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Gary Stix Illiterate women in northern Indian learned how to read and write in Hindi for six months after which they had reached a level comparable to a first-grader. Credit: Max Planck Institute for Human Cognitive and Brain Sciences The brain did not evolve to read. It uses the neural muscle of pre-existing visual and language processing areas to enable us to take in works by Tolstoy and Tom Clancy. Reading, of course, begins in the first years of schooling, a time when these brain regions are still in development. What happens, though, when an adult starts learning after the age of 30? A study published May 24 in Science Advances turned up a few unexpected findings. In the report, a broad-ranging group of researchers—from universities in Germany, India and the Netherlands—taught reading to 21 women, all about 30 years of age from near the city of Lucknow in northern India, comparing them to a placebo group of nine women. The majority of those who learned to read could not recognize a word of Hindi at the beginning of the study. After six months, the group had reached a first-grade proficiency level. When the researchers conducted brain scans—using functional magnetic resonance imaging—they were startled. Areas deep below the wrinkled surface, the cortex, in the brains of the new learners had changed. Their results surprised them because most reading-related brain activity was thought to involve the cortex. The new research may overturn this presumption and may pertain pertain to child learners as well. After being filtered through the eyes, visual information may move first to evolutionarily ancient brain regions before being relayed to the visual and language areas of the cortex typically associated with reading. © 2017 Scientific American

Keyword: Language
Link ID: 23661 - Posted: 05.25.2017

James Gorman Darwin’s finches, those little birds in the Galápagos with beaks of different sizes and shapes, were instrumental in the development of the theory of evolution. Similar birds had large and small beaks and beaks in between, all related to what kinds of insects and seeds they ate. From one ancestor, it seemed, different adaptations to the environment had evolved, giving the birds that adapted a survival edge in a particular ecological niche — evolution by natural selection. Biologists who came later went on to identify the genetic changes that had produced different beak shapes. Now another group of finch-like birds has provided a similar example, but of a different kind of evolution, one driven not by the demands of the environment, but by the demands of female birds. Their preferences in color and pattern caused the evolution of different species of seedeater, all with the same behavior and diet, but with males that look different. That’s a process called sexual selection, which Darwin also wrote about. Leonardo Campagna, a researcher at Cornell University and the Cornell Lab of Ornithology, and a group of scientists from the United States and South America investigated nine species of southern capuchino seedeaters, doing full genomes for each one and reported their findings in Science Advances. They found that the DNA of all the species is remarkably similar, as are the birds. All the females look alike and all of the species feed on grass seeds plucked from grass stalks of living plants. Only the males are different. They have a wide variety of colorations and their courting songs are also distinct. Dr. Campagna and the other researchers found that differences between species DNA were all minimal, ranging from as little as 0.03 percent to as great as 0.3 percent. All the species showed variation in the same area, DNA that appeared to have a role in regulating genes for the pigment melanin. © 2017 The New York Times Company

Keyword: Evolution; Sexual Behavior
Link ID: 23660 - Posted: 05.25.2017

A cannabis compound has been proven for the first time to reduce the frequency of seizures in people with a rare, severe form of epilepsy, according to the results of a randomized trial. For years, parents have pointed to anecdotal benefits of cannabidiol (CBD), a compound in the marijuana plant that does not produce a high, saying it reduces seizures in treatment-resistant epilepsy. Now doctors have performed a randomized trial to show cause and effect, with the findings published in Wednesday's issue of the New England Journal of Medicine. To conduct the study, the researchers focused on Dravet syndrome, a rare form of epilepsy that begins in infancy and is linked to a particular mutation that often resists combinations of up to 10 conventional seizure medications. They enrolled 120 patients who ranged in age from 2.5 to 18 years. Sixty-one patients were randomly assigned to cannabidiol, and the 59 others to placebo. Neither the researchers nor the families knew who received the medication to prevent bias. All continued to take their existing medications. "The message is that cannabidiol does work in reducing convulsing seizures in children with Dravet syndrome," said lead author Dr. Orrin Devinksy, who is director of NYU's Langone Comprehensive Epilepsy Center. For those in the cannabinoid group, the median number of convulsive seizures per month dropped from 12.4 per month before treatment, to 5.9 seizures, the researchers reported. The placebo group, in comparison, only saw their convulsive seizures fall from 14.9 per month, to 14.1. ©2017 CBC/Radio-Canada.

