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    A modelling technique for calculating stress intensity factors for structures reinforced by bonded straps. Part II: Validation

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    In this second part of the two-part paper validation of the 2D FE modelling technique described in the first part is presented for a range of test configurations. Each mechanism that influences crack growth behaviour of strap reinforced structures is modelled for different substrate geometries, strap materials and dimensions in order to test the accuracy and robustness of the methodology. First, calculated through-thickness strain energy release rate distribution is compared with the result of a 3D FE model to validate this 2D model. Second, calculated disbond areas, thermal residual stresses and their redistribution with crack propagation are validated against experimental measurements. Third, influence of geometric nonlinearity and the need to use the alternate analysis method described in part I are demonstrated by examples, and errors generated by not following this analysis rule are given. Finally, using the 2D model calculated stress intensity factors, fatigue crack growth rates and lives are predicted for different specimens, strap materials and applied stress levels and are compared with the experimental tests. Good or acceptable agreement has been achieved for each case

    PPM1D phosphatase, a target of p53 and RBM38 RNA-binding protein, inhibits p53 mRNA translation via dephosphorylation of RBM38.

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    PPM1D phosphatase, also called wild-type p53-induced phosphatase 1, promotes tumor development by inactivating the p53 tumor suppressor pathway. RBM38 RNA-binding protein, also called RNPC1 and a target of p53, inhibits p53 messenger RNA (mRNA) translation, which can be reversed by GSK3 protein kinase via phosphorylation of RBM38 at serine 195. Here we showed that ectopic expression of RBM38 increases, whereas knockdown of RBM38 inhibits, PPM1D mRNA translation. Consistent with this, we found that RBM38 directly binds to PPM1D 3'-untranslated region (3'-UTR) and promotes expression of a heterologous reporter gene that carries PPM1D 3'-UTR in a dose-dependent manner. Interestingly, we showed that PPM1D directly interacts with and dephosphorylates RBM38 at serine 195. Furthermore, we showed that PPM1D modulates p53 mRNA translation and p53-dependent growth suppression through dephosphorylation of RBM38. These findings provide evidence that the crosstalk between PPM1D and RBM38, both of which are targets and modulators of p53, has a critical role in p53 expression and activity

    Giant magnetoimpedance in crystalline Mumetal

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    We studied giant magnetoimpedance (GMI) effect in commercial crystalline Mumetal, with the emphasis to sample thickness dependence and annealing effects. By using appropriate heat treatment one can achieve GMI ratios as high as 310%, and field sensitivity of about 20%/Oe, which is comparable to the best GMI characteristics obtained for amorphous and nanocrystalline soft magnetic materials.Comment: 8 pages, 3 figure
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