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Barbara C. Furie

Researcher at Beth Israel Deaconess Medical Center

Publications -  135
Citations -  9851

Barbara C. Furie is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Thrombus & Platelet. The author has an hindex of 49, co-authored 135 publications receiving 9397 citations. Previous affiliations of Barbara C. Furie include Harvard University & Icahn School of Medicine at Mount Sinai.

Papers
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Journal ArticleDOI

Intravascular but Not Extravascular Tissue Factor Is Required for Fibrin Generation During Thrombus Formation in Cremaster Arterioles in Living Mice Subjected to Laser Injury.

TL;DR: Compared fibrin generation and platelet thrombus formation between mice lacking tissue factor in either the intravascular or the extravascular compartment using the laser injury model of thrombosis in the mouse cremaster muscle concludes that when endothelial disruption is minimized, intrav vascular TF plays a significant role in fibr in formation, while smooth muscle cell derived TF does not.
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Rapid Activation of Unstimulated Endothelial Cells Containing Tissue Factor Following Laser-Induced Injury as Monitored Via Calcium Mobilization.

TL;DR: This work has determined if endothelial cells are activated in response to the injury induced by a pulsed laser, and indicates the presence of a preformed intracellular pool of TF within HUVECs that under resting conditions is not detectable on the cell surface.
Journal ArticleDOI

Extracellular Protein Disulfide Isomerase Regulates Vitronectin during the Initiation of Thrombus Formation

TL;DR: The combined results demonstrate that extracellular PDI regulates vitronectin in a growing thrombus to promote platelet accumulation and fibrin generation and suggest that plasma-derived vitronctin and not platelet- derived vitronECTin is the primary substrate of PDI.
Patent

Crystal structure of human factor VIII and uses thereof

TL;DR: In this article, a B-domain deleted human Factor VIII and its three-dimensional structure were provided, and methods for identifying compounds that modulate Factor VIII activity, for determining structures of Factor VIII homologs or analogs, and for designing drug candidates for the treatment of hemophilia based on the structural information.
Journal ArticleDOI

Affinity-Purified Anti-Beta-2 Glycoprotein-1 Antibodies from a Patient with Lupus Anticoagulant-Associated Thrombosis Amplify Thrombus Formation in the Living Mouse.

TL;DR: It is demonstrated using intravital microscopy that purified anti- beta-2 glycoprotein 1 antibodies isolated from the serum of a patient with APS greatly amplify thrombus size following laser-induced vessel wall injury in live mice, providing evidence that anti-beta- 2 glycop protein 1 antibodies are not only a marker but are directly involved in the pathogenesis of thrombosis.