The F.D.A. declined to provide further details. But in a statement posted on its website, Dr. Robert M. Califf, the agency’s commissioner, said: “Lowering nicotine levels to minimally addictive or non-addictive levels would decrease the likelihood that future generations of young people become addicted to cigarettes and help more currently addicted smokers to quit.” “This one rule could have the greatest impact on public health in the history of public health,” said Mitch Zeller, the recently retired F.D.A. tobacco center director. “That’s the scope and the magnitude we’re talking about here because tobacco use remains the leading cause of preventable disease and death.” © 2022 The New York Times Company

Keyword: Drug Abuse
Link ID: 28377 - Posted: 06.25.2022

Allison Whitten When our phones and computers run out of power, their glowing screens go dark and they die a sort of digital death. But switch them to low-power mode to conserve energy, and they cut expendable operations to keep basic processes humming along until their batteries can be recharged. Our energy-intensive brain needs to keep its lights on too. Brain cells depend primarily on steady deliveries of the sugar glucose, which they convert to adenosine triphosphate (ATP) to fuel their information processing. When we’re a little hungry, our brain usually doesn’t change its energy consumption much. But given that humans and other animals have historically faced the threat of long periods of starvation, sometimes seasonally, scientists have wondered whether brains might have their own kind of low-power mode for emergencies. Now, in a paper published in Neuron in January, neuroscientists in Nathalie Rochefort’s lab at the University of Edinburgh have revealed an energy-saving strategy in the visual systems of mice. They found that when mice were deprived of sufficient food for weeks at a time — long enough for them to lose 15%-20% of their typical healthy weight — neurons in the visual cortex reduced the amount of ATP used at their synapses by a sizable 29%. But the new mode of processing came with a cost to perception: It impaired how the mice saw details of the world. Because the neurons in low-power mode processed visual signals less precisely, the food-restricted mice performed worse on a challenging visual task. “What you’re getting in this low-power mode is more of a low-resolution image of the world,” said Zahid Padamsey, the first author of the new study. All Rights Reserved © 2022

Keyword: Vision
Link ID: 28376 - Posted: 06.15.2022

By Emily Bazelon Scott Leibowitz is a pioneer in the field of transgender health care. He has directed or worked at three gender clinics on the East Coast and the Midwest, where he provides gender-affirming care, the approach the medical community has largely adopted for embracing children and teenagers who come out as transgender. He also helps shape policy on L.G.B.T. issues for the American Academy of Child and Adolescent Psychiatry. As a child and adolescent psychiatrist who is gay, he found it felt natural to work under the L.G.B.T. “umbrella,” as he put it, aware of the overlap as well as the differences between gay and trans identity. It was for all these reasons that Leibowitz was selected, in 2017, to be a leader of a working group of seven clinicians and researchers drafting a chapter on adolescents for a new version of guidelines called the Standards of Care to be issued by the World Professional Association for Transgender Health (WPATH). The guidelines are meant to set a gold standard for the field of transgender health care, and this would be the first update since 2012. What Leibowitz and his co-authors didn’t foresee, when they began, was that their work would be engulfed by two intersecting forces: a significant rise in the number of teenagers openly identifying as transgender and seeking gender care, and a right-wing backlash in the United States against allowing them to medically transition, including state-by-state efforts to ban it. During the last decade, the field of transgender care for youth has greatly shifted. A decade ago, there were a handful of pediatric gender clinics in the United States and a dozen or so more in other countries. The few doctors and therapists who worked in them knew one another, and the big debate was whether kids in preschool or elementary school should be allowed to live fully as the gender they identified as when they strongly and consistently asserted their wishes. Now there are more than 60 comprehensive gender clinics in the United States, along with countless therapists and doctors in private practice who are also seeing young patients with gender-identity issues. The number of young people who identify as transgender nationally is about 300,000, according to a new report by the Williams Institute, a research center at U.C.L.A.’s law school, which is much higher than previous estimates. In countries that collect national data, like the Netherlands and Britain, the number of 13-to-17-year-olds seeking treatment for gender-identity issues has also increased, from dozens to hundreds or thousands a year. © 2022 The New York Times Company

