简介：Regulatingserotoninexpressioncanbeusedtotreatpsychoticdepression.Mifepristone,aglucocorticoidreceptorantagonist,isaneffectivecandidateforpsychoticdepressiontreatment.However,theunderlyingmechanismrelatedtoserotonintransporterexpressionispoorlyunderstood.Inthisstudy,weclonedthehumanbrainserotonintransporterintoXenopusoocytes,toestablishaninvitroexpressionsystem.Two-electrodevoltageclamprecordingswereusedtodetectserotonintransporteractivity.Ourresultsshowthatmifepristoneattenuatesserotonintransporteractivitybydirectlyinhibitingtheserotonintransporter,andsuggeststhattheserotonintransporterisapharmacologicaltargetofmifepristoneforthetreatmentofpsychoticdepression.

简介：Anewwaveletvarianceanalysismethodbasedonwindowfunctionisproposedtoinvestigatethedynamicalfeaturesofelectroencephalogram(EEG).TheexprienmentalresultsshowthatthewaveletenergyofepilepticEEGsaremorediscretethannormalEEGs,andthevariationofwaveletvarianceisdifferentbetweenepilepticandnormalEEGswiththeincreaseoftime-windowwidth.Furthermore,itisfoundthatthewaveletsubbandentropy(WSE)oftheepilepticEEGsarelowerthanthenormalEEGs.

简介：Thebraincontrolsvirtuallyallbodyfunctions,bothinternallyandininteractionwiththeexternalenvironment.Asthebasicbodyanatomyofallvertebrateshasabilateralsymmetry,structuresandfunctionsofvertebratebrainsarealsoorganizedaccordingtothisfundamentalanatomicalprincipletomeetallsensory,motor,andinternalrequirementsofbodycontrol.Consequently,particularpartsorfunctionsofthebodyarecontrolledbyparticularbrainstructures.Formammalswhosebrainsonlyhaveaverylimitedcapacityto

简介：AIM:Todeterminethealterationsinratenterocytemitochondrialrespiratoryfunctionandenzymeactivitiesfollowingtraumaticbraininjury(TBI).METHODS:Fifty-sixmaleSDratswererandomlydividedintosevengroups(8ratsineachgroup):acontrolgroup(ratswithshamoperation)andtraumaticbraininjurygroupsat6,12,24h,days2,3,and7afteroperation.TBImodelswereinducedbyFeendy’sfree-fallingmethod.Mitochondrialrespiratoryfunction(respiratorycontrolratioandADP/Oratio)wasmeasuredwithaClarkoxygenelectrode.TheactivitiesofrespiratorychaincomplexⅠ-Ⅳandrelatedenzymesweredeterminedbyspectrophotometry.RESULTS:Comparedwiththecontrolgroup,themitochondrialrespiratorycontrolratio(RCR)declinedat6handremainedatalowleveluntilday7afterTBI(control,5.42±0.46;6h,5.20±0.18;12h,4.55±0.35;24h,3.75±0.22;2d,4.12±0.53;3d,3.45±0.41;7d,5.23±0.24,P<0.01).Thevalueofphosphate-to-oxygen(P/O)significantlydecreasedat12,24h,day2andday3,respectively(12h,3.30±0.10;24h,2.61±0.21;2d,2.95±0.18;3d,2.76±0.09,P<0.01)comparedwiththecontrolgroup(3.46±0.12).Twotroughsofmitochondrialrespiratoryfunctionwereseenat24handday3afterTBI.TheactivitiesofmitochondrialcomplexⅠ(6h:110±10,12h:115±12,24h:85±9,day2:80±15,day3:65±16,P<0.01)andcomplexⅡ(6h:105±8,12h:110±92,24h:80±10,day2:76±8,day3:68±12,P<0.01)wereincreasedat6hand12hfollowingTBI,andthensignificantlydecreasedat24h,day2andday3,respectively.However,therewerenodifferencesincomplexⅠandⅡactivitiesbetweenthecontrolandTBIgroups.Furthermore,pyruvatedehydrogenase(PDH)activitywassignificantlydecreasedat6handcontinuedupto7dafterTBIcomparedwiththecontrolgroup(6h:90±8,12h:85±10,24h:65±12,day2:60±9,day3:55±6,day7:88±11,P<0.01).Thechangesinα-ketoglutaricdehydrogenase(KGDH)activityweresimilartoPDH,exceptthatthedecreaseinKGDHactivitybeganat12hafterTBI(12h:90±12,24h:80±9,day2:76±15,day3:68±7,

