Supersymmetric Non-Abelian Born-Infeld Theory

Using the natural curvature invariants as building blocks in a superfield construction, we show that the use of a symmetric trace is mandatory if one is to reproduce the square root structure of the non-Abelian Dirac-Born-Infeld Lagrangian in the bosonic sector. We also discuss the BPS relations in connection with our supersymmetry construction.Comment: 13 pages, Latex, no figure

Bogomol'nyi Bounds and the Supersymmetric Born-Infeld Theory

We study N=2 supersymmetric Born-Infeld-Higgs theory in 3 dimensions and derive Bogomol'nyi relations in its bosonic sector. A peculiar coupling between the Higgs and the gauge field (with dynamics determined by the Born-Infeld action) is forced by supersymmetry. The resulting equations coincide with those arising in the Maxwell-Higgs model. Concerning Bogomol'nyi bounds for the vortex energy, they are derived from the N=2 supersymmetry algebra.Facultad de Ciencias Exacta

Bogomol'nyi Bounds and the Supersymmetric Born-Infeld Theory

We study N=2 supersymmetric Born-Infeld-Higgs theory in 3 dimensions and derive Bogomol'nyi relations in its bosonic sector. A peculiar coupling between the Higgs and the gauge field (with dynamics determined by the Born-Infeld action) is forced by supersymmetry. The resulting equations coincide with those arising in the Maxwell-Higgs model. Concerning Bogomol'nyi bounds for the vortex energy, they are derived from the N=2 supersymmetry algebra.Comment: 24 pages, Latex fil

Stabilization of the Yang-Mills chaos in non-Abelian Born-Infeld theory

We investigate dynamics of the homogeneous time-dependent SU(2) Yang-Mills fields governed by the non-Abelian Born-Infeld lagrangian which arises in superstring theory as a result of summation of all orders in the string slope parameter $\alpha'$. It is shown that generically the Born-Infeld dynamics is less chaotic than that in the ordinary Yang-Mills theory, and at high enough field strength the Yang-Mills chaos is stabilized. More generally, a smothering effect of the string non-locality on behavior of classical fields is conjectured.Comment: 7 pages, 5 figure

Non-Linear/Non-Commutative Non-Abelian Monopoles

Using recently proposed non-linearly realized supersymmetry in non-Abelian gauge theory corrected to the order (alpha')^2, we derive the non-linear BPS equations in the background B-field for the U(2) monopoles and instantons. We show that these non-Abelian non-linear BPS equations coincide with the non-commutative anti-self-dual equations via the Seiberg-Witten map.Comment: 9 pages, LaTe

Dynamics of BPS States in the Dirac-Born-Infeld Theory

The Dirac-Born-Infeld action with transverse scalar fields is considered to study the dynamics of various BPS states. We first describe the characteristic properties of the so-called 1/2 and 1/4 BPS states on the D3 brane, which can be interpreted as F/D-strings ending on a D3-brane in Type IIB string theory picture. We then study the response of the BPS states to low energy excitations of massless fields on the brane, the scalar fields representing the shape fluctuation of the brane and U(1) gauge fields describing the open string excitations on the D-brane. This leads to an identification of interactions between BPS states including the static potentials and the kinetic interactions.Comment: 19 pages, 4 figures References added, Typographical errors are correcte

Primordial fluctuations from nonlinear couplings

We study the spectrum of primordial fluctuations in theories where the inflaton field is coupled to massless fields and/or to itself. Conformally invariant theories generically predict a scale invariant spectrum. Scales entering the theory through infrared divergences cause logarithmic corrections to the spectrum, tiltilng it towards the blue. We discuss in some detail whether these fluctuations are quantum or classical in nature.Comment: 12 pages, Revtex, we added an appendix clarifying our assumptions about the initial conditions at the beggining of inflatio

Dyonic BIon black hole in string inspired model

We construct static and spherically symmetric particle-like and black hole solutions with magnetic and/or electric charge in the Einstein-Born-Infeld-dilaton-axion system, which is a generalization of the Einstein-Maxwell-dilaton-axion (EMDA) system and of the Einstein-Born-Infeld (EBI) system. They have remarkable properties which are not seen for the corresponding solutions in the EMDA and the EBI system.Comment: 13 pages, 15 figures, Final version in PR

Dihydropyridine receptor (DHPR, CACNA1S) congenital myopathy

Muscle contraction upon nerve stimulation relies on excitation–contraction coupling (ECC) to promote the rapid and generalized release of calcium within myofibers. In skeletal muscle, ECC is performed by the direct coupling of a voltage-gated L-type Ca2+ channel (dihydropyridine receptor; DHPR) located on the T-tubule with a Ca2+ release channel (ryanodine receptor; RYR1) on the sarcoplasmic reticulum (SR) component of the triad. Here, we characterize a novel class of congenital myopathy at the morphological, molecular, and functional levels. We describe a cohort of 11 patients from 7 families presenting with perinatal hypotonia, severe axial and generalized weakness. Ophthalmoplegia is present in four patients. The analysis of muscle biopsies demonstrated a characteristic intermyofibrillar network due to SR dilatation, internal nuclei, and areas of myofibrillar disorganization in some samples. Exome sequencing revealed ten recessive or dominant mutations in CACNA1S (Cav1.1), the pore-forming subunit of DHPR in skeletal muscle. Both recessive and dominant mutations correlated with a consistent phenotype, a decrease in protein level, and with a major impairment of Ca2+ release induced by depolarization in cultured myotubes. While dominant CACNA1S mutations were previously linked to malignant hyperthermia susceptibility or hypokalemic periodic paralysis, our findings strengthen the importance of DHPR for perinatal muscle function in human. These data also highlight CACNA1S and ECC as therapeutic targets for the development of treatments that may be facilitated by the previous knowledge accumulated on DHPR

Improving genetic diagnosis in Mendelian disease with transcriptome sequencing

Exome and whole-genome sequencing are becoming increasingly routine approaches in Mendelian disease diagnosis. Despite their success, the current diagnostic rate for genomic analyses across a variety of rare diseases is approximately 25 to 50%. We explore the utility of transcriptome sequencing [RNA sequencing (RNA-seq)] as a complementary diagnostic tool in a cohort of 50 patients with genetically undiagnosed rare muscle disorders. We describe an integrated approach to analyze patient muscle RNA-seq, leveraging an analysis framework focused on the detection of transcript-level changes that are unique to the patient compared to more than 180 control skeletal muscle samples. We demonstrate the power of RNA-seq to validate candidate splice-disrupting mutations and to identify splice-altering variants in both exonic and deep intronic regions, yielding an overall diagnosis rate of 35%. We also report the discovery of a highly recurrent de novo intronic mutation in COL6A1 that results in a dominantly acting splice-gain event, disrupting the critical glycine repeat motif of the triple helical domain. We identify this pathogenic variant in a total of 27 genetically unsolved patients in an external collagen VI–like dystrophy cohort, thus explaining approximately 25% of patients clinically suggestive of having collagen VI dystrophy in whom prior genetic analysis is negative. Overall, this study represents a large systematic application of transcriptome sequencing to rare disease diagnosis and highlights its utility for the detection and interpretation of variants missed by current standard diagnostic approaches