By Meghan Rosen David Ferrero wasn’t expecting the jaguar to pounce. When he approached the holding pens at Massachusetts’ Stone Zoo, the big cat watched but looked relaxed, lounging on her cage’s concrete floor. Two other jaguars rested in separate cages nearby. The jaguars usually prowled outside, in the grassy grounds of the zoo’s enclosure. But this afternoon, zookeepers kept the animals inside so that Ferrero and a colleague could grab a behind-the-scenes peek. Here, the jaguars slept at night — and fed. Here, only metal bars stood between the humans and the cats. As Ferrero stepped closer to the cages, the watchful female sprang up, twisting her body toward him, front paws thumping the bars. Fully extended, she was as tall as Ferrero. “I think she wanted to eat me,” he says. The zookeepers weren’t afraid, but Ferrero flinched. He wasn’t familiar with the lean, black-spotted feline. He was just there to pick up some pee. Ferrero, a neurobiologist from Harvard, was visiting the zoo to gather urine specimens for a study linking odors to instinctual behavior in rodents. Early lab results had hinted that a whiff of a chemical in carnivore pee flashed a sort of billboard message, blinking “DANGER” in neon lights — enough to make animals automatically shrink away in fear. © Society for Science & the Public 2000 - 2012

Keyword: Chemical Senses (Smell & Taste)
Link ID: 17334 - Posted: 10.06.2012

By Katherine Harmon A bite from the black mamba snake (Dendroaspis polylepis) can kill an adult human within 20 minutes. But mixed in with that toxic venom is a new natural class of compound that could be used to help develop new painkillers. Named “mambalgins,” these peptides block acute and inflammatory pain in mice as well as morphine does, according to a new study. Researchers, led by Sylvie Diochot, of the Institute of Molecular and Cellular Pharmacology at Nice University, Sophia Antipolis in France, purified the peptides from the venom and profiled the compounds’ structure. They then were able to test the mambalgins in strains of mice with various genetic tweaks to their pain pathways. Diochot and her colleagues determined that the mambalgins work by blocking an as-yet untargeted set of neurological ion channels associated with pain signals. The findings were published online October 3 in Nature (Scientific American is part of Nature Publishing Group). As a bonus, mambalgins did not have the risky side effect of respiratory depression that morphine does. And the mice developed less tolerance to them over time than is typical with morphine. Experimenting with the newfound compounds should also help researchers learn more about the mechanisms that drive pain. As the researchers noted in their paper, “It is essential to understand pain better to develop new analgesics. The black mamba peptides discovered here have the potential to address both of these aims.” © 2012 Scientific American,

Keyword: Pain & Touch; Neurotoxins
Link ID: 17333 - Posted: 10.04.2012

By Anna-Marie Lever Health reporter, BBC News An aspirin a day may slow brain decline in elderly women at high risk of cardiovascular disease, research finds. Around 500 at risk women, between the ages of 70 to 92, were tracked for five years - their mental capacity was tested at the start and end of the study. Those taking aspirin for the entire period saw their test scores fall much less than those who had not. The Swedish study is reported in the journal BMJ Open. Dr Silke Kern, one of paper's authors, said: "Unlike other countries - Sweden is unique, it is not routine to treat women at high risk of heart disease and stroke with aspirin. This meant we had a good group for comparison." The women were tested using a mini mental state exam (MMSE) - this tests intellectual capacity and includes orientation questions like, "what is today's date?", "where are we today?" and visual-spatial tests like drawing two interlinking pentagons. But the report found that while aspirin may slow changes in cognitive ability in women at high risk of a heart attack or stroke, it made no difference to the rate at which the women developed dementia - which was also examined for by a neuropsychiatrist. BBC © 2012

