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Страна 1 од 31 резултати
[The effect of ionol on oxidative-reductive processes in the kidney during heat stroke].
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Heat stroke was induced in intact rats in a thermal chamber (45 degrees C) and simultaneously a group of animals was subjected to overheating for the same time but was given intraperitoneal injections of ionol (120 mg/kg) for 2 days and 30 minutes before exposure in the chamber. Significant increase
Anti-ischemia/reperfusion injury effects of notoginsenoside R1 on small molecule metabolism in rat brain after ischemic stroke as visualized by MALDI-MS imaging
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Ischemic stroke is a syndrome of severe neurological responses that cause neuronal death, damage to the neurovascular unit and inflammation. Notoginsenoside R1 (NG-R1) is a neuroprotective drug that is commonly used to treat neurodegenerative and cerebrovascular diseases. However, its potential
Succinate links atrial dysfunction and cardioembolic stroke.
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METHODS
A totalQuantitative clinical proteomic study of autopsied human infarcted brain specimens to elucidate the deregulated pathways in ischemic stroke pathology.
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Ischemic stroke, still lacking an effective neuroprotective therapy is the third leading cause of global mortality and morbidity. Here, we have applied an 8-plex iTRAQ-based 2D-LC-MS/MS strategy to study the commonly regulated infarct proteome from three different brain regions (putamen, thalamus
[Morphologo-histochemical characteristics of ischemic cerebral infarcts in the acute stage of the stroke in patients with atherosclerosis].
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Morphological and histochemical investigations of the activity of succinate, malate, lactate, isocitrate, and glucoso-6-phosphate dehydrogenases, and NAD-diaphorase in the central, marginal, borderline and perifocal zones of ischemic brain infarctions were carried out. Deep changes in the activity
Altered mitochondrial function in fibroblasts containing MELAS or MERRF mitochondrial DNA mutations.
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A number of human diseases are caused by inherited mitochondrial DNA mutations. Two of these diseases, MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) and MERRF (myoclonic epilepsy and ragged-red fibres), are commonly caused by point mutations to tRNA genes
Microcirculatory, mitochondrial, and histological changes following cerebral ischemia in swine.
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BACKGROUND
Ischemic brain injury due to stroke and/or cardiac arrest is a major health issue in modern society requiring urgent development of new effective therapies. The aim of this study was to evaluate mitochondrial, microcirculatory, and histological changes in a swine model of global cerebral
Effects of naftidrofuryl oxalate on microsphere embolism-induced changes in tricarboxylic acid cycle intermediates of rats.
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The present study was undertaken to determine whether naftidrofuryl oxalate, a cerebral vasodilator, may improve or attenuate microsphere embolism-induced damage to the mitochondrial tricarboxylic acid cycle. For this purpose, the intermediates in the tricarboxylic acid cycle were determined using
Antioxidant effects of JM-20 on rat brain mitochondria and synaptosomes: mitoprotection against Ca²⁺-induced mitochondrial impairment.
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Because mitochondrial oxidative stress and impairment are important mediators of neuronal damage in neurodegenerative diseases and in brain ischemia/reperfusion, in the present study, we evaluated the antioxidant and mitoprotective effect of a new promising neuroprotective molecule, JM-20, in
Fluid use in adult intensive care.
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Methods for the restoration of circulating blood volume, including the use of intravenous fluids, have been widely discussed over many years. There are no clear guidelines regarding the type of solutions, the total volume that should be transfused, or time schedules. Colloid solutions, usually
Effects of carboxylic acids on the uptake of non-transferrin-bound iron by astrocytes.
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The concentrations of non-transferrin-bound iron are elevated in the brain during pathological conditions such as stroke and Alzheimer's disease. Astrocytes are specialised for sequestering this iron, however little is known about the mechanisms involved. Carboxylates, such as citrate, have been
Oxidative stress is involved in the permeabilization of the inner membrane of brain mitochondria exposed to hypoxia/reoxygenation and low micromolar Ca2+.
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From in vivo models of stroke it is known that ischemia/reperfusion induces oxidative stress that is accompanied by deterioration of brain mitochondria. Previously, we reported that the increase in Ca2+ induces functional breakdown and morphological disintegration in brain mitochondria subjected to
[Ergometric and pathologic study of a family with complex I deficiency].
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We studied a family with a myopathic form of complex I deficiency with regard to the clinical symptoms, usefulness of the exercise tolerance test with an ergometer for screening of mitochondrial abnormalities, pathological findings in biopsied muscles and genetics. In this family, none of the
[A case of complex I deficiency with episodic respiratory distress].
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A 7-year-old girl with normal psychomotor development during infancy began to have easy fatigability about 3 years of age. At the age of 5 years, she developed respiratory distress and became unconscious when the serum lactate and pyruvate levels were markedly elevated and a blood gas analysis
Neuroproteomics: a biochemical means to discriminate the extent and modality of brain injury.
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Diagnosis and treatment of stroke and traumatic brain injury remain significant health care challenges to society. Patient care stands to benefit from an improved understanding of the interactive biochemistry underlying neurotrauma pathobiology. In this study, we assessed the power of
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