简介:目的探讨室管膜下瘤的临床、影像学和病理特点。方法对9例室管膜下瘤患者的临床资料进行回顾性分析,对手术切除的肿瘤组织标本进行病理及免疫组化检查。结果本组患者的男女比例为2∶1,平均年龄54岁;术后随访10~109个月,均无转移和复发。MRI检查示,肿瘤位于侧脑室内8例、右颞叶1例,T1WI呈等信号6例、低信号及高信号各1例,T2WI高信号6例、等信号2例;增强扫描轻度增强、无明显强化各4例。病理检查示,瘤组织胶质纤维丰富,瘤细胞成簇状分布其间;除1例右颞叶肿瘤无微囊结构外,其余均有微囊形成。免疫组化检查:瘤细胞胶质纤维酸性蛋白(GFAP)、S-100、波形蛋白(Vimentin)阳性表达,突触素(SYN)、上皮膜抗原(EMA)、神经元特异性核心抗原(Neu-N)为阴性;Ki-67标记指数4%1例,1%~3%8例。结论室管膜下瘤多发于老年男性,进展缓慢,预后较好。其大多发生在侧脑室内,发生在脑实质的少见。认识其临床、影像学和病理特点有利于诊断及治疗。
简介:BACKGROUND:Matrixmetalloproteinase-9(MMP-9)expressionincreaseswithintracerebralhemorrhage,andparticipatesinthepathophysiologicalprocessesofsecondarybraininjuryafterintracerebralhemorrhage.OBJECTIVE:ToinvestigatetheeffectsofmildhypothermiaonMMP-9expressionandbrainedemaintheperihematomalregionofexperimentalintracerebralhemorrhagerats.DESIGN,TIMEANDSETTING:Therandomized,controlledexperimentwasperformedattheCentralLaboratoryofShandongProvincialHospitalbetweenMayandSeptember2007.MATERIALS:Seventy-two,Wistar,malerats,12-weeksold,wereusedforthisstudy.Rabbitanti-MMP-9primaryantibodywaspurchasedfromBoster,China.METHODS:Wistarratswereequallyandrandomlydividedintonormothermiaandmildhypothermiagroups.Thetwogroupseachcomprisedcontrol,6-hourintracerebralhemorrhage,24-hourintracerebralhemorrhage,48-hourintracerebralhemorrhage,72-hourintracerebralhemorrhage,and1-weekintracerebralhemorrhagesubgroups,withsixratsineachsubgroup.Ratmodelsofintracerebralhemorrhagewereestablishedbyinjecting100μLofautologousbloodintotheratcaudatenucleus.Ratsinthemildhypothermiagroupreceivedfourhoursoflocalmildhypothermiaimmediatelyfollowingtheinjection.Intracerebraltemperaturewasmaintainedat(33±0.5)℃.Subsequently,intracerebraltemperaturewasspontaneouslyrecoveredat25℃.Ratsinthecontrolsubgroupwerenotinjectedwithautologousbloodandreceivedonlywithintracerebralhemorrhage.MAINOUTCOMEMEASURES:BrainwatercontentandMMP-9expressionsurroundingthehematomaregion.RESULTS:MMP-9expressionincreasedat6hours,andbrainedemareachedapeakat48hoursafterintracerebralhemorrhage.MMP-9expressionwassignificantlydecreasedinthemildhypothermiagroupcomparedwiththenormothermiagroupateachtimepoint(P<0.05).CONCLUSION:MildhypothermiacansignificantlyinhibitMMP-9overexpressionandrelievebrainedemafollowingintracerebralhemo
简介:目的分析急性颅内血肿清除术后继发对侧颅内血肿的发生时间,形成原因及预防治疗.方法我们自1989年9月~2001年8月收集共9例,行颅内血肿清除术.结果9例第一次手术回病房后,昏迷4例,手术对侧瞳孔逐渐增大24h内再次CT复查,发现对侧颅内血肿.另5例在第一次手术后48h复查CT,均提示手术对侧颅内血肿,血肿量在30-80ml,其中5例为脑挫裂伤伴硬脑膜下血肿,中线结构移位明显,2例为颞枕部硬膜外血肿,2例为颞叶脑内血肿.硬膜外血肿2例和颞叶脑内血肿2例手术治疗,预后良好.5例脑挫裂伤伴硬膜下血肿立即行手术治疗,清除血肿,4例血肿清除后脑搏动较弱,5例均行硬膜减张缝合并去骨瓣.手术后死亡3例,2例手术后有偏瘫.结论一侧外伤性颅内血肿在手术后继发血肿的发生率为0.8%~2.2%,多发生在48~72h之内[1].其形成原因是多方面的:急性颅内压增高引起的血管自主调节丧失,血管床扩张淤血,脑血管内外压力差增大可能也是重要因素[2].并且常在脑挫裂伤的基础上继发出血,亦可因过度换气,使用脱水降压剂及去骨瓣减压不当使颅内压骤降有关.
