By Gretchen Reynolds Can exercise help us shed pounds? An interesting new study involving overweight men and women found that working out can help us lose weight, in part by remodeling appetite hormones. But to benefit, the study suggests, we most likely have to exercise a lot — burning at least 3,000 calories a week. In the study, that meant working out six days a week for up to an hour, or around 300 minutes a week. The relationship between working out and our waistlines is famously snarled. The process seems as if it should straightforward: We exercise, expend calories and, if life and metabolisms were just, develop an energy deficit. At that point, we would start to use stored fat to fuel our bodies’ continuing operations, leaving us leaner. But our bodies are not always cooperative. Primed by evolution to maintain energy stores in case of famine, our bodies tend to undermine our attempts to drop pounds. Start working out and your appetite rises, so you consume more calories, compensating for those lost. The upshot, according to many past studies of exercise and weight loss, is that most people who start a new exercise program without also strictly monitoring what they eat do not lose as much weight as they expect — and some pack on pounds. But Kyle Flack, an assistant professor of nutrition at the University of Kentucky, began to wonder a few years ago if this outcome was inevitable. Maybe, he speculated, there was a ceiling to people’s caloric compensations after exercise, meaning that if they upped their exercise hours, they would compensate for fewer of the lost calories and lose weight. © 2020 The New York Times Company

Keyword: Obesity
Link ID: 27617 - Posted: 12.09.2020

by Laura Dattaro In 1983, psychologist Christopher Gillberg posed a provocative question to the readers of the British Journal of Psychiatry: Could autism and anorexia nervosa share underlying causes? Gillberg’s curiosity came in part from his observations of three autistic boys whose female cousins all had the eating disorder, which is characterized by food restrictions, low body weight, an intense fear of gaining weight and a distorted body image. Gillberg, professor of child and adolescent psychiatry at the University of Gothenburg in Sweden, initially suggested that anorexia is the ‘female form of autism.’ Although that idea wasn’t entirely accurate, his suspicions that eating disorders and autism are linked have borne out: People with anorexia are more likely to be autistic than those without it, studies show. There are fewer data demonstrating that autistic people are at particularly high risk for eating disorders, but experts say it’s likely. How often do anorexia and autism overlap? Estimates vary, though most researchers agree that roughly 20 percent of people with anorexia are autistic. Both conditions are rare — about 1 percent of people are autistic and 0.3 percent have anorexia — and most research so far has examined the prevalence of autism in people with anorexia, not the reverse. Among 60 women receiving treatment for an eating disorder at a clinic in the United Kingdom, for example, 14 of them, or 23 percent, scored above the diagnostic cutoff on a test called the Autism Diagnostic Observation Schedule (ADOS). Similarly, about one-third of people with anorexia have been diagnosed with autism, according to a long-running study that has followed 51 people with anorexia and 51 controls in Sweden since the 1980s. © 2020 Simons Foundation

Keyword: Autism; Anorexia & Bulimia
Link ID: 27616 - Posted: 12.09.2020

Sarah Sloat Patience, you might have heard, is a virtue. That’s why so many Puritans named their daughters “Patience” in the 1600s. It is the ability to wait calmly in the face of frustration or adversity. Like Penelope weaving while waiting for Odysseus, patient people wait for their partners to finish a Netflix show they’re binging. Impatient people do not. But despite the societal framing of patience as a measurement of character, in its purest sense, patience is a chemically induced output of the brain. However, exactly what goes on in the brain that leads to patience isn’t well understood. A new study involving mice takes a step toward understanding patience by pointing to the role of serotonin, and how it interacts with different brain structures. Serotonin is a chemical and a neurotransmitter, meaning it sends messages throughout the brain. It influences many behaviors, including mood and sleep. In a paper recently released in the journal Science Advances, scientists argue that serotonin influences specific areas of the brain to promote patient behavior. But critically, this process only occurs if there’s already “high expectation or confidence” that being patient will lead to future rewards. First author Katsuhiko Miyazaki is a scientist at the Okinawa Institute of Science and Technology in Japan who researches the relationship between serotonergic neural activity and animal behavior. He tells me this study originated from an interest in revealing how projections of serotonin promote waiting for future rewards.

