671 research outputs found
Development of High Performance Firefighting Gloves Prototype Applied to Ergonomic Design
The aim of this paper is to clarify firefighters’ design needs for their firefighting gloves and to determine ergonomic design elements which could provide the best compromise between protection and comfort
Diesel exhaust particles increase IL-1β-induced human β-defensin expression via NF-κB-mediated pathway in human lung epithelial cells
BACKGROUND: Human β-defensin (hBD)-2, antimicrobial peptide primarily induced in epithelial cells, is a key factor in the innate immune response of the respiratory tract. Several studies showed increased defensin levels in both inflammatory lung diseases, such as cystic fibrosis, diffuse panbronchiolitis, idiopathic pulmonary fibrosis and acute respiratory distress syndrome, and infectious diseases. Recently, epidemiologic studies have demonstrated acute and serious adverse effects of particulate air pollution on respiratory health, especially in people with pre-existing inflammatory lung disease. To elucidate the effect of diesel exhaust particles (DEP) on pulmonary innate immune response, we investigated the hBD-2 and interleukin-8 (IL-8) expression to DEP exposure in interleukin-1 beta (IL-1β)-stimulated A549 cells. RESULTS: IL-1β markedly up-regulated the hBD-2 promoter activity, and the subsequent DEP exposure increased dose-dependently the expression of hBD-2 and inflammatory cytokine IL-8 at the transcriptional level. In addition, DEP further induced the NF-κB activation in IL-1β-stimulated A549 cells more rapidly than in unstimulated control cells, which was showed by nuclear translocation of p65 NF-κB and degradation of IκB-α. The experiment using two NF-κB inhibitors, PDTC and MG132, confirmed that this increase of hBD-2 expression following DEP exposure was regulated through NF-κB-mediated pathway. CONCLUSION: These results demonstrated that DEP exposure increases the expression of antimicrobial peptide and inflammatory cytokine at the transcriptional level in IL-1β-primed A549 epithelial cells and suggested that the increase is mediated at least partially through NF-κB activation. Therefore, DEP exposure may contribute to enhance the airway-responsiveness especially on the patients suffering from chronic respiratory disease
Analysis of different tumor volume thresholds of insignificant prostate cancer and their implications for active surveillance patient selection and monitoring
PurposeWe compared oncological outcomes according to tumor volume (TV) thresholds defining both classical and updated insignificant prostate cancer (IPC), since the TV threshold can be used as clinical parameter for active surveillance.MethodsBetween 2001 and 2012, we retrospectively analyzed 331 organ-confined prostate cancer patients who had preoperative Gleason score 6, preoperative PSA under 10 ng/mL and pathologic TV less than 1.3 mL. Among them, 81 of 331 (24.5%) had Gleason grade 4/5 disease postoperatively. Patients were stratified into two groups: (1) TV less than 0.5 mL, using the classical definition; and (2) TV between 0.5 mL and 1.3 mL, using the range of updated definition. We compared biochemical recurrence (BCR)-free survival and identified independent predictors of BCR in each group.ResultsGroup 2 had more Gleason grade 4/5 disease than group 1 (P<0.001). On multivariate analysis, Gleason grade 4/5 disease was not associated with BCR in group 1 (P=0.132). However, it was an independent predictor for BCR in group 2 (P=0.042). BCR-free survival were not significantly different according to the presence of Gleason grade 4/5 disease in group 1 (P=0.115). However, in group 2, it was significantly different according to the presence of Gleason grade 4/5 disease (P=0.041).ConclusionsAlthough the TV thresholds of the two definitions of IPC vary only slightly, this difference was enough to result in different clinical course if Gleason grade 4/5 disease was present. Therefore, the updated IPC TV threshold should be carefully applied as clinical parameter for active surveillance
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