简介：1-methyl-4-phenylpyridiniumion(MPP+)inducesendoplasmicreticulumstressandactivatescaspase-12inPC12cells,leadingtoneuronalapoptosis.However,theunderlyingmolecularmechanismremainsunknown.Thepresentstudyinvestigatedtheregulatoryeffectsofnervegrowthfactor(Aktactivator)andlithiumchloride(glycogensynthasekinase-3βinhibitor)ontheendoplasmicreticulumstresssignalingpathway.TheresultsrevealedthatMPP+inducedexpressionofBipandC/EBPhomologousprotein.TheupregulationofBipandC/EBPhomologousprotein,aswellasthedecreasedpro-caspase-12levelinducedbyMPP+wereinhibitedbypretreatmentofthenervegrowthfactororlithiumchloride.Theseresultssuggestthatthephosphatidylinositol3kinase-Akt-glycogensynthasekinase-3βpathwayisinvolvedinMPP+-inducedendoplasmicreticulumstress.

简介：BACKGROUND:ToevaluateandsummarizetheeffectsofcerebralperfusionandvascularreserveonthetreatmentofSICAS.Recently,researchonβ-amyloidproteinhasfocusedontheregulatoryeffectsofes-trogenorphytoestrogenonitsdeposition.However,therehavebeenonlyafewreportsondynamicchangesofβ-amyloidproteindepositioninhippocampusofovariectomizedrats.OBJECTIVE:Tomeasureβ-amyloidproteindepositioninthehippocampalformationofovariectomizedratsbyusingimmunohistochemistry;toobservetime-dependentdynamicchanges.DESIGN:Randomizedcontrolledanimalstudy.SETTING:ThirdXiangyaHospitalofCentralSouthUniversity.MATERIALS:TheexperimentwascarriedoutintheCentralLaboratoryoftheThirdXiangyaHospitalofCentralSouthUniversityfromNovember2005toDecember2006.FiftyhealthyfemaleSpragueDawley(SD)rats,weighing(293±10)g,wereprovidedbytheAnimalLaboratoryofXiangyaMedicalCollege,CentralSouthUniversity.Allratshadneitherachildbearinghistorynorhepaticorrenaldisease,orskeletaldeformity.β-amyloidproteinimmunohistochemicalkitwasprovidedbyWuhanBosterCompany.Theex-perimentwasinaccordancewithanimalethicsstandards.METHODS:Allratswererandomlydividedintofivegroups,includingnormalcontrolgroup(n=10),shamoperationgroup(n=10),andovariectomizedgroup(n=30).Afteranesthesiaintheovariectomizedgroup,thebilateralovarieswereseparatedandresected.Thesamevolumeoffatwasresectedintheshamoperationgroup.Ratsfromthenormalcontrolgroup,however,didnotreceiveanysurgicaltreatments.Ratsinthenormalcontrolgroupandshamoperationgroupweresacrificedbyanesthesia7weeksaftersurgery.Everytenratsfromtheovariectomizedgroupwasrespectivelysacrificedat7,15,and30weeksaftersurgery.Immunohistochemistrywasusedtodetectβ-amyloidproteindepositioninhippocampalsections.Cellcountingandgrayvaluemeasurementsservedtorecordthedynamicchangesin�

简介：Age-relatedmaculardegeneration(AMD)causesirreversiblelossofcentralvisionforwhichthereisnoeffectivetreatment.IncipientpathologyisthoughttooccurintheretinaformanyyearsbeforeAMDmanifestsfrommidlifeonwardstoaffectalargeproportionoftheelderly.Althoughgeneticaswellasnon-genetic/environmentalrisksarerecognized,itscomplexaetiologymakesitdifficulttoidentifysusceptibility,orindeedwhattypeofAMDdevelopsorhowquicklyitprogressesindifferentindividuals.HerewesummarizetheliteraturedescribinghowtheAlzheimer's-linkedamyloidbeta(Aβ)groupofmisfoldingproteinsaccumulateintheretina.ThediscoveryofthiskeydriverofAlzheimer'sdiseaseinthesenescentretinawasunexpectedandsurprising,enablinganaltogetherdifferentperspectiveofAMD.WearguethatAβfundamentallydiffersfromothersubstanceswhichaccumulateintheageingretina,anddiscussourlatestfindingsfromamousemodelinwhichphysiologicalamountsofAβweresubretinally-injectedtorecapitulatesalientfeaturesofearlyAMDwithinashortperiod.OurdiscoveriesaswellasthoseofotherssuggestthepatternofAβaccumulationandpathologyindonoraged/AMDtissuesarecloselyreproducedinmice,includinglate-stageAMDphenotypes,whichmakesthemhighlyattractivetostudydynamicaspectsofAβ-mediatedretinopathy.Furthermore,wediscussourfindingsrevealinghowAβbehavesatsingle-cellresolution,andconsiderthelong-termimplicationsforneuroretinalfunction.WeproposeAβasakeyelementinswitchingtoadiseasedretinalphenotype,whichisnowbeingusedasabiomarkerforlatestageAMD.

