Search Results (375)

Background: Cigarette smoking promotes persistent systemic alterations in COPD, yet the interplay among genetic susceptibility, oxidative stress, immune dysregulation, impaired control of persistent viral replication, and long-term outcomes remains incompletely understood. Methods: We conducted an observational study in 102 patients aged ≥70 years with severe-to-very-severe COPD undergoing pulmonary rehabilitation. Current smokers (n = 38) were compared with never/former smokers (n = 64). Analyses included Chr15q25 genotyping (rs16969968), oxidative stress biomarkers (tail intensity, 8-OHdG, MDA, and bilirubin), hematological and immunological parameters, α7nAChR expression, TTV load as a surrogate marker of immune competence, latent virus prevalence, and five-year survival assessed by multivariable Cox regression. Results: Current smokers exhibited significantly higher DNA damage (tail intensity, p = 0.001; 8-OHdG, p = 0.002), lower bilirubin levels (p = 0.031), increased neutrophil and CD4⁺ T-cell counts (p = 0.031 and p = 0.028, respectively), altered α7nAChR expression on CD4⁺ T cells (p = 0.030), and higher TTV load (p = 0.002) than never/former smokers. The rs16969968 AA genotype was more frequent among current smokers. In survival analyses, an elevated WBC count was independently associated with increased mortality risk (HR 1.12, 95% CI 1.01–1.23; p = 0.035), whereas higher bilirubin levels showed a protective association. TTV load, smoking status, and FEV1 were not independently associated with mortality. Conclusions: In severe-to-very-severe COPD, smoking is associated with a distinct biological profile characterized by enhanced oxidative DNA damage, systemic inflammation, immune remodeling, reduced antioxidant defenses, and impaired control of persistent viral replication. WBC and bilirubin emerged as the biomarkers most consistently associated with long-term outcomes. These findings support integrated biological profiling as a tool for risk stratification and precision-guided rehabilitation in advanced COPD. Full article

Objectives: To identify factors influencing influenza vaccination willingness and uptake among adults aged ≥60 years in Henan Province and to evaluate the effect of a brief educational intervention on vaccination willingness and behavior. Methods: In September 2024, a cross-sectional survey based on the Behavioral and Social Drivers (BeSD) framework was conducted among adults aged ≥60 years across five counties in Henan. For participants without baseline willingness, a 3 min one-on-one educational intervention was delivered. In May 2025, following the end of the 2024–2025 influenza vaccination season (which runs from 1 October to 31 March in Henan Province), we retrieved vaccination records for all participants from the Henan Provincial Immunization Information System. This system captures all influenza vaccinations administered at designated vaccination clinics across the province. To ensure completeness for doses administered outside the provincial system (e.g., in other provinces or at private healthcare facilities), we conducted telephone follow-up interviews with all participants whose baseline vaccination intention was inconsistent with their actual vaccination behavior (i.e., willing but unvaccinated or unwilling but vaccinated). During these interviews, for those who reported receiving the vaccine outside Henan Province or at private facilities, we inquired about the specific date and location of vaccination to supplement the registry data. We also explored the reasons behind the intention–behavior discrepancy. For these participants, we requested vaccination certificates or other supporting documentation to confirm their vaccination status. Results: Baseline vaccination willingness was 68.20% (1630/2390), whereas the actual vaccination rate was only 6.95% (166/2390), yielding a willingness-to-behavior conversion rate of 9.51% (155/1630) among those with baseline willingness. Of the 760 participants without baseline willingness, 543 (71.45%) completed the 3 min one-on-one instant educational intervention and the follow-up assessment; the remaining 217 were excluded due to refusal or loss to follow-up. Among these 543 completers, 46 (8.47%) became willing to vaccinate, and eight (1.47%) were subsequently vaccinated. Multivariate analysis identified the social processes dimension as the strongest correlate of both willingness (OR = 1.38 per 1-point increase, 95% CI: 1.33–1.44) and uptake (OR = 1.12, 95% CI: 1.03–1.22). Urban residence was associated with higher willingness (OR = 1.41, 95% CI: 1.12–1.78) and higher uptake (OR = 1.64, 95% CI: 1.11–2.42). Current smokers had a significantly lower uptake than never smokers (OR = 0.43, 95% CI: 0.22–0.85). Among the 11 participants without baseline willingness who were eventually vaccinated (eight from the intervention group and three from the non-intervention group), family/friend influence (63.64%, 7/11) and physician recommendation (36.36%, 4/11) were the primary drivers. For those with willingness but no action (n = 1475), the main barriers were perceived good health (33.29%), high vaccine cost (27.12%), and lack of time (26.31%). Conclusions: Influenza vaccination among older adults in Henan exhibits a “high willingness, low conversion” pattern, with social processes as the strongest driver bridging the intention–behavior gap. A brief educational intervention improved willingness but failed to translate into meaningful uptake, underscoring that knowledge transfer alone is insufficient. We recommend a multi-component strategy that (1) mobilizes family members and community doctors as trusted vaccine advocates; (2) leverages family and village doctor networks to reduce urban–rural disparities; (3) counters the “perceived good health” barrier with age-specific risk communication; and (4) integrates vaccine recommendations into routine care for high-risk groups, particularly frequent outpatient attendees and smokers. Full article

