Matthew Warren Scientists have uncovered the most complete remains yet from the mysterious ancient-hominin group known as the Denisovans. The jawbone, discovered high on the Tibetan Plateau and dated to more than 160,000 years ago, is also the first Denisovan specimen found outside the Siberian cave in which the hominin was uncovered a decade ago — confirming suspicions that Denisovans were more widespread than the fossil record currently suggests. The research marks the first time an ancient human has been identified solely through the analysis of proteins. With no usable DNA, scientists examined proteins in the specimen’s teeth, raising hopes that more fossils could be identified even when DNA is not preserved. “This is fantastic work,” says Katerina Douka, an archaeologist at the Max Planck Institute for the Science of Human History in Jena, Germany, who runs a separate project aiming to uncover Denisovan fossils in Asia. “It tells us that we are looking at the right area.” Until now, everything scientists have learnt about Denisovans has come from a handful of teeth and bone fragments from Denisova Cave in Russia’s Altai Mountains. DNA from these remains revealed that the Denisovans were a sister group to Neanderthals, both descending from a population that split away from modern humans about 550,00–765,000 years ago. And at Denisova Cave, the two groups seem to have met and interbred: a bone fragment described last year belonged an ancient-human hybrid individual who had a Denisovan father and Neanderthal mother.

Keyword: Evolution
Link ID: 26198 - Posted: 05.02.2019

By Kelly Servick Many people with autism have trouble making eye contact, reading the emotions in other faces, and sharing affection. And no drugs are approved to treat such social impairments. Now, results from a small academic clinical trial suggest boosting levels of vasopressin—a hormone active in the brain that’s known to promote bonding in many animals—can improve social deficits in children with autism. But in a confusing twist, a larger, company-sponsored trial that took the reverse approach, tamping down vasopressin’s effects, also found some improvements in adults with autism. “I’ve never seen this before,” Kevin Pelphrey, a neuroscientist who studies autism at the University of Virginia in Charlottesville, says of the conflicting results. He and others say the vasopressin-blocking approach doesn’t have much support from previous animal research. The new study showed some benefits but failed to meet the main endpoint set out by investigators. Still, he says, both studies suggest vasopressin’s signaling in the brain plays a key role in autism and “give me a lot of renewed excitement” for treating the condition. Though vasopressin seems to stimulate social bonding in animals, the hormone’s activity in the brain isn’t fully understood, and its effects vary by species and context. Blocking its activity in the brains of some rodents prevents them from forming an attraction to a mate. But in a species of asocial hamster, injecting it into a male’s brain seems to stimulate aggression. © 2019 American Association for the Advancement of Science.

Keyword: Autism; Hormones & Behavior
Link ID: 26197 - Posted: 05.02.2019

By Gina Kolata The Court of Arbitration for Sport in Zurich has ruled that women with very high testosterone levels — far above the normal range — cannot compete against other women in races from 400 meters to one mile unless they take drugs to suppress production of the hormone. The ruling prevents Caster Semenya, 28, an elite runner and Olympic champion from South Africa, from competing in those races because her testosterone levels are naturally very high. She had challenged attempts to disqualify her from racing as a woman. The science underpinning that decision is complicated, raising difficult questions about biology, fairness and gender identity. What is testosterone? Where does it come from in women? It’s a hormone, an androgen, that has a variety of effects on the body. Women and men produce testosterone, but women don’t make nearly as much In men, high levels of testosterone are made by the testes. Much lower levels are produced in the adrenal glands, which rest above the kidneys. Women also make testosterone in their adrenal glands, and in their ovaries. But testes produce much more: Testosterone levels in men are 295 to 1,150 nanograms per deciliter of blood, while the levels in the women are 12 to 61 nanograms per deciliter of blood. Testosterone “builds muscle,” said Dr. Benjamin D. Levine, who studies sex differences in athletic performance at the University of Texas Southwestern Medical Center. “It builds skeletal muscle, it builds cardiac muscle. It increases the number of red blood cells.” The effects are seen whether the hormone is naturally present or introduced with drugs. In one of the most infamous examples, women who represented East Germany at the Olympic Games in the ’70s and ’80s achieved astounding success after they were unknowingly doped with anabolic steroids including testosterone. “The science is quite clear,” said Dr. Aaron Baggish of Massachusetts General Hospital, who is an expert on testosterone’s effects. “An androgenized body has a performance advantage.” © 2019 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 26196 - Posted: 05.02.2019