Keyword: Alzheimers
Link ID: 17332 - Posted: 10.04.2012

By ANDREW POLLACK An experimental drug preserved and even improved the walking ability of boys with Duchenne muscular dystrophy in a clinical trial, raising hopes that the first effective treatment for the disease may be on the horizon. Boys with the disease who received the highest dose of the drug had a slightly improved ability to walk after 48 weeks of treatment, the drug’s developer, Sarepta Therapeutics, announced Wednesday. By contrast, the boys who received a placebo suffered a sharp decline in how well they could walk. The drug, called eteplirsen, also appeared to restore levels of the crucial protein that muscular dystrophy patients lack to about half of normal levels, Sarepta said. “I think this changes the entire playing field for muscular dystrophy,” said Dr. Jerry R. Mendell, director of the gene therapy and muscular dystrophy programs at Nationwide Children’s Hospital in Columbus, Ohio, and the lead investigator in the trial. There are many caveats. The trial had only 12 patients, with only four receiving the high dose and four the placebo, and the data has not been reviewed by experts. It is also unclear how long the effects of the drug would last or if safety issues would arise with longer treatment. Also, eteplirsen would be appropriate for only about 13 percent to 15 percent of Duchenne patients, those with the particular genetic mutation the drug is meant to counteract. However, a similar approach might work for some other mutations. © 2012 The New York Times Company

Keyword: Movement Disorders; Muscles
Link ID: 17331 - Posted: 10.04.2012

By Susan Milius A patch over a male Gouldian finch’s right eye works like beer goggles, though the bird doesn’t need booze to flirt unwisely. If limited to using his left eye when checking out possible mates, he risks making really stupid choices. Gouldian finches have caps of black, red or yellow feathers on their heads. In nature, the birds prefer to mate with partners with the same cap color. Yet black-headed males rendered temporarily left-eyed by a tiny removable eye patch flirted as readily with red-heads as with black-heads, says cognitive ecologist Jennifer Templeton of Knox College in Galesburg, Ill. That’s not smart because daughters typically fail to survive when Gouldian finches mate outside their cap color. Also the male himself “becomes less attractive,” Templeton says. When the bird’s right eye was covered, he sang, bowed and posed less during his attempts at courtship. Some left-eyed males didn’t manage to make up their minds at all, but “just hopped around randomly,” Templeton says. Moving the eye patch to the right eye, however, restored male Gouldian finches to their senses. Males then spent more time perching near same-cap-color females and flirting with them. “Beauty is in the right eye of the beholder,” Templeton and her colleagues conclude online October 3 in Biology Letters. Birds make fine subjects for comparing eye biases because many species’ eyes sit on opposite sides of their skulls with very different fields of view. A bird’s right eye connects to the left hemisphere of its brain, and the left eye to the right hemisphere. Unlike mammals, birds don’t have a high-speed connection between hemispheres. © Society for Science & the Public 2000 - 2012

Keyword: Laterality; Sexual Behavior
Link ID: 17330 - Posted: 10.04.2012

by Marissa Miley A virus that may encourage the body to grow more fat cells could, paradoxically, lower diabetes risk. Nikhil Dhurandhar at the Pennington Biomedical Research Center in Baton Rouge, Louisiana, and colleagues examined the long-term effects of a common virus – adenovirus-36 (Ad-36) – on humans. The team analysed blood samples made available from 1400 volunteers in a decades-long epidemiological study. The researchers detected antibodies to Ad-36 in 14.5 per cent of the subjects when they first joined the study – a prevalence in line with studies on the US adult population. Ten years later, those individuals naturally infected with Ad-36 had a higher body mass index and body fat percentage than those who were not infected – but their blood sugar and insulin levels were healthier. Animal and cell studies offer an explanation, says Dhurandhar. They suggest that Ad-36 increases the number and size of fat cells, or adipocytes, providing additional "depots" for any fat coming from excessive calorie consumption. Under normal circumstances, the number of these fat storage cells stays constant in adulthood, no matter what dietary choices people make. The extra cells from Ad-36 may make the body more likely to store excess fat, but that means less fat is left to travel to other areas, like the liver, where it can have toxic effects. The adipocytes may also store more sugar, helping to keep blood sugar levels under control and maintaining insulin sensitivity to glucose. © Copyright Reed Business Information Ltd.

