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Background: Sex steroid hormones, including testosterone and estradiol, play significant roles in various aspects of pulmonary health and diseases. However, although there were a few studies trying to link sex hormones with COPD, their effect remained limited due to small sample size and insufficient causal results. This study aims to investigate the association between sex hormones and chronic obstructive pulmonary disease (COPD) based on the National Health and Nutrition Examination Survey (NHANES) database and evaluate causality via a two-sample Mendelian randomization (MR)., Methods: Data from NHANES 2013-2016 were enrolled for the cross-sectional study. The association between sex hormones and COPD was evaluated via multivariable logistic regression. Sex-stratified analysis, subgroup analyses and interaction tests were performed to further evaluate the correlation. For MR analysis, data were collected from genome-wide association studies and FinnGen datasets. The inverse-variance-weighted (IVW) approach, along with four other approaches, was applied in the analysis. Further sensitivity analysis was conducted to assess the existence of pleiotropy and heterogeneity., Results: 7,617 eligible participants were enrolled in the cross-sectional analysis. Negative associations were observed in both testosterone-COPD (OR 0.770, 95% CI 0.626, 0.948, p = 0.018) and estradiol-COPD (OR 0.794, 95% CI 0.688, 0.915, p = 0.005) relationships after covariate adjustments. However, the results from IVW-MR analysis showed that no causal relationship was observed in either the testosterone-COPD (OR 0.83, 95% CI 0.53, 1.29, p = 0.407) or estradiol-COPD (OR 0.74, 95% CI 0.23, 2.38, p = 0.616) relationship, which was also supported by the other four approaches (all p values > 0.05)., Conclusion: Although a significant negative association was observed between sex hormones and COPD, the results of MR analysis did not support the causality of this relationship. Our study suggested that sex hormones may indirectly rather than directly affect the development of COPD via potential covariates, which warranted further investigations., Competing Interests: The authors report no conflicts of interest in this work., (© 2024 Du et al.)

Objectives: Innate and adaptive immunity play different roles in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, previous studies on the relationship between immune cells and COPD reported inconsistent results., Methods: The causal connection between 731 immune cells and COPD was established using a two-sample Mendelian randomization (MR) analysis through publicly accessible genetic data. The heterogeneity and horizontal pleiotropism of the findings were confirmed using sensitivity analysis., Results: In the B-cell panel, B-cell activating factor receptor (BAFF-R) on CD20 - and CD20 on IgD - CD38 bright (OR (95% CI): 0.93 (0.88, 0.99) and 0.97 (0.95, 0.98), respectively) were discovered to be protective. In the cDC panel, CD62L - plasmacytoid DC AC, CD80 on monocytes and CD11c on myeloid DCs (OR (95% CI): 0.94 (0.92, 0.97), 0.97 (0.94, 0.99) and (0.97 (0.95, 0.98), respectively) exerted protective effects. However, unswitched memory AC (OR (95%CI): 1.08 (1.01,1.15)) and CD 19 on IgD - CD 27 - (OR (95%CI): 1.06 (1.02,1.10)) were hazardous in the B-cell panel. However, among the 731 immune cell phenotypes, no causal relationship was found for COPD on immune cells., Conclusion: This study found a potential causal relationship between immune cells in COPD, ruling out reverse causation. This study provides new avenues for studying the mechanisms of COPD.

Background: People are constantly exposed to phthalates, but few reliable studies have focused on the connection between phthalate exposure and latent tuberculosis infection (LTBI)., Methods: Data were obtained from the National Health and Nutrition Examination Survey (NHANES) database (2011-2012). The LTBI was assessed by QuantiFERON®-TB Gold-In-Tube (QFT) or tuberculin skin testing (TST). The odds ratios (ORs) and 95% confidence intervals (CIs) per log10 unit change in the concentration of phthalate metabolites were calculated using crude and adjusted logistic regression models. The relationships between mixed phthalate concentrations and LTBI were assessed using Bayesian kernel machine regression (BKMR) models., Results: According to the results of the multivariable logistic regression, in a fully adjusted model, only monobenzyl phthalate (MBZP) was negatively associated with LTBI in Q3 (OR (95% CI): 0.485 (0.286,0.823), P  = 0.007). According to the restricted cubic spline (RCS) model, there was a linear dose‒response association between all 11 phthalate metabolites and LTBI ( p for nonlinearity >0.05). We found a significant positive correlation between mixed phthalate metabolites and LTBI by using fully adjusted BKMR model., Conclusions: Our analysis demonstrated that LTBI in the general U.S. population is linearly linked with exposure to single or combined phthalates., Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Fuqiang Wen reports financial support was provided by 10.13039/501100013365West China Hospital of 10.13039/501100004912Sichuan University., (© 2024 The Authors.)

