Inside this issueCover storiesPreserving options, sustaining hope$2 million gift will support training of physician-scientistsBoehringer and Yale combine strengths in new research alliancePartnershipsGift honors Nobelist, sponsors visits by top neuroscientistsGrants & contractsPeopleLifelines: Mending the human machineYale scientist shares $1 million Dan David prize for work on cell signaling and cancerCT scanning expert is new leader of Yale radiologistsMedical historian Warner is appointed to Avalon ProfessorshipOut & aboutAwards & honorsScienceCan microRNAs put the brakes on cancer?Advances: Bullies are no match for gene knockout | Parasite’s accomplice gets genetic mug | Along for the ride when cells divide | Are skin cells guards or go-betweens?HealthStudent-run clinic is a HAVEN for uninsuredThe power of Botox, a drug with many facesEducationYale innovation in the art of observation extends its reach 
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AdvancesHealth and science news from YaleBullies are no match for gene knockout
After repeated harassment by larger, more aggressive members of their species, mice withdraw from social contact, exhibiting behavior that is strikingly similar to that seen in humans with depression, social phobia and post-traumatic stress disorder. Using a video system that creates a map of a mouse’s movements, Assistant Professor of Psychiatry Ralph J. DiLeone, Ph.D., and colleagues found that a normal mouse (white trail in left panel) will frequently interact with another mouse placed at one side of its enclosure, but a mouse “defeated” by aggressors (black trail) will shy away. Pleasurable social experiences activate reward pathways in the brain that are also stimulated by drugs of abuse, so the team wondered whether this socially withdrawn behavior might be governed by those same circuits. As reported in the February 10 issue of Science, when the scientists selectively shut down the gene for a protein known as BDNF in an important brain reward center, mice did not develop social withdrawal in response to aggression, suggesting that BDNF in the reward pathway may be a fruitful target for new psychiatric drugs. Parasite’s accomplice gets genetic mugAs many as 500,000 people per year in sub-Saharan Africa contract sleeping sickness, which can cause severe, irreversible damage to the nervous system. The illness is transmitted by blood-sucking tsetse flies, but only when they are themselves infected by the protozoan parasite Trypanosoma brucei, which is passed into humans when the tsetse bites. In addition to T. brucei, the tsetse gut is also host to two so-called good bacteria that manufacture nutrients not found in the fly’s blood diet but crucial to its survival. In a joint project with colleagues in Japan reported online in the February issue of Genome Research, Professor of Epidemiology Serap Aksoy, Ph.D., sequenced the complete genome of Sodalis, a beneficial bacterium passed on by tsetse mothers to their larvae. The new sequence will allow scientists to better manipulate the functions of Sodalis to gain insights into tsetse biology that could lead to novel ways to fight sleeping sickness, Aksoy says. “If we get rid of these symbiotic bacteria, the flies become sterile. Understanding what they provide to the flies is very important from a vector-control point of view.” Along for the ride when cells divide
When a daughter leaves home, she packs her bags with provisions she’ll need to strike out on her own. A daughter cell—the new cell formed when a cell reproduces by dividing—does the same, gathering up copies of its parent cell’s organelles before it separates. One organelle, the Golgi apparatus, sorts and modifies proteins and packages them to be shuttled to proper sites in the cell. In most animal cells the Golgi comprises several hundred stacks stitched together into a ribbon, but in Trypanosome brucei, the parasite that causes sleeping sickness, there is just one Golgi stack. Professor of Cell Biology Graham B. Warren, Ph.D., capitalized on this simplicity in a study published in the November 18 issue of Science that illuminates how new Golgi are formed in daughter cells. When Warren and his colleagues tagged T. brucei organelles with fluorescent labels and watched through microscopes as the parasite divided, they discovered a new, as yet unnamed structure (lower green form in photo) that orchestrates the duplication of Golgi (red) in daughter cells. Are skin cells guards or go-betweens?Accounting for 15 percent of our body weight, and with an average surface area of 20 square feet, the skin is the body’s largest organ. In addition to providing a rugged protective sheath, the skin is studded with immune system cells. Langerhans cells (LCs) in the epidermis have long been thought to spur the immune system into action when we encounter pathogens, and overactive LCs have been implicated in autoimmune diseases of the skin. But an unexpected result reported on the cover of the December 15 issue of Immunity by Daniel H. Kaplan, M.D., Ph.D., assistant professor of dermatology, and Mark J. Shlomchik, M.D., Ph.D., professor of laboratory medicine and immunobiology, may force a rethinking of these ideas. When the researchers engineered mice that lacked LCs at birth, they expected the animals to be resistant to allergic skin reactions. Instead, these mice have skin that is far more sensitive than normal mice. “We now view these cells not just as sentinels or stimulators of immune
reactions, but as peacekeepers with the environment,” says Shlomchik. “Failure
of this mechanism could result in chronic inflammatory skin conditions like
lupus and psoriasis.” 
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