Chapter 16. None
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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
By Helen Thomson High levels of inflammation as a child may predict a higher risk of manic behaviour in later life, a finding that could lead to new ways of treating conditions like bipolar disorder. Hypomania involves spells of hyperactivity and is often a symptom of mood disorders, including bipolar disorder, seasonal affective disorder and some kinds of psychosis. People experiencing hypomania may take more risks, feel more confident and become impatient with others. After spells like this, they may “crash”, needing to sleep for long periods and sometimes remembering little about the previous few days. Earlier studies suggested a link between inflammation and mood disorders, prompting Joseph Hayes at University College London and his team to see if inflammation as a child might lead to mental health problems later. Analysing data from more than 1700 people, his team identified a significant link between high levels of a chemical involved in inflammation at age 9, and experiencing aspects of hypomania at age 22. The chemical, called IL-6, is normally secreted by white blood cells to stimulate an inflammatory immune response to infection or trauma. Hayes’s team says it is unclear how inflammation in childhood could induce symptoms of hypomania but IL-6 is known to affect the brain. A study that used injections to increase IL-6 in the blood of healthy volunteers found that this caused symptoms of anxiety, and reduced performance in memory tests. © Copyright Reed Business Information Ltd.
Link ID: 22636 - Posted: 09.07.2016
By JANE E. BRODY As a woman of a certain age who consumes a well-balanced diet of all the usual food groups, including reasonable amounts of animal protein, I tend to dismiss advice to take a multivitamin supplement. I’ve been told repeatedly by nutrition experts that the overuse of dietary supplements for “nutritional insurance” has given Americans the most expensive urine in the world. I do take a daily supplement of vitamin D, based on considerable evidence of its multiple health benefits, especially for older people. However, based on advice from the National Academy of Medicine and an examination of accumulating research, I’m prompted to consider also taking a vitamin B12 supplement in hopes of protecting my aging brain. Animal protein foods — meat, fish, milk, cheese and eggs — are the only reliable natural dietary sources of B12, and I do get ample amounts of several in my regular diet. But now at age 75, I wonder whether I’m still able to reap the full benefit of what I ingest. You see, the ability to absorb B12 naturally present in foods depends on the presence of adequate stomach acid, the enzyme pepsin and a gastric protein called intrinsic factor to release the vitamin from the food protein it is attached to. Only then can the vitamin be absorbed by the small intestine. As people age, acid-producing cells in the stomach may gradually cease to function, a condition called atrophic gastritis. A century ago, researchers discovered that some people — most likely including Mary Todd Lincoln — had a condition called pernicious anemia, a deficiency of red blood cells ultimately identified as an autoimmune disease that causes a loss of stomach cells needed for B12 absorption. Mrs. Lincoln was known to behave erratically and was ultimately committed to a mental hospital. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22634 - Posted: 09.06.2016
By Clare Wilson Traffic fumes go to your head. Tiny specks of metal in exhaust gases seem to fly up our noses and travel into our brains, where they may contribute to Alzheimer’s disease. Iron nanoparticles were already known to be present in the brain – but they were thought to come from the iron naturally found in our bodies, derived from food. Now a closer look at their structure suggests the particles mostly come from air pollution sources, like traffic fumes and coal burning. The findings are a smoking gun, says Barbara Maher of Lancaster University in the UK. Iron is present harmlessly in our bodies in different forms, as it is part of many biological molecules. But the form known as magnetite, or iron oxide, which is highly reactive and magnetic, has been implicated in Alzheimer’s disease. Maher’s team looked at the brains of 37 people who had lived either in Manchester in the UK or Mexico City. All contained millions of magnetite particles per gram of brain tissue, detected by measuring how magnetic the brain tissue was. The surprise came when the team used electron microscopes to take a close look at particles in the front part of the brains of six people. Round particles of magnetite outnumbered angular magnetite crystals by about one hundred to one. Crystal forms are more likely to have a natural source – such as iron that has come out of the body’s cells. But round particles normally come from melting iron at high temperatures, which happens when fuel is burned. © Copyright Reed Business Information Ltd.
