简介:WehaverecentlyclonedapathogeninducibleblastresistancegenePi-khfromtheindicaricelineTetepusingapositionalcloningapproach.Inthisstudy,wecarriedoutstructuralorganizationanalysisofthePi-khlocusinbothindicaandjaponicaricelines.A100kbregioncontaining50kbupstreamand50kbdown-streamsequencesflankingtothePi-khlocuswasselectedfortheinvestigation.Atotalof16genesinindicaand15genesinjaponicawerepredictedandanno-tatedinthisregion.TheaverageGCcontentofindicaandjaponicagenesinthisregionwas53.15%and49.3%,respectively.Bothindicaandjaponicasequenceswerepolymorphicforsimplesequencerepeatshavingmono-,di-,tri-,tetra-,andpentanucleotides.SequenceanalysisofthespecificblastresistantPi-khalleleofTetepandthesusceptiblePi-khalleleofthejaponicaricelineNipponbareshoweddifferencesinthenumberanddistributionofmotifsinvolvedinphosphorylation,resultingintheresistancephenotypeinTetep.
简介:<正>WeandothershavefirmlyestablishedthatsurfaceIgMreceptor(sIgM-R)crosslinkingwithantibodiestotheiheavychain(anti-i)leadstogrowtharrestandapoptosisinaseriesofwellcharacterizedB-celllymphomas.Thisrequiresablationofc-Mycproteinexpressionandtheconcomitantinductionofthecyclin-dependent-kinaseinhibitor,p27Kip1.Thesignalingmechanismsregulatingc-Mycandp27Kip1proteinexpressionarepoorlyunderstood.However,werecentlyestablishedthatsIgM-Rmediateddown-modulationofthePI-3Kpathwaydirectlyaffectedc-Mycandp27Kip1expressionandaccuratelypredictedgrowtharrest
简介:目的了解2000~2008年间原发性皮肤隐球菌病(PCC)的流行病学及临床特征。方法检索并回顾性分析2000~2008年文献报道的原发性皮肤隐球菌病病例资料,对比分析2000~2008年与1985~2000年报道的PCC病例及免疫正常与免疫受损PCC病例的特征是否存在差异。结果共检索出2000~2008年间符合PCC诊断标准的病例28例。近8a来PCC仍好发于年龄较大者,但男性更多见;免疫正常或受损宿主均可发生PCC;HIV感染患者发生PCC几率更小;外伤可能为PCC重要的诱发因素;皮疹部位仍以四肢等暴露部位为主;皮疹性质由以前较特异的化脓性指头炎或蜂窝织炎为主变迁到以溃疡、结节、红斑、肿块等非特异性皮疹为主;治疗仍以抗真菌药物口服或与手术联合为主,氟康唑仍为一线药物;预后一般较好。结论近年来PCC表现出一些新的特点。宿主的免疫状态可能不影响其发生PCC的机率或影响较小,而仅影响隐球菌感染后的转归。
简介:OverexpressionandactivationofHER-2/neu(alsoknownasc-erbB-2),aproto-oncogene,wasfoundinabout30%ofhumanbreastcancers,promotingcancergrowthandmakingcancercellsresistanttochemo-andradio-therapy.Wild-typep53iscrucialinregulatingcellgrowthandapoptosisandisfoundtobemutatedordeletedin60-70%ofhumancancers.Andsomecancerswithawild-typep53donothavenormalp53function,suggestingthatitisimplicatedinacomplexprocessregulatedbymanyfactors.Inthepresentstudy,weshowedthattheoverexpressionofHER-2/neucoulddecreasetheamountofwild-typep53proteinviaactivatingPI3Kpathway,aswellasinducingMDM2nucleartranslocationinMCF7humanbreastcancercells.BlockageofPI3KpathwaywithitsspecificinhibitorLY294002causedG1-Sphasearrest,decreasedcellgrowthrateandincreasedchemo-andradio-therapeuticsensitivityinMCF7cellsexpressingwild-typep53.However,itdidnotincreasethesensitivitytoadriamycininMDA-MB-453breastcancercellscontainingmutantp53.OurstudyindicatesthatblockingPI3KpathwayactivationmediatedbyHER-2/neuoverexpressionmaybeusefulinthetreatmentofbreasttumorswithHER-2/neuoverexpressionandwild-typep53.
简介:目的观察鱼腥草素钠对慢性阻塞性肺疾病模型大鼠肺组织中PI3K、AKT1及mTORmRNA表达的影响,并探讨其作用机制。方法选取Wistar雄性大鼠24只,体重(220±20)g,随机分为正常组、模型组、地塞米松组和鱼腥草素钠组(每组6只)。采用烟熏和脂多糖气管滴注联合方法建立慢性阻塞性肺疾病(chronicobstructivepulmonarydisease,COPD)大鼠模型,采用实时荧光定量聚合酶链反应检测PI3K、AKT1及mTORmRNA表达,并观察大鼠肺组织病理变化。结果与正常组相比,模型组大鼠肺组织PI3K、AKT1mRNA表达显著增高(P〈0.01,P〈0.05),mTORmRNA表达显著降低(P〈0.01);与模型组相比,鱼腥草素钠组和地塞米松组肺组织PI3K、AKT1mRNA表达显著降低(P〈0.01,P〈0.05),mTORmRNA表达显著增高(P〈0.01);与地塞米松组相比,鱼腥草素钠组肺组织mTORmRNA表达显著增高(P〈0.05)。病理观察结果显示,与正常组比较,模型组局部肺实变,肺泡腔内大量中性粒细胞浸润,胶原染色显示肺间质纤维组织大量增生;鱼腥草素钠组和地塞米松组肺组织病理改变明显轻于模型组,鱼腥草素钠组和地塞米松组肺组织呈轻度间质性肺炎,仅见少量的纤维组织增生。结论鱼腥草素钠能够减轻慢性阻塞性肺疾病模型大鼠肺组织损伤,其机制可能与其能够下调PI3K、AKT1mRNA的表达、上调mTORmRNA表达有关。