简介:瞄准:把在病人之间的标准肝炎B(HBV)种痘的反应与长期的丙肝作比较病毒(HCV)感染和健康个人。方法:这是未来的盒子控制研究。有长期的HCV感染和40健康控制的38个病人的一个总数被包括。种痘被20大杯recombinantHBsAg的注射在瞬间0,1和6点执行进三角肌肌肉。Anti-HBs集中是在最后剂量以后决定了3瞬间并且在二个组之间比较了。反应模式是被描绘(1)高反应当anti-HBs抗体效价是>时100IU/L,(2)低反应当效价是10-100IU/L时并且(3)没有反应当效价是<时10IU/L。结果:在耐心的组,有10/38(26.3%)非应答者,8/38(21.1%)低应答者并且20/38(52.6%)高应答者。在控制组的相应价值是2/40(5.0%),7/40(17.5%)和31/40(77.5%)分别地。反应模式在二个组之间是统计上不同的。在里面多变量分析,吸烟是重要confounder,当HCV感染与更低的抗体反应失去了它的重要关联时。结论:有长期的HCV感染的病人趋于与健康个人相比对HBV种痘微弱地作出回应,尽管这关联不是独立的根据多变量分析。
简介:Liverinjuryisacharacteristicfeatureofhumanimmunodeficiencyvirus(HIV)infection,whichisthesecondmostcommoncauseofmortalityinHIV-infectedpatients.NowitisrecognizedthatliverplaysakeyroleinHIVinfectionpathogenesis.Antiretroviraltherapy(ART),whichsuppressesHIVinfectioninpermissiveimmunecells,islesseffectiveinhepatocytes,therebymakingthesecellsasilentreservoirofHIVinfection.InadditiontodirecthepatotoxiceffectsofHIV,certainARTtreatmentmodalitiesprovidehepatotoxiceffects.TheexactmechanismsofHIV-triggeredchronichepatitisprogressionarenotelucidated,buttheliverisadverselyaffectedbyHIV-infectionandlivercellsareprominentlyinvolvedinHIV-elicitedinjury.Theseeffectsarepotentiatedbysecondhitslikealcohol.Here,wewillfocusontheincidenceofHIV,clinicalevidenceofHIVrelatedliverdamage,interactionsbetweenHIVandlivercellsandtheroleofalcoholandco-infectionwithhepatotropicvirusesinliverinflammationandfibrosisprogression.
简介:流行病学的研究为长期的肝炎B的一个原因的角色提供了压到优势的证据在hepatocellular癌(HCC)的发展的病毒(HBV)感染。然而,HBV感染的致病和联系HBV的HCC的carcinogenesis仍然是逃犯的。这评论将在涉及HBV相关的肝carcinogenesis的机制上总结当前的知识。在肿瘤形成的HBV的角色出现到复杂,并且可以包含直接、间接的机制。进主人染色体的HBVDNA的集成发生在同种细胞的肿瘤的早步扩大,和它被显示了提高主人chromosomal不稳定性,导致大转换复制,删除和chromosomaltranslocations。chromosomal改变的率在HBV相关的肿瘤显著地被增加,这被显示出。病毒的规章的HBVx蛋白质的延长表示可以贡献调整表明小径的细胞的抄写,蛋白质降级,增长,和apoptotic,并且它在hepatocellular癌的发展起一个关键作用。
简介:PolyomavirusBK(BKV)infectsupto90%ofthegeneralpopulation.Afterprimaryinfection,occurringearlyduringchildhood,astateofnon-replicativeinfectionisestablishedinthereno-urinarytract,withoutcomplicationsforimmunocompetenthosts.Inimmunocompromisedindividuals,particularlytransplantedpatients,asymptomaticBKVviremiaand/orviruriacanbeobserved.RenalgraftsmayalsobesourcesofinfectionasBKVpreferskidneysratherthanothersolidorgansfortransplantationsuchastheliver.ThemechanismbehindthehigherincidenceofBKVinfectioninkidneytransplantpatients,comparedtoliverorhearttransplantation,isunclearandtheprevalenceofBKVinfectioninnon-renalsolidorgantransplantshasnotbeenyetthoroughlyinvestigated.WeevaluatedtheprevalenceofPolyomavirusBKinfectionamonglivertransplantrecipients.APubMedsearchwasconductedusingthetermsBKVinfectionANDlivertransplantrecipients;BKVANDnon-renalsolidorgantransplant*;BKVinfectionANDimmunosuppression;thesearchwaslimitedtotitle/abstractandEnglish-languagearticlespublishedfrom2000,toMarch2015.ElevenrelevantstudiessuggestthattheprevalenceofBKVviruriaand/orviremiaamonglivertransplantrecipientsislessthanthatreportedinkidneyorhearttransplantrecipients,exceptwhenchronickidneydisease(CKD)ispresentatthesametime.DataalsosuggestthatviruricandviremicpatientshavehigherlevelsofserumcreatininethanBKVnegativepatients.Moreover,nospecificimmunosuppressivedrugsareassociatedwiththeonsetofBKVnephropathy.ThecomorbidityoftransplantationandCKDcouldplayamajorroleinpromotingBKVreplication.
