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intracranial hemorrhages/protease
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Risk of intracranial hemorrhage with protease-activated receptor-1 antagonists.
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OBJECTIVE
Recent clinical trial data suggest that protease-activated receptor-1 (PAR-1) antagonists may increase the risk of intracranial hemorrhage. Our objective was to investigate the qualitative and quantitative risks of intracranial hemorrhage in patients receiving PAR-1 antagonist
Risk of intracranial hemorrhage with protease-activated receptor-1 antagonists.
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[Experimental intracranial hemorrhage. Protective action of drugs with anti-protease activity].
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[Protease inhibitors in the treatment of intracranial hemorrhage].
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Vorapaxar: a novel protease-activated receptor-1 inhibitor.
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BACKGROUND
Platelet activation and reactivity are pivotal for both acute and chronic atherothrombotic event occurrences.
METHODS
Only 20% relative risk (∼ 2% absolute risk) reduction associated with newer P2Y(12) receptor blocker therapy such as prasugrel and ticagrelor compared with clopidogrel
A Novel Inhibitor of Protease-activated Receptor 1: A Review of Chemical Structure and Mode of Action.
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Limitations of current antiplatelet therapies have led to the discovery of new antiplatelet agents with new modes of action. Vorapaxar has been developed as a thrombin receptor antagonist. This drug works against the protease-activated receptor 1 (PAR1) and inhibits platelet aggregation mediated by
Vorapaxar: A Protease-Activated Receptor Antagonist for the Prevention of Thrombotic Events.
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Antiplatelet therapy reduces the risks for cardiovascular morbidity and mortality in patients with atherosclerotic disease, and it is also beneficial in managing peripheral arterial disease (PAD). These agents work through various therapeutic pathways to achieve antithrombotic effects. Although
Activation-resistant homozygous protein C R229W mutation causing familial perinatal intracranial hemorrhage and delayed onset of thrombosis.
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BACKGROUND
We describe a family with two first-degree cousins who presented with similar phenotypes characterized by neonatal intracranial hemorrhage and subsequent onset of thrombosis.
METHODS
We enrolled the two affected patients, five unaffected family members and fifty-five normal controls.
Intracranial hemorrhage and liver-associated deaths associated with tipranavir/ritonavir: review of cases from the FDA's Adverse Event Reporting System.
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Tipranavir (TPV), a protease inhibitor, has box warnings for intracranial hemorrhage (ICH) and hepatotoxicity (including hepatic failure and death). A box warning is a labeling statement about serious adverse events leading to significant injury and/or death. A box warning is the most serious
Thrombin-induced cerebral hemorrhage: role of protease-activated receptor-1.
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Thrombin causes blood-brain barrier disruption, and this study examined whether thrombin can cause brain hemorrhage through protease-activated receptor-1 (PAR-1). Male wild type and PAR-1 knockout mice had an intracerebral injection of thrombin or saline. Mice then underwent serial T2 magnetic
Proteomic Protease Substrate Profiling of tPA Treatment in Acute Ischemic Stroke Patients: A Step Toward Individualizing Thrombolytic Therapy at the Bedside.
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Tissue plasminogen activator (tPA) is the only FDA-approved medical therapy for acute ischemic stroke. But as a serine peptidase, intravenous tPA can affect the expression of other proteases that may be implicated in blood-brain barrier breakdown. Such parallel cascades of cell signaling may be
Tipranavir: a novel protease inhibitor for HIV therapy.
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Tipranavir (TPV) is a nonpeptidic protease inhibitor with potent in vitro activity against most HIV-1 strains resistant to other protease inhibitors. In vitro data have shown that resistance to TPV develops slowly. When coadministered with ritonavir (RTV) as a booster, TPV has shown potent antiviral
Overexpression of vascular endothelial growth factor in the germinal matrix induces neurovascular proteases and intraventricular hemorrhage.
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Intracranial hemorrhage in preterm neonates may result in neonatal mortality and functional disabilities, but its pathogenic mechanisms are poorly defined and better therapies are needed. We used a tetracycline-regulated transgenic system to test whether the induction of vascular endothelial growth
Early Tranexamic Acid Administration After Traumatic Brain Injury Is Associated With Reduced Syndecan-1 and Angiopoietin-2 in Patients With Traumatic Intracranial Hemorrhage
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Objective: To evaluate the effect of early tranexamic acid (TXA) administration on circulating markers of endotheliopathy.
Setting: Twenty trauma centers in the United States
Activated protein C inhibits tissue plasminogen activator-induced brain hemorrhage.
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Brain hemorrhage is a serious complication of tissue plasminogen activator (tPA) therapy for ischemic stroke. Here we report that activated protein C (APC), a plasma serine protease with systemic anticoagulant, anti-inflammatory and antiapoptotic activities, and direct vasculoprotective and
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