Total and selective reuse of Krylov subspaces for the resolution of sequences of nonlinear structural problems

This paper deals with the definition and optimization of augmentation spaces for faster convergence of the conjugate gradient method in the resolution of sequences of linear systems. Using advanced convergence results from the literature, we present a procedure based on a selection of relevant approximations of the eigenspaces for extracting, selecting and reusing information from the Krylov subspaces generated by previous solutions in order to accelerate the current iteration. Assessments of the method are proposed in the cases of both linear and nonlinear structural problems.Comment: International Journal for Numerical Methods in Engineering (2013) 24 page

Substructured formulations of nonlinear structure problems - influence of the interface condition

We investigate the use of non-overlapping domain decomposition (DD) methods for nonlinear structure problems. The classic techniques would combine a global Newton solver with a linear DD solver for the tangent systems. We propose a framework where we can swap Newton and DD, so that we solve independent nonlinear problems for each substructure and linear condensed interface problems. The objective is to decrease the number of communications between subdomains and to improve parallelism. Depending on the interface condition, we derive several formulations which are not equivalent, contrarily to the linear case. Primal, dual and mixed variants are described and assessed on a simple plasticity problem.Comment: in International Journal for Numerical Methods in Engineering, Wiley, 201

Bridging Proper Orthogonal Decomposition methods and augmented Newton-Krylov algorithms: an adaptive model order reduction for highly nonlinear mechanical problems

This article describes a bridge between POD-based model order reduction techniques and the classical Newton/Krylov solvers. This bridge is used to derive an efficient algorithm to correct, "on-the-fly", the reduced order modelling of highly nonlinear problems undergoing strong topological changes. Damage initiation problems are addressed and tackle via a corrected hyperreduction method. It is shown that the relevancy of reduced order model can be significantly improved with reasonable additional costs when using this algorithm, even when strong topological changes are involved

On the control of the load increments for a proper description of multiple delamination in a domain decomposition framework

In quasi-static nonlinear time-dependent analysis, the choice of the time discretization is a complex issue. The most basic strategy consists in determining a value of the load increment that ensures the convergence of the solution with respect to time on the base of preliminary simulations. In more advanced applications, the load increments can be controlled for instance by prescribing the number of iterations of the nonlinear resolution procedure, or by using an arc-length algorithm. These techniques usually introduce a parameter whose correct value is not easy to obtain. In this paper, an alternative procedure is proposed. It is based on the continuous control of the residual of the reference problem over time, whose measure is easy to interpret. This idea is applied in the framework of a multiscale domain decomposition strategy in order to perform 3D delamination analysis

Atypical nested 22q11.2 duplications between LCR22B and LCR22D are associated with neurodevelopmental phenotypes including autism spectrum disorder with incomplete penetrance

Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc. Background: Chromosome 22q11.2 is susceptible to genomic rearrangements and the most frequently reported involve deletions and duplications between low copy repeats LCR22A to LCR22D. Atypical nested deletions and duplications are rarer and can provide a valuable opportunity to investigate the dosage effects of a smaller subset of genes within the 22q11.2 genomic disorder region. Methods: We describe thirteen individuals from six families, each with atypical nested duplications within the central 22q11.2 region between LCR22B and LCR22D. We then compared the molecular and clinical data for patients from this study and the few reported atypical duplication cases, to the cases with larger typical duplications between LCR22A and LCR22D. Further, we analyzed genes with the nested region to identify candidates highly enriched in human brain tissues. Results: We observed that atypical nested duplications are heterogeneous in size, often familial, and associated with incomplete penetrance and highly variable clinical expressivity. We found that the nested atypical duplications are a possible risk factor for neurodevelopmental phenotypes, particularly for autism spectrum disorder (ASD), speech and language delay, and behavioral abnormalities. In addition, we analyzed genes within the nested region between LCR22B and LCR22D to identify nine genes (ZNF74, KLHL22, MED15, PI4KA, SERPIND1, CRKL, AIFM3, SLC7A4, and BCRP2) with enriched expression in the nervous system, each with unique spatiotemporal patterns in fetal and adult brain tissues. Interestingly, PI4KA is prominently expressed in the brain, and this gene is included either partially or completely in all of our subjects. Conclusion: Our findings confirm variable expressivity and incomplete penetrance for atypical nested 22q11.2 duplications and identify genes such as PI4KA to be directly relevant to brain development and disorder. We conclude that further work is needed to elucidate the basis of variable neurodevelopmental phenotypes and to exclude the presence of a second disorder. Our findings contribute to the genotype–phenotype data for atypical nested 22q11.2 duplications, with implications for genetic counseling

