Chapter 16. None

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By Jen Christiansen I threw down a bit of a challenge last month at the Association of Medical Illustrators Conference in Minnesota. But first, I had to—somewhat unexpectedly—accept some challenges presented by others. And face the reality that some of us simply do not have the constitution of an anatomist. I love classic anatomical illustrations such as the vintage works of Andreas Vesalius and the more modern stylings of Frank Netter. And on that front, this conference definitely delivered. Talks by Daniel Garrison and Francine Netter were drool-worthy, and I snapped photos of quickly advancing slides presented by W. Bruce Fye on the history of the illustrated heart, so I could reverse-image search them later and spend more time checking out the details and context. Videos of Robert Beverly Hale’s Art Students League lectures on anatomy charmed me (as presented by Glen Hintz), as well as new videos of clean architectural microstructures like the inner ear, presented by Robert Acland. I had to make myself walk quickly by one vendor table to avoid blowing my book budget for the year (and then some) on an impulse buy of Vesalius’ 1543 De Humani Corporis Fabrica, newly translated to English. But I averted my gaze when surgeons presented on the topic of facial transplantation and skull reconstruction. Shoot, I couldn’t even look at the screen through the entirety of a fascinating talk by Elizabeth Weissbrod and Valerie Henry on creating and using virtual and prosthetic simulations for military emergency response training. I avoided the hands-on human cadaveric dissection workshop sessions, telling myself and others that my travel schedule would simply not allow me to get to the Mayo Clinic in Rochester, Minn., early enough to participate or observe. © 2014 Scientific American

Keyword: Brain imaging
Link ID: 19957 - Posted: 08.14.2014

|By Melinda Wenner Moyer For most people, “fat,” particularly the kind that bulges under the skin, is a four-letter word. It makes our thighs jiggle; it lingers despite our torturous attempts to eliminate it. Too much of it increases our risk for heart disease and type 2 diabetes (the most common form of the condition). For decades researchers have looked for ways to reduce our collective stores of fat because they seemed to do more harm than good. But biology is rarely that simple. In the late 2000s several research groups independently discovered something that shattered the consensus about the absolute dangers of body fat. Scientists had long known that humans produce at least two types of fat tissue—white and brown. Each white fat cell stores energy in the form of a single large, oily droplet but is otherwise relatively inert. In contrast, brown fat cells contain many smaller droplets, as well as chestnut-colored molecular machines known as mitochondria. These organelles in turn burn up the droplets to generate heat. Babies, who have not yet developed the ability to shiver to maintain their body temperature, rely on thermogenic deposits of brown fat in the neck and around the shoulders to stay warm. Yet investigators assumed that all brown fat disappears during childhood. The new findings revealed otherwise. Adults have brown fat, too. Suddenly, people started throwing around terms like holy grail to describe the promise of brown fat to combat obesity. The idea was appealingly simple: if researchers could figure out how to incite the body to produce extra brown fat or somehow rev up existing brown fat, a larger number of calories would be converted into heat, reducing deposits of white fat in the process. © 2014 Scientific American

Keyword: Obesity
Link ID: 19953 - Posted: 08.13.2014

By GRETCHEN REYNOLDS Regular exercise may alter how a person experiences pain, according to a new study. The longer we continue to work out, the new findings suggest, the greater our tolerance for discomfort can grow. For some time, scientists have known that strenuous exercise briefly and acutely dulls pain. As muscles begin to ache during a prolonged workout, scientists have found, the body typically releases natural opiates, such as endorphins, and other substances that can slightly dampen the discomfort. This effect, which scientists refer to as exercise-induced hypoalgesia, usually begins during the workout and lingers for perhaps 20 or 30 minutes afterward. But whether exercise alters the body’s response to pain over the long term and, more pressing for most of us, whether such changes will develop if people engage in moderate, less draining workouts, have been unclear. So for the new study, which was published this month in Medicine & Science in Sports & Exercise, researchers at the University of New South Wales and Neuroscience Research Australia, both in Sydney, recruited 12 young and healthy but inactive adults who expressed interest in exercising, and another 12 who were similar in age and activity levels but preferred not to exercise. They then brought all of them into the lab to determine how they reacted to pain. Pain response is highly individual and depends on our pain threshold, which is the point at which we start to feel pain, and pain tolerance, or the amount of time that we can withstand the aching, before we cease doing whatever is causing it. © 2014 The New York Times Company

