By KENNETH CHANG Sir Peter Mansfield, who shared a Nobel Prize for discoveries that underpinned the invention of magnetic resonance imaging, the method of peering inside the human body that revolutionized medicine, died on Wednesday. He was 83. The University of Nottingham in England, where Dr. Mansfield had been a professor of physics, announced his death but not did say where he died. He lived in England. Magnetic resonance imaging, or M.R.I., has enabled doctors to diagnose and examine injuries to ligaments, bones and organs without cutting open the body or risking the radiation dangers of X-rays. “It’s hugely important,” said Charles P. Slichter, an emeritus physics professor at the University of Illinois at Urbana-Champaign. “It’s such an all-pervasive technique.” Dr. Mansfield worked in his laboratory as a postdoctoral researcher in the 1960s. Dr. Mansfield was awarded the Nobel Prize in Physiology or Medicine in 2003, along with Paul C. Lauterbur, a professor at the University of Illinois at Urbana-Champaign. The two had worked independent of each other in studying magnetic resonance imaging. Their research proceeded from an understanding that the nuclei of most atoms act as tiny magnets that line up when placed in a magnetic field. If the field is set at a specific strength, the atoms can absorb and emit radio waves. Scientists initially used the technique, called nuclear magnetic resonance, or N.M.R., to study atoms and molecules, deducing properties from the emitted waves. In his early research, Dr. Mansfield developed N.M.R. techniques to study crystals. Later, in 1972, as he worked to refine and sharpen N.M.R. data, he had a conversation with two colleagues about what applications such advances might lead to. He soon realized that if an object were placed in a nonuniform magnetic field — one that is stronger at one end than the other — scientists might be able to piece together a three-dimensional image of its atomic structure. © 2017 The New York Times Company

Keyword: Brain imaging
Link ID: 23217 - Posted: 02.13.2017

By Matt Blois A ruthless killer may soon help brain cancer patients. The rabies virus, which kills tens of thousands of people a year, has a rare ability to enter nerve cells and use them as a conduit to infect brain tissue. Now, scientists are trying to mimic this strategy to ferry tumor-killing nanoparticles into brain tumors. So far the approach has been shown to work only in mice. If successful in people, these nanoparticles could one day help doctors send treatment directly to tumors without harming healthy cells. The rabies virus, transmitted largely through the bites of infected animals, has evolved over thousands of years to hijack nerve cells, which it uses to climb from infected muscle tissue into the brain. That allows it to bypass a major hurdle: the blood-brain barrier, a selective membrane that keeps out most pathogens that travel through the bloodstream. But the barrier also prevents treatments—like cancer drugs—from reaching infected cells, limiting options for patients. To get around this problem, scientists are looking to the virus for inspiration. Already, researchers have packaged cancer-fighting drugs into nanoparticles coated with part of a rabies surface protein that lets the virus slip into the central nervous system. Now, a team of researchers from Sungkyunkwan University in Suwon, South Korea, has taken things one step further. Nanoparticle expert Yu Seok Youn and his team have engineered gold particles so that they have the same rodlike shape and size as the virus. The nanoparticle’s shape gives it more surface area than spherical particles, improving the surface protein’s ability to bind with receptors on nerve cells that serve as a gateway to the nervous system. The particles don’t carry any drugs, but the tiny gold rods readily absorb laser light, which heats them up and kills surrounding tissue. © 2017 American Association for the Advancement of Science.

Keyword: Neuroimmunology; Glia
Link ID: 23216 - Posted: 02.11.2017

By KATHARINE Q. SEELYE and ABBY GOODNOUGH MANCHESTER, N.H. — Chad Diaz began using heroin when he was 12. Now 36 and newly covered by Medicaid under the Affordable Care Act, he is on Suboxone, a substitute opioid that eases withdrawal symptoms and cravings, and he is slowly pulling himself together. “This is the best my life has gone in many, many years,” Mr. Diaz, a big man wearing camouflage, said as he sat in a community health center here. If Congress and President Trump succeed in dismantling the Affordable Care Act, he will have no insurance to pay for his medication or counseling, and he fears he will slide back to heroin. “If this gets taken from me, it’s right back to Square 1,” he said. “And that’s not a good place. I’m scary when I’m using. I don’t care who I hurt.” As the debate over the fate of the health law intensifies, proponents have focused on the lifesaving care it has brought to people with cancer, diabetes and other physical illnesses. But the law has also had a profound, though perhaps less heralded, effect on mental health and addiction treatment, vastly expanding access to those services by designating them as “essential benefits” that must be covered through the A.C.A. marketplaces and expanded Medicaid. The Center on Budget and Policy Priorities, a left-leaning research group, calculates that 2.8 million people with substance use disorders, including 220,000 with opioid disorders, have coverage under the A.C.A. As the opioid epidemic continues to devastate communities nationwide, public health officials say the law has begun to make a critical difference in their ability to treat and rehabilitate people. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 23215 - Posted: 02.11.2017