Keyword: Sexual Behavior; Development of the Brain
Link ID: 28375 - Posted: 06.15.2022

Michael Marshall Researchers are finally making headway in understanding how the SARS-CoV-2 coronavirus causes loss of smell. And a multitude of potential treatments to tackle the condition are undergoing clinical trials, including steroids and blood plasma. Once a tell-tale sign of COVID-19, smell disruption is becoming less common as the virus evolves. “Our inboxes are not as flooded as they used to be,” says Valentina Parma, a psychologist at the Monell Chemical Senses Center in Philadelphia, Pennsylvania, who helped field desperate inquiries from patients throughout the first two years of the pandemic. A study published last month1 surveyed 616,318 people in the United States who have had COVID-19. It found that, compared with those who had been infected with the original virus, people who had contracted the Alpha variant — the first variant of concern to arise — were 50% as likely to have chemosensory disruption. This probability fell to 44% for the later Delta variant, and to 17% for the latest variant, Omicron. But the news is not all good: a significant portion of people infected early in the pandemic still experience chemosensory effects. A 2021 study2 followed 100 people who had had mild cases of COVID-19 and 100 people who repeatedly tested negative. More than a year after their infections, 46% of those who had had COVID-19 still had smell problems; by contrast, just 10% of the control group had developed some smell loss, but for other reasons. Furthermore, 7% of those who had been infected still had total smell loss, or ‘anosmia’, at the end of the year. Given that more than 500 million cases of COVID-19 have been confirmed worldwide, tens of millions of people probably have lingering smell problems. For these people, help can’t come soon enough. Simple activities such as tasting food or smelling flowers are now “really emotionally distressing”, Parma says. © 2022 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28374 - Posted: 06.15.2022

By Oliver Whang Cats, so often, are a mystery, even to those that know them best. Why do they sleep so much? Why do they want your full attention one minute, none the next? How can they find their way back home after being stranded miles away for years? The writer Haruki Murakami, who is known for putting cats in his novels and essays, once confessed to not knowing why he does so; a cat “sort of naturally slips in,” he said. Another mystery: Why do cats love catnip? When exposed to the plant, which belongs to the mint family, the majority of domestic cats will lick it, rub against it, chew it and roll around in it. They brim with euphoria, getting high off the stuff. They also go wild for other plants, particularly silver vine, which is not closely related to catnip but elicits the same response from felines, including big cats like jaguars and tigers. For years, this behavior was just another cat-related enigma. But a new study, published Tuesday in the journal iScience, suggests that the reaction to catnip and silver vine might be explained by the bug repellent effect of iridoids, the chemicals in the plants that induce the high. Researchers, led by Masao Miyazaki, an animal behavior scientist at Iwate University in Japan, found that the amount of these iridoids released by the plant increased by more than 2,000 percent when the plant was damaged by cats. So perhaps kitty’s high confers an evolutionary advantage: keeping bloodsucking insects at bay. Kristyn Vitale, a cat behavior expert at Unity College who was not associated with the research, noted that the study built on strong previous work. Last year, the same lab published a study that found that cats would try their best to coat themselves in DEET-like iridoids, whether by rolling on the chemicals or by rising up to nuzzle them with their cheeks. “This indicates there may be a benefit to the cat physically placing the compounds on their body,” Dr. Vitale said. © 2022 The New York Times Company

