INTRODUCTION:Neonatal lung biopsy guides management of unusually severe, diffuse lung disease with an uncertain diagnosis. Childhood interstitial lung disease (chILD) constitutes a diverse group of uncommon respiratory diseases which are associated with major morbidity and mortality. The incidence, outcome and mortality of chILD and other severe respiratory diseases in resource-limited settings (RLS) are unclear. OBJECTIVE:This retrospective, descriptive study examined lung biopsy in an RLS on infants up to 3 months of age to diagnose and facilitate management. This study included neonates with severe respiratory distress not responding to surfactant replacement. RESULTS:Lung biopsy was diagnostic in 94% (29/31) of patients without procedure-related mortality. The mean gestational age at birth was 35.8 weeks (SD ± 4.6). The mean presentation age was 20 days of life (IQR 1-28). Of 31 participants, 16% (n = 5) had histological findings in keeping with pulmonary interstitial glycogenosis (PIG) only. Sixteen percent (n = 5) of biopsies showed findings in keeping with adenosine triphosphate (ATP)-binding cassette subfamily A member 3 (ABCA3) deficiency in combination with features of PIG on electron microscopy. Surfactant protein (SFTP)-B deficiency and undefined surfactant deficiency were equally prevalent (6% (n = 2). Pulmonary hypertension (PHT) featured in 61% (n = 17) of infants. Genetic testing was performed on 29% (n = 9) of infants, with 56% (n = 5) showing normal results. The cohort mortality was 42% (n = 13). CONCLUSIONS:ChILD should be considered in neonates with severe respiratory distress and PHT not responding to surfactant replacement. Lung biopsy is safe and diagnostic and may prevent long and futile treatment. Histopathological diagnosis frequently assists treatment decisions. Future multicentre studies should include children from an RLS to collect information on diagnoses, genetics and treatment responses.
BACKGROUND:BAE has become a well-established, minimally invasive first-line therapy for hemoptysis. Coils may be useful in selected vascular lesions, including pseudoaneurysms and arteriovenous malformations, but their more proximal occlusive effect may limit distal access and could affect later retreatment and whether adding coils to embosphere embolization improves clinical outcomes remains uncertain. We compared recurrence and safety after embosphere-based BAE performed with or without adjunctive coils. METHODS:We retrospectively reviewed all consecutive adult patients who underwent first-time BAE for hemoptysis at our single tertiary care center between January 2019 and December 2024. Patients treated with embosphere were grouped according to whether coils were also deployed. Residual confounding arising from baseline covariate imbalances was mitigated via 1:1 propensity score-based matching, with matched pairs constrained to a caliper of 0.2 standard deviations of the logit of the propensity score. Kaplan-Meier analysis was used to estimate survival without hemoptysis recurrence, and the results were further analyzed based on the cause of hemoptysis. Factors linked to recurrent hemoptysis were evaluated using Cox proportional hazards models. RESULTS:The study cohort included 260 patients (median age, 56 years; 161 women), of whom 82 received embosphere plus coils and 178 received embosphere without coils. Propensity score matching yielded 62 patients in each group. At 1, 3, and 5 years prior to matching, recurrence-free survival stood at 92.6%, 75.0%, and 59.2% in the coil cohort, respectively, compared with 90.9%, 76.0%, and 50.3% in the control cohort (p = 0.979). After matching, the corresponding rates were 91.8%, 73.8%, and 51.8% versus 85.2%, 66.8%, and 40.5% (p = 0.358). Etiology-stratified analyses also showed no significant benefit from coil use after matching (bronchiectasis, p = 0.770; tuberculosis [TB] sequelae, p = 0.868; non-TB and nonbronchiectasis, p = 0.835). The duration of the procedure varied significantly between the groups (p = 0.003), while the rates of complications showed no significant difference (p = 0.181). On multivariable analysis, TB sequelae emerged as an independent predictor of recurrent bleeding, with a hazard ratio (HR) of 1.69 (95% CI 1.20-2.15, p = 0.002). Systemic arterial-pulmonary shunts (SPSs) were also independently tied to recurrence, carrying an HR of 1.52 (95% CI 1.32-3.72, p = 0.048). CONCLUSIONS:In patients undergoing embosphere-based BAE for hemoptysis, adjunctive coils did not improve long-term recurrence-free survival or reduce complications. Coil use was associated with shorter procedure duration.
