简介：ＩＮＴＲＯＤＵＣＴＩＯＮＭａｇｎｅｔｉｃｓｔｉｍｕｌａｔｉｏｎｉｓｔｈｅｐｒｏｃｅｓｓｏｆｓｔｉｍｕｌａｔｉｎｇｅｘｃｉｔａｂｌｅｔｉｓｓｕｅｂｙａｔｉｍｅ－ｖａｒｙｉｎｇ，ｉｎｔｅｎｓｅｍａｇｎｅｔｉｃｆｉｅｌｄｗｈｉｃｈｉｎｄｕｃｅｓａｎｅｌｅｃ...

简介：TotesttheosteoinductiveactivityoftheRBXdevelopedbyus,eightdifferentdoses(4,2,1,0.5,0.25,0.125,0.075,and0.0325milligrams)ofbovinebonemorpho-geneticprotein(bBMP)wereselectedonthebasisoftheresultsofectopicassaysandwerereconstitutedwithtenmilligramsoftheantigen-extracted,partialdecalcifiedcalfcancellonsbonewhichservedasacarrierforthebBMP.Theywereimplantedin

简介：客观：导出施主的不成熟的树枝状的房间(imDC)的使用成为了一条有希望的途径导致有免疫力的忍耐或有免疫力的hyporesponsiveness。然而，导出施主的imDC需要被收获一些天并且在移植前在5-10天内输了进接受者，它在施主机关主要从死尸被收获的一个临床的背景实际上是不可能的。而且，导出施主的imDC可能被抵消导致的有免疫力的忍耐或有免疫力的hyporesponsiveness的allogeneic反应清除。在我们的学习，我们进一步探索了donor-antigen-unloaded导致的有免疫力的hyporesponsiveness的内在的机制由在肝移植前在1天内输这些imDC进老鼠的导出接受者的imDC。这份报纸是导出接受者的imDC和它在老鼠的肝接枝的保护到有免疫力的hyporesponsiveness的机制由donor-antigen-unloaded导致了的学习。方法：40只SD老鼠(施主)和40只男Wistar老鼠(接受者)随机被划分成4个组：控制，cyclosporineA(CsA)，成熟DC(mDC)，和imDC；带着为每个组的10只SD老鼠和10只Wistar老鼠。尖锐接枝拒绝的动物模型带着这些老鼠被建立。相应治疗在移植前后被给。在控制组，Wistar老鼠没接受除肝移植以外的处理。在CsA组，Wistar老鼠加CsA治疗经历了肝移植(10mg/kg湩?湵敮散獳牡?楴敭愠摮洠瑡牥慩獬椠?桴?潣牵敳漠?硥数楲敭瑮琠?敧?摩慥?浩条獥

简介：Objective:Thispaperaimsatmeasurementenhancedeffectofoxidizedlipoprotien(a)[oxLp(a)]onpermeabilityofmonolayerendothelialcellsandrelationshipwithreactiveoxygenspecies(ROS)generationanddesmogleins(DSGs)expression.MethodsandResults:Transendothelialpermeabilitywasassayedbytranswellandreactiveoxygenspecies(ROS)wasdeterminedbyDCFH-DAstaining.RT-PCRwascarriedouttodetermineDSGlandDSC2expressioninmRNA,respectively.TransendothelialpermeabilitywasenhancedbyoxLP(a)doseandtimedependently.Themostmarkedeffectappearedataconcentrationof100mg/L,Transendothelialpermeabilityreachedthemaximumvalueafter2hofFITC-dextranaddition,andthengraduallydecreasedafter4h.oxLp(a)inducesthegenerationofcellularreactiveoxygenspecies(ROS),andthiseffectcouldbeinhibitedbysuperoxidedismutase(SOD).IncubationofHUVECswithoxLp(a)resultedinadoseandtime-dependentdown-regulationofDSGlandDSC2expressionattranscriptionallevel.Conclusion:PermeabilityofmonolayerendothelialcellswasenhancedbyoxLp(a)whichisrelatedtoup-regulatingROSformationanddown-regulatingdesmogleinsexpression.

