简介：Coronaryarterychronictotalocclusion(CTO)isdefinedasanoccludedcoronaryarterysegmentwithoutanterogradeflowforatleastthreemonths.Itcanbeclassifiedasa“true”or“functional”CTObasedonflowcharacteristics.In“true”CTO,thereisnoanterogradeflow.In“functional”CTO,thereisminimalanterogradeflowthroughtheoccludedsegmentofthecoronaryartery.CTOisacommonfindingduringcoronaryangiographyanditsprevalencemayvarydependingonthereportedliterature.Amongpatientswithoutpreviouscoronaryarterybypassgrafting(CABG),CTOisfoundinabout20–30%ofthepatients.CTOmaydevelopinsidiouslyoveraperiodoftimeandinvolveacomplexinterplaybetweenintracellularandextracellularfactors,smoothmuscleandfoamcells,calcification,andneovascularization.ThereisagrowingbodyofevidencetosupportthatCTOrevascularizationmayimproveclinicaloutcomewhencomparedtomedicalmanagement.BoththeEuropeanandAmericancardiovascularsocietiessupportCTOrevascularizationwithaclass2arecommendation(levelofevidenceB).Historically,duetolowproceduralsuccessrate,apparentinefficientresourceutilization,potentialincreaseincomplicationratesanduncertainclinicalbenefits,onlyabout10–20%ofpatientswithCTOaretreatedwithpercutaneouscoronaryintervention(PCI).RecentadvancesusingnovelandinnovativetechniqueswithdedicatedequipmenthavesignificantlyimprovedtheproceduralsuccessrateforCTOPCItoabout90%inthehandsofexperiencedoperators.WithincreasinginterestinCTOPCIcoupledwithincreasededucationaleffort,CTOPCIlikelywillbecomemoreaccessibletopatientsinneedofCTOrevascularization.OngoingadvancementininnovativetechniquesandequipmentwillcontinuetoimproveproceduralsuccessratesandreduceproceduralcomplicationrateforCTOPCI.Furthermore,thereareanumberofprospectiveclinicaltrialsonthehorizonwhichshouldhelpdefinetheclinicalbenefitsandlimitationsofCTOPCIinthenear

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简介：嗜中性的渗入是含酒精的steatohepatitis的一个特点；然而，内在的机制仍然保持不清楚。我们以前报导synergistically喂的chronic-plus-binge乙醇导致neutrophils的肝的招募，它贡献肝损害。在这份报纸，我们在chronic-plus-binge乙醇喂导致调查了不变的自然漂亮T(iNKT)房间的角色肝的嗜中性的渗入和肝损害。野类型并且iNKT的二紧张房间缺乏的老鼠(CD1d缺乏并且Jα；18-deficient老鼠)受到喂的chronic-plus-binge乙醇。肝损害和发炎被检验。synergistically喂的Chronic-plus-binge乙醇增加了肝的iNKT房间的数字并且导致了他们的激活，与独自的长期的喂或饮酒作乐相比。iNKT房间缺乏的老鼠被保护免受chronic-plus-binge的伤害导致乙醇的肝的嗜中性的渗入和肝损害。而且，显著地喂几基因的肝的表示在野类型的老鼠与发炎和嗜中性的招募联系了的upregulated的chronic-plus-binge乙醇，而是这些基因的正式就职在iNKT被废除房间缺乏的老鼠。重要地，几cytokines和chemokines(例如，MIP-2，MIP-1，IL-4，IL-6和osteopontin)在嗜中性的渗入包含了在肝的NKT房间的upregulated从chronic-plus-binge被孤立与喂对的老鼠相比的喂乙醇的老鼠。最后，有堵住抗体的CD1d的处理，堵住iNKT房间激活，部分阻止了chronic-plus-binge导致乙醇的肝损害和发炎。喂的Chronic-plus-binge乙醇激活肝的iNKT房间，它在早含酒精的肝损害的发展起一个关键作用，部分地由释放招募的调停人neutrophils到肝，并且这样，iNKT房间为含酒精的肝的治疗代表一个潜在的治疗学的目标疾病。