Phil McKenna What do you do when your only means of attracting members of the opposite sex also puts your life in jeopardy? For field crickets on the Hawaiian island of Kauai, shutting up seems to work. According to a new study, rapid evolution in the Kauain population of the oceanic field cricket Teleogryllus oceanicus has rendered nine-tenths of the males there incapable of producing their iconic night-time call. The genetic mutation, which changes the shape of the male’s wing to make it silent, means the crickets are better adapted to avoid a deadly parasite. The finding dumbfounded biologist Marlene Zuk, at the University of California in Riverside, US, who first thought the dwindling population of crickets she was studying had gone extinct when she no longer heard their calls. “If you’re a cricket and you’re a male, your life is defined by calling,” Zuk explains. “How are you going to find a female, and once you do, how are you going to get her to mate with you without your call?” Zuk found that the quiet crickets maintained their reproductive chances by congregating near to the few remaining male crickets that are still capable of calling. © Copyright Reed Business Information Ltd.

Keyword: Sexual Behavior; Evolution
Link ID: 9367 - Posted: 06.24.2010

Vitamin shots may help protect multiple sclerosis patients from severe long-term disability, a study suggests. Currently, there is no effective treatment for the chronic progressive phase of MS, when serious disability is most likely to appear. Researchers cut the risk of nerve degeneration in mice with MS-type symptoms by giving them a form of vitamin B3 called nicotinamide. The Children's Hospital Boston study appears in the Journal of Neuroscience. MS, which affects about 85,000 people in the UK, is a disease of the central nervous system. It causes the break down of the myelin sheath, a fatty protein, which coats nerve fibres, disrupting the ability to conduct electrical impulses to and from the brain. Many patients develop a form of the disease called relapsing-remitting MS, in which bouts of illness are followed by complete or partial recovery. In this early phase anti-inflammatory drugs can help. But eventually patients can enter the chronic progressive phase, for which there is no good treatment. The Boston team worked on mice with an MS-like disease called experimental autoimmune encephalitis (EAE). They found that daily nicotinamide shots protected the animals' nerve cells from myelin loss, and stabilised the condition of those cells that had already been affected. The greater the dose of nicotinamide, the greater the protective effect. Rating disability on a scale of one to five, mice receiving the highest doses of nicotinamide scored between one and two, while animals who received no shots at all scored between three and four. (C)BBC

Keyword: Muscles
Link ID: 9366 - Posted: 09.20.2006

By JANE E. BRODY For an older woman I know who was suffering from “implacable depression” that refused to yield to any medications, electroconvulsive therapy — popularly called shock therapy — was a lifesaver. And Kitty Dukakis, wife of the former governor of Massachusetts and 1988 Democratic presidential nominee, says ECT, as doctors call it, gave her back her life, which had been rendered nearly unlivable by unrelenting despair and the alcohol she used to assuage it. Neither woman has experienced the most common side effect of ECT: memory disruption, though Mrs. Dukakis recalls nothing of a five-day trip to Paris she took after her treatment. The television host Dick Cavett, who also had the treatment, wrote in People magazine, “In my case, ECT was miraculous.” Mr. Cavett added, “It was like a magic wand.” But for a man I know who was suicidally depressed and given ECT as a last resort, it did nothing to relieve his depression but destroyed some of his long-term memory. Such differences in effectiveness and side effects are not unusual in medicine and psychiatry, and they are not played down in a new book called “Shock,” which Mrs. Dukakis wrote with Larry Tye, a former Boston Globe reporter. The book, in which Mrs. Dukakis details her experience with depression and ECT, explores the history, effectiveness and downsides of this nearly 70-year-old treatment, a remedy that has been repeatedly portrayed in film and literature as barbaric, inhuman, even torturous. Copyright 2006 The New York Times Company

