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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.

Keyword: Biological Rhythms; Sleep
Link ID: 22656 - Posted: 09.15.2016

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

Keyword: Sleep
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

Keyword: Obesity
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

Keyword: Attention
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.

Keyword: Vision
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

Carrie Arnold Could a protein that originated in a virus explain why men are more muscular than women? Viruses are notorious for their ability to cause disease, but they also shape human biology in less obvious ways. Retroviruses, which insert their genetic material into our genomes to copy themselves, have left behind genes that help to steer our immune systems and mold the development of embryos and the placenta. Now researchers report in PLOS Genetics that syncytin, a viral protein that enables placenta formation, also helps to increase muscle mass in male mice1. These results could partially explain a lingering mystery in biology: why the males of many mammalian species tend to be more muscular than females. “As soon as I read it, my mind started racing with the potential implications,” says evolutionary virologist Aris Katzourakis of the University of Oxford, UK. About 8% of the 3 billion pairs of As, Ts, Gs and Cs that make up our DNA are viral detritus. Many of those viral hand-me-downs have degraded into useless junk — but not all, as a series of discoveries over the past 15 years has revealed. In 2000, scientists discovered that syncytin, a protein that enables the formation of the placenta, actually originated as a viral protein that humans subsequently ‘borrowed’2. That original viral protein enables the retrovirus to fuse with host cells, depositing its entire genome into the safe harbour of the cytoplasm. Syncytin has changed little from this ancestral protein form; it directs certain placental cells to fuse with cells in the mother’s uterus, forming the outer layer of the placenta. © 2016 Macmillan Publishers Limited

Keyword: Muscles; Sexual Behavior
Link ID: 22650 - 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

Keyword: Obesity
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

Laura Sanders By sneakily influencing brain activity, scientists changed people’s opinions of faces. This covert neural sculpting relied on a sophisticated brain training technique in which people learn to direct their thoughts in specific ways. The results, published September 8 in PLOS Biology, support the idea that neurofeedback methods could help reveal how the brain’s behavior gives rise to perceptions and emotions. What’s more, the technique may ultimately prove useful for easing traumatic memories and treating disorders such as depression. The research is still at an early stage, says neurofeedback researcher Michelle Hampson of Yale University, but, she notes, “I think it has great promise.” Takeo Watanabe of Brown University and colleagues used functional MRI to measure people’s brain activity in an area called the cingulate cortex as participants saw pictures of faces. After participants had rated each face, a computer algorithm sorted their brain responses into patterns that corresponded to faces they liked and faces they disliked. With this knowledge in hand, the researchers then attempted to change people’s face preferences by subtly nudging brain activity in the cingulate cortex. In step 2 of the experiment, returning to the fMRI scanner, participants saw an image of a face that they had previously rated as neutral. Just after that, they were shown a disk. The goal, the participants were told, was simple: make the disk bigger by using their brains. They had no idea that the only way to make the disk grow was to think in a very particular way. |© Society for Science & the Public 2000 - 201

Keyword: Attention; Learning & Memory
Link ID: 22646 - Posted: 09.12.2016

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

Keyword: Obesity
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 GRETCHEN REYNOLDS A busy brain can mean a hungry body. We often seek food after focused mental activity, like preparing for an exam or poring over spreadsheets. Researchers speculate that heavy bouts of thinking drain energy from the brain, whose capacity to store fuel is very limited. So the brain, sensing that it may soon require more calories to keep going, apparently stimulates bodily hunger, and even though there has been little in the way of physical movement or caloric expenditure, we eat. This process may partly account for the weight gain so commonly seen in college students. Scientists at the University of Alabama at Birmingham and another institution recently experimented with exercise to counter such post-­study food binges. Gary Hunter, an exercise physiologist at U.A.B., oversaw the study, which was published this month in the journal Medicine & Science in Sports & Exercise. Hunter notes that strenuous activity both increases the amount of blood sugar and lactate — a byproduct of intense muscle contractions — circulating in the blood and augments blood flow to the head. Because the brain uses sugar and lactate as fuel, researchers wondered if the increased flow of fuel-rich blood during exercise could feed an exhausted brain and reduce the urge to overeat. Thirty-­eight healthy college students were invited to U.A.B.’s exercise lab to determine their fitness and metabolic rates — and to report what their favorite pizza was. Afterward, they sat quietly for 35 minutes before being given as much of their favorite pizza as they wanted, which established a baseline measure of self-­indulgence. At a later date, the volunteers returned and spent 20 minutes tackling selections from college and graduate-­school entrance exams. Hunter says this work has been used in other studies “to induce mental fatigue and hunger.” Next, half the students sat quietly for 15 minutes, before being given pizza. The rest of the volunteers spent those 15 minutes doing intervals on a treadmill: two minutes of hard running followed by about one minute of walking, repeated five times. This is the sort of brief but intensive routine, Hunter says, that should prompt the release of sugar and lactate into the bloodstream. These students were then allowed to gorge on pizza, too. But by and large, they did not overeat. © 2016 The New York Times Company

