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Biotech / Medical : Regeneron Pharmaceuticals -- Ignore unavailable to you. Want to Upgrade?


To: Miljenko Zuanic who wrote (250)12/18/1998 12:39:00 AM
From: Miljenko Zuanic  Respond to of 3557
 
Who care?

(not ones who are selling at this price)

immunity.com

Critical Role of the TIE2 Endothelial Cell Receptor in the Development of Definitive Hematopoiesis
Nobuyuki Takakura1, Xu-Ling Huang1, Takeshi Naruse1, Isao Hamaguchi1, Daniel J. Dumont2, George D. Yancopoulos3, Toshio Suda1
1 Department of Cell Differentiation, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, 2-2-1 Honjo, Kumamoto 860-0811, Japan
2 Division of Cancer Biology, Sunnybrook and Women's College Health Sciences Centre, 2075 Bayview Avenue, Toronto, Ontario, Canada M4N 3M5
3 Regeneron Pharmaceuticals, Incorporated, 777 Old Saw Mill River Road, Tarrytown, New York 10591
Corresponding author: Toshio Suda, 81 96 373 5328 (phone), 81 96 373 5332 (fax), sudato@gpo.kumamoto-u.ac.jp.

We have investigated the function of TIE2/TEK receptor tyrosine kinase in the development of definitive hematopoiesis. In the vitelline artery at 9.5 days postcoitum (d.p.c.), TIE2+ hematopoietic cells aggregated and adhered to TIE2+ endothelial cells. Soluble TIE2-Fc chimeric protein inhibited the development of hematopoiesis and angiogenesis in the para-aortic splanchnopleural mesoderm (P-Sp) explant culture, and TIE2-deficient mice showed severely impaired definitive hematopoiesis. An in vitro study revealed that Angiopoietin-1 but not Angiopoietin-2 promoted the adhesion to fibronectin (FN) through integrins in TIE2-transfected cells and primary TIE2+ cells sorted from 9.5 d.p.c. P-Sp. Adhesion of TIE2+ cells induced by Angiopoietin-1 enhanced the proliferation of hematopoietic progenitor cells.



To: Miljenko Zuanic who wrote (250)12/22/1998 12:04:00 PM
From: geewiz  Read Replies (1) | Respond to of 3557
 
Very important article in todays' NYT;

FOR PRIVATE USE ONLY;

Two Studies Find That Heart Injections
Offer Lasting Relief From Angina

By LAWRENCE K. ALTMAN

Two small studies have shown that over the course of just a few weeks, one dose of experimental drugs injected directly into the heart can greatly relieve, or even eliminate, the chest pain of coronary artery disease by encouraging the growth of new blood vessels to bypass clogged arteries, according to researchers in the United States and Germany.

The research is at a preliminary stage, and the drugs have yet to be tested in large groups of people. Even if the results hold up, it may be years before any therapy is available for patients who suffer fom such chest pain, or angina. One of the treatments under study is gene therapy to produce a protein called vegF, for vascular endothelial growth factor. The other entails injection of a protein called FGF-1, for fibroblast growth factor.

Each drug is given in a single injection, through a surgical incision in the chest. In effect, both treatments aim to allow patients to grow their own heart bypasses by sprouting thin "collateral" blood vessels, in a strategy called therapeutic angiogenesis.

The same gene therapy as is involved in one of these treatments has been shown to be effective in building new blood vessels in the legs, but these reports are the first to assert that gene therapy has produced new vessels in the heart.

The coronary gene therapy research, led by Dr. Jeffrey M. Isner of St. Elizabeth's Hospital in Brighton, Mass., and Tufts University, is reported in today's issue of Circulation, a journal published by the American Heart Association. The protein therapy is being developed by Dr. Thomas-Joseph Stegmann of Fulda, Germany, a leading figure in the field.
.............

Copywrie NYT 12/22/98

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