By JAMES GORMAN SEATTLE — When Clay Reid decided to leave his job as a professor at Harvard Medical School to become a senior investigator at the Allen Institute for Brain Science in Seattle in 2012, some of his colleagues congratulated him warmly and understood right away why he was making the move. Others shook their heads. He was, after all, leaving one of the world’s great universities to go to the academic equivalent of an Internet start-up, albeit an extremely well- financed, very ambitious one, created in 2003 by Paul Allen, a founder of Microsoft. Still, “it wasn’t a remotely hard decision,” Dr. Reid said. He wanted to mount an all-out investigation of a part of the mouse brain. And although he was happy at Harvard, the Allen Institute offered not only great colleagues and deep pockets, but also an approach to science different from the classic university environment. The institute was already mapping the mouse brain in fantastic detail, and specialized in the large-scale accumulation of information in atlases and databases available to all of science. Now, it was expanding, and trying to merge its semi-industrial approach to data gathering with more traditional science driven by individual investigators, by hiring scientists like Christof Koch from the California Institute of Technology as chief scientific officer in 2011 and Dr. Reid. As a senior investigator, he would lead a group of about 100, and work with scientists, engineers and technicians in other groups. Without the need to apply regularly for federal grants, Dr. Reid could concentrate on one piece of the puzzle of how the brain works. He would try to decode the workings of one part of the mouse brain, the million neurons in the visual cortex, from, as he puts it, “molecules to behavior.” © 2014 The New York Times Company

Keyword: Vision
Link ID: 19291 - Posted: 02.25.2014

|By Beth Skwarecki Prions, the protein family notorious for causing "mad cow" and neurodegenerative diseases like Parkinson's, can play an important role in healthy cells. "Do you think God created prions just to kill?" mused Nobel laureate Eric Kandel. "These things must have evolved initially to have a physiological function." His work on memory helped reveal that animals make and use prions in their nervous systems as part of an essential function: stabilizing the synapses that constitute long-term memories. These natural prions aren't infectious but on a molecular level they chain up exactly the same way as their disease-causing brethren. (Some researchers call them "prionlike" to avoid confusion.) This week, work from neuroscientist Kausik Si of the Stowers Institute for Medical Research, one of Kandel's former students, shows that the prion's action is tightly controlled by the cell, and can be turned on when a new long-term memory needs to be formed. Prions are proteins with two unusual properties: First, they can switch between two possible shapes, one that is stable on its own and an alternate conformation that can form chains. Second, the chain-forming version has to be able to trigger others to change shape and join the chain. Say that in the normal version the protein is folded so that one portion of the protein structure—call it "tab A"—fits into its own "slot B." In the alternate form, though, tab A is available to fit into its neighbor's slot B. That means the neighbor can do the same thing to the next protein to come along, forming a chain or clump that can grow indefinitely. © 2014 Scientific American,

Keyword: Learning & Memory; Prions
Link ID: 19290 - Posted: 02.25.2014

By JoNel Aleccia The first of 18,000 University of California, Santa Barbara, students lined up for shots Monday as the school began offering an imported vaccine to halt an outbreak of dangerous meningitis that sickened four, including one young man who lost his feet. "My dad's a pediatrician and he's been sending me emails over and over to go get it," said Carly Chianese, 20, a junior from Bayville, N.Y., who showed up a half-hour before the UCSB clinic opened. It’s the second time in three months that government health officials have inoculated U.S. college students with an emergency vaccine, Bexsero, to protect against the B strain of meningitis. More than 5,400 students at Princeton University in New Jersey received the vaccine in December after an outbreak sickened eight there. Another 4,400 got booster shots last week. No new cases have been detected at UCSB since November, but health officials said the vaccine licensed in Europe, Australia and Canada but not in the U.S. would stop future spread of the infection. Current vaccines available in the U.S. protect against four strains of meningitis, but not the B strain. Bacterial meningitis is a serious infection that kills 1 in 10 affected and leaves 20 percent with severe disabilities. Shots will be offered at UCSB from Monday through March 7, with a second series planned for later this spring. “During the last couple of outbreaks on college campuses, there have been additional cases over a year or two years,” said Dr. Amanda Cohn, a medical epidemiologist with the Centers for Disease Control and Prevention. “There is certainly that possibility. We strongly recommend that students get vaccinated.”

