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简介：Inthepresentstudy,weconstructedalentivirus,FIV-CMV-GFP-miR-7-3,containingthemicroRNA-7-3geneandthegreenfluorescentproteingene,andusedittotransfecthumangliomaU251cells.Fluorescencemicroscopyshowedthat80%ofU251cellsexpressedgreenfluorescence.Real-timereversetranscriptionPCRshowedthatmicroRNA-7-3RNAexpressioninU251cellswassignificantlyincreased.ProliferationwasslowedintransfectedU251cells,andmostcellswereintheG1phaseofthecellcycle.Inaddition,theexpressionoftheserine/threonineproteinkinase2wasdecreased.ResultssuggestedthattransfectionwithalentiviruscarryingmicroRNA-7-3caneffectivelysuppressepidermalgrowthfactorreceptorpathwayactivityinU251cells,arrestcellcycletransitionfromG1phasetoSphaseandinhibitgliomacellgrowth.

简介：2008年3月～2009年3月，我科在神经导航辅助下行再次经蝶入路手术治疗垂体腺瘤7例。取得良好效果，现报道如下。1对象与方法男4例，女3例；年龄22～46岁，平均34岁。距离上次手术时间4个月～7年，平均3．6年。主要临床表现：头痛2例，视力、视野障碍4例．肢端肥大1例。术前MRI检查显示：大腺瘤（直径1—3cm）5例，巨大腺瘤（直径〉3cm）2例。

简介：由南京军区南京总医院．世界卒中组织、南京大学医学院、江苏省医学会神经病学分会联合主办的第7届国际脑血管病高峰论坛定于2011年7月8-10日在南京召开。会议将邀请国际、国内知名专家就脑血管病及神经介八的热点问题进行研讨。参会注册代表将获得国家继续医学教育I类学分8分。

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简介：Overthepastdecade,nineseparategenetherapyclinicaltrialsforadvancedParkinson’sdisease(PD)havebeenlaunchedandcompleted,involvingthedosingofnearly12-dozenPDvolunteerswhoincurredsignificantriskstohopefullyreducesymptomsand

简介：目的分析尿激酶动脉内溶栓治疗急性缺血性脑梗死的安全性和临床疗效.方法对7例发病在6h内的急性缺血性脑梗死患者用尿激酶行动脉内溶栓治疗,比较溶栓前后的NIHSS评分.结果7例患者经溶栓治疗后血管完全再通;7例患者在14d内神经功能缺损均明显改善;未发生症状性颅内出血及颅外出血并发症.结论我们小样本的研究发现,尿激酶动脉内溶栓治疗急性缺血性脑梗死有一定疗效,但尚需进行大样本随机对照研究证实.

简介：Alzheimer’sdisease(AD)isoneofthemostdevastatingdiseasesaffectingthelifeandhealthofagingpopulation.TwohallmarksofADaresenileplaquesandneurofibrillarytangles,andADiswellknownforthemassivelossofneuronsandimpairedcognitivefunctionsespeciallymemoryloss.Despiteextensivesearchforeffectivetreatment,available

