简介：ObjectiveTodetectearlysignsofnoise-inducedhearingloss(NIHL)inmilitarypilotswithouthearingcomplaints.MethodsPuretoneaudiometryandacousticreflexthresholdsweretestedin36militarypilots(72ears)withnoiseexposurehistorybutnocomplaintsofhearingloss.Conventionaltestfrequencies(0.25-8kHz)andextendedhighfrequencies(EHF,10and12.5kHz)wereincludedinaudiometry.Whitenoiseandpuretonesat0.5,1,2,and4kHzwereusedforacousticreflextests.Twentynormalhearingsubjects(40ears)withnoexposuretooccupationalnoisewereusedascontrols.ResultsPuretonethresholdsatallconventionalfrequenciesandatEHFswereelevatedinthepilots,withthemaximumshiftat4kHz,comparedwithcontrols(p<0.01).ThepilotsalsoshowedelevatedARTtowhitenoiseanddecreaseddifferentialsbetweenwhitenoiseandpuretoneARTs(p<0.01).ConclusionEarlysignsofNIHLarepresentinsomesymptom-freemilitarypilots.Highfrequencyhearingthresholdshift,elevatedwhitenoiseARTanddecreaseddifferentialbetweenwhitenoiseandpuretoneARTsmaybeobjectiveindicatorsofearlyNIHL.

简介：ObjectiveToinvestigatetheprotectiveeffectsofsoundconditioningagainstsubsequenthigh-levelnoisetraumainrats.MethodRatswereexposedtoa4kHzoctavebandnoiseat95dBSPLfor10hours,thentoatraumaticexposuredose(105dBSPLfor13hours)delivered12hlater.Controlanimalswereexposuredtothetraumaticdoseonly.ABRthresholdswereobtainedbeforeandafternoiseexposure.ResultAnimalsthathadbeensoundconditioneddemonstratedlessABRthresholdshiftcomparedtothosethathadnot.ConclusionModeratelevelsoundexposureappearstohaveatougheningeffectontheratcochlea(or'conditioning')leadingtodecreasedhearinglossfromsubsequenttraumaticexposure.

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简介：ObjectiveTostudyeffectsofsaturatedhydrogensalineinpreventingnoise-inducedhearingloss.MethodsFifteenguineapigswererandomlydividedinto3groups(5each),grouponewasforcontrol,grouptwowastreatedwithnormalsalineandgroupthreewastreatedwithsaturatedhydrogensaline,whichwasgivenintraperitoneallyat1hourbeforenoiseexposureat1ml/100g.Onehundredroundsofimpulsenoise(157dBSPLpeak)weredeliveredasnoiseexposure.ImmediatelyafterexposuretoimpulsenoiseandonDays1,2,4and8followingexposure,auditorybrainstemresponse(ABR)thresholdsweremeasured.Outerhaircellmorphologicalchangesandsuccinatedehydrogenase(SDH)activitywereexaminedonDay8post-exposure.ResultsImmediatelyafternoiseexposure,ABRthresholdsinsaturatedhydrogensalinetreatedanimalswerelowerthanthenon-treatedanimals(P<0.05).MicroscopyshowedlittleSDHstaining,cellswellingandirregularcellarrangementinthenon-treatedornormalsalinetreatedanimals.Whereasinthesaturatedhydrogensalinetreatedanimals,therewasdeepSDHstainingwithsignificantlyreducedcelllossandmoreregularcellulararrangementcomparedtotheothertwogroups.Thesurvivingcellscountswas45.17±12.15fornon-treatedanimals,44.50±10.02fornormalsalinetreatedanimalsand,116.50±2.38foranimalstreatedwithsaturatedhydrogensaline.Whilethecountwassimilarbetweennon-treatedandnormalsalinetreatedanimals,itwassignificantlyhigherinsaturatedhydrogensalinetreatedanimals(P<0.05).ConclusionsIntraperitonealinjectionofsaturatedhydrogensalineappearstoprotectthecochleaagainstnoise-induceddamage.