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

简介：BACKGROUND:PreparationofGinkgoleafhasbeenwidelyusedtoimprovecognitivedeficitsanddementia,inparticularinAlzheimer'sdiseasepatients.However,theprecisemechanismofactionofGinkgoleafremainsunclear.OBJECTIVE:ToexploretheeffectofGinkgoBilobaextract(Egb761),Ginaton,onβ-secretaseexpressioninrathippocampalneuronalculturesfollowingchronichypoxicandhypoglycemicconditions.DESIGN,TIMEANDSETTNG:Completelybyrandomized,groupingstudy.TheexperimentwasperformedattheLaboratoryofMolecularImaging,SoutheastUniversitybetweenAugust2006andAugust2007.MATERIALS:Atotalof128Wistarratsaged24hourswereselected,andhippocampalneuronswereharvestedforprimarycultures.METHODS:Onday7,primaryhippocampalneuronalculturesweretreatedwithEgb761(0,25,50,100,150,and200μg/mL)underhypoxic/hypoglycemicorhypoglycemiccultureconditionsfor12,24,and36hours,respectively.Hippocampalneuronsculturedinprimaryculturemediumservedascontrol.MAINOUTCOMEMEASURES:Cellviabilitywasassayedusing3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide(MTT);fluorescencedetectionofβ-secretaseactivitywasperformed;WesternBlotwasusedtomeasureβ-secretaseexpression.RESULTS:Cellviabilityunderhypoxic/hypoglycemicorhypoglycemiccultureconditionswassignificantlylessthancontrolcells(P<0.05).Underhypoxic/hypoglycemicorhypoglycemiccultureconditions,treatmentwith25μg/mLEgb761didnotaltercellviability.However,>25μg/mLEgb761inducedgreatercellviability(P<0.05).Nodifferenceswereobservedbetweenhypoxic/hypoglycemicorhypoglycemiccells(P>0.05).α-secretaseactivitywasincreasedafter12hoursinhypoxic/hypoglycemicculture(P<0.01).Therewerenosignificantdifferencesbetweenthe12-,24-,or36-hourEgb761groupsandthehypoxic/hypoglycemicgroups(P>0.05).β-secretaseactivitywasgreaterafter12,24,and36hoursinhypoxic/hypoglycemiccultureconditions,comp

简介：Severalstudieshavedemonstratedthattheamountofbeta-amyloid(Aβ)proteininthebraincanbeloweredbydown-regulatingAβproduction,promotingAβdegradation,reducingAβoligomerizationordeposition,therebyalleviatingsymptomsofAlzheimer'sdisease.Curcuminhasbeenknowntobeaperoxisomeproliferatoractivatedreceptorgamma(PPARγ)agonistandcanobviouslyinhibitAβproductionandoligomerization.Thisstudyinvestigatedtheeffectsofcurcuminontheβ-siteAPPcleavingenzyme1(BACE1)activityandPPARγexpressioninhumanneuroblastomaSH-SY5Ycells,andvalidatedtheinhibitoryeffectsofcurcuminonAβ40/42expressioninthebrain.ResultsrevealedthatPPARγmRNAandproteinexpressioninthehumanneuroblastomaSH-SY5Ycellssignificantlyincreasedwithincreasingcurcuminconcentrationandtimecourse(P<0.05);BACE1mRNAandproteinexpressionandAβ40/42productionsignificantlydecreasedwithincreasingcurcuminconcentrationandtimecourse(P<0.05).ThechangesinPPARγandBACE1expressionduringAβproductioncouldbereversedbythePPARγantagonistGW9662.ThesefindingsindicatethatcurcuminreducedAβproductionbyactivatingPPARγexpressionandinhibitingBACE1expressioninaconcentration-andtime-dependentmanner.

