By Jane E. Brody Tiffany Martinez was a 17-year-old college freshman when she began hearing voices, seeing shadowy figures and experiencing troubling, intrusive thoughts. Her friends at the University of Southern Maine, where she was majoring in psychology, noticed that she was acting strangely and urged her to get help. They most likely saved her from a crippling mental health crisis, prevented the derailment of her education and ultimately enabled her to become a psychiatric nurse practitioner who can help other young people avert a psychiatric crisis. Tiffany’s friends convinced her to go to the university’s health center, where she met with a nurse who had just attended an educational seminar about identifying the early signs of mental illness in young adults. The nurse suspected that Tiffany was at risk of developing a psychotic episode and referred her to the Portland Identification and Early Referral, or PIER, program at the Maine Health Center. The program was developed in 2001 by Dr. William R. McFarlane, a psychiatrist who suspected that if early intervention could reverse the course of diseases like cancer and heart disease, it should do likewise for psychosis. Despite conventional wisdom suggesting otherwise, he persevered in the belief that an impending psychotic break could be identified and prevented if it was recognized early and appropriate steps taken to head it off. Tiffany, who said her father had schizophrenia, was an early beneficiary of his vision and has become a poster child for what can be done to prevent a devastating, costly illness that afflicts up to 3 percent of the population. After the PIER program was extended to 25 school districts in and around Portland, there was a 35 percent decline in new hospital admissions for psychotic symptoms, Dr. McFarlane said. © 2019 The New York Times Company

Keyword: Schizophrenia
Link ID: 26562 - Posted: 09.02.2019

By Sheila Kaplan and Matt Richtel An 18-year-old showed up in a Long Island emergency room, gasping for breath, vomiting and dizzy. When a doctor asked if the teenager had been vaping, he said no. The patient’s older brother, a police officer, was suspicious. He rummaged through the youth’s room and found hidden vials of marijuana for vaping. “I don’t know where he purchased it. He doesn’t know,” said Dr. Melodi Pirzada, chief pediatric pulmonologist at NYU Winthrop Hospital in Mineola, N.Y., who treated the young man. “Luckily, he survived.” Dr. Pirzada is one of the many physicians across the country treating patients — now totaling more than 215 — with mysterious and life-threatening vaping-related illnesses this summer. The outbreak is “becoming an epidemic,” she said. “Something is very wrong.” Patients, mostly otherwise healthy and in their late teens and 20s, are showing up with severe shortness of breath, often after suffering for several days with vomiting, fever and fatigue. Some have wound up in the intensive care unit or on a ventilator for weeks. Treatment has been complicated by patients’ lack of knowledge — and sometimes outright denial — about the actual substances they might have used or inhaled. Health investigators are now trying to determine whether a particular toxin or substance has sneaked into the supply of vaping products, whether some people reused cartridges containing contaminants, or whether the risk stems from a broader behavior, like heavy e-cigarette use, vaping marijuana or a combination. On Friday, the Centers for Disease Control and Prevention issued a warning to teenagers and other consumers, telling them to stop buying bootleg and street cannabis and e-cigarette products, and to stop modifying devices to vape adulterated substances. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26561 - Posted: 09.02.2019

By Roni Caryn Rabin Every year, hundreds of thousands of obese Americans undergo weight-loss surgery in a last-ditch effort to shed pounds and control their Type 2 diabetes. Now a new study suggests that bariatric surgery may also have other significant health benefits, cutting the overall risk of serious cardiovascular events and premature death by almost half. The study, published in the medical journal JAMA on Monday, is not definitive. Though it compared the long-term outcomes of about 2,300 bariatric surgery patients with some 11,500 closely matched patients who had not undergone surgery, it was an observational study, not a randomized controlled trial of the kind considered the gold standard in medicine. But the findings were so striking that an editorial accompanying the paper suggested that weight-loss surgery, rather than medications, should be the preferred treatment for Type 2 diabetes in certain patients with obesity. “The new information here is the ability of bariatric surgery to control macrovascular events like strokes, heart attacks, heart failure and kidney disease,” not just improve weight and diabetes control, said Dr. Edward H. Livingston, the editorial’s author. “That’s a big deal.” A bariatric surgeon himself, Dr. Livingston said he had long been known as a “curmudgeon” who was reluctant to make claims about the long-term health benefits of weight-loss surgery. “This is the first time I’ve come out publicly saying, ‘You know what, this may be a better way to go,’” he said, adding that insurers should cover the procedure more liberally. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26560 - Posted: 09.02.2019