简介：ObjectiveTounderstandthemechanismofnoiseexposureinducedouterhaircells(OHCs)deathpathways.MethodsThirtytwoguineapigswereusedinthisstudy.Theanimalswereeitherexposedfor4h/daytobroadbandnoiseat122dBSPL(A-weighted)for2consecutivedaysorperfusedwithMNNG.Afterauditorytest,thecochleaeofanimalsweredissected.Propidiumiodide(PI),aDNAintercalatingfluorescentprobe,wasusedtotracemorphologicalchangesinOHCnuclei.F-actinstainingwasusedtodeterminemissingOHCs.Caspase-3wasdetectedinlivingorganofCortiwholemountsusingthefluorescentprobe.ThesinglestrandDNA(ssDNA)inapoptoticOHCsinguineapigsandapoptosisinducingfactor(AIF)inhaircellsinguineapigswereexaminedbyimmunohistologymethod.WholemountsoforganofCortiwereprepared.Morphologicalandfluorescentchangeswereexaminedunderaconfocalmicroscope.Results(1)Bothapoptoticandnecrotichaircellsappearedfollowingnoiseexposure.(2)NoiseexposureinducedsinglestrandDNAinapoptoticOHCsbutnotinthenormalOHCs.(3)EitherafternoiseexposureorafterMNNGperfusion,apoptoticOHCswerefeaturedbynuclearcondensationorfragmentationwithcaspase-3activation,whereasnecroticOHCswerecharacterizedbynuclearswellingwithoutcaspase-3activation.(4)InnormalorganofCorti,AIFwaslocatedinthemitochondriaareas.Afternoiseexposure,AIFwastranslocatedfrommitochondriainapoptoticandnecroticOHCs.ConclusionThesefindingsindicatethatnoiseexposuredamagesDNAintheOHC,whichtriggersactionofCaspase-3.Subsequently,AIFistranslocatedtothenucleus,leadingtoDNAdamageandOHCsdeath.

简介：Hearinglossandtinnitusareamongthemostcommonconsequencesoflongtermnoiseexposureandre-mainanunder-addressedheathissueinmostdevelopingnationsincludingChina.Therapidindustrializa-tionandlifestylechangesinChinaincreasetheconcernovernoiseexposureandnoiseinducedhearingloss(NIHL).ResearchonNIHLinChinaislimited.ThecurrentpaperreviewsstudiespublishedinEnglishandChineselanguageliteraturesregardingnoiseexposureandNIHLinChina.TheirimplicationontheChi-nesepopulationisdiscussed.ThepossibleutilityofaresearchmodelsuchastheDangerousDecibels?asameanstoincreaseunderstandingofthescopeofNIHLamongtheChinesepopulation,toeducatethegener-alpublicinChina(especiallytheyoung)aboutNIHLanditsprevention,andtostudyeffectsoflanguageandculturalfactorsoninternationalinformationdisseminationandbehavioralinterventionsisproposed.

简介：Objective:TodemonstratetheperformancebenefitoftheAutomaticSceneClassifier（SCAN）algorithmavailableintheNucleus6（CP900series）soundprocessoroverthedefaultprocessingalgorithmsofthepreviousgenerationNucleus5（CP810）andFreedomHybridTMsoundprocessors.Methods:Eighty-twocochlearimplantrecipients（40Nucleus5processorusersand42FreedomHybridprocessorusers）listenedtoandrepeatedAzBiosentencesinnoisewiththeircurrentprocessorandwiththeNucleus6processor.Results:TheSCANalgorithmwhenenabledyieldedstatisticallysignificantnon-inferiorandsuperiorperformancewhencomparedtotheNucleus5andFreedomHybridsoundprocessorsprogrammedwithASCtADRO.Conclusion:TheresultsofthesestudiesdemonstratethesuperiorperformanceandclinicalutilityoftheSCANalgorithmintheNucleus6processorovertheNucleus5andFreedomHybridprocessors.