Background: Lung cancer carries a high psychosocial burden. Tobacco use, the stigma attached to the disease, and coping strategies are thought to interact and shape psychological outcomes, yet they have rarely been examined together. This review aimed to synthesise the evidence on the relationship between tobacco use, lung cancer stigma, and coping, and how these factors interact and influence patients’ psychological outcomes. Methods: Following the PRISMA 2020 guideline, PubMed/MEDLINE and Dialnet were searched (window 2014–April 2026) for empirical studies conducted in adults with lung cancer that addressed stigma, coping, or relevant psychological outcomes (e.g., anxiety, depression, distress, or quality of life). Study selection and data extraction were performed independently by two reviewers, with discrepancies resolved by consensus and, where needed, by a third reviewer. Methodological quality was appraised with design-specific tools (JBI for cross-sectional and cohort studies, CASP for qualitative studies, and COSMIN-oriented criteria for the psychometric study). Given the clinical and methodological heterogeneity, a structured narrative synthesis was conducted following the SWiM guideline. The protocol was registered in the Open Science Framework. Results: Twenty-four studies were included. Stigma was prevalent and consistently associated with depression, anxiety, distress, and poorer quality of life, with longitudinal evidence indicating that stigma precedes and predicts distress. Internalised stigma (guilt, shame, self-blame) was the facet most strongly linked to depression and anxiety. Smoking history graded stigma intensity (current > former > never smokers) but did not determine it, since clinically significant stigma also affected never-smokers. Adaptive coping (e.g., fighting spirit, positive reappraisal) and social support were consistently associated with better psychological adjustment and quality of life, while maladaptive coping (e.g., helplessness, avoidance, anxious preoccupation) was associated with worse outcomes; cross-sectional evidence further indicated that coping modes mediated the relationship between stigma and quality of life and that social support and self-compassion attenuated the impact of stigma on distress. Conclusions: Internalised stigma is a central, modifiable psychosocial stressor in lung cancer that affects smokers and never-smokers alike. Systematic screening for stigma, coping, and social support, together with non-stigmatising care, is warranted. Full article

