Brian Owens The hordes of microbes that inhabit every nook and cranny of every animal are not just passive hitchhikers: they actively shape their hosts’ well-being and even behaviour. Now, researchers have found evidence that bacteria living in the scent glands of hyenas help to produce the smells that the animals use to identify group members and tell when females are ready to mate. Kevin Theis, a microbial ecologist at Michigan State University in East Lansing, had been studying hyena scent communication for several years when, after he gave a talk on the subject, someone asked him what part the bacteria might play. “I just said, ‘I don’t know’,” he says. He started investigating. He found that for 40 years, scientists had wondered whether smelly bacteria were involved in animals' chemical communication. But experiments to determine which bacteria were present had been inconclusive, because the microbes had to be grown in culture, which is not possible with all bacteria. However, next-generation genetic sequencing would enable Theis to identify the microbes in a sample without having to grow them in a dish. Using this technique, Theis and his colleagues last year published a study1 that identified more types of bacterium living in the hyenas’ scent glands than the 15 previous studies of mammal scent glands combined. In both spotted hyenas (Crocuta crocuta) and striped hyenas (Hyaena hyaena), most of the bacteria were of a kind that ferments nutrients exuded by the skin and produces odours. “The diversity of the bacteria is enough to potentially explain the origin of these signals,” says Theis. Now, they have found that the structure of the bacterial communities varied depending on the scent profiles of the sour, musky-smelling 'pastes' that the animals left on grass stalks to communicate with members of their clan. In addition, in the spotted hyenas, both the bacterial and scent profiles varied between males and females, and with the reproductive state of females — all attributes that hyenas are known to be able to infer from scent pastes. The work is published this week in Proceedings of the National Academy of Sciences. © 2013 Nature Publishing Group

Keyword: Chemical Senses (Smell & Taste); Sexual Behavior
Link ID: 18915 - Posted: 11.12.2013

By PAM BELLUCK It is probably no accident that the pivotal object in Martin Cruz Smith’s newest detective thriller, “Tatiana,” is a notebook nobody can read. Early on, Mr. Smith worried that his novel, being published Tuesday by Simon & Schuster, would be unreadable too — or wouldn’t be written at all. Author of the 1981 blockbuster “Gorky Park” and many acclaimed books since, Mr. Smith writes about people who uncover and keep secrets. But for 18 years, he has had a secret of his own. In 1995, he received a diagnosis of Parkinson’s disease. But he kept it hidden, not only from the public, but from his publisher and editors. He concealed it, although for years, tremors and stiffness have kept him from taking detailed notes and sketching people, places and objects for his research — and even as he became unable to type the words he needed to finish his 2010 best seller “Three Stations.” “I didn’t want to be judged by that,” Mr. Smith, 71, explained recently in his light-filled Victorian home north of San Francisco. “Either I’m a good writer or I’m not. ‘He’s our pre-eminent Parkinson’s writer.’ Who needs that?” In talking about his Parkinson’s odyssey, including a relatively new but promising treatment, Mr. Smith is opening a window on the still incurable disorder affecting four million people worldwide, a disease that is becoming increasingly prevalent as baby boomers age. His experience reflects a common desire to conceal often-stigmatizing symptoms, like shaking, slowness, and rigidity. (He mostly didn’t mind his Parkinsonian hallucinations: a black cat in his lap, whirlwinds spiraling from computer keys, a butler, a British military officer in full regalia. “Having hallucinations for a fiction writer is redundant,” he said.) Copyright 2013 The New York Times Company

Keyword: Parkinsons
Link ID: 18914 - Posted: 11.12.2013

By Michelle Roberts Health editor, BBC News online Depression can make us physically older by speeding up the ageing process in our cells, according to a study. Lab tests showed cells looked biologically older in people who were severely depressed or who had been in the past. These visible differences in a measure of cell ageing called telomere length couldn't be explained by other factors, such as whether a person smoked. The findings, in more than 2,000 people, appear in Molecular Psychiatry. Experts already know that people with major depression are at increased risk of age-related diseases such as cancer, diabetes, obesity and heart disease. This might be partly down to unhealthy lifestyle behaviours such as alcohol use and physical inactivity. But scientists suspect depression takes its own toll on our cells. To investigate, Josine Verhoeven from the VU University Medical Centre in the Netherlands, along with colleagues from the US, recruited 2,407 people to take part in the study. More than one third of the volunteers were currently depressed, a third had experienced major depression in the past and the rest had never been depressed. The volunteers were asked to give a blood sample for the researchers to analyse in the lab for signs of cellular ageing. The researchers were looking for changes in structures deep inside cells called telomeres. BBC © 2013

