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简介：Inthepresentstudy,theeffectofblockageofthecostimulatorysignalCD86attimeofimplantationontheexpressionsofTGF-β1,MMP-9,TIMP-3andPAI-1proteinsatthematernal-fetalinterfaceandtheoutcomeofpregnancyinmurineabortion-pronemodelwasinvestigated,inwhichtheCBA/JxDBA/2matingswereusedastheabortion-pronemodelandtheCBA/J×BALB/cmatingsusedasthenormalpregnantmodel.Thestudywasperformedinfollowingthreegroups:2groupsoftheabortion-pronemodel,whichwereexperimentalgroupandcontrolexperimentalgroup,and1groupofnormalpregnantmodel,andeachgrouphad10pregnantCBA/Jmiceexclusively.FemalepregnantCBA/Jmiceintheexperimentalgroupreceivedanintraperitoneal(i.p.)injectionof100μgofantimouseCD86mAbin200μlofPBSatday4.5ofgestation,andtheirrelevant-isotopematchedratIgG2bwasadministratedinthecontrolexperimentalgroupwiththesamedosageandatsametime.Forthenormalpregnantgroup,notreatmentwasgiven.ThepregnantCBA/Jmicewerekilledonday13.5ofgestation.Then,theembryoresorptionratewascalculatedandtheexpressionsofTGF-β1,MMP-9,TIMP3andPAI-1weredetectedbyusingimmunohistochemicalmethods.Itwasdemonstratedthattheembryoresorptionrateintheexperimentalgroupwassignificantlyreducedincomparisonwiththatinthecontrolexperimentalgroup(x2=7.441,P=0.006),buttherewasnosignificantdifferencewiththatinnormalpregnantgroup(x2=0.016,P=0.898).TheexpressionsofTGF-β1andPAI-1intheexperimentalgroupweresignificantlyincreasedincomparisonwiththatinthecontrolexperimentalgroup(P=0.010,P=0.003,respectively),withnosignificantdifferencefromthatinthenormalpregnantgroup(P=0.500).However,theexpressionofMMP-9intheexperimentalgroupwassignificantlyreducedincomparisonwiththatinthecontrolexperimentalgroup(P=0.012)withnosignificantdifferencefromthatinthenormalpregnantgroup(P=0.500).Theexpression

简介：ExposureofnaivemurineCD4^+TlymphocytestosuperantigensuchasstaphylococcalenterotoxinB(SEB)inducesastrongproliferativeresponse.ProlongedexposureorsubsequentrestimulationoftherespondingTcellpopulationwithSEBleadstotheapoptoticeventsofactivation-inducedcelldeath(AICD).ThesignalingmechanismresponsiblefortheAICDisatargetofintensiveinvestigation.However,theprecisedownstreamsignahngpathwaysofSEB-inducedAICDremainsunclear.Ourresultshereshowthatthesequentialactivationofcaspase-1/ICE-hkeandcaspase-3/CPP32-hkecysteineproteasesprobablyplaysaroleinthesignalingtransductionofSEB-inducedAICD,butcaspase-3/CPP32-hkeproteasesactivationdoesnotdependoncaspase-1-likeproteasesactivation.HerbimycinA,aspecificinhibitorofproteintyresinekinases,inhibitcaspase-3/CPP32-1ikecysteineproteasesactivation.However,itdoesnotpreventDNAfragmentationofCD4^+TcellsapoptosisinducedbySEB.TheseresultsindicatethatproteintyrosinekinasespathwayisprobablyinvolvedinthesignalingtransductionofCD4^+TcellsapoptosisinducedbySEBand“crosstalks”withthepathwayofcaspase-3/CPP32-1ikeproteasesactivation.

