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actinomycin d/infarto
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 24 risultati
Effect of actinomycin D and cycloheximide on experimental myocardial infarction in rats.
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Actinomycin D, an inhibitor of DNA-directed RNA synthesis, or cycloheximide, a protein synthesis inhibitor, administered 24 h and 1 or 4 h respectively, before inducing coronary occlusion in conscious rats, offered marked protection against postinfarction ventricular fibrillation and sudden death.
Effect of actinomycin D and cycloheximide on ischemic preconditioning-induced delayed cardioprotective effect in rats.
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The present study was designed to investigate the effect of actinomycin D, a transcription inhibitor, and cycloheximide, a translation inhibitor, on the delayed cardioprotective effect of ischemic preconditioning. Left thoracotomy was performed in anaesthetized rats at 4th/5th intercostal space and
Myocardin-related transcription factor-A-overexpressing bone marrow stem cells protect cardiomyocytes and alleviate cardiac damage in a rat model of acute myocardial infarction.
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Myocardin-related transcription factor-A (MRTF-A) can transduce biomechanical and humoral signals, which can positively modulate cardiac damage induced by acute myocardial infarction (AMI). In the clinic, bone marrow stem cell (BMSC) therapy is being increasingly utilized for AMI; however, the
RNA synthesis in pons necessary for maintenance of bladder overactivity after cerebral infarction in rat.
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OBJECTIVE
The maintenance of long lasting bladder overactivity caused by cerebral infarction is believed to require transcription in the pontine micturition center. Therefore, we examined the influence of the RNA synthesis inhibitor actinomycin D (Banyu Pharmaceutical Co., Ltd., Tokyo, Japan) on
CircRNA ACAP2 induces myocardial apoptosis after myocardial infarction by sponging miR-29.
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Both GPER and membrane oestrogen receptor-α activation protect ventricular remodelling in 17β oestradiol-treated ovariectomized infarcted rats.
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Clinical and experimental studies have established that gender is a factor in the development of ventricular hypertrophy. We investigated whether the attenuated hypertrophic effect of oestradiol was via activation of phosphatidylinositol 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)
Differential recovery of prostacyclin synthesis in cultured vascular endothelial vs. smooth muscle cells after inactivation of cyclooxygenase with aspirin.
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Conflicting findings from clinical trials on the use of aspirin in preventing myocardial infarction emphasize the importance of understanding the effects of aspirin on vascular cells. Cultured vascular endothelial cells and smooth muscle cells of human, rat and bovine origin synthesized
Antiapolipoprotein A-1 IgG chronotropic effects require nongenomic action of aldosterone on L-type calcium channels.
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Autoantibodies to apolipoprotein A-1 (antiapoA-1 IgG) have been shown to be associated with higher resting heart rate and morbidity in myocardial infarction patients and to behave as a chronotropic agent in the presence of aldosterone on isolated neonatal rat ventricular cardiomyocytes (NRVC). We
Cyclooxygenase-2-dependent prostacyclin formation is regulated by low density lipoprotein cholesterol in vitro.
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Reduction of plasma low density lipoprotein (LDL) levels is associated with a reduced risk of myocardial infarction, stroke, and death. Some of this clinical benefit may be derived from an improvement in endothelium-dependent vasodilation. In the present study, we examined the effects of LDL
Coated stents to prevent restenosis in coronary heart disease.
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BACKGROUND
In-stent-restenosis (ISR) is considered to be an essential limiting factor of stenting in coronary heart disease (CHD). The development of coated stents has raised expectations on substantial lowering restenosis after stenting with decreasing the rate of restenosis and a reduction in the
Ischemic but not pharmacological preconditioning requires protein synthesis.
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BACKGROUND
Ischemic preconditioning (IPC) and pharmacological preconditioning (PPC) have both been shown to confer cardioprotective effects. However, the role of protein synthesis in preconditioning is unclear.
RESULTS
Isolated rabbit hearts were treated with cycloheximide (CHx, 10 micromol/L), a
The possible mechanism of protection induced by dexamethasone against sudden death due to coronary ligation in conscious rats.
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Rat isolated peritoneal cells (10(7) cells ml-1) incubated in the presence of dexamethasone (3 X 10(-9) M, for 90 min) were shown to release some factor(s), having a mol. wt. of 15 k, as determined by size exclusion chromatography, which inhibited phospholipase A2 activity and offered significant
Coronary artery embolism following cancer chemotherapy.
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A 16-year-old patient underwent partial gastrectomy for leiomyosarcoma of the stomach. Following resection, he received combination chemotherapy that included Adriamycin and dimethyltriazenoimidazole carboxamide (DTIC), with the cumulative Adriamycin dose being 405 mg/m2. The patient was
Glucocorticoid regulation of angiotensin-converting enzyme in primary culture of adult cardiac fibroblasts.
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The effect of dexamethasone on angiotensin-converting enzyme (ACE) in primary culture of adult cardiac fibroblasts was analyzed in this study. ACE is central to cardiac remodeling in conditions such as myocardial infarction (MI). Some studies indicate that glucocorticoids are often increased
Results of low-dose methotrexate treatment of persistent gestational trophoblastic disease in Sheffield 1980-1987.
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Between January 1980 and October 1987, 115 evaluable patients were treated in Sheffield for persistent gestational trophoblastic disease (GTD) with a low dose methotrexate regimen (LD-MTX). Each course comprised MTX 50 mg given by i.m. injection for 4 doses on alternate days. Courses were repeated
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