Sarah Boseley Health editor Low back and neck pain is an increasingly widespread and expensive condition worldwide, costing the US alone $88bn a year – the third highest bill for any health condition – despite evidence most treatments do not work. Millions of people worldwide suffer from low back and neck pain, most of it unexplained, although some professionals think it may be worsened by sitting at desks all day, carrying bags and general bad posture. Episodes of acute pain are very common, but experts say that medical investigations only make things worse and the best cure is often to take painkillers, exercise gently and wait for the pain to pass. The rising bill for treatment in the US has been uncovered in a new study by the Institute of Health Metrics and Evaluation (IHME) at the University of Washington, which looked at public and private spending on all diseases in 2013. Diabetes was in first place on $101.4bn and heart disease was second with $88.1bn. But neck and lower back pain treatment costs were close behind, at $87.6bn. The team split cancer into 29 separate conditions, which meant that none of them made the top 20, although combined the costs of treatment came to $115bn. The most remarkable thing, said Joseph Dieleman, lead author of the paper published in the Journal of the American Medical Association, was the increase in treatment costs for lower back and neck pain, running at 6.5% a year against 3.5% overall. “In absolute terms, there was an increase from $30bn in 1996 to $88bn in 2013,” he told the Guardian. © 2017 Guardian News and Media Limited

Keyword: Pain & Touch
Link ID: 23214 - Posted: 02.11.2017

After A Stroke At 33, A Writer Relies On Journals To Piece Together Her Own Story On New Year's Eve, 2006, Christine Hyung-Oak Lee developed a splitting headache. She was 33, and her world turned upside down — as in, she literally saw the world upside down. Suddenly, she could hold things in her mind for only 15 minutes at a time. She was a writer who now couldn't recall words or craft sentences. She remembers looking at the phone and thinking to herself: What is the phone number for 911? Days later, she learned she'd had a stroke. "I had a 15-minute short-term memory, like Dory the fish in Finding Nemo," Lee wrote in a Buzzfeed essay chronicling her experience. "My doctors instructed me to log happenings with timestamps in my Moleskine journal. That, they said, would be my working short-term memory. My memento to my mori." Lee used those journals to reconstruct her experience in a new memoir called Tell Me Everything You Don't Remember. She talks with NPR's Scott Simon about the silver linings of memory loss and the unexpected grief that came with her recovery. Interview Highlights On what it's like to have a 15-minute memory You don't even fathom the magnitude of your loss — or at least I didn't. I couldn't plan for the future. I couldn't think of the past. I had no regrets. So it's literally living in the moment. I was experiencing something that people go to yoga and Zen retreats to achieve. So it was quite pleasant. It was not pleasant for the people around me. But in that period of my recovery, where I couldn't remember everything, I think I was incredibly at peace and happy. On having an "invisible" disability It was frustrating. On the one hand, you want people to know: Hey, slow down for me. Hey, I'm going through a crisis. On the other hand, I was also privileged to be disabled in a way that wasn't visible. So people also didn't treat me any differently. So it was very isolating. ... When I told people that I was sick and I needed them to slow down, along with that came this need to explain my position and I ... felt a lot of resentment for having to do with that. © 2017 npr

