Chapter 16. None
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Laura Sanders In growing brains, billions of nerve cells must make trillions of precise connections. As they snake through the brain, nerve cell tendrils called axons use the brain’s stiffness to guide them on their challenging journey, a study of frog nerve cells suggests. The results, described online September 19 in Nature Neuroscience, show that along with chemical guidance signals, the brain’s physical properties help shape its connections. That insight may be key to understanding how nerve cells wire the brain, says study coauthor Kristian Franze. “I strongly believe that it’s not enough to look at chemistry,” says Franze, a mechanobiologist at the University of Cambridge. “We need to look at environmental factors, too.” The notion that physical features help guide axons is gaining momentum, says neuroscientist Samantha Butler of UCLA. “It’s a really intriguing study.” A better understanding of how nerve cells find their targets could help scientists coax new cells to grow after a spinal cord injury or design better materials for nerve cell implants. Franze and colleagues studied nerve cells from the retina of frogs. Experiments on cells in dishes suggested that axons, signal-transmitting tendrils led by tiny pioneering structures called growth cones, grew differently on hard and soft material. Axons grew longer and straighter on stiff surfaces and seemed to meander more on softer material. © Society for Science & the Public 2000 - 2016.
Keyword: Development of the Brain
Link ID: 22672 - Posted: 09.20.2016
By SABRINA TAVERNISE WASHINGTON — The Food and Drug Administration approved the first drug to treat patients with the most common childhood form of muscular dystrophy, a vivid example of the growing power that patients and their advocates wield over the federal government’s evaluation of drugs. The agency’s approval went against the recommendation of its experts. The main clinical trial of the drug was small, involving only 12 boys with the disease known as Duchenne muscular dystrophy, and did not have an adequate control group of boys who had the disease but did not take the drug. A group of independent experts convened by the agency this spring said there was not enough evidence that it was effective. But the vote was close. Large and impassioned groups of patients, including boys in wheelchairs, and their advocates, weighed in. The muscular dystrophy community is well organized and has lobbied for years to win approval for the drug, getting members of Congress to write letters to the agency. A decision on the drug had been delayed for months. The approval was so controversial that F.D.A. employees fought over it, a dispute that was taken to the agency’s commissioner, Dr. Robert M. Califf, who ultimately decided that it would stand. The approval delighted the drug’s advocates and sent the share price of the drug’s maker, Sarepta Therapeutics, soaring. But it was taken as a deeply troubling sign among drug policy experts who believe the F.D.A. has been far too influenced by patient advocates and drug companies, and has allowed the delicate balance in drug approvals to tilt toward speedy decisions based on preliminary data and away from more conclusive evidence of effectiveness and safety. © 2016 The New York Times Company
By Meredith Wadman Last year, in a move to counter charges that it has neglected the health and safety of its players, the National Football League (NFL) tapped Elizabeth “Betsy” Nabel as its first chief health and medical adviser, a paid position to which she told The Boston Globe she devotes about 1 day a month, plus some nights and weekends. (She and NFL have not disclosed her salary.) And last week, Nabel answered Science’s questions on the heels of NFL’s 14 September announcement that it will devote $40 million in new funding to medical research, primarily neuroscience relevant to repetitive head injuries—with grant applications judged by an NFL-convened panel of scientists, rather than by National Institutes of Health (NIH) study sections. Nabel is well known to many medical scientists as the cardiologist who directed the National Heart, Lung, and Blood Institute at NIH, then left that job in 2009 to become president of a prestigious Harvard University–affiliated teaching hospital: Brigham and Women’s Hospital in Boston. Nabel’s new role with NFL came under media scrutiny in May, when a report by Democrats on the House of Representatives Energy and Commerce Committee found that NFL inappropriately tried to influence the way its “unrestricted” donation to NIH was spent. It revealed, for example, that last year Nabel contacted NIH’s neurology institute director Walter Koroshetz