Structures in Mo-Ru-Si system by powder and anomal X-ray diffraction

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Solution numérique des équations compressibles de Navier-Stokes

Les équations de base -- Résolution numérique des équations -- Résultats numériques

Mott Transition in the A15 Phase of Cs3C60 : Absence of a Pseudogap and Charge Order

We present a detailed NMR study of the insulator-to-metal transition induced by an applied pressure p in the A15 phase of Cs3C60. We evidence that the insulating antiferromagnetic (AFM) and superconducting (SC) phases coexist only in a narrow p range. At fixed p, in the metallic state above the SC transition T-c, the Cs-133 and C-13 NMR spin-lattice relaxation data are seemingly governed by a pseudogaplike feature. We prove that this feature, also seen in the (CsNMR)-Cs-133 shift data, is rather a signature of the Mott transition which broadens and smears out progressively for increasing (p,T). The analysis of the variation of the quadrupole splitting nu(Q) of the Cs-133 NMR spectrum precludes any cell symmetry change at the Mott transition and only monitors a weak variation of the lattice parameter. These results open an opportunity to consider theoretically the Mott transition in a multiorbital three-dimensional system well beyond its critical point.Peer reviewe

Evidence of multiple sorption modes in layered double hydroxides using Mo as structural probe

Layered double hydroxides (LDHs) have been considered as effective phases for the remediation of aquatic environments, to remove anionic contaminants mainly through anion exchange mechanisms. Here, a combination of batch isotherm experiments and X-ray techniques was used to examine molybdate (MoO ) sorption mechanisms on CaAl LDHs with increasing loadings of molybdate. Advanced modeling of aqueous data shows that the sorption isotherm can be interpreted by three retention mechanisms, including two types of edge sites complexes, interlayer anion exchange, and CaMoO precipitation. Meanwhile, Mo geometry evolves from tetrahedral to octahedral on the edge, and back to tetrahedral coordination at higher Mo loadings, indicated by Mo K-edge X-ray absorption spectra. Moreover, an anion exchange process on both CaAl LDHs was followed by in situ time-resolved synchrotron-based X-ray diffraction, remarkably agreeing with the sorption isotherm. This detailed molecular view shows that different uptake mechanisms - edge sorption, interfacial dissolution-reprecipitation - are at play and control anion uptake under environmentally relevant conditions, which is contrast to the classical view of anion exchange as the primary retention mechanism. This work puts all these mechanisms in perspective, offering a new insight into the complex interplay of anion uptake mechanisms by LDH phases, by using changes in Mo geometry as powerful molecular-scale probe.This work has been supported by a grant from Labex OSUG@2020 (Investissements d’avenir - ANR10 LABX56). B.M., A.F.-M., L.C., S.G. and F.C. thank the NEEDS program from the CNRS for funding support. B.M. also thanks the financial support from the China Scholarship Council (CSC)

Magnetic and structural properties of the iron silicide superconductor LaFeSiH

The magnetic and structural properties of the recently discovered pnictogen/chalcogen-free superconductor LaFeSiH ($T_c\simeq10$~K) have been investigated by $^{57}$Fe synchrotron M{\"o}ssbauer source (SMS) spectroscopy, x-ray and neutron powder diffraction and $^{29}$Si nuclear magnetic resonance spectroscopy (NMR). No sign of long range magnetic order or local moments has been detected in any of the measurements and LaFeSiH remains tetragonal down to 2 K. The activated temperature dependence of both the NMR Knight shift and the relaxation rate $1/T_1$ is analogous to that observed in strongly overdoped Fe-based superconductors. These results, together with the temperature-independent NMR linewidth, show that LaFeSiH is an homogeneous metal, far from any magnetic or nematic instability, and with similar Fermi surface properties as strongly overdoped iron pnictides. This raises the prospect of enhancing the $T_c$ of LaFeSiH by reducing its carrier concentration through appropriate chemical substitutions. Additional SMS spectroscopy measurements under hydrostatic pressure up to 18.8~GPa found no measurable hyperfine field

Patterning enhanced tetragonality in BiFeO3 thin films with effective negative pressure by helium implantation

Helium implantation in epitaxial thin films is a way to control the out-of-plane deformation independentlyfrom the in-plane strain controlled by epitaxy. In particular, implantation by means of a helium microscopeallows for local implantation and patterning down to the nanometer resolution, which is of interest for deviceapplications. We present here a study of bismuth ferrite (BiFeO3) films where strain was patterned locally byhelium implantation. Our combined Raman, x-ray diffraction, and transmission electron microscopy (TEM)study shows that the implantation causes an elongation of the BiFeO3unit cell and ultimately a transition towardsthe so-called supertetragonal polymorph via states with mixed phases. In addition, TEM reveals the onset ofamorphization at a threshold dose that does not seem to impede the overall increase in tetragonality. The phasetransition from the R-like to T-like BiFeO3appears as first-order in character, with regions of phase coexistenceand abrupt changes in lattice parameters

