简介:目的探讨P53家族新成员P73及P63在脑星形细胞瘤中的表达和在不同恶性程度中的表达变化.方法采用免疫组化方法检测61例不同恶性程度的星形细胞瘤P73及P63基因的表达情况,与置换一抗的空白对照组比较,并同时进行组间对照.结果P73与P63总的阳性表达率为31.15%和40.98%.组间对照:P73组3~4级与1~2级比较P<0.05,2~3级与1~2级比较P>0.05;P63组3~4级与1~2级比较P<0.01.,2~3级与1~2级比较P<0.05.结论P73及P6.3作为P53家族的新成员可能是候选的抑癌基因,且随着恶性程度的增加其表达越明显.
简介:目的探讨不同病理级别人脑神经胶质瘤组织中p57^kip2/p21^cip1mRNA的表达变化及其关系。方法采用实时荧光定量PCR检测p57^kip2/p21^cip1mRNA在68例脑胶质瘤组织和16例非肿瘤脑组织中的表达水平。结果①p57^kip2mRNA在脑胶质瘤中的表达水平显著低于非肿瘤脑组织(P〈0.01),且其表达水平与肿瘤病理级别呈显著负相关(rs=-0.495;P〈0.01)。②p21^cip1mRNA在脑胶质瘤中的表达水平与非肿瘤脑组织相比无显著差异(P〉0.05),但其表达水平与肿瘤病理级别呈显著负相关(rs=-0.615;P〈0.01)。结论p57^kip2/p21^cip1的异常表达可能与人脑胶质瘤的发生和发展有密切相关,其表达水平可反映肿瘤的恶性程度。
简介:PreliminaryworkbyourresearchteamrevealedthatSchisandra,arenownedtraditionalChinesemedicine,causeslearningandmemoryimprovementsinovariectomizedmice.ThisactivitywasattributedtoactiveingredientsextractedwithN-butylalcohol,namedSchisandraN-butanolextract.Inthisstudy,ovariectomizedmicewerepretreatedwithSchisandraN-butanolextractgivenbyintragastricadministration.Thistreatmentledtotheenhancementoflearning,andanincreaseinhippocampalCA1synaptic,surfaceandpostsynapticdensity.Adecreaseintheaveragesizeofthesynapticactivezonewasalsoobserved.TheseexperimentalfindingsshowingthatSchisandraN-butanolextractimprovedsynapticmorphologyindicateanunderlyingmechanismbywhichtheabilityoflearningisenhancedinovariectomizedmice.
简介:ExogenoussubstancePaccelerateswoundhealingindiabetes,butthemechanismremainspoorlyunderstood.Here,weestablishedaratmodelbyintraperitoneallyinjectingstreptozotocin.Fourwounds(1.8cmdiameter)weredrilledusingaself-madepunchontotheback,bilateraltothevertebralcolumn,andthentreatedusingamnioticmembranewithepidermalstemcellsand/orsubstanceParoundandinthemiddleofthewounds.Withthecombinedtreatmentthewound-healingratewas100%at14days.Withprolongedtime,typeIcollagencontentgraduallyincreased,yettypeIIIcollagencontentgraduallydiminished.Abundantproteingeneproduct9.5-andsubstanceP-immunoreactivenervefibersregenerated.Partialnervefiberendingsextendedtotheepidermis.ThetherapeuticeffectsofcombinedsubstancePandepidermalstemcellswerebetterthanwithamnioticmembraneandeitherfactoralone.OurresultssuggestthatthecombinationofsubstancePandepidermalstemcellseffectivelycontributestonerveregenerationandwoundhealingindiabeticrats.
