简介:目的研究白细胞介素13受体α2(IL-13Rα2)在脑胶质瘤中的表达及其临床意义。方法采用免疫组化SABC法检测66例胶质瘤(其中Ⅰ-Ⅱ级31例,Ⅲ-Ⅳ级35例)标本中IL-13Rα2蛋白的表达,并利用RT-PCR法检测20例胶质瘤(其中Ⅰ~Ⅱ级8例,Ⅲ-Ⅳ级12例)新鲜标本中IL-13Rα2mRNA的表达,并与5例正常脑组织对照,分析胶质瘤中IL-13Rα2的表达强度与其病理级别的关系。结果Ⅰ-Ⅱ级胶质瘤和Ⅲ-Ⅳ级胶质瘤IL-13Rα2蛋白和mRNA的表达强度均有显著性差异(P〈0.01),病理级别越高其表达越强。在5例正常脑组织中,IL-13Rα2mRNA和蛋白的表达均为阴性,与胶质瘤相比,差异显著(P〈0.01)。结论IL-13Rα2在脑恶性胶质瘤中高表达,在低级别胶质瘤和正常脑组织仅低表达或不表达。提示在某些情况下IL-13Rα2检测有助于良性与恶性胶质瘤的鉴别诊断。而IL-13Rα2也可作为脑恶性胶质瘤靶向治疗的特异性靶标。
简介:BACKGROUND:Alpha-actinin(α-actinin)playsakeyroleinneuronalgrowthconemigrationduringdirectionaldifferentiationfromneuralstemcells(NSCs)toneurons.OBJECTIVE:Todetectinsitumicrodistributionandquantitativeexpressionofα-actininduringdirectionaldifferentiationofNSCstoneuronsinthetemporallobecerebralcortexofneonatalrats.DESIGN,TIMEANDSETTING:BetweenJanuary2006andDecember2008,cultureanddirectionaldifferentiationofNSCswereperformedatDepartmentofHistologyandEmbryology,PreclinicalMedicalCollege,ChinaMedicalUniversity.ImmuneelectronmicroscopywasperformedatDepartmentofHistologyandEmbryologyandDepartmentofElectronMicrology,PreclinicalMedicalCollege,ChinaMedicalUniversity.SpectrumanalysiswasperformedatLaboratoryofElectronMicroscopy,MentalResearchInstitute,ChineseAcademyofSciences.MATERIALS:Basicfibroblastgrowthfactor,epidermalgrowthfactor,brain-derivednervegrowthfactor,type-1insulinlikegrowthfactor,andα-actininantibodywereprovidedbyGibcoBRL,USA;rabbit-anti-ratnestinmonoclonalantibody,rabbit-anti-ratneuronspecificenolasepolyclonalantibody,andEDAX-9100energydispersiveX-rayanalysiswereprovidedbyPHILIPSCompany,Netherlands.METHODS:NSCs,followingprimaryandpassageculture,weredifferentiatedwithserumculturemedium(DMEM/F_(12)+10%fetalbovineserum+2ng/mLbrain-derivednervegrowthfactor+2ng/mLtype-1insulinlikegrowthfactor).MAINOUTCOMEMEASURES:Expressionofα-actinininneuron-likecellswasquantitativelyandqualitativelydetectedwithimmunocytochemistryusingenergydispersiveX-rayanalysis.RESULTS:Immunocytochemistry,combinedwithelectronmicroscopy,indicatedthatpositiveα-actininexpressionwaslikeaspheroidparticlewithhighelectrondensity.Inaddition,theexpressionwasgraduallyconcentratedfromthenuclearedgetothecytoplasmandexpandedintodevelopingneurites,duringdifferentiationofneuralstemcellstoneurons.Conversely,energydispersive
