356 research outputs found

    Higher-U(2,2)-spin fields and higher-dimensional W-gravities: quantum AdS space and radiation phenomena

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    A physical and geometrical interpretation of previously introduced tensor operator algebras of U(2,2) in terms of algebras of higher-conformal-spin quantum fields on the anti-de Sitter space AdS_5 is provided. These are higher-dimensional W-like algebras and constitute a potential gauge guide principle towards the formulation of induced conformal gravities (Wess-Zumino-Witten-like models) in realistic dimensions. Some remarks on quantum (Moyal) deformations are given and potentially tractable versions of noncommutative AdS spaces are also sketched. The role of conformal symmetry in the microscopic description of Unruh and Hawking's radiation effects is discussed.Comment: LaTeX, 30 pages, 2 figures, final version to appear in Class. and Quant. Gra

    Structure Constants for New Infinite-Dimensional Lie Algebras of U(N+,N-) Tensor Operators and Applications

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    The structure constants for Moyal brackets of an infinite basis of functions on the algebraic manifolds M of pseudo-unitary groups U(N_+,N_-) are provided. They generalize the Virasoro and W_\infty algebras to higher dimensions. The connection with volume-preserving diffeomorphisms on M, higher generalized-spin and tensor operator algebras of U(N_+,N_-) is discussed. These centrally-extended, infinite-dimensional Lie-algebras provide also the arena for non-linear integrable field theories in higher dimensions, residual gauge symmetries of higher-extended objects in the light-cone gauge and C^*-algebras for tractable non-commutative versions of symmetric curved spaces.Comment: 8 pages, LaTeX, no figures; minor comments added; to appear in J. Phys A (Math. Gen.

    Kinin B1 receptors mediate depression-like behavior response in stressed mice treated with systemic E. coli lipopolysaccharide

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    <p>Abstract</p> <p>Background</p> <p>Kinin B<sub>1 </sub>receptors are inducible molecules up-regulated after inflammatory stimuli. This study evaluated the relevance of kinin B<sub>1 </sub>receptors in a mouse depression behavior model.</p> <p>Methods</p> <p>Mice were exposed to a 5-min swimming session, and 30 min later they were injected with <it>E. coli </it>lipopolysaccharide (LPS). Depression-like behavior was assessed by determining immobility time in a tail suspension test. Different brain structures were collected for molecular and immunohistochemical studies. Anhedonia was assessed by means of a sucrose intake test.</p> <p>Results</p> <p>Our protocol elicited an increase in depression-like behavior in CF1 mice, as assessed by the tail-suspension test, at 24 h. This behavior was significantly reduced by treatment with the selective B<sub>1 </sub>receptor antagonists R-715 and SSR240612. Administration of SSR240612 also prevented an increase in number of activated microglial cells in mouse hippocampus, but did not affect a reduction in expression of mRNA for brain-derived neurotrophic factor. The increased immobility time following LPS treatment was preceded by an enhancement of hippocampal and cortical B<sub>1 </sub>receptor mRNA expression (which were maximal at 1 h), and a marked production of TNFÎą in serum, brain and cerebrospinal fluid (between 1 and 6 h). The depression-like behavior was virtually abolished in TNF<it>Îą </it>p55 receptor-knockout mice, and increased B<sub>1 </sub>receptor mRNA expression was completely absent in this mouse strain. Furthermore, treatment with SSR240612 was also effective in preventing anhedonia in LPS-treated mice, as assessed using a sucrose preference test.</p> <p>Conclusion</p> <p>Our data show, for the first time, involvement of kinin B<sub>1 </sub>receptors in depressive behavioral responses, in a process likely associated with microglial activation and TNFÎą production. Thus, selective and orally active B<sub>1 </sub>receptor antagonists might well represent promising pharmacological tools for depression therapy.</p

    The Role of Kinin Receptors in Preventing Neuroinflammation and Its Clinical Severity during Experimental Autoimmune Encephalomyelitis in Mice

