简介：ObjectiveTostudytheauditionandinnerearstructureinanormalswinemodel.MethodsAuditorybrainstemresponses(ABRs)weredeterminedinswineat1dayand1monthafterbirth.Theformofthecochleaandhaircellswereexaminedunderascanningelectronmicroscopeandoncochlearslices.ResultsABRthresholdsat1dayand1monthpost-birthwerebetween40and50dBSPL.ThelatenciesofwavesI,IIIandVin1dayoldswinewere1.97±0.13,3.01±0.16and4.26±0.20ms,respectively.At1month,thelantanciesofwavesI,IIIandVwere2.01±0.05,3.11±0.08and4.65±0.14ms,respectively,slightlylongerthanthoseat1day,althoughnotstatisticallysignificant(p>0.05).Theswinecochleawasconstitutedof3andahalfturnsandthecochlearhaircellslinedupinfourrows.Haircellciliaintheapicalturnwerelongerthanthoseinotherturns.ConclusionsTheswinecochleaismatureatthetimeofbirth.SwineABRthresholdsareslightlyhigherthanhumansandrats.Swineappearstobeaprecocialanimalspecies.

简介：ObjectiveTostudyeffectsofJiangtangFanglongWan(glucose-loweringanddeafness-preventingcapsule)onhearinginananimalmodelofdiabetes.MethodsWistarratswereusedtocreateadiabetesmodelbyintraperitonealinjectionofstreptozotocin(STZ,55mg/kg).FortyratswererandomlyselectedtoreceiveJiangtangFanglongWan(10g/kg/day)throughintragastricgavage(treatmentgroup)ornormalsaline(controlgroup).Auditorybrainstemresponses(ABRs)wererecordedatMonths1,2and3.ResultsABRlatenciesandwaveintervalsweresimilarbetweenthetwogroupsatMonth1(P>0.05).ABRlatenciesandwaveintervalswereshorterinthetreatmentgroupthanthoseofthecontrolgroupatMonths2and3(P<0.05andP<0.01,respectively).ConclusionOurresultssuggestthatJiangtangFanglongWanmayhaveabeneficialeffectinpreventingandtreatinghearingimpairmentassociatedwithdiabetes.

简介：Aratmodelofchronictympanicmembraneperforationwasdevelopedtobeusedinthesearchofnewmaterialsforthesealingoftheseperforations.AlongitudinalstudywascarriedoutinratssubjectedtoincisionalmyringotomyfollowedbytheapplicationofmitomycinCaloneorwithdexamethasone.Ratswerecheckedatdays3,7,10,14andweeklythereafteruntilperforationclosure,forupto6months.Theadditionofdexamethasoneisakeycomponentinordertoobtainachronicopening.Myringotomiestreatedwithsalinehadameanhealingtimeof8.5days.At8weeks,between62.5%and77.7%oftympanicmembranestreatedwithmitomycinCanddexamethasoneremainedperforatedandat6monthsthisnumberfellto21.4%.Thistechniqueisabletomaintainmosttympanicmembraneperforationspatentforatleast8weeks.Thisratmodelisadequateforitsuseinpreclinicalortranslationalresearch.