Keyword: Attention; Learning & Memory
Link ID: 27615 - Posted: 12.09.2020

Alison Abbott In October 2013, I attended the launch of the Human Brain Project in Lausanne, Switzerland, as correspondent for Nature. I hoped to leave with a better understanding of the exact mission of the baffling billion-euro enterprise, but I was frustrated. Things became clear the following year, when the project fell spectacularly, and very publicly, apart. Noah Hutton’s documentary In Silico captures a sense of what it was like behind the scenes of the project, which was supported with great fanfare by the European Commission. It had been hyped as a quantum leap in understanding how the human brain works. Instead, it left a trail of angry neuroscientists across Europe. Yet aspects of what went so expensively wrong still remain elusive. In Silico is more about the back story of the Human Brain Project (HBP). Hutton was 22 years old when he watched a 2009 talk by Henry Markram, the controversial figure who later became the first director of the HBP. Markham was speaking about the Blue Brain Project, a major initiative he had launched a few years before at one of Europe’s top universities, the Swiss Federal Institute of Technology in Lausanne, with generous funding from the Swiss government. He claimed that he would — with the help of a supercomputer related to the one that beat world chess champion Garry Kasparov in 1997 — simulate an entire rodent brain within a decade. He planned to build it from information about the brain’s tens of millions of individual neurons. © 2020 Springer Nature Limited

Keyword: Brain imaging
Link ID: 27614 - Posted: 12.09.2020

Carrie Arnold In her job as a physician at the Boston Medical Center in Massachusetts, Sondra Crosby treated some of the first people in her region to get COVID-19. So when she began feeling sick in April, Crosby wasn’t surprised to learn that she, too, had been infected. At first, her symptoms felt like those of a bad cold, but by the next day, she was too sick to get out of bed. She struggled to eat and depended on her husband to bring her sports drinks and fever-reducing medicine. Then she lost track of time completely. For five days, Crosby lay in a confused haze, unable to remember the simplest things, such as how to turn on her phone or what her address was. She began hallucinating, seeing lizards on her walls and smelling a repugnant reptilian odour. Only later did Crosby realize that she had had delirium, the formal medical term for her abrupt, severe disorientation. “I didn’t really start processing it until later when I started to come out of it,” she says. “I didn’t have the presence of mind to think that I was anything more than just sick and dehydrated.” Physicians treating people hospitalized with COVID-19 report that a large number experience delirium, and that the condition disproportionately affects older adults. An April 2020 study in Strasbourg, France, found that 65% of people who were severely ill with coronavirus had acute confusion — a symptom of delirium1. Data presented last month at the annual meeting of the American College of Chest Physicians by scientists at the Vanderbilt University Medical Center in Nashville, Tennessee, showed that 55% of the 2,000 people they tracked who were treated for COVID-19 in intensive-care units (ICUs) around the world had developed delirium. These numbers are much higher than doctors are used to: usually, about one-third of people who are critically ill develop delirium, according to a 2015 meta-analysis2 (see ‘How common is delirium?’). © 2020 Springer Nature Limited