简介：Tomakecleartheprecisehemodynamicmechanismunderlyingtheanti-atherogenesisbenefitofenhancedexternalcouterpulsation(EECP)treatment,andtoinvestigatetheproperroleofsomeimportanthemodynamicfactorsduringtheatheroscleroticprogress,acomprehensivestudycombininglong-termanimalexperimentandnumericalsolvingwasconductedinthispaper.AnexperimentallyinducedhypercholesterolemicporcinemodelwasdevelopedandthechronicEECPinterventionwassubjected.Basichemodynamicmeasurementwasperformedinvivo,aswellasthearterialendothelialsampleswereextractedforphysiologicalexamination.Meanwhile,anumericalmodelwasintroducedtosolvethecomplexhemodynamicfactorssuchasWSSandOSI.TheresultsshowthatEECPtreatmentresultedinsignificantincreaseoftheinstantlevelsofarterialWSS,bloodpressure,andOSI.DuringEECPtreatment,theinstantOSIlevelofthecommoncarotidarteriesovercardiaccyclesraisedtoameanvalueof8.58×10-2±2.13×10-2.Meanwhile,thechronicinterventionofEECPtreatmentsignificantlyreducedtheatheroscleroticlesionsinabdominalaortasandtheendothelialcellularadherence.ThepresentstudysuggeststhattheuniquebloodflowpatterninducedbyEECPtreatmentandtheaugmentationofWSSlevelincardiaccyclesmaybethemostimportanthemodynamicmechanismthatcontributetoitsanti-atherogenesiseffect.Andasoneoftheindicesthatcausegreatconcernincurrenthemodynamicstudy,OSImaynotplayakeyroleduringtheinitiationofatherosclerosis.更多还原

简介：Glioblastoma(GBM)isoneofthemostlethalhumancancers.GenomicanalysesdefinethemoleculararchitectureofGBMandhighlightacentralfunctionformechanistictargetofrapamycin(mTOR)signaling.mTORkinaseexistsintwomultiproteincomplexes,namely,mTORC1andmTORC2.Thesecomplexesdifferintermsoffunction,regulationandrapamycinsensitivity.mTORC1iswellestablishedasacancerdrugtarget,whereasthefunctionsofmTORC2incancer,includingGBM,remainspoorlyunderstood.ThisstudyreviewstherecentfindingsthatdemonstrateacentralfunctionofmTORC2inregulatingtumorgrowth,metabolicreprogramming,andtargetedtherapyresistanceinGBM,whichmakesmTORC2asacriticalGBMdrugtarget.

简介：目的将观察在浆液嗜曙红血球cationic蛋白质(ECP)上联合传播艾灸和点注射的效果，类脂化合物peroxidase(LPO)和在有咳嗽变体气喘的病人的细胞的免疫。150个盒子全部的方法A满足了包括标准的人，被使随机化进三个组，50在每个组。传播艾灸和点注射在观察组被采用，在点注射组独自在传播艾灸组和点注射独自散布艾灸。然后，治疗学的功效在治疗的一堂功课以后被评估。结果恢复率和全部的有效的率在观察组分别地是50.0%和98.0%，对18.0%和86.0%在传播艾灸组织，14.0%和82.0%在点注射组织，显示出统计上重要的差别(P<0.01)。在治疗前，在ECP，LPO，CD3+，CD4+，CD4+/CD8+和CD8+的层次没有团体之间的统计上重要的差别，强迫的重要能力(FCV)，强迫的吐气的体积1(FEV1)，并且山峰吐气的流动(PEF)(P<0.05)。在治疗以后，在观察组的ECP和LPO层次是显著地在另外的二个组比那些减少的更多，显示出统计上重要的差别(P<0.01)；在观察组的CD3+，CD4+和CD4+/CD8+的层次显著地被提高，但是CD8+显著地被减少，显示出在另外的二个组的与那些相比的统计上重要的差别(P<0.01)；并且在观察组的肺功能索引(FVC，FEV1和PEF)是显著地在另外的二个组比那些提高的更多(P<0.05)。结论联合散布艾灸和点注射能显著地与咳嗽变体气喘在病人减少ECP和LPO的内容，改进细胞的免疫，增加CD3+，CD4+和CD4+/CD8+的内容，减少CD8+的内容并且改进肺功能。