Background/Objectives: Periodontitis can elevate systemic inflammation and negatively impact glucose regulation. This cross-sectional study investigated relationships between periodontal inflammatory burden, measured by periodontal inflamed surface area (PISA), and insulin resistance and systemic inflammation in never-smokers attending a periodontal clinic with unknown diabetes status. Methods: A total of 154 adults underwent full-mouth periodontal assessments to determine PISA. Fasting blood samples were taken for glucose, insulin, and hs-CRP, and HOMA-IR was calculated. An inflammation composite was created from z-scored log(hs-CRP), IL-6, and TNF-α. Primary analysis involved regressing log(HOMA-IR) and log(hs-CRP) on PISA, scaled by interquartile range (IQR) increases, with sequential adjustments. Mediation analysis, adjusted for age, sex, and waist circumference, used bootstrap testing to evaluate inflammation as a mediator. Results: HOMA-IR and hs-CRP increased across PISA tertiles (HOMA-IR: 2.01 to 3.17; hs-CRP: 0.73 to 2.48 mg/L; both p < 0.001). In the prespecified primary adjusted model (age, sex, waist circumference, education, physical activity, family history of diabetes, and medication use), each IQR increase in log(PISA) was associated with 85.2% higher hs-CRP (95% CI 53.1% to 124.1%; p < 0.001) and 15.7% higher HOMA-IR (95% CI −0.8% to 34.9%; p = 0.064). Estimates were similar with additional adjustment for BMI and SBP, whereas adding plaque (% sites) attenuated associations (hs-CRP: +15.2%; p = 0.234; HOMA-IR: +1.0%; p = 0.925). Mediation analysis (adjusted for age/sex/waist circumference) was consistent with an indirect pathway via the inflammation composite (a × b = 0.212; 95% CI 0.094 to 0.337), while the direct effect was not supported (c′ = −0.047; 95% CI −0.207 to 0.125). Conclusions: Higher periodontal inflammatory burden was strongly associated with systemic inflammation and showed weaker, model-dependent associations with insulin resistance; the findings were consistent with an inflammation-linked pathway in exploratory, partially adjusted mediation analyses; given the cross-sectional design, causal inference is not possible. Full article

Alpha-1 antitrypsin deficiency (AATD) is a genetically heterogeneous disorder with well-established pulmonary and hepatic manifestations; however, the clinical significance of rare compound heterozygous SERPINA1 variants remains incompletely defined. We report the case of a 61-year-old never-smoking woman with chronically elevated liver transaminase who was found to carry a compound heterozygous SERPINA1 genotype (PI*V/M_procida) previously classified as non-polymerogenic and not previously associated with hepatic inclusions. This case expands the phenotypic spectrum of AATD and highlights the importance of considering SERPINA1 genotyping in adults with unexplained chronic transaminase elevation, while raising clinically relevant questions regarding surveillance and management in atypical AATD phenotypes. Full article

Background/Objectives: There has been a growing concern about excessive caffeine consumption among heavy green tea drinkers on health outcomes, such as cardiovascular diseases or cancer. We evaluated the association between green tea consumption and risk of all-cause mortality in Vietnam. Methods: We used data from the Hanoi Prospective Cohort Study, an ongoing study comprising 42,146 participants aged 10 or older in Northern Vietnam who have been followed up between 2007 and 2019. Green tea intake was derived from a validated semi-quantitative food frequency questionnaire. We performed a Cox proportional hazard regression model to calculate the hazard ratio (HR) and respective 95% confidence intervals (95% CIs) for the association between green tea consumption and risk of all-cause mortality, adjusted for potential confounding factor. Results: After a median follow-up of 11 years (range: 0.13–11.64 years), we identified 2494 deaths. Overall, there was an inverse association between green tea intake and risk of all-cause mortality (HR_{perSDincrement} = 0.93; 95% CI, 0.89–0.97, P_trend < 0.001). This pattern was more pronounced in males (HR_{perSDincrement} = 0.93; 95% CI, 0.89–0.97, P_trend < 0.001) but not in females (HR_{perSDincrement} = 0.94; 95% CI, 0.86–1.02, P_trend = 0.12; P_{heterogeneity} = 0.81). In stratified analysis, the inverse association pattern was seen in both younger and old age groups, in individuals with BMI < 23 kg/m², in both ever and never smokers, among ever alcohol drinkers and never coffee drinkers, and in individuals with and without history of type 2 diabetes (P_{heterogeneity} = 0.31). Conclusions: Findings from the current study, the first prospective cohort study in Vietnam, suggest a protective effect of green tea consumption on risk of all-cause mortality. Further studies are warranted to validate our findings in similar population and settings. Full article

