Arrhythmogenic effects of acute electronic cigarette compared to tobacco cigarette smoking in people living with HIV.

The leading cause of death in people living with HIV (PLWH) is cardiovascular disease, and the high prevalence of tobacco cigarette (TC) smoking is a major contributor. Switching to electronic cigarettes (ECs) has been promoted as a harm reduction strategy. We sought to determine if acute EC compared to TC smoking had less harmful effects on arrhythmogenic risk factors including acute changes in hemodynamics, heart rate variability (HRV), and ventricular repolarization (VR). In PLWH who smoke, changes in hemodynamics, HRV, and VR were compared pre/post acutely using an EC, TC, or puffing on an empty straw on different days in random order, in a crossover study. Thirty-seven PLWH (36 males, mean age 40.5 ± 9.1 years) participated. Plasma nicotine was greater after TC versus EC use (10.12 ± 0.96 vs. 6.18 ± 0.99 ng/mL, respectively, p = 0.004). HR increased significantly, and similarly, after acute EC and TC smoking compared to control. Changes in HRV that confer increased cardiac risk (LF/HF ratio) were significantly smaller after acute EC versus TC use, consistent with a harm reduction effect. In a post-hoc analysis of PLWH with and without positive concurrent recreational drug use as indicated by point of care urine toxicology testing, this differential effect was only seen in PLWH not currently using recreational drugs. Changes in VR were not different among the three exposures. In PLWH who smoke, EC compared to TC smoking resulted in smaller adverse changes in HRV. This differential effect was accompanied by a smaller increase in plasma nicotine, and was negated by concurrent recreational drug use. Additional studies are warranted in this vulnerable population disproportionately affected by tobacco-related health disparities.

Effect of Donor Cigarette Smoking in Kidney Transplantation: Re-Evaluation of Long-Term Outcomes.

Cigarette smoking is a common risk factor associated with negative long-term outcomes in kidney transplant recipients. However, whether donor smoking decreases graft longevity or negatively impacts recipient survival after kidney transplantation remains unknown. Therefore, this study aims to investigate the long-term outcome in patients who received a kidney graft from a deceased smoking or non-smoking donor. A total of 580 patients were divided into two groups: patients who received a graft from a smoking donor (n = 276) and those who received a graft from a non-smoking donor (n = 304). Analysis of demographic factors showed that the non-smoking cohort was older, had more extended criteria donors and longer warm ischemia times. The primary composite endpoint of patient and graft survival was better in the smoking donor cohort when analyzed using Kaplan-Meier method but not when controlled for covariates in multivariate analyses. These findings do not support a previously reported negative impact of deceased donor smoking on kidney transplant recipients. Thus, the underlying results should not be interpreted in favor of a positive donor smoking history, but rather remind the transplant community that donor smoking should not be considered as a deciding factor in refusing an otherwise acceptable kidney graft.

Heavy metal concentrations and clinical symptoms in patients diagnosed with schizophrenia related to cigarette smoking.

In our study, blood concentrations of lead (Pb), arsenic (As), and cadmium (Cd) and urine concentrations of thallium (Tl) were measured together with related symptoms of heavy metal poisoning in cigarette smoking volunteers diagnosed with schizophrenia, in cigarette smokers not diagnosed with schizophrenia, and in the control group of non-smokers and not diagnosed with schizophrenia volunteers. Our study was performed on 171 volunteers divided into the following subgroups: patients diagnosed with schizophrenia with at least 1 year of continuous cigarette smoking experience (56 participants), cigarette smokers not diagnosed with schizophrenia with at least one year of continuous smoking experience (58), and control group (not diagnosed with schizophrenia and non-smoking volunteers) (57). Smoking durations of cigarette smokers diagnosed with schizophrenia and cigarette smokers not diagnosed with schizophrenia are not similar (p = 0.431). Blood Pb, As, and Cd concentrations and urine Tl concentrations were the highest in the subgroup of cigarette smokers not diagnosed with schizophrenia, followed by the subgroup of cigarette smokers diagnosed with schizophrenia, and the control group. Only blood Pb concentrations were significantly higher (probability value p < 0.05) in the group of cigarette smokers not diagnosed with schizophrenia (5.16 µg/dL), comparing to the group of cigarette smokers diagnosed with schizophrenia (3.83 µg/dL) and to the control group (3.43 µg/dL). Blood Cd and As concentrations and urine Tl concentrations were significantly higher (p < 0.05) in cigarette smokers not diagnosed with schizophrenia than in the control group. The results revealed a statistically significant positive correlation (p < 0.001) in the cigarette smokers in the schizophrenia diagnosed group between blood Pb, blood As, and urine Tl concentrations and the duration of cigarette smoking.