BACKGROUND:There is a lack of evidence related to weaning noninvasive ventilation in bronchiolitis. The purpose of this study was to identify variables related to NIV weaning readiness and approach in bronchiolitis. METHODS:A retrospective cohort study of 74 children less than two years of age with bronchiolitis, requiring NIV and admitted to a pediatric intensive care unit (PICU) from 2022 to 2023. Demographic variables, clinical metrics, NIV mode, and weaning metrics were collected. RESULTS:Mean total duration of NIV therapy was 40 h with weans lasting 13 h. Duration for children on CPAP alone was shorter (26 h) than for children on combination of BiPAP and CPAP (45 h, 95% CI 4.258 to 33.742, p = 0.0123). Wean times were also shorter for children on CPAP alone (mean 5 h) than children on BiPAP and CPAP (mean 16 h) (95% CI 1.899 to 20.101, p = 0.0185). Patients were more likely to have a "complex wean," defined as escalation and de-escalation between multiple settings, with BiPAP (44.6%) than with CPAP (18.8%). RR at first wean was a significant predictor of NIV weaning duration (p = 0.007). CONCLUSION:There is a need for NIV weaning guidelines. RR may be an important predictor of NIV weaning readiness and approach. A "complex wean" may be a potential outcome variable for weaning NIV in children with bronchiolitis. This study may be used to inform future research and guidelines for weaning NIV in children with bronchiolitis.
BACKGROUND:To assess the clinical relevance of high-mobility group box 1 (HMGB1) in bronchopulmonary dysplasia (BPD), we conducted a systematic review and meta-analysis comparing HMGB1 levels in neonates with and without BPD. METHODS:Eight databases (PubMed, Cochrane Library, Web of Science, Embase, CNKI, VIP, Wanfang, and CBM) were searched up to March 1, 2025. Cohort studies reporting serum or bronchoalveolar lavage fluid (BALF) HMGB1 levels in neonates were included. Meta-analysis was performed using RevMan 5.4. RESULTS:Seven studies (n = 527 neonates; 308 BPD, 219 controls) were included. HMGB1 concentrations in BALF were significantly higher in neonates with BPD than in those without BPD (mean difference [MD], 5.04 ng/mL; 95% confidence interval [CI], 4.09-5.99; p < 0.00001). Serum HMGB1 concentrations were also higher in neonates with BPD (MD, 7.24 ng/mL; 95% CI, 4.53-9.96; p < 0.00001). Subgroup analyses across postnatal time points indicated that serum HMGB1 levels tended to be higher in infants with BPD than in controls; however, the progressive increase observed from Stage I to Stage III plateaued thereafter, with no further increase in Stage IV (> 20 days). CONCLUSION:Total HMGB1 concentrations in serum and BALF are elevated in neonates with BPD, which may reflect BPD-associated inflammatory lung injury. However, the clinical utility of HMGB1 is limited by its lack of disease specificity and the inability of current assays to distinguish among biologically distinct redox isoforms. Further prospective studies are needed to clarify its diagnostic and therapeutic relevance.
Cellular stress is implicated in the progression of lipopolysaccharide (LPS)-evoked acute lung injury (ALI). The goal of this study was to evaluate the effect of oral supplementation with rosiglitazone (RSG), which is an agonist of peroxisome proliferator-activated receptor (PPAR)-γ, on pulmonary inflammatory response, oxidative stress, and endoplasmic reticulum (ER) stress during LPS-evoked ALI in mice. The mice were randomly divided into four groups and orally supplemented with or without RSG (10 mg/kg) once daily for 5 consecutive days before LPS (1 mg/kg) intraperitoneal injection. The mice were sacrificed at 12 h after LPS injection. As expected, LPS-evoked ALI and death were attenuated in mice that were pretreated with RSG. LPS-evoked increase in chemokines (KC, MIP-2, and MCP-1) and proinflammatory cytokines (TNF-α and IL-1β) was inhibited in the mouse lungs by RSG. RSG pretreatment significantly mitigated LPS-evoked nuclear translocation of NF-κB p65 and p50, which regulate inflammatory gene transcription in the lungs. Additionally, LPS-evoked glutathione depletion and lipid peroxidation were alleviated by RSG. The abnormal expression of NADPH oxidases and antioxidant enzymes was restored in the lung tissues by RSG. Further experiments revealed that LPS-evoked upregulation of GRP78, p-IRE1α, and p-EIF2α was blocked by RSG pretreatment. Mechanistically, RSG pretreatment enhanced PPARγ activity in the mouse lungs and bronchial epithelial cells. RSG promoted the interaction between NF-κB p65 and PPARγ in the mouse lungs. Overall, RSG pretreatment protects against LPS-evoked ALI partially through enhancing PPARγ activity and inhibiting the cellular stress response in the mouse lungs.