to question the objectivity of an NIH study section and of a principal investigator whose team the peer reviewers had just awarded a $16 million grant. Robert Stern and his group at Boston University, with others, were proposing to image the brains and chart the symptoms of scores of college and professional football players across time. NFL suggested that the scientists, who have led in establishing the link between repetitive head injury and the neurodegenerative brain disease chronic traumatic encephalopathy (CTE), were not objective; Nabel described them in one email as “a more marginal group” whose influence it would be well to “dilute.” The scientists were to have been paid from $30 million that NFL donated to NIH in 2012. After the league objected to its $16 million going to fund the Boston University–led team—it did offer to fund $2 million of the amount—NIH’s neurology institute ended up wholly funding the 7-year grant with its own money. © 2016 American Association for the Advancement of Scienc
Keyword: Brain Injury/Concussion
Link ID: 22669 - Posted: 09.20.2016
By PAGAN KENNEDY In 1914, The Lancet reported on a clergyman who was found dead in a pool; he had left behind this suicide note: “Another sleepless night, no real sleep for weeks. Oh, my poor brain, I cannot bear the lengthy, dark hours of the night.” I came across that passage with a shock of recognition. Many people think that the worst part of insomnia is the daytime grogginess. But like that pastor, I suffered most in the dark hours after midnight, when my desire for sleep, my raging thirst for it, would drive me into temporary insanity. On the worst nights, my mind would turn into a mad dog that snapped and gnawed itself. Though one in 10 American adults suffer from chronic insomnia, we have yet to answer the most fundamental questions about the affliction. Scientists are still arguing about the mechanisms of sleep and the reasons it fails in seemingly healthy people. There are few — if any — reliable treatments for insomnia. At the same time, medical journals warn that bad sleep can fester into diseases like cancer and diabetes. Deep in the night, those warnings scuttle around my mind like rats. About 18 months ago, during a particularly grueling period, I felt so desperate that I consulted yet another doctor — but all he did was suggest the same drugs that had failed me in the past. I was thrown back once again on my own ways of coping. As a child, I had invented mental games to distract myself. For instance, I would compile a list of things and people that made me happy, starting with words that began with A and moving through the alphabet. One night, I was in the Qs, trying to figure out what to add to quesadillas, queer theory and Questlove. Then, suddenly, the game infuriated me — why, why, why did I have to spend hours doing this? In the red glare of the digital clock, my brain rattled its cage. I prepared for a wave of lunacy. But instead of a meltdown, I had a wild idea: What if there was another, easier, way to drive the miserable thoughts from my mind? I began to fantasize about a machine that would do the thinking for me. I pictured it like another brain that would fit on top of my head. The next day, I cobbled together my first insomnia machine. © 2016 The New York Times Company
Link ID: 22667 - Posted: 09.19.2016
By Colin Barras It is not just about speed. The only songbird known to perform a rapid tap dance during courtship makes more noise with its feet during its routines than at other times. The blue-capped cordon-bleu (Uraeginthus cyanocephalus) from East Africa is blessed with the attributes of a Broadway star: striking good looks, a strong singing voice – and fine tap-dancing skills. The dances are so fast that they went unnoticed until 2015, when Masayo Soma at Hokkaido University in Japan and her colleagues captured the performances on high-speed film. The bird’s speciality is a left-right-left shuffle – only with the feet striking the perch up to 50 times a second. The vision of some birds operates at a faster rate than that of humans, so the cordon-bleu’s dance may simply be about creating an impressive visual performance. But it could also be about winning over a potential mate with rhythm. To explore the idea, Soma and her colleagues recorded audio of the courtship dances, which both males and females perform. They found that the tap dances are unusually loud: the feet strike the branch with enough force to generate sound averaging 30 decibels. This typically drops to just 20 decibels when a bird’s feet strike the branch as it hops around when it is not performing, which means the step sounds are not just a by-product of movement. © Copyright Reed Business Information Ltd.
