ObjectiveTo explore ways so as to improve smoking cessation rates by studying relevant cases in Hong Kong.MethodsPatients attending the clinical pilot project in Hong Kong from 2010 to 2022 were retrospectively surveyed and analyzed. Information such as patients' general information, reasons for smoking for the first time, situations that enable smoking, barriers to smoking cessation, and withdrawal symptoms were obtained using a pre-designed case report form and analyzed.ResultsA total of 10436 patients, 6936 males and 3500 females, were included. Influenced by friends (67.70%), relieving mental stress (33.12%) and curiosity (30.52%) were the main reasons for smoking for the first time; depression (57.14%), after meals (49.08%) and nervousness (41.26%) were the situations that enable smoking; the main barriers to smoking cessation were physiologic dependence (87.06%) friends or colleagues smoking (37.03%) and compulsiveness to use tobacco (32.45%), top withdrawal symptoms smoking stoppage were craving for cigarettes (50.33%), restlessness (38.33%), and difficulty concentrating (26.63%).ConclusionsThe proportion of patients actively choosing to quit smoking is high in Hong Kong, and smoking cessation methods should be publicized to prompt smokers to take effective measures to quit. A majority of people are influenced by friends to smoke for the first time; thus, adolescent smoking behavior should be supervised to reduce first-time smokers. Moreover, as the most difficult thing to overcome in the process of quitting smoking is psychological addiction, behavioral interventions must be promoted to improve the rate of successful quitting, Steps should be taken to enable the management of withdrawal symptoms to prevent relapse.
ObjectiveTo understand the prevalence,risk factors,clinical features and the medication of coal worker's pneumoconiosis(CWP) complicated with chronic obstructive pulmonary disease (COPD). MethodsPulmonary function testing results,clinical symptoms,medication of 451 patients with CWP were collected. Then, the risk factors relevant to the incidence of COPD in CWP were analyzed with Cox multivariate regression. ResultsThe prevalence of COPD in CWP was 44.6%,and the incidence was rising with the increasing of CWP phases, exposure duration,smoking index,with the odds ratio of 3.20,1.09,and 1.01,respectively.The patients with CWP and COPD were suffered more symtoms with a CAT score of 25.5 but received less regular medications. ConclusionsThe incidence of COPD in CWP is obviously higher than that in common populaton.Exposure duration, smoking index and phases of CWP are the high risk factors for COPD in the population of CWP. The patients with CWP and COPD are suffered more symtoms but receive irregular medications.
Objective To explore the anti-inflammatory effects of ambroxol hydrochloride in chronic obstructive pulmonary disease（COPD）.Methods Thirty Wistar rats were randomly divided into three groups，ie.a control group，a smoking group and an ambroxol group.The rats in the smoking and ambroxol groups were exposed to cigarettes smoking for 12 weeks.Ambroxol hydrochloride was administered via intragastric gavage after 4 weeks smoking in the ambroxol group.After 12 weeks，the expiratory airway resistance(Re) and dynamic lung compliance(CLdyn) were measured.The expression levels of nuclear factor kappa B（NF-κB）and intercellular adhesion molecule-1(ICAM-1) in airway epithelium cell were observed by immunohistochemical method.Results Re was increased and CLdyn was decreased significantly in the smoking and ambroxol groups compared with the control group(all Plt;0.01).Re was lower (Plt;0.01) and CLdyn was higher(Plt;0.05) in the ambroxol group than those in the smoking group.B.The level of NF-κB and ICAM-1 in smoking and ambroxol groups were obviously increased compared with the control group (all Plt;0.05)，which was decreased in the ambroxol group compared with the smoking group(both Plt;0.05).C.The expression of NF-κB was positively correlated with ICAM-1 expression in airway epithelial cells（r=0.924，Plt;0.01）.Conclusions Smoking can increase the airway resistance，reduce the lung compliance and increase the expression of NF-κB and ICAM-1 in airway epithelium.Ambroxol hydrochloride can relieve those effects of smoking，which suggested an anti-inflammatory therapeutic role in COPD.
Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
ObjectiveTo systematically review the efficacy of different non-pharmacological interventions for smoking cessation. MethodsPubMed, EMbase, The Cochrane Library, Web of Science, CBM, WanFang Data, VIP and CNKI databases were electronically searched to collect randomized controlled trials (RCTs) of different non-pharmacological interventions for smoking cessation from inception to November, 2021. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies; then, network meta-analysis was performed by using Stata 15.1 software. ResultsA total of 27 RCTs involving 14 interventions were included. The results of the network meta-analysis showed that compared with conventional advice, video counseling (OR=2.34, 95%CI 1.32 to 4.15), mobile phone text message (OR=1.82, 95%CI 1.03 to 3.20), motivational interview (OR=2.00, 95%CI 1.11 to 3.59) and health education (OR=3.40, 95%CI 1.52 to 7.57) were higher in quitting rate (P<0.05). The sort results showed that health education was the most likely to be the best intervention (86.20%), followed by video consultation (74.10%). ConclusionCurrent evidence shows that the smoking cessation effects of health education, video counseling, telephone counseling, mobile phone text message and motivational interview. Among them, health education may be the best. Due to the limited quality and quantity of the included studies, more high-quality studies are needed to verify the above conclusion.
ObjectiveThrough the analysis on outcome measurements in domestic and overseas randomized controlled trials (RCTs) of smoking cessation, this study aimed to provide references for clinical trial design in the future. MethodsWe searched CNKI, WanFang Data, VIP, PubMed, EMbase, ScienceDirect and SpringLink databases to collect RCTs regarding smoking cessation from January 1998 to December 2013. Two reviewers screened literature according to the inclusive and exclusive criteria, extracted the data, and analyzed the outcome measurements of included RCTs. ResultsA total of 68 RCTs regarding smoking cessation were included. As for the baseline measurements, the frequency from high to low were age, sex, daily cigarette, smoking duration, Fagerstrom Test For Nicotine Dependence (FTND), race and education, etc.; there were significant differences of race, education level, smoking duration, smoking, starting age of smoking, attempts of trying to stop smoking, the presence of other basic disease, FTND and quit date between English and Chinese RCTs (all P<0.05). As for efficacy measurements, the continuous abstinence rate (77.8%) was mainly adopted in Chinese RCTs, while point abstinence rate (95.1%) and continuous abstinence rate (82.9%) was selected in English RCTs. As for the follow-up measurements, 22.1% of the included RCTs did not report it, 70.6% of the RCTs reported abstinence rate, and the follow-up time in Chinese RCTs was shorter than that in the English RCTs (P<0.05). ConclusionThe selection of outcome measurements is significantly different among RCTs regarding smoking cessation, the Chinese RCTs are inferior to English RCTs, and these are needed to be improved in the future clinical trials.
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 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 analyze the burden of digestive diseases attributed to smoking in China from 1990 to 2019 and forecast its change in the next 10 years. MethodsThe Global Burden of Disease database 2019 was used to analyze the burden of digestive diseases attributed to smoking in China from 1990 to 2019. Joinpoint regression model was used to analyze the time variation trend. A time series model was used to predict the burden of digestive diseases attributable to smoking over the next 10 years. ResultsIn 2019, there were 12 900 deaths from digestive diseases attributed to smoking in China, with a DALY of 398 600 years, a crude death rate of 0.91/100 000 and a crude DALY rate of 28.02/100 000. The attributed standardized mortality rate was 0.69 per 100 000, and the standardized DALY rate was 19.79 per 100 000, which was higher than the global level. In 2019, the standardized mortality rate and DALY rate of males were higher than those of females (1.48/ 100 000 vs. 0.11/ 100 000, 38.42/ 100 000 vs. 293/100 000), and the standardized rates of males and females showed a downward trend over time. In 2019, both mortality and DALY rates from digestive diseases attributed to smoking increased with age. ARIMA predicts that over the next 10 years, the burden of disease in the digestive system caused by smoking will decrease significantly. ConclusionFrom 1990 to 2019, the burden of digestive diseases attributed to smoking showed a decreasing trend in China, and the problem of disease burden is more serious in men and the elderly population. A series of effective measures should be taken to reduce the smoking rate in key groups. The burden of digestive diseases caused by smoking will be significantly reduced in the next 10 years.
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.