By Abby Sher The rules were simple. Whenever Madonna sang, we strutted our stuff up and down the matted blue carpet. If the music stopped, we struck a pose in front of the full-length mirror. “Your face is crooked!” my friend Diana shrieked. “Your legs are 10 feet long!” I yelled back. It wasn’t an insult; it was true. The mirror in my bedroom was old and warped, like in a fun house. We spent hours in front of it, jutting out our hips and crossing our eyes; laughing at how ugly we looked. How round and pointy, long and short we could be, all at the same time. I don’t know exactly when it became painful for me to look at my reflection. Maybe when I was told to cover the mirrors in our house for my father’s funeral (a Jewish tradition). I was 11 at the time and couldn’t understand how these pale lips and string bean legs of mine were here, while my dad was forever gone. So I kept staring at my body in that glass, feeling a new kind of grief and confusion rip through me. A few weeks later, I started junior high, where looks were everything. I used a mirror so I could run turquoise eyeliner across my lids or zero in on a blooming pimple. But I got more and more frustrated by what I saw. My splotchy skin and bushy eyebrows felt untamable; my arms too long. By high school, I grew out my frizzy bangs to hide my face and wore baggy overalls with a tiny cowbell around my neck, as if I were lost in the fields and needed to find my way home. It wasn’t until after college that I dove headlong into an eating disorder. There was no definitive moment where I said, I’m going to try starving myself today. Instead it was a gradual whittling away at my body. I became obsessed with shrinking myself down to a size 0; spending hours at the gym until I was dizzy and frantic, fueling myself on coffee and sugarless gum. © 2020 The New York Times Company

Keyword: Anorexia & Bulimia; Attention
Link ID: 27068 - Posted: 02.25.2020

By Susanne Antonetta Last September, I believed my brain was on fire. Not in some metaphorical way. It was, as far as I was concerned, on fire. I am bipolar and I was hallucinating. My hallucinations can be sensory, like the brain burn, but many are auditory — I know hallucinations are coming when I hear birds speak. I can tell you what the birds say, but what matters is how intensely personal it is, being shouted at by a fierce small crowd: persist persist persist from one, six degrees yes yes yes from another. I couldn’t sleep in all the chatter. Then I heard whispering everywhere, semi trucks coming to a halt right under my bedroom window. A small part of me sensed all this was not really happening, but most of me thought it was. There’s another hallucinatory change that’s harder to describe, one that comes every time, mild episode or intense. The world feels malleable, like felt, or soft paper. Walls rock and steady themselves. What’s around me becomes alive, air itself humming and moving. As with the birds, these changes feel intensely personal — everything around me shifts as I watch. During the six months leading up to this brain-fire time, I’d been having milder hallucinations, on and off. I took a medication that controlled my psychotic symptoms until my cholesterol skyrocketed and kept going up. The drugs used to treat people like me — atypical antipsychotics like Zyprexa and the one I take, Seroquel — have metabolic side effects. These include soaring cholesterol and triglycerides, as well as diabetes. There may be no way out of these side effects except dropping the medication, going, as I did, from one that works to one that doesn’t. Doctors, and the occasional friend, kept telling me something meant to be cheering: “This is just a disease, the same as a broken bone or a bout of pneumonia.” As though my antipsychotic could just as easily be penicillin. I’ve heard this statement in one form or another for several decades, since my diagnosis at age 29. I don’t accept this mechanistic view of the brain, which suggests that if you pump in drugs (at levels often determined by drug company-funded research), the cogs will start working smoothly again. This model dismisses patients’ individual experience of medications, which vary wildly. © 2020 The New York Times Company