Keyword: Miscellaneous
Link ID: 19289 - Posted: 02.25.2014

|By Jenni Laidman People born with Down syndrome have always been considered to be incurably developmentally delayed—until now. In the past few years a number of laboratories have uncovered critical drug targets within disabled chemical pathways in the brain that might be restored with medication. At least two clinical trials are currently studying the effects of such treatments on people with Down syndrome. Now geneticist Roger Reeves of Johns Hopkins University may have stumbled on another drug target—this one with the potential to correct the learning and memory deficits so central to the condition. Down syndrome occurs in about one in 1,000 births annually worldwide. It arises from an extra copy of chromosome 21 and the overexpression of each of the 300 to 500 genes the chromosome carries. “If you go back even as recently as 2004, researchers didn't have much of a clue about the mechanisms involved in this developmental disability,” says Michael Harpold, chief scientific officer with the Down Syndrome Research and Treatment Foundation. But all that has changed. “In the past six or seven years there have been several breakthroughs—and ‘breakthroughs’ is not by any means too big a word—in understanding the neurochemistry in Down syndrome,” Reeves says. This improved knowledge base has led to a series of discoveries with therapeutic promise, including the latest by Reeves. He and his team were attempting to restore the size of the cerebellum in mice engineered to show the hallmarks of Down syndrome. The cerebellum lies at the base of the brain and controls motor functions, motor learning and balance. In people with Down syndrome and in the Down mouse model the cerebellum is about 40 percent smaller than normal. By restoring its size, Reeves hoped to gain a clearer picture of the developmental processes that lead to anomalies in a brain with Down syndrome. © 2014 Scientific American

Keyword: Development of the Brain; Genes & Behavior
Link ID: 19288 - Posted: 02.25.2014

by Nathan Seppa Women who take acetaminophen during pregnancy are more likely to have a child with attention-deficit/hyperactivity disorder than are women who don’t, according to an analysis of nearly 41,000 pairs of mothers and children in a Danish birth registry. Researchers found that more than half of the women, who gave birth between 1996 and 2002, had used the pain reliever during pregnancy. Calls to the women when the children were 7 years old revealed that children whose moms used any acetaminophen during pregnancy were 37 percent more apt to be diagnosed with ADHD or a related disorder than children whose moms didn’t use the drug. If the women used it in all three trimesters, the apparent risk for offspring was 61 percent higher than for children whose mothers didn’t use the drug. Out of nearly 41,000 children, fewer than 1,000 were diagnosed with ADHD and related disorders. The data establish an association and not cause and effect. But the researchers note that acetaminophen, also sold as Tylenol or Panadol, can cross the placental barrier and may affect hormones in a fetus. Citations Z. Liew et al. Acetaminophen use during pregnancy, behavioral problems, and hyperkinetic disorders. JAMA Pediatrics. Online February 24, 2014. doi:10.1001/jamapediatrics.2013.4914. © Society for Science & the Public 2000 - 2013.

Keyword: ADHD; Development of the Brain
Link ID: 19287 - Posted: 02.25.2014

By Meeri Kim, How often, and how well, do you remember your dreams? Some people seem to be super-dreamers, able to recall effortlessly their dreams in vivid detail almost every day. Others struggle to remember even a vague fragment or two. A new study has discovered that heightened blood flow activity within certain regions of the brain could help explain the great dreamer divide. In general, dream recall is thought to require some amount of wakefulness during the night for the vision to be encoded in longer-term memory. But it is not known what causes some people to wake up more than others. A team of French researchers looked at brain activation maps of sleeping subjects and homed in on areas that could be responsible for nighttime wakefulness. When comparing two groups of dreamers on the opposite ends of the recall spectrum, the maps revealed that the temporoparietal junction — an area responsible for collecting and processing information from the external world — was more highly activated in high-recallers. The researchers speculate that this allows these people to sense environmental noises in the night and wake up momentarily — and, in the process, store dream memories for later recall. In support of this hypothesis, previous medical cases have found that when these same portions of the brain are damaged by stroke, patients lose the ability to remember their dreams, even though they can still achieve the REM (rapid eye movement) stage of sleep in which dreaming usually occurs. © 1996-2014 The Washington Post

