Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.
ObjectiveTo observe the asynchrony patterns between left and right lungs in smokers and non-smokers,to assess the role of vibration response imaging(VRI) in the early detection and evaluation of smoking-related lung abnormalities. MethodsData were collected as follows:(1)past history and smoking history were collected;(2)exhaled CO test to confirm smoking status was performed;(3)VRI test was performed and the curve of Breath Energy Unit(BEU)was drawn,which is an energy versus time graph of the breath energy.The asynchrony between left and right lungs was derived from this graph;(4)pulmonary function test was performed.In the end,26 villagers with normal spirometry findings were included in the study.The subjects were divided into an ever-smoking group and a never-smoking group. ResultsThe BEU lung asynchrony was 2.0(3.0) frame in the never-smoking group,and 2.0(3.0) frame too in the ever-smoking group.Rank sum test showed that there was no significant difference(Z=-0.29,P=0.77) between the never-smokers and the ever-smokers in the lung asynchrony.Rank correlation analysis suggested that in the ever-smoking group,smoking index and BEU asynchrony had significant correlation(r=0.61,P=0.03).In the never-smoking group,the coefficient of passive smoking index and lung asynchrony was 0.52(P=0.07).The P value of the coefficient between passive smoking index and lung asynchrony was nearly 0.05,scatter between them could be seen a presence of a certain trend. ConclusionThe lung asynchrony in VRI has dose-effect relationship with ever-smokers' smoking level(smoking index).Thus,the lung abnormalities in VRI caused by the exposure to passive smoking is maybe the same as the abnormalities caused by direct smoking.
Objective To investigate the effects of smoking on β-defensin-2 ( BD-2) expression in induced sputumand lung tissue, and its role in chronic obstructive pulmonary disease ( COPD) . Methods Patients suffering with early peripheral squamous celled lung cancer and underwent lobectomy were divided into a smoking COPD group ( COPD group) , a non-COPD smoking group ( smoker group) , and a nonsmoking group ( control group) . Preoperative induced sputumsamples were collected after hypertonic saline induction. Lung tissue samples were intraoperatively collected far from the tumor site. The sputum samples were prepared for total and differential cell count, while the lung tissue samples for pathology examination. The BD-2 concentration in sputumand lung homogenate were measured by ELISA. Correlation were analyzed between BD-2 concentration and smoking index, airway inflammation, and lung function. Results The lung pathology were highly consistent with the experimental grouping. The total cell count and neutrophils proportion in sputum and BD-2 concentration in lung homogenate were ( 2. 32 ±0. 51) ×106 / g, ( 35. 7 ±9. 8) % , and ( 14. 5 ±5. 7) ng/L in the control group respectively, while increased in the smoker group [ ( 4. 57 ±0. 87) ×106 / g, ( 52. 5 ±10. 9) % , and ( 78. 3 ±13. 1) ng/L, P lt;0. 05] , and further increased in the COPD group [ ( 6. 61 ±1. 03) ×106 / g, ( 65. 5 ±12. 3) % , and ( 127. 0 ±35. 0) ng/L, P lt; 0. 05] . The lymphocytes proportion and BD-2 concentration in sputum increased in the COPD group [ ( 3. 2 ±1. 7) % and ( 298. 0 ±135. 0) ng/L] as well as in the smoker group [ ( 2. 5 ±1. 2) % and ( 315. 0 ±124. 0) ng/L] ,as compared with the control group [ ( 1. 1 ±0. 3) % and ( 132. 0 ±48. 0) ng/L] ( P lt; 0. 05) . Linear correlation analysis revealed that BD-2 concentration in sputumwas positively correlated with smoking index,sputum total cell count and neutrophils proportion, whereas BD-2 concentration in lung homogenate wasreversely correlated with pulmonary ventilation function ( P lt; 0. 05) . Conclusions Smoking up-regulates the BD-2 level in sputum and lung tissues. Further more, the BD-2 expression status in lung tissue of smoking individuals might be associated with COPD susceptibility.
