18 research outputs found
Gamma phonons and microscopic structure of orthorhombic KNbO3 from first-principles calculations
{}From a series of total energy calculations by the full-potential linear
muffin-tin orbital method, the total energy hypersurface as function of atomic
displacements from equilibrium positions has been fitted for different Gamma
phonon modes in orthorhombic KNbO3. Frequencies and eigenvectors of all TO
Gamma phonons have been calculated in the harmonic approximation, and in the
quantum oscillator scheme -- for A2 and B2 modes. The microscopic structure of
the orthorhombic phase has been analyzed in a series of supercell calculations
for different patterns of Nb displacements, providing indications in favour of
the chain structure, with oppositely directed neighboring chains.Comment: 10 pages, including 3 LaTeX figure
Genetic diversity of a large set of horse breeds raised in France assessed by microsatellite polymorphism
After the recent publication of our article (Leroy, Genetics Selection Evolution 2009 41:5), we found several errors in the published Table Three, concerning the computation of contribution to within-breed diversity (CW). We apologize to the readers for these errors, which are corrected in the present erratum
Generation of induced pluripotent stem cell lines IRMBi003-A and IRMBi003-B from a healthy donor to model Alzheimer’s disease
International audienceInduced Pluripotent Stem Cell (iPSC) lines derived from healthy individuals are helpful and essential tools for disease modelling. Here, we described the reprogramming of skin fibroblasts obtained from a healthy 59-year-old individual without Alzheimer's disease. The generated iPSC lines have a normal karyotype, expressed pluripotency markers, and demonstrated the ability to differentiate into the three germ layers. The iPSC lines will be used as controls to study Alzheimer's disease mechanisms
Heparan sulfate mimetics are neuroprotective and neuroregenerative agents for ischemic stroke.
CERVOXY COLLInternational audienc
Stomatin-deficient cryohydrocytosis results from mutations in SLC2A1: a novel form of GLUT1 deficiency syndrome.
International audienceThe hereditary stomatocytoses are a series of dominantly-inherited hemolytic anemias in which the permeability of the erythrocyte membrane to monovalent cations is pathologically increased. The causative mutations for some forms of hereditary stomatocytosis have been found in the transporter protein genes, RHAG and SLC4A1. Glut1 deficiency syndromes (glut1DS) result from mutations in SLC2A1, encoding glucose transporter 1 (glut1). Glut1 is the major glucose transporter in the mammalian blood-brain barrier and glut1DS are manifested by an array of neurological symptoms. We have previously reported two cases of stomatin-deficient cryohydrocytosis (sdCHC), a very rare form of stomatocytosis associated with a cold-induced cation leak, hemolytic anemia and hepatosplenomegaly but also with cataracts, seizures, mental retardation and movement disorder. We now show that sdCHC is associated with mutations in SLC2A1 that cause both loss of glucose transport and a cation leak, as shown by expression studies in Xenopus oocytes. Based on a 3D model of glut1, we propose potential mechanisms underlying the phenotypes of the two mutations found. We investigated the loss of stomatin during erythropoiesis and find this occurs during reticulocyte maturation and involves endocytosis. The molecular basis of the glut1DS, paroxysmal exercise-induced dyskinesia (PED) and sdCHC phenotypes are compared and discussed