简介:AIM:ToinvestigateFusobacteriumnucleatum(F.nucleatum)abundanceincolorectalcancer(CRC)tissuesanditsassociationwithCRCinvasivenessinChinesepatients.METHODS:Theresectedcancerandadjacentnormaltissues(10cmbeyondcancermargins)from101consecutivepatientswithCRCwerecollected.Fluorescentquantitativepolymerasechainreaction(FQ-PCR)wasappliedtodetectF.nucleatuminCRCandnormaltissues.ThedifferenceofF.nucleatumabundancebetweencancerandnormaltissuesandtherelationshipofF.nucleatumabundancewithclinicalvariableswereevaluated.Fluorescenceinsituhybridization(FISH)analysiswasperformedon22CRCtissueswiththehighestF.nucleatumabundancebyFQ-PCRtestingtoconfirmFQ-PCRresults.RESULTS:ThemedianabundanceofF.nucleatuminCRCtissues[0.242(0.178-0.276)]wassignificantlyhigherthanthatinnormalcontrols[0.050(0.023-0.067)](P<0.001).F.nucleatumwasover-representedin88/101(87.1%)CRCsamples.TheabundanceofF.nucleatumdeterminedby2-ΔCTwassignificantlygreaterintumorsamples[0.242(0.178,0.276)]thaninnormalcontrols[0.050(0.023,0.067)](P<0.001).Thefrequencyofpatientswithlymphnodemetastaseswashigherintheover-abundancegroup[52/88(59.1%)]thanintheunder-abundancegroup[0/13(0%)](P<0.005).NosignificantassociationofF.nucleatumwithotherclinico-pathologicalvariableswasobserved(P>0.05).FISHanalysisalsofoundmoreF.nucleatuminCRCthaninnormaltissues(mediannumber6,25th3,75th10vs2,25th1,75th5)(P<0.01).CONCLUSION:F.nucleatumwasenrichedinCRCtissuesandassociatedwithCRCdevelopmentandmetastasis.
简介:瞄准:在首先有教养的人的胎儿的hepatocytes(HFH)调查肝炎B(HBV)的感染和复制。方法:人的胎儿的hepatocytes在没有浆液的中等、HBV积极的浆液是有教养的被增加进媒介学习hepatocytes的危险性到HBV感染。上层清液为ELISA被收集HBsAg和HBeAg的试金,和为HBV-DNA的量的荧光PCR试金日报。白朊和HBcAg,CK8和CK18表情被免疫组织化学在有教养的hepatocytes检测。lactatedehydrogenate(LDH)的内容被测量发现房间膜的正直。结果:一个稳定的hepatocyte文化系统被建立。HBV能感染hepatocytes并且复制,并且HBcAg表示能被免疫组织化学在象hepatocyte一样房间检测。在上层清液的HBV-DNA能从d被检测2到d18并且HBsAg和HBeAg在d3-d上是积极的18在HBV感染以后。在媒介的HBV从d增加了0到d6并且当房间日益增多地正在松开他们的hepatocyte显型,随后减少了。结论:HBV能感染人的胎儿的hepato-cytes并且复制。这个在试管内模型在与人的HBV入口联系进房间和随后的复制的早事件上允许详细研究。
简介:瞄准:为了由学习在IFN-gamma基因多型性,包括的IFN-gamma+874A/T单个核苷酸多型性(SNP)和CA之间的关系探索孩子的危险性到子宫内的HBV感染,重复微卫星多型性和子宫内的HBV感染。方法:在IFN-gamma+874A/T单个核苷酸多型性的TaqMan荧光聚合酶链反应在子宫内的HBV感染组被测试(组我)并且孩子们组织的正常免疫者(组II)。毛状的电气泳动在上述二个组被执行到试金IFN-gammaCA重复微卫星多型性。结果:AA的频率,在并且TT遗传型在感染组织的子宫内的HBV是67.4%,19.6%和13.0%,并且45.2%,30.1%和24.7%分别地在正常有免疫力的孩子组织。有效差量在在二个组之间的IFN-gamma+874遗传型的频率分发被发现(chi2=5.102,P=0.02389)。在子宫内的HBV感染组,AA遗传型比在正常免疫者组织是更普通的。IFN-gamma+874A等位基因的频率在子宫内的HBV感染组是77.17%,并且60.27%在正常有免疫力的孩子组织。在子宫内的HBV感染组,IFN-gamma+874A等位基因比在正常免疫者组织是更普通的。有效差量在在二个组之间的频率分发被发现(chi2=7.238,P=0.02389,或=2.228,95%CI=1.244-3.992)。(CA12)IFN-gammaCA微卫星多型性的+/(CA12)+在子宫内的HBV感染组是11.90%,26.47%在正常有免疫力的孩子组织。有效差量在在二个组之间的频率分发被发现(chi2=5.64,P=0.0176)。IFN-gammaCA重复的频率在子宫内的HBV感染组是25%,43.38%在正常有免疫力的孩子组织。IFN-gammaCA重复的频率比在正常免疫者组织是在子宫内的HBV感染组的更少。有效差量在在二个组之间的频率分发被发现(chi2=7.548,P=0.0060)。结论:在IFN-gamma+874A/TSNP和子宫内的HBV感染之间以及在IFN-gammaCA微卫星多型性和子宫内的HBV感染之间有一种关系。IFN-gamma基因多型性可能在决定个人的危险�
