Philip Ball Last week, I was told my other brain is fully grown. It doesn’t look like much. A blob of pale flesh about the size of a small pea, it floats in a bath of blood-red nutrient. It would fit into the cranium of a foetus barely a month old. Still, it’s a “brain” after a fashion and it’s made from me. From a piece of my arm, to be precise. I’m not going to pretend this isn’t strange. But neither is it an exercise in gratuitously ghoulish biological engineering, a piece of Frankensteinian scientific hubris 200 years after Mary Shelley’s tale. The researchers who made my mini-brain are trying to understand how neurodegenerative diseases develop. With mini-brains grown from the tissues of people who have a genetic susceptibility to the early onset of conditions such as Alzheimer’s, they hope to unravel what goes awry in the mature adult brain. It’s this link to studies of dementia that led me to the little room in the Dementia Research Centre of University College London last July, where neuroscientist Ross Paterson anaesthetised my upper arm and then sliced a small plug of flesh from it. This biopsy was going to be the seed for growing brain cells – neurons – that would organise themselves into mini-brains. The Brains in a Dish project is one of many strands of Created Out of Mind, an initiative hosted at the Wellcome Collection in London and funded by the Wellcome Trust for two years to explore, challenge and shape perceptions and understanding of dementias through science and the creative arts. Neuroscientist Selina Wray at UCL is studying the genetics of Alzheimer’s and other neurodegenerative diseases and she and her PhD student Christopher Lovejoy gamely agreed to culture mini-brains from cells taken from four of the Created Out of Mind team: artist Charlie Murphy, who is leading Brains in a Dish, BBC journalist Fergus Walsh, neurologist Nick Fox and me. © 2018 Guardian News and Media Limited

Keyword: Development of the Brain
Link ID: 24809 - Posted: 04.02.2018

Scott Simon One spring morning in 2015, Barbara Lipska got up as usual, dyed her hair and went for a jog in her suburban Virginia neighborhood. But when she returned from a much longer than expected run, her husband Mirek was completely taken aback. "I was lost in my own neighborhood," Lipska says. "The hair dye that I put in my hair that morning dripped down my neck. I looked like a monster when I came back home." Although she now lucidly recalls that moment, at the time she was oblivious to her unusual appearance and behavior. Lipska studies the neuroscience of mental illness and brain development at the National Institute of Mental Health. In her work she's examined the molecular structure of the brains of people who were so afflicted with schizophrenia or other disorders that they took their own lives. And for two months in 2015, she developed similar symptoms of dementia and schizophrenia — only to learn they were the effects of cancerous tumors, growing in her brain. © 2018 npr

Keyword: Miscellaneous
Link ID: 24808 - Posted: 04.02.2018

by Erin Blakemore April is Parkinson’s Disease Awareness Month, a time to think about how much you know about the disease. You may know about the tremors and stiffness that gradually take over patients’ bodies. You may know about famous people with the disease, including Michael J. Fox. For what you may not know, there’s the PD Library. If you have Parkinson’s disease or care for someone who does, you need information. And you might just find answers in the PD Library. The free online resource — maintained by the Parkinson’s Foundation — is a gold mine for anyone with an interest in the disease. About 60,000 Americans get a Parkinson’s diagnosis every year. The movement disorder happens when brain cells can’t produce enough dopamine. There is no cure for Parkinson’s disease, but there is help for those experiencing symptoms. The library includes PSAs, podcasts and pamphlets about such things as hallucinations, medication adherence and nutrition. Medical providers might want to take a look: There are videos of webcasts for nurses who care for patients with Parkinson’s disease and for caregivers who need help with such things as engaging patients in their own care and administering medication. One helpful tool on the site is a series of slides from expert briefings. There are free booklets, too, including one on psychosis and one on sleep. © 1996-2018 The Washington Post