Keyword: Sleep; Brain imaging
Link ID: 19286 - Posted: 02.24.2014

Sara Reardon Freddie Lee Hall loved to gamble, although he usually lost. Winning was better: then he gladly gave the money back to the friends he'd won it from, along with all the wages he earned picking fruit in rural Florida. His friends praised him for this. It made him feel good. And Hall needed to feel good — as court documents make abundantly clear. As a child growing up in the impoverished town of Webster, Florida, he had struggled to keep up with 16 brothers and sisters, who were much smarter than he was. If he failed to understand something, his mother beat him, once while he was tied up in a bag strung over a fire. He stuttered, never learned to read and feared the dark. He was unable to live alone. “Even though he was full grown, mentally he was a child,” his sister Diana told the court. “I had hoped to protect Freddie Lee from the outside world.” But the outside world found him. In 1978, Hall and his friend Mack Ruffin decided to rob a convenience store. They needed a car, so they forced 21-year-old Karol Hurst, who was pregnant, to drive into the woods, where they raped and killed her. Later, one of the pair also shot and killed a sheriff's deputy. When the two men were caught, tried and convicted of murder, the court decided that Hall was the likely ringleader. Ruffin was eventually sentenced to life in prison; Hall was sentenced to death. Next month, after 35 years of failed appeals to have that death sentence commuted to life imprisonment, Hall will have his case heard before the US Supreme Court. His guilt is not in question: the issue is Florida's use of IQ test scores in sentencing him to death. © 2014 Nature Publishing Group,

Keyword: Intelligence; Attention
Link ID: 19285 - Posted: 02.24.2014

By SABRINA TAVERNISE Dr. Michael Siegel, a hard-charging public health researcher at Boston University, argues that e-cigarettes could be the beginning of the end of smoking in America. He sees them as a disruptive innovation that could make cigarettes obsolete, like the computer did to the typewriter. But his former teacher and mentor, Stanton A. Glantz, a professor of medicine at the University of California, San Francisco, is convinced that e-cigarettes may erase the hard-won progress achieved over the last half-century in reducing smoking. He predicts that the modern gadgetry will be a glittering gateway to the deadly, old-fashioned habit for children, and that adult smokers will stay hooked longer now that they can get a nicotine fix at their desks. These experts represent the two camps now at war over the public health implications of e-cigarettes. The devices, intended to feed nicotine addiction without the toxic tar of conventional cigarettes, have divided a normally sedate public health community that had long been united in the fight against smoking and Big Tobacco. The essence of their disagreement comes down to a simple question: Will e-cigarettes cause more or fewer people to smoke? The answer matters. Cigarette smoking is still the single largest cause of preventable death in the United States, killing about 480,000 people a year. Dr. Siegel, whose graduate school manuscripts Dr. Glantz used to read, says e-cigarette pessimists are stuck on the idea that anything that looks like smoking is bad. “They are so blinded by this ideology that they are not able to see e-cigarettes objectively,” he said. Dr. Glantz disagrees. “E-cigarettes seem like a good idea,” he said, “but they aren’t.” © 2014 The New York Times Company

Keyword: Drug Abuse
Link ID: 19284 - Posted: 02.24.2014

By James Gallagher Health and science reporter, BBC News US doctors are warning of an emerging polio-like disease in California where up to 20 people have been infected. A meeting of the American Academy of Neurology heard that some patients had developed paralysis in all four limbs, which had not improved with treatment. The US is polio-free, but related viruses can also attack the nervous system leading to paralysis. Doctors say they do not expect an epidemic of the polio-like virus and that the infection remains rare. Polio is a dangerous and feared childhood infection. The virus rapidly invades the nervous system and causes paralysis in one in 200 cases. It can be fatal if it stops the lungs from working. There have been 20 suspected cases of the new infection, mostly in children, in the past 18 months, A detailed analysis of five cases showed enterovirus-68 - which is related to poliovirus - could be to blame. In those cases all the children had been vaccinated against polio. Symptoms have ranged from restricted movement in one limb to severe weakness in both legs and arms. Dr Emanuelle Waubant, a neurologist at the University of California, San Francisco, told the BBC: "There has been no obvious increase in the pace of new cases so we don't think we're about to experience an epidemic, that's the good news. BBC © 2014