Keyword: Depression
Link ID: 9365 - Posted: 06.24.2010

Early to bed and early to rise may be a prescription for prosperity, but for some morning larks, it's an unfortunate condition written in their genes. These people suffer from familial advanced sleep phase syndrome (FASPS), a rare condition in which people hit the hay and wake up about four hours before everyone else. A simple expulsion of protein from the cell nucleus seems to be at the root of the syndrome, report researchers who studied the way that a previously identified mutant protein behaved in cultured human skin cells. The circadian clock is our body's inborn tool for keeping us on a roughly 24-hour schedule, sleeping and eating at regular intervals, but it can go awry. In many of those with FASPS, researchers had identified a mutation in a protein called PERIOD2. Some hypothesized that the mutant protein's effects arise from the lack of a key phosphate group, but nobody had identified a mechanism, says circadian researcher Achim Kramer of Charité Universitätsmedizin Berlin. Proteins of PERIOD2's family are thought to be more stable when studded with fewer phosphates, but Kramer and co-workers discovered that in this case the opposite is true. The team's research, published online September 18 in Genes and Development, found that the mutant protein degrades more than twice as fast, apparently because it is quickly transported from the nucleus to the cytoplasm, which is rife with protein-digesting enzymes. "Usually the protein is made in the cytosol, and then it goes into the nucleus and inhibits its own synthesis," Kramer explains. The inhibition erodes as the protein is pumped back outside the nucleus. © 1996-2006 Scientific American, Inc.

Keyword: Biological Rhythms; Genes & Behavior
Link ID: 9364 - Posted: 06.24.2010

After Susan Zilber's father died from Alzheimer's disease she wanted to know if she'd share his fate. "Information is key to figuring out how you're going to deal with something," she says. "That's part of who I am, and I think that I'd be able to deal with it. I'd rather know than not know." The problem is, there isn't a single test for Alzheimer's. Now, researchers have developed new software, called HipMask, that can potentially assess a person's risk for cognitive impairment by scanning of a tiny brain area called the hippocampus, which is known to be affected in the early stages of Alzheimer's. When applied to patient PET and MRI scans taken over the course of a longitudinal study of Alzheimer's, the software proved to be 85 percent accurate in predicting who would get the disease nine years before patients showed symptoms. "What we are trying to do is to find the measure that would predict decline from normal aging to Alzheimer's disease," explains Lisa Mosconi, a brain researcher at New York University School of Medicine's Center for Brain Health. "It looks like the hippocampus is particularly involved in early Alzheimer's disease, so by studying how the hippocampus [is working] in Alzheimer's patients — or in Alzheimer's patients it's actually not working — we can probably find a predictor for Alzheimer's disease." © ScienCentral, 2000-2006.

Keyword: Alzheimers; Brain imaging
Link ID: 9363 - Posted: 06.24.2010

A drug commonly used to treat severe acne can lead to depressive behaviour in mice, according to research published in the journal Neuropsychopharmacology. Since the drug’s introduction in the early 1980s there have been controversial reports of depression and suicidal behaviour that may have occurred in some people taking Roaccutane (Accutane in the US). This has led to the drug’s manufacturers, Roche, including a warning in the product information that taking the medication may cause depression, psychosis and suicidal behaviour. However, the chemical mechanism by which this might happen has never been established. In new independent research, scientists at the universities of Bath and Texas at Austin gave Roaccutane to mice over a period of six weeks, and then monitored the rodents’ behaviour. They found that whilst there was no change in the physical abilities of the mice, the rodents spent significantly more time immobile in a range of laboratory assessments designed to test their stress responsiveness – suggesting that administration of Roaccutane increases depression-related behaviour in mice. comms@bath.ac.uk © 2004

Keyword: Depression
Link ID: 9362 - Posted: 06.24.2010

Roxanne Khamsi Birdsongs are so distinctive they are often used by ornithologists to identify individual birds. Now a novel study shows that birds are not "pre-programmed" to sing their song – rather, birds listen closely to their tune to keep their songs note perfect. The same mechanism may operate in humans, perhaps shedding light on speech disorders, the researchers say. Songbirds do not start out life as virtuosos: they often begin by ‘babbling’ random pitches and then advance to sing sophisticated tunes with the help of a tutor. Once they develop their own particular melody, they use it to announce territorial claims or to attract a mate. The slight variations in the song identify one bird from another, so birds take great pains to preserve their unique tune throughout life. To establish how birds keep tabs on their singing, scientists have conducted experiments that involved disabling the birds’ ability to hear by removing a collection of sensory cells known as the cochlea. Over time, each animal produced songs that diverged further and further from its particular identifying tune. But an operation that leaves birds deaf could have other unintended cognitive effects that affect song production, argues Jon Sakata at the University of California in San Francisco, US. He and his colleague, Michael Brainard, set up an experiment that disrupted the hearing of the birds without an invasive procedure. © Copyright Reed Business Information Ltd.

