By RONI CARYN RABIN A. Studies have found a link between low levels of magnesium, an essential mineral that plays a crucial role in a wide range of bodily processes, and sleep disorders. But if you are concerned you aren’t getting enough magnesium, changing your diet may be a better option than taking a supplement, as “there is really sparse evidence that taking super-therapeutic doses of magnesium will give you a benefit,” said Dr. Raj Dasgupta, a professor of pulmonary and sleep medicine at the University of Southern California. The mineral is widely available in both plant and animal-based foods, and the kidneys limit urinary excretion of magnesium, so deficiencies are rare in healthy people. Leafy green vegetables, nuts, legumes and whole grains are good sources of magnesium; fish, chicken and beef also contain magnesium. Older adults and people with certain disorders, such as Type 2 diabetes, gastrointestinal diseases and alcoholism, however, may have inadequate amounts. “Magnesium deficiency has been associated with higher levels of stress, anxiety and difficulty relaxing, which are key ingredients to getting good sleep at night,” Dr. Dasgupta said. He noted that magnesium interacts with an important neurotransmitter that favors sleep. One small double-blinded clinical trial of 43 elderly people in Tehran who were randomly assigned to receive either 500 milligrams of magnesium or a placebo for eight weeks found that those who received the supplement fell asleep faster and spent more of their time in bed asleep, but their total sleep time was not necessarily longer. An even smaller study of 10 people done nearly 20 years ago found that taking a magnesium supplement helped people with restless leg syndrome get more sleep. © 2018 The New York Times Company

Keyword: Sleep
Link ID: 24489 - Posted: 01.05.2018

By Meredith Wadman Chya* (pronounced SHY-a), who is not quite 10 years old, recently spent an unusual day at the University of Maryland School of Medicine in Baltimore. Part of the time she was in a "cool" brain scanner while playing video games designed to test her memory and other brain-related skills. At other points, she answered lots of questions about her life and health on an iPad. A slender Baltimore third grader who likes drawing, hip hop, and playing with her pet Chihuahua, Chya is one of more than 6800 children now enrolled in an unprecedented examination of teenage brain development. The Adolescent Brain Cognitive Development Study—or ABCD Study—will complete its 2-year enrollment period in September, and this month will release a trove of data from 4500 early participants into a freely accessible, anonymized database. Ultimately, the study aims to follow 10,000 children for a decade as they grow from 9- and 10-year-olds into young adults. Supported by the first chunk of $300 million pledged by several institutes at the National Institutes of Health (NIH) in Bethesda, Maryland, teams at 21 sites around the United States are regularly using MRI machines to record the structure and activity of these young brains. They're also collecting reams of psychological, cognitive, and environmental data about each child, along with biological specimens such as their DNA. In addition to providing the first standardized benchmarks of healthy adolescent brain development, this information should allow scientists to probe how substance use, sports injuries, screen time, sleep habits, and other influences may affect—or be affected by—a maturing brain. © 2017 American Association for the Advancement of Science.

Keyword: Development of the Brain; Schizophrenia
Link ID: 24488 - Posted: 01.04.2018

Amy Maxmen Name a remedy, and chances are that Elizabeth Allen has tried it: acupuncture, antibiotics, antivirals, Chinese herbs, cognitive behavioural therapy and at least two dozen more. She hates dabbling in so many treatments, but does so because she longs for the healthy days of her past. The 34-year-old lawyer was a competitive swimmer at an Ivy-league university when she first fell ill with chronic fatigue syndrome, 14 years ago. Her meticulous records demonstrate that this elusive malady is much worse than ordinary exhaustion. “Last year, I went to 117 doctor appointments and I paid $18,000 in out-of-pocket expenses,” she says. Dumbfounded that physicians knew so little about chronic fatigue syndrome — also known as myalgic encephalomyelitis or ME/CFS — Allen resolved several years ago to take part in any study that would have her. In 2017, she got her chance: she entered a study assessing how women with ME/CFS respond to synthetic hormones. After decades of pleading, people with the condition have finally caught the attention of mainstream science — and dozens of exploratory studies are now under way. Scientists entering the field are using the powerful tools of modern molecular biology to search for any genes, proteins, cells and possible infectious agents involved. They hope the work will yield a laboratory test to diagnose ME/CFS — which might have several different causes and manifestations — and they want to identify molecular pathways to target with drugs. © 2018 Macmillan Publishers Limited,

