309 research outputs found
Irregular AC losses with long time constants in large cable-in-conduit conductors
科研費報告書収録論文(課題番号:15360491/研究代表者:濱島高太郎/大型超伝導コイルに発生する不規則な交流損失の原因究明)44
Electronic superlattice revealed by resonant scattering from random impurities in Sr3Ru2O7
Resonant elastic x-ray scattering (REXS) is an exquisite element-sensitive
tool for the study of subtle charge, orbital, and spin superlattice orders
driven by the valence electrons, which therefore escape detection in
conventional x-ray diffraction (XRD). Although the power of REXS has been
demonstrated by numerous studies of complex oxides performed in the soft x-ray
regime, the cross section and photon wavelength of the material-specific
elemental absorption edges ultimately set the limit to the smallest
superlattice amplitude and periodicity one can probe. Here we show -- with
simulations and REXS on Mn-substituted SrRuO -- that these
limitations can be overcome by performing resonant scattering experiments at
the absorption edge of a suitably-chosen, dilute impurity. This establishes
that -- in analogy with impurity-based methods used in electron-spin-resonance,
nuclear-magnetic resonance, and M\"ossbauer spectroscopy -- randomly
distributed impurities can serve as a non-invasive, but now momentum-dependent
probe, greatly extending the applicability of resonant x-ray scattering
techniques
Crystal-field level inversion in lightly Mn-doped Sr3Ru2O7
Sr3(Ru1-xMnx)2O7, in which 4d-Ru is substituted by the more localized 3d-Mn,
is studied by x-ray dichroism and spin-resolved density functional theory. We
find that Mn impurities do not exhibit the same 4+ valence of Ru, but act as 3+
acceptors; the extra eg electron occupies the in-plane 3dx2-y2 orbital instead
of the expected out-of-plane 3d3z2-r2. We propose that the 3d-4d interplay, via
the ligand oxygen orbitals, is responsible for this crystal-field level
inversion and the material's transition to an antiferromagnetic, possibly
orbitally-ordered, low-temperature state.Comment: A high-resolution version can be found at
http://www.physics.ubc.ca/~quantmat/ARPES/PUBLICATIONS/Articles/MnSr3Ru2O7_XAS.pd
Cell senescence, apoptosis and DNA damage cooperate in the remodeling processes accounting for heart morphogenesis
During embryonic development, organ morphogenesis requires major tissue rearrangements that are tightly regulated at the genetic level. A large number of studies performed in recent decades assigned a central role to programmed cell death for such morphogenetic tissue rearrangements that often sculpt the shape of embryonic organs. However, accumulating evidence indicates that far from being the only factor responsible for sculpting organ morphology, programmed cell death is accompanied by other tissue remodeling events that ensure the outcome of morphogenesis. In this regard, cell senescence has been recently associated with morphogenetic degenerative embryonic processes as an early tissue remodeling event in development of the limbs, kidney and inner ear. Here, we have explored cell senescence by monitoring ?-galactosidase activity during embryonic heart development where programmed cell death is believed to exert an important morphogenetic function. We report the occurrence of extensive cell senescence foci during heart morphogenesis. These foci overlap spatially and temporally with the areas of programmed cell death that are associated with remodeling of the outflow tract to build the roots of the great arteries and with the septation of cardiac cavities. qPCR analysis allowed us to identify a gene expression profile characteristic of the so-called senescence secretory associated phenotype in the remodeling outflow tract of the embryonic heart. In addition, we confirmed local upregulation of numerous tumor suppressor genes including p21, p53, p63, p73 and Btg2. Interestingly, the areas of cell senescence were also accompanied by intense lysosomal activation and non-apoptotic DNA damage revealed by ?H2AX immunolabeling. Considering the importance of sustained DNA damage as a triggering factor for cell senescence and apoptosis, we propose the coordinated contribution of DNA damage, senescence and apoptotic cell death to assure tissue remodeling in the developing vertebrate heart.Funding: Thanks are due to Montse Fernandez-Calderon, Sonia Perez-Mantecon and Susana Dawalibi for technical assistance. This work was supported by Grant BFU2017-84046-P from the Spanish Ministry of Science, Innovation and Universities. C S-F is a recipient of a FPI predoctoral fellowship from the Spanish Ministry of Science, Innovation and Universitie
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