Keyword: Alzheimers
Link ID: 27613 - Posted: 12.07.2020

By Jamie Talan After 20 years of marriage, after raising two kids, after building a farm in Kentucky and tending horses and dogs, Laura Prewitt knew this much about her husband: He was tenderhearted, fun-loving and never let stress land too long on his shoulders. But in 2014, old Ted somehow morphed into a new guy, one who is not so communicative. A guy who lost his social edge and seemed unable to read faces or feelings. Who is tired and withdrawn. “He’s just not the same guy,” she says. “I want him back.” At 59, the old Ted, the sensitive husband who cried during sad movies, is gone. A scan of Ted’s brain helps explain it: Discrete regions of the right temporal lobe that regulate emotion are getting smaller; the tissue is shrinking. Ted can still do some of the things he has done for decades. Until a few years ago, he was the president at a construction company. Lately, he’ll see someone he is supposed to know but forgets who they are. He sleeps a lot. And he can’t be left alone for too long or his wife may find him trying to eat a battery or a hammer. He’s agitated. He’s always putting things in his mouth. Ted Prewitt, who has behavioral variant frontotemporal dementia (bvFTD), is one of a growing number of people in midlife diagnosed with an atypical form of dementia. Unlike Alzheimer’s, which generally occurs in older people, these are rarer dementias — including bvFTD; another frontotemporal variant that leads to language disturbances called primary progressive aphasia; a visual and spatial dementia called posterior cortical atrophy; Lewy body dementia; and early-onset Alzheimer’s in people with no family history. These conditions show up in people in their 50s and 60s, sometimes even earlier and sometimes a bit later. No one knows whether these conditions are becoming more common or doctors are better at diagnosing them. © 1996-2020 The Washington Post

Keyword: Alzheimers
Link ID: 27612 - Posted: 12.07.2020

by Angie Voyles Askham Many people with mutations that disrupt a gene called NCKAP1 have autism or autism traits — along with speech and language problems, motor delays and learning difficulties — according to a new study. The results, from a large international team of researchers and clinicians, clarify how mutations in NCKAP1 affect people and solidify its position as a top autism gene. Sequencing studies over the past decade have turned up three autistic people with de novo, or non-inherited, variants that likely disrupt NCKAP1, putting it on a list of genes strongly tied to autism. Other work has shown that mice that do not express the gene have atypical brain development. But those reports contain little information about the outward characteristics of people with NCKAP1 mutations — which are challenging to study because variants in the gene are rare, says Hui Guo, associate professor of life sciences at Central South University in Changsha, China. In the new work, Guo teamed up with scientists and clinicians across the globe to identify and characterize 18 additional people with NCKAP1 mutations. “This study demonstrates that international cooperation among many institutions is becoming fundamental to advancing our understanding of rare variants,” says Abha Gupta, assistant professor of pediatrics at Yale University, who was not involved in the study. Painting a detailed picture of traits associated with NCKAP1 mutations can also improve a person’s chance of being diagnosed and provide guidance about expected outcomes, she says. Guo asked colleagues who collect genetic data for other research to sift through their records for people with NCKAP1 variants. He also used GeneMatcher, a site that connects researchers to clinicians interested in the same genetic variants. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27611 - Posted: 12.07.2020

Anil K Seth What is the best way to understand consciousness? In philosophy, centuries-old debates continue to rage over whether the Universe is divided, following René Descartes, into ‘mind stuff’ and ‘matter stuff’. But the rise of modern neuroscience has seen a more pragmatic approach gain ground: an approach that is guided by philosophy but doesn’t rely on philosophical research to provide the answers. Its key is to recognise that explaining why consciousness exists at all is not necessary in order to make progress in revealing its material basis – to start building explanatory bridges from the subjective and phenomenal to the objective and measurable. In my work at the Sackler Centre for Consciousness Science at the University of Sussex in Brighton, I collaborate with cognitive scientists, neuroscientists, psychiatrists, brain imagers, virtual reality wizards and mathematicians – and philosophers too – trying to do just this. And together with other laboratories, we are gaining exciting new insights into consciousness – insights that are making real differences in medicine, and that in turn raise new intellectual and ethical challenges. In my own research, a new picture is taking shape in which conscious experience is seen as deeply grounded in how brains and bodies work together to maintain physiological integrity – to stay alive. In this story, we are conscious ‘beast-machines’, and I hope to show you why. Let’s begin with David Chalmers’s influential distinction, inherited from Descartes, between the ‘easy problem’ and the ‘hard problem’. The ‘easy problem’ is to understand how the brain (and body) gives rise to perception, cognition, learning and behaviour. The ‘hard’ problem is to understand why and how any of this should be associated with consciousness at all: why aren’t we just robots, or philosophical zombies, without any inner universe? It’s tempting to think that solving the easy problem (whatever this might mean) would get us nowhere in solving the hard problem, leaving the brain basis of consciousness a total mystery. © Aeon Media Group Ltd. 2012-2020.

