Search Results (10,262)

Background/Objectives: Interstitial pneumonia with autoimmune features (IPAF) is a recently defined entity characterized by interstitial lung disease (ILD) with clinical, serological, and radiological features suggestive of autoimmunity that do not fulfil the criteria for a defined connective tissue disease (CTD). This study aimed to evaluate the clinical characteristics, treatment modalities, and outcomes of patients with IPAF in a tertiary referral center. Methods: We retrospectively analyzed 72 patients who fulfilled the IPAF classification criteria. Demographic, clinical, serological, radiological, pulmonary function, treatment, and survival data were collected and evaluated. Logistic regression analysis was performed to identify factors associated with mortality. Results: The cohort consisted of 62.5% female patients, with a mean age of 62.7 (SD, 10.4) years at diagnosis. The most frequent radiological pattern was nonspecific interstitial pneumonia (83.3%). Raynaud’s phenomenon (6.9%) and arthritis (2.8%) were the most common rheumatological manifestations. Antinuclear antibodies positivity at titers ≥1:320 was observed in 27.8% of patients. Azathioprine was the most frequently prescribed agent (20.8%), followed by mycophenolate mofetil (11.1%). After a median follow-up of 30.1 months (IQR, 52.8), 16 patients (22.22%) died, with a 5-year survival rate of 70%. Glucocorticoid therapy at doses ≥20 mg/day was independently associated with increased mortality (OR 6.13 (95% CI 1.17–32.21). Conclusions: IPAF predominantly affects middle-aged females. Glucocorticoid use at doses ≥20 mg/day was associated with mortality; however, this observational association may reflect underlying disease severity rather than a causal effect of high-dose treatment. Further prospective studies are needed to optimize management strategies in patients with IPAF. Full article

Background: Primary fibula tumours are rare, representing approximately 0.25% of all primary bone tumours. While benign lesions are often asymptomatic, malignant ones typically present with pain and functional impairment. Most tumours arise in the proximal third of the fibula, yet the literature regarding their epidemiology and clinicopathological features remains limited. This systematic review aims to synthesise current evidence on presentation, diagnosis, management, and prognosis of primary malignant tumours of the proximal fibula. Methods: A systematic review was conducted following PRISMA guidelines. PubMed, Scopus, and the Cochrane Register were searched on 28 October 2025 for English-language case reports and case series on primary malignant tumors of the proximal fibula. Two reviewers independently performed study selection and data extraction, collecting information on demographics, tumor characteristics, diagnostic approaches, treatments, and outcomes, with disagreements resolved by a third reviewer. Results: Thirty-three papers involving 228 patients (78 females, 128 males, 22 unknown) were included. The mean age at diagnosis was 22.8 years (range 4–79). The most common symptoms were painful mass and neurological complaints. Osteosarcoma and Ewing’s sarcoma were predominant histological types. Limb-sparing surgeries were most common, although 16 patients underwent amputation. At mean follow-up of 48.9 months, local recurrence occurred in 44 cases, and 12 developed distant metastases, most commonly in the lungs. Overall, 38 patients died, 37 due to disease progression. Conclusions: Primary malignant tumours of the proximal fibula, while rare, pose significant therapeutic challenges. Accurate diagnosis, appropriate multimodal treatment, and careful surgical planning are crucial to optimise oncological control and functional outcomes. Full article

