Serum angiotensin converting enzyme activity in ex-smokers

A low activity of angiotensin converting enzyme (ACE) has been reported in people who smoke. To determine whether this low ACE activity would be reversible on cessation of smoking, we measured serum ACE activity in 107 healthy male volunteers. They included 27 active cigarette smokers, 28 non-smokers, 24 ex-smokers who had stopped smoking for less than 10 yr, and 28 ex-smokers who had stopped smoking for more than 10 yr. The mean value (±SD) of serum ACE in those who had stopped smoking for more than 10 yr was comparable to that of non-smokers: 23.2 ± 5.1 and 23.5 ± 4.5, respectively. ACE activity in smokers and the ex-smokers who had stopped smoking for less than 10 yr was significantly lower (17.8 ± 4.5 and 17.8 ± 3.9, respectively) than values obtained in non-smokers and the group who had not smoked for more than 10 yr (p < 0.001). These findings suggest that the effect of chronic smoking on the serum ACE activity may be reversible.     

吸烟与非吸烟慢性阻塞性肺疾病患者血清CC-16的表达水平

目的:探讨慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者中吸烟人群和不吸烟人群血清Clara细胞蛋白(Clara cell protein,CC-16)的表达水平。方法:入选COPD稳定期患者,记录入选者的基本情况、临床症状及肺功能等资料,并留取血清,采用ELISA法检测CC-16水平。按照是否有吸烟史将患者分为吸烟COPD和非吸烟COPD,以吸烟和非吸烟的健康体检者为对照。结果:共入选COPD患者34例,吸烟组17例,非吸烟组17例;健康人吸烟组15例,健康人非吸烟对照组19例。吸烟COPD组男性比例高于非吸烟COPD组,差异有统计学意义(P0.05)。吸烟和非吸烟COPD患者年龄、肺功能差异无统计学意义。与健康对照组相比,COPD患者血清CC-16水平降低(P0.001)。吸烟和非吸烟COPD患者血清CC-16水平差异无统计学意义;与非吸烟健康者相比,吸烟健康者血清CC-16呈现下降趋势,但差异无统计学意义。结论:COPD患者血清CC-16表达水平低于健康体检者,但吸烟与不吸烟COPD患者血清CC-16表达无明显差异,相关结论有待大样本研究证实。     

Serum thiocyanate, smoking habits and smoking cessation trial in patients with peripheral atherosclerosis

The smoking habits in patients with atherosclerosis in the lower limbs and the effect of advising them to stop smoking was studied by means of self-declaration of the number of cigarettes smoked per day and determination of serum thiocyanate. Ninety-six per cent of males and 70 per cent of the females were smokers or ex-smokers. The number of years of smoking was about 40 for the smokers of both sexes and the male ex-smokers and 23 for the female ex-smokers. The number of cigarettes smoked per day reported by the patients was less than that reported by the smokers in a reference population. The serum thiocyanate levels confirmed the smoking status of the non-smokers and showed that about one-sixth of the ex-smokers had smoked in the last month prior to the study, and that the smokers on the average were heavy smokers smoking much more than the self-reported number of cigarettes. The effect of advising the patients to quit smoking was very disappointing. A maximum of 15 per cent of the smokers stopped smoking while some of the ex-smokers resumed smoking.     

Chronological change of serum carcinoembryonic antigen (CEA) concentrations and pulmonary function data after cessation of smoking in subjects with smoking-associated CEA abnormality

We evaluated changes in serum carcinoembryonic antigen (CEA), peripheral neutrophil concentrations, and ratio of the forced expiratory volume in 1 s to the forced vital capacity (FEV1%) values after cessation of smoking in subjects with smoking-associated CEA abnormality (>5.0 ng/ml) (n=119). In all 25 subjects who gave up smoking (ex-smokers), CEA concentrations 1 year after the cessation decreased within the reference range and neutrophil concentrations were lower than those while smoking. However, both concentrations after 3 years were still higher than those who have never smoked (non-smokers) (n=86). Average CEA and neutrophil concentrations in 94 subjects who continued to smoke (smokers) were stable. There was no difference between chronological changes of FEV1% over 3 years in ex-smokers and in smokers. However, FEV1% values for 3 years in ex-smokers were lower than those in non-smokers. These findings suggest that the ex-smokers who gave up smoking 3 years ago are still affected by past smoking.     