Keyword: Depression
Link ID: 18913 - Posted: 11.12.2013

By PAULA SPAN Jim Cooke blames his hearing loss on the constant roar of C-119 aircraft engines he experienced in the Air Force. He didn’t wear protective gear because, like most 20-year-olds, “you think you’re indestructible,” he said. By the time he was 45, he needed hearing aids for both ears. Still, he had a long career as a telephone company executive while he and his wife, Jean, raised two children in Broadview Heights, Ohio. Only after retirement, he told me in an interview, did he start having trouble communicating. Jean and Jim Cooke Jean and Jim Cooke Mr. Cooke had to relinquish a couple of part-time jobs he enjoyed because “I felt insecure about dealing with people on the phone,” he said. He withdrew from a church organization he led because he couldn’t grasp what members were saying at meetings. “He didn’t want to be in social situations,” Mrs. Cooke said. “It gave him a feeling of inadequacy, and anger at times.” Two years ago, when their grandchildren began saying that Granddad needed to replace his hearing aid batteries — although the batteries were fine — the Cookes went to the Cleveland Clinic, where an audiologist there, Dr. Sarah Sydlowski, told Jim that at 76, he might consider a cochlear implant. Perhaps the heart-tugging YouTube videos of deaf toddlers suddenly hearing sounds have led us to think of cochlear implants as primarily for children. Or perhaps, said Dr. Frank R. Lin, a Johns Hopkins University epidemiologist, we consider late-life hearing loss normal (which it is), “an unfortunate but inconsequential aspect of aging,” and don’t explore treatment beyond hearing aids. In any case, the idea of older adults having a complex electronic device surgically implanted has been slow to catch on, even though by far the greatest number of people with severe hearing loss are seniors. © 2013 The New York Times Company

Keyword: Hearing; Robotics
Link ID: 18912 - Posted: 11.12.2013

by Ashley Yeager The compound that gives mold its musty smell can cause changes in fruit flies’ brains that mimic those of patients with Parkinson’s disease. Scientists do not know the exact cause of Parkinson’s disease, but studies have shown that exposure to human-made chemicals may be a risk factor for developing the movement disorder. Now researchers have found that the chemical 1-octen-3-ol, which mold naturally emits, kills flies’ brain cells that transmit dopamine, a compound involved in controlling movement. The mold molecule also reduces dopamine levels in the flies’ brains. In experiments with human cells, the mold chemical also blocked the cells from taking in dopamine, researchers report November 11 in the Proceedings of the National Academy of Sciences. The results offer insight into cases of movement problems that doctors have associated with fungi exposure, the scientists say. © Society for Science & the Public 2000 - 2013

Keyword: Movement Disorders; Neurotoxins
Link ID: 18911 - Posted: 11.12.2013

SAN DIEGO, CALIFORNIA—How do we recognize emotions in the facial expressions of others? A small, almond-shaped structure called the amygdala, located deep within the brain (yellow in image above), plays a key role, but exactly what it responds to is unclear. To learn more, neuroscientists implanted electrodes into the amygdalae of seven epileptic patients who were about to undergo brain surgery for their condition. They recorded the activity of 200 single amygdala neurons and determined how they responded while the patients viewed photographs of happy and fearful faces. The team found a subset of cells that distinguish between what the patients thought to be happy and fearful faces, even when they perceived ambiguous facial expressions incorrectly. (The team carefully manipulated some of the photos of fearful faces, so that some of the subjects perceived them as being neutral.) The findings, presented here yesterday at the 43rd annual meeting of the Society for Neuroscience, suggest that amygdala neurons respond to the subjective judgement of emotions in facial expressions, rather than the visual characteristics of faces that convey emotions. The scientists also found that the cellular responses persisted long after each of the photographs disappeared, further suggesting that the amygdala cooperates with other brain regions to create awareness of the emotional content of faces. Thus, when it comes to recognizing the facial expressions of others, what we think we see seems to be more important than what we actually see. © 2013 American Association for the Advancement of Science.

