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Stran 1 iz 58 rezultatov
[CATECHOLAMINE EXCRETION AND THE CLINICAL PICTURE IN THE MANAGEMENT OF CARDIAC INFARCTION AND CORONARY INSUFFICIENCY WITH N 3-PHENYLPROPYL -(2) 1, 1-DIPHENYL-PROPYL-(3)-AMINE].
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Prijava / prijava
Reduction of myocardial infarct size in rabbits by a novel indole derivative with antioxidant and free radical scavenging properties.
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Prijava / prijava
We investigated the cardioprotective efficacy of a new compound, 3-[(1H-1-indolyl)methyl] -4-amino 4,5-dihydro-1H,1,2,4 triazole-5-thione (C6458). The effect of C6458 on the reduction of the infarct size and its protective ability against oxidative damage of the myocardium after ischemia-reperfusion
Effects of neuropeptide Y2 receptor blockade on ventricular arrhythmias in rats with acute myocardial infarction.
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Excessive sympathetic activity is believed to be the key arrhythmogenic factor both in the setting of acute myocardial infarction and during chronic heart failure. The aim of this study was to evaluate the effect of neuropeptide Y2 blockade on malignant ventricular arrhythmias in rats with acute
MicroRNA-147 inhibits myocardial inflammation and apoptosis following myocardial infarction via targeting HIPK2
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Objective: The incidence of acute myocardial infarction (AMI) is increasing year by year, and it has become one of the diseases with the highest mortality in humans. MicroRNAs (miRNAs) are involved in the regulation of many diseases,
LU135252, an endothelin(A) receptor antagonist did not prevent pulmonary vascular remodelling or lung fibrosis in a rat model of myocardial infarction.
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The early intervention with endothelin(A) (ET(A)) receptor antagonists following coronary artery ligation has been shown to reduce the development of pulmonary hypertension, despite a lack of improvement in left ventricular function. The present study examined the contribution of pulmonary vascular
Resveratrol protects myocardial apoptosis induced by ischemia-reperfusion in rats with acute myocardial infarction via blocking P13K/Akt/e-NOS pathway.
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Ghrelin suppresses cardiac fibrosis of post-myocardial infarction heart failure rats by adjusting the activin A-follistatin imbalance.
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Ghrelin, a growth hormone-releasing peptide, potentially improves cardiac function, but the mechanisms remain unclear. In the study, the rat heart failure (HF) model was established by ligating the left anterior descending coronary artery (LAD) and treated with ghrelin (100μg/kg, subcutaneous
Impairment of the erythrocyte membrane fluidity in survivors of acute myocardial infarction. A prospective study.
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Erythrocytes have to constantly adapt themselves to the varying circulatory system shear stress forces and capillaries diameter. Membrane lipid and protein content have an important role in determining the erythrocyte shape and are main determinants of the membrane solid and fluid behaviour which
Effect of DPPD (diphenyl-para-phenylenediamine) on stroke and cerebral edema in gerbils.
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Diphenyl-para-phenylenediamine (DPPD) is an antioxidant that has been shown to decrease liver damage due to the peroxidative process of carbon tetrachloride in rats and to ameliorate cold-induced cerebral edema in cats. Because lipid peroxidation disrupts the integrity of the plasma membrane, a
mi R -15a/15b Cluster Modulates Survival of Mesenchymal Stem Cells to Improve Its Therapeutic Efficacy of Myocardial Infarction.
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Background The poor viability of transplanted mesenchymal stem cells (MSCs) hampers their therapeutic efficacy for ischemic heart disease. Micro RNA s are involved in regulation of MSC survival and function. The present study was designed to investigate the molecular effects of mi R -15a/15b on MSC
[Alterations of antiproliferative effects of serum obtained from patients with acute cerebral infarction treated with a radical scavenger, edaravone, with or without amlodipine using an in vitro cultured basilar artery smooth muscle cells].
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The guinea-pig basilar artery smooth muscle cell (GBa-SM3) culture system in the Dulbecco's modified Eagle's medium for 3 days serves as a useful in vitro model for assessing antiproliferative effects of various therapeutic agents on vessels. With use of this system we studied whether human serum
MiRNA-26a promotes angiogenesis in a rat model of cerebral infarction via PI3K/AKT and MAPK/ERK pathway.
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OBJECTIVE
To investigate the specific role of microRNA-26 (miRNA-26a) in a rat model of cerebral ischemic stroke and the underlying mechanism.
METHODS
A rat model of middle cerebral artery occlusion (MCAO) was established to induce permanent cerebral infarction. Neuro-behavior was observed and
lncRNA GAS5 regulates myocardial infarction by targeting the miR-525-5p/CALM2 axis.
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Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of cardiovascular diseases, especially in myocardial infarction (MI). However, the underlying molecular mechanism of how lncRNA involves and affect MI still remains unclear. This study aimed to investigate the expression of lncRNA
Ox-LDL influences peripheral Th17/Treg balance by modulating Treg apoptosis and Th17 proliferation in atherosclerotic cerebral infarction.
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BACKGROUND
CD4(+)CD25(+) regulatory T (Treg) cells and T-helper 17 (Th17) cells play important roles in acute cerebral infarction (ACI). Our previous findings have suggested that oxidized low-density lipoprotein (Ox-LDL) could influence Treg/Th17 ratio in ACI patients. However, the mechanisms are
Hydrogen peroxide preconditioning enhances the therapeutic efficacy of Wharton's Jelly mesenchymal stem cells after myocardial infarction.
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BACKGROUND
Exposure of cells to sublethal concentrations of hydrogen peroxide (H2O2) can alleviate subsequent oxidative stress-induced apoptosis. We assessed the effects of H2O2 preconditioning on the therapeutic potential of human umbilical cord Wharton's Jelly mesenchymal stem cells (WJ-MSCs) in a
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