Cardiac diastolic dysfunction by cigarette smoking is associated with mitochondrial integrity in the heart.

Cigarette smoking behaviors are harmful and cause one out of ten deaths due to cardiovascular disease. As population sizes grow and number of cigarette smokers increases, it is vital that we understand the mechanisms leading to heart failure in cigarette smokers. We have reported that metabolic regulation of a histone deacetylase, SIRT1, modulates cardiovascular and mitochondrial function under stress. Given this conclusion, we hypothesized that chronic cigarette smoking led to cardiovascular dysfunction via a reduction SIRT1. Mice were randomly organized into smoking or nonsmoking groups, and the smoking group received cigarette smoke exposure for 16 weeks. Following 16-week exposure, diastolic function of the heart was impaired in the smoking group as compared to sham, indicated by a significant increase in E/e'. The electrical function of the heart was also impaired in the smoking group compared to the sham group, indicated by increased PR interval and decreased QTc interval. This diastolic dysfunction was not accompanied by increased fibrosis in mouse hearts, although samples from human chronic smokers indicated increased fibrosis compared to their nonsmoker counterparts. As well as diastolic dysfunction, mitochondria from the 16-week smoking group showed significantly impaired function, evidenced by significant decreases in all parameters measured by the mitochondrial stress test. We further found biochemical evidence of a significantly decreased level of SIRT1 in left ventricles of both mouse and human smoking groups compared to nonsmoking counterparts. Data from this study indicate that decreased SIRT1 levels by cigarette smoking are associated with diastolic dysfunction caused by compromised mitochondrial integrity.

Treatment outcomes of oral leukoplakia on the irradiated or nonirradiated mucosa among survivors of head and neck cancer in the papulation where practice of betel nut chewing and cigarette smoking are widespread.

BACKGROUND: Radiotherapy (RT) has numerous effects on the oral mucosa, primarily genetic alterations and changes in the microenvironment. The characteristics of oral leukoplakia (OL) may differ between patients who have received previous head and neck cancer (HNC) treatment with radiation therapy and those who have not. Due to a lack of data on this scenario, we aimed to investigate the surgical outcomes of OL by comparing these two patient groups. METHODS: This retrospective cohort study enrolled a total of 224 OL lesions in 124 patients who underwent carbon dioxide laser (CO2 laser) surgery from July 2002 to Aug 2021. All patients had received previous treatments for HNC, with 59 patients undergoing only surgical approach, 65 patients undergoing RT, and 46 patients undergoing concurrent chemotherapy during RT. The analysis was performed on a per-lesion basis, not a per-capita basis. We investigated the associations of clinicopathological characteristics and treatment outcomes of OL lesions that developed from irradiated or nonirradiated oral mucosa. RESULTS: The median follow-up time was 5.87 years. Postoperative recurrence of OL occurred in 30 patients. Malignant transformation occurred in 17 patients with the incidence rate 4.19% annually and 13.7% cumulatively. The average time for OL transforming into squamous cell carcinoma was 3.27 ± 3.26 years (median 1.82, range 0.11 - 11.90). In univariate analysis, non-homogeneous morphology (P = 0.042), moderate to high-grade dysplasia (P = 0.041), and nonirradiated oral mucosa (P = 0.0047) were predictors for malignant transformation. However, in the Cox proportional hazard model, only nonirradiated oral mucosa remained an independent prognostic factor related to postoperative malignant transformation of OL (P = 0.031, HR 5.08, CI95 1.16 - 22.25). CONCLUSION: In the population whose OL is strongly aetiologically linked to environmental carcinogens such as betel nut and tobacco, OL lesions that develop on previously irradiated oral mucosa have a lower risk for postoperative malignant transformation compared to those that develop on nonirradiated mucosa. This finding highlights the potential impacts of radiation on OL. Further research is needed to confirm this observation and elucidate the underlying mechanism.

