Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic and fatal interstitial lung disease. The etiology of IPF remains to be fully elucidated and its prognosis remains poor with a short survival period. Solute carrier family 7 member 5 (SLC7A5) is an amino acid transporter that is responsible for the transportation of large neutral amino acids. The expression of SLC7A5 was found to be significantly upregulated in patients with IPF, as well as in the lung tissues of mice with bleomycin (BLM)‑induced pulmonary fibrosis and in human lung fibroblasts induced by transforming growth factor‑β1 (TGF‑β1). Both SLC7A5 knockdown and the use of the selective SLC7A5 inhibitor JPH203 affected the function of TGF‑β1‑induced myofibroblasts by inhibiting the PI3K/AKT/mTOR pathway. In vivo, JPH203 improved BLM‑induced pulmonary fibrosis in mice by inhibiting the activation of the PI3K/AKT/mTOR signaling pathway. Therefore, SLC7A5 may represent a new therapeutic target for IPF. Future research should focus on therapeutic strategies regulating this target for translation into potential effective treatments for IPF in clinical practice.

Foreign body incidents are common pediatric emergencies, but evidence on factors associated with first recurrence is limited. This study aims to identify risk factors for first recurrence using large single-center data.

We conducted a retrospective cohort study of 48 197 children at a tertiary hospital (2020-2025). Kaplan-Meier analysis and multivariate Cox regression were performed. Schoenfeld residuals assessed the PH assumption; piecewise Cox models served as sensitivity analyses for age group and anatomical location, which violated it.

In a large single-center retrospective cohort of 48 197 children (median follow-up 1096 days), 3469 (7.2%) experienced a first recurrence. Adjusted recurrence hazards were higher for children aged 3 to <7 years (hazard ratio (HR)=1.19, 95% confidence interval (CI) 1.08 to 1.31), 1 to <3 years (HR=1.51, 95% CI 1.37 to 1.66) and <1 year (HR=1.30, 95% CI 1.10 to 1.55) than for children aged ≥7 years. Compared with the location of respiratory tract incidents, hazards were higher for the urogenital tract (HR=5.13, 95% CI 4.29 to 6.14) and soft-tissue incidents (HR=1.39, 95% CI 1.20 to 1.61), but lower for the digestive tract (HR=0.86, 95% CI 0.79 to 0.94) and nasal incidents (HR=0.85, 95% CI 0.77 to 0.95). Piecewise Cox regression in follow-up-window analyses showed that associations with age and anatomical location varied over time.

Recurrence risk after a first foreign-body event in children varies during follow-up. These findings may help clinicians identify children, particularly younger children and those with urogenital foreign-body events, who could benefit from targeted caregiver counseling and early follow-up. Risk-stratified prevention strategies could account for the time-varying nature of risk recurrence.

Industrial air pollution has been linked to respiratory diseases due to pulmonary function impairment, which are poorly documented in low-and middle-income countries. This study aimed to assess the pulmonary function of a community exposed to air pollution in an Industrial Area (IA) in Ouagadougou, Burkina Faso. Thus, a cross-sectional study was conducted among 146 residents of the IA and 146 residents of Nioko 2, constituting respectively, the target and control populations, from November to December 2023. A medical team collected data on respiratory symptoms experienced by the study population through a questionnaire followed by a clinical examination. Pulmonary function tests (PFTs) were then performed by spirometry according to ATS/ERS guidelines. The results showed that the study population suffered from both upper airway (87% IA, 70.50% Nioko 2) and lower airway (89% IA, 64.40% Nioko 2) symptoms whose prevalence was higher among the residents of the IA. The PFTs revealed a decrease in the predicted average percentage of FEV1% (p = 0.002) and FET % (p = 0.002) before bronchodilation among the residents of the IA compared to Nioko 2. These spirometric parameters still remained decreased among residents of the IA compared with Nioko 2 even after bronchodilation, but with only a significant difference for FET % (p = 0.011). Furthermore, the pulmonary impairment diagnosed among the residents of the IA before bronchodilation was restrictive defects (p = 0.035), with a strong representation of females (37.50% IA, 11.11% Nioko 2). Univariate logistic regression revealed that residence in the IA was significantly associated with restrictive ventilatory defects (OR, 1.697; p = 0.035). The restrictive defects diagnosed were the main pulmonary function impairment observed in the residents of the IA notably in women. The findings in this study highlight the impact of air pollution on the pulmonary function of the residents of the IA specifically on the lower respiratory tract.