Keyword: Animal Communication; Language
Link ID: 9361 - Posted: 06.24.2010

By Sandra G. Boodman Motherhood and depression share a long common border, author Tracy Thompson observes in "The Ghost in the House" (HarperCollins, $24.95), her exploration of the often-overlooked mental health problem. The book blends memoir with research on the topic. Thompson's focus is not the more-familiar postpartum form that can follow the birth of a baby, but the longer-term illness that affects an estimated 12 million American women, many of them diagnosed in the prime childbearing years between 25 and 44. In Thompson's view, unrealistic expectations about motherhood may be increasing the risk of depression in women who feel they can't measure up. A former Washington Post reporter who chronicled her battle with suicidal depression in her 1995 book "The Beast," Thompson explores the legacy of an illness that is often passed from grandmother to mother to daughter. She discusses ways the intergenerational link might be broken, based on insights gleaned from her own history and interviews with some of the 400 mothers whose accounts of depression she collected over several years. Following are excerpts from a recent question-and-answer session with the author: What do you mean by maternal depression? Maternal depression, the way I define it, is depression that is created or exacerbated by the stresses of being a mother in this culture at this time. It can be transmitted from mother to child via genetics, environment or through learned behavior -- or more likely a combination of all three things. It's depression as it intersects with motherhood, with the lifetime job of rearing a child. © 2006 The Washington Post Company

Keyword: Depression; Genes & Behavior
Link ID: 9360 - Posted: 06.24.2010

By BENEDICT CAREY In the hour before he was killed, on Sunday, Sept. 3, Dr. Wayne S. Fenton, a prominent schizophrenia specialist, was helping his wife clear the gutters of their suburban Washington house. He was steadying the ladder, asking her to please stop showering debris on his clean shirt; he had just made an appointment to see a patient and wanted to look presentable. She said she would be happy to go along, to help control the patient. It was a running joke between them. For in this part of the country, Dr. Fenton was the therapist of last resort, the one who could settle down and get through to the most severely psychotic, resistant patients, seemingly by sheer force of sympathy and good will. An associate director at the National Institute of Mental Health, he met with patients on weekends, sometimes late at night, at all hours. “Absolutely the most nonthreatening person you ever, ever met,” his wife, Nancy Fenton, said in an interview last week. At 4:52 p.m. that Sunday, the Montgomery County police found the 53-year-old psychiatrist dead in his small office, a few minutes’ drive from his house. They soon tracked down the patient he had agreed to meet that afternoon, Vitali A. Davydov, 19, of North Potomac, who admitted he had beaten the doctor with his fists, according to charging documents. When the young man left the office, “Dr. Fenton was on the ground, bleeding from the face,” the documents said. Copyright 2006 The New York Times Company

Keyword: Schizophrenia
Link ID: 9359 - Posted: 06.24.2010

In their hunt for genes and proteins that explain how animals discern bitter from sweet, a team of Johns Hopkins researchers began by testing whether mutant fruit flies prefer eating sugar over sugar laced with caffeine. Using a simple behavioral test, the researchers discovered that a single protein missing from the fly-equivalent of our taste buds caused them to ignore caffeine's taste and consume the caffeine as if it were not there. "No, you won't see jittery Drosophila flitting past your bananas to slurp your morning java anytime soon," says Craig Montell, Ph.D., a professor of biological chemistry in the Institute of Basic Biomedical Sciences at Hopkins. "The bottom line is that our mutant flies willingly drink caffeine-laced liquids and foods because they can't taste its bitterness -- their taste receptor cells don't detect it." The Hopkins flies, genetically mutated to lack a certain taste receptor protein, have been the focus of studies to sort out how animals taste and why we like the taste of some things but are turned off by the taste of others. By color-coding sweet and bitter substances eaten by fruit flies and examining the coloring that shows up in their translucent bellies, the Hopkins team hoped to learn whether flies missing a specific "taste-receptor" protein changed their taste preferences.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 9358 - Posted: 09.19.2006