Keyword: Obesity; Learning & Memory
Link ID: 22643 - Posted: 09.10.2016

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

Keyword: Parkinsons
Link ID: 22642 - Posted: 09.10.2016

By NATALIE ANGIER The female bonobo apes of the Wamba forest in the Democratic Republic of Congo had just finished breakfast and were preparing for a brief nap in the treetops, bending and crisscrossing leafy branches into comfortable day beds. But one of the females was in estrus, her rump exceptionally pink and swollen, and four males in the group were too excited to sleep. They took turns wildly swinging and jumping around the fertile female and her bunkmates, shaking the branches, appearing to display their erections and perforating the air with high-pitched screams and hoots. Suddenly, three older, high-ranking female bonobos bolted up from below, a furious blur of black fur and swinging limbs and, together with the female in estrus, flew straight for the offending males. The males scattered. The females pursued them. Tree boughs bounced and cracked. Screams on all sides grew deafening. Three of the males escaped, but the females cornered and grabbed the fourth one — the resident alpha male. He was healthy, muscular and about 18 pounds heavier than any of his captors. But no matter. The females bit into him as he howled and struggled to pull free. Finally, “he dropped from the tree and ran away, and he didn’t appear again for about three weeks,” said Nahoko Tokuyama, of the Primate Research Institute at Kyoto University in Japan, who witnessed the encounter. When the male returned, he kept to himself. Dr. Tokuyama noticed that the tip of one of his toes was gone. “Being hated by females,” she said in an email interview, “is a big matter for male bonobos.” The toe-trimming incident was extreme but not unique. Describing results from their long-term field work in the September issue of Animal Behaviour, Dr. Tokuyama and her colleague Takeshi Furuichi reported that the female bonobos of Wamba often banded together to fend off male aggression, and in patterns that defied the standard primate rule book. © 2016 The New York Times Company

Keyword: Aggression; Sexual Behavior
Link ID: 22641 - Posted: 09.10.2016

By Karen Zusi At least one type of social learning, or the ability to learn from observing others’ actions, is processed by individual neurons within a region of the human brain called the rostral anterior cingulate cortex (rACC), according to a study published today (September 6) in Nature Communications. The work is the first direct analysis in humans of the neuronal activity that encodes information about others’ behavior. “The idea [is] that there could be an area that’s specialized for processing things about other people,” says Matthew Apps, a neuroscientist at the University of Oxford who was not involved with the study. “How we think about other people might use distinct processes from how we might think about ourselves.” During the social learning experiments, the University of California, Los Angeles (UCLA) and CalTech–based research team recorded the activity of individual neurons in the brains of epilepsy patients. The patients were undergoing a weeks-long procedure at the Ronald Reagan UCLA Medical Center in which their brains were implanted with electrodes to locate the origin of their epileptic seizures. Access to this patient population was key to the study. “It’s a very rare dataset,” says Apps. “It really does add a lot to the story.” With data streaming out of the patients’ brains, the researchers taught the subjects to play a card game on a laptop. Each turn, the patients could select from one of two decks of face-down cards: the cards either gave $10 or $100 in virtual winnings, or subtracted $10 or $100. In one deck, 70 percent of the cards were winning cards, while in the other only 30 percent were. The goal was to rack up the most money. © 1986-2016 The Scientist

Keyword: Learning & Memory; Attention
Link ID: 22640 - Posted: 09.10.2016

By Jessica Hamzelou As any weight-watcher knows, carb cravings can be hard to resist. Now there’s evidence that carbohydrate-rich foods may elicit a unique taste too, suggesting that “starchy” could be a flavour in its own right. It has long been thought that our tongues register a small number of primary tastes: salty, sweet, sour and bitter. Umami – the savoury taste often associated with monosodium glutamate – was added to this list seven years ago, but there’s been no change since then. However, this list misses a major component of our diets, says Juyun Lim at Oregon State University in Corvallis. “Every culture has a major source of complex carbohydrate. The idea that we can’t taste what we’re eating doesn’t make sense,” she says. Complex carbohydrates such as starch are made of chains of sugar molecules and are an important source of energy in our diets. However, food scientists have tended to ignore the idea that we might be able to specifically taste them, says Lim. Because enzymes in our saliva break starch down into shorter chains and simple sugars, many have assumed we detect starch by tasting these sweet molecules. Her team tested this by giving a range of different carbohydrate solutions to volunteers – who it turned out were able to detect a starch-like taste in solutions that contained long or shorter carbohydrate chains. “They called the taste ‘starchy’,” says Lim. “Asians would say it was rice-like, while Caucasians described it as bread-like or pasta-like. It’s like eating flour.” © Copyright Reed Business Information Ltd.

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 22639 - 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

Keyword: Prions
Link ID: 22638 - Posted: 09.10.2016

By JACK HEALY CINCINNATI — On the day he almost died, John Hatmaker bought a packet of Oreos and some ruby-red Swedish Fish at the corner store for his 5-year-old son. He was walking home when he spotted a man who used to sell him heroin. Mr. Hatmaker, 29, had overdosed seven times in the four years he had been addicted to pain pills and heroin. But he hoped he was past all that. He had planned to spend that Saturday afternoon, Aug. 27, showing his son the motorcycles and enjoying the music at a prayer rally for Hope Over Heroin in this region stricken by soaring rates of drug overdoses and opioid deaths. But first, he decided as he palmed a sample folded into a square of paper, he would snort this. As he crumpled to the sidewalk, Mr. Hatmaker became one of more than 200 people to overdose in the Cincinnati area in the past two weeks, leaving three people dead in what the officials here called an unprecedented spike. Similar increases in overdoses have rippled recently through Indiana, Kentucky and West Virginia, overwhelming ambulance crews and emergency rooms and stunning some antidrug advocates. Addiction specialists said the sharp increases in overdoses were a grim symptom of America’s heroin epidemic, and of the growing prevalence of powerful synthetic opiates like fentanyl. The synthetics are often mixed into batches of heroin, or sprinkled into mixtures of caffeine, antihistamines and other fillers. In Cincinnati, some medical and law enforcement officials said they believed the overdoses were largely caused by a synthetic drug called carfentanil, an animal tranquilizer used on livestock and elephants with no practical uses for humans. Fentanyl can be 50 times stronger than heroin, and carfentanil is as much as 100 times more potent than fentanyl. Experts said an amount smaller than a snowflake could kill a person. © 2016 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 22637 - Posted: 09.07.2016