Objective To investigate the role of endogenous Hydrogen Sulfide ( H2S) in airway inflammation and responsiveness in a rat model of chronic passive-smoking. Methods Male SD rats were randomly divided into a control group ( breathing fresh air) and a passive smoking group [ cigarette smoking( CS) passively] , with 18 rats in each group. Six rats in each group were randomly intraperitoneally injected with normal saline, sodium hydrosulfide ( NaHS) or propargylglycine ( PPG, an irreversible inhibitor of cystathionine- γ-lyase) . The animals were divided into six subgroups, ie. Con group, NaHS group, and PPG group, CS group, CS+ NaHS group, and CS + PPG group. After 4 months, lung histological change and airway tension were measured. The H2S levels of plasma and lung tissue were analyzed by the sensitive sulphur electrode assay. The expression of cystathionine-γ-lyase ( CSE) was measured by western blot. Results Compared with the Con group, CSE protein expression in lung tissues was increased in CS group( P lt;0. 05) ; the H2 S levels of plasma were significantly higher in CS group, NaHS group and CS + NaHS group, and much lower in PPG group ( P lt; 0. 05, respectively) . Compared with CS group, the H2S levels of plasma were significantly higher in CS + NaHS group, and much lower in CS + PPG group( P lt; 0. 05, respectively) . The H2S level of lung tissue in each group had no significant difference ( P gt; 0. 05) . Compared with Con group,score of lung pathology was significant elevated, and the responsiveness of airway smooth muscles to ACh and KCl was significant augmented in CS group. Compared with CS group, the score of lung pathology was decreased, and the responsiveness of airway smooth muscles was decreased in CS +NaHS group( P lt;0. 05) , and vise versa in CS + PPG group( P lt; 0. 01) . Conclusion H2S can alleviate airway inflammation and hyperresponsiveness induced by CS, and administration of H2S might be of clinical benefit in airwayinflammation and airway responsiveness.
Objective To explore the characteristics of vibration response imaging ( VRI) among heavy smokers whose pulmonary function is normal. Methods 67 heavy smokers with normal pulmonary function, 60 healthy non-smokers, and 60 patients with COPD were recruited. History taking, physical examination, lung function test, chest X-ray, and VRI examination were performed. The difference of VRI dynamic imaging between the three groups was analyzed. Results VRI vibration energy curve which appeared low, flat, sunken-in, and single peak accounted for 43.3% , 16.4% , 16.4% , and 14.9% respectively in the heavy smokers, accounted for 6.7% , 3.3% ,0% , and 0% respectively in the healthy nonsmokers, accounted for 60% , 33.3% , 18.3% , and 16.7% respectively in the COPD patients. The results between the heavy smokers and the healthy non-smokers were significantly different. Compared with the heavy smokers, the COPD patients exhibited more low and flat in expiration period. The energy peak value ratio of inspiration and expiration phase in the heavy smokers, the healthy non-smokers, and the COPD patients were 0.56,0.74, and 0.54 respectively. There was no significant difference between the heavy smokers and the COPD patients in peak value ratio of inspiration and expiration phase. Conclusion The vibration energy curve of the VRI in heavy smokers with normal pulmonary function is significantly different fromhealthy nonsmokers, but there is no significant difference between heavy smokers and COPD patients.
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.
ObjectiveTo systematically evaluate the association between passive smoking during pregnancy and adverse birth outcomes in Chinese, as well as to provide evidence for the prevention of adverse birth outcomes. MethodsWe electronically searched the CNKI, VIP, WanFang Data, PubMed and EMbase databases to collected cohort studies about the association between passive smoking during pregnancy and adverse birth outcomes in Chinese. The search date was from January 1st 1980 to 30th August, 2014. Two reviewers independently screened literature according to the inclusion and exclusion criteria, extracted data and assessed the risk bias of included studies. Then meta-analysis was performed using RevMan 5.1 software. ResultsA total of 24 studies were included in the meta-analysis. The results of meta-analysis showed that, the passive smoking during pregnancy was associated with increased risks of preterm (RR=1.97, 95%CI 1.38 to 2.80), low birth weight (RR=1.94, 95%CI 1.37 to 2.76), birth defects (RR=2.01, 95%CI 1.58 to 2.56), neonatal asphyxia (RR=3.34, 95%CI 1.76 to 6.33), small-for-gestational age (RR=2.62, 95%CI 1.49 to 4.63), stillbirth (RR=3.10, 95%CI 2.00 to 4.80) and spontaneous abortion (RR=1.37, 95%CI 1.19 to 1.59). ConclusionPassive smoking during pregnancy is associated with increased risks of adverse birth outcomes.
The aim of this paper is to reveal the change of the brain function for nicotine addicts after smoking cessation, and explore the basis of neural physiology for the nicotine addicts in the process of smoking cessation. Fourteen subjects, who have a strong dependence on nicotine, have agreed to give up smoking and insist on completing the test, and 11 volunteers were recruited as the controls. The resting state functional magnetic resonance imaging and the regional homogeneity (ReHo) algorithm have been used to study the neural activity before and after smoking cessation. A two factors mixed design was used to investigate within-group effects and between-group effects. After 2 weeks’ smoking cessation, the increased ReHo value were exhibited in the brain area of supplementary motor area, paracentral lobule, calcarine, cuneus and lingual gyrus. It suggested that the synchronization of neural activity was enhanced in these brain areas. And between-group interaction effects were appeared in supplementary motor area, paracentral lobule, precentral gyrus, postcentral gyrus, and superior frontal gyrus. The results indicate that the brain function in supplementary motor area of smoking addicts would be enhanced significantly after 2 weeks’ smoking cessation.
