简介:Ithasbeenfoundthatexpressionof15-lipoxygenasc-1(15-LOX-1)anditsmainproduct,13-C-hydroxyoctadecadienoicacid(13-S-HODE),aredecreasedinhumancolorectalandesophagealcancersandthatnonsteroidalanti-inflammatorydrugs(NSAIDs)cantherspeuticallyinduce15-LOC-1expressiontotriggerapoptosisinthosecancercellsindependentlyCOX-2.WefoundthataspecificCOX-2inhibitorSC-236similarlyinduceapoptosisingastriccancercells,althoughthemechanismsoftheseeffectsremaintobedefined.Inthepresentstudy,wetestedwhetherSC-236inducedapoptosisthroughup-regulationof15-LOX-1ingastriccancercells.Wefoundthat,(a)SC-236inhibitedgrowthofgastriccancercellsmainlybyapoptosisinduced;(b)SC-236induced15-LOX-1expressionandincreasedendogenous13-S-HODEproduct,insteadof15-S-HETEduringapoptosisingastriccancercellswithout15-LOX-1expressionbeforetreatmentbySC-236;(c)sc-236didn'teffectexpressionofCOX-1,COX-2,5-LOXand12-LOX;and(d)15-LOX-1inhibitionsuppressedSC-236inducedapoptosis.ThesefindingsdemonstratedthatSC-236inducedapoptosisingastriccancercellsviaup-regulationof25-LOX-1.Theyalsosupporttheconceptthatthelossoftheproapopoticroleof15-LOX-1inepithelialcancersisnotlimitedtohumancolorectalandesophagealcancers.
简介:AIM:Toanalyzethemismatchrepair(MMR)statusandtheARID1Aexpressionaswellastheirclinicopathologicalsignificanceingastricadenocarcinomas.METHODS:WeexaminedtheexpressionsofMMRproteinsandARID1Abyimmunohistochemistryinconsecutive489primarygastricadenocarcinomas.Theresultswerefurthercorrelatedwithclinicopathologicalvariables.RESULTS:ThelossofanyMMRproteinexpression,indicativeofMMRdeficiency,wasobservedin38cases(7.8%)andwassignificantlyassociatedwithanolderage(68.6±9.2vs60.4±11.7,P<0.001),afemalesex(55.3%vs31.3%,P=0.004),anantrallocation(44.7%vs25.7%,P=0.021),andadifferentiatedhistology(57.9%vs39.7%,P=0.023).AbnormalARID1Aexpression,includingreducedorlossofARID1Aexpression,wasobservedin109cases(22.3%)andwassignificantlycorrelatedwithlymphaticinvasion(80.7%vs69.5%,P=0.022)andlymphnodemetastasis(83.5%vs73.7%,P=0.042).ThetumorswithabnormalARID1AexpressionmorefrequentlyindicatedMMRdeficiency(47.4%vs20.2%,P<0.001).AmultivariateanalysisidentifiedabnormalARID1Aexpressionasanindependentpoorprognosticfactor(HR=1.36,95%CI:1.01-1.84;P=0.040).CONCLUSION:OurobservationssuggestthattheAIRD1Ainactivationisassociatedwithlymphaticinvasion,lymphnodemetastasis,poorprognosis,andMMRdeficiencyingastricadenocarcinomas.
