subarachnoid hemorrhage/protease

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Broad-spectrum and selective serine protease inhibitors prevent expression of platelet-derived growth factor-BB and cerebral vasospasm after subarachnoid hemorrhage: vasospasm caused by cisternal injection of recombinant platelet-derived growth factor-BB.

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OBJECTIVE Plasma serine protease cascade, including the complement system and thrombin, is activated in the subarachnoid space during the acute phase after subarachnoid hemorrhage (SAH). To examine the effect of protease cascade-based inflammation and subsequent vascular repair in the development of

[Expression of protease-activated receptor 1 in the basilar artery of rats following subarachnoid hemorrhage].

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OBJECTIVE To assess the relationship between protease-activated receptor 1 (PAR1) expression in the basilar artery and cerebral vasospasm (CVS) in a rat model of subarachnoid hemorrhage (SAH). METHODS Twenty-four SD rats were randomized into normal control group, SAH 3-days group, SAH 5-days group

Alterations in the expression of protease-activated receptor 1 and tumor necrosis factor-α in the basilar artery of rats following a subarachnoid hemorrhage.

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The present study aimed to investigate the expression of protease-activated receptor 1 (PAR1) and tumor necrosis factor (TNF)-α in a rat model of subarachnoid hemorrhage (SAH)-induced cerebral vasospasm (CVS). The rat models were established by twice injecting blood into the cisterna magna, after

Combination of serine protease inhibitor FUT-175 and thromboxane synthetase inhibitor OKY-046 decreases cerebral vasospasm in patients with subarachnoid hemorrhage.

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The preventive effect of the serine protease inhibitor FUT-175 (nafamostat mesilate), a potent inhibitor of the complement system, against vasospasm was evaluated in 34 high risk patients with thick and diffuse subarachnoid hemorrhage (SAH) demonstrated by computed tomography corresponding to Fisher

Effects of protease inhibitor and immunosuppressant on cerebral vasospasm after subarachnoid hemorrhage in rabbits.

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The possible role of the immune-defense system in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH) was investigated in rabbits. We used a synthetic serine protease inhibitor, gabexate mesilate (GM), a glucocorticoid, betamethasone sodium phosphate (B-P), and an

Therapeutic trial of cerebral vasospasm with the serine protease inhibitor, FUT-175, administered in the acute stage after subarachnoid hemorrhage.

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The therapeutic effect of the synthetic serine protease inhibitor, FUT-175, on cerebral vasospasm after subarachnoid hemorrhage (SAH) was investigated. Twenty-three patients with severe SAH who were admitted between February and July 1990 and who underwent surgery within 48 hours of the initial

Nexilin Regulates Oligodendrocyte Progenitor Cell Migration and Remyelination and Is Negatively Regulated by Protease-Activated Receptor 1/Ras-Proximate-1 Signaling Following Subarachnoid Hemorrhage.

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Progressive white matter (WM) impairments caused by subarachnoid hemorrhage (SAH) contribute to cognitive deficits and poor clinical prognoses; however, their pathogenetic mechanisms are poorly understood. We investigated the role of nexilin and oligodendrocyte progenitor cell (OPC)-mediated repair

Protease inhibitors for delayed cerebral ischemia after subarachnoid haemorrhage?

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Absence of plasma protease-antiprotease imbalance in the formation of saccular cerebral aneurysms.

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OBJECTIVE We examined the hypothesis that a plasma protease-antiprotease imbalance contributes to the formation of saccular cerebral aneurysms and the suggestion that the assay of these enzymes might be a screening tool for people at higher risk for aneurysm formation. METHODS From June 1997 through

Possible Involvement of Caspase-Independent Pathway in Neuronal Death After Subarachnoid Hemorrhage in Mice.

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Early brain injury is now considered as an important cause of delayed neurological deterioration after aneurysmal subarachnoid hemorrhage (SAH), and neuronal apoptosis is one of the constituents of early brain injury. Caspase family is popular proteases in apoptotic pathways, but there also exist

Activity of alpha 1-antitrypsin and cigarette smoking in subarachnoid haemorrhage from ruptured aneurysm.

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An altered equilibrium of protease/protease-inhibitor factors may be involved in the pathogenesis of aneurysm rupture: alpha 1-antitrypsin (alpha 1-AT) represents the most relevant inhibitor of elastase, a proteolytic enzyme enhancing catabolic processes of collagen metabolism. Cigarette smoking has

Interference of apoptosis in the pathophysiology of subarachnoid hemorrhage.

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Programmed cell death is crucial for the correct development of the organism and the clearance of harmful cells like tumor cells or autoreactive immune cells. Apoptosis is initiated by the activation of cell death receptors and in most cases it is associated with the activation of the cysteine

Matrix Metalloproteinases in Cerebral Vasospasm following Aneurysmal Subarachnoid Hemorrhage.

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Delayed cerebral vasospasm is a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). While the cellular mechanisms underlying vasospasm remain unclear, it is believed that inflammation may play a critical role in vasospasm. Matrix metalloproteinasees

Cystain C and neuropeptid Y levels in brain tissues after experimental subarachnoid hemorrhage.

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The aim of this study was to investigate the changes in the levels of cystatin C, which protects neurodegeneration in the central nervous system with the inhibition of cysteine protease and by inducing autophagy in the pathogenesis of cerebral vasospasm and levels of vasoconstrictive neuropeptid Y

Expression and cell distribution of SENP3 in the cerebral cortex after experimental subarachnoid hemorrhage in rats: a pilot study.

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Subarachnoid hemorrhage (SAH) is one of the life-threatening diseases with high morbidity and mortality rates. Small ubiquitin-like modifier (SUMO)-specific proteases 3 (SENP3), a member of the SUMO-specific protease family, was identified as an isopeptidase that deconjugates SUMOylation (The

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