Link ID: 22632 - Posted: 09.06.2016
Susan Milius Contrary to many adorable children’s stories, hibernation is so not sleeping. And most animals can’t do both at the same time. So what’s with Madagascar’s dwarf lemurs? The fat-tailed dwarf lemur slows its metabolism into true hibernation, and stays there even when brain monitoring shows it’s also sleeping. But two lemur cousins, scientists have just learned, don’t multitask. Like other animals, they have to rev their metabolisms out of hibernation if they want a nap. Hibernating animals, in the strictest sense, stop regulating body temperature, says Peter Klopfer, cofounder of the Duke Lemur Center in Durham, N.C. “They become totally cold-blooded, like snakes.” By this definition, bears don’t hibernate; they downregulate, dropping their body temperatures only modestly, even when winter den temperatures sink lower. And real hibernation lasts months, disqualifying short-termers such as subtropical hummingbirds. The darting fliers cease temperature regulation and go truly torpid at night. “You can pick them out of the trees,” Klopfer says. The fat-tailed dwarf lemur, Cheirogaleus medius, was the first primate hibernator discovered, snuggling deep into the softly rotting wood of dead trees. “You’d think they’d suffocate,” he says. But their oxygen demands plunge to somewhere around 1 percent of usual. As trees warm during the day and cool at night, so do these lemurs. When both a tree and its inner lemur heat up, the lemur’s brain activity reflects mammalian REM sleep. |© Society for Science & the Public 2000 - 2016
By Andy Coghlan Antidepressants may be bad for your bones. People who take some selective serotonin reuptake inhibitors (SSRI) have been found to have a higher risk of fractures, but it wasn’t clear whether this was due to the drug or their depression. “It’s a puzzling question,” says Patricia Ducy at Columbia University, New York. But her team have now found that giving mice fluoxetine – the active ingredient in Prozac – for six weeks causes them to lose bone mass. The team identified a two-stage process by measuring bones, blood and gene activity. During the first three weeks, bones grew stronger as the fluoxetine impaired osteoclasts, cells that usually deplete bone tissue. But by six weeks, the higher levels of serotonin prompted by the drug disrupted the ability of the hypothalamus region of the brain to promote bone growth. “We see bone gain, but it’s not long-lasting, and is rapidly overwhelmed by the negative effects,” says Ducy. She says this two-phase pattern is also seen in people. In the short term, those who take fluoxetine are less likely to break a bone, but the risk of bone depletion and fractures rises when they have been taking the drug for a year or more. © Copyright Reed Business Information Ltd.
Link ID: 22630 - Posted: 09.06.2016
By Alison F. Takemura A stationary Carolina sphinx moth (Manduca sexta) is the Cinderella of the animal kingdom. The hummingbird-size insect has dull, dark wings that are mottled like charred wood, and a plump body reminiscent of a small breakfast sausage. Casual observers of M. sexta often see little else. “They say, ‘Oh, it doesn’t look so nice. It’s just grey.’ But as soon as [the moths] start flying, they’re completely impressed,” says Danny Kessler, a pollination ecologist at the Max Planck Institute of Chemical Ecology in Germany. “They change their minds completely.” Hawkmoths, the group to which M. sexta belongs, whir their wings like hummingbirds as they flit between flowers, hovering to drink nectar. M. sexta’s proboscis, longer than its 2-inch body, stays unfurled, a straw ready to sip. Kessler studies the interaction between the Carolina sphinx moth, whose larvae are known as tobacco hornworms, and its preferred food source, the coyote tobacco plant (Nicotiana attenuata), to better understand how insect behavior affects a plant’s reproductive success. M. sexta adults drink nectar from tobacco’s skinny, white, trumpet-shape flowers, foraging from them at night and pollinating them in the process. Scientists have known for decades that the moth uses its antennae to detect the flowers’ scent—even from several miles away, Kessler says. © 1986-2016 The Scientist
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22626 - Posted: 09.05.2016
ByAnna Vlasits The next revolution in medicine just might come from a new lab technique that makes neurons sensitive to light. The technique, called optogenetics, is one of the biggest breakthroughs in neuroscience in decades. It has the potential to cure blindness, treat Parkinson’s disease, and relieve chronic pain. Moreover, it’s become widely used to probe the workings of animals’ brains in the lab, leading to breakthroughs in scientists’ understanding of things like sleep, addiction, and sensation. So it’s not surprising that the two Americans hailed as inventors of optogenetics are rock stars in the science world. Karl Deisseroth at Stanford University and Ed Boyden at the Massachusetts Institute of Technology have collected tens of millions in grants and won millions in prize money in recent years. They’ve stocked their labs with the best equipment and the brightest minds. They’ve been lauded in the media and celebrated at conferences around the world. They’re considered all but certain to win a Nobel Prize. There’s only one problem with this story: It just may be that Zhuo-Hua Pan invented optogenetics first. Even many neuroscientists have never heard of Pan. Pan, 60, is a vision scientist at Wayne State University in Detroit who began his research career in his home country of China. He moved to the United States in the 1980s to pursue his PhD and never left. He wears wire-rimmed glasses over a broad nose framed by smile-lines in his cheeks. His colleagues describe him as a pure scientist: modest, dedicated, careful.