Keyword: Epilepsy; Drug Abuse
Link ID: 23659 - Posted: 05.25.2017

By Meredith Wadman In 2013, a U.S. Department of Agriculture (USDA) inspector visited Thomas D. Morris, Inc., a Maryland animal breeder that sells to U.S. government and academic scientists. The inspector found numerous violations of the federal Animal Welfare Act (AWA), which sets standards for humane treatment. Fifteen unshorn sheep were penned in a sweltering building, while a group of calves and sheep had no shelter at all. A goat and a lamb were lame; another goat had an egg-sized swelling on its shoulder. In a subsequent letter, USDA warned the firm, which had 18 employees and $5 million in revenue in 2013, that future violations could result in fines or criminal prosecution. But it’s difficult for the public to know whether the company—which supplied animals used in at least 48 biomedical studies published since 2012—has kept a clean record. That’s because, on 3 February, USDA abruptly removed inspection reports, warning letters, and other documents on nearly 8000 animal facilities that the agency regulates, including Thomas D. Morris, from public databases. Some of the documents, which are maintained by USDA’s Animal and Plant Health Inspection Service (APHIS), have since been restored. But thousands remain hidden, and animal welfare advocates are now in court trying to force USDA to restore the records, and post all new documents, too. USDA officials said the removal was prompted by their commitment to “maintaining the privacy rights of individuals” identified in the documents, which animal rights groups, journalists, and others have regularly used to publicize the failings of AWA violators. And they say they are still reviewing the withdrawn documents, with an eye toward blacking out information that shouldn’t be public before reposting them. © 2017 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 23658 - Posted: 05.25.2017

By Andy Coghlan Burning the midnight oil may well burn out your brain. The brain cells that destroy and digest worn-out cells and debris go into overdrive in mice that are chronically sleep-deprived. In the short term, this might be beneficial – clearing potentially harmful debris and rebuilding worn circuitry might protect healthy brain connections. But it may cause harm in the long term, and could explain why a chronic lack of sleep puts people at risk of Alzheimer’s disease and other neurological disorders, says Michele Bellesi of the Marche Polytechnic University in Italy. Bellesi reached this conclusion after studying the effects of sleep deprivation in mice. His team compared the brains of mice that had either been allowed to sleep for as long as they wanted or had been kept awake for a further eight hours. Another group of mice were kept awake for five days in a row – mimicking the effects of chronic sleep loss. The team specifically looked at glial cells, which form the brain’s housekeeping system. Earlier research had found that a gene that regulates the activity of these cells is more active after a period of sleep deprivation. One type of glial cell, called an astrocyte, prunes unnecessary synapses in the brain to remodel its wiring. Another type, called a microglial cell, prowls the brain for damaged cells and debris. © Copyright New Scientist Ltd.

Keyword: Sleep; Glia
Link ID: 23657 - Posted: 05.24.2017

Susan Milius A question flamingo researchers get asked all the time — why the birds stand on one leg — may need rethinking. The bigger puzzle may be why flamingos bother standing on two. Balance aids built into the birds’ basic anatomy allow for a one-legged stance that demands little muscular effort, tests find. This stance is so exquisitely stable that a bird sways less to keep itself upright when it appears to be dozing than when it’s alert with eyes open, two Atlanta neuromechanists report May 24 in Biology Letters. “Most of us aren’t aware that we’re moving around all the time,” says Lena Ting of Emory University, who measures what’s called postural sway in standing people as well as in animals. Just keeping the human body vertical demands constant sensing and muscular correction for wavering. Even standing robots “are expending quite a bit of energy,” she says. That could have been the case for flamingos, she points out, since effort isn’t always visible. Translate that improbably long flamingo leg into human terms, and the visible part of the leg would be just the shin down. A flamingo’s hip and knee lie inside the bird’s body. Ting and Young-Hui Chang of the Georgia Institute of Technology tested balance in fluffy young Chilean flamingos coaxed onto a platform attached to an instrument that measures how much they sway. Keepers at Zoo Atlanta hand-rearing the test subjects let researchers visit after feeding time in hopes of catching youngsters inclined toward a nap — on one leg on a machine. “Patience,” Ting says, was the key to any success in this experiment. |© Society for Science & the Public 2000 - 2017

