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Sida 1 från 24 resultat
Effects of supplemental cystine or methionine on growth and lifespan of stroke-prone spontaneously hypertensive rats.
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Stroke-prone spontaneously hypertensive (SHRSP) rats are considered a suitable model for studying the effects of dietary and other environmental factors on human essential hypertension and haemorrhagic stroke. To investigate the suitability of a control diet for this strain of rats, we studied the
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
Homocysteine and stroke.
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During the past year epidemiological studies have linked elevated plasma total homocysteine concentrations with an increased risk of ischaemic stroke because of arterial disease. Laboratory studies have further explored the mitogenic effects of total homocysteine on vascular smooth muscle, and
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,
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
Histidine, cystine, glutamine, and threonine collectively protect astrocytes from the toxicity of zinc.
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In epilepsy, traumatic brain injury, and ischemic stroke, toxic levels of zinc released from neurons contribute to the brain damage associated with these disorders. Zinc causes oxidative stress by increasing the generation of reactive oxygen species and by inhibiting glutathione reductase (GR). This
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
Homocystine solubility and vascular disease.
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There is evidence that mild elevations of tHcy are associated with an increased risk for occlusive vascular disease, thrombosis, and stroke. It is hypothesized here that cellular toxicity could indirectly result from auto-oxidation of homocysteine to homocystine. Elevated levels of total plasma
Glutamate transporters in brain ischemia: to modulate or not?
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In this review, we briefly describe glutamate (Glu) metabolism and its specific transports and receptors in the central nervous system (CNS). Thereafter, we focus on excitatory amino acid transporters, cystine/glutamate antiporters (system xc-) and vesicular glutamate transporters, specifically
Nrf2-mediated redox signalling in vascular health and disease.
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Cells have evolved endogenous defence mechanisms to counteract oxidative stress, and the redox sensitive transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) plays a key role in the defence against oxidative stress via the induction of phase II and antioxidant enzymes.1-3 Under
Permanent dynamic transporter-mediated turnover of glutamate across the plasma membrane of presynaptic nerve terminals: arguments in favor and against.
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Mechanisms for maintenance of the extracellular level of glutamate in brain tissue and its regulation still remain almost unclear, and criticism of the current paradigm of glutamate transport and homeostasis has recently appeared. The main premise for this study is the existence of a definite and
Sampling glutamate and GABA with microdialysis: suggestions on how to get the dialysis membrane closer to the synapse.
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Microdialysis is currently optimized to sample the extrasynaptic pool. As such, the technique has facilitated discovery of ischemia-induced excitotoxic glutamate overflow (Benveniste H, Drejer J, Schousboe A, Diemer NH, 1987, Regional cerebral glucose phosphorylation and blood flow after insertion
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
Central nervous system complications in adult cystinosis patients.
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Little is known about the long-term progression of adult nephropathic cystinosis patients. Our objective was to study central nervous system complications in cystinosis patients in the era of early cysteamine treatment, using advanced neuroimaging techniques. Neurological examination and multimodal
Edaravone, a free radical scavenger, protects against ferroptotic cell death in vitro.
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Ferroptosis is characterized by an iron-dependent cell death with increased lipid peroxidation and is typically induced by either a decrease in glutathione (GSH) levels due to an insufficient supply of cysteine (Cys) or the inhibition of phospholipid hydroperoxide glutathione peroxidase (Gpx4).
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