Keyword: Depression; Neuroimmunology
Link ID: 24487 - Posted: 01.04.2018

By Catherine Offord Graduate student Anne Murphy had run out of rats. Or rather, she’d run out of male rats, the animals she was using to study brain regions involved in pain modulation for her PhD at the University of Cincinnati in the early 1990s. At a time when neuroscientists almost exclusively used male animals for research, what Murphy did next was unusual: she used a female rat instead. “I had the hardest time to get the female to go under the anesthesia; she wasn’t acting right,” Murphy says. Her advisor’s explanation? “‘Well, you know those females, they have hormones, and those hormones are always fluctuating and they’re so variable,’” Murphy recalls. The comments struck a nerve. “It really got to me,” she says. “I’m a female. I have hormones that fluctuate. . . . It made me determined to investigate the differences between males and females in terms of pain processing and alleviation.” Her decision was timely. Since the ’90s, evidence has been accumulating to suggest that not only do women experience a higher incidence of chronic pain syndromes than men do—fibromyalgia and interstitial cystitis, for example—females also generally report higher pain intensities. Additionally, Murphy notes, a handful of clinical studies has suggested that women require higher doses of opioid pain medications such as morphine for comparable analgesia; plus, they experience worse side effects and a higher risk of addiction. © 1986-2018 The Scientist

Keyword: Pain & Touch; Sexual Behavior
Link ID: 24486 - Posted: 01.04.2018

Beyond the usual suspects of snakes, spiders, and scorpions, the animal kingdom is filled with noxious critters: snails, frogs, fish, anemones, and more make toxins for defense or predation. The noxious chemicals these animals produce are potent, and they often strike where it hurts: pain pathways. These compounds have long captivated researchers hoping to understand their effects and use that knowledge to develop drugs that suppress pain in a wide variety of ailments affecting humans. Paradoxically, some of these toxins are themselves analgesic, and researchers have worked to develop synthetic derivatives that can be tested as painkillers. Such is the case for the only toxin-derived analgesic to be approved by the US Food and Drug Administration (FDA): ziconotide (Prialt), a compound 1,000 times more potent than morphine that was inspired by a component of the venom of the cone snail Conus magus. Other toxins elicit pain, and researchers have used these compounds to identify inhibitors of ion channels on the pain-sensing neurons they target. Despite more than half a century of research in this field, however, scientists have had a frustrating time developing effective analgesics. Challenges include ensuring that the drugs are highly specific to their targets—each family of ion channels involved in pain sensing in humans contains several conserved proteins—and getting them to those targets, which often lie beyond the blood-brain barrier in the central nervous system. Nevertheless, several toxin-derived candidates are beginning to prove their worth in preclinical experiments and a handful of clinical trials, and bioprospectors continue to mine the animal kingdom’s vast library of venoms and poisons for more leads. The next big thing in painkillers could soon be slithering, creeping, hopping, or swimming into the pipeline. © 1986-2018 The Scientist

Keyword: Pain & Touch; Neurotoxins
Link ID: 24485 - Posted: 01.04.2018

Phil Plait I can't think of a better way to start off a new year than scrambling your brains. Just a little bit! But still: enough to make you scratch your head and wonder just what is wrong with that sack of wrinkly pink goo in your skull. One of my favorite optical illusionists is Akiyoshi Kitaoki. He has created hundreds, maybe thousands, of guaranteed brain-melting illusions that will make you swear that what you're seeing is real when it really, really isn't. He has ones that appear to move, that warp your sense of shape and size, destroy your notion of color, and will make you seriously question whether your eyes and brain are talking to each other in any sort of coherent way. He just posted a new one to Twitter, and I love it for its simplicity and efficiency: It creates two illusions at once. Are you ready? Here it is: I don't know about you, but when I look at this I see alternating squarish shapes (Kitaoka called them turtles, so I'll go with that) arranged like a chessboard, with half darked and half lighter. What's disturbing immediately though is that they don't appear to be separated along straight lines. The vertical border of the turtles on the left appear to curve to the right a bit, and the ones on the right curve left. It makes it look like there's a mound or bulge in the middle of the image.