Keyword: Schizophrenia
Link ID: 27067 - Posted: 02.24.2020

Dominique Sisley Nothing is quite as shattering as a broken heart. A bad breakup has been known to trigger a range of psychological and physical symptoms, from nausea and insomnia to clinical depression. In more extreme scenarios, broken heart syndrome – when a person’s heart stops pumping blood properly after an emotional shock – can lead to death. Fortunately, recent breakthroughs suggest we may soon be able to beat it. In March, a Spanish study found propofol, a sedative used for anaesthesia, may also be able to mute the painful memories that come with heartbreak. Participants were injected with the drug immediately after recalling a distressing story and, when asked to recount it again 24 hours later, they found the memory to be less vivid. Advertisement The principal goal of the research was to relieve the symptoms of post-traumatic stress disorder (PTSD), but it seems there may be scope for the drug to be used to suppress other upsetting memories. An unexpected loss such as heartbreak can also be traumatic, and some people report similar symptoms. Dr Bryan Strange, who led the study, says: “Combining anaesthesia with evoking an emotionally charged memory impairs its subsequent recall. We will need to derive a set of criteria that identify people for whom it works well, and where the benefit justifies the risk of anaesthesia. There may well be those for whom heartbreak is so distressing that the criteria is fulfilled.” In the past year, a wave of apps such as Mend, Rx Breakup and Break-Up Boss have been released, promising guidance, advice and distracting activities to help soothe the pain of heartbreak. It is a lofty promise, but one that appears to be rooted in logic: a study in 2017 found similar brain-training style exercises could help curb embarrassing or impulsive post-breakup behaviour and strengthen self-control. © 2020 Guardian News & Media Limited

Keyword: Depression; Sexual Behavior
Link ID: 27066 - Posted: 02.24.2020

By Aimee Cunningham The stories that Judith Feinberg hears from people with substance use disorder are riddled with loss: of jobs, opportunity, security, dignity. “People really are struggling to see that they have a viable future,” Feinberg says. “Then you take a drug … and you don’t care until you need the drug again.” For years, that drug was very likely an opioid. But Feinberg, a physician at West Virginia University School of Medicine in Morgantown who studies infectious diseases and injection drug use, recently has seen shifts in the addictive substances used. And it’s occurring not just in West Virginia — which has the highest rate of drug overdose deaths in the nation, at 51.5 deaths per 100,000 people — but across the country, the U.S. Centers for Disease Control and Prevention reported January 30. Fueled by a plentiful supply, people have increasingly been turning to such stimulants as cocaine and methamphetamine — so much so that the rates of overdose deaths for those drugs each surpassed that of prescription opioids in 2018. There’s a small bit of hope: After two decades of rising numbers, around 3,000 fewer people overall died of a drug overdose in 2018 than in 2017. But with 67,367 deaths, 2018 ranks as the second-worst year for drug overdoses in U.S. history. It’s too soon to say whether the nudge downward is a blip or the start of a meaningful drop. In part, that may depend upon whether the rise in stimulant use over much of the last decade continues. In 2018, the rate of overdose deaths involving cocaine was 4.5 per 100,000, more than triple what it was in 2012; for methamphetamine and similar drugs, the rate jumped from 0.8 to 3.9 per 100,000 during that period. Each now surpasses the death rate from prescription opioids, and cocaine’s rate is just shy of heroin’s. © Society for Science & the Public 2000–2020

Keyword: Drug Abuse
Link ID: 27065 - Posted: 02.24.2020

By Jane Wakefield Technology reporter An ambitious project to develop a wearable device to detect early signs of Alzheimer's disease has been launched. The Early Detection of Neurodegenerative diseases (Edon) is being spearheaded by charity Alzheimer's Research UK. It will initially analyse data from continuing studies into the disease, using artificial intelligence. And this data will be used to design a prototype device within three years. Wearables collect a variety of data including gait, heart rate and sleep patterns and the hope is by analysing this data, researchers can begin to map signs of the disease years before symptoms develop. The global initiative has already won funding from tech founder turned philanthropist Bill Gates. But it also forms part of the UK government's wider ambition to use artificial intelligence and data to help better understand and prevent chronic diseases. Initially, EDoN will work with the UK's national institute for data science and artificial intelligence, The Alan Turing Institute, to trawl through data from continuing studies into Alzheimer's disease. Prof Chris Holmes, health programme director at the institute, said: "Artificial intelligence has the potential to transform the learning opportunities from large-scale data studies such as Edon by integrating information from multiple sources. "We will use AI to deliver new insights into the early signals of disease by combining digital data measurements with traditional sources such as brain imaging and memory tests." There are currently 850,000 people living with dementia in the UK, according to Alzheimer's Research UK. © 2020 BBC.