Keyword: Movement Disorders
Link ID: 19283 - Posted: 02.24.2014

Brain cell regeneration has been discovered in a new location in human brains. The finding raises hopes that these cells could be used to help people recover after a stroke, or to treat other brain diseases. For years it was unclear whether or not we could generate new brain cells during our lifetime, as the process – neurogenesis – had only been seen in animals. Instead, it was thought that humans, with our large and complex brains, are born with all the required neurons. Then last year Jonas Frisén of the Karolinska Institute in Stockholm, Sweden, and his colleagues found that neurogenesis occurs in the hippocampi of the human brain. These structures are crucial for memory formation (Cell, DOI: 10.1016/j.cell.2013.05.002) Now they have found more new brain cells in a second location – golf-ball-sized structures called the striata. These seem to be involved in many different functions, including in learning and memory. These particular aspects, related as they are to the hippocampi, lead Frisén to speculate that these new brain cells may also be involved with learning. "New neurons may convey some sort of plasticity," he says, which might help people learn and adapt to new situations. To reveal the new brain cells, the team exploited the fact that there have been varying levels of a radioactive isotope of carbon – carbon-14 – in the atmosphere since nuclear bomb tests during the cold war. This means that the year of creation of many cells in the body can be found by measuring the ratio of carbon-14 to carbon-12 in its DNA. Analysis of 30 donated brains revealed which brain cells had been born during the lifetimes of the donors. © Copyright Reed Business Information Ltd.

Keyword: Neurogenesis
Link ID: 19282 - Posted: 02.22.2014

There is no biological cure for deafness—yet. We detect sound using sensory cells sporting microscopic hairlike projections, and when these so-called hair cells deep inside the inner ear are destroyed by illness or loud noise, they are gone forever. Or so scientists thought. A new study finds specific cells in the inner ear of newborn mice that regenerate these sensory cells—even after damage, potentially opening up a way to treat deafness in humans. Researchers knew that cells in the inner ear below hair cells—known as supporting cells—can become the sensory cells themselves when stimulated by a protein that blocks Notch signaling, which is an important mechanism for cell communication. Albert Edge, a stem cell biologist at Harvard Medical School in Boston, and his colleagues, attempted to identify the exact type of supporting cells that transform into sensory ones and fill in the gaps left by the damaged cells. The researchers removed the organ of Corti, which is housed within a seashell-shaped cavity called the cochlea and contains sensory hair cells, from newborn mice and kept the cells alive in culture plates. They damaged the hair cells using the antibiotic gentamicin, which destroys its sound-sensing projections. When they examined the organ of Corti under the microscope, they saw that small numbers of hair cells had regenerated on their own. But if they blocked Notch signaling, they saw even more regenerated hair cells, the team reports today in Stem Cell Reports. The number that developed varied, but in the base of cochlea, where the tissue received the most damage, hair cell numbers returned to about 40% of the original. “It’s interesting and encouraging that they are capable of regenerating,” Edge says. © 2014 American Association for the Advancement of Science.

