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Hypoxia down-regulates cyclic guanidine monophosphate-dependent protein kinase in fetal pulmonary vascular smooth muscle cell through generation of reactive oxygen species and promotes development of pulmonary hypertension.

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KR-32570, a novel Na+/H+ exchanger-1 inhibitor, attenuates hypoxia-induced cell death through inhibition of intracellular Ca2+ overload and mitochondrial death pathway in H9c2 cells.

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A novel Na+/H+ exchanger-1 (NHE-1) inhibitor [5-(2-methoxy-5-chloro-5-phenyl)furan-2-ylcarbonyl]guanidine (KR-32570) has been previously demonstrated to elicit cardioprotective effect against ischemic injury in rat heart. In the present study, we examined the effects of KR-32570 on cell death

Action of creatinol-O-phosphate on the contractility changes evoked by hypoxia and ischemia in rat isolated heart.

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The effect of creatinol-O-phosphate (N-methyl-N-(beta-hydroxyethyl)guanidine O-phosphate, creatinolfosfate, Aplodan) pretreatment has been studied on the recovery of contractility of rat isolated heart after hypoxia or ischemia. In normoxia creatinol-O-phosphate (100 mumol/l) evoked a positive

Na(+)/H(+) exchange subtype 1 inhibition during extracellular acidification and hypoxia in glioma cells.

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Lactacidosis is a common feature of ischaemic brain tissue, but its role in ischaemic neuropathology is still not fully understood. Na(+)/H(+) exchange, a mechanism involved in the regulation of intracellular pH (pH(i)), is activated by low pH(i). The role of Na(+)/H(+) exchange subtype 1 was

Exposure to chronic hypoxia induces qualitative changes of collagen in the walls of peripheral pulmonary arteries.

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Qualitative changes of vascular wall matrix collagens in chronic hypoxic pulmonary hypertension were studied by gel electrophoresis. Male adult rats (n = 12) were exposed to hypoxia (FiO2 = 0.1, 3 wks). Control rats (n = 13) were kept in air. Samples of peripheral pulmonary arteries (PPA, diam.

Near-Infrared Fluorescence Probe for Monitoring the Metabolic Products of Vitamin C in HepG2 Cells under Normoxia and Hypoxia.

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Vitamin C (ascorbic acid; AA) is a well-known reducing agent and has been evaluated for its antitumor activity. However, the mechanism for its antitumor action remains unclear. Tracking the metabolism of AA may help to elucidate its antitumor mechanism. In this study, a near-infrared fluorescent

Recent advances in the management of malignant pheochromocytoma and paraganglioma: focus on tyrosine kinase and hypoxia-inducible factor inhibitors.

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Inactivating mutations of the succinate dehydrogenase subunit B ( SDHB) gene and the subsequent stabilization and activation of the hypoxia-inducible factor 2-alpha (HIF2α) unit are recognized hallmarks associated with the development of metastatic pheochromocytomas and paragangliomas (MPPG).

The Expression of CNS-Specific PPARGC1A Transcripts Is Regulated by Hypoxia and a Variable GT Repeat Polymorphism.

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PPARGC1A encodes a transcriptional co-activator also termed peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1-alpha (PGC-1α) which orchestrates multiple transcriptional programs. We have recently identified CNS-specific transcripts that are initiated far upstream of the reference

Creatine salts provide neuroprotection even after partial impairment of the creatine transporter.

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Creatine, a compound that is critical for energy metabolism of nervous cells, crosses the blood-brain barrier (BBB) and the neuronal plasma membrane with difficulty, and only using its specific transporter. In the hereditary condition where the creatine transporter is defective (creatine transporter

Regulation of Extracellular Matrix Synthesis by Shell Extracts from the Marine Bivalve Pecten maximus in Human Articular Chondrocytes- Application for Cartilage Engineering.

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The shells of the bivalve mollusks are organo-mineral structures predominantly composed of calcium carbonate, but also of a minor organic matrix, a mixture of proteins, glycoproteins, and polysaccharides. These proteins are involved in mineral deposition and, more generally, in the spatial

Pathophysiological mechanism of lung injury in patients with leptospirosis.

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OBJECTIVE Acute lung injury (ALI) is a serious clinical problem. We investigated the pathogenetic mechanisms of ALI caused by leptospirosis. METHODS The study included five cases of leptospirosis. We monitored the arterial pressure (AP) and heart rate (HR) and analysed the AP and HR variabilities

Pharmacological profile of KR-33028, a highly selective inhibitor of Na+/H+ exchanger.

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We evaluated the cardioprotective effects of 4-cyano (benzo[b]thiophene-2-carbonyl)guanidine (KR-33028), a recently developed inhibitor of the Na+/H+ exchanger (NHE), on hypoxia-induced H9c2 cell death and on perfused rat hearts subjected to ischemia/reperfusion. KR-33028 inhibited in a

[Acupoint Catgut Embedding Improves Gastric Mucosal Injury by Down-Regulating Expression of HIF-1α and VEGF in Chronic Atrophic Gastritis Rats]

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Objective: To observe the effect of acupoint catgut embedding on histopathological changes of gastric mucosa and expression of mucosal hypoxia inducible factor (HIF)-1α and vascular endothelial growth factor (VEGF) proteins in chronic atrophic gastritis (CAG) rats,

The role of HCO3(-)-dependent mechanisms in pHi regulation during O2 deprivation.

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We have reported in our previous work that, in the absence of HCO(3)(-), Na(+)/H(+) exchanger is responsible for an anoxia-induced alkalinization in hippocampal CA1 neurons. HCO(3)(-)-dependent mechanisms have been reported to play a key role in pH(i) regulation in nerve cells, but how their

Drugs preventing Na+ and Ca2+ overload.

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Cardiac intracellular Na+and Ca2+homeostasis is regulated by the concerted action of ion channels, pumps and exchangers. The Na+, K+-ATPase produces the electrochemical concentration gradient for Na+, which is the driving force for Ca2+removal from the cytosol via the Na+/Ca2+exchange. Reduction of

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