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Cedars-Sinai Medical Center Physicians And Scientists Present Findings At Annual Meeting Of The Pediatric Academic Societies

LOS ANGELES (May 2, 1999) -- Researchers at Cedars-Sinai Medical Center are presenting three scientific lectures and several poster-session exhibits at the Pediatric Academic Societies' 1999 Annual Meeting May 1 through 4 in San Francisco.

The first lecture was presented at 9:45 a.m. Sunday, May 2, as part of a program on neuroprotective strategies for hypoxic-ischemic encephalopathy - the effort to reduce or prevent damage to brain cells when blood supply to the brain is reduced or blood to the brain contains insufficient oxygen.

For some time, researchers have thought that the administration of magnesium may have a "protective effect" on brain cells, although the exact mechanism has not been understood. Neonatologist Richard C. Krueger, Jr., M.D., Ph.D., discussed the results of a study that advances this theory, suggesting that the administration of magnesium "could have a dramatic impact on neural development." The study was conducted by researchers at Cedars-Sinai and Chicago Children's Hospital.

The researchers placed brain cells of embryonic chickens into a culture containing only a small amount of magnesium. After five days, they added another measured amount of magnesium, analyzing the cells 24 hours later for overall viability (the ability to live, grow and develop), apoptosis (disintegration), and proliferation (reproduction).

No change was seen in the level of disintegration but both cell viability and proliferation increased. A subsequent test indicated that the cells proliferating during the initial 24-hour period were precursors to glia cells - the supportive structures of the nervous system.

This rapid reproduction of glial precursors is believed to be at least partly due to activation of PI3 Kinase, an enzyme that interacts with other cell proteins and plays an instrumental role in cell growth and other activities. When wortmannin -- a substance that inhibits the activity of PI3 Kinase and is known to cause cell disintegr
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Contact: Sandra Van
Sandy@VanCommunications.com
1-800-396-1002
Cedars-Sinai Medical Center
4-May-1999


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