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acetaldehyde/инфаркт
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Страница 1 от 24 полученные результаты
Efficient expression of codon-adapted human acetaldehyde dehydrogenase 2 cDNA with 6xHis tag in Pichia pastoris.
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Human mitochondrial acetaldehyde dehydrogenase 2 (ALDH2) catalyzes the oxidation of acetaldehyde to acetic acid. Therefore, ALDH2 has therapeutic potential in detoxification of acetaldehyde. Furthermore, ALDH2 catalyzes nitroglycerin to nitrate and 1, 2-glyceryldinitrate during therapy for angina
The polymorphism in acetaldehyde dehydrogenase 2 gene, causing a substitution of Glu > Lys(504), is not associated with coronary atherosclerosis severity in Han Chinese.
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Alcohol consumption has an important effect on coronary atherosclerotic heart disease (CAD). Acetaldehyde dehydrogenase 2 (ALDH2) is a key enzyme in alcohol metabolism. A G-to-A missense mutation of ALDH2 gene, which causes a Glu > Lys(504) substitution, was recently shown to be associated with
Altered metabolism of acetaldehyde in blood is not a specific marker of diabetic macroangiopathy.
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Previous studies have demonstrated altered acetaldehyde metabolism in diabetics with macroangiopathy. Elimination of acetaldehyde in blood homogenates was studied in 20 non-diabetic survivors of myocardial infarction and 22 healthy controls. The half-life of acetaldehyde was shorter in patients,
ALDH2 Glu504Lys polymorphism and susceptibility to coronary artery disease and myocardial infarction in East Asians: a meta-analysis.
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OBJECTIVE
Emerging evidences have shown that the Glu504Lys variant in ALDH2 gene may greatly reduce the ability of ALDH2 to metabolize acetaldehyde, which could increase the risk of coronary artery disease (CAD) and myocardial infarction (MI). However, the reported results are still conflicting. To
[Anterior myocardial infarction in a chronic alcoholic man on disulfiram therapy: a case report].
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Disulfiram is a drug used since 1940 in the treatment of alcohol dependence. However, it is not a completely safe drug; there are in the literature some case reports of more severe reaction than the usual "acetaldehyde syndrome" secondary to ingestion of disulfiram and alcohol. We describe a case of
Acute myocardial infarction associated with disulfiram-alcohol interaction in a young man with normal coronary arteries.
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Acute myocardial infarction due to acetaldehyde syndrome has been rarely reported. A 22-year-old, chronic alcoholic man was admitted to our hospital with typical angina pectoris that developed after oral intake of disulfiram and alcohol together. The electrocardiogram showed hyperacute inferior
Combined effects of current-smoking and the aldehyde dehydrogenase 2*2 allele on the risk of myocardial infarction in Japanese patients.
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Aldehyde dehydrogenase 2 (ALDH2) detoxifies toxic aldehydes, e.g. acetaldehyde in cigarette smoke; however, the interactive effects between smoking status and the ALDH2 genotype on coronary artery disease (CAD) have not been reported. We investigated the effects of smoking status and the ALDH2
Association of East Asian Variant Aldehyde Dehydrogenase 2 Genotype (ALDH2*2*) with Coronary Spasm and Acute Myocardial Infarction.
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Coronary spasm plays an important role in the pathogenesis of ischemic heart disease, including angina pectoris, acute myocardial infarction (AMI), silent myocardial ischemia, and sudden death. The prevalence of coronary spasm is higher among East Asians probably due to genetic as well as
Unique antibody responses to malondialdehyde-acetaldehyde (MAA)-protein adducts predict coronary artery disease.
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Malondialdehyde-acetaldehyde adducts (MAA) have been implicated in atherosclerosis. The purpose of this study was to investigate the role of MAA in atherosclerotic disease. Serum samples from controls (n = 82) and patients with; non-obstructive coronary artery disease (CAD), (n = 40), acute
Cardioprotection induced by a brief exposure to acetaldehyde: role of aldehyde dehydrogenase 2.
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UNASSIGNED
We previously demonstrated that acute ethanol administration protects the heart from ischaemia/reperfusion (I/R) injury thorough activation of aldehyde dehydrogenase 2 (ALDH2). Here, we characterized the role of acetaldehyde, an intermediate product from ethanol metabolism, and its
S1P receptor 1-Mediated Anti-Renin-Angiotensin System Cardioprotection: Pivotal Role of Mast Cell Aldehyde Dehydrogenase Type 2.
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In the ischemic-reperfused (I/R) heart, renin-containing mast cells (MC) release enzymatically active renin, activating a local renin-angiotensin system (RAS), causing excessive norepinephrine release and arrhythmic dysfunction. Activation of Gi-receptors on MC and/or ischemic preconditioning (IPC)
Heavy ethanol consumption aggravates the ischemic cerebral injury by inhibiting ALDH2.
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BACKGROUND
Heavy ethanol consumption is widely accepted as a risk for ischemic stroke. The molecular mechanisms of ethanol-induced brain injury have not been fully understood.
OBJECTIVE
This study aims to find out the mechanism of the ischemic cerebral injury.
METHODS
We used Sprague-Dawley rats
Disruption of the aldehyde dehydrogenase 2 gene increases the bone anabolic response to intermittent PTH treatment in an ovariectomized mouse model.
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Aldehyde dehydrogenase 2 (ALDH2) is the enzyme that oxidizes the acetaldehyde produced by alcohol metabolism. This variant not only affects the response to alcohol but is also associated with several diseases, such as esophageal cancer, myocardial infarction, and particularly osteoporosis. In our
Disulfiram--alcohol reaction mimicking an acute coronary syndrome.
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Disulfiram treatment for alcohol dependence is used with acceptable outcomes. By inhibiting the aldehyde dehydrogenase enzyme, this treatment increases acetaldehyde concentration after the ingestion of alcohol causing an unpleasant disulfiram-alcohol reaction. Typical symptoms include flushing,
Mitochondrial aldehyde dehydrogenase in myocardial ischemia-reperfusion injury: from bench to bedside.
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Acute myocardial infarction is one of the major causes of mortality worldwide. Reperfusion in a timely fashion is the most effective way to limit infarct size. However, reperfusion can itself prompt further myocardial injury. This phenomenon is commonly known as myocardial ischemia-reperfusion (IR)
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