Wireless networks are built upon a shared medium that makes it easy for adversaries to launch jamming-style attacks. These attacks can be easily accomplished by an adversary emitting radio frequency signals that do not follow an underlying MAC protocol. Jamming attacks can severely interfere with the normal operation of wireless networks and, consequently, mechanisms are needed that can cope with jamming attacks. In this paper, we examine radio interference attacks from both sides of the issue: first, we study the problem of conducting radio interference attacks on wireless networks, and second we examine the critical issue of diagnosing the presence of jamming attacks. Specifically, we propose four different jamming attack models that can be used by an adversary to disable the operation of a wireless network, and evaluate their effectiveness in terms of how each method affects the ability of a wireless node to send and receive packets. We then discuss different measurements that serve as the basis for detecting a jamming attack, and explore scenarios where each measurement by itself is not enough to reliably classify the presence of a jamming attack. In particular, we observe that signal strength and carrier sensing time are unable to conclusively detect the presence of a jammer. Further, we observe that although by using packet delivery ratio we may differentiate between congested and jammed scenarios, we are nonetheless unable to conclude whether poor link utility is due to jamming or the mobility of nodes. The fact that no single measurement is sufficient for reliably classifying the presence of a jammer is an important observation, and necessitates the development of enhanced detection schemes that can remove ambiguity when detecting a jammer. To address this need, we propose two enhanced detection protocols that employ consistency checking. The first scheme employs signal strength measurements as a reactive consistency check for poor packet delivery ratios, while the second scheme employs location information to serve as the consistency check. Throughout our discussions, we examine the feasibility and effectiveness of jamming attacks and detection schemes using the MICA2 Mote platform.

-Dynamic capacity provisioning is a useful technique for handling the multi-time-scale variations seen in Internet workloads. In this paper, we propose a novel dynamic provisioning technique for multi-tier Internet applications that employs (i) a flexible queuing model to determine how much resources to allocate to each tier of the application, and (ii) a combination of predictive and reactive methods that determine when to provision these resources, both at large and small time scales. We propose a novel data center architecture based on virtual machine monitors to reduce provisioning overheads. Our experiments on a forty-machine Xen/Linux-based hosting platform demonstrate the responsiveness of our technique in handling dynamic workloads. In one scenario where a flash crowd caused the workload of a three-tier application to double, our technique was able to double the application capacity within five minutes, thus maintaining response time targets. Our technique also reduced the overhead of switching servers across applications from several minutes to less than a second, while meeting the performance targets of residual sessions.

No abstract

Abstract. Next Generation Data Centers are transforming labor-intensive, hard-coded systems into shared, virtualized, automated, and fully managed adaptive infrastructures. Virtualization technologies promise great opportunities for reducing energy and hardware costs through server consolidation. However, to safely transition an application running natively on real hardware to a virtualized environment, one needs to estimate the additional resource requirements incurred by virtualization overheads.In this work, we design a general approach for estimating the resource requirements of applications when they are transferred to a virtual environment. Our approach has two key components: a set of microbenchmarks to profile the different types of virtualization overhead on a given platform, and a regression-based model that maps the native system usage profile into a virtualized one. This derived model can be used for estimating resource requirements of any application to be virtualized on a given platform. Our approach aims to eliminate error-prone manual processes and presents a fully automated solution. We illustrate the effectiveness of our methodology using Xen virtual machine monitor. Our evaluation shows that our automated model generation procedure effectively characterizes the different virtualization overheads of two diverse hardware platforms and that the models have median prediction error of less than 5% for both the RUBiS and TPC-W benchmarks.

Previous observations have shown that binding of growth hormone to its receptor leads to activation of transcription factors via a mechanism involving phosphorylation on tyrosine residues. In order to establish whether the prolactin-activated transcription factor Stat 5 (mammary gland factor) is also activated by growth hormone, nuclear extracts were prepared from COS-7 cells transiently expressing transfected Stat 5 and growth hormone receptor cDNA. Gel electrophoresis mobility shift analyses revealed the growth hormone-dependent presence of specific DNA-binding proteins in these extracts. The complexes formed could be supershifted by polyclonal anti-Stat 5 antiserum. In other experiments nuclear extracts from growth hormone-treated Chinese hamster ovary cells stably expressing transfected growth hormone receptor cDNA and liver from growth hormone-treated hypophysectomized rats were used for gel electrophoresis mobility shift analyses. These also revealed the presence of specific DNA-binding proteins sharing antigenic determinants with Stat 5. Stat 5 cDNA was shown to be capable of complementing the growth hormone-dependent activation of transcription of a reporter gene in the otherwise unresponsive COS-7 cell line. This complementation was dependent on the presence of Stat 5 tyrosine 694, suggesting a role for phosphorylation of this residue in growth hormone-dependent activation of DNA-binding and transcription.