Keyword: Pain & Touch
Link ID: 19952 - Posted: 08.13.2014

By EDWARD LARKIN and IRENE HURFORD PHILADELPHIA — A FEW months ago, a patient came to our hospital, seeking help. One of us, Edward, was on the team that treated him. He was pleasant, if slightly withdrawn, and cogent. He was a college graduate in his 20s and had recently been fired from his job as a high school math teacher, because of unexpected absences. He had come to believe that government agents were conspiring against him, and he had taken to living out of a truck and sleeping in different parking lots. By the time he came to us, he was exhausted. A diagnosis became clear: he had schizophrenia. We admitted him to the hospital, and after a few days, with his symptoms under control, we released him. Unfortunately, we prescribed a medication for him that could cause significant, permanent harm, instead of an equally effective drug with milder side effects — all because he was uninsured. Schizophrenia, which affects 1 percent of the population and emerges in the late teens to early 20s, is deeply misunderstood. People who suffer from it are often suspected of being dangerous, but this is not usually the case, and antipsychotic drugs are very effective. Our patient was exactly the kind of person who, with the right treatment, could have weakened the stigma surrounding schizophrenia. Antipsychotic drugs fall into two classes: the older ones, like Haldol, and newer ones, like Abilify and Latuda. Both classes are equally effective at treating some of the worst symptoms of schizophrenia, specifically the hallucinations, delusions and paranoia that cause social alienation. (They’re not effective for treating “negative symptoms,” like low motivation.) But the older drugs can cause a multitude of serious side effects, including a potentially devastating one called tardive dyskinesia. This condition involves unsettling, animalistic smacking and wagging of the lips and tongue. At its extreme, it can affect the entire body. It occurs in 20 percent or more of patients who take the drugs long-term, and it tends to start so mildly that patients can’t identify it in time to stop taking the drugs. It is often irreversible. © 2014 The New York Times Company

Keyword: Schizophrenia
Link ID: 19950 - Posted: 08.13.2014

By MICHAEL CIEPLY and BROOKS BARNES LOS ANGELES — Peering through his camera at Robin Williams in 2012, the cinematographer John Bailey thought he glimpsed something not previously evident in the comedian’s work. They were shooting the independent film “The Angriest Man in Brooklyn,” and Mr. Williams was playing a New York lawyer who, facing death, goes on a rant against the injustice and banality of life. His performance, Mr. Bailey said Tuesday, was a window into the “Swiftian darkness of Robin’s heart.” The actor, like his character, was raging against the storm. That defiance gave way on Monday to the personal demons that had long tormented Mr. Williams. With his suicide at age 63, Mr. Williams forever shut the window on a complicated soul that was rarely visible through the cracks of an astonishingly intact career. Given his well-publicized troubles with depression, addiction, alcoholism and a significant heart surgery in 2009, Mr. Williams should have had a résumé filled with mysterious gaps. Instead, he worked nonstop. At the very least — if his life had followed the familiar script of troubled actors — there would have been whispers of on-set antics: lateness, forgotten lines, the occasional flared temper. Not so with Mr. Williams. “He was ready to work, he was the first one on the set,” said Mr. Bailey, speaking of Mr. Williams’s contribution to “The Angriest Man in Brooklyn,” of which he was the star. “Robin was always 1,000 percent reliable,” said a senior movie agent, speaking on the condition of anonymity to conform to the wishes of Mr. Williams’s family. “He was almost impossibly high functioning.” As Hollywood struggled on Tuesday to understand how Mr. Williams — effervescent in the extreme — could take his own life, authorities released details of his death. A clothed Mr. Williams hanged himself with a belt from a door frame in his bedroom in Tiburon, Calif., according to Lt. Keith Boyd, assistant deputy chief coroner for Marin County. © 2014 The New York Times Company