Clinical and immunologic phenotype associated with activated phosphoinositide 3-kinase δ syndrome 2: A cohort study

Background Activated phosphoinositide 3-kinase δ syndrome (APDS) 2 (p110δ-activating mutations causing senescent T cells, lymphadenopathy, and immunodeficiency [PASLI]–R1), a recently described primary immunodeficiency, results from autosomal dominant mutations in PIK3R1, the gene encoding the regulatory subunit (p85α, p55α, and p50α) of class IA phosphoinositide 3-kinases. Objectives We sought to review the clinical, immunologic, and histopathologic phenotypes of APDS2 in a genetically defined international patient cohort. Methods The medical and biological records of 36 patients with genetically diagnosed APDS2 were collected and reviewed. Results Mutations within splice acceptor and donor sites of exon 11 of the PIK3R1 gene lead to APDS2. Recurrent upper respiratory tract infections (100%), pneumonitis (71%), and chronic lymphoproliferation (89%, including adenopathy [75%], splenomegaly [43%], and upper respiratory tract lymphoid hyperplasia [48%]) were the most common features. Growth retardation was frequently noticed (45%). Other complications were mild neurodevelopmental delay (31%); malignant diseases (28%), most of them being B-cell lymphomas; autoimmunity (17%); bronchiectasis (18%); and chronic diarrhea (24%). Decreased serum IgA and IgG levels (87%), increased IgM levels (58%), B-cell lymphopenia (88%) associated with an increased frequency of transitional B cells (93%), and decreased numbers of naive CD4 and naive CD8 cells but increased numbers of CD8 effector/memory T cells were predominant immunologic features. The majority of patients (89%) received immunoglobulin replacement; 3 patients were treated with rituximab, and 6 were treated with rapamycin initiated after diagnosis of APDS2. Five patients died from APDS2-related complications. Conclusion APDS2 is a combined immunodeficiency with a variable clinical phenotype. Complications are frequent, such as severe bacterial and viral infections, lymphoproliferation, and lymphoma similar to APDS1/PASLI-CD. Immunoglobulin replacement therapy, rapamycin, and, likely in the near future, selective phosphoinositide 3-kinase δ inhibitors are possible treatment options

PI3Kδ and primary immunodeficiencies.

Primary immunodeficiencies are inherited disorders of the immune system, often caused by the mutation of genes required for lymphocyte development and activation. Recently, several studies have identified gain-of-function mutations in the phosphoinositide 3-kinase (PI3K) genes PIK3CD (which encodes p110δ) and PIK3R1 (which encodes p85α) that cause a combined immunodeficiency syndrome, referred to as activated PI3Kδ syndrome (APDS; also known as p110δ-activating mutation causing senescent T cells, lymphadenopathy and immunodeficiency (PASLI)). Paradoxically, both loss-of-function and gain-of-function mutations that affect these genes lead to immunosuppression, albeit via different mechanisms. Here, we review the roles of PI3Kδ in adaptive immunity, describe the clinical manifestations and mechanisms of disease in APDS and highlight new insights into PI3Kδ gleaned from these patients, as well as implications of these findings for clinical therapy

Proteome-wide identification of poly(ADP-ribose) binding proteins and poly(ADP-ribose)-associated protein complexes

Poly(ADP-ribose) (pADPr) is a polymer assembled from the enzymatic polymerization of the ADP-ribosyl moiety of NAD by poly(ADP-ribose) polymerases (PARPs). The dynamic turnover of pADPr within the cell is essential for a number of cellular processes including progression through the cell cycle, DNA repair and the maintenance of genomic integrity, and apoptosis. In spite of the considerable advances in the knowledge of the physiological conditions modulated by poly(ADP-ribosyl)ation reactions, and notwithstanding the fact that pADPr can play a role of mediator in a wide spectrum of biological processes, few pADPr binding proteins have been identified so far. In this study, refined in silico prediction of pADPr binding proteins and large-scale mass spectrometry-based proteome analysis of pADPr binding proteins were used to establish a comprehensive repertoire of pADPr-associated proteins. Visualization and modeling of these pADPr-associated proteins in networks not only reflect the widespread involvement of poly(ADP-ribosyl)ation in several pathways but also identify protein targets that could shed new light on the regulatory functions of pADPr in normal physiological conditions as well as after exposure to genotoxic stimuli