Keyword: Alzheimers
Link ID: 27064 - Posted: 02.24.2020

By James Gorman There’s something about a really smart dog that makes it seem as if there might be hope for the world. China is in the midst of a frightening disease outbreak and nobody knows how far it will spread. The warming of the planet shows no signs of stopping; it reached a record 70 degrees in Antarctica last week. Not to mention international tensions and domestic politics. But there’s a dog in Norway that knows not only the names of her toys, but also the names of different categories of toys, and she learned all this just by hanging out with her owners and playing her favorite game. So who knows what other good things could be possible? Right? This dog’s name is Whisky. She is a Border collie that lives with her owners and almost 100 toys, so it seems like things are going pretty well for her. Even though I don’t have that many toys myself, I’m happy for her. You can’t be jealous of a dog. Or at least you shouldn’t be. Whisky’s toys have names. Most are dog-appropriate like “the colorful rope” or “the small Frisbee.” However, her owner, Helge O. Svela said on Thursday that since the research was done, her toys have grown in number from 59 to 91, and he has had to give some toys “people” names, like Daisy or Wenger. “That’s for the plushy toys that resemble animals like ducks or elephants (because the names Duck and Elephant were already taken),” he said. During the research, Whisky proved in tests that she knew the names for at least 54 of her 59 toys. That’s not just the claim of a proud owner, and Mr. Svela is quite proud of Whisky, but the finding of Claudia Fugazza, an animal behavior researcher from Eötvös Loránd University in Budapest, who tested her. That alone makes Whisky part of a very select group, although not a champion. You may recall Chaser, another Border collie that knew the names of more than 1,000 objects and also knew words for categories of objects. And there are a few other dogs with shockingly large vocabularies, Dr. Fugazza said, including mixed breeds, and a Yorkie. These canine verbal prodigies are, however, few and far between. “It is really, really unusual, and it is really difficult to teach object names to dogs,” Dr. Fugazza said. © 2020 The New York Times Company

Keyword: Language; Learning & Memory
Link ID: 27063 - Posted: 02.21.2020

By Sara Reardon To many people’s eyes, artist Mark Rothko’s enormous paintings are little more than swaths of color. Yet a Rothko can fetch nearly $100 million. Meanwhile, Pablo Picasso’s warped faces fascinate some viewers and terrify others. Why do our perceptions of beauty differ so widely? The answer may lie in our brain networks. Researchers have now developed an algorithm that can predict art preferences by analyzing how a person’s brain breaks down visual information and decides whether a painting is “good.” The findings show for the first time how intrinsic features of a painting combine with human judgment to give art value in our minds. Most people—including researchers—consider art preferences to be all over the map, says Anjan Chatterjee, a neurologist and cognitive neuroscientist at the University of Pennsylvania who was not involved in the study. Many preferences are rooted in biology–sugary foods, for instance, help us survive. And people tend to share similar standards of beauty when it comes to human faces and landscapes. But when it comes to art, “There are relatively arbitrary things we seem to care about and value,” Chatterjee says. To figure out how the brain forms value judgments about art, computational neuroscientist Kiyohito Iigaya and his colleagues at the California Institute of Technology first asked more than 1300 volunteers on the crowdsourcing website Amazon Mechanical Turk to rate a selection of 825 paintings from four Western genres including impressionism, cubism, abstract art, and color field painting. Volunteers were all over the age of 18, but researchers didn’t specify their familiarity with art or their ethnic or national origin. © 2020 American Association for the Advancement of Science