By R. Douglas Fields From his sniper’s perch on the 32nd floor of the Mandalay Bay hotel in Las Vegas, a lone gunman fired 1,000 bullets from high-powered rifles into a crowd of concertgoers in 2017, murdering 58 innocent people and injuring 869 others. After he committed suicide at the crime scene, the mass murderer’s brain was shipped to Stanford University to seek a possible biological explanation for this depraved incident. What could the scientists possibly find during such an inspection? Quite a lot, in fact. No genetic test for homicidal behavior is in the offing. But this type of investigation can add insight into how violence is controlled by the brain. Using the same experimental methods that have enabled the tracing of brain circuits responsible for other complex human activities—including walking, speech and reading—neuroscientists now can pinpoint pathways that underlie aggressive behaviors. These new findings help to expose the underlying mechanisms at work in acts of extreme violence, such as the Las Vegas atrocity, but they also help to explain the more commonplace road rage and even a mother’s instantaneous response to any threat to her child. Physical, sometimes deadly violence is the hub of nature’s survival-of-the fittest struggle, and all animals have evolved specialized neural circuitry to execute—and control—aggressive behavior. In pioneering experiments on cats beginning in the late 1920s, Walter Hess discovered a locus deep within the hypothalamus, a brain area that unleashes violent aggression. It turns out that this is the same spot where other powerful compulsive urges and behaviors are activated, including sex, eating and drinking. When Hess stimulated this knot of neurons using a wire electrode inserted into the brain of a docile cat, the feline instantly launched into a hissing rage, attacking and killing another animal in its cage. The human brain has this same neural structure, labeled the hypothalamic attack area.

Keyword: Aggression; Hormones & Behavior
Link ID: 26195 - Posted: 05.02.2019

By Nicholas Bakalar Girls who have serious or repeated infections in childhood are at higher risk for developing eating disorders in adolescence, a new study has found. The study, in JAMA Psychiatry, tracked 525,643 girls — every girl born in Denmark from 1989 through 2006. The researchers recorded all prescriptions that were filled for antibiotics and other anti-infective medications, as well as hospitalizations for infection, through 2012. There were 4,240 diagnoses of eating disorders during that time. Compared with girls who had never been hospitalized for infection, those who had been hospitalized were at a 22 percent increased risk for anorexia, a 35 percent increased risk for bulimia and a 39 percent increased risk for other eating disorders. Filling three or more prescriptions for anti-infective drugs was associated with similar increases in the risk, and the more infections or hospitalizations a girl had, the more likely she was to develop an eating disorder. This is an observational study so it cannot determine cause and effect, and the authors acknowledge that other mechanisms — genetic factors, or stress and anxiety, for example — could increase the risk of both eating disorders and infection. The lead author, Lauren Breithaupt, a research fellow at Harvard, said that the reasons for the link are unknown, but “it could be that the anti-infective agents are upsetting the microbes in the gut. Changing the microbiome could affect behaviors through the connection of the gut to the brain through the vagus nerve.” © 2019 The New York Times Company

Keyword: Anorexia & Bulimia; Neuroimmunology
Link ID: 26194 - Posted: 05.02.2019

By Benedict Carey Federal health regulators announced on Tuesday that they would require manufacturers of sleeping pills such as Ambien and related drugs to post strongly worded warnings in boxes on labels and patient guides. The Food and Drug Administration, in what it called a safety announcement, noted that the drugs’ side effects included risky behaviors, such as sleepwalking and sleep driving, that can lead to injury and even death. The F.D.A. singled out Ambien and two other popular sleep aids, Lunesta and Sonata, as well as three formulations of zolpidem, the generic name for Ambien. The boxed warnings — the most prominent form of warning required by the agency — must list side effects such as sleepwalking and sleep driving, in which people using the drugs take risks without being fully awake. The agency said such reactions were rare but could lead to injuries or death; it advised doctors not to prescribe the drugs to people who have had such side effects in the past. “Patients, stop taking your insomnia medicine and contact your health care professional right away if you experience a complex sleep behavior where you engage in activities while you are not fully awake,” the agency’s safety alert said, “or if you do not remember activities you have done while taking the medicine.” Prescriptions for sleeping pills grew to more than 20 million in 2010 from 5.3 million in 1999, according to national estimates. About one in eight people with sleeping difficulty report using the drugs; among people of retirement age, more than a third report taking a sleeping aid. The F.D.A. warned about such effects in 2007, after doctors reported that some patients were having strange nighttime experiences, mostly while taking zolpidem (Ambien), the first of the so-called z-drugs. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26193 - Posted: 05.01.2019

