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Background: Exudative pleural effusion (EPE) is one of the common pleural manifestations of various diseases. Differential diagnosis of EPE is imperative clinically as it identifies different causes of EPE, thereby, enabling effective treatments. Thoracoscopy is a useful tool for differential diagnosis of EPE; however, some patients refuse thoracoscopic examination due to its invasive nature. In addition, the specificity and sensitivity of existing routine tests of EPE are unsatisfactory. Therefore, there is a great need to establish an effective method for the differential diagnosis of EPE.Methods: This study was a single-institution retrospective analysis of diagnostic efficiency of C-reactive protein (CRP) and procalcitonin (PCT) between March 2018 and September 2018. A total of 87 patients diagnosed with EPE were enrolled. All participants underwent diagnostic thoracentesis. The EPE was examined using biochemical, routine, microbiological, and cytological methods. Pathological cytology detection was necessary for those suspected of malignant PE. Benign PE originates in patients with pneumonia, empyema, and tuberculosis. The levels of CRP and PCT in EPE and serum were measured before treatment.Correlation analysis and receiver-operating characteristic (ROC) curve analysis were conducted to determine the underlying relationship between levels of CRP and PCT, and for differential diagnosis. Results:The ROC analysis showed that the sensitivity and specificity for the analysis of pleural fluid CRP (p-CRP) were higher (cut-off: 17.55 pg/mL; sensitivity: 75.00%, specificity: 83.90%) than that of serum CRP (s-CRP, cut-off: 23.90 pg/mL; sensitivity: 71.00%, specificity: 80.4%) in the differential diagnosis for EPE. However, the analysis of pleural fluid PCT (p-PCT) and serum PCT (s-PCT) did not demonstrate correlations with EPE. Combined analysis of p-CRP (cut-off: 17.55 mg/dL) with s-CRP (cut-off: 23.9 pg/mL) showed the highest diagnostic accuracy (88.4%) in diagnosing infectious EPE. Conclusions:The data support the close relationship between combined analysis of p-CRP with s-CRP and effective and accurate differential diagnosis of EPE, due to its higher sensitivity and specificity. However, as a highly sensitive marker for diagnosing bacterial infections, neither s-PCT nor p-PCT, showed correlations with the differential diagnosis of EPE.

Background Homologous recombination deficiency (HRD) is a well‐known biomarker which could predict poly‐ADP ribose polymerase 1 (PARP) inhibitor and platinum drug response. As an aggressive cancer, small‐cell lung cancer (SCLC) is sensitive to platinum drugs, but relapse occurs rapidly. Herein, we aim to illustrate the genomic alteration patterns of homologous recombination repair (HRR)‐related genes in a Chinese SCLC cohort and further analyze the relationship among HRR gene mutations and known biomarkers of immune checkpoint inhibitor (ICI) response, including tumor mutation burden (TMB) and programmed cell death‐ligand 1 (PD‐L1) expression. Methods Next‐generation sequencing (NGS)‐based target capture sequencing of 543 cancer‐related genes was performed to analyze the genomic profiles of 133 Chinese SCLC patients, and TMB was calculated. PD‐L1 expression was evaluated in 90 out of 133 patients using the SP142 PD‐L1 immunohistochemistry assay. Results Among the 133 patients with SCLC, 47 (35.3%) had HRR gene mutations. ATM (8.3%) was the most frequently mutated HRR gene in the cohort, followed by NBN (4.5%). Pathogenic somatic and germline mutations of HRR genes were identified in 11 (23.4%) and 4 (8.5%) patients, respectively. HRR gene mutations cooccurred with KMT2D gene mutations. There were several differences in genomic alterations between patients with HRR gene mutations (HRR‐Mut) and without HRR mutations (HRR‐WT). The results revealed that TP53 and RB1 were commonly mutated genes in both groups. Mutations in the KMT2D gene and genes in the RTK‐RAS pathway occurred more frequently in the HRR‐Mut group. Furthermore, we found that mutations in HRR genes were associated with high TMB (Wilcoxon, p = 0.048), but there was no correlation of HRR gene mutation status with PD‐L1 expression. Conclusions We exhaustively describe the genomic alteration profile of Chinese SCLC patients and provide further evidence that HRR gene mutations are prevalent in SCLC patients.

Background: Pulmonary rehabilitation (PR) is a widely recognized nonpharmacologic therapy for chronic obstructive pulmonary disease (COPD), but most of the current studies on whether PR can benefit COPD patients are based on the evaluation of symptoms and pulmonary function, which is limited to a certain extent. Because COPD is characterized by potential regional lung changes in morphology and pathophysiology, this study was designed to evaluate the effects of individualized PR on regional lung function in patients with stable COPD.Methods: In this study, patients with stable COPD who met the criteria were included, and they were treated with PR for 2 weeks using the respiratory rehabilitation training instrument. The symptoms, and global and regional lung function before and after 2 weeks of PR treatment were evaluated using surveys, spirometry, and electrical impedance tomography (EIT), respectively. The spatial coefficient of variation (CV) of regional spirometry parameters were calculated to quantify spatial heterogeneity of lung function.Temporal inhomogeneity was determined by the regional expiration time.Results: A total of 34 participants were recruited in this study, of whom 24 completed the PR. After 2 weeks of intervention, the modified Medical Research Council (mMRC) dyspnea scale and the COPD assessment test (CAT) score was significantly lower compared to those measured before the treatment (2.3±1.17 vs. 2.1±0.93, P=0.034; and 15.0±7.18 vs. 10.9±6.06, P<0.001, respectively). Global spirometry forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), FEV1 predicted percentage (%pred), and peak expiratory flow (PEF) were significantly better than they were pre-rehabilitation (2.1±0.86 vs.