OBJECTIVE:This study aimed to identify factors that predict progression to necrotizing pneumonia (NP) in children with Mycoplasma pneumoniae pneumonia (MPP) who fail to respond to initial therapy and to develop a predictive model to support early clinical decision-making. METHODS:We retrospectively analyzed clinical and laboratory data of children with macrolide-unresponsive Mycoplasma pneumoniae pneumonia (MUMPP) admitted to Tianjin Children's Hospital from January 2021 to January 2025. MUMPP was defined as persistent fever (≥ 38.5°C, lasting ≥ 4 h/day) after ≥ 72 h of standardized intravenous macrolide therapy. Patients were classified into an observation group (n = 106, those who developed NP) and a control group (n = 130, those who did not). Independent predictors of NP were identified by multivariable logistic regression and incorporated into a nomogram. Model performance was evaluated using ROC analysis, calibration plots, and decision curve analysis. RESULTS:In multivariable analysis, increased white blood cell (WBC) count (OR = 2.484, 95% CI: 1.406-4.613), longer fever duration (OR = 1.618, 95% CI: 1.217-2.193), pleural effusion (OR = 3.955, 95% CI: 1.664-10.00), and elevated C-reactive protein (CRP) (OR = 2.152, 95% CI: 1.547-3.074) were independently associated with NP among children with MPP after initial treatment failure. Calibration curves indicated close agreement between predicted and observed risks in both the derivation cohort (p = 0.588) and the validation cohort (p = 0.424). The model showed good discrimination, with an AUC of 0.848 (95% CI: 0.789-0.908) in the derivation cohort and 0.889 (95% CI: 0.815-0.963) in the validation cohort. Decision curve analysis suggested net clinical benefit across relevant threshold probabilities. CONCLUSION:Among children with MUMPP, higher WBC count, prolonged fever, pleural effusion, and higher CRP identify increased risk of NP.
BACKGROUND:The Bronchiectasis Health Questionnaire (BHQ) was developed to assess the health-related quality of life (HRQOL) in patients with noncystic fibrosis (CF) bronchiectasis. This study aimed to translate, culturally adapt, and validate the BHQ for use among Chinese patients. METHODS:The traditional Chinese version of the BHQ (TC-BHQ) was created through a process of translation, cognitive debriefing interviews, and expert panel reviews. The psychometric evaluation of the TC-BHQ encompassed assessments of factor structure, convergent validity, known-group comparison, internal consistency, and test-retest reliability. RESULTS:We recruited 150 non-CF bronchiectasis patients. Confirmatory factor analysis (CFA) supported the one-factor structure of the BHQ. In terms of concurrent validity, the TC-BHQ total score showed a significant correlation with the St. George's Respiratory Questionnaire (SGRQ) total score (r = -0.77, p < 0.01). In addition, the TC-BHQ total score significantly correlated with all SGRQ subscale scores, including the symptom score (r = -0.62, p < 0.01), activity score (r = -0.60, p < 0.01), and impact score (r = -0.75, p < 0.01). There was a statistically significant change in the total score between baseline and follow-up (p = 0.007). Both internal consistency and test-retest reliability of the TC-BHQ were acceptable. CONCLUSION:TC-BHQ is a promising tool for assessing HRQOL in patients with non-CF bronchiectasis. It has the potential to be a useful instrument in both clinical and research settings.