Influence of BMI, Cigarette Smoking and Cryopreservation on Tyrosine Phosphorylation during Sperm Capacitation.

Capacitation involves tyrosine phosphorylation (TP) as a key marker. Lifestyle-related factors, such as obesity and smoking, are recognized for their adverse effects on semen quality and male fertility, yet the underlying mechanisms, including their potential impact on TP, remain unclear. Moreover, the effect of sperm cryopreservation on TP at the human sperm population level is unexplored. Flow cytometry analysis of global TP was performed on pre-capacitated, post-capacitated and 1- and 3-hours' incubated fresh and frozen-thawed samples from sperm donors (n = 40). Neither being overweight nor smoking (or both) significantly affected the percentage of sperm showing TP. However, elevated BMI and smoking intensity correlated with heightened basal TP levels (r = 0.226, p = 0.003) and heightened increase in TP after 3 h of incubation (r = 0.185, p = 0.017), respectively. Cryopreservation resulted in increased global TP levels after capacitation but not immediately after thawing. Nonetheless, most donors' thawed samples showed increased TP levels before and after capacitation as well as after incubation. Additionally, phosphorylation patterns in fresh and frozen-thawed samples were similar, indicating consistent sample response to capacitation stimuli despite differences in TP levels. Overall, this study sheds light on the potential impacts of lifestyle factors and cryopreservation on the dynamics of global TP levels during capacitation.

Effect of conventional cigarette smoking and recent heated tobacco products on CAD/CAM restorative materials.

OBJECTIVE: To determine the effects of conventional cigarette smoking (CS) and recent heated tobacco products (HTPs) on the surface roughness and color stability of different indirect restorative materials. MATERIALS AND METHODS: One hundred disc-shaped samples were constructed of three different restorative CAD/CAM materials: lithium disilicate glass-ceramic (IPS e.max CAD; Ivoclar Vivadent, Liechtenstein), zirconia (BruxZir® Zirconia, Glidewell, USA) and polyetheretherketone (BioHPP® bredent GmbH, Germany). Of the IPS e.max CAD and the Bruxzir samples, 20 samples were glazed, and 20 samples were polished, while the BioHPP samples were all polished according to the manufacturer's instructions. Fifty samples were subjected to conventional cigarette smoking (LM, Philip Morris International Inc., Egypt) (Groups: IPS e.max CAD_Glazed exposed to CS (LD_G_Cig), IPS e.max CAD_Polished exposed to CS (LD_P_Cig), Bruxzir_Glazed exposed to CS (Zr_G_Cig), Bruxzir _Polished exposed to CS (Zr_P_Cig) and BioHPP exposed to CS (PEEK_Cig) and fifty samples were exposed to heated tobacco product smoking (Heets, Russet selection, Philip Morris International Inc., Italy) (Groups: IPS e.max CAD_Glazed exposed to HTP (LD_G_HTP), IPS e.max CAD_Polished exposed to HTP (LD_P_HTP), Bruxzir_Glazed exposed to HTP (Zr_G_HTP), Bruxzir CAD_Polished exposed to HTP (Zr_P_HTP) and BioHPP exposed to HTP (PEEK_HTP).. Six hundred cigarettes/heets representing 30 days of medium smoking behavior (20 cigarettes/day) were used. Before and after exposure to smoke, the surface roughness of all the samples was measured using JITAI8101 surface roughness tester (Beijing Jitai Tech Detection Device Co., Ltd, China, and the color parameters were assessed using VITA Easyshade Advance 4.01 (VITA shade, VITA made, VITA). The data were analyzed using One-way ANOVA, paired sample t-test and independent sample t-test. The significance level was set at α < 0.05. The surface topography was evaluated by scanning electron microscopy (SEM) and analyzed using energy-dispersive X-ray (EDX) spectroscopy to determine changes in the surface chemical composition. RESULTS: Both types of smoking caused significant increases in the surface roughness of all the samples. There was a significant difference in color change between CS and HTP for all materials with different surface finish (P < 0.01) and zirconia had the greatest effect on color change (P < 0.001). In contrast, polyetheretherketone (PEEK) "BioHPP" had the least effect (P < 0.001). CONCLUSION: Exposure to different types of smoking induce changes in the surface topography and color of different esthetic restorative materials. Compared with HTP, conventional cigarette smoke has a greater effect on the surface roughness and color stability of esthetic restorative materials. The glazed surfaces showed less change in surface topography than did the polished surfaces. Zirconia showed better color stability when compared to polyetheretherketone (PEEK).