Keyword: Brain imaging
Link ID: 22625 - Posted: 09.03.2016
By LISA SANDERS, M.D. On Thursday, we challenged Well readers to take on the complicated case of a 50-year-old woman who felt feverish and couldn’t stop vomiting and who ended up losing a lot of weight. Like the doctors who saw her as she searched for a diagnosis, many of you focused on her recent journey to Kenya as the source of her symptoms. It was a completely reasonable approach, and one that was extensively explored by the doctors who cared for her. But ultimately it was incorrect. This was a really tough case. Indeed, only three of you got it right. The correct diagnosis was: Hyperthyroidism Thyroid hormone controls metabolism. The more of this hormone flowing in the body, the harder the body works. Because this hormone plays such an important role in how we function, the body tightly regulates how much of it is released and when. But just like every other system in the body, that regulatory mechanism can mess up, releasing either too little hormone (hypothyroidism) or, as in this case, too much. The usual symptoms of hyperthyroidism are pretty apparent: The heart races; patients are sweaty, shaky, itchy and sometimes feverish. The appetite increases, but because the entire body is revved up, there is often weight loss. Bowel movements become more frequent and sleep harder to come by. Frequent and uncontrolled vomiting is less common but has been reported. This patient had all of these symptoms. The most common cause of hyperthyroidism is an autoimmune disorder known as Graves’ disease, named after Dr. Robert Graves, a 19th-century Irish physician who wrote about the phenomenon of rapid and violent palpitations associated with an enlarged thyroid gland. In the 20th century it was discovered that the symptoms result when antibodies, the foot soldiers of the immune system, cause excess stimulation of the thyroid gland, resulting in the uncontrolled production and release of thyroid hormone. © 2016 The New York Times Company
Keyword: Hormones & Behavior
Link ID: 22624 - Posted: 09.03.2016
By JOHN P. GLUCK Albuquerque, N.M. — Five years ago, the National Institutes of Health all but ended biomedical and behavioral research on chimpanzees, concluding that, as the closest human relative, they deserved “special consideration and respect.” But chimpanzees were far from the only nonhuman primates used in research then, or now. About 70,000 other primates are still living their lives as research subjects in labs across the United States. On Wednesday, the N.I.H. will hold a workshop on “continued responsible research” with these animals. This sounds like a positive development. But as someone who spent decades working almost daily with macaque monkeys in primate research laboratories, I know firsthand that “responsible” research is not enough. What we really need to examine is the very moral ground of animal research itself. Like many researchers, I once believed that intermittent scientific gains justified methods that almost always did harm. As a graduate student in the late 1960s, I came to see that my natural recoil from intentionally harming animals was a hindrance to how I understood scientific progress. I told myself that we were being responsible by providing good nutrition, safe cages, skilled and caring caretakers and veterinarians for the animals — and, crucially, that what we stood to learn outweighed any momentary or prolonged anguish these animals might experience. The potential for a medical breakthrough, the excitement of research and discovering whether my hypotheses were correct — and let’s not leave out smoldering ambition — made my transition to a more “rigorous” stance easier than I could have imagined. One of my areas of study focused on the effects of early social deprivation on the intellectual abilities of rhesus monkeys. We kept young, intelligent monkeys separated from their families and others of their kind for many months in soundproof cages that remained lit 24 hours a day, then measured how their potential for complex social and intellectual lives unraveled. All the while, I comforted myself with the idea that these monkeys were my research partners, and that by creating developmental disorders in monkeys born in a lab, we could better understand these disorders in humans. © 2016 The New York Times Company
Keyword: Animal Migration
Link ID: 22622 - Posted: 09.03.2016
Laura Sanders An experimental drug swept sticky plaques from the brains of a small number of people with Alzheimer’s disease over the course of a year. And preliminary results hint that this cleanup may have staved off mental decline. News about the new drug, an antibody called aducanumab, led to excitement as it trickled out of recent scientific meetings. A paper published online August 31 in Nature offers a more comprehensive look at the drug’s effects. “Overall, this is the best news that we’ve had in my 25 years doing Alzheimer’s clinical research,” study coauthor Stephen Salloway of Brown University said August 30 at a news briefing. “It brings new hope for patients and families most affected by the disease.” The results are the most convincing evidence yet that an antibody can reduce amyloid in the brain, says Alzheimer’s researcherRachelle Doody of Baylor College of Medicine in Houston, who was not involved in the study. Still, experts caution that the results come from 165 people, a relatively small number. The seemingly beneficial effects could disappear in larger clinical trials, which are under way. “These new data are tantalizing, but they are not yet definitive,” says neuroscientist John Hardy of University College London. Like some other drug candidates for Alzheimer’s, aducanumab is an antibody that targets amyloid-beta, a sticky protein that accumulates in the brains of people with the disease. Delivered by intravenous injection, aducanumab appeared to get inside the brains of people with mild Alzheimer’s (average age about 73) and destroy A-beta plaques, the results suggest. After a year of exposure to the drug, A-beta levels had dropped. This reduction depended on the dose — the more drug, the bigger the decline in A-beta. In fact, people on the highest dose of the drug had almost no A-beta plaques in their brains after a year. |© Society for Science & the Public 2000 - 2016.