Objective To explore the effect of smoking on pulmonary function parameters of male patients with chronic obstructive pulmonary disease (COPD) and to analyze the correlation between smoking and pulmonary function parameters. Methods From January 2014 to October 2015, the pulmonary function parameters of 223 male outpatients or hospitalized patients with COPD in the Department of Respiratory Medicine were retrospectively analyzed by using SPSS 17.0 software. The patients were randomly divided into smoking group (n=98), smoking cessation group (n=82) and non-smoking group (n=43). Results Various degrees of damage or abnormality of lung capacity, ventilatory function, gas exchange function and airway resistance (Raw) existed in the patients with COPD. Compared with smoking cessation group and non-smoking group, residual volume/ total lung capacity (RV/TLC) and Raw were significantly higher (P< 0.05), maximum ventilatory volume, ventilation reserve percent, forced vital capacity, the percent of first second forced expiratory volume compared its predicted value (FEV1%pred), maximum mid-expiratory flow (MMEF), forced expiratory flow 50%, forced expiratory flow 75% and diffusing capacity of carbon monoxide were significantly lower (P<0.05) in the smoking group. There was a negative relationship between MMEF, FEV1%pred and smoking index (r=–0.352, –0.381, P<0.05), and a positive relationship between Raw, RV/TLC and smoking index (r=0.403, 0.378, P<0.05). Conclusions Most of the male COPD patients smoke or used to smoke. Smoking leads to ventilation and gas exchange function decrease, small airway limitation aggravation, airway resistance and emphysema degree increase in COPD patients. Smoking index has a negative relationship with MMEF, FEV1%pred and a positive relationship with Raw and RV/TLC.
Objective To explore the status of smoking and passive smoking of the population with the high risk of stroke in the community and their attitude towards smoking control. Methods In March 2015, under the direction of Stroke Screening and Prevention Projection, the residents with the high risk of stroke were sought out in Longfeng Community, Suining City, Sichuan Province. And then their status of smoking and passive smoking and their attitude towards smoking control was investigated by Passive Smoking Questionnaire for Adults from National Smoking Control Office. Results A total of 354 residents with the high risk of stroke were sought out, in whom 152 (42.9%) were smokers, and the smoking rate of males (70.1%) and females (1.4%) was significantly different (P<0.001). Those aged 40-49 had the highest smoking rate (55.0%), followed by those aged 50-59 (51.7%), and smokers of the two age groups accounted for 73.0% of all smokers. There was significant difference in smoking rate among different age groups (P<0.001). The smoking rate of those with a lower education level of primary school (57.9%) was the highest, and there were significant differences in smoking rates among the population with different education levels (P<0.001). The smoking rate of the solitary (95.7%) was higher than that of the non solitary (34.9%) (P<0.001). In 202 non-smokers, 67 (33.2%) was suffered from passive smoking, and the rate of passive smoking was 31.3% in males and 62.3% in females with a significant difference (P<0.001). The proportion of the female non-smokers against passive smoking (84.1%) was higher than that of the male non-smokers (57.8%). According to the participants report, 79.9% of participants approved completely non-smoking in hospital, school and public transport, 66.4% approved non-smoking in the office and traffic station, and only 10.2% approved non-smoking in the restaurants. Conclusions The rates of smoking and passive smoking among the population with the high risk of stroke are high, and most of the population are supportive to smoke prohibition in public places except restaurants. The population with a low cultural level is short of smoking harm knowledge.