简介：Multiplesclerosis(MS)isachronicautoimmunediseaseofthecentralnervoussystem(CNS)characterizedbycoexistingprocessesofinflammation,demyelination,axonalneurodegeneration,andgliosis.Itisthemostcommondisablingneurologicaldiseaseinyoungadulthood.Althoughautoimmuneinflammationcontributestoaxonalpathology

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简介：BACKGROUND:Ithasbeendemonstratedthattransforminggrowthfactor-β(TGF-β)andbrain-derivedneurotrophicfactor(BDNF)caninducestemcelldifferentiationintoneuron-likecells.OBJECTIVE:ToinvestigatetheefficacyofTGF-βandBDNFatinducingthedifferentiationofadultratbonemarrowstromalcells(BMSCs)intoneuron-likecells,bothincombinationoralone.DESIGN,TIMEANDSETTING:AcomparativeobservationexperimentwasperformedattheDepartmentofOrthopedics,FirstAffiliatedHospitalofLiaoningMedicalUniversitybetweenOctober2007andJanuary2008.MATERIALS:TGF-βandBDNFwerepurchasedfromSigma,USA;mouseanti-ratneuronspecificenolase,neurofilamentandglialfibrillaryacidicproteinwerepurchasedfromBeijingHMHLBiochemLtd.,China.METHODS:BMSCswereisolatedfromratsaged4weeksandincubatedwithTGF-β(1μg/L)and/orBDNF(50μg/mL).MAINOUTCOMEMEASURES:Expressionofneuron-specificenolase,neurofilamentandglialfibrillaryacidicproteinweredeterminedbyimmunocytochemistry.RESULTS:BMSCsdifferentiatedintoneuron-likecellsfollowinginductionofTGF-βandBDNF,andexpressedbothneuron-specificenolaseandneurofilament.ThepercentofpositivecellswassignificantlygreaterinthecombinationgroupthanthoseinducedwithTGF-βorBDNFalone(P<0.01).CONCLUSION:TreatmentofBMSCswithacombinationofTGF-βandBDNFinduceddifferentiationintoneuron-likecells,withtheinductionbeingsignificantlygreaterthanwithTGF-βorBDNFalone.

简介：目的构建大鼠神经营养因子3（NT-3）基因真核表达载体并观察其在真核细胞内的表达情况。方法采用逆转录聚合酶链式反应（RT-PCR）技术从大鼠脑组织总RNA中扩增NT-3基因cDNA序列,将其克隆到真核表达载体pcDNA3中,经酶切鉴定和序列分析后,以阳离子脂质体Li-pofectamine2000介导转染L929细胞,应用免疫细胞化学和westernblot鉴定NT-3在细胞内的表达。结果RT-PCR产物为822bp的特异片段,重组质粒pcDNA3/NT-3酶切后产生822bp和5.2kb的片段,DNA测序证实822bp片段的碱基序列与大鼠NT-3基因序列完全一致,成功构建了pcDNA3/NT-3重组质粒。将其转染真核细胞后,免疫细胞化学、westernblot结果表明NT-3能在真核细胞中正确表达。结论成功构建了重组真核表达质粒载体pcDNA3/NT-3,为后续的研究奠定基础。

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：MEG3a是功能未知的母本印记基因MEG3的新型转录产物，研究表明MEG3a在正常垂体组织中高表达．而几乎在全部无功能性垂体腺瘤、大部分功能性垂体腺瘤中不表达。同时，该基因的异位表达能抑制许多癌细胞株的增殖。包括Hela细胞．MCF-7和H4组蛋白等，因而它可能是一种抑癌基因，其生物学功能与细胞增殖有关。本文就MEG3和MEG3a基因与无功能性垂体腺瘤的关系作简要综述。

简介：脊髓肠源性囊肿(spinalenterogenouscysts,SEC)是一罕见的先天性、发育性畸形.以往命名较纷杂[1-6],WHO的命名是肠源性囊肿(enterogenouscysts)[6-8],并将其定义为"囊肿内壁衬有类似于胃肠道上皮、能分泌粘液的上皮".现将我院救治的3例脊髓肠源性囊肿患者报道如下.