Background: Chest X-ray (CXR) is widely used for the assessment of thoracic diseases, yet automated multi-label interpretation remains challenging due to subtle visual patterns, overlapping anatomical structures, and frequent co-occurrence of abnormalities. While recent deep learning models have shown strong performance, limitations in interpretability, anatomical awareness, and robustness continue to hinder their clinical adoption. Methods: The proposed framework employs a hybrid ConvNeXtV2–Vision Transformer (ViT) architecture that combines convolutional feature extraction for capturing fine-grained local patterns with transformer-based global reasoning to model long-range contextual dependencies. The model is trained exclusively using image-level annotations. In addition to classification, three complementary post hoc components are integrated to enhance model trust and interpretability. A segmentation-aware Gradient-weighted class activation mapping (Grad-CAM) module leverages CheXmask lung and heart segmentations to highlight anatomically relevant regions and quantify predictive evidence inside and outside the lungs. An ontology-driven neuro-symbolic reasoning layer translates Grad-CAM activations into structured, rule-based explanations aligned with clinical concepts such as “basal effusion” and “enlarged cardiac silhouette”. Furthermore, a lightweight out-of-distribution (OOD) detection module based on confidence scores, energy scores, and Mahalanobis distance scores is employed to identify inputs that deviate from the training distribution. Results: On the VinBigData test set, the model achieved a macro-AUROC of 0.9525 and a Micro AUROC of 0.9777 when trained solely with image-level annotations. External evaluation further demonstrated strong generalisation, yielding macro-AUROC scores of 0.9106 on NIH ChestXray14 and 0.8487 on CheXpert (frontal views). Both Grad-CAM visualisations and ontology-based reasoning remained coherent on unseen data, while the OOD module successfully flagged non-thoracic images. Conclusions: Overall, the proposed approach demonstrates that hybrid convolutional neural network (CNN)–vision transformer (ViT) architectures, combined with anatomy-aware explainability and symbolic reasoning, can support automated chest X-ray diagnosis in a manner that is accurate, transparent, and safety-aware. Full article

Chronic obstructive pulmonary disease (COPD) is a major health burden worldwide and in Taiwan, ranking as the third leading cause of death globally, and its prevalence in Taiwan continues to rise. Readmission within 14 days is a key indicator of disease instability and care efficiency, driven jointly by patient-level physiological vulnerability (such as reduced lung function and multiple comorbidities) and healthcare system-level deficiencies in transitional care. To mitigate the growing burden and improve quality of care, it is urgently necessary to develop an AI-based prediction model for 14-day readmission. Such a model could enable early identification of high-risk patients and trigger multidisciplinary interventions, such as pulmonary rehabilitation and remote monitoring, to effectively reduce avoidable early readmissions. However, medical data are commonly characterized by severe class imbalance, which limits the ability of conventional machine learning methods to identify minority-class cases. In this study, we used real-world clinical data from multiple hospitals in Kaohsiung City to construct a prediction framework that integrates data generation and ensemble learning to forecast readmission risk among patients with chronic obstructive pulmonary disease (COPD). CTGAN and kernel density estimation (KDE) were employed to augment the minority class, and the impact of these two generation approaches on model performance was compared across different augmentation ratios. We adopted a stacking architecture composed of six base models as the core framework and conducted systematic comparisons against the baseline models XGBoost, AdaBoost, Random Forest, and LightGBM across multiple recall thresholds, different feature configurations, and alternative data generation strategies. Overall, the results show that, under high-recall targets, KDE combined with stacking achieves the most stable and superior overall performance relative to the baseline models. We further performed ablation experiments by sequentially removing each base model to evaluate and analyze its contribution. The results indicate that removing KNN yields the greatest negative impact on the stacking classifier, particularly under high-recall settings where the declines in precision and F1-score are most pronounced, suggesting that KNN is most sensitive to the distributional changes introduced by KDE-generated data. This configuration simultaneously improves precision, F1-score, and specificity, and is therefore adopted as the final recommended model setting in this study. Full article

The reasons for disease outbreaks caused by Actinobacillus pleuropneumoniae (APP) in vaccinated pigs are often unknown and remain a challenge for farmers and veterinarians. One hypothesis for APP vaccine failure is the timing of APP vaccination during field or vaccine-induced viremia with Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), which may negatively affect the immune response to APP vaccination. In this study, fattening pigs were vaccinated with a modified live vaccine (MLV) against PRRSV either at the beginning of the fattening period (group G1) or six weeks later (group G2). All pigs were vaccinated against APP five days after the start of fattening, which coincided with MLV-PRRSV viremia in G1. Within both G1 and G2, four subgroups of pigs (n = 10) were vaccinated with three different APP vaccines or remained unvaccinated to assess serological responses to various APP antigens. MLV-PRRSV viremia had no significant effect on APP-ApxII (p = 0.127), APP-LPS (p = 0.120), or opsonophagocytic antibody responses on day 40 of fattening. Lung lesion scores at slaughter were significantly higher (p = 0.004) in pigs from G2 (1.82 ± 2.38) compared with those from G1 (0.65 ± 0.88). All APP vaccines elicited presumably protective opsonophagocytic antibodies. In conclusion, no effects of MLV-PRRSV viremia on serological responses following APP vaccination were observed. Full article