简介:AIM:ToelucidatethemolecularmechanismsunderlyinghepatitisBvirus(HBV)occultinfectionofgenotypeC.METHODS:Atotalof10typesofhepatitisBsurfaceantigen(HBsAg)variantsfromaKoreanoccultcohortwereused.AfteracompleteHBVgenomeplasmidmutatedsuchthatitdoesnotexpressHBsAgandplasmidencoding,eachHBsAgvariantwastransientlyco-transfectedintoHuH-7cells.ThesecretioncapacityandintracellularexpressionoftheHBVvirionsandHBsAgsintheirrespectivevariantswereanalyzedusingreal-timequantitativepolymerasechainreactionassaysandcommercialHBsAgenzyme-linkedimmunosorbentassays,respectively.RESULTS:AllvariantsexhibitedlowerlevelsofHBsAgsecretionintothemediumcomparedwiththewildtype.Inparticular,ineightofthetenvariants,verylowlevelsofHBsAgsecretionthatweresimilartothenegativecontrolweredetected.Incontrast,mostvariants(9/10)exhibitednormalvirionsecretioncapacitiescomparablewith,orevenhigherthan,thewildtype.ThisprovidednewinsightintotheintrinsicnatureofoccultHBVinfection,whichleadstoHBsAgsero-negativenessbuthashorizontalinfectivity.Furthermore,mostvariantsgeneratedhigherreactiveoxidativespeciesproductionthanthewildtype.ThisfindingprovidespotentiallinksbetweenoccultHBVinfectionandliverdiseaseprogression.CONCLUSION:ThepresentlyobtaineddataindicatethatdeficiencyinthesecretioncapacityofHBsAgvariantsmayhaveapivotalfunctionintheoccultinfectionsofHBVgenotypeC.
简介:AIM:Toinvestigatethefactorsinfluencingtheoccurrenceofgastricvarioliformlesions(GVLs)andtheirpossiblelinkwithgastriccancer.METHODS:A1:1matchedcase-controlstudywasperformedtoretrospectivelyanalyzedatafrom1638chronicgastritispatientswhohadundergonegastroscopyatoneoftwoChinesehospitalsbetween2009and2014.PatientswithGVLs(cases)werecomparedtothosewithoutsuchlesions(controls).Endoscopicandpathologicalfindingswererecorded,alongwithinterviewinformationonHelicobacterpylori(H.pylori)infection,medical,drugandfamilyhistories,lifestyleandeatinghabits.TheassociationbetweeneachfactorandtheoccurrenceofGVLswasestimated,andthenmultivariateconditionallogisticregressionwasusedtoevaluatetheindependentfactors.RESULTS:Thefrequencyandseverityofglandularatrophy,intestinalmetaplasia(IM)andlow-gradeintraepithelialneoplasiaweresignificantlyincreasedintheGVLgroup(P<0.01).OverallanalysisshowedthatH.pyloriinfection[3.051(2.157,4.317),P<0.001],allergicrespiratorydiseases[3.636(2.183,6.055),P<0.001],work-relatedstress[2.019(1.568,2.600),P<0.001],irregularmeals[2.300(1.462,3.619),P<0.001],highintakeofspicyfood[1.754(1.227,2.507),P=0.002]andhighintakeoffreshfruit[0.231(0.101,0.529),P=0.001]weresignificantlycorrelatedwiththeoccurrenceofGVLs(positively,exceptforthelatter).Stratifiedanalysesindicatedthatpickledfoodconsumptioninpatientsover50yearsold[7.224(2.360,22.115),P=0.001]andexcessivesmokinginmen[2.013(1.282,3.163),P=0.002]werealsopositivelycorrelated,andthat,forantralGVLs,vegetableconsumption[0.491(0.311,0.776),P=0.002]wasnegativelycorrelated.CONCLUSION:SevenriskfactorsandtwoprotectivefactorsaredeterminedforGVLs,whichwerefoundtobeassociatedwithpremalignantabnormalities.