Nursing staff anxiety versus smoking habits

The aim of this study was to assess smoking habits versus anxiety levels of 114 female nurses. The Spielberger State-Trait Anxiety Inventory Scale (STAI, Questions 21-40) was used. Current smokers (n=52) had the highest levels of anxiety (STAI score: mean+/-SD, 43.04+/-8.48) compared to non-smokers (n=30), and ex-smokers (n=32) (38.94+/-6.45 and 36.56+/-6.62, respectively; P<0.02). Differences in STAI scores were greater between non-smokers and ex-smokers (P<0.01), while the STAI scores of current smokers were positively correlated with their per day quota of cigarettes (Pearson's: +0.65; P<0.002). We concluded that even in people who are well-acquainted with the ill-effects of nicotine abuse, smoking habits persist and are correlated with levels of anxiety. Apparently the (perceived) stress-relieving effects of nicotine outweigh anxiety of nursing staff. Preventive programs, if based exclusively on information on the effects of smoking on health, seem to be ineffective. Alternatively, techniques aimed at the relief of anxiety may yield better results.     

Cigarette smoking and hypertension influence nitric oxide release and plasma levels of adhesion molecules.

Progression of atherosclerosis is currently believed to involve interactions between leukocytes and vascular endothelium. Epidemiological risk factors for atherosclerosis such as hypertension and smoking are known to cause endothelial dysfunction, which is an early event in the atherosclerotic process; they also may be considered in the light of their effects on adhesion molecule expression and release. Little is known about the additive effect between these two risk factors on endothelial adhesion molecule expression and nitric oxide release. Soluble adhesion molecules and the nitric oxide were quantified in smoking hypertensive patients in comparison to those from patients with hypertension alone. Cotinine, a stable metabolite of nicotine, has been used to identify smokers. One hundred and three hypertensive patients were selected: 51 smokers (plasma cotinine levels >25 ng/ml) and 52 non-smokers. Plasma concentrations of soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble endothelial leukocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-I) were quantified with ELISA methods. Plasma concentration of nitric oxide metabolites was measured by HPLC, whilst plasma concentration of cotinine was measured by RIA. Significant increases of sICAM-1 and sVCAM-1 were demonstrated in smokers (p<0.001 and p<0.05, respectively). In the same patients, a positive significant correlation between sVCAM-1 and plasma cotinine levels was observed (p<0.002). Nitric oxide metabolites were reduced significantly (p<0.04) in smokers. In conclusion, our data show that the two risk factors, smoking and hypertension, are additive risk factors in generating endothelial dysfunction and vascular damage, which plays a key role in atherogenesis.     

H型高血压患者吸烟与血清同型半胱氨酸的相关性研究

目的 分析H型高血压患者吸烟、戒烟对血清同型半胱氨酸(Hcy)水平的影响,分析吸烟指数、戒烟时间与Hcy水平的相关性.方法 对2018年10月至2019年10月在北京老年医院就诊的高血压患者进行Hcy检测,高血压合并Hcy≥10μmol/L者为H型高血压患者,筛选出H型高血压人群587例.对该人群全部进行调查问卷.分析...     

Smoking and prognosis in women with breast cancer

The hypothesis was that smokers might have more aggressive types of breast cancer because of either delayed diagnosis or higher grade and hence have a worse prognosis. A cohort of breast cancer patients completed a lifestyle questionnaire at the time of diagnosis, including whether they were current smokers, ex-smokers or lifelong non-smokers. Ex-smokers were asked when they had stopped. The participants were 166 women with stage I/II invasive breast cancer diagnosed between October 1984 and March 1987. Participants were divided into three groups: current smokers, ex-smokers and non-smokers. Survival curves were produced by using Cox proportional hazards analysis, with outcome variables for overall and breast cancer-specific survival together with distant relapse-free survival. Smoking was the third most important predictor of distant relapse-free, breast cancer-specific and overall survival after stage and age at diagnosis. These results suggest that smokers are not only more likely to die of other diseases, but also have a higher mortality from breast cancer, compared with those with the disease who have never smoked. The best prognosis, however, was found in those who had given up smoking.     