简介:目的探讨抑制细胞外信号调节激酶1/2(ERK1/2)对大鼠弥漫性脑损伤(DBI)后脑组织细胞凋亡的影响。方法按随机数字表法将228只成年SD大鼠随机分为假手术组(n=12)、DBI组(n=72)、阻滞剂组(n=72)、对照组(n=72),后三组按动物处死时间分为30min、3h、24h、48h、72h和7d六个亚组,每亚组12只。参照Mamarou自由落体方法制作重型DBI模型。阻滞剂组损伤后尾静脉注射ERK1/2特异性阻滞剂U0126(0.05mg/kg),对照组注射等量溶剂二甲基亚砜。免疫印迹法法检测脑组织磷酸化ERK1/2(pERK1/2)的表达水平,免疫组化法检测Caspase-3表达,流式细胞术检测细胞凋亡率。结果伤后30min,脑组织pERK1/2表达水平显著增高(P<0.05),并持续高水平表达至72h,伤后7d与假手术组无统计学差异(P>0.05)。伤后3h,脑组织Caspase-3表达水平和细胞凋亡率均明显增高,72h达到高峰,伤后7d仍明显高于假手术组(P<0.05)。伤后30min、3h、24h、48h、72h和7d,阻滞剂组脑组织Caspase-3表达水平和细胞凋亡率均明显低于DBI组和对照组(P<0.05),而DBI组和对照组均无统计学差异(P>0.05)。结论阻滞ERK1/2通路,可显著抑制DBI大鼠脑组织Caspase-3的表达,降低细胞凋亡率。
简介:目的探讨小鼠脑室管膜bcl-2和caspase-3在低氧预适应中的表达变化。方法将Blb/c近交系小鼠随机分为空白对照组(H0组)、低氧对照组(H1组)和低氧预适应组(H4组)。用免疫荧光和激光共聚焦显微镜等技术,测定bcl-2和caspase-3表达的荧光强度。结果H1和H4组的bcl-2表达均显著高于H0组,其中H4组又显著高于H1组。H1和H4组caspase-3的表达显著高于H0组,H4组显著低于H1组。结论低氧预适应过程中,小鼠脑室管膜区通过bcl-2的高表达和caspase-3的低表达,抵御室管膜细胞凋亡,参与脑保护机制。
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简介:BACKGROUND:Drugaddictioninvolvestwomaincentralnervoussystems,namelythedopamineandnoradrenalinesystems.Thesesystemsareprimarilydistributedinfivebrainregions:theventraltegmentalarea,thenucleusaccumbens,theprefrontalcortex,thehippocampus,andthelocuscoeruleus.OBJECTIVE:Toinvestigateregionalchangesofguaninenucleotidebindingprotein-inhabitant2(Gi2)indopaminergicandnoradrenergicneuronsinbrainsofmorphine-tolerantand-dependentrats.DESIGN,TIME,ANDSETTING:ArandomizedcontrolstudywasperformedattheDepartmentofNeu-robiologyintheSecondMilitaryMedicalUniversityofChinesePLA(Shanghai,China)betweenSeptember2002andMarch2004.MATERIALS:Thirty-six,healthy,male,Sprague-Dawley(SD)ratswereusedtoestablishmorphine-dependentmodels.MorphinehydrochloridewasaproductofShenyangFirstPharmaceuticalFactory(China);naloxonehydrochloridewasaproductofBeijingFour-RingPharmaceuticalFactory(China);andαsubunitofGi2antibodywasofferedbySantaCruzBiotechnology,Inc(USA).METHODS:Thirty-sixSDratswererandomlydividedintosixgroups(n=6):(1)acutemor-phine-dependentgroup,(2)acuteabstinentgroup,(3)acutecontrolgroup,(4)chronicmorphine-dependentgroup,(5)chronicabstinentgroup,and(6)chroniccontrolgroup.Ratsintheacutemorphine-dependentandtheacutegroupswereinjectedwithmorphine(5mg/kg),oneinjectioneverytwohours,foratotalofeightinjections.Intheacuteandchronicmorphine-dependentratmodels,morphinewithdrawalsyndromewasprecipitatedbyaninjectionofnaloxone(5mg/kg).Ratsintheacutecontrolgroupweregivenaperitonealinjectionofphysiologicalsalineatthesameadministrationtimeastheabovetwogroups.Ratsinthechronicmorphine-dependentandchronicabstinentgroupswereinjectedwithmorphinethreetimesperday.Theadministrationdoseonday1wasinitially5mg/kgat20:00,whichincreasedby5mg/kgat8:00,12:00,and20:00untilday7.Onday
简介:BACKGROUND:Calciumion(Ca2+)overloadplaysanimportantroleincerebralischemia/reperfusioninjury.Anisodamine,atypeofalkaloid,canprotectthemyocardiumfromischemiaandreperfusioninjurybyinhibitingintracellularcalcium[Ca2+]ioverload.OBJECTIVE:Toinvestigateeffectsofanisodamineon[Ca2+]iconcentrationandcortexultrastructurefol-lowingacutecerebralischemia/reperfusioninrabbits.DESIGN,TIMEANDSETTING:RandomizedandcontrolledtrialwasperformedattheDepartmentofEmergency,TongjiHospital,TongjiMedicalCollegeofHuazhongUniversityofScienceandTechnologyfromSeptembertoDecember2006.MATERIALS:Fortyhealthyrabbitswereusedtoestablishmodelsofacutecerebralischemia/reperfusion.AnisodaminewasprovidedbyLianyungangDongfengPharmaceuticalFactory;Fura-2waspurchasedfromNanjingJianchengBioengineeringInstitute;dual-wavelengthfluorescentspectrophotometrysystemandDM-300softwarewereprovidedbyBio-Rad,USA;OPTON-EM10CtransmissionelectronmicroscopewasproductofSiemens,Germany.METHODS:Fortyrabbitswererandomlydividedintothefollowinggroups:shamoperation,ischemia,ischemia/reperfusion,andanisodamine,withtenrabbitsineachgroup.Modelsofcompletecerebralischemiainjurywereestablished.Inaddition,bloodwascollectedfromthefemoralarteryofratsintheischemia/reperfusionandanisodaminegroupstoinducehypotensionandestablishreperfusioninjurymodels.Thebilateralcommoncarotidarteryclampwasremovedfromtheanisodaminegroup20minutesafterischemia,andanisodamine(10mg/kgbodymass)wasinjectedviathefemoralvein.Rabbitsintheshamoperationgroupunderwentonlyvenouscannulation.MAINOUTCOMEMEASURES:[Ca2+]iconcentrationwasdeterminedusingadual-wavelengthfluorescentspectrophotometrysystem,andcorticalultrastructurewasobservedfollowinguranyl-leadcitratestaining.RESULTS:Thelevelsof[Ca2+]iintheischemiaandischemia/reperfusiongroupsweresignificantlyin-creased,c