Keyword: Vision; Emotions
Link ID: 18910 - Posted: 11.12.2013

Ian Sample, science correspondent in San Diego Criminal courts in the United States are facing a surge in the number of defendants arguing that their brains were to blame for their crimes and relying on questionable scans and other controversial, unproven neuroscience, a legal expert who has advised the president has warned. Nita Farahany, a professor of law who sits on Barack Obama's bioethics advisory panel, told a Society for Neuroscience meeting in San Diego that those on trial were mounting ever more sophisticated defences that drew on neurological evidence in an effort to show they were not fully responsible for murderous or other criminal actions. Lawyers typically drew on brain scans and neuropsychological tests to reduce defendants' sentences, but in a substantial number of cases the evidence was used to try to clear defendants of all culpability. "What is novel is the use by criminal defendants to say, essentially, that my brain made me do it," Farahany said following an analysis of more than 1,500 judicial opinions from 2005 to 2012. The rise of so-called neurolaw cases has caused serious concerns in the country where brain science first appeared in murder cases. The supreme court has begun a review of how such evidence can be used in criminal cases. But legal and scientific experts nevertheless foresee the trend spreading to other countries, including the UK, and Farahany said she was expanding her work abroad. The survey even found cases where defendants had used neuroscience to argue that their confessions should be struck out because they were not competent to provide them. "When people introduce this evidence for competency, it has actually been relatively successful," Farahany said. © 2013 Guardian News and Media Limited

Keyword: Brain imaging; Aggression
Link ID: 18909 - Posted: 11.11.2013

Jessica Wright A new test of mouse intelligence closely mimics the types of assays used with people and detects a subtle learning deficit reminiscent of one seen in teenagers with autism, according to findings presented Saturday at the2013 Society for Neuroscience annual meeting in San Diego. Another behavioral test, also presented Saturday, uncovers an unexpected social deficit in an autism mouse model. The test in the first study could be used to screen for drugs that improve cognitive deficits associated with autism, says Jill Silverman, a postdoctoral associate in Jacqueline Crawley’s lab at the University of California, Davis MIND Institute. Silverman presented the work at a poster session. To measure learning in mice, researchers typically place them in a water maze, or see if they learn to anticipate an electric shock. “But you don’t shock people or put them in a pool to swim,” notes Silverman. Silverman instead trained the mice in a human activity: using a touchscreen. In the most basic form of the test, the mice see two graphic images (such as a plane and a spider) and learn that they get “yummy” strawberry milkshake if they touch the spider, Silverman says. (She says she uses milkshakes because the mice work hard for them, even if they aren’t hungry.) BTBR mice, which have many autism-like features, learn to go for the spider just as readily as control mice do. So Silverman made things much more complicated. The complex test follows the logic of transitive properties. For example, if John is taller than Anne and Anne is taller than Jane, we are able to infer that John is taller than Jane. © Copyright 2013 Simons Foundation

Keyword: Autism; Learning & Memory
Link ID: 18908 - Posted: 11.11.2013

The long-term impact of roadside bombings on the brains of Canadian soldiers in Afghanistan is the focus of two research projects underway in Western Canada. "In recent years, encounters with improvised explosive devices or IEDs in Afghanistan have inflicted traumatic brain injury on a number of Canadian soldiers," said Dr. Robert Thirsk, a former Canadian astronaut who is now a vice-president with the Canadian Institute of Health Research. "The impact of these blasts may not be immediately apparent. Months after the event the soldiers can suffer from the neurological problems and the mental disorders like anxiety that we're reading about in the newspapers. These weapons may be improvised, but our response to them needs to be strategic." Dr. Yu Tian Wang of the Brain Research Center at the University of British Columbia is looking at the biological changes that occur in the brain at the cellular level following an injury by an explosive device. Wang is studying whether a drug can reduce the death and dysfunction of brain cells following injury. "We know that during traumatic brain injuries some synaptic connections become weakened and the information from one neuron to another is slowed down," Wang said. "Now we know the underlying reason is due to a particular memory surface protein being reduced." Wang said an injection of peptides could provide protection to brain cells before a blast and possibly help repair damage if given immediately after an explosion. © CBC 2013