Laura Sanders A newly described dementia strikes people in their last decades of life. The disease, aptly named LATE, comes with symptoms that resemble Alzheimer’s disease, but is thought to be caused by something completely different. An international team of scientists and clinicians describe the disease and officially christen it LATE, which stands for the more technical description, “limbic-predominant age-related TDP-43 encephalopathy,” online April 30 in Brain. Study coauthor Peter Nelson, a neuropathologist at the University of Kentucky in Lexington, helped organize a meeting last year that addressed a growing realization among doctors and scientists: “There’s this disease, and it doesn’t have a name,” he says. Estimates vary, but it’s possible that about a quarter of people age 85 and older have LATE, Nelson says. “This is a disease that really attacks the very latest portion of the human aging spectrum,” he says. LATE comes with memory trouble and dementia — symptoms that mirror Alzheimer’s, Nelson says. But instead of the plaques and tangles that mark the brains of people with Alzheimer’s disease, LATE is characterized by a lesser-known protein called TDP-43. In LATE, that protein accumulates and spreads through parts of the brain that are key to thinking and memory, including the amygdala and hippocampus. In Brain, Nelson and his colleagues describe the signs of LATE in the brain in a series of stages, from less severe to most severe. But the trouble is that these signs, which include the spread of TDP-43 and occasionally signs of damage to the hippocampus, can be found only after a person has died. There are currently no surefire clinical tests that identify LATE in a living person. |© Society for Science & the Public 2000 - 2019.

Keyword: Alzheimers
Link ID: 26192 - Posted: 05.01.2019

By Lisa Sanders, M.D. “I don’t know where I am,” said a terrified voice on the phone. It was the woman’s husband, and he was scared. “I’m lost,” he said in a panicked tone. It’s O.K., she told him, sounding as calm and reassuring as she could. Her husband, a former high school English teacher in his 60s, left his mother-in-law’s that morning to return to their home several hours away in Pinon Hills, just north of San Bernardino, Calif. It was a route he drove often enough to know well. But after making his way through towns that seemed familiar, he lost his sense of how to get home. With her voice on the speakerphone, she guided him. His voice shook, and she knew he was crying. She wanted to cry, too, but forced herself to be the strength he needed. She still loved her husband, but he’d changed so much. Where was the man she married over 30 years ago? Twenty years earlier, he found out he had multiple sclerosis. It started with numbness in his arms and hands. Sometimes his vision would darken on the periphery, as if he were in a tunnel. And then, after a couple of hours or so, he’d be fine. He was referred to a local neurologist, who did some testing. An M.R.I. of his brain showed patchy white clouds among the normal gray swirls of brain. That finding was suggestive of multiple sclerosis. In M.S., the immune system goes awry and attacks the fatty sleeves that surround the nerves in the brain and spine; that’s what causes the characteristic M.R.I. findings. But it wasn’t a perfect fit. The fluid taken from his spine did not show the proteins that are usually seen in M.S. Moreover, while M.S. is characterized by episodes of unusual neurological symptoms that come and go, they usually last days or weeks rather than hours. Still, there are different forms of the disorder, and they can vary widely in symptom intensity and rate of progression. And there are few diseases that result in the M.R.I. findings and intermittent symptoms that this man had. Subsequent neurologists confirmed the diagnosis of M.S. © 2019 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 26191 - Posted: 05.01.2019

