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.
Objective To make an evidence-based treatment plan for a smoker with periimplantitis. Methods Based on the clinical problems raised from the case, we searched The Cochrane Library (Issue 2, 2009), ACP Journal Club (1991 to July 2009), MEDLINE (1950 to July 2009), EMbase (1980 to July 2009) and Chinese Journal Fulltext Database (1994 to July 2009) for guidelines, systematic reviews, meta-analyses and randomized controlled trials (RCTs). The quality of the included studies was assessed. Results A total of 4 systematic reviews, 8 RCTs were included. The following methods were supported by Level A evidence: (1) Scaling combined with local antibiotics; (2) Guided bone regeneration; (3) Non-surgical debridement with titanium hand-instruments or with an ultrasonic device. Based on the available evidence, we proposed a three-stage therapy plan for the patient: In the first stage, full mouth ultrasonic scaling was performed. The peri-implant pocket was debrided with plastic curettes, and then minocycline gel was applied once a week for four times. The patient was persuaded to maintain oral hygiene and quit smoking. In the second stage, four weeks later, open flap debridement and guided bone regeneration were conducted. In the third stage, long-term care of oral hygiene and dental implants were performed. After 6 months of follow-up, the peri-implant tissues were healthy with no evidence of inflammation, bleeding or suppuration. Conclusion Based on the approach of evidence-based medicine, we accomplished the treatment of the case with reliable outcomes.
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.
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 evaluate the effect of long-term systemic education management program on intervention of chronic obstructive pulmonary disease (COPD). MethodsTwo hundred forty-six stable patients were interviewed face-to-face from March to August in 2013.They were divided into a systemic education group, a follow-up group and a control group according to different management program.The investigation contained general conditions, commonly used medicines, the effects of smoking cessation, the frequency of acute exacerbation in the year before investigation, COPD Assessment Test (CAT) and modified British Medical Research Council (mMRC). ResultsThe success rate for smoking cessation in the systemic education group was 97.6%, which was higher than 81.0% in the follow-up group and 73.8% in the control group(P < 0.01).97.6% of patients in the systemic education group and 93.7% of patients in the follow-up group used bronchodilator.Whereas only 65.5% of patients in the control group inhaled bronchodilator, significantly lower than other two groups (P < 0.01).Mucolytic agents were taken by 14.5% and 19.0% of patients in the systemic education group and the follow-up group, and by 36.9% of patients in the control group (P < 0.01).The frequency of acute exacerbation was 0.9±0.9 both in the systemic education group and the follow-up group, which was lower than 1.2±1.0 in the control group (P < 0.05).CAT and mMRC in the systemic education group (10.2±5.7 and 1.5±1.0) and the follow-up group (11.1±5.8 and 1.5±0.9) were significantly lower than those in the control group (15.0±6.6 and 1.9±1.1, P < 0.01). ConclusionsLong-term systemic education management program can improve success rate for smoking cessation and bronchodilator use, reduce the frequency of acute exacerbation, and improve quality of life effectively in COPD patients.
