No abstract

IP prefix hijacking remains a major threat to the security of the Internet routing system due to a lack of authoritative prefix ownership information. Despite many efforts in designing IP prefix hijack detection schemes, no existing design can satisfy all the critical requirements of a truly effective system: real-time, accurate, light-weight, easily and incrementally deployable, as well as robust in victim notification. In this paper, we present a novel approach that fulfills all these goals by monitoring network reachability from key external transit networks to one's own network through lightweight prefix-owner-based active probing. Using the prefix-owner's view of reachability, our detection system, ISPY, can differentiate between IP prefix hijacking and network failures based on the observation that hijacking is likely to result in topologically more diverse polluted networks and unreachability. Through detailed simulations of Internet routing, 25-day deployment in 88 ASes (108 prefixes), and experiments with hijacking events of our own prefix from multiple locations, we demonstrate that ISPY is accurate with false negative ratio below 0.45% and false positive ratio below 0.17%. Furthermore, ISPY is truly real-time; it can detect hijacking events within a few minutes.

No abstract

Background Cancer cachexia is characterized by weight loss, especially ongoing skeletal muscle loss, and is associated with poor patient outcomes. However, the molecular mechanism of skeletal muscle wasting is not fully understood. Objectives We aimed to investigate muscle fiber morphology and proteolysis system activity changes that may account for cancer cachexia and to relate these changes to patients’ clinical phenotypes. Methods We divided 39 patients with resectable gastric cancer into 4 groups based on the presence of cachexia (weight loss) and/or sarcopenia (low muscularity), including a noncachexia/nonsarcopenia group (N, n = 10), a cachexia/sarcopenia group (CS, n = 13), a cachexia/nonsarcopenia group (C, n = 9), and a noncachexia/sarcopenia group (S, n = 7). Rectus abdominis muscle biopsy specimens were obtained intraoperatively. Muscle fiber size, ultrastructural architecture, and the expression of autophagic-lysosomal system (ALS) and ubiquitin proteasome system (UPS) markers were assayed. Results Mean ± SD muscle fiber cross-sectional areas were significantly decreased in the CS (460 ± 120 μm2) and S groups (480 ± 135 μm2) compared with the N (1615 ± 388 μm2, both P < 0.05) and C groups (1219 ± 302 μm2, both P < 0.05). In the C, S, and CS groups, the muscle exhibited tissue disorganization and autophagosome formation to different degrees. The levels of ALS and UPS markers were significantly increased in the CS, C, and S groups compared with the N group. Alterations in muscle fiber morphology and increased ALS and UPS activity were related to severe muscle loss, but not weight loss. Conclusions The ALS and UPS are simultaneously activated in cancer cachexia and may play coordinated roles in cachexia-induced muscle loss.