简介：BACKGROUND:GenetherapyforParkinson'sdiseaseisbeingexploredasaneffectivestrategytorestoreandprotectthefunctionofneuronalcellsinthesubstantianigra.Regulationofgeneexpressionisnecessaryforgenetherapytoavoidadverseeffectsduetoexcessivesynthesisoftransgeneproducts.OBJECTIVE:Herewedevelopedrecombinantadeno-associatedvirus(AAV)asaviralvector-mediatedgeneregulationsystembasedonCrerecombinasefusedtothemutatedligand-bindingdomainoftheestrogenreceptor(CreERT2)+inducingagenttamoxifen.InducibleCrerecombinasewasusedtoreducetyrosinehydroxylasegeneexpressionandtopreventtheexcessiveincreaseindopamine.DESIGN,TIMEANDSETTING:Ageneticengineeringinvitrocomparativestudyandrandomizedcontrolledanimalexperiment.ThisstudywasconductedattheGeneTherapyCenter,JichiMedicalSchool,JapanfromJune2002toJune2004.METHODS:ToconstructarecombinantAAVvectorcarryingadopaminesynthasegene.ThetyrosinehydroxylasegenewasinsertedusingaloxPfragmentthatcouldberegulatedbyCrerecombinase.TherecombinantAAVvectorcarryingtheCreERT2genewasco-transducedwithHEK293cellsandthecorpusstriatuminaratmodelofParkinson'sdisease,withinducingagenttamoxifentoregulategeneexpression.MAINOUTCOMEMEASURES:ThelevelsofdopamineandaromaticL-aminoaciddecarboxylase(AADC)activityweredetectedinHEK293cellmediumandinthecorpusstriatuminaratmodelofParkinson'sdiseaseusinghigh-performanceliquidchromatography.ImmunofluorescencedoublestainingwasusedtoobservetyrosinehydroxylaseandCreorAADCco-expressioninHEK293cellmedium.ImmunohistochemicalstainingwasemployedtoobservetyrosinehydroxylaseandAADCexpressionandbehavioralchangesweremeasuredinParkinson'srats.RESULTS:TransfectedAAV-CreERT2andAAVexpressingdopaminesynthesisenzymescouldincreasethesynthesisofdopamineinHEK293mediumandParkinson'sratstriatum(P<0.01)andimprovetherotationalbehaviorofParkin

简介：Tourette'ssyndromeistreatedbybehavioralorpharmacologicaltherapy.However,patientswithmalignantTourette'ssyndromealsoexhibitlife-threateningsymptoms,whichareunresponsivetoconservativetreatmentsorneurosurgicalprocedures,suchasdeepbrainstimulation.Inrecentyears,mesenchymalstemcells(MSCs)haveshowntherapeuticpotentialinmanyneurologicaldiseases.Therefore,thepresentstudyproposedtouseMSCtransplantationasanoveltherapyforTourette'ssyndrome.StereotypicbehaviorsinTourette'ssyndromeratsdecreasedsignificantlyat21daysafterhumanMSCstransplantationintothestriatum.ImmunohistochemistryanalysesrevealedsurvivaloftransplantedhumanMSCsanddifferentiationintoneuronsandastrocytesintheratbrain.ResultssuggestthatintrastriataltransplantationofhumanMSCscouldprovidetherapeuticpotentialforTourette'ssyndrome.

简介：S100蛋白是一种分子量较小（10～12ku）的EF-手型钙结合蛋白，通过对钙离子的调节及与靶蛋白的相互作用，在体内发挥多种生物学作用．在细胞增殖、分化，肌肉收缩、基因表达、分泌及细胞凋亡中发挥重要作用。1965年Moore等首先在牛脑组织中发现S100蛋白，因其在中性饱和硫酸铵中100％溶解而得名。现已发现S100蛋白家族成员20个，S100B蛋白为其中一员，

简介：Alzheimer’sdisease(AD)isthemostcommontypeofdementiainelderlypopulation.WithagrowingagingpopulationnotonlyintheUnitedStatesbutalsointheworldwide,ADconstitutesanemergentpublichealthproblem.Overdecades,theprevailinghypothesiswasthatneurodegenerationmightresultfromoneortwoofthespecificlesions

简介：Despitetheadvancesincombinatorialorsyntheticchemistryandbioinformatics,recentliteraturehasdemonstratedtherelevanceofnatureandbiomassasasourceofnewmoleculestotreatdifferentpathologies,i.e.,bioactivecompoundsobtainedfromEcteinascidiaturbinatetotreatsometypesofcancerorrapamycinfromStreptomyceshygroscopicustopreventorganrejectionaftertransplant.Thistrend