Cigarette Smoke Extract Induces MUC5AC Expression Through the ROS/ IP3R/Ca2+ Pathway in Calu-3 Cells.

Background: Chronic obstructive pulmonary disease (COPD) is caused by exposure to noxious external particles, air pollution, and the inhalation of cigarette smoke. Airway mucus hypersecretion particularly mucin5AC (MUC5AC), is a crucial pathological feature of COPD and is associated with its initiation and progression. In this study, we aimed to investigate the effects of cigarette smoke extract (CSE) on MUC5AC expression, particularly the mechanisms by which reactive oxygen species (ROS) induce MUC5AC expression. Methods: The effects of CSE on the expression of MUC5AC and mucin5B (MUC5B) were investigated in vitro in Calu-3 cells. MUC5AC and MUC5B expression levels were measured using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), immunofluorescence staining, and enzyme-linked immunosorbent assay (ELISA). Total cellular levels of ROS and Ca2+ were determined using DCFH-DA and Fluo-4 AM. Subsequently, the expression levels of IP3R, IRE1α, p-IRE1α and XBP1s were measured by Western blotting. Gene silencing was achieved by using small-interfering RNAs. Results: Our findings revealed that exposure to CSE increased MUC5AC levels and upregulated ROS, IP3R/Ca2+ and unfolded protein response (UPR)-associated factors. In addition, knockdown of IP3R using siRNA decreased CSE-induced Ca2+ production, UPR-associated factors, and MUC5AC expression. Furthermore, 10 mM N-acetyl-l-cysteine (NAC) treatment suppressed the effects of CSE, including ROS generation, IP3R/ Ca2+, UPR activation, and MUC5AC overexpression. Conclusion: Our results suggest that ROS regulates CSE-induced UPR and MUC5AC overexpression through IP3R/ Ca2+ signaling. Additionally, we identified NAC as a promising therapeutic agent for mitigating CSE-induced MUC5AC overexpression.

Coexistence of Standard Modifiable, Other Classical, and Novel and Classical Atherosclerotic Cardiovascular Disease Risk Factors in Middle Eastern Young Women.

Background: The coexistence of multiple standard modifiable risk factors (SMuRFs),classical and novel risk factors (RFs) for atherosclerotic cardiovascular disease (ASCVD) is common in the Middle East (ME). There is a paucity of data on the coexistence of these RFs in ME young women. Aim: Comparing the prevalence and the statistical patterns of the SMuRFs, classical and novel RFs in target population. Methods: In this case-control (1:2) study, consecutive young women aged 18-50 years were enrolled in 12 centers (July 2021 to October 2023). Prevalence and coexistence of 19 RFs were compared between cases with ASCVD and their controls. The RFs included SMuRFs (hypertension, type 2 diabetes, dyslipidemia, and cigarette smoking), other classical RF (obesity, family history of premature ASCVD, and physical inactivity), novel RFs and social determinants of health (health insurance, place of residence, depression, and level of education). Results: The study included 627 subjects; 209 had ASCVD (median age 46 years, IQR 49-42 years) and 418 controls (median age 45 years, IQR 48-41 years). The presence of 1-2 RFs; (ASCVD: 63.2%, Control: 54.1%, p=0.037) and 3-4 RFs; (ASCVD: 27.8%, Control: 3.3%, p < 0.001) SMuRFs was more prevalent in women with ASCVD. Similarly, the presence of 4-5 RFs; (ASCVD: 40.7%, Control: 14.6%, p<0.001), and 6-7 (ASCVD: 10.5%, Control: 1%, p < 0.001). The classical RF were also significantly common in these women. The distribution of multiple novel RF was not statistically significant across both groups. Finally, regarding the socioeconomic RFs in women with ASCVDs, the presence of 1-2 RFs (ASCVD: 59.8%, Control: 76.1%, p < 0.001) was significantly less common while the presence of 3-4 RFs (ASCVD: 39.2%, Control: 21.8%, p < 0.001) was vastly more common. Conclusion: An elevated rate of coexistence of classical RF in the case group, mainly socioeconomic and SMuRFs. By managing them primary and secondary ASCVDs prevention attained.