Rho kinase inhibition by fasudil suppresses lipopolysaccharide-induced apoptosis of rat pulmonary microvascular endothelial cells via JNK and p38 MAPK pathway

Apoptosis of microvascular endothelial cells plays a crucial role in the progression of various lung diseases and triggers microcirculatory disorder and organ dysfunction. LPS, an outer membrane component of Gram-negative bacteria, is one of the major virulence factors for lung diseases. Recent studies have shown that the Rho/Rho kinase (ROCK) pathway plays an important role in the regulation of apoptosis, inflammatory cell migration and chemokine production in various cell types and animal models. We therefore undertake this study to investigate the inhibitory effect of fasudil, a potent and selective inhibitor of ROCK, on LPS-induced apoptosis of rat pulmonary microvascular endothelial cells (PMVECs). The results suggested that fasudil effectively prevented LPS-induced injury of rat PMVECs, as determined by MTT assay, LDH activity assay, apoptosis and western blot analysis of apoptosis-related proteins Bcl-2 and Bax. Furthermore, the mechanisms underlying the protective effect were evaluated. We found that LPS-induced MYPT-1 phosphorylation was markedly suppressed by fasudil. Moreover, fasudil pretreatment obviously inhibited the activation of JNK and p38 MAPKs induced by LPS, whereas that of ERK1/2 was not affected by fasudil. In addition, inhibiting the JNK and p38 pathways by SP600125 and SB203580 respectively attenuated the LPS-induced apoptosis and regulated the expression of apoptosis-related proteins Bcl-2 and Bax. Taken together, these results demonstrate that fasudil exerts an anti-apoptotic effect in rat PMVECs, which is mediated by the inhibition of Rho/ROCK and its downstream JNK and p38 MAPKs.     

Smoking and serum alpha 1-antitrypsin in 1296 healthy men (author's transl)]

Serum alpha 1-antitrypsin (alpha 1AT) was measured by radial immunodiffusion in 1296 healthy men aged 18--50 years. Other biological criteria, including leukocyte count and alpha 2-globulins were measured and the subjects were given a detailed questionnaire on their smoking habits. Results showed a very strong positive relationship between smoking and serum alpha 1AT: the heavy smokers had a serum alpha 1AT 20% higher than the non-smokers, and among subjects who stopped smoking, the level returned rapidly to normal. There were also close interrelationships between serum alpha 1AT, smoking, leukocyte count and a alpha 2-globulins. A discussion of these results is presented.     

Advanced glycation endproducts increase EPC apoptosis and decrease nitric oxide release via MAPK pathways

Objective

Previous studies have shown that advanced glycation endproducts (AGE) can induce endothelial progenitor cells (EPC) apoptosis, which contributes to the pathogenesis of diabetes mellitus. Nitric oxide (NO) signaling is closely associated with apoptosis. We therefore investigated the effects of AGE on human EPC apoptosis, NO release and related signal transduction pathways.

Methods

EPC isolated from healthy human subjects were cultured with various concentrations of AGE (0, 2, 20 and 200 mg/L) for 0, 24, 48 and 72 h in the presence or absence of various MAPK (ERK/P38/JNK) inhibitors, respectively. EPC apoptosis (detected by flow cytometric analyses) and NO concentration in culture supernatant were determined. The mRNA levels of eNOS, COX-2, Bcl-2 and Bax were assessed by RT-PCR and the protein expressions of NF-κB and Caspase-3 assessed by Western blot.

Results

Increased EPC apoptosis and reduced NO release were induced by 200 mg/L AGE, accompanied by a downregulation of eNOS and Bcl-2 expressions as well as an elevation in COX-2, Bax, NF-κB and Caspase-3 expressions in a time-dependent manner (all P < 0.05). These changes were significantly attenuated by pretreatment with various MAPK (ERK/P38/JNK) inhibitors (P < 0.05).

Conclusions

AGE can promote EPC apoptosis and decrease NO release via MAPK pathways.     

Lipolysis in smokers during tobacco withdrawal: a pilot study

OBJECTIVE: Nicotine has an influence on several metabolic events, such as lipid metabolism. Habitual smoking increases plasma levels of glycerol as well as noradrenaline, which is the main stimulating hormone of adipose tissue lipolysis. However, the long-term effect of smoking on lipolysis is unclear. We compared nocturnal lipolysis in habitual smokers during short-term tobacco withdrawal with a control group of non-smokers. MATERIAL AND METHODS: Sixteen healthy subjects (9 heavy smokers and 7 non-smokers) were recruited in the study. The smokers were not permitted to smoke for at least 7 h before the test. The microdialysis technique was used to measure glycerol levels, the end-product of lipolysis, in subcutaneous adipose tissue. Variations in adipose tissue blood flow were measured using the ethanol technique. Glycerol, lactate and glucose concentrations as well as ethanol outflow/inflow ratio were measured between 2400 and 0600 h. RESULTS: There were no significant differences in subcutaneous glycerol or glucose concentrations between smokers and non-smokers. Between 0300 and 0600 h, lactate levels in smokers were lower than those in non-smokers. Adipose tissue blood flow did not differ between the groups. CONCLUSIONS: Despite potent acute and direct effects of smoking on lipolysis, we could not find any significant differences in basal lipolysis rate between smokers during short-term tobacco withdrawal and non-smokers.     