Background: Despite a decline in lung cancer in the U.S., lung cancer among never-smoking Asian American (AsA) women is rising, and subgroup aggregation obscures heterogeneity. We compared primary lung cancer prevalence across disaggregated AsA subgroups and examined factors associated with prevalence such as personal- and family-cancer histories versus Non-Hispanic Whites (NHWs). Methods: This cross-sectional study analyzed electronic health records of AsA women (≥18) in a large Northern California health system (2010–2022). Lung cancer cases were obtained from the hospital registry and categorized by smoking status and self-reported ethnicity. Adjusted prevalence ratios (aPRs) were estimated using targeted maximum likelihood estimation, accounting for sociodemographic, smoking, and clinical covariates. Results: Among 1,843,119 women, 8651 had primary lung cancer; 2429 were never-smokers. In AsA never-smokers, aPRs and 95% confidence intervals versus age-matched NHW were: Chinese (3.36, [3.20–3.53]), Filipino (2.68, [2.55–2.82]), Vietnamese (2.07, [1.96–2.18]), Japanese (1.99, [1.89–2.10]), Korean (1.90, [1.80–2.00]), and Other Asian (0.35, [0.33–0.37]). Personal cancer-history reflected an increase in prevalence among Korean patients (2.91, [2.76–3.06]) while family cancer-history demonstrated increased prevalence among Chinese patients (1.51, [1.42–1.60]). Among women with uterine cancer, Chinese patients had higher lung-cancer prevalence than NHW (1.91, [1.58–2.31]). Conclusions: Never-smoking disaggregated AsA women show heterogeneous lung cancer prevalence, with higher prevalence in Korean women with personal cancer-history and in Chinese women with family cancer-history compared with NHW, supporting history-informed and ethnic-specific lung cancer screenings. Full article

Periodontitis and type 2 diabetes mellitus (T2DM) are linked through systemic inflammation and endothelial dysfunction, yet it remains uncertain whether periodontal inflammatory burden independently reflects early, multi-organ microvascular vulnerability beyond glycemic exposure. This study aimed to assess the independent association between periodontal inflammatory burden, measured by PISA, and retinal microvascular impairment on OCT-A, and to examine relationships with renal trajectories, small-fiber neuropathy, and inflammatory/endothelial biomarkers. This cross-sectional observational study included 285 never-smoking adults with T2DM. The primary outcome was a pre-specified OCT-A microvascular impairment composite. Secondary outcomes included eGFR slope and log(UACR) slope, corneal nerve fiber length (CNFL), and a multi-organ microvascular burden score. Biomarkers comprised hsCRP, IL-6, sICAM-1, sVCAM-1, sE-selectin, PAI-1, angiopoietin-2 (Ang-2), and vWF:Ag. Multivariable linear regression estimated associations per 1 SD higher PISA, adjusting for age, sex, diabetes duration, HbA1c, CGM time in range, CGM coefficient of variation, systolic blood pressure, LDL cholesterol, BMI, and medication classes (SGLT2 inhibitors, GLP-1 receptor agonists, ACEi/ARB, statins). False discovery rate (FDR) control (q = 0.10) was applied for secondary endpoints. Higher PISA was independently associated with worse OCT-A microvascular impairment (adjusted β = 0.138, 95% CI 0.061–0.216; p = 0.0005). Although statistically significant, the effect sizes were modest in magnitude, and their translation into clinically meaningful differences in microvascular outcomes warrants investigation in prospective settings. Higher PISA was also associated with greater multi-organ microvascular burden (β = 0.101, 95% CI 0.040–0.163; p = 0.0014; FDR q = 0.005) and lower CNFL (β = −0.224, 95% CI −0.397 to −0.052; p = 0.0113; FDR q = 0.023). PISA was associated with higher levels of inflammatory and endothelial activation/injury biomarkers (all FDR q < 0.10). In this cross-sectional study, periodontal inflammatory burden was independently associated with quantitative retinal microvascular impairment, lower corneal nerve fiber length, and a consistent pattern of endothelial activation biomarker elevations in never-smoking adults with T2DM. The clinical significance of the observed effect sizes requires further evaluation, and longitudinal studies are needed to establish temporality. Full article