Keyword: Sexual Behavior
Link ID: 22665 - Posted: 09.19.2016
Tina Hesman Saey Color vision may actually work like a colorized version of a black-and-white movie, a new study suggests. Cone cells, which sense red, green or blue light, detect white more often than colors, researchers report September 14 in Science Advances. The textbook-rewriting discovery could change scientists’ thinking about how color vision works. For decades, researchers have known that three types of cone cells in the retina are responsible for color vision. Those cone cells were thought to send “red,” “green” and “blue” signals to the brain. The brain supposedly combines the colors, much the way a color printer does, to create a rainbow-hued picture of the world (including black and white). But the new findings indicate that “the retina is doing more of the work, and it’s doing it in a more simpleminded way,” says Jay Neitz, a color vision scientist at the University of Washington in Seattle who was not involved in the study. Red and green cone cells each come in two types: One type signals “white”; another signals color, vision researcher Ramkumar Sabesan and colleagues at the University of California, Berkeley, discovered. The large number of cells that detect white (and black — the absence of white) create a high-resolution black-and-white picture of a person’s surroundings, picking out edges and fine details. Red- and green-signaling cells fill in low-resolution color information. The process works much like filling in a coloring book or adding color to a black-and-white film, says Sabesan, who is now at the University of Washington. |© Society for Science & the Public 2000 - 2016
Link ID: 22660 - Posted: 09.15.2016
By Brian Owens It’s certainly something to crow about. New Caledonian crows are known for their ingenious use of tools to get at hard-to-reach food. Now it turns out that their Hawaiian cousins are adept tool-users as well. Christian Rutz at the University of St Andrews in the UK has spent 10 years studying the New Caledonian crow and wondered whether any other crow species are disposed to use tools. So he looked for crows that have similar features to the New Caledonian crow – a straight bill and large, mobile eyes that allow it to manipulate tools, much as archaeologists use opposable thumbs as an evolutionary signature for tool use in early humans. “The Hawaiian crow really stood out,” he says. “They look quite similar.” Hawaiian crows are extinct in the wild, but 109 birds still live in two captive breeding facilities in Hawaii. That meant Rutz was able to test pretty much every member of the species. He stuffed tasty morsels into a variety of holes and crevices in a log, and gave the birds a variety of sticks to see if they would use them to dig out the food. Almost all of them did, and most extracted the food in less than a minute, faster than the researchers themselves could. “It’s mind-blowing,” says Rutz. “They’re very good at getting the tool in the right position, and if they’re not happy with it they’ll modify it or make their own.” © Copyright Reed Business Information Ltd.
By Krystnell A. Storr This one goes out to the head bobbers, the window seat sleepers, and the open-mouth breathers — there is no shame in being able to fall asleep anywhere, and at any time. Be proud, and, if you can’t help it, snore loud. Scientists have come to a consensus that our bodies definitely need sleep, but we don’t all need the same amount. The next step for them is to figure out where the process of sleep starts and ends in the body. And, like a good movie, one revelation about sleep only leads to another. Think of yourself as a very minor character in the scientific story of fatigue. The real star of this cozy mystery is the fruit fly, an A-lister in sleep science. Thanks to fruit flies, we understand two of the basic factors that govern sleep: a biological clock, which scientists know a lot about, and a homeostatic switch, which they only just discovered and are beginning to understand. Let’s start with this biological clock. The clock that is connected to sleep is controlled by a circadian rhythm and uses environmental cues such as sunlight to tell the body when to wake up. This sun-sleep connection in humans and flies alike got scientists like Russell Foster, a professor at Oxford University in the United Kingdom, asking questions such as: What happens when we don’t have the mechanisms in our eye to distinguish dawn from dusk and send that message to the brain? Why can we still fall asleep according to the circadian rhythm? The answer, Foster said, is that mammals have a third layer of photoreceptors in the eye. It used to be that scientists thought rods and cones, cells that help us process images, were the only ones in the eye that worked to detect light. But when they removed these cells in mice, they noticed that the mice could still keep up with the circadian rhythm. The hidden cells, they found, were intrinsically sensitive to light and acted as a backup measure to keep us on our sleep schedule, whether we can see that the sun is up or not.
