Clinical Respiratory Journal最新文献

Background

Children with asthma living in highly polluted megacities are at increased risk of poor asthma control and airway inflammation. Breastfeeding has immunomodulatory effects, but its potential to buffer pollution-related inflammation remains understudied.

Objective

To evaluate whether breastfeeding duration is associated with asthma control and airway eosinophilic inflammation (FeNO), and whether it modifies the impact of urban air pollution in children with asthma living in Mexico City.

Methods

We conducted a multicenter retrospective study (2022–2025) including children aged 6–17 years with physician-diagnosed asthma. Asthma control (ACT), airway inflammation (FeNO, NIOX VERO), breastfeeding duration (0–12 months), and borough-level pollution categories (high/medium/low) were evaluated. Multivariable logistic and linear regression models assessed associations and breastfeeding × pollution interactions.

Results

A total of 162 children were included (mean age 10.8 years; 51.2% female). Breastfeeding ≥ 6 months was associated with better asthma control (ACT ≥ 20: OR 2.1; 95% CI 1.3–3.5) and significantly lower FeNO (β −0.24; p < 0.01). High-pollution residence was linked to lower ACT scores and higher FeNO (both p < 0.01). A significant interaction indicated that breastfeeding ≥ 6 months attenuated the detrimental effect of pollution on airway inflammation and asthma control (p for interaction < 0.05).

Conclusions

Prolonged breastfeeding was independently associated with improved asthma control and reduced airway eosinophilic inflammation, partially mitigating the respiratory burden of chronic pollution exposure.

Clinical Implications

Breastfeeding may serve as an accessible, low-cost protective strategy for children with asthma living in polluted urban environments, supporting its integration into respiratory health policies and early-life preventive care.

Background

Noninvasive ventilation (NIV) is the treatment of choice in cases of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). However, depressed mental status, frequently caused by AECOPD, represents a relative contraindication to NIV. This study evaluates the efficacy of NIV in patients with AECOPD with moderate to severe impairment of consciousness.

Methods

In this monocentric, retrospective study, we included patients admitted to the emergency department (ED) from January 2018 to December 2022 for AECOPD, altered mental status (GCS ≤ 13 and/or KMS ≥ 2) and treated with NIV.

Results

Out of 919 patients admitted with acute respiratory failure, 228 (24.8%) met the inclusion criteria for AECOPD. Of these, 205 (90%) underwent NIV during the ED admissions without adverse events. In 48 patients (21.1%), NIV was withdrawn due to clinical improvement. Only 23 (10.1%) experienced NIV failure with worsening of hypoxemia and occurrence of hypotension, of whom 16 (7% of the total population) died in the ED. Severe neurological impairment (low GCS) was an independent predictor of mortality. Systolic and diastolic blood pressure, SpO₂, pH value and lactate levels were predictive of early mortality. COVID-19 status did not significantly affect mortality rates.

Conclusion

NIV was feasible and associated with successful outcomes in a majority of patients with AECOPD and moderate to severe neurological impairment. Specific parameters, including initial GCS, blood pressure, SpO₂, and blood gas profiles, can help predict outcomes and treatment efficacy.

Introduction

Thoracic SMARCA4-deficient undifferentiated tumors (SMARCA4-UT) are rare and aggressive epithelioid neoplasms characterized by the loss of the SMARCA4 gene. These tumors are typically diagnosed at advanced stages and exhibit a dismal prognosis. Currently, there are no standardized treatment protocols or approved targeted therapies.

Methods

We present a case series of nine patients diagnosed of thoracic SMARCA4-UT, detailing demographic, pathological, imaging, and treatment data. Moreover, a comprehensive literature review and genomic analysis of SMARCA4 mutations in lung cancer were also performed.

Results

The cohort comprised predominantly male smokers (mean age: 63.0 ± 9.6 years). All cases exhibited loss of BRG1 expression, with negative staining for TTF-1 and p40, while SMARCB1/INI-1 expression was preserved. Patients showed poor responses to conventional chemotherapy but demonstrated partial responsiveness to immunotherapy or targeted agents. Genomic analysis of SMARCA4 mutations in lung cancer demonstrates that SMARCA4 mutations, primarily located in the SNF2-related and helicase conserved C-terminal domains, are associated with a poorer prognosis in lung cancer.

Conclusion

Immunotherapy and targeted therapies show promise in managing thoracic SMARCA4-UT, warranting further investigation. Further exploring the genetic and molecular landscape of this tumor might reveal potential therapeutic targets.

Background

Traditional biometric systems are vulnerable to forgery, highlighting the need for secure alternatives. Electroencephalography (EEG) offers inherent advantages in liveness detection and antispoofing but typically requires external stimuli. We propose a novel paradigm leveraging intrinsic respiratory-evoked EEG signals for identity authentication, with potential applications in clinical settings where unobtrusive monitoring is critical.

Methods

We developed a 64-channel EEG acquisition system with synchronized respiratory event monitoring. Thirteen healthy volunteers performed four breathing patterns: oral, nasal, slow nasal, and rapid nasal breathing. A hybrid deep learning model was designed to optimize spatial–temporal feature extraction from EEG signals.

Results

The model achieved 98.3% accuracy in identity recognition using rapid nasal breathing-evoked EEG, outperforming traditional biometric methods. Nasal breathing patterns consistently yielded higher accuracy than oral breathing, with rapid nasal breathing showing the strongest discriminative power.