简介：Oxaliplatin,ananticancerdrugcommonlyusedtotreatcolorectalcancerandothertumors,hasanumberofserioussideeffects,mostnotablyneuropathyandototoxicity.Togaininsightsintoitsototoxicprofile,oxaliplatinwasappliedtoratcochlearorgancultures.Consistentwithitneurotoxicpropensity,oxaliplatinselectivelydamagednervefibersataverylowdose1μM.Incontrast,thedoserequiredtodamagehaircellsandspiralganglionneuronswas50foldhigher(50μM).Oxailiplatin-inducedcochlearlesionsinitial-lyincreasedwithdose,butunexpectedlydecreasedatveryhighdoses.Thisnon-lineardoseresponsecouldberelatedtodepressedoxaliplatinuptakeviaactivetransportmechanisms.Previousstudieshavedemon-stratedthataxonaldegenerationinvolvesbiologicallyactiveprocesseswhichcanbegreatlyattenuatedbynicotinamideadeninedinucleotide(NAD+).TodetermineifNAD+wouldprotectspiralganglionaxonsandthehaircellsfromoxaliplatindamage,cochlearculturesweretreatedwithoxaliplatinaloneatdosesof10μMor50μMrespectivelyascontrolsorcombinedwith20mMNAD+.Treatmentwith10μMoxaliplatinfor48hoursresultedinminordamagetoauditorynervefibers,butsparedcochlearhaircells.However,whencochlearculturesweretreatedwith10μMoxaliplatinplus20mMNAD+,mostauditorynervefiberswereintact.50μMoxaliplatindestroyedmostofspiralganglionneuronsandcochlearhaircellswithapop-toticcharacteristicsofcellfragmentations.However,50μMoxaliplatinplus20mMNAD+treatmentgreat-lyreducedneuronaldegenerationsandhaircellmissing.TheresultssuggestedthatNAD+providessignifi-cantprotectionagainstoxaliplatin-inducedneurotoxicityandototoxicity,whichmaybeduetoitsactionsofantioxidant,antiapoptosis,andenergysupply.

简介：Objective:Toestablishananimalmodeloflike-auditoryneuropathyinneonatalrat.MethodsTheani-malswereinjectedwithphenylhydrazinehydrochlorideorsalineat7-dayofage.ABRandDPOAEwereperformedtoassesstheauditoryfunction.Thecochleabasilarmembranestretchedpreparationandcochlearfrozensectionswerepreparedforimmunohistochemicalstainingtoexaminethemorphologicalchangeofhaircellsandspiralganglioncells(SGNs).ResultsAt7-dayagetheABRwaveI,III,V,latenciesandI-III,I-VIWIsintheexperimentalgroupweresignificantlyprolongedcomparedwiththoseinthecontrolgroup.TheABRthresholdswerealsoelevatedintheexperimentalgroup.Wefoundthereisnosignificantdiffer-enceinDPOAEinphenylhydrazinehydrochlorideexposuregroupcomparetocontrolgroup.Thecochlearhaircellsshowednosignsoflossinbothgroup,butthetotalnumberofneurofilamentspositivecellsinSGNsweresignificantlyreducedinthephenylhydrazinetreatedanimals.ConclusionOurstudysuggeststhatphenylhydrazinehydrochloridecanchangetheauditoryfunctionandinduceperipheralnervepathologybytargetedmainlytheSGNsinneonatalrat.

简介：Inmedicallaboratoryanimals,thepigistheclosestspeciestohumaninevolution,exceptforprimates.Asananimalmodel,thepigishighlyconcernedbymanyscientists,includingcomparativebiology,developmentalbiology,medicalgenetics.Rodentsasanimalmodelforhumanhearingdefectshasarepoorproducibilityandreliability,duetodifferencesinanatomicalstructure,evolutionaryrateandmetabolicrate,butthesehappenstobetheadvantagesofthepigmodel.Inthispaper,wewillsummarizetheapplicationofminiaturepiginthestudyofhumanhereditarydeafness.