Keyword: Drug Abuse
Link ID: 28373 - Posted: 06.15.2022

By Erika Engelhaupt To Charles Darwin, nature had a certain order. And in that order, males always came out on top. They were the leaders, the innovators, the wooers and the doers. “The males of almost all animals have stronger passions than the females,” Darwin wrote in 1871. “The female, on the other hand, with the rarest of exceptions, is less eager.” The founder of evolutionary theory posited that throughout the animal kingdom, males are active, females are passive, and that’s pretty much that. Females, in sum, are boring. That’s poppycock, Lucy Cooke writes in her latest book, Bitch. This blinkered view of nature as a man’s world was conceived and promulgated by Victorian men who imposed their values and world view on animals, she says. Cooke, a documentary filmmaker and the author of The Truth About Animals and two children’s books (SN: 4/14/18, p. 26), has traveled the world and met scientists who are exposing the truth about the sexes. She takes readers on a wild ride as she observes the ridiculous mating rituals of sage grouse, searches for orca poop (to monitor sex hormones) and watches female lemurs boss around males. Through such adventures, Cooke learns that females are anything but boring. “Female animals are just as promiscuous, competitive, aggressive, dominant and dynamic as males,” she writes. That may not sound radical to today’s feminists, but in the field of evolutionary biology, such a pronouncement has long bordered on the heretical. Generations of biologists have focused on male behavior and physiology, on the assumption that females are little more than baby-making machines to be won over by the strongest, showiest males. © Society for Science & the Public 2000–2022.

Keyword: Sexual Behavior; Evolution
Link ID: 28372 - Posted: 06.15.2022

By Benjamin Mueller Taking a scan of an injured brain often produces a map of irretrievable losses, revealing spots where damage causes memory difficulties or tremors. But in rare cases, those scans can expose just the opposite: plots of brain regions where an injury miraculously relieves someone’s symptoms, offering clues about how doctors might accomplish the same. A team of researchers has now taken a fresh look at a set of such brain images, drawn from cigarette smokers addicted to nicotine in whom strokes or other injuries spontaneously helped them quit. The results, the scientists said, showed a network of interconnected brain regions that they believe underpins addiction-related disorders affecting potentially tens of millions of Americans. The study, published in the scientific journal Nature Medicine on Monday, supports an idea that has recently gained traction: that addiction lives not in one brain region or another, but rather in a circuit of regions linked by threadlike nerve fibers. The results may provide a clearer set of targets for addiction treatments that deliver electrical pulses to the brain, new techniques that have shown promise in helping people quit smoking. “One of the biggest problems in addiction is that we don’t really know where in the brain the main problem lies that we should target with treatment,” said Dr. Juho Joutsa, one of the study’s lead authors and a neurologist at the University of Turku in Finland. “We are hoping that after this, we have a very good idea of those regions and networks.” Research over the last two decades has solidified the idea that addiction is a disease of the brain. But many people still believe that addiction is voluntary. © 2022 The New York Times Company

Keyword: Drug Abuse; Stroke
Link ID: 28371 - Posted: 06.14.2022

By John Horgan Have you ever been gripped by the suspicion that nothing is real? A student at Stevens Institute of Technology, where I teach, has endured feelings of unreality since childhood. She recently made a film about this syndrome for her senior thesis, for which she interviewed herself and others, including me. “It feels like there’s a glass wall between me and everything else in the world,” Camille says in her film, which she calls Depersonalized; Derealized; Deconstructed Derealization and depersonalization refer to feelings that the external world and your own self, respectively, are unreal. Lumping the terms together, psychiatrists define depersonalization/derealization disorder as “persistent or recurrent … experiences of unreality, detachment, or being an outside observer with respect to one’s thoughts, feelings, sensations, body, or actions,” according to the Diagnostic and Statistical Manual of Mental Disorders. For simplicity, I’ll refer to both syndromes as derealization. Some people experience derealization out of the blue, others only under stressful circumstances—for example, while taking a test or interviewing for a job. Psychiatrists prescribe psychotherapy and medication, such as antidepressants, when the syndrome results in “distress or impairment in social, occupational, or other important areas of functioning.” In some cases, derealization results from serious mental illness, such as schizophrenia, or hallucinogens such as LSD. Extreme cases, usually associated with brain damage, may manifest as Cotard delusion, also called walking corpse syndrome, the belief that you are dead; and Capgras delusion, the conviction that people around you have been replaced by imposters. © 2022 Scientific American,

