340 research outputs found

    Floroindole confers protection against cecal ligation and puncture-induced sepsis via inhibition of NF-kB p65 phosphorylation

    Get PDF
    Purpose: To investigate the protective effect of floroindole against cecal ligation and puncture (CLP)- induced sepsis, as well as the underlying mechanism of action. Methods: Thirty-five 10–week-old male Wistar rats weighing 190 - 210 g (mean: 200.00 ± 10.10 g) were used for this study. The rats were randomly assigned to seven groups of five rats each, viz, normal control group, and six CLP groups. The CLP groups were those subjected to cecal ligation and puncture (CLP). The first 5 CLP groups received 2, 4, 6, 8 or 10 mg/kg floroindole, respectively, 1 h after CLP, via intraperitoneal route (i.p.) while the 6th CLP group served as untreated control. Western blotting, enzyme-linked immunosorbent assay (ELISA) and real-time quantitative polymerase chain reaction (qRT-PCR) were used for the assessment of the expression levels of tumor necrosis factor-α (TNF- α), interleukn-6 (IL-6), nucleotide-binding oligomerization domain 2 (NOD2) and p-NF-κB p65. Results: Cecal ligation and puncture (CLP) significantly and time-dependently upregulated the expressions of TNF-α, IL-6 and NOD2 in intestinal tissues of rats (p < 0.05). However, treatment with floroindole significantly, and dose-dependently down-regulated CLP-induced expressions of these proteins (p < 0.05). Treatment of rats with floroindole also significantly and dose-dependently inhibited CLP-induced phosphorylation of NF-κB p65 in rat ileum (p < 0.05). Conclusion: The results obtained in this study demonstrate that floroindole confers some degree of protection against CLP-induced sepsis via inhibition of NF-κB p65 phosphorylation

    Experimental Investigation on the Vertical Distribution of Cohesive Sediment Concentration in Weak Dynamical Flow

    Get PDF
    Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

    Visible Light Communication System Evaluations with Integrated Hardware and Optical Parameters

    Get PDF

    Optical Wireless Communication Channel Measurements and Models

    Get PDF

    Joint transmit power allocation and splitting for swipt aided OFDM-IDMA in wireless sensor networks

    Get PDF
    In this paper, we propose to combine Orthogonal Frequency Division Multiplexing-Interleave Division Multiple Access (OFDM-IDMA) with Simultaneous Wireless Information and Power Transfer (SWIPT), resulting in SWIPT aided OFDM-IDMA scheme for power-limited sensor networks. In the proposed system, the Receive Node (RN) applies Power Splitting (PS) to coordinate the Energy Harvesting (EH) and Information Decoding (ID) process, where the harvested energy is utilized to guarantee the iterative Multi-User Detection (MUD) of IDMA to work under sufficient number of iterations. Our objective is to minimize the total transmit power of Source Node (SN), while satisfying the requirements of both minimum harvested energy and Bit Error Rate (BER) performance from individual receive nodes. We formulate such a problem as a joint power allocation and splitting one, where the iteration number of MUD is also taken into consideration as the key parameter to affect both EH and ID constraints. To solve it, a sub-optimal algorithm is proposed to determine the power profile, PS ratio and iteration number of MUD in an iterative manner. Simulation results verify that the proposed algorithm can provide significant performance improvement

    LncEGFL7OS Regulates Human Angiogenesis by Interacting with MAX at the EGFL7/miR-126 locus

    Get PDF
    In an effort to identify human endothelial cell (EC)-enriched lncRNAs,~500 lncRNAswere shown to be highly restricted in primary human ECs. Among them,lncEGFL7OS, located inthe opposite strand of theEGFL7/miR-126gene, is regulated by ETS factors through abidirectional promoter in ECs. It is enriched in highly vascularized human tissues, and upregulatedin the hearts of dilated cardiomyopathy patients. LncEGFL7OS silencing impairs angiogenesis asshown by EC/fibroblast co-culture, in vitro/in vivo and ex vivo human choroid sproutingangiogenesis assays, while lncEGFL7OS overexpression has the opposite function. Mechanistically,lncEGFL7OS is required for MAPK and AKT pathway activation by regulating EGFL7/miR-126expression. MAX protein was identified as a lncEGFL7OS-interacting protein that functions toregulate histone acetylation in the EGFL7/miR-126 promoter/enhancer. CRISPR-mediated targetingof EGLF7/miR-126/lncEGFL7OS locus inhibits angiogenesis, inciting therapeutic potentialargeting this locus. Our study establishes lncEGFL7OS as a human/primate-specific EC-restricted lncRNA critical for human angiogenesis
    • …
    corecore