Myocardial injury in severe community-acquired pneumonia (SCAP) is often under-recognized, and interpretation of high-sensitivity cardiac troponin I (hs-cTnI) may be complicated by renal dysfunction and critical illness. We evaluated whether admission interleukin-8 (IL-8) and soluble suppression of tumorigenicity 2 (sST2) could support early risk stratification of guideline-consistent myocardial injury in patients with SCAP.

In this prospective cohort of 146 patients with SCAP, guideline-consistent myocardial injury was defined as hs-cTnI elevation above the assay-specific 99th percentile upper reference limit. Admission IL-8, sST2, and their combination were assessed using receiver operating characteristic curve analysis and 10-fold cross-validation. Fixed and estimated glomerular filtration rate (eGFR)-stratified hs-cTnI thresholds were compared in an exploratory analysis. An exploratory subgroup analysis was performed among patients with CURB-65 ≤ 1.

The median age was 71 years; 91 patients (62.3%) were male and 55 (37.7%) were female. Myocardial injury occurred in 88 patients (60.3%). The IL-8 + sST2 model showed good discrimination for myocardial injury, with an AUC of 0.825 (95% CI: 0.751-0.895) and an internally cross-validated AUC of 0.812. Admission IL-8 showed stronger individual discrimination than sST2. eGFR-stratified hs-cTnI thresholds did not reduce discordant hs-cTnI elevations in this cohort, likely because few patients had moderate-to-severe renal dysfunction. Among patients with CURB-65 ≤ 1 (n = 38), IL-8 > 43.53 pg/mL was associated with a higher prevalence of myocardial injury (76.2% vs. 29.4%, p = 0.004). An exploratory 0-2 biomarker score showed a graded increase in myocardial injury prevalence across score categories: 15.4%, 62.5%, and 78.6%.

Admission IL-8 was associated with guideline-consistent myocardial injury in patients with SCAP, whereas sST2 showed weaker individual discrimination. The combined model had numerically higher discrimination than IL-8 alone, but the incremental contribution of sST2 remains uncertain. These findings represent an initial evaluation and require external validation before clinical implementation.

Globally, 85% of the population uses traditional medicine. Ethiopia is a country with various traditional medicinal practices. However, various studies also reported traditional medicine used in children by their parents has had adverse outcomes and hospitalized them with complications. Various studies had also reported that traditional medicine use was high during COVID-19. Despite the fact that, children are particularly vulnerable population, limited studies exists regarding the prevalence, types, and determinants of parental TM use during COVID-19. In addition the existing studies were also confined to quantitative methods. Therefore, this study uses a mixed study design to explore indigenous methods of traditional medicine knowledge acquisition, preservation, preparation, storage, and dosage of herbs; barriers of disclosure; and prevalence of concomitant use.

A community-based concurrent mixed study design was conducted among 941 randomly selected parents from Dec 01/2023 to March 01/2024. The data was cleaned, coded, and entered in Epi-Data version 4.6 and transferred to Stata version 14.1 for analysis. Finally, an AOR with a 95% CI was computed, and variables with a p-value < 0.05 in the multivariable analysis were taken as significant factors. The qualitative data was collected from 16 selected key informants by in-depth face-to-face interviews and analyzed by using thematic analysis.

The prevalence of parental TM use for children was 87.6%. Sibling relation to child (AOR: 0.45, 95% CI, 0.01-0.77), religion (AOR: 0.11, 95% CI, 0.04-0.29), parental TM use for themselves (AOR: 6.55, 95% CI, 1.67-25.69), easy accessibility (AOR: 2.72, 95% CI, 1.16-6.40), safety & efficacy (AOR: 4.53, 95% CI, 2.3-13.61), and TM skill in the family (AOR: 0.47, 95% CI, 0.19-0.84) were determinants of TM utilization. Lack of awareness, misperception of TM, lack of trust in HCP and negative judgment from HCP were the main-barriers for non-disclosure of TM use.

This result indicated traditional medicine use was high; nearly 9 out of 10 parents had used TM for their children during COVID-19. There was high concomitant utilization (90.6%) and high non-disclosure rate (98.1%) of traditional medicine use to health workers. Hence, it is better to give priority to strengthening the implementation of TM policy and manage accordingly.

The elevation of neutrophil-lymphocyte ratio (NLR) has been shown to be critically involved in unfavorable outcomes among patients with chronic obstructive pulmonary disease (COPD). The mechanism underlying NLR changes during COPD progression remains unclear. This study evaluates the association between neutrophil PD-L1 expression and acute exacerbation of AECOPD and examines its correlation with the NLR.

In this prospective observational study from June 1 to December 30 2024, we enrolled 14 patients with acute exacerbation, 27 with stable conditions, and 9 healthy control subjects. Blood samples were collected for neutrophil isolation, and the CD15+CD274+ neutrophil percentage was measured using flow cytometry. We also recorded and analyzed smoking history, pulmonary function test results, and blood routine test data.