Keyword: Obesity
Link ID: 17329 - Posted: 10.04.2012

By Deborah Kotz, Globe Staff Is Alzheimer’s disease really a form of diabetes? Let’s call it type 3, because that’s what a Brown Medical School researcher dubbed it back in 2005 when she autopsied the brains of Alzheimer’s patients and found that they had signs of insulin resistance -- an early indicator of diabetes. Since then, however, we haven’t seen a sea-change in preventive treatments based on this idea. Those who carry the gene for hereditary Alzheimer’s aren’t given diabetes drugs to help stave off dementia. Nor are Alzheimer’s patients given insulin injections. What has been getting attention, however, is whether we should make extra efforts to eat a low glycemic diet -- which is low in processed foods, sugar, and starchy carbohydrates that cause quick spikes in blood sugar -- to help protect our brains from developing those gunky amyloid plaques associated with Alzheimer’s. The September issue of the New Scientist advocates for changing our eating patterns with a frightening image of a cracked chocolate brain on its cover. (Chocolate consumption, though, hasn’t been linked to cognitive decline, much to my relief.) New York Times food columnist Mark Bittman pointed out in a recent post that the latest studies provide some persuasive evidence linking diet to the development of Alzheimer’s. I’ve covered those studies too, including this one that measured a smaller Alzheimer’s risk in people who eat a diet rich in fish, veggies, and fruit compared with those who eat a diet centered on processed foods containing trans fats. © 2012 NY Times Co.

Keyword: Alzheimers
Link ID: 17328 - Posted: 10.03.2012

By PAUL CHRISTOPHER, M.D. “I’m addicted to painkillers,” J., a thickset construction worker, told me on a recent afternoon in the emergency room, his wife at his side. Two years before, after months of pain, stiffness and swelling in his hands and neck, his primary physician had diagnosed rheumatoid arthritis and had prescribed three medications: two to slow the disease and one, oxycodone, for pain. Bolstered by the painkiller, J. had felt more limber and energetic than he had in years. “I could finally keep up with the other guys,” he told me. He worked harder, and his pain worsened. His primary physician increased the oxycodone dose. Soon, J. was looking forward more to the buzz than to the relief the pills brought. He went to see two other physicians who, unaware that he was double-dipping, prescribed similar medications. When a co-worker offered to sell him painkillers directly, J.’s use spiraled out of control. By the time I saw him, he was taking dozens of pills a day, often crushing and snorting them to speed the onset of his high. With remarkable candor, he described how the drugs had marred every facet of his life — from days of missed work to increasing debt, deteriorating health and marital strain. But when I listed the treatment options that might help, J. shook his head, looked from me to his wife, and got up. “I’m all set,” he said, holding up his hands. Then he walked out of the room. Despair fell on his wife’s face. “Please,” she said, grabbing my arm, “you can’t let him leave.” Copyright 2012 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 17327 - Posted: 10.03.2012

By Jennifer Viegas Bats may have more in common with the fictional Batman than previously believed, since both successfully combine work with courting sexy potential mates -- a lot of them. A new study, published in the latest Proceedings of the Royal Society B, reveals that bat echolocation calls, primarily used for orientation and foraging, also contain information about sex, which helps the flying mammals to acquire and keep mates. The info is especially helpful to certain male bats with harems of adoring females that are actually huskier than the males. This holds true for the greater sac-winged bat (Saccopteryx bilineata), which was the focus of the study. Lead author Mirjam Knörnschild told Discovery News that "male S. bilineata court females whenever the opportunity arises. The social information in echolocation calls about the sex of the calling bat benefits listening harem males because they can distinguish between females and male rivals. It might also benefit calling females because they are greeted friendly." athletes Knörnschild, a researcher at the University of Ulm's Institute of Experimental Ecology, and her team analyzed greater sac-winged bat echolocation calls. The scientists discovered that the calls contain "pronounced vocal signatures encoding sex and individual identity." This can include species identity, age, sex, group affiliation, and other more specific information about the individual. © 2012 Discovery Communications, LLC.