Keyword: Parkinsons
Link ID: 24807 - Posted: 04.02.2018

By Adrian Cho When a football player takes a big hit to the head and gets his “bell rung,” it’s more than an expression: Like a real bell, the player’s brain can oscillate at different frequencies, a new modeling study finds. The results bolster the notion that concussions originate not so much from the collision of the brain with the skull, but in the stretching and shearing of tissue that the ringing causes deep within the brain. The researchers suggest that better helmets could be designed to dampen the most damaging low-frequency vibrations. The work could significantly simplify the modeling of concussions, says Philip Bayly, a mechanical engineer specializing in head impacts at Washington University in St. Louis in Missouri, who was not involved in the study. “To me, that’s the main thing,” he says. “It’s the low frequencies that dominate and you can simulate the brain with just a few low-frequency modes.” Every year hundreds of thousands of Americans suffer concussions while participating in sports or other recreational activities. However, scientists don’t know exactly how a blow to the head produces the injury. In the popular conception, a concussion occurs when the cranium comes to a sudden stop and the brain crashes into it, like a car driver flying into the dashboard. But research suggests that concussions are more complicated. For example, a violent rotation of the skull—as can happen when a skateboarder’s head slams sideways into the pavement—can cause more damage than a simple sudden stop. Clinical data also suggest that concussions involve more than the surface of the brain, as their severity correlates with damage deeper inside, such as deformations around the corpus callosum, the bridge between the brain’s hemispheres. © 2018 American Association for the Advancement of Science

Keyword: Brain Injury/Concussion
Link ID: 24806 - Posted: 03.31.2018

By TARA PARKER-POPE Today’s teenagers have been raised on cellphones and social media. Should we worry about them or just get out of their way? A recent wave of student protests around the country has provided a close-up view of Generation Z in action, and many adults have been surprised. While there has been much hand-wringing about this cohort, also called iGen or the Post-Millennials, the stereotype of a disengaged, entitled and social-media-addicted generation doesn’t match the poised, media-savvy and inclusive young people leading the protests and gracing magazine covers. There’s 18-year-old Emma González, whose shaved head, impassioned speeches and torn jeans have made her the iconic face of the #NeverAgain movement, which developed after the 17 shooting deaths in February at Marjory Stoneman Douglas High School in Parkland, Fla. Naomi Wadler, just 11, became an overnight sensation after confidently telling a national television audience she represented “African-American girls whose stories don’t make the front page of every national newspaper.” David Hogg, a high school senior at Stoneman Douglas, has weathered numerous personal attacks with the disciplined calm of a seasoned politician. Sure, these kids could be outliers. But plenty of adolescent researchers believe they are not. “I think we must contemplate that technology is having the exact opposite effect than we perceived,” said Julie Lythcott-Haims, the former dean of freshmen at Stanford University and author of “How to Raise an Adult.” “We see the negatives of not going outside, can’t look people in the eye, don’t have to go through the effort of making a phone call. There are ways we see the deficiencies that social media has offered, but there are obviously tremendous upsides and positives as well.” “I am fascinated by the phenomenon we are seeing in front of us, and I don’t think it’s unique to these six or seven kids who have been the face of the Parkland adolescent cohort,” says Lisa Damour, an adolescent psychologist and author of “Untangled: Guiding Teenage Girls Through the Seven Transitions Into Adulthood.” © 2018 The New York Times Company

Keyword: Intelligence; Development of the Brain
Link ID: 24805 - Posted: 03.31.2018

by Amy Ellis Nutt and Dan Keating The first warning came a dozen years ago, when the Food and Drug Administration accused the drug company AstraZeneca of “false or misleading” information about health risks in the marketing material for its blockbuster medication Seroquel, an antipsychotic developed to treat schizophrenia but increasingly prescribed “off label” for insomnia. What followed was an onslaught of litigation by state attorneys general, who charged AstraZeneca with fraudulently promoting Seroquel for unapproved uses, and by individual patients, who claimed that it had failed to alert consumers about some of the drug’s most pernicious side effects. Although the company never admitted wrongdoing, by the end of 2011 it had paid out more than $1 billion to settle many of the cases. Another product might have been derailed, but not Seroquel. Despite generic competition and lingering lawsuits, AstraZeneca’s annual reports show Seroquel remained a blockbuster, with $3.6 billion in sales from 2014 to 2016. In the drug’s titanic success and its strong link to off-label prescribing lies a cautionary tale — about the sometimes conflicting forces within health care, the relationship between medications and marketing, and the limits of regulatory protections. These days, the powerful antipsychotic is used for an expansive array of ills, including insomnia, post-traumatic stress disorder and agitation in patients with dementia. Many of the doctors who turn to it for off-label uses are physicians with minimal training in psychiatry and, medical experts say, too little understanding of the potential downsides. © 1996-2018 The Washington Post