Background/Objectives: Cigarette smoking is a major risk factor for periodontitis, but the salivary host-response profile associated with smoking-related periodontal inflammation remains incompletely characterized. This study compared salivary NETosis-related and oxidative-inflammatory biomarkers among current smokers, former smokers, and never-smokers with periodontitis. Methods: This cross-sectional study included 159 systemically healthy adults with periodontitis (53 per group: current smokers, former smokers, never-smokers). Individuals with systemic diseases or concomitant medications that could interfere were excluded. Unstimulated whole saliva was analyzed for NETosis-related biomarkers (MPO-DNA complexes, citrullinated histone H3, neutrophil elastase, cell-free DNA) and oxidative-inflammatory markers (MMP-8, IL-1β, IL-6, TNF-α, 8-OHdG, total antioxidant capacity). Results: Salivary MPO-DNA complexes differed significantly among groups (current smokers 33.52 ± 9.96, former smokers 26.90 ± 8.38, never-smokers 19.20 ± 7.50 ng/mL; p < 0.001, η² = 0.317). The composite NETosis score (η² = 0.702) and oxidative-inflammatory score (η² = 0.718) showed the same graded pattern. Biochemical verification confirmed clear group separation (salivary cotinine: current smokers 312.3 ± 77.0, former smokers 9.7 ± 5.1, never-smokers 3.2 ± 1.4 ng/mL). Smoking exposure was positively correlated with biomarker levels and the severity of periodontal disease. Smoking status remained independently associated with MPO-DNA complexes and the NETosis score after covariate adjustment. Conclusions: Current smoking was associated with an enhanced salivary NETosis-related and oxidative-inflammatory phenotype. Former smokers displayed an intermediate profile. Salivary MPO-DNA complexes and composite biomarker scores warrant further investigation as candidate non-invasive indicators of smoking-associated periodontal inflammatory burden, pending diagnostic performance analyses and prospective validation. Full article

Background: Pre-Chronic Obstructive Pulmonary Disease (pre-COPD) and Preserved Ratio Impaired Spirometry (PRISm) phenotypes represent important components of the early obstructive lung disease spectrum, characterized by respiratory symptoms and structural lung abnormalities prior to the development of overt airflow limitation. Emphysema is considered one of the major structural phenotypes underlying airway disease and the COPD spectrum. Although cigarette smoking is the best recognized risk factor for these conditions, non-tobacco exposures may also contribute to early structural lung changes. In this study, we evaluated the radiological features, pulmonary function parameters, and dyspnea severity of CT-detected emphysema in symptomatic patients classified as having pre-COPD or PRISm, with particular attention paid to the potential influence of smoking status on disease characteristics. Methods: In this retrospective, single-center study, symptomatic patients aged 20–50 years classified as having pre-COPD or PRISm and in whom emphysema was detected on high-resolution computed tomography (HRCT) were evaluated. Only symptomatic patients who underwent HRCT for clinical indications and in whom emphysema was identified were included. Demographic characteristics, emphysema type and quantitative emphysema severity, pulmonary function parameters, and Modified Medical Research Council (mMRC) dyspnea scores were analyzed. The PRISm and pre-COPD groups were compared in terms of clinical and symptomatic characteristics. In addition, smoking-related clinical and radiological characteristics were also evaluated. Results: A total of 232 patients were included in the study. The median age was 43 years (38–48), and 84.1% of the participants were male. Among the study population, 68.5% were classified in the pre-COPD group and 31.5% in the PRISm group. The most frequently identified emphysema patterns were paraseptal (44.4%) and centrilobular (40.5%). The median total lung emphysema area was 18% (13–22). A weak negative correlation was observed between the degree of emphysema and FEV₁ (r = −0.185; p = 0.005), whereas a weak positive correlation was found between emphysema extent and the mMRC dyspnea score (r = 0.214; p = 0.001). Dyspnea severity was significantly higher in the PRISm group compared with the pre-COPD group (p < 0.001). In the smoking-status subgroup analysis, ever-smokers demonstrated significantly greater dyspnea severity and lower FEV₁ values, whereas never-smokers had a significantly higher proportion of emphysema extent > 18% (all p < 0.05). Conclusions: Radiologically detected emphysema in symptomatic patients without airflow limitation was associated with statistically significant but weak alterations in pulmonary function and dyspnea burden. Dyspnea severity was significantly higher in the PRISm phenotype. In a smoking-status subgroup analysis, ever-smokers had significantly greater dyspnea severity, whereas never-smokers showed a significantly higher proportion of extensive emphysema (>18%), despite similar functional impairment across groups. These findings underscore the importance of non-tobacco exposures in the development of emphysema within pre-obstructive spirometric phenotypes. Multicenter prospective studies incorporating healthy controls and systematic exposure documentation are needed to confirm these observations. Full article