Keyword: Vision
Link ID: 24484 - Posted: 01.04.2018

by Ben Guarino The next time a friend tells you that you look sick, hear the person out. We are better than chance at detecting illness in others simply by looking at their faces, according to new research led by a Swedish psychologist. “We can detect subtle cues related to the skin, eyes and mouth,” said John Axelsson of the Karolinska Institute, who co-wrote the study published Tuesday in the journal Proceedings of the Royal Society B. “And we judge people as sick by those cues.” Other species have more finely tuned disease radars, relying primarily on the sense of smell. And previous research, Axelsson noted, has shown that animals can sniff sickness in other animals. (A Canadian hospital enlisted the help of an English springer spaniel trained to smell bacterial spores that infect patients.) Yet while there is some evidence that an unhealthy person gives off odors that another individual can identify as sickness, the face is our primary source of “social information for communication,” Axelsson said. He and his colleagues, a team that included neuroscientists and psychologists in Germany and Sweden, injected eight men and eight women with a molecule found in bacterial membranes. Like animals — from insects to mammals — people react very strongly to this substance, lipopolysaccharide. “People did not really become sick from the bacteria,” Axelsson said, but their bodies did not know the bacteria weren't actually attacking. Their immune systems kicked into action, complete with feelings of sickness. The subjects, all white, received about $430 for their trouble. © 1996-2018 The Washington Post

Keyword: Attention; Neuroimmunology
Link ID: 24483 - Posted: 01.03.2018

By Mark R. Hutchinson When someone is asked to think about pain, he or she will typically envision a graphic wound or a limb bent at an unnatural angle. However, chronic pain, more technically known as persistent pain, is a different beast altogether. In fact, some would say that the only thing that acute and persistent pain have in common is the word “pain.” The biological mechanisms that create and sustain the two conditions are very different. Pain is typically thought of as the behavioral and emotional results of the transmission of a neuronal signal, and indeed, acute pain, or nociception, results from the activation of peripheral neurons and the transmission of this signal along a connected series of so-called somatosensory neurons up the spinal cord and into the brain. But persistent pain, which is characterized by the overactivation of such pain pathways to cause chronic burning, deep aching, and skin-crawling and electric shock–like sensations, commonly involves another cell type altogether: glia.1 Long considered to be little more than cellular glue holding the brain together, glia, which outnumber neurons 10 to 1, are now appreciated as critical contributors to the health of the central nervous system, with recognized roles in the formation of synapses, neuronal plasticity, and protection against neurodegeneration. And over the past 15 to 20 years, pain researchers have also begun to appreciate the importance of these cells. Research has demonstrated that glia seem to respond and adapt to the cumulative danger signals that can result from disparate kinds of injury and illness, and that they appear to prime neural pathways for the overactivation that causes persistent pain. In fact, glial biology may hold important clues to some of the mysteries that have perplexed the pain research field, such as why the prevalence of persistent pain differs between the sexes and why some analgesic medications fail to work. © 1986-2018 The Scientist

Keyword: Pain & Touch; Glia
Link ID: 24482 - Posted: 01.03.2018

Samantha Raphelson Jennifer Brea was a PhD candidate at Harvard University when flu-like symptoms and a high fever brought her down for more than five years. After her condition stumped several doctors, the 28-year-old filmed herself on her iPhone, including an episode when she was unable to move or speak. She showed the footage to her doctor, and in 2012 – a year and a half after her initial fever – she was diagnosed with a condition called myalgic encephalomyelitis, or chronic fatigue syndrome. Even though an estimated 836,000 to 2.5 million Americans suffer from ME/CFS, the disease is largely misunderstood and many sufferers have not been diagnosed. The annual federal research budget for the disease is $4 million to $6 million, which is slim compared to, for example, the nearly $109 million allocated annually to multiple sclerosis research. That's part of the problem, Brea says. "It's a disease that is twice as common as multiple sclerosis and on average can be even more debilitating, and yet we get almost no research funding and no access to medical care," she says. Brea tells Here & Now's Robin Young that her new documentary, Unrest, seeks to lift the veil on this invisible illness. The Sundance-award-winning film, which began with that initial iPhone footage, premieres on PBS next Monday. ME/CFS follows an infection that leaves 75 percent of those affected unable to work and 25 percent homebound or bedridden. The disease is characterized by severe physical and mental fatigue, sleep problems and cognitive dysfunction, according to the Centers for Disease Control and Prevention. © 2018 npr

