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By Sara Chodosh When a single neuron fires, it is an isolated chemical blip. When many fire together, they form a thought. How the brain bridges the gap between these two tiers of neural activity remains a great mystery, but a new kind of technology is edging us closer to solving it. The glowing splash of cyan in the photo above comes from a type of biosensor that can detect the release of very small amounts of neurotransmitters, the signaling molecules that brain cells use to communicate. These sensors, called CNiFERs (pronounced “sniffers”), for cell-based neurotransmitter fluorescent engineered reporters, are enabling scientists to examine the brain in action and up close. This newfound ability, developed as part of the White House BRAIN Initiative, could further our understanding of how brain function arises from the complex interplay of individual neurons, including how complex behaviors like addiction develop. Neuroscientist Paul Slesinger at Icahn School of Medicine at Mount Sinai, one of the senior researchers who spearheaded this research, presented the sensors Monday at the American Chemical Society’s 252nd National Meeting & Exposition. Current technologies have proved either too broad or too specific to track how tiny amounts of neurotransmitters in and around many cells might contribute to the transmission of a thought. Scientists have used functional magnetic resonance imaging to look at blood flow as a surrogate for brain activity over fairly long periods of time or have employed tracers to follow the release of a particular neurotransmitter from a small set of neurons for a few seconds. But CNiFERs make for a happy medium; they allow researchers to monitor multiple neurotransmitters in many cells over significant periods of time. © 2016 Scientific American

Keyword: Brain imaging
Link ID: 22600 - Posted: 08.25.2016

James Hamblin Like ​The Atlantic? Subscribe to ​the Daily​, our free weekday email newsletter. Elite tennis players have an uncanny ability to clear their heads after making errors. They constantly move on and start fresh for the next point. They can’t afford to dwell on mistakes. Peter Strick is not a professional tennis player. He’s a distinguished professor and chair of the department of neurobiology at the University of Pittsburgh Brain Institute. He’s the sort of person to dwell on mistakes, however small. “My kids would tell me, dad, you ought to take up pilates. Do some yoga,” he said. “But I’d say, as far as I’m concerned, there's no scientific evidence that this is going to help me.” Still, the meticulous skeptic espoused more of a tennis approach to dealing with stressful situations: Just teach yourself to move on. Of course there is evidence that ties practicing yoga to good health, but not the sort that convinced Strick. Studies show correlations between the two, but he needed a physiological mechanism to explain the relationship. Vague conjecture that yoga “decreases stress” wasn’t sufficient. How? Simply by distracting the mind? The stress response in humans is facilitated by the adrenal glands, which sit on top of our kidneys and spit adrenaline into our blood whenever we’re in need of fight or flight. That stress response is crucial in dire circumstances. But little of modern life truly requires it (especially among academic scientists). Most of the time, our stress responses are operating as a sort of background hum, keeping us on edge. Turn that off, and we relax. © 2016 by The Atlantic Monthly Group

Keyword: Stress
Link ID: 22599 - Posted: 08.25.2016

By Alice Callahan As new parents, Penn State researcher Doug Teti and his wife were co-sleepers, sharing their bed at night with all three of their children, now grown. So when Dr. Teti, a professor of human development and family studies, embarked on an usual study of co-sleeping, bringing cameras into the bedrooms of 139 Pennsylvania couples, he did not expect to see co-sleeping associated with family stress. But to his surprise, many of the parents in the study who co-slept with their children beyond 6 months of age, a group he called “persistent co-sleepers,” did show signs of stress, particularly the mothers. Dr. Teti emphasized that the research isn’t an indictment against co-sleeping, but does suggest that a number of factors, including cultural pressures and an unsupportive spouse, can make longer-term co-sleeping a more stressful experience for some families. “Co-sleeping is simply a practice, just like solitary sleep is a practice,” he said. “It is important for parents to be on the same page about whatever practices with their children they choose to put into effect.” The study, published this month in the journal Developmental Psychology, was unusual in that it tracked 139 couples, mostly married or living together, who generously allowed researchers to peek into their bedrooms with video cameras, recording nighttime interactions with their new babies at five time points in the first year of life. Co-sleeping — defined in this study as room-sharing or bed-sharing, often a mix of the two — was surprisingly common in early infancy. Nearly 75 percent of the parents co-slept with infants early on, and about half were still co-sleeping three months after the birth. But once the babies reached 6 months of age, only one in four babies continued to share a bed or a room with their parents. © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22598 - Posted: 08.25.2016