ObjectiveTo investigate the effects of smoking combined with intermittent hypoxia on the pathophysiology of lung tissue and thoracic aorta, and the endothelial injury.MethodsTwenty-four rats (SPF, female, six weeks old) were divided randomly into 4 groups (n=6). The control group was given false smoking and normal oxygen exposure, the smoking-exposed group was exposed in smoking, the intermittent hypoxia group was exposed in intermittent hypoxia environment, and the overlap group was exposed to smoking and intermittent hypoxia. After 8 weeks, body weight, right ventricular hypertrophy index (RVHI), the pathological changes of lung tissue and thoracic aorta were measured, and the level of endothelin-1 (ET-1), endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1α (SDF-1α) in serum of rats were evaluated.ResultsRVHI of rats in the smoking-exposed group, intermittent hypoxia group, overlap group were higher than that in the control group. In addition, RVHI in the overlap group was higher than that in the smoking-exposed group, intermittent hypoxia group (all P<0.05). The levels of ET-1, VEGF and SDF-1α in the serum of the smoking-exposed group, intermittent hypoxia group and overlap group were higher than those in the control group, while the level of eNOS was lower than that in the control group, (all P<0.05), the most significant difference was between control group and the overlap group. Pathological observation of lung tissue and thoracic aorta showed obvious emphysema in the smoking-exposed group and overlap group, which was more obvious in the overlap group than that in the smoking-exposed group (all P<0.05). Lung interstitial inflammatory infiltration, bronchial wall lymphocyte hyperplasia and pulmonary fibrosis were shown in different degrees in the smoking-exposed group, intermittent hypoxia group and overlap group, and the pulmonary arteriole wall showed thickening, fibrosis and peripheral inflammatory infiltration also were found in these groups. Thoracic aorta in the smoking-exposed group, intermittent hypoxia group and overlap group showed different degrees of endothelial cell injury, middle membrane thickening, and collagen fiber hyperplasia. The pathological features of the overlap group were most obvious compared to the other two groups.ConclusionsSmoking and intermittent hypoxia exposure can lead to different degrees of lung tissue and vascular endothelial injury and decrease of vascular endothelial protective factors in rats, resulting in dysfunction of vascular endothelial cells, which leads to the structural remodeling of pulmonary arterioles and aorta, such as thickening, fibrosis, etc. Combined smoking and intermittent hypoxia exposure can lead to more serious pathological damage.
Objective To investigate the relationship between smoking and lung cancer by evidence-based evaluation. Methods Using Meta-analysis method, the results of 29 case-control studies involving the relationship between smoking and lung cancer in recent decade were analyzed by Review Manager 4. 2 software. Results The association between smoking and lung cancer was significant ( Z =12. 16, P lt; 0. 000 01) , and the pooled OR value was 5. 75( 4. 34, 7. 62) . The population attributable risk percentage( PARP) of smoking was 69. 16% . The pooled OR of 1-10 cpd( cigarettes per day) , 10-20 cpd, 20-40 cpd and more than 40 cpd were 1. 97( 1. 69, 2. 30) , 5. 20( 3. 54, 7. 62) , 7. 46( 5. 22, 10. 67) and 15. 14 ( 5. 27, 43. 44) respectively. The pooled OR of less than 20 years of smoking duration, 20-40 years and more than 40 years were 1. 25( 1. 01, 1. 53) , 5. 10( 3. 03, 8. 57) and 10. 77( 7. 30, 15. 89) respectively. While the pooled ORof less than 10 pack-years, 10-20 pack-years, 20-40 pack-years and more than 40 pack-years were 1. 73( 1. 01, 2. 96) , 3. 73 ( 3. 02, 4. 61) , 5. 69 ( 3. 79, 8. 54) and 8. 41 ( 4. 56, 15. 51) respectively. The pooled OR of initial smoking age less than 15 years old, 15-20 years old and more than 20 years old were 13. 31( 7. 09, 24. 97) , 7. 21( 4. 51, 11. 52) and 4. 74( 3. 47, 6. 47) respectively. The pooled OR of quitting smoking for 1-10 years, 10-20 years and more than 20 years were 7. 16( 4. 70, 10. 91) , 2. 12( 1. 16, 3. 86)and 1. 47 ( 0. 67, 3. 20 ) respectively, and more than 20 years of quitting smoking had no significant difference. The pooled OR of light smoking and deep smoking were 3. 26( 1. 24, 8. 58) and 8. 07( 4. 67, 13. 94) respectively. Conclusions Smoking is an important risk factor of lung cancer. Meta-anlalysis revealed cigarettes comsuption per day, smoking duration, total amount of cigarettes ( pack-years) , smoking behaviour( depth) , initial age of smoking and duration of quitting smoking can increase the risk of lung cancer.
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 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 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.