Keyword: Depression
Link ID: 19948 - Posted: 08.13.2014

Jia You Premature babies are more likely to produce piercing cries than their full-term peers are, researchers report online today in Biology Letters. Scientists have studied infant crying as a noninvasive way to assess how well a baby’s nervous system develops. Previous research of full-term babies indicates that an abnormally high pitch is associated with disturbances in an infant’s metabolism and neurological development. The team recorded spontaneous crying in preterm babies and full-term babies of the same age and compared the pitch of their sobs. They found that preterm babies whimper in a shriller voice, but not because they are smaller in size or grew at a slower rate in their mothers’ wombs. Instead, the researchers suspect the high pitch could reflect lower levels of activities in a premature baby’s vagal nerve, which extends from the brain stem to the abdomen. Vagal nerve activities are believed to decrease tension in the vocal cords, thus producing a lower pitch. Previous studies show that giving preterm babies massage therapies can stimulate their vagal activities, improve their ingestion, and help them gain weight. © 2014 American Association for the Advancement of Science

Keyword: Development of the Brain
Link ID: 19946 - Posted: 08.13.2014

James Gorman Deep in the mouse brain, scientists recently found that a very small network of cells, a few thousand at most, turns appetite on and off. They used the most sophisticated of modern techniques, but as has often happened in science — witness penicillin, Velcro and Viagra — the researchers discovered something they weren’t looking for. “This was an accidental discovery,” said David Anderson, of the California Institute of Technology, the senior scientist on the team that reported the finding, in Nature Neuroscience. The discovery may eventually lead to a better understanding and treatment of eating disorders. The surprise and drama of the finding are immediately clear, however, in lab videos. A mouse busily munches lab chow until a light signal is sent to its brain, and the mouse wanders off, no longer interested in food. His lab had previously studied this small group of neurons, in a part of the brain called the amygdala. That earlier research was on fear, an emotion strongly associated with the amygdala in both mice and humans. As a technique called optogenetics became more and more refined, he said, it seemed worth revisiting the neurons with this new tool. Optogenetics requires genetic manipulation of specific cells to make them sensitive to light in a certain wavelength, in this case blue light. Then fiber-optic cables are inserted into the brain, and when the light is turned on, neurons can be activated or turned off. Researchers in Dr. Anderson’s lab, including Haijiang Cai, a postdoctoral researcher and a co-author of the report, prepared the mice and conducted the experiment with the entirely unexpected result. © 2014 The New York Times Company

Keyword: Obesity
Link ID: 19945 - Posted: 08.12.2014

By Rachel Feltman Bioengineers have created the most realistic fake brain tissue ever – and it’s built like a jelly doughnut. The 3-D tissue, described in a paper published Monday in Proceedings of the National Academy of Sciences, is so structurally similar to a real rat brain (a common substitute for human brains in the lab) that it could help scientists answer longstanding questions about brain injuries and disease. Currently, the best way to study brain tissue is to grow neurons in a petri dish, but those neurons can only be grown flat. A real brain contains a complicated structure of 3-D tissue. Simply giving the neurons room to grow in three dimensions didn’t prove successful: While neurons will grow into more complicated structures in the right kind of gel, they don’t survive very long or mimic the structure of a real brain. Led by David Kaplan, the director of the Tissue Engineering Resource Center at Tufts University, researchers developed a new combination of materials to mimic the gray and white matter of the brain. The new model relies on a doughnut-shaped, spongy scaffold made of silk proteins with a collagen-based gel at the center. The outer scaffold layer, which is filled with rat neurons, acts as the grey matter of the brain. As the neurons grew networks throughout the scaffold, they sent branches out across the gel-filled center to connect with neurons on the other side. And that configuration is about as brain-like as lab-grown tissue can get. The basic structure can be reconfigured, too.