简介:瞄准:为了学习流行和风险因素,与人的免疫不全与三倍的感染联系了在一张城市的诊所人口的病毒(HIV)/hepatitisB(HBV)/hepatitisC病毒(HCV)。方法:5639个病人的回顾的图表评论在纽约城市里在圣卢凯斯鲁塞韦尔特医院HIV诊所(全面照顾的中心)列在后面,从1999年1月的美国到2007年5月。下列人口统计的特征被分析:年龄,性别,种族和HIV冒因素的风险。多重逻辑回归分析被执行在这些病毒的获得上评估人口统计的因素的影响。结果:HIV/HBV,HIV/HCV和HIV/HBV/HCV感染在252/5639(4.47%)被检测,1411/5639(25.02%)和89/5639(1.58%)病人分别地。HIV/HBV合作感染与男性被联系(或1.711;P=0.005),黑色跑(或2.091;P<0.001),人与\O性交人(MSM)(或1.747;P=0.001),静脉内的药使用(IDU)(或0.114;P<0.001),IDU和异性爱的活动(或0.247;P=0.018),或未知(或1.984;P=0.004)。HIV/HCV合作感染与男性被联系(或1.241;P=0.011),黑色跑(或0.788;P=0.036),MSM(或0.565;P<0.001),IDU(或8.956;P<0.001),IDU和异性爱的活动(或9.106;P<0.001),IDU和MSM(或9.179;P<0.001),或输送(或3.224;P<0.001)。HIV/HBV/HCV合作感染与男性被联系(或2.156;P=0.015),IDU(或6.345;P<0.001),IDU和异性爱的活动(或9.731;P<0.001),IDU和MSM(或9.228;P<0.001),或未知(或4.219;P=0.007)。结论:我们的学习证明有HBV/HCV/HIV的合作感染显著地与IDU被联系。这些结果加亮需要加强教育和综合照顾的最佳的模型,特别地为有IDU的人口,到减少病毒的传播的风险。
简介:瞄准:调查白酒剂量的协会,与反常白酒相关的肝损伤指示物喝和肥胖的持续时间,在中国的岛人口的白酒相关的肝损伤的流行。方法:从中国的岛人口的使随机化的多级式的成层的簇采样在基于人口的盒子控制学习被使用。然后,会见,体格检查,实验室评价和ultrasonography被做。结果:每日的白酒吸入>=20g,喝5年和肥胖是的>=的持续时间仔细与白酒相关的肝损伤有关(P<0.05)。机会比率(或)(95%CI)是1.965(1.122-3.442),3.412(1.789-6.507)并且1.887(1.261-2.824)分别地。在20g日报白酒吸入组织的>=和20g日报白酒吸入组织的<的白酒相关的肝损伤的流行率分别地是37.14%和12.06%。在喝的5年组织的>=和喝的5年组织的<的白酒相关的肝损伤的流行率分别地是34.44%和8.53%。没有重要剂量反应关系在每日的白酒吸入和反常白酒相关的肝损伤指示物之间以及在喝和反常白酒相关的肝损伤指示物的持续时间之间被发现。在在喝组和黄米饭酒喝酒组,的啤酒之间的白酒相关的肝损伤的流行没有有效差量烈性酒喝酒组,多重喝酒组。结论:每日的白酒吸入的风险阀值是喝导致白酒相关的肝损伤的20g和持续时间在中国的岛人口的5年。肥胖导致的肝损伤应该被担心。