Objective This study aims to investigate the changes of inflammatory markers of oropharynx and its correlation with prognosis in the stable phase of chronic obstructive pulmonary disease (COPD). Methods Sixty-two patients with COPD in stable stage were divided into smoking and non-smoking groups, and 31 healthy persons were selected as controls. The pharyngeal swabs were collected to determine tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), collagen type Ⅳ (COL-4), and fibronectin (FN) by an enzyme-linked immunosorbent assay. Meanwhile, eosinophil count and C-reactive protein (CRP) in peripheral blood were measured. The correlations between the above metrics and COPD and the prognosis of the patients were analyzed. Results TNF-α, IL-8, COL-4, FN and CRP levels in patients with COPD were significantly higher compared with control groups (P<0.05), and there were significant differences between smoking and non-smoking groups in inflammatory markers such as TNF-α, IL-8, FN, CRP (P<0.05). The forced expiratory volume in one second (FEV1) and FEV1%pred of patients with COPD were significantly lower than the control group (P<0.05). The smoking index of patients with COPD in smoking group was significantly higher than that in smoking control group (P<0.05). TNF- α and IL-8 were positively associated with blood CRP in patients with COPD. Conclusion The inflammatory markers of oropharynx in patients with COPD are different from those in healthy persons and smoking may promote the increase of inflammatory markers of oropharynx in patients with COPD; the non-invasive detection of paired pharyngeal inflammatory markers may be helpful in determining acute onset and prognosis.
Objective To study the expression of human Runt-related transcription factor 1 (RUNX1) in rat airway epithelial cells stimulated by cigarette smoking extract (CSE), and explore the role of RUNX1 in regulating epithelial-mesenchymal transition (EMT). Methods Primary rat bronchial epithelial cells were cultured by enzyme digestion and stimulated with different concentrations of CSE. The viability of cells was detected by CCK-8 to explore the appropriate concentration of CSE. After the cells were treated with CSE, the Runx1 interference and overexpression vectors were constructed and transfected into the cells to silence or overexpress the Runx1 gene. Immunocytochemical method was used to detect RUNX1 expression and Western blot analysis was used to detect the expression of RUNX1, nuclear factor-κB (NF-κB), Snail, E-cadherin, and vimentin. Results The survival rate of bronchial epithelial cells could be reduced by CSE, and the degree of reduction was directly positively correlated to the concentration of CSE. After CSE stimulation, the expression level of E-cadherin in primary rat bronchial epithelial cells decreased significantly (P<0.05); the expression levels of RUNX1, NF-κB, Snail and vimentin significantly increased (P<0.05). After interfering with RUNX1 gene, the expression level of E-cadherin was up-regulated (P<0.05), and the expression levels of NF-κB, Snail and vimentin were down-regulated (P<0.05). After overexpression of RUNX1 gene, the expression level of E-cadherin decreased (P<0.05), and the expression levels of NF-κB, Snail and vimentin increased (P<0.05). Conclusions CSE promotes the expression of RUNX1 in rat airway epithelial cells. RUNX1 might regulate EMT process by involving in the regulation of NF-κB /Snail expression.
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 expression of dipeptidyl peptidase 4 (DPP4) and angiotensin-converting enzyme 2 (ACE2) in lung tissues of patients with four different diseases including coronavirus disease 2019 (COVID-19), chronic obstructive pulmonary disease (COPD), pulmonary sarcoidosis and pulmonary bullae, and to find out the potential risk factors affecting COVID-19. Methods This study retrospectively analyzed the clinical data of 40 patients admitted to Renmin Hospital of Wuhan University with COVID-19 (COVID-19 group), COPD (COPD group), pulmonary sarcoidosis (pulmonary sarcoidosis group) and pulmonary bullae (pulmonary bullae group) and surgically resected paraffin-embedded pathological lung tissues were obtained from their lung tissue pathological specimens after surgery and paraffin embedding. The GEO database (https://www.ncbi.nlm.nih.gov/geo/) was used for bioinformatics analysis to explore the expression difference of DPP4 and ACE2 mRNA in COVID-19, COPD, pulmonary sarcoidosis and normal lung tissues. Immunohistochemistry method was used to detect the expression of DPP4 and ACE2 protein in lung tissues of each group and the average optical density was measured by image analysis software. Results The results of GEO database analysis showed that compared with pulmonary bullae group, the expression level of DPP4 mRNA had no significant difference in the COPD group and pulmonary sarcoidosis group (both P>0.05), but it was increased in the COVID-19 group (P<0.05); There was no significant difference in the expression level of ACE mRNA in the pulmonary sarcoidosis group (P>0.05), but it was increased in the lung tissue of COVID-19 group and COPD group (both P<0.05). The results of immunohistochemistry showed that DPP4 and ACE2 proteins were lowly expressed in the pulmonary sarcoidosis group and pulmonary bullae group, while their expression level was high in COVID-19 and COPD groups without significant difference (P>0.05). The expression of DPP4 and ACE2 proteins in COVID-19 group was not related to the patient’s gender and age (P>0.05), but was related to smoking and long smoking duration (P<0.05), and there was a positive correlation between DPP4 and ACE2 expression (P<0.05). Conclusions DPP4 and ACE2 proteins are lowly expressed in the pulmonary sarcoidosis group and pulmonary bullae group, while their expression level is high in COVID-19 and COPD groups. There is no significant difference in the expression level of DPP4 and ACE2 protein in the COVID-19 and COPD lung tissues. There may be a positive correlation between DPP4 and ACE2 proteins expression in lung tissue, and smoking may be a potential risk factor for COVID-19.
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.