简介:目的探讨细胞周期蛋白p21^Waf1/cip1和p27^Kip1在功能性垂体腺瘤中的表达,及其与患者临床特征、预后的关系。方法构建包含6例正常垂体、36例侵袭性腺瘤(侵袭组)和58例非侵袭性腺瘤(非侵袭组)石蜡标本的组织芯片;免疫组化染色检测p21^Waf1/cip1和p27^Kip1蛋白的表达水平;MALDI-TOF法分析p21^Waf1/cip1和p27^Kip1启动子甲基化水平。分析垂体腺瘤患者p21^Waf1/cip1和p27^Kip1蛋白表达水平与其临床特征的关系。结果侵袭组高表达p21^Waf1/cip1者为8例(22.2%),H-Score值为148±28.4;非侵袭组高表达p21^Waf1/cip1者为39例(67.2%),H-Score值为217.2±43.2;侵袭组高表达p27^Kip1者为10例(27.8%),H-Score值为122.1±31.1;非侵袭组高表达p27^Kip1者为37例(63.8%),H-Score值为187.2±36.6。两组的p21^Waf1/cip1和p27^Kip1表达水平的差异均有统计学意义(χ^2=18.01,P=0.000;χ^2=11.52,P=0.001)。p27^Kip1表达水平与血清促乳素水平呈负相关(r=-0.237,P〈0.01)。CpG位点甲基化检测显示,p27^Kip1启动子甲基化水平〉50%的为7/33,其中4个位点的差异有统计学意义(P〈0.01)。结论功能性垂体腺瘤的p21^Waf1/cip1和p27^Kip1表达水平降低与肿瘤的侵袭行为有明显关系;启动子甲基化程度影响p27^Kip1的表达水平。
简介:目的探讨热休克蛋白(HSP70)在人胶质瘤细胞BT-325p38MAPK信号通路中的作用.方法用脂质体介导法将hsp70基因导入人胶质瘤细胞BT-325中,倒置显微镜观察转染细胞的形态学及粘附性变化,紫外线照射30min后,采用免疫组化和Western-blot方法测定转染前后HSP70的表达水平及照射前后p38MAPK表达情况.结果免疫组化和Western-blot证实hsp70基因成功转染入BT-325中,转染细胞受到紫外线照射后p38MAPK表达减弱.结论体外转染hsp70基因可抑制紫外线照射后BT-325细胞p38MAPK的表达.
简介:BACKGROUND:Previousstudieshaveshownthatp75neurotrophinreceptorplaysanimportantroleinperipheralnerveinjury.However,theroleofp75neurotrophinreceptorintheregenerationofperipheralnervesremainspoorlyunderstood.OBJECTIVE:Tostudytheeffectofp75neurotrophinreceptoronfacialnerveregeneration.DESIGN,TIMEANDSETTING:ArandomizedcontrolledexperimentwasperformedintheRegenerationLaboratoryofFlindersUniversity,AustraliaandtheBiomedicalLaboratoryofDentistrySchool,ShandongUniversityfromMarch2005toFebruary2006.MATERIALS:CholeratoxinBsubunit,fastblue,andbiotinrabbit-antigoatIgGwereprovidedbySigma,USA;goat-anticholeratoxinBsubunitantibodywasprovidedbyListBiologicals,USA.METHODS:Inp75neurotrophinreceptorknockoutandwildtype129/svmice,thefacialnervesononesidewerecrushed.Atdays2and4followinginjury,regeneratingmotorneuronsinthefacialnucleiwerelabeledbyfastblue,andtheregeneratingaxonwaslabeledbytheanterogradetracercholeratoxinBsubunit.MAINOUTCOMEMEASURES:AxonalregenerativevelocityandnumberweredetectedbyimmunohistochemicalstainingofcholeratoxinBsubunit,growth-associatedprotein,proteingeneproduct9.5,andcalcitonin-gene-relatedpeptide;survivalofmotorneuronsinthefacialnucleiwasdetectedbyretrogradefastblue.RESULTS:Axonalgrowthinthefacialnerveofp75neurotrophinreceptorknockoutmicewassignificantlylessthaninwildtypemice.Atday7afterinjury,thenumberofregeneratingmotorneuronsinp75neurotrophinreceptorknockoutmiceremainedsignificantlylessthaninwildtypemice(P<0.05).Thenumberofpositivelystainedfibersforgrowth-associatedprotein-43,proteingeneproduct9.5,andcalcitonin-gene-relatedpeptideinp75neurotrophinreceptorknockoutmicewassignificantlylessthaninwildtypemice(P<0.01).CONCLUSION:p75neurotrophinreceptorpromotedaxonalregenerationandenhancedthesurvivalrateofmotorneuronsfollowingfacialnerveinjury.