Keyword: Schizophrenia; Sleep
Link ID: 24804 - Posted: 03.31.2018

By Liz Tormes When I first started working as a photo researcher for Scientific American MIND in 2013, a large part of my day was spent looking at brains. Lots of them. They appeared on my computer screen in various forms—from black-and-white CT scans featured in dense journals to sad-looking, grey brains sitting on the bottom of glass laboratory jars. At times they were boring, and often they could be downright disturbing. But every now and then I would come across a beautiful 3D image of strange, rainbow-colored pathways in various formations that looked like nothing I had ever seen before. I was sure it had been miscategorized somehow—no way was I looking at a brain! Through my work I have encountered countless images of multi-colored Brainbows, prismatic Diffusion Tensor Imaging (DTI), and even tiny and intricate neon mini-brains grown from actual stem cells in labs. Increasingly I have found myself dazzled, not just by the pictures themselves, but by the scientific and technological advances that have made this type of imaging possible in only the past few years. It was through my photo research that I happened upon the Netherlands Institute for Neuroscience’s (NIN) annual Art of Neuroscience contest. This exciting opportunity for neurologists, fine artists, videographers and illustrators, whose work is inspired by human and animal brains, was something I wanted to share with our readers. © 2018 Scientific American

Keyword: Brain imaging
Link ID: 24803 - Posted: 03.31.2018

By Simon Makin Neuroscientists today know a lot about how individual neurons operate but remarkably little about how large numbers of them work together to produce thoughts, feelings and behavior. What is needed is a wiring diagram for the brain—known as a connectome—to identify the circuits that underlie brain functions. The challenge is dizzying: There are around 100 billion neurons in the human brain, which can each make thousands of connections, or synapses, making potentially hundreds of trillions of connections. So far, researchers have typically used microscopes to visualize neural connections, but this is laborious and expensive work. Now in a paper published March 28 in Nature, an innovative brain-mapping technique developed at Cold Spring Harbor Laboratory (CSHL) has been used to trace the connections emanating from hundreds of neurons in the main visual area of the mouse cortex, the brain’s outer layer. The technique, which exploits the advancing speed and plummeting cost of genetic sequencing, is more efficient than current methods, allowing the team to produce a more detailed picture than previously possible at unprecedented speed. Once the technology matures it could be used to provide clues to the nature of neuro-developmental disorders such as autism that are thought to involve differences in brain wiring. The team, led by Anthony Zador at CSHL and neuroscientist Thomas Mrsic-Flogel of the University of Basel in Switzerland, verified their method by comparing it with a previous gold-standard means of identifying connections among nerve cells—a technique called fluorescent single neuron tracing. This involves introducing into cells genes that produce proteins that fluoresce with a greenish glow, so they and their axons (neurons’ output wires) can be visualized with light microscopy. © 2018 Scientific American

Keyword: Brain imaging; Schizophrenia
Link ID: 24802 - Posted: 03.30.2018

A new report says an estimated one in every 66 Canadian children and youth aged five to 17 has autism spectrum disorder. The report by the Public Health Agency of Canada, released on Thursday, is the first detailing the national prevalence of the neurodevelopmental disorder and is in line with estimates in the United States. Autism spectrum disorder is typically detected in early childhood and causes impairments in communication skills and social interactions, often combined with repetitive behaviours and restricted interests or activities. Boys are four to five times more likely to be diagnosed with autism spectrum disorder, or ASD, than girls. "Understanding trends and patterns in ASD diagnosis is essential to developing meaningful programs and services to support people living with ASD and their families," said Dr. Theresa Tam, chief public health officer, noting that the estimates establish a baseline that will help researchers determine if prevalence rates are changing over time. The report includes data from six provinces and one territory and found prevalence ranged from a high of one in 57 children in Newfoundland and Labrador, to one in 126 in Yukon. Newfoundland and Labrador, Nova Scotia, Prince Edward Island, New Brunswick, Quebec, British Columbia and Yukon all contributed data to the report, a spokesperson for the Public Health Agency of Canada said. ©2018 CBC/Radio-Canada.

