HEALTH-related quality of life (HRQL) is increasingly used as an outcome in clinical trials, effectiveness research, and research on quality of care. Factors that have facilitated this increased usage include the accumulating evidence that measures of HRQL are valid and "reliable,"1the publication of several large clinical trials showing that these outcome measures are responsive to important clinical changes,2-5and the successful development and testing of shorter instruments that are easier to understand and administer.6-13Because these measures describe or characterize what the patient has experienced as the result of medical care, they are useful and important supplements to traditional physiological or biological measures of health status. Given this improved ability to assess patients' health status, how can physicians and health care systems intervene to improve HRQL? Implicit in the use of measures of HRQL in clinical trials and in effectiveness research is the concept that clinical

Linking clinical variables with health-related quality of life. A conceptual model of patient outcomes

Disseminated intravascular coagulation is characterized by the widespread activation of coagulation, which results in the intravascular formation of fibrin and ultimately thrombotic occlusion of small and midsize vessels.1–3 Intravascular coagulation can also compromise the blood supply to organs and, in conjunction with hemodynamic and metabolic derangements, may contribute to the failure of multiple organs. At the same time, the use and subsequent depletion of platelets and coagulation proteins resulting from the ongoing coagulation may induce severe bleeding (Figure 1). Bleeding may be the presenting symptom in a patient with disseminated intravascular coagulation, a factor that can complicate decisions about . . .

Disseminated Intravascular Coagulation

Endothelial cells, which form the inner cellular lining of blood vessels and lymphatics, display remarkable heterogeneity in structure and function. This is the first of a 2-part review focused on phenotypic heterogeneity of blood vessel endothelium. This review provides an historical perspective of our understanding of endothelial heterogeneity, discusses the scope of phenotypic diversity across the vascular tree, and addresses proximate and evolutionary mechanisms of endothelial cell heterogeneity. The overall goal is to underscore the importance of phenotypic heterogeneity as a core property of the endothelium.

Phenotypic Heterogeneity of the Endothelium: I. Structure, Function, and Mechanisms

▪ Abstract Von Willebrand factor (VWF) is a blood glycoprotein that is required for normal hemostasis, and deficiency of VWF, or von Willebrand disease (VWD), is the most common inherited bleeding disorder. VWF mediates the adhesion of platelets to sites of vascular damage by binding to specific platelet membrane glycoproteins and to constituents of exposed connective tissue. These activities appear to be regulated by allosteric mechanisms and possibly by hydrodynamic shear forces. VWF also is a carrier protein for blood clotting factor VIII, and this interaction is required for normal factor VIII survival in the circulation. VWF is assembled from identical ≈250 kDa subunits into disulfide-linked multimers that may be >20,000 kDa. Mutations in VWD can disrupt this complex biosynthetic process at several steps to impair the assembly, intracellular targeting, or secretion of VWF multimers. Other VWD mutations impair the survival of VWF in plasma or the function of specific ligand binding sites. This growing...

Alan R. Giles

Papers

Synergistic mixture of phospholipid vesicles and blood factor xa