Nonlinear reduced basis using mixture Wasserstein barycenters: application to an eigenvalue problem inspired from quantum chemistry

The aim of this article is to propose a new reduced-order modelling approach for parametric eigenvalue problems arising in electronic structure calculations. Namely, we develop nonlinear reduced basis techniques for the approximation of parametric eigenvalue problems inspired from quantum chemistry applications. More precisely, we consider here a one-dimensional model which is a toy model for the computation of the electronic ground state wavefunction of a system of electrons within a molecule, solution to the many-body electronic Schr\"odinger equation, where the varying parameters are the positions of the nuclei in the molecule. We estimate the decay rate of the Kolmogorov n-width of the set of solutions for this parametric problem in several settings, including the standard L2-norm as well as with distances based on optimal transport. The fact that the latter decays much faster than in the traditional L2-norm setting motivates us to propose a practical nonlinear reduced basis method, which is based on an offline greedy algorithm, and an efficient stochastic energy minimization in the online phase. We finally provide numerical results illustrating the capabilities of the method and good approximation properties, both in the offline and the online phase

Le genre des controverses : approches féministes et queer

Durant les vingt dernières années, plusieurs controverses ont ouvert un espace de conflictualité autour de la définition et des usages politiques de la « différence des sexes ». Les controverses relatives à la loi sur la « parité », au Pacs, au port du « voile » et de la « burqa », au « mariage pour tous » ou encore aux plans d’action publique pour l’égalité filles-garçons à l’école ont toutes participé d’une mise en délibération des conceptions hégémoniques des identités de genre et des rapp..

Genomic plasticity of the immune-related Mhc class I B region in macaque species

<p>Abstract</p> <p>Background</p> <p>In sharp contrast to humans and great apes, the expanded <it>Mhc</it>-<it>B </it>region of rhesus and cynomolgus macaques is characterized by the presence of differential numbers and unique combinations of polymorphic class I <it>B </it>genes per haplotype. The MIB microsatellite is closely linked to the single class I <it>B </it>gene in human and in some great apes studied. The physical map of the <it>Mhc </it>of a heterozygous rhesus monkey provides unique material to analyze MIB and <it>Mamu</it>-<it>B </it>copy number variation and then allows one to decipher the compound evolutionary history of this region in primate species.</p> <p>Results</p> <p><it>In silico </it>research pinpointed 12 MIB copies (duplicons), most of which are associated with expressed <it>B</it>-genes that cluster in a separate clade in the phylogenetic tree. Generic primers tested on homozygous rhesus and pedigreed cynomolgus macaques allowed the identification of eight to eleven MIB copies per individual. The number of MIB copies present per haplotype varies from a minimum of three to six in cynomolgus macaques and from five to eight copies in rhesus macaques. Phylogenetic analyses highlight a strong transpecific sharing of MIB duplicons. Using the physical map, we observed that, similar to MIB duplicons, highly divergent <it>Mamu</it>-<it>B </it>genes can be present on the same haplotype. Haplotype variation as reflected by the copy number variation of class I <it>B </it>loci is best explained by recombination events, which are found to occur between MIBs and <it>Mamu</it>-<it>B</it>.</p> <p>Conclusion</p> <p>The data suggest the existence of highly divergent MIB and <it>Mamu-B </it>lineages on a given haplotype, as well as variable MIB and <it>B </it>copy numbers and configurations, at least in rhesus macaque. Recombination seems to occur between MIB and <it>Mamu</it>-<it>B </it>loci, and the resulting haplotypic plasticity at the individual level may be a strategy to better cope with pathogens. Therefore, evolutionary inferences based on the multiplicated MIB loci but also other markers close to <it>B</it>-genes appear to be promising for the study of <it>B</it>-region organization and evolution in primates.</p

On the relationship between residual zonal flows and bump-on tail saturated instabilities

A connection is established between two classical problems: the non linear saturation of a bump-on tail instability in collisionless regime, and the decay of a zonal flow towards a finite amplitude residual. Reasons for this connection are given and commented

Myogenesis modelled by human pluripotent stem cells uncovers Duchenne muscular dystrophy phenotypes prior to skeletal muscle commitment

Duchenne muscular dystrophy (DMD) causes severe disability of children and death of young men, with an incidence of approximately 1/5,000 male births. Symptoms appear in early childhood, with a diagnosis made around 4 years old, a time where the amount of muscle damage is already significant, preventing early therapeutic interventions that could be more efficient at halting disease progression. In the meantime, the precise moment at which disease phenotypes arise - even asymptomatically - is still unknown. Thus, there is a critical need to better define DMD onset as well as its first manifestations, which could help identify early disease biomarkers and novel therapeutic targets. In this study, we have used human induced pluripotent stem cells (hiPSCs) from DMD patients to model skeletal myogenesis, and compared their differentiation dynamics to healthy control cells by a comprehensive multi-omics analysis. Transcriptome and miRnome comparisons combined with protein analyses at 7 time points demonstrate that hiPSC differentiation 1) mimics described DMD phenotypes at the differentiation endpoint; and 2) homogeneously and robustly recapitulates key developmental steps - mesoderm, somite, skeletal muscle - which offers the possibility to explore dystrophin functions and find earlier disease biomarkers. Starting at the somite stage, mitochondrial gene dysregulations escalate during differentiation. We also describe fibrosis as an intrinsic feature of skeletal muscle cells that starts early during myogenesis. In sum, our data strongly argue for an early developmental manifestation of DMD whose onset is triggered before the entry into the skeletal muscle compartment, data leading to a necessary reconsideration of dystrophin functions during muscle development

Myogenesis modelled by human pluripotent stem cells uncovers Duchenne muscular dystrophy phenotypes prior to skeletal muscle commitment

Duchenne muscular dystrophy (DMD) causes severe disability of children and death of young men, with an incidence of approximately 1/5,000 male births. Symptoms appear in early childhood, with a diagnosis made around 4 years old, a time where the amount of muscle damage is already significant, preventing early therapeutic interventions that could be more efficient at halting disease progression. In the meantime, the precise moment at which disease phenotypes arise - even asymptomatically - is still unknown. Thus, there is a critical need to better define DMD onset as well as its first manifestations, which could help identify early disease biomarkers and novel therapeutic targets. In this study, we have used human induced pluripotent stem cells (hiPSCs) from DMD patients to model skeletal myogenesis, and compared their differentiation dynamics to healthy control cells by a comprehensive multi-omics analysis. Transcriptome and miRnome comparisons combined with protein analyses at 7 time points demonstrate that hiPSC differentiation 1) mimics described DMD phenotypes at the differentiation endpoint; and 2) homogeneously and robustly recapitulates key developmental steps - mesoderm, somite, skeletal muscle - which offers the possibility to explore dystrophin functions and find earlier disease biomarkers. Starting at the somite stage, mitochondrial gene dysregulations escalate during differentiation. We also describe fibrosis as an intrinsic feature of skeletal muscle cells that starts early during myogenesis. In sum, our data strongly argue for an early developmental manifestation of DMD whose onset is triggered before the entry into the skeletal muscle compartment, data leading to a necessary reconsideration of dystrophin functions during muscle development