Keyword: Vision; Attention
Link ID: 27062 - Posted: 02.21.2020

By Viviane Callier In 1688 Irish philosopher William Molyneux wrote to his colleague John Locke with a puzzle that continues to draw the interest of philosophers and scientists to this day. The idea was simple: Would a person born blind, who has learned to distinguish objects by touch, be able to recognize them purely by sight if he or she regained the ability to see? The question, known as Molyneux’s problem, probes whether the human mind has a built-in concept of shapes that is so innate that such a blind person could immediately recognize an object with restored vision. The alternative is that the concepts of shapes are not innate but have to be learned by exploring an object through sight, touch and other senses, a process that could take a long time when starting from scratch. An attempt was made to resolve this puzzle a few years ago by testing Molyneux's problem in children who were congenitally blind but then regained their sight, thanks to cataract surgery. Although the children were not immediately able to recognize objects, they quickly learned to do so. The results were equivocal. Some learning was needed to identify an object, but it appeared that the study participants were not starting completely from scratch. Lars Chittka of Queen Mary University of London and his colleagues have taken another stab at finding an answer, this time using another species. To test whether bumblebees can form an internal representation of objects, Chittka and his team first trained the insects to discriminate spheres and cubes using a sugar reward. The bees were trained in the light, where they could see but not touch the objects that were isolated inside a closed petri dish. Then they were tested in the dark, where they could touch but not see the spheres or cubes. The researchers found that the invertebrates spent more time in contact with the shape they had been trained to associate with the sugar reward, even though they had to rely on touch rather than sight to discriminate the objects. © 2020 Scientific American

Keyword: Development of the Brain; Vision
Link ID: 27061 - Posted: 02.21.2020

By Richard Klasco, M.D. A. The theory of the “sugar high” has been debunked, yet the myth persists. The notion that sugar might make children behave badly first appeared in the medical literature in 1922. But the idea did not capture the public’s imagination until Dr. Ben Feingold’s best-selling book, “Why Your Child Is Hyperactive,” was published in 1975. In his book, Dr. Feingold describes the case of a boy who might well be “patient zero” for the putative connection between sugar and hyperactivity: [The mother’s] fair-haired, wiry son loved soft drinks, candy and cake — not exactly abnormal for any healthy child. He also seemed to go completely wild after birthday parties and during family gatherings around holidays. In the mid-’70s, stimulant drugs such as Ritalin and amphetamine were becoming popular for the treatment of attention deficit hyperactivity disorder. For parents who were concerned about drug side effects, the possibility of controlling hyperactivity by eliminating sugar proved to be an enticing, almost irresistible, prospect. Some studies supported the theory. They suggested that high sugar diets caused spikes in insulin secretion, which triggered adrenaline production and hyperactivity. But the data were weak and were soon questioned by other scientists. An extraordinarily rigorous study settled the question in 1994. Writing in the New England Journal of Medicine, a group of scientists tested normal preschoolers and children whose parents described them as being sensitive to sugar. Neither the parents, the children nor the research staff knew which of the children were getting sugary foods and which were getting a diet sweetened with aspartame and other artificial sweeteners. Urine was tested to verify compliance with the diets. Nine different measures of cognitive and behavioral performance were assessed, with measurements taken at five-second intervals. © 2020 The New York Times Company

Keyword: ADHD; Obesity
Link ID: 27060 - Posted: 02.21.2020

By David Grimm More than 3 years after it hosted a workshop on the science and ethics of biomedical studies on monkeys, the National Institutes of Health (NIH) this week convened another workshop on nonhuman primate research. And much like the previous event, the meeting is drawing sharply divergent reactions from biomedical and animal advocacy groups. “It was a very good look at the opportunities and challenges of doing this type of research,” says Alice Ra’anan, director of government relations and science policy at the American Physiological Society, a group that represents nearly 10,000 scientists, doctors, and veterinarians. It was “an excellent and robust discussion around fostering rigorous research in nonhuman primates,” adds Matthew Bailey, president of that National Association for Biomedical Research. But Emily Trunnell, a research associate at People for the Ethical Treatment of Animals, an animal rights group, counters that the event was a wasted opportunity to talk about the ethics of using nonhuman primates in the first place. “It was just a bunch of scientists clamoring for more money and more monkeys.” The workshop comes at a time when scientists are using a near-record number of rhesus macaques, marmosets, and other nonhuman primates in biomedical research. The animals, many researchers say, have become increasingly important in revealing how the human brain works and in developing treatments for infectious diseases. There’s been a particular surge in demand for marmosets, which are being genetically engineered to serve as models for autism, Parkinson’s, and other neurological disorders. © 2020 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 27059 - Posted: 02.21.2020