Keyword: Autism
Link ID: 24801 - Posted: 03.30.2018

Rachel Ehrenberg BOSTON — Getting your groove on solo with headphones on might be your jam, but it can’t compare with a live concert. Just ask your brain. When people watch live music together, their brains waves synchronize, and this brain bonding is linked with having a better time. The new findings, reported March 27 at a Cognitive Neuroscience Society meeting, are a reminder that humans are social creatures. In western cultures, performing music is generally reserved for the tunefully talented, but this hasn’t been true through much of human history. “Music is typically linked with ritual and in most cultures is associated with dance,” said neuroscientist Jessica Grahn of Western University in London, Canada. “It’s a way to have social participation.” Study participants were split into groups of 20 and experienced music in one of three ways. Some watched a live concert with a large audience, some watched a recording of the concert with a large audience, and some watched the recording with only a few other people. Each person wore EEG caps, headwear covered with electrodes that measure the collective behavior of the brain’s nerve cells. The musicians played an original song they wrote for the study. The delta brain waves of audience members who watched the music live were more synchronized than those of people in the other two groups. Delta brain waves fall in a frequency range that roughly corresponds to the beat of the music, suggesting that beat drives the synchronicity, neuroscientist Molly Henry, a member of Grahn’s lab, reported. The more synchronized a particular audience member was with others, the more he or she reported feeling connected to the performers and enjoying the show. |© Society for Science & the Public 2000 - 2018

Keyword: Hearing
Link ID: 24800 - Posted: 03.30.2018

By KAREN BARROW Creepy-crawly, itchy, tingly, aching legs — while different people may describe restless leg syndrome differently the results are the same: sleepless nights and restless days. What is it like to be diagnosed with R.L.S.? Six men and women speak about their experiences. Lynne Kaiser, an artist, believes she has had restless leg syndrome for most of her life. She recalls waking up in the middle of the night as a child to take a hot bath or fill a hot water bottle to try to relieve the prickly sensations in her legs. It wasn’t until recently that a specialist confirmed the diagnosis. Today, Mrs. Kaiser advocates for R.L.S. patients. Dopaminergic medications, as well as art and needlework, help her to “get in a tunnel” where she can be distracted from the uncomfortable sensations, she said. Mrs. Kaiser says the symptoms of R.L.S. strained her relationship with her husband. He couldn’t understand why she couldn’t just relax in bed with him, or why she would get up at night to stretch her legs or sit in a scalding hot bath. Because of R.L.S., Mrs. Kaiser finds it difficult to travel. She also knows that R.L.S. medications tend to lose their effectiveness over time, so she focuses on how good she feels today. “I really try not to think about the future,” she said. Dr. David Rye, a professor of neurology at Emory University in Atlanta, discovered that he had restless leg syndrome several years after he began researching the disease. He says that many in the medical community believe that R.L.S. is a psychological disease rather than a physical ailment. However, Dr. Rye and his colleagues were among the first to discover a gene variant linked to R.L.S. Genetic factors help to explain why R.L.S. is so much more prevalent among Caucasians than other ethnicities. © 2018 The New York Times Company