ObjectiveTo investigate the influence of endoplasmic reticulum stress (ERS) on smoking-induced nucleus pulposus cells apoptosis and inflammatory response.MethodsBetween October 2016 and October 2018, 25 patients with cervical disc herniation receiving discectomy were collected and divided into smoking group (14 cases) and non-smoking group (11 cases). The baseline data of age, gender, herniated segment, and Pfirrmann grading showed no significant difference between the two groups (P>0.05). The obtained nucelus pulposus tissues were harvested to observe the cell apoptosis via detecting the apoptosis-related proteins (Caspase-3 and PRAP) by TUNEL staining and Western blot test. The nucleus pulposus cells were isolated and cultured with enzyme digestion, of which the third generation cells were used in follow-up experiments. Then, the expressions of inflammatory factors [interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α)] were detected by ELISA; the nuclear translocation of P65 was monitored by cell immunofluorescence staining. Furthermore, ERS-related proteins (GRP78 and CHOP) were detected by Western blot; and endoplasmic reticulum ultrastructure was observed under transmission electron microscope. To verify the regulatory effect of ERS, cells were pretreated by ERS specific inhibitor (4-PBA), then cell apoptosis and inflammatory response were tested.ResultsThe nucleus pulposus tissue observation showed that the cell apoptotic rate and the expressions of apoptosis-related proteins (Caspase-3 and PARP) were obviously higher in smoking group than in non-smoking group (P<0.05). The nucleus pulposus cells observation indicated that the expressions of the inflammatory factors (IL-1β and TNF-α) and the ERS-related proteins (GRP78 and CHOP) were also higher in smoking group than in non-smoking group (P<0.05). The results of cell immunofluorescence staining further confirmed that smoking stimulated nuclear translocation of P65 in nucleus pulposus cells. The ERS injury was much more serious in smoking group than in non-smoking group. Furthermore, after 4-PBA inhibiting ERS, the expressions of GRP78, CHOP, IL-1β, TNF-α, and P65 were significantly decreased (P<0.05), and flow cytometry results showed that cell apoptotic rate in smoking group was decreased, showing significant difference compared with the non-smoking group (P<0.05).ConclusionSomking can stimulate cell apoptosis and inflammatory response in nucleus pulposus cells via ESR pathway. Suppressing ESR may be a novel target to suspend smoking-induced intervertebral disc degeneration.
Objective To explore the ultrastructure characteristics of pulmonary arteries in smokers with normal lung function and with chronic obstructive pulmonary disease ( COPD) . Methods 33 patients who undertook surgery for peripheral lung cancer were collected. According to smoking history and pulmonary function, the patients were divided into three groups, ie. non-smokers with normal pulmonary function ( group A, n = 10) , smokers with normal pulmonary function ( group B, n = 13) , and smokers in stable phase of COPD ( group C, n = 10) . Normal lung tissues without cancer were sampled and observed under light and electric microscope. Results ①Compared with group A, the thickness of intimal layer of intra-acinar pulmonary muscular arteries of group B and C were significantly higher, the area of their lumenwas lower, and the proportion of their muscular arteries was higher( P lt; 0. 01) . ②Ultrastructure of small pulmonary arteries of group A showed that intimal layer was normal, so as to endothelial cells and smooth muscle cells. Collagen fiber was not increased. Ultrastructure observation of group B showed that endothelialcells were distorted, basal membrane was thick, and collagen fiber increased in vessels. Ultrastructure observation of group C showed that endothelial cells degenerated, vascular intima thickness increased, andsynthetic phenotype smooth muscle cells increased. ③ Smoking index was positively correlated with the proportion of muscular arteries and the proportion of intimal area( r =0. 464,0. 635, P lt;0. 05, respectively) ,and negatively correlated with the proportion of lumen area( r= - 0. 603, P lt;0. 05) . Conclusions Smokers with normal lung fuction and with COPD show the similar ultrastructural characterizations in endothelial cells, smooth muscle cells, and pulmonary arterial remodeling, which related closely to smoking.