By Rachel Feltman In the age of the quantified self, products that promise to track your habits and fix your behavior are a dime a dozen. Find out how much you walk; do that more. Find out how much junk you eat; do that less. Correct your posture in real time, and get feedback as you strengthen your pelvic floor muscles. More and more companies are built on the notion that any problem can be solved if you get enough numbers to find a pattern. In that sense, Sense — a sleep tracker made by the start-up Hello — isn't all that unusual. But the company's new lead scientist is just getting his hands on two years of user sleep data, and he seems particularly passionate about using it for good. Matthew Walker, a professor of neuroscience and psychology at the University of California in Berkeley, and director of the U.C. Berkeley Sleep and Neuroimaging Laboratory, does not mince words when it comes to snoozing. "It’s very clear right now that the sleep-loss epidemic is the greatest public health crisis in First World nations of the 21st century," Walker told The Washington Post. "Every disease that is killing us, in First World countries, can be linked to loss of sleep." Indeed, the Centers for Disease Control and Prevention states that lack of sleep — in addition to causing fatal accidents and injuries — has been linked to an increase risk of hypertension, diabetes, depression, obesity and even cancer. Just about all scientists and medical professionals agree that good sleep helps keep the body healthy. © 1996-2016 The Washington Post
Link ID: 22655 - Posted: 09.15.2016
By GINA KOLATA A few years ago, Richard Kahn, the now-retired chief scientific and medical officer of the American Diabetes Association, was charged with organizing a committee to prescribe a diet plan for people with diabetes. He began by looking at the evidence for different diets, asking which, if any, best controlled diabetes. “When you look at the literature, whoa is it weak. It is so weak,” Dr. Kahn said in a recent interview. Studies tended to be short term, diets unsustainable, differences between them clinically insignificant. The only thing that really seemed to help people with diabetes was weight loss — and for weight loss there is no magic diet. But people want diet advice, Dr. Kahn reasoned, and the association really should say something about diets. So it, like the National Institutes of Health, went with the Department of Agriculture’s food pyramid. Why? “It’s a diet for all America,” Dr. Kahn said. ”It has lots of fruits and vegetables and a reasonable amount of fat.” That advice, though, recently came under attack in a New York Times commentary written by Sarah Hallberg, an osteopath at a weight loss clinic in Indiana, and Osama Hamdy, the medical director of the obesity weight loss program at the Joslin Diabetes Center at Harvard Medical School. There is a diet that helps with diabetes, the two doctors said, one that restricts — or according to Dr. Hallberg, severely restricts — — carbohydrates. “If the goal is to get patients off their medications, including insulin, and resolve rather than just control their diabetes, significant carb restriction is by far the best nutrition plan,” Dr. Hallberg said in an email. “This would include elimination of grains, potatoes and sugars and all processed foods. There is a significant and ever growing body of literature that supports this method.” She is in private practice at Indiana University Health Arnett Hospital and is medical director of a startup developing nutrition-based medical interventions. © 2016 The New York Times Company
Link ID: 22654 - Posted: 09.15.2016
André Corrêa d’Almeida and Amanda Sue Grossi Development. Poverty. Africa. These are just three words on a page – almost no information at all – but how many realities did our readers just conjure? And how many thoughts filled the spaces in-between? Cover yourselves. Your biases are showing. In the last few decades, groundbreaking work by psychologists and behavioural economists has exposed unconscious biases in the way we think. And as the World Bank’s 2015 World Development Report points out, development professionals are not immune to these biases. There is a real possibility that seemingly unbiased and well-intentioned development professionals are capable of making consequential mistakes, with significant impacts upon the lives of others, namely the poor. The problem arises when mindsets are just that – set. As the work of Daniel Kahneman and Amos Tversky has shown, development professionals – like people generally – have two systems of thinking; the automatic and the deliberative. For the automatic, instead of performing complex rational calculations every time we need to make a decision, much of our thinking relies on pre-existing mental models and shortcuts. These are based on assumptions we create throughout our lives and that stem from our experiences and education. More often than not, these mental models are incomplete and shortcuts can lead us down the wrong path. Thinking automatically then becomes thinking harmfully. © 2016 Guardian News and Media Limited
Link ID: 22653 - Posted: 09.15.2016
By Rachel Becker Optical illusions have a way of breaking the internet, and the latest visual trick looks like it’s well on its way. On Sunday afternoon, game developer Will Kerslake tweeted a picture of intersecting gray lines on a white background. Twelve black dots blink in and out of existence where the gray lines meet. In the six hours since he posted the photo to Twitter, it’s been shared more than 6,000 times, with commenters demanding to know why they can’t see all 12 dots at the same time. The optical illusion was first posted to Facebook about a day ago by Japanese psychology professor Akiyoshi Kitaoka, and it has been shared more than 4,600 times so far. But the origin of this bit of visual trickery is a scientific paper published in the journal Perception in 2000. To be clear, there really are 12 black dots in the image. But (most) people can’t see all 12 dots at the same time, which is driving people nuts. "They think, 'It’s an existential crisis,'" says Derek Arnold, a vision scientist at the University of Queensland in Australia. "'How can I ever know what the truth is?'" But, he adds, scientists who study the visual system know that perception doesn’t always equal reality. In this optical illusion, the black dot in the center of your vision should always appear. But the black dots around it seem to appear and disappear. That’s because humans have pretty bad peripheral vision. If you focus on a word in the center of this line you’ll probably see it clearly. But if you try to read the words at either end without moving your eyes, they most likely look blurry. As a result, the brain has to make its best guess about what’s most likely to be going on in the fuzzy periphery — and fill in the mental image accordingly. © 2016 Vox Media, Inc.
