Structure and magnetism of self-organized Ge(1-x)Mn(x) nano-columns

We report on the structural and magnetic properties of thin Ge(1-x)Mn(x)films grown by molecular beam epitaxy (MBE) on Ge(001) substrates at temperatures (Tg) ranging from 80deg C to 200deg C, with average Mn contents between 1 % and 11 %. Their crystalline structure, morphology and composition have been investigated by transmission electron microscopy (TEM), electron energy loss spectroscopy and x-ray diffraction. In the whole range of growth temperatures and Mn concentrations, we observed the formation of manganese rich nanostructures embedded in a nearly pure germanium matrix. Growth temperature mostly determines the structural properties of Mn-rich nanostructures. For low growth temperatures (below 120deg C), we evidenced a two-dimensional spinodal decomposition resulting in the formation of vertical one-dimensional nanostructures (nanocolumns). Moreover we show in this paper the influence of growth parameters (Tg and Mn content) on this decomposition i.e. on nanocolumns size and density. For temperatures higher than 180deg C, we observed the formation of Ge3Mn5 clusters. For intermediate growth temperatures nanocolumns and nanoclusters coexist. Combining high resolution TEM and superconducting quantum interference device magnetometry, we could evidence at least four different magnetic phases in Ge(1-x)Mn(x) films: (i) paramagnetic diluted Mn atoms in the germanium matrix, (ii) superparamagnetic and ferromagnetic low-Tc nanocolumns (120 K 400 K) and (iv) Ge3Mn5 clusters.Comment: 10 pages 2 colonnes revTex formatte

Réorganisation des personnels non médicaux du DIM au CHRU de Nancy

International audienceLe codage centralisé du PMSI est effectué par 29 techniciens d'information médicale (TIM). En 2019, une démarche de réorganisation a été instaurée avec trois objectifs : assurer la continuité du codage, améliorer la qualité du codage et la qualité de vie au travail

Growth mechanism of Si nanowhiskers and SiGe heterostructures in Si nanowhiskers: X-ray scattering and electron microscopy investigations

International audienc

High throughput screening for inhibitors of REST in neural derivatives of human embryonic stem cells reveals a chemical compound that promotes expression of neuronal genes

Decreased expression of neuronal genes such as brain-derived neurotrophic factor (BDNF) is associated with several neurological disorders. One molecular mechanism associated with Huntington disease (HD) is a discrete increase in the nuclear activity of the transcriptional repressor REST/NRSF binding to repressor element-1 (RE1) sequences. High-throughput screening of a library of 6,984 compounds with luciferase-assay measuring REST activity in neural derivatives of human embryonic stem cells led to identify two benzoimidazole-5-carboxamide derivatives that inhibited REST silencing in a RE1-dependent manner. The most potent compound, X5050, targeted REST degradation, but neither REST expression, RNA splicing nor binding to RE1 sequence. Differential transcriptomic analysis revealed the upregulation of neuronal genes targeted by REST in wild-type neural cells treated with X5050. This activity was confirmed in neural cells produced from human induced pluripotent stem cells derived from a HD patient. Acute intraventricular delivery of X5050 increased the expressions of BDNF and several other REST-regulated genes in the prefrontal cortex of mice with quinolinate-induced striatal lesions. This study demonstrates that the use of pluripotent stem cell derivatives can represent a crucial step toward the identification of pharmacological compounds with therapeutic potential in neurological affections involving decreased expression of neuronal genes associated to increased REST activity, such as Huntington disease

Drug screening on Hutchinson Gilford progeria pluripotent stem cells reveals aminopyrimidines as new modulators of farnesylation

International audienceHutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disorder characterized by a dramatic appearance of premature aging. HGPS is due to a single-base substitution in exon 11 of the LMNA gene (c.1824C>T) leading to the production of a toxic form of the prelamin A protein called progerin. Because farnesylation process had been shown to control progerin toxicity, in this study we have developed a screening method permitting to identify new pharmacological inhibitors of farnesylation. For this, we have used the unique potential of pluripotent stem cells to have access to an unlimited and relevant biological resource and test 21 608 small molecules. This study identified several compounds, called monoaminopyrimidines, which target two key enzymes of the farnesylation process, farnesyl pyrophosphate synthase and farnesyl transferase, and rescue in vitro phenotypes associated with HGPS. Our results opens up new therapeutic possibilities for the treatment of HGPS by identifying a new family of protein farnesylation inhibitors, and which may also be applicable to cancers and diseases associated with mutations that involve farnesylated proteins