Keyword: Consciousness
Link ID: 27610 - Posted: 12.07.2020

By Sally Satel For over a half-century, steroid drugs have been a mainstay of medical care, widely used to treat inflammatory illness such as asthma, skin conditions and autoimmune diseases. Less is known about their dramatic and sometimes frightening long-term effects on mood, personality and thinking. I took steroids years ago, and the side effects changed my life. Steroid medications mimic a natural hormone in the body called glucocorticoid, which suppresses immune system processes that trigger inflammation, the sources of many autoimmune and chronic disease. In 1948, glucocorticoid was first used for a chronic inflammatory disease, rheumatoid arthritis, which causes joint deformity and chronic pain. Two years later, the American physician behind the breakthrough therapy was one of the winners of the Nobel Prize. Steroids have been prescribed for many other conditions since then. One steroid, dexamethasone, has been used for people with severe cases of covid-19 and President Trump was given it when he was hospitalized for the disease in October. My story starts in 1977. I was finishing my senior year as a biology major at Cornell University when I was diagnosed with Crohn’s disease, a form of inflammatory disease in which the body’s immune system attacks the gastrointestinal tract. I had a relatively mild case — transient pain, causing me to rush to the nearest ladies’ room, and find some blood in the bowl — and so I was able to finish my final year on time and begin a PhD program in evolutionary biology that summer. My predoctoral project entailed measuring the jaw muscles of tadpoles using jewelers’ tools and a dissecting microscope. Within weeks, though, I had a “flare” in the parlance of gastroenterology — I felt weak and was having increased bouts of blood-streaked diarrhea. In mid-October, I spent five days at the hospital where my symptoms resolved on a daily regimen of 60 mg of the potent steroid prednisone. I was discharged on 60 mg per day and felt fine for a week. But soon my brain began to feel like cotton wrapped in yards of gauze. I tried to study for an upcoming quiz but I couldn’t concentrate. © 1996-2020 The Washington Post

Keyword: Hormones & Behavior
Link ID: 27609 - Posted: 12.07.2020

By Kelly Servick Do old and damaged cells remember what it was like to be young? That’s the suggestion of new study, in which scientists reprogrammed neurons in mouse eyes to make them more resistant to damage and able to regrow after injury—like the cells of younger mice. The study suggests that hallmarks of aging, and possibly the keys to reversing it, lie in the epigenome, the proteins and other compounds that decorate DNA and influence what genes are turned on or off. The idea that aging cells hold a memory of their young epigenome “is very provocative,” says Maximina Yun, a regenerative biologist at the Dresden University of Technology who was not involved in the work. The new study “supports that [idea], but by no means proves it,” she adds. If researchers can replicate these results in other animals and explain their mechanism, she says, the work could lead to treatments in humans for age-related disease in the eye and beyond. Epigenetic factors influence our metabolism, our susceptibility to various diseases, and even the way emotional trauma is passed through generations. Molecular biologist David Sinclair of Harvard Medical School, who has long been on the hunt for antiaging strategies, has also looked for signs of aging in the epigenome. “The big question was, is there a reset button?” he says. “Would cells know how to become younger and healthier?” In the new study, Sinclair and his collaborators aimed to rejuvenate cells by inserting genes that encode “reprogramming factors,” which regulate gene expression—the reading of DNA to make proteins. The team chose three of the four factors scientists have used for more than 10 years to turn adult cells into induced pluripotent stem cells, which resemble the cells of an early embryo. (Exposing animals to all four factors can cause tumors.) © 2020 American Association for the Advancement of Science.