Keyword: Depression; Neuroimmunology
Link ID: 24481 - Posted: 01.03.2018

/ By Drew Smith For decades, no industry has been a more reliable moneymaker than pharmaceuticals. Immune to recession, drug companies regularly score 15 percent profit margins year after year. There is no danger of market saturation and, in the U.S., little prospect of government restraint of prices. Nearly all regulatory submissions win approval, and turnaround times are steadily decreasing. If you are an investor, what’s not to like? But all dominant and expanding industries are fueled by resources of one type or another. Some of these are tangible and obvious, like gold deposits. Their exploitation follows a familiar arc. There is an initial rush to simply pick nuggets up off the ground. When the nuggets have been picked, miners must search for pebbles, then sand, then dust. There are still fortunes to be made, but more and more capital investment is needed to separate the gold from the dross. If you are a drug company, drug targets are your resource. Our conception of disease has progressed through many understandings — as demonic possession, humoral imbalance, blockage of chi, disordering of machinery — and has now landed on the notion that it is either an invasion by microscopic creatures or bad behavior by large protein molecules. Health is restored by poisoning the invaders or correcting the proteins. Drugs are the agents that accomplish these goals. To a first approximation, drugs are small molecules that bind to specific large molecules. This is the one-disease, one-protein, one-drug paradigm, and it is the essential value proposition of the pharmaceutical industry. Companies identify protein targets and make drugs that alter target behavior. They are very, very good at this. So good that the supply of new drugs largely depends on the supply of new drug targets. Copyright 2018 Undark

Keyword: Depression; Schizophrenia
Link ID: 24480 - Posted: 01.03.2018

By James Hartzell A hundred dhoti-clad young men sat cross-legged on the floor in facing rows, chatting amongst themselves. At a sign from their teacher the hall went quiet. Then they began the recitation. Without pause or error, entirely from memory, one side of the room intoned one line of the text, then the other side of the room answered with the next line. Bass and baritone voices filled the hall with sonorous prosody, every word distinctly heard, their right arms moving together to mark pitch and accent. The effect was hypnotic, ancient sound reverberating through the room, saturating brain and body. After 20 minutes they halted, in unison. It was just a demonstration. The full recitation of one of India´s most ancient Sanskrit texts, the Shukla Yajurveda, takes six hours. I spent many years studying and translating Sanskrit, and became fascinated by its apparent impact on mind and memory. In India's ancient learning methods textual memorization is standard: traditional scholars, or pandits, master many different types of Sanskrit poetry and prose texts; and the tradition holds that exactly memorizing and reciting the ancient words and phrases, known as mantras, enhances both memory and thinking. I had also noticed that the more Sanskrit I studied and translated, the better my verbal memory seemed to become. Fellow students and teachers often remarked on my ability to exactly repeat lecturers’ own sentences when asking them questions in class. Other translators of Sanskrit told me of similar cognitive shifts. So I was curious: was there actually a language-specific “Sanskrit effect” as claimed by the tradition? © 2018 Scientific American

