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decarboxylase/hypoxia
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Activation of hypoxia-inducible factor-1 regulates human histidine decarboxylase expression.
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Histidine decarboxylase (HDC) catalyzes the formation of histamine from histidine. Histamine has various effects in physiological and pathological reactions, such as inflammation, cell growth, and neuro-transmission. We investigated the role of hypoxia-inducible factor (HIF)-1 on hypoxia-induced HDC
Developmental changes of glutamate acid decarboxylase-67 in mouse brain after hypoxia ischemia.
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Objective To study the developmental changes of glutamic acid decarboxylase-67 (GAD-67, a GABA synthetic enzyme) in normal and hypoxic ischemic (HI) brain. Methods C57/BL6 mice on postnatal day (P) 5, 9, 21and 60, corresponding developmentally to premature, term, juvenile and adult human brain were
Regulation of ornithine decarboxylase and polyamine import by hypoxia in pulmonary artery endothelial cells.
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In rat lung and cultured lung vascular cells, hypoxia decreases ornithine decarboxylase (ODC) activity and increases polyamine import. In this study, we used rat cultured pulmonary artery endothelial cells to explore the mechanism of hypoxia-induced reduction in ODC activity and determined whether
Acute hypoxia increases ornithine decarboxylase activity and polyamine concentrations in fetal rat brain.
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The cellular responses to hypoxia are poorly understood. To test the hypothesis that ornithine decarboxylase (ODC; L-ornithine carboxy-lyase; EC 4.1.1.17) activity and polyamine concentrations change in response to acute hypoxia, we performed the following studies. Pregnant Sprague-Dawley rats
Fetal dexamethasone exposure affects basal ornithine decarboxylase activity in developing rat brain regions and alters acute responses to hypoxia and maternal separation.
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Although glucocorticoids are widely used to stimulate fetal/neonatal lung function, they also interfere with cellular development in the central nervous system. Dexamethasone was administered to pregnant rats in late gestation at a dose (0.8 mg/kg) that lies just above the threshold for stimulation
Ornithine decarboxylase activity and polyamine concentrations in fetal rat brain: response to chronic hypoxic-hypoxia and/or carbon monoxide-hypoxia.
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Ornithine decarboxylase activity (ODC; E.C. 4.1.1.17), is significantly elevated in fetal and newborn rat brain in response to acute hypoxia. Because relatively little is known about ODC activities and polyamine metabolism in hypoxia and also because ODC and the polyamines are essential for normal
Acute hypoxia induces elevation of ornithine decarboxylase activity in neonatal rat brain slices.
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Recent studies in vivo have demonstrated that ornithine decarboxylase (ODC) activity in the fetal rat brain is elevated 4-5-fold by acute maternal hypoxia. This hypoxic-associated increase is seen in the rat brain in both the newborn and the adult. Because of the intimate involvement of ODC in
Ornithine decarboxylase activity in vitro in response to acute hypoxia: a novel use of newborn rat brain slices.
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In fetal as well as newborn rats, acute hypoxic exposure results in significantly elevated brain ornithine decarboxylase (ODC) activity, polyamine concentrations, and ODC mRNA. The interpretations of these in vivo hypoxic-induced changes, however, are complicated by maternal confounding effects. To
Permanent increase of immunocytochemical reactivity for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase, mitochondrial enzymes, and glial fibrillary acidic protein in rat cerebral cortex damaged by early postnatal hypoxia-ischemia.
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A former study indicated that hypoxic-ischemic encephalopathy in rat sustained during early postnatal life may result in permanent epileptic activity in the baseline electroencephalogram. We, therefore, investigated whether the presumed higher firing frequency and metabolic activity of neurons in
Cocaine exacerbates hypoxia-induced cell damage in the developing brain: effects on ornithine decarboxylase activity and protein synthesis.
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The immature brain is resistant to cell damage from hypoxia, such as that experienced during parturition. Because cocaine causes cerebral ischemia, we examined whether cocaine interferes with this resistance. On postnatal days 1, 4 or 8, neonatal rats were given an acute injection of saline or
Post-translational modification of glutamic acid decarboxylase 67 by intermittent hypoxia: evidence for the involvement of dopamine D1 receptor signaling.
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Intermittent hypoxia (IH) associated with sleep apnea leads to cardio-respiratory morbidities. Previous studies have shown that IH alters the synthesis of neurotransmitters including catecholamines and neuropeptides in brainstem regions associated with regulation of cardio-respiratory functions.
L-arginine Attenuates Hypobaric Hypoxia-Induced Increase in Ornithine Decarboxylase 1.
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BACKGROUND
Chronic hypoxia-induced pulmonary hypertension and vascular remodeling have been shown to be associated with ornithine decarboxylase 1 (ODC1). However, few animal studies have investigated the role of ODC1 in acute hypoxia.
OBJECTIVE
We investigated ODC1 gene expression, morphologic and
Regulation of ornithine decarboxylase by hypoxia in pulmonary artery smooth muscle cells.
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The polyamines are a family of low-molecular-weight organic cations that play essential intracellular regulatory roles in cell growth and differentiation. Elevations in cellular polyamine contents necessary for most physiological and pathological events in the lung appear to be driven by increase de
The effects of hypoxia, hypertrophy, and diet on rat myocardial ornithine decarboxylase activity.
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We have shown that there is a highly significant difference between right and left ventricular ornithine decarboxylase activity. The left ventricle had a much higher activity compared with the right ventricle. A restricted diet caused a decrease in ornithine decarboxylase activity after 24 hr.
Ornithine decarboxylase activity in fetal and newborn rat brain: responses to hypoxic and carbon monoxide hypoxia.
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In response to acute maternal hypoxia, ornithine decarboxylase (ODC) activity increased significantly in fetal rat brain, peaking at 4 h. This was associated with increased ODC mRNA and elevated polyamine concentrations. To correlate this response with development, we measured ODC activity in the
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