Keyword: Hearing; Regeneration
Link ID: 19281 - Posted: 02.22.2014

By DEBORAH BLUM Toxicologists have long considered ethylene glycol, the active ingredient in many antifreeze and engine coolant formulas, to be a seductive and uniquely dangerous poison. For one thing, it’s sweet. “We actually had a mechanic who developed a taste for it,” recalled Dr. Marsha Ford, director of the Carolinas Poison Center in Charlotte, N.C. “He’d pour himself a little and sip it. And he kept doing that until he got sick.” And that’s the other danger: Ethylene glycol is a slow-acting poison. Even following a high dose, symptoms can take up to 48 hours to appear. The country’s poison control centers record more than 5,000 ethylene glycol ingestions annually; some 2,000 cases require medical treatment. Most are accidental, but ethylene glycol also figures in hundreds of suicide attempts every year — not to mention the occasional murder. Recently an Ohio woman was convicted of killing her fiancé by spiking raspberry iced tea with antifreeze. The situation for animals has been even more dangerous than for despised spouses. According to the Humane Society of the United States, as many as 90,000 pets and wild animals are poisoned annually by drinking spilled or carelessly stored products containing ethylene glycol. Now the manufacturers of those products have determined to do something about all the carnage. They are making antifreeze taste awful — so very bitter that it will be nigh impossible to drink by accident. © 2014 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Neurotoxins
Link ID: 19280 - Posted: 02.22.2014

If you ever feel like your emotions are getting the best of you, you may want to try dimming the lights. According to researchers at the University of Toronto Scarborough, bright light can make us more emotional — for better or for worse — making us experience both positive and negative feelings more intensely. The findings seem to contradict commonly held notions that people feel happier and more optimistic on bright, sunny days and gloomier on dark, cloudy days. In fact, the idea for the study was spurred by findings that suicide rates peak in the late spring and summer, when sunshine is most abundant. “I was very surprised by this,” study author Alison Jing Xu told CBC News. Xu is an assistant professor of management at UTSC and the Rotman School of Management. “Normally I would say if brighter days generally increase people’s affect, then suicide rates should peak in winter — but actually it does not,” she said. Xu, along with the study’s co-author Aparna Labroo of Northwestern University in the U.S., conducted six experiments to explore the relationship between light and emotion. Their paper is published in the Journal of Consumer Psychology. Participants in each case were divided into two groups: Some were placed in a brightly lit room where fluorescent ceiling lights were turned on, while others were placed in a dimly lit room where the only light came from computer monitors. © CBC 2014

Keyword: Emotions; Biological Rhythms
Link ID: 19279 - Posted: 02.22.2014

When you hear a friend’s voice, you immediately picture her, even if you can’t see her. And from the tone of her speech, you quickly gauge if she’s happy or sad. You can do all of this because your human brain has a “voice area.” Now, scientists using brain scanners and a crew of eager dogs have discovered that dog brains, too, have dedicated voice areas. The finding helps explain how canines can be so attuned to their owners’ feelings. “It’s absolutely brilliant, groundbreaking research,” says Pascal Belin, a neuroscientist at the University of Glasgow in the United Kingdom, who was part of the team that identified the voice areas in the human brain in 2000. “They’ve made the first comparative study using nonhuman primates of the cerebral processing of voices, and they’ve done it with a noninvasive technique by training dogs to lie in a scanner.” The scientists behind the discovery had previously shown that humans can readily distinguish between dogs’ happy and sad barks. “Dogs and humans share a similar social environment,” says Attila Andics, a neuroscientist in a research group at the Hungarian Academy of Sciences at Eötvös Loránd University in Budapest and the lead author of the new study. “So we wondered if dogs also get some social information from human voices.” To find out, Andics and his colleagues decided to scan the canine brain to see how it processes different types of sounds, including voices, barks, and natural noises. In humans, the voice area is activated when we hear others speak, helping us recognize a speaker’s identity and pick up on the emotional content in her voice. If dogs had voice areas, it could mean that these abilities aren’t limited to humans and other primates. © 2014 American Association for the Advancement of Science

