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Recently, there has been a constant barrage of worms over the Internet. Besides threatening network security, these worms create an enormous economic burden in terms of loss of productivity not only for the victim hosts, but also for other hosts, as these worms create unnecessary network traffic. Further, measures taken to filter these worms at the router level incur additional network delays because of the extra burden placed on the routers. To develop appropriate tools for thwarting the quick spread of worms, researchers are trying to understand the behavior of worm propagation with the aid of epidemiological models. In this study, we present an optimization model that takes into account infection and treatment costs. Using this model we can determine the level of treatment to be applied for a given rate of infection spread.

To directly define the role of phospholipase CQ Q1 (PLCQ Q1) in NF-U UB activation, NF-U UB promoted luciferase reporter gene plasmid (pNF-U UB-Luc) was transfected into rat-3Y1 fibroblasts that overexpress whole PLCQ Q1 (PLCQ Q1-3Y1), src homology domains SH2-SH2-SH3 of PLCQ Q1 (SH223-3Y1) and v-src (Src-3Y1). Transient transfection with pNF-U UB-Luc remarkably increased the luciferase activity in all three transformants compared with normal rat-3Y1 cells. Pretreatment with inhibitors of protein tyrosine kinase reduced this increase in luciferase activity, but U73122 (a PLC inhibitor) did not. While PD98059, an inhibitor of mitogen activated protein kinase (MAPK), significantly reduced the luciferase activity, there was no effect by wortmannin and Ro-31-8220, inhibitors of phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC), respectively. This study shows a direct evidence that the SH2-SH2-SH3 region of PLCQ Q1 contributes to the NF-U UB signaling and that MAPK, but not PI3K and PKC, is involved in SH2-SH2-SH3 mediated NF-U UB activation in these cells.z 2000 Federation of European Biochemical Societies.

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