Inside this issueCover storiesThree decades at the helm, and a legacyExperts on mental illness, multiple sclerosis are newest chairs
Emergency Medicine rises to independent academic department
PeopleLifelines: Fred Volkmar
Immunobiologist earns new award for top young scientistsTo honor his mother and fight melanoma, a rower shows his mettleDiabetes expert is appointed inaugural Cowgill ProfessorLeading geriatrics researcher is Humana Foundation ProfessorImmunobiologist is named Eugene Higgins Professor
Out & aboutScienceIn Yale autism research, the eyes have it
Advances: How to unleash an appetite suppressant | Genetic footprints on the trail of Lyme disease | Viruses make a move to infect new cellsHealthKeeping needs of young families in mindAdvances: Best use of flu shots? Kids and young adultsPartnershipsGrants & contracts  
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AdvancesHealth and science news from YaleBest use of flu shots? Kids and young adultsTo prepare for outbreaks of influenza, both seasonal flu and the H1N1 (“swine flu”) strain, the Centers for Disease Control and Prevention (CDC) and its Advisory Committee on Immunization Practices (ACIP) have compiled mass vaccination guidelines. But in the August 20 issue of Sciencexpress, Alison P. Galvani, Ph.D., associate professor of epidemiology, and Clemson University’s Jan Medlock, Ph.D., published mathematical models predicting that current CDC/ACIP recommendations would produce far from optimal results in a pandemic. The team found that prioritizing vaccination for the 5 to 19 age group—which is responsible for most flu transmissions—and the 30 to 39 age group would be more effective than CDC/ACIP guidelines. For example, the model showed that if 40 million doses of H1N1 vaccine were distributed by ACIP guidelines in an outbreak following the pattern seen in the 1918 flu epidemic, there would be 59 million infections, 853,000 deaths, and a total cost of $939 billion. Under Medlock and Galvani’s proposal, those numbers were cut to 44 million, 645,000, and $703 billion, respectively. How to unleash an appetite suppressantFirst isolated by the late Aaron B. Lerner, M.D., Ph.D., a renowned Yale researcher and dermatologist, α-melanocyte-stimulating hormone, or α-MSH, is a pituitary hormone with a variety of effects. In the skin and hair, α-MSH stimulates the release of melanin, causing dark pigmentation; in the brain, the hormone acts as a powerful, but short-lived, appetite suppressant. To discern why α-MSH is deactivated so rapidly, a group led by Sabrina Diano, Ph.D., associate professor of obstetrics, gynecology, and reproductive sciences and of neurobiology, examined two closely related mouse strains, one fat and one lean. As Diano and her colleagues report in the July 20 issue of The Journal of Clinical Investigation, the leaner mice lacked a gene that codes for an enzyme known as PRCP. The team then demonstrated that PRCP blunts α-MSH’s action by knocking off a single amino acid. Moreover, the group showed that PRCP is abundant in nerve cells of the hypothalamus, a brain region known to govern eating behavior. “Our findings provide a possible new target for the development of drugs to control metabolic disorders such as obesity and type 2 diabetes,” says Diano.
Genetic footprints on the trail of Lyme diseaseIn post-Colonial America, settlers’ need for fuel, building materials, and tillable land led to unprecedented deforestation. Between 1830 and 1880, nearly 80 percent of New England’s forests disappeared. A genetic analysis of the bacterium that causes Lyme disease, reported by School of Medicine scientists in the August 14 online issue of Proceedings of the National Academy of Sciences, suggests that the disease, which is transmitted by deer ticks, largely disappeared from New England along with the trees, but roared back when the region was reforested and deer returned. Samples of the Lyme disease bacterium Borrelia burgdorferi from ticks in the Midwest and Northeastern U.S. showed genetic variations that suggest the disease was widespread for thousands of years but retreated to pockets of the northern Midwest and isolated islands off the New England coast after deforestation. “The current epidemic of Lyme disease is the result of infected ticks expanding their range independently from these isolated refuges,” says Durland Fish, Ph.D., professor of epidemiology and senior author of the paper. “This expansion is likely to continue until the ticks, and the diseases they carry, return to their former range.” Viruses make a move to infect new cellsRetroviruses, which cause HIV/AIDS and some forms of leukemia, spread 1,000 times more efficiently when uninfected cells are in physical contact with infected cells. But scientists have been unsure exactly why cell-to-cell contact has such a strong influence on this process. Walther Mothes, Ph.D., associate professor of microbial pathogenesis, and colleagues used four-dimensional imaging (in 3-D space over time) to track the assembly and movement of individual particles of murine leukemia virus (MLV) in living cells. As reported in the July issue of PLoS Biology, the study, led by Postdoctoral Fellow Jing Jin, Ph.D., found that MLV expresses an adhesion protein that docks with uninfected cells and recruits other viral proteins to these sites to assemble new viruses. When the team deleted the “tail” of this protein, new viral particles did not assemble at the jumping-off point between cells. “We are just opening the door to this whole process,” Mothes says. “Our hope is that somewhere down the road we will have a completely new antiviral strategy based on targeting cell-to-cell transmission.” |
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