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Previous Volume 340:1555-1564 May 20, 1999 Number 20 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Hemostasis is a physiologic mechanism that maintains blood in a fluid state within the circulation. The coagulation of blood is mediated by cellular components and soluble plasma proteins. In response to vascular injury, circulating platelets adhere, aggregate, and provide cell-surface phospholipid for the assembly of blood-clotting enzyme complexes. The extrinsic pathway of blood coagulation is initiated when blood is exposed to non-vascular-cell–bound tissue factor in the subendothelial space (Figure 1). Tissue factor binds to activated factor VII, and the resulting enzyme complex activates factors IX and X of the intrinsic and common coagulation pathways, respectively. Factor IX activated . . . [Full Text of this Article]

The Systemic-Defect–Local-Phenotype Paradox

Hypercoagulability in Humans

Animal Models of Hypercoagulability

Vascular-Bed–Specific Signaling Pathways

Extracellular Signals

Cell-Subtype–Specific Signaling Pathways

Transcriptional Regulation

Coronary-Artery Thrombosis

Conclusions

Source Information

From the Department of Medicine, Divisions of Molecular Medicine and Hematology–Oncology, Beth Israel Deaconess Medical Center, Boston (R.D.R., W.C.A.); and the Department of Biology, Massachusetts Institute of Technology, Cambridge (R.D.R.).

Address reprint requests to Dr. Aird at the Division of Molecular Medicine, RW-663, Beth Israel Deaconess Medical Center, Boston, MA 02215, or at waird@caregroup.harvard.edu.

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