Keyword: Robotics; Aggression
Link ID: 19944 - Posted: 08.12.2014

By PAM BELLUCK The 40-year-old man showed up in Dr. Mary Malloy’s clinic with sadly disfiguring symptoms. His hands, elbows, ears and feet were blemished with protruding pustules and tuber-like welts, some so painful it was hard for him to walk. He suffered from a rare genetic condition called dysbetalipoproteinemia, which caused his cholesterol levels to soar so high that pools of fatty tissue seemed to bubble up under his skin. But there was something else about this patient. He was missing a gene that, when present in one form, greatly increases the risk of developing Alzheimer’s disease. Dr. Malloy, who co-directs the Adult Lipid Clinic at the University of California, San Francisco, and her colleagues saw an opportunity to answer an important neurological riddle: Does the absence of the gene — named apolipoprotein E, or APOE, after the protein it encodes — hurt the brain? If a person with this rare condition were found to be functioning normally, that would suggest support for a new direction in Alzheimer’s treatment. It would mean that efforts — already being explored by dementia experts — to prevent Alzheimer’s by reducing, eliminating or neutralizing the effects of the most dangerous version of APOE might succeed without causing other problems in the brain. The researchers, who reported their findings on Monday in the journal JAMA Neurology, discovered exactly that. They ran a battery of tests, including cognitive assessments, brain imaging and cerebrospinal fluid analyses. The man’s levels of beta-amyloid and tau proteins, which are markers of Alzheimer’s, gave no indication of neurological disease. His brain size was unaffected, and the white matter was healthy. His thinking and memory skills were generally normal. “This particular case tells us you can actually live without any APOE in the brain,” said Dr. Joachim Herz, a neuroscientist and molecular geneticist at University of Texas Southwestern Medical Center, who was not involved in the research. “So if they were to develop anti-APOE therapies for Alzheimer’s, we would not have to worry about serious neurological side effects.” © 2014 The New York Times Company

Keyword: Alzheimers
Link ID: 19943 - Posted: 08.12.2014

By ZACH SCHONBRUN EAST RUTHERFORD, N.J. — Victor Cruz dumped a bucket of ice water on his head at home on Sunday and then stepped out on thin ice himself — challenging the Giants’ co-owners to do the same. Taking part in the Ice Bucket Challenge — a social media craze that raises awareness for Lou Gehrig’s disease (amyotrophic lateral sclerosis) — Cruz, a wide receiver, posted the video on his Twitter feed. “That water was cold, man,” Cruz said Monday. The Ice Bucket Challenge was started by friends and family members of Pete Frates, a 29-year-old from Beverly, Mass., who played baseball at Boston College and was found to have A.L.S., a neurodegenerative condition, in 2012. As a reward for withstanding the icy punishment, the participant gets to nominate another person, who has 24 hours to complete the task. Cruz aimed high, calling out the co-owners John Mara and Steve Tisch to step under the bucket themselves. Just before practice on Monday, the 59-year-old Mara, wearing a white Giants T-shirt and black shorts, allowed Cruz to dump a Gatorade tub filled with ice water over his head. Before doing so, Mara nominated the Jets’ owner, Woody Johnson; the Patriots’ owner, Robert K. Kraft; and Patriots Coach Bill Belichick to do the same. “Feels good,” a smiling Mara said in a video posted on the Giants’ team website. It is unclear if Tisch will follow suit. Those who fail to complete the task within 24 hours are asked to donate to A.L.S. research. © 2014 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 19937 - Posted: 08.12.2014

|By William Skaggs One of the most frustrating and mysterious medical conditions affecting the mind is impaired consciousness, as can occur with brain damage. Patients in a coma or a vegetative or minimally conscious state sometimes spontaneously recover to varying degrees, but in most cases there is little that doctors can do to help. Now a rigorous study by a group at Liège University Hospital Center in Belgium has found that a simple treatment called transcranial direct-current stimulation (tDCS) can temporarily raise awareness in minimally conscious patients. In tDCS, electrodes are glued to the scalp, and a weak electric current is passed through them to stimulate the underlying brain tissue. Scientists led by neurologist Steven Laureys applied the electric current for 20 minutes to patients' left prefrontal cortex, an area known to be involved in attentiveness and working memory. Afterward, the effects on consciousness were measured by doctors who did not know whether the patient had received real tDCS or a sham treatment, in which the apparatus ran, but no current was delivered. For patients in a vegetative state, who display no communication or purposeful behavior, the stimulation might have led to improvement in two patients, but no statistically compelling evidence emerged. Yet 13 of 30 patients in a minimally conscious state—defined by occasional moments of low-level awareness—showed measurable gains in their responses to questions and sensory stimuli. Some had only recently been injured, but others had been minimally conscious for months. © 2014 Scientific American