Keyword: Vision
Link ID: 27608 - Posted: 12.05.2020

By Lisa Sanders, M.D. “You need to call an ambulance,” the familiar voice from her doctor’s office urged the frightened 59-year-old woman. “Or should I do it for you?” No, she replied shakily. I can do it. The woman looked down at the phone in her hand; there were two of them. She closed one eye and the second phone disappeared. Then she dialed 911. It had been a hellish few days. Five days earlier, she noticed that she was having trouble walking. Her legs couldn’t or wouldn’t follow her brain’s instructions. She had to take these ungainly baby steps to get anywhere. Her muscles felt weak; her feet were inert blocks. Her hands shook uncontrollably. She vomited half a dozen times a day. The week before, she decided to stop drinking, and she recognized the shaking and vomiting as part of that process. The trouble walking, that was new. But that’s not why she called her doctor. The previous day, she was driving home and was just a block away when suddenly there were two of everything. Stone-cold sober and seeing double. There were two dotted lines identifying the middle of her quiet neighborhood street in South Portland, Maine. Two sets of curbs in front of two sets of sidewalks. She stopped the car, rubbed her eyes and discovered that the second objects slid back into the first when one eye stayed covered. She drove home with her face crinkled in an awkward wink. At home, she immediately called her doctor’s office. They wanted to send an ambulance right then. But she didn’t have health insurance. She couldn’t afford either the ambulance or the hospital. She would probably be better by the next day, she told the young woman on the phone. But the next day was the same. And when she called the doctor’s office this time, the medical assistant’s suggestion that she call an ambulance made a lot more sense. The woman was embarrassed by the siren and flashing lights. Her neighbors would be worried. But she couldn’t deny the relief she felt as she watched the ambulance pull up. The E.M.T.s helped her to her feet and onto the stretcher, then drove her to nearby Northern Light Mercy Hospital. © 2020 The New York Times Company

Keyword: Language
Link ID: 27607 - Posted: 12.05.2020

By Mekado Murphy Creating an audioscape for a movie about a musician losing his hearing is more complicated than it may seem. The filmmakers behind the new drama “Sound of Metal” wanted to take audiences into the experience of its lead character, Ruben (Riz Ahmed), a punk-metal drummer who is forced to look at his life differently as he goes deaf. Judging by the overwhelmingly positive reviews, the filmmakers pulled off that difficult feat. In The New York Times, Jeannette Catsoulis raved about “an extraordinarily intricate sound design that allows us to borrow Ruben’s ears.” The film (streaming on Amazon) often places us in Ruben’s aural perspective as he navigates his new reality. (It’s worth watching with headphones or a good sound system.) “I had many conversations with people who have lost their hearing and not two people’s experience is the same,” said Darius Marder, the film’s co-writer and director. “But one thing that’s pretty much true for all people who are deaf is that they don’t lose sound entirely. It isn’t silence.” Instead, Marder and his sound designer, Nicolas Becker, wanted to capture those low-frequency vibrations and other tones. The approach was adjusted for different moments in Ruben’s experience. In separate Zoom interviews, Marder and Becker focused on three scenes as they spoke about some of the techniques and ideas they used to tap into Ruben’s aural experience, including putting microphones inside skulls and mouths. If the first times there’s a notable change in Ruben’s hearing comes before a show, as he is setting up the merchandise table with his bandmate and girlfriend, Lou (Olivia Cooke). At one point, he experiences a high-pitched ringing, then voices are muffled. Ahmed’s response in that moment isn’t just acting. The filmmakers had custom-fit earpieces made for the actor so they could feed him a high-frequency sound they had created. © 2020 The New York Times Company

Keyword: Hearing
Link ID: 27606 - Posted: 12.05.2020

By Veronique Greenwood The ibis and the kiwi are dogged diggers, probing in sand and soil for worms and other buried prey. Sandpipers, too, can be seen along the shore excavating small creatures with their beaks. It was long thought that these birds were using trial and error to find their prey. But then scientists discovered something far more peculiar: Their beaks are threaded with cells that can detect vibrations traveling through the ground. Some birds can feel the movements of their distant quarry directly, while others pick up on waves bouncing off buried shells — echolocating like a dolphin or a bat, in essence, through the earth. There’s one more odd detail in this story of birds’ unusual senses: Ostriches and emus, birds that most definitely do not hunt this way, have beaks with a similar interior structure. They are honeycombed with pits for these cells, though the cells themselves are missing. Now, scientists in a study published Wednesday in Proceedings of the Royal Society B report that prehistoric bird ancestors dating nearly as far back as the dinosaurs most likely were capable of sensing vibrations with their beaks. The birds that use this remote sensing today are not closely related to one another, said Carla du Toit, a graduate student at the University of Cape Town in South Africa and an author of the paper. That made her and her co-authors curious about when exactly this ability evolved, and whether ostriches, which are close relatives of kiwis, had an ancestor that used this sensory ability. “We had a look to see if we could find fossils of early birds from that group,” Ms. du Toit said. “And we’re very lucky.” There are very well-preserved fossils of birds called lithornithids dating from just after the event that drove nonavian dinosaurs to extinction. © 2020 The New York Times Company