Objective To study the correlation between smoking and obstructive sleep apnea (OSA). Methods A total of 454 patients from October 2015 to July 2021 were retrospectively collected for nocturnal polysomnography monitoring (no less than 7 hours). The patients were divided into an OSA group (n=405) and a control group (n=49, patients with primary snoring) according to the results of polysomnography monitoring. According to the apnea hypopnea index (AHI) and the lowest oxygen saturation during sleep, the severity of OSA was classified into a mild to moderate group (5 times/h ≤ AHI<30 times/h) and a severe group (AHI ≥30 times/h). The patients were inquired about their smoking history, then the patients diagnosed with OSA were further divided into a smoking group, a smoking cessation group, and a non-smoking group based on their smoking history. Results The smoking rate of the patients in the OSA group was higher than that in the control group (50.9% vs. 32.7%, P<0.05), while the smoking rate in the severe OSA group was higher than that in the mild to moderate group (55.7% vs. 39.8%, P<0.05). Smoking was positively correlated with AHI, cumulative percentages of time spent at oxygen saturation below 90% (Ts90%), and total apnea time (r value was 0.196, 0.197, 0.163, P<0.05), while negatively correlated with the lowest and average SpO2 during sleep (r value was –0.202, –0.214, P<0.05). The logistic regression analysis with severe OSA as the outcome variable showed that smoking (OR=1.781) and obesity (OR=1.930) were independent risk factors of severe OSA (P<0.05). The comparison between groups of the OSA patients with different smoking states showed that the proportion of severe OSA, AHI, Ts90%, and total apnea time (77.8%, 53.55 times/h, 18.35%, and 111.70 minutes, respectively) of the smoking group were higher than those of the non-smoking group (62.8%, 40.20 times/h, 8.40%, and 76.20 minutes, respectively, P<0.05). The lowest SpO2 and average SpO2 during sleep (69.50%, 93.00%, respectively) of the smoking group were lower than those of the non-smoking group (75.00%, 94.00%, respectively, both P<0.05). The average SpO2 of the smoking cessation group was higher than that of the smoking group (94.00% vs. 93.00%, P<0.05), and the Ts90% of the smoking cessation group was lower than that of the smoking group (6.75% vs. 18.35%, P<0.05). Conclusions Smoking significantly affects the degree of sleep-disordered breathing and may be an independent risk factor for severe OSA. Smoking can exacerbate the severity of OSA and the degree of hypoxia, while smoking cessation can improve the degree of hypoxia in OSA patients.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.
ObjectiveTo investigate the effect of supervised smoking cessation program on COPD Assessment Test (CAT), modified British Medical Research Council (mMRC) and St George’s Respiratory Questionnaire (SGRQ) score and readmission risk in smoking patients with chronic obstructive pulmonary disease (COPD). Methods A total of 200 patients with COPD were enrolled in the study from the Department of Respiratory and Critical Care Medicine of Ganmei Hospital Affiliated to Kunming Medical University (The First People’s Hospital of Kunming) from April 2018 to December 2019. They were randomized divided into a control group (100 cases) and a supervision group (100 cases). The control group stopped smoking by their own will, and the supervision group was interfered on the basis of self-quit. Repeated measure analysis of variance was used to compare the CAT, mMRC, SGRQ scores and hospitalization times of the enrolled subjects before intervention, at the end of 6 months and 12 months of intervention, to evaluate the impact of supervised smoking cessation on the quality of life in smoking patients with COPD. Results CAT scores and mMRC scores were lower in the supervision group than in the control group after 6 months of follow-up compared with the baseline enrollment. There was a significant decrease in the supervision group, from 2.39 to 0.58 respectively; the decrease of control group was not obvious, from 0.15 to 0.01 respectively. After 12 months of follow-up, compared with enrollment and after 6 months of follow-up, the supervision group had a significant decrease, and the CAT score decreased from 4.45 to 2.06, respectively. The mMRC scores decreased by 1.03 and 0.45 points, respectively. The CAT scores of the control group were increased by 0.02 and 0.17 points, respectively, which showed an opposite trend to that of the supervision group. The mMRC score was decreased to a certain extent by 0.16 and 0.15 points, respectively, which was significantly less than that of the supervision group. The differences were statistically significant (P<0.05). After 1 year, compared with enrollment, the average SGRQ score decreased in both the supervision group and the control group. SGRQ symptom score decreased by 4.95 points and 3.51 points respectively; SGRQ activities decreased by 4.01 points and 10.00 points respectively; SGRQ effect score decreased by 5.33 points and 8.65 points respectively; SGRQ total scores were decreased by 6.26 points and 8.95 points respectively. And the number of cigarettes was reduced by 19.01 and 17.15 respectively. The differences were statistically significant (P<0.05). The decreasing range of CAT score, mMRC score, SGRQ symptom score and smoking counts in the supervision group was significantly higher than that in the control group. Considering the supervision to quit smoking can well reflect the improvement of clinical symptoms in COPD patients. In terms of the times of hospitalization, the risk of readmission was lower in the supervision group. Conclusions The mMRC, CAT and SGRQ scores showed that supervised smoking cessation could better improve the quality of life and reduce the risk of readmission in smoking patients. Lung function and quality of life were significantly better after intervention than before.