Keyword: Sleep
Link ID: 23656 - Posted: 05.24.2017

By James Hendrix Having witnessed the success of combination therapy in HIV, cancer and heart disease, the time has come for Alzheimer’s disease. At meetings convened by the Alzheimer’s Association and others, a consensus is emerging that the most effective Alzheimer’s treatments may be those that attack the disease on multiple fronts. Looking back for a moment… In the 1980s, the world faced a new, unknown virus. HIV/AIDS was spreading virtually unchecked, devastating millions of lives and spurring lively scientific debate. Today, an HIV diagnosis is no longer a death sentence. AIDS-related deaths have fallen by 45 percent since their peak in 2005 according to UNAIDS, a United Nations program for global action against the spread of the virus. As researchers learned more about HIV, they developed new classes of antiviral medications—each attacking the virus in a unique way. Physicians eventually began prescribing two or more of these drugs together and emerging scientific evidence started revealing the most effective combinations. Today, a powerful three-drug antiviral “cocktail” is allowing people with HIV to live long lives. Advances in understanding the progression of Alzheimer’s point to a number of underlying biological processes involved in the development of the disease. By leveraging this knowledge, we now have a singular opportunity to pioneer new approaches against Alzheimer’s, including combination therapies. © 2017 Scientific American,

Keyword: Alzheimers
Link ID: 23655 - Posted: 05.24.2017

By Diana Kwon Age as a state of mind is not just the stuff of birthday card clichés. In recent years, scientists have plumbed the molecular depths of the body and surfaced with tell-tale biomarkers of aging, some of which extend to the brain. Now, researchers are harnessing another tool, neuroimaging, to measure the organ’s age, and using that to predict how long a person will live. “People are searching for the tree rings of humans,” James Cole, a research associate at Imperial College London, told The Scientist. Cole and his colleagues recently devised their own technique of predicting the biological age of people’s brains using a combination of machine learning and magnetic resonance imaging (MRI) scans. In a study published last month (April 25) in Molecular Psychiatry, the team reported that this technique was able to predict mortality in humans—people with “older” brains, they found, had greater risk of dying before age 80. To create this marker of brain aging, the researchers first trained a machine-learning algorithm to analyze structural brain scans from a healthy reference sample containing 2,001 individuals between 18 and 90 years old. Then, they used this tool to predict brain age in the Lothian Birth Cohort, a group of 669 adults, all born in 1936. Based on the algorithm’s assessment, individuals who had brains that were “older” than their actual, chronological age also tended to have an increased risk of dying sooner and lower performance on various fitness measures, such as lung function, walking speed, and fluid intelligence. © 1986-2017 The Scientist

Keyword: Development of the Brain; Alzheimers
Link ID: 23654 - Posted: 05.24.2017

