In 2021, the fifth edition of the World Health Organization (WHO) classification of thoracic tumors introduced a new category, “Thoracic SMARCA4-deficient undifferentiated tumor”, highlighting SMARCA4 deficiency as a key molecular marker for classifying as “other pulmonary epithelial tumors”. SMARCA4 is a gene encoding a protein involved in chromatin remodeling, and approximately 8% of non-small cell lung cancer (NSCLC) patients exhibit SMARCA4 deletions. These patients are more prone to drug resistance, early recurrence, and unfavorable clinical outcomes. Moreover, NSCLC patients with concomitant SMARCA4 mutations may not benefit from currently available treatments, underscoring the distinctiveness of this subgroup. Thoracic SMARCA4-deficient undifferentiated tumors (SMARCA4-UT) represent distinct entities from SMARCA4-deficient non-small cell lung cancer (SMARCA4-dNSCLC). This distinction is supported by their divergent pathological characteristics, demographic profiles, and survival outcomes. NSCLC cases deficient in SMARCA4 exhibit high malignancy, yet the precise biological mechanisms underlying this phenomenon remain under intensive investigation. Pathological examination and immunohistochemistry can effectively differentiate SMARCA4-UT from SMARCA4-dNSCLC. SMARCA4-UT typically manifests as adenocarcinoma or, more rarely, as squamous cell carcinoma with undifferentiated rhabdomyoblastic morphology. Therefore, elucidating the mechanisms underlying SMARCA4 alterations in NSCLC and their regulatory roles in tumorigenesis and the microenvironment is crucial. This article aims to discuss the structure, biological functions, significance in NSCLC development, and emerging potential therapeutic strategies related to SMARCA4 while providing clinical practice guidance for NSCLC patients with SMARCA4 deletions.

Limited data exists on the impact of inflammatory cells and clinical characteristics on lung function in individuals with asthma. The objective is to examine the correlation between increased inflammatory cells, asthma symptoms, and lung function in patients with asthma in a clinical setting. A retrospective cohort study was conducted on 234 individuals suspected of having asthma in Xian, China between January 2008 and December 2021. Of those, 143 patients with complete clinical feature and lung function data were enrolled to examine the relationship between increased inflammatory cells, asthma symptoms, and lung function. Basic characteristics, blood eosinophil count, blood neutrophil count, blood platelet count, blood C-reactive protein (CRP), and comprehensive lung function analysis were evaluated at each inpatient for the 143 adult asthmatics. The association between inflammatory cells and clinical parameters with pulmonary function was compared. The results of the study showed that individuals in the alcohol intake group had elevated blood eosinophil count compared to those in the non-alcohol intake group (P = 0.024). Long-acting inhaled beta 2 agonists and antibiotic therapy were associated with lower blood eosinophil count (P = 0.021 and P = 0.049, respectively) compared to other therapy. There was a independent association between blood eosinophil counts and FEV1 pre- and post-therapy in asthma but there was a markedly correlation between blood eosinophil counts and FEV1/FVC pre-and post-therapy in Asthma (P = 0.007). Blood neutrophil counts were inversely correlated with FEV1/FVC after treatment (P = 0.032). Night onset in asthma was positively correlated with blood neutrophil counts, while fever was negatively correlated with blood CRP (P = 0.028). Platelet counts >300 × 109/L after treatment were significantly associated with a decline in FEV (<0.001) in patients with asthma. Elevated blood eosinophil count was independently associated with clinical features in asthma. Based on the study's findings, there is a significant decline in FEV1/FVC among individuals with elevated blood eosinophil count, both pre- and post-bronchodilator while there was a independent relationship between blood eosinophil counts and FEV1 pre-and post-therapy in asthma. This suggests that increased levels of eosinophils may independently associated contribute to reduced lung function in asthma patients.