Keyword: Pain & Touch; Evolution
Link ID: 27605 - Posted: 12.05.2020

A study led by researchers at the National Institutes of Health has made a surprising connection between frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), two disorders of the nervous system, and the genetic mutation normally understood to cause Huntington’s disease. This large, international project, which included a collaboration between the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA), opens a potentially new avenue for diagnosing and treating some individuals with FTD or ALS. Several neurological disorders have been linked to “repeat expansions,” a type of mutation that results in abnormal repetition of certain DNA building blocks. For example, Huntington’s disease occurs when a sequence of three DNA building blocks that make up the gene for a protein called huntingtin repeats many more times than normal. These repeats can be used to predict whether someone will develop the illness and even when their symptoms are likely to appear, because the more repeats in the gene, the earlier the onset of disease. “It has been recognized for some time that repeat expansion mutations can give rise to neurological disorders,” said Sonja Scholz, M.D., Ph.D., investigator, NINDS Intramural Research Program. “But screening for these mutations throughout the entire genome has traditionally been cost-prohibitive and technically challenging.” Taking advantage of technology available at NIH, the researchers screened the entire genomes from large cohorts of FTD/ALS patients and compared them to those of age-matched healthy individuals. While several patients had a well-established genetic marker for FTD/ALS, a small subset surprisingly had the same huntingtin mutation normally associated with Huntington’s disease. Remarkably, these individuals did not show the classical symptoms of Huntington’s but rather those of ALS or FTD.

Keyword: ALS-Lou Gehrig's Disease ; Huntingtons
Link ID: 27604 - Posted: 12.05.2020

By Emily Willingham When a male sand-sifting sea star in the coastal waters of Australia reaches out a mating arm to its nearest neighbor, sometimes that neighbor is also male. Undaunted, the pair assume their species’ pseudocopulation position and forge ahead with spawning. Mating, pseudo or otherwise, with a same-sex neighbor obviously does not transfer a set of genes to the next generation—yet several sea star and other echinoderm species persist with the practice. They are not alone. From butterflies to birds to beetles, many animals exhibit same-sex sexual behaviors despite their offering zero chance of reproductive success. Given the energy expense and risk of being eaten that mating attempts can involve, why do these behaviors persist? One hypothesis, hotly debated among biologists, suggests this represents an ancient evolutionary strategy that could ultimately enhance an organism’s chances to reproduce. In results published recently in Nature Ecology & Evolution, Brian Lerch and Maria R. Servedio, from the University of North Carolina, Chapel Hill, offer theoretical support for this proposed explanation. They created a mathematical model that calculated scenarios in which mating attempts, regardless of partner sex, might be worth it. The results predicted that, depending on life span and mating chances, indiscriminate mating with any available candidates could in fact yield a better reproductive payoff than spending precious time and energy sorting out one sex from the other. Although this study does not address sexual orientation or attraction, both of which are common among vertebrate species, it does get at some persistent evolutionary questions: when did animals start distinguishing mates by sex, based on specific cues, and why do some animals apparently remain indiscriminate in their choices? © 2020 Scientific American

