2019
Minocycline mitigates the effect of neonatal hypoxic insult on human brain organoids
Boisvert EM, Means RE, Michaud M, Madri JA, Katz SG. Minocycline mitigates the effect of neonatal hypoxic insult on human brain organoids. Cell Death & Disease 2019, 10: 325. PMID: 30975982, PMCID: PMC6459920, DOI: 10.1038/s41419-019-1553-x.Peer-Reviewed Original ResearchConceptsNeonatal hypoxic injuryBrain developmentEfficacy of minocyclineLow birth weightUse of minocyclineEffects of hypoxiaNormal brain developmentCerebral organoid modelHuman brain organoidsLater time pointsAnimal model systemsNeonatal hypoxicDevastating causeCerebral palsySignificant morbidityHuman brain developmentNeurological consequencesBirth weightHypoxic injuryNeuronal deathCortical neuronsInjury resultsGlial cellsForebrain markersPotential treatment
2009
Fgfr1 Is Required for Cortical Regeneration and Repair after Perinatal Hypoxia
Fagel DM, Ganat Y, Cheng E, Silbereis J, Ohkubo Y, Ment LR, Vaccarino FM. Fgfr1 Is Required for Cortical Regeneration and Repair after Perinatal Hypoxia. Journal Of Neuroscience 2009, 29: 1202-1211. PMID: 19176828, PMCID: PMC2768410, DOI: 10.1523/jneurosci.4516-08.2009.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnalysis of VarianceAnimalsAnimals, NewbornBromodeoxyuridineCell ProliferationCerebral CortexCreatinineDNA-Binding ProteinsGlial Fibrillary Acidic ProteinHypoxiaMiceMice, Inbred C57BLMice, TransgenicNerve RegenerationNeurogenesisNeuronsOlfactory BulbParvalbuminsPhosphopyruvate HydrataseReceptor, Fibroblast Growth Factor, Type 1T-Box Domain ProteinsConceptsWild-type miceCortical neuronsOlfactory bulbSubventricular zoneChronic postnatal hypoxiaNeonatal hypoxic injuryPersistent behavioral deficitsExcitatory cortical neuronsSVZ cell proliferationCell proliferationPostnatal day 3Receptor 1 geneNormoxic miceOB neurogenesisReactive neurogenesisPerinatal hypoxiaPostnatal hypoxiaNeuronal recoveryFibroblast growth factor receptor 1 (FGFR1) geneHypoxic miceChronic hypoxiaGABAergic interneuronsHypoxic injuryResidual deficitsCortical regeneration
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