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    Background: Multiple sclerosis (MS) is a demyelinating and neuroinflammatory disease of the human central nervous system (CNS). the expression of kinins is increased in MS patients, but the underlying mechanisms by which the kinin receptor regulates MS development have not been elucidated.Methodology/Principal Findings: Experimental autoimmune encephalomyelitis (EAE) was induced in female C57BL/6 mice by immunization with MOG(35-55) peptide emulsified in complete Freund's adjuvant and injected with pertussis toxin on day 0 and day 2. Here, we report that blockade of the B(1)R in the induction phase of EAE markedly suppressed its progression by interfering with the onset of the immune response. Furthermore, B(1)R antagonist suppressed the production/expression of antigen-specific T(H)1 and T(H)17 cytokines and transcription factors, both in the periphery and in the CNS. in the chronic phase of EAE, the blockade of B(1)R consistently impaired the clinical progression of EAE. Conversely, administration of the B(1)R agonist in the acute phase of EAE suppressed disease progression and inhibited the increase in permeability of the blood-brain barrier (BBB) and any further CNS inflammation. of note, blockade of the B(2)R only showed a moderate impact on all of the studied parameters of EAE progression.Conclusions/Significance: Our results strongly suggest that kinin receptors, mainly the B(1)R subtype, play a dual role in EAE progression depending on the phase of treatment through the lymphocytes and glial cell-dependent pathways.Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Programa de Apoio aos Nucleos de Excelencia (PRONEX), BrazilFundacaode Apoio a Pesquisa Cientifica Tecnologica do Estado de Santa Catarina (FAPESC), BrazilUniv Fed Santa Catarina, Dept Pharmacol, Ctr Biol Sci, Florianopolis, SC, BrazilUniversidade Federal de São Paulo, Dept Biophys, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biophys, São Paulo, BrazilWeb of Scienc

    Symmetries of Non-Linear Systems: Group Approach to their Quantization

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    We report briefly on an approach to quantum theory entirely based on symmetry grounds which improves Geometric Quantization in some respects and provides an alternative to the canonical framework. The present scheme, being typically non-perturbative, is primarily intended for non-linear systems, although needless to say that finding the basic symmetry associated with a given (quantum) physical problem is in general a difficult task, which many times nearly emulates the complexity of finding the actual (classical) solutions. Apart from some interesting examples related to the electromagnetic and gravitational particle interactions, where an algebraic version of the equivalence principle naturally arises, we attempt to the quantum description of non-linear sigma models. In particular, we present the actual quantization of the partial-trace non-linear SU(2) sigma model as a representative case of non-linear quantum field theory.Comment: 24 pages, LaTeX, no figure

    Calculation of Grounding Grids Parameter at Arbitrary Geometry

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    This paper deals with the computation of ground resistance, surface voltage, touch voltage and step voltage, to mesh with horizontal wires arranged in different angles. The computer program implemented used in the mathematical modeling is based on the method proposed by Heppe, which allows obtaining the grounding parameters for homogeneous soil and soil stratified in two layers. The results obtained with the proposed method will be compared with other methods in literature. Also will be presented the results of a grounding grid using wires at various angles

    Evolutionary relationships among barley and <i>Arabidopsis</i> core circadian clock and clock-associated genes

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    The circadian clock regulates a multitude of plant developmental and metabolic processes. In crop species, it contributes significantly to plant performance and productivity and to the adaptation and geographical range over which crops can be grown. To understand the clock in barley and how it relates to the components in the Arabidopsis thaliana clock, we have performed a systematic analysis of core circadian clock and clock-associated genes in barley, Arabidopsis and another eight species including tomato, potato, a range of monocotyledonous species and the moss, Physcomitrella patens. We have identified orthologues and paralogues of Arabidopsis genes which are conserved in all species, monocot/dicot differences, species-specific differences and variation in gene copy number (e.g. gene duplications among the various species). We propose that the common ancestor of barley and Arabidopsis had two-thirds of the key clock components identified in Arabidopsis prior to the separation of the monocot/dicot groups. After this separation, multiple independent gene duplication events took place in both monocot and dicot ancestors. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00239-015-9665-0) contains supplementary material, which is available to authorized users

    Adaptation and Validation of QUick, Easy, New, CHEap, and Reproducible (QUENCHER) Antioxidant Capacity Assays in Model Products Obtained from Residual Wine Pomace