Pediatric asthma is a chronic inflammatory airway disease with high heterogeneity. Its onset and progression are closely related to environmental exposures in early life and impaired immune regulation. Gut microbiota dysbiosis not only alters the production of metabolites such as short-chain fatty acids, 12,13-diHOME, and succinate, but also drives airway inflammation through multiple immunoregulatory mechanisms. Gut microbial dysbiosis can affect the production of metabolites, such as short-chain fatty acids, and promote airway inflammation through complex immune regulatory mechanisms. In addition, multi-axis interactions, including the gut-brain-lung and gut-bone-lung axis, may influence inflammatory phenotypes and disease heterogeneity in pediatric asthma. This review summarizes the characteristics of gut microbiota dysbiosis in pediatric asthma and focuses on the core mechanisms by which the gut-lung axis contributes to asthma pathogenesis, including metabolite-mediated regulation, disruption of immune homeostasis, mucosal barrier dysfunction, and multi-axis crosstalk. It also summarizes potential intervention approaches targeting the gut microbiota. Elucidating the gut microbiota-immune-multi-organ regulatory network may provide a theoretical basis for the early identification and precision intervention of pediatric asthma.

Human rhinovirus (HRV) is the predominant viral pathogen causing community-acquired upper respiratory tract infections, typically manifesting as mild coryzal symptoms. Severe neurological complications, including febrile infection-related epilepsy syndrome (FIRES), are exceptionally rare.

We report a case of febrile infection-related epilepsy syndrome (FIRES) with bilateral claustral involvement occurring in temporal association with an HRV-positive febrile respiratory illness, identified at the General Hospital of Ningxia Medical University in April 2025. The patient presented with acute refractory status epilepticus following a prodromal febrile illness. Neuroimaging revealed bilateral claustral hyperintensities and symmetrical thalamic lesions, while continuous electroencephalographic monitoring demonstrated burst-suppression patterns with frontotemporal discharges. HRV was detected in a respiratory tract specimen by nucleic acid testing but was not detected in the cerebrospinal fluid; the relationship between HRV detection and the neurological syndrome is therefore interpreted as a temporal association rather than a proven causal one, since a single respiratory detection may represent asymptomatic carriage rather than active infection.

This case underscores the importance of considering FIRES in patients with acute encephalopathy following a respiratory infection, even when the implicated pathogen-human rhinovirus in this case-is detected only in the respiratory tract, where it may represent either active infection or asymptomatic carriage. Early recognition through comprehensive neuroimaging and electroencephalographic monitoring, combined with multimodal immunomodulatory and antiseizure therapy, was followed by clinical and electrographic improvement and a favorable functional outcome in this patient; however, because corticosteroids, intravenous immunoglobulin, tocilizumab, a ketogenic diet, multiple antiseizure medications, and intravenous anesthetics were administered concurrently or sequentially, the contribution of any specific treatment cannot be determined, and no conclusions regarding treatment efficacy or the clinical utility of cytokine monitoring can be drawn from this single case. The hypothesized cytokine-mediated mechanisms underlying this clinico-radiological entity are discussed in a narrative review of the literature.

Sarcopenia in chronic obstructive pulmonary disease (COPD) is driven by elevated tumor necrosis factor-alpha (TNF-α), yet the underlying mechanism remains unclear. Here, we identify the mitochondrial metabolic enzyme Prodh2 as a pivotal mediator. Prodh2 was significantly upregulated in sarcopenic COPD patients and a corresponding mouse model. Mechanistically, TNF-α induced Prodh2 transcription in myoblasts via a p53-dependent pathway. This upregulation triggered excessive mitochondrial reactive oxygen species, leading to the release of mitochondrial DNA (mtDNA). Cytosolic mtDNA subsequently activated the cGAS/STING innate immune pathway, causing myoblast apoptosis, proliferation arrest, and atrophy. While Prodh2 knockdown reversed these effects in vitro, muscle-specific knockdown of Prodh2 in vivo critically ameliorated muscle atrophy and restored strength. Our study unveils a novel TNF-α-p53-Prodh2-cGAS/STING axis that links chronic inflammation to sarcopenia through metabolic-immune crosstalk, validating Prodh2 as a promising therapeutic target.

