A software framework for alleviating the effects of MAC-aware jamming attacks in wireless access networks

The IEEE 802.11 protocol inherently provides the same long-term throughput to all the clients associated with a given access point (AP). In this paper, we first identify a clever, low-power jamming attack that can take advantage of this behavioral trait: the placement of a lowpower jammer in a way that it affects a single legitimate client can cause starvation to all the other clients. In other words, the total throughput provided by the corresponding AP is drastically degraded. To fight against this attack, we design FIJI, a cross-layer anti-jamming system that detects such intelligent jammers and mitigates their impact on network performance. FIJI looks for anomalies in the AP load distribution to efficiently perform jammer detection. It then makes decisions with regards to optimally shaping the traffic such that: (a) the clients that are not explicitly jammed are shielded from experiencing starvation and, (b) the jammed clients receive the maximum possible throughput under the given conditions. We implement FIJI in real hardware; we evaluate its efficacy through experiments on two wireless testbeds, under different traffic scenarios, network densities and jammer locations. We perform experiments both indoors and outdoors, and we consider both WLAN and mesh deployments. Our measurements suggest that FIJI detects such jammers in realtime and alleviates their impact by allocating the available bandwidth in a fair and efficient way. © Springer Science+Business Media

Inhibition of Interleukin 10 Signaling after Fc Receptor Ligation and during Rheumatoid Arthritis

Interleukin-10 (IL-10) is a potent deactivator of myeloid cells that limits the intensity and duration of immune and inflammatory responses. The activity of IL-10 can be suppressed during inflammation, infection, or after allogeneic tissue transplantation. We investigated whether inflammatory factors suppress IL-10 activity at the level of signal transduction. Out of many factors tested, only ligation of Fc receptors by immune complexes inhibited IL-10 activation of the Jak-Stat signaling pathway. IL-10 signaling was suppressed in rheumatoid arthritis joint macrophages that are exposed to immune complexes in vivo. Activation of macrophages with interferon-γ was required for Fc receptor–mediated suppression of IL-10 signaling, which resulted in diminished activation of IL-10–inducible genes and reversal of IL-10–dependent suppression of cytokine production. The mechanism of inhibition involved decreased cell surface IL-10 receptor expression and Jak1 activation and was dependent on protein kinase C delta. These results establish that IL-10 signaling is regulated during inflammation and identify Fc receptors and interferon-γ as important regulators of IL-10 activity. Generation of macrophages refractory to IL-10 can contribute to pathogenesis of inflammatory and infectious diseases characterized by production of interferon-γ and immune complexes

Gene Network Analysis of Bone Marrow Mononuclear Cells Reveals Activation of Multiple Kinase Pathways in Human Systemic Lupus Erythematosus

Background: Gene profiling studies provide important information for key molecules relevant to a disease but are less informative of protein-protein interactions, post-translational modifications and regulation by targeted subcellular localization. Integration of genomic data and construction of functional gene networks may provide additional insights into complex diseases such as systemic lupus erythematosus (SLE). Methodology/Principal Findings: We analyzed gene expression microarray data of bone marrow mononuclear cells (BMMCs) from 20 SLE patients (11 with active disease) and 10 controls. Gene networks were constructed using the bioinformatic tool Ingenuity Gene Network Analysis. In SLE patients, comparative analysis of BMMCs genes revealed a network with 19 central nodes as major gene regulators including ERK, JNK, and p38 MAP kinases, insulin, Ca2+ and STAT3. Comparison between active versus inactive SLE identified 30 central nodes associated with immune response, protein synthesis, and post-transcriptional modification. A high degree of identity between networks in active SLE and non-Hodgkin's lymphoma (NHL) patients was found, with overlapping central nodes including kinases (MAPK, ERK, JNK, PKC), transcription factors (NF-kappaB, STAT3), and insulin. In validation studies, western blot analysis in splenic B cells from 5-month-old NZB/NZW F1 lupus mice showed activation of STAT3, ITGB2, HSPB1, ERK, JNK, p38, and p32 kinases, and downregulation of FOXO3 and VDR compared to normal C57Bl/6 mice. Conclusions/Significance: Gene network analysis of lupus BMMCs identified central gene regulators implicated in disease pathogenesis which could represent targets of novel therapies in human SLE. The high similarity between active SLE and NHL networks provides a molecular basis for the reported association of the former with lymphoid malignancies

Efficient Load-Aware Channel Allocation in Wireless Access Networks

Dense deployments of hybrid WLANs result in high levels of interference and low end-user throughput. Many frequency allocation mechanisms for WLANs have been proposed by a large body of previous studies. However, none of these mechanisms considers the load that is carried by APs in terms of channel conditions, number of affiliated users as well as communication-load, in conjunction. In this paper, we propose LAC, a load-aware channel allocation scheme for WLANs, which considers all the above performance determinant factors. LAC incorporates an airtime cost metric into its channel scanning process, in order to capture the effects of these factors and select the channel that will provide approximately maximum long-term throughput. We evaluate LAC through extensive OPNET simulations, for many different traffic scenarios. Our simulations demonstrate that LAC outperforms other frequency allocation policies for WLANs in terms of total network throughput by up to 135%