logical significance of tissue prothrombin remains unclear. Although the thrombin of the atrial tissue may be derived from the cleared thrombin from the circulation across the endocardium and the vascular endothelium, the possibility of local production of thrombin in the atria cannot be ruled out. In conclusion, the expression of thrombin in the atrial tissues of human autopsied hearts was demonstrated. Further research is needed to determine the 
physiological and pathological roles of atrial tissue thrombin. Acknowledgments We thank Dr. Brian Quinn for his kind advice regarding the use of the English language. We also thank to Dr. Shun Sato for his valuable contributions to the immunohistochemical analyses. Chronic exposure to inorganic arsenic, in the most prevalent form of arsenite from drinking water is one of the most significant and widespread environmental health risks in the U.S. and throughout the world. Epidemiologic evidence links iAs exposure to an increased risk of lung, bladder, skin and other cancers, type 2 diabetes, vascular and cardiovascular disease, and reproductive and developmental anomalies, all of which can be linked to inappropriate steroid or nuclear receptormediated gene regulation which can have deleterious effects on every metabolic 21150909 system and is associated with many forms of cancer. Micromolar amounts of iAs inhibit transcription mediated by the glucocorticoid receptor, the progesterone receptor, the androgen receptor, the estrogen receptor and the mineralocorticoid receptor , as well as the thyroid hormone and the retinoic acid receptors. This suggests an iAs target common to all or many nuclear receptorregulated gene promoters but a mechanism has yet to be identified. Steroid hormone-regulated receptors belong to the superfamily of nuclear receptors that includes the GR, PR, ER, MR, and AR. All use similar transcriptional activation mechanisms to regulate physiological responses to a broad range of internal and external stimuli. Following ligand binding, transcription by steroid receptors is initiated by receptor-DNA binding and changes in chromatin structure contributed to by changes in histone post-translational modifications . Arsenic-associated changes in histone PTMs have been identified in transcriptional activation from some non-steroid regulated promoters and global changes have been reported in response to iAs at histone H3. Histone PTMs, are regulated by coactivator or corepressor proteins that interact with promoters via protein-protein interactions with the steroid receptor itself, or with other promoter-associated proteins. These co-regulatory proteins act as transducers between Arsenic Inhibits CARM1 internal or external stimuli and a genetic response by providing targets for PTMs mediated by cell signaling pathways. Thiazovivin site Coactivators such as CARM1 have enzymatic activities on histones and nonhistone, promoter-associated proteins. CARM1 targets histone H3R17 and H3R26 for methylation upon activation of both ER and GR-regulated promoters and associates 16476508 with these promoters by binding to one of the three p160 coactivators which in turn bind directly to the DNA-bound steroid receptor. To understand how iAs represses steroid hormone-mediated gene transcription we sought to determine when in the transcription process an iAs effect could be detected and whether histone modification patterns changed in response to hormone alone compared to hormone plus iAs at the MMTV promoter. We found that iAs repres