By Francie Diep For as long as Brad Johnson can remember, he has never been able to sleep more than six hours a night. Most nights, he sleeps even less. Mr. Johnson, 63, always wakes without an alarm clock, feeling rested and ready for the day. “If you paid me $100,000 to sleep eight hours tonight, I couldn’t do it,” he said. He’s not the only one in his family like this. Two of his seven siblings also are natural short sleepers. He suspects that their father was one, too. At least 15 years ago, he said, one of his brothers reached out to a sleep doctor at the University of Utah, who took an interest in the family, collecting blood samples and conducting interviews at a reunion. Ultimately, researchers identified six members of Mr. Johnson’s extended family, men and women, who get by on an average of less than six hours of sleep a night, much less than the eight and a half hours that people typically need to function at their best. Researchers wondered whether there was something about their genetics that might help explain how sleep works for the rest of us. “The problem is, we know so little about what sleep really is and what it’s for,” said Dr. Louis Ptacek, a neurologist at the University of California, San Francisco. “As we identify more and more genes, hopefully this will outline a system, or systems, that are critically important to sleep.” Dr. Ptacek and his colleagues identified a gene mutation that shows up in every naturally short-sleeping member of Mr. Johnson’s family. When the scientists took the mutated version of the gene and put it in lab mice, they found that the mice needed about an hour less sleep a day than their siblings that did not have the gene. The researchers, who published their findings in the journal Neuron on Wednesday, determined that the gene, ADRB1, has a direct bearing on how much sleep people need. Their findings, they said, could be used to design therapies to help people with sleep problems. © 2019 The New York Times Company

Keyword: Sleep; Genes & Behavior
Link ID: 26559 - Posted: 08.31.2019

By Joanne Chen The only thing worse than feeling completely wired at 11 p.m. when you’re ready for sleep is being stark awake at 3 a.m. Blissfully passing out at an appropriate bedtime is cold comfort when the brain wakes up too soon and refuses to take advantage of those eight full hours. I toss and turn and scrunch up my pillow every which way, exasperated and fixated on the impending doom of the alarm clock set to go off at 6 a.m. About half of all insomnia sufferers experience this middle-of-the-night “sleep-maintenance” insomnia, either by itself or along with the “sleep-onset” sort, trouble falling asleep in the first place, said Jennifer Martin, Ph.D., a professor of medicine at the University of California at Los Angeles. If, after 20 minutes, you’re still up, the American Academy of Sleep Medicine recommends stepping out of the bedroom and doing some reading or other quiet activity. But I didn’t realize that it’s actually a last-resort tactic. “Get up only when you’re so upset you can’t fall asleep anyway,” said Dr. Martin, an insomnia specialist. In fact, some of the best first-line strategies are pursued (more or less) lying down. The next time you find yourself staring at the ceiling at 3 a.m., try these six things: Remain in bed For you to fall asleep, your heart rate needs to slow down, said Michael Breus, Ph.D., a Los Angeles area clinical sleep psychologist. But when you get up, you elevate it. So my impulse to use the bathroom just because I’m awake only makes matters worse. “Do that only if you need to,” said Breus, who is also the author of “The Power of When.” © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26558 - Posted: 08.31.2019

By Tam Hunt How do you know your dog is conscious? Well, she wags her tail when she’s happy, bounces around like a young human child when excited, and yawns when sleepy— among many other examples of behaviors that convince us (most of us, at least) that dogs are quite conscious in ways that are similar to, but not the same as, human consciousness. Most of us are okay attributing emotions, desires, pain and pleasure—which is what I mean by consciousness in this context—to dogs and many other pets. What about further down the chain. Is a mouse conscious? We can apply similar tests for “behavioral correlates of consciousness” like those I’ve just mentioned, but, for some of us, the mice behaviors observed will be considerably less convincing than for dogs in terms of there being an inner life for the average mouse. Advertisement What about an ant? What behaviors do ants engage in that might make us think an individual ant is at least a little bit conscious? Or is it not conscious at all? Let me now turn the questions around: how do I know you, my dear reader, are conscious? If we met, I’d probably introduce myself and hear you say your name and respond to my questions and various small talk. You might be happy to meet me and smile or shake my hand vigorously. Or you might get a little anxious at meeting someone new and behave awkwardly. All of these behaviors would convince me that you are in fact conscious much like I am, and not just faking it! Now here’s the broader question? How can we know anybody or any animal or any thing is actually conscious and not just faking it? The nature of consciousness makes it by necessity a wholly private affair. The only consciousness I can know with certainty is my own. Everything else is inference. © 2019 Scientific American