By Sayuri Hayakawa, Viorica Marian As Emperor Akihito steps down from the Chrysanthemum Throne in Japan’s first abdication in 200 years, Naruhito officially becomes the new Emperor on May 1, 2019, ushering in a new era called Reiwa (令和; “harmony”). Japan’s tradition of naming eras reflects the ancient belief in the divine spirit of language. Kotodama (言霊; “word spirit”) is the idea that words have an almost magical power to alter physical reality. Through its pervasive impact on society, including its influence on superstitions and social etiquette, traditional poetry and modern pop songs, the word kotodama has, in a way, provided proof of its own concept. For centuries, many cultures have believed in the spiritual force of language. Over time, these ideas have extended from the realm of magic and mythology to become a topic of scientific investigation—ultimately leading to the discovery that language can indeed affect the physical world, for example, by altering our physiology. Our bodies evolve to adapt to our environments, not only over millions of years but also over the days and years of an individual’s life. For instance, off the coast of Thailand, there are children who can “see like dolphins.” Cultural and environmental factors have shaped how these sea nomads of the Moken tribe conduct their daily lives, allowing them to adjust their pupils underwater in a way that most of us cannot. © 2019 Scientific American

Keyword: Language
Link ID: 26190 - Posted: 05.01.2019

By Sheila Kaplan WASHINGTON — The Food and Drug Administration said Tuesday that it would permit the sale of IQOS, a “heat not burn” tobacco device made by Philip Morris International, in the United States. While the agency stopped short of declaring that the device was safer than traditional cigarettes, the F.D.A. did say the heated tobacco-stick system could help people to quit smoking. Philip Morris has waited two years for the agency to clear IQOS (pronounced EYE-kose), a penlike electronic device that comes with a sleek battery pack resembling a cigarette case. The product includes an electronically controlled heating blade that warms a tobacco stick and releases a vapor with the taste of tobacco but fewer harmful chemicals than cigarette smoke. It differs from e-cigarettes already on the market because it contains tobacco rather than liquid nicotine. But IQOS still delivers an amount of nicotine that’s similar to traditional cigarettes. “The F.D.A.’s decision to authorize IQOS in the U.S. is an important step forward for the approximately 40 million American men and women who smoke,” said André Calantzopoulos, the chief executive of Philip Morris International. “Some will quit. Most won’t, and for them IQOS offers a smoke-free alternative to continued smoking.” Howard A. Willard III, chief executive of Altria, which will distribute the product in this country, said the company planned to begin sales of IQOS in Atlanta. A few years ago, the F.D.A.’s decision would have been a clear win for both Philip Morris and Altria. But IQOS products will now have to compete with the extremely popular devices sold by the vaping giant Juul Labs, in which Altria has a 35 percent stake. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26189 - Posted: 05.01.2019

April Dembosky Amelia and her roommate had been awake for two days straight. They decided to spray-paint the bathroom hot pink. After that, they laid into building and rebuilding the pens for the nine pit bull puppies they were raising in their two-bedroom apartment. Then the itching started. It felt like pin pricks under the skin of her hands. Amelia was convinced she had scabies, skin lice. She spent hours in front of the mirror checking her skin, picking at her face. She even got a health team to come test the apartment. All they found were a few dust mites. "At first, with meth, I remember thinking, 'What's the big deal?' " says Amelia, who asked that we not reveal her last name to protect her family's privacy. "But when you look at how crazy things got, everything was so out of control. Clearly, it is a big deal." While public health officials have focused on the opioid epidemic in recent years, another epidemic has been brewing quietly, but vigorously, behind the scenes. Methamphetamine use is surging in parts of the U.S., particularly the West, leaving first responders and addiction treatment providers struggling to handle a rising need. Across the country, overdose deaths involving methamphetamine doubled from 2010 to 2014. Admissions to treatment facilities for meth are up 17%. Hospitalizations related to meth jumped by about 245% from 2008 to 2015. And throughout the West and Midwest, 70% of local law enforcement agencies say meth is their biggest drug threat. © 2019 npr

