506 research outputs found
Nicotine coregulates multiple pathways involved in protein modification/degradation in rat brain
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
Recently the BES collaboration has announced observation of a resonant state
in the spectrum in
decay. Fitting the data with a state, the mass is determined to be
1833.7 MeV with statistic significance. This state is consistent
with the one extracted from previously reported threshold
enhancement data in . 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 and for
and for , respectively.
Combining the calculated branching ratio of and data on
threshold enhancement in , we determine the
coupling for interaction. We finally study branching ratios of
other decay modes. We find that 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
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 and , 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 and
already leads to a large difference between and , even the decay amplitude is not chirally suppressed. Moreover,
the small ratio of of
measured in experiment does not imply to be a pure glueball. With
our results it is helpful to understand the partonic contents if or is measured reliably.Comment: revised versio
Effect of Intensity Modulator Extinction on Practical Quantum Key Distribution System
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
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
The global rotational degrees of freedom in the Schr\"{o}dinger equation for
an -body system are completely separated from the internal ones. After
removing the motion of center of mass, we find a complete set of
independent base functions with the angular momentum . 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
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
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 quarkonium into and
Recently CLEO has studied the radiative decay of into 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 or
, in which the later is parameterized by distribution amplitudes of
gluons in . 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 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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