by Angela Chen@chengela What happens when you look up and see a ball headed toward you? Without even thinking about it, you flinch. That might be because our brains are constantly living our lives in fast-forward, playing out the action in our head before it happens. Humans have to navigate, and respond to, an environment that is always changing. Our brain compensates for this by constantly making predictions about what’s going to happen, says Mattias Ekman, a researcher at Radboud University Nijmegen in the Netherlands. We’ve known this for a while, but these predictions are usually associative. An example: if you see a hamburger, your brain might predict that there will be fries nearby. In a study published today in the journal Nature Communications, Ekman and other scientists focused instead on how the brain predicts motion. So they used brain scans to track what happened as participants observed a moving dot. First, 29 volunteers looked at a white dot the size of a ping-pong ball. The dot went from left to right and then reversed directions. The volunteers watched the dot for about five minutes while scientists scanned their brains with ultra-fast fMRI. This way, the researchers know what pattern of brain activity was activated in the visual cortex while they watched the dot. After these five minutes, the researchers showed only the beginning of the sequence to the volunteers. Here, the scans showed that the brain “autocompletes” the full sequence — and it does it at twice the rate of the actual event. So if a dot took two seconds to go across the screen, the brain predicted the entire sequence in one second. “You’re actually already trying to predict what’s going to happen,” says Ekman. “These predictions are hypothetical, so in a way you’re trying to generate new memories that match the future.” © 2017 Vox Media, Inc.

Keyword: Attention
Link ID: 23653 - Posted: 05.24.2017

By Bob Holmes As soon as I decided to write a book on the science of flavor, I knew I wanted to have myself genotyped. Every one of us, I learned through my preliminary research for Flavor: The Science of Our Most Neglected Sense, probably has a unique set of genes for taste and odor receptors. So each person lives in their own flavor world. I wanted to know what my genes said about my own world. Sure enough, there was a lesson there—but not the one I expected. Our senses of smell and taste detect chemicals in the environment as they bind to receptors on the olfactory epithelium in the nose or on taste buds studding the mouth. From these two inputs, plus a few others, the brain assembles the compound perception we call flavor. Taste is pretty simple: basically, one receptor type each for sweet, sour, salty, and the savory taste called umami, and a family of maybe 20 or more bitter receptors, each of which is sensitive to different chemicals. Smell, on the other hand, relies on more than 400 different odor receptor types, the largest gene family in the human genome. Variation in any of these genes—and, probably, many other genes that affect the pathways involved in taste or smell—should affect how we perceive the flavors of what we eat and drink. Hence the genotyping. One April morning a few years ago, I drooled into a vial and sent that DNA sample off to the Monell Chemical Senses Center in Philadelphia, home to what is likely the world’s biggest research group dedicated to the basic science of flavor. A few months later, I visited Monell to take a panel of perceptual tests and compare the results to my genetic profile. © 1986-2017 The Scientist

Keyword: Chemical Senses (Smell & Taste)
Link ID: 23652 - Posted: 05.24.2017

By Jack Turban We all know that person. Her Instagram is covered with more pictures of feline friends than human companions. Not an insignificant number of these pictures feature mini cat-sized lattes with the caption “Fluffy simply adores her morning coffee.” And let us not forget that the archetype of crazy cat man may be just as prevalent. When you look at these pictures, you probably wonder: is he like this because of the cat? Or does he have the cat because he is like this? It turns out that cats have a mischievous and somewhat dark reputation in neuroscience. There is research to suggest that a cat’s proximity to other mammals can cause them to behave strangely. This feline power has been attributed to a protozoan that lives in their stool, called Toxoplasma gondii (or Toxo for short). In one classic story, researchers showed that Toxo can travel into a rat’s brain and cause the rat to no longer avoid areas where cats live. The rats, in fact, become attracted to the smell of cat urine. Previously repulsed by the smell, these brain-infected rodents run joyously through urine-laden environments. They walk right through the cat’s trap, until their young rodent lives come to an end under a forceful paw. These same protozoans can affect the brains of humans. Immuno-compromised patients, like those with AIDS, can contract the infection from a litter box and develop dangerous brain abscesses. We treat these patients with powerful antibiotics and frequently recommend that they give away their cats. Pregnant women are also advised not to handle cat litter, as a fetus does not yet have the immune system needed to fight Toxo. Fetuses exposed to the protozoan can suffer from seizures, cognitive problems, and blindness. But what about your immunocompetent and decidedly non-pregnant Instagram friend; is she under the influence of this cat’s protozoan minion? . © 2017 Scientific American,