Keyword: Drug Abuse
Link ID: 26188 - Posted: 05.01.2019

By Shubham Saharan Thomas Jessell, renowned neurologist and former director of and key contributor to the founding of Columbia’s Mortimer B. Zuckerman Mind Brain Behavior Institute, has died. He was 67. In a statement to MBBI affiliates, Institute co-directors Rui Costa, Eric Kandel, and Richard Axel attributed Jessell’s death to a rapidly-progressing neurodegenerative disorder. Jessell was endowed under the Claire Tow Professorship in Motor Neuron Disorders in the neuroscience and biochemistry and molecular biophysics departments. He was well known for his research on chemical signals and neurological circuits. Originally an assistant professor in the department of neurobiology at Harvard Medical School, Jessell moved to Columbia in 1985 to work as an investigator for the Howard Hughes Medical Institute, a philanthropic organization that provides funding for biological and medical research as well as scientific education. Jessell, along with Axel and Kandel from the department of neuroscience, played a significant role in founding the MBBI, a center dedicated to neuroscience research, which is located at the Jerome L. Greene Science Center on the Manhattanville campus. In March 2018, HHMI stripped Jessell of all titles and grants and announced that it would stop funding his lab starting May 31. Columbia began investigating Jessell’s misconduct in December 2017, after which he was removed from all administrative positions, including his co-directorship of the MBBI, for engaging in a years-long relationship that violated the University policy on consensual romantic and sexual relationships between faculty and students. Copyright Spectator Publishing Company

Keyword: Development of the Brain
Link ID: 26187 - Posted: 05.01.2019

By Benedict Carey Ever since its premiere, on March 31, 2017, the Netflix series “13 Reasons Why,” about a teenage girl’s suicide, has alarmed many health experts, who believe it glamorizes the topic for some young people. The show also has impressed critics, along with viewers young and old, who see it as an honest portrayal of adolescent distress. Now, a new study finds that suicide rates spiked in the month after the release of the series among boys aged 10 to 17. That month, April 2017, had the highest overall suicide rate for this age group in the past five years, the study found; the rate subsequently dropped back into line with recent trends, but remained elevated for the year. Suicide rates for girls aged 10 to 17 — the demographic expected to identify most strongly with the show’s protagonist — did not increase significantly. The study, posted Monday by the Journal of Child and Adolescent Psychiatry, is likely to fuel further debate about the merits of “13 Reasons Why,” the third season of which is in production. “Suicide is a problem worldwide, and it’s so hard to knock these rates down,” said Lisa M. Horowitz, a staff scientist in the National Institute of Mental Health’s Intramural Research Program, and an author of the paper. “The last thing we need is something that increases them.” In a statement, a Netflix spokesperson said: “We’ve just seen this study and are looking into the research, which conflicts with last week’s study from the University of Pennsylvania,” which focused on young adults. “This is a critically important topic and we have worked hard to ensure that we handle this sensitive issue responsibly.” © 2019 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 26186 - Posted: 04.30.2019

By Simon Baron-Cohen At the annual meeting of the International Society for Autism Research (INSAR) in Montreal, Canada, this week, one topic likely to be widely debated is the concept of neurodiversity. It is dividing the autism community, but it doesn’t have to. The term “neurodiversity” gained popular currency in recent years but was first used by Judy Singer, an Australian social scientist, herself autistic, and first appeared in print in the Atlantic in 1998. Neurodiversity is related to the more familiar concept of biodiversity, and both are respectful ways of thinking about our planet and our communities. The notion of neurodiversity is very compatible with the civil rights plea for minorities to be accorded dignity and acceptance, and not to be pathologized. And whilst the neurodiversity movement acknowledges that parents or autistic people may choose to try different interventions for specific symptoms that may be causing suffering, it challenges the default assumption that autism itself is a disease or disorder that needs to be eradicated, prevented, treated or cured. Many autistic people—especially those who have intact language and no learning difficulties such that they can self-advocate—have adopted the neurodiversity framework, coining the term “neurotypical” to describe the majority brain and seeing autism as an example of diversity in the set of all possible diverse brains, none of which is “normal” and all of which are simply different. © 2019 Scientific American

Keyword: Autism
Link ID: 26185 - Posted: 04.30.2019

Nicola Davis Olfactory tests could help doctors spot older adults who are at greater risk of developing dementia, researchers say. The sense of smell is known to deteriorate with age. However, researchers have previously found it might also hint at health problems: older adults who struggle to identify odours have a greater chance of dying in the near future regardless of how old they are. Other studies have found older adults who have difficulties in identifying and remembering smells are more likely to have characteristics linked to a greater risk of developing Alzheimer’s disease even if there is no current sign of cognitive decline. Get Society Weekly: our newsletter for public service professionals Read more It is thought the sense of smell is one of the first faculties affected by certain neurodegenerative diseases. Now experts say they have probed further, and those diseases alone do not explain why a poor sense of smell might bode ill. “My suspicion is [the] process of smell in older adults probably has much broader potential health implications than what we already know about,” said Prof Honglei Chen, a co-author of the research from Michigan State University. He suggested it could be linked to conditions of the immune system and even psychiatric disorders. © 2019 Guardian News & Media Limited

