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disulfide/мозочен удар
Врската е зачувана во таблата со исечоци
Страница 1 од 89 резултати
Analysis of Neutrophil/Lymphocyte ratio and Thiol/Disulfide homeostasis parameters in patients admitted to the emergency department with ischemic stroke.
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Dynamic thiol-disulfide homeostasis in acute ischemic stroke patients.
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Dynamic thiol-disulfide homeostasis plays a critical role in the cellular protection provided by antioxidation. The aim of this study was to investigate whether there is a change in thiol-disulfide homeostasis in acute ischemic stroke patients. Patients diagnosed with acute ischemic stroke that had
Eight at one stroke - a synthetic tetra-disulfide peptide epitope.
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We have designed a cysteine-rich β-hairpin peptide which dimerises spontaneously to the antiparallel double β-hairpin motif C1-C12', C1'-C12, C5-C8, C5'-C8'-tricyclo-(CHWECCitGCRLVC)2. The highly regioselective oxidation of eight cysteines yields an intermolecular bi-disulfide 24mer hinge peptide
Disturbance of thiol/disulfide aminothiols homeostasis in patients with acute ischemic stroke stroke: Preliminary findings.
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[Blood cell aggregation and oxidative stress in pathogenesis of ischemic stroke].
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Rheologic properties of blood cells and a state of oxidative-reductive processes and blood systems have been studied in 75 patients in acute period of ischemic stroke. The signs of oxidative stress development and simultaneous augmentation of blood cells aggregation were found. Shifts of
Severe hypotension and ischemic stroke after disulfiram-ethanol reaction.
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Disulfiram (tetraethylthiuram disulfide) has been used for almost 60 years in the treatment of alcohol addiction. It causes aversive behavior due to disulfiram-ethanol reaction (DER). The classical DER includes flush, sweating, tremor, nausea, vomiting, tachycardia, moderate decrease in blood
Mortality among workers exposed to carbon disulfide.
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Mortality experience was investigated at a plant in Ontario that produced viscose rayon, with carbon disulfide as a main raw material. Work-history records for 279 deceased workers at the plant (plant A) were obtained and compared with those for 511 deceased workers at a pulp and paper plant in the
Recovery of brain biomarkers following peroxisome proliferator-activated receptor agonist neuroprotective treatment before ischemic stroke.
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BACKGROUND
Lipid lowering agent such as agonists of peroxisome proliferator-activated receptors (PPAR) are suggested as neuroprotective agents and may protect from the sequelae of brain ischemic stroke. Although the demonstration is not clearly established in human, the underlying molecular
Targeting the Role of Lipoprotein (a) in Stroke.
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Stroke is the third leading cause of death in the United States, behind only heart disease and cancer, with over 140,000 associated deaths per year.
Considerable research is ongoing to examine the role of modifiable risk factors which may cause or contribute to stroke. Although age and family
Thiol-Disulfide Homeostasis in Cerebral Venous Sinus Thrombosis.
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Distinct structural changes in wild-type and amyloidogenic chicken cystatin caused by disruption of C95-C115 disulfide bond.
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Human cystatin C (HCC) amyloid angiopathy (HCCAA) is characterized by tissue deposition of amyloid fibrils in blood vessels, which can lead to recurrent hemorrhagic stroke. Wild-type HCC forms part of the amyloid deposits in brain arteries of elderly people with amyloid angiopathy. A point mutation
Elevated plasma homocyst(e)ine concentration as a possible independent risk factor for stroke.
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Homocyst(e)ine refers to the sulfur-containing amino acids homocysteine, homocystine, and homocysteine-cysteine mixed disulfide, which normally exist in plasma in both the free and protein-bound forms. Marked hyperhomocyst(e)inemia is associated with well-recognized complications of occlusive
Experimental stroke protection induced by 4-hydroxybenzyl alcohol is cancelled by bacitracin.
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Induction of protein disulfide isomerase (PDI) is validated as a main mechanism by which 4-hydroxybenzyl alcohol (4-HBA), an active principle of Gastrodia elata Blume, reduces cerebral infarct volumes in a murine model of focal brain ischemia/reperfusion. In contrast to its position isomers, i.e.
Carbon disulfide neurotoxicity: Taiwan experience.
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Carbon disulfide (CS2) intoxication may induce peripheral neuropathy, encephalopathy, and cardiovascular diseases. In our studies, abnormalities of the peripheral nerves including clinical symptoms and electrophysiological findings were still present 3 years after cessation of CS2 exposure. The data
Up-regulation of protein-disulfide isomerase in response to hypoxia/brain ischemia and its protective effect against apoptotic cell death.
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We isolated and identified a stress protein that is up-regulated in response to hypoxia in primary-cultured glial cells. Protein-disulfide isomerase (PDI) was up-regulated not only by hypoxia in glia in vitro, but also by transient forebrain ischemia in rats in vivo. To determine whether newly
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