Keyword: Consciousness; Attention
Link ID: 28370 - Posted: 06.14.2022

By Pam Belluck An experimental therapy for A.L.S., the paralyzing and fatal neurological disorder, has been approved in Canada, adding a new treatment option for a disease for which there are few effective therapies. The approval, the first in the world for the treatment — AMX0035, to be marketed in Canada as Albrioza — comes with the condition that the drug company later provide better evidence that the treatment works. It is likely to be of major interest to patients with A.L.S. (amyotrophic lateral sclerosis) in the United States, where the same therapy is being evaluated by the Food and Drug Administration, which has raised questions about the treatment’s effectiveness. An F.D.A. review earlier this year found the treatment to be safe, but said there was not enough evidence that it was effective either in helping patients live longer or slowing the rate at which they lose functions like muscle control, speaking or breathing without assistance. A committee of independent advisers to the F.D.A. voted by a narrow margin in March that the therapy was not ready for approval. The F.D.A. had been scheduled to issue a final decision this month, but recently extended the deadline to Sept. 29, saying it needed more time to review additional analyses of data submitted by the company. In the meantime, Calaneet Balas, president and chief executive of the A.L.S. Association, one of several patient advocacy organizations pressing for F.D.A. approval, said, “We expect that Americans living with A.L.S. will try to access Albrioza in Canada, just as we have heard reports of people trying to buy the ingredients on Amazon.” © 2022 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28369 - Posted: 06.14.2022

Sofia Quaglia When they are in the deep, dark ocean, seals use their whiskers to track down their prey, a study has confirmed after observing the sea mammals in their natural habitat. It’s hard for light to penetrate the gloom of the ocean’s depths, and animals have come up with a variety of adaptations in order to live and hunt there. Whales and dolphins, for example, use echolocation – the art of sending out clicky noises into the water and listening to their echo as they bounce off possible prey, to locate them. But deep-diving seals who don’t have those same acoustic projectors must have evolutionarily learned to deploy another sensory technique. Scientists have long hypothesised that the secret weapons are their long, cat-like whiskers, conducting over 20 years of experiments with artificial whiskers or captive seals blindfolded in a pool, given the difficulties of directly observing the hunters in the tenebrous depths of the ocean. Now a study may have confirmed the hypothesis, according to Taiki Adachi, assistant project scientist of University of California, Santa Cruz, and one of the lead authors of the study published in Proceedings of the National Academy of Science. Adachi and his team positioned small video cameras with infrared night-vision on the left cheek, lower jaw, back and head of five free-ranging northern elephant seals, the Mirounga angustirostris, in Año Nuevo state park in California. They recorded a total of approximately nine and a half hours of deep sea footage during their seasonal migration. By analysing the videos the scientists noted that diving seals held back their whiskers for the initial part of their dives and, and once they reached a depth suitable for foraging, they rhythmically whisked their whiskers back and forth, hoping to sense any vibration caused by the slightest water movements of swimming prey. © 2022 Guardian News & Media Limited o

