Our previous work demonstrated that both polymorphonuclear leukocytes (PMNs) and protein fractions released from PMNs induced de novo synthesis of fibroblast growth factor 2 (FGF-2), which in turn becomes the direct mediator of endothelial mesenchymal transformation observed in corneal endothelial cells (CECs). To identify the protein factor, we used ProteinChip Array technology. Protein fractions obtained from the conditioned medium released by PMNs were resolved by twodimensional electrophoresis with immobilized pH gradient strips. Most of the protein spots, with molecular masses of 17 kDa, were sequentially subjected to in-gel trypsin digestion and mass spectrometry. The 17-kDa peptide band was identified as interleukin-1␤ (IL-1␤). Biological activities of IL-1␤ were further determined; IL-1␤ altered the shape of CECs from polygonal to fibroblastic morphologies in a time-and dose-dependent manner, whereas neutralizing IL-1␤ antibody, neutralizing antibody to FGF-2, and LY294002 blocked the action of IL-1␤. IL-1␤ greatly increased the levels of FGF-2 mRNA in a time-and dose-dependent manner; IL-1␤ stimulated expression of all isoforms of FGF-2. IL-1␤ initially induced nuclear accumulation of FGF-2 and facilitated translocation of FGF-2 to plasma membrane and extracellular matrix. IL-1␤ activated phosphatidylinositol (PI) 3-kinase, the enzyme activity of which was greatly stimulated after a 5-min exposure to IL-1␤. This early and rapid activation of PI 3-kinase greatly enhanced FGF-2 production in CECs; pretreatment with LY294002 hampered the induction activity of IL-1␤. These observations suggest that IL-1␤ takes part in endothelial to mesenchymal transformation of CECs through its inductive potential on FGF-2 via the action of PI 3-kinase.

These data indicate that PI 3-kinase ultimately leads to activation of the cell cycle machinery in response to FGF-2. It does so by upregulating expression of Cdk4, facilitating the nuclear import of Cdk4, and sequestering Cdk4 in the nuclei as it simultaneously downregulates expression of p27 and facilitates the proteolysis of the molecule by phosphorylation.

These data support the hypothesis that cAMP inhibits the proliferation of CECs, preventing them from entering the S phase by negatively regulating PI 3-kinase.

The main purpose of this study is to propose a security control system model, which enables to strictly monitor the web for security and detect the damages caused by malicious code when using random devices for transits and disposals. This model is significantly different in comparison to other existing monitoring systems. It connects the crawler not just to the main-URL but further extends its connection to the sub-URL, enabling it to sequentially detect vicious links and the status of the website. Moreover, the model includes an algorithm that enables the detection of malicious code in an internetdownloaded file through analyzing its behavioral patterns.To validate this model, this study has developed and implemented the core algorithm to a prototype, conducting various experiments. As a result, the new module which anticipated in this study was considered as a representative factor to monitor and detect the malfunctions of the website. Furthermore, the website's security could be effectively identified utilizing the proposed modules.