Inside this issueCover storiesA continuous infusion of philanthropyNew Cancer Center head: ‘aspire to cure cancers’Alpern reappointed to new term as dean of medical school
PeopleLifelines: Jorge GalánExpert on spinal cord injury receives VA's highest scientific awardDean of Public Health is Anna M.R. Lauder ProfessorBerliner Professor envisions blood vessel growth as therapyExpert on kidney development, repair is named Long ProfressorFive medical school faculty are elected to a venerable groupOut & aboutScienceA protein's surprise role in Alzheimer'sHow membranes get the bendsAdvances: Living dangerously, in more ways than one | A new syndrome, a new role for a geneHealthAdvances: Relax—for your heart's sake | Drug can curb both smoking and drinkingPartnershipsGrants & contractsSupporting medical educationDownload this issue in PDF format |
AdvancesHealth and science news from YaleRelax—for your heart’s sake
It is well known that stress and anger are not heart-healthy, but a
new School of Medicine study, published in the March 3 issue of the Journal of the American College of Cardiology, provides new evidence of the harmful effects of mental stress on the heart. Rachel J. Lampert, M.D., associate professor of medicine, and colleagues sought to learn whether anger would increase T-wave alternans (TWA), which measure electrical instability in the heart, and whether anger-induced electrical instability would predict future problems in patients being treated for arrhythmias. Asking 62 patients with enlarged hearts and recently implanted defibrillators to perform math problems under pressure and to recall situations in which they were angry while undergoing standard heart monitoring, they found that those with greater anger-induced TWA were more likely to experience arrhythmias in the future. “Further studies are needed to determine whether there is a role for therapies which may reduce anger and the body’s response to stress,” Lampert says, “thereby preventing arrhythmias in those at risk.” Drug can curb both smoking and drinkingThat roughly 60 percent of alcoholics smoke is not surprising, since
scientists have shown that nicotine appears to enhance alcohol’s
“buzz.” And while the harm that can be caused by abusing either drug is
widely acknowledged, trying to quit using them has long proven an
elusive challenge. Now, it may be easier to fight both addictions at once. A new School
of Medicine study has found that varenicline, a popular smoking
cessation drug sold under the trade name Chantix, also dramatically
reduces the amount of alcohol a heavy drinker will consume. In an advance issue of Biological Psychiatry published online in February, first author Sherry McKee, Ph.D., associate professor of psychiatry, and colleagues report that, after taking varenicline in a laboratory setting, 80 percent of heavy-drinking smokers did not drink alcohol that was made available to them, compared to 30 percent of those who were given a placebo. At the doses studied, there were no adverse effects when varenicline was combined with alcohol. “A medication such as varenicline, which may target shared biological systems in alcohol and nicotine abuse, holds promise as a treatment for individuals with both disorders,” says McKee. Living dangerously, in more ways than one
Evolutionary biologists are intrigued by Methanopyrus kandleri,
a single-celled organism that thrives near hydrothermal vents on the
ocean floor where water temperatures can reach 752 degrees Fahrenheit
(see photo). Thanks to new work in the laboratory of Dieter Söll,
Ph.D., Sterling Professor of Molecular Biophysics and Biochemistry, M. kandleri may soon be a darling of virologists. In the May 1 edition of Science a Yale team reports that M. kandleri carries a mutation that swaps cytosine (C) for uracil (U) in 30 crucial genes. The mutation would probably be fatal, but the researchers found that M. kandleri also has an enzyme that corrects the mutation. The enzyme is a member of a family that interests HIV researchers
because of its antiviral activity, and “may be of biotechnological
interest if we can engineer it to mutate C to U at any desired location
within an RNA molecule,” says Lennart Randau, Ph.D., postdoctoral
associate in the Söll lab and a lead author of the paper. A new syndrome, a new role for a geneAn international team led by Richard P. Lifton, M.D., Ph.D., chair
and Sterling Professor of Genetics, and Ute I. Scholl, M.D., a
postdoctoral associate in Lifton’s lab, has implicated a gene known as KCNJ10 in a previously unreported medical syndrome. Mutations in KCNJ10, which codes for an ion channel that is
expressed in the brain, kidney, and inner ear, cause seizures and
deafness in mice. In the April 7 issue of Proceedings of the National Academy of Sciences, Scholl and colleagues report KCNJ10
mutations in five patients from four families with a syndrome that
features—in addition to complex neurological problems—a defect in the
kidney’s ability to manage potassium and magnesium levels. These electrolyte abnormalities are attributed to a
loss of the ion channel’s contribution to maintaining the activity of
the kidney’s sodium-potassium pump. The authors dubbed the disorder SeSAME syndrome because
it features seizures, sensorineural deafness, ataxia, mental
retardation and electrolyte imbalance. “A study like this would have taken years in the past,” says Lifton, a Howard Hughes Medical Institute investigator, but with new techniques, “it was accomplished in a few weeks by a single fellow in the lab.” |
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