呼吸困难鉴别指数在慢性阻塞性肺病的应用

目的:探讨呼吸困难鉴别指数(dyspnea differentiation index,DDI)在慢性阻塞性肺病(chronic obstructive pulmonary disease,COPD)病情评估中的应用。方法:测定62例COPD患者(吸烟者32例、非吸烟者30例)的PaO2和PEF值,根据Rajesh K. Ailani等创立的公式计算呼吸困难鉴别指数DDI,用治疗前后的DDI与二组(吸烟组、非吸烟组)气急患者改善情况分别进行对比,观察其相关性。结果:DDI值与吸烟组COPD患者的临床严重度分级标准呈明显相关性,与非吸烟组COPD患者的病情改善相关不确定。结论:用DDI判别吸烟组COPD病情是一种敏感、简便可行的方法,值得临床上应用。     

Asiatic acid, a triterpene, induces apoptosis and cell cycle arrest through activation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase pathways in human breast cancer cells

This study first investigates the anticancer effect of asiatic acid in two human breast cancer cell lines, MCF-7 and MDA-MB-231. Asiatic acid exhibited effective cell growth inhibition by inducing cancer cells to undergo S-G2/M phase arrest and apoptosis. Blockade of cell cycle was associated with increased p21/WAF1 levels and reduced amounts of cyclinB1, cyclinA, Cdc2, and Cdc25C in a p53-independent manner. Asiatic acid also reduced Cdc2 function by increasing the association of p21/WAF1/Cdc2 complex and the level of inactivated phospho-Cdc2 and phospho-Cdc25C. Asiatic acid treatment triggered the mitochondrial apoptotic pathway indicated by changing Bax/Bcl-2 ratios, cytochrome c release, and caspase-9 activation, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8. We also found that mitogen-activated protein kinases (MAPKs), extracellular signal-regulated kinase (ERK1/2), and p38, but not c-Jun NH2-terminal kinase (JNK), are critical mediators in asiatic acid-induced cell growth inhibition. U0126 [1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene] or SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole], specific inhibitors of mitogen-activated protein kinase kinase and p38 kinase activities, significantly decreased or delayed apoptosis. Asiatic acid was likely to confine the breast cancer cells in the S-G2/M phase mainly through the p38 pathway, because both SB203580 and p38 small interfering RNA (siRNA) inhibition significantly attenuated the accumulation of inactive phospho-Cdc2 and phospho-Cdc25C proteins and the cell numbers of S-G2/M phase. Moreover, U0126 and ERK siRNA inhibition completely suppressed asiatic acid-induced Bcl-2 phosphorylation and Bax up-regulation, and caspase-9 activation. Together, these results imply a critical role for ERK1/2 and p38 but not JNK, p53, and Fas/Fas ligand in asiatic acid-induced S-G2/M arrest and apoptosis of human breast cancer cells.     

稳定期慢性阻塞性肺疾病患者非侵入性标记物研究

目的比较慢性阻塞性肺疾病（COPD）患者和健康受试者非侵入性标记物,评估其与吸烟的关系。方法选取在我院治疗的稳定期COPD戒烟患者52例（COPD EX组）,稳定期COPD吸烟患者36例（COPD S组）,在我院体检的健康的吸烟者23例（HE S组）,健康的戒烟者23例（HE EX组）。比较所有受试者呼出气冷凝物（EBC）、痰液中前列腺素E2（PGE2）和异构前列腺素15 F2t isoprostane（15 F2t IsoP）的水平、呼出气一氧化氮（FeNO）、痰细胞计数和肺功能。结果与COPD S组比较,COPD EX组的FeNO值明显提高;与两健康组比较,两COPD组EBC中15 F2t IsoP水平明显升高（P＜0.05）;与同等健康状况的戒烟者比较,吸烟者尿液中15 F2t IsoP水平升高（P＜0.05）。结论不同类型炎症性标志物的联合检测分析可用于对COPD患者呼吸炎症的综合评估。     

