Ional Science (UL1TR000100) (GSF) and funding from Ignyta, Inc. (DLB).Whitaker et al. Genome Medicine 2013, 5:40 http://genomemedicine/content/5/4/Page 12 of20.21. 22.23.24. 25.26.of differentially methylated regions in regular and cancerous tissues. Nat Genet 2012, 44:1207-1214. Nakano K, Boyle DL, Firestein GS: Regulation of DNA methyltransferases and DNA methylation in rheumatoid arthritis synoviocytes. J Immunol 2012, 190:1297-1303. Kyburz D, Corr M: The KRN mouse model of inflammatory arthritis. Springer Semin Immunopathol 2003, 25:79-90. Maciejewska Rodrigues H, Jungel A, Gay RE, Gay S: Innate immunity, epigenetics and autoimmunity in rheumatoid arthritis. Mol Immunol 2009, 47:12-18. Firestein GS, Paine MM, Littman BH: Gene expression (collagenase, tissue inhibitor of metalloproteinases, complement, and HLA-DR) in rheumatoid arthritis and osteoarthritis synovium. Quantitative evaluation and impact of intraarticular corticosteroids. Arthritis Rheum 1991, 34:1094-1105. Brentano F, Kyburz D, Schorr O, Gay R, Gay S: The part of Toll-like receptor signalling within the pathogenesis of arthritis. Cell Immunol 2005, 233:90-96. Carrion M, Juarranz Y, Perez-Garcia S, Jimeno R, Pablos JL, Gomariz RP, Gutierrez-Canas I: RNA sensors in human osteoarthritis and rheumatoid arthritis synovial fibroblasts: immune regulation by vasoactive intestinal peptide. Arthritis Rheum 2011, 63:1626-1636. Ospelt C, Brentano F, Jungel A, Rengel Y, Kolling C, Michel BA, Gay RE, Gay S: Expression, regulation, and signaling with the pattern-recognition receptor nucleotide-binding oligomerization domain two in rheumatoid arthritis synovial fibroblasts. Arthritis Rheum 2009, 60:355-363.doi:ten.1186/gm444 Cite this article as: Whitaker et al.: An imprinted rheumatoid arthritis methylome signature reflects pathogenic phenotype. Genome Medicine 2013 5:40.Submit your next manuscript to BioMed Central and take full advantage of:Easy on-line submission Thorough peer critique No space constraints or colour figure charges Instant publication on acceptance Inclusion in PubMed, CAS, Scopus and Google Scholar Study that is freely obtainable for redistributionSubmit your manuscript at www.biomedcentral/submit
The oxidative strain hypothesis proposed that cell injury in chronic pancreatitis (CP) was mediated at the acinar level by short-lived oxygen absolutely free radicals developed as a result of imbalance in the physiological processes making these agents and those pathways involved in deactivating them[1].Ublituximab A key component of this theory was that the methionine transsulfuration pathway which yields glutathione (vital inside the quenching of antioxidants) is overwhelmed in individuals with CP because the detoxification of xenobiotics by cytochrome P450 led to overproduction of oxygen-derived totally free radicals[1].Levofloxacin There was evidence that the dietary intake of some sufferers with CP was deficient in selenium, methionine and vitamin C, crucial cofactors in these transsulfuration pathways[2].PMID:23514335 This obtaining was supported by evidence showing that plasma/ blood levels of circulating antioxidants were low in CP in comparison to control[3]. The logical completion of this paradigm was the development of antioxidant therapy – a pharmacological preparation containing methionine, vitamin C, vitamin E and selenium and designed to restore these crucial co-factors to patients with CP[1]. Early clinical trials of antioxidant therapy failed to establish proof of clinical efficacy and as a result the treatment was not extensively accepted.
