When Mobile Blockchain Meets Edge Computing

Blockchain, as the backbone technology of the current popular Bitcoin digital currency, has become a promising decentralized data management framework. Although blockchain has been widely adopted in many applications, e.g., finance, healthcare, and logistics, its application in mobile services is still limited. This is due to the fact that blockchain users need to solve preset proof-of-work puzzles to add new data, i.e., a block, to the blockchain. Solving the proof-of-work, however, consumes substantial resources in terms of CPU time and energy, which is not suitable for resource-limited mobile devices. To facilitate blockchain applications in future mobile Internet of Things systems, multiple access mobile edge computing appears to be an auspicious solution to solve the proof-of-work puzzles for mobile users. We first introduce a novel concept of edge computing for mobile blockchain. Then, we introduce an economic approach for edge computing resource management. Moreover, a prototype of mobile edge computing enabled blockchain systems is presented with experimental results to justify the proposed concept.Comment: Accepted by IEEE Communications Magazin

TAS-Based Incremental Hybrid Decode–Amplify–Forward Relaying for Physical Layer Security Enhancement

In this paper, a transmit antenna selection (TAS)- based incremental hybrid decode-amplify-forward (IHDAF) scheme is proposed to enhance physical layer security in cooperative relay networks. Specifically, TAS is adopted at the source in order to reduce the feedback overhead. In the proposed TAS-based IHDAF scheme, the network transmits signals to the destination adaptive select direction transmission mode, AF mode or DF mode depending on the capacity of the source-relay link and source-relay link. In order to fully examine the benefits of the proposed TAS-based IHDAF scheme, we first derive its secrecy outage probability (SOP) in a closed-form expression. We then conduct asymptotic analysis on the SOP, which reveals the secrecy performance floor of the proposed TAS-based IHDAF scheme when no channel state information is available at the source. Theoretical analysis and simulation results demonstrate that the proposed TAS-based IHDAF scheme outperforms the selective decode-and-forward (SDF), the incremental decodeand-forward (IDF), and the noncooperative direction transmission (DT) schemes in terms of the SOP and effective secrecy throughout, especially when the relay is close to the destination. Furthermore, the proposed TAS-based IHDAF scheme offer a good trade-off between complexity and performance compare with using all antennas at the source.ARC Discovery Projects Grant DP150103905

Minocycline and sulforaphane inhibited lipopolysaccharide-mediated retinal microglial activation

PURPOSE: To elucidate the inhibitory effect of minocycline and sulforaphane on lipopolysaccharide (LPS)-induced retinal microglial activation and the mechanisms through which they exerted their inhibitory effects. METHODS: Primary retinal microglial cultures were exposed to LPS with or without minocycline and sulforaphane. The mRNA expression of monocyte chemotactic protein (MCP)-1, MCP-3, macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, eotaxin, regulated upon activation normal T-cell expressed and secreted (RANTES) protein, and interleukin (IL)-10 were examined by reverse transcription polymerase chain reaction (RT-PCR) assay. The mRNA expression of inducible nitric oxide synthase (iNOS) and subsequent nitric oxide (NO) production were examined by RT-PCR assay and Griess reagent assay. Protein expression of the p65 subunit of nuclear factor-kappa B (NF-kappa B) and p-p38, p-p44/42 and p-JNK mitogen-activated protein kinases (MAPKs) were examined by Western blot and immunofluorescent analysis. RESULTS: Cultured retinal microglial cells were activated following exposure to LPS. The mRNA expression and protein production of eotaxin, RANTES, and IL-10 and the mRNA expression of iNOS and subsequent NO production were upregulated. The protein expression of p-p38, p-JNK, and the p65 subunit of NF-kappa B were also upregulated. However, the protein expression of p-p44/42 was not significantly changed. Pretreatment with minocycline or sulforaphane for 1 h before LPS administration inhibited LPS-induced microglial morphological change and inhibited LPS-induced upregulation of p-p38, but had no effect on the expression of p-p44/42, p-JNK, and the p65 subunit of NF-kappa B. CONCLUSIONS: Minocycline and sulforaphane inhibited LPS-induced retinal microglial activation, Western blot and immunofluorescent studies showed decreased p-p38 MAPK expression. We suggested that the inhibitory effect of minocycline and sulforaphane was partly through a p38 MAPK-dependent mechanism.Biochemistry & Molecular BiologyOphthalmologySCI(E)PubMed18ARTICLE117-181083-10931