Disease relevance of Hypoxia-Ischemia, Brain

• Outcome from coma caused by cerebral hypoxia-ischemia (eg, cardiac arrest) was compared with serial neurological findings in 210 patients [1].
• In contrast, targeted deletion of Jnk3 not only reduces the stress-induced JNK activity, but also protects mice from brain injury after cerebral ischemia-hypoxia [2].
• Calpastatin is up-regulated in response to hypoxia and is a suicide substrate to calpain after neonatal cerebral hypoxia-ischemia [3].
• Combination of systemic hypothermia and N-acetylcysteine attenuates hypoxic-ischemic brain injury in neonatal rats [4].
• In a randomized prospective trial, we studied the effect of early high-dose phenobarbital treatment on the early (intraventricular hemorrhage) and late (neurodevelopmental abnormalities) manifestations of hypoxic-ischemic encephalopathy in preterm infants weighing 1500 g or less at birth [5].

High impact information on Hypoxia-Ischemia, Brain

• CONCLUSIONS: Measurement of the urinary lactate: creatinine ratio soon after birth may help identify infants at high risk for hypoxic-ischemic encephalopathy [6].
• Caspase inhibitor affords neuroprotection with delayed administration in a rat model of neonatal hypoxic-ischemic brain injury [7].
• Presynaptic inhibition of Ca(2+)-dependent glutamate release may be a valuable approach to attenuating hypoxic-ischemic brain injury [8].
• We now report that minocycline administered either immediately before or immediately after a hypoxic-ischemic insult substantially blocks tissue damage in a rodent model of neonatal hypoxic-ischemic brain injury [9].
• The extracellular acidity that accompanies brain hypoxia-ischemia is known to reduce both NMDA and AMPA-kainate receptor-mediated currents and NMDA receptor-mediated neurotoxicity [10].

Chemical compound and disease context of Hypoxia-Ischemia, Brain

• Magnetic resonance spectroscopy of N-acetylaspartate in hypoxic-ischemic encephalopathy [11].
• Hypoxic preconditioning (8% O2, 3 h) produces tolerance 24 h after hypoxic-ischemic brain injury in neonatal rats [12].
• Glucose affects the severity of hypoxic-ischemic brain injury in newborn pigs [13].
• We examined the impact of pre-treatment with the calcium antagonist flunarizine on the development of hypoxic-ischemic brain injury in the immature rat [14].
• CONCLUSIONS: Deferoxamine administered after induction of cerebral hypoxia-ischemia reduces injury in 7-day-old rats [15].

Biological context of Hypoxia-Ischemia, Brain

• The mini-review describes recently accomplished research pertaining to the use of the immature rat model, specifically, investigations involving energy metabolism, glucose transporter proteins, free radical injury, and seizures superimposed upon cerebral hypoxia-ischemia [16].
• Transient global brain hypoxia-ischemia in adult rats: neuronal damage, glial proliferation, and alterations in inositol phospholipid hydrolysis [17].
• Down-regulation of excitatory amino acid transporter 1 expression by intraventricular administration of specific antisense oligonucleotide exacerbated neuronal damage in hypoxia-ischemia brain [18].
• The iron chelator deferoxamine is efficacious in ameliorating hypoxic-ischemic brain injury in some models, perhaps by decreasing oxidative stress [19].
• Although the role of magnesium in neonatal hypoxic-ischemic brain injury related to N-methyl-D-aspartate receptors has been widely studied; the effects of magnesium on neuronal apoptosis have not been known exactly in hypoxia-ischemia [20].

Anatomical context of Hypoxia-Ischemia, Brain

• Cerebrospinal fluid activin a measurement in asphyxiated full-term newborns predicts hypoxic ischemic encephalopathy [21].
• In an experimental model of perinatal hypoxic-ischemic brain injury, we examined quisqualic acid (Quis)-stimulated phosphoinositide (PPI) turnover in hippocampus and striatum [22].
• The postsynaptic neuronal dendrite is selectively vulnerable to hypoxic-ischemic brain injury and glutamate receptor overactivation [23].
• This study was designed to investigate how neutrophils contribute to perinatal hypoxic ischemic brain injury and how neutropenia compared with allopurinol in its neuroprotective effects [24].
• OBJECTIVE: The aim of this study was to establish whether abnormal signal intensity in the posterior limb of the internal capsule (PLIC) on magnetic resonance imaging is an accurate predictor of neurodevelopmental outcome at 1 year of age in infants with hypoxic-ischemic encephalopathy (HIE) [25].

Gene context of Hypoxia-Ischemia, Brain

• The effects of insulin-like growth factor (IGF)-1, IGF-2, and des-IGF-1 on neuronal loss after hypoxic-ischemic brain injury in adult rats: evidence for a role for IGF binding proteins [26].
• TGF-beta1 has been shown to be induced following hypoxic-ischemic brain injury and may play a critical role in the pathophysiology of degenerative processes in the CNS [27].
• The present results show that BDNF can be detected in human CSF and that the levels increase following hypoxic-ischemic brain injury [28].
• Hsp70 overexpression sequesters AIF and reduces neonatal hypoxic/ischemic brain injury [29].
• Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury [30].

Analytical, diagnostic and therapeutic context of Hypoxia-Ischemia, Brain

• Twenty-seven rat pups received a subcutaneous injection of 0.1 ml mannitol in a dosage of 4 mg/kg body wt immediately following cerebral hypoxia-ischemia and every 12 hours thereafter for a total of four doses [31].
• D2 receptor imaging with iodine-123-iodobenzamide brain SPECT in infants with hypoxic-ischemic brain injury [32].
• The effect of unilateral perinatal hypoxic-ischemic brain injury on striatal dopamine uptake sites and on D1 and D2 receptors was investigated in rat by using in vitro quantitative receptor binding autoradiography, 9-11 weeks after the insult [33].
• To examine the effect of valproic acid in this condition, hypoxic-ischemic brain injury was induced in 7-day-old rat pups by ligation of the right common carotid and then the pups were exposed to 1 hour of hypoxia in 8% oxygen [34].
• Clinically this series is manifested by hypoxic-ischemic encephalopathy (HIE), a syndrome that includes coma, seizures, a burst suppression EEG, respiratory depression and severe hypotonia [35].

References