Keyword: Consciousness
Link ID: 26557 - Posted: 08.31.2019

By Laura Sanders It’s baby’s first brain wave, sort of. As lentil-sized clusters of nerve cells grow in a lab dish, they begin to fire off rhythmic electrical signals. These oscillations share some features with those found in the brains of developing human babies, researchers report October 3 in Cell Stem Cell. Three-dimensional spheres of human brain cells, called cerebral organoids, are extremely simplistic models of the human brain. Still, these easy-to-obtain organoids may offer a better way to study how a brain is made, and how that process can go wrong (SN: 2/20/18). “The field is white-hot,” with fast progress in both making and understanding brain organoids, says John Huguenard, a neuroscientist at Stanford University not involved in the study. Finding this sort of coordinated electrical activity in organoids’ nerve cells, or neurons, is a first, he says. “The neurons are growing up and becoming mature enough where they can not only start to behave like neurons and fire individually, but now they can be coordinated.” For the study, researchers coaxed stem cells into forming some of the neurons that make up the outer layer of the brain. These cortical organoids grew in lab dishes that held arrays of electrodes printed along the bottom, allowing the scientists to monitor electrical activity as the organoids developed. © Society for Science & the Public 2000–2019

Keyword: Development of the Brain
Link ID: 26556 - Posted: 08.30.2019

By Pam Belluck How do genes influence our sexuality? The question has long been fraught with controversy. An ambitious new study — the largest ever to analyze the genetics of same-sex sexual behavior — found that genetics does play a role, responsible for perhaps a third of the influence on whether someone has same-sex sex. The influence comes not from one gene but many, each with a tiny effect — and the rest of the explanation includes social or environmental factors — making it impossible to use genes to predict someone’s sexuality. “I hope that the science can be used to educate people a little bit more about how natural and normal same-sex behavior is,” said Benjamin Neale, a geneticist at the Broad Institute of M.I.T. and Harvard and one of the lead researchers on the international team. “It’s written into our genes and it’s part of our environment. This is part of our species and it’s part of who we are.” The study of nearly half a million people, funded by the National Institutes of Health and other agencies, found differences in the genetic details of same-sex behavior in men and women. The research also suggests the genetics of same-sex sexual behavior shares some correlation with genes involved in some mental health issues and personality traits — although the authors said that overlap could simply reflect the stress of enduring societal prejudice. Even before its publication Thursday in the journal Science, the study has generated debate and concern, including within the renowned Broad Institute itself. Several scientists who are part of the L.G.B.T.Q. community there said they were worried the findings could give ammunition to people who seek to use science to bolster biases and discrimination against gay people. One concern is that evidence that genes influence same-sex behavior could cause anti-gay activists to call for gene editing or embryo selection, even if that would be technically impossible. Another fear is that evidence that genes play only a partial role could embolden people who insist being gay is a choice and who advocate tactics like conversion therapy. © 2019 The New York Times Company

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 26555 - Posted: 08.30.2019

By Lindsey Bever There is no one gene that determines a person’s sexual orientation, but genetics — along with environment — play a part in shaping sexuality, a massive new study shows. Researchers analyzed DNA from hundreds of thousands of people and found that there are a handful of genes clearly connected with same-sex sexual behavior. The researchers say that, although variations in these genes cannot predict whether a person is gay, these variants may partly influence sexual behavior. Andrea Ganna, lead author and European Molecular Biology Laboratory group leader at the Institute of Molecular Medicine in Finland, said the research reinforces the understanding that same-sex sexual behavior is simply “a natural part of our diversity as a species.” The new study, published Thursday in the journal Science, is not the first to explore the link between genetics and same-sex behavior, but it is the largest of its kind, and experts say it provides one of the clearest pictures of genes and sexuality. Ganna, who is also an instructor at Massachusetts General and Harvard, and an international team of scientists examined data from more than 470,000 people in the United States and the United Kingdom to see whether certain genetic markers in their DNA were linked to their sexual behavior. Specifically, the researchers used data from the UK Biobank study and from the private genomics company 23andMe, which included their DNA data and responses to questions about sexual behaviors, sexual attraction and sexual identity. More than 26,000 participants reported at least one sexual encounter with someone of the same sex. Earlier studies, the researchers said, weren’t large enough to reveal the subtle effects of individual genes. © 1996-2019 The Washington Post