BACKGROUND:Bronchiolitis obliterans (BO) is a rare chronic pulmonary condition in pediatric patients, characterized by irreversible fibrotic constriction of the small airways. This study aims to analyze the risk factors for BO caused by severe adenovirus pneumonia (SAP) and to develop a nomogram model for personalized prediction. METHODS:We retrospectively analyzed 251 children with SAP admitted to the Children's Hospital of Nanjing Medical University between January 2017 and March 2024. Among them, 77 were classified into the BO group and 174 into the non-BO group. A predictive nomogram was developed based on independent risk factors identified through univariate analysis, least absolute shrinkage and selection operator (LASSO) regression, and multivariate logistic regression. RESULTS:Multivariable analysis identified the following independent risk factors for BO: wheezing (odds ratio [OR] = 4.78; 95% confidence interval [CI], (2.00∼11.40); p < 0.001), large lobar consolidation (OR = 8.53; 95% CI, 3.63∼20.02; p < 0.001), length of hospital stay (OR = 1.20; 95% CI, 1.08-1.33; p < 0.001), and duration of fever (OR = 1.20; 95% CI, 1.09-1.32; p < 0.001). Mechanical ventilation showed a trend toward increased risk but did not reach statistical significance (OR = 5.35; 95% CI, 0.74-38.56; p = 0.096). The nomogram demonstrated excellent discriminative ability, with an area under the curve of 0.90 (95% CI: 0.85-0.94). Calibration curves indicated good agreement between predicted and observed outcomes. Decision curve analysis showed a net clinical benefit within a clinically relevant threshold probability range of 0.10-0.70. CONCLUSIONS:A nomogram incorporating five independent risk factors-wheezing, duration of fever, length of hospital stay, mechanical ventilation, and large lobar consolidation-was developed to predict BO risk in children with SAP.
BACKGROUND:While the individual effects of biologics in asthma are well demonstrated, the potential impact of the use of biologics on overall asthma-related hospitalization at a population-based level has not been reported. METHODS:A territory-wide study conducted in Hong Kong, involving all adult patients with asthma managed in Hospital Authority. The primary outcome was the change in asthma-related hospitalization from 2014 to 2023, correlating with the number of biologic use among patients with asthma and adjusted for Air Quality Health Index and influenza case number. RESULTS:The weekly asthma-related hospitalization was 96 episodes at the start of the study period and 78 episodes at the end of the study period. There was a significant reduction of asthma-related hospitalization associated with biologic usage, giving the estimated risk ratio of 0.994 (95% CI = 0.991-0.996, p value < 0.05). The estimated break-point for the change in asthma-related hospitalization was at Week 169 (95% CI = 130.3-207.7), which was the week of 19/3/2017 to 25/3/2017. The slopes before and after the break-point were 0.022 and -0.191 with the difference in the two slope estimates being significant (p < 0.001) according to the Davies test. The significant difference in the slope before and after the break-point suggested that beyond Week 169, there was a trend of significant reduction in asthma-related hospitalization. CONCLUSION:We observed a reduction in asthma-related hospitalizations throughout the study period with a potential temporal association with the increase in biologic prescription. While biologics provided benefits in individual level, the possible benefits in a population-based level could be related to a more comprehensive care in severe asthma patients from the introduction of biologics for severe asthma.
OBJECTIVE:To clarify the predictive role of club cell 10-kDa protein (CC10) and cysteinyl leukotrienes (CysLTs) for subsequent wheezing after RSV infection. METHODS:From October 1, 2022, to October 31, 2023, children diagnosed with RSV-induced bronchiolitis hospitalized in the pediatric ward were included. Nasopharyngeal aspirates (NPAs) were obtained on the day of admission. NPAs from hospitalized children without respiratory infections served as the control group. We analyzed the correlation between CC10 and CysLTs levels in NPAs and disease severity. Follow-up assessments were conducted to observe the subsequent wheezing. RESULTS:There were 169 hospitalized infants diagnosed with RSV-bronchiolitis, and 22 healthy controls matched for age were selected. The levels of CC10 in the NPAs were significantly lower in the RSV group (219.4 ± 83.1 pg/mL) than those in the control group (284.1 ± 68.1 pg/mL; p < 0.001). Levels of CysLTs were significantly greater in the RSV group (346.3 ± 98.1 pg/mL) than in the control group (288.3 ± 82.5 pg/mL; p < 0.05). Pearson correlation analysis showed that CC10 protein level was negatively correlated with severity (r2 = 0.34, p < 0.001). Conversely, the level of CysLTs was positively correlated with severity (r2 = 0.09, p < 0.001). 142 cases were completed with follow-up within a year after discharge. 47 cases (33.1%) had experienced subsequent wheezing, and 95 cases (66.9%) did not have subsequent wheezing. The multivariate logistic regression analysis indicates a higher likelihood of subsequent wheezing in children with CysLTs levels over 335.3 pg/mL (OR = 5.496), allergy history (OR = 3.466), and longer ventilation duration (OR = 1.364). CONCLUSIONS:While CC10 and CysLTs levels correlated with the severity of RSV-bronchiolitis, only CysLTs, along with allergy history and duration of ventilation, showed a suggestive link to subsequent wheezing, but further validation is needed.