Keyword: Emotions; Hearing
Link ID: 19278 - Posted: 02.22.2014

National Institutes of Health researchers have identified gene variants that cause a rare syndrome of sporadic fevers, skin rashes and recurring strokes, beginning early in childhood. The team’s discovery coincides with findings by an Israeli research group that identified an overlapping set of variants of the same gene in patients with a similar type of blood vessel inflammation. The NIH group first encountered a patient with the syndrome approximately 10 years ago. The patient, then 3 years old, experienced fevers, skin rash and strokes that left her severely disabled. Because there was no history of a similar illness in the family, the NIH group did not at first suspect a genetic cause, and treated the patient with immunosuppressive medication. However, when the NIH team evaluated a second patient with similar symptoms two years ago — a child who had experienced recurrent fevers and six strokes by her sixth birthday — they began to suspect a common genetic cause and embarked on a medical odyssey that has led not only to a diagnosis, but to fundamental new insights into blood vessel disease. In their study, which appears in the Feb. 19, 2014, advance online edition of the New England Journal of Medicine, the researchers describe how next-generation genome sequencing, only recently available, facilitated a molecular diagnosis for patients in their study. The researchers found that harmful variants in the CECR1 gene impede production of a protein vital to the integrity of healthy blood vessel walls. The researchers showed that faulty variants in their patients’ DNA that encode the CECR1 gene cause a loss of function of the gene’s ability to produce of an enzyme called adenosine deaminase 2 (ADA2). Without it, abnormalities and inflammation in blood vessel walls result. The researchers call the new syndrome, deficiency of ADA2, or DADA2.

Keyword: Stroke; Development of the Brain
Link ID: 19277 - Posted: 02.22.2014

By ANAHAD O'CONNOR Many people occasionally wake up in the middle of the night and find themselves unable to get back to sleep. But if it happens often, and you are consistently tired and not functioning well during the day, that is indicative of a problem, said Dr. Meir H. Kryger, a professor at Yale School of Medicine and the author of “The iGuide to Sleep.” Stressful events, a loud pet or a snoring bedmate may be to blame, or the problem could be a medical issue such as a cough, sleep apnea or getting up to urinate — which could be a sign of diabetes. Dr. Kryger said he has had patients who are stirred awake by the sensation of their heart beating rapidly because of a cardiac rhythm problem. Worrying about being awake only makes the problem worse. “We see that in patients who’ve had insomnia for a while,” Dr. Kryger said. “They wake up and become so angry, frustrated and aroused that they can’t fall asleep.” In some cases better habits can help. Nicotine or alcohol levels fall during sleep and can cause people to awaken, so quitting smoking or avoiding alcoholic beverages, especially before bedtime, can help. Steer clear of heavy or spicy meals before trying to sleep if heartburn or acid reflux is keeping you up. You may be tempted to nap during the day to compensate for lost sleep time, but this can just prolong the problem, Dr. Kryger said. Avoid taking naps that are longer than 20 minutes, particularly in the evening. If you wake up at night and find that you still cannot get back to asleep after 20 minutes, do not lie there in anguish staring at your clock. Get out of bed and do something that distracts and relaxes you, like reading a book. Then return to bed when you feel sleepy. © 2014 The New York Times Company

Keyword: Sleep
Link ID: 19276 - Posted: 02.22.2014

Adrienne LaFrance For the better part of the past decade, Mark Kirby has been pouring drinks and booking gigs at the 55 Bar in New York City's Greenwich Village. The cozy dive bar is a neighborhood staple for live jazz that opened on the eve of Prohibition in 1919. It was the year Congress agreed to give American women the right to vote, and jazz was still in its infancy. Nearly a century later, the den-like bar is an anchor to the past in a city that's always changing. For Kirby, every night of work offers the chance to hear some of the liveliest jazz improvisation in Manhattan, an experience that's a bit like overhearing a great conversation. "There is overlapping, letting the other person say their piece, then you respond," Kirby told me. "Threads are picked up then dropped. There can be an overall mood and going off on tangents." Brain areas linked to meaning shut down during improvisational jazz interactions. In other words, this music is syntactic, not semantic. The idea that jazz can be a kind of conversation has long been an area of interest for Charles Limb, an otolaryngological surgeon at Johns Hopkins. So Limb, a musician himself, decided to map what was happening in the brains of musicians as they played. He and a team of researchers conducted a study that involved putting a musician in a functional MRI machine with a keyboard, and having him play a memorized piece of music and then a made-up piece of music as part of an improvisation with another musician in a control room. What researchers found: The brains of jazz musicians who are engaged with other musicians in spontaneous improvisation show robust activation in the same brain areas traditionally associated with spoken language and syntax. In other words, improvisational jazz conversations "take root in the brain as a language," Limb said. © 2014 by The Atlantic Monthly Group