Keyword: Sexual Behavior; Hearing
Link ID: 17326 - Posted: 10.03.2012

By Ferris Jabr In the 1970s biologist Sydney Brenner and his colleagues began preserving tiny hermaphroditic roundworms known as Caenorhabditis elegans in agar and osmium fixative, slicing up their bodies like pepperoni and photographing their cells through a powerful electron microscope. The goal was to create a wiring diagram—a map of all 302 neurons in the C. elegans nervous system as well as all the 7,000 connections, or synapses, between those neurons. In 1986 the scientists published a near complete draft of the diagram. More than 20 years later, Dmitri Chklovskii of Janelia Farm Research Campus and his collaborators published an even more comprehensive version. Today, scientists call such diagrams "connectomes." So far, C. elegans is the only organism that boasts a complete connectome. Researchers are also working on connectomes for the fruit fly nervous system and the mouse brain. In recent years some neuroscientists have proposed creating a connectome for the entire human brain—or at least big chunks of it. Perhaps the most famous proponent of connectomics is Sebastian Seung of the Massachusetts Institute of Technology, whose impressive credentials, TED talk, popular book, charisma and distinctive fashion sense (he is known to wear gold sneakers) have made him a veritable neuroscience rock star. Other neuroscientists think that connectomics at such a large scale—the human brain contains around 86 billion neurons and 100 trillion synapses—is not the best use of limited resources. It would take far too long to produce such a massive map, they argue, and, even if we had one, we would not really know how to interpret it. To bolster their argument, some critics point out that the C. elegans connectome has not provided many insights into the worm's behavior. In a debate* with Seung at Columbia University earlier this year, Anthony Movshon of New York University said, "I think it's fair to say…that our understanding of the worm has not been materially enhanced by having that connectome available to us. We don't have a comprehensive model of how the worm's nervous system actually produces the behaviors. What we have is a sort of a bed on which we can build experiments—and many people have built many elegant experiments on that bed. But that connectome by itself has not explained anything." © 2012 Scientific American

Keyword: Development of the Brain
Link ID: 17325 - Posted: 10.03.2012

by Elizabeth Norton Baboons, like people, really do get by with a little help from their friends. Humans with strong social ties live longer, healthier lives, whereas hostility and "loner" tendencies can set the stage for disease and early death. In animals, too, strong social networks contribute to longer lives and healthier offspring—and now it seems that personality may be just as big a factor in other primates' longevity status. A new study found that female baboons that had the most stable relationships with other females weren't always the highest up in the dominance hierarchy or the ones with close kin around—but they were the nicest. Scientists are increasingly seeing personality as a key factor in an animal's ability to survive, adapt, and thrive in its environment. But this topic isn't an easy one to study scientifically, says primatologist Dorothy Cheney of the University of Pennsylvania. "Research in mammals, birds, fish, and insects shows individual patterns of behavior that can't be easily explained. But the many studies of personality are based on human traits like conscientiousness, agreeableness, or neuroticism. It isn't clear how to apply those traits to animals," Cheney says. Along with a group of scientists—including co-authors Robert Seyfarth, also at the University of Pennsylvania, and primatologist Joan Silk of Arizona State University, Tempe—Cheney has studied wild baboons at the Moremi Game Reserve in Botswana for almost 20 years. Besides providing detailed, long-term observations of behavior in several generations of baboons, the research has yielded a wealth of biological and genetic information. © 2010 American Association for the Advancement of Science.