Diana Kwon In the 16th century, when the study of human anatomy was still in its infancy, curious onlookers would gather in anatomical theaters to catch of a glimpse of public dissections of the dead. In the years since, scientists have carefully mapped the viscera, bones, muscles, nerves, and many other components of our bodies, such that a human corpse no longer holds that same sense of mystery that used to draw crowds. New discoveries in gross anatomy—the study of bodily structures at the macroscopic level—are now rare, and their significance is often overblown, says Paul Neumann, a professor who specializes in the history of medicine and anatomical nomenclature at Dalhousie University. “The important discoveries about anatomy, I think, are now coming from studies of tissues and cells.” Over the last decade, there have been a handful of discoveries that have helped overturn previous assumptions and revealed new insights into our anatomy. “What’s really interesting and exciting about almost all of the new studies is the illustration of the power of new [microscopy and imaging] technologies to give deeper insight,” says Tom Gillingwater, a professor of anatomy at the University of Edinburgh in the UK. “I would guess that many of these discoveries are the start, rather than the end, of a developing view of the human body.” © 1986–2020 The Scientist

Keyword: Brain imaging
Link ID: 27058 - Posted: 02.20.2020

By Kim Tingley Hearing loss has long been considered a normal, and thus acceptable, part of aging. It is common: Estimates suggest that it affects two out of three adults age 70 and older. It is also rarely treated. In the U.S., only about 14 percent of adults who have hearing loss wear hearing aids. An emerging body of research, however, suggests that diminished hearing may be a significant risk factor for Alzheimer’s disease and other forms of dementia — and that the association between hearing loss and cognitive decline potentially begins at very low levels of impairment. In November, a study published in the journal JAMA Otolaryngology — Head and Neck Surgery examined data on hearing and cognitive performance from more than 6,400 people 50 and older. Traditionally, doctors diagnose impairment when someone experiences a loss in hearing of at least 25 decibels, a somewhat arbitrary threshold. But for the JAMA study, researchers included hearing loss down to around zero decibels in their analysis and found that they still predicted correspondingly lower scores on cognitive tests. “It seemed like the relationship starts the moment you have imperfect hearing,” says Justin Golub, the study’s lead author and an ear, nose and throat doctor at the Columbia University Medical Center and NewYork-Presbyterian. Now, he says, the question is: Does hearing loss actually cause the cognitive problems it has been associated with and if so, how? Preliminary evidence linking dementia and hearing loss was published in 1989 by doctors at the University of Washington, Seattle, who compared 100 patients with Alzheimer’s-like dementia with 100 demographically similar people without it and found that those who had dementia were more likely to have hearing loss, and that the extent of that loss seemed to correspond with the degree of cognitive impairment. But that possible connection wasn’t rigorously investigated until 2011, when Frank Lin, an ear, nose and throat doctor at Johns Hopkins School of Medicine, and colleagues published the results of a longitudinal study that tested the hearing of 639 older adults who were dementia-free and then tracked them for an average of nearly 12 years, during which time 58 had developed Alzheimer’s or another cognitive impairment. They discovered that a subject’s likelihood of developing dementia increased in direct proportion to the severity of his or her hearing loss at the time of the initial test. The relationship seems to be “very, very linear,” Lin says, meaning that the greater the hearing deficit, the greater the risk a person will develop the condition. © 2020 The New York Times Company

