Weeks before they took their first breaths, two babies had their spinal cords delicately repaired by surgeons in the first operations of their kind in the UK. The spina bifida surgeries were successfully performed by a team at University College hospital in London this summer on two babies while they were still in the womb. Spina bifida is usually treated after birth, but research shows repairing the spine earlier can stop the loss of spinal fluid and lead to better long-term health and mobility outcomes. A 30-strong team carried out the two operations, coordinated by the UCL professor Anna David, who had worked for three years to bring the procedure to patients in the UK. She said mothers previously had to travel to the US, Belgium or Switzerland. “It’s fantastic. Women now don’t have to travel out of the UK,” David said. “They can have their family with them. There are less expenses. So all good things.” Advertisement The surgery team from University College London hospitals (UCLH) and Great Ormond Street hospital travelled to Belgium to train at a facility in Leuven, where more than 40 of the operations have been carried out. Spina bifida is a condition that develops during pregnancy when the bones of the spine do not form properly, creating a gap that leaves the spinal cord unprotected. It can cause a baby’s spinal fluid to leak and affect brain development, potentially leading to long-term health and mobility problems. © 2018 Guardian News and Media Limited

Keyword: Development of the Brain
Link ID: 25614 - Posted: 10.25.2018

Sukanya Charuchandra L. Wu et al., “Human ApoE isoforms differentially modulate brain glucose and ketone body metabolism: Implications for Alzheimer’s disease risk reduction and early intervention,” J Neurosci, 38:6665­–81, 2018. Humans carry three different isoforms of the ApoE gene, which affects Alzheimer’s risk. Liqin Zhao of the University of Kansas and her colleagues previously found that the gene plays a role in brain metabolism when expressed in mice; in a new study, they looked for the pathways involved. LEAVING AN IMPRESSION Zhao’s team engineered female mice to express the human versions of either ApoE2, ApoE3, or ApoE4, and analyzed expression of 43 genes involved in energy metabolism in their cortical tissue. BLOCKADE Mice with ApoE2 showed higher levels of proteins needed for glucose uptake and metabolism in their brains relative to animals harboring the most common isoform in humans, ApoE3. Mice with ApoE4 had lower levels of such proteins. The brain tissue’s glucose transport efficiency also varied across the genotypes, and levels of a key glucose-metabolizing enzyme, hexokinase, were reduced in ApoE4 brains. However, ApoE2 and ApoE4 brains contained similar levels of proteins involved in using ketone bodies, a secondary source of energy, while ApoE3 brains had lower levels of those proteins. “Brain glycolytic function may serve as a significant mechanism underlying the differential impact of ApoE genotypes,” Zhao says. © 1986 - 2018 The Scientist.

Keyword: Obesity; Alzheimers
Link ID: 25613 - Posted: 10.25.2018

Laura Sanders Researchers have found a new link between gut and brain. By signaling to nerve cells in the brain, certain microbes in the gut slow a fruit fly’s walking pace, scientists report. Fruit flies missing those microbes — and that signal — turn into hyperactive speed walkers. With the normal suite of gut microbes, Drosophila melanogaster fruit flies on foot cover an average of about 2.4 millimeters a second. But fruit flies without any gut microbes zip along at about 3.5 millimeters a second, Catherine Schretter, a biologist at Caltech, and her colleagues report October 24 in Nature. These flies with missing microbes also take shorter breaks and are more active during the day. “Our work suggests that microbes assist in maintaining a certain level of locomotion,” Schretter says. An enzyme made by Lactobacillus brevis bacteria normally serves as the brakes, the researchers found. When researchers supplied the enzyme, called xylose isomerase, to flies lacking bacteria, the flies began walking at a slower, more normal pace. Xylose isomerase acts on a sugar that’s thought to influence nerve cells in fruit flies’ brains that control walking. For still mysterious reasons, the bacterial influence on walking speed occurred only in female fruit flies, not males. Studying that difference will be “a very interesting potential direction for this work,” Schretter says. |© Society for Science & the Public 2000 - 2018

