The Abelian Higgs Model as an Ensemble of Vortex Loops

In the London limit of the Ginzburg-Landau theory (Abelian Higgs model), vortex dipoles (small vortex loops) are treated as a grand canonical ensemble in the dilute gas approximation. The summation over these objects with the most general rotation- and translation invariant measure of integration over their shapes leads to effective sine-Gordon theories of the dual fields. The representations of the partition functions of both grand canonical ensembles are derived in the form of the integrals over the vortex dipoles and the small vortex loops, respectively. By virtue of these representations, the bilocal correlator of the vortex dipoles (loops) is calculated in the low-energy limit. It is further demonstrated that once the vortex dipoles (loops) are considered as such an ensemble rather than individual ones, the London limit of the Ginzburg-Landau theory (Abelian Higgs model) with external monopoles is equivalent up to the leading order in the inverse UV cutoff to the compact QED in the corresponding dimension with the charge of Cooper pairs changed due to the Debye screening.Comment: 17 pages, LaTeX2e, no figures, dedicated to Prof. Yu.A. Simonov on the occasion of his 65-th birthday, final published version (minor corrections, references added

Ensemble of Vortex Loops in the Abelian-Projected SU(3)-Gluodynamics

Grand canonical ensemble of small vortex loops emerging in the London limit of the effective Abelian-projected theory of the SU(3)-gluodynamics is investigated in the dilute gas approximation. An essential difference of this system from the SU(2)-case is the presence of two interacting gases of vortex loops. Two alternative representations for the partition function of such a grand canonical ensemble are derived, and one of them, which is a representation in terms of the integrals over vortex loops, is employed for the evaluation of the correlators of both kinds of loops in the low-energy limit.Comment: 10 pages, LaTeX2e, no figures, minor corrections, to appear in Mod. Phys. Lett.

Direct numerical simulation of homogeneous nucleation and growth in a phase-field model using cell dynamics method

Homogeneous nucleation and growth in a simplest two-dimensional phase field model is numerically studied using the cell dynamics method. Whole process from nucleation to growth is simulated and is shown to follow closely the Kolmogorov-Johnson-Mehl-Avrami (KJMA) scenario of phase transformation. Specifically the time evolution of the volume fraction of new stable phase is found to follow closely the KJMA formula. By fitting the KJMA formula directly to the simulation data, not only the Avrami exponent but the magnitude of nucleation rate and, in particular, of incubation time are quantitatively studied. The modified Avrami plot is also used to verify the derived KJMA parameters. It is found that the Avrami exponent is close to the ideal theoretical value m=3. The temperature dependence of nucleation rate follows the activation-type behavior expected from the classical nucleation theory. On the other hand, the temperature dependence of incubation time does not follow the exponential activation-type behavior. Rather the incubation time is inversely proportional to the temperature predicted from the theory of Shneidman and Weinberg [J. Non-Cryst. Solids {\bf 160}, 89 (1993)]. A need to restrict thermal noise in simulation to deduce correct Avrami exponent is also discussed.Comment: 9 pages, 8 figures, Journal of Chemical Physics to be publishe

The finiteness of the four dimensional antisymmetric tensor field model in a curved background

A renormalizable rigid supersymmetry for the four dimensional antisymmetric tensor field model in a curved space-time background is constructed. A closed algebra between the BRS and the supersymmetry operators is only realizable if the vector parameter of the supersymmetry is a covariantly constant vector field. This also guarantees that the corresponding transformations lead to a genuine symmetry of the model. The proof of the ultraviolet finiteness to all orders of perturbation theory is performed in a pure algebraic manner by using the rigid supersymmetry.Comment: 23 page

The time of the Roma in times of crisis: Where has European neoliberal capitalism failed?

This paper argues that the economic and financial crisis that has ensnared Europe from the late 2000s has been instrumental in reshaping employment and social relations in a detrimental way for the majority of the European people. It argues that the crisis has exacerbated the socio-economic position of most Roma people, immigrants as well as of other vulnerable groups. This development is approached here as an outcome of the widening structural inequalities that underpin the crisis within an increasingly neoliberalised Europe. Through recent policy developments and public discourses from a number of European countries I show how rising inequalities nurture racialised social tensions. My account draws on classic and contemporary theoretical propositions that have been propounded about the nature of capitalism, its contemporary re-articulation as well as its ramification for the future of Europe

Vacuum polarisation induced coupling between Maxwell and Kalb-Ramond Fields

We present here a manifestly gauge invariant calculation of vacuum polarization to fermions in the presence of a constant Maxwell and a constant Kalb-Ramond field in four dimensions. The formalism is a generalisation of the one used by Schwinger in his famous paper on gauge invariance and vacuum polarization. We get an explicit expression for the vacuum polarization induced effective Lagrangian for a constant Maxwell field interacting with a constant Kalb-Ramond field. In the weak field limit we get the coupling between the Maxwell field and the Kalb-Ramond field to be $(\tilde{H}.\tilde{F})^2$, where ${\tilde H}_{\mu}= {1\over {3!}}\epsilon_{\mu\alpha\beta\lambda}H^{\alpha\beta\lambda}$ and $\tilde F$ is the dual of $F_{\mu\nu}$.Comment: 16 pages, Revte

Extraction of BoNT/A, /B, /E, and /F with a Single, High Affinity Monoclonal Antibody for Detection of Botulinum Neurotoxin by Endopep-MS

Botulinum neurotoxins (BoNTs) are extremely potent toxins that are capable of causing respiratory failure leading to long-term intensive care or death. The best treatment for botulism includes serotype-specific antitoxins, which are most effective when administered early in the course of the intoxication. Early confirmation of human exposure to any serotype of BoNT is an important public health goal. In previous work, we focused on developing Endopep-MS, a mass spectrometry-based endopeptidase method for detecting and differentiating the seven serotypes (BoNT/A-G) in buffer and BoNT/A, /B, /E, and /F (the four serotypes that commonly affect humans) in clinical samples. We have previously reported the success of antibody-capture to purify and concentrate BoNTs from complex matrices, such as clinical samples. However, to check for any one of the four serotypes of BoNT/A, /B, /E, or /F, each sample is split into 4 aliquots, and tested for the specific serotypes separately. The discovery of a unique monoclonal antibody that recognizes all four serotypes of BoNT/A, /B, /E and /F allows us to perform simultaneous detection of all of them. When applied in conjunction with the Endopep-MS assay, the detection limit for each serotype of BoNT with this multi-specific monoclonal antibody is similar to that obtained when using other serotype-specific antibodies

Genetically altering organismal metabolism by leptin-deficiency benefits a mouse model of amyotrophic lateral sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal, neurodegenerative disease that causes death of motor neurons. ALS patients and mouse models of familial ALS display organismal level metabolic dysfunction, which includes increased energy expenditure despite decreased lean mass. The pathophysiological relevance of abnormal energy homeostasis to motor neuron disease remains unclear. Leptin is an adipocyte-derived hormone that regulates whole-animal energy expenditure. Here, we report that placing mutant superoxide dismutase 1 (SOD1) mice in a leptin-deficient background improves energy homeostasis and slows disease progression. Leptin-deficient mutant SOD1 mice possess increased bodyweight and fat mass, as well as decreased energy expenditure. These observations coincide with enhanced survival, improved strength and decreased motor neuron loss. These results suggest that altering whole-body energy metabolism in mutant SOD1 mice can mitigate disease progression. We propose that manipulations that increase fat mass and reduce energy expenditure will be beneficial in the setting of motor neuron diseas

Controlled iris radiance in a diurnal fish looking at prey

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