Lung cancer is a leading cause of global cancer mortality, with EGFR mutations serving as a primary therapeutic target. Although EGFR tyrosine kinase inhibitors (TKIs) are initially effective, acquired resistance inevitably develops. While ROS1 rearrangements are well-known baseline drivers, they are exceptionally rare as acquired resistance mechanisms. We utilized next-generation sequencing (NGS) to identify a rare ROS1 intragenic rearrangement (exons 35–37) in three never-smoking women with EGFR-mutant lung adenocarcinoma following progression on EGFR TKIs. Clinical courses were heterogeneous: one patient achieved a durable partial response using combined osimertinib and crizotinib. A second patient, intolerant to dual TKI therapy due to QTc prolongation and grade 3 edemas, achieved a sustained partial response with platinum-pemetrexed chemotherapy. The third patient exhibited polyclonal resistance, including EGFR C797S and TP53 mutations, with fatal central nervous system progression. In this three-patient case series, ROS1 exon 35–37 RNA-level intragenic rearrangements were repeatedly detected after EGFR-TKI progression, suggesting a rare transcript-level alteration within heterogeneous resistance evolution. However, its biological significance, driver versus passenger role, and therapeutic relevance remain uncertain. Combined EGFR and ROS1 inhibition may be considered in selected cases, but further validation is required. Full article

Background/Objectives: Interstitial lung disease (ILD) occurs commonly in systemic sclerosis (SSc) and is the leading cause of mortality. There are limited data on the accuracy of lung auscultation in identifying the presence of ILD in patients with SSc. Methods: We retrospectively identified patients with newly diagnosed SSc who had documented lung auscultation findings and chest high-resolution computed tomography (HRCT) available for review. Diagnoses were made by rheumatologists at Mayo Clinic, Rochester, Minnesota, USA over a 4-year period. Pulmonary function measurements included lung volumes, spirometry, and single-breath diffusing capacity. Results: Among 151 patients with SSc (median age, 62 years), 72.2% were female and 55.0% were never smokers. Limited cutaneous SSc was the most common phenotype (67.3%). Seventy (46.4%) patients were evaluated by pulmonologists. There was evidence of ILD by HRCT in 69 patients (45.7%); the most common pattern of ILD was fibrotic nonspecific interstitial pneumonia (59.2%). Respiratory symptoms were present in 46.4% of those with ILD compared to 15.9% among those without. The sensitivity and specificity for crackles heard by rheumatologists in detecting ILD were 50.7% and 97.6%, respectively; for pulmonologists, 71.4% and 85.7%, respectively. Presence of crackles was associated with high positive predictive values (94.6% for rheumatologists vs. 92.1% for pulmonologists, respectively); negative predictive values were moderate (70.2% vs. 56.3%, respectively). Crackles correlated with lower pulmonary function measures but did not differ across ILD patterns. Conclusions: Detection of crackles on lung auscultation appears to be a specific and moderately sensitive indicator of ILD (often asymptomatic) in patients with newly diagnosed SSc. The presence of crackles correlates with worse pulmonary function but may be absent in early ILD. Full article

