Chapter 16. None

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By STEPH YIN For animals that hibernate, making it to spring is no small feat. Torpor — the state of reduced bodily activity that occurs during hibernation — is not restful. By the time they emerge, hibernating animals are often sleep-deprived: Most expend huge bursts of energy to arouse themselves occasionally in the winter so their body temperatures don’t dip too low. This back-and-forth is exhausting, and hibernators do it with little to no food and water. By winter’s end, some have shed more than half their body weight. But just because it’s spring doesn’t mean it’s time to celebrate. Spring means getting ready for the full speed of summer — and after spending a season in slow motion, that requires some ramping up. Here’s a look at what different animals have on the agenda after coming out of winter’s slumber. Black bears emerge from their dens in April, but stay lethargic for weeks. During this so-called walking hibernation, they sleep plenty and don’t roam very far. Though they have lost up to one-third of their body weight over winter, they don’t have a huge appetite right away — their metabolism is not yet back to normal. They snack mostly on pussy willows and bunches of snow fleas. In January or February, some females give birth, typically to two or three cubs. New mothers continue to hibernate, but they go in and out of torpor, staying alert enough to respond to their cubs’ cries. When they emerge from their dens, mama bears find trees with rough bark that her cubs can easily climb for safety. “Slowly, the bears’ metabolism gears up to normal, active levels,” said Lynn Rogers, a bear expert and principal biologist at the Wildlife Research Institute, a nonprofit in Minnesota. “When plants start sprouting on the forest floor, that’s when they start really moving around.” © 2017 The New York Times Company

Keyword: Biological Rhythms
Link ID: 23406 - Posted: 03.25.2017

By Diana Kwon Astrocytes, star-shape glial cells in the brain, were once simply considered support cells for neurons. However, neuroscientists have recently realized they have many other functions: studies have shown that astrocytes are involved in metabolism, learning, and more. In the latest study to investigate astrocytes’ roles in the brain, researchers confirmed these cells played a key role in regulating mouse circadian rhythms. The team’s results were published today (March 23) in Current Biology. “Recent results have indicated that [glia] are actively modulating synaptic transmission, the development of the nervous system, and changes in the nervous system in response to changes in the environment,” said coauthor Erik Herzog, a neuroscientist at Washington University in St. Louis. “So circadian biologists recognized that the system that we study in the brain also had astrocytes and have wondered what role that they might play.” In 2005, Herzog’s team published a seminal study linking glia to mammalian circadian rhythms. By investigating rat and mouse astrocytes in a dish, the researchers discovered that these glial cells showed circadian rhythms in gene expression. Since then, several independent groups have reported evidence to suggest that astrocytes help regulate daily rhythms. However, linking astrocytes to circadian behaviors in mice remained difficult. “I had several folks in the lab over many years [who] were unable to find the tools that would allow us to answer the question definitively: Do astrocytes play a role in scheduling our day?” Herzog recalled. “Then, within the last year or so, some new tools . . . became available for us.”. © 1986-2017 The Scientist

Keyword: Biological Rhythms; Glia
Link ID: 23405 - Posted: 03.25.2017

USA Today Network Josh Hafner , For college students, new parents and employees dogged by deadlines, the all-nighter is nothing new. But going without sleep leaves you basically drunk, putting you at the equivalent of a .1% blood alcohol content as you drive to work, make decisions and interact with others. “The first thing that goes is your ability to think," said Joseph Ojile, M.D., a board member with the National Sleep Foundation. Judgement, memory and concentration all suffer impairment by the body's 17th hour without sleep, he said. “We know at 17 hours, you're at .08% blood alcohol level," he said, the legal standard for drunk driving. "At 24 hours, you’re at 0.1%." Coordination deteriorates as well in those intervening hours, said Ojile, a professor at Saint Louis University School of Medicine. Irritability sets in, too. Pain becomes more acute and the immune system suffers, he said, leaving the body more open to infection. "Here’s the worst part about the lack of judgement," Ojile said. "The person is unaware of their impairment. How scary is that? ‘I’m fine, I’ll just drive home. I’ll do my work at the nuclear plant, no problem. Or fly the plane, no problem.’" It's not entirely clear how the effects worsen past 24 hours, Ojile said, other than they do. The brain starts shutting down in trance-like microsleeps, 15- to 30-second spells that occur without the person noticing. Eventually, not sleeping results in death.