Keyword: Consciousness
Link ID: 19934 - Posted: 08.11.2014

By SERGE F. KOVALESKI Nearly four years ago, Dr. Sue Sisley, a psychiatrist at the University of Arizona, sought federal approval to study marijuana’s effectiveness in treating military veterans with post-traumatic stress disorder. She had no idea how difficult it would be. The proposal, which has the support of veterans groups, was hung up at several regulatory stages, requiring the research’s private sponsor to resubmit multiple times. After the proposed study received final approval in March from federal health officials, the lone federal supplier of research marijuana said it did not have the strains the study needed and would have to grow more — potentially delaying the project until at least early next year. Then, in June, the university fired Dr. Sisley, later citing funding and reorganization issues. But Dr. Sisley is convinced the real reason was her outspoken support for marijuana research. “They could never get comfortable with the idea of this controversial, high-profile research happening on campus,” she said. Dr. Sisley’s case is an extreme example of the obstacles and frustrations scientists face in trying to study the medical uses of marijuana. Dating back to 1999, the Department of Health and Human Services has indicated it does not see much potential for developing marijuana in smoked form into an approved prescription drug. In guidelines issued that year for research on medical marijuana, the agency quoted from an accompanying report that stated, “If there is any future for marijuana as a medicine, it lies in its isolated components, the cannabinoids and their synthetic derivatives.” Scientists say this position has had a chilling effect on marijuana research. © 2014 The New York Times Company

Keyword: Drug Abuse
Link ID: 19933 - Posted: 08.11.2014

by Aviva Rutkin What can the human brain do for a computer? There's at least one team of researchers that thinks it might have the answer. Working at IBM Research–Almaden in San Jose, California, they have just released more details of TrueNorth, a computer chip composed of one million digital "neurons". Under way for several years, the project abandons traditional computer architecture for one inspired by biological synapses and axons. The latest results, published in Science, provide a timely reminder of the promise of brain-inspired computing. The human brain still crushes any modern machines when it comes to tasks like vision or voice recognition. What's more, it manages to do so with less energy than it takes to power a light bulb. Building those qualities into a computer is an alluring prospect to many researchers, like Kwabena Boahen of Stanford University in California. "The first time I learned how computers worked, I thought it was ridiculous," he says. "I basically felt there had to be a better way." Aping the brain's structure could help us build computers that are far more powerful and efficient than today's, says TrueNorth team leader Dharmendra Modha. "We want to approximate the anatomy and physiology, the structure and dynamics of the brain, within today's silicon technology," he says. "I think that the chip and the associated ecosystem have the potential to transform science, technology, business, government and society." But how best to go about building a proper artificial brain is a matter of debate. © Copyright Reed Business Information Ltd

Keyword: Robotics
Link ID: 19932 - Posted: 08.09.2014

Posted by Ewen Callaway More than 130 leading population geneticists have condemned a book arguing that genetic variation between human populations could underlie global economic, political and social differences. “A Troublesome Inheritance“, by science journalist Nicholas Wade, was published in June by Penguin Press in New York. The 278-page work garnered widespread criticism, much of it from scientists, for suggesting that genetic differences (rather than culture) explain, for instance, why Western governments are more stable than those in African countries. Wade is former staff reporter and editor at the New York Times, Science and Nature. But the letter — signed by a who’s who of population genetics and human evolution researchers, and to be published in the 10 August New York Times — represents a rare unified statement from scientists in the field and includes many whose work was cited by Wade. “It’s just a measure of how unified people are in their disdain for what was done with the field,” says Michael Eisen, a geneticist at the University of California, Berkeley, who co-drafted the letter. “Wade juxtaposes an incomplete and inaccurate explanation of our research on human genetic differences with speculation that recent natural selection has led to worldwide differences in I.Q. test results, political institutions and economic development. We reject Wade’s implication that our findings substantiate his guesswork. They do not,” states the letter, which is a response to a critical review of the book published in the New York Times. “This letter is driven by politics, not science,” Wade said in a statement. “I am confident that most of the signatories have not read my book and are responding to a slanted summary devised by the organizers.” © 2014 Macmillan Publishers Limited

