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cystine/infarction
Врската е зачувана во таблата со исечоци
11 резултати
64Cu-Labeled Divalent Cystine Knot Peptide for Imaging Carotid Atherosclerotic Plaques.
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The rupture of vulnerable atherosclerotic plaques that lead to stroke and myocardial infarction may be induced by macrophage infiltration and augmented by the expression of integrin αvβ3. Indeed, atherosclerotic angiogenesis may be a promising marker of inflammation. In this study, an engineered
Central post stroke pain: clinical, MRI, and SPECT correlation.
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OBJECTIVE
The objective of this study was to report clinical spectrum of central post stroke pain (CPSP) and correlate these with magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) findings.
METHODS
The study was designed as a prospective study.
METHODS
The study
SPECT changes and their correlation with EEG changes in tuberculous meningitis.
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OBJECTIVE
In tuberculous meningitis (TBM) blood flow may be altered due to associated vasculitis, hydrocephalus and raised intracranial pressure. Electroencephalography (EEG) and single photon emission computed tomography (SPECT) provide information about electrical activity and regional cerebral
Single photon emission computed tomography in tuberculous meningitis.
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BACKGROUND
Data on single photon emission computed tomography (SPECT) in tuberculous meningitis are lacking and prompted this study. SPECT findings in tuberculous meningitis are reported and correlated with clinical and radiological findings.
METHODS
Seventeen patients with tuberculous meningitis
Neuroprotective Effects of a Novel Antioxidant Mixture Twendee X in Mouse Stroke Model.
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BACKGROUND
Oxidative stress and inflammation are important aggravating factors in acute ischemic stroke.
METHODS
In the present study, the neuroprotective effects of a novel antioxidant mixture Twendee X containing multiple antioxidative ingredients, such as coenzyme Q10, ascorbic acid, and cystine,
System x(c)- activity and astrocytes are necessary for interleukin-1 beta-mediated hypoxic neuronal injury.
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The purpose of this study was to elucidate the cellular/biochemical pathway(s) by which interleukin-1beta (IL-1beta) contributes to the pathogenesis of hypoxic-ischemic brain damage. In vivo, IL-1 receptor type I (IL-1RI)-deficient mice showed smaller infarcts and less neurological deficits than
[Free amino-acids of the plasma in atherosclerotic patients (author's transl)].
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18 free amino-acids have been valuated in a group of patients recovering from myocardial infarction dating more than one year back and in another group of healthy active athlets. In the group of the ill persons the mean values of the following amino-acids were significantly higher: Arginine,
HIF-1α triggers long-lasting glutamate excitotoxicity via system xc- in cerebral ischaemia-reperfusion.
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Hypoxia-inducible factor 1α (HIF-1α) controls many genes involved in physiological and pathological processes. However, its roles in glutamatergic transmission and excitotoxicity are unclear. Here, we proposed that HIF-1α might contribute to glutamate-mediated excitotoxicity during cerebral
Lactacidosis modulates glutathione metabolism and oxidative glutamate toxicity.
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Lactate and acidosis increase infarct size in humans and in animal models of cerebral ischemia but the mechanisms by which they exert their neurotoxic effects are poorly understood. Oxidative glutamate toxicity is a form of nerve cell death, wherein glutamate inhibits cystine uptake via the
Potent neuroprotection after stroke afforded by a double-knot spider-venom peptide that inhibits acid-sensing ion channel 1a.
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Stroke is the second-leading cause of death worldwide, yet there are no drugs available to protect the brain from stroke-induced neuronal injury. Acid-sensing ion channel 1a (ASIC1a) is the primary acid sensor in mammalian brain and a key mediator of acidosis-induced neuronal damage following
Novel Biomarker of Oxidative Stress Is Associated With Risk of Death in Patients With Coronary Artery Disease.
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BACKGROUND
Free radical scavengers have failed to improve patient outcomes, promoting the concept that clinically important oxidative stress may be mediated by alternative mechanisms. We sought to examine the association of emerging aminothiol markers of nonfree radical mediated oxidative stress
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