简介:患者,女,32岁,以“头颈部反复酸痛3年,伴视物模糊半年”为主诉于2013年12月3日入院,神经系统体格检查未见明显异常.入院后头颅MRI平扫示:右侧后颅窝可见1个类圆形异常信号软组织块影,大小约5.5cm×3.7cm×3.2cm,T1WI等低信号,T2WI高低混杂信号,内可见血管流空信号,未见“脑膜尾征”.磁共振扩散加权成像(diffusionweightedimaging,DWI)信号稍高,增强扫描肿块明显强化,未见明显坏死区,其后上缘宽基底与小脑幕相连,与右侧横窦分界不清,邻近小脑组织明显受推压并见水肿带,第四脑室明显受压变窄并左移,桥脑轻度受压,第三脑室及双侧侧脑室明显扩张,蝶鞍稍扩
简介:目的分析我国急性脑梗死患者院前延误的影响因素。方法中国国家卒中登记数据库于200侔9月到2008年8月连续收集来自全国各地152家二级和三级医院的急性卒中住院患者。本研究利用该数据库中的患者信息,以发病至到院时间大于3h为院前延误,通过单因素和多因素Logistic回归分析,探讨急性缺血性卒中患者院前延误的影响因素。结果本研究对来自中国国家卒中登记数据库的10505例急性脑梗死患者进行院前延误影响因素的分析,结果发现仅有21.58%的患者(n=2267)在发病5h内到达医院。导致院前延误时间缩短的因素有:老龄[调整后的比值比(oddsratio,OR)0.992,95%可信区间(confidenceinterval,CI)0.988~0.9971、使用急救车到达医院(调整后的OR0.540,95%C/0.500~0.584)、饮酒史(调整后的DR0.895,95%C/0.802~0.999)、冠状动脉粥样硬化性心脏病史(调整后的OR0.786,95%C/0.684~0.905)、心房颤动病史(调整后的OR0.555,95%引0.452.~0.635)、首发症状为意识障碍(调整后的OR0.660,95%010.561~0.776)。导致院前延误时间延长的因素:单独居住(调整后的OR1.760,95%纠1.507~2.571)、自费医疗(调整后的OR1.255,95%C/1.081~1.411)、睡醒时发现症状(调整后的OR1.678,95%C/1.489~1.891)、发病前改良Rankin量表(modifiedRankinScale,mRS)评分≥2分(调整后的OR1.445,95%C/1.207-1.750)、高血压病史(调整后的OR1.114,95%C/1.004-1.2-38)、糖尿病病史(调整后的0R1.141,95%C/1.006~1.295)、首发症状为失语(调整后的DR1.580,95%C/1.259~1.556)、首发症状为视野缺损(调整后的OR1.458,95%d1.056~2.051)。结论我国脑梗死患者的院前延误现象比较严重,提高公众对卒中的认识,加强院前急救系统的�
简介:ThedefiningneuropathologicalfeatureofParkinson’sdisease(PD)isthelossofnigrostriataldopaminergic(DA)projections.Thisresultsinabiochemicalreductionofstriataldopaminelevelsandmovementdisorders,suchasatremoratrest,rigidityofthelimbs,bradykinesia,andposturalinstability(Kimetal.,2011;Kimetal.,2012;BurkeandO’Malley,2013;Leemetal.,2014;Nametal.,2014).BecausetheetiologyofPDisnotfullyunderstood,itcannotguidethedevelopmentofknowledge-basedtargetedtherapeutics.