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简介：ToobservetheeffectofGardeniaextractZGontheadsorptionquantityofherpessimplexvirustype1(HSV-1)soastoexplorethemechanismofitsantiviralactivity,fluoresceinisothiocyanate(FITC)wasusedasthefluorescentprobetolabelvirusesandheparinsodiumwasusedascontrol.Meanwhile,theeffectofGardeniaextractZGontheadsorptionquantityonthesurfaceofHep-2cellswasdeterminedbyflowcytometry.ItwasdemonstratedthatadsorptionofHSV-1onthesurfaceofHep-2cellsexhibitedthecharacterofsaturationandspecificityandheparinsodiumcouldpreventattachmentofvirusesonthesecells.Theseresultsareinaccordwiththosereportedpreviously.Itwasalsoprovedthatthemannerofdrug-usepriortoadsorptionorsimultaneoususeofdrugandadsorptionwasbetterthanadsorptionpriortodrug-use,andtheinhibitionratesoftheformerandlattermannerwere84.76%and82.92%respectively.Threemannersofdrug-usewithGardeniaextractZGwerealleffectivetoreducetheadsorptionquantityofviruses,especiallythemannerofsimultaneoususeofdrugandadsorptionwithanadsorptioninhibitionrateof68.46%.Fromtheaboveobservation,itisapparentthatthemechanismofanti-viralactivityofGardeniaextractZGmaybeviaseveralstepsinvolvedintheHSV-1adsorption.

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简介：WeareracingwithHIV-1,theetiologicagentforAIDSinhumanbeings[1,2],withtwopossibleendconsequences:ifwewin,HIV-1willbeunderourcontrolbyimmunologicortherapeuticmeasures;ifHIV-1wins,theSIVAfricanmonkeys'storywouldrepeatinhumans,i.e.,onlythefewindividualsthatarenotkilledbythevirus

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简介：Wehavepreviouslydemonstratedtheabilityofmalariaparasitestointerferewithspecificimmuneresponses.CD4Tcellsspecifictoparasiteantigens,butnotCD4Tcellsspecifictoanirrelevantantigen,ovalbumin(OVA),aredeletedviaapoptosisduringmalariainfection.Itisofinterest,therefore,toinvestigatetheimmuneresponsesthatdevelopedfollowingvaccinationwiththe19kDacarboxylterminusofthemerozoitesurfaceprotein1(MSP119)inmicethathadpreviouslyexperiencedmalariainfection.Inthisstudy,pre-exposureofmicetoPlasmodiumyoeliielicitednativeanti-MSP119antibodyresponses,whichcouldbeboostedbyvaccinationwithrecombinantMSP119，Likewise,infectionofMSP119-primedmicewithPlasmodiumyoelii(P.yoelii)ledtoanincreaseofanti-MSP119antibodies.MSP119vaccinationofmalariapreexposedmiceorimmunizationbyinfection/cureofMSP119-primedmiceenabledthemicetosurvivechallengeinfection,withtheformergrouphavingslightlylowerparasitaemia.Thedatasuggestthatexposuretomalariainfectionprimesanaturalimmuneresponsewhichcanbeboostedbyvaccination.Thisinformationisrelevanttothedevelopmentofavaccineforuseinindividualslivinginmalaria-endemicareas.

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简介：ToexplorethemechanismoftheinhibitionofHIV-1byMycoplasmafermerttans,culturesupernatantsandthallodicproteinsfromM.fermerttansPG18werepreparedandtheproteincomponentsofthesupernatantswerepurifiedwithhighperformanceliquidchromatography(HPLC).Theinhibitoryactivitiestoreversetranscriptase(RT)andthenucleaseactivitiesweredetected;theinfluenceofM.fermerttansonIL-10secretionbybothnormalandH1V-1infectedhumanPBMCweredetermined,andtheinhibitoryeffectofrhIL-10onH1V-1replicationwasdetectedwithEI,ISAmethod.Theresultsshowedthatthepurifiedproteinswithamolecularweightof67-100kDaor10-25kDashoweda36%or34%inhibitoryac-tivitytoRTandpartialnucleaseactivity.ThethallodicproteincouldinducebothnormalandH1V-1infectedPBMCtosecretIL-10remarkably,andtothelatter,thiseffectwasmoreapparent.WhilerhIL-10couldinhibitreplicationofH1V-1inPB-MCinvitroinadose-dependantmanner.ItconcludesthattheinhibitoryeffectoftheM.fermentansPG18culturesupernatantsonRTandthepromotingeffectofPG18thallodicproteinonIL-10secretioninPBMCexplainthemechanismsofinhibitiontoHIV-1byM.fermentansPG18.

