Background: There have been many studies on the effectiveness and complications of airway stent, but few had focused on factors that affect survival after stent placement. This study intended to assess the factors associated with the survival in patients with malignant central airway obstruction (MCAO) after airway metallic stent placement. Methods: The clinical data of adult MCAO patients who underwent stent placement form February 2003 to June 2017 in the First Affiliated Hospital of Soochow University in China were retrospectively analyzed.The survival rates were compared using Log-rank tests. Potential prognostic factors were identified using multivariate Cox hazard regression models. Results: Total 102 MCAO patients were included in this study. The median survival time of these patients after airway metallic stent placement was 4.1 months. Multivariate analysis showed that MCAO patients receiving radiotherapy [hazard ratio (HR) 0.554; 95% confidence interval (CI): 0.308-0.999] or chemoradiotherapy (HR 0.251; 95% CI: 0.126-0.499) after stenting had better prognosis. However, ECOG PS ≥3 score prior to the stenting (HR 2.193; 95% CI: 1.364-3.526) and stents placed in both trachea and main bronchus (HR 2.458; 95% CI: 1.384-4.366) were associated with worse survival.Conclusions: In our results, survival of MCAO patients after airway metallic stenting was related to ECOG PS score prior to the stenting, the site of stent placement and we have hereby proposed for the first time that having opportunity to receive radiotherapy or chemoradiotherapy after stenting contribute to better prognosis.

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ObjectData on the characteristics and related factors of fungal empyema thoracis (FET) are limited. Our aim is to investigate the clinical characteristics and related factors of FET.MethodsWe conducted a retrospective study of patients with positive culture from pleural effusion who were admitted to the First Affiliated Hospital of Soochow University between January 2007 and January 2018. The clinical and laboratory characteristics of all study participants were collected. Logistic regression models were used to assess the related factors of FET.ResultsThere were 30 patients diagnosed with FET. The median age of patients with FET was 62.7 years old and 24 (80.0%) were male. The most frequent pathogens of FET were Candida albicans (55.9%). Diabetes mellitus (23.3% vs. 7.9%, P = 0.019) and upper gastrointestinal tract perforation or rupture (20.0% vs. 2.1%, P < 0.001) were associated with increased risk of FET. The adjusted odds ratios (95% confident interval) were 3.11 (1.02–9.56) for diabetes mellitus and 12.71 (3.47–46.55) for upper gastrointestinal tract perforation or rupture. There were 10 deaths (33.3%) among FET patients after one-year of follow-up.ConclusionsDiabetes mellitus and upper gastrointestinal tract perforation or rupture were associated with increased risk of FET.

Background Forkhead box L2 (FOXL2) has been recognized as a transcription factor in the progression of many malignancies, but its role in non‐small cell lung cancer (NSCLC) remains unclear. This research clarified on the role of FOXL2 and the specific molecular mechanism in NSCLC. Methods RNA and protein levels were detected by quantitative real‐time polymerase chain reaction (qRT–PCR) and western blotting assays. Cell proliferation was examined by cell counting kit‐8 (CCK‐8) and clonogenic assays. Transwell and wound healing assays were used to detect cell invasion and migration. Cell cycle alterations were assessed by flow cytometry. The relationship between FOXL2 and miR‐133b was verified by dual‐luciferase reporter assays. In vivo metastasis was monitored in the tail vein‐injected mice. Results FOXL2 was upregulated in NSCLC cells and tissues. Downregulation of FOXL2 restrained cell proliferation, migration, and invasion and arrested the cell cycle of NSCLC cells. Moreover, FOXL2 promoted the epithelial–mesenchymal transition (EMT) process of NSCLC cells by inducing the transforming growth factor‐β (TGF‐β)/Smad signaling pathway. miR‐133b directly targeted the 3′‐UTR of FOXL2 and negatively regulated FOXL2 expression. Knockdown of FOXL2 blocked metastasis in vivo. Conclusions miR‐133b downregulates FOXL2 by targeting the 3′‐UTR of FOXL2, thereby inhibiting cell proliferation, EMT and metastasis induced by the TGF‐β/Smad signaling pathway in NSCLC. FOXL2 may be a potential molecular target for treating NSCLC.