简介：AlexiswritingastoryforRob＇sshow.Alocalwomanfoundagiantratinherhouse.Itwassittingonamatinherlivingroom,anditchasedherblackcataway.Thestorysoundslikeakid,spoembecausemanyofthewordshavesimilarsounds.＂Afatratchasesawoman＇sblackcat!＂

简介：感谢可爱的cat，感谢机敏的rat，猫和老鼠之间的那点事儿，永远带给我们无穷的乐趣!而这一次，它们之间又发生了怎样的故事呢？期待你来翻译。别忘了将你的译作e-mail或邮寄给我们哦!

简介：反复、大声地朗读这首童谣：Q：童谣中出现了哪几种事物？请按发音的不同，把它们分为两类。

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简介：瞄准：为了建立老鼠乙醇胃炎，当模特儿，我们在胃的mucosa上评估了乙醇的效果并且在导致乙醇的长期的胃炎上学习了geranylgeranylacetone的预防效果。方法：100只男Sprague-Dawley老鼠随机被划分成4个相等的组：正常控制组，经历正常的胃的灌注盐(NS)由gastrogavage；为控制组和为4wk由gastrogavage与乙醇(有56%乙醇内容的精华精神)经历了胃的灌注的2个模型治疗组建模。geranylgeranylacetone的低或高的剂量被增加，在在2模型治疗的乙醇灌注前的1h组织NS的一样的数量，而不是geranylgeranylacetone在那个模型控制组被使用。老鼠然后被牺牲，胃被移开。胃的mucosa的损害水平被光和电子观察前列腺素2的显微镜学，和层次，endothelin-1(ET-1)和氮的氧化物(PGE2)(没有)被放射性免疫测定和Griess方法测量。结果：胃的mucosal表皮的损坏分数(版本；4.5)并且溃疡索引(UI；12.0)模型控制，组比正常控制组的显著地高级(0和0分别地，所有P=0.000)。胃的mucosal版本和2个模型治疗组的UI(版本：2.5和2.0；UI：3.5和3.0)比模型控制组的显著地低(所有P<0.01)。低剂量、高剂量的模型治疗组之间没有统计上重要的差别。模型控制组的血浆ET-1的表达式值比正常控制组的高(P<0.01)并且2个模型治疗组(所有P<0.01)。胃的mucosalPGE2和浆液的表示价值不模型控制组是比正常控制组的那些低的(所有P<0.05)并且2个模型治疗组(所有P<0.05)。胃的有粘液的layerand的厚度在模型控制组的hexosamine内容在正常控制组是比那显著地低的(所有P<0.01)并且2个模型治疗组(所有P<0.05)。扫描并且传播电子显微镜学观察在模型控制组，显示出那上皮的连接是含糊的，细胞间的关节消失了，细胞内部的细胞器的损坏是比在正常控制组的那些显著地更

简介：Leadisamajorenvironmentaltoxicantthroughouttheworld.Leadcaninducesevereneurotoxicityincludingirreversiblehearingimpairment.Manyinvivostudieshaveshownthatleaddamagestheauditorynervoussystem,buthaslittleornoeffectoncochlearsensoryhaircells.Togaininsightsonleadototoxicandneurotoxiceffectsinvitro,leadacetate(LA)wasappliedtopostnatalday3-4ratcochlearorganotypicculturesfor24or72hwithdosesof0.1,0.5,1,2or4mM.After24or72htreatmentwithleadacetate,nearlyallofcochlearsensoryhaircellswereintact.However,after72htreatment,theperipheralauditorynervefibersprojectingtothehaircellsandthespiralganglionneurons(SGN)weredamagedwhenleadconcentrationexceeded2mM.Ourresultsindicatedthat72htreatmentwithonlythehighdoses(>2mM)ofleadactatedamagedSGNsandperipheralnervefibers;haircellsremainedstructurallyintactevenafter4mMtreatment.TheseresultsshowthatleadprimarilydamagescochlearnervefibersandSGNratherthanhaircells.