Keyword: Pain & Touch
Link ID: 28368 - Posted: 06.14.2022

Philip Ball How do you spot an optimistic pig? This isn’t the setup for a punchline; the question is genuine, and in the answer lies much that is revealing about our attitudes to other minds – to minds, that is, that are not human. If the notion of an optimistic (or for that matter a pessimistic) pig sounds vaguely comical, it is because we scarcely know how to think about other minds except in relation to our own. Here is how you spot an optimistic pig: you train the pig to associate a particular sound – a note played on a glockenspiel, say – with a treat, such as an apple. When the note sounds, an apple falls through a hatch so the pig can eat it. But another sound – a dog-clicker, say – signals nothing so nice. If the pig approaches the hatch on hearing the clicker, all it gets is a plastic bag rustled in its face. What happens now if the pig hears neither of these sounds, but instead a squeak from a dog toy? An optimistic pig might think there’s a chance that this, too, signals delivery of an apple. A pessimistic pig figures it will just get the plastic bag treatment. But what makes a pig optimistic? In 2010, researchers at Newcastle University showed that pigs reared in a pleasant, stimulating environment, with room to roam, plenty of straw, and “pig toys” to explore, show the optimistic response to the squeak significantly more often than pigs raised in a small, bleak, boring enclosure. In other words, if you want an optimistic pig, you must treat it not as pork but as a being with a mind, deserving the resources for a cognitively rich life. We don’t, and probably never can, know what it feels like to be an optimistic pig. Objectively, there’s no reason to suppose that it feels like anything: that there is “something it is like” to be a pig, whether apparently happy or gloomy. Until rather recently, philosophers and scientists have been reluctant to grant a mind to any nonhuman entity. Feelings and emotions, hope and pain and a sense of self were deemed attributes that separated us from the rest of the living world. To René Descartes in the 17th century, and to behavioural psychologist BF Skinner in the 1950s, other animals were stimulus-response mechanisms that could be trained but lacked an inner life. To grant animals “minds” in any meaningful sense was to indulge a crude anthropomorphism that had no place in science. © 2022 Guardian News & Media Limited

Keyword: Evolution; Intelligence
Link ID: 28367 - Posted: 06.11.2022

William E. Pelham, Jr. For decades, many physicians, parents and teachers have believed that stimulant medications help children with ADHD learn because they are able to focus and behave better when medicated. After all, an estimated 6.1 million children in the U.S. are diagnosed with attention-deficit/hyperactivity disorder, and more than 90% are prescribed stimulant medication as the main form of treatment in school settings. However, in a peer-reviewed study that several colleagues and I published in the Journal of Consulting and Clinical Psychology, we found medication has no detectable effect on how much children with ADHD learn in the classroom. At least that’s the case when learning – defined as the acquisition of performable skills or knowledge through instruction – is measured in terms of tests meant to assess improvements in a student’s current academic knowledge or skills over time. Compared to their peers, children with ADHD exhibit more off-task, disruptive classroom behavior, earn lower grades and score lower on tests. They are more likely to receive special education services and be retained for a grade, and less likely to finish high school and enter college – two educational milestones that are associated with significant increases in earnings. In this study, funded by the National Institute of Mental Health, we evaluated 173 children between the ages of 7 and 12. They were all participants in our Summer Treatment Program, a comprehensive eight-week summer camp for children with ADHD and related behavioral, emotional and learning challenges. Children got grade-level instruction in vocabulary, science and social studies. The classes were led by certified teachers. The children received medication the first half of summer and a placebo during the other half. They were tested at the start of each academic instruction block, which lasted approximately three weeks. They then took the same test at the end to determine how much they learned. © 2010–2022, The Conversation US, Inc.

Keyword: ADHD; Learning & Memory
Link ID: 28366 - Posted: 06.11.2022

By Maria Temming The Terminator may be one step closer to reality. Researchers at the University of Tokyo have built a robotic finger that, much like Arnold Schwarzenegger’s titular cyborg assassin, is covered in living human skin. The goal is to someday build robots that look like real people — albeit for more altruistic applications. Super realistic-looking robots could more seamlessly interact with humans in medical care and service industries, say biohybrid engineer Shoji Takeuchi and his colleagues June 9 in Matter. (Whether cyborgs masked in living tissue would be more congenial or creepy is probably in the eye of the beholder.) To cover the finger in skin, Takeuchi and colleagues submerged the robotic digit in a blend of collagen and human skin cells called dermal fibroblasts. The mixture settled into a base layer of skin, or dermis, covering the finger. The team then poured a liquid containing human keratinocyte cells onto the finger, which formed an outer skin layer, or epidermis. After two weeks, skin covering the finger measured a few millimeters thick — comparable to the thickness of human skin. The lab-made skin was strong and stretchy enough to withstand the robotic finger bending. It could also heal itself: When researchers made a small cut on the robotic finger and covered it with a collagen bandage, the skin’s fibroblast cells merged the bandage with the rest of the skin within a week. Researchers at the University of Tokyo covered this robotic finger in living human skin to pave the way for ultrarealistic cyborgs. “This is very interesting work and an important step forward in the field,” says Ritu Raman, an MIT engineer who also builds machines with living components. “Biological materials are appealing because they can dynamically sense and adapt to their environments.” For instance, she’d like to see a future version of the living robot skin embedded with nerve cells to make robots more aware of their surroundings. © Society for Science & the Public 2000–2022.

