Tobacco Induced Diseases最新文献

{"title":"Oral symptoms potentially associated with mild-to-moderate COVID-19 in tobacco users.","authors":"Hanaa E Alkharobi","doi":"10.18332/tid/186531","DOIUrl":"10.18332/tid/186531","url":null,"abstract":"<p><strong>Introduction: </strong>Coronavirus disease (COVID-19) is a worldwide infection characterized by various symptoms. Few studies have examined its oral manifestations. However, there is insufficient information on the oral manifestations of patients with COVID-19 who use tobacco products. Therefore, this cross-sectional study investigated oral symptoms of tobacco-using patients with mild-to-moderate COVID-19.</p><p><strong>Methods: </strong>This study used a convenience sample of non-hospitalized patients (aged ≥18 years) with mild-to-moderate COVID-19 diagnosed by polymerized chain reaction (PCR). This study excluded pregnant or lactating women or patients with serious COVID-19 complications, including those who required hospitalization or were on specific medications (antiviral, corticosteroid, antimicrobial, or immunosuppressive). Oral examinations were performed, including labial, buccal, and gingival mucosa, tongue, floor of the mouth, and palate, for any newly developed lesions associated with the onset of COVID-19. The salivary flow was determined using the passive drool collection technique.</p><p><strong>Results: </strong>Lip dryness, gingivitis, tongue lesions, and taste loss were the most commonly reported oral symptoms in patients with mild-to-moderate COVID-19. The most common general symptoms were tiredness and headache (63.9%), followed by dry cough, myalgia, sore throat, and fever. This study found 139 occurrences of oral symptoms, of which 52 were dry lips (27 tobacco non-users, and 25 tobacco users), and 11 were gingivitis (five non-users, and six tobacco users), and 12 tongue changes (eight non-users, and four tobacco users). Ageusia, or loss of taste sensation, was most commonly reported with or without other oral COVID-19 symptoms (55 occurrences: 36 non-users and 19 tobacco users). No significant differences were found in oral symptoms between tobacco non-users and tobacco users.</p><p><strong>Conclusions: </strong>There is a need to expand the routine examination protocol for patients during future respiratory pandemics, as monitoring oral health allows dentists to improve the management of oral sequelae during a pandemic.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11089344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140917246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E-cigarette use, perceived risks, attitudes, opinions of e-cigarette policies, and associated factors among Thai university students.","authors":"Tippanart Vichayanrat, Warungkana Chidchuangchai, Raksanan Karawekpanyawong, Kanisorn Phienudomkitlert, Nichawee Chongcharoenjai, Naphada Fungkiat","doi":"10.18332/tid/186536","DOIUrl":"10.18332/tid/186536","url":null,"abstract":"<p><strong>Introduction: </strong>Although many countries, including Thailand, currently ban the sale of e-cigarettes, their use continues to rise, especially among young adults. Since the study of e-cigarette use among university students is limited, this study aimed to determine factors associated with e-cigarette use and explore university students' attitudes toward e-cigarettes, perceived risk, and opinion of e-cigarette policies.</p><p><strong>Methods: </strong>This cross-sectional study was conducted among undergraduate students using convenience sampling in a university, in central Thailand from November 2022 to February 2023. A self-administered online questionnaire was distributed to 19 faculties representing health sciences, science and technology, social and arts faculties, and the International College.</p><p><strong>Results: </strong>A total of 548 students completed the online questionnaire, and 20.4% reported ever using e-cigarettes, while 40% of e-cigarette users were unsure about the nicotine content. About 28% agreed, and 22% were unsure whether e-cigarettes could help quit smoking. Most students perceived that e-cigarettes are addictive and harmful, while about half of the participants agreed with the policy related to e-cigarettes in Thailand. Students with positive attitudes towards e-cigarettes were more likely to use e-cigarettes (AOR=1.15; 95% CI: 1.08-1.22), and those with lower perceived risk (AOR=0.89; 95% CI: 0.82-0.96) and who disagreed with e-cigarettes policy (AOR=0.93; 95% CI: 0.89-0.97) were more likely to use e-cigarettes. Personal income and having friends who use e-cigarettes were the significant predictors for e-cigarette use, while studying in the faculty of science and technology was a predictor of using e-cigarettes last month.</p><p><strong>Conclusions: </strong>Although the perceived risk was high, about half of the students thought that e-cigarettes could help them quit smoking and were unsure or disagreed with e-cigarette banning policies. Attitude, perceived risk, policy opinions, personal income, and having friends who used e-cigarettes, were associated with e-cigarette use. Thus, correcting misunderstandings and increasing risk perceptions about e-cigarettes must be advocated among university students.