Background: Post-COVID-19 syndrome (PCS) is defined as the persistence or development of new symptoms 3 months after the initial infection with the SARS-CoV-2 virus, these clinical aspects being most often associated with functional respiratory changes, as well as imagistic modifications. This study aimed to evaluate longitudinal changes in pulmonary function among patients with PCS, in relation to the severity of the acute COVID-19 episode and the time elapsed since infection. Methods: A retrospective, observational study was conducted at the Clinical Hospital of Pulmonary Diseases Iași, Romania, between January 2021 and December 2022, including 97 adult patients with confirmed PCS. Demographic, clinical, and functional data were collected from medical records. Pulmonary function tests (PFTs) were performed according to ATS/ERS standards, assessing Forced Vital Capacity (FVC), Forced Expiratory Volume in the First Second (FEV₁), FEV₁/FVC ratio (Tiffeneau Index), Maximal Expiratory Flow at 50% and 25% of FVC (MEF50, MEF25), Diffusing Capacity of the Lung for Carbon Monoxide (adjusted for haemoglobin) (DLCO), Carbon Monoxide Transfer Coefficient (KCO), Alveolar Volume (AV), Total Lung Capacity (TLC) and Residual Volume (RV). Patients were grouped by time elapsed since infection (1–3, 4–7, 9–12, and up to 22 months). Statistical analyses included the Mann–Whitney U test, Spearman’s correlation, ROC curve analysis, and Principal Component Analysis (PCA). Results: A progressive improvement in FVC was observed up to 9–18 months post-infection (p < 0.05), while FEV₁ remained stable, suggesting a predominantly restrictive ventilatory pattern. Patients with moderate acute COVID-19 presented significantly lower FVC%, FEV₁%, DLCO%, and KCO% values compared with those with mild disease (p < 0.05). Diffusion abnormalities (DLCO and KCO) persisted beyond 12 months, indicating lasting alveolar-capillary impairment. ROC analysis identified TLC (AUC = 0.857), AV (AUC = 0.855), and KCO (AUC = 0.805) as the most discriminative parameters for residual dysfunction. PCA revealed three major functional domains—airflow limitation, diffusion capacity, and lung volume—explaining up to 70% of total variance. Conclusions: We are facing the emergence of a new phenomenon, namely a secondary post-COVID-19 pandemic of patients confronting with persistent post-COVID-19 symptoms who present with functional respiratory changes and who require careful monitoring in dynamics, personalized treatments and a multidisciplinary approach. Full article

Background: Sarcoidosis is a multisystem inflammatory disorder characterized by non-caseating granulomas, most commonly affecting the lungs and intrathoracic lymph nodes. Angiotensin-converting enzyme (ACE) levels and calcium abnormalities are recognized biomarkers, while ^18F-fluorodeoxyglucose positron emission tomography/computed tomography (FDG-PET/CT) is increasingly used to assess disease activity. However, neither provides sufficient diagnostic accuracy alone. Therefore, this study aimed to investigate the relationship between FDG-PET/CT metabolic findings and serum ACE and calcium (Ca²⁺) levels as surrogate indicators of inflammatory metabolic intensity in sarcoidosis. Methods: In this retrospective single-center study, 127 patients with pulmonary sarcoidosis who underwent PET/CT at diagnosis were evaluated. Demographic and clinical data, ACE, and Ca²⁺ levels were recorded. FDG uptake in mediastinal, pulmonary, and extrapulmonary sites was analyzed, and correlations with biomarkers were assessed. Results: The cohort included 89 females (70.1%) and 38 males (29.9%), mean age 51.3 ± 11.9 years. FDG uptake was most frequent in mediastinal lymph nodes (84.3%) and lung parenchyma (40.9%). ACE levels correlated weakly with total SUVmax (r = 0.214, p = 0.019). Calcium levels correlated with extrapulmonary SUVmax (r = 0.327, p = 0.001) and were higher in patients with extrapulmonary involvement (p = 0.045). No associations were found between symptom presence and biomarkers or SUVmax values. Conclusions: FDG-PET/CT metabolic parameters, particularly total and extrapulmonary SUVmax, demonstrated modest yet statistically significant associations with ACE and calcium levels. These findings suggest that a combined biomarker-imaging approach may provide complementary information regarding inflammatory metabolic intensity and systemic involvement; however, the results should be interpreted as exploratory and require validation in prospective studies. Full article

