Herbert Eradat.

Centralized reference diagnostic methods were performed at Ulm University or Cancer Genetics with the use of fluorescence in situ hybridization for genomic aberrations, DNA sequencing for IGHV mutation position, and WAVE DNA fragment confirmatory and analysis Sanger sequencing for TP53 analyses, as described previously.25-27 Adverse events were graded with the use of the National Cancer Institute Common Terminology Criteria for Adverse Events , version 4.03. End Points The principal end point of the trial was progression-free survival. Secondary end factors were rates of complete and overall response, lymph-node response, and general survival.Discussion Studies in germ-free of charge mice and cross-sectional clinical research in humans have suggested a role for the intestinal microbiota in the pathogenesis of atherosclerosis in sufferers with a diet abundant with phosphatidylcholine through the formation of the metabolite trimethylamine and transformation to TMAO.7,15 In our study, we describe the generation of the proatherogenic metabolite TMAO from dietary phosphatidylcholine through the use of stable-isotope-tracer feeding studies. We further discovered a role for the intestinal microbiota in the creation of TMAO through its suppression through oral broad-spectrum antibiotics and then reacquisition of trimethylamine and the production of TMAO from dietary phosphatidylcholine following the withdrawal of antibiotics and subsequent intestinal recolonization.