Keyword: Sleep
Link ID: 24799 - Posted: 03.29.2018

Martha Bebinger A pipe was the only sign of drug use found near Chris Bennett's body in November. But it looked like the 32-year-old Taunton, Mass. native had stopped breathing and died of an opioid overdose. Bennett's mother Liisa couldn't understand what happened. Then she saw the toxicology report. "I'm convinced he was smoking cocaine that was laced," she says. "That's what he had in his system, [it] was cocaine and fentanyl." Liisa Bennett was shocked. Chris had developed an addiction to pain pills and then heroin in his late teens but had not used opioids for at least 10 years, as far as she knew. Bennett had warned her son that if he ever used opioids again, he'd be in greater danger of an overdose because fentanyl, an opioid drug more powerful than heroin, was mixed into much of the supply. "My focus was making sure that he wasn't going to do the heroin that was laced," Bennett says. She never suspected the crack cocaine Chris smoked occasionally would kill him. "Absolutely not." The Centers for Disease Control and Prevention says fentanyl, which is up to 50 times more powerful than heroin, was found in more than half of overdose deaths last year in 10 states including Massachusetts. Now, there's concern as it creeps into cocaine. © 2018 npr

Keyword: Drug Abuse
Link ID: 24798 - Posted: 03.29.2018

By Laura Sanders U.S. deaths from opioid overdoses are mounting with breathtaking speed. These powerful drugs — including heroin, morphine and fentanyl — can relieve pain and evoke intense feelings of pleasure. But the same drugs, whether prescribed by a doctor or bought on the street, can quickly turn deadly by simultaneously messing with crucial systems in the body. Among the many rapid effects that opioids have on the body, one is particularly lethal: Breathing is restricted. “Opioids kill people by slowing the rate of breathing and the depth of breathing,” says medical toxicologist and emergency physician Andrew Stolbach of Johns Hopkins University School of Medicine. Breathing delivers fresh oxygen to the body’s cells and eliminates carbon dioxide. Opioids can interfere with that life-sustaining process in multiple, dangerous ways. Here’s how opioids kill. In the brain stem, regions called the medulla and the pons control the depth and rate of breathing. Both are loaded with opioid receptors — proteins that sit on the surface of cells and grab onto opioids. Upon activating, the receptors change the behavior of cells in ways that can slow or even stop breathing.

Keyword: Drug Abuse
Link ID: 24797 - Posted: 03.29.2018

By Catherine Offord A tadpole has a lot of growing to do to get up to the size it needs to be to metamorphose into an adult frog or toad. Now, researchers at the University of Michigan suggest that this rapid growth is made possible by a lack of inhibitory feeding controls prior to metamorphosis. The team reports the absence of these controls, along with the hormonal regulation that accompanies it, today (March 28) in Proceedings of the Royal Society B. “Our findings are consistent with the hypothesis that the strong drive to eat prior to metamorphosis is due to the absence, or the relative immaturity of hypothalamic feeding control circuits,” the authors write in their paper. This lack of inhibition helps allow “the animal to maximize growth during this critical life-history stage.” Previous work by the researchers had implicated a role for leptin, a hormone that acts as a hunger inhibitor in vertebrates, in regulating the changing feeding habits of toads during early development. To investigate how this hormone might prepare juvenile amphibians for metamorphosis, the team analyzed levels of mRNA transcripts for leptin receptor proteins and for the hormone itself in tadpoles of the African clawed frog (Xenopus laevis). The researchers found that the tadpoles were essentially unresponsive to leptin, unlike their adult counterparts, and showed minimal expression of the leptin receptor in the hypothalamus—a key brain region in the regulation of feeding behavior. Instead, these responses develop as the relevant neural circuits mature during metamorphosis, the authors write. © 1986-2018 The Scientist

