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staurosporine/krwotok

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Microvascular endothelial cell hyperpermeability induced by endogenous caspase 3 activator staurosporine.

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BACKGROUND Microvascular hyperpermeability following conditions such as hemorrhagic shock occurs mainly owing to disruption of the adherens junctional protein complex in endothelial cells. The objective of this study was to examine the action of staurosporine, a potent activator of endogenous

The role of calcium desensitization in vascular hyporeactivity and its regulation after hemorrhagic shock in the rat.

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The objectives of the present study were to investigate the role of calcium desensitization in vascular hyporeactivity, and the regulatory effects of Rho-kinase, protein kinase C (PKC), and protein kinase G (PKG) on calcium sensitivity. The vascular reactivity and calcium sensitivity with superior
Studies indicate that simple hemorrhage induces profound suppression in splenic and peritoneal macrophage (Mphi) functions such as antigen presentation, reduced major histocompatibility complex class II antigen expression, as well as cytokine release. Since many of these macrophage functions require

[Regulatory effect of protein kinase C and protein kinase G on calcium sensitivity of vascular smooth muscle cells following hemorrhagic shock].

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OBJECTIVE To observe the effect of protein kinase C (PKC) and protein kinase G (PKG) on calcium desensitization following hemorrhagic shock in rats. METHODS The model of hemorrhagic shock was replicated by blood letting and maintaining mean arterial pressure at 40 mm Hg (1 mm Hg=0.133 kPa) for 2

[Involvement of protein kinase C in enhancement of vascular calcium sensitivity by blocking mesenteric lymph return in hemorrhagic shock rats].

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The aim of the present study was to investigate whether protein kinase C (PKC) was involved in the effect of mesenteric lymph duct ligation or mesenteric lymph drainage on vascular calcium sensitivity in hemorrhagic shock rats. Male Wistar rats were randomly divided into Sham, Shock (hemorrhagic

Beneficial effects of activation of PKC on hemorrhagic shock in rats.

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BACKGROUND The reduced vascular reactivity after severe trauma or shock played an important role in the development and outcome of shock. Our previous study showed that protein kinase C (PKC) took part in the regulation of vascular reactivity after hemorrhagic shock. The objective of this study was

Relaxation of subarachnoid hemorrhage-induced spasm of rabbit basilar artery by the K+ channel activator cromakalim.

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OBJECTIVE Cerebral vasospasm resulting from subarachnoid hemorrhage (SAH) is refractory to most vasodilators. However, despite evidence that a mechanism underlying the vasospasm may be smooth muscle cell membrane depolarization resulting from decreased K+ conductance, the ability of K+ channel

Crimean-Congo haemorrhagic fever replication interplays with regulation mechanisms of apoptosis.

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Pathogenesis of viral haemorrhagic fevers is associated with alteration of vascular barrier function and haemorrhage. To date, the specific mechanism behind this is unknown. Programmed cell death and regulation of apoptosis in response to viral infection is an important factor for host or virus

Staurosporine Induces Platelet Apoptosis Through p38 Mitogen-Activated Protein Kinase Signaling Pathway.

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BACKGROUND Staurosporine (STS), a microbial alkaloid and potent PKC inhibitor, has become one of the most promising anti-cancer drugs. STS effectively induces apoptosis in many nucleated cells; however, it is still unclear whether STS induces apoptosis in enucleated platelets. METHODS Apoptotic

Beneficial effect of cyclosporine A on traumatic hemorrhagic shock.

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BACKGROUND Vascular hyporeactivity plays an important role in severe trauma and shock. We investigated the beneficial effect of cyclosporine A (CsA) on traumatic shock and its relationship to vascular reactivity improvement and mitochondrial permeability transition pore (MPTP). METHODS Sodium
In addition to an anticoagulant activity, activated protein C (APC) also exhibits anti-inflammatory and cytoprotective properties. These properties may contribute to the beneficial effect of APC in treating severe sepsis patients. A higher incidence of bleeding because of its anticoagulant function

No effect of apolipoprotein E on neuronal cell death due to excitotoxic and apoptotic agents in vitro and neonatal hypoxic ischaemia in vivo.

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The epsilon4 allele of apolipoprotein E (apoE) is a genetic risk factor for Alzheimer's disease. Studies also suggest that the epsilon4 allele may be a risk factor for poor outcome following head trauma, brain haemorrhage and ischaemia. The mechanism by which the presence of an apoE epsilon4 allele

Possible role of protein kinase C-dependent smooth muscle contraction in the pathogenesis of chronic cerebral vasospasm.

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In the present study, we investigate the possible role of protein kinase C (PKC)-dependent smooth muscle contraction in cerebral vasospasm following subarachnoid hemorrhage (SAH), employing the beagle "two-hemorrhage" model. The occurrence of chronic vasospasm was angiographically confirmed on day 7

Phenotype-based identification of host genes required for replication of African swine fever virus.

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African swine fever virus (ASFV) produces a fatal acute hemorrhagic fever in domesticated pigs that potentially is a worldwide economic threat. Using an expressed sequence tag (EST) library-based antisense method of random gene inactivation and a phenotypic screen for limitation of ASFV replication

Vasorelaxing effect of the Rho-kinase inhibitor, Y-27632, in isolated canine basilar arteries.

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OBJECTIVE Increased calcium sensitization mediated by Rho/Rho-kinase may be important in the pathogenesis of cerebral vasospasm. The effects of a highly selective Rho-kinase inhibitor, Y-27632, were investigated on spasmogen-induced contractions of canine basilar artery. METHODS Typical spasmogenic
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