简介：目的检测KA致痫后鼠海马Caspase-3酶活性动态变化.方法运用FIENA法特异性体外检测Caspase-3的活性.结果KA致痫后6h,鼠海马即有Caspase-3活性显著增高,一周内保持高水平,10天开始下降;而正常鼠海马几乎无活性Caspase-3检出.结论Caspase-3参与癫痫后神经细胞的凋亡损害,特异性Caspase-3酶抑制剂能预防癫痫后凋亡的发生.

简介：我院收治3例垂体腺瘤合并脑血管病,现报告如下:例1,男,45岁,因'视力下降、性欲减退2年,头痛2个月'入院.体检:神志清,胡须、阴毛稀少.视力:左0.8,右眼前手动.左眼颞侧、右眼周边视野缺损.双乳房可挤出稀白乳汁.血皮质醇:上午8时为422.29nmol/l,下午4时为313.68nmol/l;血泌乳素(prolactin,PRL)>9.1nmol/l;雌二醇(estradiol,E)<70pmol/l,睾酮(testosterone,T)为5.86nmol/l,其余正常.颅脑CT、MRI示3.7cm×2.8cm大小囊、实性肿块,位于鞍内及鞍上区,视交叉明显受压.行右翼点入路肿瘤切除术.术中见右侧颈内动脉床突上段有大小为3mm的动脉瘤,给予夹闭.肿瘤位于视交叉前下方,有囊性变,质软易吸除.病理报告:垂体腺瘤.诊断:垂体腺瘤并动脉瘤.恢复顺利出院.随访5年无复发.

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简介：目的探讨术前三维稳态构成干扰（3D-CISS）序列和三维时间飞跃（3D-TOF）序列MRI在原发性三叉神经痛责任血管判断中价值。方法回顾性分析2016年1~12月首次行微血管减压术（MVD）治疗的79例原发性三叉神经痛的临床资料。术前均行3D-CISS和3D-TOF序列MRI检查。以术中发现为判断责任血管的标准。结果术中发现单一责任血管56例（70.8%），2支及以上责任血管19例（24.1%），无责任血管4例（5.1%）；责任血管中包含至少一条动脉73例（92.4%），单纯静脉2例（2.5%）。术前影像学检查阳性75例，阴性4例。75例阳性中，术中发现责任血管73例，未发现责任血管2例；4例阴性中，术中发现责任血管2例，2例未发现责任血管。术前3D-CISS和3D-TOF序列MRI判断责任血管的灵敏性为97.3%（73/75），特异性为50.0%（2/4），准确率为94.9%[（73＋2）/79]；判断责任血管包含动脉的灵敏性为98.6%（72/73），特异性为50.0%（3/6），准确率为94.9%[（72＋3）/79]。结论术前3D-CISS联合3D-TOF序列MRI可用于判断原发性三叉神经痛责任血管，尤其对于包含动脉的责任病变，准确率较高，为MVD提供参考信息。

简介：近年来关于糖尿病性癫痫已多有文献报道．而由非酮症性单纯高血糖所引起的癫疴发作则鲜见论述。我院自1996年2月-2006年8月诊断、治疗非酮症性高血糖癫痫患者3例，结果报告如下。

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简介：目的：评价高分辨率3D-FIESTA+c成像及图像处理技术显示脑神经及其病变的价值。方法采用3D-FIESTA+c对20例健康志愿者和20例临床疑是因血管等原因压迫相应脑神经具有临床症状的患者进行扫描及图像后处理。由2名神经放射学医师根据20名健康志愿者480支脑神经显示的清晰程度分为清晰、较清晰、不清晰3个等级，清晰和较清晰定义为显示，不清晰定义为未显示；临床病例中，脑神经与血管关系分为无接触、接触、压迫。结果12对脑神经显示率分别为：嗅神经84.3%，视神经100%，动眼神经100%，滑车神经43.8%，三叉神经100%，外展神经100%，面神经100%，前庭蜗神经100%，舌咽神经、迷走神经及副神经复合体100%，舌下神经47.1%。20例脑神经症状患者，16例确诊为脑神经与周围血管接触或压迫，且均被临床治疗证实。结论高分辨3D-FIESTA+c成像与图像后处理技术相结合可显示脑神经及其病变，能准确定位血管走向及其与脑神经的关系，为临床医生提供准确、全面的影像学资料。