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简介：Asmostgenesequencesandfunctionalstructuresofinternalorgansinratshavebeenwellstudied,ratmodelsarcwidelyusedinexperimentalmedicalstudies.Alargenumberofdescriptionsandatlasoftherattemporalbonehavebeenpublished,butsomedetailedanatomyofitssurfaceandinsidestructuresremainstobestudied.Byfocusingonsomeuniquecharacteristicsoftherattemporalbone,thecurrentpaperaimstoprovidemoreaccurateanddetailedinformationonrattemporalboneanatomyinanattempttocompletemissingorunclearareasintheexistedknowledge.Wealsohopethispapercanlayasolidfoundationforexperimentalrattemporalbonesurgeries,andpromoteinformationexchangeamongcolleagues,aswellasprovidingusefulguidancefornoviceresearchersinthefieldofhearingresearchinvolvingrats.

简介：Trimethyltin(TMT)isanoccupationalandenvironmentalhealthhazardbehavingasapotentneurotoxinknowntoaffectthecentralnervoussystemaswellastheperipheralauditorysystem.However,themechanismsunderlyingTMT-inducedototoxicityarepoorlyunderstood.ToelucidatetheeffectsofTMTonthecochlea,asingleinjectionof4or8mg/kgTMTwasadministeredintraperitoneallytoadultrats.Thecompoundactionpotential(CAP)thresholdwasusedtoassessthefunctionalstatusofthecochleaandhistologicaltechniqueswereusedtoassesstheconditionofthehaircellsandauditorynervefibers.TMTat4mg/kgproducedatemporaryCAPthresholdelevationof25-60dBthatrecoveredby28dpost-treatment.Althoughtherewasnohaircelllosswiththe4mg/kgdose,therewasanoticeablelossofauditorynervefibersparticularlybeneaththeinnerhaircells.TMTat8mg/kgproducedalargepermanentCAPthresholdshiftthatwasgreatestatthehighfrequencies.TheCAPthresholdshiftwasassociatedwiththelossofouterhaircellsandinnerhaircellsinthebasal,high-frequencyregionofthecochlea,considerablelossofauditorynervefibersandasignificantlossofspiralganglionneuronsinthebasalturn.Spiralganglionneuronsshowedevidenceofsomashrinkageandnuclearcondensationandfragmentation,morphologicalfeaturesofapoptoticcelldeath.TMT-induceddamagewasgreatestinthehigh-frequency,basalregionofthecochleaandthenervefibersbeneaththeinnerhaircellswerethemostvulnerablestructures.

简介：AbstractObjective:The study objective was to investigate whether endogenous glucocorticoids directly impact the functions and proliferation/apoptosis of ovarian granulosa cells.Methods:Primary rat ovarian granulosa cells were cultured and treated with graded concentrations of corticosterone either alone or in the presence of the indicated drugs. After 48 h of treatment, the cells and growth media were collected to measure intracellular and extracellular progesterone/estradiol concentrations, and steroid secretion ratios were obtained by parameter calculation. The number of granulosa cells was determined by Cell Counting Kit-8. To determine the impact on cell numbers, granulosa cell proliferation was detected using the BrdU incorporation method and cell apoptosis was detected by flow cytometry.Results:First, high corticosterone concentrations significantly stimulated progesterone synthesis/secretion and inhibited estradiol synthesis in cultured granulosa cells. Second, accompanied by follicle-stimulating hormone, high corticosterone concentrations promoted progesterone synthesis/release and estradiol release. Last, high corticosterone concentrations increased the cell number and suppressed apoptosis but did not induce cell proliferation.Conclusions:These indicate that high glucocorticoid concentrations may play luteotropic roles in the functions and number of corpora lutea.

