2013
Gene–environment interactions in severe intraventricular hemorrhage of preterm neonates
Ment LR, Ådén U, Lin A, Kwon SH, Choi M, Hallman M, Lifton RP, Zhang H, Bauer CR. Gene–environment interactions in severe intraventricular hemorrhage of preterm neonates. Pediatric Research 2013, 75: 241-250. PMID: 24192699, PMCID: PMC3946468, DOI: 10.1038/pr.2013.195.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApgar ScoreBlood CoagulationCerebral VentriclesCerebrovascular CirculationCollagen Type IVFactor VGene-Environment InteractionGenetic Predisposition to DiseaseGenetic VariationGestational AgeHumansHypoxia, BrainInfantInfant, PrematureInflammation MediatorsIntracranial HemorrhagesMethylenetetrahydrofolate Reductase (NADPH2)PhenotypePremature BirthPrognosisRisk FactorsConceptsIntraventricular hemorrhageCerebral injuryPreterm neonatesFactor V Leiden geneRisk of IVHEnvironmental triggersSevere intraventricular hemorrhageCerebral blood flowMethylenetetrahydrofolate reductase (MTHFR) variantsUnknown environmental triggersPresence of mutationsPeriventricular infarctionApgar scorePerinatal hypoxiaPreclinical dataFetal environmentGerminal matrixCerebral vasculatureBlood flowT polymorphismGene-environment interactionsMTHFR 677CHemorrhageNeonatesVascular pathways
2004
Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity
Weiss J, Takizawa B, McGee A, Stewart WB, Zhang H, Ment L, Schwartz M, Strittmatter S. Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity. Experimental Neurology 2004, 189: 141-149. PMID: 15296844, DOI: 10.1016/j.expneurol.2004.05.018.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornAxonsBehavior, AnimalBiotinCentral Nervous SystemDextransDisease Models, AnimalExploratory BehaviorHumansHypoxia, BrainImmunoblottingImmunohistochemistryInfant, NewbornInfant, PrematureMiceMice, Inbred C57BLMyelin Basic ProteinMyelin ProteinsMyelin-Associated GlycoproteinNogo ProteinsOligodendrogliaReceptors, Cell SurfaceTime FactorsConceptsChronic sublethal hypoxiaPeriventricular leukomalaciaMyelin associated glycoproteinCorticospinal tractWhite matterLow birth weight infantsCerebral white matter volumeBirth weight infantsLow birth weightAnterograde axonal tracingPeriventricular white matterPremature human infantsCNS white matterWhite matter volumeHypoxia-induced reductionWeight infantsAxonal sproutingCerebral ventriculomegalyCorticofugal fibersLocomotor hyperactivityNeonatal hypoxiaPersistent abnormalitiesMotor cortexBirth weightHuman prematurity
2002
Disrupted synaptic development in the hypoxic newborn brain
Curristin SM, Cao A, Stewart WB, Zhang H, Madri JA, Morrow JS, Ment LR. Disrupted synaptic development in the hypoxic newborn brain. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 15729-15734. PMID: 12438650, PMCID: PMC137784, DOI: 10.1073/pnas.232568799.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornApoptosisAtmosphere Exposure ChambersBrain Damage, ChronicCell DifferentiationCytoskeletonDisease Models, AnimalDNA, ComplementaryEndothelial Growth FactorsGene Expression ProfilingHypoxiaHypoxia, BrainHypoxia-Inducible Factor 1, alpha SubunitIntercellular Signaling Peptides and ProteinsLymphokinesMembrane ProteinsMiceMice, Inbred C57BLMicrotubulesNerve Tissue ProteinsOligodendrogliaOligonucleotide Array Sequence AnalysisStress, PhysiologicalSynapsesSynaptic TransmissionTranscription FactorsTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsPostnatal hypoxiaCerebral maturationGlial maturationNewborn brainSynaptic maturationPresynaptic functionPostsynaptic functionSublethal hypoxiaSynaptic developmentHealth crisisHypoxiaCognitive disabilitiesBrainMaturation programMaturationDysynchronyNeuropathologyInfantsNeurotransmissionCohortProtein assaysMiceHypoxic