Keyword: Hearing; Alzheimers
Link ID: 27057 - Posted: 02.20.2020

By Judith Graham, Kaiser Health News Do I know I’m at risk for developing dementia? You bet. My father died of Alzheimer’s disease at age 72; my sister was felled by frontotemporal dementia at 58. And that’s not all: Two maternal uncles had Alzheimer’s, and my maternal grandfather may have had vascular dementia. (In his generation, it was called senility.) So what happens when I misplace a pair of eyeglasses or can’t remember the name of a movie I saw a week ago? “Now comes my turn with dementia,” I think. Then I talk myself down from that emotional cliff. Am I alone in this? Hardly. Many people, like me, who’ve watched this cruel illness destroy a family member, dread the prospect that they, too, might become demented. The lack of a cure or effective treatments only adds to the anxiety. It seems a common refrain, the news that another treatment to stop Alzheimer’s has failed. How do we cope as we face our fears and peer into our future? Andrea Kline, whose mother, as well as her aunt and uncle, had Alzheimer’s disease, just turned 71 and lives in Boynton Beach, Fla. She’s a retired registered nurse who teaches yoga to seniors at community centers and assisted-living facilities. “I worry about dementia incessantly: Every little thing that goes wrong, I’m convinced it’s the beginning,” she told me. Because Ms. Kline has had multiple family members with Alzheimer’s, she’s more likely to have a genetic vulnerability than someone with a single occurrence in their family. But that doesn’t mean this condition lies in her future. A risk is just that: It’s not a guarantee. The age of onset is also important. People with close relatives struck by dementia early — before age 65 — are more likely to be susceptible genetically. Ms. Kline was the primary caregiver for her mother, Charlotte Kline, who received an Alzheimer’s diagnosis in 1999 and passed away in 2007 at age 80. “I try to eat very healthy. I exercise. I have an advance directive, and I’ve discussed what I want” in the way of care “with my son,” she said. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27056 - Posted: 02.20.2020

Maternal obesity may increase a child’s risk for attention-deficit hyperactivity disorder (ADHD), according to an analysis by researchers from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), part of the National Institutes of Health. The researchers found that mothers — but not fathers — who were overweight or obese before pregnancy were more likely to report that their children had been diagnosed with attention-deficit hyperactivity disorder (ADHD) or to have symptoms of hyperactivity, inattentiveness or impulsiveness at ages 7 to 8 years old. Their study appears in The Journal of Pediatrics. The study team analyzed the NICHD Upstate KIDS Study, which recruited mothers of young infants and followed the children through age 8 years. In this analysis of nearly 2,000 children, the study team found that women who were obese before pregnancy were approximately twice as likely to report that their child had ADHD or symptoms of hyperactivity, inattention or impulsiveness, compared to children of women of normal weight before pregnancy. The authors suggest that, if their findings are confirmed by additional studies, healthcare providers may want to screen children of obese mothers for ADHD so that they could be offered earlier interventions. The authors also note that healthcare providers could use evidence-based strategies to counsel women considering pregnancy on diet and lifestyle. Resources for plus-size pregnant women and their healthcare providers are available as part of NICHD’s Pregnancy for Every Body initiative.

Keyword: ADHD; Development of the Brain
Link ID: 27055 - Posted: 02.20.2020

Merrit Kennedy As doctors in London performed surgery on Dagmar Turner's brain, the sound of a violin filled the operating room. The music came from the patient on the operating table. In a video from the surgery, the violinist moves her bow up and down as surgeons behind a plastic sheet work to remove her brain tumor. The King's College Hospital surgeons woke her up in the middle of the operation in order to ensure they did not compromise parts of the brain necessary for playing the violin, such as parts that control precise hand movements and coordination. "We knew how important the violin is to Dagmar, so it was vital that we preserved function in the delicate areas of her brain that allowed her to play," Keyoumars Ashkan, a neurosurgeon at King's College Hospital, said in a press release. Turner, 53, learned that she had a slow-growing tumor in 2013. Late last year, doctors found that it had become more aggressive and the violinist decided to have surgery to remove it. In an interview with ITV News, Turner recalled doctors telling her, "Your tumor is on the right-hand side, so it will not affect your right-hand side, it will affect your left-hand side." "And I'm just like, 'Oh, hang on, this is my most important part. My job these days is playing the violin,' " she said, making a motion of pushing down violin strings with her left hand. Ashkan, an accomplished pianist, and his colleagues came up with a plan to keep the hand's functions intact. © 2020 npr

