Objective To examine the relationship between smoking and tobacco-related mortality in a cohort of the aged Chinese armymen.Methods A cohort study was carried out in Xi'an,China from 1987 to 2005.A total of 1 268 retired male military cadres aged 55 or older were examined in 1987 and followed up in the next 18 years.At baseline,388 men were non-smokers,461 were former smokers,and 419 were current smokers.The current smoking rate was 33.04%,Quitted rate was 52.39%.The terminal main observation items included all-cause and tobacco-associated mortality.Results Up to Jun 30,2005,a total of 491 subjects died.Compared with non-smokers,the relative risks(95% confidence intervals(CI)) of ever-smokers for all-cause deaths,chronic obstructive pulmonary disease(COPD),lung cancer,and coronary heart disease(CHD) were 1.24(1.01-1.53),1.91(1.06-3.46),2.91(1.36-6.23),and 1.15(0.68-1.93),respectively.Compared with current smokers,the risks of total mortality and death from lung cancer for former smokers were decreased by 66.7% and 14.98%,respectively.Conclusions Cigarette smoking was a major death risk factor in the cohort and quitting smoking could save lives.

[摘 要] 目的：研究环状RNA nei样DNA糖化酶3（circNEIL3）和微小RNA（miR）-4784对乳腺癌细胞MDA-MB-231的增殖、迁移和侵袭的影响。方法：收集2018年1月至2019年12月在济南市中西医结合医院经组织病理诊断为乳腺癌并行手术切除的45例乳腺癌患者的癌组织和配对癌旁组织，qPCR法检测乳腺癌组织、癌旁组织中circNEIL3和miR-4784的相对水平。将circNEIL3的小干扰RNA（si-circNEIL3）、miR-4784模拟物、si-circNEIL3+miR-4784抑制物分别转染MDA-MB-231细胞，采用CCK-8法、平板克隆实验、划痕愈合实验、Transwell实验检测circNEIL3和miR-4784表达对细胞活力、克隆形成、迁移和侵袭的影响。双荧光素酶报告基因实验、RNA免疫沉淀（RIP）和RNA pull-down实验检测circNEIL3和miR-4784之间相互作用。结果：乳腺癌组织中circNEIL3呈高表达（P<0.05），miR-4784呈低表达（P<0.05）。干扰circNEIL3显著降低MDA-MB-231细胞活力、克隆形成数、划痕愈合率以及侵袭数（均P<0.05）。过表达miR-4784显著降低MDA-MB-231细胞活力、克隆形成数、划痕愈合率以及侵袭数（均P<0.05）。双荧光素酶报告基因实验、RIP和RNA pull-down实验均证实circNEIL3与miR-4784可直接结合，干扰circNEIL3能明显上调miR-4784表达（P<0.05），过表达circNEIL3能明显下调miR-4784表达（P<0.05）。抑制miR-4784表达部分逆转干扰circNEIL3对MDA-MB-231细胞活力、克隆形成、迁移和侵袭的抑制作用（P<0.05）。结论：干扰circNEIL3通过靶向上调miR-4784表达抑制MDA-MB-231细胞的增殖、迁移和侵袭。