Finally, it was possible that some missing and unpublished data may lead to bias in effect size. In conclusion, despite its various limitations, our study is clinically valuable because it revealed that carvedilol leads to lower incidence of POAF than control and appears to be superior to metoprolol as the current study clearly delineated. Carvedilol may effectively reduce the incidence of POAF in patients undergoing cardiac surgery. On the basis of this encouraging finding, we believe that research on the field is promising and should be continued. At least the ongoing COMPACT, which is a prospective, multi-center, randomized, open-label, active-controlled trial, will answer the question of whether or not carvedilol is more superior to metoprolol in preventing POAF in patients undergoing CABG. The focus of this paper is to understand the dynamics of interaction between two major signaling pathways in the innate immune response controlled by the nuclear factor-kB and interferon response factor -3 transcription factors that mediate inflammation and antiviral responses, respectively. The IIR is a signaling Albaspidin-AA mechanism designed to limit the spread of infecting pathogen at mucosal surfaces before the adaptive immune response is activated. The presence of “foreign” pathogen-associated molecular pa erns, such as dsRNA and lipopolysaccharide, is recognized by a family of pa ern recognition receptors that subsequently trigger signal transduction cascades. These cascades include the NF-kB and IRF transcription factors. The link to adaptive immune protection is conferred by the expression of cytokine and protective interferons downstream of the NF-kB and IRF pathways. Interestingly, the intracellular IIR is not mediated by second messengers, but instead by signaling complexes produced by intracellular adapter molecules. These enzymes perform the functions of ubiquitylation, serine/threonine phosphorylation, and cysteinyl oxidation cascades that release and activate cytoplasmic TF complexes to enter the nucleus. Despite the finding that this pathway is activated in a robust manner, it is under very tight negative-feedback control. The properties of negative feedback of this system have been modeled using deterministic ordinary differential equations to understand the roles of negative feedback of inducible IkB-a,b and -e isoforms in regulating the temporal control of NF-kB, and our studies have modeled the roles of the NF-kB -TNFAIP3 feedback loop. Not much is known about how the activation of these two major signaling arms of the IIR is controlled. Recent work by our group and others has shown that adapter molecules regulating the IRF3 signaling pathway are inter-connected with those of NF-kB at multiple Coptisine-chloride stages, with the final shared component being the IkB kinase-c subunit. More recently, single-cell imaging experiments have provided informative approaches to understanding the sources of cellular heterogeneity. Despite these and other experimental and modeling a empts, li le has been known about how the NF-kB and IRF3 pathways interact with each other. In addition to its tight control by intracellular negative cross-talk pathways, a full understanding of the IIR must incorporate celltype dependent differences.