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glyceraldehyde 3 phosphate/infarzierung
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Seite 1 von 29 Ergebnisse
Glyceraldehyde-3-phosphate dehydrogenase versus toluidine blue as a marker for infarct volume estimation following permanent middle cerebral artery occlusion in mice.
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Infarct size is a good predictor of the neurological outcome following stroke. Estimation of infarct size in the early phase following experimental stroke depends on the availability of reliable techniques that can distinguish ischemic from nonischemic tissue. The objective of this study was to
Biochemical mechanism of infarct size reduction by pyruvate.
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We have explored the biochemical mechanism of the infarct size reduction found after intracoronary pyruvate infusion. Using the double infarct model, we simultaneously produced in nine dogs a control- and a therapy-infarct and compared the infarct sizes in each dog after 90 min of occlusion and 90
Regional biochemical remodeling in non-infarcted tissue of rat heart post-myocardial infarction.
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Changes in the capacities of ATP-synthesizing reactions were analysed in residual non-infarcted myocardium following myocardial infarction. Rats were subjected to left coronary artery ligation (MI; n = 11) or to sham operation (sham; n = 18). Two months later, hearts were excised, rinsed and
Phenylephrine protects cardiomyocytes from starvation-induced apoptosis by increasing glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity.
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Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is known to be a "housekeeping" protein; studies in non-cardiomyocytic cells have shown that GAPDH plays pro-apoptotic role by translocating from cytoplasm to the nucleus or to the mitochondria. However, the cardiovascular roles of GAPDH are unknown.
Reciprocal change in angiotensinogen mRNA expression in rat myocardium and liver after myocardial infarction.
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The aim of this study was to analyze sequential change of angiotensinogen (Ao) mRNA expression in rat liver and noninfarcted myocardium after myocardial infarction (MI). Female sprague-Dawley rats were subjected either to left coronary artery occlusion or sham operation. Three weeks after MI,
Decreased type VI adenylyl cyclase mRNA concentration and Mg(2+)-dependent adenylyl cyclase activities and unchanged type V adenylyl cyclase mRNA concentration and Mn(2+)-dependent adenylyl cyclase activities in the left ventricle of rats with myocardial infarction and longstanding heart failure.
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OBJECTIVE
To address the effect of longstanding left ventricular (LV) hypertrophy and failure on LV adenylyl cyclase (AC) gene expression, mRNA concentrations of the main cardiac AC isoforms were measured in the non-infarcted area of LV from rats with myocardial infarction (MI), without (H) or with
Transforming growth factor beta-1 in acute myocardial infarction in rats.
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TGF-beta 1 has been examined in the heart during myocardial infarction caused by ligation of the left coronary artery. Infarcted and uninfarcted myocardium have been compared by immunohistochemical staining of TGF-beta 1 and by Northern blot analysis of mRNA. Normal ventricular myocytes are strongly
Increased mRNA expression of tumour necrosis factor-alpha and its converting enzyme in circulating leucocytes of patients with acute myocardial infarction.
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Tumour necrosis factor-alpha (TNF-alpha) plays an important role in myocardial damage in acute myocardial infarction (AMI). It has recently been discovered that TNF-alpha-converting enzyme (TACE) cleaves precursor TNF-alpha into its mature form. However, it remains unknown whether TNF-alpha
Experiments on infarct genesis caused by blockage of carbohydrate metabolism in guinea pig placentae.
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The poisoning of pregnant guinea pigs with monoiodineacetate, an inhibitor of carbohydrate metabolism in the glyceraldehyde-3-phosphate dehydrogenase phase, leads within a few minutes to the formation of syncytial plasma protrusions in the maternal blood lacunae of the placenta. These protusions
An appropriate loading control for western blot analysis in animal models of myocardial ischemic infarction.
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An appropriate loading control is critical for Western blot analysis. Housekeeping proteins (HKPs), such as β-actin, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and β-tubulin, are commonly used to normalize protein expression. But HKP expression can be impacted by certain experimental
Bone Marrow Mesenchymal Stem Cells (BM-MSCs) Improve Heart Function in Swine Myocardial Infarction Model through Paracrine Effects.
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Stem cells are promising for the treatment of myocardial infarction (MI) and large animal models should be used to better understand the full spectrum of stem cell actions and preclinical evidences. In this study, bone marrow mesenchymal stem cells (BM-MSCs) were transplanted into swine heart
Time-dependent increases in syndecan-1 and fibroglycan messenger RNA expression in the infarct zone after experimentally induced myocardial infarction in rats.
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BACKGROUND
Syndecan-1 and fibroglycan, heparan sulphate proteoglycans, play important roles in extracellular matrix formation via their biological functions.
OBJECTIVE
To examine experimentally the sequential changes in syndecan-1 and fibroglycan messenger RNA (mRNA) expression after acute
Low myocardial transcript variant alt-a of cyclin dependent kinase inhibitor p21 expression differentiates hypothermia from cardiac/respiratory causes of death.
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Gene expressions in the myocardium have been shown to vary between different causes of death, which can be utilized in the recognition of varied processes. Our previous work with a limited number of cases showed a high messenger ribonucleic acid expression of the transcript variant alt-a of cyclin
Differential regulation of ventricular adrenomedullin and atrial natriuretic peptide gene expression in pressure and volume overload in the rat.
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1. Adrenomedullin is a recently discovered vasodilating and natriuretic peptide whose physiological and pathophysiological roles remain to be established. Like atrial natiuretic peptide adrenomedullin is expressed in the left ventricle. Ventricular expression of atrial natriuretic peptide is known
Nuclear localization of the mitochondrial factor HIGD1A during metabolic stress.
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Cellular stress responses are frequently governed by the subcellular localization of critical effector proteins. Apoptosis-inducing Factor (AIF) or Glyceraldehyde 3-Phosphate Dehydrogenase (GAPDH), for example, can translocate from mitochondria to the nucleus, where they modulate apoptotic death
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