Inside this issueCover storiesFor patients, research ... and for Yale‘Thriving survivor’ tells his taleOpportunities for giving to Smilow Cancer HospitalPartnershipsGrants & contractsPeopleLifelines: Sukru EmreStructural biologist wins top science prizeThree faculty members elected to Institute of MedicineExpert on protein-folding is named Sterling ProfessorSurgical oncologist is appointed Lampman Professor of SurgeryYoung scientists honored at White HouseNew AAAS FellowsOut & aboutScienceNew building is a ‘place for great science’Connecticut high schoolers get a taste of real-world researchNew NIH program funds scientific ‘innovators’ at YaleAdvances: Does breastfeeding build better brains? | An Akt against heart disease | Of bugs, bivalves and breathing | Adding staying power to brain tumor drugs  
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Advances
Health and science news from YaleDoes breastfeeding build better brains?
For some infants, being breastfed means a higher IQ later in life. But for others, breastfeeding doesn’t boost IQ score at all. A small difference in one gene, it turns out, makes all the difference. The gene, FADS2, helps turn the fatty acids found in breast milk into compounds important to brain development. A team of researchers including Julia Kim-Cohen, Ph.D., assistant professor of psychology at Yale, discovered that children who have one version of FADS2 and who were breastfed scored 7 points higher on IQ tests administered up to age 13 than those who carry the same gene variant but drank formula milk. But for children who don’t have the special version of the gene, there was no IQ difference associated with being fed breast milk versus formula, the scientists report in the November 20 issue of Proceedings of the National Academy of Sciences. “Previous research linking breastfeeding to IQ has been somewhat inconsistent. This gene may help explain that inconsistency,” says Kim-Cohen, who is now studying whether FADS2 and other genes play a role not only in cognitive development but in the emotional development of children. An Akt against heart diseaseAs blood courses through the 100,000 miles of vessels in an adult’s circulatory system, cholesterol, fats and other debris can coat the walls of arteries, forming the dangerous, rupture-prone plaques of atherosclerosis. Scientists believe that atherosclerosis begins after damage to the endothelium, the innermost layer of cells that lines artery walls, but they are still learning about the genes that prevent—or promote—its progression. In the December issue of Cell Metabolism, a team led by William C. Sessa, Ph.D., professor of pharmacology and director of the medical school’s program in Vascular Biology and Therapeutics, describes a key gene in the development of coronary atherosclerosis. In mice prone to atherosclerosis, the loss of the gene Akt1 decreased endothelial production of the gas nitric oxide, leaving the endothelium even more susceptible to damage and the formation of fatty plaques. Mice lacking Akt1 also had more plaques in the aorta and coronary arteries, making them a valuable new model to understand acute coronary syndromes, such as unstable angina and heart attacks, in humans. Of bugs, bivalves and breathing
Chitin, a tough natural polymer, is an important component of fungal cell walls and the bodies and eggs of parasitic worms, so both plants and mammals have evolved chitin-degrading enzymes known as chitinases to ward off infection. But chitin is also found in crustacean and clam shells and in insect exoskeletons, making it the second-most abundant biopolymer on Earth. According to Geoffrey L. Chupp, M.D., associate professor of medicine, and colleagues in Paris and Wisconsin, the chitin-related mechanism that protects us from fungi and parasites may also be contributing to a global rise in asthma rates by reacting to shellfish or the chitin-encased dust mites that roam about in our mattresses and carpets. As reported in the November 15 issue of the New England Journal of Medicine, Chupp’s research group found that levels of YKL-40, a chitinase-like protein, are significantly elevated in patients with severe asthma, defined as those who use rescue inhalers and oral corticosteroids most frequently and require hospitalization for their asthma most often. Although the study doesn’t prove that YKL-40 is involved in causing asthma, it demonstrates that the protein can be used as a reliable measure of asthma severity. Jack A. Elias, M.D., chair and Waldemar Von Zedtwitz Professor of Medicine and senior author of the new paper, says the study is among the first to define a parameter for asthma that can be assessed with a blood test. “This may allow us to identify a subpopulation of patients with severe asthma and give us insights into the biologic processes that make the disease so severe in these individuals," Elias notes. "Our studies also have demonstrated that eliminating YKL–40 decreases specific types of tissue inflammation—which could be of particular benefit to asthmatic patients with an elevated level of this protein.” Adding staying power to brain tumor drugsWhen a surgeon removes a brain tumor, it’s routine to leave chemotherapy drugs in place of the cancer. But it’s notoriously tricky to get these drugs to sufficiently penetrate the brain; blood flowing through capillaries sweeps the small molecules out of the dense tissue before they can make much of an impact. But W. Mark Saltzman, Ph.D., Goizueta Foundation Professor of Chemical and Biomedical Engineering, and colleagues at Cornell University have made one drug, camptothecin, stick around the brain longer by attaching water-soluble polymers to it. The larger compound doesn’t get taken up by capillaries, and is more amenable to the brain’s chemistry, the group reports in the November issue of Bioconjugate Chemistry. Saltzman’s team designed the drug to release the polymer once it’s had a chance to seep throughout the brain, so the drug can then do its job in killing cancerous cells. “Like a stealth fighter,” says Saltzman, chair of Yale’s department of biomedical engineering, “it can get through war zones.”  |
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