Keyword: Language; Attention
Link ID: 24479 - Posted: 01.03.2018

Brian Mann When Bella Doolittle heard her diagnosis last February of early-onset Alzheimer's, she sat in the car outside the doctor's office and cried. "He said, 'Well, we figured out what's going on with you and this is it.' And I'm like, 'No it's not.' " Doolittle's husband, Will Doolittle, sits next to her on the couch, recalling how she grilled the doctor. "You asked, 'How long does this take? How long do I have?' And he said, 'On average, eight years.' That really upset you." "That really pissed me off," Bella says, laughing now at the memory. "Absolutely. I mean, I was pretty devastated. I'm like, eight years? I'm not even wrinkly yet." Researchers say as many as 200,000 Americans experience Alzheimer's younger than the typical age of 65, developing dementia-like symptoms in their 40s and 50s. For people like Bella, the diagnosis can feel overwhelming and bring feelings of shame. They fear losing memories, careers, and parts of their identity. Bella is a young-looking 59, wearing a T-shirt and a mop of red hair. On the day NPR visited her home in Glens Falls in upstate New York, where they raised four kids, Bella was in the kitchen making her signature Christmas gift. "It's homemade Kahlúa, the best you will ever drink," she says. "I have my vanilla beans imported from Madagascar." Bella Doolittle remembers how she first became aware that something was wrong. For a while before the diagnosis, she just felt "off." Her brain would get fuzzy and then it got worse. © 2018 npr

Keyword: Alzheimers
Link ID: 24478 - Posted: 01.02.2018

By Catherine Offord As a physiotherapist at University Hospital Zurich in the mid-2000s, Annina Schmid often encountered people with chronic pain. “My interest in research got sparked while I was seeing my patients,” she says. “It was very difficult to treat them, or to understand why pain persists in some people, while it doesn’t even occur in others.” Schmid, who grew up in Switzerland, had earned her master’s degree in clinical physiotherapy in 2005 at Curtin University in Perth, Australia, and she was keen to return down under. In 2008, she secured an Endeavour Europe Scholarship from the Australian Government and moved to the University of Queensland in Brisbane for a PhD in neuroscience. “She’s very motivated,” says Schmid’s colleague and collaborator Brigitte Tampin, a musculoskeletal physiotherapist at Curtin University and at Osnabrück University of Applied Sciences in Germany. Tampin adds that Schmid’s physiotherapy background was an asset for her PhD work and beyond. “She can think as a clinician and as a researcher.” For her PhD, Schmid focused on animal models of mild nerve compression, also called entrapment neuropathy, in which pressure on nerve fibers—from bone, for example—can cause pain and loss of motor function. Using a tube to compress the sciatic nerves of rats, Schmid was able to replicate not only local symptoms seen in humans, but also inflammation at distant sites, a possible explanation for why patients often report pain in other parts of the body.1 © 1986-2018 The Scientist

Keyword: Pain & Touch
Link ID: 24477 - Posted: 01.02.2018

Just 10 minutes of aerobic exercise can improve executive function by priming parts of the brain used to laser focus on the task at hand, according to a new study. This paper, “Executive-Related Oculomotor Control Is Improved Following a 10-minute Single-Bout of Aerobic Exercise: Evidence from the Antisaccade Task,” was published in the January 2018 issue of Neuropsychologia. This research was conducted by Matthew Heath, who is a kinesiology professor and supervisor in the Graduate Program in Neuroscience at the University of Western Ontario, along with UWO master’s student Ashna Samani. For this study, Samani and Heath asked a cohort of healthy young adults to either sit quietly and read magazines or perform 10 minutes of moderate-to-vigorous physical activity (MVPA) on a stationary bicycle. (MVPA aerobic intensity is hard enough that you might break a sweat but easy enough that you can carry on a conversation.) Immediately after the 10-minute reading task or time spent doing aerobic exercise, the researchers used eye-tracking equipment to gauge antisaccades, which is a way to measure varying degrees of executive control. As the authors explain in the study abstract, “Antisaccades are an executive task requiring a goal-directed eye movement (i.e., a saccade) mirror-symmetrical to a visual stimulus. The hands- and language-free nature of antisaccades coupled with the temporal precision of eye-tracking technology make it an ideal tool for identifying executive performance changes.” © 1991-2018 Sussex Publishers, LLC

