20 research outputs found

    Luttinger model approach to interacting one-dimensional fermions in a harmonic trap

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    A model of interacting one--dimensional fermions confined to a harmonic trap is proposed. The model is treated analytically to all orders of the coupling constant by a method analogous to that used for the Luttinger model. As a first application, the particle density is evaluated and the behavior of Friedel oscillations under the influence of interactions is studied. It is found that attractive interactions tend to suppress the Friedel oscillations while strong repulsive interactions enhance the Friedel oscillations significantly. The momentum distribution function and the relation of the model interaction to realistic pair interactions are also discussed.Comment: 12 pages latex, 1 eps-figure in 1 tar file, extended Appendix, added and corrected references, new eq. (53), corrected typos, accepted for PR

    Information and digital literacies; a review of concepts

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    A detailed literature reviewing, analysing the multiple and confusing concepts around the ideas of information literacy and digital literacy at the start of the millennium. The article was well-received, and is my most highly-cited work, with over 1100 citations

    Histones from dying renal cells aggravate kidney injury via TLR2 and TLR4.

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    In AKI, dying renal cells release intracellular molecules that stimulate immune cells to secrete proinflammatory cytokines, which trigger leukocyte recruitment and renal inflammation. Whether the release of histones, specifically, from dying cells contributes to the inflammation of AKI is unknown. In this study, we found that dying tubular epithelial cells released histones into the extracellular space, which directly interacted with Toll-like receptor (TLR)-2 (TLR2) and TLR4 to induce MyD88, NF-κB, and mitogen activated protein kinase signaling. Extracellular histones also had directly toxic effects on renal endothelial cells and tubular epithelial cells in vitro. In addition, direct injection of histones into the renal arteries of mice demonstrated that histones induce leukocyte recruitment, microvascular vascular leakage, renal inflammation, and structural features of AKI in a TLR2/TLR4-dependent manner. Antihistone IgG, which neutralizes the immunostimulatory effects of histones, suppressed intrarenal inflammation, neutrophil infiltration, and tubular cell necrosis and improved excretory renal function. In summary, the release of histones from dying cells aggravates AKI via both its direct toxicity to renal cells and its proinflammatory effects. Because the induction of proinflammatory cytokines in dendritic cells requires TLR2 and TLR4, these results support the concept that renal damage triggers an innate immune response, which contributes to the pathogenesis of AKI
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