 Inside this issueCover storiesA brother’s gift launches Yale ScholarsCity vote clears way for building of cancer treatment centerMedical school names new dean of public healthPartnershipsGrants & contractsPeopleTwo Yale biologists receive Gairdner AwardsLifelines: A steadying influenceOut & aboutAwards & honorsEducationYale scientist named “million-dollar professor” for teaching planPediatric neurologist is new associate dean for YSM admissionsScienceMeeting the demand for blood supply: Yale makes strides in vessel engineeringDiving deep into a data wave to help make surgery saferAn eye for scienceAdvances: Why 2 percent is a world of difference | This is your brain on an empty stomach | Cells fall on sword to stop Legionnaire's| Maki de Sade: wasabi really hurts!HealthMinimizing pain, accelerating healingWith surgical simulation, practice makes perfectDisability is no dead-end for elders, Yale research finds 
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AdvancesHealth and science news from YaleWhy 2 percent is a world of difference
Genomically speaking, we are 98 percent chimp, and for decades, biologists have puzzled over how this small genetic modification could create such vastly different creatures. To explore this question, Kevin P. White, Ph.D., associate professor of genetics, and his colleagues developed a gene chip to compare the activity of more than 1,000 genes from humans, chimpanzees, orangutans and rhesus macaques, four species spanning 70 million years of evolution. As reported in the March 9 issue of Nature, the team found that genes that code for regulatory proteins are four times more likely to have increased their expression during human evolution than those that govern housekeeping or metabolic functions. Monkeying with gene regulators can give rise to dramatically different new traits, like brain size or body shape, because the proteins serve as master switches that influence the activity of many other genes. “For 30 years scientists suspected that gene regulation has played a central role in human evolution,” says White. “This helps open the door to a functional dissection of the role of gene regulation during the evolution of modern humans.” This is your brain on an empty stomachCutting calories can definitely make you trimmer, and may help you live longer. Now a new Yale study suggests that dieting might also keep you mentally sharper. Blood levels of a gut hormone called ghrelin (rhymes with “melon”) rise when the stomach is empty, flooding the brain’s eating control center and stimulating neurons that govern appetite. When Tamas L. Horvath, D.V.M., Ph.D., chair and associate professor of comparative medicine, and colleagues injected mice with ghrelin, the hormone rapidly altered circuits in the hippocampus, a brain region that is crucial to learning and memory. Ghrelin-treated mice were significantly better at learning and remembering their way around a maze. In people, aging and obesity—two factors associated with memory loss in Alzheimer’s disease—cause ghrelin levels to fall. Horvath’s results, published in the March issue of Nature Neuroscience, suggest that shoring up ghrelin levels with weight reduction or drugs that mimic its action could help stave off dementia. Cells fall on sword to stop Legionnaire’s
Like a deadly stowaway, Legionella pneumophila, the bacterium that causes Legionnaire’s disease, (see photo) hides inside cells to evade detection by the immune system. Holed up in sealed vacuoles, the germs multiply, causing fatal pneumonia in up to a quarter of those infected. But the immune system usually outwits Legionella. In the March issue of the journal Nature Immunology, Associate Professor of Microbial Pathogenesis Craig R. Roy, Ph.D., and colleagues show that immune cells detect Legionella and destroy it by inducing cells to commit suicide. Roy’s team found that a protein called Birc1e detects any bits of bacteria that escape vacuoles and activates the caspase-1 protease, a master regulator of cell death. Caspase-1 degrades proteins in infected cells, starting a cascade of events that end with the cell’s demise—and the elimination of Legionella. “Identification of Birc1e and the caspase cascade gives us information about the process of how the body fights off infection by a potentially lethal microbe, as well as possible targets for treatments,” says Roy. Maki de Sade: wasabi really hurts!For pain researchers, the recent discovery of a neuronal receptor that relays the zip of wasabi holds more than gastronomic interest: the sinus-clearing kick of the Japanese condiment registers not on the taste buds, but in pain-sensing nerve cells in the nose. According to Assistant Professor of Pharmacology Sven-Eric Jordt, Ph.D., and collaborators, the newly identified receptor is also key to garlic’s bite, and to the toxic and inflammatory effects of many environmental irritants. As reported in the March 24 issue of Cell, mice lacking the TRPA1 receptor experience little pain or irritation when mustard oil, the pungent ingredient in wasabi and mustard, is applied to their paws. Neurons in these mice also failed to respond to the main irritant found in tear gas, wood smoke and car exhaust, and the animals were less sensitive to some types of inflammatory pain. Jordt says that finding ways to shut down the TRPA1 receptor in people could yield much-needed new pain therapies for injuries and diseases from arthritis to cancer, and that manipulating the receptor might also help pollution-related diseases like asthma and chronic cough. 
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