Grouping and sponsoring centric green coverage model for Internet of Things

Recently, green computing has received significant attention for Internet of Things (IoT) environments due to the growing computing demands under tiny sensor enabled smart services. The related literature on green computing majorly focuses on a cover set approach that works efficiently for target coverage, but it is not applicable in case of area coverage. In this paper, we present a new variant of a cover set approach called a grouping and sponsoring aware IoT framework (GS-IoT) that is suitable for area coverage. We achieve non-overlapping coverage for an entire sensing region employing sectorial sensing. Non-overlapping coverage not only guarantees a sufficiently good coverage in case of large number of sensors deployed randomly, but also maximizes the life span of the whole network with appropriate scheduling of sensors. A deployment model for distribution of sensors is developed to ensure a minimum threshold density of sensors in the sensing region. In particular, a fast converging grouping (FCG) algorithm is developed to group sensors in order to ensure minimal overlapping. A sponsoring aware sectorial coverage (SSC) algorithm is developed to set off redundant sensors and to balance the overall network energy consumption. GS-IoT framework effectively combines both the algorithms for smart services. The simulation experimental results attest to the benefit of the proposed framework as compared to the state-of-the-art techniques in terms of various metrics for smart IoT environments including rate of overlapping, response time, coverage, active sensors, and life span of the overall network

The 4-hydroxynonenal mediated oxidative damage of blood proteins and lipids involves secondary lipid peroxidation reactions

Lipid peroxidation is associated with several metabolic diseases. Lipid peroxidation causes cellular damage through reactive aldehyde species such as 4-hydroxyonenal (4-HNE). The exact mechanism(s) by which 4-HNE causes damage in the intravascular compartment is not yet exactly understood. Using an in vitro system, the damage induced by 4-HNE on the blood was investigated by measuring protein carbonyl groups and thiobarbituric acid reactive substances (TBARS) following 4-HNE treatment. The findings demonstrated that treatment with 4-HNE increased the carbonylation of protein and the formation of TBARS in the blood plasma. It was also tested whether phenelzine, a scavenger of aldehyde species, or U-83836E, a scavenger of lipid peroxy radicals, attenuated the damage caused by 4-HNE. It was demonstrated that phenelzine or U-83836E both mitigated the effects of 4-HNE on the proteins and the lipids of the blood plasma. The findings of the current study suggest that phenelzine, U-83836E or functionally similar therapeutics may prevent or treat diseases that involve an increased production of 4-HNE in the intravascular compartment.The present study was supported by the Deanship of Research at Jordan University of Science and Technology (grant no. 301/2014)

Glucagon-like peptide-1 exerts anti-inflammatory effects on mouse colon smooth muscle cells through the cyclic adenosine monophosphate/nuclear factor-κB pathway in vitro

Ahmed Al-Dwairi,1 Tamara E Alqudah,1 Othman Al-Shboul,1 Mohammad Alqudah,1 Ayman G Mustafa,2 Mahmoud A Alfaqih1 1Department of Physiology and Biochemistry, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan; 2Department of Anatomy, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan Background: Intestinal smooth muscle cells (SMCs) undergo substantial morphological, phenotypic, and contractile changes during inflammatory bowel disease (IBD). SMCs act as a source and target for different inflammatory mediators, however their role in IBD pathogenesis is usually overlooked. Glucagon-like peptide-1 (GLP-1) is an incretin hormone reported to exert multiple anti-inflammatory effects in different tissues including the gastrointestinal tract through various mechanisms. Aim: The aim of this research is to explore the effect of GLP-1 analog exendin-4 on the expression and secretion of inflammatory markers from mouse colon smooth muscle cells (CSMCs) after stimulation with lipopolysaccharide (LPS). Materials and methods: Freshly isolated CSMCs from male BALB/c mice were cultured in DMEM and treated with vehicle, LPS (1 µg/mL), LPS+exendin-4 (50 nM), or LPS+exendin-4 (100 nM) for 24 h. Expression of inflammatory cytokines was then evaluated by antibody array membrane. Results: CSMCs showed basal expression of several cytokines which was enhanced with the induction of inflammation by LPS. However, exendin-4 (50 and 100 nM) significantly (p<0.05) reduced the expression of multiple cytokines including tumor necrosis factor-α (TNF-α), interleukin-1α (IL-1α), T cell activation gene-3 (TCA-3), stromal cell-derived factor-1 (SDF-1), and macrophage colony stimulating factor (M-CSF). To confirm these results, expression of these cytokines was further assessed by enzyme-linked immunosorbent assay and real-time polymerase chain reaction and similar results were also observed. Moreover, secretion of TNF-α and IL1-α into the conditioned media was significantly downregulated by exendin-4 when compared to LPS-treated cells. Furthermore, LPS increased NF-κB phosphorylation, while exendin-4 significantly reduced levels of NF-κB phosphorylation. Conclusion: These data indicate that GLP-1 analogs can exert significant anti-inflammatory effects on CSMCs and can potentially be used as an adjunct treatment for inflammatory bowel conditions. Keywords: GLP-1, inflammation, inflammatory bowel disease, smooth muscl