Identifying treatable traits in critically ill patients offers potential to enable a precision medicine approach to treatment. The aim of this exploratory analysis of the REMAP-CAP immune modulation domain was to evaluate whether plasma ferritin or soluble urokinase plasminogen activator receptor (suPAR) represent treatable traits for anakinra in critically ill patients with coronavirus disease (COVID-19).

An exploratory analysis of patients randomised within the COVID-19 immune modulation domain of the REMAP-CAP trial was conducted. Adults within 24 h of receiving respiratory or cardiovascular organ support in an ICU with suspected or microbiologically confirmed COVID-19 were included. Plasma ferritin was measured at study sites, and plasma suPAR measured in stored plasma samples. The primary outcome was organ support-free days (OSFD) until day 21. Analyses were performed using a Bayesian cumulative logistic regression model, and results are presented as the posterior median odds ratio (OR), along with 95% credible intervals (CrI), for anakinra being superior to control.

In ferritin analyses, 1243 patients were included. Patients with increasing ferritin levels had numerically fewer OSFDs. The posterior probabilities of anakinra having benefit (OR > 1) were 64%, 71%, and 21% across increasing ferritin terciles, compared to 53% in analyses that did not adjust for ferritin levels. 145 patients were included in the suPAR analyses. Patients with high baseline plasma suPAR (≥ 6 ng/ml; n = 85) had numerically fewer OSFDs than patients with low plasma suPAR (-1.0 (-1.0, 9.0) vs. 13.0 (-1.0, 17.0)). The posterior probabilities of anakinra having benefit (OR > 1) were 94.8% (OR 2.28 [0.85-6.06]) in patients with low baseline suPAR, and 38.6% (OR 0.88 [0.39-2.00]) in patients with high baseline suPAR.

Plasma ferritin does not identify patients with COVID-19 who benefit from treatment with anakinra, whilst anakinra may be beneficial in patients with low, rather than high, baseline plasma suPAR. These hypothesis-generating findings contrast with the results of clinical trials in non-critically ill patients with COVID-19.

NCT02735707. Date of trial registration: 06/04/2016.

Chronic lung disease, which is the third leading cause of death globally, places a disproportionate burden of morbidity and mortality on sub-Saharan Africa, where limited infrastructure results in a lack of understanding of how lung function changes over time, whether it varies among susceptible populations, or whether at-risk individuals could be identified before abnormal lung function develops. To address this gap, we aimed to characterise lung function patterns and identify correlates of lung function decline in rural Uganda.

Adults completed health questionnaires and American Thoracic Society/European Respiratory Society-acceptable spirometry up to three times over four years (2015-2019). Our primary outcome was lung function (forced expiratory volume in 1 second (EV₁) and FEV₁/forced vital capacity (FVC)); our secondary outcome was spirometry patterns. We characterised baseline patterns using Global Lung Initiative (GLI)-Global prediction equations and identified correlates of decline using generalised mixed effects linear regression. We then explored effect modification by sex, smoking, and socioeconomic status using interaction terms, with inverse probability of treatment weights balancing baseline characteristics.

A total of 902 participants completed 1,471 ATS/ERS-acceptable spirometry tests. Their median age was 35 years, 56% were women, 75% were never-smokers, and 31% experienced chronic respiratory symptoms. Abnormal lung function affected 14% of the cohort, more commonly women and those with respiratory symptoms. FEV₁ declined by 10mL/year (95% CI = -17, -2), and FEV₁/FVC declined by 0.006/year (95% CI = -0.008, -0.005) or 0.53% predicted/year (95% CI = -0.68, -0.37). Among those with normal baseline lung function, FEV₁ and FEV₁/FVC declined more rapidly (FEV₁ -18mL/year; FEV₁/FVC -0.66% predicted). There was no effect modification by sex, smoking, or SES.

