简介：Coloncancersdevelopadaptivemechanismstosurviveunderextremeconditionsanddisplayhallmarksofunlimitedproliferationandresistancetocelldeath.Thederegulationofcelldeathisakeyfactorthatcontri-butestochemoresistanceintumors.Inaphysiologicalcontext,balancebetweencellproliferationanddeath,andprotectionagainstcelldamagearefundamentalprocessesformaintaininggutepithelialhomeostasis.Themechanismsunderlyinganti-deathcytoprotectionandtumorresistanceoftenbearcommonpathways,andalthoughdistinguishingthemwouldbeachallenge,itwouldalsoprovideanopportunitytodevelopadvancedanti-cancertherapeutics.Thisreviewwilloutlinecelldeathpathways(i.e.,apoptosis,necrosis,andnecroptosis),anddiscusscytoprotectivestrategiesinnormalintestinalepitheliumanddeathresistancemechanismsofcolontumor.Incolorectalcancers,theintracellularmechanismsofdeathresistanceincludethedirectalterationofapoptoticandnecroptoticmachineryandtheupstreameventsmodulatingdeatheffectorssuchastumorsuppressorgeneinactivationandpro-survivalsignalingpathways.Theautocrine,paracrineandexogenousfactorswithinatumormicroenvironmentcanalsoinstigateresistanceagainstapoptoticandnecroptoticcelldeathincoloncancersthroughchangesinreceptorsignalingortransporteruptake.Therolesofcyclooxygenase-2/prostaglandinE2,growthfactors,glucose,andbacteriallipopolysaccharidesincolorectalcancerwillbehighlighted.Targetinganti-deathpathwaysinthecoloncancertissuemightbeapromisingapproachoutsideofanti-proliferationandanti-angiogenesisstrategiesfordevelopingnoveldrugstotreatrefractorytumors.

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简介：瞄准：为了在病人调查胰岛素抵抗和糖尿病的临床的参数的流行，由长期的丙肝(CHC)或长期的肝炎B(CHB)影响了。方法：我们回顾地评估了经历了肝活体检视的852个连续病人(726CHC和126CHB)。我们记录了年龄，性别，中高音，类型2糖尿病或新陈代谢的症候群(MS)，身体团索引(BMI)，和明显的疾病持续时间(增加)。结果：年龄，增加，BMI，在有温和/中等的肝纤维变性的病人的MS和糖尿病的流行在CHC是显著地更高的。然而，脂肪变性的度和在肝活体检视评估的肝纤维变性没在CHC和CHB病人之间不同。在多变量分析，年龄，性别，BMI，中高音和糖尿病是为在CHC的肝纤维变性的独立风险因素，而仅仅年龄与在CHB的肝纤维变性有关。我们也评估了在重要脂肪变性之间的协会(>30%)并且年龄，性别，BMI，糖尿病，MS和肝纤维变性。糖尿病，BMI和肝纤维变性与脂肪变性>被联系30%在CHC，而仅仅年龄和BMI与在CHB的脂肪变性有关。结论：这些数据可以显示丙肝病毒感染是为胰岛素抵抗的一个风险因素。

简介：AIM:Toobservethereversaleffectsofwide-typep53geneonmulti-drugresistanceto5-FU(LOVO/5-FU).METHODS:AftertreatmentwithAd-p53,LOVO/5-FUsensitivityto5-Fuwasinvestigatedusingtetrazoliumdyeassay.Multidrugresistancegene-1(MDR1)geneexpressionwasassayedbysemi-quantitativereversetranscriptionpolymerasechainreactionandtheexpressionofp53proteinwasexaminedbyWesternblotting.RESULTS:Thereversalactivityaftertreatmentwithwidetypep53genewasincreasedupto4.982foldat48h.TheexpressionofMDR1genedecreasedsignificantlyaftertreatmentwithwide-typep53gene,andtheexpressionofp53proteinlastedforabout5d,withapeakat48h,andbegantodecreaseat72h.CONCLUSION:Wide-typep53genehasaremarkablereversalactivityforthehighexpressionofMDR1geneincolorectalcancers.Thereversaleffectsseemtobeinatimedependentmanner.Itmighthavegoodprospectsinclinicalapplication.