Laura Sanders Brain scientists Eric Jonas and Konrad Kording had grown skeptical. They weren’t convinced that the sophisticated, big data experiments of neuroscience were actually accomplishing anything. So they devised a devilish experiment. Instead of studying the brain of a person, or a mouse, or even a lowly worm, the two used advanced neuroscience methods to scrutinize the inner workings of another information processor — a computer chip. The unorthodox experimental subject, the MOS 6502, is the same chip that dazzled early tech junkies and kids alike in the 1980s by powering Donkey Kong, Space Invaders and Pitfall, as well as the Apple I and II computers. Of course, these experiments were rigged. The scientists already knew everything about how the 6502 works. “The beauty of the microprocessor is that unlike anything in biology, we understand it on every level,” says Jonas, of the University of California, Berkeley. A barrel-hurling gorilla is the enemy in Donkey Kong, a video game powered by the MOS 6502 microprocessor. Along with Space Invaders and Pitfall, this game served as the “behavior” in a recent experiment. Using a simulation of MOS 6502, Jonas and Kording, of Northwestern University in Chicago, studied the behavior of electricity-moving transistors, along with aspects of the chip’s connections and its output, to reveal how it handles information. Since they already knew what the outcomes should be, they were actually testing the methods. By the end of their experiments, Jonas and Kording had discovered almost nothing. |© Society for Science & the Public 2000 - 2016

Keyword: Brain imaging
Link ID: 22597 - Posted: 08.24.2016

Neuroscience News Researchers have identified a brain mechanism that could be a drug target to help prevent tolerance and addiction to opioid pain medication, such as morphine, according to a study by Georgia State University and Emory University. The findings, published in the Nature journal Neuropsychopharmacology in August, show for the first time that morphine tolerance is due to an inflammatory response produced in the brain. This brain inflammation is caused by the release of cytokines, chemical messengers in the body that trigger an immune response, similar to a viral infection. Researchers’ results show blocking a particular cytokine eliminated morphine tolerance, and they were able to reduce the dose of morphine required to alleviate pain by half. “These results have important clinical implications for the treatment of pain and also addiction,” said Lori Eidson, lead author and a graduate student in the laboratory of Dr. Anne Murphy in the Neuroscience Institute of Georgia State. “Until now, the precise underlying mechanism for opioid tolerance and its prevention have remained unknown.” Over 67 percent of the United States population will experience chronic pain at some point in their lives. Morphine is the primary drug used to manage severe and chronic pain, with 3 to 4 percent of adults in the U.S. receiving long-term opioid therapy. However, tolerance to morphine, defined as a decrease in pain relief over time, significantly impedes treatment for about 60 percent of patients. Long-term treatment with opioids is associated with increased risk of abuse, dependence and fatal overdoses.

Keyword: Drug Abuse; Pain & Touch
Link ID: 22596 - Posted: 08.24.2016

Nicola Davis Children who suffer a traumatic brain injury, including mild concussion from a blow to the head, are less likely to do well at school and are at increased risk of early death, researchers have revealed. As adults they are also more likely to receive a disability pension, have failed to gain secondary school qualifications and nearly twice as likely to have been hospitalised for psychiatric reasons. The team analysed data from more than a million people born between 1973 and 1985, finding that around 9% had been diagnosed with at least one traumatic brain injury before the age of 25. More than 75% of these were mild injuries. The researchers compared the outcomes for these individuals with those of others who had not experienced a head injury, as well as carrying out a second comparison, where possible, with siblings who had not been injured. Once factors such as age and sex were taken into account, the team found that those diagnosed with a traumatic brain injury have an increased risk of experiencing a number of health and social problems. Those who had suffered a traumatic brain injury were 76% more likely to receive a disability pension, 58% more likely to have failed to gain secondary school qualifications and nearly twice as likely to have been hospitalised for psychiatric reasons, compared to those who had sustained no injury. When the researchers looked at patients who had siblings that had not sustained a traumatic brain injury, they found similar - although smaller - effects, suggesting that genetics could also play a role. © 2016 Guardian News and Media Limited

