26 research outputs found

    Assessment of the LES-FGM framework for capturing stable and unstable modes in a hydrogen / methane fuelled premixed combustor

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    The main objective of this paper is to assess the capability of compressible Large Eddy Simulations (LES) to capture azimuthal combustion instability. The thickened flame model coupled with Flamelet Generated Manifold (FGM) tabulated chemistry is used as the combustion model. LES of an annular combustor is performed for five cases featuring stable and unstable combustion of hydrogen-methane mixtures. The unstable modes feature azimuthal instabilities and this annular combustor is used to test the LES-FGM framework. A consistent methodology is applied across all cases. It is found that LES predicts azimuthal modes for stable cases but these modes are weak and intermittent with pressure fluctuation amplitudes within the order of experimental noise. In addition, the unstable cases capture azimuthal modes that have approximately the same frequency as that of the experiment though the amplitudes of the modes are over-predicted. This suggests that the described LES-FGM framework is able to predict the onset of thermoacoustic instabilities and their qualitative changes with addition of hydrogen. © 2023 The Combustion InstituteAssessment of the LES-FGM framework for capturing stable and unstable modes in a hydrogen / methane fuelled premixed combustoracceptedVersio

    Switch activation of PI-PLC downstream signals in activated macrophages with wortmannin

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    AbstractPhosphatidylinositol (4,5)-bisphosphate (PtdIns(4,5)P2) has been known to serve as a substrate for phosphatidylinositol 3-kinase (PI3K) and phosphoinositide-specific phospholipase C (PI-PLC), which can produce PtdIns(3,4,5)P3 and inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) and diacylglycerol (DAG), respectively. In this study, we elucidated the role of PI-PLC during the LPS-activated mouse macrophages RAW264.7 treated with PI3K inhibitor wortmannin. First, wortmannin treatment enhanced Ins(1,4,5)P3 production and iNOS expression in LPS-activated macrophages. Inhibition of PI3K by p85 siRNA also showed an enhancement of iNOS expression. On the other hand, overexpression of PI3K by ras-p110 expression plasmid significantly decreased iNOS expression in LPS-activated macrophages. In addition, overexpression of wild-type or dominant-negative Akt expression plasmid did not affect the iNOS expression in LPS-activated macrophages. Second, treatment of PI-PLC inhibitor U73122 reversed the enhancement of iNOS expression, the increase of phosphorylation level of ERK, JNK and p38, and the increase of AP-1-dependent gene expression in wortmannin-treated and LPS-activated macrophages. However, NF-κB activity determined by EMSA assay and reporter plasmid assay did not change during LPS-activated macrophages with or without wortmannin. We propose that the inhibition of PI3K by wortmannin in mouse macrophages enhances the PI-PLC downstream signals, and subsequently increases the LPS induction of iNOS expression independently of Akt pathway

    Gut mucosal DAMPs in IBD: From mechanisms to therapeutic implications

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    Endogenous damage-associated molecular patterns (DAMPs) are released during tissue damage and have increasingly recognized roles in the etiology of many human diseases. The inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohn’s disease (CD), are immune-mediated conditions where high levels of DAMPs are observed. DAMPs such as calprotectin (S100A8/9) have an established clinical role as a biomarker in IBD. In this review, we use IBD as an archetypal common chronic inflammatory disease to focus on the conceptual and evidential importance of DAMPs in pathogenesis and why DAMPs represent an entirely new class of targets for clinical translation. </p

    Detection of GAP43 expression in the sciatic nerve of 808-nm LLLT laser-treated site using immunofluorescent staining.

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    <p>Groups: sham-operated rats without (normal) or with 8 J/cm<sup>2</sup> LLLT (normal+8J) and rats with sciatic nerve crush injury without (crush) or with LLLT at 3 J/cm<sup>2</sup> (crush+3J), 8 J/cm<sup>2</sup> (crush+8J) or 15 J/cm<sup>2</sup> (crush+15J). Sections were labeled with DAPI (blue), GAP43 (green) and neurofilament (red), which is specifically expressed in neurites. Original magnification: 100×. White boxes show the enlarged views with a magnification of 400×. Scale bar, 200 um.</p

    The 3 J/cm<sup>2</sup> and 8 J/cm<sup>2</sup> LLLT treatments improved the sciatic functional index (SFI) in rats with a sciatic nerve crush injury.

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    <p>Representative images of (A) the sham-operated rat left hindlimb and (B) the sciatic-injured rat right hindlimb. (C) Functional assessment of the recovery of injured sciatic nerves by calculating the SFI in the normal rats without (normal) or with 8 J/cm<sup>2</sup> LLLT (normal+8J) and in the sciatic nerve-crushed rats without (crush) or with LLLT at 3 J/cm<sup>2</sup> (crush+3J), 8 J/cm<sup>2</sup> (crush+8J) or 15 J/cm<sup>2</sup> (crush+15J). *P<0.05, compared with crush group.</p

    The 8 J/cm<sup>2</sup> dosage of 808-nm laser enhanced the range of motion (ROM).

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    <p>(A) Representative images show the sham-operated left rat hindlimb at mid-stance phase and (B) the sciatic-injured right rat hindlimb at mid-stance phase. (C) Functional assessment of the recovery of the injured sciatic nerve using ROM analysis by comparing the right hindlimb with the left hindlimb (ratio) in the normal rats without (normal) or with 8 J/cm<sup>2</sup> LLLT (normal+8J) and in the sciatic nerve-crushed rats without (crush) or with LLLT at 3 J/cm<sup>2</sup> (crush+3J), 8 J/cm<sup>2</sup> (crush+8J) or 15 J/cm<sup>2</sup> (crush+15J). *P<0.05, compared with the crush group.</p

    Detection of GAP43 protein expression in rats with sciatic nerve crush injury after 808-nm LLLT treatments using western blot analysis.

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    <p>Representative western blotting and quantitative analyses of GAP43 protein expression in the sciatic nerve of normal rats with 8 J/cm<sup>2</sup> LLLT (normal+8J) and in the rats with sciatic nerve crush injury without (crush) or with LLLT at 3 J/cm<sup>2</sup> (crush+3J), 8 J/cm<sup>2</sup> (crush+8J) or 15 J/cm<sup>2</sup> (crush+15J) were shown. We detected the expression of the GAP43 protein in the sciatic nerve of left sham-operated hindlimb (left normal control; N) and in the sciatic nerve of right hindlimb at the laser-treated site (T) or a distal site (D). *P<0.05, **P<0.01, compared with the left sham-operated hindlimb (left normal control; N). <sup>#</sup>P<0.05, compared with the crush group at the laser-treated site (T). <sup>&</sup>P<0.05, compared between the crush groups at the distal site (D).</p

    LLLT-treated (808 nm) sciatic nerve presented thicker myelin sheaths.

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    <p>Representative TEM images (A) and quantitative analyses of myelin sheath thickness (B) in the sciatic nerves of sham-operated rats without (normal) or with 8 J/cm<sup>2</sup> LLLT (normal+8J) and in the rats with sciatic nerve crush injury without (crush) or with LLLT at 3 J/cm<sup>2</sup> (crush+3J), 8 J/cm<sup>2</sup> (crush+8J) or 15 J/cm<sup>2</sup> (crush+15J). <sup>#</sup>P<0.05, compared with the crush group. Scale bar, 5 um.</p
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