Does breathing other people's tobacco smoke cause lung cancer?

The available epidemiological studies of lung cancer and exposure to other people's tobacco smoke, in which exposure was assessed by whether or not a person classified as a non-smoker lived with a smoker, were identified and the results combined. There were 10 case-control studies and three prospective studies. Overall, there was a highly significant 35% increase in the risk of lung cancer among non-smokers living with smokers compared with non-smokers living with non-smokers (relative risk 1.35, 95% confidence interval 1.19 to 1.54). Part of this increase was almost certainly caused by the misclassification of some smokers as non-smokers. As smokers, who are more likely to get lung cancer than non-smokers, tend to live with smokers this misclassification probably exaggerated the estimated increase in risk. Adjustment for this error reduced the estimate to 30% (relative risk 1.30), but as people who live with non-smokers may still be exposed to other people's smoke this estimate was revised again to allow for the fact that a truly unexposed reference group was not used. The increase in risk among non-smokers living with smokers compared with a completely unexposed group was thus estimated as 53% (relative risk of 1.53). This analysis, and the fact that non-smokers breathe environmental tobacco smoke, which contains carcinogens, into their lungs and that the generally accepted view is that there is no safe threshold for the effect of carcinogens, leads to the conclusion that breathing other people's tobacco smoke is a cause of lung cancer. About a third of the cases of lung cancer in non-smokers who live with smokers, and about a quarter of the cases in non-smokers in general, may be attributed to such exposure.     

Apoptosis and diseases: regulation and clinical relevance

It is increasingly clear that apoptosis plays a central role in the pathogenesis of several human diseases. For instance, an increase in apoptosis leads to cell loss accompanied by neurodegenerative diseases, whereas we know that genetically determined defects of apoptosis result in deregulated cell proliferation, typical of cancer. Hence, apoptosis may be relevant as therapeutic targets for many human diseases. This article reviews briefly the regulation and the clinical relevance of apoptotic mechanisms in several different human diseases.     

慢性阻塞性肺疾病与肺癌关系的研究进展

慢性阻塞性肺疾病(COPD)是临床的常见疾病,肺癌是最常见的恶性肿瘤之一,发病率和病死率均很高。近年来,国内外多项研究提示两者存在相关性,但机制尚未完全明确;推测两者具有共同的病理生理学基础,可能与烟雾暴露、慢性炎性反应、肺功能下降、遗传易患因素以及免疫调节异常有关。该文就COPD与肺癌的关系研究进展予以综述,为两者的早期预防、诊断提供帮助。     

Lung disease in farmers.

Lung diseases in farmers attributable to their occupation include (a) farmer's lung, caused by exposure to mouldy hay, (b) the asthma caused by exposure to grain dust and (c) silo-filler's disease. Their prevalence in Canada is unknown. Farmer's lung results from inhalation of mould spores in hay; the mechanism is immunologic. The exact cause and mechanism of grain dust asthma are unknown but may be immunologic. Silo-filler's disease is caused by the toxic effects of inhaled nitrogen dioxide.     

香烟烟雾引起的氧化应激在肺泡Ⅱ型上皮细胞损伤中的作用

香烟烟雾中含有自由基等大量的强氧化剂,因而可以导致氧化应激。氧化应激可对肺泡Ⅱ型上皮细胞(AECⅡ)造成损伤,但是其对AECⅡ造成损伤的机制至今还未完全清楚,近期这个领域研究的热点集中在三个方面:氧化应激诱导的AECⅡ凋亡、氧化应激与炎性反应的相互作用对AECⅡ的损伤以及氧化应激对AECⅡ结构和功能的直接损伤。AECⅡ损伤与肺部损伤有密切关系,对其损伤机制的研究,有助于呼吸道疾病的诊断和治疗。     

