2015
Pannexin 1 deficiency can induce hearing loss
Zhao H, Zhu Y, Liang C, Chen J. Pannexin 1 deficiency can induce hearing loss. Biochemical And Biophysical Research Communications 2015, 463: 143-147. PMID: 26002464, PMCID: PMC4464954, DOI: 10.1016/j.bbrc.2015.05.049.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCaspase 3CochleaConnexinsDisease Models, AnimalEvoked Potentials, Auditory, Brain StemHearing LossMiceMice, KnockoutNerve Tissue ProteinsOtoacoustic Emissions, SpontaneousConceptsDistortion product otoacoustic emissionsHearing lossAuditory brainstem response recordingsProgressive hearing lossProduct otoacoustic emissionsHigh incidenceCell degenerationOtoacoustic emissionsGap junction proteinAcoustic stimulationCell apoptotic pathwaysHair cellsResponse recordingsGene mutationsJunction proteinsExtensive expressionCochleaActive cochlear mechanicsGap junctionsApoptotic pathwayDeficiencyHearingCritical roleCochlear mechanics
2014
Connexin26 (GJB2) deficiency reduces active cochlear amplification leading to late-onset hearing loss
Zhu Y, Chen J, Liang C, Zong L, Chen J, Jones R, Zhao H. Connexin26 (GJB2) deficiency reduces active cochlear amplification leading to late-onset hearing loss. Neuroscience 2014, 284: 719-729. PMID: 25451287, PMCID: PMC4268423, DOI: 10.1016/j.neuroscience.2014.10.061.Peer-Reviewed Original ResearchConceptsLate-onset hearing lossActive cochlear amplificationDistortion product otoacoustic emissionsHearing lossNonsyndromic hearing lossTherapeutic interventionsProgressive hearing lossHair cell lossPostnatal day 5Cochlear amplificationProduct otoacoustic emissionsConditional knockout miceKnockout miceClinical observationsDay 5Cell lossEndocochlear potentialOtoacoustic emissionsNormal hearingCx26 expressionDeafness mechanismMiceCx26 deficiencyCochleaIntervention
2013
The effects and outcomes of electrolyte disturbances and asphyxia on newborns hearing
Liang C, Hong Q, Jiang T, Gao Y, Yao X, Luo X, Zhuo X, Shinn J, Jones R, Zhao H, Lu G. The effects and outcomes of electrolyte disturbances and asphyxia on newborns hearing. International Journal Of Pediatric Otorhinolaryngology 2013, 77: 1072-1076. PMID: 23648318, PMCID: PMC3738180, DOI: 10.1016/j.ijporl.2013.03.031.Peer-Reviewed Original ResearchMeSH KeywordsAsphyxiaChinaFemaleHearing DisordersHearing TestsHumansInfant, NewbornInfant, PrematureLogistic ModelsMaleNeonatal ScreeningOtoacoustic Emissions, SpontaneousRisk FactorsWater-Electrolyte ImbalanceConceptsElectrolyte disturbancesInfant HearingTEOAE testHearing outcomesFull-term infantsOtoacoustic emission testHigh-risk factorsMonths of agePreterm infantsNewborn hearingAsphyxiaSignificant impairmentInfantsHypocalcaemiaPass rateSignificant reductionOutcomesHearingLow recovery ratesNewbornsImpairmentRecovery rateMonthsActive cochlear amplification is dependent on supporting cell gap junctions
Zhu Y, Liang C, Chen J, Zong L, Chen G, Zhao H. Active cochlear amplification is dependent on supporting cell gap junctions. Nature Communications 2013, 4: 1786. PMID: 23653198, PMCID: PMC3675877, DOI: 10.1038/ncomms2806.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAuditory ThresholdCochlear Microphonic PotentialsConnexin 26ConnexinsEvoked Potentials, Auditory, Brain StemGap JunctionsGene DeletionGene TargetingHair Cells, Auditory, OuterHearing LossLabyrinth Supporting CellsMiceMice, KnockoutMolecular Motor ProteinsNonlinear DynamicsOtoacoustic Emissions, SpontaneousSpiral GanglionConceptsActive cochlear amplificationOuter hair cellsCell gap junctionsHearing lossCochlear amplificationHair cellsGap junctionsDistortion product otoacoustic emissionsOuter hair cell electromotilityHair cell electromotilitySevere hearing lossProduct otoacoustic emissionsShorter outer hair cellsHair-bundle movementsOuter pillar cellsLeftward shiftOtoacoustic emissionsAcoustic stimulationDeiters' cellsHearing sensitivityConnexin 26Active cochlear mechanicsNovel findingsPillar cellsBundle movement
2008
Prestin up-regulation in chronic salicylate (aspirin) administration: An implication of functional dependence of prestin expression
Yu N, Zhu M, Johnson B, Liu Y, Jones R, Zhao H. Prestin up-regulation in chronic salicylate (aspirin) administration: An implication of functional dependence of prestin expression. Cellular And Molecular Life Sciences 2008, 65: 2407-2418. PMID: 18560754, PMCID: PMC2548279, DOI: 10.1007/s00018-008-8195-y.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsGuinea PigsHair Cells, Auditory, OuterMiceMolecular Motor ProteinsOtoacoustic Emissions, SpontaneousRNA, MessengerSalicylatesSignal TransductionTime FactorsTinnitusTranscription FactorsUp-RegulationConceptsLong-term administrationPrestin expressionSalicylate administrationChronic salicylate administrationDistortion product otoacoustic emissionsNuclear transcription factors c-fosProduct otoacoustic emissionsTranscription factor c-FosOHC electromotilityHearing lossNF-κBAcute inhibitionOtoacoustic emissionsAdministrationC-fosProtein levelsOuter hair cell electromotilityHair cell electromotilityEgr-1Incremental increaseExpressionSalicylateElectromotilityFour-fold