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简介：提高transdermal药交货技术的非侵略的激光被调查了。切换Q的Nd的532nm的第二泛音波长:有15ns的脉搏持续时间的钇铝柘榴石激光被用来聚乙烯表在药答案的表面上盖住在一个黑人上照耀，并且因此在答案生产了压力波浪。当皮肤模型和试剂respectively.Fluorescence显微镜被雇用在激光处理以后经由皮肤样品检验药交货的机制，猪的皮肤和玫瑰精B被使用。实验表明在激光的照明下面的玫瑰精B的穿入深度与激光横梁的精力密度增加了。在70mJ/cm2的激光精力密度的20个激光机会以后，插入深度在30分钟到达了440m，没有激光照明，它作为那是大约三次。一可能的解释是导致激光的压力波浪在皮肤织物的阶层corneum形成了microchannels。这些microchannels比小囊、细胞间的路径通过SC为玫瑰精B的渗入提供了更有效的路径。药答案通过隧道在集中坡度下面扩散了进SC。

简介：Curcumin,adietaryphytochemical,exhibitsmultifunctionalnaturalproductwithregulatoryeffectsoninflammation.However,thepoorbioavailabilitylimitsitsclinicalapplications.Thus,wedesignedandsynthesizedanovelmonocarbonylanalogueofcurcuminB7andtheirinhibitionagainstmonocytechemotacticprotein-1（MCP-1）andinterleukin-8（IL-8）releasewasevaluatedinH2O2-stimulatedhumanvascularendothelialcells（ECs）inadose-responsivemanner,whileexhibitingnocytotoxicityinECs.Takentogether,theseinsightsonthenovelcompoundB7mayserveaspotentialagentsforthetreatmentofatherosclerosis.

简介：Thispaperaimstotheresearchoftheimpactoffluidshearstressontheadhesionbetweenvascularendothelialcellsandleukocyteinducedbytumornecrosisfactor-α(TNF-α)bymicrofliudicchiptechnology.Microfluidicchipwasfabricatedbysoftlithograph;Endothelialmicrofluidicchipwasconstructedbyoptimizingtypesoftheextracellularmatrixproteinsmodifiedinthemicrochannelandcellincubationtime;humanumbilicalveinendothelialcellsEA.Hy926linedinthemicrochannelwereexposedtofluidshearstressof1.68dynes/cm~2and8.4dynes/cm~2respectively.Meanwhile,adhesionbetweenEA.Hy926cellsandleukocytewasinducedbyTNF-αunderaflowcondition.EA.Hy926cellculturedinthestaticconditionwasusedascontrolgroup.Thenumbersoffluorescently-labeledleukocyteinmicrochannelwerecountedtoquantizetheadhesionlevelbetweenEA.Hy926cellsandleukocyte;cellimmunofluorescencetechniquewasusedtodetecttheintercellularadhesionmolecule(ICAM-1)expression.TheconstructedendothelialmicrofluidicchipcanaffordtothefluidshearstressandrespondtoexogenousstimulusofTNF-α;comparedwiththeadhesionnumbersofleukocyteincontrolgroup,adhesionbetweenEA.Hy926cellsexposedtolowfluidshearstressandleukocytewasreducedunderthestimulusofTNF-αataconcentrationof10ng/ml(P<0.05);leukocyteadhesionwithEA.Hy926cellsexposedtohighfluidshearstresswasreducedsignificantlythanEA.Hy926cellsincontrolgroupandEA.1Hy926cellsexposedtolowfluidshearstress(P<0.01);theregulationmechanismoffluidshearstresstotheadhesionbetweenEA.Hy926cellsandleukocyteinducedbyTNF-αwasthroughthewayofICAM-1.Theendothelialmicrofluidicchipfabricatedinthispapercouldbeusedtostudythefunctionsofendothelialcellinvitroandprovideanewtechnicalplatformforexploringthepathophysiologyoftherelatedcardiovascularsystemdiseasesunderaflowenvironment.