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 22595 - Posted: 08.24.2016

By PAM BELLUCK The images tell a heartbreaking story: Zika’s calamitous attack on the brains of babies — as seen from the inside. A study of brain scans and ultrasound pictures of 45 Brazilian babies whose mothers were infected with Zika in pregnancy shows that the virus can inflict serious damage to many different parts of the fetal brain beyond microcephaly, the condition of unusually small heads that has become the sinister signature of Zika. The images, published Tuesday in the journal Radiology, also suggest a grim possibility: Because some of the damage was seen in brain areas that continue to develop after birth, it may be that babies born without obvious impairment will experience problems as they grow. “It really brings to the forefront the importance of truly understanding the impact of Zika virus and the fact that we need to follow children who not only are exposed to Zika in pregnancy, but even those who don’t appear to have any complications at birth,” said Dr. Catherine Y. Spong, chief of the pregnancy and perinatology branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development, who was not involved in the study. Most of the babies in the study were born with microcephaly, although three were not. Each also suffered other impairments, almost all of which emerge earlier than microcephaly because a smaller head is really a consequence of brain that has failed to develop fully or has been damaged along the way, experts said. “The brain that should be there is not there,” said Dr. Deborah Levine, an author of the study and a professor of radiology at Harvard Medical School in Boston. “The abnormalities that we see in the brain suggest a very early disruption of the brain development process.” © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22594 - Posted: 08.24.2016

Ian Sample Science editor For Jules Verne it was the friend who keeps us waiting. For Edgar Allan Poe so many little slices of death. But though the reason we spend a third of our lives asleep has so far resisted scientific explanation, research into the impact of sleepless nights on brain function has shed fresh light on the mystery - and also offered intriguing clues to potential treatments for depression. In a study published on Tuesday, researchers show for the first time that sleep resets the steady build-up of connectivity in the human brain which takes place in our waking hours. The process appears to be crucial for our brains to remember and learn so we can adapt to the world around us. The loss of a single night’s sleep was enough to block the brain’s natural reset mechanism, the scientists found. Deprived of rest, the brain’s neurons seemingly became over-connected and so muddled with electrical activity that new memories could not be properly laid down. Lack of sleep alters brain chemicals to bring on cannabis-style 'munchies' But Christoph Nissen, a psychiatrist who led the study at the University of Freiburg, is also excited about the potential for helping people with mental health disorders. One radical treatment for major depression is therapeutic sleep deprivation, which Nissen believes works through changing the patient’s brain connectivity. The new research offers a deeper understanding of the phenomenon which could be adapted to produce more practical treatments. © 2016 Guardian News and Media Limited

Keyword: Sleep; Learning & Memory
Link ID: 22593 - Posted: 08.24.2016

by Laura Sanders When someone uses the phrase “sleeping like a baby,” it’s obvious that they don’t really know how babies sleep. Many babies, especially newborns, are lousy sleepers, waking up every few hours to rustle around, cry and eat. For creatures who sleep up to 18 hours per 24-hour period, newborns are exhausting. That means that bone-tired parents are often desperate to get their babies to sleep so they can rest too. A study published in the September Pediatrics captured this nightly struggle in the homes of 162 Pennsylvanian families. And the results revealed something disturbing: Despite knowing that they were being videotaped, many parents didn’t put their babies into a safe sleeping spot. The risk of sleep-related infant deaths, including those caused by strangulation or sudden infant death syndrome, goes up when babies are put in unsafe sleeping positions or near suffocation hazards. Babies should be on their back on a firm mattress free of any objects. But that wasn’t the case for the majority of babies in the study, says Ian Paul, a pediatrician at Penn State. As a parent to three, Paul is sympathetic to the difficulties of soothing babies to sleep. “The first few months are really exhausting,” he says. But as a pediatrician, he also sees the risks of ignoring safe sleep guidelines. “Parents need to realize that these risks are real and might happen to them.” The videos taken for the study revealed that at 1 month of age, nearly all of the babies were put onto a sleep surface that had a loose or ill-advised item. |© Society for Science & the Public 2000 - 2016