By Rhitu Chatterjee When her nest is invaded by bloodsucking mites, the female house finch juggles the birth order of her future offspring. She first lays eggs that will bear daughters--which tend to be hardier--and saves the eggs of her more sensitive sons for last. The strategy ensures that vulnerable male chicks spend less time with the mites and may help explain why the house finch has been so successful in adapting to new environments. The house finch (Carpodacus mexicanus) is the conquistador of the bird world. Confined to the western United States and Mexico until about 1940, the bird quickly set up shop around the country when a few individuals were set loose in New York. Each population has had to overcome the hardships of its new environment, and scientists have long suspected that the secret to the bird's success is an ability to adapt very quickly to small changes in its surroundings. To find how these birds fare in the face of an aggressive adversary, evolutionary biologist Alexander Badyaev and his colleagues at the University of Arizona in Tucson turned to a group of house finches that has lived in Arizona for hundreds of years. During the breeding season in late spring, the bloodsucking nest mite (Pellonyssus reedi) attacks mothers and chicks. As in most bird species, the male chicks are especially vulnerable to danger when born. © 2006 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Evolution
Link ID: 9357 - Posted: 06.24.2010

Neuroscience is tackling a problem that obsessed Hamlet: What is the difference in our minds between talk and action? Less than you would expect, an international research group reports in the Sept. 19 issue of Current Biology. The brain's premotor cortex shows the same activity pattern when subjects observe an action as when they hear words describing the same action, the study's authors said. "If you hear the word 'grasp,' it's actually the premotor cortex that's active, not just a separate, abstract semantic area in the brain," said lead investigator Lisa Aziz-Zadeh, assistant professor of occupational sciences with a joint appointment in the Brain and Creativity Institute of the USC College of Letters, Arts and Sciences. The premotor cortex has long been identified as a center of activity for actions. The notion that it could also process verbal descriptions of those actions has met some resistance. "Neuroscience is coming around to this idea, but there hasn't been much data supporting it," Aziz-Zadeh said.

Keyword: Language
Link ID: 9356 - Posted: 09.19.2006

Helen Pearson In the name of science (and for a small fee), 35 brave individuals volunteered to take part in an extensive taste test of raw broccoli, cauliflower, Brussels sprouts and 25 other bitter vegetables. The results help to explain why some people have a natural aversion to these veggies. Researchers previously knew that the tongue carries a receptor called TAS2R, which comes in several different forms. Only those people carrying a 'sensitive' form of this receptor have been found to be able to taste bitter chemicals such as phenylthiocarbamide (PTC), and researchers had suspected that these same people may be turned off vegetables that contain chemically similar compounds called glucosinolates. But this conclusion was uncertain: in vegetables, the taste of these compounds may be masked by other chemicals. Mari Sandell and Paul Breslin of Monell Chemical Senses Center in Philadelphia, Pennsylvania, wanted to test the theory. They gave the willing victims 17 raw vegetables known to be rich in glucosinolates — a shopping list that includes some vegetables that have nauseated generations of school kids, such as broccoli, cauliflower, Brussels sprouts, radish and turnips. The volunteers also swallowed 11 vegetables that are bitter but lack glucosinolates, including aubergine, bitter melon and spinach. ©2006 Nature Publishing Group

Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 9355 - Posted: 06.24.2010

Rowan Hooper Ever wondered how some people can “put themselves into another person's shoes” and some people cannot? Our ability to empathise with others seems to depend on the action of "mirror neurons" in the brain, according to a new study. Mirror neurons, known to exist in humans and in macaque monkeys, activate when an action is observed, and also when it is performed. Now new research reveals that there are mirror neurons in humans that fire when sounds are heard. In other words, if you hear the noise of someone eating an apple, some of the same neurons fire as when you eat the apple yourself. So-called auditory mirror neurons were known only in macaques. To determine if they exist in humans Valeria Gazzola, at the school of behavioural and cognitive neurosciences neuroimaging centre at the University of Groningen, the Netherlands, and colleagues, put 16 volunteers into functional magnetic resonance imaging (fMRI) scanners and observed their brains as they were played different noises. The volunteers heard noises such as a sheet of paper being torn, or of someone crunching potato chips. Then the same subjects were scanned again, this time whilst tearing a piece of paper, or eating potato chips. “We combined the data from listening and execution and looked to see if the activity in the brain overlaps,” says Gazzola’s colleague Christian Keysers, also at the University of Groningen. Sure enough, it did overlap. Motor neurons associated with mouth actions (crunching) and hand actions (ripping) were activated in both cases. © Copyright Reed Business Information Ltd

Keyword: Autism
Link ID: 9354 - Posted: 06.24.2010

BY ALEX WILLIAMS A FEW days after the terror arrests in London last month, a small commuter plane with three tourists was banking off the coast of Costa Rica when a sudden sound, like a muffled explosion, shattered the calm. The rear door of the plane, improperly shut, had blown open. There was a moment of panic for two of the passengers. But Roger Knox, a graphic designer making a connecting flight before boarding a jetliner home to San Francisco, was not worried. He had just doubled his usual preflight dose of Ativan, a prescription anti-anxiety drug, in anticipation of the ride on the small plane. Mr. Knox, 46, said he is generally so drug-phobic that he doesn’t take aspirin for a headache. But he is also a white-knuckle flier, and over the last few years, with advice from his doctor, he has experimented with drugs to massage his nerves before flying. “My meds never give me a feeling of being high or stoned,” Mr. Knox said. “They can make me a bit drowsy, but for someone used to adrenaline-pumping, think-I’m-going-to-freak-out anxiety, that’s a welcome change.” Terror alerts. Long security lines. Overstuffed transcontinental jets. It’s all more tolerable with a prescription drug to round off the edges, many people have found. Copyright 2006 The New York Times Company

Keyword: Emotions; Learning & Memory
Link ID: 9353 - Posted: 06.24.2010

Roxanne Khamsi An experimental cancer drug has slowed muscular dystrophy in mice with the disease, raising hopes that a simple pill could one day treat the fatal condition in humans. “The results the researchers are reporting are very dramatic and impressive,” says Jeff Chamberlain at the University of Washington School of Medicine in Seattle, US. The researchers caution that the results are preliminary, but say that the approach might offer advantages over other medicines for muscular dystrophy currently in clinical trials. There are many forms of the muscle-wasting disease, but no cure for any of them. The most common form of the illness among children, known as Duchenne muscular dystrophy, involves a mutation for a muscle protein known as dystrophin. Without functioning copies of this protein, muscles weaken, leading to breathing problems and, ultimately, death in the victims' teens or early twenties. Pier Puri at the Burnham Institute in La Jolla, California and colleagues tried to boost muscle function in mice carrying a mutation in the dystrophin gene, by treating the animals with a cancer drug called trichostatin A (TSA). © Copyright Reed Business Information Ltd.

Keyword: Muscles; Movement Disorders
Link ID: 9352 - Posted: 06.24.2010

David Perlman, Chronicle Science Editor Argentine ants, those aggressive unstoppable pests that invade homes and farms throughout California and many other states, live in peace and harmony with each other inside their enormous colonies, but scientists are finally discovering how to make those ants destroy their own relatives in spasms of chemical warfare. In laboratory experiments, researchers have found that when they alter the chemical coding those common household ants carry on the skeletons outside their bodies, all hell breaks loose. The ants, unable to recognize their altered nest mates, will tear the strangers' legs apart, rip off their sensitive antennae and battle them to the death. The research is only in its earliest stages, but the scientists who conducted the experiments say they could be on track to finding a method to wipe out the common Argentine ants without harming any other benign creatures that share their environment. The key to the scientists' research is the unique chemicals the ants carry on the exoskeletons that cover their bodies. The chemicals enable the insects to recognize each other as genetically similar, but when researchers interfered with those recognition signals, the untreated ants became bitter enemies of the ants whose chemical coatings were altered. ©2006 San Francisco Chronicle