Keyword: Brain Injury/Concussion
Link ID: 18907 - Posted: 11.11.2013

Sarah DeWeerdt Parts of the brain that process vision and control movements are poorly connected in children with autism, according to results presented Saturday at the 2013 Society for Neuroscience annual meeting in San Diego. In addition to the social deficits that are a core feature of autism, children with the disorder often have clumsy movements. Studies have also found that people with autism have trouble imitating others. The new study uncovers patterns of brain activity suggesting all three of these deficits may be related. The researchers used functional magnetic resonance imaging (fMRI) to measure resting-state activation — brain activity that occurs while individuals are resting quietly in the scanner — in 45 children with autism and 45 controls. Parts of the brain that tend to activate and deactivate together during this procedure are said to be functionally connected. The researchers zeroed in on two sets of brain structures involved in motor activity. One of them, the ventral motor component, includes parts of the cortex, the thalamus and lobule 6 of the cerebellum. They also focused on three areas of the brain involved in visual processing. The most interesting is a region at the back of the brain responsible for complex interpretation of visual information. © Copyright 2013 Simons Foundation

Keyword: Autism; Vision
Link ID: 18906 - Posted: 11.11.2013

By SENDHIL MULLAINATHAN Why is obesity soaring? The answer seems pretty clear. In 1955, a standard soda at McDonald’s was only seven ounces. Today, a medium is three times as large, and even a child’s-size version is 12 ounces. It’s a widely held view that obesity is a consequence of our behaviors, and that behavioral economics thus plays a central role in understanding it — with markets, preferences and choices taking center stage. As a behavioral economist, I subscribed to that view — until recently, when I began to question my thinking. For many health problems, of course, behavior plays some role but biology is often a major villain. “Biology” here is my catchall term for the myriad bodily mechanics that are only weakly connected to our choices. A few studies have led me to wonder whether the same is true with obesity. Have I been the proverbial owner of a (behavioral) hammer, looking for (behavioral) nails everywhere? Have I failed to appreciate the role of biology? A first warning sign comes from looking at other animals. Our pets have been getting fatter along with us. In 2012, some 58.3 percent of cats were, literally, fat cats. That is taken from a survey by the Association for Pet Obesity Prevention. (The very existence of this organization is telling.) Pet obesity, however, can easily be tied to human behavior: a culture that eats more probably feeds its animals more, too. And yet, a study by a group of biostatisticians in the Proceedings of the Royal Society challenges this interpretation. They collected data from animals raised in captivity: macaques, marmosets, chimpanzees, vervets, lab rats and mice. The data came from labs and centers and spanned several decades. These captive animals are also becoming fatter: weight gain for female lab mice, for example, came out to 11.8 percent a decade from 1982 to 2003. But this weight gain is harder to explain. Captive animals are fed carefully controlled diets, which the researchers argue have not changed for decades. Animal obesity cannot be explained through eating behavior alone. We must look to some other — biological — driver. © 2013 The New York Times Company

Keyword: Obesity
Link ID: 18905 - Posted: 11.10.2013

Anjan Chatterjee Before I realized what was happening, the patient reached down between my legs and grabbed my genitals. It was 1985, in the middle of the night during my medicine internship. I was working about 110 hours a week. Every third night I was on call and felt lucky if I got a couple of hours of sleep. That night, I was taking care of this patient for another intern. On my endless “to do” list was the task of placing an intravenous line. When I got to her room it was dark. I didn’t know what her medical condition was. I was focused on starting her IV and then moving on to my next task. I turned on the soft light over her hospital bed and gently woke her. She seemed calm. I loosened her restrained arm to look for a good vein. That was when she grabbed me. Even in my sleep-, food-, and sex-deprived state, I recognized that my charms were not the reason for her attention. She acted indiscriminately. She grabbed nurse’s breasts and students’ buttocks with the same enthusiasm. I had not yet started my neurology residency and did not know that she was suffering from a human version of Klüver-Bucy syndrome. The syndrome is named after Heinrich Klüver, a psychologist, and Paul Bucy, a neurosurgeon, who observed that rhesus monkeys changed profoundly when their anterior-medial temporal lobes were removed. They became placid. They were no longer fearful of objects they would normally avoid. They became “hyper-oral,” meaning they would put anything and everything in their mouth. They also became hypersexual. A similar syndrome occurs in humans. The patient I encountered that night had an infection affecting parts of her brain analogous to those parts in monkeys that Paul Bucy removed. All the cultural and neural machinery that puts a check on such behavior was dissolved by her infection. She displayed sexual desire, the deep-rooted instinct that ensures the survival of our species, in its most uninhibited form. © 2013 Salon Media Group, Inc.

