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Determination of Hund's coupling in 5d oxides using resonant inelastic x-ray scattering
Yuan, Bo,Clancy, J. P.,Cook, A. M.,Thompson, C. M.,Greedan, J.,Cao, G.,Jeon, B. C.,Noh, T. W.,Upton, M. H.,Casa, D.,Gog, T.,Paramekanti, A.,Kim, Young-June American Physical Society 2017 Physical Review B Vol.95 No.23
<P>We report resonant inelastic x-ray scattering (RIXS) measurements on ordered double-perovskite samples containing Re5+ and Ir5+ with 5d(2) and 5d(4) electronic configurations, respectively. In particular, the observedRIXS spectra of Ba2YReO6 and Sr2MIrO6 (M = Y, Gd) show sharp intra-t(2g) transitions, which can be quantitatively understood using a minimal 'atomic' Hamiltonian incorporating spin-orbit coupling. and Hund's coupling J(H). Our analysis yields lambda = 0.38(2) eV with J(H) = 0.26(2) eV for Re5+ and lambda = 0.42(2) eV with J(H) = 0.25(4) eV for Ir5+. Our results provide sharp estimates for Hund's coupling in 5d oxides and suggest that it should be treated on equal footing with spin-orbit interaction in multiorbital 5d transition-metal compounds.</P>
Hozoi, L.,Gretarsson, H.,Clancy, J. P.,Jeon, B.-G.,Lee, B.,Kim, K. H.,Yushankhai, V.,Fulde, Peter,Casa, D.,Gog, T.,Kim, Jungho,Said, A. H.,Upton, M. H.,Kim, Young-June,van den Brink, Jeroen American Physical Society 2014 Physical review. B, Condensed matter and materials Vol.89 No.11
In the search for topological phases in correlated electron systems, materials with 5d transition-metal ions, in particular the iridium-based pyrochlores A2Ir2O7, provide fertile grounds. Several topological states have been predicted but the actual realization of such states is believed to critically depend on the strength of local potentials arising from distortions of the IrO6 cages. We test this hypothesis by measuring with resonant inelastic x-ray scattering the electronic level splittings in the A = Y, Eu systems, which we show to agree very well with ab initio quantum chemistry electronic-structure calculations for the series of materials with A = Sm, Eu, Lu, and Y. We find, however, that the primary source for quenching the spin-orbit interaction is not a distortion of the IrO6 octahedra but longer-range lattice anisotropies which inevitably break the local cubic symmetry.
Dae-Kee, Kim,Lu Long,Alexi Crosby,Xudong, Yang,Mark Southwood,D. Upton,Nicholas W. Morrell 이화여자대학교 약학연구소 2010 藥學硏究論文集 Vol.- No.20
Background— Recent genetic studies have highlighted the role of the bone morphogenetic protein (BMP)/transforming growth factor (TGF)-β signaling pathways in the pathogenesis of familial pulmonary arterial hypertension (PAH). It remains unclear whether alterations in these pathways contribute to other forms of pulmonary hypertension and to what extent these changes can be exploited for therapeutic intervention. Methods and Results— We studied BMP/TGF-β signaling in 2 rat models of PAH due to chronic hypoxia and monocrotaline. In both models, there was a significant reduction in lung BMP type IA receptor and BMP type II receptor mRNA expression, although these changes were more pronounced in the monocrotaline model. This was accompanied by a reduction in lung levels of phospho-Smad1/5 and Id (inhibitor of DNA binding) gene expression in the monocrotaline model. In contrast, we observed increased TGF-β activity, again more marked in the monocrotaline model, as evidenced by increased phospho-Smad2/3 and increased expression of TGF-β–regulated genes. Immunohistochemistry revealed increased TGF-β1 expression in pulmonary artery smooth muscle cells and macrophages surrounding remodeled pulmonary arteries in monocrotaline rats. Inhibition of activin receptor-like kinase-5 signaling in vivo with the selective small-molecule inhibitor IN-1233 prevented PAH, right ventricular hypertrophy, and vascular remodeling after monocrotaline injection and inhibited the progression of established PAH in this model. No significant effect was observed in hypoxic PAH. In vitro studies confirmed that TGF-β stimulated migration of distal rat pulmonary artery smooth muscle cells and that this effect was inhibited by IN-1233. Conclusions— Disruption of BMP/TGF-β signaling is more pronounced in the monocrotaline model of PAH than in the chronic hypoxia model. Increased TGF-β activity is associated with greater macrophage recruitment with monocrotaline treatment. Inhibition of TGF-β signaling via activin receptor-like kinase-5 prevents development and progression of PAH in the monocrotaline model and may involve inhibition of pulmonary artery smooth muscle cell migration.