简介:AIM:ToinvestigatetheroleoftheoverexpressionofB7-H3inapoptosisincolorectalcancercelllinesandtheunderlyingmolecularmechanisms.METHODS:SW620cellsthathighlyoverexpressedB7-H3(SW620-B7-H3-EGFP)andHCT8cellsstablytransfectedwithB7-H3shRNA(HCT8-shB7-H3)werepreviouslyconstructedinourlaboratory.CellstransfectedwithpIRES2-EGFPwereusedasnegativecontrols(SW620-NCandHCT8-NC).Real-timePCRandwesternblottinganalysiswereusedtodetectthemRNAandproteinexpressionsoftheapoptosisregulatorproteinsBcl-2,Bcl-xlandBax.Acellproliferationassaywasusedtoevaluatethesurvivalrateanddrugsensitivityofthecells.Theeffectofdrugresistancewasdetectedbyacellcycleassay.Activecaspase-3westernblottingwasusedtoreflecttheanti-apoptoticabilityofcells.WesternblottingwasalsoperformedtodeterminetheexpressionofproteinsassociatedwiththeJak2-STAT3signalingpathwayandtheapoptosisregulatorproteinsafterthetreatmentwithAG490,aJak2specificinhibitor,inB7-H3overexpressingcells.ThedatawereanalyzedbyGraphPadPrism6usinganon-pairedt-test.RESULTS:WhetherbyoverexpressioninSW620cellsordownregulationinHCT8,B7-H3significantlyaffectedtheexpressionofanti-andpro-apoptoticproteins,atboththetranscriptionalandtranslationallevels,comparedwiththenegativecontrol(P<0.05).AcellproliferationassayrevealedthatB7-H3overexpressionincreasedthedrugresistanceofcellsandresultedinahighersurvivalrate(P<0.05).Inaddition,theresultsofcellcycleandactivecaspase-3westernblottingprovedthatB7-H3overexpressioninhibitedapoptosisincolorectalcancercelllines(P<0.05).B7-H3overexpressionimprovedJak2andSTAT3phosphorylationand,inturn,increasedtheexpressionofthedownstreamanti-apoptoticproteinsB-cellCLL/lymphoma2(Bcl-2)andBcl-xl,basedonwesternblotting(P<0.05).AftertreatingB7-H3overexpressingcellswiththeJak2-specificinhibitorAG490,thephosphorylationofJak2andSTAT3,andtheexp
简介:AIM:ToevaluatethecompletionrateanddiagnosticyieldofthePillCamSB2-exincomparisontothePillCamSB2.METHODS:Twohundredcasesusingthe8-hPillCamSB2wereretrospectivelycomparedto200casesusingthe12hPillCamSB2-exatatertiaryacademiccenter.Endoscopicallyplacedcapsuleswereexcludedfromthestudy.Demographicinformation,indicationsforcapsuleendoscopy,capsuletype,studylength,completionofexam,clinicallysignificantfindings,timestampofmostdistantfinding...
简介:目的研究代谢综合征组分与非酒精性脂肪性肝病的关系。方法采用二分类组间比较与多分类趋势分析,比较MS组与非MS组之间、MS组分分组之间样本特征;对符合MS组分标准的患者发生NAFLD的影响因素进行二项Logistic回归分析,并拟合预测方程。结果MS组的BMI、TC、DBP、SBP、TG、SUA水平值和NAFLD的患病率显著髙于非MS组(P<0.05);HDL-C与MAU水平值显著低于非MS组(P<0.05)。MS组分分组中,随着代谢异常组分的增加,BMI、FPG、DBP、SBP、TG、MAU、SUA水平与NAFLD患病率升髙。年龄、BMI、TC、FPG和TG是MS患者发生NAFLD的独立影响因素(P<0.05);拟合方程为:Logit(P)=-19.476+0.08年龄+0.457BMI-1.326TC+0.918FPG+2.679TG。结论MS组分与NAFLD关系密切;年龄、BMI、TC、FPG和TG是MS患者发生NAFLD的独立影响因素;拟合方程可用于NAFLD的预测判断,为临床筛查识别髙风险患者。
简介:LongbeforethediscoveryofHelicobacterpylori,thereweremanyexcellentobservationalstudiesthatdocumenteddifferencesinthepatternsofgastroduodenaldisease.Itwasclearthatinthedevelopingworld,gastriculcerandgastriccancerweremorecommonthaninthedevelopedworldwhereduodenalulcerpredominated.Thiscorrelatedwiththedistributionofgastritisinduodenalulcerpatientswheretheinflammationwasantralpredominantwhileingastriculcerpatientsthegastritiswasmoreevenlydistributedthroughthestomach.Gastriculcersusuallyappearedinafairlyrestricteddistributioninthestomachneartheangulusandclosetothetransitionalzonebetweenantrumandbodymucosa.Asasocietydevelopedsothesepatternsofdiseasechanged.