Keyword: Obesity
Link ID: 25612 - Posted: 10.25.2018

By Kelly Servick WASHINGTON, D.C.—A hand-size monkey called Callithrix jacchus—the common marmoset—is in great demand in labs and yet almost nowhere to be found. Marmosets’ small size, fast growth, and sophisticated social life were already enough to catch the eye of neuroscientists. They’ve now been genetically engineered to make their brains easier to image and to serve as models for neurological disorders such as autism and Parkinson’s. The problem: “There are just no monkeys,” says Cory Miller, a neuroscientist at the University of California, San Diego. At a meeting here this week, convened by the National Academies of Sciences, Engineering, and Medicine’s (NASEM’s) Institute for Laboratory Animal Research, neuroscientist Jon Levine, who directs the Wisconsin National Primate Research Center at the University of Wisconsin in Madison, likened the surge in demand to “a 10-alarm fire that’s about to be set.” In response, the National Institutes of Health (NIH) plans to launch funding to expand marmoset research. And established marmoset researchers, including Miller, are working together to help new labs get animals. When Miller’s lab started to work with marmosets in 2009, many colleagues who studied macaques—the most popular genus of research monkey—didn’t even know that marmosets were monkeys, he remembers. “They were like, ‘Is it those chipmunks that were in the Rocky Mountains?’” (They were thinking of marmots.) © 2018 American Association for the Advancement of Science

Keyword: Animal Rights; Autism
Link ID: 25611 - Posted: 10.24.2018

By JoAnna Klein Lavender bath bombs; lavender candles; deodorizing lavender sachets for your shoes, car or underwear drawer; lavender diffusers; lavender essential oils; even lavender chill pills for humans and dogs. And from Pinterest: 370 recipes for lavender desserts. Take a deep breath. Release. People like lavender. We’ve been using this violet-capped herb since at least medieval times. It smells nice. But Google “lavender” and results hint at perhaps the real fuel for our obsession: “tranquillity,” “calm,” “relaxation,” “soothing,” and “serenity.” Lavender has purported healing powers for reducing stress and anxiety. But are these effects more than just folk medicine? Yes, said Hideki Kashiwadani, a physiologist and neuroscientist at Kagoshima University in Japan — at least in mice. “Many people take the effects of ‘odor’ with a grain of salt,” he said in an email. “But among the stories, some are true based on science.” In a study published Tuesday in the journal Frontiers in Behavioral Neuroscience, he and his colleagues found that sniffing linalool, an alcohol component of lavender odor, was kind of like popping a Valium. It worked on the same parts of a mouse’s brain, but without all the dizzying side effects. And it didn’t target parts of the brain directly from the bloodstream, as was thought. Relief from anxiety could be triggered just by inhaling through a healthy nose. Their findings add to a growing body of research demonstrating anxiety-reducing qualities of lavender odors and suggest a new mechanism for how they work in the body. Dr. Kashiwadani believes this new insight is a key step in developing lavender-derived compounds like linalool for clinical use in humans. Dr. Kashiwadani and his colleagues became interested in learning how linalool might work for anti-anxiety while testing its effects on pain relief in mice. In this earlier study, they noticed that the presence of linalool seemed to calm mice. © 2018 The New York Times Company

Keyword: Emotions; Chemical Senses (Smell & Taste)
Link ID: 25610 - Posted: 10.24.2018

By: A. Benjamin Srivastava, M.D., and Mark S. Gold, M.D. T he opioid epidemic is one of the foremost public health crises in the United States. A recent analysis from Stanford University suggested that without any changes in currently available treatment, prevention, and public health approaches, we should expect to have 510,000 deaths from prescription opioids and street heroin from 2016 to 2025 in the US.1 Both the lay press and scientific literature are full of proposals, analyses, and potential solutions. Most focus on expanding access to and dissemination of overdose reversal treatment (naloxone), and the medication-assisted treatment (MAT) drugs methadone, buprenorphine, and naltrexone. Obviously, expanding the availability of naloxone and MAT drugs are important steps that can be readily implemented, especially using an approach similar to what was done during the HIV epidemic.2,3 But in addition to such efforts, we must invest in research to develop new treatments informed by neuroscientific evidence. A comprehensive discussion of naltrexone should be understood within the context of naloxone, which is considered its short-acting version based on relative half-lives (three hours for naloxone, 13 hours for oral naltrexone). When first synthesized, naloxone was a novel medication as well as a cornerstone of research into the pharmacology of the opioid system. Naloxone successfully competes against opioids to bind to the “Mu” opioid receptor on neurons, completely blocking the opioid’s downstream effects. As a “Mu opioid receptor (MOR) antagonist,” it reverses the potentially deadly effects of opioid overdose. © 2018 The Dana Foundation