简介:目的探讨重T2加权灰阶反转成像检查对大垂体腺瘤及其周围结构的显示作用。方法对15例术前有视力障碍的垂体瘤病人行重T2加权灰阶反转成像及常规T1加权成像,前者TR/TE为5800ms/259ms,后者为600ms/20ms;层厚3mm。结果重T2加权灰阶反转成像可清晰显示肿瘤与终板、前连合及前交通动脉丛的空间关系;其视神经、视交叉和视束的检测率分别为93.3%、100%和86.7%,而在T1加权成像中则分别为66.7%、93.3%和66.7%,前者对视路的检测率显著性高于后者。结论重T2加权灰阶反转成像可清楚显示垂体大腺瘤与视路的位置关系,有助于垂体瘤经颅手术的术前策略制定。
简介:目的筛选小鼠嗅球发育中凋控同源盒转录因子2(DLX2)的相关基因,探讨室管膜前下区神经干细胞在嗅球中向多巴胺神经元分化的机制。方法利用16844点的高密度Oligo芯片检测发育期嗅球的基因表达情况,采用基因神经网络分析,筛选与DLX2相关的基因。结果从2398个在4个时间点都表达的基凶中筛选出623个差异基因,在相关系数设定为0.95水平上,共筛选出29个与DLX2相关的基因。29个基因中,已知功能的基因有13个,主要与代谢、凋亡、发育及信号传导功能相关,未知功能的基因有16个。结论在嗅球中可能有29个基因参与了DLX2的表达调控,对它们进一步的研究将有助于理解室管膜前下区神经干细胞在嗅球中向多巴胺神经元分化的机制。
简介:目的研究阻滞弥漫性脑损伤急性期ERKI/2信号通路过度激活对星形胶质细胞反应的影响。方法制作大鼠外伤性弥漫性脑损伤模型,打击损伤前30min自尾静脉注射U0126。Westemblot法检测损伤脑皮层pERKl/2表达水平,免疫组化染色法检测pERKl/2和GFAP在损伤脑组织中的表达。结果pERKl/2表达在损伤后迅速、显著升高,5min为表达高峰,其后下降,但直到损伤后72h都有高水平表达,至7d下降至基础水平。损伤后各个时间点,U0126组pERKl/2水平较DBI组明显降低(P〈0.05)。U0126组与DBI组比较,12~72h各时间点GFAP阳性细胞平均光密度值降低(P〈0.05)。结论弥漫性脑损伤诱导了强烈的ERKl/2信号通路激活和星形胶质细胞反应。U0126能够剂量依赖性抑制GFAP的表达,抑制急性期星形胶质细胞反应。
简介:目的:通过监护仪所示的呼吸率、心率和血氧饱和度(SpO2)参数探索肺源性心脏病病理生理变化的昼夜生物节律特征。方法,15例样本均符合肺源性心脏病诊断标准,其中男12例,女4例,平均年龄68岁,设置6个时点:0点、4点、8点、12点、16点、20点,从24h监护仪中获取呼吸率(次数)、心率(次数)和SpO2(百分率)的监测数据,分项输入余弦法程序进行生物节律分析。结果:在所观测的15个病例中,呼吸率9例和心率10例的峰值相位位于356.89°--84.50°(23点44分-4点36分),其中5例其中5例P〈0.05,提示有显著生物节律特征。SpO2的峰值相位,12例位于-130.60°--310.16°(8点20-20点20分),其中5例P〈0.05,提示有显著生物节律特征。结论:肺源性心脏病例的呼吸率和心率夜间明显快于白天,SpO2明显夜间低于白天,提示该病的病理生理具有昼夜生物节律特征。
简介:目的:探讨合并睡眠障碍的2型糖尿病患者在干预过程中采用短期胰岛素强化治疗方案对血糖水平和预后的影响。方法:选取2017年7月至2018年7月新疆医科大学附属医院收治的2型糖尿病合并睡眠障碍的患者120例,随机分为观察组和对照组,每组60例。对照组采用常规降糖治疗方案,观察组采用短期胰岛素强化治疗方案。对血糖水平、睡眠质量评分展开比较。结果:2组治疗前,经测定空腹及餐后2h血糖比较,差异无统计学意义(P>0.05),治疗后检测值均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05)。观察组治疗后睡眠质量各维度日间功能、睡眠质量、睡眠障碍、睡眠效率、入睡时间评分均高于对照组,差异有统计学意义(P<0.05)。结论:2型糖尿病合并睡眠障碍的患者,在干预过程中,应和短期胰岛素强化治疗方案,可有效稳定血糖水平,增强睡眠质量。
简介:目的探讨亚低温治疗对颅脑损伤后Calpain、MAP-2基因和蛋白表达的影响。方法将54只SD大鼠随机分为假手术组(n=6)、常温脑损伤组(n=24)和亚低温脑损伤组(n=24)。亚低温脑损伤组在液压打击伤后即接受持续4h的亚低温治疗。伤后6h、12h、24h和72h4个时间点分别处死3只常温脑损伤组和亚低温脑损伤组大鼠。荧光PCR、Westernblot半定量检测皮质Calpain及MAP-2基因转录和蛋白的表达。结果颅脑损伤后12h及24h亚低温使CalpainmRNA表达增加(P〈0.05),伤后6h、12h、24h和72h亚低温均可减少Calpain蛋白的升高,伤后12h及72h尤其显著(P〈0.05)。与假手术组比较,常温脑损伤组和亚低温脑损伤组MAP-2基因转录均减少(P〈0.05);与常温脑损伤组比较,伤后6h、12h和24h亚低温可抑制MAP-2基因转录的下调,但亚低温脑损伤组MAP-2蛋白的表达均比同时间点常温组低(P〈0.05)。结论颅脑损伤后亚低温治疗的脑保护机制可能与调节Calpain蛋白的表达有关,而亚低温与MAP-2的关系还有待进一步研究。