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To evaluate their prognostic value, five different non-invasive techniques were used on 34 full term infants with hypoxic- ischaemicencephalopathy (HIE) within six hours of delivery.
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However, the mechanisms underlying its neuroprotective effects following cerebralischemia remain unclear.
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These data suggest that general anesthesia increased the tolerance to cerebralischemia.
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Rehabilitation therapy through physical exercise also provides therapeutic efficacy for cerebralischemia.
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These findings suggest that baicalin has a neuroprotective effect on cerebralischemia.
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However, selective neuronal death in transient focal cerebralischemia needs more investigation.
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Ranibizumab was not associated with any cases of cerebrovascular hemorrhage and cerebrovascularischemia.
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The presence of TCD-detected microemboli could be a risk factor for cerebrovascularischemia.
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Conclusions: These data suggest that TCD-detected microemboli are associated with an increased prevalence of prior cerebrovascularischemia.
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The outcomes of hypoxic- ischemicencephalopathy vary between death and intact survival.
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We conclude that diffusion tensor imaging can quantify white matter injury in neonates with hypoxic- ischemicencephalopathy.
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His death certificate lists the cause of death as hypoxic ischemicencephalopathy caused by cardiopulmonary arrest.
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Outcome measures consisted of previously reported indices that were modified including the addition of hypoxic ischemicencephalopathy.
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This makes it increasingly important to assess, soon after birth, the prognosis of children with hypoxic- ischemicencephalopathy.
Usage of brain ischemia in English
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The role of TLR4 in brainischemia has not been examined yet.
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Enhanced glucose uptake protects cells during energy depletion including brainischemia.
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Summary: Reversible brainischemia is a harbinger for subsequent ischemic stroke.
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Four-vessel occlusion model of transient global brainischemia was used.
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PGA1 treatment also significantly ameliorated motor dysfunction after brainischemia.
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Here we report that PHD1 deficiency provides neuroprotection in a murine model of permanent brainischemia.
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Masitinib reduced significantly brainischemia induced by experimental stroke and potentiated the therapeutic effect of rt-PA.
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Background: Cognitive dysfunction and delirium after ICU are frequent and may partially result from brainischemia episodes.
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These studies represent evidence that changes in the HPA axis play an important role in brainischemia.
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Neuronal injury from even brief periods of global brainischemia seems to be associated with deteriorating neurocognitive function.
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Taken together, our results suggest that PAFR activation might be crucial for the global brainischemia and reperfusion injury.
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Objective: To review the pathophysiology of acute brainischemia and infarction and the evidence supporting various stroke reperfusion treatments.
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The pathogenesis of acute brainischemia (ABI) is highly complex and involves multiple mechanisms including free radical generation.
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Heat shock proteins (HSPs) induced by brainischemia may play an important role in neuroprotection from neuronal degeneration.
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Mobilization after heart or brainischemia is well established, but it is unclear if this occurs after intestinal ischemia-reperfusion injury.
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Edaravone is the active substance of a Japanese medicine, which aids neurological recovery following acute brainischemia and subsequent cerebral infarction.