ABSTRACT
Severe community-acquired pneumonia (SCAP) in elderly has more atypical clinical presentation compared to younger patients. Timely recognition could improve clinical care. This study investigated the value of soluble urokinase-type plasminogen activator receptor (suPAR) on severity assessment and outcome prediction in elderly patients with CAP. We conducted a prospective, observational study between January 2014 and December 2016. A total of 230 patients ≥65 were enrolled in this study, of which 151 were CAP and 79 were SCAP. Serum suPAR levels were determined by ELISA essays within 24 h after hospitalization. Thirty-day and 1-year mortalities were recorded as outcomes. Serum suPAR level was significantly increased in patients with SCAP. Positive correlation was found between suPAR levels with CURB-65 and PSI score (r = 0.423 and r = 0.489; p < .001 for both). The AUC for suPAR to discriminate SCAP patients from CAP was 0.783 at a cut-off value 4.27 ng/mL. AUCs of suPAR for predicting 30-day and 1-year mortalities were 0.815 (95% CI 0.746-0.866) and 0.820 (95% CI 0.770-0.870). Regression result shows suPAR (≥8.92 ng/mL) was independent factor for 30-day mortality (HR = 2.83, 95% CI 1.04-7.69) and suPAR with cut-off value 6.18 ng/mL could predict 1-year mortality (HR = 2.44, 95% CI 1.09-5.44). suPAR was strongly associated with CAP severity and could be a prognostic indicator for 1-year survival in elderly.
Subject(s)
Community-Acquired Infections/blood , Pneumonia/blood , Receptors, Urokinase Plasminogen Activator/blood , Aged , Aged, 80 and over , Biomarkers/blood , Community-Acquired Infections/mortality , Enzyme-Linked Immunosorbent Assay , Female , Humans , Male , Pneumonia/mortality , Prognosis , Prospective Studies , Severity of Illness Index , Survival AnalysisABSTRACT
BACKGROUND/AIMS: The polycomb protein Bmi-1 plays oncogenic roles in various cancers. Here we aimed to investigate the contribution of Bmi-1 on the malignant behaviors of pancreatic cancer such as chemoresistance, invasion and tumorigenesis. METHODS AND RESULTS: The MTT cell proliferation assay showed that shRNA mediated Bmi-1 knockdown and enhanced the chemosensitivity of pancreatic cancer cells to gemcitabine. The transwell invasion assay showed that Bmi-1 knockdown inhibited the invasion of pancreatic cancer cells in vitro. Notably, the reduced abilities of chemoresistance and invasion were associated with the transition from the mesenchymal phenotype to the epithelial phenotype of pancreatic cancer cells. Moreover, Bmi-1 knockdown led to the inhibition of the PI3K-Akt pathway and disrupted the sphere-forming abilities of pancreatic cancer cells. A nude mouse xenograft experiment demonstrated that pancreatic cancer cells depleted of Bmi-1 showed weak tumorigenicity in vivo. CONCLUSION: Our data suggest that Bmi-1 plays an important role in the progression of pancreatic cancer and represents a novel target for antitumor therapy of pancreatic cancer.
