59 research outputs found

    Effect of NiO nanoparticle addition on the structural, microstructural, magnetic, electrical, and magneto-transport properties of La0.67Ca0.33MnO3 nanocomposites

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    Incorporation of the secondary oxide phase into the manganite composite capable of enhancing low-field magnetoresistance (LFMR) for viability in high-performance spintronic applications. Polycrystalline La0.67Ca0.33MnO3 (LCMO) was prepared via the sol–gel route in this study. The structural, microstructural, magnetic, electrical, and magneto-transport properties of (1−x) LCMO: x NiO, x = 0.00, 0.05, 0.10, 0.15 and 0.20 were investigated in detail. The X-ray diffraction (XRD) patterns showed the coexistence of LCMO and NiO in the composites. The microstructural analysis indicated the amount of NiO nanoparticles segregated at the grain boundaries or on the surface of LCMO grains increased with the increasing secondary phase content. LCMO and NiO still retained their individual magnetic phase as observed from AC susceptibility (ACS) measurement. This further confirmed that there is no interfacial diffusion reaction between these two compounds. The NiO nanoparticle acted as a barrier to charge transport and caused an increase in resistivity for composite samples. The residual resistivity due to the grain/domain boundary is responsible for the scattering mechanism in the metallic region as suggested by the theoretical model fitting, ρ(T)=ρ0+ρ2T2+ρ4.5T4.5. The magnetoresistance values of LCMO and its composites were found to increase monotonically with the decrease in temperature. Hence, the LFMR was observed. Nonetheless, the slight reduction of LFMR in composites was attributed to the thick boundary layer created by NiO and impaired the spin polarised tunnelling process

    Disseminated and Congenital Toxoplasmosis in a Mother and Child With Activated PI3-Kinase δ Syndrome Type 2 (APDS2): Case Report and a Literature Review of Toxoplasma Infections in Primary Immunodeficiencies

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    Phosphoinositide 3-kinase (PI3K) plays an integral role in lymphocyte function. Mutations in PIK3CD and PIK3R1, encoding the PI3K p110δ and p85α subunits, respectively, cause increased PI3K activity and result in immunodeficiency with immune dysregulation. We describe here the first cases of disseminated and congenital toxoplasmosis in a mother and child who share a pathogenic mutation in PIK3R1 and review the mechanisms underlying susceptibility to severe Toxoplasma gondii infection in activated PI3Kδ syndrome (APDS) and in other forms of primary immunodeficiency
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