Keyword: Chemical Senses (Smell & Taste); Aggression
Link ID: 9351 - Posted: 06.24.2010

By Laura Blackburn If you've ever wondered why the same pint of beer makes you feel slightly more buzzed in the summer than it does in the winter, scientists may finally have your answer. Work with drunk fruit flies suggests that the same molecular mechanisms that help control the body's response to temperature are also involved in alcohol tolerance. Just like in humans, too much alcohol has a toxic effect on a fly. Once imbibed, alcohol--ethanol, actually--makes its way to cell membranes, for example in the nervous system, where it increases their fluidity, much like milk makes cereal soggy. This somehow disrupts the cell's function, translating into what we feel as an alcohol buzz. A cell's membrane fluidity also depends on temperature, becoming more solid as it cools. To keep things from getting too rigid, the cell cranks up its production of fatty acids, which squeeze into the membrane and loosen it up. Because these fatty acids are regulated by proteins that are also involved in ethanol detoxification, evolutionary geneticist Kristi Montooth of Brown University came up with an idea: The regulatory proteins activated during cold weather might help flies better cope with ethanol. © 2006 American Association for the Advancement of Science

Keyword: Drug Abuse
Link ID: 9350 - Posted: 06.24.2010

A new vaccine being tested in a human clinical trial holds a great deal of promise for treating type 1 diabetes, a disease that newly afflicts 35,000 children each year. The research that established the foundation for this vaccine was conducted in UCLA research laboratories. The drug is still being tested and is not likely to be available for at least a few years. "It's the only thing so far that really slows this disease down without adverse side effects," Allan J. Tobin, a UCLA professor emeritus of physiological science and neurology, said about the new drug. "The amazing thing about this emerging story, however, is that it started from basic research on the brain." Tobin, whose laboratory conducted critical neuroscience research in the late 1980s and 1990s, is a member and former director of UCLA's Brain Research Institute. Type I diabetes — also known as insulin-dependent diabetes or juvenile diabetes (because it usually begins in childhood or adolescence) — afflicts more than 1 million Americans. It is characterized by a failure of the body to produce insulin because the immune system attacks and destroys the body's insulin-producing cells of the pancreas. On Sunday, Sept. 17, at a meeting in Copenhagen of the European Association for the Study of Diabetes, Johnny Ludvigsson — pediatrics professor at Sweden's University Hospital, Linköping University — will present results from the phase II study conducted in eight hospitals in Sweden in collaboration with Diamyd Medical (www.diamyd.com), a life science company located in Stockholm, Sweden.

Keyword: Obesity
Link ID: 9349 - Posted: 06.24.2010

A new study directed by Mount Sinai School of Medicine extends and strengthens the research that experimental dietary regimens might halt or even reverse symptoms of Alzheimer's Disease (AD). The study entitled "Calorie Restriction Attenuates Alzheimer's Disease Type Brain Amyloidosis in Squirrel Monkeys" which has been accepted for publication and will be published in the November 2006 issue of the Journal of Alzheimer's Disease, demonstrates the potential beneficial role of calorie restriction in AD type brain neuropathology in non-human primates. Restricting caloric intake may prevent AD by triggering activity in the brain associated with longevity. "The present study strengthens the possibility that CR may exert beneficial effects on delaying the onset of AD- amyloid brain neuropathology in humans, similar to that observed in squirrel monkey and rodent models of AD," reported Mount Sinai researcher Dr. Pasinetti and his colleagues, who published their study, showing how restricting caloric intake based on a low-carbohydrate diet may prevent AD in an experimental mouse model, in the July 2006 issue of the Journal of Biological Chemistry. "This new breakthrough brings great anticipation for further human study of caloric restriction, for AD investigators and for those physicians who treat millions of people suffering with this disease" says Giulio Maria Pasinetti, M.D., Ph.D., Professor of Psychiatry and Neuroscience, Director of the Neuroinflammation Research Center at Mount Sinai School of Medicine and lead author of the study. "The findings offer a glimmer of hope that there may someday be a way to prevent and stop this devastating disease in its tracks."

Keyword: Alzheimers; Obesity
Link ID: 9347 - Posted: 09.16.2006