2012
Oligodendrocyte Regeneration after Neonatal Hypoxia Requires FoxO1-Mediated p27Kip1 Expression
Jablonska B, Scafidi J, Aguirre A, Vaccarino F, Nguyen V, Borok E, Horvath TL, Rowitch DH, Gallo V. Oligodendrocyte Regeneration after Neonatal Hypoxia Requires FoxO1-Mediated p27Kip1 Expression. Journal Of Neuroscience 2012, 32: 14775-14793. PMID: 23077062, PMCID: PMC3517297, DOI: 10.1523/jneurosci.2060-12.2012.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornCell DifferentiationCells, CulturedCyclin-Dependent Kinase Inhibitor p27Forkhead Box Protein O1Forkhead Transcription FactorsGene Expression Regulation, DevelopmentalHumansHypoxia, BrainInfantInfant, NewbornMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, TransgenicNerve RegenerationOligodendrogliaConceptsDiffuse white matter injuryNeonatal hypoxiaOligodendrocyte regenerationOligodendrocyte progenitor cell proliferationWhite matter injuryWhite matter lesionsPermanent neurodevelopmental disabilityCritical developmental time windowWhite matter developmentOverexpression of FoxO1Preterm infantsProgenitor cell proliferationDevelopmental time windowMatter lesionsOligodendrocyte deathAbnormal myelinationNeurodevelopmental disabilitiesMouse modelBiphasic effectP27Kip1 expressionNull miceOligodendrogenesisHypoxiaOligodendrocyte differentiationOligodendrocyte development
2009
Modeling premature brain injury and recovery
Scafidi J, Fagel DM, Ment LR, Vaccarino FM. Modeling premature brain injury and recovery. International Journal Of Developmental Neuroscience 2009, 27: 863-871. PMID: 19482072, PMCID: PMC2783901, DOI: 10.1016/j.ijdevneu.2009.05.009.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsBrain injuryAnimal modelsSignificant public health problemPremature brain injuryPublic health problemRelevant animal modelsNeurodevelopmental sequelaePreterm brainPreterm infantsPremature birthPreclinical modelsHealth problemsInjuryBrain structuresCellular mechanismsBrainInfantsSchool ageNeuroanatomical structuresVariable degreesRecent insightsEpigenetic mechanismsSequelaeTherapyRecoveryHypoxic Injury during Neonatal Development in Murine Brain: Correlation between In Vivo DTI Findings and Behavioral Assessment
Chahboune H, Ment LR, Stewart WB, Rothman DL, Vaccarino FM, Hyder F, Schwartz ML. Hypoxic Injury during Neonatal Development in Murine Brain: Correlation between In Vivo DTI Findings and Behavioral Assessment. Cerebral Cortex 2009, 19: 2891-2901. PMID: 19380380, PMCID: PMC2774398, DOI: 10.1093/cercor/bhp068.Peer-Reviewed Original ResearchConceptsChronic sublethal hypoxiaLow birth weight preterm infantsBirth weight preterm infantsHypoxia-induced modificationNeonatal rodent modelPreterm birth resultsWeight preterm infantsSignificant neurodevelopmental disabilitiesOpen field taskGreater locomotor activityPreterm infantsPreterm birthNeurodevelopmental consequencesBirth resultsHypoxic injurySomatosensory cortexCaudate putamenCallosal connectivityCorpus callosumBehavioral deficitsNeurodevelopmental disabilitiesRodent modelsNeonatal developmentDTI findingsSublethal hypoxia