896 resultados para System B
Resumo:
Cocaine is a widely used drug and its abuse is associated with physical, psychiatric and social problems. Abnormalities in newborns have been demonstrated to be due to the toxic effects of cocaine during fetal development. The mechanism by which cocaine causes neurological damage is complex and involves interactions of the drug with several neurotransmitter systems, such as the increase of extracellular levels of dopamine and free radicals, and modulation of transcription factors. The aim of this review was to evaluate the importance of the dopaminergic system and the participation of inflammatory signaling in cocaine neurotoxicity. Our study showed that cocaine activates the transcription factors NF-κB and CREB, which regulate genes involved in cellular death. GBR 12909 (an inhibitor of dopamine reuptake), lidocaine (a local anesthetic), and dopamine did not activate NF-κB in the same way as cocaine. However, the attenuation of NF-κB activity after the pretreatment of the cells with SCH 23390, a D1 receptor antagonist, suggests that the activation of NF-κB by cocaine is, at least partially, due to activation of D1 receptors. NF-κB seems to have a protective role in these cells because its inhibition increased cellular death caused by cocaine. The increase in BDNF (brain-derived neurotrophic factor) mRNA can also be related to the protective role of both CREB and NF-κB transcription factors. An understanding of the mechanisms by which cocaine induces cell death in the brain will contribute to the development of new therapies for drug abusers, which can help to slow down the progress of degenerative processes.
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The photosensitivity of dye mixture-doped polymethyl methacrylate (PMMA) films are investigated as a function of laser power, concentration of the dyes, modulation frequency and the irradiation wavelength. Energy transfer from a donor molecule to an acceptor molecule affects the emission output of the dye mixture system. Photosensitivity is found to change with changes in donor–acceptor concentrations. PMMA samples doped with the dye mixture are found to be more photosensitive when the dyes are mixed in the same proportion.
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In this article a simple and effective controller design is introduced for the Hammerstein systems that are identified based on observational input/output data. The nonlinear static function in the Hammerstein system is modelled using a B-spline neural network. The controller is composed by computing the inverse of the B-spline approximated nonlinear static function, and a linear pole assignment controller. The contribution of this article is the inverse of De Boor algorithm that computes the inverse efficiently. Mathematical analysis is provided to prove the convergence of the proposed algorithm. Numerical examples are utilised to demonstrate the efficacy of the proposed approach.
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A simple and effective algorithm is introduced for the system identification of Wiener system based on the observational input/output data. The B-spline neural network is used to approximate the nonlinear static function in the Wiener system. We incorporate the Gauss-Newton algorithm with De Boor algorithm (both curve and the first order derivatives) for the parameter estimation of the Wiener model, together with the use of a parameter initialization scheme. The efficacy of the proposed approach is demonstrated using an illustrative example.
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In this paper a new system identification algorithm is introduced for Hammerstein systems based on observational input/output data. The nonlinear static function in the Hammerstein system is modelled using a non-uniform rational B-spline (NURB) neural network. The proposed system identification algorithm for this NURB network based Hammerstein system consists of two successive stages. First the shaping parameters in NURB network are estimated using a particle swarm optimization (PSO) procedure. Then the remaining parameters are estimated by the method of the singular value decomposition (SVD). Numerical examples including a model based controller are utilized to demonstrate the efficacy of the proposed approach. The controller consists of computing the inverse of the nonlinear static function approximated by NURB network, followed by a linear pole assignment controller.
Resumo:
In this article a simple and effective algorithm is introduced for the system identification of the Wiener system using observational input/output data. The nonlinear static function in the Wiener system is modelled using a B-spline neural network. The Gauss–Newton algorithm is combined with De Boor algorithm (both curve and the first order derivatives) for the parameter estimation of the Wiener model, together with the use of a parameter initialisation scheme. Numerical examples are utilised to demonstrate the efficacy of the proposed approach.
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A Li(2)O-B(2)O(3)-Al(2)O(3) glass system, un-doped and doped with LiF, and/or TiO(2) was synthesized by the fusion method and its physical properties were investigated by thermoluminescence (TL), X-ray diffraction (XRD), electron paramagnetic resonance (EPR), atomic force microscopy (AFM) and differential thermal analysis (DTA). The samples were subjected to gamma-rays from a colbalt-60 ((60)Co) source. These techniques provided evidence of LiF and LiF doped with Ti crystal formation in the glass system. A TL glow peak at about 433 K was sensitive to (60)Co gamma-rays and showed good linearity with doses and consequently could be used to quantify radiation doses. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.
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We construct the finite temperature field theory of the two-dimensional ghost-antighost system within the framework of thermo field theory. (C) 2000 Elsevier B.V. B.V. All rights reserved.
