Fourth, microarray studies are directed towards GDC-0449 analysis of defined genes and increasing evidence points to the importance of critical regulatory elements outside the protein-coding regions which will not be captured with this approach. In conclusion, these results indicate that anti-TNF treatment modulates different disease pathways in specific immune-mediated inflammatory disorders. Thus, clinical and tissue responses can be achieved with TNF inhibition by divergent mechanisms dependent on the underlying disease. Moreover, careful analysis of differential gene expression in involved tissues and possibly blood cells following treatment with biologic therapies may provide insights into disease pathogenesis and unveil new disease targets. These two commercial materials have been commonly used in the manufacture of various consumer goods, industrial products, and medical devices. Given the prevalence of BPA in our environment and daily lives, it can be detected in serum, urine, breast milk and saliva in the majority of populations in different countries. Thus, concern has grown regarding whether BPA exposure can cause health problems in humans, as underscored by recent cross-sectional and longitudinal studies that show that urinary or serum levels of BPA are positively associated with various cardiovascular diseases. Recent epidemiological studies have also shown that either urinary or serum BPA levels were positively associated with coronary artery stenosis, carotid atherosclerosis, and peripheral arterial disease, suggesting that BPA exposure may be an emerging risk factor for the development of atherosclerosis. However, this latter hypothesis has not been verified experimentally using appropriate animal models. This is an important issue because it is not clear whether BPA exposure is causal for the development of atherosclerosis. In fact, the toxicological mechanisms of BPA in terms of atherosclerosis remain largely unknown. Several studies have shown that BPA exposure increases atherosclerosis in mice and alters cardiac functions in both mice and rats. Although these rodent studies are informative, it is not known whether these results can be extrapolated to humans because rodents are quite different from humans in terms of lipid metabolism, glucose metabolism, cardiovascular systems, and responses to inflammatory stimuli. Furthermore, regional distributions of fat depots, their cellular compositions, and regulations of resistin, agouti protein, adipsin, and adrenergic receptors are dissimilar between rodents and humans. In this regard, there are advantages to studying lipid metabolism and atherosclerosis in rabbits rather than mice. In addition, rabbits are phylogenetically closer to humans than are rodents.