Serum angiotensin converting enzyme activity in cigarette smokers

Low activity of angiotensin converting enzyme (ACE) has been reported in patients with smoking related diseases, such as chronic bronchitis, emphysaema and carcinoma of the lung [1] but this has not been reported in healthy, chronic smokers. Serum ACE was measured in 40 healthy cigarette smokers and in 42 healthy non-smokers. The mean value was significantly lower in the smokers. Hence a non-smokers. The mean value was significantly lower in the smokers. Hence a patient's smoking habits should be taken into consideration when assessing the significance of his serum ACE levels.     

Effect of cigarette smoking on the antibody response to inhaled antigens and the prevalence of extrinsic allergic alveolitis among pigeon breeders

There was a reduced prevalence of symptoms of Extrinsic Allergic Alveolitis (EAA) among the cigarette smokers in a survey of 102 volunteer pigeon breeders. These smokers had a significantly lower antibody response against the inhaled antigens associated with the disease; only one of twenty-three smokers (4.3%), but thirty-nine of sixty-five non-smokers (55.4%) had elevated serum IgG antibody levels, despite similar degrees of avian exposure in each group. The appearance of antibody in six of fourteen ex-smokers (42.9%) suggested that the apparent inhibitory effect of smoking on the antibody response was reversible. The smoking group had lower total serum IgG and IgA, higher serum IgD, and their total IgM and IgE levels were similar to the nonsmokers.     

The effects of cigarette smoking on serum levels of HDL cholesterol and HDL apolipoprotein A-I. Findings of a prospective epidemiological study on employees of several companies in Westphalia, West Germany

In preventive studies of company employees in Westphalia, HDL cholesterol was measured in the sera of 4933 men and 2365 women, as well as HDL apolipoprotein A-I in the sera of 3509 men and 1648 women. Three subgroups were compared: non-smokers = persons who have never smoked; ex-smokers = persons who do not smoke at present but did in the past; smokers = persons who smoke cigarettes at present. Mean values for HDL cholesterol and for HDL apolipoprotein A-I were significantly lower in smokers than in non-smokers or in ex-smokers, while there were no differences between the last two groups. These differences appeared in both sexes but were more pronounced in women than in men. To answer the question whether the observed differences are caused by the consumption of cigarettes by itself or whether they are caused by the presence of other risk factors, further subgroups were compared to assess the influence of the risk factors obesity, hypertension, hypercholesterolaemia, hyperglycaemia and hyperuricaemia. It was found that - regardless of the presence of no, one, two or more risk factors - the frequency of probands with low HDL cholesterol values (less than 0.907 mmol/l (men); less than 1.166 mmol/l (women] was about 10% higher in smokers than in non-smokers or ex-smokers. Subgroups based on the number of risk factors did not exhibit the same clear distribution for apolipoprotein A-I values as were seen for HDL cholesterol. The results are interpreted in the light of the existing literature.     

Smoking depresses adipose lipoprotein lipase response to oral glucose

Adipose tissue lipoprotein lipase was studied in smokers (n = 17) aged 18-47 years and compared with enzyme activity in non-smokers of comparable age (n = 8) and a second time in some of the subjects 5-9 weeks after cessation of smoking (n = 7). Serum cotinine levels served to validate the smoking status of the subjects. Fasting enzyme activity was similar in smokers and non-smokers, when expressed per 10(6) cells, but was significantly increased when normalized for cell size. When lipoprotein lipase was determined in the same individual 4 h after an oral glucose load, a significant decrease (P less than 0.002) occurred in the smokers, while enzyme activity rose in the nonsmokers (P less than 0.02). A tendency for enzyme activity to rise after oral glucose was seen in ex-smokers, which did not reach statistical significance. Even though the mean serum insulin and glucose levels did not differ in the three groups of subjects, the per cent decrease in lipoprotein lipase after oral glucose in smokers was negatively correlated with insulin release into serum in the same subject, i.e., the greater the insulin release, the less the decrease in lipoprotein lipase activity. We would like to propose that the lower body weight in smokers is related to the paradoxical response of adipose tissue lipoprotein lipase to carbohydrate and that the reversal of this behaviour contributes to the weight gain often observed after cessation of smoking.