506 research outputs found

    Nicotine coregulates multiple pathways involved in protein modification/degradation in rat brain

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    Previously, we used cDNA microarrays to demonstrate that the phosphatidylinositol and MAP kinase signaling pathways are regulated by nicotine in different rat brain regions. In the present report, we show that, after exposure to nicotine for 14 days, ubiquitin, ubiquitin-conjugating enzymes, 20S and 19S proteasomal subunits, and chaperonin-containing TCP-1 protein (CCT) complex members are upregulated in rat prefrontal cortex (PFC) while being downregulated in the medial basal hypothalamus (MBH). In particular, relative to saline controls, ubiquitins B and C were upregulated by 33% and 47% (P<0.01), respectively, in the PFC. The proteasome beta subunit 1 (PSMB1) and 26S ATPase 3 (PSMC3) genes were upregulated in the PFC by 95% and 119% (P<0.001), respectively. In addition to the protein degradation pathway of the ubiquitin-proteasome complexes, we observed in the PFC an increase in the expression of small, ubiquitin-related modifiers (SUMO) 1 and 2 by 80% and 33%, respectively (P<0.001), and in 3 of 6 CCT subunits by up to 150% (P<0.0001). To a lesser extent, a change in the opposite direction was obtained in the expression of the same gene families in the MBH. Quantitative real-time RT-PCR was used to validate the microarray results obtained with some representative genes involved in these pathways. Taken together, our results suggest that, in response to systemic nicotine administration, the ubiquitin-proteasome, SUMO, and chaperonin complexes provide an intricate control mechanism to maintain cellular homeostasis, possibly by regulating the composition and signaling of target neurons in a region-specific manner. © 2004 Elsevier B.V. All rights reserved

    Some properties of the newly observed X(1835) state at BES

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    Recently the BES collaboration has announced observation of a resonant state in the π+πη\pi^+\pi^- \eta' spectrum in J/ψγπ+πηJ/\psi \to \gamma \pi^+\pi^-\eta' decay. Fitting the data with a 0+0^{-+} state, the mass is determined to be 1833.7 MeV with 7.7σ7.7\sigma statistic significance. This state is consistent with the one extracted from previously reported ppˉp \bar p threshold enhancement data in J/ψγppˉJ/\psi \to \gamma p \bar p. We study the properties of this state using QCD anomaly and QCD sum rules assuming X(1835) to be a pseudoscalar and show that it is consistent with data. We find that this state has a sizeable matrix element leading to branching ratios of (2.617.37)×103(2.61\sim 7.37)\times 10^{-3} and (2.2110.61)×102(2.21\sim 10.61)\times 10^{-2} for J/ψγGpJ/\psi \to \gamma G_p and for Gpπ+πηG_p \to \pi^+\pi^- \eta', respectively. Combining the calculated branching ratio of J/ψγGpJ/\psi \to \gamma G_p and data on threshold enhancement in J/ψγppˉJ/\psi \to \gamma p \bar p, we determine the coupling for GpppˉG_p- p-\bar p interaction. We finally study branching ratios of other J/ψγ+threemesonsJ/\psi \to \gamma + {three mesons} decay modes. We find that J/ψγGpγ(π+πη,KKπ0)J/\psi \to \gamma G_p \to \gamma (\pi^+\pi^- \eta, K K \pi^0) can provide useful tests for the mechanism proposed.Comment: 13 pages, 3 figures. The final version to appear at EPJ

    On Two-Body Decays of A Scalar Glueball

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    We study two body decays of a scalar glueball. We show that in QCD a spin-0 pure glueball (a state only with gluons) cannot decay into a pair of light quarks if chiral symmetry holds exactly, i.e., the decay amplitude is chirally suppressed. However, this chiral suppression does not materialize itself at the hadron level such as in decays into π+π\pi^+\pi^- and K+KK^+K^-, because in perturbative QCD the glueball couples to two (but not one) light quark pairs that hadronize to two mesons. Using QCD factorization based on an effective Lagrangian, we show that the difference of hadronization into ππ\pi\pi and KKKK already leads to a large difference between Br(π+π){\rm Br} (\pi^+\pi^-) and Br(K+K){\rm Br}(K^+K^-), even the decay amplitude is not chirally suppressed. Moreover, the small ratio of R=Br(ππ)/Br(KKˉ)R={\rm Br}(\pi\pi)/{\rm Br}(K\bar K) of f0(1710)f_0(1710) measured in experiment does not imply f0(1710)f_0(1710) to be a pure glueball. With our results it is helpful to understand the partonic contents if Br(ππ){\rm Br}(\pi\pi) or Br(KKˉ){\rm Br}(K\bar K) is measured reliably.Comment: revised versio

    Effect of Intensity Modulator Extinction on Practical Quantum Key Distribution System

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    We study how the imperfection of intensity modulator effects on the security of a practical quantum key distribution system. The extinction ratio of the realistic intensity modulator is considered in our security analysis. We show that the secret key rate increases, under the practical assumption that the indeterminable noise introduced by the imperfect intensity modulator can not be controlled by the eavesdropper.Comment: 6 pages, 5 figures. EPJD accepte

    Statistical analysis and the equivalent of a Thouless energy in lattice QCD Dirac spectra