Keyword: Attention
Link ID: 24476 - Posted: 01.02.2018

By C. CLAIBORNE RAY Q. Did cranial deformation as practiced by the ancient Mayans change or impair brain function? A. The famous slanted forehead that was apparently a mark of high rank among pre-Columbian Mayans was achieved by various forms of compression of the head in infancy. It is believed by many researchers to have had no significant effect on cranial capacity and how the brain worked, the conclusion of a 1989 study of skulls in The American Journal of Physical Anthropology. But there is no direct evidence to support this contention, no large study comparing brain development in living populations that do and do not practice head flattening. An extensive review article in the journal Anthropology in 2003 speculated that the practice of compression had the potential to damage the delicate developing frontal lobe, as is seen in certain conditions. The authors speculated that such damage could have impaired vision, object recognition, hearing ability, memory, attentiveness and concentration. These factors in turn might have contributed to behavior disorders and difficulty in learning new information. Still other researchers suggest that the diverging conclusions can be attributed to how the skull measurements are done. The compression may have affected the shape of the face more than the brain itself, they said. © 2018 The New York Times Company

Keyword: Development of the Brain
Link ID: 24475 - Posted: 01.02.2018

Linda Bauld Search for the term ‘vaping’ online and you’d be forgiven for thinking that it is an activity fraught with risks. The top stories relate to health problems, explosions and that vaping leads to smoking in teenagers. For the average smoker seeking information on vaping, a quick internet search offers little reassurance. Might as well continue smoking, the headlines imply, if these products are so dangerous. But the reality is that they are not. In the past year, more than any other, the evidence that using an e-cigarette is far safer than smoking has continued to accumulate. 2017 saw the publication of the first longer term study of vaping, comparing toxicant exposure between people who’d stopped smoking and used the products for an average of 16 months, compared with those who continued to smoke. Funded by Cancer Research UK, the study found large reductions in carcinogens and other toxic compounds in vapers compared with smokers, but only if the user had stopped smoking completely. A further recent study compared toxicants in vapour and smoke that can cause cancer, and estimated excess cancer risk over a lifetime from smoking cigarettes or vaping. Most of the available data on e-cigarettes in this study suggested a cancer risk from vaping around 1% of that from smoking. E-cigarettes are less harmful than smoking because they don’t contain tobacco. Inhaling burnt tobacco - but also chewing it - is hugely damaging to human health. Remove the tobacco and the combustion and it is hardly surprising that risk is reduced. That doesn’t mean e-cigarettes are harmless. But it does mean that we can be relatively confident that switching from smoking to vaping will have health benefits. © 2017 Guardian News and Media Limited

Keyword: Drug Abuse
Link ID: 24474 - Posted: 12.30.2017

By Jessica Hamzelou Did you pile on the pounds this Christmas? At least you can take some comfort in the fact that not all fat is bad. Evidence in mice and monkeys suggests it is important for storing important immune cells and may even make them more effective at fighting infection. Yasmine Belkaid at the US National Institutes of Health and her team have found that a type of immune cell – called a memory T-cell – seems to be stored in the body fat of mice. These cells learn to fight infection. Once exposed to a pathogen, they mount a stronger response the next time they encounter it. When the researchers infected mice with parasites or bacteria, they found that memory T-cells clustered densely in the animals’ body fat. Tests showed that these cells seemed to be more effective than those stored in other organs, being better at replicating and at releasing infection-fighting chemicals, for example. After exposing the mice to the same pathogens again, the memory T-cells stored in their fat were the fastest to respond. Belkaid’s team found that monkeys also have plenty of memory T-cells in their body fat, and that these cells worked better than those from other organs. “It means that fat tissue is not only a reservoir for memory cells, but those memory cells have enhanced function,” says Belkaid. “The tissue is like a magic potion that can optimally activate the T-cells.” © Copyright New Scientist Ltd.

