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Primary Insomnia Linked to Neurochemical Abnormality

For the first time, researchers have identified a specific neurochemical abnormality in adults with primary insomnia. Primary insomnia is difficulty getting to sleep or staying asleep, or having non-refreshing sleep, for at least one month without any known physical or mental condition. The current study results indicate that gamma-aminobutyric acid (GABA), the most common inhibitory transmitter in the brain, is reduced by nearly 30 percent in individuals who suffer from primary insomnia for more than six months. These findings suggest that primary insomnia is a manifestation of a neurobiological state of hyperarousal, which is present during both waking and sleep at physiological and cognitive levels. "Recognition that insomnia has manifestations in the brain may increase the legitimacy of those who have insomnia and report substantial daytime consequences," said Dr. John Winkelman, of Brigham and Women’s Hospital at Harvard Medical School, the principal investigator on the study. "Insomnia is not just a phenomenon observed at night, but has daytime consequences for energy, concentration, and mood." This work was reported June 9 at SLEEP 2000, the 23rd Annual Meeting of the Associated Professional Sleep Societies. [Press release]

Active Microenvironment May Provide Treatment Targets for Prostate Cancer

In a study of the response of prostate stroma (the surrounding structural framework of the prostate gland) to prostate cancer, researchers at the Baylor College of Medicine have identified 1,141 genes whose expression is altered in this response. Among the gene expression changes are ones that induce the formation of new structures such as blood vessels, nerves, and parts of nerves. These changes may explain why men with reactive stroma face a more aggressive disease, said Dr. Michael Ittmann, a senior author of the report. "Often in prostate cancer, you don't see much change in the stromal cells," said Dr. Ittmann. "However, in this subgroup of patients (in which the stroma become visibly reactive), you see a histologically recognizable change in the appearance of the stroma. Dr. (Gustavo) Ayala (another senior author of the report) has shown previously that this correlates with a bad prognosis. We know the stroma are doing something to promote bad behavior in cancer cells." "These findings are very important as this is the first step in discovering pathways and mechanisms in the tumor microenvironment that could be targeted as a novel therapeutic approach to treat prostate cancer by treating the cancer microenvironment niche,” said Dr. David Rowley, another author of the report, which was published in Clinical Cancer Research. [Press release]

Genetic Roots of Animal Tameness Discovered in Rats

In breeding studies conducted in rats, an international team of researchers has identified genomic regions associated with tameness. The discovery could help animal breeders, farmers, zoologists, and anyone else who handles and raises animals to more fully understand what makes some animals interact with humans better than do others. It may also lead to more precise breeding strategies designed to pass specific genes from one generation to the next as a way to produce tame animals. “I hope our study will ultimately lead to a detailed understanding of the genetics and biology of tameness," said Dr. Frank Albert, the lead author of the research report. "Maybe we'll then be able to domesticate a few of those species where humans have historically not been successful, like the wild African Buffalo." For this study, two groups of rats, one bred for tameness toward humans and the other bred for aggressiveness toward humans, were mated with each other and genomic regions associated with tameness and with aggressiveness were identified. The senior author of this study was Dr. Svante Paabo. The research was published in the June issue of Genetics. [Press release] [Genetics abstract]

New Class of Alkaloids Found in Amazonian Poison Frogs

Scientists have identified a new class of alkaloids in some Amazonian poison frogs (family Dendrobatidae). The class of alkaloids, N-methyldecahydroquinolines, has not been previously identified in the frogs or, it is believed, in nature. Senior author Dr. H. Martin Garraffo and colleagues noted that there are more than 500 alkaloids, potentially toxic substances, known to exist in the skin of poison frogs of the family Dendrobatidae. The frogs use the alkaloids as a chemical defense to discourage predators from biting and eating them. Western Colombian natives have used skin extracts from another group of frogs, unrelated to those in the new study, to coat blow-darts for hunting. The frogs obtain nearly all of the alkaloids from their diet--removing the chemicals from ants, mites, small beetles, millipedes, and possibly other small arthropods; concentrating them with incredible efficiency; and storing them in their skin. Although the researchers speculate that the frogs could get the new alkaloids from ants, they are, in fact, not certain about the origin of the chemicals, which could also be produced in the frogs' own bodies. Feeding experiments with alkaloids fed to captive frogs are planned, which might settle this point. This work was published online ahead-of-print in the American Chemical Society’s Journal of Natural Products and is scheduled for publication in the June 26 issue of the journal. [Journal of Natural Products article]

