protease/edema

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Studies of four Japanese families with hereditary angioneurotic edema: simultaneous activation of plasma protease systems and exogenous triggering stimuli.

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Forty-five relatives of 4 families with hereditary angioneurotic edema (HANE) were studied. Twenty-five, including 11 asymptomatic kindreds with the disposition, showed typical changes in complement system compatible with HANE. Follow-up study of HANE patients showed that, even in remission period,

Cystoid macular edema in a patient with acquired immunodeficiency syndrome and past ocular history of cytomegalovirus retinitis after initiation of protease inhibitors.

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OBJECTIVE To describe a patient with acquired immunodeficiency syndrome (AIDS) who presented with cystoid macular edema (CME) which was not associated with active cytomegalovirus (CMV) retinitis or AIDS-related microvasculopathy. METHODS A 32-year-old man with AIDS and a past ocular history of

Effects of focal mild hypothermia on thrombin-induced brain edema formation and the expression of protease activated receptor-1, matrix metalloproteinase-9 and aquaporin 4 in rats.

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Hypothermia is an effective neuroprotective treatment for brain injury caused by intracerebral hemorrhage (ICH). It is reported to reduce brain edema and neuronal cell death. Thrombin, a coagulation protease released from blood clots, is critical in brain edema formation following ICH. Protease

The expression and the role of protease nexin-1 on brain edema after intracerebral hemorrhage.

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Brain edema is one of the most frequent and serious complications of intracerebral hemorrhage (ICH), but how the ICH cause brain edema is unknown. Our studies were designed to investigate the regulation and distribution of protease nexin-1 (PN-1), thrombin and aquaporin-4 (AQP-4) in brain edema

Serine protease inhibitor attenuates intracerebral hemorrhage-induced brain injury and edema formation in rat.

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Our previous studies have demonstrated that thrombin plays an important role in intracerebral hemorrhage (ICH)-induced brain injury and edema formation. We, therefore, examined whether nafamostat mesilate (FUT), a serine protease inhibitor, can reduce ICH-induced brain injury. Anesthetized male

Protease activated receptor-1 and brain edema formation in glioma models.

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OBJECTIVE Our previous studies showed that thrombin contributes to brain edema in gliomas. The present study investigated the role of a thrombin receptor, protease activated receptor-1 (PAR-1), in edema formation in glioma models. METHODS These experiments were performed in Fischer 344 rats, PAR-1

Using a Caesalpinia echinata Lam. protease inhibitor as a tool for studying the roles of neutrophil elastase, cathepsin G and proteinase 3 in pulmonary edema.

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Acute lung injury (ALI) is characterized by neutrophil infiltration and the release of proteases, mainly elastase (NE), cathepsin G (Cat G) and proteinase 3 (PR3), which can be controlled by specific endogenous inhibitors. However, inhibitors of these proteases have been isolated from different

Protease-activated receptor 1 inhibitor improves brain edema in rats with intracerebral hemorrhage

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Aim: To investigate the changes of water content in brain tissue, the expression of AQP4mRNA after cerebral hemorrhage in rats, and the intervention effect of Protease activated receptor 1 inhibitor (PAR1 inhibitor) on both.

Edema Induced by a Crotalus durissus terrificus Venom Serine Protease (Cdtsp 2) Involves the PAR Pathway and PKC and PLC Activation.

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Snake venom serine proteases (SVSPs) represent an essential group of enzymatic toxins involved in several pathophysiological effects on blood homeostasis. Some findings suggest the involvement of this class of enzymatic toxins in inflammation. In this paper, we purified and isolated a new gyroxin

Inhibitory effects of a novel synthetic protease inhibitor, FUT-175, on the paw edema in rats and zymosan-induced complement activation in vitro.

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FUT-175 inhibited the zymosan-induced rat paw edema in a dose-dependent manner, while indomethacin exhibited no significant activities in this model. FUT-175 also inhibited the decrease in hemolytic complement (CH50) induced by zymosan in vitro, and indomethacin was inactive. These results suggest

Basophil-derived mouse mast cell protease 11 induces microvascular leakage and tissue edema in a mast cell-independent manner.

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Mouse mast cell protease 11 (mMCP-11) is the most recently identified member of the mouse mast cell tryptase family. This tryptase is preferentially produced by basophils in contrast to other members that are expressed by mast cells but not basophils. Although blood-circulating basophils have long

A mutation unique in serine protease inhibitors (serpins) identified in a family with type II hereditary angioneurotic edema.

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BACKGROUND Hereditary angioneurotic edema (HANE) is an autosomal dominant disease due to genetic alterations at the C1 inhibitor gene. Mutations within the C1 inhibitor gene are responsible for the molecular defect in type II HANE. Most of the dysfunctional proteins result from mutations involving

Treatment of alpha-1-antitrypsin deficiency, massive edema, and panniculitis with alpha-1 protease inhibitor.

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Use of a protease inhibitor, ulinastatin, for reexpansion pulmonary edema following evacuation of bilateral pleural effusion.

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[On the significance of proteases for the Arthus reaction and pharmacologically induced edema in rat paws].

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