简介:目的建立高表达缓激肽受体(B2R)的大鼠胶质瘤模型,为研究缓激肽选择性开放血脑屏障的机制及解决目前临床应用中存在的问题提供必要的模型.方法①大鼠B2R的真核细胞的表达和其载体(prB2R)侵染C6胶质瘤细胞株;②Real-timeRT-PCR测定B2R的转录;③WesternBlot法测定B2R的表达水平.结果①大鼠胶质瘤细胞株C6高表达B2R;②Real-timeRT-PCR测定C6-B2R1和C6-B2R2克隆的B2R分别比C6对照高7.6和6.9倍;③C6-B2R1和C6-B2R2克隆的蛋白表达水平高于C6对照克隆的3.8和3.78倍.移植C6-B2R1肿瘤1周后的B2R表达水平高于C6对照肿瘤的3.6倍.结论高表达B2R的大鼠胶质瘤模型已被成功建立.
简介:目的高同型半胱氨酸血症可能为认知功能损害的独立危险因素,干预高同型半胱氨酸血症是否能改善认知功能,尚需进一步研究证实。方法2009年1月~2011年3月宣武医院神经内科门诊患者,头部MRI证实存在脑白质疏松,同时不合并重要部位或大面积脑梗死患者。简易智能状态检查(MMSE)11~24分(为轻,中度病人)。共入组87例,高同型半胱氨酸血症组45例,合并高同型半胱氨酸血症组42例。两组均采用抗血小板、降血压、降血脂的药物和维生素B6、叶酸、甲钴胺治疗。两组分别于服药前及服药后8周、12周,采用简易智能状态量表(MMSE)对患者进行评价,同时复查血同型半胱氨酸水平。结果在治疗后12周末以高同型半胱氨酸血症组MMSE评分改善较好(P〈0.05)。结论高同型半胱氨酸血症可能为认知功能损害的独立危险因素,对高同型半胱氨酸血症进行药物干预可能达到改善认知功能障碍及痴呆或延缓其进展的作用。
简介:BACKGROUND:Duetothelackofautografttransplantrejection,Schwanncells(SCs)canpromotetheproliferationofembryonicstemcellsandtheinductionofdopaminergicneurons.Mesencephalicstemcellscanbeinducedtoproducedopaminergicneurons.Thetherapeuticeffectsofco-graftsofSCsandneuralstemcells(NSCs)deservesfurtherstudyandverificationinParkinsoniananimalmodels.OBJECTIVE:ToinvestigatetheeffectsofSchwanncellsandmesencephalicNSCco-graftsinParkinsoniananimalmodelsonanimalbehaviorandhistology.DESIGN:Randomizedcontrolledexperiment.SETTING:FudanUniversity;InstituteofNeuroscience,ChineseAcademyofSciences.MATERIALS:ThefollowinganimalswereobtainedfromtheExperimentalAnimalCenter,ShanghaiInstituteforBiologicalScience,ChineseAcademyofSciences:5Sprague-Dawleyrats,embryonicday(E)13-16;16neonatalSprague-Dawleyrats,postnatalday1-3;and18adultSDratsofbothgenders.Animalexperimentationmetanimalethicalapproval.METHODS:TheexperimentwasperformedattheDepartmentofAnatomy,HistologyandEmbryology,ShanghaiMedicalCenter,FudanUniversityfromSeptember2005toJanuary2007.ThemesencephalicNSCswereobtainedfromthebrainsofSDratsatE13-16,andSCswereharvestedfromthesciaticnervesofneonatalratsatday1-3.Hemiparkinsonianrats(n=18)wereselectedfortransplantationafterestimatingrotationalbehaviorinresponsetoapomorphineandwererandomlyassignedtothreegroups:controlgroup,NSCgroup,andco-graftgroup.Therewere6ratsineachgroup.Eitherphosphatebufferedsaline(PBS),NSCs,orSCsplusNSCsweretransplantedintotherightneostriatumofParkinsonianrats,respectively.MAINOUTCOMEMEASURES:①Rotationalbehaviorwasinducedbyapomorphine(0.05mg/kg,i.p.)2,4,6,8,and10weeksaftertransplantation,andthenumberofrotationswerecounted.②Differentiationandsurvivalofdopaminergicneuronsintherightneostriatumwerequantifiedbytyrosinehydroxylaseimmu