Keyword: Sexual Behavior
Link ID: 18904 - Posted: 11.10.2013

By ANDREW HIGGINS BRUSSELS — Facing a decision on whether to impose tight restrictions on a booming market for electronic cigarettes, members of the European Parliament received a pleading letter in September that was signed by thousands of former smokers worried that “the positive story of e-cigarettes may be about to come to an abrupt halt.” The signatures had been collected via a website, saveecigs.com, which proclaimed itself the voice of the “forgotten millions in this debate” — people who had taken up e-cigarettes to stop smoking, and their grateful families. The website, however, was not quite the grass-roots effort it claimed to be. The text of the letter it asked people to sign was drafted by a London lobbyist hired by Totally Wicked, an e-cigarette company. The website had been set up by a British woman living in Iceland who had previously worked for the owners of Totally Wicked. As the headquarters of the European Union, Brussels sets regulatory standards that resonate around the world. It rivals Washington as a focus for corporate lobbying, with an estimated 30,000 professional lobbyists with registered lobbying firms and thousands more who operate beneath the radar. In this case, a determined lobbying campaign, marrying corporate interests in a fledgling but fast-growing industry with voices elicited from the general public, was aimed at a compelling public health issue: whether e-cigarettes, which deliver nicotine without burning tobacco, should be regulated as medicinal products, just as nicotine patches are. The stakes were substantial. Although e-cigarettes have not been linked to any serious health issues, they have been in widespread use for such a short time that researchers have no basis yet for determining if there are long-term risks. © 2013 The New York Times Company

Keyword: Drug Abuse
Link ID: 18903 - Posted: 11.10.2013

by Guest Writer, Emilie Reas! My first trip to a haunted house is as vivid today as when I was 5 years old. As I made my way past a taunting witch and a rattling skeleton, my eyes fell upon a blood-soaked zombie. My heart raced, my throat swelled, and the tears began to flow. Even now, as a mature (ahem) adult, the ghosts and goblins don’t faze me. But those vacant zombie eyes and pale skin? Oh, the horror! My rational brain knows how irrational my fear is, yet still I shudder, gripped by the same terror that first overwhelmed me decades ago. Unsettling experiences occur daily that we easily brush off – a creepy movie, a turbulent plane ride, or a nip at your ankle by the neighbor’s dog. But occasionally, the fear sticks, establishing a permanent memory that can haunt us for years. At their mildest, such fear memories cause discomfort or embarrassment, but at their worst, they can be downright debilitating. Do spiders make you scream? Are you unable to speak in public without a trembling voice and hands? Maybe you suffered a traumatic accident that’s made you terrified to get back behind the wheel of a car. We’ve all experienced the disruptive effects of a fearful experience we just can’t shake. Yet scientists don’t fully understand why some traumatic events are fleeting, while others are stored as lasting memories. Past research has shown that particular areas of the brain, such as the anterior cingulate and insula, are active during fearful experiences, but also during many other situations, including while monitoring surroundings and emotions or paying attention to important information. Other regions, including the amygdala, hippocampus and prefrontal cortex, are more specialized to support memory for emotional experiences, as they play important roles in emotional processing, memory and attention. While it’s clear that establishing fear memories relies on cross-talk between these regions, it’s not known how they solidify fears into memory and determine which particular ones will endure for the long-term. © Society for Science & the Public 2000 - 2013

Keyword: Learning & Memory; Stress
Link ID: 18902 - Posted: 11.09.2013

By JACKIE CALMES and ROBERT PEAR WASHINGTON — The Obama administration on Friday will complete a generation-long effort to require insurers to cover care for mental health and addiction just like physical illnesses when it issues long-awaited regulations defining parity in benefits and treatment. The rules, which will apply to almost all forms of insurance, will have far-reaching consequences for many Americans. In the White House, the regulations are also seen as critical to President Obama’s program for curbing gun violence by addressing an issue on which there is bipartisan agreement: Making treatment more available to those with mental illness could reduce killings, including mass murders. In issuing the regulations, senior officials said, the administration will have acted on all 23 executive actions that the president and Vice President Joseph R. Biden Jr. announced early this year to reduce gun crimes after the Newtown, Conn., school massacre. In planning those actions, the administration anticipated that gun control legislation would fail in Congress as pressure from the gun lobby proved longer-lasting than the national trauma over the killings of first graders and their caretakers last Dec. 14. “We feel actually like we’ve made a lot of progress on mental health as a result in this year, and this is kind of the big one,” said a senior administration official, one of several who described the outlines of the regulations that Kathleen Sebelius, the secretary of health and human services, will announce at a mental health conference on Friday in Atlanta with the former first lady Rosalynn Carter. While laws and regulations dating to 1996 took initial steps in requiring insurance parity for medical and mental health, “here we’re doing full parity, and we’ve also taken steps to extend it to the people covered in the Affordable Care Act,” the senior official said. “This is kind of the final word on parity.” © 2013 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 18901 - Posted: 11.09.2013