Keyword: Drug Abuse; Pain & Touch
Link ID: 25609 - Posted: 10.24.2018

By Gretchen Reynolds Ten minutes of mild, almost languorous exercise can immediately alter how certain parts of the brain communicate and coordinate with one another and improve memory function, according to an encouraging new neurological study. The findings suggest that exercise does not need to be prolonged or intense to benefit the brain and that the effects can begin far more quickly than many of us might expect. We already know that exercise can change our brains and minds. The evidence is extensive and growing. Multiple studies with mice and rats have found that when the animals run on wheels or treadmills, they develop more new brain cells than if they remain sedentary. Many of the new cells are clustered in the hippocampus, a portion of the brain that is essential for memory creation and storage. The active animals also perform better on tests of learning and memory. Equivalent experiments examining brain tissue are not possible in people. But some past studies have shown that people who exercise regularly tend to have a larger, healthier hippocampus than those who do not, especially as they grow older. Even one bout of exercise, research suggests, can help most of us to focus and learn better than if we sit still. But these studies usually have involved moderate or vigorous exercise, such as jogging or brisk walking and often for weeks or months at a time. Whether a single, brief spurt of very easy exercise will produce desirable changes in the brain has remained unclear. So for the new study, which was published in September in Proceedings of the National Academy of Sciences, scientists from the University of California, Irvine, and the University of Tsukuba in Japan turned to a group of healthy, young college students. © 2018 The New York Times Company

Keyword: Learning & Memory
Link ID: 25608 - Posted: 10.24.2018

By Mitch Leslie Male mice that work out spawn healthier offspring than their lethargic counterparts, according to a new study. Whether the results hold true for humans remains uncertain, but they support the notion that some of the benefits of exercise are somehow passed on to the next generation. “The science is solid, and it’s pretty exciting,” says epigeneticist Sarah Kimmins of McGill University in Montreal, Canada, who wasn’t connected to the work. Scientists already know that a parent’s bad exercise or dietary habits can affect their offspring. Mothers who are obese during pregnancy, for example, give birth to children who are more likely to be obese as adults and develop metabolic illnesses such as cardiovascular disease. Another study found that male rats that snarfed high-fat chow fathered offspring that didn’t respond normally to glucose, a hallmark of type 2 diabetes. To determine whether the opposite is true, molecular exercise physiologist Kristin Stanford of The Ohio State University College of Medicine in Columbus and colleagues fed male mice a fat-rich diet for 3 weeks. One group of animals had access to running wheels, scampering nearly 6 kilometers per night on average, but the rest were couch potatoes. After dissecting some of the rodents to obtain samples of their sperm, the researchers allowed the remaining mice to mate. Stanford and her colleagues tracked the resulting offspring until they were a year old, about middle age for a mouse. Even though the offspring of exercising and nonexercising dads all ate a high-fat diet their entire lives and didn’t get any physical activity, the offspring of healthy fathers seemed to inherit their dads’ metabolism. The progeny of the runners showed a better response to increases in blood glucose and had lower insulin levels—both hallmarks of a sound metabolism—the researchers report today in Diabetes. “Exercise was completely negating the effect of a high-fat diet” on the offspring, Stanford says. © 2018 American Association for the Advancement of Scienc

Keyword: Epigenetics; Obesity
Link ID: 25607 - Posted: 10.23.2018

By Kristina R. Olson On arrival at a friend's house for dinner one night in the fall of 2008, I joined the evening's youngest guest, five-year-old Noah, who was playing on the couch. Little did I know he would single-handedly change the course of my career. As a professor of developmental psychology, hanging out at the kids' table is not unusual for me. I study how children think about themselves and the people around them, and some of my keenest insights have come from conversations like this one. After some small talk, I saw Noah glance around the room, appear to notice that no one was looking and retrieve something from inside his pocket. The reveal was slow but the result unmistakable: a beloved set of Polly Pocket dolls. Over the next few years I got to know Noah well and learned more about his past (all names of children here are pseudonyms to protect their privacy). Noah's parents had first noticed that he was different from his brother in the preschool years. He preferred female playmates and toys more commonly associated with girls, but his parents were unfazed. As he got older, Noah grew out his previously short hair and replaced his fairly gender-neutral wardrobe with one that prominently featured Twinkle Toes—shoes that lit up in pink as he stepped. Unlike many similar kids, Noah's family, friends and school fully accepted him. They even encouraged him to meet other kids like himself, boys who flouted gender norms. Along with the other adults in Noah's life, I couldn't help but wonder: What did Noah's behavior mean? Was he gay? Could he just be a kid who paid less attention to gender norms than most? At the time I had no idea that these questions would soon guide my scientific research. © 2018 Scientific American

Keyword: Sexual Behavior
Link ID: 25606 - Posted: 10.23.2018

Claire Ainsworth As a clinical geneticist, Paul James is accustomed to discussing some of the most delicate issues with his patients. But in early 2010, he found himself having a particularly awkward conversation about sex. A 46-year-old pregnant woman had visited his clinic at the Royal Melbourne Hospital in Australia to hear the results of an amniocentesis test to screen her baby's chromosomes for abnormalities. The baby was fine — but follow-up tests had revealed something astonishing about the mother. Her body was built of cells from two individuals, probably from twin embryos that had merged in her own mother's womb. And there was more. One set of cells carried two X chromosomes, the complement that typically makes a person female; the other had an X and a Y. Halfway through her fifth decade and pregnant with her third child, the woman learned for the first time that a large part of her body was chromosomally male1. “That's kind of science-fiction material for someone who just came in for an amniocentesis,” says James. Sex can be much more complicated than it at first seems. According to the simple scenario, the presence or absence of a Y chromosome is what counts: with it, you are male, and without it, you are female. But doctors have long known that some people straddle the boundary — their sex chromosomes say one thing, but their gonads (ovaries or testes) or sexual anatomy say another. Parents of children with these kinds of conditions — known as intersex conditions, or differences or disorders of sex development (DSDs) — often face difficult decisions about whether to bring up their child as a boy or a girl. Some researchers now say that as many as 1 person in 100 has some form of DSD2. © 2018 Macmillan Publishers Limited

Keyword: Sexual Behavior
Link ID: 25605 - Posted: 10.23.2018

By Amanda Montañez Humans are socially conditioned to view sex and gender as binary attributes. From the moment we are born—or even before—we are definitively labeled “boy” or “girl.” Yet science points to a much more ambiguous reality. Determination of biological sex is staggeringly complex, involving not only anatomy but an intricate choreography of genetic and chemical factors that unfolds over time. Intersex individuals—those for whom sexual development follows an atypical trajectory—are characterized by a diverse range of conditions, such as 5-alpha reductase deficiency (highlighted in graphic below). A small cross section of these conditions and the pathways they follow is shown here. In an additional layer of complexity, the gender with which a person identifies does not always align with the sex they* are assigned at birth, and they may not be wholly male or female. The more we learn about sex and gender, the more these attributes appear to exist on a spectrum. *The English language has long struggled with the lack of a widely recognized nongendered third-person singular pronoun. A singular form of “they” has grown in widespread acceptance, and many people who do not identify with a binary gender use it. © 2018 Scientific American