Keyword: Alzheimers; Chemical Senses (Smell & Taste)
Link ID: 26184 - Posted: 04.30.2019

By Rahul Desikan What is it like to be locked into your body, to be alive but not living? I’m dying — fast. My lungs are at 20 percent of vital capacity and it’s a matter of time before the nerves supplying my breathing muscles degenerate. I have a rapid form of ALS — amyotrophic lateral sclerosis, or Lou Gehrig’s disease. Two years ago, I was running around with my kids, hiking with my wife. All that is over. My body no longer moves. I cannot talk — my only voice is the one in my head, telling me over and over that I am going to die. Soon. I can’t even breathe for myself anymore — I am tethered to a ventilator that breathes for me. I don’t want you to feel sorry for me. At all. It is just ironic, this new, condensed life of mine. I went into medicine to take care of patients with brain diseases. Now, I have one of the diseases that I study. Even with this lethal disease, I continue to find neurology fascinating and beautiful. I wish you knew the old me. ALS has completely destroyed my body and parts of my brain. The new version has stripped me of control over regulating my emotions. I laugh and cry inappropriately during movies, and even during conversations. The cognitive parts of my brain are still working perfectly fine so I’m able to get through the day. But because swallowing has become increasingly difficult, eating and drinking are a battle: continuous bouts of choking, vomiting, crying, sweating, drooling — until finally, it goes through. It is not a pretty picture. What is it like to be locked in? When I swallow, I imagine my childhood in India — driving with my parents and sister in our sky-blue Maruti minivan through the wide roads of New Delhi, relishing my grandmother’s sambar, a savory soup of lentils and vegetables. In my mind, I am always in Boston where I lived for 15 years during college and then medical school and for my doctorate in neurobiology. In my mind, which is all I have left, I am playing house music records at Satellite Records in the Back Bay or trying the Persian eggplant dish at Lala Rokh with my wife or going out with my friends to River Gods or the Enormous Room in Central Square. I am so good at imagining the old me that I see, taste, hear, touch everything. And relive every single detail. © 1996-2019 The Washington Post

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26183 - Posted: 04.29.2019

By Jane E. Brody I was packing up at the end of a family vacation in Florida when my back went into an excruciating spasm unrelieved by a fistful of pain medication. As my twin sons, then 8 years old, wheeled me through the airport, one of them suggested, “Mom, if you think about something else, it won’t hurt so much.” At the time, I failed to appreciate the wisdom of his advice. Now, four decades later, a sophisticated distraction technique is being used to help patients of all ages cope with pain, both acute and chronic. The method, called Virtual Reality Therapy, goes beyond simple distraction, as might result from watching television. Rather, it totally immerses the patient in an entertaining, relaxing, interactive environment that so occupies the brain, it has no room to process pain sensations at the same time. “It’s not just a distraction — it’s like an endogenous narcotic providing a physiological and chemical burst that causes you to feel good,” said Jeffrey I. Gold, director of the pediatric pain management clinic at Children’s Hospital Los Angeles. “It’s different from reading a book or playing with a toy. It’s a multisensory experience that engages a person’s attention on a much deeper level.” Virtual Reality Therapy is the new kid on the block for pain management, now gradually growing in use as the opioid epidemic continues to soar and the price of the needed equipment has plummeted. VR, as it is called, has been most widely and successfully used so far to help children and adults weather acute pain, as can accompany an IV insertion or debridement of burns. But it can also enhance the effectiveness of established techniques like physical therapy, hypnosis and cognitive behavioral therapy to treat debilitating chronic pain. © 2019 The New York Times Company