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    Random Matrix Theory (RMT) is a powerful statistical tool to model spectral fluctuations. This approach has also found fruitful application in Quantum Chromodynamics (QCD). Importantly, RMT provides very efficient means to separate different scales in the spectral fluctuations. We try to identify the equivalent of a Thouless energy in complete spectra of the QCD Dirac operator for staggered fermions from SU(2) lattice gauge theory for different lattice size and gauge couplings. In disordered systems, the Thouless energy sets the universal scale for which RMT applies. This relates to recent theoretical studies which suggest a strong analogy between QCD and disordered systems. The wealth of data allows us to analyze several statistical measures in the bulk of the spectrum with high quality. We find deviations which allows us to give an estimate for this universal scale. Other deviations than these are seen whose possible origin is discussed. Moreover, we work out higher order correlators as well, in particular three--point correlation functions.Comment: 24 pages, 24 figures, all included except one figure, missing eps file available at http://pluto.mpi-hd.mpg.de/~wilke/diff3.eps.gz, revised version, to appear in PRD, minor modifications and corrected typos, Fig.4 revise

    Independent Eigenstates of Angular Momentum in a Quantum N-body System

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    The global rotational degrees of freedom in the Schr\"{o}dinger equation for an NN-body system are completely separated from the internal ones. After removing the motion of center of mass, we find a complete set of (2+1)(2\ell+1) independent base functions with the angular momentum \ell. These are homogeneous polynomials in the components of the coordinate vectors and the solutions of the Laplace equation, where the Euler angles do not appear explicitly. Any function with given angular momentum and given parity in the system can be expanded with respect to the base functions, where the coefficients are the functions of the internal variables. With the right choice of the base functions and the internal variables, we explicitly establish the equations for those functions. Only (3N-6) internal variables are involved both in the functions and in the equations. The permutation symmetry of the wave functions for identical particles is discussed.Comment: 24 pages, no figure, one Table, RevTex, Will be published in Phys. Rev. A 64, 0421xx (Oct. 2001

    Application of a customized pathway-focused microarray for gene expression profiling of cellular homeostasis upon exposure to nicotine in PC12 cells

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    Maintenance of cellular homeostasis is integral to appropriate regulation of cellular signaling and cell growth and division. In this study, we report the development and quality assessment of a pathway-focused microarray comprising genes involved in cellular homeostasis. Since nicotine is known to have highly modulatory effects on the intracellular calcium homeostasis, we therefore tested the applicability of the homeostatic pathway-focused microarray on the gene expression in PC-12 cells treated with 1 mM nicotine for 48 h relative to the untreated control cells. We first provided a detailed description of the focused array with respect to its gene and pathway content and then assessed the array quality using a robust regression procedure that allows for the exclusion of unreliable measurements while decreasing the number of false positives. As a result, the mean correlation coefficient between duplicate measurements of the arrays used in this study (control vs. nicotine treatment, three samples each) has increased from 0.974±0.017 to 0.995±0.002. Furthermore, we found that nicotine affected various structural and signaling components of the AKT/PKB signaling pathway and protein synthesis and degradation processes in PC-12 cells. Since modulation of intracellular calcium concentrations ([Ca2+]i) and phosphatidylinositol signaling are important in various biological processes such as neurotransmitter release and tissue pathogenesis including tumor formation, we expect that the homeostatic pathway-focused microarray potentially can be used for the identification of unique gene expression profiles in comparative studies of drugs of abuse and diverse environmental stimuli, such as starvation and oxidative stress. © 2003 Elsevier B.V. All rights reserved

    Strain- and region-specific gene expression profiles in mouse brain in response to chronic nicotine treatment

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    A pathway-focused complementary DNA microarray and gene ontology analysis were used to investigate gene expression profiles in the amygdala, hippocampus, nucleus accumbens, prefrontal cortex (PFC) and ventral tegmental area of C3H/HeJ and C57BL/6J mice receiving nicotine in drinking water (100 μg/ml in 2% saccharin for 2 weeks). A balanced experimental design and rigorous statistical analysis have led to the identification of 3.5-22.1% and 4.1-14.3% of the 638 sequence-verified genes as significantly modulated in the aforementioned brain regions of the C3H/HeJ and C57BL/6J strains, respectively. Comparisons of differential expression among brain tissues showed that only a small number of genes were altered in multiple brain regions, suggesting presence of a brain region-specific transcriptional response to nicotine. Subsequent principal component analysis and Expression Analysis Systematic Explorer analysis showed significant enrichment of biological processes both in C3H/HeJ and C57BL/6J mice, i.e. cell cycle/proliferation, organogenesis and transmission of nerve impulse. Finally, we verified the observed changes in expression using real-time reverse transcriptase polymerase chain reaction for six representative genes in the PFC region, providing an independent replication of our microarray results. Together, this report represents the first comprehensive gene expression profiling investigation of the changes caused by nicotine in brain tissues of the two mouse strains known to exhibit differential behavioral and physiological responses to nicotine. © 2007 Blackwell Publishing Ltd

    Reexamining radiative decays of 11^{--} quarkonium into η\eta' and η\eta

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    Recently CLEO has studied the radiative decay of Υ\Upsilon into η\eta' and an upper limit for the decay has been determined. Confronting with this upper limit,most of theoretical predictions for the decay fails. After briefly reviewing these predictions we re-examine the decay by separating nonperturbative effect related to the quarkonium and that related to η\eta' or η\eta, in which the later is parameterized by distribution amplitudes of gluons in η\eta'. With this factorization approach we obtain theoretical predictions which are in agreement with experiment. Uncertainties in our predictions are discussed. The possibly largest uncertainties are from relativistic corrections for J/ΨJ/\Psi and the value of the charm quark mass. We argue that the effect of these uncertainties can be reduced by using quarkonium masses instead of using quark masses. An example of the reduction is shown with an attempt to explain the violation of the famous 14% rule in radiative decays of charmonia.Comment: 9 Pages, Latex fil
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