peroxidase/beroerte

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Plasma glutathione peroxidase deficiency and platelet insensitivity to nitric oxide in children with familial stroke.

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In a previous report by Freedman et al (J Clin Invest. 1996;97:979-987), plasma from 2 brothers with stroke or transient ischemic attack inactivated the antiplatelet effects of nitric oxide (NO), and this effect was found to be a consequence of a deficiency of plasma glutathione peroxidase (GSH-Px).

Cell age distribution of erythrocytes at the incidence of cerebral stroke in stroke-prone spontaneously hypertensive rats, and their glutathione peroxidase activity.

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To study the mechanism of the fall of glutathione peroxidase (GSH-Px) activity in erythrocyte after cerebral strokes in stroke-prone spontaneously hypertensive rats (SHRSP), erythrocytes were fractionated into low density erythrocytes (LD-E) and high density erythrocytes (HD-E) by a density gradient

Effect of glutathione peroxidase mimic ebselen (PZ51) on endothelium and vascular structure of stroke-prone spontaneously hypertensive rats.

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BACKGROUND To investigate whether extrinsic antioxidant seleno-glutathione peroxidase mimic ebselen (PZ51) can protect endothelium and vascular structure of stroke-prone spontaneously hypertensive rats (SHRsp) during the chronic process of hypertension. METHODS Twenty-two 8-week-old SHRsp were

Relationship between erythrocytes glutathione peroxidase and incidence of stroke lesion in the stroke-prone spontaneously hypertensive rat.

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1. To determine biochemically the incipient timing of cerebral stroke in stroke-prone spontaneously hypertensive rats (SHRSP) the relation between the glutathione peroxidase (GSH-Px) activity in erythrocytes and the extent of stroke lesion was investigated. 2. When the blood pressure of SHRSP was

Plasma glutathione peroxidase in pediatric stroke families.

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OBJECTIVE Promoter polymorphisms in the plasma glutathione peroxidase gene (GPX3), which encodes a major antioxidant enzyme implicated in post-translational modification of fibrinogen, have been implicated as risk factors for arterial ischemic stroke (AIS) and cerebral sinovenous thrombosis (CSVT)

Inflammatory response and glutathione peroxidase in a model of stroke.

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Stroke is one of the leading causes of death in major industrial countries. Many factors contribute to the cellular damage resulting from ischemia/reperfusion (I/R). Experimental data indicate an important role for oxidative stress and the inflammatory cascade during I/R. We are testing the

Changes in vascular permeability in stroke-prone spontaneously hypertensive rats studied with peroxidase as a tracer.

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Cerebrovascular permeability in stroke-prone spontaneously hypertensive rats (SHR) at various ages was histologically studied using horseradish peroxidase as a tracer and such was related to the cerebrovascular lesions in the animals. An increase in permeability was demonstrated in the brain of SHR,

Promoter polymorphisms in the plasma glutathione peroxidase (GPx-3) gene: a novel risk factor for arterial ischemic stroke among young adults and children.

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OBJECTIVE Plasma glutathione peroxidase (GPx-3)-deficiency increases extracellular oxidant stress, decreases bioavailable nitric oxide, and promotes platelet activation. The aim of this study is to identify polymorphisms in the GPx-3 gene, examine their relationship to arterial ischemic stroke (AIS)

Glutathione peroxidase inhibits cell death and glial activation following experimental stroke.

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Stroke is a leading cause of morbidity and mortality in major industrial countries. Many factors contribute to the cellular damage resulting from ischemia-reperfusion (I-R). Growing evidence indicates that reactive oxygen species (ROS) contribute significantly to this process, though their exact

Prediction of stroke lesions in stroke-prone spontaneously hypertensive rats by glutathione peroxidase in erythrocytes.

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The incipient timing of cerebral strokes in the stroke-prone spontaneously hypertensive rats (SHRSP) was biochemically determined by investigating the relationship between the glutathione peroxidase (GSH-Px) activity in erythrocytes and the extent of stroke lesions. When the blood pressure of SHRSPs

Glutathione peroxidase overexpression inhibits cytochrome C release and proapoptotic mediators to protect neurons from experimental stroke.

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OBJECTIVE Ischemic injury and reperfusion increases superoxide (O2-) production and reduces the ability of neurons to scavenge free radicals, leading to the release of cytochrome c and apoptosis. Here we test whether overexpression with the use of gene therapy of the antioxidant glutathione

The C718T polymorphism in the 3'-untranslated region of glutathione peroxidase-4 gene is a predictor of cerebral stroke in patients with essential hypertension.

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In the present study we have investigated the association of three single nucleotide polymorphisms in glutathione peroxidase (GPx) genes GPX1 rs1050450 (P198L), GPX3 rs2070593 (G930A) and GPX4 rs713041 (T718C) with the risk of cerebral stroke (CS) in patients with essential hypertension (EH). A

Mitochondrial HMG-CoA synthase partially contributes to antioxidant protection in the kidney of stroke-prone spontaneously hypertensive rats.

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OBJECTIVE Increased oxidative stress plays an important role in cardiovascular diseases including hypertension and stroke. Evidence has indicated that ketone bodies could exert antioxidative effects. We explored the role of renal mitochondrial 3-hydroxy-3-methylglutaryl-coenzyme A synthase (HMGCS2)

Manganese-enhanced MRI of brain plasticity in relation to functional recovery after experimental stroke.

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Restoration of function after stroke may be associated with structural remodeling of neuronal connections outside the infarcted area. However, the spatiotemporal profile of poststroke alterations in neuroanatomical connectivity in relation to functional recovery is still largely unknown. We

Evidence for a Beneficial Effect of Oral N-acetylcysteine on Functional Outcomes and Inflammatory Biomarkers in Patients with Acute Ischemic Stroke

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Purpose: Numerous preclinical studies have demonstrated the potential neuroprotective effects of N-acetylcysteine (NAC) in the treatment of brain ischemia. Accordingly, the present study aimed to assess the potential therapeutic effects

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