Keyword: Pain & Touch; Attention
Link ID: 26182 - Posted: 04.29.2019

By Susana Martinez-Conde Human night vision is not as precise as day vision. That’s why getting up barefoot in the middle of the night comes with a much higher risk of stepping on painful Lego pieces than walking along the same path during the day. I have three kids of ages twelve and under, so I know. But the specific ways in which our night vision is worse than our day vision are surprisingly counterintuitive to most of us. I remember learning in college that night-vision is achromatic (meaning that we only see in grayscale at night) and not really believing it. It took some careful night-time observation to conclude that my professor was right: objects that were colorful during the day had no hue at night. Most shocking of all was the realization that, though I had always suffered from night-time color blindness (as all of us do), I had never been aware of my deficiency. A recent study by Alejandro Gloriani and Alexander Schütz, from the University of Marburg, Germany, published earlier this month in Current Biology, shows that our night vision self-delusion is even more pervasive than previously thought. Advertisement To appreciate Gloriani and Schütz’s discovery, the first thing to understand is that day and night vision rely on the activity of different types of photoreceptors (these are the retinal cells that convert light energy into electrical signals, which your brain can then process). ‘Cones’ are active during the day (or when you turn the lights on at night). ‘Rods’ are active during the night (or at very dim light levels). © 2019 Scientific American

Keyword: Vision
Link ID: 26181 - Posted: 04.29.2019

Lisa Wehrstedt Researchers in Philadelphia revealed last week that tastebuds also bear odour-detecting proteins, calling into question the idea that smell and taste come together in the brain to produce flavour. According to Dr Mehmet Hakan Ozdener, his findings open up the possibility of using smells to trick us into healthier eating, for example by adding a low-concentration odour to food to make it taste sweeter and thereby reduce sugar intake. It is believed that we all experience a form of motion-induced blindness while driving at night, when the red lights of the cars in front temporarily disappear if we move our eyes to the oncoming traffic. This phenomenon, where the brain ignores or discards visual information when it is placed in front of a moving background, was first observed in the lab in 1965. First described in 1976, the McGurk effect is a connection between hearing and vision in speech perception. When the auditory component of a syllable is paired with the visual component of another, this can lead to the perception of a third sound. Research conducted by the University of Oxford in 2013 suggests that the sight of cutlery and the perception of its size, weight, shape and colour have an effect on how we determine flavour, suggesting that the brain makes judgments on food even before it goes in our mouths. Yoghurt, for example, tastes sweeter on a white spoon than it does on a black spoon. © 2019 Guardian News & Media Limited

Keyword: Chemical Senses (Smell & Taste); Vision
Link ID: 26180 - Posted: 04.29.2019

By Amy Barnhorst SACRAMENTO — If suicide is preventable, why are so many people dying from it? Suicide is the 10th leading cause of death in the United States, and suicide rates just keep rising. A few years ago, I treated a patient, a flight attendant, whose brother had brought her in to the psychiatric crisis unit after noticing her unusual behavior at a wedding. After the ceremony, she quietly handed out gifts and heartfelt letters to her family members. When her brother took her home, he noticed many of her furnishings and paintings were missing. In her bathroom he found three unopened bottles of prescription sleep medication. He confronted her, and she admitted that she had donated her possessions to charity. She had also cashed out her retirement account and used the money to pay off her mortgage, her car loan and all of her bills. When I interviewed her, she said that for the last four months, doing anything — eating, cleaning her house, talking to her neighbors — had taken colossal effort, and brought her no joy. She felt exhausted by having to live through each day, and the thought of sustaining this for years to come was an intolerable torment. After evaluating her, I told her that I thought she was experiencing an episode of bipolar depression, and needed to be committed to the hospital while we started treatment. She shrugged and gave me her most troubling response yet: “I don’t care.” One of the reasons I remember this woman so well is that, of all the patients I have evaluated for suicide risk, she was an anomaly. She had a sustained and thought-out commitment to ending her life. Fortunately, that allowed her to be discovered, and her family was able to quickly get her into emergency care. She responded well to lithium, one of only two psychiatric medications shown to reduce suicide (the other is an antipsychotic, clozapine). Her depression lifted slowly and she began to remember the things that made her life worth living. © 2019 The New York Times Company

Keyword: Depression; Schizophrenia
Link ID: 26179 - Posted: 04.29.2019