1,374 research outputs found

    Chern-Simons Reduction and non-Abelian Fluid Mechanics

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    We propose a non-Abelian generalization of the Clebsch parameterization for a vector in three dimensions. The construction is based on a group-theoretical reduction of the Chern-Simons form on a symmetric space. The formalism is then used to give a canonical (symplectic) discussion of non-Abelian fluid mechanics, analogous to the way the Abelian Clebsch parameterization allows a canonical description of conventional fluid mechanics.Comment: 12 pages, REVTeX; revised for publication in Phys Rev D; email to [email protected]

    Creation and evolution of magnetic helicity

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    Projecting a non-Abelian SU(2) vacuum gauge field - a pure gauge constructed from the group element U - onto a fixed (electromagnetic) direction in isospace gives rise to a nontrivial magnetic field, with nonvanishing magnetic helicity, which coincides with the winding number of U. Although the helicity is not conserved under Maxwell (vacuum) evolution, it retains one-half its initial value at infinite time.Comment: Clarifying remarks and references added; 12 pages, 1 figure using BoxedEPSF, REVTeX macros; submitted to Phys Rev D; email to [email protected]

    Nonuniform symmetry breaking in noncommutative λΊ4\lambda \Phi^4 theory

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    The spontaneous symmetry breaking in noncommutative λΊ4\lambda\Phi^4 theory has been analyzed by using the formalism of the effective action for composite operators in the Hartree-Fock approximation. It turns out that there is no phase transition to a constant vacuum expectation of the field and the broken phase corresponds to a nonuniform background. By considering =Acos⁥(Q⃗⋅x⃗)=A \cos(\vec Q \cdot \vec x) the generated mass gap depends on the angles among the momenta k⃗\vec k and Q⃗\vec Q and the noncommutativity parameter ξ⃗\vec\theta. The order of the transition is not easily determinable in our approximation.Comment: 18 pages, 4 figures, added reference

    In vivo antiviral efficacy of prenylation inhibitors against hepatitis delta virus

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    Hepatitis delta virus (HDV) can dramatically worsen liver disease in patients coinfected with hepatitis B virus (HBV). No effective medical therapy exists for HDV. The HDV envelope requires HBV surface antigen proteins provided by HBV. Once inside a cell, however, HDV can replicate its genome in the absence of any HBV gene products. In vitro, HDV virion assembly is critically dependent on prenyl lipid modification, or prenylation, of its nucleocapsid-like protein large delta antigen. To overcome limitations of current animal models and to test the hypothesis that pharmacologic prenylation inhibition can prevent the production of HDV virions in vivo, we established a convenient mouse-based model of HDV infection capable of yielding viremia. Such mice were then treated with the prenylation inhibitors FTI-277 and FTI-2153. Both agents were highly effective at clearing HDV viremia. As expected, HDV inhibition exhibited duration-of-treatment dependence. These results provide the first preclinical data supporting the in vivo efficacy of prenylation inhibition as a novel antiviral therapy with potential application to HDV and a wide variety of other viruses

    Non-Abelian Chern-Simons Particles and their Quantization

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    A many--body Schr\"odinger equation for non--Abelian Chern--Simons particles is obtained from both point--particle and field--theoretic pictures. We present a particle Lagrangian and a field theoretic Lagrange density, and discuss their properties. Both are quantized by the symplectic method of Hamiltonian reduction. An NN--body Schr\"odinger equation for the particles is obtained from both starting points. It is shown that the resulting interaction between particles can be replaced by non--trivial boundary conditions. Also, the equation is compared with the one given in the literature.Comment: 18 pages, MIT preprint CTP # 227

    VEGF Induces More Severe Cerebrovascular Dysplasia in Eng+/− than in Alk1+/− Mice

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    Brain arteriovenous malformations (BAVMs) are an important cause of intracranial hemorrhage (ICH) in young adults. A small percent of BAVMs is due to hereditary hemorrhagic telangiectasia 1 and 2 (HHT1 and 2), which are caused by mutations in two genes involved in transforming growth factor-ÎČ signaling: endoglin (Eng), and activin-like kinase 1 (Alk1). The BAVM phenotype has incomplete penetrance in HHT patients, and the mechanism is unknown. We tested the hypothesis that a “response-to-injury” triggers abnormal vascular (dysplasia) development, using Eng and Alk1 haploinsufficient mice. Adeno-associated virus (AAV) expressing vascular endothelial growth factor (VEGF) was used to mimic the injury conditions. VEGF overexpression caused a similar degree of angiogenesis in the brain of all groups, except that the cortex of Alk1+/− mice had a 33% higher capillary density than other groups. There were different levels of cerebrovascular dysplasia observed in haploinsufficient mice (Eng+/− > Alk1+/−), which simulates the relative penetrance of BAVM in HHT patients (HHT1 > HHT2). Few dysplastic capillaries were observed in AAV-LacZ-injected mice. Our data indicate that both angiogenic stimulation and genetic alteration are necessary for the development of vascular dysplasia, suggesting that anti-angiogenic therapies might be adapted to slow the progression of the disease and decrease the risk of spontaneous ICH

    Chicken Embryos as a Potential New Model for Early Onset Type I Diabetes

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    Diabetic retinopathy (DR) is the leading cause of blindness among the American working population. The purpose of this study is to establish a new diabetic animal model using a cone-dominant avian species to address the distorted color vision and altered cone pathway responses in prediabetic and early diabetic patients. Chicken embryos were injected with either streptozotocin (STZ), high concentration of glucose (high-glucose), or vehicle at embryonic day 11. Cataracts occurred in varying degrees in both STZ- and high glucose-induced diabetic chick embryos at E18. Streptozotocin-diabetic chicken embryos had decreased levels of blood insulin, glucose transporter 4 (Glut4), and phosphorylated protein kinase B (pAKT). In STZ-injected E20 embryos, the ERG amplitudes of both a- and b-waves were significantly decreased, the implicit time of the a-wave was delayed, while that of the b-wave was significantly increased. Photoreceptors cultured from STZ-injected E18 embryos had a significant decrease in L-type voltage-gated calcium channel (L-VGCC) currents, which was reflected in the decreased level of L-VGCCα1D subunit in the STZ-diabetic retinas. Through these independent lines of evidence, STZ-injection was able to induce pathological conditions in the chicken embryonic retina, and it is promising to use chickens as a potential new animal model for type I diabetes
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