Keyword: Stroke; Learning & Memory
Link ID: 23213 - Posted: 02.11.2017

By STEPH YIN If you’re reading this at home, pause and put on a song you can’t resist dancing to. Go on, bop your head to the beat. Let yourself wiggle a bit. Throw in some arms and legs. If you’re reading this at work, maybe imagine these things at your desk. As you’re dancing, pay attention to where and how you’re moving. How much are you swaying your hips? Are your legs moving together or independently of each other? How vigorously are you moving your torso? You should note those movements, because very specific patterns may make some people appear to be better dancers than others. That’s the conclusion of a study published on Thursday in Scientific Reports, in which researchers asked 200 people to rate 39 female dancers. A few features stood out as contributing to higher-quality dance: big hip swings, and the right and left limbs moving independently of one another (which the researchers describe as asymmetric arm and thigh movements). The researchers speculate that those moves serve two purposes for heterosexual women. “One is, they’re showing off their reproductive quality, perhaps their hormonal status, to males,” said Nick Neave, an associate professor of psychology at Northumbria University in England and an author of the paper. “Another is, they’re showing off how good they are to female rivals.” In 2011, the same researchers reported that women preferred certain dance moves by men, especially exaggerated movements in the upper body. In other studies, Dr. Neave and his colleagues have found links between male dance attractiveness and risk-taking, as well as handgrip strength, a marker for overall body strength. “We know that dance moves are signaling strength and vigor in males,” Dr. Neave said. “Now we’re beginning to do the same research with females.” In the study, his team asked 39 female university students in Britain to dance alone to a drum beat. The researchers used a motion-capture system to track the women’s moves. They animated each dancer as an avatar to try to make sure that only the dance movements — and no other physical features — would affect ratings. Then they recruited 57 men and 143 women to watch 15-second clips of the avatars and rate them each on a numeric scale. © 2017 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 23212 - Posted: 02.10.2017

Ian Sample Science editor Dozens of British children who developed narcolepsy as a result of a swine flu vaccine could be compensated after the high court rejected a government appeal to withhold payments. Six million people in Britain, and more across Europe, were given the Pandemrix vaccine made by GlaxoSmithKline during the 2009-10 swine flu pandemic, but the jab was withdrawn after doctors noticed a sharp rise in narcolepsy among those who received it. The sleep disorder is permanent and can cause people to fall asleep dozens of times a day. Some narcoleptics have night terrors and a muscular condition called cataplexy that can lead them to collapse on the spot. In 2015, a 12-year-old boy, known as John for the proceedings, was awarded £120,000 by a court that ruled he had been left severely disabled by narcolepsy caused by the vaccine. He was seven when he had the jab and developed symptoms within months. Because of his tiredness, John became disruptive at school and found it almost impossible to make friends. He takes several naps a day, cannot shower or take a bus on his own, and may never be allowed to drive a car. Despite paying out, the Department for Work and Pensions argued John’s disability was not serious enough to warrant compensation and said the court was wrong to take into account how the illness would affect him in the future. But the high court on Thursday rejected the government’s appeal that only the boy’s disability at the time should have been considered. The ruling paves the way for more than 60 other people to claim compensation. © 2017 Guardian News and Media Limited

Keyword: Narcolepsy; Neuroimmunology
Link ID: 23211 - Posted: 02.10.2017

Katherine Bourzac Kristopher Boesen, who broke his neck in a car accident, regained the ability to move his arms and hands after his spinal cord was injected with stem cells. Two years after having a stroke at 31, Sonia Olea Coontz remained partially paralysed on her right side. She could barely move her arm, had slurred speech and needed a wheelchair to get around. In 2013, Coontz enrolled in a small clinical trial. The day after a doctor injected stem cells around the site of her stroke, she was able to lift her arm up over her head and speak clearly. Now she no longer uses a wheelchair and, at 36, is pregnant with her first child. Coontz is one of stem-cell therapy's “miracle patients”, says Gary Steinberg, chair of neurosurgery at Stanford School of Medicine in California, and Coontz's doctor. Conventional wisdom said that her response was impossible: the neural circuits damaged by the stroke were dead. Most neuroscientists believed that the window for functional recovery extends to only six months after the injury. Stem-cell therapies have shown great promise in the repair of brain and spinal injuries in animals. But animal models often behave differently from humans — nervous-system injuries in rats, for example, heal more readily than they do in people. Clinical trial results have been mixed. Interesting signals from small trials have faded away in larger ones. There are plenty of unknowns: which stem cells are the right ones to use, what the cells are doing when they work and how soon after an injury they can be used. © 2016 Macmillan Publishers Limited,

Keyword: Regeneration; Stem Cells
Link ID: 23210 - Posted: 02.10.2017

“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.

