26 research outputs found

    Nucleon Structure from Lattice QCD Using a Nearly Physical Pion Mass

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    We report the first Lattice QCD calculation using the almost physical pion mass mpi=149 MeV that agrees with experiment for four fundamental isovector observables characterizing the gross structure of the nucleon: the Dirac and Pauli radii, the magnetic moment, and the quark momentum fraction. The key to this success is the combination of using a nearly physical pion mass and excluding the contributions of excited states. An analogous calculation of the nucleon axial charge governing beta decay has inconsistencies indicating a source of bias at low pion masses not present for the other observables and yields a result that disagrees with experiment.Comment: journal version; 15 pages, 6 figure

    Probabilistic models to evaluate effectiveness of steel bridge weld fatigue retrofitting by peening

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    The purpose of this study was to evaluate, with two probabilistic analytical models, the effectiveness of several alternative fatigue management strategies for steel bridge welds. The investigated strategies employed, in various combinations, magnetic particle inspection, gouging and rewelding, and postweld treatment by peening. The analytical models included a probabilistic strain-based fracture mechanics model and a Markov chain model. For comparing the results obtained with the two models, the fatigue life was divided into a small, fixed number of condition states based on crack depth, similar to those often used by bridge management systems to model deterioration due to other processes, such as corrosion and road surface wear. The probabilistic strain-based fracture mechanics model was verified first by comparison with design S-N curves and test data for untreated welds. Next, the verified model was used to determine the probability that untreated and treated welds would be in each condition state in a given year; the probabilities were then used to calibrate transition probabilities for a much simpler Markov chain fatigue model. Then both models were used to simulate a number of fatigue management strategies. From the results of these simulations, the performance of the different strategies was compared, and the accuracy of the simpler Markov chain fatigue model was evaluated. In general, peening was more effective if preceded by inspection of the weld. The Markov chain fatigue model did a reasonable job of predicting the general trends and relative effectiveness of the different investigated strategies

    Evolution of a Metal to Insulator Transition in Ca2x_{2-x}Nax_{x}CuO2_{2}Cl2_{2}, as seen by ARPES

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    We present angle resolved photoemission (ARPES) data on Na-doped Ca2_2CuO2_2Cl2_2. We demonstrate that the chemical potential shifts upon doping the system across the insulator to metal transition. The resulting low energy spectra reveal a gap structure which appears to deviate from the canonical dx2y2 cos(kxa)cos(kya)d_{x2-y2} ~ |cos(k_x a)-cos(k_y a)| form. To reconcile the measured gap structure with d-wave superconductivity one can understand the data in terms of two gaps, a very small one contributing to the nodal region and a very large one dominating the anti-nodal region. The latter is a result of the electronic structure observed in the undoped antiferromagnetic insulator. Furthermore, the low energy electronic structure of the metallic sample contains a two component structure in the nodal direction, and a change in velocity of the dispersion in the nodal direction at roughly 50 meV. We discuss these results in connection with photoemission data on other cuprate systems.Comment: 10 pages, 12 figures, accepted by PRB; a high quality pdf is available at http://helios.physics.utoronto.ca/~fronning/RonningNaCCOCResub.pdf (2.2MB

    PTPA variants and impaired PP2A activity in early-onset parkinsonism with intellectual disability

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    The protein phosphatase 2A complex (PP2A), the major Ser/Thr phosphatase in the brain, is involved in a number of signalling pathways and functions, including the regulation of crucial proteins for neurodegeneration, such as alpha-synuclein, tau and LRRK2. Here, we report the identification of variants in the PTPA/PPP2R4 gene, encoding a major PP2A activator, in two families with early-onset parkinsonism and intellectual disability. We carried out clinical studies and genetic analyses, including genome-wide linkage analysis, whole-exome sequencing, and Sanger sequencing of candidate variants. We next performed functional studies on the disease-associated variants in cultured cells and knock-down of ptpa in Drosophila melanogaster. We first identified a homozygous PTPA variant, c.893T&gt;G (p.Met298Arg), in patients from a South African family with early-onset parkinsonism and intellectual disability. Screening of a large series of additional families yielded a second homozygous variant, c.512C&gt;A (p.Ala171Asp), in a Libyan family with a similar phenotype. Both variants co-segregate with disease in the respective families. The affected subjects display juvenile-onset parkinsonism and intellectual disability. The motor symptoms were responsive to treatment with levodopa and deep brain stimulation of the subthalamic nucleus. In overexpression studies, both the PTPA p.Ala171Asp and p.Met298Arg variants were associated with decreased PTPA RNA stability and decreased PTPA protein levels; the p.Ala171Asp variant additionally displayed decreased PTPA protein stability. Crucially, expression of both variants was associated with decreased PP2A complex levels and impaired PP2A phosphatase activation. PTPA orthologue knock-down in Drosophila neurons induced a significant impairment of locomotion in the climbing test. This defect was age-dependent and fully reversed by L-DOPA treatment. We conclude that bi-allelic missense PTPA variants associated with impaired activation of the PP2A phosphatase cause autosomal recessive early-onset parkinsonism with intellectual disability. Our findings might also provide new insights for understanding the role of the PP2A complex in the pathogenesis of more common forms of neurodegeneration.</p
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