The first appearance of viruses can date back to the late last century. As an effective form of malware, viruses reside in the permanent storage of target hosts. Before a virus can execute, that must load into memory from the persistent storage included in the associated file. Due to the reliable destructive power of viruses, many mechanisms have been developed to defend computer systems against these hazardous threats. Antivirus software is one of the most famous and popular among these mechanisms. Most antivirus software uses static analysis (signature-based) technology on files stored in permanent storage, such as hard disks or USB flashes, to detect viruses hidden in files. Fileless malware was developed to enhance the survivability of malware by circumventing detection. Fileless malware only exists in the target hosts’ memory, not files. Antivirus software cannot even access the fileless malware code, much less analyze it, since it may be performed in memory directly without needing to load it from a disk. As a result, it is difficult for an antivirus engine to defend a system against fileless malware attacks. This paper proposes a kernel-based solution called Check-on-Execution (CoE) to detect fileless malware on a Linux system. When a program is going to execute a piece of code in a writable and executable memory area of a process, CoE suspends the code execution first. Coe retrieves the code from memory, packs the code with an ELF header to create an ELF file, and uses VirusTotal to check the file to prevent a Linux system from executing fileless malware. Experimental results show that CoE noticeably enhances the ability of a Linux system to defend itself again fileless malware. CoE is also suitable for protecting a system from shell code injection attacks, such as buffer and heap overflow attacks. It is capable of handling even packed malware. But in this paper, we only focus on fileless malware.

The effects of environmental media on the corrosion fatigue fracture behavior of 25CrMo steel were investigated. The media include air, and a 3.5 wt.% and a 5.0 wt.% NaCl solutions. Experimental results indicate that the media induces the initiation of corrosion fatigue cracks at multiple sites. The multi-cracking sites cause the changes in the crack growth directions, the crack growth rate during the coupling action of the media and the stress amplitude. The coupling effects are important for engineering applications and research. The probability and predictions of the corrosion fatigue characteristic life can be estimated using the 3-parameter Weibull distribution function.

The current study was designed to investigate the anti-inflammatory effect of salidroside (SDS) and the underlying mechanism by using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages in vitro and a mouse model of binge drinking induced liver injury in vivo. SDS downregulated protein expression of toll-like receptor 4 (TLR4) and CD14. SDS inhibited LPS-triggered phosphorylation of LPS-activated kinase 1 (TAK1), p38, c-Jun terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Degradation of IκB-α and nuclear translocation of nuclear factor (NF)-κB were effectively blocked by SDS. SDS concentration-dependently suppressed LPS mediated inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein levels, as well as their downstream products, NO. SDS significantly inhibited protein secretion of interleukin (IL)-1β. Additionally C57BL/6 mice were orally administrated SDS for continuous 5 days, followed by three gavages of ethanol every 30 min. Alcohol binge drinking caused the increasing of hepatic lipid accumulation and serum transaminases levels. SDS pretreatment significantly alleviated liver inflammatory changes and serum transaminases levels. Further investigation indicated that SDS markedly decreased protein level of IL-1β in serum. Taken together, these data implied that SDS inhibits liver inflammation both in vitro and in vivo, and may be a promising candidate for the treatment of inflammatory liver injury.