The oxygen free radicals originating from mitochondrial complex I contribute to oxidative brain injury following hypoxia-ischemia in neonatal mice. - Wikidata - awgldk - TriplyDB

The oxygen free radicals originating from mitochondrial complex I contribute to oxidative brain injury following hypoxia-ischemia in neonatal mice.

The oxygen free radicals originating from mitochondrial complex I contribute to oxidative brain injury following hypoxia-ischemia in neonatal mice.

http://www.wikidata.org/entity/Q35811566

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Metabolic Changes Following Perinatal Asphyxia: Role of Astrocytes and Their Interaction with Neurons Oxidative Stress and the Use of Antioxidants in Stroke Mitochondrial reactive oxygen species: a double edged sword in ischemia/reperfusion vs preconditioning Phenolic Melatonin-Related Compounds: Their Role as Chemical Protectors against Oxidative Stress Ischemic A/D transition of mitochondrial complex I and its role in ROS generation The membrane-active tri-block copolymer pluronic F-68 profoundly rescues rat hippocampal neurons from oxygen-glucose deprivation-induced death through early inhibition of apoptosis Brain adaptation to hypoxia and hyperoxia in mice N-3 fatty acid rich triglyceride emulsions are neuroprotective after cerebral hypoxic-ischemic injury in neonatal mice Glucose and Intermediary Metabolism and Astrocyte-Neuron Interactions Following Neonatal Hypoxia-Ischemia in Rat.Opposing effects of glucose on stroke and reperfusion injury: acidosis, oxidative stress, and energy metabolism.Protective effect of oxysophoridine on cerebral ischemia/reperfusion injury in mice.Dynamic spatio-temporal imaging of early reflow in a neonatal rat stroke model.Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS.Nelfinavir inhibits intra-mitochondrial calcium influx and protects brain against hypoxic-ischemic injury in neonatal mice Inhibitors of ROS production by the ubiquinone-binding site of mitochondrial complex I identified by chemical screening Isoflurane anesthesia initiated at the onset of reperfusion attenuates oxidative and hypoxic-ischemic brain injury Mitochondrial bioenergetic alterations after focal traumatic brain injury in the immature brain.DHA but Not EPA Emulsions Preserve Neurological and Mitochondrial Function after Brain Hypoxia-Ischemia in Neonatal Mice.Persistently Altered Brain Mitochondrial Bioenergetics After Apparently Successful Resuscitation From Cardiac Arrest.Neuroprotective Effect of 3-(Naphthalen-2-Yl(Propoxy)Methyl)Azetidine Hydrochloride on Brain Ischaemia/Reperfusion Injury.Apoptosis-inducing factor downregulation increased neuronal progenitor, but not stem cell, survival in the neonatal hippocampus after cerebral hypoxia-ischemia.AIF, reactive oxygen species, and neurodegeneration: a "complex" problem Sex-dependent mitochondrial respiratory impairment and oxidative stress in a rat model of neonatal hypoxic-ischemic encephalopathy.Hyperglycemic Conditions Prime Cells for RIP1-dependent Necroptosis.Clinical significance of elevated serum A-FABP and free fatty acid in neonates with hypoxic ischemic brain damage.Convergence of genetic and environmental factors on parvalbumin-positive interneurons in schizophrenia.Antioxidant gene therapy against neuronal cell death.Prohibitin viral gene transfer protects hippocampal CA1 neurons from ischemia and ameliorates postischemic hippocampal dysfunction.Mitochondrial mechanisms of neuronal rescue by F-68, a hydrophilic Pluronic block co-polymer, following acute substrate deprivation.Mitochondrial dysfunction in alveolar and white matter developmental failure in premature infants.Modulation of the conformational state of mitochondrial complex I as a target for therapeutic intervention.Inhibition of Ectodermal-Neural Cortex 1 Protects Neural Cells from Apoptosis Induced by Hypoxia and Hypoglycemia.Metabolomic analysis of survival in carbohydrate pre-fed pigs subjected to shock and polytrauma.Sex-dependent mitophagy and neuronal death following rat neonatal hypoxia-ischemia.A synthetic cell permeable antioxidant protects neurons against acute oxidative stress.Hypoxic-ischemic injury in the developing brain: the role of reactive oxygen species originating in mitochondria.Mitochondrial dynamics: cell-type and hippocampal region specific changes following global cerebral ischemia.Bioenergetic regulation of microglia.Krebs cycle metabolites and preferential succinate oxidation following neonatal hypoxic-ischemic brain injury in mice.Reverse electron transfer results in a loss of flavin from mitochondrial complex I: Potential mechanism for brain ischemia reperfusion injury.

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P2860

The oxygen free radicals originating from mitochondrial complex I contribute to oxidative brain injury following hypoxia-ischemia in neonatal mice.

http://www.wikidata.org/entity/Q35811566

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The oxygen free radicals origi ...... xia-ischemia in neonatal mice.

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The oxygen free radicals origi ...... xia-ischemia in neonatal mice.

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The oxygen free radicals origi ...... xia-ischemia in neonatal mice.

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JNEUROSCI.6303-11.2012

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Journal of Neuroscience

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The oxygen free radicals origi ...... xia-ischemia in neonatal mice.

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Anatoly A Starkov

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Dzmitry Matsiukevich

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Irina V Utkina-Sosunova

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Sergei A Sosunov

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Vadim S Ten

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Veniamin I Ratner

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Zoya V Niatsetskaya

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P2860

Allopurinol for preventing mortality and morbidity in newborn infants with suspected hypoxic-ischaemic encephalopathy

Developmental shift of cyclophilin D contribution to hypoxic-ischemic brain injury

How mitochondria produce reactive oxygen species

Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death

Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death

Mitochondrial calcium and the permeability transition in cell death

The mitochondrial generation of hydrogen peroxide. General properties and effect of hyperbaric oxygen

Late measures of brain injury after neonatal hypoxia-ischemia in mice.

Delayed neuronal preconditioning by NS1619 is independent of calcium activated potassium channels.

Complement component c1q mediates mitochondria-driven oxidative stress in neonatal hypoxic-ischemic brain injury.

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