Link ID: 22652 - Posted: 09.15.2016
By Julia Shaw The brain, with its 100 billion neurons, allows us to do amazing things like learn multiple languages, or build things that send people into outer space. Yet despite this astonishing capacity, we routinely can’t remember where we put our keys, we forget why we went to the grocery store, and we fail when trying to recall personal life events. This apparent contradiction in functionality opens up the question of why we forget some things but remember others. Or, more fundamentally, what causes forgetting? This week my book ‘The Memory Illusion’ drops in Canada, and as a Canadian girl I want to celebrate this by showcasing some Canadian researchers who have given us insight into precisely this question. An article published recently in Psychological Science by Talya Sadeh and colleagues at the Rotman Research institute in Toronto addresses a long-running debate in the world of memory science; do we forget things because of decay or interference? Decay. Advocates of the decay account posit that our memories slowly disappear, fading because of a passage of time during which they have not been accessed. You can picture this much like a message written in sand, with every ocean wave that flows over the shore making the writing less legible until it eventually disappears entirely. The sand represents the web of brain cells that form a memory in the brain, and the ocean waves represent time passing. © 2016 Scientific American,
Keyword: Learning & Memory
Link ID: 22651 - Posted: 09.13.2016
By ANAHAD O’CONNOR The sugar industry paid scientists in the 1960s to play down the link between sugar and heart disease and promote saturated fat as the culprit instead, newly released historical documents show. The internal sugar industry documents, recently discovered by a researcher at the University of California, San Francisco, and published Monday in JAMA Internal Medicine, suggest that five decades of research into the role of nutrition and heart disease, including many of today’s dietary recommendations, may have been largely shaped by the sugar industry. “They were able to derail the discussion about sugar for decades,” said Stanton Glantz, a professor of medicine at U.C.S.F. and an author of the JAMA paper. The documents show that a trade group called the Sugar Research Foundation, known today as the Sugar Association, paid three Harvard scientists the equivalent of about $50,000 in today’s dollars to publish a 1967 review of research on sugar, fat and heart disease. The studies used in the review were handpicked by the sugar group, and the article, which was published in the prestigious New England Journal of Medicine, minimized the link between sugar and heart health and cast aspersions on the role of saturated fat. Even though the influence-peddling revealed in the documents dates back nearly 50 years, more recent reports show that the food industry has continued to influence nutrition science. Last year, an article in The New York Times revealed that Coca-Cola, the world’s largest producer of sugary beverages, had provided millions of dollars in funding to researchers who sought to play down the link between sugary drinks and obesity. In June, The Associated Press reported that candy makers were funding studies that claimed that children who eat candy tend to weigh less than those who do not. The Harvard scientists and the sugar executives with whom they collaborated are no longer alive. One of the scientists who was paid by the sugar industry was D. Mark Hegsted, who went on to become the head of nutrition at the United States Department of Agriculture, where in 1977 he helped draft the forerunner to the federal government’s dietary guidelines. Another was Dr. Fredrick J. Stare, the chairman of Harvard’s nutrition department. © 2016 The New York Times Company
Link ID: 22649 - Posted: 09.13.2016
Martha Bebinger Five states are voting this fall on whether marijuana should be legal, like alcohol, for recreational use. That has sparked questions about what we know – and don't know – about marijuana's effect on the brain. Research is scarce. The U.S. Drug Enforcement Agency classifies marijuana as a Schedule I drug. That classification puts up barriers to conducting research on it, including a cumbersome DEA approval application and a requirement that scientists procure very specific marijuana plants. One long-term study in New Zealand compared the IQs of people at age 13 and then through adolescence and adulthood to age 38. Those who used pot heavily from adolescence onward showed an average 8 percent drop in IQ. People who never smoked, by contrast, showed slightly increased IQ. Critics pounced on the study, which was published in 2012, because it didn't adjust for many other things that affect IQ such as home life or family income. And there's no proof the IQ differences are due to pot. One of those critics, Nicholas Jackson, now a senior statistician at the University of California, Los Angeles, wondered what would happen if he could rule out some of those elements by comparing twins. "Individuals that share the same genes, grew up in the same household, where the difference between them was that one of the twins was using marijuana and one was not," Jackson says. © 2016 npr