Keyword: Evolution; Emotions
Link ID: 17323 - Posted: 10.02.2012

Zoë Corbyn Conventional wisdom says that most retractions of papers in scientific journals are triggered by unintentional errors. Not so, according to one of the largest-ever studies of retractions. A survey1 published in Proceedings of the National Academy of Sciences has found that two-thirds of retracted life-sciences papers were stricken from the scientific record because of misconduct such as fraud or suspected fraud — and that journals sometimes soft-pedal the reason. The survey examined all 2,047 articles in the PubMed database that had been marked as retracted by 3 May this year. But rather than taking journals’ retraction notices at face value, as previous analyses have done, the study used secondary sources to pin down the reasons for retraction if the notices were incomplete or vague. These sources included investigations by the US Office of Research Integrity, and evidence reported by the blog Retraction Watch. The analysis revealed that fraud or suspected fraud was responsible for 43% of the retractions. Other types of misconduct — duplicate publication and plagiarism — accounted for 14% and 10% of retractions, respectively. Only 21% of the papers were retracted because of error (see ‘Bad copy’). Earlier studies had found that the percentage of retractions attributable to error was 1.5–3 times higher2–4. “The secondary sources give a very different picture,” says Arturo Casadevall, a microbiologist at Yeshiva University in New York, and a co-author of the latest study. “Retraction notices are often not accurate.” © 2012 Nature Publishing Group

Keyword: Miscellaneous
Link ID: 17322 - Posted: 10.02.2012

By AMANDA SCHAFFER For years, researchers have investigated how the body loses the ability to produce enough insulin, a hallmark of diabetes. Now an intriguing theory is emerging, and it suggests a potential treatment that few scientists had considered. The hormone insulin helps shuttle glucose, or blood sugar, from the bloodstream into individual cells to be used as energy. But the body can become resistant to insulin, and the beta cells of the pancreas, which produce the hormone, must work harder to compensate. Eventually, the thinking goes, they lose the ability to keep up. “We used to say that the beta cells poop out,” said Alan Saltiel, director of the Life Sciences Institute at the University of Michigan. In reality, he added, this shorthand meant “we have no idea what’s going on.” Some evidence suggested that large numbers of these cells died through a process of programmed cell death called apoptosis. But that was at best a partial explanation. Now, researchers at Columbia University have put forth a surprising alternative. In mice with Type 2 diabetes, the researchers showed that beta cells that had lost function were not dead at all. Most remained alive, but in a changed form. They reverted to an earlier developmental, “progenitor,” state. It’s as if these cells are “stepping back in time to a point where they look like they might have looked during their development,” said Dr. Domenico Accili, director of the Columbia University Diabetes and Endocrinology Research Center, who led the new work. © 2012 The New York Times Company

Keyword: Stress; Obesity
Link ID: 17321 - Posted: 10.02.2012

By Gregory Thomas, During an introductory psychology course at Britain’s University of Essex in 2009, Arnold Wilkins asked his class to participate in a quick experiment. Wilkins projected two images on a wall and asked students to write down whether they found either of them disturbing. One was a photograph of a woody landscape. The other was a close-up of a lotus-flower seedpod — a flat-faced pod pocked with small holes. Most of the students were unmoved, but one, freshman An Le, recalls being both transfixed and revolted by the lotus image. “It felt like I was in shock,” he says. Le is far from alone in his response. Thousands of people claim to suffer trypophobia, a term derived from the Greek “trypo,” which means punching, drilling or boring holes. It refers to an irrational fear of clusters of small holes, such as beehives, ant holes and even bubbles in a pancake on the griddle or air pockets in a chocolate bar. On Web sites and blogs, self-diagnosed trypophobes share tales of vomiting, sleep loss and anxiety attacks at the sight of such objects as honeycombs and rotting wood. They say the fears are haunting and disruptive of their daily lives. But the medical world hasn’t yet embraced the phobia as real. Trypophobia isn’t listed in any major dictionary or in the Diagnostic and Statistical Manual of Mental Disorders. Attempts to add trypophobia to the Oxford English Dictionary and even to establish a Wikipedia page have been rebuffed because there hasn’t been any research published on the subject. A Wikipedia editor who deleted an entry on trypophobia in 2009 noted that trypophobia is “likely hoax and borderline patent nonsense.” © 1996-2012 The Washington Post