Lung function decline may be more rapid in this young, mostly non-smoking population. Our findings extend the understanding of non-obstructive lung disease in sub-Saharan Africa and emphasise that risk persists despite normal spirometry. These data can inform regional public health strategies for risk mitigation, early disease detection, and building healthcare infrastructure for the growing population at risk for or living with chronic lung disease.

Prolonged QTc interval is a common electrophysiological abnormality in patients with chronic liver disease, but limited evidence exists regarding its occurrence in acute-on-chronic liver failure (ACLF), particularly in hepatitis B virus-related ACLF (HBV-ACLF). Given the rapid progression, high mortality, and severe complications associated with ACLF, understanding cardiac electrophysiological changes is clinically important. This study aimed to determine the incidence of QTc prolongation in patients with HBV-ACLF and to identify independent factors associated with QTc abnormalities. A retrospective study was conducted on 206 consecutive patients with HBV-ACLF admitted between January 2016 and December 2023. Heart rate and QT interval data were obtained from 12-lead electrocardiograms performed at admission. QTc was calculated using Bazett's formula. Patients were categorized into prolonged and non-prolonged QTc groups using a cutoff of 440 ms. Demographic, clinical, and laboratory variables were compared, and significant factors (P < .05) were entered into multivariate logistic regression to determine independent predictors. Of the 206 patients included, 68 (33%) exhibited prolonged QTc intervals. Univariate analysis revealed significant differences in red blood cell count (RBC), total cholesterol (CHOL), creatinine (CRE), potassium (K), fibrinogen (FIB), ascites, HBV-DNA level, and Child-Pugh classification (all P < .05). Multivariate logistic regression identified K, CRE, HBV-DNA, and ascites as independent predictors of QTc prolongation (P < .05 for all). Approximately one-third of patients with HBV-ACLF demonstrated prolonged QTc intervals. Electrolyte imbalance, renal dysfunction, viral replication activity, and ascites were independently associated with QTc prolongation. Routine QTc monitoring may provide a simple and noninvasive tool for early identification of patients at increased risk of cardiac complications.

Although drug-coated balloons (DCBs) are increasingly used in acute coronary syndrome (ACS), evidence regarding mid-term clinical outcomes after DCB angioplasty remains limited. Real-world data evaluating whether intravascular ultrasound (IVUS)-guided lesion preparation is associated with improved outcomes compared with angiography-guided intervention are scarce, particularly in patients with complex coronary lesions. This study compares clinical outcomes associated with IVUS versus coronary angiography (CAG) guidance for DCB angioplasty in patients with ACS, focusing on major adverse cardiovascular events (MACE) and net adverse clinical events (NACE) within the prespecified 24-month observation window. This retrospective study included 229 patients with ACS treated with DCB angioplasty between October 2017 and June 2025. Patients were categorized into IVUS-guided (n = 122) and CAG-guided (n = 107) groups according to the imaging strategy used during the procedure. Inverse probability of treatment weighting (IPTW) was applied to adjust for baseline confounders. The primary endpoints were MACE and NACE occurring within the prespecified 24-month observation window after DCB angioplasty. Secondary outcomes included individual clinical events, procedural characteristics, length of stay, and biochemical parameters assessed at predefined follow-up time points. After IPTW adjustment, baseline characteristics were balanced between groups. Procedural parameters, including DCB diameter, number of DCBs deployed, and bailout stenting rate, were comparable (all P > .05). Within the prespecified 24-month observation window, MACE occurred less frequently in the IVUS group than in the CAG group (8.2% vs 17.8%; IPTW P = .038). Major bleeding was also lower in the IVUS group (1.6% vs 11.2%; IPTW P = .015), contributing to a lower incidence of NACE (9.8% vs 26.2%; IPTW P = .001). IVUS guidance was additionally associated with a shorter hospital stay (4.2 vs 5.8 days; P < .001), while biochemical parameters remained comparable during follow-up. In patients with ACS treated with DCB, IVUS‑guided angioplasty was associated with significantly lower MACE and improved NACE outcomes during follow-up compared with angiography‑guided therapy alone. This benefit was largely attributable to an improved safety profile (e.g., fewer bleeding events). The associations remained consistent across subgroups, suggesting that IVUS‑guided lesion preparation may offer clinical value in this population and warrants further investigation.