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11087886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140912757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How does the e-cigarette industry respond to tax adjustments? Evidence from China.","authors":"Rong Zheng, Lingyun Meng, Shidong Su, Mark Goodchild","doi":"10.18332/tid/186355","DOIUrl":"10.18332/tid/186355","url":null,"abstract":"<p><strong>Introduction: </strong>China enacted an excise tax on e-cigarettes in November 2022, which offers a distinctive opportunity to examine the industry's reactions to this fiscal adjustment. This study delves into the industry's pricing strategies following the introduction of the excise tax, facilitating a thorough assessment of the subsequent impact on market dynamics and the government's revenue streams.</p><p><strong>Methods: </strong>We developed a TaXSiM model specifically tailored for e-cigarettes in China by integrating the country's e-cigarette tax framework. Our approach involved leveraging market data obtained from a representative product, the RELX Phantom Series, to ensure the model's effectiveness and relevance.</p><p><strong>Results: </strong>The excise implementation of 2022 significantly heightened the tax burden on e-cigarettes, marking an increase of approximately 150 RMB per device and 19 RMB per cartridge. Despite these financial pressures, electronic cigarette firms exemplified by RELX, strategically endeavored to sustain competitiveness. Their approach involved initially implementing a 'Razor blade model' and eventually a 'comprehensive under-shifting' strategy, which mitigated the health impact of the tax hike, resulting in a relatively minor decline in sales while amplifying the impact on tax revenue. However, this strategic pricing maneuver came at a cost, as it led to a substantial decrease in profits, and therefore expedited a reshuffling of the industry by compelling smaller brands to leave the market rapidly.</p><p><strong>Conclusions: </strong>To effectively curb the use of e-cigarettes through tax policies, it is advisable to relocate the imposition of excise taxes on electronic cigarettes to the retail stage. This shift aims to narrow the scope for industry-level pricing strategies. Furthermore, this approach should be coupled with the introduction of an additional specific tax, strategically crafted to accentuate the health-related benefits associated with the excise taxation on electronic cigarettes.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11080932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LRG1 promotes the apoptosis of pulmonary microvascular endothelial cells through KLK10 in chronic obstructive pulmonary disease.","authors":"Wei Cheng, Qing Song, Aiyuan Zhou, Ling Lin, Yiyang Zhao, Jiaxi Duan, Zijing Zhou, Yating Peng, Cong Liu, Yuqin Zeng, Ping Chen","doi":"10.18332/tid/186404","DOIUrl":"https://doi.org/10.18332/tid/186404","url":null,"abstract":"<p><strong>Introduction: </strong>Cigarette smoking is one of the most important causes of COPD and could induce the apoptosis of pulmonary microvascular endothelial cells (PMVECs). The conditional knockout of LRG1 from endothelial cells reduced emphysema in mice. However, the mechanism of the deletion of LRG1 from endothelial cells rescued by cigarette smoke (CS) induced emphysema remains unclear. This research aimed to demonstrate whether LRG1 promotes the apoptosis of PMVECs through KLK10 in COPD.</p><p><strong>Methods: </strong>Nineteen patients were divided into three groups: control non-COPD (n=7), smoker non-COPD (n=7), and COPD (n=5). The emphysema mouse model defined as the CS exposure group was induced by CS exposure plus cigarette smoke extract (CSE) intraperitoneal injection for 28 days. Primary PMVECs were isolated from the mouse by magnetic bead sorting method via CD31-Dynabeads. Apoptosis was detected by western blot and flow cytometry.</p><p><strong>Results: </strong>LRG1 was increased in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. KLK10 was over-expressed in lung tissue of COPD patients and CS exposure mice, and CSE-induced PMVECs apoptosis model. LRG1 promoted apoptosis in PMVECs. LRG1 knockdown reversed CSE-induced apoptosis in PMVECs. The mRNA and protein expression of KLK10 were increased after over-expressed LRG1 in PMVECs isolated from mice. Similarly, both the mRNA and protein levels of KLK10 were decreased after LRG1 knockdown in PMVECs. The result of co-immunoprecipitation revealed a protein-protein interaction between LRG1 and KLK10 in PMVECs. KLK10 promoted apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. KLK10 knockdown could reverse CSE-induced apoptosis in PMVECs.</p><p><strong>Conclusions: </strong>LRG1 promotes apoptosis via up-regulation of KLK10 in PMVECs isolated from mice. KLK10 promotes apoptosis via the down-regulation of Bcl-2/Bax in PMVECs. There was a direct protein-protein interaction between LRG1 and KLK10 in PMVECs. Our novel findings provide insights into the understanding of LRG1/KLK10 function as a potential molecule in COPD.