Hyperoxia causes maturation-dependent cell death in the developing white matter. - Wikidata - awgldk - TriplyDB

Hyperoxia causes maturation-dependent cell death in the developing white matter.

Hyperoxia causes maturation-dependent cell death in the developing white matter.

http://www.wikidata.org/entity/Q35009330

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Alzheimer's disease as homeostatic responses to age-related myelin breakdown Parkinson disease protein DJ-1 converts from a zymogen to a protease by carboxyl-terminal cleavage Focal necrosis and disturbed myelination in the white matter of newborn infants: a tale of too much or too little oxygen Mammalian lipoxygenases and their biological relevance Oligodendroglial alterations and the role of microglia in white matter injury: relevance to schizophrenia.Brain development after neonatal intermittent hyperoxia-hypoxia in the rat studied by longitudinal MRI and immunohistochemistry.Pathophysiology of glia in perinatal white matter injury.Oxygen delivery, consumption, and conversion to reactive oxygen species in experimental models of diabetic retinopathy A transcription factor map as revealed by a genome-wide gene expression analysis of whole-blood mRNA transcriptome in multiple sclerosis.RIP1 kinase mediates arachidonic acid-induced oxidative death of oligodendrocyte precursors.The challenge of understanding cerebral white matter injury in the premature infant.Early blood gas abnormalities and the preterm brain.Damaged mitochondria in Fanconi anemia - an isolated event or a general phenomenon?Cellular changes underlying hyperoxia-induced delay of white matter development.Oxygen toxicity and reactive oxygen species: the devil is in the details.N-methyl-D-aspartate receptor subtype 3A promotes apoptosis in developing mouse brain exposed to hyperoxia.Future applications of antioxidants in premature infants.Interaction of inflammation and hyperoxia in a rat model of neonatal white matter damage.Blood protein concentrations in the first two postnatal weeks associated with early postnatal blood gas derangements among infants born before the 28th week of gestation. The ELGAN Study.Elevated NADPH oxidase activity contributes to oxidative stress and cell death in Huntington's disease.Injury and differentiation following inhibition of mitochondrial respiratory chain complex IV in rat oligodendrocytes Impact of bronchopulmonary dysplasia on brain and retina.Structural modulation of brain development by oxygen: evidence on adolescents migrating from high altitude to sea level environment.Neonatal hyperoxia exposure disrupts axon-oligodendrocyte integrity in the subcortical white matter.Aberrant Rab11-dependent trafficking of the neuronal glutamate transporter EAAC1 causes oxidative stress and cell death in Huntington's disease.12/15-lipoxygenase expression is increased in oligodendrocytes and microglia of periventricular leukomalacia Perinatal inflammation results in decreased oligodendrocyte numbers in adulthood.Oxidative stress and executive function in children receiving chemotherapy for acute lymphoblastic leukemia.Arginase 2 deficiency reduces hyperoxia-mediated retinal neurodegeneration through the regulation of polyamine metabolism.Hyperoxia in the term newborn: more evidence is still needed for optimal oxygen therapy.Neonatal encephalopathy: pre-clinical studies in neuroprotection.SOD1 overexpression improves features of the oligodendrocyte precursor response in vitro.Intratracheal transplantation of mesenchymal stem cells simultaneously attenuates both lung and brain injuries in hyperoxic newborn rats.Neurite transection produces cytosolic oxidation, which enhances plasmalemmal repair.Oxidative stress, prefrontal cortex hypomyelination and cognitive symptoms in schizophrenia Erythropoietin Restores Long-Term Neurocognitive Function Involving Mechanisms of Neuronal Plasticity in a Model of Hyperoxia-Induced Preterm Brain Injury.Oxidative-nitrosative stress in a rabbit pup model of germinal matrix hemorrhage: role of NAD(P)H oxidase.Cerebral near infrared spectroscopy oximetry in extremely preterm infants: phase II randomised clinical trial.Cardiopulmonary bypass in the newborn: effects of circulatory cell-free hemoglobin and hyperoxia evaluated in a novel rat pup model.Inflammatory response in preterm infants is induced early in life by oxygen and modulated by total parenteral nutrition.

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P2860

Hyperoxia causes maturation-dependent cell death in the developing white matter.

http://www.wikidata.org/entity/Q35009330

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Hyperoxia causes maturation-dependent cell death in the developing white matter.

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Hyperoxia causes maturation-dependent cell death in the developing white matter.

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Hyperoxia causes maturation-dependent cell death in the developing white matter.

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Hyperoxia causes maturation-dependent cell death in the developing white matter.

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Hyperoxia causes maturation-dependent cell death in the developing white matter.

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JNEUROSCI.3213-07.2008

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Journal of Neuroscience

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Hyperoxia causes maturation-dependent cell death in the developing white matter

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Amy Armstrong

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Bettina Gerstner

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Felix Brehmer

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Joseph J Volpe

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Kerstin Genz

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Rachael L Neve

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Tara M DeSilva

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Ursula Felderhoff-Mueser

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P2860

Trends in severe brain injury and neurodevelopmental outcome in premature newborn infants: the role of cystic periventricular leukomalacia

12-Lipoxygenase plays a key role in cell death caused by glutathione depletion and arachidonic acid in rat oligodendrocytes

Eicosanoid regulation of angiogenesis: role of endothelial arachidonate 12-lipoxygenase

Bcl-2-related protein family gene expression during oligodendroglial differentiation

Peroxynitrite-induced neuronal apoptosis is mediated by intracellular zinc release and 12-lipoxygenase activation

Avoiding hyperoxia in infants 1250 g is associated with improved short- and long-term outcomes

Can Changes in Clinical Practice Decrease the Incidence of Severe Retinopathy of Prematurity in Very Low Birth Weight Infants?

12-Lipoxygenase: classification, possible therapeutic benefits from inhibition, and inhibitors.

Lipoxygenases: occurrence, functions, catalysis, and acquisition of substrate.

Genetic analysis of neuronal physiology with defective herpes simplex virus vectors.

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