Keyword: Emotions; Learning & Memory
Link ID: 17320 - Posted: 10.02.2012

By BENEDICT CAREY Proposed changes to the official diagnosis of autism will not reduce the proportion of children found to have it as steeply as many have feared, scientists reported on Tuesday, in an analysis that contradicts several previous studies. Earlier research had estimated that 45 percent or more of children currently on the “autism spectrum” would not qualify under a new definition now being refined by psychiatric researchers — a finding that generated widespread anxiety among parents who rely on state-financed services for their children. The new report, posted online Tuesday by The American Journal of Psychiatry, concluded that the number who would be excluded is closer to 10 percent. The finding may soothe the anxieties of some parents, but will not likely settle the debate over the effect of the new diagnosis. All sides agree that the proposed criteria are narrower and will likely result in fewer diagnoses of autism, but until doctors begin using the new definition widely, the predictions of its effect are just that: predictions. The debate has simmered over the past year as an expert panel appointed by the American Psychiatric Association has updated its proposals for the association’s Diagnostic and Statistical Manual of Mental Disorders, scheduled to take effect in May 2013. The manual is the field’s standard reference, and several recent studies suggested that the amended autism definition was far narrower than intended. © 2012 The New York Times Company

Keyword: Autism
Link ID: 17319 - Posted: 10.02.2012

By Simon J Makin Humans are born to a longer period of total dependence than any other animal we know of, and we also know that mistreatment or neglect during this time often leads to social, emotional, cognitive and mental health problems in later life. It’s not hard to imagine how a lack of proper stimulation in our earliest years – everything from rich sensory experiences and language exposure to love and care – might adversely affect our development, but scientists have only recently started to pull back the curtain on the genetic, molecular and cellular mechanisms that might explain how these effects arise in the brain. You’ll often hear it said that human beings are “social animals”. What biologists tend to mean by that phrase is behaviour like long-lasting relationships or some kind society, whether that’s the social hierarchy of gorillas or the extreme organisation of bees and ants. But, to an extent, most animals are social. A mother usually bonds with its offspring in any species of bird or mammal you care to mention, and almost all animals indulge in some kind of social behaviour when they mate. But there is another sense in which most animals seem to be fundamentally social. There is an emerging scientific understanding of the way social experience moulds the biochemistry of the brain and it looks like most species don’t just prefer the company of others – they need it to develop properly. Take that staple of genetics research, drosophila – aka the fruit fly. While they are not as social as primates or bees, they are more social than you might think, and there have been studies showing that social isolation can disrupt their mating behaviour or even reduce their lifespan. © 2012 Scientific American,

Keyword: Development of the Brain; Glia
Link ID: 17318 - Posted: 10.02.2012

By NICHOLAS BAKALAR A small study has found that obese children are more likely than others to have a weak sense of taste. German researchers tested tasting ability in 99 obese and 94 normal-weight children, whose average age was 13, by having them try to identify tastes on strips of filter paper and asking them to distinguish among sweet, sour, salty, umami (savory) and bitter. The children also were asked to rate the taste’s intensity on a five-point scale. Girls were better than boys at distinguishing tastes, and older children scored higher than younger; there were no differences by ethnicity. Obese children scored an average of 12.6 out of a possible 20, while the normal-weight children averaged 14.1, a statistically significant difference. On the intensity scale, obese children rated all flavor concentrations lower than did those in the normal-weight group. “We think it’s important, especially for young children, to get different tastes so that they can improve their taste sensitivity,” said the lead author, Dr. Johanna Overberg, a pediatrician at Charité Children’s Hospital in Berlin. “If you taste more and different things at younger ages, you can do this.” The authors, writing online in the Archives of Disease in Childhood, say the reason for the association is unclear, but they suggest that the hormone leptin may affect both body weight and the sensitivity of taste buds. Copyright 2012 The New York Times Company