简介:瞄准:调查影响他我有教养的老鼠小岛的生存能力和功能上的oxygenase-1(HO-1)基因转移在试管内。方法:小岛被管内胶原酶消化从Sprague-Dawley老鼠的胰孤立,并且由不连续的Ficoll密度坡度远心沉淀净化了。净化的老鼠小岛是有包含人的HO-1基因(Ad-HO-1)的adenoviral向量的transfected或提高了绿荧光灯的蛋白质基因(Ad-EGFP),然后为七天有教养。Transfection被萤光显微镜检查和西方的污点证实。小岛生存能力被氮蒽orange/propidium碘化物评估荧光灯的染色。刺激葡萄糖的胰岛素版本用胰岛素放射性免疫测定工具包被检测并且被用来估计小岛的功能。刺激索引(SI)被在低葡萄糖刺激之上由胰岛素版本在高葡萄糖刺激之上划分胰岛素版本计算。结果:在七种天文化以后,有教养的老鼠小岛的生存能力显著地减少了(92%+/-6%对52%+/-13%,P<0.05),并且刺激葡萄糖的胰岛素版本也显著地减少了(6.47+/-0.55mIU/L/30IEQ对4.57+/-0.40mIU/L/30IEQ,14.93+/-1.17mIU/L/30IEQ对9.63+/-0.71mIU/L/30IEQ,P<0.05)。有在20的MOI的adenoviral向量的老鼠小岛的Transfection是有效的,并且没损害小岛功能。在7dpost-transfection,Ad-HO-1transfected小岛的生存能力比控制小岛的高(71%+/-15%对52%+/-13%,P<0.05)。在Ad-HO-1transfected组之中在在低葡萄糖刺激(2.8mmol/L)之上的胰岛素版本没有有效差量,Ad-EGFPtransfected组织,并且控制组织P>0.05),当时当由高葡萄糖(16.7mmol/L)刺激了时答案,在Ad-HO-1transfected组的胰岛素版本比在Ad-EGFP,transfected组织并且控制组显著地高,分别地(12.50+/-2.17mIU/L/30IEQ对8.87+/-0.65mIU/L/30IEQ;12.50+/-2.17mIU/L/30IEQ对9.63+/-0.71mIU/L/30IEQ,P<0.05)。Ad-HO-1transfected组的SI比Ad-EGFP,transfected组织并且控制组也显著地高,分
简介:瞄准:检验在试验性的严重尖锐胰腺炎(树液)抵销抗体的反高的活动性组盒子1的效果(HMGB1)。方法:傻瓜被在C3H/HeN老鼠创造关上的十二指肠的循环劝诱。傻瓜在抵销抗体(200大杯)的anti-HMGB1的intraperitonealinjection以后立即被劝诱。胰腺炎,机关损害(肝,肾和肺),和到胰的细菌的translocation的严厉被检验在树液的正式就职以后的12h。结果:显著地抵销抗体的Anti-HMGB1在树液改进了浆液淀粉酶水平的举起和胰和肺的组织学的改变。Anti-HMGB1抗体显著地也改善了在SAP.However的浆液丙氨酸aminotransferase和creatinine的举起,anti-HMGB1抗体变得更坏细菌的translocation到胰。结论:BlockadeofHMGB1稀释了树液的发展并且联系了机关机能障碍,建议HMGB1may充当为在树液的煽动性的反应和机关损害的一个关键调停人。
简介:目的了解先天性肝外门腔静脉分流(Abernethy畸形)的临床特点。方法回顾分析1例Abernethy畸形并下消化道出血患者的临床资料,并进行文献复习。结果本例患者男性,20岁。反复间歇性便血20年。重度贫血貌,外周血WBC2.0×109/L,RBC2.6×1012/L,HB41g/L,PLT125×109/L;粪红色软便,OB(+++),血液(++);经电子胃镜、电子结肠镜、腹部血管彩超、腹部CT血管重建和磁共振成像检查诊断,行结直肠周围血管离断和直肠下段曲张静脉缝扎术,术后恢复良好,随访2年,生活质量好。结论Abernethy畸形分为Ⅰ型和Ⅱ型,Ⅱ型患者肝外门静脉广泛扩张并导致门腔静脉分流,以下消化道出血为主要临床表现。
简介:病人男性,46岁,左上腹部疼痛不适、消瘦1月,于2002年1月20日入院。病人自述1个月前开始左上腹部隐痛不适,呈持续性疼痛,夜间加重,伴有乏力,体重下降明显(约10kg)。无其它不适。查体:未触及表浅淋巴结肿大。腹部膨隆,以左侧为主。可触及脾脏肿大,脾下界达左肋下约3cm。向右越过中线2cm,质韧,边界清,触痛明显,推之不移动。B超:肝脏正常。脾脏体积显著增大,30cm×28cm×15cm大小,
