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hypoxia/nekros

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Interleukin-17 (IL-17) and tumor necrosis factor (TNF)-α are able to cooperatively alter the expression levels of a number of genes. In the present study, the mRNA expression levels of hypoxia-inducible factor (HIF)-1α were analyzed in MDA-MB-231 breast cancer cells following treatment with IL-17,

Hypoxia influences linearly patterned programmed cell necrosis and tumor blood supply patterns formation in melanoma.

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To investigate the possibility that tumor cells undergoing linearly patterned programmed cell necrosis (LPPCN) establish a spatial foundation for vasculogenic mimicry (VM) and to reveal that hypoxia influences LPPCN formation as well as Endo G and DNase 1 expression, 78 C57 mice were divided evenly

Tumor necrosis factor-α potentiates long-term potentiation in the rat dentate gyrus after acute hypoxia.

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An inadequate supply of oxygen in the brain may lead to an inflammatory response through neuronal and glial cells that can result in neuronal damage. Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that is released during acute hypoxia and can have neurotoxic or neuroprotective effects

Apoptosis, necrosis and hypoxia inducible factor-1 in human head and neck squamous cell carcinoma cultures.

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The objective of this study was to examine the mode of cell death and the hypoxia inducible factor-1 (HIF-1) expression of human head and neck squamous cell carcinoma (HNSCC) exposed to hypoxia in vitro. Apoptosis and necrosis rates were examined using flow cytometry. The findings suggest that HNSCC

Experimental cardiac necrosis in hypobaric and anemic hypoxia.

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Resistance to isoproterenol-induced cardiac necrosis (IPRO) was compared in rats exposed to two types of hypoxia (i.e., hypobaric and anemic). IPRO was induced by two consecutive, subcutaneous injections of isoproterenol (80 mg/kg) at 24-h intervals. The animals were killed on the third day and the

Counteracting apoptosis and necrosis with hypoxia responsive expression of Bcl-2Delta.

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In the encapsulated environment of biohybrid artificial organs, cells often encounter a deficiency in oxygen, which lead to apoptosis, necrosis, and lost of productivity. Two vectors with constitutive CMV promoters were constructed to examine the ability of Bcl-2Delta to help C2C12 mouse myoblasts
Many studies in the literature have been carried out to evaluate the various cellular and molecular processes involved in osteogenesis.Angiogenesis and bone formation work closely together in this group of disorders. Hypoxia-inducible factor (HIF) which is stimulated in tissue hypoxia triggers a

Silencing HIF-1α aggravates growth inhibition and necrosis of proximal renal tubular epithelial cell under hypoxia.

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The kidney is particularly susceptible to ischemia/hypoxia insult while dysfunction of proximal tubular epithelial cells (PTEC) is a primary pathologic hallmark in acute kidney injury. Hypoxia-inducible factor-1 (HIF-1) is a key regulator responsible for cellular hypoxic responses. Therefore, we
We have previously reported that human umbilical cord blood mononuclear cells (HUCBC), which contain hematopoietic, mesenchymal, and endothelial stem cells, can significantly reduce acute myocardial infarction size. To determine the mechanism whereby HUCBC increase myocyte and vascular endothelial

Hypoxia causes ischemic bowel necrosis in rats: the role of platelet-activating factor (PAF-acether).

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We have previously shown that injection of platelet-activating factor causes necrotizing enterocolitis in the rat and that platelet-activating factor is an endogenous mediator in lipopolysaccharide-induced bowel necrosis. Because hypoxia is a known predisposing factor for neonatal necrotizing

Cardioprotective effect of chronic hyperglycemia: effect on hypoxia-induced apoptosis and necrosis.

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It is generally accepted that mild forms of diabetes render the heart resistant to an ischemic insult. Because myocytes incubated chronically in medium containing high concentrations of glucose (25 mM) develop into a diabetes-like phenotype, we tested the hypothesis that high-glucose treatment

[Heatstroke: a rare cause of massive hepatic necrosis due to hypoxia].

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The authors report the case of a 76 year-old woman affected by heatstroke complicated by massive liver cell necrosis and fulminant liver failure, with a favorable outcome. Liver cell necrosis was localized in centro- and medio-lobular areas and was not associated with hepatic vein congestion. These

Deficient of LRRC8A attenuates hypoxia-induced necrosis in 3T3-L1 cells.

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Under acute hypoxia, multiple ion channels on the cell membrane are activated, causing cell swelling and eventually necrosis. LRRC8A is an indispensable protein of the volume-regulated anion channel (VRAC), which participates in swelling and the acceleration of cell necrosis. In this study,

NURR1 inhibition reduces hypoxia-mediated cardiomyocyte necrosis via blocking Mst1-JNK-mPTP pathway.

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Context: Although many studies have investigated the molecular mechanisms underlying hypoxia-related cardiomyocyte damage, the role of necrosis in cardiomyocyte death.Objective: The aim of our study is to explore the pathological role of nuclear receptor related 1 protein (NURR1) in

Dual-tracer PET of viable tumor volume and hypoxia for identification of necrosis-containing radio-resistant Sub-volumes.

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Introduction: Positron emission tomography (PET) using hypoxia-selective tracers like FAZA may guide radiation dose-escalation approaches. However, poor resolution combined with slow tracer retention in relatively inaccessible target cells and slow clearance of unbound tracer results in
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