Conclusions

Respiratory-evoked EEG signals provide a viable, noninvasive biometric identifier. The high accuracy of rapid nasal breathing opens avenues for clinical integration, such as continuous patient authentication in respiratory monitoring devices or secure access to electronic health records.

Objective

Continuous positive airway pressure (CPAP) therapy for obstructive sleep apnea (OSA) results in a modest reduction in blood pressure. This study aimed to identify parameters from 24-h ambulatory blood pressure monitoring (ABPM) that are predictive of treatment response.

Methods

Treatment-naïve patients with OSA were prospectively recruited from the Centre for Sleep Medicine and Science at Beijing Anzhen Hospital between July 2023 and April 2025. All participants underwent 24-h ABPM assessments before and after 3-month CPAP therapy. Correlations between the baseline ABPM data and post-CPAP changes in blood pressure were analyzed. Multivariate analysis was used to determine whether specific baseline blood pressure cutoffs independently predicted a clinically significant reduction in blood pressure.

Results

Good CPAP adherence (median usage: 6.1 h/night and 6.0 days/week; residual apnea–hypopnea index: 1.7 events/h) was achieved among 51 recruited patients (92.2% male, median age 40.5 years). After 3 months of CPAP treatment, significant reductions were observed in nearly all blood pressure measurements. Baseline 24-h mean arterial pressure (MAP) was positively correlated with the reduction in all 24-h blood pressure measures, all nighttime blood pressure measures, and daytime MAP. Compared with patients with 24-h MAP < 96 mmHg, those with baseline 24-h MAP ≥ 96 mmHg experienced relatively high absolute and relative reductions in all blood pressure measures.

Conclusions

Baseline 24-h MAP effectively predicts blood pressure reduction following CPAP therapy in patients with OSA, demonstrating the clinical value of an ABPM-guided strategy for managing patients with comorbid OSA and hypertension.

Trial Registration: ChiCTR2300067728

Background

Preserved ratio impaired spirometry (PRISm) is associated with elevated cardiovascular disease (CVD) risk and progression to COPD, but the underlying mechanisms remain unclear. Frailty is known to worsen outcomes in COPD; however, its role in PRISm has not been well defined. This study examined factors associated with cardiovascular events and mortality in PRISm and developed risk models.

Methods

We analyzed 8882 adults (aged 20–79 years) from NHANES 2007–2012, identifying 763 (8.6%) with PRISm (FEV₁/FVC ≥ 0.70 and FEV₁ < 80% predicted). Frailty was assessed using the 23-item laboratory frailty index (FI-LAB; cut-off ≥ 0.23). The primary outcome was all-cause mortality, obtained from linked National Death Index records; the secondary outcome was major adverse cardiovascular events (MACEs: myocardial infarction, stroke, heart failure, or angina), assessed cross-sectionally. LASSO regression and multivariable logistic/Cox models were used to identify variables independently associated with the outcomes, and nomograms were constructed.

Results

PRISm participants had higher frailty prevalence (53.9% vs. 45.5%) and more MACEs (16.2% vs. 6.0%) than those with normal spirometry (both p < 0.0001). Frailty was independently associated with prevalent MACEs (adjusted OR = 18.87, p < 0.001) and was bidirectionally associated with PRISm (OR = 1.40, p < 0.001). Key factors independently associated with MACEs included frailty index, age, sex, anemia, and emphysema (AUC = 0.786). Over 9.9 years, mortality was higher in frail vs. non-frail PRISm individuals (15.2% vs. 7.0%; adjusted HR = 30.66). Frailty severity demonstrated a clear mortality gradient, and a mortality nomogram integrating age and frailty achieved an AUC of 0.81.

Conclusion

Frailty is strongly and independently associated with cardiovascular morbidity and mortality. FI-LAB offers a practical tool for risk stratification and may help guide targeted preventive strategies.

Objective

It was found that the levels of antineutrophil cytoplasmic antibodies (ANCA) are elevated and linked to disease severity of bronchiolitis obliterans (BO) in children. This study aims to explore the mechanism of ANCA in the process of BO.

Methods

Plasma from BO patients (n = 40) and healthy controls (n = 11) was analyzed for ANCA and neutrophil extracellular traps (NETs) components. Plasma IgG from ANCA-positive BO children and normal controls were used to stimulate neutrophils, measuring reactive oxygen species (ROS) and NETs production. Small airway epithelial cells (SAECs) were exposed to NETs, assessing viability by CCK8 and cytokine release by ELISA. The IgG treated neutrophils were co-cultured with SAECs, and cytokines were measured by ELISA.

Results

The levels of ANCA and NETs components including dsDNA, neutrophil elastase (NE) and myeloperoxidase (MPO) in the plasma of BO children were significantly higher than those of healthy controls. ANCA-positive IgG induced neutrophils produce ROS and NETs. The cell viability of SAECs was significantly reduced upon treatment with NETs in a concentration-dependent manner. The levels of IL-8, IL-17, TNF-α, and TGF-β secreted by SAECs treated with NETs were increased significantly, and the degree of increase was positively correlated with the concentration of NETs. The co-culture of neutrophils stimulated by ANCA IgG with SAECs significantly increased the expression of cytokines including IL-8, IL-17, TNF-α, and TGF-β.

Conclusions

NETs induced by ANCA may exacerbate airway inflammation in children with BO.