Keyword: Emotions
Link ID: 23651 - Posted: 05.24.2017

Carl Zimmer In a significant advance in the study of mental ability, a team of European and American scientists announced on Monday that they had identified 52 genes linked to intelligence in nearly 80,000 people. These genes do not determine intelligence, however. Their combined influence is minuscule, the researchers said, suggesting that thousands more are likely to be involved and still await discovery. Just as important, intelligence is profoundly shaped by the environment. Still, the findings could make it possible to begin new experiments into the biological basis of reasoning and problem-solving, experts said. They could even help researchers determine which interventions would be most effective for children struggling to learn. “This represents an enormous success,” said Paige Harden, a psychologist at the University of Texas, who was not involved in the study. For over a century, psychologists have studied intelligence by asking people questions. Their exams have evolved into batteries of tests, each probing a different mental ability, such as verbal reasoning or memorization. In a typical test, the tasks might include imagining an object rotating, picking out a shape to complete a figure, and then pressing a button as fast as possible whenever a particular type of word appears. Each test-taker may get varying scores for different abilities. But over all, these scores tend to hang together — people who score low on one measure tend to score low on the others, and vice versa. Psychologists sometimes refer to this similarity as general intelligence. It’s still not clear what in the brain accounts for intelligence. Neuroscientists have compared the brains of people with high and low test scores for clues, and they’ve found a few. Brain size explains a small part of the variation, for example, although there are plenty of people with small brains who score higher than others with bigger brains. © 2017 The New York Times Company

Keyword: Intelligence; Genes & Behavior
Link ID: 23650 - Posted: 05.23.2017

Nicola Davis Air pollution might be linked to poor sleep, say researchers looking into the impact of toxic air on our slumbers. The study explored the proportion of time participants spent asleep in bed at night compared with being awake – a measure known as sleep efficiency. The results reveal that greater exposure to nitrogen dioxide and small particulates known as PM 2.5s are linked with a greater chance of having low sleep efficiency. That, researchers say, could be down to the impact of air pollution on the body. “Your nose, your sinuses and the back of your throat can all be irritated by those pollutants so that can cause some sleep disruption as well as from breathing issues,” said Martha Billings, assistant professor of medicine at the University of Washington and co-author of the research. Billings added that pollutants entering the blood could have an effect on the brain and hence the regulation of breathing. The study, presented at the American Thoracic Society’s annual international conference, drew on air pollution data captured for nitrogen dioxide and PM2.5 levels over a five-year period in six US cities, including data captured near the homes of the 1,863 participants. The data was then used to provide estimates of pollution levels in the home. Researchers then captured data from medical-grade wearable devices worn by the participants on their wrists over a period of seven consecutive days to monitor fine movements while they slept – an approach that offers insights into how long each participant spent asleep or awake.

Keyword: Sleep; Neurotoxins
Link ID: 23649 - Posted: 05.23.2017

By PERRI KLASS, M.D. Why do children wake up early when they are young but want to stay in bed till noon as teenagers? Experts say it’s biology. Adolescents’ bodies want to stay up late and sleep late, putting them out of sync with what their school schedules demand of them. So kids have trouble waking up, and they often find themselves feeling drowsy in morning algebra class. But that chronic sleepiness can affect their health and well-being, their behavior, and even their safety; it becomes genuinely dangerous when sleepy teenagers get behind the wheel. At a recent conference on adolescent sleep, health and school start times, at which I gave a brief keynote, several experts made compelling arguments supporting the idea that middle and high school start times should shift to 8:30 a.m. or later, as recommended by the American Academy of Pediatrics and the American Academy of Sleep Medicine. Brian Tefft, a senior researcher with the AAA Foundation for Traffic Safety, talked about “drowsy driving.” He cited an annual study that asks, “In the past 30 days how often have you driven when you were so tired that you had a hard time keeping your eyes open?” Over the past five years, on average, a quarter of the 16- to 18-year-old licensed drivers reported driving in that condition at least once, and 2 percent said fairly often or regularly. The argument is that teenagers who face very early school start times are at risk of regular sleep deprivation. Driving after sleeping only four to five hours a night is associated with a similar crash risk as driving with an alcohol level at the legal limit. Sleeping less than four hours puts you at the same risk as driving with double the legal alcohol limit. (This is not only true for adolescents, but for all of us.) Drowsy driving may not be the only risk that tired teenagers take. Wendy Troxel, a clinical psychologist and senior behavioral and social scientist at RAND, talked about the “adolescent health paradox,” that teenagers, who are in a developmental period of physical strength and resilience, face disproportionately high mortality rates. Unintentional injury (especially car crashes) is high on the list of causes, followed by homicide and suicide. © 2017 The New York Times Company

