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disulfide/infarction

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页 1 从 91 结果

Histochemistry of sulfhydryls in acute myocardial infarction.

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To study the changes in sulfhydryl and disulfide distribution in myocardial infarction we applied the fluorescent sulfhydryl reagent, monobromobimane to sections of myocardium from patients dying of infarction of 24 h to 7 days duration. Staining for both sulfhydryls and for disulfide after

Brain MRI findings of carbon disulfide poisoning.

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OBJECTIVE To evaluate the findings of brain MRI in patients with carbon disulfide poisoning. METHODS Ninety-one patients who had suffered carbon disulfide poisoning [male:female=87:4; age, 32-74 (mean 53.3) years] were included in this study. To determine the extent of white matter hyperintensity

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
Myocardial physiology in the aftermath of myocardial infarction (MI) before remodeling is an under-explored area of investigation. Here, we describe the effects of MI on the cardiac sarcomere with focus on the possible contributions of reactive oxygen species. We surgically induced MI in

Ten-year coronary mortality of workers exposed to carbon disulfide.

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Two cohorts, one comprising 343 viscose rayon workers exposed for at least five years to carbon disulfide (CS2) and the other made up of 343 nonexposed men, were followed from 1967 to 1977 with respect to coronary heart disease (CHD) mortality. In the examination in 1967 known risk factors of CHD

Association of thiol/disulfide ratio with syntax score in patients with NSTEMI.

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OBJECTIVE The aim of this study was to investigate the relation between native thiol/disulfide ratio (TDR) and severity of coronary atherosclerosis as assessed by the Syntax score (SXscore) in patients with non-ST elevation myocardial infarction (NSTEMI) who underwent coronary angiography. METHODS A
In this study, we present nanofiber-mediated gene delivery for myocardial infarction (MI). Branched polyethylenimine cross-linked via disulfide bonds (ssPEI) complexed with vascular endothelial growth factor (VEGF) were immobilized on electrospun polycaprolactone (PCL)/polyethylenimine (PEI)
Protein disulfide isomerase (PDI) family members including PDI and ERp57 emerge as novel targets for anti-thrombotic treatments, but chemical agents with selectivity remain to be explored. We previously reported a novel derivative of danshensu (DSS), known as ADTM, displayed strong cardioprotective
OBJECTIVE The aim of the study was to analyze the molecular mechanisms activated during postinfarction remodeling in human hearts. BACKGROUND The molecular mechanisms of initial response to ischemic insult in the heart and the pathways involved in compensation and remodeling are still largely
Considerable efforts have been made to exploit cardioprotective drugs and gene delivery systems for myocardial infarction (MI). The promising cardioprotective effects of recombinant human erythropoietin (rHuEPO) protein in animal experiments have not been consistently reproduced in clinical human
Thrombin-like enzymes (TLEs) are studied widely because of their therapeutic potential in myocardial infarction and thrombotic diseases. But they are always produced in Escherichia coli BL21 (DE3) as inclusion bodies because they are single chain Cys-rich proteins. In this work, coexpressing of
Previous studies have shown that exposure to chronic hypoxia protects against myocardial infarction, but little is known about the cellular and molecular mechanisms involved. Here we observed that chronic hypoxia for 3 wk resulted in improved survival of mice (from 64% to 83%), reduced infarction
Increased O(2)(*-) and NO production is a key mechanism of mitochondrial dysfunction in myocardial ischemia/reperfusion injury. In complex II, oxidative impairment and enhanced tyrosine nitration of the 70 kDa FAD-binding protein occur in the post-ischemic myocardium and are thought to be mediated
OBJECTIVE The mechanisms underlying numerous biological roles of hydrogen sulfide (H2S) remain largely unknown. We have previously reported an inhibitory role of H2S in the L-type calcium channels in cardiomyocytes. This prompts us to examine the mechanisms underlying the potential regulation of H2S
This study aimed to explore the cardioprotective effect of new synthesized coumarin (E)-4-hydroxy-N'-(1-(7-hydroxy-2-oxo-2H-chromen-3-yl) ethylidene) benzohydrazide denoted (Hyd.Cou) against myocardial infarction disorders. Male Wistar rats were divided into four groups; Control, ISO, ISO+ Ac
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