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1、国外文献1(1).txt爱空空情空空,自己流浪在街中;人空空钱空空,单身苦命在打工;事空空业空空,想来想去就发疯;碗空空盆空空,生活所迫不轻松。总之,四大皆空!(MODSandTLR4)1.AdvExpMedBiol.2010;667:59-68.LipidAReceptorTLR4-MediatedSignalingPathways.YamamotoM,AkiraS.DepartmentofHostDefense,ResearchInstituteforMicrobialDiseases,Os
2、akaUniversity,Osaka,565-0871,Japan.AbstractLipidAisastrongactivatorofmonocytestoreleaseimmunestimulatorssuchasproinflammatorycytokines.OverproductionofinflammatorycytokinessuchasTNFandIL-6isknowntocausesepticshockthatfrequentlyleadstomultipleorganfai
3、lureandfinallytodeath.Inrecentyears,LipidAhasalsobeenrecognizedbyaToll-likereceptor,TLR4.ActivationofTLR4byLPSorLipidAtriggerssignaltransductionviathecytoplasmicdomaincalledtheToll/IL-1Receptor(TIR)domain.IntracellularTIRdomain-containingadaptormolec
4、ulesareinvolvedintheTLR4-mediatedsignalingpathways.Moreover,asubsetofLPS-induciblegenesisregulatedintwostepsbytheinduciblenuclearprotein.Additionally,theTLR4-mediatedactivationofsignalingcascadesiselaboratelydown-regulatedbyanumberofnegativeregulator
5、s.Inthischapter,wediscussthemechanismsoftheactivationorde-activationprogrammediatedbytheLipidAreceptorTLR4.脂质A受体TLR4介导的信号通路脂质A是一种强有力的单核细胞激活剂,能促使单核细胞释放免疫刺激因子,如炎症细胞因子。我们知道,产生过量的炎症细胞因子(如肿瘤坏死因子和白细胞介素-6)会引起脓毒性休克,最后经常是因为多器官衰竭而导致死亡。近年来,研究者认为脂质A也被Toll样受体TLR4
6、识别。由细菌脂多糖和脂质A激活的TLR-4经过胞质域所触发的信号传导被称为Toll/IL-1受体域(TIR)。细胞内的TIR域所包含的接合分子与TLR-4介导的信号转到有关。而且,一组脂多糖诱导基因是由诱导核蛋白在两个步骤来调控的。此外,由TLR-4介导的信号级联激活是由一定数量的负调节器来下调的。在这个章节,我们讨论由脂质A的受体TLR-4介导的激活或取消激活程序的机制。2.Biologicals.2010Sep;38(5):552-6.Epub2010Jun19.Ulinastatin-me
7、diatedprotectionagainstzymosan-inducedmultipleorgandysfunctioninrats.YangQ,LiuX,LiuM,ZhangL,GuanY.IntensiveCareUnit,FirstHospitalofJilinUniversity,71XinminStreet,Changchun,Jilin130021,China.AbstractThepurposeofthisstudywastoevaluatethepotentialorgan-
8、protectiveactivityofulinastatin(aurinarytrypsininhibitor)andtoinvestigatetheunderlyingmechanism(s)inaratmodelofmultipleorgandysfunctionsyndrome(MODS).WhenadultWistarratswerechallengedintraperitoneallywithyeastpolysaccharide(zymosan),theydevelopedbioc