92 research outputs found

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

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    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

    Magnetic and structural properties of the iron silicide superconductor LaFeSiH

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    The magnetic and structural properties of the recently discovered pnictogen/chalcogen-free superconductor LaFeSiH (Tc10T_c\simeq10~K) have been investigated by 57^{57}Fe synchrotron M{\"o}ssbauer source (SMS) spectroscopy, x-ray and neutron powder diffraction and 29^{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/T11/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 TcT_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

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

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    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.

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    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

    Cardiovascular disease and the role of oral bacteria

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    In terms of the pathogenesis of cardiovascular disease (CVD) the focus has traditionally been on dyslipidemia. Over the decades our understanding of the pathogenesis of CVD has increased, and infections, including those caused by oral bacteria, are more likely involved in CVD progression than previously thought. While many studies have now shown an association between periodontal disease and CVD, the mechanisms underpinning this relationship remain unclear. This review gives a brief overview of the host-bacterial interactions in periodontal disease and virulence factors of oral bacteria before discussing the proposed mechanisms by which oral bacterial may facilitate the progression of CVD
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