Superspace formulation of general massive gauge theories and geometric interpretation of mass-dependent BRST symmetries

A superspace formulation is proposed for the osp(1,2)-covariant Lagrangian quantization of general massive gauge theories. The superalgebra os0(1,2) is considered as subalgebra of sl(1,2); the latter may be considered as the algebra of generators of the conformal group in a superspace with two anticommuting coordinates. The mass-dependent (anti)BRST symmetries of proper solutions of the quantum master equations in the osp(1,2)-covariant formalism are realized in that superspace as invariance under translations combined with mass-dependent special conformal transformations. The Sp(2) symmetry - in particular the ghost number conservation - and the "new ghost number" conservation are realized as invariance under symplectic rotations and dilatations, respectively. The transformations of the gauge fields - and of the full set of necessarily required (anti)ghost and auxiliary fields - under the superalgebra sl(1,2) are determined both for irreducible and first-stage reducible theories with closed gauge algebra.Comment: 35 pages, AMSTEX, precision of reference

G_2 invariant 7D Euclidean super Yang-Mills theory as a higher-dimensional analogue of the 3D super-BF theory

A formulation of the N_T=1, D=8 Euclidean super Yang-Mills theory with generalized self-duality and reduced Spin(7)-invariance is given which avoids the peculiar extra constraints of Nishino and Rajpoot, hep-th/0210132. Its reduction to 7 dimensions leads to the G_2-invariant N_T=2, D=7 super Yang-Mills theory which may be regarded as a higher-dimensional analogue of the N=2, D=3 super-BF theory. When reducing further that G_2-invariant theory to 3 dimensions one gets the N_T=2 super-BF theory coupled to a spinorial hypermultiplet.Comment: 9 pages, Late

Direct EPR Detection of Nitric Oxide in Mice Infected with the Pathogenic Mycobacterium Mycobacterium tuberculosis

It has been shown that treatment of mice preinfected with Mycobacterium tuberculosis with spin NO traps (iron complexes with diethyldithiocarbamate) enables detection of large amounts of NO in internal organs 2 and 4 weeks after infection (up to 55–57 μmol/kg of wet lung tissue accumulated with spin NO traps during 30 min). The animals were infected with the drug-sensitive laboratory strain H37Rv and a clinical isolate nonrespondent to antituberculous drugs (the multidrug-resistant strain of M. tuberculosis) obtained from a patient with an active form of tuberculosis. Two weeks after infection with the multidrug-resistant strain, the NO level in the lungs, spleen, liver and kidney increased sharply concurrently with slight lesions of lung tissue. A reverse correlation, i.e., low level of NO in the lungs and other internal organs and extensive injury of lung tissue, was established for H37Rv-infected mice. Four weeks after infection, NO production in the lungs increased dramatically for both M. tuberculosis strains resulting in 80–84% damage of lung tissue. The lesion is suggested to be due to the development of defense mechanisms in M. tuberculosis counteracting NO effects

Mechanism of the interaction between ribosomal protein S1 and oligonucleotides.

The interaction of the ribosomal protein S1 from E. coli MRE 600 with oligonucleotides was studied by hydrodynamic, spectrophotometric, and kinetic methods. UV-difference spectra which are induced by the complex formation could be separated into a hyperchromic contribution originating from the nucleic acid moiety and a hypochromic contribution from the protein. Systematic determination of binding and rate constants was carried out by the temperature-jump relaxation technique. From the quantitative evaluation of the relaxation times and the relaxation amplitudes, the following conclusions could be drawn: The stoichiometry of the complex formation is one mole S1 per one mole oligonucleotide. The binding constant K, the recombination rate constant kR, and the dissociation rate constant kD, respectively, were measured at different temperatures. The values at 10 degrees C are K = 2 x 10(6) M-1, kR = 1.3 x 10(8) M-1S-1, kD = 65 s-1 for A(pA) 12 and K = 7.5 x 10(5) M-1, kR = 6.8 x 10(7) M-1S-1, kD = 90 S-1 for U(pU) 12. Discrepancies with data reported elsewhere are discussed. The stacking-unstacking equilibrium of the free oligonucleotide is frozen if the oligonucleotide is bound to the protein. The conformational change of the oligonucleotide does not occur in the form of a preequilibrium, but is induced after the primary binding step