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Page 1 od 54 rezultati
Protective Effects of Brain Infarction by N-Acetylcysteine Derivatives.
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OBJECTIVE
We recently found that acrolein (CH2=CH-CHO) is more strongly involved in brain infarction compared with reactive oxygen species. In this study, we looked for acrolein scavengers with less side effects.
METHODS
Photochemically induced thrombosis model mice were prepared by injection of
Lipid peroxidation and protective enzymes during myocardial infarction.
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Fasting blood taken from 34 patients with myocardial infarction, 19 with unstable angina and 40 healthy controls, was analysed for malondialdehyde and erythrocyte detoxification enzymes, superoxide dismutase and glutathione peroxidase. Malondialdehyde concentration was raised in the patients with
Glutathione S-transferase gene polymorphism as a susceptibility factor for acute myocardial infarction and smoking in the North Indian population.
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OBJECTIVE
Glutathione S-transferase (GST) plays a key role in the detoxification of xenobiotic atherogens generated by smoking. We investigated whether functional GST gene polymorphism might be associated with acute myocardial infarction (AMI) and smoking. No such investigation has previously been
Association of manganese superoxide dismutase Ala16Val polymorphism in the incidence of acute myocardial infarction in the Egyptians.
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Background: Oxidative stress has been implicated in various diseases including atherosclerosis; the most common pathologic process underlying acute myocardial infarction (AMI). The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against reactive oxygen
Glutathione S-transferase M1 null genotype is associated with a decreased risk of myocardial infarction.
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Tobacco smoke is a major cause of both cancer and vascular disease. Although its carcinogenic role via induction of DNA damage and mutation is well established, the mechanisms involved in vascular disease remain unclear. One possibility is that DNA damage causes smooth muscle cell proliferation in
CYP1A1 and GSTM1/T1 genetic variation in predicting risk for cerebral infarction.
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Cytochrome P450 1A1 (CYP1A1) is involved in the production of arachidonic acid-derived vasoactive substance. We hypothesized that CYP1A1 polymorphism might be related to pathological conditions associated with cerebral infarction (CI). We investigated the effect of genetic polymorphism in the
Loss of Nrf2 promotes rapid progression to heart failure following myocardial infarction.
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Nrf2 gene encodes a transcription factor regulating the expression of antioxidant and detoxification genes. We test here whether Nrf2 plays a role for cardiac protection during ischemic injury in an effort to establish Nrf2 as a target for cardiac protection therapies. Cardiac ischemia induced by
Successful treatment of refractory cerebral oedema in ecstasy/cocaine-induced fulminant hepatic failure using a new high-efficacy liver detoxification device (FPSA-Prometheus).
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Ecstasy-induced fulminant hepatic failure is associated with high mortality. If complicated by cerebral oedema, orthotopic liver transplantation is the only established treatment. We report a case of combined ecstasy/cocaine-induced fulminant hepatic failure presenting with severe rhabdomyolysis,
Skin cornification proteins provide global link between ROS detoxification and cell migration during wound healing.
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Wound healing is a complex dynamic process characterised by a uniform flow of events in nearly all types of tissue damage, from a small skin scratch to myocardial infarction. Reactive oxygen species (ROS) are essential during the healing process at multiple stages, ranging from the initial signal
Cocaine use and acute myocardial infarction.
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Cocaine use in the United States is widespread, affecting more than 30 million Americans. Although many of these persons do not seek healthcare, the overriding cause for hospitalization is cocaine-associated chest pain. Because only a minority of these patients suffer myocardial injury, it is
Cardiovascular complications of cocaine abuse.
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Cocaine abuse may lead to serious cardiac complications, including myocardial ischemia and infarction, myocarditis, cardiomyopathy and arrhythmias. With concomitant use of alcohol and cocaine, cocaethylene is produced by hepatic transformation. Cocaethylene is now thought to be primarily responsible
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
Glutathione S-transferase 8-8 is localized in smooth muscle cells of rat aorta and is induced in an experimental model of atherosclerosis.
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Allylamine (AA) is an electrophilic amine with a long history of experimental usage because of its extremely potent and relatively specific cardiovascular toxicity; it has been utilized in a variety of experimental models attempting to mimic human atherosclerotic lesions, myocardial infarction, and
Augmented glutathione synthesis decreases acrolein toxicity.
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We have shown recently that acrolein is more strongly involved in cell damage than reactive oxygen species during brain infarction. Thus, we tried to isolate cells with reduced susceptibility to acrolein toxicity to clarify how acrolein is detoxified under cell culture conditions. The IC(50) of
Decrease in acrolein toxicity based on the decline of polyamine oxidases.
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We have shown recently that acrolein is strongly involved in cell damage during brain infarction and chronic renal failure. To study the mechanism of acrolein detoxification, we tried to isolate Neuro2a cells with reduced sensitivity to acrolein toxicity (Neuro2a-ATD cells). In one cell line,
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