A three-scale domain decomposition method for the 3D analysis of debonding in laminates

The prediction of the quasi-static response of industrial laminate structures requires to use fine descriptions of the material, especially when debonding is involved. Even when modeled at the mesoscale, the computation of these structures results in very large numerical problems. In this paper, the exact mesoscale solution is sought using parallel iterative solvers. The LaTIn-based mixed domain decomposition method makes it very easy to handle the complex description of the structure; moreover the provided multiscale features enable us to deal with numerical difficulties at their natural scale; we present the various enhancements we developed to ensure the scalability of the method. An extension of the method designed to handle instabilities is also presented

Adaptation d'une technique de quantification de l'ARN messager du facteur tissulaire sur sang total par RT-PCR, appliquée à l'étude préliminaire d'une population témoin

Le facteur tissulaire (FT) est le principal initiateur de la coagulation in vivo. Il intervient également dans d'autres grandes fonctions comme l'angiogénèse, la réaction inflammatoire, la carcinogénèse et la prolifération tumorale. Sa distribution n'est pas uniforme dans l'organisme : il est exprimé de manière constitutive par certains types cellulaires et inductibles par d'autres. Une surexpression du FT est potentiellement responsable d'un état d'hypercoagulabilité qui, associé à des lésions endothéliales et/ou à une stase sanguine, peut induire une thrombose. Nous avons développé une technique de quantification relative de l'ARNm du FT sur sang total par RT-PCR, avec une sonde TaqMan® comme système de détection. Nous avons rapporté ce niveau de transcription à celui d'un gène de référence (GAPDH). Nous avons appliqué cette technique, reproductible, efficace et performante, à la quantification relative, par la méthode comparative des Ct, de l'ARNm du FT sur sang total dans une population témoin. Nous avons ainsi démontré qu'à l'état basal, chez l'adulte sain sans antécédent de thrombose, la quantification relative FT/GAPDH, pour chaque échantillon, rapportée à un calibrant, était proche de 1 (en moyenne : 0,73 +/- 0,41). Ce groupe de témoins semble donc constituer une population relativement homogène, confirmant les données de la littérature quant à la faible transcription du gène du FT au niveau sanguin dans des conditions physiologiques. Nous souhaiterions utiliser cette technique pour étudier la transcription du gène du FT chez des patients atteints de syndromes myéloprolifératifs (SMP) qui présentent un risque élevé de thromboses, dont le mécanisme, probablement multifactoriel, n'est encore que partiellement élucidé ; il pourrait allier une activation des monocytes sanguins, principale source de FT dans le sang circulant et l'influence, longtemps controversée, des leucocytes. En parallèle, nous pourrions rechercher une éventuelle corrélation entre la présence de la mutation JAK2 V617F et un niveau de transcription élevé du gène du FT. Si ce test offrait une bonne valeur prédictive positive, la quantification de l'ARNm du FT dans le sang total pourrait être considérée comme un paramètre de choix dans l'évaluation du risque thrombotique chez les patients atteints de SMP.CLERMONT FD-BCIU-Santé (631132104) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Optimisation d'une technique de dosage de l'activité procoagulante du facteur tissulaire (application à l'étude de l'état d'hypercoagulabilité des patients atteints de syndromes myeloprolifératifs)

CLERMONT FD-BCIU-Santé (631132104) / SudocLYON1-BU Santé (693882101) / SudocSudocFranceF