Keyword: Epilepsy; Movement Disorders
Link ID: 27054 - Posted: 02.20.2020

Amy Schleunes New Zealand’s North Island robins (Petroica longipes), known as toutouwai in Maori, are capable of remembering a foraging task taught to them by researchers for up to 22 months in the wild, according to a study published on February 12 in Biology Letters. These results echo the findings of a number of laboratory studies of long-term memory in animals, but offer a rare example of a wild animal retaining a learned behavior with no additional training. The study also has implications for conservation and wildlife management: given the birds’ memory skills, researchers might be able to teach them about novel threats and resources in their constantly changing habitat. “This is the first study to show [memory] longevity in the wild,” says Vladimir Pravosudov, an animal behavior researcher at the University of Nevada, Reno, who was not involved in the study. Rachael Shaw, a coauthor and behavioral ecologist at Victoria University in New Zealand, says she was surprised that the birds remembered the new skill she had taught them. “Wild birds have so much that they have to contend with in their daily lives,” she says. “You don’t really expect that it’s worth their while to retain this learned task they hardly had the opportunity to do, and they can’t predict that they will have an opportunity to do again.” Shaw is generally interested in the cognitive abilities of animals and the evolution of intelligence, and the toutouwai, trainable food caching birds that can live up to roughly 10 years, make perfect subjects for her behavioral investigations. “They’ve got this kind of boldness and curiosity that a lot of island bird species share,” says Shaw. These qualities make them vulnerable to predation by invasive cats, rats, and ermines (also known as stoats), but also inquisitive and relatively unafraid of humans, an ideal disposition for testing memory retention in the field. © 1986–2020 The Scientist

Keyword: Learning & Memory; Evolution
Link ID: 27053 - Posted: 02.20.2020

By Rachel Cericola A year ago, I was diagnosed with nasal polyps and regularly snored like a wild boar. I’ve had the polyps removed, but the snoring continues. I’m not alone. According to Principles and Practice of Sleep Medicine (Fifth Edition), “about 40 percent of the adult population” snores. Sometimes my snoring wakes up my husband (and vice versa), so I decided to try out six popular over-the-counter anti-snoring contraptions. To get a baseline measurement of how much I was snoring without any intervention, I used SnoreLab, a highly rated app that listens for snoring sounds, records clips, and analyzes your resting audio. After calculating an average of four nights’ intervention-free snoring readings to get a starting “sleep score,” I then slept with each anti-snoring device for several nights and tracked my SnoreLab results against that baseline. (Note that some of these devices may work for you and not me — and none of them should be used to treat sleep apnea. If you’re having restless sleep, gasping awake, or even feeling tired and foggy in the daytime, see a doctor.) While longer-term testing is needed before we could confidently recommend any of these, a few devices showed promise in our preliminary — and far from scientific — trials. Here’s how they did, in order of how much I found they helped: Smart Nora, $329 at the time of publication This system will slightly move your head when it catches you snoring. It includes a wireless, mic-equipped device that can sit bedside or be wall-mounted to detect snoring. Once it does that, it communicates with an under-bed base station that pumps air through a tube to an insert that lives inside your pillow. That motion gently adjusts your head position to reduce snoring (in my case, it effectively did so without waking me up). It sounds bizarre, but this was actually the most effective device I tried, cutting my total snoring in half, according to my SnoreLab sleep scores. It is also the most expensive. There are many options for personalization, which we will continue to test. © 2020 The New York Times Company

