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Biotech / Medical : Gliatech (GLIA) -- Ignore unavailable to you. Want to Upgrade?

To: dalroi who wrote (864)	7/23/1999 8:43:00 AM
From: scaram(o)uche	Read Replies (1) \| Respond to of 2001

04:05 PM ET 07/22/99 Drug May Help Stroke Victims Drug May Help Stroke Victims By PAUL RECER= AP Science Writer= WASHINGTON (AP) _ Brain damage caused by stroke was reduced by half in laboratory tests of an experimental drug that someday may offer hope for the 500,000 Americans who suffer strokes each year. In mouse experiments, the new drug appeared to stop two brain cell-killing reactions that usually follow a stroke caused by a blocked blood vessel, said Dr. David Pinsky, a researcher at the Columbia University's College of Physicians and Surgeons. A report on the study will be published Friday in the journal Science. ''After a stroke, there is an immune system reaction that acts like a cluster bomb attack in the brain,'' said Pinsky. One type of immune cell kills neurons directly, while other cells cause inflammation that can slow blood flow to the stroke area and injure still more cells. Both of these actions cause ''collateral damage,'' killing neurons that may not have been involved in the original stroke, said Pinsky. The new drug molecule appears to at least partially block both of these stroke reactions and significantly limit the collateral damage to the brains in mice who had been artificially induced to have strokes, said Pinsky. Dr. Pan Ganguly, a researcher at the National Heart Lung and Blood Institute, said the Pinsky study ''is an important piece of work'' that could lead to a new way to treat strokes. He said that ''after a stroke, the damaging process can continue for quite a while,'' and finding a drug to stop this process is ''an important advance.'' But Ganguly cautioned the drug, so far, has been studied only in animals and that it may be a long time before its benefits are proven in human patients. ''I still have a lot of reservations about this drug, but it is a novel approach in an area where we desperately need new therapeutics,'' he said. According to the American Heart Association, about 500,000 Americans suffer strokes annually. Also called ''brain attacks'', strokes kill about 150,000 Americans each year and are the third biggest cause of death behind heart disease and cancer. Stroke is the leading cause of long-term disability. There are about 4 million American stroke survivors, many of whom have difficulties with speech, walking or caring for themselves. The direct and indirect annual cost of strokes has been estimated at about $41 billion annually. Strokes caused by vessel blockage, ischemic strokes, are often treated now by drugs called ''clot busters.'' These dissolve clots that cause strokes when they block the flow of blood and oxygen to brain cells. Pinsky said the drug he is studying has a different function than the clot busters and the two drugs, in theory, would be used together to limit stroke damage. Following a stroke, the researcher said, nearby neurons are often damaged. They respond to the damage by showing a molecule, called C1q, on the cell surface. This triggers a type of immune response, called complement, and activates a type of cell called the microglia. ''Microglia are responsible for basically consuming debris or injured cells,'' said Pinsky. Following a stroke, the microglia will kill the injured neurons that might otherwise survive, he said. The complement process, he said, ''sets off a cascade'' that includes inflammation of nearby vessels. This reduces blood and oxygen flow to nearby neurons. Pinsky said the new drug blocks microglia from attacking damaged neurons and prevents the inflammation of nearby vessels.

To: dalroi who wrote (864)	7/23/1999 8:57:00 AM
From: scaram(o)uche	Read Replies (2) \| Respond to of 2001

The work is from Avant. Relevant to the properdin work (and ongoing chemistry efforts at Janssen??). Interesting concept.... sialyl Lewis A and analogs have largely failed (CYTL, AMGN.... TXB has one in development, and PDLI has anti-selectin MAbs). GLIA and Janssen were into an interesting field much earlier than most..... Neuronal Protection in Stroke by an sLex-Glycosylated Complement Inhibitory Protein Judy Huang, 1 Louis J. Kim, 1 Richard Mealey, 2 Henry C. Marsh Jr., 2 Yuan Zhang, 1 Andrea J. Tenner, 3 E. Sander Connolly Jr., 1 David J. Pinsky 1* Glycoprotein adhesion receptors such as selectins contribute to tissue injury in stroke. Ischemic neurons strongly expressed C1q, which may target them for complement-mediated attack or C1qRp-mediated clearance. A hybrid molecule was used to simultaneously inhibit both complement activation and selectin-mediated adhesion. The extracellular domain of soluble complement receptor-1 (sCR1) was sialyl Lewis x glycosylated (sCR1sLex) to inhibit complement activation and endothelial-platelet-leukocyte interactions. sCR1 and sCR1sLex colocalized to ischemic cerebral microvessels and C1q-expressing neurons, inhibited neutrophil and platelet accumulation, and reduced cerebral infarct volumes. Additional benefit was conferred by sialyl Lewis x glycosylation of the unmodified parent sCR1 molecule. 1 Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA. 2 Avant Immunotherapeutics, Inc., 119 Fourth Avenue, Needham, MA 02494, USA. 3 University of California, Department of Molecular Biology and Biochemistry, Irvine, CA 92697, USA.