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11069109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140851464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perception of the oral health risks of passive smoking from traditional cigarettes, electronic cigarettes, and heated tobacco products: A cross-sectional study.","authors":"Francesco Saverio Ludovichetti, Andrea Zuccon, Adolfo Di Fiore, Giulia Zambon, Adriana Bargan, Edoardo Stellini, Sergio Mazzoleni","doi":"10.18332/tid/186588","DOIUrl":"https://doi.org/10.18332/tid/186588","url":null,"abstract":"<p><strong>Introduction: </strong>Tobacco smoke is a major health risk factor for smokers but also for non-smokers due to passive smoking. These risks come from conventional cigarette smoke but also from aerosol produced by electronic cigarettes and heated tobacco products (HTPs). The aim of this study was to investigate population knowledge about the adverse effects of passive smoking from traditional cigarettes, electronic cigarettes, and HTPs.</p><p><strong>Methods: </strong>Between February and October 2023, 504 subjects among the general population responded to a questionnaire with 8 questions in Italian, via a link to the Google Forms platform. The questions related to the oral health effects of active and passive smoking. Descriptive analyses of all variables in the questionnaire were performed, and statistical analyses between variables were carried out using the chi-squared test and Fisher's exact test.</p><p><strong>Results: </strong>A large subset of individuals interviewed stated that active smoking is harmful to health and consider active smoking more damaging compared with passive smoking (86.3%). The majority believed that passive smoking of cigarettes is more harmful to oral health than passive smoking of HTPs (79.4%) or electronic cigarettes (e-cigarettes) (84.9%).</p><p><strong>Conclusions: </strong>Results suggest that most people in this study had good knowledge about the adverse effects of active or passive smoking on health; however, knowledge regarding e-cigarettes and HTPs was poor and confused. These results reveal the complexity of perceptions regarding different types of smoking and the need for further research to fully understand the risks associated with each type of passive smoking.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11064127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140866637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of smoking cessation medications on intracranial aneurysm risk: A Mendelian randomization study.","authors":"Xin Liang, Xin Tong, Yan Miao, Xiaopeng Xue, Aihua Liu, Feng Guan","doi":"10.18332/tid/186171","DOIUrl":"https://doi.org/10.18332/tid/186171","url":null,"abstract":"<p><strong>Introduction: </strong>We aim to assess the association between smoking behavior and intracranial aneurysms (IAs) and the effect of smoking cessation medications on IAs at the genetic level.</p><p><strong>Methods: </strong>Causal effects of four phenotypes: 1) age at initiation of regular smoking, 2) cigarettes smoked per day, 3) smoking cessation, and 4) smoking initiation on IAs, were analyzed using two-sample inverse-variance weighted Mendelian randomization analyses. The effects of genes interacting with the smoking cessation medications were analyzed using cis-expression quantitative trait loci genetic instruments on IAs using summary statistics-based Mendelian randomization analyses. Colocalization analyses were then used to test whether the genes shared causal variants with IAs. The role of confounding phenotypes as potential causative mechanisms of IAs at these gene loci was tested.</p><p><strong>Results: </strong>Cigarettes smoked per day (OR=2.89; 95% CI:1.85-4.51) and smoking initiation on IAs (OR=4.64; 95% CI: 2.64-8.15) were significantly associated with IA risk. However, age at initiation of regular smoking (OR=0.54; 95% CI: 0.10-2.8) and smoking cessation (OR=6.80; 95% CI: 0.01-4812) had no overall effect on IAs. Of 88 genes that interacted with smoking cessation medications, two had a causal effect on IA risk. Genetic variants affecting HYKK levels showed strong evidence of colocalization with IA risk. Higher HYKK levels in the blood were associated with a lower IA risk. Gene target analyses revealed that cigarettes/day could be a main mediator of HYKK's effect on IA risk.</p><p><strong>Conclusions: </strong>This study provides evidence supporting that smoking initiation on IAs and cigarettes/day may increase IA risk. Increased HYKK gene expression may reduce IA risk. This can be explained by the increased number of cigarettes consumed daily. HYKK could also reduce IA risk due to the positive effect of continuous abstinence and varenicline therapy on smoking cessation.