Superconducting proximity effect to the block antiferromagnetism in Ky_{y}Fe2−x_{2-x}Se2_{2}

Recent discovery of superconducting (SC) ternary iron selenides has block antiferromagentic (AFM) long range order. Many experiments show possible mesoscopic phase separation of the superconductivity and antiferromagnetism, while the neutron experiment reveals a sizable suppression of magnetic moment due to the superconductivity indicating a possible phase coexistence. Here we propose that the observed suppression of the magnetic moment may be explained due to the proximity effect within a phase separation scenario. We use a two-orbital model to study the proximity effect on a layer of block AFM state induced by neighboring SC layers via an interlayer tunneling mechanism. We argue that the proximity effect in ternary Fe-selenides should be large because of the large interlayer coupling and weak electron correlation. The result of our mean field theory is compared with the neutron experiments semi-quantitatively. The suppression of the magnetic moment due to the SC proximity effect is found to be more pronounced in the d-wave superconductivity and may be enhanced by the frustrated structure of the block AFM state.Comment: 6 pages, 6 figure

Theory for charge and orbital density-wave states in manganite La0.5_{0.5}Sr1.5_{1.5}MnO4_4

We investigate the high temperature phase of layered manganites, and demonstrate that the charge-orbital phase transition without magnetic order in La$_{0.5}$Sr$_{1.5}$MnO$_4$ can be understood in terms of the density wave instability. The orbital ordering is found to be induced by the nesting between segments of Fermi surface with different orbital characters. The simultaneous charge and orbital orderings are elaborated with a mean field theory. The ordered orbitals are shown to be $d_{x^2-y^2} \pm d_{3z^2-r^2}$.Comment: published versio

Progressive amorphization of GeSbTe phase-change material under electron beam irradiation

Fast and reversible phase transitions in chalcogenide phase-change materials (PCMs), in particular, Ge-Sb-Te compounds, are not only of fundamental interests, but also make PCMs based random access memory (PRAM) a leading candidate for non-volatile memory and neuromorphic computing devices. To RESET the memory cell, crystalline Ge-Sb-Te has to undergo phase transitions firstly to a liquid state and then to an amorphous state, corresponding to an abrupt change in electrical resistance. In this work, we demonstrate a progressive amorphization process in GeSb2Te4 thin films under electron beam irradiation on transmission electron microscope (TEM). Melting is shown to be completely absent by the in situ TEM experiments. The progressive amorphization process resembles closely the cumulative crystallization process that accompanies a continuous change in electrical resistance. Our work suggests that if displacement forces can be implemented properly, it should be possible to emulate symmetric neuronal dynamics by using PCMs

Macrophage colony-stimulating factor and its receptor signaling augment glycated albumin-induced retinal microglial inflammation in vitro

<p>Abstract</p> <p>Background</p> <p>Microglial activation and the proinflammatory response are controlled by a complex regulatory network. Among the various candidates, macrophage colony-stimulating factor (M-CSF) is considered an important cytokine. The up-regulation of M-CSF and its receptor CSF-1R has been reported in brain disease, as well as in diabetic complications; however, the mechanism is unclear. An elevated level of glycated albumin (GA) is a characteristic of diabetes; thus, it may be involved in monocyte/macrophage-associated diabetic complications.</p> <p>Results</p> <p>The basal level of expression of M-CSF/CSF-1R was examined in retinal microglial cells <it>in vitro</it>. Immunofluorescence, real-time PCR, immunoprecipitation, and Western blot analyses revealed the up-regulation of CSF-1R in GA-treated microglial cells. We also detected increased expression and release of M-CSF, suggesting that the cytokine is produced by activated microglia via autocrine signaling. Using an enzyme-linked immunosorbent assay, we found that GA affects microglial activation by stimulating the release of tumor necrosis factor-α and interleukin-1β. Furthermore, the neutralization of M-CSF or CSF-1R with antibodies suppressed the proinflammatory response. Conversely, this proinflammatory response was augmented by the administration of M-CSF.</p> <p>Conclusions</p> <p>We conclude that GA induces microglial activation via the release of proinflammatory cytokines, which may contribute to the inflammatory pathogenesis of diabetic retinopathy. The increased microglial expression of M-CSF/CSF-1R not only is a response to microglial activation in diabetic retinopathy but also augments the microglial inflammation responsible for the diabetic microenvironment.</p