Link ID: 22621 - Posted: 09.01.2016
By CATHERINE SAINT LOUIS In seven countries that recently experienced Zika outbreaks, there were also sharp increases in the numbers of people suffering from a form of temporary paralysis, researchers reported Wednesday. The analysis, published online in The New England Journal of Medicine, adds to substantial evidence that Zika infections — even asymptomatic ones — may bring on a paralysis called Guillain-Barré syndrome. The syndrome can be caused by a number of other factors, including infection with other viruses. Researchers studying the Zika epidemic in French Polynesia had estimated that roughly 1 in 4,000 people infected with the virus could develop the syndrome. The Centers for Disease Control and Prevention has said that the Zika virus is “strongly associated” with Guillain-Barré, but has stopped short of declaring it a cause of the condition. The new data suggest a telling pattern: Each country in the study saw unusual increases in Guillain-Barré that coincided with peaks in Zika infections, the researchers concluded. “It’s pretty obvious that in all seven sites there is a clear relationship,” said Dr. Marcos A. Espinal, the study’s lead author and the director of communicable diseases at the Pan American Health Organization, which collected data on confirmed and suspected cases of Zika infection and on the incidence of Guillain-Barré. “Something is going on.” In Venezuela, officials expected roughly 70 cases of Guillain-Barré from December 2015 to the end of March 2016, as mosquitoes were spreading the virus. Instead, there were 684 cases. Similarly, during five months in which the Zika virus was circulating in Colombia, officials recorded 320 cases of Guillain-Barré when there should have been about 100. From September 2015 to March 2016, while Zika infections peaked in El Salvador, cases of Guillain-Barré doubled to 184 from 92. © 2016 The New York Times Company
Keyword: Movement Disorders
Link ID: 22618 - Posted: 09.01.2016
By JAMES GORMAN Who’s a good dog? Well, that depends on whom you’re asking, of course. But new research suggests that the next time you look at your pup, whether Maltese or mastiff, you might want to choose your words carefully. “Both what we say and how we say it matters to dogs,” said Attila Andics, a research fellow at Eotvos Lorand University in Budapest. Dr. Andics, who studies language and behavior in dogs and humans, along with Adam Miklosi and several other colleagues, reported in a paper to be published in this week’s issue of the journal Science that different parts of dogs’ brains respond to the meaning of a word, and to how the word is said, much as human brains do. Photo A dog waiting for its brain activity to be measured in a magnetic resonance imaging machine for research reported in the journal Science. Credit Enik Kubinyi As with people’s brains, parts of dogs’ left hemisphere react to meaning and parts of the right hemisphere to intonation — the emotional content of a sound. And, perhaps most interesting to dog owners, only a word of praise said in a positive tone really made the reward system of a dog’s brain light up. The experiment itself was something of an achievement. Dr. Andics and his colleagues trained dogs to enter a magnetic resonance imaging machine and lie in a harness while the machine recorded their brain activity. A trainer spoke words in Hungarian — common words of praise used by dog owners like “good boy,” “super” and “well done.” The trainer also tried neutral words like “however” and “nevertheless.” Both the praise words and neutral words were offered in positive and neutral tones. The positive words spoken in a positive tone prompted strong activity in the brain’s reward centers. All the other conditions resulted in significantly less action, and all at the same level. © 2016 The New York Times Company
Laurel Hamers The brains of human ancestors didn’t just grow bigger over evolutionary time. They also amped up their metabolism, demanding more energy for a given volume, a new study suggests. Those increased energy demands might reflect changes in brain structure and organization as cognitive abilities increased, says physiologist Roger Seymour of the University of Adelaide in Australia, a coauthor of the report, published online August 31 in Royal Society Open Science. Blood vessels passing through bones leave behind holes in skulls; bigger holes correspond to bigger blood vessels. And since larger vessels carry more blood, scientists can use hole size to estimate blood flow in extinct hominids’ brains. Blood flow in turn indicates how much energy the brain consumed. (In modern humans, the brain eats up 20 to 25 percent of the energy the body generates when at rest.) Seymour and colleagues focused on the carotid arteries, the vessels that deliver the bulk of the brain’s blood. The team looked at nearly three dozen skulls from 12 hominid species from the last 3 million years, including Australopithecus africanus, Homo neanderthalensis and Homo erectus. In each, the researchers compared the brain’s overall volume with the diameter of the carotid artery’s tiny entrance hole at the base of the skull. “We expected to find that the rate of blood flow was proportional to the brain size,” Seymour says. “But we found that wasn’t the case.” Instead, bigger brains required more blood flow per unit volume than smaller brains. |© Society for Science & the Public 2000 - 2016.