Keyword: Pain & Touch; Robotics
Link ID: 28365 - Posted: 06.11.2022

Researchers from the National Eye Institute (NEI) have identified a new disease that affects the macula, a small part of the light-sensing retina needed for sharp, central vision. Scientists report their findings on the novel macular dystrophy, which is yet to be named, in JAMA Ophthalmology. NEI is part of the National Institutes of Health. Macular dystrophies are disorders that usually cause central visual loss because of mutations in several genes, including ABCA4, BEST1, PRPH2, and TIMP3. For example, patients with Sorsby Fundus Dystrophy, a genetic eye disease specifically linked to TIMP3 variants, usually develop symptoms in adulthood. They often have sudden changes in visual acuity due to choroidal neovascularization– new, abnormal blood vessels that grow under the retina, leaking fluid and affecting vision. TIMP3 is a protein that helps regulate retinal blood flow and is secreted from the retinal pigment epithelium (RPE), a layer of tissue that nourishes and supports the retina’s light-sensing photoreceptors. All TIMP3 gene mutations reported are in the mature protein after it has been “cut” from RPE cells in a process called cleavage. “We found it surprising that two patients had TIMP3 variants not in the mature protein, but in the short signal sequence the gene uses to ‘cut’ the protein from the cells. We showed these variants prevent cleavage, causing the protein to be stuck in the cell, likely leading to retinal pigment epithelium toxicity,” said Bin Guan, Ph.D., lead author. The research team followed these findings with clinical evaluations and genetic testing of family members to verify that the two new TIMP3 variants are connected to this atypical maculopathy.

Keyword: Vision
Link ID: 28364 - Posted: 06.11.2022

by Charles Q. Choi The primordial cells that give rise to most other brain cells do not proliferate in a typical way in autistic people — and that could explain how common traits emerge from a range of genetic origins, according to a new study. The idea that autism disrupts the proliferation of neural precursor cells isn’t new, but until now, few studies had investigated how that difference arises. In the new study, scientists fashioned neural precursor cells out of cord blood cells from five autistic boys ages 4 to 14 and, to serve as controls, either their non-autistic brothers or unrelated non-autistic people. Three of the autistic children have idiopathic cases, in which there is no known genetic cause for their autism; the other two have deletions in 16p11.2, a chromosomal region linked to autism and other neuropsychiatric conditions. Three of the autistic children have macrocephaly, or a large head. Neural precursors from the autistic boys all proliferated in atypical ways, the scientists found. Among children with macrocephaly, this growth was accelerated, leading to 28 to 55 percent more cells than in the non-autistic controls after six days. In contrast, cells from the other two boys, both with idiopathic autism, grew more slowly and more of those cells died, yielding 40 to 65 percent fewer cells than in controls after six days. “Despite the fact that these individuals are genetically distinct, especially the idiopathic individuals, it is amazing they have a common developmental process dysfunction — control of proliferation,” says study co-lead investigator Emanuel DiCicco-Bloom, professor of neuroscience, cell biology and pediatrics at Rutgers University in Piscataway, New Jersey. © 2022 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28363 - Posted: 06.11.2022