The percentage of CD15+CD274+ neutrophils was notably higher in patients with COPD compared to healthy controls and was even more elevated in those experiencing acute exacerbations of COPD (AECOPD) than in patients with stable COPD. This increased percentage was positively correlated with NLR but negatively correlated with FEV1% (FEV1 percentage of the predicted value). The AUC of CD15+CD274+ neutrophil percentage for predicting AECOPD was 0.894 with 95% CI 0.8-0.989 and a ratio above 3.273 (odds ratio 1.386; 95% CI 1.016-1.891; P = 0.039) independently associated with AECOPD.

Peripheral blood neutrophil PD-L1 expression was elevated in AECOPD and independently associated with exacerbation status in this pilot cohort. Larger, multi-center studies with mechanistic validation are required to determine its clinical utility.

Widespread adoption of transbronchial lung cryobiopsy (TBLC) using a 1.9 or 2.4 mm touch cryoprobe in interstitial lung disease (ILD) has been limited by high bleeding risk. Recent studies have demonstrated that the 1.1 mm cryoprobe via conventional bronchoscope may achieve diagnostic yields comparable to larger probes while maintaining a favorable safety profile. Studies of the 1.1 mm touch cryoprobe in the diagnosis of ILD have been flawed and conflicting.

The aim of this study is to describe the complication rate, diagnostic yield, and factors that increase diagnostic yield of TBLC using a 1.1 mm touch cryoprobe in patients with ILD.

The retrospective cohort study included patients that were prospectively identified in the ILD clinic registry at University of Texas Southwestern Medical Center (UTSW) who underwent TBLC from 2022-2026. Procedural characteristics were recorded. Patients were assigned a pre-TBLC, post-TBLC, and final diagnosis.

This study demonstrates that TBLC using a 1.1 mm probe added to BAL significantly increases diagnostic yield with an 11% risk of pneumothorax and a 6.5% risk of bleeding. The combination of BAL and TBLC was diagnostic in 27 (43.5%) of patients and led to a change in diagnosis in 27 (43.5%) of patients. The number of TBLC samples taken is associated with a higher diagnostic yield.

The diagnostic yield and complication rates of the 1.1 mm touch probe in our study are higher than previously reported studies with TBBx but lower than 1.9 and 2.4 mm touch probes, though there was no direct comparison group in our study. To increase yield of the procedure, multiple lobes should be biopsied and more samples taken.

There is limited evidence on how reduced healthcare resource utilization during the COVID-19 pandemic has affected the detection of inflammatory and immunologic diseases. We aimed to describe the observed incidence rates (IRs) of asthma, atopic dermatitis (AD), and multiple sclerosis (MS) before, during, and after the pandemic. Individuals aged ≥6 years were identified in Optum's de-identified Clinformatics® Data Mart Database from 2018 to 2022 to make 20 season-based cohorts. Age- and sex-standardized IRs of asthma, AD, and MS were estimated. Incidence rate ratios (IRR) and 95% confidence intervals (CI) were calculated comparing IRs in seasonal cohorts in 2019-2022 to the corresponding timeframe in 2018. Compared to spring 2018, IRs of asthma, AD, and MS in spring 2020 decreased by 14% (IRR: 0.86, 95% CI: 0.84-0.87), 28% (IRR: 0.72, 95% CI: 0.69-0.75), and 23% (IRR: 0.77, 95% CI: 0.68-0.87), respectively. The observed incidence reduction was most profound in children (6-11 years) and adolescents (12-17 years), followed by senior adults (≥65 years). There was no sex difference. IRs returned to or exceeded pre-pandemic levels for AD and MS in summer 2020 and for asthma in spring 2021. COVID-19 led to an apparent decline in incidence for selected inflammatory and immunologic diseases, which was more pronounced for pediatric and senior populations. The observed decrease in incidence likely reflects delayed access to healthcare, resulting in unrecorded (but still occurring) diagnoses for those time periods. Future studies using data that encompass the pandemic period should exercise caution in the design of study and interpretation of incidence or prevalence data.