Keyword: Drug Abuse
Link ID: 22648 - Posted: 09.13.2016
By Bob Grant Lab rats that compulsively drink are cured of their addiction by a drug that silences neural networks that strengthened as they became dependent on alcohol.FLICKR, SARAH LAVAL Alcohol dependence involves neural reward networks that are strengthened by the regular consumption of alcohol. Using rat models of compulsive drinking, researchers at The Scripps Research Institute (TSRI) have now shown that they can interfere with those specific networks to curb the behavior. They reported their findings last week (September 7) in The Journal of Neuroscience. “We can completely reverse alcohol dependence by targeting a network of neurons,” coauthor Olivier George, a TSRI neuroscientist, said in a statement. “It is very challenging to target such a small population of neurons in the brain, but this study helps to increase our knowledge of a part of the brain that is still a mystery,” added coauthor and TSRI postdoc Giordano de Guglielmo. The researchers used a drug called Daun02 to shut down a specific group of neurons in the amygdalas of rats that drank compulsively. The treated rats stopped imbibing as much, and this behavioral change lasted for several days. “With classic pharmacology we usually observe a 20-40 percent decrease in drinking because the individuals are highly dependent (we model heavy alcoholism),” George told Medical News Today. “Instead, here, the drinking went all the way back down to normal drinking, and without noticeable side effects; very unusual. And, usually, to have long lasting effects like that, you need daily treatment, not a single one; it shows that we might have found alcoholism's Achilles' heel.” © 1986-2016 The Scientist
Keyword: Drug Abuse
Link ID: 22647 - Posted: 09.13.2016
By SARAH HALLBERG and OSAMA HAMDY Earlier this year, the Food and Drug Administration approved a new weight-loss procedure in which a thin tube, implanted in the stomach, ejects food from the body before all the calories can be absorbed. Some have called it “medically sanctioned bulimia,” and it is the latest in a desperate search for new ways to stem the rising tides of obesity and Type 2 diabetes. Roughly one-third of adult Americans are now obese; two-thirds are overweight; and diabetes afflicts some 29 million. Another 86 million Americans have a condition called pre-diabetes. None of the proposed solutions have made a dent in these epidemics. Recently, 45 international medical and scientific societies, including the American Diabetes Association, called for bariatric surgery to become a standard option for diabetes treatment. The procedure, until now seen as a last resort, involves stapling, binding or removing part of the stomach to help people shed weight. It costs $11,500 to $26,000, which many insurance plans won’t pay and which doesn’t include the costs of office visits for maintenance or postoperative complications. And up to 17 percent of patients will have complications, which can include nutrient deficiencies, infections and intestinal blockages. It is nonsensical that we’re expected to prescribe these techniques to our patients while the medical guidelines don’t include another better, safer and far cheaper method: a diet low in carbohydrates. Once a fad diet, the safety and efficacy of the low-carb diet have now been verified in more than 40 clinical trials on thousands of subjects. Given that the government projects that one in three Americans (and one in two of those of Hispanic origin) will be given a diagnosis of diabetes by 2050, it’s time to give this diet a closer look. © 2016 The New York Times Company
Link ID: 22645 - Posted: 09.12.2016
