digoxigenin/hypoxia

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Anti-apoptotic effect of heat shock protein 90 on hypoxia-mediated cardiomyocyte damage is mediated via the phosphatidylinositol 3-kinase/AKT pathway.

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1. Hypoxia-induced cardiomyocyte apoptosis contributes significantly to cardiac dysfunction following trauma, shock and burn injury. There is evidence that heat shock protein (HSP) 90 is anti-apoptotic in cardiomyocytes subjected to a variety of apoptotic stimuli. Because HSP90 acts as an upstream

Effect of c-myc antisense oligodeoxynucleotides on hypoxia-induced proliferation of pulmonary vascular pericytes.

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To study the effect of c-myc antisense oligodeoxynucleotides (ODNs) on proliferation of pulmonary vascular pericytes (PC) induced by hypoxia, cell culture, dot hybridization using probe of digoxigenin-11-dUTP-labeled cDNA, 3H-thymidine incorporation, immunocytochemical technique and image analysis

Hypoxia-reoxygenation-induced apoptosis in cultured neonatal rat cardiomyocyets and the protective effect of prostaglandin E.

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The aim of the present study was to investigate the effect of prostaglandin (PG) E1 on hypoxia/re-oxygenation (H/R) apoptosis and the expression of bcl-2 and bax in cultured neonatal rat cardiomyocytes. The H/R model was made using the first generation of cultured neonatal rat cardiomyocytes.

Expression of CD95 and CD95L on astrocytes in the CA1 area of the immature rat hippocampus after hypoxia-ischemia injury.

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The immature brain is affected profoundly by hypoxia-ischemia (HI) injury, which can lead to permanent neurologic sequelae in survivors. Neuronal degeneration after HI injury usually is achieved through apoptosis. Both CD95 and its natural ligand, CD95L, which are key molecules in the regulation of

Soluble guanylate cyclase gene expression and localization in rat lung after exposure to hypoxia.

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The nitric oxide (NO)-cGMP signal transduction pathway plays an important role in the regulation of pulmonary vascular tone and resistance in pulmonary hypertension. A number of studies have demonstrated that endothelial (e) and inducible nitric oxide synthases (NOS) are upregulated in

Thermal preconditioning protects the human internal mammary artery from hypoxia/re-oxygenation-induced damage.

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1. Preconditioning has been demonstrated to ameliorate ischaemia/reperfusion injury in several cells and tissues. Therefore, in the present study we investigated whether preconditioning of human bypass grafts, internal mammary artery (IMA) and saphenous vein (SV) induces heat shock protein (Hsp)

Methylprednisolone inhibits low-flow hypoxia-induced mitochondrial dysfunction in isolated perfused rat liver.

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OBJECTIVE To investigate the mechanism by which methylprednisolone protects the liver from hypoxia-induced injury. METHODS Prospective control study using the isolated rat liver. METHODS Animal research facility. METHODS Male, fasted, pathogen-free Sprague-Dawley rats. METHODS Low-flow hypoxia was

Localization of erythropoietin gene expression in proximal renal tubular cells detected by digoxigenin-labelled oligonucleotide probes.

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Erythropoietin (EPO) is the main humoral stimulus of erythropoiesis. In adult mammals, the kidney releases EPO in response to hypoxic stress. Conflicting data have suggested either renal tubular or peritubular cell origins of EPO synthesis in vivo. In situ hybridization studies were performed to

The effect of hypoxia on expression of basic fibroblast growth factor in pulmonary vascular pericytes.

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To examine whether hypoxia exerts effect on the expression of basic fibroblast growth factor (bFGF) in pulmonary vascular pericytes (PC), cell culture, in situ hybridization with probe of digoxigenin-11-dUTP-labled cDNA, immunocytochemistry and image analysis were employed in this study. The results

Hypoxia-inducible factor-2α promotes hepatocyte apoptosis during cholestasis.

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OBJECTIVE Hypoxia-inducible factor-2α (HIF-2α) has been reported to play an important role in a host of pathophysiological processes, including cellular survival. This study explores the role of HIF-2α in cholestasis-mediated hepatocyte apoptosis. METHODS Hypoxia-inducible factor-2α expression was

Hypoxia confers protection against apoptosis via the PI3K/Akt pathway in endothelial progenitor cells.

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OBJECTIVE The recruitment of endothelial progenitor cells (EPC) to ischemia has recently been suggested as an important mechanism of tissue repair. Although tissue ischemia can facilitate EPC mobilization, recruitment, and retention at the hypoxic site, the effects of hypoxia on EPC survival are not

Chronic hypoxia enhances endothelin-1-induced intracellular calcium elevation in rat carotid body chemoreceptors and up-regulates ETA receptor expression.

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Endothelin-1 (ET-1) excites carotid body (CB) chemoreceptors and induces mitosis of the chemoreceptors in chronic hypoxia. The aim of the present study was to examine the hypothesis that up-regulation of both ETA receptor and endogenous ET-1 expression in CB chemoreceptors enhances the response of

Angiopoietin-1 protects mesenchymal stem cells against serum deprivation and hypoxia-induced apoptosis through the PI3K/Akt pathway.

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OBJECTIVE The angiopoietin-1 (Ang1)/Tie-2 signaling system not only plays a pivotal role in vessel growth, remodeling, and maturation, but also reduces apoptosis of endothelial cells, neurons, and cardiomyocytes. However, relatively little is known as to whether Ang1 has a protective effect on

[Expression and distribution of bFGF mRNA in lung tissue of rat with chronic pulmonary hypertension].

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To evaluate the role of basic fibroblast growth factor (bFGF) in the development of hypoxic pulmonary hypertension, 30 wistarmale rats were divided into hypoxic group and control group. Rat models with chronic hypoxia induced pulmonary hypertension were established. The pulmonary hemodynamics was

Endogenous digitalislike factors in obstructive sleep apnea.

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Recent studies have provided evidence that hypoxia may stimulate the release of endogenous digitalislike factors (EDLF). Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia during sleep and may be associated with sympathetic activation and a high risk of developing hypertension.

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