简介:BACKGROUND:Calciumion(Ca2+)overloadplaysanimportantroleincerebralischemia/reperfusioninjury.Anisodamine,atypeofalkaloid,canprotectthemyocardiumfromischemiaandreperfusioninjurybyinhibitingintracellularcalcium[Ca2+]ioverload.OBJECTIVE:Toinvestigateeffectsofanisodamineon[Ca2+]iconcentrationandcortexultrastructurefol-lowingacutecerebralischemia/reperfusioninrabbits.DESIGN,TIMEANDSETTING:RandomizedandcontrolledtrialwasperformedattheDepartmentofEmergency,TongjiHospital,TongjiMedicalCollegeofHuazhongUniversityofScienceandTechnologyfromSeptembertoDecember2006.MATERIALS:Fortyhealthyrabbitswereusedtoestablishmodelsofacutecerebralischemia/reperfusion.AnisodaminewasprovidedbyLianyungangDongfengPharmaceuticalFactory;Fura-2waspurchasedfromNanjingJianchengBioengineeringInstitute;dual-wavelengthfluorescentspectrophotometrysystemandDM-300softwarewereprovidedbyBio-Rad,USA;OPTON-EM10CtransmissionelectronmicroscopewasproductofSiemens,Germany.METHODS:Fortyrabbitswererandomlydividedintothefollowinggroups:shamoperation,ischemia,ischemia/reperfusion,andanisodamine,withtenrabbitsineachgroup.Modelsofcompletecerebralischemiainjurywereestablished.Inaddition,bloodwascollectedfromthefemoralarteryofratsintheischemia/reperfusionandanisodaminegroupstoinducehypotensionandestablishreperfusioninjurymodels.Thebilateralcommoncarotidarteryclampwasremovedfromtheanisodaminegroup20minutesafterischemia,andanisodamine(10mg/kgbodymass)wasinjectedviathefemoralvein.Rabbitsintheshamoperationgroupunderwentonlyvenouscannulation.MAINOUTCOMEMEASURES:[Ca2+]iconcentrationwasdeterminedusingadual-wavelengthfluorescentspectrophotometrysystem,andcorticalultrastructurewasobservedfollowinguranyl-leadcitratestaining.RESULTS:Thelevelsof[Ca2+]iintheischemiaandischemia/reperfusiongroupsweresignificantlyin-creased,c
简介:目的构建pEGFP-N1-GGF2质粒,观察其在大鼠脑组织中的表达。方法采用RT-PCR方法从人胚胎脑组织总RNA中扩增出人GGF2全长序列.并克隆到增强型绿色荧光蛋白(EGFP)基因真核表达载体pEGFP-N1上,构建pEGFP-N1-GGF2质粒.通过脂质体将pEGFP-NI-GGF2质粒转染大鼠脑组织.荧光显微镜下观察GGF2融合蛋白在大鼠脑内表达的时间和空间分布特征。结果成功构建了pEGFP-N1-GGF2表达载体,荧光显微镜观察可见,pEGFP-N1-GGF2表达载体转染6h大鼠脑内即可见GGF2融合蛋白表达.3d时融合蛋白表达最多,7d时表达量稍有下降但仍高,14d时表达量已明显下降。GGF2融合蛋白在脑内的表达以针道为中心向周围扩散.荧光信号可达皮层深部。结论脂质体介导的pEGFP-NI-GGF2质粒能够在大鼠脑内表达GGF2融合蛋白。
简介:目的探讨神经-钙粘素(N—cadherin),上皮-钙粘素(E—cadherin)及B—catenin在人脑胶质瘤中的表达及意义。方法采用S—P免疫组化方法检测N—cadherin、E—cadherin、β—catenin在42例不同级别胶质瘤及8例正常脑组织中的表达。结果N—cadherin,E—cadherin及β—catenin的表达在正常脑组织与胶质瘤之间以及胶质瘤的高低级别组间存在显著差异(P〈0.05),并且在生存时间〉2年组与生存时间≤2年组间差别显著(P〈0.05);N—cadherin与β—catenin的表达随着肿瘤级别的升高而增高,且二者在胶质瘤中的表达呈正相关(P〈0.05,r=0.778)。E—cadherin的表达随着肿瘤级别的升高而下降,E—cadherin与N—cadherin、β—catenin的表达呈负相关(P〈0.05,r1=-0.747,r2=-0.783);结论提示N—cadherin与β—catenin的过度表达和E—cadherin的表达下调在胶质瘤的侵袭及恶性进展中起着重要作用。N—cadherin与β—catenin的表达可能与胶质瘤患者的预后密切相关,提示可作为反映胶质瘤恶性程度与预后的指标。
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: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:目的动态监测血清基因间长链非编码RNA—p21(1incRNA-p21)表达水平与急性蛛网膜下腔出血(SAH)的相关性,从而为临床早期诊断SAH提供可靠的实验依据。方法将105只SD雄性大鼠随机分为SAH手术组(63只)、假手术组(21只)和正常对照组(21只),采用颈内动脉穿刺法制作SAH模型,实时荧光定量聚合酶链式反应法(RT-PCR)检测血清中lincRNA—p21水平,于预定时间进行神经行为学评估和干湿重法测定脑组织含水量。结果相对于正常对照组,急性SAH组在2—18hlincRNA—p21表达呈下降趋势(P〈0.05),18—48h呈急剧上升趋势后恢复至正常水平(P〈0.05),而0~2h、48~72h和假手术组相对于正常对照组差异无统计学意义(P〉0.05)。对神经行为学评分、脑组织含水量与lincRNA—p21表达相关性分析结果显示神经行为学(P=0.924)和脑组织含水量(P=0.224)均与lincRNA—p21表达无相关性。结论血清lincRNA—p21的表达水平可以作为急性蛛网膜下腔出血潜在的生物学诊断标志和治疗靶点,但不能作为病情严重程度指标。