By David Grimm Depending on whom you ask, yesterday’s U.S. government workshop on the state of nonhuman primate research was either a raging success or a complete fiasco. The event, held at the National Institutes of Health (NIH) in Bethesda, Maryland, brought together dozens of scientists, veterinarians, and bioethicists to discuss how research on monkeys and related animals is contributing to human medicine and to review the welfare policies that surround this work. But observers differed widely on whether it accomplished what Congress had in mind when it told NIH to hold the event. “It was a great showcase of the importance nonhuman primates have played and continue to play in human health,” says Anne Deschamps, a senior science policy analyst at the Federation of American Societies for Experimental Biology in Bethesda, one of several scientific organizations that signed onto a white paper released in advance of the meeting that promoted the use of these animals in biomedical research. She contends that research on these animals has been critical for our understanding of HIV and the human brain. But the animal rights group People for the Ethical Treatment of Animals (PETA), whose lobbying efforts led to the workshop, says the meeting was supposed to determine whether monkeys and their relatives belong in laboratories in the first place. “It was an infomercial for the use of monkeys in experiments,” says PETA Senior Vice President Kathy Guillermo in Norfolk, Virginia. “It was a wasted opportunity.” © 2016 American Association for the Advancement of Science
Keyword: Animal Rights
Link ID: 22644 - Posted: 09.12.2016
By Karen Weintraub Researchers have long believed that problems with mitochondria—the power plants of cells—underlie some cases of Parkinson’s disease. Now a new study details those problems, and suggests that they may form a common thread linking previously unexplained cases of the disease with those caused by different genetic anomalies or toxins. Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it, says Marco Baptista, research director at the nonprofit Michael J. Fox Foundation, a leading center for study and advocacy in the fight against Parkinson’s. The study, published Thursday in Cell Stem Cell, did identify a possible way to reverse the damage of Parkinson’s—but only in individual cells and fruit flies. Finding a treatment that does the same thing in people will be challenging, Baptista says. Roughly one million Americans have Parkinson’s disease, which is characterized by motor problems and can cause other symptoms including cognitive and gastrointestinal difficulties. About 1 to 2 percent of cases are linked to mutations in the LRRK2 gene, with far fewer associated with genes known as PINK1 and Parkin. Exposure to environmental factors such as toxic chemicals can also lead to Parkinson’s, although most cases have no obvious cause. In the new paper Xinnan Wang, an assistant professor of neurosurgery at Stanford University, and her colleagues show that mitochondria are underpowered in several types of Parkinson’s and that these mitochondria also release toxic chemicals. Looking at fly models of the disease as well as cells taken from patients, the researchers found that they could correct these problems and reverse neurodegeneration if they reduced levels of a protein involved in mitochondrial activity. © 2016 Scientific American
Link ID: 22642 - Posted: 09.10.2016
By Abby Olena Mammalian prions are notoriously difficult as structural biology subjects, given their insolubility and tendency to aggregate. Researchers have now overcome these challenges to figure out the preliminary structure of a shortened form of infectious prion (PrPSc), which they report today (September 8) in PLOS Pathogens. “For the first time, we have a structure of an infectious mammalian prion,” said Giuseppe Legname of Scuola Internazionale Superiore di Studi Avanzati in Trieste, Italy, who was not involved in this study. “It’s a very important paper,” he added. “What we have done is to obtain a very simple, very preliminary idea of what the structure of these mammalian prions are,” said study coauthor Jesús Requena of the University of Santiago de Compostela in Spain. Requena and colleagues generated a shortened form of PrPSc by injecting a laboratory strain of prions into transgenic mice that express a truncated form of normal cellular prion protein (PrPC), which lacks the attachment of a membrane anchor present in full-length PrPSc. In nature, PrPC transforms into full-length PrPSc, which causes Creutzfeldt-Jakob disease in humans, scrapie in sheep, and mad cow disease. The absence of the membrane anchor in shortened PrPSc from the transgenic mice allowed the researchers to isolate a fairly homogeneous population of PrPSc. They confirmed that this population was infectious by inoculating wild-type mice, which then developed symptoms of prion disease. © 1986-2016 The Scientist
Link ID: 22638 - Posted: 09.10.2016