Background: The advanced lung cancer inflammation index (ALI) is an important characteristic of cancer and other diseases. This retrospective study aimed to explore the prognostic value of the ALI in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) using noninvasive ventilation (NIV). Methods: This is a retrospective cohort study. A nonrandom sampling method was employed to collect the inpatients diagnosed with AECOPD and used noninvasive ventilators in the Department of Respiratory and Critical Medicine, Beijing Chao-yang Hospital, affiliated with Capital Medical University, from January 2017 to December 2022. Participants were categorized into a success group (NIV-S) and a failure group (NIV-F) based on the outcome of their noninvasive ventilator use in hospitals. The laboratory indices of both groups were compared. A multivariate logistic regression analysis was conducted to identify the risk factors influencing patient prognosis when using noninvasive ventilators, and the subject working a characteristic curve was employed to assess the predictive power of associated risk factors for the failure of noninvasive ventilators. Results: A total of 137 patients suffering from AECOPD complicated with respiratory failure were included, including 117 cases in the NIV successful group (NIV-S, 85.4%) and 20 cases in the NIV failed group (NIV-F, 14.6%). The arterial blood carbon dioxide partial pressure (PaCO2), fibrinogen, and urea nitrogen in the NIV-S were lower. At the same time, the total protein, albumin, body mass index (BMI), and ALI were higher than those in the NIV-F. Moreover, our data revealed that ALI could be considered a reliable biomarker for predicting NIV-F (AUC: 0.822 and 95% CI: 0.710-0.934). The ALI group, along with an OR of 12.206 (95% CI: 3.086-48.279; p < 0.001). Conclusions: Low ALI is associated with NIV-F in patients with AECOPD and is a practical and valuable tool for prognostic assessment.
BACKGROUND:Patients with obstructive sleep apnea (OSA) are at increased risk of perioperative complications, such as hypoxemia, respiratory depression, and airway obstruction. This study aims to evaluate the effectiveness of individualized nursing in the perioperative management of patients with OSA. METHODS:We retrospectively analyzed 107 patients with OSA undergoing elective surgery between January 2023 and January 2025, who were allocated to a conventional group (n = 55) or an individualized group (n = 52) according to the nursing approach. Perioperative respiratory safety (postanesthesia care unit [PACU], minimum oxygen saturation [SpO2], Aldrete score, and respiratory adverse events within 48 h), analgesia and functional recovery (visual analog scale [VAS] scores, opioid consumption, time to first ambulation), postoperative Epworth Sleepiness Scale (ESS) scores, continuous positive airway pressure (CPAP) adherence, Short Form-36 (SF-36) quality of life, complications, ICU transfer, length of stay, and hospitalization costs were compared between groups. RESULTS:Compared with the conventional group, the individualized nursing group showed significantly higher PACU minimum SpO2 (p = 0.001) and Aldrete scores (p < 0.001), a lower incidence of postoperative respiratory adverse events within 48 h (p < 0.05), reduced 24-h and 48-h VAS scores and opioid consumption (p < 0.05), and earlier ambulation (p < 0.001). During the 6-month follow-up, the individualized group demonstrated lower ESS scores, improved CPAP adherence, and greater improvements across all SF-36 domains (all p < 0.001), as well as reduced overall complications, ICU transfer rates, length of hospital stay, and hospitalization costs (p < 0.05). CONCLUSION:Individualized nursing is associated with improved perioperative respiratory safety and recovery quality, better long-term sleep outcomes and quality of life, and reduced complications and healthcare resource use in patients with OSA.