Lifespan-Extending Mutations Activate Germ Cell Pathways in Somatic Cells

Scientists at Massachusetts General Hospital and Harvard Medical School have shown that mutations extending lifespan in the experimental roundworm C. elegans induce expression of germline genes and pathways in somatic cells. "C. elegans mutants with extreme longevity accomplish this feat, in part, by adopting genetic programs, normally restricted to the germline, into somatic cells," said Dr. Sean Curran, the study's lead author. "We know that germline cells are more stable than somatic cells--they live longer and are more resistant to stresses that damage other cells--and understanding the molecular pathways involved in that stability may someday allow us to devise therapies protective against age-related decline in other tissues." Earlier, senior author Dr. Gary Ruvkun and other researchers had discovered that simple mutations in genetic pathways conserved throughout evolution can double or triple the lifespan of C. elegans, and that similar mutations in the corresponding pathways also dramatically extend mammalian lifespan. "The idea that somatic cells can reacquire genetic pathways usually restricted to germline cells is fascinating, and since germline protection is seen across species, the activity of these genes may play a role in controlling mammalian lifespan," said Dr. Ruvkun. "Understanding the mechanisms involved in this transformation could help us develop new ways to repair and even regenerate key cells and tissues." Dr. Ruvkun was a co-recipient of the 2008 Lasker Award for Basic Medical Research for his role in discovering that tiny molecules of RNA can control the activity of critical genes. The current research was published online in Nature on June 7.

Deep-Sea Bacterium May Be Potent Anti-Pollutant Tool

Scientists in China have shown that a particular strain of bacterium isolated from sediments deep beneath the Pacific Ocean might provide a powerful clean-up tool for heavy metal pollution. The researchers showed that Brachybacterium, strain Mn32, is highly effective in removing manganese from solutions, converting it to insoluble manganese oxides. Not only did the bacterium directly oxidize the manganese but the resulting oxides themselves also absorbed the metal from the culture solution, making Brachybacterium, strain Mn32, a potentially useful candidate for use in bioremediation and cleaning up pollution. In addition to removing manganese from its environment, the Brachybacterium also absorbed significant amounts of zinc and nickel. All of these metals are found as pollutants in water and soils contaminated by heavy industries such as steel-making. Senior author Dr. Gejiao Wang said that “the next stage of our research is to immobilize this bacterial strain into a bioreactor to test its ability to remove manganese and other heavy metals in such a system. If successful, it could provide a more efficient way to clean up heavy metal pollutants." This work was reported in the June issue of Microbiology. [Press release] [Microbiology abstract]

Electronic “Smart Pill” Used to Measure Acidity in Ulcerative Colitis

A recently developed electronic diagnostic tool called the SmartPill has been used to measure the pH in the digestive tracts of patients with the chronic inflammatory disease ulcerative colitis (UC). Using the SmartPill, researchers at NewYork-Presbyterian/Weill Cornell Medical Center have shown that patients with mild to moderate UC have significantly more acidic pH in their colons, compared with the average person--a finding that may impact treatment strategy. "By using the SmartPill to measure the pH throughout the digestive tract, we were able to see how the pH levels can vary in patients with ulcerative colitis. This may help us understand why some drug treatments are more effective than others," said Dr. Brian Bosworth, the lead investigator on the study. Administered in the physician's office, the SmartPill allows the patient to go about his or her normal routine during the course of the test. As the wireless SmartPill capsule passes through the gastrointestinal tract, it transmits data--including pressure, pH, and temperature--to a SmartPill data receiver worn by the patient. Once the single-use capsule has passed from the body, the patient returns the data receiver to the physician who can then download the collected data to a computer, where it can be analyzed. This particular study was presented on June 3 at the Digestive Disease Week meeting in Chicago. [Press release] [SmartPill information] [Ulcerative colitis information]