Keyword: Sleep
Link ID: 23404 - Posted: 03.25.2017

By Linda Searing The precise cause, or causes, of dementias such as Alzheimer’s disease remain unclear, but one theory points to molecules called free radicals that can damage nerve cells. This damage, called oxidative stress, may lead to changes in the brain over time that result in dementia. Might antioxidant supplements prevent this? The study involved 7,540 men 60 and older (average age, 67) with no indications of dementia and no history of serious head injury, substance abuse or neurological conditions that affect cognition. They were randomly assigned to take vitamin E (an antioxidant, 400 International Units daily), selenium (also an antioxidant, 200 micrograms daily), both vitamin E and selenium or a placebo. The men also had their memory assessed periodically. In just over five years, 325 of the men (about 4 percent) developed dementia, with essentially no difference in the rate of occurrence between those who took one or both supplements and those who took the placebo. The researchers concluded that the antioxidant supplements “did not forestall dementia and are not recommended as preventive agents.” Who may be affected? Older men. The risk for dementia increases with advanced age and is most common among the very elderly. Memory loss is the most well-known symptom, but people with dementia may also have problems thinking, speaking, controlling emotions and doing daily activities such as getting dressed and eating. Alzheimer’s disease is the most common type of dementia, affecting more than 5.5 million Americans, including more than 10 percent of those 65 and older and more women than men. Caveats Participants took the supplements for a relatively short time. Whether the findings would apply to women was not tested. The study did not prove that the dementia developed by the study participants was caused by oxidative stress. © 1996-2017 The Washington Post

Keyword: Alzheimers
Link ID: 23403 - Posted: 03.25.2017

If your parrot is feeling glum, it might be tweetable. Wild keas spontaneously burst into playful behaviour when exposed to the parrot equivalent of canned laughter – the first birds known to respond to laughter-like sounds. The parrots soared after one another in aerobatic loops, exchanged foot-kicking high fives in mid-air and tossed objects to each other, in what seems to be emotionally contagious behaviour. And when the recording stops, so does the party, and the birds go back to whatever they had been doing. We already knew that these half-metre-tall parrots engage in playful behaviour, especially when young. What’s new is that a special warbling call they make has been shown to trigger behaviour that seems to be an equivalent of spontaneous, contagious laughter in humans. Moreover, it’s not just the young ones that respond, adults of both sexes join in the fun too. Raoul Schwing of the University of Veterinary Medicine in Vienna, Austria, and his team played 5-minute recordings to gatherings of between two and a dozen wild keas on a mountainside of New Zealand’s Arthur’s Pass National Park, on the southern island. The group played recordings of the warble sound, or other sounds, including two other frequent kea sounds – a screech and a whistle – plus the alarm call of a local robin species and a bland tone. © Copyright Reed Business Information Lt

Keyword: Emotions; Evolution
Link ID: 23400 - Posted: 03.24.2017

By DENISE GRADY Dr. Lewis P. Rowland, a neurologist who made fundamental discoveries in nerve and muscle diseases and clashed with government investigators during the McCarthy era, died on March 16 in Manhattan. He was 91. The cause was a stroke, his son Steven said. Dr. Rowland, the chairman of Columbia University’s neurology department for 25 years, died at NewYork-Presbyterian/Columbia University Medical Center. Dr. Rowland was a prolific researcher and writer, with nearly 500 published scientific articles that focused on devastating neuromuscular diseases, including muscular dystrophy, myasthenia gravis and many rare syndromes. He took a special interest in amyotrophic lateral sclerosis, or A.L.S., also called Lou Gehrig’s disease, which causes degeneration of nerves in the brain and spinal cord, leading to weakness, paralysis and death. Dr. Rowland led research teams that delineated a number of uncommon diseases that had been poorly understood. They also found that in a subgroup of A.L.S. patients, the disease was linked to lymphoma, a cancer of the immune system. Other studies led to the discovery that a gene defect causes an unusual form of dementia in some patients with A.L.S. In myasthenia gravis, Dr. Rowland and his colleagues documented its high death rate and helped identify treatments that prolonged survival. In the 1970s, long before the tools existed to study DNA’s role in neurological diseases like A.L.S., Alzheimer’s and Parkinson’s, Dr. Rowland predicted correctly that genetics would be the key to understanding them. One of his accomplishments at Columbia was the expansion in 1982 of an intensive care unit that added beds for patients who were severely ill with neurological disorders. Before then, it was often difficult to find I.C.U. space for them. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Muscles
Link ID: 23399 - Posted: 03.24.2017