Keyword: Sleep; Development of the Brain
Link ID: 23648 - Posted: 05.23.2017

Claude Messier, Alexandria Béland-Millar, The short answer is yes: certain brain regions do indeed consume more energy when engaged in particular tasks. Yet the specific regions involved and the amount of energy each consumes depend on the person’s experiences as well as each brain’s individual properties. Before we delve into the answer, it is important to understand how we measure a brain’s energy expenditure. Picture the colorful brain images researchers use to display neural activity. The colors typically represent the amount of oxygen or glucose various brain regions use during a task. Our brain is always active on some level—even when we are not engaged in a task—but it requires more energy to accomplish something that demands concentration such as moving, seeing or thinking. A simple example is that our primary visual cortex lights up more in brain scans—consuming more energy—when our eyes are open than when they are closed. Similarly, our primary motor cortex uses more energy if we move our hands than if we keep them still. Say you are learning a new skill—how to juggle or speak Spanish. Neuroscientists have made the fascinating observation that when we do something completely novel, a broad range of brain areas becomes active. As we become more skilled at the task, however, our brain becomes more focused: we require only the essential brain regions and need increasingly less energy to perform that task. Once we have mastered a skill—we become fluent in Spanish—only the brain areas directly involved remain active. Thus, learning a new skill requires more brainpower than a well-practiced activity. © 2017 Scientific American

Keyword: Brain imaging
Link ID: 23647 - Posted: 05.23.2017

By GRETCHEN REYNOLDS Mice do not, so far as we know, practice meditation. But in order to study how that activity affects human brains at the cellular level, researchers at the University of Oregon managed to put murine brains into a somewhat equivalent state. Their experiments, reported in March in the Proceedings of the National Academy of Sciences, suggest new ways of investigating how a person’s brain can constantly reshape itself. Past studies have suggested that people who meditate tend to have more white matter in and around the anterior cingulate cortex, a part of the brain involved in regulating emotions. Meditation also seems to intensify theta-wave activity, a type of rhythmic electrical pulsation often associated with a state of calm. Psychologists at Oregon speculated that the surge in theta waves stimulated the production of cells in the white matter. But they needed to develop an animal model of this activity; they obviously couldn’t examine the living brain tissue in meditating humans. So the psychologists asked colleagues in the university’s neuroscience department if they could increase theta-wave activity in mice, which were already being used to study brain states and neural plasticity, or the brain’s ability to rewire itself. Could the neuroscientists create a comparable effect in mice? Yes, it turned out, using a brain-research technique known as optogenetics, which uses light to turn on and off neurons, and mice that have been bred with specific genes responsive to light. The Oregon group, by pulsing the light at the same frequency found in human theta waves (eight hertz), were able to switch on the neurons in the anterior cingulate cortexes of the mice. They also exposed some mice to light at higher and lower frequencies and left others alone. Each treated mouse received 30 minutes of light therapy for 20 days, in an attempt to mimic the amount of meditation done in earlier human studies. Afterward, those mice exposed to the eight-hertz, thetalike light waves proved to be relatively calm in behavioral tests: they lingered in lighted portions of a special cage, while their twitchier counterparts ran for the shadows. © 2017 The New York Times Company