基于网络药理学探讨九痛丸治疗肺癌胸痛可行性验证分析

现代医家临床应用九痛丸多依据《金匮要略》中“治九种心痛”的注解用以治疗心系疾病所致的心胸疼痛,但由于其用药峻猛,理论上与心系疾病常见的气虚血瘀、痰湿毒邪内阻的发病机理并不完全符合,因此临床研究较少。宋鲁成教授在临床诊疗中发现,九痛丸可能是张仲景治疗癌性胸痛的处方,效用极佳,但是近现代文献中尚未有人对九痛丸与治疗肺癌进行系统的研究。因此文中基于网络药理学和生物信息学等方法,研究应用九痛丸治疗肺癌胸痛的具体作用通路与可能机制,并通过实验验证九痛丸治疗肺癌胸痛的理论以及可行性。文章主要通过药理学数据库检索,得到九痛丸药物组成中的活性成分及对应靶点,然后再挖掘肺癌已知发病相关基因靶点,将药物与疾病靶点做成靶点网络后取交集进行分析,筛选九痛丸与肺癌相关性最强的特异性靶点并进行信号通路富集分析,显示九痛丸作用于肺癌的关键节点涉及的信号通路主要被富集在细胞周期调控、细胞增殖、凋亡、肿瘤转录调控失调、病毒致癌及其他肿瘤通路等100余条信号通路。筛选其中肿瘤细胞周期调控这一关键作用机制,选择人肺癌细胞(SPC-A1)进行实验验证,结果发现流式细胞分析显示九痛丸可明显抑制SPC-A1的增殖,明显促进其凋亡。提示九痛丸能通过抑制肿瘤细胞增殖来治疗肺癌。     

c-Met活化与肺癌的关系及其靶向药物的研究进展

c-Met为酪氨酸激酶受体的一种,肝细胞生长因子(HGF)为其天然配体。c-Met的激活主要有HGF配体依赖型和非HGF配体依赖型两种形式。许多恶性肿瘤包括肺癌中存在c-Met的多种活化机制,c-Met的异常激活亦与肺癌的发生发展及恶性生物学行为关系密切。本文就c-Met的活化与非小细胞肺癌及小细胞肺癌的关系及其靶向药物在肺癌中的研究进展作一综述。     

Deaths in Canada from lung cancer due to involuntary smoking.

Recently published evidence indicates that involuntary smoking causes an increased risk of lung cancer among nonsmokers. Information was compiled on the proportion of people who had never smoked among victims of lung cancer, the risk of lung cancer for nonsmokers married to smokers and the prevalence of such exposure. On the basis of these data we estimate that 50 to 60 of the deaths from lung cancer in Canada in 1985 among people who had never smoked were caused by spousal smoking; about 90% occurred in women. The total number of deaths from lung cancer attributable to exposure to tobacco smoke from spouses and other sources (mainly the workplace) was derived by applying estimated age- and sex-specific rates of death from lung cancer attributable to such exposure to the population of Canadians who have never smoked; about 330 deaths from lung cancer annually are attributable to such exposure.     

Tobacco smoke in the workplace: an occupational health hazard

Tobacco smoke, which contains over 50 known carcinogens and many other toxic agents, is a health hazard for nonsmokers who are regularly exposed to it while at work. Involuntary exposure to tobacco smoke annoys and irritates many healthy nonsmokers. Serious acute health effects are probably limited to the one fifth of the population with pre-existing health conditions that are aggravated by exposure to tobacco smoke. The consequences of long-term exposure include decreased lung function and lung cancer. Existing air quality standards for workplaces do not directly specify an acceptable level for tobacco smoke. The evidence on the composition of tobacco smoke and on the health hazards of involuntary exposure suggests that there may not be a "safe" level for such exposure.     

非电离辐射损害男性生育功能生物学机制的研究现状

越来越多的证据表明,长期暴露于某些非电离辐射（NIR: non-ionizing radiation）是诱发男性不育、癌症等疾病的危险因素。目前的研究表明了NIR对精子参数、激酶在生殖细胞代谢和内分泌系统中作用的不利影响,且产生遗传毒性、基因组不稳定性和氧化应激。然而,迄今为止非电离辐射作用于男性性腺造成不育的生物学、分子生物学机制尚不清楚。本综述旨在总结现有的NIR造成男性不育机制的生物医学研究。