ich neurons and glia cells migrate out to form all the layers of the brain," said Ballabh, an associate professor in the Department of Pediatrics, Cell Biology, and Anatomy at New York Medical College, and a neonatologist at Westchester Medical Center.
The problem is that the germinal matrix is as fragile as it is critical during its short life. In a normally developing fetus, the blood vessels do their job and then fade away by the time the baby is born. But when a baby is born prematurely, the structure is suddenly pushed into a role for which it is not designed, handling high rates of blood flow and pressure, increasing the risk of a total collapse.
Babies most at risk are those born between 24 and 32 weeks gestation that weigh less than 1500 grams, or about 3 lbs., 5 ounces. About 20 percent of such infants have a bleed, known as a germinal matrix hemorrhage or an intraventricular hemorrhage. While the problem sometimes is very small and hardly perceptible, other times the bleed causes tremendous brain damage.
With funding from the National Institute of Neurological Disorders and Stroke and the Philip Morris Organization, the team started out to lessen the risk, focusing much of their endeavour on a molecule known as VEGF, which is mainly in charge for answering the brain's call for more oxygen by vigorously building new blood vessels.
The goal was to make the germinal matrix a little hardier in cases of premature birth, by eradicating the vigorous building of new, but very delicate, blood vessels that bleed more easily than established blood vessels. The team used celecoxib to hit down the production of cox-2, which consecutively slowed production of VEGF. The team also studied an anti-cancer drug known as ZD6474, which affects another molecule, angiopoietin-2, that the body uses to build blood vessels.
The team found that in human brain tissue, the compounds significantly abridged the pro
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