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Effect of stagnant hypoxia on acid ribonuclease activity in the rat prosencephalon during ontogenesis.

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In the rat prosencephalon it proved possible to differentiate lysosomal ribonuclease from alkaline ribonuclease activity, which could be detected only in the presence of p-chlormercuribenzoate. Acid RNase activity related to the amount of protein in the prosencephalon fell during ontogenesis. It was

Hypoxia-sensitive supramolecular nanogels for the cytosolic delivery of ribonuclease A as a breast cancer therapeutic.

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As the most common malignancy in women, breast cancer causes >40,000 deaths annually. Ribonuclease A (RNase), a new anti-cancer agent, has attracted intense interest due to its high efficacy and specificity. However, RNase suffers from instability, a short half-life in the circulation and poor

New insights into hypoxia-related mechanisms involved in different microvascular patterns of bronchopulmonary carcinoids and poorly differentiated neuroendocrine carcinomas. Role of ribonuclease T2 (RNASET2) and HIF-1α.

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Ribonuclease T2 (RNASET2) is a pleiotropic and polyfunctional protein, which exerts several different activities in neoplastic cells since the early steps of tumor development. Besides having an antitumorigenic activity, RNASET2 inhibits both bFGF-induced and VEGF-induced angiogenesis and has a role

Effect of anoxia and ischemia on ribonuclease activity in brain.

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Modulated vasodilator responses to natriuretic peptides in rats exposed to chronic hypoxia.

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Natriuretic peptides (NPs), such as atrial natriuretic peptide (ANP), C-type natriuretic peptide (CNP), and adrenomedullin (ADM), are endogenous vasodilators acting via specific receptors. This study addressed the question of how pulmonary artery (PA) responses to these peptides and the gene

Effects of NF-kappaB oligonucleotide "decoys" on gene expression in P7 rat hippocampus after hypoxia/ischemia.

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"Decoy" oligonucleotides can be used as gene-specific nuclear factor (NF-kappaB) inhibitors to regulate gene expression. We applied two different decoy oligonucleotides that contained the NF-kappaB binding consensus sequences present in the immunoglobulin G (IgG)-kappaB and Bcl-x promoter into

Transcriptional initiation under conditions of anoxia-induced quiescence in mitochondria from Artemia franciscana embryos.

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In response to anoxia, embryos of the brine shrimp Artemia franciscana are able coordinately to downregulate metabolism to levels low enough to permit survival for several years at room temperature. In addition to dramatic decreases in free ATP levels and heat production, intracellular pH drops from

Effect of hypoxia on lung, heart, and liver insulin-like growth factor-I gene and receptor expression in the newborn rat.

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OBJECTIVE We examined the effect of 7 days of hypoxia in the newborn rat on: a) body, heart, and lung growth; b) circulating insulin-like growth factor-I (IGF-I); c) lung, heart, and liver IGF-I gene expression; and d) lung IGF-I type 1 receptor gene expression and IGF-I receptor binding. We

Prolonged mild fetal hypoxia up-regulates type I nitric oxide synthase expression in discrete areas of the late-gestation fetal sheep brain.

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OBJECTIVE Our purpose was to study the effects of prolonged mild hypoxemia on type I nitric oxide synthase (NOS) messenger RNA, protein, and enzymatic activity in the fetal sheep brain. METHODS Pregnant sheep were randomly allocated to receive maternal nitrogen (n = 8) or compressed air (controls, n

Acute hypoxia upregulates NOS gene expression in rats.

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This study aimed to investigate the influence of acute tissue hypoxygenation on the expression of NO synthase (NOS) genes in vivo. To this end, male Sprague-Dawley rats were exposed either to 9% oxygen or to 0.1% carbon monoxide for 6 h, and mRNA levels of NOS-I, -II, and -III in kidneys, livers,

Chronic myocardial hypoxia increases nitric oxide synthase and decreases caveolin-3.

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Nitric oxide synthase (NOS) is believed to play an important role in protecting the myocardium against ischemia. Chronic hypoxia from birth increases NOS activity in the myocardium resulting in enhanced nitric oxide production and increased resistance to ischemia. We examined the effects of chronic

[Ribonuclease improves the function of hippocampal slices in the postischemic period].

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Population spike amplitude was measured in hippocampal slices under conditions of 20-min glucose and oxygen deficit ("in vitro ischemia") with or without ribonuclease A. In control slices the response was gradually decreased within 3 +/- 2 min after the onset of hypoxia/hypoglycemia. This process

Genome-Wide Expression Analysis Suggests Hypoxia-Triggered Hyper-Coagulation Leading to Venous Thrombosis at High Altitude.

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Venous thromboembolism (VTE), a multi-factorial disease, is the third most common cardiovascular disease. Established genetic and acquired risk factors are responsible for the onset of VTE. High altitude (HA) also poses as an additional risk factor, predisposing individuals to VTE; however, its

Suppression of hypoxia-associated vascular endothelial growth factor gene expression by nitric oxide via cGMP.

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OBJECTIVE To investigate the suppressive effect of nitric oxide (NO) on vascular endothelial growth factor (VEGF) gene expression and to elucidate its mechanism of action. METHODS Immortalized human retinal epithelial (RPE) cells, H-ras-transfected murine capillary endothelial cells, and nuclear

Hypoxia enhances stimulus-dependent induction of E-selectin on aortic endothelial cells.

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In many diseases, tissue hypoxia occurs in conjunction with other inflammatory processes. Since previous studies have demonstrated a role for leukocytes in ischemia/reperfusion injury, we hypothesized that endothelial hypoxia may "superinduce" expression of an important leukocyte adhesion molecule,

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