简介:BACKGROUND:Theintegrityofthebloodbrainbarrier(BBB)playsanimportantroleinthepatho-physiologicalprocessofcerebralischemia/reperfusioninjury.Ithasbeenrecentlyobservedthatmetalloproteinase-9(MMP-9)iscloselyrelatedtocerebralischemia/reperfusioninjuryOBJECTIVE:ThisstudywasdesignedtoobserveMMP-9expressionintheratbrainaftercerebralischemia/reperfusioninjuryandtoinvestigateitscorrelationtoBBBpermeability.DESIGN,TIMEANDSETTING:Thisstudy,arandomizedcontrolledanimalexperiment,wasperformedattheInstituteofNeurobiology,CentralSouthUniversitybetweenSeptember2005andMarch2006.MATERIALS:NinetyhealthymaleSDrats,aged3–4months,weighing200–280g,wereusedinthepresentstudy.Rabbitanti-ratMMP-9polyclonalantibody(Boster,Wuhan,China)andEvansblue(Sigma,USA)werealsoused.METHODS:Allratswererandomlydividedinto9groupswith10ratsineachgroup:normalcontrolgroup,sham-operatedgroup,andischemiafor2hoursfollowedbyreperfusionfor3,6,12hours,1,2,4and7daysgroups.Intheischemia/reperfusiongroups,ratsweresubjectedtoischemia/reperfusioninjurybysutureocclusionoftherightmiddlecerebralartery.Inthesham-operatedgroup,ratsweremerelysubjectedtovesseldissociation.Inthenormalcontrolgroup,ratswerenotmodeled.MAINOUTCOMEMEASURES:BBBpermeabilitywasassessedbydeterminingthelevelofeffusionofEvansblue.MMP-9expressionwasdetectedbyanimmunohistochemicalmethod.RESULTS:All90ratswereincludedinthefinalanalysis.BBBpermeabilityalterationwascloselycorrelatedtoischemia/reperfusiontime.BBBpermeabilitybegantoincreaseatischemia/reperfusionfor3hours,thenitgraduallyreachedapeaklevelatischemia/reperfusionfor1day,andthereafteritgraduallydecreased.MMP-9expressionbegantoincreaseatischemia/reperfusionfor3hours,thengraduallyreacheditspeaklevel2daysafterperfusion,andthereafteritgraduallydecreased.CONCLUSION:
简介:目的研究不同级别人脑胶质瘤MMP-9、E-cad、nm23的表达变化。方法采用免疫组化方法检测96例人脑胶质瘤组织中MMP-9、E-cad、nm23的表达。按照2007年WHO中枢神经系统肿瘤分类标准分级:Ⅰ级4例,Ⅱ级35例,Ⅲ级27例,Ⅳ级30例。另选取5例正常脑组织作为对照组,均为非颅内疾病死亡的尸检标本。结果随着胶质瘤病理级别增高,MMP-9表达显著增加(rs=-0.322,P〈0.01),nm23表达显著降低(rs=-0.355,P〈0.05)。E-cad阳性表达与胶质瘤级别无明显相关性(P〉0.05)。MMP-9与E-cad表达呈显著负相关(rs=-0.440,P〈0.01),E-cad与nm23表达呈显著正相关(rs=0.325,P〈0.01)。结论MMP-9、E-cad、nm23在不同级别胶质瘤中表达水平不一样。
