5,279 research outputs found

    Tripartite Entanglement in Noninertial Frame

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    The tripartite entanglement is examined when one of the three parties moves with a uniform acceleration with respect to other parties. As Unruh effect indicates, the tripartite entanglement exhibits a decreasing behavior with increasing the acceleration. Unlike the bipartite entanglement, however, the tripartite entanglement does not completely vanish in the infinite acceleration limit. If the three parties, for example, share the Greenberger-Horne-Zeilinger or W-state initially, the corresponding π\pi-tangle, one of the measures for tripartite entanglement, is shown to be π/60.524\pi/6 \sim 0.524 or 0.176 in this limit, respectively. This fact indicates that the tripartite quantum information processing may be possible even if one of the parties approaches to the Rindler horizon. The physical implications of this striking result are discussed in the context of black hole physics.Comment: 19 pages, 5 figure

    Green's function approach to transport through a gate-all-around Si nanowire under impurity scattering

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    We investigate transport properties of gate-all-around Si nanowires using non-equilibrium Green's function technique. By taking into account of the ionized impurity scattering we calculate Green's functions self-consistently and examine the effects of ionized impurity scattering on electron densities and currents. For nano-scale Si wires, it is found that, due to the impurity scattering, the local density of state profiles loose it's interference oscillations as well as is broaden and shifted. In addition, the impurity scattering gives rise to a different transconductance as functions of temperature and impurity scattering strength when compared with the transconductance without impurity scattering.Comment: 8 pages, 4 figure

    Deficiency of Capicua disrupts bile acid homeostasis

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    Capicua (CIC) has been implicated in pathogenesis of spinocerebellar ataxia type 1 and cancer in mammals; however, the in vivo physiological functions of CIC remain largely unknown. Here we show that Cic hypomorphic (Cic-L-/-) mice have impaired bile acid (BA) homeostasis associated with induction of proinflammatory cytokines. We discovered that several drug metabolism and BA transporter genes were down-regulated in Cic-L-/- liver, and that BA was increased in the liver and serum whereas bile was decreased within the gallbladder of Cic-L-/- mice. We also found that levels of proinflammatory cytokine genes were up-regulated in Cic-L-/- liver. Consistent with this finding, levels of hepatic transcriptional regulators, such as hepatic nuclear factor 1 alpha (HNF1 alpha), CCAAT/enhancer-binding protein beta (C/EBP beta), forkhead box protein A2 (FOXA2), and retinoid X receptor alpha (RXR alpha), were markedly decreased in Cic-L-/- mice. Moreover, induction of tumor necrosis factor alpha (Tnf alpha) expression and decrease in the levels of FOXA2, C/EBP beta, and RXRa were found in Cic-L-/- liver before BA was accumulated, suggesting that inflammation might be the cause for the cholestasis in Cic-L-/- mice. Our findings indicate that CIC is a critical regulator of BA homeostasis, and that its dysfunction might be associated with chronic liver disease and metabolic disorders.open11810Ysciescopu

    Integrated analysis of global proteome, phosphoproteome, and glycoproteome enables complementary interpretation of disease-related protein networks

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    Multi-dimensional proteomic analyses provide different layers of protein information, including protein abundance and post-translational modifications. Here, we report an integrated analysis of protein expression, phosphorylation, and N-glycosylation by serial enrichments of phosphorylation and N-glycosylation (SEPG) from the same tissue samples. On average, the SEPG identified 142,106 unmodified peptides of 8,625 protein groups, 18,846 phosphopeptides (15,647 phosphosites), and 4,019 N-glycopeptides (2,634 N-glycosites) in tumor and adjacent normal tissues from three gastric cancer patients. The combined analysis of these data showed that the integrated analysis additively improved the coverages of gastric cancer-related protein networks; phosphoproteome and N-glycoproteome captured predominantly low abundant signal proteins, and membranous or secreted proteins, respectively, while global proteome provided abundances for general population of the proteome. Therefore, our results demonstrate that the SEPG can serve as an effective approach for multi-dimensional proteome analyses, and the holistic profiles of protein expression and PTMs enabled improved interpretation of disease-related networks by providing complementary information.11103Ysciescopu

    Characterization of developmental defects in the forebrain resulting from hyperactivated mTOR signaling by integrative analysis of transcriptomic and proteomic data

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    Hyperactivated mTOR signaling in the developing brain has been implicated in multiple forms of pathology including tuberous sclerosis complex (TSC). To date, various phenotypic defects such as cortical lamination irregularity, subependymal nodule formation, dysmorphic astrocyte differentiation and dendritic malformation have been described for patients and animal models. However, downstream networks affected in the developing brain by hyperactivated mTOR signaling have yet to be characterized. Here, we present an integrated analysis of transcriptomes and proteomes generated from wild-type and Tsc1/Emx1-Cre forebrains. This led to comprehensive lists of genes and proteins whose expression levels were altered by hyperactivated mTOR signaling. Further incorporation of TSC patient data followed by functional enrichment and network analyses pointed to changes in molecular components and cellular processes associated with neuronal differentiation and morphogenesis as the key downstream events underlying developmental and morphological defects in TSC. Our results provide novel and fundamental molecular bases for understanding hyperactivated mTOR signaling-induced brain defects which can in turn facilitate identification of potential diagnostic markers and therapeutic targets for mTOR signaling-related neurological disorders. ? The Author(s) 2017.11Ysciescopu
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