Background: The development of lung cancer is strongly influenced by oxidative stress (OS), which results when the balance between oxidants and antioxidants is disturbed. Evaluation of both specific redox markers such as thiol/disulfide homeostasis (TDH) and overall indicators including total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) may provide a more comprehensive view of oxidative imbalance in lung cancer. We examined OS indices and TDH in patients with lung cancer versus healthy controls. Methods: Eighty participants were enrolled, consisting of 40 patients with newly diagnosed lung cancer and 40 age- and sex-matched healthy controls. Serum levels of native thiol (NT), total thiol (TT), and disulfide were determined using an automated spectrophotometric method. Additionally, TAS, TOS, and the OSI were evaluated to provide an overall assessment of oxidative balance. Routine hematological and biochemical parameters were compared between groups. Results: White blood cell and neutrophil counts were notably higher in lung cancer patients compared with controls (p < 0.05). NT and TT levels were remarkably decreased, whereas disulfide levels, TOS, and OSI were significantly elevated in the lung cancer group (p < 0.05). TAS levels tended to be lower in patients, although not reaching statistical significance. No significant association was observed between oxidative parameters and tumor stage or localization. Conclusions: Patients with lung cancer exhibited a marked oxidative imbalance, characterized by elevated oxidant burden and impaired TDH. Combined assessment of TAS, TOS, OSI, and thiol/disulfide parameters may provide valuable insight into the oxidative pathophysiology of lung cancer and hold potential as complementary biomarkers for disease evaluation. Further large scale studies are needed to confirm these findings. Full article

Background: Lung carcinoids—typical and atypical—are rare neuroendocrine tumors (NETs) representing 1–2% of lung cancers. Despite clinicopathological differences, their clinical management often mirrors lung cancer protocols rather than NET-specific recommendations. Objectives: Portray a 12-year real-world experience with lung carcinoids at a Comprehensive Cancer Center, identifying gaps in diagnostic work-up, treatment decision-making, and follow-up. Methods: Retrospective observational cohort study of adult patients with histologically confirmed lung carcinoids diagnosed at IPO Porto between January 2013 and December 2024. Demographic, clinical, imaging, and treatment data were collected from electronic patient records. Analyses were descriptive. Results: Among 179 identified cases, 129 met eligibility criteria. Median age was 62 years (range 18–84); 53.6% were women and 53.5% were non-smokers; 84.5% had ECOG-PS 0–1. The most frequent presentation was respiratory symptoms (34.1%), followed by incidental findings (43.4%, of which ~20% were during staging or surveillance of other cancers). Typical carcinoids accounted for 49.6% and atypical for 43.4%. FDG-PET/CT was requested in 70.9% of cases, including many with typical carcinoid, and SSTR-PET/CT in 64.6% (dual PET in 38.8%). Most patients (65.1%) presented with stage I disease; 17.1% were stage IV. Mean time-to-first treatment was 83 days (range 1–259). Surgery was the first treatment option for 78.3% of patients. Conclusions: This real-world series highlights heterogeneity in diagnostic pathways, excessive FDG-PET use in typical carcinoids, and non-standardized follow-up. Dedicated multidisciplinary lung-NET boards and national reference centers are needed to homogenize and streamline patient management. Full article