简介：摘要：目的 通过建立骨关节炎模型探讨整合素pI和GIT 1对软骨细胞的影响，及二者之间的调控关系。对临床上骨性关节炎的治疗起指导作用。 方法 采用约一周龄的年乳大鼠20只，用定量PCR和Western Blotting检测对照组、pcDNA3.1空载体转染组、pcDNA3.1-GIT 1过表达组、pcDNA3 . I -integrin-p1过表达组、integrin-p 1 siRNA组和NC siRNA组中，integrin-p1和GIT1的mRNA和蛋白质的表达水平，来判断integrin-p1和GIT1之间的调控关系。结论 integrin-p1可以调控GIT1的表达，GTI1可能是位于integrin-pI下游的一个关键分子。

简介：ToclarifytheroleofAPOBEC3G(A3G)incellulardefenseagainsthepatitisBvirus(HBV),theexpressionofA3GinnormalhumanliverandtheregulationoftheA3Gexpressioninhep-atomacellline(HuH-7)wereinvestigated.ExpressionlevelofAPOBEC3smRNAinhumanliverwasdeterminedbyRT-PCR.HuH-7andHepG2cellsweretreatedwithvariousconcentrationsofIFN-α(0U/ml,100U/ml,500U/ml,1000U/ml)for12h.ThemRNAlevelsweremeasuredbyaquantitativeRT-PCR,theresultswerenormalizedrelativetothespecimenswithoutIFN-αstimulation.TotalproteinofHuH-7cellstreatedwithvariousconcentrationsofIFN-αfor48hwassubjectedtoWesternblotanalysis.Forreportergeneassay,HuH-7cellsweretransfectedwiththereporterplasmidscontainingIRF-Esitesanditsmutantswithdifferentlengths.Thenthecellsweretreatedwithorwithout1200U/mlIFN-aforadditional12h(1000U/ml)after24hoftransfection,andthecelllysatewaspreparedandassayedforluciferaseactivity.ItwasfoundthatnormalhumanliverexpressedthemRNAofA3G.A3GmRNAexpressioninHuH-7andHepG2cellswereup-regulatedbyIFN-αstimulationinadose-depen-dentmanner.WesternblotanalysisindicatedthatA3GproteinexpressionwasalsoenhancedbyIFN-αstimulation.SequenceanalysisshowedtheexistenceofputativesitesofIFNregulatoryfactorelement(IRF-E)in5'regionofA3Ggeneupstreamtheinitiationcodon.IFN-αstimulationresultsin6-to8-foldincreaseinluciferaseactivityincellstransfectedwiththeplasmidcontainingIRF-Esitesofthe5'upstreamsequences,whereasluciferaseactivitydidnotchangeincellstransfectedwiththeplasmidcontainingmutantIRF-EsitesorwithoutIRF-Esites.Asaconclusion,A3Gareexpressedinnormalhumanliver.A3Gexpressionwasup-regulatedbyIFN-αstimulationinhepatomacellsandcouldbeinvolvedinhostdefensemechanismsagainstHBV.ERF-Esitein5'regionofAP0BEC3Ggeneupstreamtheinitiationcodonplaysanimportantroleinthisp

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简介：ToinvestigatethephenotypicknockoutofHIV-1chemokinecoreceptorCXCR4andCCR5byintrakinesanditsinhibitoryeffectonHIV-1infection.PrimaryhumanPBLsweretransducedwiththerecombinantvectorpLNCX-R-K-S-K(△NGFR),followedbyanti-NGFR/anti-IgG-magneticbeadmethodselectionandFCMdetection.ThetransducedPBLswereinfectedwithDP1HIV-1virusthereafterenvelope-mediatedsyncytiumformationandp24detectionwerecarriedouttostudytheblockageofHIV-1infectionbyco-inactivationofCCR5andCXCR4.pLNCX-R-K-S-K(△NGFR)-transducedPBILswereisolatedwithananti-NGFR/anti-IgG-magneticbeadmethod.Afterisolation,about70%ofthePBLswerepositivefortheNGFRmarker.WhenthetransducedPBLswereinfectedwithDP1HIV-1virus,envelop-mediatedsyncytiumformationwasalmostcompletelyinhibitedbypLNCX-R-K-S-K(△NGFR)transfection.Also,p24antigenwasverylowintheculturesofpLNCX-R-K-S-K(△NGFR)transducedPBLs.pLNCX-R-K-S-K(△NGFR)transductioninhibitedtheproductionofDP1p24antigenby15%,43%and19%ondays4,7and10respectively.ThelymphocyteswiththephenotypicknockoutofCCR5andCXCR4couldprotectprimaryhumanPBLsfromDP1HIV-1virusinfection.