A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017

By Jia Naqvi A drug frequently prescribed for pain is no more effective than a placebo at controlling sciatica, a common source of pain in the lower back and leg, according to a study published Wednesday in the New England Journal of Medicine. The researchers at the George Institute for Global Health in Australia followed 209 sciatica patients in Sydney who were randomly assigned to receive either the drug pregabalin, more commonly known as Lyrica, or a placebo. The results showed no significant differences in leg pain intensity between the group on the placebo and that on Lyrica after eight weeks taking the drug or during the rest of the year on follow-up exams. Similarly, there were no differences for other outcomes such as back pain, quality of life and degree of disability. After Lyrica was approved in 2004, it has become the most commonly prescribed medicine for neuropathic pain, which is caused by damage to the nervous system. The drug was ranked as the 19th-highest-earning pharmaceutical in 2015, with worldwide sales rising annually at a rate of 9 percent and sale revenue of more than $3 billion in 2015 in the United States. “We have seen a huge rise in the amount of prescriptions being written each year for patients suffering from sciatica. It’s an incredibly painful and disabling condition, so it’s no wonder people are desperate for relief and medicines such as pregabalin have been widely prescribed,” Christine Lin, one of the authors of the study and an associate professor at the George Institute for Global Health, said in a news release. © 1996-2017 The Washington Post

Keyword: Pain & Touch
Link ID: 23395 - Posted: 03.23.2017

By Sam Wong It takes brains to choose a good partner. In one of the first experiments to look at the cognitive demands of choosing a mate, female guppies with big brains showed a preference for more colourful males, while those with smaller brains showed no preference. In guppies, like most animals, females are choosy about who to mate with, since they invest more in their offspring than males, which don’t help care for them. They tend to prefer males with striking colour patterns and big tails, traits that have been linked to good foraging ability and health. By choosing a male with these qualities, female guppies give their offspring a good chance of inheriting the same useful traits. Despite this, females often go on to make different choices. Alberto Corral López and colleagues at Stockholm University wanted to find out if brain size could account for this. Corral López and his team tested 36 females bred to have large brains, 36 bred to have small brains, and 16 females similar to guppies found in the wild. Previous studies have shown that large-brained guppies perform better in cognitive tests, suggesting that they are smarter. Each female was given the opportunity to associate with two males, one more colourful than the other. Females are known to spend more time close to males they would prefer to mate with, so the team timed how long they spent with each male. © Copyright Reed Business Information Ltd

Keyword: Sexual Behavior; Evolution
Link ID: 23394 - Posted: 03.23.2017

By Mo Costandi This map of London shows how many other streets are connected to each street, with blue representing simple streets with few connecting streets and red representing complex streets with many connecting streets. Credit: Joao Pinelo Silva The brain contains a built-in GPS that relies on memories of past navigation experiences to simulate future ones. But how does it represent new environments in order to determine how to navigate them successfully? And what happens in the brain when we enter a new space, or use satellite navigation (SatNav) technology to help us find our way around? Research published Tuesday in Nature Communications reveals two distinct brain regions that cooperate to simulate the topology of one’s environment and plan future paths through it when one is actively navigating. In addition, the research suggests both regions become inactive when people follow SatNav instructions instead of using their spatial memories. In a previous study researchers at University College London took participants on a guided tour through the streets of London’s Soho district and then used functional magnetic resonance imaging (fMRI) to scan their brains as they watched 10 different simulations of navigating those streets. Some of the movies required them to decide at intersections which way would be the shortest path to a predetermined destination; others came with instructions about which way to go at each junction. © 2017 Scientific American,

