Summary With the growing number of malware, malware analysis technologies need to be advanced continuously. Malware authors use various packing techniques to hide their code from malware detection tools and techniques. The packing techniques are generally used to compress and encrypt executable code in executable files, and the unpacking code is usually embedded in the executable files. Therefore, packed executable files can be executed by itself, and the information associated with packing can be used to analyze and detect malware. Since different packing tools will generate different packed executable files, packing tools can be identified by analyzing packed executable files, and packer identification can reduce malware‐analyzing overheads, and the executable files can even be unpacked. However, most previous studies focused on packing detection using signatures of unpacking code, and these approaches can be avoided by placing unpacking code in other locations or by distributing unpacking code in multiple locations. In this paper, we propose a new packer identification method by analyzing only code sections to extract features of malware generated by different packing tools. Experimental results show that our approach can identify different packing tools with the accuracy of 91.6% on average. Considering packer identification is the harder problem than packing detection, we argue that our approach can contribute to reducing overheads of malware analysis.

Background4-Nonylphenol is a ubiquitous environmental toxin that is formed as a byproduct in the manufacturing and/or sewage treatment of regular household items. Previous work in our lab has implicated 4-NP in the progression of autoimmune diseases such as inflammatory bowel disease in which macrophages mistakenly attack the intestinal linings, causing chronic inflammation. Several key pro-and anti-inflammatory molecules have been shown to be involved in the manifestation of this disease, including IL-23A, COX-2, IL-8, TLR-4, and IL-10.Material/Methods4-NP’s effects on these known mediators of IBD were effectively analyzed using a novel model for IBD, by which 4-NP may promote an inflammatory response. Data were collected using DNA Microarray, RT-PCR, and ELISA, after 48 hour treatment of U937 histiocytic lymphocyte cells and COLO320DM human intestinal epithelial cells with 1 nM and 5 nM concentrations of 4-NP.ResultsSignificant dysregulation of the expression of both pro- and anti-inflammatory genes was observed in U937 cells that would promote and prolong inflammation. However, TLR-4, IL-8, and COX-2 gene expressions showed unprecedented effects in COLO320DM cells suggesting that these genes mediate apoptotic processes within the gastrointestinal tract.ConclusionsOverall, our results suggest that 4-NP administration engenders immune responses linked to apoptotic processes via dysregulation of macrophage signaling. In sum, 4-NP appears to increases the risk of developing inflammatory bowel disease by promoting or prolonging adverse progression of inflammation in the gastrointestinal tract.