Enumerating pelvic recurrence following radical cystectomy for bladder cancer: A canadian multi-institutional study

Introduction: We aimed to enumerate the rate of pelvic recurrence following radical cystectomy at university-affiliated hospitals in Canada. Methods: Canadian, university-affiliated hospitals were invited to participate. They were asked to identify the first 10 consecutive patients undergoing radical cystectomy starting January 1, 2005, who had urothelial carcinoma stages pT3/T4 N0-2 M0. The first 10 consecutive cases starting January 1, 2005 who met these criteria were the patients submitted by that institution with information regarding tumour stage, age, number of nodes removed, and last known clinical status in regard to recurrence and patterns of failure. Results: Of the 111 patients, 80% had pT3 and 20% pT4 disease, with 62% being node-negative, 14% pN1, and 27% pN2; 57% had 10 or more nodes removed. Cumulative incidence of pelvic relapse was 40% among the entire group Conclusions: This review demonstrates a high rate of pelvic tumour recurrence following radical cystectomy for pT3/T4 urothelial cancer

Niacin Ameliorates Neuro-Inflammation in Parkinson’s Disease via GPR109A

In this study, we used macrophage RAW264.7 cells to elucidate the molecular mechanism underlying the anti-inflammatory actions of niacin. Anti-inflammatory actions of niacin and a possible role of its receptor GPR109A have been studied previously. However, the precise molecular mechanism of niacin’s action in reducing inflammation through GPR109A is unknown. Here we observed that niacin reduced the translocation of phosphorylated nuclear kappa B (p-NF-κB) induced by lipopolysaccharide (LPS) in the nucleus of RAW264.7 cells. The reduction in the nuclear translocation in turn decreased the expression of pro-inflammatory cytokines IL-1β, IL-6 in RAW264.7 cells. We observed a decrease in the nuclear translocation of p-NF-κB and the expression of inflammatory cytokines after knockdown of GPR109A in RAW264.7 cells. Our results suggest that these molecular actions of niacin are mediated via its receptor GPR109A (also known as HCAR2) by controlling the translocation of p-NF-κB to the nucleus. Overall, our findings suggest that niacin treatment may have potential in reducing inflammation by targeting GPR109A