Keyword: Epilepsy; Development of the Brain
Link ID: 23209 - Posted: 02.10.2017

By Tamar Haspel In his new book “The Case Against Sugar,” journalist Gary Taubes makes, as you might easily guess, a spirited case against sugar. His argument is based on the straightforward idea that sugar contributes to obesity and disease well beyond its calorie content, because it affects human metabolism in a way that encourages fat storage. In his new book, the science journalist Gary Taubes takes a hard-nosed look at sugar — and further advances the idea that not all calories are created equal. But there are competing theories of obesity. Who’s right? The debate is often framed as being over the nature of calories themselves, with scientists holding that calories are units of energy — each one no different than the other. Sugar is a carbohydrate, and the body converts carbs to glucose which is then absorbed into the bloodstream. This, in turn, triggers the pancreas to release insulin, the hormone that enables the body to use energy or store it as fat. If a person doesn’t eat many carbohydrates, the pancreas doesn’t release as much insulin, and less fat is stored, forcing the body’s metabolism to increase and burn off that energy. In practical terms, the theory goes, such a person will have an easier time losing weight — or avoiding gaining it. This hypothesis is called, appropriately, the carbohydrate/insulin, or C/I, model, and it is the basis for any number of popular low-carb diets, including Atkins, the Paleo diet, and others. It is also a “minority position” among food scientists, Taubes concedes, and many mainstream nutrition authorities reject it. Copyright 2017 Undark

Keyword: Obesity
Link ID: 23208 - Posted: 02.09.2017

By Meredith Wadman A pair of Boston University (BU) brain researchers is pushing back against demands by the National Hockey League (NHL) that they release data, brain pathology slides, and interview records of former NHL players and their families. The scientists accumulated the records during their research on chronic traumatic encephalopathy (CTE), a neurodegenerative disease that has been linked to repetitive head trauma. In affidavits unsealed yesterday in a class action lawsuit brought against the league by former players, BU neuroscientists Robert Stern and Ann McKee argued that giving the league the records would compromise both their ongoing research and the privacy of the players and families involved. The affidavits were first reported on yesterday by Rick Westhead of the Canadian sports network TSN. The NHL first subpoenaed the documents in September 2015. Stern and McKee, a neuropsychologist and a neuropathologist, respectively, at BU’s Chronic Traumatic Encephalopathy Center, have studied the brains of former professional athletes, including hockey players, and are currently using MRI imaging to study scores of living National Football League and college football players in a large study funded by the National Institutes of Health. They say that assurances that players’ privacy will be protected are essential for the success of that $16 million study. In the current litigation, the NHL’s medical expert, Rudy Castellani, asked the BU scientists for copies of gross pathology photographs, all brain slides, and clinical data of former NHL players in order to “verify the accuracy of the reports, evaluate for other pathological processes that may be significant, and conduct a full, independent neuropathological analysis of the cases.” (The scientists interviewed the former NHL players in some cases, and, in others, their surviving family members.) © 2017 American Association for the Advancement of Science.

Keyword: Brain Injury/Concussion
Link ID: 23207 - Posted: 02.09.2017

Swedish researchers say a simple blood test is effective at differentiating symptoms of Parkinson's disease from similar disorders, but it isn't ready for clinical use. In its early stages, neurologists say Parkinson's is difficult to distinguish from rarer disorders, called atypical parkinsonian disorders. They have overlapping symptoms that tend to worsen more quickly and are more likely to lead to death. Researchers are on the hunt for biomarkers to help diagnosis these disorders. One potential biomarker, a nerve protein that can be detected when nerve cells die, is found in higher concentrations in spinal fluid collected by lumbar puncture. Now medical scientists have also found the protein in less invasive blood tests. For the study published in Wednesday's online issue of the journal Neurology, Dr. Oskar Hansson of Sweden's Lund University and his team examined 504 people in three groups. Two of the groups, in England and Sweden, included healthy people and those who had been living with one of the disorders for an average of four to six years. The third group of 109 patients had the diseases for three years or less. "The results of the present study strongly indicate that NfL when measured in blood can be used to distinguish between patients with Parkinson's disease and patients with progressive supranuclear palsy multiple system atrophy and corticobasal degeneration with high diagnostic accuracy," the study's authors said. ©2017 CBC/Radio-Canada.