Keyword: Sleep; Development of the Brain
Link ID: 22592 - Posted: 08.24.2016

By Roni Caryn Rabin We’ve all heard about the power of positive thinking. But will it help me sleep? My problem isn’t falling asleep – it’s staying asleep. This particular form of torture has been dubbed “sleep-maintenance” insomnia. Call me a high-functioning sufferer: I’m usually O.K. once I’ve had my morning coffee. But I worry about the long-term health ramifications of losing sleep. Now several medical organizations have endorsed a treatment known as cognitive behavioral therapy for insomnia or C.B.T.-I. In May the American College of Physicians advised its members that C.B.T.-I. was the first treatment they should offer patients with insomnia. I wanted to try it, but there is a shortage of trained therapists with expertise in C.B.T.-I. I didn’t want to wait for an appointment; I just wanted to solve the problem. So I decided to try an online sleep program. Convincing data that internet-based programs are effective is piling up, and a recent review of clinical trials reported that insomniacs improved their sleep as much after online C.B.T.-I. programs as they did after face-to-face C.B.T.-I. counseling. Internet programs are likely to be cheaper than most therapists, too. I downloaded a five-week course called Conquering Insomnia for $40. Another online C.B.T. program called SHUTi charges $135 for 16 weeks of access to a program, which includes a series of six sessions and follow-up for 10 weeks. Both programs provide individualized feedback on your weekly sleep logs. The developers of these programs say they want them to be accessible to as many people as possible. One in 10 people suffer from insomnia. “The number of clinicians nationally who know how to do C.B.T. for insomnia is a couple of thousand. We need 100,000,” said Dr. Gregg Jacobs, a sleep medicine specialist and assistant professor of psychiatry at the University of Massachusetts Medical School who developed the Conquering Insomnia program. “There are tens of millions of people out there who have insomnia.” © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22591 - Posted: 08.24.2016

By NICHOLAS ST. FLEUR Neuroscientists have developed a way to turn an entire mouse, including its muscles and internal organs, transparent while illuminating the nerve paths that run throughout its body. The process, called uDisco, provides an alternate way for researchers to study an organism’s nervous system without having to slice into sections of its organs or tissues. It allows researchers to use a microscope to trace neurons from the rodent’s brain and spinal cord all the way to its fingers and toes. “When I saw images on the microscope that my students were obtaining, I was like ‘Wow, this is mind blowing,’” said Ali Ertürk, a neuroscientist from the Ludwig Maximilians University of Munich in Germany and an author of the paper. “We can map the neural connectivity in the whole mouse in 3D.” They published their technique Monday in the journal Nature Methods. So far, the technique has been conducted only in mice and rats, but the scientists think it could one day be used to map the human brain. They also said it could be particularly useful for studying the effects of mental disorders like Alzheimer’s disease or schizophrenia. Dr. Ertürk and his colleagues study neurodegenerative disorders, and are particularly interested in diseases that occur from traumatic brain injuries. Researchers often study these diseases by examining thin slices of brain tissue under a microscope. “That is not a good way to study neurons because if you slice the brain, you slice the network,” Dr. Ertürk said. “The best way to look at it is to look at the entire organism, not only the brain lesion but beyond that. We need to see the whole picture.” To do this, Dr. Ertürk and his team developed a two-step process that renders a rodent transparent while keeping its internal organs structurally sound. The mice they used were dead and had been tagged with a special fluorescent protein to make specific parts of their anatomy glow. © 2016 The New York Times Company

