On a functional satisfying a weak Palais-Smale condition

In this paper we study a quasilinear elliptic problem whose functional satisfies a weak version of the well known Palais-Smale condition. An existence result is proved under general assumptions on the nonlinearities.Comment: 18 page

Long time dynamics and coherent states in nonlinear wave equations

We discuss recent progress in finding all coherent states supported by nonlinear wave equations, their stability and the long time behavior of nearby solutions.Comment: bases on the authors presentation at 2015 AMMCS-CAIMS Congress, to appear in Fields Institute Communications: Advances in Applied Mathematics, Modeling, and Computational Science 201

Orbital stability: analysis meets geometry

We present an introduction to the orbital stability of relative equilibria of Hamiltonian dynamical systems on (finite and infinite dimensional) Banach spaces. A convenient formulation of the theory of Hamiltonian dynamics with symmetry and the corresponding momentum maps is proposed that allows us to highlight the interplay between (symplectic) geometry and (functional) analysis in the proofs of orbital stability of relative equilibria via the so-called energy-momentum method. The theory is illustrated with examples from finite dimensional systems, as well as from Hamiltonian PDE's, such as solitons, standing and plane waves for the nonlinear Schr{\"o}dinger equation, for the wave equation, and for the Manakov system

Symbiotic Bright Solitary Wave Solutions of Coupled Nonlinear Schrodinger Equations

Conventionally, bright solitary wave solutions can be obtained in self-focusing nonlinear Schrodinger equations with attractive self-interaction. However, when self-interaction becomes repulsive, it seems impossible to have bright solitary wave solution. Here we show that there exists symbiotic bright solitary wave solution of coupled nonlinear Schrodinger equations with repulsive self-interaction but strongly attractive interspecies interaction. For such coupled nonlinear Schrodinger equations in two and three dimensional domains, we prove the existence of least energy solutions and study the location and configuration of symbiotic bright solitons. We use Nehari's manifold to construct least energy solutions and derive their asymptotic behaviors by some techniques of singular perturbation problems.Comment: to appear in Nonlinearit

On the stability of standing waves of Klein-Gordon equations in a semiclassical regime

We investigate the orbital stability and instability of standing waves for two classes of Klein-Gordon equations in the semi-classical regime.Comment: 9 page

Preparation and Characterization of Fluorescence Probe from Assembly Hydroxyapatite Nanocomposite

A new nanocomposite fluorescence probe with thioglycolic acid (TA) functional layers embedded inside the hydroxyapatite nanoribbon spherulites has been synthesized. The fluorescence intensity of the novel probe is about 1.5–3.3-fold increase compared with the probe containing no TA. When used to detect cadmium ion, the most of original assembly nanoribbon spherulites structure in the novel probe is found to have been damaged to new flake structures. The mechanism of determining cadmium ion in alcohol solution has been studied. The present systematic study provides significant information on the effect of assembly nanostructure on the metal-enhanced fluorescence phenomenon

Results of final focus test beam

International audienceThe beam experiments of Final Focus Test Beam (FFTB) started in September 1993 at SLAC, and have produced a 1.7 μm×75 nm spot of 46 GeV electron beam. A number of new techniques involving two nanometer spot-size monitors have been developed. Several beam diagnostic/tuning schemes are applied to achieve and maintain the small spot. This experiment opens the way toward the nanometer world for future linear collider

Pathogenic NR2F1 variants cause a developmental ocular phenotype recapitulated in a mutant mouse model.

Pathogenic NR2F1 variants cause a rare autosomal dominant neurodevelopmental disorder referred to as the Bosch-Boonstra-Schaaf Optic Atrophy Syndrome. Although visual loss is a prominent feature seen in affected individuals, the molecular and cellular mechanisms contributing to visual impairment are still poorly characterized. We conducted a deep phenotyping study on a cohort of 22 individuals carrying pathogenic NR2F1 variants to document the neurodevelopmental and ophthalmological manifestations, in particular the structural and functional changes within the retina and the optic nerve, which have not been detailed previously. The visual impairment became apparent in early childhood with small and/or tilted hypoplastic optic nerves observed in 10 cases. High-resolution optical coherence tomography imaging confirmed significant loss of retinal ganglion cells with thinning of the ganglion cell layer, consistent with electrophysiological evidence of retinal ganglion cells dysfunction. Interestingly, for those individuals with available longitudinal ophthalmological data, there was no significant deterioration in visual function during the period of follow-up. Diffusion tensor imaging tractography studies showed defective connections and disorganization of the extracortical visual pathways. To further investigate how pathogenic NR2F1 variants impact on retinal and optic nerve development, we took advantage of an Nr2f1 mutant mouse disease model. Abnormal retinogenesis in early stages of development was observed in Nr2f1 mutant mice with decreased retinal ganglion cell density and disruption of retinal ganglion cell axonal guidance from the neural retina into the optic stalk, accounting for the development of optic nerve hypoplasia. The mutant mice showed significantly reduced visual acuity based on electrophysiological parameters with marked conduction delay and decreased amplitude of the recordings in the superficial layers of the visual cortex. The clinical observations in our study cohort, supported by the mouse data, suggest an early neurodevelopmental origin for the retinal and optic nerve head defects caused by NR2F1 pathogenic variants, resulting in congenital vision loss that seems to be non-progressive. We propose NR2F1 as a major gene that orchestrates early retinal and optic nerve head development, playing a key role in the maturation of the visual system

Pathogenic <i>NR2F1</i> variants cause a developmental ocular phenotype recapitulated in a mutant mouse model.

Funder: National Institute of Health Research Biomedical Research Centre at Moorfields Eye Hospital and UCL Institute of OphthalmologyPathogenic NR2F1 variants cause a rare autosomal dominant neurodevelopmental disorder referred to as the Bosch-Boonstra-Schaaf Optic Atrophy Syndrome. Although visual loss is a prominent feature seen in affected individuals, the molecular and cellular mechanisms contributing to visual impairment are still poorly characterized. We conducted a deep phenotyping study on a cohort of 22 individuals carrying pathogenic NR2F1 variants to document the neurodevelopmental and ophthalmological manifestations, in particular the structural and functional changes within the retina and the optic nerve, which have not been detailed previously. The visual impairment became apparent in early childhood with small and/or tilted hypoplastic optic nerves observed in 10 cases. High-resolution optical coherence tomography imaging confirmed significant loss of retinal ganglion cells with thinning of the ganglion cell layer, consistent with electrophysiological evidence of retinal ganglion cells dysfunction. Interestingly, for those individuals with available longitudinal ophthalmological data, there was no significant deterioration in visual function during the period of follow-up. Diffusion tensor imaging tractography studies showed defective connections and disorganization of the extracortical visual pathways. To further investigate how pathogenic NR2F1 variants impact on retinal and optic nerve development, we took advantage of an Nr2f1 mutant mouse disease model. Abnormal retinogenesis in early stages of development was observed in Nr2f1 mutant mice with decreased retinal ganglion cell density and disruption of retinal ganglion cell axonal guidance from the neural retina into the optic stalk, accounting for the development of optic nerve hypoplasia. The mutant mice showed significantly reduced visual acuity based on electrophysiological parameters with marked conduction delay and decreased amplitude of the recordings in the superficial layers of the visual cortex. The clinical observations in our study cohort, supported by the mouse data, suggest an early neurodevelopmental origin for the retinal and optic nerve head defects caused by NR2F1 pathogenic variants, resulting in congenital vision loss that seems to be non-progressive. We propose NR2F1 as a major gene that orchestrates early retinal and optic nerve head development, playing a key role in the maturation of the visual system