Comparative effects of e-cigarette smoking on periodontal status, salivary pH, and cotinine levels.

BACKGROUND: The nicotine in e-cigarette liquid can negatively impact periodontal tissues by altering the salivary pH and elevating cotinine levels. Thus, the study aimed to determine the periodontal parameters, salivary pH, and cotinine levels among cigarette, e-cigarette, and never-smokers. METHODS: A total of 144 participants were recruited (48 cigarette smokers, 48 e-cigarette smokers, and 48 never-smokers). Clinical periodontal parameters, including plaque index (PI), gingival index (GI), periodontal probing pocket depth (PPD), and clinical attachment loss (CAL) were recorded, excluding third molars. The level of unstimulated whole salivary pH was measured using a portable pH meter and the levels of salivary cotinine were measured using Enzyme-Linked Immunosorbent Assay (ELISA). RESULTS: Data were analysed statistically using analysis of variance. Mean scores of PPD, percentage of pocket depth ≥ 4 mm, and CAL (p < 0.05) were significantly higher among cigarette smokers than those in e-cigarette and never-smokers, while GI (p < 0.05) were significantly higher among e-cigarette smokers. The unstimulated salivary pH was more acidic among cigarette smokers (p < 0.05) and e-cigarette smokers (p < 0.05) than in never-smokers. The cotinine levels were higher among cigarette smokers (p < 0.05) and e-cigarette smokers (p < 0.05) than in never-smokers. CONCLUSIONS: Clinical periodontal parameters were poorer in cigarette smokers than in e-cigarette smokers and never-smokers. Meanwhile, cigarette and e-cigarette smokers have more acidic salivary pH and higher cotinine levels than in never-smokers.

Protective Effect of the Total Alkaloid Extract from Bulbus Fritillariae pallidiflorae in a Mouse Model of Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease.

Purpose: In recent years, the incidence of chronic obstructive pulmonary disease (COPD) has been increasing year by year, but therapeutic drugs has no breakthrough. The total alkaloid extract from Bulbus Fritillariae pallidiflorae (BFP-TA) is widely used in treating lung diseases. Therefore, this study aimed to investigate the protective effect and mechanism of BFP-TA in COPD mice. Methods: BFP-TA was prepared by macroporous adsorbent resin, and the material basis of BFP-TA was analyzed by HPLC-ELSD and UHPLC-MS/MS. Then, the COPD mouse model was induced by cigarette smoke (CS) for 12 weeks, administered at weeks 9-12. Subsequently, the body weight, lung-body ratio, pulmonary function, histopathology, and the levels of pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and oxidative stress markers in the serum of mice were determined. The expressions of related protein of EMT and MAPK signaling pathways in the lung tissues of mice were detected by Western blot. Results: The alkaloid relative content of BFP-TA is 64.28%, and nine alkaloids in BFP-TA were identified and quantified by UHPLC-MS/MS. Subsequently, the animal experiment showed that BFP-TA could improve pulmonary function, and alleviate inflammatory cell infiltration, pulmonary emphysema, and collagen fiber deposition in the lung of COPD mice. Furthermore, BFP-TA could decrease the levels of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1ß), MMPs (MMP-9 and MMP-12) and MDA, while increase the levels of TIMP-1 and SOD. Moreover, BFP-TA could decrease the protein expressions of collagen I, vimentin, α-SMA, MMP-9, MMP-9/TIMP-1, Bax, p-JNK/JNK, p-P38/P38, and p-ERK/ERK, while increase the level of E-cadherin. Conclusion: This study is the first to demonstrate the protective effect of BFP-TA in CS-induced COPD mouse model. Furthermore, BFP-TA may improve airway remodeling by inhibiting the EMT process and potentially exert anti-inflammatory effect by inhibiting the MAPK signaling pathway.

Effect of Cigarette Smoking on Clinical and Molecular Endpoints in COPD Patients.