Keyword: Obesity
Link ID: 24796 - Posted: 03.29.2018

by Ariana Eunjung Cha) Sally Clark lost both her infant sons shortly after their births. In 1996, 11-week-old Christopher fell unconscious after being put to bed and never woke up. Two years later, 8-week-old Harry was found dead slumped forward in his bouncy chair. Doctors initially concluded the first boy had died of sudden infant death syndrome (SIDS) — in which a seemingly healthy baby dies without warning and without an obvious cause. But after Clark's second child died, prosecutors in the United Kingdom charged her with murder and put her on trial. According to scholars analyzing the widely publicized case, Clark was wrongly convicted based on a statistic. An expert witness for the prosecution claimed the chance of two cases of SIDS, in an affluent family like hers, was astronomically high — 1 in 73 million. Her defenders said the numbers assumed that SIDS strikes at random, even though we had no idea back then whether that was true. An important study published Wednesday in the Lancet shows a link between SIDS and a rare genetic mutation that would make some families more vulnerable than others — providing a possible explanation for situations like Clark's. The research involved 278 infants who died of SIDS, also called “crib death” or “cot death,” and 729 healthy controls. Four of those who died of SIDS had a variant of a gene called SCN4A associated with an impairment of breathing muscles, while no babies in the control group had it. Authors Michael Hanna from the United Kingdom's Medical Research Council's Center for Neuromuscular Diseases and Michael Ackerman from the Mayo Clinic in the United States wrote that these mutations are typically found in fewer than 5 out of 100,000 people. © 1996-2018 The Washington Post

Keyword: Sleep; Genes & Behavior
Link ID: 24795 - Posted: 03.29.2018

By NICHOLAS BAKALAR Being physically fit in midlife may reduce a woman’s risk for dementia. In 1968, Swedish researchers evaluated the cardiovascular fitness of 191 women ages 38 to 60, testing their endurance with an ergometer cycling test. Then they examined them periodically through 2012. Over the years, 44 women developed dementia. They categorized the women into three fitness groups based on peak workload in their cycling tests: low, medium and high. The incidence of all-cause dementia was 32 percent in the low fitness group, 25 percent for the medium, and 5 percent among those with a high fitness level. The average age at dementia was 11 years older in the high-fitness group than in the medium fitness group. Compared with medium fitness, high fitness decreased the risk of dementia by 88 percent. The study, in Neurology, controlled for many variables, including smoking, drinking, blood pressure and cholesterol, and the follow-up was very long. But the sample was small and the study is observational, and the authors draw no conclusions about cause and effect. Still, the senior author, Dr. Ingmar Skoog, a professor of psychiatry at the University of Gothenburg, said that women should get moving for many reasons. “If you start exercising,” he said, “you reduce your risk for cardiovascular disease, cancer and dementia. And you get immediate gratification by feeling better.” © 2018 The New York Times Company

Keyword: Alzheimers
Link ID: 24794 - Posted: 03.29.2018

Sara Reardon Jhon Kennedy was building a house for his family when he realized that his 45-year-old father was beginning to struggle with daily life. His dad tried to help with the construction project but often forgot to complete simple tasks. And he kept getting lost on the way home from work. Jhon Kennedy wasn’t surprised: his four uncles had also started to lose their memories, one by one. But their doctors in Colombia's rural Antioquia region, which is known for its mountainous terrain and coffee plantations, had never heard of early-onset dementia. It wasn’t until a cousin learned about a study of Alzheimer’s disease at the University of Antioquia in Medellín that Jhon Kennedy’s relatives understood the illness they faced. For more than three decades, researchers there have been tracking a genetic mutation — common in the region — that causes Alzheimer’s to strike people in their 40s and 50s. Later this year, a team at the university will begin scanning the brains of some Alzheimer’s-study participants with a technique that is available only in a few major medical centres worldwide. It will allow the researchers to track a protein called tau, which accumulates rapidly in the brains of people with the disease as symptoms begin to emerge. Watching tau form in real time could reveal the role it plays in Alzheimer’s, says Francisco Lopera, the neurologist who is leading the research. Many scientists have long believed that the disease is triggered by another protein, amyloid, that builds up in the brains of people with Alzheimer’s. But several drugs that reduce amyloid levels have failed to relieve the symptoms of the disease in clinical trials, increasing researchers’ interest in the role of tau. © 2018 Macmillan Publishers Limited,