Keyword: Sexual Behavior
Link ID: 25604 - Posted: 10.23.2018

By Benedict Carey A generation ago, depression was viewed as an unwanted guest: a gloomy presence that might appear in the wake of a loss or a grave disappointment and was slow to find the door. The people it haunted could acknowledge the poor company — I’ve been a little depressed since my father died — without worrying that they had become chronically ill. Today, the condition has been recast in the medical literature as a darker, more permanent figure, a monster in the basement poised to overtake the psyche. For decades, researchers have debated the various types of depression, from mild to severe to “endogenous,” a rare, near-paralyzing despair. Hundreds of studies have been conducted, looking for markers that might predict the course of depression and identify the best paths to recovery. But treatment largely remains a process of trial and error. A drug that helps one person can make another worse. The same goes for talk therapies: some patients do very well, others don’t respond at all. “If you got a depression diagnosis, one of the most basic things you want to know is, what are the chances of my life returning to normal or becoming optimal afterward?” said Jonathan Rottenberg, a professor of psychology at the University of South Florida. “You’d assume we’d have an answer to that question. I think it’s embarrassing that we don’t.” In a paper in the current issue of Perspectives on Psychological Science, Dr. Rottenberg and his colleagues argue that, in effect, the field has been looking for answers in the wrong place. In trying to understand how people with depression might escape their condition, scientists have focused almost entirely on the afflicted, overlooking a potentially informative group: people who once suffered from some form of depression but have more or less recovered. Indeed, while this cohort almost certainly exists — every psychiatrist and psychologist knows someone in it — it is so neglected that virtually nothing is known about its demographics, how well its members are faring and, fundamentally, how many individuals it contains. © 2018 The New York Times Company

Keyword: Depression
Link ID: 25603 - Posted: 10.23.2018

Richard Harris Powerful drugs that have been used for decades to treat delirium are ineffective for that purpose, according to a study published online Monday in the New England Journal of Medicine. Antipsychotic medications, such as haloperidol (brand name, Haldol), are widely used in intensive care units, emergency rooms, hospital wards and nursing homes. "In some surveys up to 70 percent of patients [in the ICU] get these antipsychotics," says Dr. E. Wesley "Wes" Ely, an intensive care specialist at Vanderbilt University Medical Center. They're prescribed by "very good doctors at extremely good medical centers," he says. "Millions of people worldwide are getting these drugs to treat their delirium." But the drugs can have serious side effects. And Ely says there is no solid research showing that they are effective at treating delirium. Patients with delirium are often confused and incoherent and sometimes can suffer hallucinations. This condition can lead to long-term cognitive problems, including a form of dementia. Ely and colleagues at 16 U.S. medical centers decided to put antipsychotic drugs to a rigorous test. They divided nearly 600 patients who were suffering from delirium into three groups. One group got the powerful antipsychotic haloperidol. A second group got ziprasidone, which is a related medication from a class of drugs called "atypical antipsychotics." A third group got a placebo. © 2018 npr

Keyword: Alzheimers; Schizophrenia
Link ID: 25602 - Posted: 10.23.2018

Tina Hesman Saey SAN DIEGO — For some people, choosing a same-sex partner may be in their DNA. In a large study of more than 490,000 men and women in the United States, United Kingdom and Sweden, researchers discovered four genetic variants that occur more often in people who indicated on questionnaires that they had had same-sex sexual partners. Andrea Ganna, a geneticist at the Broad Institute of MIT and Harvard reported the results October 19 at the annual meeting of the American Society of Human Genetics. Two of the variants were specific to men’s sexual partner choice. The other two influence sex partner choice for both men and women. Collectively, the DNA differences explained only 8 to 12 percent of the heritability of having same-sex partners. “There is no gay gene,” Ganna said, “but rather non-heterosexuality is influenced by many tiny-effect genetic factors.” The new study is an advance over previous attempts to find “gay genes,” says J. Michael Bailey, a psychologist at Northwestern University in Evanston, Ill., who was not involved in the new work. The study’s size is its main advantage, Bailey says. “It’s huge. Huge.” Researchers examined DNA data from more than 400,000 participants in the U.K. Biobank and more than 69,000 people who had their DNA tested by the consumer testing company 23andMe. People who have given their DNA data to those research projects also answered a battery of questions, including ones about whether they had ever had a partner of the same sex and how many sexual partners they have had. The findings were replicated with data from three other studies, including one from Sweden. Findings from such large studies are more likely to be replicated than the small studies in the past, Bailey says. Researchers have “really gotten these studies down now and if they find things, it’s pretty sure that they’re true.” |© Society for Science & the Public 2000 - 2018

