简介：cAMPsignalingandthecontrolofSchwanncellfate:Theubiquitoussecondmessengercyclicadenosinemonophosphate(cAMP)controlsavarietyofcellularresponsesinacelltype-specificandstimulus-dependentmannerthroughanelaboratenetworkofsignalingintermediariesthatconnectstimulationofcellmembranereceptors(typicallyG

简介：磷脂酶C（phospholipaseC，PLC）是肌醇磷脂信号通路的关键酶，自20世纪50年代发现以来，在哺乳动物中已鉴定出六个族：PLCβ、PLCγ、PLCδ、PLCε、PLCζ、PLC-η，至少13个同工酶。除PLCζ外其他各种PLC同工酶广泛分布于机体各组织器官。它受G蛋白耦联受体、酪氨酸激酶受体和非酪氨酸激酶受体等活化，

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：目的探讨和研究血清高敏C-反应蛋白(high-sensitivityC-reactiveproteinhsCRP)与老年急性缺血性脑卒中(AIS)的关系及其可能机制.方法对72例老年AIS患者和56例健康查体者,检测血浆hsCRP水平,以多项临床及生化指标为危险因素进行统计学分析.结果老年AIS组的hsCRP水平(4.68±3.16)mg/L明显高于对照组(1.65±1.89)mg/L,差异具有显著性意义.单因素Logistic回归分析,发现hsCRP是AIS发生的一个独立危险因素,高hsCRP(≥1.5mg/L)发生AIS的OR值为6.9.且随hsCRP水平的增高,AIS临床病情严重程度增加.年龄、BMI、总胆固醇、HDL-C以及临床病情严重程度与hsCRP显著相关,但校正年龄和BMI后,只有临床病情严重程度与hsCRP仍保持显著相关.结论老年AIS患者的体内炎症反应水平是升高的,hsCRP是老年AIS患者临床病情严重程度的一个敏感指标.

简介：目的采用反映血管新生状态的指标经模糊C均值聚类对星形细胞肿瘤病理学分级进行探讨。方法采用含有正常成人脑组织、弥漫性星形细胞瘤（WHOⅡ级）、间变性星形细胞瘤（WHOⅢ级）、胶质母细胞瘤（WHOⅣ级）及阳性对照组织的168点矩阵的组织芯片,通过免疫组织化学SABC双标法标记内皮细胞和血管内皮生长因子,以Image-ProPlus5.1中文版图像分析软件对染色结果及血管内皮生长因子阳性单位、微血管密度及微血管平均周长等指标进行测定。采用单因素分析方法筛选与星形细胞肿瘤病理级别相关的参数,以矩阵实验室数学软件提供的模糊C均值聚类函数参数作为聚类对象,将不同的组织切片参数值进行模糊C均值聚类,所得聚类值分别赋值为星形细胞肿瘤病理分级值。结果（1）在不同病理分级组之间,星形细胞肿瘤血管内皮生长因子阳性单位差异具有统计学意义（P=0.000）,各病理分级组间两两比较差异亦有统计学意义（均P〈0.05）。（2）在不同病理分级组之间,星形细胞肿瘤微血管密度值差异有统计学意义（P=0.000）,两两比较差异亦有统计学意义（均P=0.000）。（3）星形细胞肿瘤微血管平均周长,Ⅱ级组与Ⅲ级组、Ⅱ级组与Ⅳ级组比较差异有统计学意义（均P=0.000）,而Ⅲ级组与Ⅳ级组之间差异无统计学意义（P=1.000）。（4）与WHO病理分级相比,模糊C均值聚类产生的星形细胞肿瘤病理分级值对Ⅱ、Ⅲ、Ⅳ级等级别的诊断符合率分别为85.71%、48.39%和78.95%,总体正确率达68.46%。结论星形细胞肿瘤血管内皮生长因子阳性单位、微血管密度和微血管平均周长等项指标的模糊C均值聚类值与星形细胞肿瘤病理分级值比较符合,可应用模糊C均值聚类法对星形细胞肿瘤的病理分级进行辅助推测。

简介：目的探讨以最近发展起来的核转染技术直接将编码绿色荧光蛋白DNA质粒转染到兔原代骨髓基质细胞的细胞核内进行基因修饰的可行性。方法从兔股骨抽取骨髓，密度梯度离心法获取原代骨髓基质细胞。以Nucleolector^TM技术转染pEGFP-C2（EGFP组），以同期培养未转染的细胞作为对照组。测定细胞的活力、贴壁率、生长曲线以及转染的效率。结果在转染后24h成功发现EGFP的表达。两组细胞具有相似的形态学变化、贴壁率以及生长曲线。EGFP的表达逐渐增强，至第6天达到最高峰（47．8％），观察一个月未发现表达减弱。结论pEGFP-C2基因核转染对兔原代骨髓基质细胞的体外增殖无明显影响；EGFP可以作为兔骨髓基质细胞有效的基因表达标记；Nucleofector^TM技术是一种简易而高效的转染兔原代骨髓基质细胞的方法。