Keyword: Learning & Memory
Link ID: 23391 - Posted: 03.22.2017

Hannah Devlin Scientists have developed a new genetic test for Alzheimer’s risk that can be used to predict the age at which a person will develop the disease. A high score on the test, which is based on 31 genetic markers, can translate to being diagnosed many years earlier than those with a low-risk genetic profile, the study found. Those ranked in the top 10% in terms of risk were more than three times as likely to develop Alzheimer’s during the course of the study, and did so more than a decade before those who ranked in the lowest 10%. Strobe lighting provides a flicker of hope in the fight against Alzheimer’s Read more Rahul Desikan, of the University of California – who led the international effort, said the test could be used to calculate any individual’s risk of developing Alzheimer’s that year. “That is, if you don’t already have dementia, what is your yearly risk for AD onset, based on your age and genetic information,” he said. The so-called polygenic hazard score test was developed using genetic data from more than 70,000 individuals, including patients with Alzheimer’s disease and healthy elderly people. It is already known that genetics plays a powerful role in Alzheimer’s. Around a quarter of patients have a strong family history of the disease, and scientists have shown this is partly explained by a gene called ApoE, which comes in three versions, and is known to have a powerful influence on the risk of getting the most common late-onset type of Alzheimer’s. One version of ApoE appears to reduce risk by up to 40%, while those with two copies (one from each parent) of the high-risk version can increase risk by 12 times.

Keyword: Alzheimers
Link ID: 23390 - Posted: 03.22.2017

By KIM SEVERSON SONOMA, Calif. — The first thing Paula Wolfert wants to make a guest is coffee blended with butter from grass-fed cows and something called brain octane oil. She waves a greasy plastic bottle of the oil around her jumble of a kitchen like a preacher who has taken up a serpent. Never mind that this is the woman who introduced tagines, Aleppo pepper and cassoulet to American kitchens, wrote nine cookbooks and once possessed a palate the food writer Ruth Reichl declared the best she’d ever encountered. Ms. Wolfert, 78, has dementia. She can’t cook much, even if she wanted to. Which, by the way, she doesn’t. She learned she probably had Alzheimer’s disease in 2013, but she suspected something wasn’t right long before. Words on a page sometimes made no sense. Complex questions started to baffle her. Since she has always been an audacious and kinetic conversationalist with a touch of hypochondria, friends didn’t notice anything was wrong. Doctors spoke of “senior moments.” But she knew. One day, Ms. Wolfert went to make an omelet for her husband, the crime novelist William Bayer. She had to ask him how. The woman who once marched up to the French chef Jean-Louis Palladin and told him a dish didn’t have enough salt can no longer taste the difference between a walnut and a pecan, or smell whether the mushrooms are burning. The list of eight languages she once understood has been reduced to English. Maybe 40 percent of the words she knew have evaporated. “What am I going to do, cry about it?” Ms. Wolfert said in an interview at her home this month, the slap of her Brooklyn accent still sharp. After all, she points out, her first husband left her in Morocco with two small children and $2,000: “I cried for 20 minutes and I thought, ‘This isn’t going to do any good.’” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 23389 - Posted: 03.22.2017

By NICHOLAS BAKALAR Some research has suggested that vitamin E and selenium supplements might lower the risk for Alzheimer’s disease, but a new long-term trial has found no evidence that they will. The study began as a randomized clinical trial in 2002 testing the supplements for the prevention of prostate cancer. When that study was stopped in 2009 because no effect was found, 3,786 of the original 7,540 men participated in a continuing study to test the antioxidants as a preventive for Alzheimer’s. The study, in JAMA Neurology, randomly assigned the men, whose average age was 67 at the start, to take either vitamin E, selenium, both supplements, or a placebo. By 2015, 4.4 percent of the men had dementia, but there was no difference between the groups. Neither selenium, vitamin E, nor both in combination were any more effective than a placebo. The study controlled for age, family history of Alzheimer’s disease, education, race, diabetes and other factors. The lead author, Richard J. Kryscio, a professor of statistics at the University of Kentucky, said that it is possible that different dosages or different types of selenium or vitamin E might show an effect. “We could have picked the wrong version or the wrong dose,” he said. “But there’s really no evidence that these supplements will make a difference down the road in preventing dementia.” © 2017 The New York Times Company

Keyword: Alzheimers
Link ID: 23388 - Posted: 03.22.2017

by Helen Thompson Aside from being adorable, sea otters and Indo-Pacific bottlenose dolphins share an ecological feat: Both species use tools. Otters crack open snails with rocks, and dolphins carry cone-shaped sponges to protect their snouts while scavenging for rock dwelling fish. Researchers have linked tool use in dolphins to a set of differences in mitochondrial DNA — which passes from mother to offspring — suggesting that tool-use behavior may be inherited. Biologist Katherine Ralls of the Smithsonian Institution in Washington, D.C., and her colleagues looked for a similar pattern in otters off the California coast. The team tracked diet (primarily abalone, crab, mussels, clams, urchins or snails) and tool use in the wild and analyzed DNA from 197 individual otters. Otters that ate lots of hard-shelled snails — and used tools most frequently — rarely shared a common pattern in mitochondrial DNA, nor were they more closely related to other tool-users than any other otter in the population. Unlike dolphins, sea otters may all be predisposed to using tools because their ancestors probably lived off mollusks, which required cracking open. However, modern otters only take up tools when their diet requires them, the researchers report March 21 in Biology Letters. |© Society for Science & the Public 2000 - 2017.