Cigarette smoking is a primary contributor to mortality risks and is associated with various diseases. Among these, COPD represents a significant contributor to global mortality and disability. The objective of this study is to investigate the effect of smoking on a selected battery of variables, with an emphasis on DNA damage. A total of 87 elderly patients diagnosed with COPD, divided into three groups based on their smoking history (current, former, never-smokers), were evaluated using a cross-sectional approach. Clinical features including mortality and inflammatory/oxidative parameters (Lymphocytes/Monocytes, Neutrophils/Lymphocytes, Platelets/Lymphocytes ratio), SII, MDA, 8-Oxo-dG, and IL6 (ELISA assay), as well as DNA damage (comet assay), were investigated. Virus infection, i.e., influenza A virus subtype H1N1, JC polyomavirus (JCPyV), BK polyomavirus (BKPyV), and Torquetenovirus (TTV), was also tested. Current smokers exhibit higher levels of comorbidity (CIRS; p < 0.001), Platelets/Lymphocytes ratio (p < 0.001), systemic immune inflammation (p < 0.05), and DNA damage (p < 0.001). Former smokers also showed higher values for parameters associated with oxidative damage and showed a much lower probability of surviving over 5 years compared to never- and current smokers (p < 0.0017). This study showed a clear interaction between events which are relevant to the oxidative pathway and cigarette smoking. A category of particular interest is represented by former smokers, especially for lower survival, possibly due to the presence of more health problems. Our findings raise also the attention to other parameters which are significantly affected by smoking and are useful to monitor COPD patients starting a program of pulmonary rehabilitation (DNA damage, inflammation parameters, and selected viral infections).

Correlation between cigarette smoking and alcohol consumption and Rosacea: A two-sample Mendelian randomization study.

BACKGROUND: Controversy persists regarding the causal relationship between Cigarette smoking, alcohol consumption, and Rosacea. This paper employs the Mendelian randomization (MR) method to elucidate the correlation between Cigarette smoking, alcohol consumption, and Rosacea. The aim is to contribute valuable insights to aid in the prevention and early treatment of Rosacea. METHOD: Summary datasets for cigarette smoking parameters (Cigarettes smoked per day, Smoking status: Previous, smoking status: Current) and alcohol consumption (Alcoholic drinks per week) were selected alongside data for Rosacea from genome-wide association studies (GWAS). The Two-sample MR method was employed to analyze the correlation between cigarette smoking, alcohol consumption, and Rosacea. Various MR analysis methods, including inverse variance weighting (IVW), MR-Egger, Simple Mode, Weighted Mode, and Weighted Median, were chosen. IVW served as the primary analysis method. RESULTS: The results indicate a significant negative association between Cigarettes smoked per day and Rosacea. Moreover, a significant positive correlation was observed between Smoking status: Previous and Rosacea. However, no significant associations were found between Smoking status: Current, Alcoholic drinks per week, and Rosacea. CONCLUSION: This study provides further clarity on the association between cigarette smoking, drinking, and Rosacea through a two-sample MR analysis. Notably, the number of cigarettes smoked per day appears to be associated with a reduced incidence of Rosacea, while cigarette smoking cessation may increase the risk. Surprisingly, alcohol consumption does not emerge as a significant risk factor for Rosacea. These findings contribute to a nuanced understanding of the complex relationship between lifestyle factors and the occurrence of Rosacea, offering potential insights for preventive measures and early intervention.

Effects of Active Chronic Cigarette-Smoke Exposure on Circulating Fibrocytes.

PURPOSE: This study aimed to evaluate the hypothesis that active smoking impacts upon mediators and abundance of circulating fibrocyte cells in smoking-related disease characterised by fibrosis. METHODS: Flow cytometry and enzyme-linked immunosorbent assays were used to investigate blood from five patient groups: healthy never-smokers, healthy current smokers, stable chronic obstructive pulmonary disease (COPD) active smokers, idiopathic pulmonary fibrosis (IPF) never-smokers, and IPF active smokers. RESULTS: A significant inverse dose-response relationship was observed in healthy smokers among cumulative smoking burden (pack-years) and fibrocyte abundance (p = 0.006, r = -0.86). Among serum profibrotic fibrocyte chemokines measured, CCL18 rose significantly alongside fibrocyte numbers in all five subject groups, while having an inverse dose-response relationship with pack-year burden in healthy smokers (p = 0.003, r = -0.89). In IPF, CCL2 rose in direct proportion to fibrocyte abundance irrespective of smoking status but had lower serum levels in those currently smoking (p = < 0.001). For the study population, CXCL12 was decreased in pooled current smokers versus never-smokers (p = 0.03). CONCLUSION: The suppressive effect of current, as distinct from former, chronic smoking on circulating fibrocyte abundance in healthy smokers, and modulation of regulatory chemokine levels by active smoking may have implications for future studies of fibrocytes in smoking-related lung diseases as a potential confounding variable.

