Background: To investigate the related risk factors of postoperative nosocomial pneumonia (POP) in patients withⅠ-Ⅲa lung cancer. Methods: Medical records of 511 patients who underwent resection for lung cancer between January 2012 to December 2012 were retrospectively reviewed. Risk factors of postoperative pneumonia were identified and evaluated by univariate and multivariate analyses. Results: The incidence of postoperative pneumonia in these lung cancer patients was 2.9% (15 cases). Compared with 496 patients who had no pneumonia infection after operation, older age (>60), histopathological type of squamous cell carcinoma and longer surgery time (>3h) were significant risk factors by univariate analysis. Other potential risk factors such as alcohol consumption, history of smoking, hypersensitivity, hypertension, diabetes mellitus and so on were not showed such significance in this study. Further, the multivariate analysis revealed that old age (>60 years) (OR 5.813, p=0.018) and histopathological type of squamous cell carcinoma (OR 5.831, p<0.001) were also statistically significant independent risk factors for postoperative pneumonia. Conclusions: This study demonstrated that being old aged (>60 years) and having squamous cell carcinoma histopathological type might be important factors in determining the risk of postoperative pneumonia in lung cancer patients after surgery.
Background/Aims: The study was designed to explore the potential relationship of TLR4 and endothelial PAS domain-containing protein 1 (EPAS1) in vivo and vitro experiments. Methods: Bronchoalveolar lavage fluid (BALF) samples were collected from 55 chronic obstructive pulmonary disease (COPD) patients and 25 healthy subjects. The differential cell count was performed using Wright-Giemsa staining. The expression levels of TLR4 and TLR5 were detected by RT-qPCR. The levels of methylation and mRNA expression of EPAS1 were assayed by bisulfite sequencing PCR and real-time PCR. The correlation of TLR4 and EPAS1 was also analyzed in TLR 4-overexpressing endothelial cells. Results: The results showed that the number of neutrophils, lymphocytes and macrophages and expression of TLR 4 were significantly increased in lower respiratory tract of COPD patients. Moreover, decreased EPAS1 mRNA and increased EPAS1 promoter methylation were detected in COPD, which were closely associated with increased TLR4 expression. According to in vitro experiments, TLR 4 inhibited EPAS1 mRNA expression and promoted promoter methylation in endothelial cells. Conclusion: These findings suggest that TLR4 over-expression decreased EPAS1expression which contributes to the progress of COPD.
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