Keyword: Genes & Behavior
Link ID: 19931 - Posted: 08.09.2014

Simon Makin Fish that have been exposed to a common anti-anxiety drug are more active and have better chances of survival than unexposed fish, researchers report in Environmental Research Letters1. The results suggest that standard methods for assessing the environmental impact of pharmaceuticals in waterways might miss some of the drugs' effects because they focus exclusively on harms, according to the authors. In the study, researchers led by Jonatan Klaminder at Umeå University in Sweden exposed Eurasian perch (Perca fluviatilis) to oxazepam, one of a widely used class of anti-anxiety drugs called benzodiazepines. Standard ecotoxicology experiments use unstressed, healthy fish that have been bred in labs. Control groups are designed to have 100% survival rates so that decreases in survival in the test group are easy to detect by comparison. But it is difficult to detect any increase in survival rates when the control group already has nearly complete survival. So Klaminder and his colleagues used the opposite approach. They exposed fish to the drug at two sensitive life stages: two-year-old wild fish taken from a Swedish lake that had only recently thawed after winter, and strings of roes — fish eggs that contain embryos undergoing development. These are more realistic conditions, the researchers say, as animals in the wild often experience high mortality. The researchers used oxazepam at a high concentration of 1,000 micrograms per litre and at a low concentration of 1 μg l−1. The low dose is relevant to aquatic environments in urban areas, because oxazepam concentrations of 1.9 μg l−1 have been measured in effluents from wastewater treatment plants. © 2014 Nature Publishing Group,

Keyword: Stress
Link ID: 19928 - Posted: 08.09.2014

By Emily Underwood The early signs of Creutzfeldt-Jakob disease (CJD)—a rare, incurable brain disorder caused by infectious, misshapen proteins called prions—are difficult to interpret. At first, people may simply feel depressed and can undergo personality changes or bouts of psychosis. By the time memory failure, blindness, and coma set in, typically within a year of infection, death is usually imminent. Now, researchers report that a simple nasal swab may help physicians detect the disease far more accurately and earlier than current methods. Finding simple, noninvasive diagnostic tests is “one of the holy grails” for CJD and other prion diseases, says biochemist Byron Caughey of the National Institute of Allergy and Infectious Diseases’ Rocky Mountain Laboratories in Hamilton, Montana, who helped lead the new work. Although there’s no cure for CJD, early diagnosis is important because it can help rule out other, treatable disorders, and it allows medical personnel to take precautions that prevent the disease from spreading to others through exposure to brain tissue or spinal fluid, he says. Researchers made a major stride toward better diagnostic methods in 2010, when Caughey and other researchers first described a new technique called the RT-QuIC test. The test requires removing cerebrospinal fluid (CSF) from patients by means of a spinal tap, putting samples into a bath of normally shaped prion proteins, and agitating the solution to encourage any abnormal prion “seeds” in the tissue to latch onto the regular proteins. If even trace amounts of pathogenic protein are present, they rapidly use the normal proteins to create millions of insoluble, fibrous amyloid strands. Researchers believe that these amyloid aggregates, also seen in other neurodegenerative diseases such as Alzheimer’s disease, ultimately cause CJD by interfering with or killing off neurons en masse. After death, the brains of people affected by CJD are so badly damaged that they often resemble Swiss cheese or sponges. © 2014 American Association for the Advancement of Science.

Keyword: Prions
Link ID: 19926 - Posted: 08.07.2014

Ian Sample, science correspondent The human brain can judge the apparent trustworthiness of a face from a glimpse so fleeting, the person has no idea they have seen it, scientists claim. Researchers in the US found that brain activity changed in response to how trustworthy a face appeared to be when the face in question had not been consciously perceived. Scientists made the surprise discovery during a series of experiments that were designed to shed light on the the neural processes that underpin the snap judgments people make about others. The findings suggest that parts of our brains are doing more complex subconscious processing of the outside world than many researchers thought. Jonathan Freeman at New York University said the results built on previous work that shows "we form spontaneous judgments of other people that can be largely outside awareness." The study focused on the activity of the amygdala, a small almond-shaped region deep inside the brain. The amygdala is intimately involved with processing strong emotions, such as fear. Its central nucleus sends out the signals responsible for the famous and evolutionarily crucial "fight-or-flight" response. Prior to the study, Freeman asked a group of volunteers to rate the trustworthiness of a series of faces. People tend to agree when they rank trustworthiness – faces with several key features, such as more furrowed brows and shallower cheekbones, are consistently rated as less trustworthy. Freeman then invited a different group of people to take part in the experiments. Each lay in an MRI scanner while images of faces flashed up on a screen before them. Each trustworthy or untrustworthy face flashed up for a matter of milliseconds. Though their eyes had glimpsed the images, the participants were not aware they had seen the faces. © 2014 Guardian News and Media Limited