OBJECTIVE:To investigate the regulatory effects of bronchial epithelial cell-released autophagosome (BA)-induced neutrophils on bronchial epithelial cells and the underlying mechanisms. METHODS:Transmission electron microscopy and western blotting were used to identify autophagosomes in 16HBE cells stimulated with house dust mite (HDM) antigen. The production of reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) was detected after BA were cocultured with human peripheral blood neutrophils. Flow cytometry was used to detect the apoptosis rate of 16HBE cells incubated with cocultured supernatant, and BAX, Bcl-2, and cleaved caspase 3 expression was detected by western blotting. In mouse acute asthma, hematoxylin and eosin (HE) staining was used to detect lung tissue injury. Apoptosis was detected by TUNEL, and neutrophils, macrophages, LC3, BAX, and Bcl-2 were detected by immunohistochemistry. RESULTS:HDM induced the release of autophagosomes by 16HBE cells. BA induced ROS production in neutrophils by activating NF-κB signaling pathway and further promotes the formation of NETs, which induced apoptosis of 16HBE cells and was mediated by the regulation of BAX, Bcl-2, and cleaved caspase 3. In the HDM-induced mouse acute asthma, the lung tissue structure was destroyed, the content of neutrophils and macrophages increased, the macrophages showed M1 polarization, and the expression of LC3, BAX, Bcl-2, and apoptosis increased. CONCLUSION:HDM-stimulated 16HBE cells released autophagosomes, which induced ROS production in neutrophils via NF-κB pathway activation and further promoted NET formation, ultimately leading to 16HBE cell apoptosis and lung injury in mice.
OBJECTIVE:To investigate the effects of mindfulness-based stress reduction (MBSR) combined with cardiopulmonary rehabilitation (CR) training on cardiopulmonary function, oxygen delivery efficiency, and psychological stress in patients with pulmonary arterial hypertension (PAH). METHODS:A total of 50 clinically stable PAH patients were randomly assigned to an intervention group (N = 25) and a control group (N = 25). The intervention group received a 6-week program combining MBSR and standardized CR, while the control group received conventional health education and standard pharmacological management. Cardiopulmonary exercise capacity, hemodynamic parameters, and psychological stress levels were assessed before and after the intervention. RESULTS:After 6 weeks, the intervention group showed significantly improved percentage of predicted peak oxygen uptake (84.3 ± 12.1% vs. 71.2 ± 13.4%, p = 0.001), oxygen delivery (1650 ± 410 mL/min vs. 1388 ± 375 mL/min, p = 0.022), and arterial oxygen content (18.5 ± 2.1 mL/dL vs. 17.1 ± 1.8 mL/dL, p = 0.015). Hemodynamically, pulmonary vascular resistance significantly decreased (415 ± 265 vs. 586 ± 310 dyn·s/cm5, p = 0.040), and pulmonary artery compliance increased (2.12 ± 0.46 mL/mmHg vs. 1.76 ± 0.42 mL/mmHg, p = 0.009). In terms of psychological stress, the intervention group showed significantly lower scores in HAMA (11.28 ± 3.94 vs. 14.22 ± 4.06, p = 0.013), HAMD (11.36 ± 4.32 vs. 15.26 ± 4.89, p = 0.011), and SPBS (18.04 ± 4.83 vs. 23.02 ± 5.44, p = 0.001) compared with the control group. CONCLUSION:MBSR combined with CR significantly improves cardiopulmonary exercise performance, oxygen transport capacity, and hemodynamic function in PAH patients, while also reducing psychological stress levels. This combined intervention demonstrates good safety and promising clinical applicability.
BACKGROUND:This study primarily analyzed differences in venous thromboembolism (VTE) characteristics across altitudes and their temporal trends during the puerperium. Additionally, it identified independent risk factors for postpartum pulmonary embolism (PE). METHODS:This retrospective study reviewed all postpartum VTE cases at People's Hospital of Xizang Autonomous Region between 2015 and 2024. RESULTS:This cohort study of 172 postpartum women (median age 31 [IQR 26-36]) compared high-altitude (HA, n = 109) and very high-altitude (VHA, n = 63) groups. PE proportion was significantly higher in VHA vs. HA ( p = 0.033). VHA subjects also showed significant elevated preterm delivery (p = 0.033) and ≥ 3 deliveries (p < 0.001). Joinpoint regression (2015-2024) revealed biphasic trends: significant early-phase escalations in VTE (APC = 18.05%) and deep vein thrombosis (DVT) (APC = 19.66%) during 2015-2022 (p < 0.05), followed by clinically relevant (though statistically nonsignificant) late-phase reductions. PE proportion demonstrated a significant overall increase (APC = 18.77%, p < 0.05). In multivariate analysis, four independent predictors significantly increased PE risk: altitude gradient (OR 1.035, p < 0.001), multiparity (OR 2.548, p = 0.004), hypertension or eclampsia (OR 1.797, p = 0.001), and structural heart disease (OR 1.988, p < 0.001). CONCLUSION:This decade-long analysis (2015-2024) revealed significant altitudinal gradients in postpartum VTE. Clinically significant escalation of postpartum VTE burden in high-altitude populations warrants urgent intervention. Integrated multiparity management and enhanced comorbidity control are critical future initiatives for resolving key perinatal thrombotic risk bottlenecks.