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    Evaluation of the total antioxidant capacity of solid matrices without extraction steps is a very interesting alternative for food researchers and also for food industries. These methodologies have been denominated QUENCHER from QUick, Easy, New, CHEap, and Reproducible assays. To demonstrate and highlight the validity of QUENCHER (Q) methods, values of Q-method validation were showed for the first time, and they were tested with products of well-known different chemical properties. Furthermore, new QUENCHER assays to measure scavenging capacity against superoxide, hydroxyl, and lipid peroxyl radicals were developed. Calibration models showed good linearity (R2 > 0.995), proportionality and precision (CV < 6.5%), and acceptable detection limits (<20.4 nmol Trolox equiv). The presence of ethanol in the reaction medium gave antioxidant capacity values significantly different from those obtained with water. The dilution of samples with powdered cellulose was discouraged because possible interferences with some of the matrices analyzed may take place.The autonomous government of Castilla y León (Project BU268A11-2

    Cannabinoid Agonists Inhibit Neuropathic Pain Induced by Brachial Plexus Avulsion in Mice by Affecting Glial Cells and MAP Kinases

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    Many studies have shown the antinociceptive effects of cannabinoid (CB) agonists in different models of pain. Herein, we have investigated their relevance in neuropathic pain induced by brachial plexus avulsion (BPA) in mice.Mice underwent BPA or sham surgery. The mRNA levels and protein expression of CB(1) and CB(2) receptors were assessed by RT-PCR and immunohistochemistry, respectively. The activation of glial cells, MAP kinases and transcription factors were evaluated by immunohistochemistry. The antinociceptive properties induced by cannabinoid agonists were assessed on the 5(th) and 30(th) days after surgery. We observed a marked increase in CB(1) and CB(2) receptor mRNA and protein expression in the spinal cord and dorsal root ganglion, either at the 5(th) or 30(th) day after surgery. BPA also induced a marked activation of p38 and JNK MAP kinases (on the 30(th) day), glial cells, such as microglia and astrocytes, and the transcription factors CREB and NF-ÎşB (at the 5(th) and 30(th) days) in the spinal cord. Systemic treatment with cannabinoid agonists reduced mechanical allodynia on both the 5(th) and 30(th) days after surgery, but the greatest results were observed by using central routes of administration, especially at the 30(th) day. Treatment with WIN 55,212-2 prevented the activation of both glial cells and MAP kinases, associated with an enhancement of CREB and NF-ÎşB activation.Our results indicate a relevant role for cannabinoid agonists in BPA, reinforcing their potential therapeutic relevance for the management of chronic pain states

    Caffeine Consumption Prevents Diabetes-Induced Memory Impairment and Synaptotoxicity in the Hippocampus of NONcZNO10/LTJ Mice

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    Diabetic conditions are associated with modified brain function, namely with cognitive deficits, through largely undetermined processes. More than understanding the underlying mechanism, it is important to devise novel strategies to alleviate diabetes-induced cognitive deficits. Caffeine (a mixed antagonist of adenosine A1 and A2A receptors) emerges as a promising candidate since caffeine consumption reduces the risk of diabetes and effectively prevents memory deficits caused by different noxious stimuli. Thus, we took advantage of a novel animal model of type 2 diabetes to investigate the behavioural, neurochemical and morphological modifications present in the hippocampus and tested if caffeine consumption might prevent these changes. We used a model closely mimicking the human type 2 diabetes condition, NONcNZO10/LtJ mice, which become diabetic at 7–11 months when kept under an 11% fat diet. Caffeine (1 g/l) was applied in the drinking water from 7 months onwards. Diabetic mice displayed a decreased spontaneous alternation in the Y-maze accompanied by a decreased density of nerve terminal markers (synaptophysin, SNAP25), mainly glutamatergic (vesicular glutamate transporters), and increased astrogliosis (GFAP immunoreactivity) compared to their wild type littermates kept under the same diet. Furthermore, diabetic mice displayed up-regulated A2A receptors and down-regulated A1 receptors in the hippocampus. Caffeine consumption restored memory performance and abrogated the diabetes-induced loss of nerve terminals and astrogliosis. These results provide the first evidence that type 2 diabetic mice display a loss of nerve terminal markers and astrogliosis, which is associated with memory impairment; furthermore, caffeine consumption prevents synaptic dysfunction and astrogliosis as well as memory impairment in type 2 diabetes
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