Keyword: Attention
Link ID: 19924 - Posted: 08.07.2014

The gurgles made by a hungry belly are familiar to us all, but they are not just the side effect of an empty stomach. Brain cells not normally associated with communication send out a signal when they detect blood glucose levels are running low, and this triggers the stomach contractions. Richard Rogers of the Pennington Biomedical Research Center at Louisiana State University and colleagues used a drug called fluorocitrate to knock out the function of certain astrocytes and neurons in the brains of rats, blocking the sensation of hunger. Only when astrocyte function was restored did the gastric grumbles return, showing that it is these cells that respond to low glucose levels (Journal of Neuroscience, DOI: 10.1523/JNEUROSCI.1406-14.2014). The feeling of discomfort you get when hungry is called "hypoglycaemia awareness". "For most people this is only slightly unpleasant, but for diabetics whose glucose levels can drop significantly, [being hungry] can be dangerous," says Rogers. "It's important to understand how this mechanism works." © Copyright Reed Business Information Ltd.

Keyword: Obesity; Aggression
Link ID: 19922 - Posted: 08.07.2014

Sarah C. P. Williams Every fall, grizzly bears pack on the pounds in preparation for their winter hibernation. In humans, such extreme weight gain would likely lead to diabetes or other metabolic diseases, but the bears manage to stay healthy year after year. Their ability to remain diabetes-free, researchers have now discovered, can be chalked up to the shutting down of a protein found in fat cells. The discovery could lead to new diabetes drugs that turn off the same pathway in humans. The findings are “provocative and interesting,” says biologist Sandy Martin of the University of Colorado, Denver, who was not involved in the new work. “They found a natural solution to a problem that we haven’t been able to solve.” As people gain weight, fat, liver, and muscle cells typically become less sensitive to the hormone insulin—which normally helps control blood sugar levels—and insulin levels rise. In turn, that increased insulin prevents the breakdown of fat cells, causing a vicious cycle that can lead to full-blown insulin resistance, or diabetes. Developing new diabetes drugs has been hampered by the fact that findings from many mouse models of diabetes have not translated to humans. So Kevin Corbit, a senior scientist at Thousand Oaks, California–based drug company Amgen, decided to start looking at obesity and metabolic disease in other animals. “When I was thinking about things that are quite fat, one of the first things I thought of was bears, and what they do to prepare to go into hibernation,” he says. “But of course you don’t see bears running around with diabetes and heart disease.” © 2014 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 19919 - Posted: 08.06.2014

Claudia M. Gold In the course of working on my new book about listening to parents and children, I have had the pleasure of immersing myself in the writing of D.W. Winnicott, pediatrician turned psychoanalyst. Winnicott's professional life included both caring for countless young children and families as a pediatrician, and psychoanalytic practice, where his adult patients "regressed to dependence," giving him an opportunity to interact with their infantile qualities, but with adult capacities for communication. This combination of experiences gave him a unique vantage point from which to make his many brilliant observations about children and the nature of the parent-child relationship. A recent New York Times Magazine article on autism prompted me to share his words of wisdom on the subject, which, though written in 1966, still have relevance today. The following is from a collection of papers, Thinking About Children: From my point of view the invention of the term autism was a mixed blessing...I would like to say that once this term has been invented and applied, the stage was set for something which is slightly false, i.e. the discovery of a disease…Pediatricians and physically minded doctors as a whole like to think in terms of diseases which gives a tidy look to the textbooks... The unfortunate thing is that in matters psychological things are not like that. Winnicott implores the reader to instead understand the child in relational and developmental context. He writes: The subject quickly becomes one not of autism and not of the early roots of a disorder that might develop in to autism, but rather one of the whole story of human emotional development and the relationship of the process in the individual child to the environmental provision which may or may not in any one particular case facilitate the maturational process. ©2014 Boston Globe Media Partners, LLC

Keyword: Autism
Link ID: 19915 - Posted: 08.05.2014