Keyword: Obesity; Neuroimmunology
Link ID: 24473 - Posted: 12.30.2017

By NEIL GENZLINGER Ben Barres, a neuroscientist who did groundbreaking work on brain cells known as glia and their possible relation to diseases like Parkinson’s, and who was an outspoken advocate of equal opportunity for women in the sciences, died on Wednesday at his home in Palo Alto, Calif. He was 63. In announcing the death, Stanford University, where Dr. Barres was a professor, said he had had pancreatic cancer. Dr. Barres was transgender, having transitioned from female to male in 1997, when he was in his 40s and well into his career. That gave him a distinctive outlook on the difficulties that women and members of minorities face in academia. and especially in the sciences. An article he wrote for the journal Nature in 2006 titled “Does Gender Matter?” took on some prominent scholars who had argued that women were not advancing in the sciences because of innate differences in their aptitude. “I am suspicious when those who are at an advantage proclaim that a disadvantaged group of people is innately less able,” he wrote. “Historically, claims that disadvantaged groups are innately inferior have been based on junk science and intolerance.” The article cited studies documenting obstacles facing women, but it also drew on Dr. Barres’s personal experiences. He recounted dismissive treatment he had received when he was a woman and how that had changed when he became a man. “By far,” he wrote, “the main difference that I have noticed is that people who don’t know I am transgendered treat me with much more respect: I can even complete a whole sentence without being interrupted by a man.” Dr. Barres (pronounced BARE-ess) was born on Sept. 13, 1954, in West Orange, N.J., with the given name Barbara. “I knew from a very young age — 5 or 6 — that I wanted to be a scientist, that there was something fun about it and I would enjoy doing it,” he told The New York Times in 2006. “I decided I would go to M.I.T. when I was 12 or 13.” © 2017 The New York Times Company

Keyword: Glia; Sexual Behavior
Link ID: 24472 - Posted: 12.30.2017

By Daniel Barron Earlier this year, I wrote about my patient, Andrew, an engineer who developed a heroin habit. An unfortunate series of joint replacements had left Andrew with terrible pain and, when his medication ran out, he turned to heroin. Months after his surgeries—after his tissue and scars had healed—Andrew remained disabled by a deep, biting pain. I recall puzzling over his pain, how it had spread throughout his body and how previous clinical teams had prescribed progressively higher doses of opioids to tame it. Andrew had transitioned from acute pain (i.e., pain from his surgical wounds) to chronic pain (i.e., pain in the absence of an obvious cause), but it was unclear to me whether this reflected a drug tolerance or a different pain process. The difference between drug tolerance and chronic pain is a difficult concept to get hold of. In the hospital workroom one morning, I realized how confused I was by the topic and paged the hospital’s on-call pain specialist. Fortune smiled and Donna-Ann M Thomas, Yale University’s Pain Medicine Division Chief, picked up the phone and patiently explained how tolerance and chronic pain are quite different. Andrew became tolerant to opioids when his body required progressively larger doses to have the same effect. Opioids activate the Mu opioid receptor, which blocks pain signals in the spinal cord. To find a way around the opioid blockade, Andrew’s body had made more Mu receptors to compensate for the drug, meaning more drug had to be present to stifle the pain signal, hence the escalating doses. © 2017 Scientific American,

Keyword: Pain & Touch; Attention
Link ID: 24471 - Posted: 12.30.2017

By Abigail Zuger, M.D. All human beings contain a frightening tangle of primal impulses struggling for dominance, and that’s true not only for the chaotic psyche, but also the sober, dependable, symmetric old hands. Even the ordinary act of reaching for a fork or throwing a ball is the product of immensely complex genetic and neurologic negotiation. In some ways we are not that much further along than we were when our ancestors linked left-handedness to the sinister and the gauche. For all its sophistication, modern science is still unable to explain exactly why some of us prefer to do these tasks with the left hand and some with the right. Many theories are proposed and debated; studies yield data invariably suggestive but never conclusive. Moreover, as Howard Kushner systematically outlines in his short but meaty survey of the science and sociology of handedness, in some ways we are not that much further along than we were back in the days when our ancestors linked left-handedness to the sinister and the gauche, among many other undesirable traits, and just left it at that. An emeritus professor at Emory University and San Diego State, as well as a visiting scholar at the University of California – San Diego, Kushner brings academic credentials in both neuroscience and the history of science to his overview. In addition, he himself is left-handed, as was his mother (who like many left-handed children of her era was forcibly retrained to use her right), and the residua of personal experience echo through the book. Copyright 2017 Undark

Keyword: Laterality
Link ID: 24470 - Posted: 12.30.2017