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We combine the D0 measurement of the width difference between the light and heavy B-s(0) mass eigenstates and of the CP-violating mixing phase determined from the time-dependent angular distributions in the B-s(0)-> J/psi phi decays along with the charge asymmetry in semileptonic decays also measured with the D0 detector. With the additional constraint from the world average of the flavor-specific B-s(0) lifetime, we obtain Delta Gamma(s)equivalent to(Gamma(L)-Gamma(H))=0.13 +/- 0.09 ps(-1) and vertical bar phi(s)vertical bar=0.70(-0.47)(+0.39) or Delta Gamma(s)=-0.13 +/- 0.09 ps(-1) and vertical bar phi(s)vertical bar=2.44(-0.39)(+0.47). The data sample corresponds to an integrated luminosity of 1.1 fb(-1) accumulated with the D0 detector at the Fermilab Tevatron Collider.
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We present a study of the decay B-s(0)-> J/psi phi. We obtain the CP-odd fraction in the final state at time zero R-perpendicular to = 0.16 +/- 0.10 (stat) +/- 0.02(syst), the average lifetime of the (B-s(0), (B) over bar (0)(s)) system, (tau) over bar (B-s(0)) = 1.39(-0.16)(+0.13)(stat)(-0.02)(+0.01)(syst) ps, and the relative width difference between the heavy and light mass eigen-states, Delta Gamma/(Gamma) over bar = (Gamma(L) - Gamma(H))/(Gamma) over bar = 0.24(-0.38)(+0.28)(stat)(-0.04)(+0.03)(syst). With the additional constraint from the world average of the B-s(0) lifetime measurements using semileptonic decays, we find (tau) over bar (B-s(0)) = 1.39 +/- 0.06 ps and Delta Gamma/(Gamma) over bar = 0.25(-0.15)(+0.14). For the ratio of the B-s(0) and B-0 lifetimes we obtain (tau) over bar (B-s(0))/tau(B-s(0)) = 0.91 +/- 0.09(stat) +/- 0.003(syst).
Resumo:
From an analysis of the decay B-s(0)-> J/psi phi, we obtain the width difference between the light and heavy mass eigenstates Delta Gamma equivalent to(Gamma(L)-Gamma(H))=0.17 +/- 0.09(stat)+/- 0.02(syst) ps(-1) and the CP-violating phase phi(s)=-0.79 +/- 0.56(stat)(-0.01)(+0.14)(syst). Under the hypothesis of no CP violation (phi(s)equivalent to 0), we obtain 1/Gamma=tau/(B-s(0))=1.52 +/- 0.08(stat)(-0.03)(+0.01)(syst) ps and Delta Gamma=0.12(-0.10)(+0.08)(stat)+/- 0.02(syst) ps(-1). The data sample corresponds to an integrated luminosity of about 1.1 fb(-1) accumulated with the D0 detector at the Fermilab Tevatron collider. This is the first direct measurement of the CP-violating mixing phase in the B-s(0) system.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Deer species of the genus Mazama show significant inter and intraspecific chromosomal variation due to the occurrence of rearrangements and B chromosomes. Given that carriers of aneuploidies and structural rearrangements often show anomalous chromosome pairings, we here performed a synaptonemal complex analysis to study chromosome pairing behavior in a red brocket deer (Mazama americana) individual that is heterozygous for a Robertsonian translocation, is a B chromosome carrier, and has a multiple sex chromosome system (XY1Y2). The synaptonemal complex in spermatocytes showed normal chromosome pairings for all chromosomes, including the autosomal and sex trivalents. The electromicrographs showed homology among B chromosomes since they formed bivalents, but they also appeared as univalents, indicating their anomalous behavior and non-Mendelian segregation. Thus, synaptonemal complex analysis is a useful tool to evaluate the role of B chromosomes and rearrangements during meiosis on the intraspecific chromosomal variation that is observed in the majority of Mazama species. © FUNPEC-RP.
Resumo:
Cocaine is a widely used drug and its abuse is associated with physical, psychiatric and social problems. Abnormalities in newborns have been demonstrated to be due to the toxic effects of cocaine during fetal development. The mechanism by which cocaine causes neurological damage is complex and involves interactions of the drug with several neurotransmitter systems, such as the increase of extracellular levels of dopamine and free radicals, and modulation of transcription factors. The aim of this review was to evaluate the importance of the dopaminergic system and the participation of inflammatory signaling in cocaine neurotoxicity. Our study showed that cocaine activates the transcription factors NF-κB and CREB, which regulate genes involved in cellular death. GBR 12909 (an inhibitor of dopamine reuptake), lidocaine (a local anesthetic), and dopamine did not activate NF-κB in the same way as cocaine. However, the attenuation of NF-κB activity after the pretreatment of the cells with SCH 23390, a D1 receptor antagonist, suggests that the activation of NF-κB by cocaine is, at least partially, due to activation of D1 receptors. NF-κB seems to have a protective role in these cells because its inhibition increased cellular death caused by cocaine. The increase in BDNF (brain-derived neurotrophic factor) mRNA can also be related to the protective role of both CREB and NF-κB transcription factors. An understanding of the mechanisms by which cocaine induces cell death in the brain will contribute to the development of new therapies for drug abusers, which can help to slow down the progress of degenerative processes.