Background/objectives: RSV is a major cause of mortality in infants, and despite recent progress to prevent RSV in the very young, an RSV vaccine for this population is still highly warranted. Clinical studies in infants in the 1960s using formalin-inactivated RSV (FI-RSV) led to life-threatening enhanced respiratory disease (ERD). Therefore, a thorough safety assessment of RSV vaccine candidates intended for RSV seronegative infants is crucial. Methods: Prior to clinical pediatric development of Ad26.RSV.preF, an adenovirus type 26 vector-encoding RSV F protein stabilized in its prefusion conformation, predisposition to ERD was extensively assessed in cotton rat and mouse models. Results: Cotton rats intramuscularly immunized with a wide dose range of Ad26.RSV.preF, including low and sub-protective vaccine doses, and challenged with vaccine homologous RSV A2 or heterologous RSV B Wash 18537, did not show signs of predisposition to ERD. Histopathology scores for alveolitis, peribronchiolitis, interstitial pneumonia, and perivasculitis after challenge were significantly lower for Ad26.RSV.preF-immunized cotton rats compared to FI-RSV-immunized cotton rats and comparable to or lower than scores in cotton rats intranasally pre-exposed to RSV prior to challenge to mimic natural repeated infection. These results were observed in animals with or without viral replication in the lung after RSV challenge, in the presence or absence of vaccine-induced antibodies. Similar results were observed in mice, where more extensive assessment of mono- and polymorphonuclear cell alveolitis, mucus cell hyperplasia, and mucus accumulation was performed. Conclusions: Based on these extensive analyses, we conclude that there are no indications of ERD predisposition after Ad26.RSV.preF vaccination in rodent models, irrespective of the vaccine dose, challenge virus strain, or presence of viral replication in the lung. These results are crucial for the pediatric development of this vaccine. Full article

Pulmonary hypertension (PH) causes morbidity and mortality in sickle cell disease (SCD). The release of heme during hemolysis triggers endothelial dysfunction and contributes to PH. Long non-coding RNAs (lncRNAs) may play a pivotal role in endothelial dysfunction and PH pathogenesis. This study assessed the regulatory role of the lncRNA–heme oxygenase-1 (HMOX1) axis in SCD-associated PH pathogenesis. Total RNAs were isolated from the lungs of 15–17-week-old sickle cell (SS) mice and littermate controls (AA) mice and subjected to lncRNA expression profiling using the Arrystar™ lncRNA array. Volcano plot filtering was used to screen for differentially expressed lncRNAs and mRNAs with statistical significance (fold change > 1.8, p < 0.05). A total of 3915 lncRNAs were upregulated and a total of 3545 lncRNAs were downregulated in the lungs of SS mice compared to AA mice. To validate differentially expressed lncRNAs, six upregulated lncRNAs and six downregulated lncRNAs were selected for quantitative PCR. MALAT1 expression was significantly upregulated in the lungs of SS mice and in hemin-treated human pulmonary artery endothelial cells (HPAECs), suggesting that hemolysis induces MALAT1. Functional studies revealed that MALAT1 depletion increased, while MALAT1 overexpression decreased, the endothelial dysfunction markers endothelin-1 (ET-1) and vascular cell adhesion molecule-1 (VCAM1), indicating a protective role of MALAT1 in maintaining endothelial homeostasis. In vivo, adenoviral MALAT1 overexpression attenuated PH, right ventricular hypertrophy (RVH), vascular remodeling, and reduced ET-1 and VCAM1 expression in SS mice. Given that HMOX1 protects endothelial cells during hemolysis, we observed that HMOX1 expression and activity were elevated in SS mouse lungs and hemin-treated HPAECs. HMOX1 knockdown enhanced ET-1 and VCAM1 expression, confirming its endothelial-protective function. Importantly, MALAT1 overexpression increased HMOX1 expression and activity, whereas MALAT1 knockdown reduced HMOX1 levels and mRNA stability. Collectively, these findings identify MALAT1 as a protective regulator that mitigates endothelial dysfunction, vascular remodeling, and PH in SCD, at least in part through the induction of HMOX1. These results suggest that SCD modulates the MALAT1–HMOX1 axis, and further characterization of MALAT1 function may provide new insights into SCD-associated endothelial dysfunction and PH pathogenesis, as well as identify novel therapeutic targets. Full article