Keyword: Brain imaging
Link ID: 22590 - Posted: 08.23.2016

Scientists and clinicians have long dreamed of helping the injured brain repair itself by creating new neurons, and an innovative NIH-funded study published today in Nature Medicine may bring this goal much closer to reality. A team of researchers has developed a therapeutic technique that dramatically increases the production of nerve cells in mice with stroke-induced brain damage. The therapy relies on the combination of two methods that show promise as treatments for stroke-induced neurological injury. The first consists of surgically grafting human neural stem cells into the damaged area, where they mature into neurons and other brain cells. The second involves administering a compound called 3K3A-APC, which the scientists have shown helps neural stem cells grown in a petri dish develop into neurons. However, it was unclear what effect the molecule, derived from a human protein called activated protein-C (APC), would have in live animals. A month after their strokes, mice that had received both the stem cells and 3K3A-APC performed significantly better on tests of motor and sensory functions compared to mice that received neither or only one of the treatments. In addition, many more of the stem cells survived and matured into neurons in the mice given 3K3A-APC. “This USC-led animal study could pave the way for a potential breakthrough in how we treat people who have experienced a stroke,” added Jim Koenig, Ph.D., a program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which funded the research. “If the therapy works in humans, it could markedly accelerate the recovery of these patients.”

Keyword: Stroke; Stem Cells
Link ID: 22589 - Posted: 08.23.2016

By Clare Wilson Taking a daily vitamin or mineral supplement is widely seen as a common-sense way of looking after yourself – a kind of insurance, like wearing a seat belt. But evidence is growing that it might not be such a healthy habit after all. The latest finding is that calcium supplements, taken by many women after the menopause to strengthen their bones, are linked to dementia. Among women who have had a stroke, taking calcium was associated with a seven-fold rise in the number who went on to have dementia. Calcium was also linked with a smaller, non-statistically significant, rise in dementia in women who had not had a stroke. The finding emerged from a study that was not a randomised trial, so it is not the most robust type of medical evidence. The researchers merely counted dementia cases in people who had chosen whether to take calcium, and so the data could be biased. But the results are striking and come on the heels of a previous study that was a randomised trial, which found a link between calcium supplements and a modestly higher risk of heart attacks – suggesting that caution over calcium is indeed warranted. If future research confirms the association with dementia, women would face a horrible dilemma: should they continue to take calcium, staving off bone weakness that can lead to fatal hip fractures, while running an increased risk of one of the most dreaded illness of ageing? So what’s going on? Team member Silke Kern at the Sahlgrenska Academy Institute of Neuroscience and Physiology in Gothenburg, Sweden, says that taking a calcium pill triggers a rapid surge in the mineral’s levels in the blood, one that you wouldn’t get from calcium in food. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers
Link ID: 22588 - Posted: 08.23.2016

By GINA KOLATA Shena Pearson nearly froze in her seat, terrified, as she stared at a power-point slide. She was at her first meeting of an epilepsy foundation, seeking help for her 12-year-old son Trysten, when a neurologist flashed the slide about something called Sudep. It stands for sudden unexpected death in epilepsy. Her son’s neurologist had never mentioned it. “Oh dear God, my child is at risk, seriously at risk,” Ms. Pearson thought to herself. Sudden death in epilepsy is a little-known and seldom-mentioned phenomenon, but now, after a push by advocates, the federal government has begun a concerted program to understand it. Yet a question remains: When, if ever, should patients be warned? In a way, the extreme reticence of many neurologists to mention sudden unexpected death to epilepsy patients harks back to the days when doctors and families often did not tell people they had cancer — too terrifying. But today, patients learn not just about cancer but about many other potentially fatal conditions, like an inoperable brain aneurysm that could burst at any time and kill a person. So the quiet about the epilepsy death risk appears to be an anomaly. Sudep’s name pretty much explains what it is: Someone with epilepsy — unprovoked seizures, which are electrical surges in the brain — dies, and there is no apparent cause. Often a person with epilepsy goes to bed and is found in the morning, unresponsive. In some cases, there is indirect evidence of a seizure, like urine on the sheets, bloodshot eyes or a severely bitten tongue, leading to the suggestion that preventing seizures as much as possible with medications could lower patients’ risks. But so much about the syndrome remains unknown. © 2016 The New York Times Company