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 25601 - Posted: 10.22.2018

By Michael Price SAN DIEGO, CALIFORNIA—How genes influence sexual orientation has sparked debate for at least a quarter century. But geneticists have had only a handful of underpowered studies to address a complex, fraught, and often stigmatized area of human behavior. Now, the largest-ever study of the genetics of sexual orientation has revealed four genetic variants strongly associated with what the researchers call nonheterosexual behavior. Some geneticists are hailing the findings as a cautious but significant step in understanding the role of genes in sexuality. Others question the wisdom of asking the question in the first place. Andrea Ganna, a research fellow with the Broad Institute in Cambridge, Massachusetts, and Harvard Medical School in Boston, and colleagues examined data from hundreds of thousands of people who provided both DNA and behavioral information to two large genetic surveys, the UK Biobank study and the private genetics firm 23andMe. They analyzed DNA markers from people who answered either “yes” or “no” to the question, “Have you ever had sex with someone of the same sex?” In total, they identified 450,939 people who said their sexual relationships had been exclusively heterosexual and 26,890 people who reported at least one homosexual experience. In Ganna’s talk yesterday at the annual meeting of the American Society of Human Genetics here, he emphasized that the researchers were cautious about exploring sexual behavior that is still illegal in many countries, and that they tried to frame their questions carefully “to avoid a fishing expedition.” The team, which includes behavioral scientists, preregistered their research design and also met regularly with members of the LGBTQ community to discuss and share results. Ganna acknowledged that what they call “nonheterosexual behavior” includes “a large spectrum of sexual experiences, that go from people who engage exclusively in same-sex behavior to those who might have experimented once or twice.” © 2018 American Association for the Advancement of Science

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 25600 - Posted: 10.22.2018

Allison Aubrey By age 40, about one in 10 adults will experience some hearing loss. It happens so slowly and gradually, says audiologist Dina Rollins, "you don't realize what you're missing." And even as it worsens, many people are in denial. By the time someone is convinced they have a hearing problem, age-related memory loss may have already set in. But, here's the good news: Restoring hearing with hearing aids can help slow down cognitive decline. Consider these findings: Researchers tracked about 2,000 older adults in the U.S. both before and after they started using hearing aids. The adults were participants in a big, national study, the Health and Retirement Study. "We found the rate of cognitive decline was slowed by 75 percent following the adoption of hearing aids," says Asri Maharani, a researcher at the University of Manchester in the division of neuroscience and experimental psychology and an author of the paper. "It is a surprising result," Maharani says. The study was published this spring in the Journal of the American Geriatrics Society. To assess cognition over time, researchers performed a battery of tests face-to-face with participants. This was done every two years from 1996 to 2014. One test to assess memory required participants to recall a list of 10 words, both immediately after the words were read aloud, and then again after the participants had been distracted by other tasks. © 2018 npr

Keyword: Alzheimers; Development of the Brain
Link ID: 25599 - Posted: 10.22.2018

By Sandra G. Boodman Ever since he was a toddler, Michael had been beset by an array of medical problems that doctors couldn’t explain. Severe leg pain came first. That was followed a few years later by recurrent, sometimes severe, stomachaches. Later, the little boy developed a wracking cough, followed by trouble breathing. In fifth grade, after he fell and smacked his tailbone, he was in so much pain he wound up in a wheelchair. His worried parents took him to four emergency rooms and an array of Washington-area specialists, among them orthopedists, neurologists, pediatricians and a gastroenterologist. Yet virtually every test failed to uncover a problem. It would take a seasoned pediatrician to pull together the disparate elements of the 10-year-old’s medical history and make an unexpected diagnosis that would prove to be a turning point for the boy and his family. Three years later, Michael, now 14 and a freshman in high school, seems to have moved beyond the disorder that dominated his first decade. His father said he believes his son’s illness resulted from “a perfect storm” of factors. He would have preferred that the doctors who saw Michael had spoken “a little more freely about their guesses” and had provided more guidance. To protect Michael’s privacy, his parents requested that he and they be identified by their middle names. When he was nearly 2, Michael, who had been previously healthy, began limping and then stopped walking. His pediatrician found no obvious explanation and sent him to a pediatric neurologist, who ordered an extensive work-up, including scans and blood tests. © 1996-2018 The Washington Post