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11059939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140851463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotine aggravates pancreatic fibrosis in mice with chronic pancreatitis via mitochondrial calcium uniporter.","authors":"Xue Wei, Yue Yuan, Miaomiao Li, Zhiren Li, Xinye Wang, Haoxuan Cheng, Xinjuan Liu, Jianyu Hao, Tong Jin","doi":"10.18332/tid/186587","DOIUrl":"https://doi.org/10.18332/tid/186587","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to investigate the effects of nicotine on the activation of pancreatic stellate cells (PSCs) and pancreatic fibrosis in chronic pancreatitis (CP), along with its underlying molecular mechanisms.</p><p><strong>Methods: </strong>This was an <i>in vivo</i> and <i>in vitro</i> study. <i>In vitro</i>, PSCs were cultured to study the effects of nicotine on their activation and oxidative stress. Transcriptome sequencing was performed to identify potential signaling pathways involved in nicotine action. And the impact of nicotine on mitochondrial Ca²⁺ levels and Ca²⁺ transport-related proteins in PSCs was analyzed. The changes in nicotine effects were observed after the knockdown of the mitochondrial calcium uniporter (MCU) in PSCs. <i>In vivo</i> experiments were conducted using a mouse model of CP to assess the effects of nicotine on pancreatic fibrosis and oxidative stress in mice. The alterations in nicotine effects were observed after treatment with the MCU inhibitor Ru360.</p><p><strong>Results: </strong><i>In vitro</i> experiments demonstrated that nicotine promoted PSCs activation, characterized by increased cell proliferation, elevated α-SMA and collagen expression. Nicotine also increased the production of reactive oxygen species (ROS) and cellular malondialdehyde (MDA), exacerbating oxidative stress damage. Transcriptome sequencing revealed that nicotine may exert its effects through the calcium signaling pathway, and it was verified that nicotine elevated mitochondrial Ca2+ levels and upregulated MCU expression. Knockdown of MCU reversed the effects of nicotine on mitochondrial calcium homeostasis, improved mitochondrial oxidative stress damage and structural dysfunction, thereby alleviating the activation of PSCs. <i>In vivo</i> validation experiments showed that nicotine significantly aggravated pancreatic fibrosis in CP mice, promoted PSCs activation, exacerbated pancreatic tissue oxidative stress, and increased MCU expression. However, treatment with Ru360 significantly mitigated these effects.</p><p><strong>Conclusions: </strong>This study confirms that nicotine upregulates the expression of MCU, leading to mitochondrial calcium overload and exacerbating oxidative stress in PSCs, and ultimately promoting PSCs activation and exacerbating pancreatic fibrosis in CP.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11057042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140872107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex disparities in the association between serum cotinine and chronic kidney disease.","authors":"Jianling Song, Ping Wang, Hong Li","doi":"10.18332/tid/185965","DOIUrl":"https://doi.org/10.18332/tid/185965","url":null,"abstract":"<p><strong>Introduction: </strong>Despite the existence of numerous studies highlighting the adverse effects of smoking on kidney function, the investigation of the correlation between serum cotinine and chronic kidney disease (CKD) remains inconclusive due to insufficient evidence. Consequently, the primary objective of this study was to ascertain the association between serum cotinine levels and CKD.</p><p><strong>Methods: </strong>This study analyzed data from 10900 Americans participating in the National Health and Nutrition Examination Survey between 2005 and 2016. The independent variable under investigation was log serum cotinine, while the dependent variable was the presence of CKD. To investigate the potential linear and non-linear correlations between serum cotinine and CKD, logistic regression models and generalized additive models (GAM) were employed. Furthermore, stratified analyses and interaction tests were conducted to evaluate potential disparities in the relationship between serum cotinine and CKD, based on sex.</p><p><strong>Results: </strong>The median age in the study participants was 49.28 ± 17.96 years, and the median log serum cotinine (ng/mL) was -0.54 ± 1.68. The prevalence of CKD was found to be 17.04%. Multifactorial regression analysis did not show a statistically significant association between log serum cotinine and CKD (OR=1.02; 95% CI: 0.98-1.06, p=0.4387). A statistically significant non-linear association between log serum cotinine and CKD was also not observed in the GAM analysis (p non-linear value=0.091). Subgroup analyses revealed sex differences in the association between log serum cotinine and CKD. Briefly, males had a positive association between log serum cotinine and incident CKD (OR=1.08; 95% CI: 1.02-1.15, p=0.0049). In females, there was a U-shaped association between log serum cotinine and CKD, with an optimal inflection point for log serum cotinine of -0.30 (serum cotinine=0.5 ng/mL).