The computer systems security arms race between attackers and defenders has largely taken place in the domain of software systems, but as hardware complexity and design processes have evolved, novel and potent hardware-based security threats are now possible. This paper presents a hybrid hardware/software approach to defending against malicious hardware.We propose BlueChip, a defensive strategy that has both a design-time component and a runtime component. During the design verification phase, BlueChip invokes a new technique, unused circuit identification (UCI), to identify suspicious circuitry-those circuits not used or otherwise activated by any of the design verification tests. BlueChip removes the suspicious circuitry and replaces it with exception generation hardware. The exception handler software is responsible for providing forward progress by emulating the effect of the exceptiongenerating instruction in software, effectively providing a detour around suspicious hardware. In our experiments, BlueChip is able to prevent all hardware attacks we evaluate while incurring a small runtime overhead.

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Attackers and defenders of computer systems both strive to gain complete control over the system. To maximize their control, both attackers and defenders have migrated to low-level, operating system code. In this paper, we assume the perspective of the attacker, who is trying to run malicious software and avoid detection. By assuming this perspective, we hope to help defenders understand and defend against the threat posed by a new class of rootkits.We evaluate a new type of malicious software that gains qualitatively more control over a system. This new type of malware, which we call a virtual-machine based rootkit (VMBR), installs a virtual-machine monitor underneath an existing operating system and hoists the original operating system into a virtual machine. Virtual-machine based rootkits are hard to detect and remove because their state cannot be accessed by software running in the target system. Further, VMBRs support general-purpose malicious services by allowing such services to run in a separate operating system that is protected from the target system. We evaluate this new threat by implementing two proof-of-concept VMBRs. We use our proof-of-concept VMBRs to subvert Windows XP and Linux target systems, and we implement four example malicious services using the VMBR platform. Last, we use what we learn from our proof-of-concept VMBRs to explore ways to defend against this new threat. We discuss possible ways to detect and prevent VMBRs, and we implement a defense strategy suitable for protecting systems against this threat.

Analyzing intrusions today is an arduous, largely manual task because system administrators lack the information and tools needed to understand easily the sequence of steps that occurred in an attack. The goal of BackTracker is to identify automatically potential sequences of steps that occurred in an intrusion. Starting with a single detection point (e.g., a suspicious file), BackTracker identifies files and processes that could have affected that detection point and displays chains of events in a dependency graph. We use BackTracker to analyze several real attacks against computers that we set up as honeypots. In each case, BackTracker is able to highlight effectively the entry point used to gain access to the system and the sequence of steps from that entry point to the point at which we noticed the intrusion. The logging required to support BackTracker added 9% overhead in running time and generated 1.2 GB per day of log data for an operating-system intensive workload.

Dietary flavonoids have been shown to be protective against various types of cancers. Here we studied the effects of 12 different flavonoids and other substances on cell proliferation and VEGF expression in human ovarian cancer cells, OVCAR-3. Cell growth was determined to pinpoint the best time for drug treatment. By LDH assay, no cytotoxicity was observed for OVCAR-3 cells with all 12 chemicals except mevinolin. Six flavonoids, including apigenin, taxifolin, luteolin, quercetin, genistein, and kaempferol, were shown to inhibit the ovarian cancer cell growth in a dose-dependent manner. From both RT-qPCR and ELISA results, all flavonoids have shown varied degrees of inhibition in VEGF expression. Taxifolin and naringin showed the least inhibition effect. They both lack a double bond in the second ring structure that may be important in inhibiting VEGF expression. The rank order of VEGF protein secretion inhibitory potency was genistein > kaempferol > apigenin > quercetin > tocopherol > luteolin > cisplatin > rutin > naringin > taxifolin. Genistein, quercetin, and luteolin have shown strong inhibition to cell proliferation and VEGF expression of human ovarian cancer cells, and they show promising in the prevention of ovarian cancers.

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Recent findings have shown an inverse association between circulating C15:0/C17:0 fatty acids with disease risk, therefore, their origin needs to be determined to understanding their role in these pathologies. Through combinations of both animal and human intervention studies, we comprehensively investigated all possible contributions of these fatty acids from the gut-microbiota, the diet, and novel endogenous biosynthesis. Investigations included an intestinal germ-free study and a C15:0/C17:0 diet dose response study. Endogenous production was assessed through: a stearic acid infusion, phytol supplementation, and a Hacl1 −/− mouse model. Two human dietary intervention studies were used to translate the results. Finally, a study comparing baseline C15:0/C17:0 with the prognosis of glucose intolerance. We found that circulating C15:0/C17:0 levels were not influenced by the gut-microbiota. The dose response study showed C15:0 had a linear response, however C17:0 was not directly correlated. The phytol supplementation only decreased C17:0. Stearic acid infusion only increased C17:0. Hacl1 −/− only decreased C17:0. The glucose intolerance study showed only C17:0

Background Dietary recommendations to limit red meat are based on observational studies linking intake to cardiovascular disease (CVD) risk together with the potential of its saturated fatty acid (SFA) content to raise low-density lipoprotein (LDL) cholesterol. However, the relation of white meat to CVD risk, and the effects of dietary protein source on lipoprotein particle subfractions, have not been extensively evaluated. Objective We tested whether levels of atherogenic lipids and lipoproteins differed significantly following consumption of diets with high red meat content compared with diets with similar amounts of protein derived from white meat or nonmeat sources, and whether these effects were modified by concomitant intake of high compared with low SFAs. Methods Generally healthy men and women, 21–65 y, body mass index 20–35 kg/m2, were randomly assigned to 1 of 2 parallel arms (high or low SFA) and within each, allocated to red meat, white meat, and nonmeat protein diets consumed for 4 wk each in random order. The primary outcomes were LDL cholesterol, apolipoprotein B (apoB), small + medium LDL particles, and total/high-density lipoprotein cholesterol. Results Analysis included participants who completed all 3 dietary protein assignments (61 for high SFA; 52 for low SFA). LDL cholesterol and apoB were higher with red and white meat than with nonmeat, independent of SFA content (P < 0.0001 for all, except apoB: red meat compared with nonmeat [P = 0.0004]). This was due primarily to increases in large LDL particles, whereas small + medium LDL and total/high-density lipoprotein cholesterol were unaffected by protein source (P = 0.10 and P = 0.51, respectively). Primary outcomes did not differ significantly between red and white meat. Independent of protein source, high compared with low SFA increased LDL cholesterol (P = 0.0003), apoB (P = 0.0002), and large LDL (P = 0.0002). Conclusions The findings are in keeping with recommendations promoting diets with a high proportion of plant-based food but, based on lipid and lipoprotein effects, do not provide evidence for choosing white over red meat for reducing CVD risk. This trial was registered at Clinicaltrials.gov as NCT01427855.