简介：Thewaltzingguineapigmaybeagoodmodeltoinvestigateifgeneticfactorcanchangethesensitivityinnoise-inducedhearingloss.Atotalof34waltzigguineapigswerestudiedandwefoundthatthereisnoanysignificantincreasedsensitivitytonoisetraumaiftheage-inducedhearinglosswasconsideredinwaltz-ingguineapig.

简介：Noisepollutionisamajorhazardousfactortohumanhealthandislikelyharmfulforvulnerablegroupssuchaspre-terminfantsunderlifesupportsysteminanintensivecareunit.Previousstudieshavesuggestedthatnoiseexposureimpairschildren’slearningabilityandcognitiveperformanceandcognitivefunctionsinanimalmodelsinwhichtheeffectismainlyattributedtotheoxidantstressofnoiseonthecognitivebrain.Thepotentialroleofnoiseinducedhearingloss(NIHL),ratherthantheoxidantstress,hasalsobeenindicatedbyadepressionofneurogenesisinthehippocampuslongafterabriefnoiseexposure,whichproducesonlyatentativeoxidantstress.ItisnotclearifnoiseexposureandNIHLduringearlydevelopmentexertsalongtermimpactoncognitivefunctionandneurogenesistowardsadulthood.Inthepresentstudy,abriefnoiseexposureathighsoundlevelwasperformedinneonatalC57BL/6Jmice(15daysafterbirth)toproduceasignificantamountofpermanenthearinglossasproved2monthsafterthenoise.Atthisage,thenoise-exposedanimalsshoweddeterioratedspatiallearningandmemoryabilitiesandareductionofhippocampalneurogenesisascomparedwiththecontrol.Theaveragedhearingthresholdwasfoundtobestronglycorrelatedwiththescoresforspatiallearningandmemory.Weconsidertheeffectsobservedarelargelyduetothelossofhearingsensitivity,ratherthantheoxidantstress,duetothelongintervalbetweennoiseexposureandtheobservations.

简介：Thepurposeofthepresentstudywastodetermineprotectivieeffectsofbasicfibroblastgrowthfactor(bFGF)oncochlearneuronsandhaircellsinvitroandinvivo.InexperimentI,culturedspiralganglionneurons(SGNs)preparedfromP3micewereexposedto20mMglutamatefor2hoursbeforetheculturemediumwasreplacedwithfreshmediumcontaining0,25,50,and100ng/mlbFGF,respectively.Fourteendayslater,allcultureswerefixedwith4%paraformaldehyde,andstainedwith1%toluidineblue.ThenumberofsurvivingSGNswerecountedandthelengthofSGNsneuritesweremeasured.Exposureto20mMglutamatefor24hoursresultedinaninhibitiononneuriteoutgrowthofSGNsandelevatedcelldeath.TreatmentofthecultureswithbFGFledtopromotionofneuriteoutgrowthandelevatednumberofsurvivingSGNs.EffectsofbFGFweredosedependentwiththehighestpotencyat100ng/ml.InexperimentⅡ,invivostudieswerecarriedoutwithguineapigsinwhichbFGForartificialperilymphwasperfusedintothecochleatoassesspossibleprotectiveeffectsofbFGFoncochlearhaircellsandcompoundactionpotentials(CAP).TheCAPsweremeasuredbefore,immediatlyand48hoursafterexposuretonoise.SignificantdifferencesinCAPwereobserved(p＜0.05)amongthebFGFperfusedgroup,controlgroup(t=3.896)andartificialperilymphperfusedgroup(t=2.520)at48hoursafternoiseexposure,CochleaewereremovedandhaircellLosswasanalyzedinsurfacepreparationspreparedfromallexperimentalanimals.Acoustictraumacausedlossof651and687innerhaircellsinthecontrolandartificialperilymphperfusedgroup,respectively.Insharpcontrast,only31innerhaircellswerelostinthebFGFperfusedears.Similarly,moreouterhaircellsdiedinthecontrolandperilymphperfuesedgroup(41830and41968,respectively)thaninthegrouptreatedwithbFGF(34258).OurresultsdemonstratethatbFGFprotectedSGNsagainstglutmateneurotoxicityinvitro.Inaddition,treatmentwithbFGFalso