Background: The prognosis of ABA-HAP patients is very poor. This study aimed to develop a scoring model to predict ABA-HAP in patients with GNB-HAP. Methods: A single center retrospective cohort study was performed among patients with HAP caused by GNB in our hospital during January 2019 to June 2019 (the derivation cohort, DC). The variables were assessed on the day when qualified respiratory specimens were obtained. A prediction score was formulated by using independent risk factors obtained from logistic regression analysis. It was prospectively validated with a subsequent cohort of GNB-HAP patients admitted to our hospital during July 2019 to Dec 2019 (the validation cohort, VC). Results: The final logistic regression model of DC included the following variables: transferred from other hospitals (3 points); blood purification (3 points); risk for aspiration (4 points); immunocompromised (3 points); pulmonary interstitial fibrosis (3 points); pleural effusion (1 points); heart failure (3 points); encephalitis (5 points); increased monocyte count (2 points); and increased neutrophils count (2 points). The AUROC of the scoring model was 0.845 (95% CI, 0.796 ∼ 0.895) in DC and 0.807 (95% CI, 0.759 ∼ 0.856) in VC. The scoring model clearly differentiated the low-risk patients (the score < 8 points), moderate-risk patients (8 ≤ the score < 12 points) and high-risk patients (the score ≥ 12 points), both in DC (P < 0.001) and in VC (P < 0.001). Conclusion: This simple scoring model could predict ABA-HAP with high predictive value and help clinicians to choose appropriate empirical antibiotic therapy.

Pneumonia is a common acute infectious disease affecting the lower respiratory tract. Innate immune cells within the lungs play a crucial role in the onset and progression of pneumonia. Various multidrug-resistant bacteria have evolved multiple strategies to evade innate immunity, posing significant challenges to the treatment of pneumonia. This review primarily explores the major innate immune cells in the lungs and their functions, the immune evasion mechanisms of common multidrug-resistant bacteria, and the latest research advances in targeted innate immunity-based anti-infective therapies. This review synthesizes recent advances in the interaction between the innate immune system of the lungs and multidrug-resistant bacteria. It systematically categorizes and compares the immune evasion mechanisms of multidrug-resistant bacteria across four core pathways. This aims to provide novel insights for treating pulmonary infections caused by these multidrug-resistant pathogens.

Objective: To propose a refined CT-based phenotypic classification of pulmonary bullae and investigate the differences in demographic characteristics, morphological features, and pulmonary function among different subtypes. Methods: This retrospective study enrolled 467 patients diagnosed with pulmonary bullae who underwent chest CT at Tangdu Hospital from January 2023 to December 2024. Patients were classified into three phenotypes: bullous emphysema, intrapulmonary bullae, and subpleural bullae. Demographic data, smoking history, BMI, bulla morphology (size, number, internal septations, wall thickness, margin regularity), and pulmonary function parameters (FVC, FEV ₁ , FEV ₁ /FVC, DLCO) were collected and compared among groups. Subgroup analyses were performed based on smoking status, BMI level, and COPD status. Results: Significant intergroup differences were observed in age, BMI, and smoking history ( P < 0.05). Patients with bullous emphysema were older, had lower BMI, and higher smoking rates. Morphologically, the bullous emphysema group exhibited significantly greater maximum bulla length, width, and surface area compared to the other two groups ( P < 0.05). Smoking was associated with larger bullae, higher proportions of internal septations and thick walls, and fewer regular margins ( P < 0.05). Low BMI patients (BMI < 23.03 kg/m ² ) demonstrated larger bullae with more complex morphology compared to high BMI patients ( P < 0.05). Functionally, the bullous emphysema group had significantly lower FEV ₁ , FEV ₁ % predicted, FEV ₁ /FVC, and DLCO% predicted ( P < 0.05). Patients with COPD ( n = 83) showed larger bullae and lower proportions of regular margins and internal septations compared to non-COPD patients ( P < 0.05). Conclusion: CT-based phenotyping of pulmonary bullae reveals distinct demographic, morphological, and functional profiles. Bullous emphysema is associated with more severe morphological abnormalities and pulmonary function impairment. Smoking and low BMI are modifiable factors promoting bulla progression. This classification provides a foundation for personalized clinical surveillance and intervention strategies.