Medicine@Yale publication

Medicine@Yale.

January/February 2006   Volume 2 Issue 1

Inside this issue

Cover stories

Making a major impact in Science

Neuroscientists target disorders of the brain and spinal cord

Banner year for Yale as six on faculty join Institute of Medicine

Partnerships

New collaboration with museum aims to improve science literacy

Yale, VA supporting troops on the home front

Unlikely allies, common goals in fight against obesity

Medical school welcomes first Gilliam Fellows

Grants & contracts

People

Lifelines: Edward Chu, moving cancer drugs into the clinic

Graduate council bestows top honor on residency dean

L. Veronica Lee champions prevention and women’s cardiovascular health

Cell biologist Mellman elected to European academy

Alumnus receives Yale Medal for his decades of service

Out & about

Science

Advances: Restoring flexibility to heal broken brains | Mad cow’s small impact explained?

Health

Advances: Take sleep apnea seriously, says study | Cool therapy helps after troubled births

 



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Advances

Health and science news from Yale

Take sleep apnea seriously, says study

It can be trying to share a bed with a person affected by obstructive sleep apnea, a common condition in which breathing stops repeatedly during sleep, since loud snoring is a telltale symptom. But a study from the Yale Center for Sleep Medicine (YCSM) provides new evidence that sleep apnea is more than an annoyance.

Since 1997, YCSM researchers had diagnosed sleep apnea in 697 patients using polysomnography, a technique that measures heart rate, breathing and other physiological variables during sleep. A follow-up study begun in 2002 revealed that 9 percent of these individuals suffered strokes or died, compared to only 1.6 percent of a control group.

As reported in The New England Journal of Medicine on November 10, after eliminating smoking, alcohol use and hypertension as factors, the scientists found that sleep apnea doubled the risk of stroke or death.

“Sleep apnea is a common and serious problem, but it is also highly treatable,” says H. Klar Yaggi, M.D., assistant professor of medicine and lead author. “If you or someone you know has symptoms of sleep apnea, it is important to discuss this with a doctor.”

Mad cow’s small impact explained?

A recent study by neuropathologist Laura Manuelidis, M.D., professor of surgery, and colleagues in Japan may offer the beginnings of a solution to an epidemiological puzzle.

In 1996, during an epidemic of bovine spongiform encephalopathy (BSE), or mad cow disease, in British cattle, some epidemiologists predicted that up to 100,000 people could contract variant Creutzfeldt-Jakob disease (vCJD), a rapidly progressing, invariably fatal neurodegenerative condition, from BSE-infected beef.

But that nightmarish scenario hasn’t yet come to pass: almost 10 years later only 151 cases of vCJD have been verified.

Manuelidis and her team reported in the October 21 issue of Science that when neuronal cell cultures were infected with either a weak or sporadic form of CJD or with agents that cause sheep scrapie, a disease similar to CJD, the cultures resisted infection by a more virulent strain of CJD agent.

The team suggests that exposure to less virulent strains of CJD may protect people against the newly evolved bovine agent.

Restoring flexibility to heal broken brains

In early life, the brain is continually sculpted by stimuli from the outside world. But soon, most neural circuits become hard-wired.

Fixed circuits are reliable but costly: the injured brain can rarely repair itself. In 2000, Stephen M. Strittmatter, M.D., Vincent Coates Professor of Neurology, identified Nogo, a protein found in the myelin sheath surrounding axons (bright green in the brain section above) that suppresses self-repair in injured neurons. A report in the September 30 issue of Science indicates that Nogo may also lock down cortical wiring during normal development.

The visual cortex is normally divided equally between inputs from each eye. But if one eye is kept shut during a “critical period” before neural circuits are fixed, the active eye appropriates more cortex. However, Strittmatter, Nigel W. Daw, Ph.D., professor of ophthalmology and visual science, and postdoctoral fellows Aaron W. McGee, Ph.D., and Yupeng Yang, Ph.D., showed that in mice bred to lack the Nogo receptor, an active eye can usurp cortical real estate well past the critical period into adulthood.

Noting that “limited plasticity is central to a range of neurological disorders,” Strittmatter is testing Nogo blockers to see if reviving the brain’s inborn flexibility can help it to heal after injury.

Cool therapy helps after troubled births

If the placenta or umbilical cord are torn or squeezed before or during childbirth, or if the uterus ruptures, many infants suffer from a severe form of oxygen deprivation known as hypoxic-ischemic encephalopathy, or HIE, that can cause disabilities, such as cerebral palsy, or death.

A new study by a nationwide network of researchers, including Richard A. Ehrenkranz, M.D., professor of pediatrics and of obstetrics, gynecology and reproductive sciences, shows that a simple therapy that lowers newborns’ brain temperature can reduce disability and death after HIE.

As reported in the October 13 issue of The New England Journal of Medicine, the researchers placed babies with HIE on water-cooled blankets that lowered their body temperature to 92.3 degrees within 6 hours after birth. Only 44 percent of the infants who received the cooling treatment developed disabilities or died, compared to 62 percent of a control group.

The cooling therapy “slows down the injury process caused by birth asphyxia,” says Ehrenkranz. “Less injury means a better out-come and fewer cases of cerebral palsy and other complications.”

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