Keyword: Parkinsons
Link ID: 23206 - Posted: 02.09.2017

In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.

Keyword: Alzheimers
Link ID: 23205 - Posted: 02.09.2017

Scientists who spent years listening to the communication calls of one of our closest ape relatives say their eavesdropping has shed light on the origin of human language. Dr Adriano Reis e Lameira from Durham University recorded and analysed almost 5,000 orangutan "kiss squeaks". He found that the animals combined these purse-lipped, "consonant-like" calls to convey different messages. This could be a glimpse of how our ancestors formed the earliest words. The findings are published in the journal Nature Human Behaviour. "Human language is extraordinarily advanced and complex - we can pretty much transmit any information we want into sound," said Dr Reis e Lameira. "So we tend to think that maybe words evolved from some rudimentary precursor to transmit more complex messages. "We were basically using the orangutan vocal behaviour as a time machine - back to a time when our ancestors were using what would become [those precursors] of consonants and vowels." The team studied kiss squeaks in particular because, like many consonants - the /t/, /p/, /k/ sounds - they depend on the action of the lips, tongue and jaw rather than the voice. "Kiss squeaks do not involve vocal fold action, so they're acoustically and articulatory consonant-like," explained Dr Reis e Lameira. In comparison to research into vowel-like primate calls, the scientists explained, the study of consonants in the evolution of language has been more difficult. But as Prof Serge Wich from Liverpool John Moores University, a lead author in the study, said, they are crucial "building blocks" in the evolution of language. "Most human languages have a lot more consonants than vowels," said Prof Wich. "And if we have more building blocks, we have more combinations." © 2017 BBC.

Keyword: Language; Evolution
Link ID: 23204 - Posted: 02.09.2017

By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist

Keyword: Drug Abuse; Learning & Memory
Link ID: 23203 - Posted: 02.09.2017

Having a thicker outer layer of the brain is linked to an increased likelihood of having autism. The cerebral cortex is the wrinkled outer layer of the brain that is responsible for many of our most human traits, including thought, language and consciousness. This layer is typically thicker in men than in women, and its structure has been linked to differences in personality. Now brain scans have shown that women who have a more male-like brain structure are three times more likely to have been diagnosed with autism. The study compared the brains of 98 men and women with high functioning autism with those of 98 people who don’t have autism. These findings provide new insights into the brain’s role in sex differences in autism, according to the team that did the study. Autism is thought to be two to five times more common in men than in women, and some think the condition is caused by having an “extreme male brain”. Journal reference: JAMA Psychiatry, DOI: 10.1001/jamapsychiatry.2016.3990 © Copyright Reed Business Information Ltd.

Keyword: Autism; Sexual Behavior
Link ID: 23202 - Posted: 02.09.2017

by Linda Rodriguez McRobbie If you ask Jill Price to remember any day of her life, she can come up with an answer in a heartbeat. What was she doing on 29 August 1980? “It was a Friday, I went to Palm Springs with my friends, twins, Nina and Michelle, and their family for Labour Day weekend,” she says. “And before we went to Palm Springs, we went to get them bikini waxes. They were screaming through the whole thing.” Price was 14 years and eight months old. What about the third time she drove a car? “The third time I drove a car was January 10 1981. Saturday. Teen Auto. That’s where we used to get our driving lessons from.” She was 15 years and two weeks old. The first time she heard the Rick Springfield song Jessie’s Girl? “March 7 1981.” She was driving in a car with her mother, who was yelling at her. She was 16 years and two months old. Price was born on 30 December 1965 in New York City. Her first clear memories start from around the age of 18 months. Back then, she lived with her parents in an apartment across the street from Roosevelt Hospital in Midtown Manhattan. She remembers the screaming ambulances and traffic, how she used to love climbing on the living room couch and staring out of the window down 9th Avenue. When she was five years and three months old, her family – her father, a talent agent with William Morris who counted Ray Charles among his clients; her mother, a former variety show dancer, and her baby brother – moved to South Orange, New Jersey. They lived in a three-storey, red brick colonial house with a big backyard and huge trees, the kind of place people left the city for. Jill loved it.