Early in the pathogenesis of pulmonary fibrosis (PF), there are multiple inflammatory cell infiltrations in the damaged lung tissue. When lung injury persists, inflammatory cytokines prompt local fibroblasts migration and hyperproliferation, triggering abnormal deposition of extracellular matrix in the lung interstitium. This excessive repair leads to interstitial cell reorganization, triggering lung tissue fibrosis and further activation of inflammatory cells. Therefore, modulation of inflammatory mediators is of great significance in the treatment and prevention in the process of fibrosis. Cortex Mori Radicis (CMR) is a traditional Chinese herb with anti-inflammatory and antifibrotic properties. In this study, we investigated the therapeutic effects of CMR on bleomycin-induced PF using in vivo and in vitro models. In vivo experiments showed that CMR treatment significantly reduced inflammation, attenuated fibrosis, and alleviated lung function decline. In vitro, CMR inhibited migration, proliferation, and epithelial-mesenchymal transition (EMT) in A549 lung epithelial cells. Network pharmacological analysis identified 25 bioactive components and 10 key therapeutic targets in CMR, with the PI3K/AKT signaling pathway emerging as the core regulatory mechanism. Subsequent in vivo validation confirmed that CMR could inhibit the activation of the PI3K/AKT pathway. In conclusion, CMR exerts protective effects against PF by modulating the PI3K/AKT pathway, thereby attenuating inflammation and fibrotic remodeling. This study provides both pharmacodynamic evidence and mechanistic insight supporting the clinical potential of CMR and underscores the advantages of multitargeted intervention strategies offered by traditional Chinese medicine in the treatment of PF.
Pulmonary fibrosis (PF) is a progressive fibrotic interstitial lung disease characterized by aberrant activation of myofibroblasts and excessive deposition of extracellular matrix. In light of the complexity of its pathogenesis and the limited availability of approved antifibrotic drugs, PF remains a refractory lung disease imposing a substantial burden on patients. Current research into the pathogenesis of PF has largely revolved around the core hypothesis of recurrent microinjuries to alveolar epithelial cells. However, in recent years, increasing attention has been directed toward the role of endothelial dysfunction in the progression of fibrosis. This review focuses on pulmonary microvascular endothelial cells and systematically examines their regulatory mechanisms in the initiation and progression of PF from three perspectives: endothelial cell senescence and programmed cell death, intercellular crosstalk between endothelial cells and surrounding cells, and endothelial-mesenchymal transition (EndoMT). Furthermore, we summarize antifibrotic drugs and therapeutic strategies targeting endothelial cells, providing theoretical insights and research directions to elucidate the pathogenesis of PF and explore novel therapeutic approaches.
INTRODUCTION:Alpha-1 antitrypsin deficiency (AATD) may be directly related to bronchiectasis. However, radiological diagnosis of mild bronchiectasis is subjective, and visual assessment of airway tapering is time-consuming. CT algorithms have been used to quantify airway tapering in other bronchiectasis aetiologies. We assessed whether this process can be used in AATD. METHODS:Historic CT scans from patients with severe AATD in the Birmingham registry were processed with YACTA software (Weinheimer et al., 2017), and data on bronchiectasis index (BEI), airway wall thickness (AWPi10) and emphysema (PD15) were extracted. Correlation with visual data was assessed using standard statistical tests. Receiver operating characteristic (ROC) curves were used to find thresholds at which algorithm data are associated with visual data. Regression models assessed the impact of algorithm data on lung function decline, exacerbation rate, mortality and bronchiectasis severity index (BSI), corrected for age, sex, smoking status and PD15. RESULTS:A total of 154 scans were analysed. BEI correlated moderately well with visual scoring of bronchial dilatation (p < 0.001), bronchial wall thickness (BWT, p < 0.001), number of lobes affected (p < 0.001) and morphology (p < 0.001). AWPi10 did not correlate with BWT (p = 0.28). Thresholds were identified for the association of BEI with bronchial dilatation ≥ 2 × arterial diameter; lobar involvement ≥ 3 lobes, and presence of varicose or cystic morphology, though sensitivity and specificity were relatively low. BEI is associated only with BSI (p = 0.002). AWPi10 did not associate with clinical outcomes. CONCLUSION:Algorithm CT analysis has value in quantifying mild bronchiectasis in AATD and may be used in trials of emerging therapies.