Background: Despite potential benefits and widespread prescription of aspirin among chronic obstructive pulmonary disease (COPD) patients, limited research has investigated its adverse effects (AEs) in COPD population., Methods: We conducted a retrospective analysis of adverse drug events (ADEs) reported in the US Food and Drug Administration Adverse Event Reporting System (FAERS) between Q1 2013 and Q2 2022. COPD patients were categorized into two groups based on aspirin use. ADEs related to aspirin use were identified using combined reporting odds ratio (ROR), proportional reporting ratio (PRR), information component (IC) methods., Results: A total of 56,660 ADEs reports associated with COPD patients were included in the study. Among these reports, 144 adverse events were linked to aspirin use in COPD patients, including fatigue (4.12%), diarrhea (3.13%), dyspnea exertional (2.03%), rhinorrhea (1.99%), weight increased (1.89%) and vomiting (1.84%), muscle spasms (1.79%), cardiac disorder (1.74%), heart rate increased (1.69%) and peripheral swelling (1.59%). Subgroup analysis indicates that age and gender might affect the AEs frequency in COPD patients using aspirin., Conclusions: Our findings identify 10 most frequently reported ADEs associated with aspirin use in COPD patients, thus offer valuable insights into the AEs of aspirin for safer clinical utilization in COPD management.

Background: Observational studies showed a bidirectional association between depression and chronic obstructive pulmonary disease (COPD). However, it is unclear whether the observed association is causal. Thus we estimated the relationship using observational studies combined with bidirectional Mendelian randomization [MR]., Materials and Methods: The study included 9977 participants from the 2013-2018 National Health and Nutrition Examination Survey and used weighted logistic regression analysis to assess the association between depression and COPD, followed by a bidirectional Mendelian randomization analysis to verify their causality., Results: Adjusted-weighted logistic regression in observational studies showed a significant association between COPD and mild depression (OR (95% CI): 1.81 (1.30, 2.52), P  = 0.002) and COPD and depression (OR (95% CI): 1.93 (1.49, 2.50), P  < 0.001). MR suggested depression may play a causal role in COPD risk (OR (95% CI): 1.45 (1.32, 1.60), P  < 0.001), but more evidence for reverse causation is lacking (reverse MR OR (95% CI): 1.03 (0.99, 1.07), P  = 0.151)., Conclusion: In conclusion, our study found depression may play a potential causal role in the morbidity of COPD suggesting depression might be the etiology of COPD. This finding needs to be validated in further prospective cohort studies with large sample sizes and adequate follow-up time.

An adjustable mounting structure is proposed to compensate for surface deformation of a mirror caused by the assembly process. The mount adopts a six-point support based on the kinematic mount principle. Three of the support points are adjustable, and they are moved along the axial direction by actuators. Surface deformation is expressed by Zernike coefficients in this paper, and a sensitivity matrix of the surface deformation is established by varying the unit displacement of each adjustment support point and getting the corresponding Zernike coefficient changes. The surface deformation is measured, and the compensation adjustment of each adjustable support point is then obtained by anti-sensitivity calculation. Finally, the feasibility of present support structure design and surface figure compensating method are verified by experiments. The experimental results show that the present structure and method could significantly reduce the surface deformation caused by the assembly process. The surface deformation is 4.6 nm RMS after assembly and it is decreased to 1.3 nm RMS after four iterations of compensation, which is close to the 1.1 nm RMS after optical polishing.