Keyword: Sleep
Link ID: 27052 - Posted: 02.20.2020

By Katherine Kornei Imagine a frog call, but with a metallic twang—and the intensity of a chainsaw. That’s the “boing” of a minke whale. And it’s a form of animal communication in danger of being drowned out by ocean noise, new research shows. By analyzing more than 42,000 minke whale boings, scientists have found that, as background noise intensifies, the whales are losing their ability to communicate over long distances. This could limit their ability to find mates and engage in important social contact with other whales. Tyler Helble, a marine acoustician at the Naval Information Warfare Center Pacific, and colleagues recorded minke whale boings over a 1200-square-kilometer swathe of the U.S. Navy’s Pacific Missile Range Facility near the Hawaiian island of Kauai from 2012 to 2017. By measuring when a single boing arrived at various underwater microphones, the team pinpointed whale locations to within 10 to 20 meters. The researchers then used these positions, along with models of how sound propagates underwater, to calculate the intensity of each boing when it was emitted. The team compared these measurements with natural ambient noise, including waves, wind, and undersea earthquakes (no military exercises were conducted nearby during the study period). They found that minke whale boings grew louder in louder conditions. That’s not surprising—creatures across the animal kingdom up their volume when there’s background noise. (This phenomenon, dubbed the Lombard effect, holds true for humans, too—think of holding a conversation at a loud concert.) © 2019 American Association for the Advancement of Science.

Keyword: Animal Communication; Hearing
Link ID: 27051 - Posted: 02.19.2020

Ian Sample Science editor Consuming a western diet for as little as one week can subtly impair brain function and encourage slim and otherwise healthy young people to overeat, scientists claim. Researchers found that after seven days on a high fat, high added sugar diet, volunteers in their 20s scored worse on memory tests and found junk food more desirable immediately after they had finished a meal. The finding suggests that a western diet makes it harder for people to regulate their appetite, and points to disruption in a brain region called the hippocampus as the possible cause. “After a week on a western-style diet, palatable food such as snacks and chocolate becomes more desirable when you are full,” said Richard Stevenson, a professor of psychology at Macquarie University in Sydney. “This will make it harder to resist, leading you to eat more, which in turn generates more damage to the hippocampus and a vicious cycle of overeating.” Previous work in animals has shown that junk food impairs the hippocampus, a brain region involved in memory and appetite control. It is unclear why, but one idea is that the hippocampus normally blocks or weakens memories about food when we are full, so looking at a cake does not flood the mind with memories of how nice cake can be. “When the hippocampus functions less efficiently, you do get this flood of memories, and so food is more appealing,” Stevenson said. To investigate how the western diet affects humans, the scientists recruited 110 lean and healthy students, aged 20 to 23, who generally ate a good diet. Half were randomly assigned to a control group who ate their normal diet for a week. The other half were put on a high energy western-style diet, which featured a generous intake of Belgian waffles and fast food. © 2020 Guardian News & Media Limited

Keyword: Learning & Memory; Obesity
Link ID: 27050 - Posted: 02.19.2020

Researchers at the National Institutes of Health found evidence that specific immune cells may play a key role in the devastating effects of cerebral malaria, a severe form of malaria that mainly affects young children. The results, published in the Journal of Clinical Investigation, suggest that drugs targeting T cells may be effective in treating the disease. The study was supported by the NIH Intramural Research Program. “This is the first study showing that T cells target blood vessels in brains of children with cerebral malaria,” said Dorian McGavern, Ph.D., chief of the Viral Immunology and Intravital Imaging Section at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) who co-directed the study with Susan Pierce, Ph.D., chief of the Laboratory of Immunogenetics at the National Institute of Allergy and Infectious Diseases (NIAID). “These findings build a bridge between mouse and human cerebral malaria studies by implicating T cells in the development of disease pathology in children. It is well established that T cells cause the brain vasculature injury associated with cerebral malaria in mice, but this was not known in humans.” More than 200 million people worldwide are infected annually with mosquito-borne parasites that cause malaria. In a subset of those patients, mainly young children, the parasites accumulate in brain blood vessels causing cerebral malaria, which leads to increased brain pressure from swelling. Even with available treatment, cerebral malaria still kills up to 25% of those affected resulting in nearly 400,000 deaths annually. Children who survive the infection will often have long-lasting neurological problems such as cognitive impairment.

Keyword: Neuroimmunology
Link ID: 27049 - Posted: 02.19.2020