简介:Basementmembranedegradationandblood-brainbarrierdamageappearaftercerebralinfarction,severelyimpactingneuronalandbrainfunctioning;however,theunderlyingpathogeneticmechanismsremainpoorlyunderstood.Inthisstudy,weinducedcerebralinfarctioninstrokepronespontaneouslyhypertensiveratsbyintragastricadministrationofhigh-sodiumwater(1.3%NaCl)for7consecutiveweeks.Immunohistochemicalandimmunofluorescenceassaysdemonstratedthat,comparedwiththenon-infarctedcontralateralhemisphere,stroke-pronespontaneouslyhypertensiveratsonnormalsodiumintakeandWistar-Kyotorats,matrixmetalloproteinase-9expression,thenumberofbloodvesselswithdiscontinuouscollagenIVexpressionandmicrovesseldensityweresignificantlyhigher,andthenumberofcontinuouscollagenIV-positivebloodvesselswaslowerintheinfarctborderzonesofstroke-pronespontaneouslyhypertensiveratsgivenhigh-sodiumwater.Linearcorrelationanalysisshowedmatrixmetalloproteinase-9expressionwaspositivelycorrelatedwiththenumberofdiscontinuouslycollagenIV-labeledbloodvesselsandmicrovesseldensityincerebralinfarctsofstroke-pronespontaneouslyhypertensiverats.Theseresultssuggestthatmatrixmetalloproteinase-9upregulationisassociatedwithincreasedregionalangiogenesisanddegradationofcollagenIV,themajorcomponentofthebasallamina,instroke-pronespontaneouslyhypertensiveratswithhigh-sodiumwater-inducedfocalcerebralinfarction.
简介:目的探讨大鼠局灶性脑缺血后脑内水通道蛋白-9(AQP-9mRNA)表达与脑水肿动态变化的关系,评价依达拉奉的干预作用。方法216只雄性Sprague—Dawley(SD)大鼠随机分为3组:假手术组(A组,6只),生理盐水组(B组,大脑中动脉阻断后6h、12h、24h、48h、72h、5d、7d7个时点,各6只),依达拉奉处理组(C组,同B组),术后即刻予以依达拉奉干预。分别测定脑组织含水量;实时荧光定量PCR(realtimequantitativepolymerasechainreaction,RT—PCR)法检测mRNA表达;用HE染色方法观察病理形态学改变。结果B组大鼠MCAO后脑组织含水量呈上升趋势,48h达高峰,各时点均高于与A组(P〈0.05)。同时,AQP-9mRNA表达量与脑含水量呈相同趋势改变,相关性分析表明AQP-9mRNA表达量(r=0.788,P〈0.05)与脑组织含水量呈正相关。B组与C组相比,各时点脑组织含水量明显下降(P〈0.05);AQP-9mRNA表达显著下调(P〈0.05);组织病理提示脑水肿及神经元损伤程度减轻。结论大鼠脑缺血后脑内AQP-9mRNA表达与脑水肿变化呈正相关,提示AQP-9可能参与大脑中动脉阻断后的脑水肿形成。依达拉奉干预可减少AQP-9mRNA的表达,从而减轻大鼠大脑中动脉阻断后脑水肿,减少神经元坏死,改善神经功能预后。