Keyword: Stress
Link ID: 23646 - Posted: 05.22.2017

By Catherine Caruso If you give a mouse a beer, he is going to want a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos or some other caloric snack. A study published in January in Nature Communications helps to explain why binge drinking, in both mice and humans, so often leads to binge eating even though alcohol is, itself, high in calories. In the first part of the study, neuroscientists Craig Blomeley and Sarah Cains, both at the Francis Crick Institute Mill Hill Laboratory in London, injected mice with the equivalent of roughly two bottles of wine once a day for three consecutive days, mimicking a weekend of heavy drinking. Sure enough, the inebriated mice ate far more than sober mice in a control group. To figure out why, the researchers then exposed thin-sliced postmortem mouse brains to alcohol and measured the resulting neural activity using fluorescent tags and electrodes. They found that ethanol exposure alters calcium exchange in the cells, causing specialized nerve cells called agouti-related protein (AgRP) neurons to fire more frequently and easily. These neurons normally fire when our body needs calories, and research has shown that activating them artificially will cause mice to chow down even when they are full. The study results suggest that alcohol activates AgRP neurons in the brain, giving drunk mice the munchies. The same is likely true for humans because this brain circuitry has been highly conserved across mammal species, Cains says: “I don't doubt that AgRP neurons are activated in humans, and that's why you see this effect.” © 2017 Scientific American

Keyword: Drug Abuse; Obesity
Link ID: 23645 - Posted: 05.22.2017

By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 23644 - Posted: 05.22.2017

Jon Hamilton It took an explosion and 13 pounds of iron to usher in the modern era of neuroscience. In 1848, a 25-year-old railroad worker named Phineas Gage was blowing up rocks to clear the way for a new rail line in Cavendish, Vt. He would drill a hole, place an explosive charge, then pack in sand using a 13-pound metal bar known as a tamping iron. But in this instance, the metal bar created a spark that touched off the charge. That, in turn, "drove this tamping iron up and out of the hole, through his left cheek, behind his eye socket, and out of the top of his head," says Jack Van Horn, an associate professor of neurology at the Keck School of Medicine at the University of Southern California. Gage didn't die. But the tamping iron destroyed much of his brain's left frontal lobe, and Gage's once even-tempered personality changed dramatically. "He is fitful, irreverent, indulging at times in the grossest profanity, which was not previously his custom," wrote John Martyn Harlow, the physician who treated Gage after the accident. This sudden personality transformation is why Gage shows up in so many medical textbooks, says Malcolm Macmillan, an honorary professor at the Melbourne School of Psychological Sciences and the author of An Odd Kind of Fame: Stories of Phineas Gage. "He was the first case where you could say fairly definitely that injury to the brain produced some kind of change in personality," Macmillan says. © 2017 npr

Keyword: Attention; Emotions
Link ID: 23643 - Posted: 05.22.2017

Elle Hunt About 150 years ago, and “almost a lifetime” either side, Charles Darwin was beleaguered by the problem of the peacock’s tail. Just the sight of a feather, he wrote in April 1860, “makes me sick!” The plumage of the male bird represented a hole in his theory of evolution. According to Victorian thinking, beauty was divine creation: God had designed the peacock for his own and humankind’s delight. In, On The Origin of Species, published the previous year, Darwin had challenged the dominant theory of creationism, arguing that man had been made not in God’s image but as a result of evolution, with new species formed over generations in response to their environment. But beauty, and a supposed aesthetic sense in animals (“We must suppose [that peahens] admire [the] peacock’s tail, as much as we do,” he wrote), took Darwin the best part of his life to justify – not least because the theory he eventually landed upon went against the grain of his entire worldview. Sexual selection was of strategic importance to Darwin, says Evelleen Richards, an honorary professor in history and philosophy of science at the University of Sydney: it was a naturalistic account for aesthetic differences between male and female animals of the same species, shoring up his defence of natural selection.

Keyword: Evolution; Sexual Behavior
Link ID: 23642 - Posted: 05.22.2017