Keyword: Epilepsy
Link ID: 22587 - Posted: 08.23.2016

By Daniel Barron After prepping for the day’s cases, “Mike Brennan,” a 63-year-old cardiology technician, sat down for his morning coffee and paper. On the front page, he discovered something troubling: he could no longer read. No matter how long he stared at a word, its meaning was lost on him. With a history of smoking and hypertension, he worried that he might have had a stroke. So, leaving his coffee, he walked himself down the hall to the emergency department, where neurologists performed a battery of tests to tease out what had happened. Mike still recognized individual letters and, with great difficulty, could sound out small words. But even some simple vocabulary presented problems, for example, he read “desk” as “dish” or “flame” as “thame.” Function words such as prepositions and pronouns gave him particular trouble. Mike couldn’t read, but there was nothing wrong with his eyes. Words heard were no problem. He could recognize colors, faces, and objects. He could speak, move, think and even write normally. Mike had “pure alexia,” meaning he could not read but showed no other impairments. An M.R.I. scan of Mike’s brain revealed a pea-sized stroke in his left inferior occipitotemporal cortex, a region on the brain’s surface just behind the left ear. © 2016 Scientific American

Keyword: Language
Link ID: 22586 - Posted: 08.23.2016

By Lydia Pyne | On August 3, 1908, the first near-complete Neanderthal skeleton was discovered in a cave near the village of La Chapelle-aux-Saints in south central France, during a survey of the region’s Paleolithic archaeological sites. For decades prior, prehistorians had collected bits and pieces of curious but not-quite-human fossils from museums and excavations alike—the odd skull here, a scrap of tooth there. In 1863, the mélange of bones was finally given its own species designation, Homo neanderthalensis. Forty-five years later, the La Chapelle discovery was the first Neanderthal specimen found in an original archaeological context and the first to be expertly excavated and carefully studied. Because the body was arranged in a flexed, fetal position and carefully placed in the floor of the cave, excavators argued that fossil—nicknamed the Old Man—had been purposefully buried by his Neanderthal contemporaries. More than any other single individual, the Old Man of La Chapelle has shaped the way that science and popular culture have thought about Neanderthals. But why? What is it about this Neanderthal’s story that is so special? In short, the Old Man was the right fossil found at the right time. He was—and still is—offered as a key bit of evidence in debates about evolution and human origins. He quickly became a scientific touchstone, an archetype for how science and popular culture create celebrity fossils. I explore the stories of similarly spectacular paleoanthropological finds in my new book Seven Skeletons: The Evolution of the World’s Most Famous Human Fossils. © 1986-2016 The Scientist

Keyword: Evolution
Link ID: 22585 - Posted: 08.23.2016

Sara Reardon Neuroscientists have invented a way to watch the ebb and flow of the brain's chemical messengers in real time. They were able to see the surge of neurotransmitters as mice were conditioned — similarly to Pavlov's famous dogs — to salivate in response to a sound. The study, presented at the American Chemical Society’s meeting in Philadelphia, Pennyslvania, on 22 August, uses a technique that could help to disentangle the complex language of neurotransmitters. Ultimately, it could lead to a better understanding of brain circuitry. The brain’s electrical surges are easy to track. But detecting the chemicals that drive this activity — the neurotransmitters that travel between brain cells and lead them to fire — is much harder. “There’s a hidden signalling network in the brain, and we need tools to uncover it,” says Michael Strano, a chemical engineer at the Massachusetts Institute of Technology in Cambridge. In many parts of the brain, neurotransmitters can exist at undetectably low levels. Typically, researchers monitor them by sucking fluid out from between neurons and analysing the contents in the lab. But that technique cannot measure activity in real time. Another option is to insert a metal probe into the space between neurons to measure how neurotransmitters react chemically when they touch metal. But the probe is unable to distinguish between structurally similar molecules, such as dopamine, which is involved in pleasure and reward, and noradrenaline which is involved in alertness. © 2016 Macmillan Publishers Limited

