754 research outputs found
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
Nonsense mutations in alpha-II spectrin in three families with juvenile onset hereditary motor neuropathy
Distal hereditary motor neuropathies are a rare subgroup of inherited peripheral neuropathies hallmarked by a length-dependent axonal degeneration of lower motor neurons without significant involvement of sensory neurons. We identified patients with heterozygous nonsense mutations in the alpha II-spectrin gene, SPTAN1, in three separate dominant hereditary motor neuropathy families via next-generation sequencing. Variable penetrance was noted for these mutations in two of three families, and phenotype severity differs greatly between patients. The mutant mRNA containing nonsense mutations is broken down by nonsense-mediated decay and leads to reduced protein levels in patient cells. Previously, dominant-negative alpha II-spectrin gene mutations were described as causal in a spectrum of epilepsy phenotypes
Regularisation, the BV method, and the antibracket cohomology
We review the Lagrangian Batalin--Vilkovisky method for gauge theories. This
includes gauge fixing, quantisation and regularisation. We emphasize the role
of cohomology of the antibracket operation. Our main example is gravity,
for which we also discuss the solutions for the cohomology in the space of
local integrals. This leads to the most general form for the action, for
anomalies and for background charges.Comment: 12 pages, LaTeX, Preprint-KUL-TF-94/2
Separability of Black Holes in String Theory
We analyze the origin of separability for rotating black holes in string
theory, considering both massless and massive geodesic equations as well as the
corresponding wave equations. We construct a conformal Killing-Stackel tensor
for a general class of black holes with four independent charges, then identify
two-charge configurations where enhancement to an exact Killing-Stackel tensor
is possible. We show that further enhancement to a conserved Killing-Yano
tensor is possible only for the special case of Kerr-Newman black holes. We
construct natural null congruences for all these black holes and use the
results to show that only the Kerr-Newman black holes are algebraically special
in the sense of Petrov. Modifying the asymptotic behavior by the subtraction
procedure that induces an exact SL(2)^2 also preserves only the conformal
Killing-Stackel tensor. Similarly, we find that a rotating Kaluza-Klein black
hole possesses a conformal Killing-Stackel tensor but has no further
enhancements.Comment: 27 page
Complicated spastic paraplegia in patients with AP5Z1 mutations (SPG48)
Objective: Biallelic mutations in the AP5Z1 gene encoding the AP-5 ζ subunit have been described in a small number of patients with hereditary spastic paraplegia (HSP) (SPG48); we sought to define genotypeâphenotype correlations in patients with homozygous or compound heterozygous sequence variants predicted to be deleterious.
Methods: We performed clinical, radiologic, and pathologic studies in 6 patients with biallelic mutations in AP5Z1.
Results: In 4 of the 6 patients, there was complete loss of AP-5 ζ protein. Clinical features encompassed not only prominent spastic paraparesis but also sensory and motor neuropathy, ataxia, dystonia, myoclonus, and parkinsonism. Skin fibroblasts from affected patients tested positive for periodic acid Schiff and autofluorescent storage material, while electron microscopic analysis demonstrated lamellar storage material consistent with abnormal storage of lysosomal material.
Conclusions: Our findings expand the spectrum of AP5Z1-associated neurodegenerative disorders and point to clinical and pathophysiologic overlap between autosomal recessive forms of HSP and lysosomal storage disorders
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