ABSTRACT
Recently, the wireless sensor network paradigm is shifting toward research aimed at enabling the robust delivery of multimedia content. A challenge is to deliver multimedia content with predefined levels of Quality of Service (QoS) under resource constraints such as bandwidth, energy, and delay. In this paper, we propose a distributed systematic network coding (DSNC) scheme for reliable multimedia content uploading over wireless multimedia sensor networks, in which a large number of multimedia sensor nodes upload their own content to a sink through a cluster head node. The design objective is to increase the reliability and bandwidth-efficient utilization in uploading with low decoding complexity. The proposed scheme consists of two phases: in the first phase, each sensor node distributedly encodes the content into systematic network coding packets and transmits them to the cluster head; then in the second phase, the cluster head encodes all successfully decoded incoming packets from multiple sensor nodes into innovative systematic network coding packets and transmits them to the sink. A bandwidth-efficient and channel-aware error control algorithm is proposed to enhance the bandwidth-efficient utilization by dynamically determining the optimal number of innovative coded packets. For performance analysis and evaluation, we firstly derive the closed-form equations of decoding probability to validate the effectiveness of the proposed uploading scheme. Furthermore, we perform various simulations along with a discussion in terms of three performance metrics: decoding probability, redundancy, and image quality measurement. The analytical and experimental results demonstrate that the performance of our proposed DSNC outperforms the existing uploading schemes.
ABSTRACT
Several mechanisms are involved in controlling intracellular survival of pathogenic mycobacteria in host macrophages, but how these mechanisms are regulated remains poorly understood. We report a role for Kelch-like ECH-associated protein 1 (Keap1), an oxidative stress sensor, in regulating inflammation induced by infection with Mycobacterium avium in human primary macrophages. By using confocal microscopy, we found that Keap1 associated with mycobacterial phagosomes in a time-dependent manner, whereas siRNA-mediated knockdown of Keap1 increased M. avium-induced expression of inflammatory cytokines and type I interferons (IFNs). We show evidence of a mechanism whereby Keap1, as part of an E3 ubiquitin ligase complex with Cul3 and Rbx1, facilitates ubiquitination and degradation of IκB kinase (IKK)-ß thus terminating IKK activity. Keap1 knockdown led to increased nuclear translocation of transcription factors NF-κB, IFN regulatory factor (IRF) 1, and IRF5 driving the expression of inflammatory cytokines and IFN-ß. Furthermore, knockdown of other members of the Cul3 ubiquitin ligase complex also led to increased cytokine expression, further implicating this ligase complex in the regulation of the IKK family. Finally, increased inflammatory responses in Keap1-silenced cells contributed to decreased intracellular growth of M. avium in primary human macrophages that was reconstituted with inhibitors of IKKß or TANK-binding kinase 1 (TBK1). Taken together, we propose that Keap1 acts as a negative regulator for the control of inflammatory signaling in M. avium-infected human primary macrophages. Although this might be important to avoid sustained or overwhelming inflammation, our data suggest that a negative consequence could be facilitated growth of pathogens like M. avium inside macrophages.