简介：Thereceptorforadvancedglycationendproducts(RAGE)isareceptoroftheimmunoglobulinsuperfamilyofcellsurfacemoleculeswhichplaysimportantcontributionsunderbothphysiologicalandpathologicalconditions.OvertheyearsextensiveresearchworksupportedthedetrimentalroleofRAGEinAlzheimer’sdisease(AD)pathophysiology,rangingfromitsinvolvementinbetaamyloid(Aβ)braininfluxandclearance,

简介：缺血性卒中仍是当今社会威胁健康的主要疾病，它是我国引起死亡以及残疾的重要原因。S100B是与神经系统紧密相关的蛋白，它在缺血性卒中过程中可以发挥神经毒作用，诱导神经元以及星形胶质细胞凋亡。临床试验发现，S100B的水平与缺血性卒中患者病灶面积大小和预后有关。由于S100B在中枢神经系统的生物学特性，提示它可能在将来作为一项诊断卒中的生物标记物。

简介：BACKGROUND:TheprogressivedegenerationofdopaminergicneuronsinParkinson’sdiseaseisassociatedwithanactivatedglialreaction,combinedwithaninflammatoryprocess.Theseresponsesleadtotheproductionofcytokines,suchasinterferon-γ,tumornecrosisfactor-α(TNF-α),andinterleukin-1β.Inaddition,14-3-3proteinisacomponentofLewybodiesinParkinson’sdisease.OBJECTIVE:Toobservetheexpressionof14-3-3γandζprotein,aswellasTNF-α,inmousemicroglia,aswellaschangesafterlipopolysaccharide(LPS)activation.Toinvestigatepossiblemechanismsofdopaminergicneuronalinjuryduetoactivatedmicroglia.ToandclarifytheimmuneresponsemechanismsofParkinson’sdisease.DESIGN:Randomizedcontrolledobservation,cellstudy.SETTING:LaboratoryofDepartmentofNeurology,theAffiliatedUnionHospitalofTongjiMedicalCollege,HuazhongUniversityofScienceandTechnology.MATERIALS:TheBV-2immortalizedmurinemicrogliacelllinewaspurchasedfromChinaUnitcellcenter.LPSwasprovidedbySigmaCompany.CellcultureswerepurchasedfromGibco.Phospho-(Ser)14-3-3bindingmotifantibodywaspurchasedfromSantaCruzBiotechnologies.FITCwasprovidedbyLinfeiBiotechnology,Wuhan,China.TNF-αELISAwasprovidedbyJingmeiBiotechCo,Wuhan,China.TheflowcytometerwasprovidedbyBectonDickinson,Canada.METHODS:ThepresentexperimentwasperformedattheLaboratoryofDepartmentofNeurology,theAffiliatedUnionHospitalofTongjiMedicalCollege,HuazhongUniversityofScienceandTechnologyfromApriltoDecember2006.Themicroglialcellline,BV-2,wasculturedinvitroandstimulatedwithLPSfor2,6,12,and24hours.BV-2cultureswithoutLPSwereusedascontrols.MAINOUTCOMEMEASURES:Expressionof14-3-3γproteinwasdetectedbyflowcytometry.14-3-3ζpercentageexpressionandthemeanfluorescenceintensitywasdetectedbyimmunofluorescence.TNF-αexpressionwasdetectedbyELISA.RESULTS:14-3-3γproteinexpressionanalysis:followi

