Loss of strength in Ni3Al at elevated temperatures

Stress decrease above the stress peak temperature (750 K) is studied in h123i single crystals of Ni3(Al, 3 at.% Hf ). Two thermally activated deformation mechanisms are evidenced on the basis of stress relaxation and strain rate change experiments. From 500 to 1070 K, the continuity of the activation volume/temperature curves reveals a single mechanism of activation enthalpy 3.8 eV/atom and volume 90 b3 at 810K with an athermal stress of 330 MPa. Over the very same temperature interval, impurity or solute diffusion towards dislocation cores is evidenced through serrated yielding, peculiar shapes of stress–strain curves while changing the rate of straining and stress relaxation experiments. This complicates the identification of the deformation mechanism, which is likely connected with cube glide. From 1070 to 1270 K, the high-temperature mechanism has an activation enthalpy and volume of 4.8 eV/atom and 20 b3, respectively, at 1250 K

Asymptotic analysis for singularly perturbed convection-diffusion equations with a turning point

Turning points occur in many circumstances in fluid mechanics. When the viscosity is small, very complex phenomena can occur near turning points, which are not yet well understood. A model problem, corresponding to a linear convection-diffusion equation (e.g., suitable linearization of the Navier-Stokes or B́nard convection equations) is considered. Our analysis shows the diversity and complexity of behaviors and boundary or interior layers which already appear for our equations simpler than the Navier-Stokes or B́nard convection equations. Of course the diversity and complexity of these structures will have to be taken into consideration for the study of the nonlinear problems. In our case, at this stage, the full theoretical (asymptotic) analysis is provided. This study is totally new to the best of our knowledge. Numerical treatment and more complex problems will be considered elsewhere.open91

Spectral modification of laser-accelerated proton beams by self-generated magnetic fields

Target normal measurements of proton energy spectra from ultrathin (50-200 nm) planar foil targets irradiated by 10(19) W cm(-2) 40 fs laser pulses exhibit broad maxima that are not present in the energy spectra from micron thickness targets (6 mu m). The proton flux in the peak is considerably greater than the proton flux observed in the same energy range in thicker targets. Numerical modelling of the experiment indicates that this spectral modification in thin targets is caused by magnetic fields that grow at the rear of the target during the laser-target interaction

Numerical Evaluation of P-Multigrid Method for the Solution of Discontinuous Galerkin Discretizations of Diffusive Equations

This paper describes numerical experiments with P-multigrid to corroborate analysis, validate the present implementation, and to examine issues that arise in the implementations of the various combinations of relaxation schemes, discretizations and P-multigrid methods. The two approaches to implement P-multigrid presented here are equivalent for most high-order discretization methods such as spectral element, SUPG, and discontinuous Galerkin applied to advection; however it is discovered that the approach that mimics the common geometric multigrid implementation is less robust, and frequently unstable when applied to discontinuous Galerkin discretizations of di usion. Gauss-Seidel relaxation converges 40% faster than block Jacobi, as predicted by analysis; however, the implementation of Gauss-Seidel is considerably more expensive that one would expect because gradients in most neighboring elements must be updated. A compromise quasi Gauss-Seidel relaxation method that evaluates the gradient in each element twice per iteration converges at rates similar to those predicted for true Gauss-Seidel

Combined Effect of Hemostatic Gene Polymorphisms and the Risk of Myocardial Infarction in Patients with Advanced Coronary Atherosclerosis

BACKGROUND: Relative little attention has been devoted until now to the combined effects of gene polymorphisms of the hemostatic pathway as risk factors for Myocardial Infarction (MI), the main thrombotic complication of Coronary Artery Disease (CAD). The aim of this study was to evaluate the combined effect of ten common prothrombotic polymorphisms as a determinant of MI. METHODOLOGY/PRINCIPAL FINDINGS: We studied a total of 804 subjects, 489 of whom with angiographically proven severe CAD, with or without MI (n = 307; n = 182; respectively). An additive model considering ten common polymorphisms [Prothrombin 20210G>A, PAI-1 4G/5G, Fibrinogen beta -455G>A, FV Leiden and "R2", FVII -402G>A and -323 del/ins, Platelet ADP Receptor P2Y12 -744T>C, Platelet Glycoproteins Ia (873G>A), and IIIa (1565T>C)] was tested. The prevalence of MI increased linearly with an increasing number of unfavorable alleles (chi(2) for trend = 10.68; P = 0.001). In a multiple logistic regression model, the number of unfavorable alleles remained significantly associated with MI after adjustment for classical risk factors. As compared to subjects with 3-7 alleles, those with few (/=8) alleles had an increased MI risk (OR 2.49, 95%CIs 1.03-6.01). The number of procoagulant alleles correlated directly (r = 0.49, P = 0.006) with endogenous thrombin potential. CONCLUSIONS: The combination of prothrombotic polymorphisms may help to predict MI in patients with advanced CAD