Superconducting mechanism for the cuprate Ba2_2CuO3+δ_{3+\delta} based on a multiorbital Lieb lattice model

For the recently discovered cuprate superconductor $\mathrm{Ba_{2}CuO_{3+\delta}}$, we propose a lattice structure which resembles the model considered by Lieb to represent the vastly oxygen-deficient material. We first investigate the stability of the Lieb-lattice structure, and then construct a multiorbital Hubbard model based on first-principles calculation. By applying the fluctuation-exchange approximation to the model and solving the linearized Eliashberg equation, we show that $s$-wave and $d$-wave pairings closely compete with each other, and, more interestingly, that the intra-orbital and inter-orbital pairings coexist. We further show that, if the energy of the $d_{3z^2-r^2}$ band is raised to make it "incipient" with the lower edge of the band close to the Fermi level within a realistic band filling regime, $s\pm$-wave superconductivity is strongly enhanced. We reveal an intriguing relation between the Lieb model and the two-orbital model for the usual K$_2$NiF$_4$ structure where a close competition between $s-$ and $d-$wave pairings is known to occur. The enhanced superconductivity in the present model is further shown to be related to an enhancement found previously in the bilayer Hubbard model with an incipient band.Comment: 19 pages, 20 figures; references and figures update

Temperature elevation enhances cell surface expression of measles virus fusion protein in infected cells

Cell fusion proceeded gradually in measles virus-infected cells incubated at 35°C. Shift-up of incubation temperature to 39°C induced rapidly increased cell fusion in spite of the cessation of de novo synthesis of the fusion (F) protein. Pulse-chase experiments showed that there was little difference in the acquisition of immunoreactivity by haemagglutinin (H) and F proteins between the two temperatures. H protein was detected on the cell surface 60 min after the chase at either temperature. However, appearance of F protein on the cell surface took less than 3 h at 39°C whereas it took 5 h at 35°C. These data indicate that temperature elevation induces more efficient expression of F protein on the cell surface accompanied by marked syncytium formation in measles virus-infected cells

Glycosylation of measles virus haemagglutinin protein in infected cells

Processing of the measles virus haemagglutinin (H) protein was analysed by the pulse-chase method, immunoprecipitation with an anti-H monoclonal antibody and SDS-polyacrylamide gel electrophoresis, combined with the addition of carbonyl cyanide m-chlorophenylhydrazone (CCCP) or monensin (inhibitors of intracellular processing of secretory proteins) to cultures and digestion of the protein with endoglycosidase H or neuraminidase. The apparent M(r) of the H protein was increased from 74K to 78K during the chase period. Addition of either CCCP or monensin to the chase medium inhibited the appearance of the 78K H protein, but not the immunoreactivity of the H protein or dimer formation, suggesting that these two events occur in the rough endoplasmic reticulum. The 74K H protein processed in the presence of CCCP was fully sensitive to endoglycosidase H digestion, whereas the 74K H protein processed in the presence of monensin was partially resistant to endoglycosidase H. In experiments using 3H-labelled sugars, [3H]galactose was incorporated into the 74K H protein in the presence of monensin. Neuraminidase treatment increased the electrophoretic mobility of the 78K H protein to 74K. Only the 78K H protein was detected on the surface of untreated cells, and it was resistant to endoglycosidase H digestion. These data suggest that after galactose addition sialic acid is added to the H protein in the trans-Golgi complex and then the mature 78K H protein is transported to the cell surface

The Mechanism of Water Cycle System in Lake Inba-Numa Watershed:A Comparative Study of Runoff Mechanisms of Small Watersheds

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

Survey of Period Variations of Superhumps in SU UMa-Type Dwarf Novae. II: The Second Year (2009-2010)

As an extension of the project in Kato et al. (2009, arXiv:0905.1757), we collected times of superhump maxima for 61 SU UMa-type dwarf novae mainly observed during the 2009-2010 season. The newly obtained data confirmed the basic findings reported in Kato et al. (2009): the presence of stages A-C, as well as the predominance of positive period derivatives during stage B in systems with superhump periods shorter than 0.07 d. There was a systematic difference in period derivatives for systems with superhump periods longer than 0.075 d between this study and Kato et al. (2009). We suggest that this difference is possibly caused by the relative lack of frequently outbursting SU UMa-type dwarf novae in this period regime in the present study. We recorded a strong beat phenomenon during the 2009 superoutburst of IY UMa. The close correlation between the beat period and superhump period suggests that the changing angular velocity of the apsidal motion of the elliptical disk is responsible for the variation of superhump periods. We also described three new WZ Sge-type objects with established early superhumps and one with likely early superhumps. We also suggest that two systems, VX For and EL UMa, are WZ Sge-type dwarf novae with multiple rebrightenings. The O-C variation in OT J213806.6+261957 suggests that the frequent absence of rebrightenings in very short-Porb objects can be a result of sustained superoutburst plateau at the epoch when usual SU UMa-type dwarf novae return to quiescence preceding a rebrightening. We also present a formulation for a variety of Bayesian extension to traditional period analyses.Comment: 63 pages, 77 figures, 1 appendix, Accepted for publication in PASJ, data correctio

cGAS Drives Noncanonical-Inflammasome Activation in Age-Related Macular Degeneration

Geographic atrophy is a blinding form of age-related macular degeneration characterized by retinal pigmented epithelium (RPE) death; the RPE also exhibits DICER1 deficiency, resultant accumulation of endogenous Alu-retroelement RNA, and NLRP3-inflammasome activation. How the inflammasome is activated in this untreatable disease is largely unknown. Here we demonstrate that RPE degeneration in human-cell-culture and mouse models is driven by a noncanonical-inflammasome pathway that activates caspase-4 (caspase-11 in mice) and caspase-1, and requires cyclic GMP-AMP synthase (cGAS)-dependent interferon-β production and gasdermin D-dependent interleukin-18 secretion. Decreased DICER1 levels or Alu-RNA accumulation triggers cytosolic escape of mitochondrial DNA, which engages cGAS. Moreover, caspase-4, gasdermin D, interferon-β, and cGAS levels were elevated in the RPE in human eyes with geographic atrophy. Collectively, these data highlight an unexpected role of cGAS in responding to mobile-element transcripts, reveal cGAS-driven interferon signaling as a conduit for mitochondrial-damage-induced inflammasome activation, expand the immune-sensing repertoire of cGAS and caspase-4 to noninfectious human disease, and identify new potential targets for treatment of a major cause of blindness