Background/Objectives: Post-COVID-19 pulmonary fibrosis (PCPF) and idiopathic pulmonary fibrosis (IPF) exhibit significant clinical and pathophysiological overlap, suggesting convergent molecular pathways driving fibrosis. This prospective longitudinal study investigates the sustained dysregulation of matrix metalloproteinases (MMP)-2 and MMP-9 and its relationship with evolving systemic inflammation and endothelial dysfunction in convalescent COVID-19 patients, with comparative analysis to IPF. Methods: We conducted a prospective observational study of 86 patients at 6 and 12 months post-SARS-CoV-2 infection, stratified by high-resolution CT evidence of PCPF (FB+ group, n = 32) or absence of fibrosis (FB− group, n = 54). Gene expression of MMP-2 and MMP-9 in peripheral blood leukocytes and circulating levels of MMP-2, MMP-9, pro-inflammatory cytokines (TNF-α, IL-6), and endothelial dysfunction markers (Endothelin-1 [ET-1], adhesion molecules) were quantified via qRT-PCR and ELISA. A pre-pandemic healthy control group (HD, n = 20) and an IPF patient group (n = 10) served as comparators. Results: A significant, sustained elevation of MMP-2 and MMP-9 was observed in all post-COVID-19 patients versus HDs, most pronounced in the FB+ group and qualitatively similar to IPF. A critical divergence emerged: FB− patients showed resolution of systemic inflammation (reduced TNF-α, IL-6), whereas FB+ patients exhibited persistent cytokine elevation. Critically, a delayed, severe endothelial dysfunction, characterized by a profound surge in ET-1 and elevated adhesion molecules, manifested exclusively in the FB+ cohort at 12 months. Positive correlations linked plasma MMP-2/9 levels with ET-1 (r_s = 0.65, p = 0.004; r_s = 0.49, p = 0.009) and ET-1 with sICAM-1 (r_s = 0.68, p = 0.01). Conclusions: The development of PCPF is associated with a distinct pathogenic triad: sustained MMP dysregulation, failure to resolve inflammation, and severe late-phase endothelial dysfunction. The correlative links between these components suggest a self-reinforcing loop. This systemic signature mirrors patterns in IPF, underscoring shared final pathways in fibrotic lung disease and identifying the MMP–inflammation–endothelial axis as a promising target for biomarker development and therapeutic intervention. Full article

Background: Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity, mortality, and healthcare utilization. Lung volume reduction surgery improves outcomes in a select cohort but portends high morbidity. Bronchoscopic lung volume reduction (BLVR) is a less invasive, reversible manner of lung volume reduction, using one-way valves to improve lung function, quality of life, and exercise capacity. Nevertheless, knowledge gaps persist regarding factors that predict procedural success. Methods: We retrospectively reviewed 142 patients who underwent BLVR at the University of Chicago between December 2018 and July 2024 to assess the relationship between comorbidities and procedural outcomes. Using logistic and multinomial regression, we determined odds ratios (ORs) for a binary outcome of success and failure and relative risk ratios (RRRs) for failure sub-categories relative to procedural success. Results: We observed a procedural success rate of 48.1% and pneumothorax prevalence of 21.8%. After adjusting for age, sex, race, and body mass index (BMI), comorbidities associated with procedural failure included chronic kidney disease (CKD), congestive heart failure (CHF), anemia, and a BMI, Obstruction, Dyspnea and Exercise (BODE) Index of 5 or greater. Obstructive sleep apnea (OSA) was associated with procedural success. Conclusions: Comorbidities associated with dyspnea appear to have a significant effect on procedural success in BLVR. Full article