Cigarette smoking-related OLC1 overexpression associated with poor prognosis in bladder urothelial carcinoma.

AIMS: To explore the clinical significance of OLC1 and cigarette smoking in bladder urothelial carcinoma (UBC). MATERIALS AND METHODS: OLC1 mRNA expression was detected in 106 UBC samples by mRNA array or reverse real-time PCR. OLC1 protein expression in 114 UBC samples was detected by immunohistochemical staining. Wild-type C57BL/6J mice were injected with cigarette smoke condensate (n = 12) or exposed to cigarette smoke (n = 6) to investigate the correlations between cigarette smoking and OLC1 expression using mRNA array. KEY FINDINGS: The mRNA and protein expression of OLC1 were higher in tumor samples (p < 0.01) and significantly correlated with tumor stage (p < 0.05). OLC1 protein expression and smoking history were correlated with disease-free survival (p < 0.05). OLC1 expression was significantly elevated in smoking patients with higher smoking intensity on both mRNA and protein levels (p < 0.05). Cigarette smoke exposure experiments revealed that OLC1 mRNA overexpressed in bladder uroepithelium of mice. SIGNIFICANCE: OLC1 could serve as a potential prognosis biomarker of UBC, especially for smoking patients.

Effects of cigarette smoking associated with sarcopenia in persons 60 years and older: a cross-sectional study in Zhejiang province.

PURPOSE: Smoking is a risk factor for sarcopenia. Nevertheless, few studies analyzed the independent effects of various smoking dimensions (duration, intensity, cumulative dose) on sarcopenia risk. This is a cross-sectional study based on an older population in Zhejiang Province to determine which smoking dimensions are mainly important for sarcopenia risk and to explore the dose-response relationship between them. METHODS: Our study included 783 patients with sarcopenia and 4918 non-sarcopenic individuals. Logistic regression and restricted cubic with logistic regression (for nonlinear dose effects) were used to obtain odds ratios (ORs) and 95% confidence intervals as well as restricted cubic splines (RCS) curves. RESULTS: Compared with never-smokers, current smokers had an increased risk of sarcopenia (OR = 1.786; 95% CI 1.387-2.301) after adjusting for confounders such as age, sex, education, alcohol consumption, disease history, etc. There was no significant association between smoking intensity and sarcopenia after more than 20 cigarettes per day (OR = 1.484; 95% CI 0.886-2.487), whereas the risk of sarcopenia increased significantly with increasing duration of smoking after more than 40 years (OR = 1.733; 95% CI 1.214-2.473). Meanwhile, there was a significant non-linear dose-response relationship between smoking duration or intensity and the risk of sarcopenia. However, the risk of sarcopenia increased linearly with the number of pack-years of smoking, which is not a significant nonlinear dose-response relationship. CONCLUSIONS: This study indicated the association between smoking and sarcopenia. Both smoking duration and cumulative dose were significantly and positively associated with sarcopenia. These findings reflect the important role of the number of years of smoking in increasing the risk of sarcopenia and provide scientific evidence that different smoking dimensions may influence the risk of the sarcopenia.

Impact of Cigarette Smoking on Clinical Presentation and Treatment Response in Coeliac Disease.

