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brain ischemia/hypoxia
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Página 1 a partir de 1897 resultados
Adeno-associated viral-vector-mediated hypoxia-inducible vascular endothelial growth factor gene expression attenuates ischemic brain injury after focal cerebral ischemia in mice.
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OBJECTIVE
Exogenous delivery of vascular endothelial growth factor gene (VEGF) may provide a useful approach to the treatment of brain ischemia. We investigated the use of a hypoxia-responsive element to control VEGF expression given for neuroprotection.
METHODS
Three groups (n=36) of mice received
Effect of intermittent hypoxia on neuro-functional recovery post brain ischemia in mice.
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Intermittent hypoxia was a simulation of a high-altitude environment. Neuro-inflammation post brain ischemia was considered as a vital impact which contributed to cognitive-functional deficit. The isoform of nitric oxide synthase (iNOS) was an inflammation factor secreted by microglias in
Hyperbaric oxygen preconditioning ameliorates hypoxia-ischemia brain damage by activating Nrf2 expression in vivo and in vitro.
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The present study aimed to investigate whether hyperbaric oxygen preconditioning (HBO-PC) could ameliorate hypoxia-ischemia brain damage (HIBD) by an increase of Nrf2 expression. P7 Sprague-Dawley rats (aged 7 d, n = 195) were used in two in vivo experiments, including BO-PC exposure experiments in
[Activation of autophagy pathway in hippocampus and deterioration of learning and memory ability by intermittent hypoxia in rats after cerebral ischemia].
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Objective To investigate the effects of different duration of intermittent hypoxia on the autophagy pathway in the hippocampus and the learning and memory ability after cerebral ischemia in rats. Methods 100 male Wistar rats were randomly divided into sham operation (SO) group, ischemia/reperfusion
Temporal and topographic profiles of tissue hypoxia following transient focal cerebral ischemia in rats.
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Intravascular accumulation of blood cells after brain ischemia-reperfusion can cause obstruction of cerebral blood flow and tissue hypoxia/ischemia as a consequence. In the present study, we examined temporal and topographic changes of tissue hypoxia/ischemia after occlusion of the middle cerebral
Protective effects of kamikihi-to, a traditional Chinese medicine, against cerebral ischemia, hypoxia and anoxia in mice and gerbils.
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The protective effects of Kamikihi-To (KMK), a traditional Chinese medicine, against cerebral ischemia, hypoxia and anoxia were investigated with various experimental models in mice and gerbils. KMK (2.0 g/kg/day, p.o. for 5 days) significantly prolonged the survival time of mice subjected to
[The role of HIF-1alpha in neuronal apoptosis after hypoxia/hypoxia ischemia brain damage in neonatal rats].
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OBJECTIVE
To investigate the relationship between HIF-1alpha expression and neuron apoptosis in hypoxia/hypoxia ischemia brain injury and elucidate the role of HIF-1alpha in regulating neuron apoptosis.
METHODS
Postnatal day 10 SD rats were divided into three groups: the hypoxia ischemia group (HI),
The neuroprotective role of TERT via an antiapoptotic mechanism in neonatal rats after hypoxia-ischemia brain injury.
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Telomerase reverse transcriptase (TERT) can regulate cell apoptosis and proliferation. It has been shown that TERT expression can be induced in models of adult brain ischemia. In the present study, we investigated the role of TERT in ischemic neuronal death in neonatal hypoxic-ischemic rats model.
Rapid noninvasive continuous monitoring of oxygenation in cerebral ischemia and hypoxia.
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The brain is most sensitively dependent on oxygen to maintain its normal function. Methods to assess the degree of its oxygenation have generally been invasive and indirect. Rapid assessment of brain oxygenation is particularly vital during cerebrospinal ischemia and hypoxia. We have developed a
A comparative study of EEG suppressions induced by global cerebral ischemia and anoxia.
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Cerebral ischemia and anoxia induce sequential changes that include ionic redistribution, alteration of enzimatic reactions governing metabolism and intracellular signaling. Despite high technology instrumentation including positron emission, tomography and magnetic resonance imaging used to unravel
Changes of hypoxia-inducible factor-1 signaling and the effect of cilostazol in chronic cerebral ischemia.
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Hypoxia-inducible factor-1 and its specific target gene heme oxygenase-1, are involved in acute cerebral ischemia. However, very few studies have examined in detail the changes in the hypoxia-inducible factor-1/heme oxygenase-1 signaling pathway in chronic cerebral ischemia. In this study, a rat
[Effect of obstructive sleep apnea hypoxia on learning memory capacity after cerebral ischemia-reperfusion in rats].
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OBJECTIVE
To investigate the effect of obstructive sleep apnea hypoxia on learning memory capacity in rat after ischemia.
METHODS
Eighty healthy male wister rats were randomly divided into: sham operation group (SO group, n=20), merely ischemia group (I/R group, n=20), and obstructive sleep apnea
Desferoxamine preconditioning protects against cerebral ischemia in rats by inducing expressions of hypoxia inducible factor 1 alpha and erythropoietin.
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OBJECTIVE
To investigate whether desferoxamine (DFO) preconditioning can induce tolerance against cerebral ischemia and its effect on the expression of hypoxia inducible factor 1alpha (HIF-1alpha) and erythropoietin (EPO) in vivo and in vitro.
METHODS
Rat model of cerebral ischemia was established
Hypoxia-inducible factor-1alpha DNA induced angiogenesis in a rat cerebral ischemia model.
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BACKGROUND
Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that regulates the adaptive response to hypoxia in mammalian cells. It consists of a regulatory subunit HIF-1alpha, which accumulates under hypoxic conditions, and a constitutively expressed subunit, HIF-1beta. In this study, we
Early expressions of hypoxia-inducible factor 1alpha and vascular endothelial growth factor increase the neuronal plasticity of activated endogenous neural stem cells after focal cerebral ischemia.
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Endogenous neural stem cells become "activated" after neuronal injury, but the activation sequence and fate of endogenous neural stem cells in focal cerebral ischemia model are little known. We evaluated the relationships between neural stem cells and hypoxia-inducible factor-1α and vascular
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