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 26554 - Posted: 08.30.2019

By Stephen L. Macknik In normal vision, light falls on the retinas inside the eyes, and is immediately transduced into electrochemical signals before being uploaded to the brain through the optic nerves. So you do not see light itself, but the brain's interpretation of electrochemical signals in the visual parts of the brain. It follows that, if your eyes do not work, but your brain is stimulated just so, your visual neurons will activate (and you will be able to see) just the same as if your eyes were in perfect condition. Sounds easy, but can we do that? Building on decades of research in visual neuroscience, my lab, in collaboration with Susana Martinez-Conde’s, has now conducted some of the studies that validate this idea, completing some of the most important preliminary steps towards a new kind of visual prosthetic. Francis Collins, the Director of the National Institutes of Health, has just posted a blog that highlights our approach. He took notice of our work when we first presented it at this year's meeting for the Principal Investigators of the BRAIN Initiative—the NIH led government funding initiative meant to spur research along on topics like brain implants. The BRAIN Initiative funds several agencies including the NIH, including the National Science Foundation, who kindly funded the grant driving our research thus far. Our starting premise is that vision is fundamentally a thumbnail sketch. Even if 99.9% of your retina works fine, but the central 1/1000th of your visual field is broken, you will be legally blind. That central 0.1% of your visual field is about the same size as your thumbnail held up at arm's length. Because that central 0.1% of the retina is the visual sweet spot, it is the place where the visual magic happens. In fact, much of the remaining 99.9% of the retina’s main job is to help you detect where to move your eyes next. This means that we need to restore central vision in the blind, or we are not really restoring functional vision at all. © 2019 Scientific American

Keyword: Vision; Robotics
Link ID: 26553 - Posted: 08.29.2019

By Annie Roth Kalutas live fast and die young — or, at least, the males do. Male kalutas, small mouselike marsupials found in the arid regions of Northwestern Australia, are semelparous, meaning that shortly after they mate, they drop dead. This extreme reproductive strategy is rare in the animal kingdom. Only a few dozen species are known to reproduce in this fashion, and most of them are invertebrates. Kalutas are dasyurids, the only group of mammals known to contain semelparous species. Only around a fifth of the species in this group of carnivorous marsupials — which includes Tasmanian devils, quolls and pouched mice — are semelparous and, until recently, scientists were not sure if kalutas were among them. Now there is no doubt that, for male kalutas, sex is suicide. In a study, published in April in the Journal of Zoology, researchers from the University of Western Australia and the University of Queensland confirmed that kalutas exhibit what is known as obligate male semelparity. “We found that males only mate during one highly synchronized breeding season and then they all die,” said Genevieve Hayes, a vertebrate ecologist and the lead author of the study. Dr. Hayes and her colleagues monitored the breeding habits of a population of kalutas in Millstream Chichester National Park in Western Australia during the 2013 and 2014 breeding seasons. In both seasons, the researchers observed a complete die-off of males. Although male kalutas have exhibited semelparity in captivity, this was the first time it had been seen in the wild. Kalutas evolved independently of other semelparous dasyurids, so the confirmation that male kalutas die after mating suggests that this unorthodox reproductive strategy has evolved not once, but twice in dasyurids.

