9 research outputs found

    Current reversals and metastable states in the infinite Bose-Hubbard chain with local particle loss

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    We present an algorithm which combines the quantum trajectory approach to open quantum systems with a density-matrix renormalization group scheme for infinite one-dimensional lattice systems. We apply this method to investigate the long-time dynamics in the Bose-Hubbard model with local particle loss starting from a Mott-insulating initial state with one boson per site. While the short-time dynamics can be described even quantitatively by an equation of motion (EOM) approach at the mean-field level, many-body interactions lead to unexpected effects at intermediate and long times: local particle currents far away from the dissipative site start to reverse direction ultimately leading to a metastable state with a total particle current pointing away from the lossy site. An alternative EOM approach based on an effective fermion model shows that the reversal of currents can be understood qualitatively by the creation of holon-doublon pairs at the edge of the region of reduced particle density. The doublons are then able to escape while the holes move towards the dissipative site, a process reminiscent---in a loose sense---of Hawking radiation

    Infection of adenovirus <i>atrogin-1</i> and microarray analysis.

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    <p><b>A.</b> Neonatal rat cardiomyocytes were infected with adenovirus green fluorescent protein (GFP) control (Ad-GFP) or <i>atrogin-1</i> (Ad-<i>atrogin-1</i>). The infection efficiency was visualized for GFP 24 hours later using fluorescence microscopy (Magnification, ×400). <b>B.</b> The levels of <i>atrogin-1</i> protein were determined by Western blot analysis with anti-<i>atrogin-1</i> antibody, using β-actin as the internal control. Quantitative analysis of protein bands was shown (n = 3). <b>C.</b> Hierarchical clustering depicting expression profiles of differentially expressed genes in Ad-<i>atrogin-1</i> (A1 and A2) and Ad-control (G1 and G2) groups. Data from individual sample are shown. A subset of genes displays significant expression changes at ≥2-fold or ≤−2-fold. Gene expression levels are shown as color variations (red: up-regulated expression; green: down-regulated expression).</p

    Effect of <i>atrogin-1</i> on inflammation.

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    <p><b>A.</b> Neonatal rat cardiomyocytes were infected with Ad-GFP or Ad-<i>atrogin-1</i>-GFP for 24 h and then treated with LPS (1 µg/ml) for additional 24 hours. The qRT-PCR analysis of gene expression was performed in triplicate using specific oligonucleotides primers. Data represent the mean ± SEM. <b><sup>#</sup></b><i>P</i><0.05, <b><sup>&</sup></b><i>P</i><0.01, <sup>P<0.05 vs. Ad-GFP; *P<0.01 vs. Ad-GFP+LPS. B. Neonatal rat cardiomyocytes were infected with Ad-siRNA-control or Ad-siRNA-atrogin-1 for 24 h and then treated with LPS (1 µg/ml) for additional 24 hours. The qRT-PCR analysis of gene expression was performed as in A. Data represent the mean ± SEM. #P<0.05, &P<0.01, </sup><i>P</i><0.05 vs. siRNA-control; *<i>P</i><0.01 vs. Ad-siRNA+LPS.</p

    Effects of <i>atrogin-1</i> overexpression on cardiomyocyte apoptosis and hypertrophy.

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    <p>Neonatal rat cardiomyocytes were infected with Ad-GFP or Ad-<i>atrogin-1</i>-GFP for 24 h and then treated with LPS (1 µg/ml) for additional 24 hours. <b>A.</b> Apoptosis was detected and quantified using TUNEL assay (red), and nuclei were counterstained with DAPI (blue). A representative field is shown for each condition (top panels), Magnification, ×400. Quantitative analysis of TUNEL-positive cells from three independent experiments (bottom panels). <b>B.</b> The cells were fixed and stained with anti-α-actinin antibody followed by Alexa Fluor 568-conjugated goat anti-mouse IgG (red), and nuclei were stained with DAPI (blue). A representative field is shown for each condition (top panels), Magnification, ×200. Quantitative analysis of cell surface area (a minimum of 100 randomly chosen cells measured in each group) (bottom panels). Data represent the mean ± SEM (n = 3). <b><sup>#</sup></b><i>P</i><0.05, <b><sup>&</sup></b><i>P</i><0.01 vs. Ad-GFP; *<i>P</i><0.05; <sup>$</sup><i>P</i><0.01 vs. Ad-GFP+LPS. <b>C.</b> The qRT-PCR analysis of ANF, Myh6 and serca2 mRNA expression was performed in triplicate using specific oligonucleotides primers. <b>D</b> and <b>E.</b> Neonatal rat cardiomyocytes were infected with Ad-siRNA-<i>atrogin-1</i> or Ad-siRNA-control for 24 hours. Analysis of apoptosis and cell surface area were performed as in A and B. Data represent the mean ± SEM (n = 3). <b><sup>#</sup></b><i>P</i><0.05, <b><sup>&</sup></b><i>P</i><0.01 vs. siRNA-control; *<i>P</i><0.05 vs. siRNA-control +LPS.</p

    Effects of <i>atrogin-1</i> on MAPK and NF-κB signaling pathways.

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    <p><b>A.</b> Neonatal rat cardiomyocytes were infected with Ad-GFP or Ad-atrogin-1-GFP for 24 h and then treated with LPS (1 µg/ml). The protein levels of total and phospho-ERK1/2, JNK1/2, p38 and p65/NF-κB were detected by Western blot analysis (left panels). Quantitative analysis of relative intensity of phosphorylated proteins was shown (right panel). Data represent the mean ± SEM (n = 3). <b><sup>#</sup></b><i>P</i><0.05, <b><sup>&</sup></b><i>P</i><0.05 vs. Ad-GFP; *<i>P</i><0.01 vs. Ad-GFP+LPS. <b>B.</b> Neonatal rat cardiomyocytes were infected with adenovirus siRNA-control or siRNA-atrogin-1 and then treated with LPS (1 µg/ml). The protein levels were detected as in A (left panels). Quantitative analysis of relative intensity of phosphorylated proteins was shown (right panel). Data represent the mean ± SEM (n = 3). <b><sup>#</sup></b><i>P</i><0.05, <b><sup>&</sup></b><i>P</i><0.05 vs. siRNA-control; *<i>P</i><0.05 vs. siRNA-control+LPS.</p

    Scatter plot of relative changes in gene expression as determined by microarray analysis and by qRT-PCR.

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    <p>Eight genes were analyzed: IL-6, DKK2, Calr, Cxcl6, Cxcl1, Axin2, IL-1r1, and Cadm1. Each symbol represents the fold change of the respective gene in ad-<i>atrogin-1</i> group over Ad-GFP control.</p
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