Keyword: Sexual Behavior; Evolution
Link ID: 27603 - Posted: 12.05.2020

Abby Olena The smallest terrestrial mammal, the Etruscan shrew (Suncus etruscus), is about as big as a person’s thumb and no heavier than a couple of paper clips. To have enough energy to survive, it must eat eight or more times its body weight daily and therefore doesn’t hibernate. Instead, according to a study published November 30 in PNAS, in winter, these shrews lose 28 percent of the volume from their somatosensory cortex, which likely helps them conserve energy. “This phenomenon of an animal that is not a hibernator still implementing these energy saving strategies is just stunning,” says Christine Schwartz, a neuroscientist who studies hibernation at the University of Wisconsin La Crosse and was not involved in the work. Scientists have shown before that red-toothed shrews, which belong to a group separate from the Etruscan shrew, are born and grow to their full body size in a single summer. Then in autumn, they start to shrink all over—in their spine length, skull, brain, bones, organs such as the liver, and body weight—reaching their smallest size in the winter. Somewhere around February, they start to grow again and reach a second size peak as they sexually mature in the spring. Then they reproduce just once, and, shortly after, die. This cycle is known as Dehnel’s phenomenon. When Saikat Ray was a graduate student in Michael Brecht's lab at the Bernstein Center for Computational Neuroscience in Berlin, he was curious to see if Dehnel’s phenomenon also exists in white-toothed shrews, the subfamily that includes the Etruscan shrew. They already had a colony of Etruscan shrews in the lab, says Ray, who is now a postdoc in Nachum Ulanovsky’s lab at the Weizmann Institute in Israel, because the animals’ tiny brains are a helpful model system for studying more of the brain at once than are the brains of larger mammals, such as mice or rats. © 1986–2020 The Scientist.

Keyword: Neurogenesis
Link ID: 27602 - Posted: 12.05.2020

By Sabrina Imbler In the spring of 2018 at the Montreal Insectarium, Stéphane Le Tirant received a clutch of 13 eggs that he hoped would hatch into leaves. The eggs were not ovals but prisms, brown paper lanterns scarcely bigger than chia seeds. They were laid by a wild-caught female Phyllium asekiense, a leaf insect from Papua New Guinea belonging to a group called frondosum, which was known only from female specimens. Phyllium asekiense is a stunning leaf insect, occurring both in summery greens and autumnal browns. As Royce Cumming, a graduate student at the City University of New York, puts it, “Dead leaf, live leaf, semi-dried leaf.” Mr. Le Tirant, the collections manager of the insectarium since 1989, specializes in scarab beetles; he estimates that he has 25,000 beetles in his private collection at home. But he had always harbored a passion for leaf insects and had successfully bred two species, a small one from the Philippines and a larger one from Malaysia. A Phyllium asekiense — rare, beautiful and, most important, living — would be a treasure in any insectarium. In the insect-rearing laboratory, Mario Bonneau and other technicians nestled the 13 eggs on a mesh screen on a bed of coconut fibers and spritzed them often with water. In the fall, and over the course of several months, five eggs hatched into spindly black nymphs. The technicians treated the baby nymphs with utmost care, moving them from one tree to another without touching the insects, only whatever leaf they clung to. “Other insects, we just grab them,” Mr. Le Tirant said. “But these small leaf insects were so precious, like jewels in our laboratory.” The technicians offered the nymphs a buffet of fragrant guava, bramble and salal leaves. Two nymphs refused to eat and soon died. The remaining three munched on bramble, molted, munched, molted, and molted some more. One nymph grew green and broad, just like her mother. © 2020 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 27601 - Posted: 12.05.2020