by Sarah Zielinski If you put two birds together and gave them a problem, would they be any better at solving it than if they were alone? A study in Animal Behaviour of common mynas finds that not only are they no better at problem solving when in a pair than when on their own, the birds actually get a lot worse when put in a group. Andrea S. Griffin and her research team from the University of Newcastle in Callaghan, Australia, began by using dog food pellets as bait to capture common mynas (a.k.a. the Indian mynah, Acridotheres tristis) from around Newcastle. Then they gave each of the birds an innovation test, consisting of a box containing a couple of drawers and some Petri dishes. To get to the food hidden in spots in the box, the birds would have to get creative and figure out how to open one of the four containers by doing things like levering up a lid or pushing open a drawer. The scientists then ranked the birds by innovative ability before pairing them up. Half the pairs consisted of a high-innovation and a low-innovation myna, and the other half were pairs of medium-innovation birds. Then the pairs each received an innovation test similar to the one with boxes. Another experiment tested the birds in same-sex groups of five. On their own, 29 of 34 birds were able to access at least one container. But in pairs, only 15 of the 34 birds did so, and they took a lot longer. Performance dropped for both high- and medium-innovation birds, and it didn’t improve for the low-ranked ones, which had done so poorly the first time around that their results couldn’t get any worse. In groups of five, birds’ results fell even further: No mynas solved any of those tasks. © Society for Science & the Public 2000 - 2013

Keyword: Intelligence; Learning & Memory
Link ID: 18900 - Posted: 11.09.2013

Where, exactly, does the sand flea have sex? On the dusty ground, where it spends the first half of its life? Or already nestled snugly in its host—such as in a human foot—where it can suck the blood it needs to nourish its eggs? The answer to this question, which has long puzzled entomologists and tropical health experts, seems to be the latter. A new study, in which a researcher let a sand flea grow inside her skin, concludes that the parasites most likely copulate when the females are already inside their hosts. Tunga penetrans, also known as the chigger flea, sand flea, chigoe, jigger, nigua, pique, or bicho de pé, is widespread in the Caribbean, South America, and sub-Saharan Africa. The immature female burrows permanently into the skin of a warm-blooded host—it also attacks dogs, rats, cattle, and other mammals—where over 2 weeks it swells up to many times its original size, reaching a diameter of up to 10 mm. Through a small opening at the end of its abdominal cone, the insect breathes, defecates, and expels eggs. The female usually dies after 4 to 6 weeks, still embedded in the skin. Native to the Caribbean, sand fleas infected crewmen sailing with Columbus on the Santa Maria after they were shipwrecked on Haiti. They and others brought the parasite back to the Old World, where it eventually became endemic across sub-Saharan Africa. Even today it is an occasional stowaway, showing up in European and North American travel clinics in the feet of tourists who have gone barefoot on tropical beaches. For people living in infested regions, however, the flea is a serious public health issue. What starts as a pale circle in the skin turns red and then black, becoming painful, itchy—and often infected, a condition called tungiasis. One flea seems to attract others, and people can be infested with dozens at once. © 2013 American Association for the Advancement of Science

