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    Effects of free surface and heterogeneous residual internal stress on stress-driven grain growth in nanocrystalline metals
    (London : Hindawi, 2013) Schneider, Andreas S.; Wang, F.; Zhao, J.; Huang, P.; Lu, T.J.; Xu, K.W.
    By reevaluating the experimental study of Zhang et al. (2005), here we demonstrate that the extent of grain growth, previously proposed to be solely driven by external stress, may have been significantly overestimated. A new physical mechanism, termed as free surface assisted stress-driven grain growth (or self-mechanical annealing), is proposed and discussed in detail. Representing the cooperative effect of free surface and heterogeneous residual internal stress, the proposed mechanism is considered more favorable than the traditional pure stress-driven mechanism for interpreting the abnormal grain growth widely observed in deforming nanocrystalline metals at room temperature.
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    Proteinase-activated receptor-2 agonist activates anti-influenza mechanisms and modulates IFNγ induced antiviral pathways in human neutrophils
    (London : Hindawi, 2013) Feld, Micha; Shpacovitch, Victoria; Ehrhardt, Christina; Fastrich, Michaela; Goerge, Tobias; Ludwig, Stephan; Steinhoff, Martin
    Proteinase-activated receptor-2 (PAR2) is expressed by human leukocytes and participates in the development of inflammatory diseases. Recent studies demonstrated an ability of PAR2 agonist to enhance IFNγ-induced antiviral responses of human leukocytes. However, the precise cellular antiviral defense mechanisms triggered in leukocytes after stimulation with IFNγ and/or PAR2 agonist remain elusive. Therefore, we aimed to identify neutrophil defense mechanisms involved in antiviral resistance. Here we demonstrated that PAR2 agonist enhanced IFNγ-related reduction of influenza A virus (IAV) replication in human neutrophils. PAR2-mediated decrease in IAV replication was associated with reduced NS-1 transcription. Moreover, PAR2-dependent neutrophil activation resulted in enhanced myeloperoxidase degranulation and extracellular myeloperoxidase disrupted IAV. The production of ROS was elevated in response to PAR2 activation. Interestingly, IFNγ did not influence both effects: PAR2 agonist-triggered myeloperoxidase (MPO) release and reactive oxygen species (ROS) production, which are known to limit IAV infections. In contrast, orthomyxovirus resistance gene A (MxA) protein expression was synergistically elevated through PAR2 agonist and IFNγ in neutrophils. Altogether, these findings emphasize two PAR2-controlled antiviral mechanisms that are independent of or modulated by IFNγ.