2 [95% CI: 1.3-3.6]; P = 0.002), infectious (OR 1.7 [95% CI: 1.1-2.7]; P = 0.01), cardiovascular (OR 2.4 [95% CI: 1.2-4.8]; P = 0.01), renal (OR 2.3 [95%

CI: 1.5-3.5]; P < 0.00,001), neurological (OR 4.3 [95% CI: 1.3-17.7]; P = 0.005), and pain (OR 1.8 [95% CI: 1.03-3.1]; P = 0.04) morbidities. Further stratification of CKD revealed preoperative eGFR <= 50 mL/min/1.73 m2 to be associated with more frequent morbidity and longer hospital stay, independent of age. Multiple regression analysis identified CKD (P = 0.006) and Proton Pump inhibitor congestive cardiac failure (P = 0.002) as preoperative factors associated with prolonged hospital stay.\n\nCONCLUSIONS: A substantial minority of patients with CKD undergoing elective orthopedic procedures are at increased risk of prolonged morbidity and hospital stay. Preoperative eGFR may enhance perioperative risk stratification beyond traditional risk factors. (Anesth Analg 2011;112:1375-81)”
“Objective. ICG-001 manufacturer MicroRNA have recently been identified as regulators that modulate target gene expression and are involved in shaping the immune response. This study was undertaken to investigate the contribution of microRNA-146a (miR-146a), which was identified in the pilot expression profiling step, to the pathogenesis of systemic lupus erythematosus

(SLE).\n\nMethods. TaqMan microRNA assays of peripheral blood leukocytes were used for comparison of expression levels of microRNA between SLE patients and controls. Transfection and stimulation of cultured cells were conducted to determine the biologic function of miR-146a. Bioinformatics prediction and validation by reporter gene assay and Western blotting ACY-241 cost were performed to identify miR-146a targets.\n\nResults. Profiling of 156 miRNA in SLE patients revealed the differential expression of multiple microRNA, including miR-146a, a

negative regulator of innate immunity. Further analysis showed that underexpression of miR-146a negatively correlated with clinical disease activity and with interferon (IFN) scores in patients with SLE. Of note, overexpression of miR-146a reduced, while inhibition of endogenous miR-146a increased, the induction of type I IFNs in peripheral blood mononuclear cells (PBMCs). Furthermore, miR-146a directly repressed the transactivation downstream of type I IFN. At the molecular level, miR-146a could target IFN regulatory factor 5 and STAT-1. More importantly, introduction of miR-146a into the patients’ PBMCs alleviated the coordinate activation of the type I IFN pathway.\n\nConclusion. The microRNA miR-146a is a negative regulator of the IFN pathway. Underexpression of miR-146a contributes to alterations in the type I IFN pathway in lupus patients by targeting the key signaling proteins. The findings provide potential novel strategies for therapeutic intervention.