简介：ObjectiveToinvestigateTcellactivationfollowingfacialnerveaxotomizationandlatentneuroimmunologicmechanismsintraumaticfacialparalysis.MethodsAmurinemodeloffacialnervetransactionwasused.LymphocytesfromcervicalandmesentericlymphnodesinBABL/cmiceatspecifictimeswerecollectedandexpressionratesofCD69onTcellswereassessedbyflowcytometry.ResultsInfiltratingTcellsweredetectedaroundthefacialneuronsinthefacialnervenucleusinmicewhosefacialnervewastransected.ImmunofluorescentstainingshowedrecruitmentofactivatedTcells.Threedayspost-facialnervetransection,theexpressionrateofCD69onTcellsfromcervicaldraininglymphoidnodes(CDLNs)wassignificantlydifferentfromthatonTcellsfrommesentericlymphnodes(MLNs)(P=0.0457),whereasthelatterwassimilartothatinanimalsundergoingshamsurgeriesandthatinblankcontrolanimals(p=0.2817and0.2724,respectively).Twoweekspost-nervetransection,theTcellCD69expressionratefromCDLNsremainedatahigherlevelandthanthatinthesham-operationanimals(p=0.0007).Attwoweeks,CD69expressionrateonTcellsfromMLNswasalsoup-regulatedanddifferentcomparedwiththesham-operationanimalsandwithitselfatthreedayspost-operation(p=0.0082and0.0133,respectively).ConclusionTcellsappeartobeactivatedandup-regulatedinCDLNsfollowingfacialnervetransection.ThereisevenevidenceofTcellactivationinMLNsat2weekspost-nervetransection.Thissuggestesanalterationofimmuneresponsefromlocaltogeneralimmunityintheacutestageoffacialnervetrauma,whichmayhelpcoordinatingandcontrollingthescalesandorientationoftheneuroimmuneresponseduringthepathogenesisandprogressionoffacialnervetrauma.

简介：BackgroundChronicotitismedia(COM)isasignificantclinicalproblem.UnderstandingthemechanismsofCOMiscriticalforitscontrolandtreatment.However,littleisknownoftheprocessesleadingtoCOMasaresultoflackofanimalmodelsofN-ethyl-N-nitrosourea(ENU)inducedmutationsinotitismediawitheffusion(OME).MethodsOtoscopyandauditorybrainresponse(ABR)evaluationwerecarriedoutundersedationinNmf391nmf/nmfmiceof2,4,6and8monthsofage.Themicewerekilledforstudyofmiddleandinnerearpathology.ResultsTympanicmembranevisualizationandABRthresholdsin1-to8-month-oldNmf391nmf/nmfmiceshowedspontaneousOMEandinnereardiseasesinapproximately100%oftheanimals.ThesignificantelevationofABRthresholdssuggestedasensorineuralcomponentinhearinglossinadditiontotheconductiveloss.Middleandinnerearhistologyshowedvariousdegreesofouterhaircellslossandmiddleearinflammationinallthemice,butnoinflammationcellsintheinnerear.TheABRthresholdat32kHzwassignificantlyelevated.ConclusionsThisstudyshowshistopathologicchangesintheNmf391nmf/nmfmousemodelofCOMwitheffusionthathavenotbeenreportedinhumanCOM.ThisENUinducedmutationmodelofCOMwillbevaluableforthecharacterizationofmiddleearinflammationandinnereardiseaseprocessesthatareinducedbymiddleearinfections.WeproposethatCOMwitheffusioninthisENUinducedmutationmodelisthecauseofthecochleahaircellsdamage.

简介：Objective:Toinvestigatetheeffectsofconductivehearingloss(CHL)onvestibularevokedmyogenicpotentials(VEMPs)usingasimulatedCHLmodel,andtoprovidethebasisforfuturestudies.Methods:Twenty-onehealthysubjectswererecruitedinthisstudy.WemeasuredocularVEMPs(oVEMPs)andcervicalVEMPs(cVEMPs)inthesesubjectsbyair-conductionsound(ACS)stimulation.CHLwassimulatedlaterbyblockingtherightexternalauditorycanalwithasoundproofearplugtoevaluateitsimpactsonVEMPs.Subjects'responsesbeforesimulatedCHLservedasthecontrol,andwerecomparedtotheirresponsesfollowingsimulatedCHL.Results:oVEMPsfollowingsimulatedCHLshoweddecreasedresponserate,elevatedthresholds,attenuatedamplitudesandprolongedN1latenciescomparedwiththosebeforesimulatedCHL,andthedifferenceswerestatisticallysignificant.Similarly,cVEMPsfollowingsimulatedCHLalsoshoweddecreasedresponserate,elevatedthresholdsandattenuatedamplitudes,withprolongedP1latenciescomparedwiththosebeforesimulatedCHL,althoughonlydifferencesinresponserate,thresholdandamplitudeweresignificant.Conclusions:ConductivehearinglossaffectstheresponserateandotherresponseparametersinoVEMPsandcVEMPs.