Genome of Honey Bee-Killing Parasite Is Sequenced

Researchers at the USDA’s Agricultural Research Service, and colleagues, have reported the draft sequencing of the genome of a parasite that can kill honey bees. The parasite, Nosema ceranae, is one of many pathogens suspected of being responsible for the current decline in honey bee populations. This decline has been attributed to what is called colony collapse disorder (CCD). In 2006, CCD began devastating commercial beekeeping operations, with some beekeepers reporting losses of up to 90 percent, according to the USDA. Researchers believe CCD may be the result of a combination of pathogens, parasites, and stress factors, but the cause remains elusive. At stake are honey bees that play a valuable part in a $15 billion industry of crop farming in the United States. The microsporidian Nosema is a fungus-related microbe that produces spores that bees consume when they forage. Infection spreads from the bee’s digestive tract to other tissues. Within weeks, colonies are either wiped out or lose much of their strength. One Nosema species, Nosema apis, was the leading cause of microsporidia infections among domestic bee colonies until recently, when N. ceranae jumped from Asian honey bees to the European honey bees used commercially in the United States. Sequencing the N. ceranae genome should help scientists trace the parasite's migration patterns, determine how it became dominant, and help resolve the spread of infection by enabling the development of diagnostic tests and treatments. This work was published June 5 in PLoS Pathogens. [Press release] [PLoS Pathogens article]

Novel Brain Protein May Be Key to Huntington Disease Mystery

Scientists at Johns Hopkins have shown evidence that a novel protein (Rhes) located chiefly in a key area of the brain (the corpus striatum), may be a clue to the mystery of why abnormal huntintin protein, although present in cells throughout the body, exerts its cell-killing and disease-causing effects primarily in the corpus striatum. The findings, according to the Hopkins scientists, explain the unique pattern of brain damage in Huntingtin disease (HD) and its symptoms, as well as offer a strategy for new therapy. “It's always been a mystery why, if the protein made by the HD gene is seen in all cells of the body, only the brain, and only a particular part of the brain, the corpus striatum, deteriorates," said Dr. Solomon H. Snyder, senior author of the report. "By finding the basic culprit (Rhes), the potential is there to develop drugs that target it and either prevent symptoms or slow them down." In their work, the researchers showed that the Rhes protein interacts with the huntingtin protein, but much more strongly with the mutant, disease-causing version than with the normal version. They further showed that presence of both the Rhes protein and the huntingtin protein in cells led to speedy cell death, while the presence of either protein alone did not. They also observed that the presence of the Rhes protein resulted in less clumping of the huntingtin protein in cells, than did the absence of Rhes protein. This could be an explanation for why, in HD, less clumping of huntingtin is observed in the corpus striatum than in the unaffected cells in the body, even though clumping has been proposed, by some, as a cause of the disease. "Here's the Rhes protein, we've known about it for years, nobody ever really knew what it did in the brain or anywhere else," said Dr. Snyder.

Personalize Medicine (Bioinformatics) Conference to be Held at San Francisco State

A one-day conference entitled “Personalized Medicine 2.0—Bioinformatics: Mining the Data” will be held at San Francisco State University on Thursday, June 4, from 9 am through 7 pm. The conference will be held in the Seven Hills Center at the University, 1600 Holloway Avenue. Full details and registration can be found at the link below. You may register online, at the door, or by contacting Jen Javernick at jjav@sfsu.edu or at 415-405-2636. The conference is described as an exciting, one-day conference and networking opportunity for scientists, educators, and health & industry professionals. Personalized medicine is the application of genomic data to ensure the delivery of the right treatments and preventive measures to the right patient at the right time, ushering in a new era of affordable healthcare delivered with laser precision. Personalized Medicine 2.0 is the second annual one-day conference focused on the perspectives of non-profit and corporate research, biotechnology, academic, and diagnostic leaders with concentration on how the evolving landscape is revolutionizing medical care. The conference will explore what happens "on the ground" when personalized medicine is put into practice, and what that means for caregivers and patients, as well as for the industries that develop products for personalized medicine. This year, the conference will concentrate on the role of bioinformatics, data mining, and systems biology in advancing personalized medicine. Speakers and panelists are from Genentech, Burrill & Company, Navigenics, UCSF, Pathwork Diagnostics, and more. The conference is an opportunity to network with the scientists, employers, and business leaders driving the future of healthcare. [Conference info and registration]

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