Keyword: Sexual Behavior
Link ID: 26552 - Posted: 08.29.2019

Colin Barras An ancient face is shedding new light on our earliest ancestors. Archaeologists have discovered a 3.8-million-year-old hominin skull in Ethiopia — a rare and remarkably complete specimen that could change what we know about the origins of one of humanity’s most famous ancestors, Lucy. The researchers who discovered the skull say it belongs to a species called Australopithecus anamensis, and it gives scientists their first good look at the face of this hominin. This species was thought to precede Lucy’s species, Australopithecus afarensis. But features of the latest find now suggest that A. anamensis shared the prehistoric Ethiopian landscape with Lucy’s species for at least 100,000 years, the researchers say. This hints that the early hominin evolutionary tree was more complicated than scientists had thought — but other researchers say the evidence isn’t yet conclusive. “Fossil hominin crania are exceptionally rare treasures,” says Carol Ward, a palaeoanthropologist at the University of Missouri in Columbia who wasn’t involved in the analysis. “This to me is the specimen we have been waiting for.” An analysis of the skull is published in Nature1 . Exceptionally preserved A. afarensis lived in East Africa between about 4 million and 3 million years ago. It is important to the understanding of human evolution because it might have been the ape-like species from which the ‘true’ human genus, Homo, evolved about 2.8 million years ago. Over the past few decades, researchers have discovered dozens of fragments of australopithecine fossils in Ethiopia and Kenya that date back more than 4 million years. Most researchers think these older fossils belong to the earlier species, A. anamensis. It’s generally thought that A. anamensis gradually morphed into A. afarensis, implying that the two species never coexisted.

Keyword: Evolution
Link ID: 26551 - Posted: 08.29.2019

By Kelly Servick Try to cheat your body out of a full night’s sleep and you’ll suffer the consequences … unless you happen to carry a rare genetic mutation. According to a new study, some people who function normally on just 6 hours of sleep harbor an altered version of a particular gene, the second gene so far linked to short sleep. In 2009, researchers described a mother and daughter with a mutation in a gene called DEC2 who felt well rested after with about 6 hours of sleep per night. (Many experts recommend that adults get at least 7 hours.) DEC2 codes for a protein that helps turn off the expression of other genes, including the gene for the hormone orexin, known to regulate wakefulness. Now, by studying another family containing naturally short sleepers, the scientists have identified another mutation, which they estimate is present in roughly four of every 100,000 people. Mice genetically engineered to have this mutation slept, on average, 1 hour less per day than controls, the researchers report online today in Neuron. The mutation affects a gene called ADRB1, which encodes a receptor for the common neural signaling molecule noradrenaline. In a part of the mouse brainstem, cells studded with this receptor were active during wakefulness and quiet during deep (non–rapid eye movement) sleep, the researchers found. And stimulating these ADRB1-bearing brainstem neurons could immediately awaken them from deep sleep. They propose that the mutation renders these wake-promoting brainstem neurons more active, which could explain why its human carriers are content to sleep less. © 2019 American Association for the Advancement of Science.

Keyword: Sleep; Genes & Behavior
Link ID: 26550 - Posted: 08.29.2019

By Anil K. Seth On the 10th of April this year Pope Francis, President Salva Kiir of South Sudan and former rebel leader Riek Machar sat down together for dinner at the Vatican. They ate in silence, the start of a two-day retreat aimed at reconciliation from a civil war that has killed some 400,000 people since 2013. At about the same time in my laboratory at the University of Sussex in England, Ph.D. student Alberto Mariola was putting the finishing touches to a new experiment in which volunteers experience being in a room that they believe is there but that is not. In psychiatry clinics across the globe, people arrive complaining that things no longer seem “real” to them, whether it is the world around them or their own selves. In the fractured societies in which we live, what is real—and what is not—seems to be increasingly up for grabs. Warring sides may experience and believe in different realities. Perhaps eating together in silence can help because it offers a small slice of reality that can be agreed on, a stable platform on which to build further understanding. Advertisement We need not look to war and psychosis to find radically different inner universes. In 2015 a badly exposed photograph of a dress tore across the Internet, dividing the world into those who saw it as blue and black (me included) and those who saw it as white and gold (half my lab). Those who saw it one way were so convinced they were right—that the dress truly was blue and black or white and gold—that they found it almost impossible to believe that others might perceive it differently. We all know that our perceptual systems are easy to fool. The popularity of visual illusions is testament to this phenomenon. Things seem to be one way, and they are revealed to be another: two lines appear to be different lengths, but when measured they are exactly the same; we see movement in an image we know to be still. The story usually told about illusions is that they exploit quirks in the circuitry of perception, so that what we perceive deviates from what is there. Implicit in this story, however, is the assumption that a properly functioning perceptual system will render to our consciousness things precisely as they are. © 2019 Scientific American

