简介:2009甲型(H1N1pdm09)流感大流行后,几个单价大流行性流感疫苗通过快速程序被许可使用。发作性睡病作为疫苗的副作用被发现,主要是在接受用欧洲的灭活纯化协议生产的AS03佐剂A(H1N1)流感疫苗的人群。感染野生甲型(H1N1)大流行流感病毒后没有接种疫苗的人群,发作性睡病的发病也在增加,这提示此种病毒抗原的作用在发作性睡病疾病发展中具有一定作用。本文进行了发作性睡病背景简介,概述了流感疫苗制剂的不同类型,探讨了自身免疫性疾病和自然感染之间的关系。
简介:目的报告1例脊髓空洞症(SM)合并Charcot关节病(CJ),通过文献复习的方法提高对该病在诊断及治疗上的认识。方法通过回顾该疾病的临床表现及典型的影像学特点,结合相关文献以求提高诊断正确率。结果该病例左肘部为典型的Charcot关节病表现,颈椎MRI确诊为Chiari畸形合并脊髓空洞症。结论临床表现及影像学特点是诊断该病的主要依据,目前尚无有效治疗手段,手术治疗有一定疗效。
简介:GinsenosideRg1(Rg1)hasanti-agingandanti-neurodegenerativeeffects.However,themechanismsunderlyingtheseactionsremainunclear.TheaimofthepresentstudywastodeterminewhetherRg1affectshippocampalsurvivalandneuriteoutgrowthinvitroafterexposuretoamyloid-betapeptidefragment25–35(Aβ25–35),andtoexplorewhethertheextracellularsignal-regulatedkinase(ERK)andAktsignalingpathwaysareinvolvedinthesebiologicalprocesses.Weculturedhippocampalneuronsfromnewbornratsfor24hours,thenaddedRg1tothemediumforanother24hours,withorwithoutpharmacologicalinhibitorsofthemitogen-activatedproteinkinase(MAPK)familyorAktsignalingpathwaysforafurther24hours.Wethenimmunostainedtheneuronsforgrowthassociatedprotein-43,andmeasuredneuritelength.Inaseparateexperiment,weexposedculturedhippocampalneuronstoAβ25–35for30minutes,beforeaddingRg1for48hours,withorwithoutAktorMAPKinhibitors,andassessedneuronalsurvivalusingHoechst33258staining,andphosphorylationofERK1/2andAktbywesternblotanalysis.Rg1inducedneuriteoutgrowth,andthiseffectwasblockedbyAPI-2(Aktinhibitor)andPD98059(MAPK/ERKkinaseinhibitor),butnotbySP600125orSB203580(inhibitorsofc-JunN-terminalkinaseandp38MAPK,respectively).Consistentwiththiseffect,Rg1upregulatedthephosphorylationofAktandERK1/2;theseeffectswerereversedbyAPI-2andPD98059,respectively.Inaddition,Rg1significantlyreversedAβ25–35-inducedapoptosis;thiseffectwasblockedbyAPI-2andPD98059,butnotbySP600125orSB203580.Finally,Rg1significantlyreversedtheAβ25–35-induceddecreaseinAktandERK1/2phosphorylation,butAPI-2preventedthisreversal.OurresultsindicatethatRg1enhancesneuriteoutgrowthandprotectsagainstAβ25–35-induceddamage,andthatitsmechanismmayinvolvetheactivationofAktandERK1/2signaling.更多还原
简介:Theactiveingredientofginseng,ginsenosidesRg1,hasbeenshowntoscavengefreeradicalsandimproveantioxidantcapacity.ThisstudyhypothesizedthatginsenosidesRg1hasaprotectiveroleinhumanneuroblastomacellsinjuredbyH_2O_2.GinsenosidesRg1atdifferentconcentrations(50and100μM)wasusedtotreatH_2O_2(150μM)-injuredSH-SY5Ycells.ResultsdemonstratedthatginsenosideRg1elevatedthesurvivalrateofSH-SY5YcellsinjuredbyH_2O_2,diminishedtheamountofleakedlactatedehydrogenase,andincreasedsuperoxidedismutaseactivity.GinsenosideRg1effectivelysuppressedcaspase-3immunoreactivity,andcontributedtoheatshockprotein70geneexpression,inadose-dependentmanner.TheseresultsindicatethatginsenosideRg1hasprotectiveeffectsonSH-SY5YcellsinjuredbyH_2O_2andthatitsmechanismofactionisassociatedwithanti-oxidationandtheinhibitionofapoptosis.
简介:MicroRNAs(miRNAs)aresmall,non-codingRNAsthatnegativelyadjustgeneexpressioninmultifariousbiologicalprocesses.However,theregulatoryeffectsofmiRNAsonSchwanncellsremainpoorlyunderstood.PreviousmicroarrayanalysisresultshaveshownthatmiRNAexpressionisalteredfollowingsciaticnervetransaction,therebyaffectingproliferationandmigrationofSchwanncells.ThisstudyinvestigatedwhethermiR-148b-3pcouldregulatemigrationofSchwanncellsbydirectlytargetingcullin-associatedandneddylation-dissociated1(Cand1).Up-regulatedexpressionofmiR-148b-3ppromotedSchwanncellmigration,whereassilencingofmiR-148b-3pinhibitedSchwanncellmigrationinvitro.FurtherexperimentsconfirmedthatCandlwasadirecttargetofmiR-148b-3p,andCandlknockdownreversedsuppressionofthemiR-148b-3pinhibitoronSchwanncellmigration.TheseresultssuggestedthatmiR-148b-3ppromotedmigrationofSchwanncellsbydirectlytargetingCandlinvitro.
简介:目的研究富含亮氨酸重复序列免疫球蛋白样蛋白1(LRIG1)、表皮生长因子受体(EGFR)、ECadherin及N-Cadherin在不同病理级别胶质瘤中表达差异,探讨LRIG1在胶质瘤恶性进展中可能的作用机制。方法收集74例胶质瘤患者手术标本,包含12对原发及复发配对胶质瘤标本,采用qRT-PCR检测LRIG1、EGFR、E-Cadherin、N-Cadherin基因的表达,并采用免疫印迹检测LRIG1、EGFR、E-Cadherin、NCadherin、Vimentin蛋白表达情况。结果随着胶质瘤病理级别的升高,LRIG1、E-Cadherin基因及蛋白表达水平降低,EGFR、N-Cadherin基因及蛋白表达水平升高,差异均具有统计学意义(均P〈0.05)。WHOⅢ-Ⅳ组胶质瘤EGFR/LRIG1及N-Cadherin/E-Cadherin比值显著高于WHOⅠ-Ⅱ组(均P〈0.05)。EGFR/LRIG1与NCadherin/E-Cadherin变化之间存在正相关(r=0.56,P〈0.05)。对原发及复发配对胶质瘤标本的研究结果与上述一致。结论胶质瘤中EGFR/LRIG1表达失衡,可能通过诱导上皮间质转化(EMT)促进胶质瘤细胞的恶性进展。LRIG1可能成为胶质瘤治疗的新靶点。