Keyword: Development of the Brain; Emotions
Link ID: 25598 - Posted: 10.22.2018

Sasa Woodruff Ryan "China" McCarney has played sports his entire life, but sometimes he has to force himself to show up on the field to play pick-up soccer with his friends. "I'm dreading and I'm anticipating the worst. But I do it anyway. And then, it's a euphoric sensation when you're done with it because you end up having a great time," says McCarney. McCarney was just 22 when he had his first panic attack. As a college and professional baseball player, he says getting help was stigmatized. It took him six years to get professional support. He still struggles with depression and social anxiety, but says exercising helps him — especially when it's with his teammates. Research shows exercise can ease things like panic attacks or mood and sleep disorders, and a recent study in the journal, Lancet Psychiatry, found that popular team sports may have a slight edge over the other forms of physical activity. The researchers analyzed CDC survey data from 1.2 million adults and found — across age, gender, education status and income — people who exercised reported fewer days of bad mental health than those who didn't. And those who played team sports reported the fewest. One of the study's authors, Adam Chekroud, an assistant adjunct professor at Yale's School of Medicine, thinks team activity could add another layer of relief for sufferers of mental illness. He says there are biological, cognitive and social aspects to mental illness. "Some sports might just be hitting on more of those elements than other sports," he says. "If you just run on a treadmill for example, it's clear that you're getting that biological stimulation. But perhaps there are other elements of depression that you're not going to be tapping into." © 2018 npr

Keyword: Depression
Link ID: 25597 - Posted: 10.22.2018

Amanda B. Keener If Leonardo da Vinci had a good eye doctor, he might not have become such a great artist. At least that’s what an analysis of paintings and sculptures believed to be modeled after da Vinci suggests. Visual neuroscientist Christopher Tyler of the City University of London examined six pieces of art, including Salvator Mundi and Vitruvian Man. Five of the pieces depict an eye misalignment consistent with a disorder called exotropia that can interfere with three-dimensional vision, Tyler reports online October 18 in JAMA Ophthalmology. Exotropia, in which one eye turns slightly outward, is one of several eye disorders collectively called strabismus. Today, strabismus, which affects 4 percent of people in the United States, is treated with special glasses, eye patches or surgery. Tyler calculated the differences in eye alignment using the same sorts of measurements that an optometrist does when tailoring a pair of glasses. Most of the portraits showed the eyes misaligned, but Vitruvian Man by da Vinci himself did not. As a result, da Vinci may have had intermittent exotropia, present only some of the time and perhaps controllable, Tyler suspects. “The person [with intermittent exotropia] can align their eyes and see in 3-D, but if they’re inattentive or tired, the eye may droop,” he says. If da Vinci could control his exotropia, Tyler speculates that it would have been an artistic advantage. “The artist’s job is to paint on a 2-D surface,” he says. “This can be difficult when you view the world three-dimensionally.” Both eyes need to focus on the same subject for 3-D vision. Many artists shut one eye when viewing their subjects to more easily translate details into two dimensions. But with intermittent exotropia, da Vinci could have switched from 3-D to 2-D and back again with ease. |© Society for Science & the Public 2000 - 201

Keyword: Vision
Link ID: 25596 - Posted: 10.22.2018

By Jocelyn KaiserO For years, a Colorado couple searched for an explanation for why their bright, active little girl was having increasing trouble walking, speaking, and seeing. In December 2016, Julia Vitarello and Alek Makovec learned that 6-year-old Mila Makovec almost certainly had Batten disease, an inherited and fatal neurodegenerative disorder. Now, in a stunning illustration of personalized genomic medicine, Mila is receiving a drug tailored to her particular disease-causing DNA mutation—and it appears to have halted the condition’s progression. Today at the annual meeting of The American Society of Human Genetics in San Diego, California, researchers told the story of how in less than a year, they went from sequencing Mila’s genome to giving her a synthetic RNA molecule that helps her cells ignore her genetic flaw and make a needed protein. The same steps could help some other patients with diseases caused by unique mutations in a single gene, they said. “It’s very exciting,” says gene therapy researcher Steven Gray of the University of Texas Southwestern Medical Center in Houston, who wasn’t involved in the research. “There couldn’t be a stronger example of how personalized medicine might work in practice.” Batten disease afflicts an estimated two to four in 100,000 births in the United States. Patients have problems with lysosomes, enzyme-filled sacs within cells that clear waste molecules. Without properly working lysosomes, waste builds up and kills neural cells, causing brain damage and death by adolescence. © 2018 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 25595 - Posted: 10.20.2018