简介：ObjectiveToestablishananimalmodelofsuddenonsetsensorineuralhearingloss(SSNHL)tostudyitsmechanisms.MaterialsandmethodsTheinnerearwasexposedto3-nitropropionicacidat0.5mol/L(3-NP(H))and0.3mol/L(3-NP(L))throughtheroundwindowmembranefor30minutesin50maleguineapigs.Thresholdsofauditorybrainstemresponses(ABR)wereestablishedbeforethetreatmentandretestedat4hours,1day,3daysand6daysfollowing3-NPexposure.Controlanimalsweretreatedwithphosphatebufferedsaline(PBS)andtheirABRswereretestedat4hoursand1dayafterthetreatment.Animalsweremonitoredfornystagmusandposturalsignsofvestibulardysfunction,usingadigitalvideocamera,followingthetreatmentprocedure.Specimensweretakenat12hours,1day,3daysand7daysfollowing3-NP(H)exposureandembeddedinJB4forlightmicroscopyobservation.ResultsABRswerelostinallanimalstestedat4hoursfollowing3-NP(H)exposure.TherateofcompleteABRlossdecreasedaspost-treatmenttesttimeincreased.ABRswerelostin80%(4/5)oftheanimalsat1dayafterexposureto3-NP(L).Spontaneoushorizontalnystagmuswithafastphaseawayfromthetreatedeardevelopedinall3-NP(H)-treatedanimalsandin20%(1/5)oftheanimalsexposedto3-NP(L),exceptfortheonetreatedbilaterally.Variousdegreeofposturaldisturbancesconsistentwithunilateralvestibulardysfunction,suchasspontaneousbarrelrollingtowardstheexposuresidewhilewalking,wereseeninallanimalsexposedto3-NP(H)and40%(2/5)ofanimalsexposedto3-NP(L),exceptfortheoneanimaltreatedbilaterally,whichshowednosignsofimbalance.Bothnystagmusandposturaldisturbancesresolvedin2daysfollowing3-NPexposure.HistologicalstudyshowedtemporaryedematintheorganorCorti,Claudiuscellsandtheinnersulcuscells3daysafter3-NP(H)treatment.Enlargementofintercellularspaceinthespiralprominencewasfirstnoticedat12hourspost-3-NP(H)exposure,progressedatd

简介：ObjectiveTostudytheinfluenceofJiangTangFangLongformulaoninsulinproductionandfunctioninananimalmodelofdiabetichearingloss.MethodsWistarrats(n=60)wererandomlydividedinto6groups(10ineach)toreceivenotreatment(thenormalcontrol,GroupA),ortoreceiveintra-peritoneal55mg/kgstreptozotocinwith(GroupsC,DandE)orwithout(GroupB)subsequentJiangTangFangLongformulatreatmentatvariousdosesorYuLongWantreatment(GroupF).After60days,fastingbloodglucose(FBG),bodyweight(BW)andfastinginsulin(FINS)wererecordedandtheHOMA-IRandHOMA-βcalcu-lated.Insulinexpressioninpancreatictissueswasmeasuredbyradioimmunoassay.ResultsComparedwithanimalsthatreceivedstreptozotocinwithoutrescuetreatment(GroupB),animalsthatreceivedhigherdosesofJiangTangFangLongformula(GroupsDandE)showedimprovedindicesofdiabetesmanifestation(P<0.05)andimprovedHOMA-β(P<0.05)inadose-dependentmanner,aswellasimprovedinsulinexpressioninpancreaticislets(P<0.05).ThedifferencebetweenlowdoseJiangTangFangLongformulatreatment(GroupC)andGroupBwasnotsignificant(P>0.05).ConclusionOurresultssuggestthatJiangTangFangLongformulamayimprovepancreaticβ-cellsfunctionwhichmayexplainitsefficacyintreatingdiabetichearingloss.