简介：Multidrug抵抗(MDR)是在癌症化疗的一个主要问题。MDR的最好已知的机制之一是ATP有约束力的盒子(ABC)的提高的表示运输ers。当人的ABC运输ers的一些成员被显示了与提高的表示引起抗药性时，另外的成员的在表示上是否能也在许多模型癌症房间线和诊所贡献抗药性，还没被知道。为介绍ABCtransporters的分析的表示的微数组和量的PCR数组的最近的开发帮助了处理这些问题。在这篇文章，有在在抗药性和chemo敏感预言识别ABCtransporter基因的ABCtransporter基因和他们的使用的有限或完整的表的各种各样的数组将被考察。

简介：TheobjectiveofthisstudyistoexploreapotentiallyeffectivetrainingmethodforthehospitalprofessionalstoeducatedrugusersandtoenhancetheirknowledgeofHIVinfection.Onehundredandsixtyonesubjects,whocamefrom13differentprovincesandwereadmittedinadrugreliefhospitalinBeijing,wererecruitedforthisstudy.Theaverageageofthesesubjectswas35.21±6.24yearold.Theaveragenumbersofyearsfordrugaddictionwere7years,andtheaveragenumbersofdrugrelieftreatmentreceivedinthepastwas5.5times.ThelevelofAIDSknowledgeofthesesubjects,includingpathogenicfactors,sourceofinfection,routeoftransmissionandpreventivemeasures,wereevaluatedbeforeandafterreceivingtheAIDSeducationaltrainingtothesedrugusers.Ourresultsshowedthattherewasastatisticallysignificantincrease(P＜0.01)intheknowledgeofHIVinfectionandpreventionamongthesesubjects.PositiveattitudeandbehavioraltendenciestowardHIVpreventionwerealsoimproved.Therefore,itisimperativeforthemedicalprofessionalstoincorporateAIDSeducationintodrugrelieftreatmenttoachievethemaximumeffectontheknowledgeofAIDSandimprovementofpositiveattitudesandbehaviorstowardHIVpreventionamongdrugusers.

简介：ApoptosisproducedinBcellsthroughFas(APO-1,CD95)triggeringisregulatedbysignalsderivedfromothersurfacereceptors:CD40engagementproducesupregulationofFasexpressionandmarkedsusceptibilitytoFas-inducedcelldeath,whereasantigenreceptorengagement,orIL-4Rengagement,inhibitsFaskillingandinsodoinginducesastateofFas-resistance,eveninotherwisesensitive,CD40-stimulatedtargets.SurfaceimmunoglobulinandIL-4RutilizeatleastpartiallydistinctpathwaystoproduceFas-resistancethatdifferentiallydependonPKCandSTAT6,respectively.Further,surfaceimmunoglobulinsignalingforinducibleFas-resistancebypassesBtk,requiresNF-κB,andentailsnewmacromolecularsynthesis.TerminaleffectorsofBcellFas-resistanceincludetheknownanti-apoptoticgeneproducts,Bcl-XLandFLIP,andanovelanti-apoptoticgenethatencodesFAIM(FasApoptosisInhibitoryMolecule).faimwasidentifiedbydifferentialdisplayandexistsintwoalternativelysplicedforms;faim-Sisbroadlyexpressed,butfaim-Lexpressionistissue-specific.TheFAIMsequenceishighlyevolutionarilyconserved,suggestinganimportantroleforthismoleculethroughoutphylogeny.InducibleresistancetoFaskillingishypothesizedtoprotectforeignantigen-specificBcellsduringpotentiallyhazardousinteractionswithFasL-bearingTcells,whereasautoreactiveBcellsfailtobecomeFas-resistantandaredeletedviaFas-dependentcytotoxicity.InadvertentoraberrantacquisitionofFas-resistancemaypermitautoreactiveBcellstoescapeFasdeletion,andmalignantlymphocytestoimpedeanti-tumorimmunity.

简介：<正>ThesusceptibilityofprimaryBcellstoFas(APO-1,CD95)-mediatedapoptosisisregulatedbysignalsderivedfromadditionalsurfacereceptors.CD40engagementproducesupregulationofFasexpressionandinducesmarkedsensitivitytoFas-inducedcelldeath,whereasBcellantigenreceptor(BCR)engagementinhibitsFaskillingandtherebyproducesFas-resistance,eveninotherwisesusceptible,CD40-stimulatedtargets.BCRsignalingforinducibleFas-resistancedevelopsoveraperiodof12hoursanddependson