Keyword: Learning & Memory
Link ID: 23201 - Posted: 02.08.2017

Bruce Bower A small, poorly understood segment of the population stays mentally healthy from age 11 to 38, a new study of New Zealanders finds. Everyone else encounters either temporary or long-lasting mental disorders. Only 171 of 988 participants, or 17 percent, experienced no anxiety disorders, depression or other mental ailments from late childhood to middle age, researchers report in the February Journal of Abnormal Psychology. Of the rest, half experienced a transient mental disorder, typically just a single bout of depression, anxiety or substance abuse by middle age. “For many, an episode of mental disorder is like influenza, bronchitis, kidney stones, a broken bone or other highly prevalent conditions,” says study coauthor Jonathan Schaefer, a psychologist at Duke University. “Sufferers experience impaired functioning, many seek medical care, but most recover.” The remaining 408 individuals (41 percent) experienced one or more mental disorders that lasted several years or more. Their diagnoses included more severe conditions such as bipolar and psychotic disorders. Researchers analyzed data for individuals born between April 1972 and March 1973 in Dunedin, New Zealand. Each participant’s general health and behavior were assessed 13 times from birth to age 38. Eight mental health assessments occurred from age 11 to 38. |© Society for Science & the Public 2000 - 2016.

Keyword: Depression
Link ID: 23200 - Posted: 02.08.2017

Squid and their cephalopod brethren have been the inspiration for many a science fiction creature. Their slippery appendages, huge proportions, and inking abilities can be downright shudder-inducing. (See: Arrival.) But you should probably be more concerned by the cephalopod’s huge brain—which not only helps it solve tricky puzzles, but also lets it converse in its own sign language. Right now, you’re probably imagining twisted tentacles spelling out creepy cephalopod communiqués. But it’s not that: Certain kinds of squid send messages by manipulating the color of their skin. “Their body patterning is fantastic, fabulous,” says Chuan-Chin Chiao, a neuroscientist at National Tsing Hua University in Taiwan. They can display bands, or stripes, or turn completely dark or light. And Chiao is trying to crack their code. Chiao got his inspiration from physiologist B. B. Boycott, who in the 1960s showed that the cuttlefish brain was the control center for changing skin color. Boycott copied his technique from neurosurgeon Wilder Penfield, who treated epilepsy patients by burning out the misbehaving bits of their brains. While their grey matter was exposed for surgery, Penfield also applied a gentle current through the electrodes in his patients’ brains. You know, just to see what would happen. A zap in one spot above the ears caused a tingle in the left hand. In another spot, tingles in the leg. And so Penfield discovered that the sensory cortex is a homunculus, with specific brain areas mapping onto different parts of your body. Over time, scientists tried the electrical stimulation technique on all kinds of animals—including Boycott’s cuttlefish.

Keyword: Animal Communication
Link ID: 23199 - Posted: 02.08.2017

By Anil Ananthaswamy Next time a nurse sticks a needle into your arm, don’t look away: it’ll be less painful. A new study shows that we feel less pain when we are looking at our body – and that this effect works with virtual reality too. In 2009, Patrick Haggard and Matthew Longo of University College London showed that looking at your own body has an analgesic effect. The researchers shone infrared laser light on the skin of volunteers. Those who were looking at their body rather than at a neutral object said that they felt less pain. Scalp electrodes revealed that this analgesic effect was linked to weaker activity in parts of the brain’s cortex that process pain – although why this happens is unclear. Since then, two different teams have tested the effect using the rubber hand illusion – in which a rubber hand is placed next to a person’s real hand, which is hidden from view. Stroking both the real and rubber hands with paint brushes convinces them that the rubber hand is their own. Extending this illusion, the teams wanted to know: can looking at a rubber hand that feels like one’s own alleviate pain in your real hand? The studies were contradictory: one study showed an analgesic effect, but the other did not. Maria Sanchez-Vives at the University of Barcelona, Spain, and her colleagues argue that differences in the position of the rubber hand and real hand may have led to the differing results. To test the effect of the rubber hand’s position, her team used virtual reality to induce the illusion. Instead of seeing a real rubber hand, participants were shown one via a VR headset instead. © Copyright Reed Business Information Ltd.

Keyword: Pain & Touch
Link ID: 23198 - Posted: 02.08.2017