Keyword: Hearing; Language
Link ID: 19275 - Posted: 02.20.2014

By Sandhya Somashekhar, The Food and Drug Administration has approved 24 drugs for the treatment of male sexual dysfunction. For women, that number is zero. The disparity reflects drugmakers’ difficulties in unlocking the secret to revving up women’s sex drive. It also has become a rallying point for women’s advocates and even some members of Congress, who suggest that federal regulators seem more eager to approve sex-enhancing drugs for men than for women. It isn’t every day that political leaders and groups such as the National Organization for Women get involved in the drug- approval process, particularly for “lifestyle” drugs. But the unsuccessful quest for a “female Viagra” is sparking complicated questions about a woman’s right to a pill that may improve her sex life — and about how much of a libido lift is enough to be judged effective by the FDA. A drug called flibanserin, touted by some as the “little pink pill,” the counterpoint to Viagra’s little blue pill, was developed 12 years ago. Last month, women’s groups were disappointed when the FDA asked for further safety tests on the medication. Some critics say the agency — consciously or not — may be succumbing to society’s squeam­ishness about women’s sexual desires compared with those of men. “It looks to me like there are more hurdles being put in front of this drug than there have been on drugs addressing male dysfunction,” said Terry O’Neill, president of NOW. “Obviously, everyone only wants drugs to get on the market if they are proven safe and effective. But we don’t want attitudes to get in the way of a good drug.” © 1996-2014 The Washington Post

Keyword: Sexual Behavior
Link ID: 19274 - Posted: 02.20.2014

by Colin Barras If it's beyond repair, you find something else to do its job. This could soon apply to rods and cones, the light-sensitive cells in our eyes that can wither with age, causing blindness. A drug has been found that coaxes neighbours of ailing cells to do their work for them. In 2012, Richard Kramer at the University of California, Berkeley, discovered that injecting a certain chemical into the eyes of blind mice made normally light-insensitive ganglion cells respond to light. These cells ferry optical signals from the rods and cones to the brain, so the mice regained some ability to see light. But it only worked with ultraviolet light. Now, Kramer's team has found a different drug that does the same with visible light. Just 6 hours after they were injected, blind mice could learn to respond to light in the same way as sighted mice – although Kramer says he doesn't know whether they regained vision or just light sensitivity. When the researchers studied the drug's impact on retinal cells in more detail, they realised it had had no effect on healthy cells. "That's what's particularly remarkable and hopeful about this," says Kramer. "It's possible that if you put this drug in a partially damaged eye it would restore vision to the damaged regions and leave the healthy areas unaffected – although we haven't done the experiments to test that." Gene therapy and stem cell treatments are also being explored as ways to restore sight, but a drug would be simpler and any side effects should be reversible, says Kramer. © Copyright Reed Business Information Ltd

Keyword: Vision
Link ID: 19273 - Posted: 02.20.2014

James Hamblin Brain training is becoming big business. Everywhere you look, someone is talking about neuroplasticity and trying to train your brain. Soon there will be no wild brains left. At the same time, everyone who spends more than two continuous hours using a computer is, according to the American Optometric Association, ruining their eyes with Computer Vision Syndrome. So, Dr. Aaron Seitz might be onto something with his new brain-training program that promises better vision. UltimEyes is a game-based app that's sold as "fun and rewarding" as it improves your vision and "reverse[s] the effects of aging eyes." It doesn't claim to work on the eyes themselves, but on the brain cortex that processes vision—the part that takes blurry puzzle pieces from the eyes and arranges them into a sweet puzzle. (Brain training for memory, the kind we hear about the most on TV, would be the part that lacquers the finished puzzle, frames it, and hangs it on the wall.) A standard 25-minute session using UltimEyes forces your eyes to work in ways they probably don't in everyday life, and its website warns that after the first use, "just like the first time that you go to the gym, your eyes may feel a bit tired. This experience typically goes away by your third session as your visual system adjusts to its new work-out routine." Seitz is a neuroscientist at the University of California, Riverside. To test out his vision-training game, he had players on the university's baseball team use the app. Half the team trained for 30 sessions. For comparison, the other half did no training. © 2014 by The Atlantic Monthly Group

Keyword: Vision; Learning & Memory
Link ID: 19272 - Posted: 02.20.2014