简介:目的探讨发病6-9h动脉溶栓治疗对美国国立卫生研究院卒中量表(NationalInstitutesofHealthStrokeScale,NIHSS)〈5分的急性缺血性卒中患者的治疗效果。方法回顾86例发病距接受治疗的时间6-9h的急性缺血性卒中(NIHSS〈5分)患者资料,比较选择性尿激酶动脉溶栓和口服阿司匹林2种治疗方法的发病7d和90d效果。结果与口服阿司匹林组相比,选择性动脉溶栓组患者发病7d的Barthel指数(Barthelindex,BI)较对照组明显改善(81.3±7.9vs54.5±9.3,P=0.034),改良Rankin量表(modifiedRankinScale,mRS)评分〈3分的患者比例明显增加(88.4%vs48.8%,P=0.028);但在90d后,两组患者的BI及mRS之间没有显著差异。结论对急性轻型缺血性卒中6-9h积极的动脉尿激酶溶栓治疗可以促进患者的早期恢复。
简介:目的以6一羟基多巴胺(6一OHDA)为工具药,建立帕金森病(PD)的细胞模型,观察褐藻多糖硫酸酯(Fuc)对细胞模型的保护作用并初步探讨其作用机制。方法用不同浓度(12.5、25、50、100、200μmol/L)的6-OHDA处理MN9D细胞24h,挑选出合适浓度50μmol/L。再以50μmolfL6-OHDA处理MN9D细胞不同时间(6、12、24及48h),建立细胞损伤模型,挑选出合适时间24h。用0.01、0.1、1.0mg/mLFuc预孵育MN9D细胞1h后加入50μmol/L6-OHDA共同作用24h,以探讨Fuc的保护作用。MTT法检测细胞存活率,生化法测定乳酸脱氢酶(LDH)释放量.二氯荧光素乙二酯(DCF—DA)染色法检测细胞内的氧化应激水平。结果随着6.OHDA浓度增加或作用时间延长,MN9D细胞MTT值逐渐降低。50μmol/L6.OHDA处理细胞24h,MTT值明显下降,LDH释放量增加。而0.1、1.0mg/mL的Fuc预孵育1h可明显减轻MN9D细胞的损伤,提高MTT值并降低LDH释放量,细胞形态学改变与生化实验结果一致。50μmol/L6-OHDA作用8h可明显升高MN9D细胞内的氧化应激水平,而1.0mg/mL的Fuc预处理1h可以拮抗6-OHDA引起的细胞内氧化应激水平增高。结论Fuc可以有效的拮抗6-OHDA对MN9D细胞的损伤作用,其作用机制可能与抗氧化活性有关。
简介:目的探讨伴高血压急性脑梗死患者血清基质金属蛋白酶-9(MMP-9)水平变化及意义。方法选择临床上发病3天内入院的伴有原发性高血压病的急性前循环脑梗死患者65例,不伴原发性高血压病的急性前循环脑梗死的患者43例,原发性高血压病患者30例,健康对照组30例,采集空腹静脉血。用ELISA法检测其血清MMP-9水平。结果伴有原发性高血压病急性脑梗死组患者血清MMP-9水平(316.18±52.26ng/ml)明显高于其他三组(均P〈0.01),不伴原发性高血压病的脑梗死组患者血清MMP-9水平(287.65±48.83ng/ml)明显高于原发性高血压病组(206.82±44.22ng/ml)和健康对照组(112.16±36.28ng/ml)(均P〈0.01)。原发性高血压组患者血清MMP-9水平明显高于对照组(P〈0.01)。结论高血压病患者及脑梗死患者血清MMP-9均有明显增高,血清MMP-9的活性增强可能是高血压导致脑梗死发生的机制之一,血清MMP-9可能在高血压脑梗死患者的发病及继发的病理损害中发挥更为重要的作用。血清MMP-9可以作为高血压病患者脑梗死前的预警指标。
简介:目的观察单唾液酸四己糖神经节苷脂(GM1)对急性低压氧后基质金属蛋白酶9(MMP9)表达的影响,探讨MMP9在GM1预防低压氧脑水肿中可能的机制。方法24只雄性C57BL/6小鼠随机分成4组(n=6):分别为对照(contr01)组、急性低压氧(HH)组、GM1治疗(GM1+HH)组、单纯给药(GM1)组。control组:置于低压氧舱外的常氧舱内;HH组:置于6000m海拔模拟舱内24h;HH+GM1组:连续腹腔注射GM13d(30mg/kg),最后一次给药后30min行急性低压氧处理,方法同HH组;GM1组:前期GM1处理同HH+GM1组,后期同control组处理。小鼠在急性低压氧处理24h后应用免疫荧光和Westernblot检测MMP9蛋白表达水平,通过湿重比和伊文思蓝定量评价脑水肿程度。结果GM1降低急性低压氧24h后血脑屏障损伤,减少湿重比(P〈0.05)和伊文思蓝渗出量(P〈0.05),并抑制MMP9表达上调(P〈0.05),减弱星形胶质细胞MMP9荧光强度。结论GM1抑制MMP9表达上调,可能参与其预防急性低压氧脑水肿的机制中。