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 17317 - Posted: 10.02.2012

by Jessica Hamzelou California has become the first US state to ban unfounded therapies that attempt to turn gay teenagers straight. "These practices have no basis in science or medicine and they will now be relegated to the dustbin of quackery," said state governor Jerry Brown in a statement to the San Francisco Chronicle. He signed a bill outlawing the therapies on 29 September. Brown's conclusions are in line with those reached a few years ago by a task force of psychologists who were commissioned by the American Psychological Association to assess all published research on the therapies. The group, led by Judith Glassgold, found no evidence that the treatment was effective. "The scientific evidence does not support such therapies," says Clinton Anderson, director of the APA's Lesbian, Gay, Bisexual and Transgender Concerns office. "They were not helpful and could be harmful," says Glassgold, who is based in Washington DC. "Most people became more depressed and anxious, and could become suicidal." "Usually these talk therapies are based on the assumption that homosexuality is a mental illness caused by poor parenting and confused gender roles," she adds. "They attempt to explain that to the patient, and try to get them to act and behave in a heterosexual manner." © Copyright Reed Business Information Ltd

Keyword: Sexual Behavior
Link ID: 17316 - Posted: 10.02.2012

By Tori Rodriguez A common complaint about wrinkle-masking Botox is that recipients have difficulty displaying emotions on their faces. That side effect might be a good thing, however, for people with treatment-resistant depression. In the first randomized, controlled study on the effect of botulinum toxin—known commercially as Botox—on depression, researchers investigated whether it might aid patients with major depressive disorder who had not responded to antidepressant medications. Participants in the treatment group were given a single dose (consisting of five injections) of botulinum toxin in the area of the face between and just above the eyebrows, whereas the control group was given placebo injections. Depressive symptoms in the treatment group decreased 47 percent after six weeks, an improvement that remained through the 16-week study period. The placebo group had a 9 percent reduction in symptoms. The findings appeared in May in the Journal of Psychiatric Research. Study author M. Axel Wollmer, a psychiatrist at the University of Basel in Switzerland, believes the treatment “interrupts feedback from the facial musculature to the brain, which may be involved in the development and maintenance of negative emotions.” Past studies have shown that Botox impairs people's ability to identify others' feelings, and the new finding adds more evidence: the muscles of the face are instrumental for identifying and experiencing emotions, not just communicating them. © 2012 Scientific American

Keyword: Depression; Emotions
Link ID: 17315 - Posted: 10.02.2012

by Melissa Lee Phillips  Giving a whole new meaning to "pregnancy brain," a new study shows that male DNA—likely left over from pregnancy with a male fetus—can persist in a woman's brain throughout her life. Although the biological impact of this foreign DNA is unclear, the study also found that women with more male DNA in their brains were less likely to have suffered from Alzheimer's disease—hinting that the male DNA could help protect the mothers from the disease, the researchers say. During mammalian pregnancy, the mother and fetus exchange DNA and cells. Previous work has shown that fetal cells can linger in the mother's blood and bone for decades, a condition researchers call fetal microchimerism. The lingering of the fetal DNA, research suggests, may be a mixed blessing for a mom: The cells may benefit the mother's health—by promoting tissue repair and improving the immune system—but may also cause adverse effects, such as autoimmune reactions. One question is how leftover fetal cells affect the brain. Researchers have shown that fetal microchimerism occurs in mouse brains, but they had not shown this in humans. So a team led by autoimmunity researcher and rheumatologist J. Lee Nelson of the Fred Hutchinson Cancer Research Center in Seattle, Washington, took samples from autopsied brains of 59 women who died between the ages of 32 and 101. By testing for a gene specific to the Y chromosome, they found evidence of male DNA in the brains of 63% of the women. (The researchers did not have the history of the women's pregnancies.) The male DNA was scattered across multiple brain regions, the team reports online today in PLoS ONE. Because some studies have suggested that the risk of Alzheimer's disease (AD) increases with an increasing number of pregnancies, the team also examined the brains for signs of the disease, allowing them to determine whether AD correlated with the observed microchimerism. Of the 59 women, 33 had AD—but contrary to the team's expectation, the women with AD had significantly less male DNA in their brains than did the 26 women who did not have AD. © 2010 American Association for the Advancement of Science

Keyword: Sexual Behavior; Stem Cells
Link ID: 17314 - Posted: 09.29.2012