Keyword: Consciousness; Vision
Link ID: 26549 - Posted: 08.29.2019

By Carolyn Wilke In learning to read, squiggles and lines transform into letters or characters that carry meaning and conjure sounds. A trio of cognitive neuroscientists has now mapped where that journey plays out inside the brain. As readers associate symbols with pronunciation and part of a word, a pecking order of brain areas processes the information, the researchers report August 19 in the Proceedings of the National Academy of Sciences. The finding unveils some of the mystery behind how the brain learns to tie visual cues with language (SN Online: 4/27/16). “We didn’t evolve to read,” says Jo Taylor, who is now at University College London but worked on the study while at Aston University in Birmingham, England. “So we don’t [start with] a bit of the brain that does reading.” Taylor — along with Kathy Rastle at Royal Holloway University of London in Egham and Matthew Davis at the University of Cambridge — zoomed in on a region at the back and bottom of the brain, called the ventral occipitotemporal cortex, that is associated with reading. Over two weeks, the scientists taught made-up words written in two unfamiliar, archaic scripts to 24 native English–speaking adults. The words were assigned the meanings of common nouns, such as lemon or truck. Then the researchers used functional MRI scans to track which tiny chunks of brain in that region became active when participants were shown the words learned in training. © Society for Science & the Public 2000–2019

Keyword: Language; Brain imaging
Link ID: 26548 - Posted: 08.27.2019

By Cara Giaimo Peppered moth caterpillars live across the Northern Hemisphere, from the forests of China to the backyards of North America. But if you’ve never seen one, don’t feel bad: They’re experts at blending in. Each caterpillar mimics the twig it perches on, straightening its knobbly body into a stick-like shape. It also changes its hue to match the twig’s color, whether birch white, willow green or dark oak brown. They’re so good at this, in fact, that they can do it blindfolded — literally. According to a paper published in Communications Biology in early August, the caterpillars sense the color of their surroundings not only with their eyes, but also with their skin. While other animals, including cuttlefish and lizards, have similar abilities, this is “the most complete demonstration so far that color change can be controlled by cells outside the eyes,” said Martin Stevens, a professor of sensory and evolutionary ecology at the University of Exeter. Dr. Stevens, who was not involved in the study, added that the exact mechanism remains a mystery. The adult peppered moth is famous for a completely different color journey; After soot from the Industrial Revolution darkened tree bark in Britain, peppered moths there evolved to be darker, too. Ilik Saccheri, a professor of ecological genetics at the University of Liverpool and an author of the new paper, normally studies the adult moth. This requires keeping a lot of caterpillars around. Years of observation sparked his curiosity about their color-changing abilities, which happen individually and in a matter of minutes rather than over generations. Each caterpillar hatches tiny and black, and in its early days is blown around by the wind. Once it falls on a plant, it must camouflage itself to avoid being spotted by hungry birds. This process, which involves producing new pigments, plays out over a period of days or weeks. “I was a bit disbelieving that they could change that accurately only using their eyes,” which are quite simple at the larval stage, Dr. Saccheri said. © 2019 The New York Times Company

Keyword: Vision; Evolution
Link ID: 26547 - Posted: 08.27.2019

Patti Neighmond The pathway to opioid abuse for women often starts with a prescription from the doctor's office. One reason is that women are more likely than men to seek help for pain. Pain researchers say that not only do women suffer more painful conditions, they actually perceive pain more intensely than men do. "The burden of pain is substantially greater for women than men," says researcher and psychologist Roger Fillingim, "and that led pain researchers like myself to wonder if the pain perception system is different in women than in men." For more than two decades, Fillingim has been studying gender differences and pain, most recently at the University of Florida's Pain Research and Intervention Center of Excellence, where he is director. He recruits healthy male and female volunteers to take part in experimental pain sessions using various painful stimuli, including pressure, heat, cold and electrical stimulation. Probes are typically applied to the hand or arm. As intensity of the stimuli is increased, volunteers are asked to rate their pain on a scale of zero to 10, where zero is no pain and 10 is the most intense pain one can imagine. If volunteers report pain levels at 10, Fillingim stops the experiment immediately. "On average, women report the same stimuli to be more painful than men," Fillingim says, emphasizing that the same stimulus is applied to everybody, so if there are differences in how painful the experience is, it can't be because of the stimulus because it's calibrated to be the same for all. © 2019 npr