Idiopathic pulmonary fibrosis (IPF) is associated with cigarette smoking, yet the relationship between the tobacco-specific nitrosamine nicotine-derived nitrosamine ketone (NNK) and IPF-associated lung transcriptional remodeling remains incompletely understood. Here, we developed an exposure-informed computational framework integrating multi-database target prediction, lung single-cell and single-nucleus transcriptomic analysis, co-expression network analysis, bulk lung cohort projection, and exploratory structure-based modeling. Putative human protein targets of NNK were predicted from ChEMBL, PharmMapper, and SwissTargetPrediction, yielding 2,505 nonredundant targets. These targets were intersected with IPF-associated intramodular hub genes identified from cell type-specific weighted gene co-expression network analysis, defining a focused 42-gene ExposureA-core gene set. Projected ExposureA-core scores showed the clearest IPF-control differences in endothelial and epithelial pseudo-bulk profiles. Functional annotation of the training-derived epithelial ExposureA-core Top30 signature highlighted MAPK and p38 MAPK signaling, PI3K-AKT signaling, angiogenesis or vasculature regulation, cell-substrate adhesion, and membrane-, adhesion-, and cytoskeleton-related cellular components, suggesting remodeling- and adhesion-related epithelial transcriptional features in IPF. The fixed epithelial ExposureA-core Top30 signature remained detectable in independent bulk lung transcriptomic cohorts without gene re-selection, coefficient fitting, or score optimization, with exploratory ROC analyses showing apparent IPF-control separation in GSE110147 and GSE92592. Exploratory docking and 100-ns molecular dynamics simulations of selected epithelial Top30-encoded candidates showed that modeled ECE1-NNK, MMP7-NNK, and TGM2-NNK complexes reached dynamic equilibrium, with relatively stable RMSD, radius of gyration, solvent-accessible surface area, residue-level fluctuation, and low-energy conformational states, supporting their structural plausibility as candidate modeled complexes. Overall, this study defines a focused exposure-informed IPF-associated transcriptional framework and prioritizes epithelial remodeling-related candidate features for future experimental validation. These findings support hypothesis-generating computational prioritization rather than direct evidence that NNK drives IPF pathogenesis.

The sheep lung has long been used to model aspects of the human lung, both its normal development and pathological changes that occur in ovine models of lung disease. The similarities between the two species provide an opportunity to investigate phases of lung development that are not accessible for investigation in humans, for example later in gestation. Here we use single cell (sc) RNA-seq to investigate the developmental dynamics of the sheep proximal and distal lung from mid gestation (80 days) through late gestation (120 days) and term (147 days). We identify changes in cell identity and abundance between the time points that illustrate many key features of mesenchymal, endothelial, and epithelial differentiation. Lastly we compare the single cell profiles through development of wildtype (WT) sheep with those of animals of the same breed engineered to have a loss-of-function mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Mutations in CFTR cause cystic fibrosis (CF) and the CFTR^-/- sheep exhibit many features of CF in humans. The results identify cellular signatures in the CFTR^-/- lung before birth that may facilitate the understanding of clinical features of CF in early postnatal life.

A woman in her early 50s presented with haemoptysis and cavitary pulmonary nodules. Initial testing showed a low-titre positive cryptococcal antigen (CrAg); however, repeat testing on two occasions was negative. Her cavitary nodules were ultimately attributed to an overlap systemic autoimmune rheumatic disease. She achieved complete clinical and radiological resolution with corticosteroid therapy. This case highlights the importance of recognising false-positive serum CrAg results.

The COVID-19 pandemic has contributed to more than 7 million deaths globally and has triggered a variety of postacute sequelae, now commonly referred to as long COVID, in millions more. Early efforts during the pandemic resulted in several therapies to mitigate the severity and mortality of acute COVID-19. However, despite effective therapies and accumulated immunity through vaccination and natural infection reducing disease severity, COVID-19 continues to contribute to hospitalizations and mortality. Long COVID encompasses several distinct yet overlapping clinical syndromes, and evidence suggests that these manifestations are mediated by numerous underlying mechanisms. There are currently no approved therapies for the treatment of long COVID, driven in part by its heterogeneity in presentation and etiology. This review will outline the current guidelines for treating acute COVID-19 and summarize information on the mechanistic rationale behind various published and ongoing clinical trials investigating potential long COVID therapeutic agents.

Advanced HIV infection is associated with profound immunosuppression, predisposing patients to opportunistic infections such as Pneumocystis jirovecii pneumonia (PJP) and Mycobacterium avium complex (MAC). PJP can cause severe respiratory disease, including acute respiratory distress syndrome (ARDS), while disseminated MAC may contribute to systemic illness and pulmonary complications. Concurrent infection with both pathogens is uncommon but may precipitate severe pulmonary failure. A man in his 40s presented with unintentional weight loss, fatigue, oral thrush, and progressive dyspnea. On arrival, oxygen saturation was 86% on room air, requiring high-flow nasal cannula. Laboratory evaluation revealed profound immunosuppression (CD4 7 cells/mm³, HIV RNA 123,000 copies/mL) and elevated β-D-glucan (>700 pg/mL). Chest CT demonstrated diffuse bilateral ground-glass opacities. He was initially treated empirically with broad-spectrum antibiotics (piperacillin-tazobactam and linezolid) and subsequently started on trimethoprim-sulfamethoxazole and corticosteroids for PJP. Despite supportive measures, the patient's respiratory status deteriorated, requiring intubation. Sputum cultures grew MAC, prompting initiation of azithromycin, rifampin, and ethambutol. The patient developed disseminated intravascular coagulation, acute tubular necrosis requiring daily hemodialysis, and septic shock requiring dual vasopressors. He was not a candidate for ECMO due to multi-organ failure in the context of advanced AIDS, and his prognosis remained guarded. This case highlights the rapid progression and complexity of opportunistic infections in advanced AIDS. Extensive diagnostic evaluation, early recognition of co-infections, and aggressive multidisciplinary management are essential, though outcomes may remain poor in patients with profound immunosuppression and multi-organ failure.