By Benedict Carey At a recent visit to the Veterans Affairs clinic in the Bronx, Barry, a decorated Vietnam veteran, learned that he belonged to a very exclusive club. According to a new A.I.-assisted algorithm, he was one of several hundred V.A. patients nationwide, of six million total, deemed at imminent risk of suicide. The news did not take him entirely off guard. Barry, 69, who was badly wounded in the 1968 Tet offensive, had already made two previous attempts on his life. “I don’t like this idea of a list, to tell you the truth — a computer telling me something like this,” Barry, a retired postal worker, said in a phone interview. He asked that his surname be omitted for privacy. “But I thought about it,” Barry said. “I decided, you know, OK — if it’s going to get me more support that I need, then I’m OK with it.” For more than a decade, health officials have watched in vain as suicide rates climbed steadily — by 30 percent nationally since 2000 — and rates in the V.A. system have been higher than in the general population. The trends have defied easy explanation and driven investment in blind analysis: machine learning, or A.I.-assisted algorithms that search medical and other records for patterns historically associated with suicides or attempts in large clinical populations. Doctors have traditionally gauged patients’ risks by looking at past mental health diagnoses and incidents of substance abuse, and by drawing on experience and medical instinct. But these evaluations fall well short of predictive, and the artificially intelligent programs explore many more factors, like employment and marital status, physical ailments, prescription history and hospital visits. These algorithms are black boxes: They flag a person as at high risk of suicide, without providing any rationale. But human intelligence isn’t necessarily better at the task. “The fact is, we can’t rely on trained medical experts to identify people who are truly at high risk,” said Dr. Marianne S. Goodman, a psychiatrist at the Veterans Integrated Service Network in the Bronx, and a clinical professor of medicine at the Icahn School of Medicine at Mount Sinai. “We’re no good at it.” © 2020 The New York Times Company

Keyword: Depression
Link ID: 27600 - Posted: 11.30.2020

By Jelena Kecmanovic Across the spectrum, mental health problems seem to be on the rise. One-quarter of Americans reported moderate to severe depression this summer and another quarter said they suffered from mild depression, a recent study reported. These findings are similar to surveys done by the Census Bureau and the Centers for Disease Control and Prevention. A third of Americans now show signs of clinical anxiety or depression, Census Bureau finds. Former first lady Michelle Obama highlighted the problem for many when she said in August that she has been dealing with “low-grade depression.” As a psychologist, I hear almost daily how the combination of coronavirus, racial unrest, economic uncertainty and political crisis are leading many people to feel a lot worse than usual. “It is not at all surprising that we are seeing the significant increase in distress. It’s a normal reaction to an abnormal situation,” said Judy Beck, president of the Beck Institute for Cognitive Behavior Therapy in Philadelphia and author of the widely used mental health textbook “Cognitive Behavior Therapy: Basics and Beyond.” But an important difference exists between having depressive symptoms — such as sadness, fatigue and loss of motivation — and a full-blown major depressive episode that can affect your ability to function at work and home for weeks or months. The amount and duration of the symptoms, as well as the degree to which they impair one’s life all play a role in diagnosing clinical depression. Extensive research suggests that certain ways of thinking and behaving can hasten the plunge into clinical depression, while others can prevent it. As we head into winter, which can stress the coping skills of many people, here are some strategies that can help you resist the depressive downward spiral. 1. Reduce overthinking. When we feel down, we tend to think about the bad things repeatedly, often trying to figure out why they’ve happened. Research shows that some people are especially prone to this kind of “depressive rumination.” They overanalyze everything, hoping to think their way out of feeling bad, and fret about consequences of their sadness.

Keyword: Depression; Emotions
Link ID: 27599 - Posted: 11.30.2020

by Laura Dattaro Autistic boys with large brains in early childhood still have large brains in adolescence, according to a new study. Autistic girls, too, have brains that grow differently from those of their non-autistic peers. The findings challenge the long-standing idea that brain enlargement in autism is temporary. Previous studies indicated that young children on the spectrum have larger brains than their non-autistic peers but older people with autism do not. To explain the difference, researchers speculated that a pruning process follows early brain overgrowth. But the changes are a mirage, the researchers behind the new study say: Because having a large brain is associated with a low intelligence quotient (IQ) and severe autism traits, and because older children with such characteristics are often excluded from imaging studies, the prior results reflect only a lack of older participants with large brains. “This whole idea of this early overgrowth followed by normalization is just an artifact of sampling bias,” says lead investigator Christine Wu Nordahl, associate professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute. “It was sort of like, ‘Wow, why didn’t we ever think about this before?’ But it’s pretty clear that that’s what’s happening.” Autistic and non-autistic children also show different development patterns in their white matter — fibers that connect regions of the brain — in early childhood, a second study from Nordahl’s group shows. Some of the differences correlate with changes in the children’s autism traits over time. © 2020 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 27598 - Posted: 11.30.2020