Inside this issueCover storiesPassing the torchAcquisition of Bayer site will accelerate biomedical researchInternational effort rewrites the book on the human genomePartnershipsFoundation supports Yale research “of practical benefit”Grants & contractsPeopleLifelines: Lawrence CohenYale scientist is new president of Wellesley CollegeTop heart surgeon is named Glenn ProfessorDiabetes experts win top scientific honorsObstetrics/gynecology chair is honored as leader and writerOut & aboutAwards & honorsScienceFinding a new chink in cancer's armorResearch center aims to make rickets historyBrewing a new treatment for kidney diseaseAdvances: Putting a squeeze on Lyme disease | These mice like to spend time chilling | Hearing voices: A brain out of sync? | Stem cells show promise in Parkinson's  
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AdvancesHealth and science news from YalePutting a squeeze on Lyme disease
The Centers for Disease Control and Prevention recently reported that the incidence of Lyme disease, caused by the tick-borne bacterium Borrelia burgdorferi, has more than doubled in the past 15 years, with most cases concentrated in New England. Now, Yale scientists have found a loophole in the bacterium’s life cycle that offers a way to stop ticks from ever carrying the disease, which they pick up as larvae when they suck blood from mice. Erol Fikrig, M.D., professor of medicine, epidemiology and microbial pathogenesis, and colleagues discovered that B. burgdorferi takes advantage of a protein that ticks inject into mice when they bite to prevent an immune response and swelling. When the researchers blocked this protein, either by stopping ticks from producing it in their salivary glands, or by coaxing the mice to obstruct it, the B. burgdorferi couldn’t go from mouse to tick. The findings, published in the inaugural issue of Cell Host & Microbe in July, may eventually help curb infections in humans by targeting the bacterium at this early stage in its lifecycle. “You could reduce the number of ticks carrying Lyme disease,” says Fikrig. “That’s the long-term goal.” These mice like to spend time chillingWhen breath mints are called “cool” on television, it’s truth in advertising, according to a new study by Sven-Eric Jordt, Ph.D., assistant professor of pharmacology, and colleagues from the University of California at San Francisco and the University of Wisconsin. The team reports in the July 12 issue of Nature that mouse neurons engineered to lack TRPM8, an ion channel receptor involved in detecting the cooling sensation produced by menthol, were profoundly less sensitive to both menthol and cool temperatures. In further experiments, when mice lacking TRPM8 were placed on test surfaces that included cool areas, they were far less likely than normal mice to avoid those spots. However, if these areas were cooled below 15 °C (59 °F), TRPM8-deficient mice avoided them as much as normal mice, suggesting that temperatures below this threshold may stimulate pain pathways that do not rely on TRPM8. The importance of TRPM8 in detecting menthol is well-established, but some researchers disputed its role in cold detection. For now, it seems, the issue’s been iced. Hearing voices: a brain out of sync?
Some 200 milliseconds before you speak, brain cells in your motor cortex fire in concert, predicting the sounds you are about to produce. This electrical discharge instructs your auditory cortex to disregard any matching signals coming from your ears, which keeps you from being distracted by the sound of your own voice. But the story may be different for patients with schizophrenia, as Judith Ford, Ph.D., and collaborators suggest in the March issue of the American Journal of Psychiatry. The researchers found that brain activity synchronized shortly before the onset of speech, possibly reflecting communication between the motor and sensory cortex. However, in patients with severe auditory hallucinations, this pre-speech synchronization is weaker, and the brain’s reaction to self-generated speech is not dampened: patients who hear voices seem less able to recognize their own. Next on the authors’ list is to repeat the study for the “inner speech” that accompanies thinking to see whether a lack of synchronization may cause patients with schizophrenia to mistakenly perceive their inner thoughts as external voices. Stem cells show promise in Parkinson’sThe symptoms of Parkinson’s disease (PD)—muscle rigidity, tremor and a general slowing of movement—have been successfully treated in monkeys using human stem cells. PD is caused when large numbers of dopamine-producing cells (DA cells) die off in a brain region known as the substantia nigra. In the July 17 issue of Proceedings of the National Academy of Sciences, a team headed by D. Eugene Redmond Jr., M.D., professor of psychiatry and neurosurgery, reports that human neural stem cells implanted into one side of the substantia nigra in monkeys with severe Parkinsonian symptoms migrated and survived on both sides, where many displayed biochemical markers indicating that they had matured into DA cells. Other implanted cells also migrated to key regions and appeared to play a nurturing role, creating a protective microenvironment that restored the function of the monkeys’ own surviving DA cells. Over a four-month period, the monkeys treated with stem cells had vastly improved. “Not only are stem cells a potential source of replacement cells,” says Redmond, “they also seem to have a whole variety of effects that normalize other abnormalities.”  |
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