Chronic obstructive pulmonary disease (COPD) and tuberculosis (TB) increasingly co-occur in low- and middle-income countries and aging populations. Prior pulmonary TB is a robust, smoking-independent determinant of COPD and is linked to persistent systemic inflammation, endothelial dysfunction, dyslipidemia, and hypercoagulability axes that also amplify cardiovascular disease (CVD) risk. We conducted a targeted narrative non-systematic review (2005–2025) of PubMed/MEDLINE, Embase, Scopus, and Web of Science, selecting studies for clinical relevance across epidemiology, clinical phenotypes, pathobiology, biomarkers, risk scores, sleep-disordered breathing, and management. No quantitative synthesis or formal risk-of-bias assessment was performed. Accordingly, findings should be interpreted as a qualitative synthesis rather than pooled estimates. Prior TB is associated with a distinctive COPD phenotype characterized by mixed obstructive–restrictive defects, reduced diffusing capacity (DLCO), radiographic sequelae, and higher exacerbation/hospitalization burden. Mechanistic insights: Convergent mechanisms chronic immune activation, endothelial injury, prothrombotic remodeling, molecular mimicry, and epigenetic reprogramming provide biologic plausibility for excess CVD, venous thromboembolism, and pulmonary hypertension. Multimarker panels spanning inflammation, endothelial injury, myocardial strain/fibrosis, and coagulation offer incremental prognostic value beyond clinical variables. While QRISK4 now includes COPD, it does not explicitly model prior TB or COPD-TB outcomes, but data specific to post-TB cohorts remain limited. Clinical implications: In resource-constrained settings, pragmatic screening, prioritized PAP access, guideline-concordant pharmacotherapy, and task-shifting are feasible adaptations. A history of TB is a clinically meaningful modifier of cardiopulmonary risk in COPD. An integrated, multimodal assessment history, targeted biomarkers, spirometry/lung volumes, DLCO, 6 min walk test, and focused imaging should guide individualized care while TB-aware prediction models and implementation studies are developed and validated in high-burden settings. Full article

Workers’ exposure to silica dust is a global occupational and public health concern and is particularly prevalent in Southern Africa, mainly because of inadequate dust control measures. It is worsened by the high prevalence of HIV/AIDS, which exacerbates tuberculosis and other occupational lung diseases. The prevalence of silicosis in the region ranges from 9 to 51%; however, silica dust exposure levels and controls, especially in the informal mining sector, particularly in artisanal small-scale mines (ASMs), leave much to be desired. This is important because silicosis is incurable and can only be eliminated by preventing worker exposure. Additionally, several studies have indicated inadequate occupational health and safety policies, weak inspection systems, inadequate monitoring and control technologies, and inadequate occupational health and hygiene skills. Furthermore, there is a near-absence of silica dust analysis laboratories in southern Africa, except in South Africa. This protocol aims to systematically evaluate the effectiveness of respirable dust and respirable crystalline silica dust exposure evaluation and control methodology for the mining industry. The study will entail testing the effectiveness of current dust control measures for controlling microscale particles using various exposure dose metrics, such as mass, number, and lung surface area concentrations. This will be achieved using a portable Fourier transform infrared spectroscope (FTIR) (Nanozen Industries Inc., Burnaby, BC, Canada), the Nanozen DustCount, which measures both the mass and particle size distribution. The surface area concentration will be analysed by inputting the particle size distribution (PSD) results into the Multiple-Path Particle Dosimetry Model (MPPD) to estimate the retained and cleared doses. The MPPD will help us understand the sub-micron dust deposition and the reduction rate using the controls. To the best of our knowledge, the proposed approach has never been used elsewhere or in our settings. The proposed approach will reduce dependence on highly skilled individuals, reduce the turnaround sampling and analysis time, and provide a reference for regional harmonised occupational exposure limit (OEL) guidelines as a guiding document on how to meet occupational health, safety and environment (OHSE) requirements in ASM settings. Therefore, the outcome of this study will influence policy reforms and protect hundreds of thousands of employees currently working without any form of exposure prevention or protection. Full article