Keyword: Evolution
Link ID: 23386 - Posted: 03.22.2017

As the father of two sons with schizophrenia, author Ron Powers is familiar with the pain and frustration of dealing with a chronic, incurable disease of the brain. Powers' younger son, Kevin, was a talented musician whose struggles with schizophrenia began at age 17. Just before his 21st birthday, in 2005, Kevin took his own life. A few years later, Powers' older son, Dean, started experiencing symptoms of schizophrenia and had a psychotic break. "There is no greater ... feeling of helplessness than to watch two beloved sons deteriorate before [your] eyes, not knowing what to do to bring them back," Powers tells Fresh Air's Terry Gross. Powers' new book, No One Cares About Crazy People, is both a memoir about his sons and a history of how the mentally ill have been treated medically, legally and socially. Although Dean is now medicated and doing well, Powers notes that many people with schizophrenia don't receive the treatment they need — in part because they often don't believe they are ill. "This unwillingness to believe that one is afflicted has led to tremendous problems," Powers says. "To force that person into being helped is a violation of his or her civil rights ... and the law may penalize the care workers who give [people with schizophrenia] medications or admit them to a hospital against their will. ... That is the great reigning Catch-22 of the way our society deals — or fails to deal — with schizophrenia." © 2017 npr

Keyword: Schizophrenia
Link ID: 23383 - Posted: 03.21.2017

By Chris Baraniuk It’s sometimes practically impossible to tell similar colours apart. Even side by side, they look the same. A special pair of spectacles gives us new power to see more distinct colours, and could one day help to spot counterfeit banknotes or counteract camouflage. The glasses, devised by a team at the University of Wisconsin-Madison, basically enhance the user’s colour vision, allowing them to see metamers – colours that look the same but give off different wavelengths of light – as recognisably distinct hues. Human colour vision relies on three types of cone cells that react to short (blue), medium (green) and long (red) wavelengths. While brushing up on his knowledge of the eye before teaching a photonics class, physicist Mikhail Kats had a brainwave. Could the eye be tricked into effectively having another type of cone cell? In theory, this could take our vision from being trichromatic, which uses three colour channels, to tetrachromatic. Some animals see in four (or more) channels. Goldfish, for example, have cells for red, blue, green and ultraviolet light. Some researchers suggest that a very small number of humans may be tetrachromats too. Read more: Human eye proteins detect red beyond red To make their glasses, Kats and his colleagues designed two colour filters, one for each eye that strip out specific parts of the blue light spectrum. With each eye receiving slightly different spectral information about blue things, the team hypothesised that any subtle differences in colour would be more pronounced. And they were right. © Copyright Reed Business Information Ltd

Keyword: Vision
Link ID: 23381 - Posted: 03.21.2017

Cris Ledón-Rettig Picture a lion: The male has a luxuriant mane, the female doesn’t. This is a classic example of what biologists call sexual dimorphism – the two sexes of the same species exhibit differences in form or behavior. Male and female lions pretty much share the same genetic information, but look quite different. We’re used to thinking of genes as responsible for the traits an organism develops. But different forms of a trait – mane or no mane – can arise from practically identical genetic information. Further, traits are not all equally sexually dimorphic. While the tails of peacocks and peahens are extremely different, their feet, for example, are pretty much the same. Understanding how this variation of form – what geneticists call phenotypic variation – arises is crucial to answering several scientific questions, including how novel traits appear during evolution and how complex diseases emerge during a lifetime. So researchers have taken a closer look at the genome, looking for the genes responsible for differences between sexes and between traits within one sex. The key to these sexually dimorphic traits appears to be a kind of protein called a transcription factor, whose job it is to turn genes “on” and “off.” In our own work with dung beetles, my colleagues and I are untangling how these transcription factors actually lead to the different traits we see in males and females. A lot of it has to do with something called “alternative gene splicing” – a phenomenon that allows a single gene to encode for different proteins, depending on how the building blocks are joined together. © 2010–2017, The Conversation US, Inc.