简介:目的探讨PreS1抗原检测的临床价值。方法采用酶联免疫吸附试验法检测421例慢性乙型肝炎患者血清PreS1抗原和HBV标记物;采用荧光定量PCR法检测HBVDNA。结果在421例慢性乙型肝炎患者中,HBVDNA阳性者367例,其中PreS1Ag阳性者188例(51.2%),HBeAg阳性者119例(32.4%),后两者有显著性差异(P〈0.01);在高HBVDNA载量(105~107copies/ml和〉107copies/ml)组患者中,PreS1Ag阳性率(60.2%,60.0%)显著高于HBVDNA阴性组(33.3%)和低载量(103~105copies/ml)组(41.9%,P〈0.01);但在421例患者中,PreS1Ag阳性率(48.9%)低于HBVDNA(87.2%,P〈0.01)。结论PreS1Ag能够较HBeAg更好地反映HBV在体内的复制状态,但尚不能代替HBVDNA的检测。
简介:INTRODUCTIONInChina,liverfibrosisinmostpatientsresultedfromthevirusesofhepatitisB.Bothanti-virusandanti-fibrosisshouldbeconsideredindesigningaprogramforthetreatmentofliverfibrosis.Therefore,40casesofliverfibrosisduetohepatitisBweretreatedbyusingIFN-α1andtraditionalmedicinalpreparationsfromFebruary1994toApril1996.Goodcurativeeffectwasachieved.
简介:AIMTotestwhetherNox1playsaroleintyphlitisinducedbySalmonellaentericaserovarTyphimurium(S.Tm)inamousemodel.METHODSEight-week-oldmalewild-type(WT)andNox1knockout(KO)C57BL6/J(B6)micewereadministeredmetronidazolewaterfor4dtomakethemsusceptibletoS.Tminfectionbytheoralroute.Themiceweregivenplainwaterandadministeredwith4differentdosesofS.Tmbyoralgavage.Themicewerefollowedforanother4d.Fromthetimeofthemetronidazoleapplication,themicewereobservedtwicedailyandweigheddaily.Theileum,cecumandcolonwereremovedforsamplingatthefourthdaypost-inoculation.PortionsofallthreetissueswerefixedforhistologyandplacedinRNAlaterformRNA/cDNApreparationandquantitativereal-timePCR.ThecontentsofthececumwererecoveredforestimationofS.TmCFU.RESULTSWefoundNox1-knockout(Nox1-KO)micewerenotmoresensitivetoS.TmcolonizationandinfectionthanWTB6mice.Thisconclusionisbasedonthefollowingobservations:(1)S.Tm-infectioninducedsimilarweightlossinNox1-KOmicecomparedtoWTmice;(2)thesameS.TmCFUwasrecoveredfromthececalcontentofNox1-KOandWTmiceregardlessoftheinoculationdose,exceptthelowestinoculationdose(2×106CFU)forwhichtheNox1-KOhadone-loglowerCFUthanWTmice;(3)thereisnodifferenceincecalpathologybetweenWTandNox1-KOgroups;and(4)therearenoS.Tminfection-inducedchangesingeneexpressionlevels(IL-1b,TNF-α,andDuox2)betweenWTandNox1-KOgroups.TheAlpigeneexpressionwasmoresuppressedbyS.TmtreatmentinWTthantheNox1-KOcecum.CONCLUSIONNox1doesnotprotectmicefromS.Tmcolonization.Nox1-KOprovidesaveryminorprotectiveeffectagainstS.Tminfection.UsingNOX1-specificinhibitorsforcolitistherapyshouldnotincreaserisksinbacterialinfection.