简介:Parkinson’sdisease(PD)isanage-relatedneurodegenerativedisordercharacterizedbytypicalmotorsignsandsymptomsthatareduetodopamine(DA)depletioninthebasalganglia.ThetreatmentofPDissymptomatic,andaimsatreplacingthelostDAinputusingeitherL-DOPAorDAagonists.ThecausesofPDareunknownin
简介:Oxidativestressiscloselyassociatedwithsecondarycelldeathinmanydisordersofthecentralnervoussystemincludingstroke,Parkinson’sdisease,Alzheimer’sdisease.Amongmanyaberrantoxidativestress-associatedproteins,DJ-1hasbeenassociatedwiththeoxidativestresscelldeathcascadeprimarilyinParkinson’sdisease.Althoughprincipallyexpressedinthecytoplasmandnucleus,DJ-1canbesecretedintotheserumunderpathologicalcondition.Recently,aclosepathologicalassociationbetweenDJ-1andoxidativestressinstrokehasbeenimplicated.Tothisend,weandothershavedemonstratedtheimportantroleofmitochondriainneuroprotectionforstrokebydemonstratingthatthetranslocationofDJ-1inthemitochondriacouldpotentiallymitigatemitochondrialinjury.Here,wediscussourrecentfindingstestingthehypothesisthatDJ-1notonlyfunctionsasaformofintracellularprotectionfromoxidativestress,butthatitalsoutilizesparacrineand/orautocrinecuesinordertoaccomplishextracellularsignalingbetweenneighboringneuronalcells,resultinginneuroprotection.ThisarticlehighlightsrecentevidencesupportingthestatusofDJ-1askeyanti-oxidativestresstherapeutictargetforstroke.
简介:Thehippocampalregionofthebrainisimportantforencodingenvironmentinputsandmemoryformation.However,theunderlyingmechanismsareunclear.ToinvestigatethebehaviorofindividualneuronsinresponsetosomatosensoryinputsinthehippocampalCA1region,werecordedandanalyzedchangesinlocalfieldpotentialsandthefiringratesofindividualpyramidalcellsandinterneuronsduringtailclampinginurethane-anesthetizedrats.Wealsoexploredthemechanismsunderlyingtheneuronalresponses.Somatosensorystimulation,intheformoftailclamping,changedlocalfieldpotentialsintothetarhythm-dominatedwaveforms,decreasedthespikefiringofpyramidalcells,andincreasedinterneuronfiring.Inaddition,somatosensorystimulationattenuatedorthodromic-evokedpopulationspikes.TheseresultssuggestthatsomatosensorystimulationsuppressestheexcitabilityofpyramidalcellsinthehippocampalCA1region.Increasedinhibitionbylocalinterneuronsmightunderliethiseffect.Thesefindingsprovideinsightintothemechanismsofsignalprocessinginthehippocampusandsuggestthatsensorystimulationmighthavetherapeuticpotentialforbraindisordersassociatedwithneuronalhyperexcitability.
简介:Hypoxia-induciblefactor1(HIF-1)attenuatesamyloid-betaproteinneurotoxicityanddecreasesapoptosisinducedbyoxidativestressorhypoxiaincorticalneurons.Inthisstudy,weconstructedarecombinantadeno-associatedvirus(rAAV)vectorexpressingthehumanHIF-1αgene(rAAV-HIF-1α),andtestedtheassumptionthatrAAV-HIF-1αrepresseshippocampalneuronalapoptosisinducedbyamyloid-betaprotein.OurresultsconfirmedthatrAAV-HIF-1αsignificantlyreducesapoptosisinducedbyamyloid-betaproteininprimaryculturedhippocampalneurons.DirectintracerebralrAAV-HIF-1αadministrationalsoinducedrobustandprolongedHIF-1αproductioninrathippocampus.SinglerAAV-HIF-1αadministrationresultedindecreasedapoptosisofhippocampalneuronsinanAlzheimer’sdiseaseratmodelestablishedbyintracerebroventricularinjectionofaggregatedamyloid-betaprotein(25–35).OurinvitroandinvivofindingsdemonstratethatHIF-1haspotentialforattenuatinghippocampalneuronalapoptosisinducedbyamyloid-betaprotein,andprovidesexperimentalsupportfortreatmentofneurodegenerativediseasesusinggenetherapy.