Link ID: 22616 - Posted: 08.31.2016
By Alison F. Takemura | In mice, severely restricting caloric intake promotes the transformation of white fat into brown fat, which contains cells that burn energy faster, according to a study published today (August 25) in Cell Metabolism. The innate immune system, researchers from the University of Geneva, Switzerland, and their colleagues reported, mediates this fat cell-transforming effect. “The paper nicely characterizes this phenomenon,” said Ajay Chawla of the University of California, San Francisco, who was not involved in the work. “And it mechanistically seems to identify a pathway that we had identified.” Whereas the present study found diet induced a “beiging” phenotype—in which white adipose tissue starts to express more energy-expending brown fat cells—Chawla and colleagues had previously shown that cold temperatures, another extreme condition, can produce the same effect. Scientists are keenly interested in learning how to generate brown fat cells. A treatment could help stem the obesity epidemic. “Finding some mechanism to activate this response—ideally, in obese or diabetic individuals—is really attractive,” said postdoctoral researcher Salvatore Fabbiano of the University of Geneva who led the present study. Several conditions are already known to make white fat tissue more brown—cold temperatures, microbe loss, and gastric bypass surgery among them. Fabbiano and colleagues hypothesized that the common feature of all these experiences was an increased expenditure of calories compared to intake. © 1986-2016 The Scientist
Link ID: 22615 - Posted: 08.31.2016
By RACHEL RABKIN PEACHMAN New research shows that athletes who leave the game immediately after a concussion recover twice as fast as athletes who keep playing. Credit Fabrizio Costantini for The New York Times High school athletes who kept playing in the minutes after a concussion took nearly twice as long to recover as those who left the game immediately after the head trauma, a new study shows. The finding, published in the journal Pediatrics, is believed to be the first to focus on one of the most difficult social challenges of treating concussions: a pervasive sports culture that encourages young athletes to keep playing through pain. Medical guidelines call for benching the athlete immediately after the head injury to prevent long-term complications and the potentially devastating consequences of a second hit. “Kids are often reluctant to acknowledge a concussion,” said Dawon Dicks, a youth football coach with CoachUp in Andover, Mass. “The kid may want a scholarship and want to go to college, or it could be that ‘Dad or Coach wants me to play.’ That’s when they’re going to start to be a little dishonest in what they’re truly feeling.” The latest study tracked the neurological symptoms of 69 athletes who visited the University of Pittsburgh Medical Center Sports Medicine Concussion Program after suffering head trauma during a contact sport. The athletes, who ranged from 12 to 19 years old, came from football, soccer, ice hockey, volleyball, field hockey, basketball, wrestling and rugby. The sample included 35 athletes who were removed from games right after getting a concussion and compared their symptoms and recovery to 34 athletes who kept playing in the game or match after taking a hit. The study found that players who stayed in the game after head trauma took an average of 44 days to recover. By comparison, athletes who left a game immediately after signs of concussion took only an average of 22 days to recover. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 22614 - Posted: 08.30.2016
By Will Boggs MD NEW YORK (Reuters Health) - Most adults in the U.S. who screen positive for depression are not being treated for depression, according to results from Medical Expenditure Panel Surveys (MEPS). "With the recent increase in prescribing of antidepressant medications, many physicians might assume that undertreatment of depression is no longer a widespread problem," Dr. Mark Olfson from College of Physicians and Surgeons, Columbia University and the New York State Psychiatric Institute in New York City told Reuters Health by email. "This study makes clear, however, that most American adults who screen positive for depression receive no treatment for their symptoms." Surveys from the early 2000s show that about half of U.S. adults with a lifetime medical history of major depressive disorder had never received treatment for depression. Still, little is known about the extent to which adults with depression in the U.S. receive depression care and the extent to which such patients are matched based on their illness severity to appropriate treatments and healthcare professionals. Dr. Olfson and colleagues used data from the 2012 and 2013 MEPS to examine the prevalence and treatment of adults with screen-positive depression (a Patient Health Questionnaire-2 score of 3 or less). They also assessed whether serious psychological distress was associated with more intensive treatment. © 2016 Scientific American