Keyword: Pain & Touch; Sexual Behavior
Link ID: 26546 - Posted: 08.27.2019

Sarah Horn, M.D., and Howard Hurtig, M.D. While people usually regard Parkinson’s disease (PD) as a disorder characterized by abnormalities of the brain’s motorfunctions (movement), such as tremor, stiffness, and difficulties with balance and walking, there is less public awareness that non-motor features, such as cognitive impairment, are equally important. At some point during the long course of this progressive disorder, most patients will be confronted with one or more non-motor symptoms, some of which develop during the premotor or prodromalstage of the illness, when a loss of neurons is accumulating throughout the nervous system before the onset of the classic motor symptoms. Understanding the full range of motor and non-motor features of PD can alert people to recognize the earliest phases of PD and thereby proactively begin a partnership with a health care provider (usually a neurologist) to develop a comprehensive plan of management. In 1817, the British neurologist James Parkinson, in his essay The Shaking Palsy, accurately described through casual observation the same motor signs and symptoms of PD that we see today. He would never learn about the disease’s non-motor abnormalities, nor would he believe that intellect was affected. Much has changed in 200 years, but only in the last two decades has it become clear that non-motor features are an integral to the pathophysiology of PD. Such features have in fact become defining markers of the disease process, particularly during the prodromal stage of the disease. The recognition of PD as a common neurological disorder—caused by a lack of the chemical dopamine in the brain—has been bolstered by its prevalence among celebrities, including Muhammad Ali, Michael J. Fox, Linda Ronstadt, Pope John Paul II, and more recently Jesse Jackson and Alan Alda. The average age at diagnosis is 62.5 years, and an estimated 10 percent of patients are diagnosed at age 50 or younger .

Keyword: Parkinsons
Link ID: 26545 - Posted: 08.27.2019

Douwe Draaisma Some 70 years ago, John Cade, an Australian psychiatrist, discovered a medication for bipolar disorder that helped many patients to regain stability swiftly. Lithium is now the standard treatment for the condition, and one of the most consistently effective medicines in psychiatry. But its rise was riddled with obstacles. The intertwined story of Cade and his momentous finding is told in Lithium, a compelling book by US psychiatrist Walter Brown. Bipolar disorder, labelled manic-depressive illness until 1980, affects around 1 in 100 people globally. Without treatment, it can become a relentless cycle of emotional highs and lows. Suicide rates for untreated people are 10–20 times those in the general population. Fortunately, lithium carbonate — derived from the light, silvery metal lithium — can reduce that figure tenfold. Brown’s telling of Cade’s eventful life covers much of the same ground as Finding Sanity (2016), a rather hagiographic biography by Greg de Moore and Ann Westmore. What Brown does superbly well is to show that Cade made his discovery without access to advances in technology or to modern facilities — and almost despite them. His finding was the happy result of being forced to work with the simplest of means. During the Second World War, Cade was interred for more than three years in the notorious Japanese prisoner-of-war camp at Changi in Singapore. He was put in charge of the psychiatric section, where he began to note the decisive link between certain food deficiencies and diseases in his fellow prisoners. A lack of B vitamins, for instance, caused beriberi and pellagra.

Keyword: Schizophrenia
Link ID: 26544 - Posted: 08.27.2019

By Laura Sanders A honeybee that’s been promoted to forager has upgrades in her nerve cells, too. Vibration-sensing nerve cells, or neurons, are more specialized in bees tasked with finding food compared with younger, inexperienced adult bees, researchers report August 26 in eNeuro. This neural refinement may help forager bees better sense specific air vibrations produced by their fellow foragers during waggle dances — elaborate routines that share information about food location, distance and quality (SN Online: 1/24/14). Researchers compared certain neurons in adult bees that had emerged from their cells one to three days earlier to neurons of forager bees, which were older than 10 days. In the foragers, these neurons had more refined shapes, the team found. These vibration-detecting cells, called DL-INT-1 neurons, appear sparser in certain areas, with fewer message-receiving tendrils called dendrites. Refined dendrites may be a sign that these cells are more selective in their connections. And in foragers, these neurons also appear to handle information more efficiently than their counterparts in the young adult bees, experiments with electrodes reveal. These changes in shape and behavior suggest that in foragers, neurons become adept at decoding vibrations produced by other foragers’ waggle dances, say computational neuroscientist Ajayrama Kumaraswamy of the Ludwig-Maximilians-Universität München in Germany and colleagues. But it’s not clear whether foraging experience in the fields or the passage of time itself prompts these refinements. © Society for Science & the Public 2000–2019

Keyword: Learning & Memory; Animal Communication
Link ID: 26543 - Posted: 08.27.2019