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glutamine/hypoxie

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Induction of macrophage glutamine: fructose-6-phosphate amidotransferase expression by hypoxia and by picolinic acid.

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We studied the expression of glutamine: fructose-6-phosphate amidotransferase (GFAT), the rate limiting enzyme in the hexosamine biosynthetic pathway controlling protein glycosylation. We obtained the first evidence that the GFAT mRNA and protein are constitutively expressed in murine mononuclear

Glutamate, glutamine and glutamine synthetase in the neonatal rat brain following hypoxia.

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Exposing 7-day-old rat pups to hypoxia, 8% oxygen/92% nitrogen, for 3 h alters glutamate (GLU), glutamine and glutamine synthetase (GS) activity in the striatum, frontal cortex and hippocampus. Immediately following the hypoxic insult there is a rapid transient elevation of GLU followed by a fall

Glutamine and glutamate limit the shortening of action potential duration in anoxia-challenged rabbit hearts.

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In clinical conditions, amino acid supplementation is applied to improve contractile function, minimize ischemia/reperfusion injury, and facilitate postoperative recovery. It has been shown that glutamine enhances myocardial ATP/APD (action potential duration) and glutathione/oxidized glutathione
OBJECTIVE The purpose of this study was to examine: 1) the association between the expression of the insulin receptor (INSR), insulin receptor substrate 1 (IRS1) and 2 (IRS2), insulin inducible gene 1 (INSIG1) and 2 (INSIG2), Ras-related associated with diabetes (RRAD), and brain-specific

Increased glutamate uptake and glutamine synthetase activity in neuronal cell cultures surviving chronic hypoxia.

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To examine the neurochemical effects of chronic hypoxia on immature nervous tissue in vitro, mixed neuronal-glial cell cultures derived from fetal mice were exposed to 5% O2 for 24 or 48 h. Those cultures subjected to longer hypoxia manifested improved neuronal survival compared to those with the

Rapid loss of glutamine synthetase from astrocytes in response to hypoxia: implications for excitotoxicity.

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We have examined brains of neonatal pigs that were rendered hypoxic. Glutamine synthetase (GS), a key enzyme in the detoxification of glutamate and ammonia, was rapidly lost from astrocytes in regions susceptible to damage, including the CA1 of hippocampus and various cortical regions. Conversely,
OBJECTIVE To study the effect of L-alanyl-L-glutamine (Ala-Gln) on the levels of insulin-like growth factor-1 (IGF-1) and IGF-1 receptor (IGF-1R) in the intestinal tissues of low-birth-weight (LBW) newborn rats with hypoxia/reoxygenation-induced intestinal injury. METHODS Pregnant rats were fed with
OBJECTIVE Tumor microenvironment is characterized by regions of fluctuating and chronic hypoxia, low extracellular pH, and nutrient depletion. Although it is well known that hypoxia stimulates the accumulation of hypoxia-inducible factor-1alpha (HIF-1alpha), the role of low extracellular pH and
Glucose and glutamine are essential energy metabolites for brain tumor growth and survival under both normoxic and hypoxic conditions. Both metabolites can contribute their carbons to lipid biosynthesis. We used uniformly labeled [(14)C]-U-D-glucose and [(14)C]-U-L-glutamine to examine the profile
The effect of hypobaric hypoxia on the activities of glutamine synthetase, glutaminase and cyclic 3'5' AMP phosphodiesterase in rat brain was studied after exposure to 25,000' for 6 h. Glutamine synthetase activity was increased in all the regions of brain studied, and addition of gamma amino
BACKGROUND Intestinal ischemia and reperfusion may lead to profuse secretion of water and electrolytes. The underlying mechanisms have been related to increased hydrostatic pressure, to denudation of intestinal villi, and, recently, to adenosine-mediated enhancement of chloride secretion. METHODS We
The aim of this study was to evaluate the combined effects of carbohydrate (CHO) and glutamine (Gln) supplementation on cytokine production by monocytes after exercise until exhaustion performed in hypoxia.Fifteen physically active men underwent three

Cerebellar glutamine synthetase in children after hypoxia or ischemia.

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BACKGROUND Glutamate has been implicated in the pathophysiology of acute hypoxic-ischemic encephalopathy. Glutamine synthetase is an enzyme found in astrocytes that converts glutamate to its nontoxic analogue, glutamine. The present study tests the hypothesis that brain glutamine synthetase activity
Nitric oxide is postulated to be involved in the pathophysiology of neurological disorders due to hypoxia/ anoxia in brain due to increased release of glutamate and activation of N-methyl-D-aspartate receptors. Reactive oxygen species have been implicated in pathophysiology of many neurological

Glutamine protects neuronal function against cerebral hypoxia: a study using the in vitro hippocampal slice preparation.

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Pretreatment of hippocampal slices with glutamine doubled the recovery rate of the synaptic function (electrically evoked population spike) from a standardized hypoxic insult in CA1 pyramidal neurons. This protective effect of glutamine was dose-dependent and biphasic; recovery of synaptic function
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