Platelet FcγRIIa expression in patients with stable coronary artery disease.

OBJECTIVES: FcÉ£RIIa amplifies platelet activation and greater expression increases platelet reactivity. In patients with myocardial infarction (MI), high platelet FcÉ£RIIa identifies patients with an approximately 4-fold greater risk of MI, stroke, and death. We compared platelet FcÉ£RIIa in 2 groups: (1) patients who had not had an MI in the previous year and were undergoing cardiac catheterization and percutaneous coronary intervention (PCI) labeled as stable coronary artery disease (CAD), and (2) previously obtained results in patients with MI (n = 197). METHODS: Patients undergoing cardiac catheterization and PCI were enrolled. FcÉ£RIIa expression was quantified with the use of flow cytometry. Comparisons were made with Mann-Whitney Rank Sum Test and Chi Squared analysis. Significance was defined as P less than .05. RESULTS: Compared to patients with MI, patients with stable CAD (n = 49) were older (70 ± 9 years vs 63 ± 12 years) and were more likely to have had prior MI (43% vs 23%), prior revascularization (62% vs 33%), diabetes (35% vs 24%), and hypertension (98% vs 66%). In patients with stable CAD, platelet FcÉ£RIIa was, on average, lower than that seen in patients with acute MI (9746 ± 4316 vs 11 479 ± 2405 molecules/platelet, P less than .001). Patients with stable CAD exhibited a range of platelet FcÉ£RIIa (~4500 to ~27 000 molecules/platelet) similar to that seen in acute MI patients (~6500 to ~30 000 molecules/platelet). CONCLUSIONS: Compared to patients with MI, patients with stable CAD had, on average, lower platelet FcÉ£RIIa. However, the range of platelet FcÉ£RIIa was similar to that seen in patients with MI. These results support future studies designed to assess the prognostic implications of platelet FcÉ£RIIa in patients with stable CAD.

Genomic and functional characterization of a mucosal symbiont involved in early-stage colorectal cancer.

Colorectal cancer is a major health concern worldwide. Growing evidence for the role of the gut microbiota in the initiation of CRC has sparked interest in approaches that target these microorganisms. However, little is known about the composition and role of the microbiota associated with precancerous polyps. Here, we found distinct microbial signatures between patients with and without polyps and between polyp subtypes using sequencing and culturing techniques. We found a correlation between Bacteroides fragilis recovered and the level of inflammatory cytokines in the mucosa adjacent to the polyp. Additional analysis revealed that B. fragilis from patients with polyps are bft-negative, activate NF-κB through Toll-like receptor 4, induce a pro-inflammatory response, and are enriched in genes associated with LPS biosynthesis. This study provides fundamental insight into the microbial microenvironment of the pre-neoplastic polyp by highlighting strain-specific genomic and proteomic differences, as well as more broad compositional differences in the microbiome.