BACKGROUND AND AIMS: The environmental factors, apart from gluten ingestion predisposing to coeliac disease are poorly known. Smoking is associated with many immune-mediated diseases, but research on coeliac disease is scarce. This study aims to investigate how smoking affects the clinical presentation, presence of comorbidities and response to gluten-free diet in coeliac disease. METHODS: Altogether 815 adults with coeliac disease participated in a nationwide cross-sectional study. Participants were interviewed and smoking habits (never, former, or current smoker), clinical presentation of coeliac disease and presence of comorbidities were elicited. Serology and severity of small bowel mucosal lesions at diagnosis were gathered from the participants' medical records and follow-up serology was measured. Gastrointestinal symptoms and psychological well-being were assessed using validated questionnaires. RESULTS: Current smokers were more often male and were diagnosed at younger ages than never or former smokers. There were no differences between the groups in clinical presentation, severity of symptoms or mucosal lesions at diagnosis or in dietary compliance and clinical, serological, and histological recovery. Musculoskeletal disorders, particularly osteoporosis and osteopenia, were more common in never smokers than in other groups (14.5% vs. 5.1% and 4.1%, p<0.001), and cardiovascular disorders were diagnosed more often in former smokers (36.2% vs. 23.5% and 21.9%, p=0.003). CONCLUSIONS: Smoking does not seem to have an impact on the clinical presentation, severity of symptoms or mucosal damage in coeliac disease. Histological and clinical recovery as well as seroconversion on gluten-free diet are not affected by smoking status.

Examining the Effect of Genes on Depression as Mediated by Smoking and Modified by Sex.

Depression is heritable, differs by sex, and has environmental risk factors such as cigarette smoking. However, the effect of single nucleotide polymorphisms (SNPs) on depression through cigarette smoking and the role of sex is unclear. In order to examine the association of SNPs with depression and smoking in the UK Biobank with replication in the COPDGene study, we used counterfactual-based mediation analysis to test the indirect or mediated effect of SNPs on broad depression through the log of pack-years of cigarette smoking, adjusting for age, sex, current smoking status, and genetic ancestry (via principal components). In secondary analyses, we adjusted for age, sex, current smoking status, genetic ancestry (via principal components), income, education, and living status (urban vs. rural). In addition, we examined sex-stratified mediation models and sex-moderated mediation models. For both analyses, we adjusted for age, current smoking status, and genetic ancestry (via principal components). In the UK Biobank, rs6424532 [LOC105378800] had a statistically significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 4.0 × 10-4) among all participants and a marginally significant indirect effect among females (p = 0.02) and males (p = 4.0 × 10-3). Moreover, rs10501696 [GRM5] had a marginally significant indirect effect on broad depression through the log of pack-years of cigarette smoking (p = 0.01) among all participants and a significant indirect effect among females (p = 2.2 × 10-3). In the secondary analyses, the sex-moderated indirect effect was marginally significant for rs10501696 [GRM5] on broad depression through the log of pack-years of cigarette smoking (p = 0.01). In the COPDGene study, the effect of an SNP (rs10501696) in GRM5 on depressive symptoms and medication was mediated by log of pack-years (p = 0.02); however, no SNPs had a sex-moderated mediated effect on depressive symptoms. In the UK Biobank, we found SNPs in two genes [LOC105378800, GRM5] with an indirect effect on broad depression through the log of pack-years of cigarette smoking. In addition, the indirect effect for GRM5 on broad depression through smoking may be moderated by sex. These results suggest that genetic regions associated with broad depression may be mediated by cigarette smoking and this relationship may be moderated by sex.

The interaction between diet quality and cigarette smoking on the incidence of hypertension, stroke, cardiovascular diseases, and all-cause mortality.

This study aimed to examine the interaction between diet quality indices (DQIs) and smoking on the incidence of hypertension (HTN), stroke, cardiovascular diseases, and all-cause mortality. We prospectively followed 5720 participants and collected dietary data via a validated food frequency questionnaire to calculate DQI-international (DQI-I) and DQI-revised (DQI-R). Considering an interaction analysis, we classified participants based on diet quality (median: higher/lower) and smoking status. Over 9 years of follow-up, higher diet quality scores were associated with a lower risk of stroke and mortality. While current smokers had a higher risk of stroke and mortality but had a lower risk of developing HTN. Compared to the current smokers with lower diet quality, nonsmokers with higher diet quality according to the DQI-I [HR 0.24; 95% CI (0.08, 0.66)], and DQI-R [HR 0.20; 95% CI (0.07, 0.57)] had a lower risk of stroke. Moreover, the lower risk of mortality was more evident in nonsmokers with higher DQI-I [HR 0.40; 95% CI (0.22-0.75)] and DQI-R scores [HR 0.34; 95% CI (0.18-0.63)] compared to nonsmokers with lower diet quality. While higher DQI-I and DQI-R scores were associated with a lower risk of stroke and mortality, this beneficial effect may be negated by smoking.