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简介：Clusterinisa75-80kDaheterodimericglycoprotein,thatisproducedinmosttissuesbutwhichexactbiologicalroleisstillnotclear.Particularly,itsroleinprotectionorpromotionofapoptosisisheavilydisputed,sincedatasupportingbothviewshavebeenreportedinseveralindependentstudies.Toclarifythisissue,andalsotodeterminewhetherclusterinexpressionitselfmightbeaffectedbyapoptosis,inthepresentstudy,ratthymocytesweretreatedwithdexamethasone,-asyntheticglucocorticoidthatelicitsapoptosisinthymocytes-,andclusterinmRNAexpressionwasanalyzedbysemi-quantitativeRT-PCRbeforeandafterinductionofapoptosis.Interestingly,neitherthetreatmentwithdexamethasoneinvitronortriggeringofapoptosisinvivoup-regulatedclusterinexpression,opposingtheviewthatclusterinisinvolvedinapoptoticprocesses.Ontheotherhand,anewclusterinmRNAisoformwasdetectedandisolated,whoseexpressionwasrestrictedtofreshlyisolatedthymocytes.Thisnovelisoformlacksthepost-translationalproteolyticcleavagesiteandisthereforepredictedtoencodeamonomericprotein.Thebiologicalfunctionundernormalcircumstances,however,willneedfurtherinvestigationsforclarification.Whileapoptosiscouldnotmodulateclusterinexpression,activationofthymocyteswithconcanavalinAandinterleukin-2resultedinup-regulationofclusterinmRNAlevel,indicatingthatclusterinexpressionisratherunderthecontrolofcellactivation-mediatedratherthanapoptosis-inducedsignals.

简介：Rats(Rattusnorvegicus)havemanyadvantagesovermiceinscientificstudies,forexample,theyaremorerelevanttohumaninphysiologicalandpharmacologicalresponses.Therefore,ratsarebroadlyusedinexperimentalstudies.Therecentbreakthroughinthegenerationofratembryonicstemcells(rESCs)opensthedoortoapplicationofgenetargetingtocreatemodelsforthestudyofhumandiseases.Inaddition,theinvitrodifferentiationofrESCsintoderivativesofthreegermlineswillserveasapowerfultoolandresourcefortheinvestigationofmammaliandevelopment,cellfunction,tissuerepair,anddrugdiscovery.However,thedistinctcultureconditionandsignalinhibitor-dependedmaintenanceofrESCsstandasaconsiderablechallengeforitsinvitrodifferentiation.Toaddressit,weinvestigatedwhetherrESCsarecapableofformingterminaldifferentiatedcardiomyocytes.Wefoundthattheembryoidbodies(EBs)-basedmethodusedinmouseESC(mESC)differentiationfailedtoworkinthecultivationofrESCs.WethenmodifiedthedifferentiationprotocolandsuccessfullydevelopedaninvitrodifferentiationsystemtodifferentiaterESCsintothreeembryonicgermlayers.Byusingthismethod,therESCsformspontaneousbeatingcardiomyocyteswiththepropertiessimilartothosederivedfromfetalratheartsandmESCs.Thisuniquecellularsystemwillprovideanewapproachtostudytheearlydevelopmentandcardiacfunctionaswellastoperformpharmacologicaltestandcelltherapystudy(Grants:theStateMajorResearchProgramofChina(2009ZX09503-024,2010CB945603)andCAS(XDA01030000).

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简介：Thereisaccumulatingevidencethatcysteinesulfenation（cys-SOH）inproteinsplaysanimportantroleincellularresponsetooxidativestress.Thepurposeofthepresentstudywastoidentifymitochondrialproteinsthatundergochangesincys-SOHduringaging.Studieswereconductedinratswhentheywere5or30monthsofage.FollowingblockingoffreeproteinthiolswithN-ethylmaleimide,proteinsulfenicacidswerereducedbyarsenitetofreethiolgroupsthatweresubsequentlylabeledwithbiotin-maleimide.Sampleswerethencomparativelyanalyzedbytwo-dimensionalWesternblots,andproteinsshowingchangesinsulfenationwereselectivelyidentifiedbymassspectrometrypeptidesequencing.Asaresult,fiveproteinswereidentified.Proteinsshowinganage-relateddecreaseinsulfenationincludepyruvatecarboxylaseandpyruvatedehydrogenase;whilethoseshowinganage-relatedincreaseinsulfenationincludeaconitase,mitofilin,andtubulin（α-1）.Resultsofthepresentstudyprovideageneralpictureofmitochondrialproteinsulfenationinbrainoxidativestressandimplicatetheinvolvementofproteinsulfenationinoveralldeclineofmitochondrialfunctionduringbrainaging.