Keyword: Sexual Behavior; Evolution
Link ID: 23380 - Posted: 03.21.2017

Sara Reardon, Jeff Tollefson, Alexandra Witze & Erin Ross Funding for the National Oceanic and Atmospheric Administration’s weather satellites, which track hurricanes, would be maintained under the Trump plan. When it comes to science, there are few winners in US President Donald Trump’s first budget proposal. The plan, released on 16 March, calls for double-digit cuts for the Environmental Protection Agency (EPA) and the National Institutes of Health (NIH). It also lays the foundation for a broad shift in the United States’ research priorities, including a retreat from environmental and climate programmes. Rumours of the White House proposal have swirled for weeks, alarming many researchers who depend on government funding — and science advocates who worry that the Trump administration’s stance will jeopardize US leadership in fields ranging from climate science to cancer biology. It is not clear, however, how much of the plan will survive negotiations in Congress over the coming months. What could Trump’s budget for science mean for you? “Cutting [research and development] funding from our budget is the same as cutting the engines off an airplane that’s too heavy for take-off,” says Jason Rao, director of international affairs at the American Society for Microbiology in Washington DC. The greatest threats to the United States, he says, are those presented by infectious diseases, climate change and energy production — none of which can be addressed effectively without scientific research. © 2017 Macmillan Publishers Limited,

Keyword: Miscellaneous
Link ID: 23376 - Posted: 03.20.2017

Obese people who get surgery to lose weight have half the risk of developing heart failure as do patients who make lifestyle changes to shed excess pounds, a recent study suggests. “We were surprised by the large difference in heart failure incidence between the two groups,” said lead study author Johan Sundstrom of Uppsala University in Sweden. It’s possible that gastric bypass patients had a lower risk of heart failure because they lost more weight than the group trying to do so without surgery. Researchers also found that losing 22 pounds by any means was tied to a 23 percent drop in heart failure risk. The study team examined data on 25,805 obese people who had gastric bypass surgery, which reduces the stomach to a small pouch, and 13,701 patients who were put on low-calorie diets. After following half of the patients for at least four years, people who had gastric bypass were found to be 46 percent less likely to have developed heart failure. After one year, surgery patients had an average weight loss 41.4 pounds greater than that of those who relied on diet and exercise, the study found. After two years, surgery was associated with an average weight loss that was 49.8 pounds more than those who undertook lifestyle changes. Some previous research has linked obesity to heart failure, and a growing body of evidence suggests that obesity might directly cause the heart condition, Sundstrom said. While the new study wasn’t designed to prove a causal relationship, it adds more evidence in support of this possibility. © 1996-2017 The Washington Post

Keyword: Obesity
Link ID: 23372 - Posted: 03.19.2017

By Anna Azvolinsky Delivering a CRISPR/Cas9–based therapy directly to the eye via a viral vector can prevent retinal degeneration in a mouse model of retinitis pigmentosa, a team led by researchers at the National Eye Institute reported in Nature Communications today (March 14). Retinitis pigmentosa, which affects around one in 4,000 people, causes retinal degeneration that eventually leads to blindness. The inherited disorder has been mapped to more than 60 genes (and more than 3,000 mutations), presenting a challenge for researchers working toward a gene therapy. The results of this latest study suggest that a broader, gene-editing–based therapeutic approach could be used to target many of the genetic defects underlying retinitis pigmentosa. “Given the lack of effective therapies for retinal degeneration, particularly the lack of therapies applicable to a broad range of different genetic varieties of this disease, this study represents a very exciting and important advance in our field,” Joseph Corbo, a neuropathologist at the Washington University School of Medicine in St. Louis who was not involved in the work, wrote in an email to The Scientist. This combination of “CRISPR technology with an adeno-associated virus vector, a system tried and true for delivering genetic information to the retina, may represent the first step in a global treatment approach for rod-mediated degenerative disease,” Shannon Boye, whose University of Florida lab develops gene replacement strategies for eye disorders, wrote in an email to The Scientist. © 1986-2017 The Scientist

Keyword: Vision
Link ID: 23364 - Posted: 03.16.2017