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Blood genomic responses differ after stroke, seizures, hypoglycemia, and hypoxia: blood genomic fingerprints of disease.

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Using microarray technology, we investigated whether the gene expression profile in white blood cells could be used as a fingerprint of different disease states. Adult rats were subjected to ischemic strokes, hemorrhagic strokes, sham surgeries, kainate-induced seizures, hypoxia, or insulin-induced

Surgical disconnection of the hypothalamus from the fetal pituitary abolishes the corticotrophic response to intrauterine hypoglycemia or hypoxemia in the sheep during late gestation.

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We have investigated the ACTH and cortisol responses to acute episodes of hypoxemia or hypoglycemia in fetal sheep in which the hypothalamus and pituitary were surgically disconnected at between 112 and 123 days gestation. Before 130 days gestation, basal plasma concentrations of ACTH were

[Morphological plasticity of hippocampal CA1 neurons in vitro after short-term anoxia/hypoglycemia followed by reoxygenation].

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Oxygen and glucose are known to modulate the neuronal plasticity. Their fluctuations have ability to induce cell damage, the degree of which is thought to depend on the intensity and duration of pathological events. Experimental investigations have shown that a short-term anoxia-hypoglycemia results

Changes in intracellular free magnesium during hypoglycaemia and hypoxia in cerebral tissue as calculated from 31P-nuclear magnetic resonance spectra.

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31P-nuclear magnetic resonance spectra of superfused cerebral tissues were obtained under normal, hypoglycaemic, and hypoxic conditions. Concentrations of free intracellular magnesium were calculated from differences in chemical shifts between the alpha- and beta-resonances of the nucleoside

Early effects on restoration of evoked field potentials in the hippocampal CA(1) region after reversible hypoxia/hypoglycemia by the radical scavenger N-tert.-butyl-alpha-phenylnitron.

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In transverse hippocampus slices a short period of hypoxia/hypoglycemia induced by perfusion with an O(2)/glucose-free medium caused early loss and incomplete restoration of evoked field potentials in the CA(1) region. In the present study a search was made for whether the formation of free

Effects of hypoglycaemia on ventilation and arousal responses to hypoxia, and newborn calves during active and quiet sleep.

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Ventilatory and arousal responses to progressive, isocapnic hypoxia were assessed in five full-term calves, aged 1-8 d, during normo-glycaemia and insulin-induced hypoglycaemia; replicate tests were made during both quiet and active sleep. Hypoxia was produced by rebreathing 8-10% (W/V) oxygen;

Egr-1 is a critical regulator of EGF-receptor-mediated expansion of subventricular zone neural stem cells and progenitors during recovery from hypoxia-hypoglycemia.

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We recently established that the EGF-R (epidermal growth factor receptor) (EGF-R) is an essential regulator of the reactive expansion of SVZ (subventricular zone) NPs (neural precursors) that occurs during recovery from hypoxic-ischemic brain injury. The purpose of the current studies was to

Transient hypoxia/hypoglycemia upregulates endothelin B receptors in cultured rat astrocytes.

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Endothelins are potent vasoactive peptides that bind to their specific receptors, playing an important role in the CNS under physiological and pathophysiological conditions. Astrocytes, which have been shown to express these receptors, also have a considerable role to play under physiological and

Neither moderate hypoxia nor mild hypoglycaemia alone causes any significant increase in cerebral [Ca2+]i: only a combination of the two insults has this effect. A 31P and 19F NMR study.

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(1) The energy state and free intracellular calcium concentration ([Ca2+]i) of superfused cortical slices were measured in moderate hypoxia (approximately 65 microM O2), in mild hypoglycaemia (0.5 mM glucose), and in combinations of the two insults using 19F and 31P NMR spectroscopy. (2) Neither

[Protect effects of Qingkailing injection on mitochondrion membrane potential during injury induced by hypoxia-hypoglycemia and reoxygenation in cultured rat hippocampal neurons].

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OBJECTIVE To investigate the protect effects of Qingkailing injection on mitochondrion membrane potential (MMP) during injury induced by hypoxia-hypoglycemia and reoxygenation in cultured rat hippocampal neurons. METHODS Mitochondrion activity was measured by methyl thiazolyl tetrazolium (MTT) test.

Ontogeny of adrenomedullary responses to hypoxia and hypoglycemia: role of splanchnic innervation.

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Adrenals of neonatal rats were denervated at 3 days of age (just before functional neuronal connections are ordinarily made). At 14 days of age, rats with denervated adrenals did not secrete catecholamines in response to a neurogenic reflex stimulus (insulin-induced hypoglycemia), confirming that

Unlike hypoxia, hypoglycemia does not preferentially destroy GABAergic neurons in developing rat neocortex explants in culture.

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We tested whether hypoglycemia, like hypoxia, would preferentially destroy GABAergic nerve cells in the neocortex. To this end, rat neocortex explants dissected from 6-day-old rat pups and cultured up to a developmental stage approximately comparable to that of the newborn human neocortex, were

[Hypoglycemia in newborn of the diabetic mother in relation to some indicators of perinatal hypoxia].

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METHODS To examine whether perinatal hypoxia increases the risk of occurrence of hypoglycaemia--between first and second hour of life--in newborn of the diabetic mother. METHODS The study material consisted of 151 newborns born to 58 pregestational and 93 gestational diabetes mothers. The occurrence

Moderate hypoglycemia aggravates effects of hypoxia in hippocampal slices from diabetic rats.

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We recorded the effects of hypoxia combined with relative hypoglycemia on pre- and post-synaptic potentials in the CA1 area of slices from 4-month-old control and diabetic (streptozotocin-treated) Wistar rats. In experiments on slices kept in 10 or 4 mM glucose (at 33 degrees C), hypoxia was applied

Hypoxia-inducible factor-2alpha (HIF-2alpha) is involved in the apoptotic response to hypoglycemia but not to hypoxia.

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Deprivation of oxygen (hypoxia) and/or glucose (hypoglycemia) represents a serious stress that affects cellular survival. The hypoxia-inducible transcription factor-1alpha (HIF-1alpha), which has been implicated in the cellular response to hypoxia (Semenza, G. L. (1999) Annu. Rev. Cell Dev. Biol.

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