OBJECTIVE:We investigated the therapeutic effects of combined erythromycin and budesonide treatment on tracheal stenosis (TS) and the associated changes in macrophage-related markers and HDAC2 expression. METHODS:A rabbit model of TS was established by mechanical scraping of the tracheal inner wall, and the animals were then treated with erythromycin, budesonide, or their combination. Treatment effects were evaluated through histological analysis. We quantified the mRNA expression of M1 and M2 macrophage markers using quantitative PCR and assessed the protein expression of histone deacetylase 2 (HDAC2) by western blotting. RAW264.7 cells were stimulated with lipopolysaccharide or interleukin-4, and macrophage phenotypic changes after erythromycin and budesonide treatment were assessed by flow cytometry. M1/M2 macrophages were co-cultured with fibroblasts, and alpha smooth muscle actin (α-SMA) expression was detected by immunofluorescence. RESULTS:The rabbit TS model exhibited TS characterized by significant thickening of the tracheal mucosa and submucosa. These histological changes were ameliorated in the treatment groups, with the greatest improvement observed in the combination therapy group. The mRNA expression levels of iNOS, CD206, CD163, and Arg1, as well as the protein expression of HDAC2, were elevated in treated groups. In vitro, erythromycin combined with budesonide altered macrophage phenotypic distribution, with the M2/M1 ratio shifting toward 1.0. Additionally, fibroblast α-SMA expression varied according to macrophage phenotype in the co-culture system. CONCLUSION:Erythromycin combined with budesonide effectively ameliorated injury-induced TS and was associated with changes in macrophage-related markers and increased HDAC2 expression.
BackgroundClimate change has emerged as a major public health challenge, with significant implications for respiratory diseases such as asthma. Environmental factors, including air pollution, aeroallergens, and extreme weather events, are closely linked to asthma exacerbations, yet the global research landscape on this topic remains fragmented. This study aimed to systematically map research trends, hotspots, and emerging frontiers in the field of climate change and asthma over the past two decades.MethodsPublications from January 1, 2005, to March 31, 2025, were retrieved from the Web of Science Core Collection (WoSCC) using a defined search strategy. Only articles and reviews in English were included, resulting in a final dataset of 1033 publications. CiteSpace was employed for bibliometric analysis, including coauthorship, cocitation, and keyword co-occurrence mapping, as well as cluster and burst detection, to identify influential contributors, collaborative networks, and thematic evolution.ResultsAnnual publications increased steadily, peaking in 2024. The United States and China were the most prolific countries, with Harvard T.H. Chan School of Public Health, Harvard University, and Columbia University among the leading institutions. Key research hotspots included climate-related environmental exposures (e.g., PM2.5, ozone, and temperature variability), allergen dynamics (e.g., pollen, ragweed, and fungal spores), vulnerable populations (particularly children), and public health impacts. Emerging frontiers encompassed interdisciplinary integration, predictive modeling, mechanistic studies focusing on oxidative stress and immune regulation, and climate adaptation strategies. Despite progress, challenges remain in integrating asthma-specific measures into climate-health policies, conducting long-term multinational studies, and advancing translational research.ConclusionsThis bibliometric analysis provides a comprehensive overview of the global research landscape on climate change and asthma, revealing thematic evolution from allergen and epidemiological studies toward mechanistic and policy-oriented research. Strengthening interdisciplinary collaboration, enhancing global data sharing, and embedding asthma prevention into broader climate mitigation and adaptation frameworks will be critical for reducing the respiratory health burden in a changing climate.