Keyword: Brain imaging; Drug Abuse
Link ID: 22584 - Posted: 08.22.2016

Laura Sanders Fractions of a second after food hits the mouth, a specialized group of energizing nerve cells in mice shuts down. After the eating stops, the nerve cells spring back into action, scientists report August 18 in Current Biology. This quick response to eating offers researchers new clues about how the brain drives appetite and may also provide insight into narcolepsy. These nerve cells have intrigued scientists for years. They produce a molecule called orexin (also known as hypocretin), thought to have a role in appetite. But their bigger claim to fame came when scientists found that these cells were largely missing from the brains of people with narcolepsy. People with narcolepsy are more likely to be overweight than other people, and this new study may help explain why, says neuroscientist Jerome Siegel of UCLA. These cells may have more subtle roles in regulating food intake in people without narcolepsy, he adds. Results from earlier studies hinted that orexin-producing nerve cells are appetite stimulators. But the new results suggest the opposite. These cells actually work to keep extra weight off. “Orexin cells are a natural obesity defense mechanism,” says study coauthor Denis Burdakov of the Francis Crick Institute in London. “If they are lost, animals and humans gain weight.” Mice were allowed to eat normally while researchers eavesdropped on the behavior of their orexin nerve cells. Within milliseconds of eating, orexin nerve cells shut down and stopped sending signals. |© Society for Science & the Public 2000 - 2016

Keyword: Obesity
Link ID: 22583 - Posted: 08.22.2016

By KATHERINE KINZLER You may not be surprised to learn that food preference is a social matter. What we choose to eat depends on more than just what tastes good or is healthful. People in different cultures eat different things, and within a culture, what you eat can signal something about who you are. More surprising is that the sociality of food selection, it turns out, runs deep in human nature. In research published this month in the Proceedings of the National Academy of Sciences, my colleagues and I showed that even 1-year-old babies understand that people’s food preferences depend on their social or cultural group. Interestingly, we found that babies’ thinking about food preferences isn’t really about food per se. It’s more about the people eating foods, and the relationship between food choice and social groups. While it’s hard to know what babies think before they can talk, developmental psychologists have long capitalized on the fact that babies’ visual gaze is guided by their interest. Babies tend to look longer at something that is novel or surprising. Do something bizarre the next time you meet a baby, and you’ll notice her looking intently. Using this method, the psychologists Zoe Liberman, Amanda Woodward, Kathleen Sullivan and I conducted a series of studies. Led by Professor Liberman, we brought more than 200 1-year-olds (and their parents) into a developmental psychology lab, and showed them videos of people visibly expressing like or dislike of foods. For instance, one group of babies saw a video of a person who ate a food and expressed that she loved it. Next they saw a video of a second person who tried the same food and also loved it. This second event was not terribly surprising to the babies: The two people agreed, after all. Accordingly, the babies did not look for very long at this second video; it was what they expected. © 2016 The New York Times Company

Keyword: Obesity; Development of the Brain
Link ID: 22582 - Posted: 08.22.2016

Laura Sanders For some people, fentanyl can be a life-saver, easing profound pain. But outside of a doctor’s office, the powerful opioid drug is also a covert killer. In the last several years, clandestine drugmakers have begun experimenting with this ingredient, baking it into drugs sold on the streets, most notably heroin. Fentanyl and closely related compounds have “literally invaded the entire heroin supply,” says medical toxicologist Lewis Nelson of New York University Langone Medical Center. Fentanyl is showing up in other drugs, too. In San Francisco’s Bay Area in March, high doses of fentanyl were laced into counterfeit versions of the pain pill Norco. In January, fentanyl was found in illegal pills sold as oxycodone in New Jersey. And in late 2015, fentanyl turned up in fake Xanax pills in California. This ubiquitous recipe-tinkering makes it impossible for users to know whether they’re about to take drugs mixed with fentanyl. And that uncertainty has proved deadly. Fentanyl-related deaths are rising sharply in multiple areas. National numbers are hard to come by, but in many regions around the United States, fentanyl-related fatalities have soared in recent years. Maryland is one of the hardest-hit states. From 2007 to 2012, the number of fentanyl-related deaths hovered around 30 per year. By 2015, that number had grown to 340. A similar rise is obvious in Connecticut, where in 2012, there were 14 fentanyl-related deaths. In 2015, that number was 188. |© Society for Science & the Public 2000 - 2016.

Keyword: Drug Abuse; Pain & Touch
Link ID: 22581 - Posted: 08.22.2016