Keyword: Alzheimers; Learning & Memory
Link ID: 24793 - Posted: 03.28.2018

By RANDI HUTTER EPSTEIN Getting a high testosterone reading offers bragging rights for some men of a certain age — and may explain in part the lure of testosterone supplements. But once you are within a normal range, does your level of testosterone, the male hormone touted to build energy, libido and confidence, really tell you that much? Probably not, experts say. Normal testosterone levels in men range from about 300 to 1,000 nanograms per deciliter of blood. Going from one number within the normal zone to another one may not pack much of a punch. “You don’t see the big improvement once men are within the normal range,” said Dr. Shalender Bhasin, an endocrinologist and professor of medicine at Harvard Medical School. The largest differences in terms of energy and sex drive are when men go from below-normal to normal levels. A 2015 study in JAMA found that sex drive improved among men who went from about 230, considered low, to 500, around the middle of what’s considered normal. There was no difference among men who moved within the normal range from 300 to 500. Testosterone does influence muscle size. The more testosterone a man takes, the larger the muscle — regardless of starting level, one reason the hormone is popular with young bodybuilders. But testosterone supplements do not seem to help frail older men walk farther or get out of chairs more easily, goals that doctors typically look for in aiding older patients. Beginning at age 30, testosterone levels drop, on average, about 1 percent a year. About 5 percent of men between the ages of 50 and 59 have low levels of testosterone along with symptoms like loss of libido and sluggishness, according to a few small studies. © 2018 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 24792 - Posted: 03.28.2018

By JAN HOFFMAN Medicare officials thought they had finally figured out how to do their part to fix the troubling problem of opioids being overprescribed to the old and disabled: In 2016, a staggering one in three of 43.6 million beneficiaries of the federal health insurance program had been prescribed the painkillers. Medicare, they decided, would now refuse to pay for long-term, high-dose prescriptions; a rule to that effect is expected to be approved on April 2. Some medical experts have praised the regulation as a check on addiction. But the proposal has also drawn a broad and clamorous blowback from many people who would be directly affected by it, including patients with chronic pain, primary care doctors and experts in pain management and addiction medicine. Critics say the rule would inject the government into the doctor-patient relationship and could throw patients who lost access to the drugs into withdrawal or even provoke them to buy dangerous street drugs. Although the number of opioid prescriptions has been declining since 2011, they noted, the rate of overdoses attributed to the painkillers and, increasingly, illegal fentanyl and heroin, has escalated. “The decision to taper opioids should be based on whether the benefits for pain and function outweigh the harm for that patient,” said Dr. Joanna L. Starrels, an opioid researcher and associate professor at Albert Einstein College of Medicine. “That takes a lot of clinical judgment. It’s individualized and nuanced. We can’t codify it with an arbitrary threshold.” Underlying the debate is a fundamental dilemma: how to curb access to the addictive drugs while ensuring that patients who need them can continue treatment. © 2018 The New York Times Company

Keyword: Pain & Touch; Drug Abuse
Link ID: 24791 - Posted: 03.28.2018

By Virginia Morell As every dog lover—and scientist—knows, man’s best friend is good at reading faces. Dogs can tell the difference between happy and not-so-happy expressions, such as anger and sadness. Like us, they watch the left sides of peoples’ faces—where emotional cues first appear. And they even seem to be able to interpret our emotions and modulate their behavior accordingly. But what are the neural mechanisms that control how dogs process human faces? To find out, scientists trained eight dogs—mostly border collies—to lie still in a functional magnetic resonance imaging scanner while viewing photos of strangers with either happy or neutral expressions. The faces matched the gender of the dogs’ chief caretakers, because dogs have been shown to score lower on tasks involving faces of the opposite sex. The results: A happy human face produces a distinctive signature in a dog’s temporal lobe and other neural regions, the scientists report online this week on the preprint server bioRxiv. In a follow-up experiment, the pooches’ brains were scanned as they looked at faces expressing happiness, anger, fear, or sadness. The happiness pattern was so distinctive that a machine learning program could pick it out from brain activity linked to all the other emotions. (A similar “happiness” signature is found in humans.) That means, the researchers say, that our human emotions are represented in our pooches’ brains—which suggests that our canine pals really do know what we’re feeling. © 2018 American Association for the Advancement of Science.

Keyword: Emotions; Animal Communication
Link ID: 24790 - Posted: 03.28.2018