简介：Nestin+neuronshavebeenshowntoexpresscholineacetyltransferase(ChAT)inthemedialseptum-diagonalbandofBrocainadultrats.Thisstudyexploredtheprojectionofnestin+neuronstotheolfactorybulbandthetimecourseofnestin+neuronsinthemedialseptum-diagonalbandofBrocainadultratsduringinjuryrecoveryafterolfactorynervetransection.Thisstudyobservedthatallnestin+neuronsweredouble-labeledwithChATinthemedialseptum-diagonalbandofBroca.Approximately53.6%ofnestin+neuronswereprojectedtotheolfactorybulbandco-labeledwithfastblue.Alargenumberofnestin+neuronswerenotpresentineachregionofthemedialseptum-diagonalbandofBroca.Nestin+neuronsinthemedialseptumandverticallimbofthediagonalbandofBrocashowedobviouscompensatoryfunction.Thenumberofnestin+neuronsdecreasedtoaminimumlaterthannestin–/ChAT+neuronsinthemedialseptum-diagonalbandofBroca.Theresultssuggestthatnestin+cholinergicneuronsmayhaveacloserconnectiontoolfactorybulbneurons.Nestin+cholinergicneuronsmayhaveastrongertolerancetoinjurythanNestin–/ChAT+neurons.Thedifferencebetweennestin+andnestin–/ChAT+neuronsduringtherecoveryprocessrequiresfurtherinvestigations.

简介：Prostatecancergene3(PCA3,alsoknownasDD3)isanewbiomarkerthatcouldimprovetheaccuracyofprostatecancerdiagnosis.Itisagreatbiomarkerwithfairlyhighspecificityandsensitivity.Theincidenceofprostatecancerisrisingsteadilyinmostcountries.Thecommonlyusedprostate-specificantigen(PSA)testoncegavepeoplehopeforearlydiagnosisofprostatecancer.However,thelowspecificityofthePSAtesthasresultedinalargenumberofunnecessarybiopsiesandovertreatment.Duringthepastdecade,manynewprostatecancerbiomarkershavebeenfound.Amongthese,PCA3isthemostpromising.Duetoitsgreatperformanceindistinguishingprostatecancerfromotherprostateconditions,PCA3couldlikelybeappliedforearlydiagnosisofprostatecancer,patientfollow-up,prognosisprediction,andtargetedtherapy.Afteryearsofresearch,wehaveobtainedsomeknowledgeaboutthesequenceofPCA3gene.WehavealsodeterminedtherelationshipbetweenPCA3andtheproliferationofprostatecancercellsandlearnedsomeinformationabouthowPCA3affectstumor-relatedgenesandproteins.APCA3scorehasbeencreated,andithasbeenusedinavarietyofstudies.SomeresearchershaveevenappliedPCA3totargetedtherapyandobtainedagoodeffectinvitro.Thisreviewdescribesthecurrentstateofresearch,andexploresthefutureprospectsforPCA3.更多还原

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.

简介：为了观察由在yin和yang顶点上呼吸增强并且减少操作的效果，与ischemic击在病人为膝关节的马达功能指。

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简介：在CD4系抄写因素ThPok和CD8系抄写因素之间的相互影响，老牛相关的抄写因素3(Runx3)，在T房间，开发广泛地被记录了。然而，很少在不变的自然漂亮T(iNKT)房间开发对这些抄写因素的角色被知道。限制CD1d的iNKT房间承诺CD4+CD8−和CD4−CD8−sublineages，它对抗原刺激作出回应与快速并且T助手(Th)的有势力版本1并且Th2cytokines。然而，以前的报告在ThPok缺乏的老鼠表明了CD8+NKT房间的一张新人口。在当前的学习，我们寻求了决定Runx3是否当ThPok不在时涉及CD8的重新表示和iNKT房间的功能。我们使用了缺乏Runx3，ThPok或两个的老鼠并且证实Runx3为在ThPok猛烈老鼠的CD8+iNKT房间的外观部分负责。另外，Runx3参予了有免疫力的反应在α的一个模型由iNKT房间调停了；-galactosylceramide-induced尖锐肝炎。这些结果显示Runx3为在ThPok缺乏的iNKT房间观察的phenotypic和功能的变化是关键的。