A Comparison of Inflammatory Responses Between Robotically Enhanced Coronary Artery Bypass Grafting and Conventional Coronary Artery Bypass Grafting: Implications for Hybrid Revascularization.

OBJECTIVE: The inflammatory response elicited by robotically enhanced coronary artery bypass grafting (r-CABG) has not been well described. When r-CABG is performed as part of hybrid coronary revascularization, the inflammatory milieu and the timing of percutaneous coronary intervention may affect the stent patency negatively in the short and long term. The goal of this study was to describe the extent and time course of cytokine release after r-CABG compared with conventional CABG (c-CABG) and to elucidate the optimal timing for r-CABG in the setting of hybrid coronary revascularization for a future study. DESIGN: Prospective, observational study. SETTING: Tertiary-care center in a university hospital. PARTICIPANTS: The study comprised patients scheduled to undergo r-CABG or c-CABG from October 2012 to November 2014. INTERVENTIONS: Cytokine levels of interleukin (IL)-6, IL-8, IL-10; tumor necrosis factor-α; and C-reactive protein (CRP) were measured at the following time points: preprocedure; at the end of the procedure; and at 4, 8, 12, 24, and 48 hours after the procedure. MEASUREMENTS AND MAIN RESULTS: Twenty-eight patients undergoing r-CABG and 10 patients undergoing c-CABG were enrolled. The levels of cytokines after r-CABG and c-CABG were compared using the mixed-effect linear regression model for longitudinal data. Cytokine release in the r-CABG group was comparatively less for IL-6, IL-10, tumor necrosis factor, and CRP levels. They all trended toward the baseline by the 48th hour in both groups, except CRP levels, which reached their peak at 48 hours in both groups. CONCLUSIONS: The inflammatory response to r-CABG was blunted compared with that of c-CABG. The high CRP levels on the second postoperative day after r-CABG were a cause for concern in regard to percutaneous coronary intervention performed at that time period, but additional studies are necessary.

miR-8 modulates cytoskeletal regulators to influence cell survival and epithelial organization in Drosophila wings.

The miR-200 microRNA family plays important tumor suppressive roles. The sole Drosophila miR-200 ortholog, miR-8 plays conserved roles in Wingless, Notch and Insulin signaling - pathways linked to tumorigenesis, yet homozygous null animals are viable and often appear morphologically normal. We observed that wing tissues mosaic for miR-8 levels by genetic loss or gain of function exhibited patterns of cell death consistent with a role for miR-8 in modulating cell survival in vivo. Here we show that miR-8 levels impact several actin cytoskeletal regulators that can affect cell survival and epithelial organization. We show that loss of miR-8 can confer resistance to apoptosis independent of an epithelial to mesenchymal transition while the persistence of cells expressing high levels of miR-8 in the wing epithelium leads to increased JNK signaling, aberrant expression of extracellular matrix remodeling proteins and disruption of proper wing epithelial organization. Altogether our results suggest that very low as well as very high levels of miR-8 can contribute to hallmarks associated with cancer, suggesting approaches to increase miR-200 microRNAs in cancer treatment should be moderate.