简介：BACKGROUND:Studieshavesuggestedthatfibronectinleucine-richtransmembraneprotein3(FLRT3)isrelatedtoinjuryandregenerationofthenervoussystem.However,theexpressionandbiologicalcharacteristicsoftheseproteinsremainpoorlyunderstood.OBJECTIVE:ToobtainFLRT3C-terminalgenefragments,toeffectivelyexpressandpurifythetargetproteins.DESIGN,TIMEANDSETTING:AnobservationalstudyofcellularandmolecularbiologywasperformedatthelaboratoryofHistologyandEmbryologyinXiangyaSchoolofMedicine,CentralSouthUniversitybetweenOctober2007andJune2008.MATERIALS:ThreeSpragueDawleyadultratswereusedtoextracttotalRNAfromratbrains.ThepGEX4T3andEscherichiacoli(E.coli)JM109werepurchasedfromPromega.E.coliBL21wasprovidedbyNovagen.METHODS:FLRT3proteincodingC-terminalDNAfragments,atalengthof786bp,wereamplifiedusingRT-PCRtechniquefromrattotalRNA.TheamplifiedproductswereclonedintotheexpressionvectorpGEX4T3.ArecombinantexpressionvectorwasthenconstructedandintroducedintoE.coliBL21.IsopropyI-D-thiogalactopyranosidewasappliedtoinduceexpressionofrecombinantGSTfusionproteins,followedbyisolation,purification,andrenaturationofinclusionbodiesthatcomprisedrecombinantproteins.Finally,thepurifiedrecombinantproteinwasobtained.MAINOUTCOMEMEASURES:DeterminationofFLRT3C-terminalDNAsequence;expressionoftargetproteinswasassayedbySDS-PAGEelectrophoresis;purifiedrecombinantproteinwasidentifiedwithWesternblotmethods.RESULTS:FLRT3proteincodingC-terminalDNAfragments,atalengthof786bp,weresuccessfullyharvestedthroughRT-PCRamplification,andwerethenclonesintotheprokaryoticexpressionvectorpGEX4T3.Theresultsofthesequencewereconsistentwiththeknowngenesequence.SDS-PAGEanalysisdemonstratedthattherewasaspecificproteinbandintherecombinantGSTfusionproteinsatarelativemolecularmassof56,600.Therecombinantproteinwasobservedintheinclusionbody,andh

简介：目的探讨脑梗死患者血清C-反应蛋白(C-reactiveprotein,CRP)水平与病情严重程度及预后的量化关系.方法对病程为2周以内的90例脑梗死患者进行入院时和1周后血清C-反应蛋白水平测定.入院时C-反应蛋白测定值为CRP1,1周后检测值为CRP2;根据入院时C-反应蛋白测定值进行分组.A组:CRP1≤2.00mg/L,B组:2.00mg/L＜CRP1≤9.50mg/L,C组:CRP1＞9.50mg/L.应用美国国立卫生研究院卒中量表(NIHSS)及Barthe1指数(BI)记分法,对入院时90例患者(NIHSS1及B11)和随访的58例患者(NIHSS2及BI2)进行神经功能缺损程度评分.结果入院时血清C-反应蛋白水平与发病时及治疗后3个月随访时的神经功能缺损严重程度呈显著相关(P≤0.001),且这种相关性存在量化关系:CRP1≤2.00mg/L时,NIHSS1中位数为5.00分,BI2中位数为100.00分;2.00mg/L＜CRP1≤9.50mg/L,NIHSS1中位数为7.00分,BI2中位数为85.00分;CRP1＞9.50mg/L时,NIHSS1中位数为13.00分,BI2中位数为47.50分.入院时血清C-反应蛋白水平与相应的神经功能缺损程度及治疗后3个月恢复期水平之间差异具有显著意义(P＜0.05或P＜0.001).血清CRP2水平与入院时及治疗后3个月时的神经功能缺损程度间差异无显著性意义(P＞0.05).结论根据脑梗死患者发病后2周内的血清C-反应蛋白水平可以对病情严重程度及预后进行量化评估.

简介：BACKGROUND:Clinicaldiagnosisofvariousneurologicaldisordersinvolvingthesensorynervesdependsprimarilyonsubjectivedescription,whichcannotbequantitativelyevaluated,andisalsolessreproducibleandspecific.QuantitativesensorytestingmethodscanovercometheseshortcomingsandiscurrentlyusedtoidentifythefunctionoftheC-andA-fibers.OBJECTIVE:Toapplythequantitativesensorytestingmethodforanalyzingchangesintemperaturesensation,cryalgesia,thermalgesia,andvibrationsenseontheskinsurfaceofhemiplegicpatientswithpost-strokeshoulder-handsyndrome,andtoanalyzetherelationshipbetweenthesechangesandshoulder-handsyndrome.DESIGN,TIMEANDSETTING:Anon-randomized,concurrent,controlstudywasperformedattheClinicandInpatientDepartmentoftheThirdXiangyaHospital,CentralSouthUniversity,betweenJune2000andApril2001.PARTICIPANTS:Thirtypost-stroke,hemiplegicpatientsweredividedintoshoulder-handsyndromeandcontrolgroups,accordingtowhetherpatientsexhibitedshoulder-handsyndrome,with15patientsineachgroup.METHODS:ATSA2001quantitativesensorytestingdevice(Medoc,Israel)wasusedforquantitativesensorytesting.Allsensorytestingemployedlimits,testingtemperaturesenseonthepalmthenareminenceandvibrationsenseonthethumbmetacarpal.Coldthresholdwas≤28℃,warmththresholdwas≥36℃,cold-evokedpainthresholdwas≤5℃,heat-evokedpainthresholdwas≥51℃,vibrationthresholdwas≥5μm/s;ifapatientmetoneoftheseitems,he/shewasconsideredtobehypoanesthesia.MAINOUTCOMEMEASURES:Cold,warm,cold-evokedpain,heat-evokedpainandvibrationthresholdchangesonskinfromtheparalyzedupperextremitywasmeasuredintheshoulder-handsyndromeandcontrolgroups.RESULTS:Incidenceofsensorydisabilityintheshoulder-handsyndromegroupincreasedmoresignificantlythaninthecontrolgroup(P<0.05),withtheprimarymanifestationsbeingdecreasedcoldthreshold(P<0.

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.