Improved gene expression programming to solve the inverse problem for ordinary differential equations

Many complex systems in the real world evolve with time. These dynamic systems are often modeled by ordinary differential equations in mathematics. The inverse problem of ordinary differential equations is to convert the observed data of a physical system into a mathematical model in terms of ordinary differential equations. Then the modelay be used to predict the future behavior of the physical system being modeled. Genetic programming has been taken as a solver of this inverse problem. Similar to genetic programming, gene expression programming could do the same job since it has a similar ability of establishing the model of ordinary differential systems. Nevertheless, such research is seldom studied before. This paper is one of the first attempts to apply gene expression programming for solving the inverse problem of ordinary differential equations. Based on a statistic observation of traditional gene expression programming, an improvement is made in our algorithm, that is, genetic operators should act more often on the dominant part of genes than on the recessive part. This may help maintain population diversity and also speed up the convergence of the algorithm. Experiments show that this improved algorithm performs much better than genetic programming and traditional gene expression programming in terms of running time and prediction precisio

Hepatitis B virus–induced imbalance of inflammatory and antiviral signaling by differential phosphorylation of STAT1 in human monocytes

It is not clear how hepatitis B virus (HBV) modulates host immunity during chronic infection. In addition to the key mediators of inflammatory response in viral infection, monocytes also express a high-level IFN-stimulated gene, CH25H, upon response to IFN-a exerting an antiviral effect. In this study, the mechanism by which HBV manipulates IFN signaling in human monocytes was investigated. We observed that monocytes from chronic hepatitis B patients express lower levels of IFN signaling/stimulated genes and higher levels of inflammatory cytokines compared with healthy donors. HBV induces monocyte production of inflammatory cytokines via TLR2/MyD88/NF-kB signaling and STAT1-Ser727 phosphorylation and inhibits IFN-a–induced stat1, stat2, and ch25h expression through the inhibition of STAT1-Tyr701 phosphorylation and in an IL-10–dependent, partially autocrine manner. Further, we found that enhancement of STAT1 activity with a small molecule (2-NP) rescued HBV-mediated inhibition of IFN signaling and counteracted the induction of inflammatory cytokines. In conclusion, HBV contributes to the monocyte inflammatory response but inhibits their IFN-a/b responsiveness to impair antiviral innate immunity. These effects are mediated via differential phosphorylation of Tyr701 and Ser727 of STAT1