简介：PTEN，phosphatidylinositol-3-kinase/AKT小径的一个否定管理者，是胰岛素发信号的一个重要调节的人。决定胰腺的Pten的新陈代谢的函数，我们产生了胰特定的Pten大美人(PPKO)鼠标。PPKO老鼠扩大了胰并且提高了acinar房间的增长。他们也展出了低血糖症，hypoinsulinemia，和改变的氨基的新陈代谢。尤其是，PPKO老鼠证明streptozotocin(STZ)的推迟的发作导致了糖尿病，到high-fat-diet(HFD)的偏导性的抵抗导致了糖尿病。在PPKO老鼠为抵抗调查机制到导致HFD的多糖症，我们在主要胰岛素应答的纸巾评估了AKTphosphorylation：肝，肌肉，和脂肪。我们发现在胰的Pten损失引起在肝发信号的AKT的举起。AKT和它的下游的底层GSK3尾的phosphorylation在PPKO老鼠的肝被增加，当没有Pten等位基因的可检测的切除，PTEN水平在PPKO老鼠的肝被减少时。戏剧性地揭示的Proteomics分析减少了在PPKO老鼠的肝78-kDa铺平调整葡萄糖的蛋白质(GRP78)，它可以也贡献用HFD喂的PPKO老鼠的更低的血葡萄糖水平。一起，我们的调查结果在新陈代谢的规定在肝揭示新奇回答到胰腺的缺点，把一种新尺寸加到理解糖尿病抵抗。

简介：

简介：Immatureembryosofricevarieties“Xiushui11”and“Chunjiang11”preculturedfor4dwereinfectedandtransformedbyAgrobacteriumtumefaciensstrainEHA101/pExT7(containingthespiderinsecticidalgene).Theresistantcalliweretransferredontothedifferentiationmediumandplantswereregenerated.Thetransformationfrequencyreached56%～72%measuredasnumbersofGeneticin(G418)-resistantcalliproducedand36%～60%measuredasnumbersoftransgenicplantsregenerated,respectively.PCRandSouthernblotanalysisoftransgenicplantsconfirmedthattheT-DNAhadbeenintegratedintothericegenome.InsectbioassaysusingT1transgenicplantsindicatedthatthemortalityoftheleaffolder(Cnaphalocrasismedinalis)after7dofleaffeedingreached38%～61%andthecorrectedmortalityofthestripedstemborer(Chilosuppressalis)after7dofleaffeedingreached16%～75%.Theinsectbioassayresultsdemonstratedthatthetransgenicplantsexpressingthespiderinsecticidalproteinconferredenhancedresistancetothesepests.

简介：WRKY抄写因素响应关於生命、不能生活的压力有许多规章的角色。在这研究，我们孤立被稻瘟病真菌Magnaporthegrisea和植物生长素导致的米饭WRKY基因(OsWRKY31)。这基因编码211氨基酸的残余的多肽并且属于可能在单音的简易窄床和dicot植物的分叉以后发源的米饭WRKY基因家庭的亚群。OsWRKY31被发现对洋葱外皮房间的原子核局部性短暂地表示OsWRKY31-eGFP熔化蛋白质。与一个Gal4DNA有约束力的领域熔化的OsWRKY31和它的异种的分析显示OsWRKY31在酵母举办transactivation活动。OsWRKY31基因的Overexpression被发现与M对感染提高抵抗。grisea，和展出的转基因的线减少了侧根形成和延伸与相比野类型并且RNAi植物。线与在表示上显示出许多防卫相关的基因的组成的表示例如PBZ1和OsSci2，以及早植物生长素反应基因，例如OsIAA4和OsCrl1基因。而且，植物与对在高集中的外长地供应的IBA，NAA和2,4-D在表示上不太敏感，在OsWRKY31基因的表示上建议那可能改变植物生长素反应或运输。这些结果也建议OsWRKY31可能在米饭是在植物生长素反应和防卫反应的信号转导小径的一个普通部件。

简介：<正>WeandothershavefirmlyestablishedthatsurfaceIgMreceptor(sIgM-R)crosslinkingwithantibodiestotheiheavychain(anti-i)leadstogrowtharrestandapoptosisinaseriesofwellcharacterizedB-celllymphomas.Thisrequiresablationofc-Mycproteinexpressionandtheconcomitantinductionofthecyclin-dependent-kinaseinhibitor,p27Kip1.Thesignalingmechanismsregulatingc-Mycandp27Kip1proteinexpressionarepoorlyunderstood.However,werecentlyestablishedthatsIgM-Rmediateddown-modulationofthePI-3Kpathwaydirectlyaffectedc-Mycandp27Kip1expressionandaccuratelypredictedgrowtharrest