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    Evidence for the decay B0→J/ψω and measurement of the relative branching fractions of meson decays to J/ψη and J/ψη′

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    First evidence of the B 0 → J / ψ ω decay is found and the B s 0 → J / ψ η and B s 0 → J / ψ η ′ decays are studied using a dataset corresponding to an integrated luminosity of 1.0 fb -1 collected by the LHCb experiment in proton-proton collisions at a centre-of-mass energy of sqrt(s) = 7 TeV. The branching fractions of these decays are measured relative to that of the B 0 → J / ψ ρ 0 decay:frac(B (B 0 → J / ψ ω), B (B 0 → J / ψ ρ 0)) = 0.89 ± 0.19 (stat) - 0.13 + 0.07 (syst),frac(B (B s 0 → J / ψ η), B (B 0 → J / ψ ρ 0)) = 14.0 ± 1.2 (stat) - 1.5 + 1.1 (syst) - 1.0 + 1.1 (frac(f d, f s)),frac(B (B s 0 → J / ψ η ′), B (B 0 → J / ψ ρ 0)) = 12.7 ± 1.1 (stat) - 1.3 + 0.5 (syst) - 0.9 + 1.0 (frac(f d, f s)), where the last uncertainty is due to the knowledge of f d / f s, the ratio of b-quark hadronization factors that accounts for the different production rate of B 0 and B s 0 mesons. The ratio of the branching fractions of B s 0 → J / ψ η ′ and B s 0 → J / ψ η decays is measured to befrac(B (B s 0 → J / ψ η ′), B (B s 0 → J / ψ η)) = 0.90 ± 0.09 (stat) - 0.02 + 0.06 (syst)

    [19] F. Lin and W. M. Wonham, 1990. Decentralized control and coordination of discrete event systems with partial observation.

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    discrete event systems. Discrete Event Dynamic Systems: Theory and Applications, 4(3), pp. 221-236. [9] M. Heymann and F. Lin, 1996. Nonblocking supervisory control of nondeterministic systems, Technion CIS Report #9620, October 1996. [10] M. Heymann and F. Lin, 1995. On observability and nondeterminism in discrete event control, Proceedings of the 33rd Allerton Conference on Communication, Control, and Computing, pp. 136-145. [11] M. Heymann and F. Lin, 1996. Discrete event control of nondeterministic discrete event systems, Proceedings of the 35th IEEE Conference on Decision and Control, to appear. [12] J. E. Hopcroft and J. D. Ullman. Introduction to Automata Theory, Languages and Computation. Addison-Wesley, 1979. [13] K. Inan, 1994. Nondeterministic supervision under partial observation. in G. Cohen and J.-P. Quadrat, Eds., 11th International Conference on Analysis and Optimization o

    The stem cell E3-ligase Lin-41 promotes liver cancer progression through inhibition of microRNA-mediated gene silencing

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    Lin-41 is a stem cell-specific E3 ligase and a known target of the tumour suppressor microRNA (miRNA) let-7. Lin-41 was recently reported to mediate ubiquitylation and degradation of the miRNA pathway protein Ago2. We demonstrate that Lin-41 is over-expressed in hepatocellular carcinoma (HCC). Lin-41 over-expression correlates with high a-fetoprotein level, high tumour grade and high tumour stage and predicts early tumour recurrence. Lin-41 is a strong predictor of poor long-term survival for patients with HCC. Lin-41 knock-down by RNA interference in HCC cell lines Huh7 and Hep3B suppressed proliferation in vitro and reduced in vivo tumour growth in NOD/SCID mice. On the other hand, over-expression of Lin-41 in the HCC cell line SK-Hep1 enhanced tumourigenicity. Over-expression and knock-down of Lin-41 led to inverse changes in the levels of Ago1 and Ago2 proteins. Over-expression of Ago1 and Ago2 reduced in vivo tumour growth. Lin-41 over-expression suppressed let-7 activity in HCC cell lines and expression of Lin-41 enhanced the expression of let-7-regulated oncogenes c-Myc, Lin-28B, HMGA2 and type 1 insulin-like growth factor receptor (IGF1R). Expression of Lin-28B and c-Myc enhanced the expression of Lin-41. Chromatin immunoprecipitation and reporter assays revealed direct association of c-Myc with the Lin-41 promoter, resulting in transcriptional transactivation. Our results indicate that Lin-41 plays an important role in the growth of HCC by regulating RISC complex proteins Ago1 and Ago2 to inhibit miRNA-mediated gene silencing and promote the expression of oncogenic proteins. Lin-41 is also a strong prognostic factor for patients with HCC. Copyright (C) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd

    Oleoylethanolamide, an endogenous PPAR-alpha agonist, lowers body weight and hyperlipidemia in obese rats

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    The fatty-acid ethanolamide, oleoylethanolamide (OEA), is a naturally occurring lipid that regulates feeding and body weight [Rodriguez de Fonseca, F., Navarro, M., Gomez, R., Escuredo, L., Nava, F., Fu, J., Murillo-Rodriguez, E., Giuffrida, A., LoVerme, J., Gaetani, S., Kathuria, S., Gall, C., Piomelli, D., 2001. An anorexic lipid mediator regulated by feeding. Nature 414, 209-212], and serves as an endogenous agonist of peroxisome proliferator-activated receptor-alpha (PPAR-alpha) [Fu, J., Gaetani, S., Oveisi, F., Lo Verme, J., Serrano, A., Rodriguez De Fonseca, F., Rosengarth., A., Luecke, H., Di Giacomo, B., Tarzia, G., Piomelli, D., 2003. Oleoylethanolamide regulates feeding and body weight through activation of the nuclear receptor PPAR-alpha. Nature 425, 90-93], a ligand-activated transcription factor that regulates several aspects of lipid metabolism [. Peroxisome proliferator-activated receptors: nuclear control of metabolism. Endocr. Rev. 20, 649-688]). OEA reduces food intake in wild-type mice, but not in mice deficient in PPAR-alpha (PPAR-alpha(-/-)), an effect that is also observed with the PPAR-alpha agonists Wy-14643 and GW7647 [Brown, P.J., Chapman, J.M., Oplinger, J.A., Stuart, L.W., Willson, T.M. and Wu, Z., 2000. Chemical compounds as selective activators of PPAR-alpha. PCT Int. Appl., 32; . The PPARs: from orphan receptors to drug discovery. J. Med. Chem. 43, 527-550]. By contrast, specific agonists of PPAR-delta/beta (GW501516) or PPAR-gamma (ciglitazone) have no such effect. In obese Zucker rats, which lack functional leptin receptors, OEA reduces food intake and lowers body-weight gain along with plasma lipid levels. Similar effects are seen in diet-induced obese rats and mice. In the present study, we report that subchronic OEA treatment (5mgkg(-1), intraperitoneally, i.p., once daily for two weeks) in Zucker rats initiates transcription of PPAR-alpha and other PPAR-alpha target genes, including fatty-acid translocase (FAT/CD36), liver fatty-acid binding protein (L-FABP), and uncoupling protein-2 (UCP-2). Moreover, OEA decreases neutral lipid content in hepatocytes, as assessed by Oil red O staining, as well as serum cholesterol and triglyceride levels. The results suggest that OEA regulates lipid metabolism and that this effect may contribute to its anti-obesity propertie

    LIN-2 and FRM-3 regulate the synaptic abundance but not surface expression level of AChRs.

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    (A-D) ACR-16::RFP and UNC-29::RFP synaptic abundance were decreased in lin-2null and frm-3null mutants. Representative images (A, C, scale bar 10 μm) and mean puncta intensity (B, D) are shown. The wild type is normalized to 1. (E-H) ACh- and Levamisole-activated currents were unaltered in lin-2null and frm-3null mutants. Representative traces (E, G) and mean current amplitude (F, H) are shown. (I, J) GABA-activated currents were decreased by 50% in lin-2null mutants but were unchanged in frm-3null mutants. Data are mean ± SEM (***, p < 0.001 when compared to control; one-way ANOVA). The number of worms analyzed for each genotype is indicated in the bar.</p

    Tz-Lin Hsu Piano Recital Program Notes

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    This is the Program Notes of Tz-Lin Hsu\ue2s piano recital held on May 20th, 2020. The recital program includes Johann Sebastian Bach\ue2s The Well-Tempered Clavier, Book 1, Prelude and Fugue No. 17 in A-flat Major, BWV 862; Ludwig van Beethoven\ue2s Sonata No. 7 in D Major, Op. 10, No. 3, Jakob Ludwig Felix Mendelssohn Bartholdy\ue2s Fantasy in F-sharp minor, Op. 28; and Ignacy Jan Paderewski\ue2s Th\uc3\ua8me vari\uc3\ua8 in A Major, Op. 16, No. 3. The program notes will briefly introduce these four composers\ue2 lives, their compositional backgrounds, and the structure of each work, including the tonal organization and thematic materials
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