Background: Despite well-documented adverse impact on both systemic and oral health, tobacco smoking remains a persistent issue in military populations. It contributes to the global burden of tobacco use and is often perceived as a means of coping with stress in military settings. Purpose: This study aimed to assess the prevalence of tobacco use among military marines, its impact on oral health, and their level of knowledge regarding smoking, as well as to identify variables associated with their smoking habits. Thus, it provides a basis for implementing appropriate tobacco cessation and harm reduction strategies, particularly within the military. This study demonstrated a high prevalence of tobacco use among military marines, despite generally high levels of knowledge regarding tobacco smoking. A knowledge gap was still evident in relation to smoking behavior. The most frequently reported oral health impacts among smokers were tooth staining, halitosis, and taste impairment. Duration of military service and level of knowledge were significantly associated with smoking behavior. Materials and Methods: A validated and reliable online survey was administered to collect socio-demographic data, including age, education level, and length of military service. The survey also assessed smoking status, smoking behavior, its impact on oral health, and participants’ knowledge of smoking-related risks. Data were analyzed descriptively, and associated factors were examined using multivariate analysis. Results: A total of 475 military marines participated in the study. Of these, 44.8% were current smokers, 25.7% were former smokers, and 29.5% had never smoked. Overall, 71% of participants demonstrated good knowledge of smoking-related risks. The most commonly reported oral health impacts were halitosis, tooth staining, and impaired taste. Smoking status did not differ significantly by age (p = 0.095) or education level (p = 0.610), but differed significantly by length of military service (p < 0.05) and level of knowledge (p < 0.05). Multivariate analysis using multinomial logistic regression indicated that length of military service was a significant predictor of smoking behavior (p = 0.005; 95% CI: 0.282–0.800), with 1–5 years of service emerging as the most influential category. Based on the odds ratio, individuals with 11–15 years of service had a 1.8-fold higher likelihood of smoking. Conclusions: Despite a generally good level of knowledge regarding the health risks of smoking, the prevalence of tobacco use remains high among military marines. The most commonly reported oral health impacts were tooth staining, halitosis, and impaired taste. Length of military service and level of knowledge regarding smoking were identified as significant factors associated with smoking status. Full article

Emphysema is a well-recognized risk factor for lung cancer; however, its influence on the immunologic tumor microenvironment in lung adenocarcinoma remains poorly defined. In this pilot, hypothesis-generating study, immune-related gene expression profiling was performed using archival formalin-fixed paraffin-embedded tumor specimens from 12 patients with lung adenocarcinoma, including the Never-smoker group (never-smokers without emphysema; n = 4), the Smoker 1 group (smokers without emphysema; n = 3), and the Smoker 2 group (smokers with CT-defined emphysema; n = 5). Expression of 770 immune-related genes was analyzed using the nCounter PanCancer IO 360 Panel (NanoString Technologies, Seattle, WA, USA). Compared with the Never-smoker group, tumors from the Smoker 1 group showed marked upregulation of SFRP1, SERPINB5, and IL6, whereas tumors from the Smoker 2 group exhibited increased expression of KIR2DL3, BLK, and WNT2B. Relative to the Smoker 1 group, the Smoker 2 group demonstrated significant upregulation of MMP7, TDO2, and CCL18. Pathway enrichment analysis revealed cytokine–cytokine receptor interaction as the most prominently enriched pathway in both smoker groups, while the IL-17 signaling pathway was preferentially enriched in the Smoker 2 group. In addition, diffusing capacity for carbon monoxide showed significant correlations with immune-related genes including IL-6 and IL-6R. Collectively, these preliminary findings suggest that lung adenocarcinoma arising in emphysematous lungs may be characterized by a distinct pro-inflammatory immune microenvironment. Given the small sample size and potential confounders, these results should be regarded as hypothesis-generating. Emphysema-associated immune remodeling may nevertheless represent an important biological factor worthy of validation in larger, independent cohorts. Full article

Oral squamous cell carcinoma (OSCC) typically develops in individuals with established risk factors such as tobacco and alcohol use, yet an increasing number of cases occur in young non-smoking, non-drinking (NSND) patients. We report a case of oral tongue OSCC in a 33-year-old woman who is a never-smoker and never-drinker without identifiable environmental or local risk factors. The patient underwent surgical treatment followed by adjuvant radiotherapy and remains disease-free 15 months after therapy. Whole-exome sequencing (WES) revealed a pathogenic truncating TP53 mutation together with additional somatic alterations affecting genes involved in DNA repair, hypoxia adaptation, mitochondrial function, and epigenetic regulation. The heterogeneous mutational profile suggests branched tumor evolution and the involvement of non-classical tumorigenic pathways. This report contributes to the growing evidence that OSCC in young NSND patients represents a biologically distinct subgroup and demonstrates the value of comprehensive genomic profiling for improving understanding of tumor heterogeneity and potential molecular drivers in the absence of traditional carcinogenic exposures. Full article