</p><p><strong>Conclusions: </strong>Cross-sectional analyses of NHANES data showed gender differences in the association between serum cotinine and the development of CKD.</p>","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11056949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140871964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role and mechanism of macrophage autophagy in the experimental model of chronic obstructive pulmonary disease","authors":"Li Zhang, Tian Cheng, Caihong Liu, Shengyang He, Junjuan Lu","doi":"10.18332/tid/186403","DOIUrl":"https://doi.org/10.18332/tid/186403","url":null,"abstract":"INTRODUCTION Macrophages play an important role in chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS) impairs autophagy in alveolar macrophages from COPD patients, and autophagic impairment leads to reduced clearance of protein aggregates, dysfunctional mitochondria, and defective bacterial delivery to lysosomes. However, the exact function of lung macrophage autophagy in the pathogenesis of CS-induced COPD remains largely unknown. METHODS Western blot detected the expression of autophagy-related proteins induced by CSE. The model of COPD mice was established by CS exposure combined with CSE intraperitoneal injection. Double immunofluorescence was used to measure the CD206+LC3B+ cells. The morphological changes and effects on lung function were observed. Masson staining detected the changes in collagen fibers in lung tissue. The expression levels of E-cadherinb and N-cadherinb were detected by immunohistochemistry. Western blot detected the expression of ATP6V1E1 in lung tissue. RESULTS At 24 hours of exposure to CSE, the expression levels of LC3B (microtubule-associated protein 1A/1B-light chain 3B) and P62 (nucleoporin 62) were highest at 1% CSE and AGT5 (nucleoporin 62) at 2.5% CSE; at 48 hours, the expression levels of LC3B, P62 and AGT5 were highest at 2.5% CSE, and as the intervention time increased.CD206+LC3B+ cells were significantly higher in the COPD group. Enhanced macrophage autophagy may promote emphysema formation and aggravate lung function damage. The expression of E-cadherinb in lung tissue of the COPD group was decreased, and N-cadherinb expression was increased; the expression of E-cadherinb was increased, and N-cadherinb expression was decreased in ATG5myeΔ COPD mice. The expression of ATP6V1E1 in the lung tissue was increased in the COPD group; ATP6V1E1 expression was decreased in the lung tissues of ATG5myeΔ COPD mice. CONCLUSIONS CSE enhanced macrophage autophagy, leads to increased lung function impairment and collagenous fiber in lung tissue, as well as promotes epithelial-mesenchymal transition, and eventually leads to small airway remodeling, which may be achieved through the ATG5/ATP6V1E1 pathway.","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140666354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of a computer-facilitated intervention on improving provider delivery of tobacco treatment in a thoracic surgery and oncology outpatient setting: A pilot study","authors":"M. Nayak, Emanuele Mazzola, M. Jaklitsch, J. Drehmer, Emara Nabi-Burza, Raphael Bueno, J. Winickoff, M. Cooley","doi":"10.18332/tid/186272","DOIUrl":"https://doi.org/10.18332/tid/186272","url":null,"abstract":"INTRODUCTION Effective tobacco treatments are available but are often not delivered to individuals with an actual or potential diagnosis of thoracic malignancy. The specific aims of this study were to identify the prevalence of tobacco use and examine the effectiveness of the Clinical and community Effort Against Smoking and secondhand smoke Exposure (CEASE), a system-level computer-facilitated intervention, to improve provider delivery of tobacco treatment in a thoracic surgery and oncology outpatient setting. METHODS A pre-post-test design was used to assess the effectiveness of CEASE. A 3-step approach was used to integrate tobacco treatment into routine care: ask about tobacco use, assist with cessation, and refer to a quitline. An end-of-visit survey was conducted to collect prevalence of tobacco use and delivery of tobacco treatment. Descriptive statistics and Fisher’s exact test were used for analysis. RESULTS A total of 218 individuals were enrolled; 105 participants were in usual care (UC) and 113 were in the CEASE group. Of those who enrolled, 27.6% were never smokers in UC and 27.7% in CEASE, 60% were former smokers in UC and 50% in CEASE, and 12.4% were current smokers in UC and 21.4% in CEASE. Significant differences were noted in delivery of tobacco treatment with 15.4% having received tobacco treatment in UC compared to 62.5% in CEASE (p<0.004). CONCLUSIONS A computer-facilitated intervention increased provider delivery of tobacco treatment in a thoracic surgery and oncology outpatient setting. This intervention provided a low-resource approach that has the potential to be scaled and implemented more broadly.","PeriodicalId":23202,"journal":{"name":"Tobacco Induced Diseases","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140674289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}