Keyword: Sexual Behavior; Evolution
Link ID: 18899 - Posted: 11.09.2013

by Laura Sanders Neonatal intensive care units are crammed full of life-saving equipment and people. The technology that fills these bustling hubs is responsible for saving the lives of fragile young babies. That technology is also responsible for quite a bit of noise. In the NICU, monitors beep, incubators whir and nurses, doctors and family members talk. This racket isn’t just annoying: NICU noise often exceeds acceptable levels set by the American Academy of Pediatrics, a 2009 analysis found. To dampen the din, many hospitals are shifting away from open wards to private rooms for preemies. Sounds like a no-brainer, right? Fragile babies get their own sanctuaries where they can recover and grow in peace. But in a surprising twist, a new study finds that this peace and quiet may actually be bad for some babies. Well aware of the noise problem in the NICU ward, Roberta Pineda of Washington University School of Medicine in St. Louis and colleagues went into their study of 136 preterm babies expecting to see benefits in babies who stayed in private rooms. Instead, the researchers found the exact opposite. By the time they left the hospital, babies who stayed in private rooms had less mature brains than those who stayed in an open ward. And two years later, babies who had stayed in private rooms performed worse on language tests. The results were not what the team expected. “It was extremely surprising,” Pineda told me. The researchers believe that the noise abatement effort made things too quiet for these babies. As distressing data from Romanian orphanages highlights, babies need stimulation to thrive. Children who grew up essentially staring at white walls with little contact from caregivers develop serious brain and behavioral problems, heartbreaking results from the Bucharest Early Intervention Project show. Hearing language early in life, even before birth, might be a crucial step in learning to talk later. And babies tucked away in private rooms might be missing out on some good stimulation. © Society for Science & the Public 2000 - 2013

Keyword: Hearing; Development of the Brain
Link ID: 18898 - Posted: 11.09.2013

Stanley Rachman. “Will these hands ne'er be clean?” In Shakespeare's play Macbeth, Lady Macbeth helps to plot the brutal murder of King Duncan. Afterwards she feels tainted by Duncan's blood and insists that “all the perfumes of Arabia” could not sweeten her polluted hands. Baffled by her compulsive washing, her doctor is forced to admit: “This disease is beyond my practise.” In the 400 years since Macbeth was first performed, other doctors, psychiatrists, neuroscientists and clinical psychologists — myself included — have also found the problem beyond the reach of their own expertise. We see compulsive washing a lot, mostly as a symptom of obsessive–compulsive disorder (OCD), but also in people who have suffered a physical or emotional trauma, for example in women who have suffered sexual assault. The events trigger a deep-seated psychological, and ultimately biological, response. We know that the driving force of compulsive washing is a fear of contamination by dirt and germs. An obsessive fear of contact with sexual fluids, for example, can drive compulsive washing in OCD and force people to restrict sexual activity to a specific room in the house. Compulsive washing fails to relieve the anxiety. Most patients with OCD continue to feel contaminated despite vigorous attempts to clean themselves. Why does repeated washing fail? There is much debate at present about the direction that psychiatric medicine and research should take. We should not underestimate what we can continue to learn from the careful observation of patients. Such observations have led my colleagues and me to diagnose a new cause of OCD and other types of compulsive washing: mental contamination. © 2013 Nature Publishing Group

Keyword: OCD - Obsessive Compulsive Disorder; Emotions
Link ID: 18897 - Posted: 11.08.2013

Roughly a year ago, I found myself at an elegant dinner party filled with celebrities and the very wealthy. I am a young professor at a major research university, and my wife and I were invited to mingle and chat with donors to the institution. To any outside observer, my career was ascendant. Having worked intensely and passionately at science for my entire adult life, I had secured my dream job directing an independent neuroscience research laboratory. I was talking to a businessman who had family members affected by a serious medical condition. He turned to me and said: “You're a neuroscientist. What do you know about Parkinson's disease?” My gaze darted to catch the eyes of my wife, but she was involved in another conversation. I was on my own, and I paused to gather my thoughts before responding. Because I had a secret. It was a secret that I hadn't yet told any of my colleagues: I have Parkinson's. I am still at the beginning of my fascinating, frightening and ultimately life-affirming journey as a brain scientist with a disabling disease of the brain. Already it has given me a new perspective on my work, it has made me appreciate life and it has allowed me to see myself as someone who can make a difference in ways that I never expected. But it took a bit of time to get here. The first signs I remember the first time I noticed that something was wrong. Four years ago, I was filling out a mountain of order forms for new lab equipment. After a few pages, my hand became a quaking lump of flesh and bone, locked uselessly in a tense rigor. A few days later, I noticed my walk was changing: rather than swinging my arm at my side, I held it in front of me rigidly, even grabbing the bottom edge of my shirt. I also had an occasional twitch in the last two fingers of my hand. © 2013 Nature Publishing Group

Keyword: Parkinsons
Link ID: 18896 - Posted: 11.08.2013