简介：BACKGROUND:Thecorticospinaltractisthecorestructureofcerebralcontrolofextremitymovementandplasticity,whichareprerequisitesformovementrehabilitationafterbraininjury.Themeasurementandassessmentofplasticitychangeswithinthecorticospinaltracthasbecomeoneofthekeygoalsinthisfield.OBJECTIVE:Toexploretheeffectsofbiotinylateddextranamine(BDA)asaneuraltracerintheratcorticospinaltractandthepossibilitiesofassessingplasticitywithinthecorticospinaltract.DESIGN:Anobservationalexperiment.SETTING:DepartmentofAcupunctureofChineseMedicalCollege,ChongqingMedicalUniversity,DepartmentofNeurology,theSecondAffiliatedHospital,ChongqingMedicalUniversity.MATERIALS:EighteenmaleadultSpragueDawley(SD)ratsofcleangrade,weighing200-250g,wereprovidedbytheexperimentalanimalcenterofChongqingMedicalUniversity.Theanimalproceduresinthisstudywereinaccordancewiththeanimalethicsstandards.BDAwasprovidedbyVectorLaboratoriesCompany(USA,catalogueSp-1140;serialnumberR0721).METHODS:ThisexperimentwasperformedintheLaboratoryofChongqingMedicalUniversitybetweenSeptemberandDecember2006.AdultSDratswereusedintheexperimentand15%BDAwasinjectedslowlywithamini-syringethroughtworound(3mmdiameter)holesintotheleftsensoryandmotorcortex.Thecenterofoneholewaslocated3mmanteriorfromtheanteriorfontaneland1.5mmleftofthemidline;thesecondholewaslocated1.5mmposteriorfromtheanteriorfontaneland4mmleftofthemidline.Threeinjectionsweremadeateachholeatthreedifferentlevels:1.4,1.2,and1mmventralfromthesurfaceoftheflatskull.After14days,thebrainsandspinalcordswereremovedandfrozen.SectionswerecutonacryostatandBDAtransportationabsorbedbyaxonswasobservedunderafluorescencemicroscope.MAINOUTCOMEMEASURES:AxonalabsorptionandtransportationofBDAwasobservedunderfluorescencemicroscope.RESULTS:EighteenS

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简介：MicroRNAs(miRNAs)aredynamicallyregulatedduringneurodevelopment,yetfewreportshaveexaminedtheirroleinspinabifida.Inthisstudy,weusedanestablishedfetalratmodelofspinabifidainducedbyintragastricallyadministeringoliveoil-containingall-transretinoicacidtodamsonday10ofpregnancy.Damsthatreceivedintragastricadministrationofall-transretinoicacid-freeoliveoilservedascontrols.ThemiRNAexpressionprofileintheamnioticfluidofratsat20daysofpregnancywasanalyzedusinganmiRNAmicroarrayassay.Comparedwiththatincontrolfetuses,theexpressionofmiRNA-9,miRNA-124a,andmiRNA-138wassignificantlydecreased(>2-fold),whereastheexpressionofmiRNA-134wassignificantlyincreased(>4-fold)intheamnioticfluidofratswithfetusesmodelingspinabifida.Theseresultswerevalidatedusingreal-timequantitativereverse-transcriptionpolymerasechainreaction.HierarchicalclusteringanalysisofthemicroarraydatashowedthatthesedifferentiallyexpressedmiRNAscoulddistinguishfetusesmodelingspinabifidafromcontrolfetuses.OurbioinformaticsanalysissuggestedthatthesedifferentiallyexpressedmiRNAswereassociatedwithmanycytologicalpathways,includinganervoussystemdevelopmentsignalingpathway.ThesefindingsindicatethatfurtherstudiesarewarrantedexaminingtheroleofmiRNAsthroughtheirregulationofavarietyofcellfunctionalpathwaysinthepathogenesisofspinabifida.Suchstudiesmayprovidenoveltargetsfortheearlydiagnosisandtreatmentofspinabifida.