Link ID: 22613 - Posted: 08.30.2016
Laura Sanders Despite its name, the newly identified GluMI cell (pronounced “gloomy”) is no downer. It’s a nerve cell, spied in a mouse retina, that looks like one type of cell but behaves like another. Like neighboring retina nerve cells that subdue, or deaden, activity of other nerve cells, GluMI cells have a single arm extending from their body. But unlike those cells, GluMI cells actually seem to ramp up activity of nearby cells in a way that could aid vision. GLuMIs don’t seem to detect light firsthand, but they respond to it, Luca Della Santina of the University of Washington in Seattle and colleagues found. GluMIs are among a growing list of unexpected and mysterious cells found in the retinas of vertebrates, the researchers write August 8 in Current Biology. Citations L. Della Santina et al. Glutamatergic monopolar interneurons provide a novel pathway of excitation in the mouse retina. Current Biology. Vol. 26, August 8, 2016. doi:10.1016/j.cub.2016.06.016. |© Society for Science & the Public 2000 - 2016
Link ID: 22610 - Posted: 08.30.2016
By Daniel Engber In the spring of 2013, a 63-year-old social psychologist in Wurzburg, Germany, made a bold suggestion in a private email chain. For months, several dozen of his colleagues had been squabbling over how to double-check the scientific literature on “social priming,” the idea that even very subtle cues—the height of a chair, the temperature of a cup of coffee, the color of a printed word—can influence someone’s behavior or judgment. Now the skeptics in the group wanted volunteers: Who among the priming experts and believers would help them with a large-scale replication effort, in which a major finding would be tested in many different labs at once? Who—if anyone—would agree to put his research to this daunting test? The experts were reluctant to step forward. In recent months their field had fallen into scandal and uncertainty: An influential scholar had been outed as a fraud; certain bedrock studies—even so-called “instant classics”—had seemed to shrivel under scrutiny. But the rigidity of the replication process felt a bit like bullying. After all, their work on social priming was delicate by definition: It relied on lab manipulations that had been precisely calibrated to elicit tiny changes in behavior. Even slight adjustments to their setups, or small mistakes made by those with less experience, could set the data all askew. So let’s say another lab—or several other labs—tried and failed to copy their experiments. What would that really prove? Would it lead anyone to change their minds about the science?
Link ID: 22609 - Posted: 08.29.2016
Doctors describe 16-year-old Sebastian DeLeon as a walking miracle — he is only the fourth person in the U.S. to survive an infection from the so-called brain-eating amoeba. Infection from Naegleria fowleri is extremely rare but almost always fatal. Between 1962 and 2015, there were only 138 known infections due to the organism, according to the Centers for Disease Control and Prevention. Just three people survived. This summer, two young people, one in Florida and one in North Carolina, became infected after water recreation. Only one had a happy ending. DeLeon is a 16-year-old camp counselor. The Florida Department of Health thinks he got the infection while swimming in unsanitary water on private property in South Florida before his family came to visit Orlando's theme parks. So many things had to go right for DeLeon to survive. On a Friday, he had a bad headache. The next day, his parents decided this was way more than just a migraine and took him to the emergency room at Florida Hospital for Children. Doctors persuaded the family to do a spinal tap to rule out meningitis, even though he didn't have a stiff neck, the telltale symptom. Sheila Black, the lab coordinator, looked at the sample and assumed she saw white blood cells. But then she took a second, longer look. "We are all detectives," Black said. "We literally had to look at this and study it for a while and watch for the movement because the amoeba can look like a white cell. So unless you're actually visually looking for this and looking for the movement, you're going to miss it." © 2016 npr
Link ID: 22608 - Posted: 08.29.2016