简介：目的：研究脑肿瘤手术前后血清S100B蛋白水平的改变，并分析其与患者临床资料的相关性，评估血清S100B对术后脑损伤的反映能力。方法30例胶质瘤、28例脑膜瘤和15例听神经瘤患者于手术前（入院时）、手术后第1d、第3d、第7d分别采集血清；同时记录患者手术时长、肿瘤WHO级别、肿瘤体积、脑水肿体积、KPS等临床资料。设正常对照组33例，采集单次血清。用双抗体夹心法ELISA检测血清S100B含量。将手术前后血清S100B水平进行重复测量方差分析；将血清S100B水平与手术时长、肿瘤体积等临床资料进行相关性分析。结果术前血清S100B水平在各脑肿瘤组之间的差异无统计学意义（P＞0．05），胶质瘤组、脑膜瘤组则高于正常对照组（均P＜0．05）。术后第1d、第3d血清S100B含量无明显改变（P＞0．05），术后第7d时高于手术前水平（P＜0．05），这种趋势在3个脑肿瘤组之间并无差别。在胶质瘤组中，术后第3、7d血清S100B含量与术后脑水肿体积呈正相关（均P＜0．05）；术后第1d、第3d血清S100B含量与胶质瘤病理级别呈正相关（均P＜0．05）。在听神经瘤组中，手术前、术后第3d血清S100B含量与听神经瘤肿瘤体积呈负相关（均P＜0．05），术后第7d血清S100B水平与手术时长呈正相关（P＜0．05）。脑膜瘤组内未见任何相关性。结论血清S100B对脑肿瘤切除术后的脑损伤反映较差，其含量升高可能与损伤后神经修复活动有关。血清S100B含量与胶质瘤的病理级别、术后脑水肿程度有一定的相关性，与听神经瘤体积及手术时长存在相关性。脑肿瘤术前血清S100B升高可能反映了肿瘤对脑实质的压迫损伤。

简介：目的研究红藻氨酸（KA）致痫大鼠海马S100B、降钙素基因相关肽（CGRP）的表达及病理改变。方法雄性SD大鼠按照完全随机数字表法分成对照组（8只）和模型组（40只），模型组再根据处死时间分为造模后6h、12h、24h、72h、1周5个亚组，每组8只。模型组采用KA建立颞叶癫痫动物模型，对照组用等体积生理盐水代替KA注射。模型组造模后6h、12h、24h、72h、1周．对照组注射后24h取大鼠海马组织行Niss1染色、Timm染色和免疫组化染色，观察S100B、CGRP蛋白的表达情况以及海马神经元和胶质细胞的病理变化。结果Nissl染色结果显示，模型组大鼠1周后CA3区出现大量固缩的坏死神经元，胞体萎缩，尼氏体消失。Timm染色结果显示，模型组大鼠1周后CA3区始层出现条带状分布的棕色颗粒，齿状回内分子层亦可见少量棕色颗粒。免疫组化染色结果显示，模型组大鼠海马CGRP蛋白大量表达，72h时达到高峰，同时伴随大量神经元丧失及胶质细胞增生。结论KA致痫大鼠出现S100B、CGRP蛋白高表达，尼氏体消失，苔藓纤维发芽等一系列病理学改变，推测S100B、CGRP蛋白参与了癫痫发生。

简介：我们经治一病例,因头痛,耳道疱疹,耳痛,面瘫,合并有听力减退,前庭功能障碍,轻度面部感觉障碍,及悬雍垂偏斜,声音嘶哑,入院治疗.

简介：目的探讨垂体Rathke＇s囊肿物理性状与患者症状和预后的关系。方法回顾性分析2005年4月至2013年5月手术治疗的104例垂体Rathke＇s囊肿患者的临床资料,其中87例病人术后随访5~92个月,平均26.6个月。结果本组囊肿直径为8~30mm,平均（15.3±5.0）mm,其中〈10mm7例,10~20mm69例,≥20mm28例。囊液含结晶54例,无结晶50例;囊液清亮37例,囊液粘稠67例。术后3个月复查MRI示囊肿全切除85例,囊肿残留2例;全切率为97.7%。术后复发3例,复发率为3.4%。头晕患者囊液含结晶的比例明显高于无头晕的患者（P〈0.05）;垂体激素水平异常的患者囊液含结晶的比例明显高于垂激素正常的患者（P〈0.05）;视力减退患者囊肿直径明显大于无视力减退者（P〈0.01）。结论垂体Rathke＇s囊肿囊内少量结晶与头晕有关,而大量结晶与垂体激素水平异常有关。手术治疗Rathke＇s囊肿的效果良好,术后并发症少,复发率低;术中处理好囊肿的分隔及囊内结晶是避免Rathke＇s囊肿残留与复发的关键。