简介：ObjectiveTostudycharacteristicsofhearinglossafterexposuretomoderatenoiseexposureinC57BL/6Jmice.MethodsMaleC57BL/6Jmicewithnormalhearingatageof5-6weekswerechosenforthisstudy.Themicewererandomlyselectedtobestudiedimmediatelyafterexposure(GroupP0),or1day(GroupP1),3days(GroupP3),7days(GroupP7)or14days(P14)afterexposure.Theirbeforeexposureconditionservedasthenormalcontrol.Allmicewereexposedtoabroad-bandwhitenoiseat100dBSPLfor2hours,ABRthresholdswereusedtoestimatehearingstatusateachtimepoint.ResultsABRthresholdelevationwasseenateverytestedfrequencyatP0(P<0.01).Elevationathigh-frequencies(16kHzand32kHz)wasgreaterthanatlowerfrequencies(4kHzand8kHz,P<0.05).FromP1toP14,ABRthresholdscontinuouslyimproved,andtherewasnosignificantdifferencebetweenP14andbeforeexposure(P>0.05).ConclusionThereisafrequencyspecificresponseto100dBSPLbroad-bandwhitenoiseinC57BL/6Jmice,withthehigh-frequencybeingmoresusceptible.HearinglossinducedbymoderatenoiseexposureappearsreversibleinC57BL/6Jmice.

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简介：Olderadultsoftenfinditdifficulttoperceivespeech,especiallyinnoisyconditions.Thoughhearingaidisoneoftherehabilitativedevicesavailabletoolderadultstoalleviatehearingloss,someofthemmayexperienceannoyancethroughhearingaidandhencerejectit.maybeduetocircuitrynoiseand/orbackgroundnoise.Acceptablenoiselevelisadirectbehaviouralmeasuretoestimatetheextentofhowmuchapersonisabletoputupwithnoisewhilesimultaneouslylisteningtospeech.Acceptablenoiselevelisacentralauditorymeasureanditisnotinfluencedbyage.gender,presentationlevelorspeaker.Usingthismeasure,wecanquantifytheannoyancelevelexperiencedbyanindividual.Thisinformationisofutmostimportanceandcautionshouldbepaidbeforesettingtheparametersinhearingaid,especiallyforthosewhoareunabletoacceptnoise.Inthisreviewarticle,anattempthasbeenmadetodocumenthowtooptimizethehearingaidprogrambysettingparameterssuchasnoisereductioncircuit,microphonesensitivityandgain.Theseadjustmentsofparametersmighthelptoreducerejectionrateofhearingaids,especiallyinthoseindividualswhoareannoyedbybackgroundnoise.

简介：Noise-inducedhearinglossisacommoncauseofacquiredhearinglossintheadultpopulation.Acousticoverstimulationcausescochleardamagethroughmechanicalstresstothetissue.Consequently,complexmolec-ularchangesareinitiated,andthesechangesleadtomorphologicalandbiologicalalterationsinthecochlea,whichinturncompromisethecochlearfunctionandcausehearingloss.Inthepast10years,therehavebeensignificantadvancesinourunderstandingofthemolecularmechanismsofnoise-inducedhearingloss.Theseadvancesareattributed,inpart,tothedevelopmentofhigh-throughputtechnologiesfortheglobalanalysesofmolecularchanges.Inthisreview,webrieflydescribethenewlydevelopedmethodsforinvestigatingthemo-lecularresponsesofthecochleatoacoustictraumaandtheknowledgegeneratedfromthesestudies.Wealsodiscussthestrengthsandlimitationsofeachtechniqueandthemajorchallengestoinvestigatecochleardegen-erationfollowingacousticinjury.