shwartzman phenomenon/protease

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Contribution of protein Z and protein Z-dependent protease inhibitor in generalized Shwartzman reaction.

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OBJECTIVE Sepsis, a leading cause of mortality in critically ill patients, is closely linked to the excessive activation of coagulation and inflammation. Protein Z, a cofactor for the protein Z-dependent protease inhibitor, enhances the inhibition of coagulation factor Xa, and protein Z-dependent

Cholera and pertussis exotoxins protect mice against the lethal Schwartzman reaction and antagonize the effects of lipopolysaccharide on second messenger systems.

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Pertussis toxin, and also cholera toxin are capable of inhibiting the effects of LPS in the elicitation of the generalized Schwartzman reaction. This is a potentially lethal generalized thrombo-haemorrhagic hypersensitivity and inflammatory-type response that occurs after two consecutive injections

Studies on the mechanism of the Shwartzman phenomenon.

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Rabbit skin which is prepared for the Shwartzman phenomenon by an intradermal injection of meningococcal toxin exhibits, in vitro, a high degree of aerobic glycolysis. This metabolic abnormality is reflected, in vivo, by a measurable increase in the concentration of lactic acid in the prepared skin.

Protease-activated receptor-4 inhibition protects from multiorgan failure in a murine model of systemic inflammation.

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Coagulation proteases may act as cell signaling molecules via protease-activated receptor (PAR) cleavage, subsequently affecting cellular and inflammatory responses. Activation of PARs in the setting of systemic inflammation and disseminated intravascular coagulation (DIC) might thus exacerbate the

Pharmacological studies of FUT-175, nafamstat mesilate. I. Inhibition of protease activity in in vitro and in vivo experiments.

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FUT-175, 6-amidino-2-naphthyl p-guanidinobenzoate dimethanesulfonate (nafamstat mesilate), a novel synthetic protease-inhibiting agent, was studied to determine its in vitro effects against various proteases and other enzymes, as well as to determine its in vivo protease inhibitory effects. FUT-175

Regulatory roles of T mu and T gamma cells in the collaborative cellular initiation of the extrinsic coagulation pathway by bacterial lipopolysaccharide.

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The Shwartzman reaction is a classic biologic response in which the coagulation system is activated in vivo. Cellular initiation of the extrinsic coagulation protease cascade can be mediated by one or more limbs of the lymphoid response to diverse biological stimuli. The T cell-instructed monocyte

Cutaneous manifestations of bacterial sepsis.

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In short, bacterial sepsis is associated with a number of peripheral manifestations involving the skin and soft tissues. The pathogenesis of the lesions observed is not fully understood and is almost certainly multifactorial. In ecthyma gangrenosum, the presence of large numbers of gram-negative

"CELL-WALL PROTEIN A" OF PSEUDOMONAS AERUGINOSA AND ITS RELATIONSHIP TO "ORIGINAL ENDOTOXIN PROTEIN".

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Homma, J. Yuzuru (University of Tokyo, Tokyo, Japan), and Nachiko Suzuki. "Cell-wall protein A" of Pseudomonas aeruginosa and its relationship to "original endotoxin protein." J. Bacteriol. 87:630-640. 1964.-To compare the properties of two kinds of proteins, one obtained from the cell wall of

Macrophage procoagulant factors--mediators of inflammatory and neoplastic tissue lesions.

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Mononuclear phagocytes, a specialized cell lineage comprising bone-marrow precursors, blood monocytes and tissue macrophages, can interact with blood coagulation mechanisms with resulting thrombus formation or extravascular fibrin accumulation. Such procoagulant activity is usually activation

Lymphoid procoagulant response to bacterial endotoxin in the rat.

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A number of species respond to bacterial endotoxin (lipopolysaccharide [LPS]) wherein cells of the monocyte-macrophage lineage are rapidly induced either directly or via T-cell collaboration to initiate the extrinsic coagulation protease pathway. This results in fibrin formation and deposition as

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