简介:背景:研究表明GEF-H1能激活Rho蛋白,与肿瘤发生、发展、浸润、迁移等密切相关。目的:构建人pEGFP-GEF-H1载体并稳定转染结肠癌HCT116细胞后检测GEF-H1表达。方法:在线合成引物软件设计人GEF-H1基因引物,构建重组质粒pEGFP-GEF-H1,并转染结肠癌HCT116细胞,以转染空质粒和未转染的细胞分别作为空质粒组和空白对照组。荧光显微镜下观察绿色荧光蛋白表达,RT-PCR和蛋白质印迹法分别检测GEF-H1mRNA和蛋白表达水平。结果:成功构建了人pEGFP-GEF-H1载体,测序结果表明序列正确。转染重组质粒pEGFP-GEF-H1后,荧光显微镜下可见较强的绿色荧光,GEF-H1mRNA和蛋白表达水平均较空质粒组和空白对照组明显上调。结论:体外成功构建了人pEGFP-GEF-H1载体,且转染结肠癌HCT116细胞后高表达GEF-H1,为进一步探讨结肠癌与GEF-H1的关系提供了必要的实验材料。
简介:ToinvestigatetheprotectiveeffectofdecoctionofliaoweiongastricmucosaofH.pyloriassociatedchronicatrophicgastritisinrats.TheH.pyloriassociatedchronicatrophicgastritismodelswereinducedwithsodiumdeoxycholate,sodiumsalicylate,ethanol,andculturebrothofH.pylori.ProtectiveeffectofdecoctionofliaoweiongastricmucosaofH.pyloriassociatedchronicatrophicgastritiswasobservedquantitatively.
简介:目的观察早期胃癌组织中GTP酶激活蛋白SH3功能区结合蛋白G3BP1和G3BP2的表达变化并探讨其意义。方法选择早期胃癌组织89例和正常对照组织35例,采用免疫组织化学方法检测两组G3BP1蛋白和G3BP2蛋白的表达情况。结果早期胃癌组和正常组G3BP1的阳性率分别为87.64%和60.00%,G3BP2阳性率分别为86.51%和54.28%,两组比较差异有统计学意义(P=0.000,0.000);早期胃癌G3BP1和G3BP2的表达均与幽门螺杆菌感染相关(P=0.000);早期胃癌组织中G3BP1与G3BP2表达呈正相关(rs=0.252,P=0.017)。结论早期胃癌组织中G3BP1和G3BP2呈高表达,可能与幽门螺杆菌感染紧密相关,两指标异常表达可能在早期胃癌的发生和发展中起重要作用。
简介:目的探讨甲状腺素(TH)水平对H—rasl2V转基因肝癌小鼠肝肿瘤的影响。方法将45只H—rasl2V转基因肝癌小鼠随机分为甲状腺机能亢进症组、甲状腺机能减退症组和对照组,分别给予甲状腺素片、丙硫氧嘧啶片或蒸馏水灌胃制造不同的TH水平状态,待小鼠7月龄后,测量肝脏肿瘤指标。结果甲状腺机能亢进症组小鼠血清T3和T4分别为(226.5±79.0)ng/dL,和(1.0±0.5)μg/dL,显著高于甲状腺机能减退症组【分别为(148.9±52.1)ng/dL和(0.8±0.4)pm01/L,P〈0.051,也显著高于对照组【分别为(175.3±63.9)n/dL和(O.9±O.4)μg/aL,P〈O.05】;甲状腺机能亢进症组小鼠游离T3和T4分别为(0.5±0.2)pm01/L和(4.3±1.4)pm01/L,显著高于甲状腺机能减退症组【分别为(0.3±0.1)pmol/L和(1.8±0.5)pm01]L,P〈0.05】,也显著高于对照组【分别为(O.4±0.2)pmol/L和(1.9±0.7)pmol/L,P〈0.05】;甲状腺机能亢进症组小鼠肿瘤数为(7.9±3.2)个,肿瘤直径超过2mm的数量为(4.1±2.7)个,肝/体质量比为(8.6±2.4),显著低于甲状腺机能减退症组【分别为(14.0±73)个、(9.9±4.8)个和(13.5±4.6),P〈O.05】,也显著低于对照组【分别为(11.4±5.3)个、(7.7±3.1)个和(11.3±3.5),P〈0.051o结论甲状腺素水平的高低能影响H—rasl2V转基因肝癌小鼠肝脏肿瘤生长,甲状腺素可以有效抑制肿瘤的发展。
简介:AIM:Toevaluatetheroleofsurvivinandcaspase-3inapoptosisofgastriccarcinoma,aswellasinprognosisofpatientswithgastriccarcinoma.METHODS:Expressionsofsurvivinandcaspase-3wereinvestigatedimmunohistochemicallyin80gastriccarcinomapatientswithoutahistoryofchemo-radiationtherapy.TumorcellapoptosiswasexaminedbyTUNELmethod.RESULTS:Immunohistochemicalanalysisshowedthatsurvivinexpressionwaspositivein61of80patients(76%)withgastriccarcinoma.Incontrast,noexpressionofsurvivininadjacentnormaltissueswasdetected.Expressionlevelofcaspase-3washigherinnormaltissuesthanincarcinoma.Patientswithhigherexpressionofsurvivinhadworsehistologicalgradesandpathologicalstages.Expressionofcaspase-3wassignificantlyassociatedwithhistologicalstages,butnotwiththepathologicalstages.Althoughsurvivinexpressionincarcinomawasnotinverselyrelatedtocaspase-3,patientswithsurvivin(-)andcaspase-3(+)hadthemaximumapoptosisindex.CONCLUSION:Expressionlevelofsurvivinwasassociatedwithhistologicalgradesandpathologicalstagesofthetumor,indicatingthatsurvivinmaybeapoorprognosisfactorforgastriccarcinoma.Unlikecaspase-3,survivin(anapoptosisinhibitor)canmarkedlyinhibittheapoptosisoftumorcells.
简介:AIM:ToexploreexpressionsofPIK3CAintheprogressionofgastriccancerfromprimarytometastasisanditseffectsonactivationofphosphatidylinositol3-kinase(PI3K)/Aktpathway.METHODS:mRNAandproteinlevelsofPIK3CAwereassessed,respectively,byreal-timequantitativepolymerasechainreactionandimmunohistochemistryinspecimensofnormalgastricmucosa,primaryfociandlymphnodeanddistantmetastasisofgastriccancer.AktandphosphorylatedAktproteinwerealsoexaminedbyWesternblottinginthesetissues,inordertoanalyzetheeffectofPIK3CAexpressionlevelchangesontheactivationofPI3K/Aktsignalingpathway.RESULTS:PIK3CAmRNAinlymphnodemetastasiswereapproximately5and2foldshigher,respectively,thanthatinthecorrespondingnormalgastricmucosaandprimarygastriccancertissues(P<0.05),whilenostatisticalsignificancewasfoundcomparedwithdistantmetastasis.Immunohistochemically,PIK3CAproteinexpressionwasdiscoveredin7(35%)specimensof20primaryfocivs10(67%)of15oflymphnodemetastasisor11(61%)of18ofdistantmetastasis(35%vs67%,P=0.015;35%vs61%,P=0.044).WiththeincreasedlevelofPIK3CAexpression,thetotalAktproteinexpressionremainedalmostunchanged,butp-Aktproteinwasupregulatedmarkedly.CONCLUSION:IncreasedexpressionofPIK3CAisexpectedtobeapromisingindicatorofmetastasisingastriccancer.Up-regulationofPIK3CAmaypromotethemetastasisofgastriccancerthroughaberrantactivationofPI3K/Aktsignaling.
简介:目的调查分析我院近3年来住院的药物性肝损伤(DILI)患者临床特点及转归,为提高医师对该病的认识以及保证患者合理用药提供参考。方法2014年3月~2017年5月我院收治115例DILI患者,回顾性分析了其临床资料。结果引起DILI的主要药物为中药、抗生素药物、免疫抑制剂、循环系统用药和抗肿瘤药物,所占比例分别为20.9%、18.3%、13.0%、10.4%、8.7%;本组胆汁淤积型66例(57.4%),肝细胞型16例(13.9%),混合型33例(28.7%);发病时血清ALT水平为(151.2±56.8)U/L,AST为(136.5±25.4)U/L,ALP为(251.6±79.4)U/L,TBIL为(39.8±11.3)μmol/L,GGT为(101.5±28.8)U/L,经2~3w治疗,分别降至(21.7±10.2)U/L、(39.3±8.3)U/L、(120.8±70.5)U/L、(15.2±9.4)μmol/L、(37.6±7.2)U/L;76例(66.1%)DILI患者完全恢复,25例(21.7%)患者病情基本恢复,10例(8.7%)患者肝功能指标反复,4例(3.5%)因肝衰竭而死亡。结论引起DILI的药物种类繁多,中药、抗生素和免疫抑制剂等为主要的诱发药物,临床表现无特异性,治疗后预后良好,但临床医生应注意用药安全,尽量避免或降低DILI的发生。