简介:目的形成高甘油三酯血症的临床实践指南。参与者工作小组包括由内分泌学会临床指南小组委员会(ClinicalGuidelinesSubcommittee,CGS)选定的主席,及另外五位此领域的专家和一位方法学家。作者没有接受任何企业的资助或报酬。证据指南采用的推荐、评估、制订与评价的分级(theGradingofBecommendations,Assessment,Development,&ndEvaluation,GBADE)系统来描述推荐的强度和证据质量。共识过程共识是通过对证据的系统回顾、电子邮件讨论、电话会议和面对面的会议为指导。本指南依次由内分泌学会CGS、临床事务核心委员会和内分泌学会理事会审议并批准。在每个阶段,工作小组根据书面意见做出修订。结论工作小组建议,高甘油三酯血症的诊断主要基于空腹水平,轻度和中度的高甘油三酯血症(甘油三酯为150~999mg/d1)可以用于心血管疾病风险因素的评估,且重度和极重度高甘油三酯血症(甘油三酯〉1000mg/dI)被认为是胰腺炎的危险因素之一。工作小组同时建议高甘油三酯血症患者评估继发性高脂血症,原发性高甘油三酯血症患者评估血脂异常和心血管疾病的家族史。工作小组建议,中度高甘油三酯血症患者的治疗目标是非高密度脂蛋白胆固醇水平与国家胆固醇教育计划成人治疗小组指南一致。初始治疗应是生活方式治疗,也可考虑饮食改变和药物联合治疗。重度或极重度高甘油三酯血症患者,贝特类药物应作为一线用药。
简介:目的探讨MMP-2和TIMP-2与胶质瘤侵袭性及恶性表型之间的关系及其意义.方法采用Elivision二步免疫组织化学法染色观察MMP-2和TIMP-2在46例不同恶性度胶质瘤及10例正常脑组织中的表达并用德国LeicaQ550cw图像分析系统测其灰度值作为表达强度的量化指标.结果在对照组、低度及高度恶性胶质瘤中,MMP-2的阳性表达率分别为10%、63.6%和95.8%;在对照组、低度及高度恶性胶质瘤中,TIMP-2的阳性表达率分别为10%、36.3%和37.5%.MMP-2在Ⅰ、Ⅱ级和Ⅲ、Ⅳ级胶质瘤中平均灰度值分别为173.27±13.26和98.63±18.20;TIMP-2在Ⅰ、Ⅱ级和Ⅲ、Ⅳ级胶质瘤中平均灰度值分别为210.44±12.95和205.65±9.75.结论MMP-2表达随胶质瘤恶性程度增加而增强,可作为胶质瘤恶性表型及侵袭性指标之一.TIMP-2表达在正常脑组织及不同级别胶质瘤中无明显差异.MMP-2/TIMP-2的比值与胶质瘤侵袭性密切相关.
简介:RolesofKeap1-Nrf2pathwayinbrain:NeuronalsurvivalandneurogenesisareimpairedinneurodegenerativediseasessuchasParkinson’sdiseaseandAlzheimer’sdisease(Winneretal.,2011).Geneticup-regulationofgrowthfactorsenhancedneuronalsurvivalandneurogenesis,improvedneuronalfunctionsandhalteddiseaseprogressioninanimalmodelsofAlzheimer’sdisease
简介:BACKGROUND:Mailuoning,aChineseherb,hasbeenwidelyusedinChinatotreatacuteischemicstroke,andthemajorcomponentexhibitsanti-oxidativeeffects.However,thepreciseanti-oxidationpathwayremainsuncertain.OBJECTIVE:TovalidatetheprotectiveeffectsofMailuoningonH2O2-inducedprimarycorticalneuroninjuryinembryonicmice.DESIGN,TIMEANDSETTING:ComparativeobservationandinvitroexperimentswereperformedattheJiangsuKeyLaboratoryforMolecularMedicinefromJanuary2008toSeptember2009.MATERIALS:Mailuoning(NanjingJinlingMedicalCompany,China),reactiveoxygenspecies(ROS)kit(BeyotimeBiotechnology,China),superoxidedismutase(SOD),Cu/ZnSODkit,malondialdehyde(MDA)kits(NanjingJiancheng,China),mitochondrialmembranepotential(GMS10013.1,GENMED,USA)andcatalaseactivityassaykit(BeyotimeBiotechnology,China)wereutilizedforthepresentstudy.METHODS:MouseembryoniccorticalneuronswereisolatedandculturedwithculturemediumcontainingH2O2(80μmol/L)and/orMailuoning(1.25μg/mL)for24hours.MAINOUTCOMEMEASURES:Neuronalviabilityanddeathweredetectedbymethylthiazolyltetrazdiumandflowcytometry;ROSproductionwasdeterminedbyflowcytometry;mitochondrialmembranepotentialwasdetectedusingfluorescentstaining;SODactivitywasdetectedusingamodifiednitrobluetetrazoliummethod;Cu/ZnSODandcatalaseactivitywasdetectedbyspectrophotometry;andMDAwasdeterminedusingthelipidperoxidationmethod.RESULTS:H2O2increasedROSproductionandMDAconcentration(P<0.05),anddecreasedmitochondrialmembranepotential,SOD,Cu/ZnSODandcatalaseactivity(P<0.05);thenumberofsurvivingneurons(P<0.05)wasalsoreduced.Mailuoningreversedthesechanges.CONCLUSION:MailuoningprotectsH2O2-inducedinjuryincorticalcellsbyinhibitingROSandMDA,increasingdepolarizationofmitochondrialmembrane,andenhancingSODandcatalaseactivity.