New Superembeddings for Type II Superstrings

Possible ways of generalization of the superembedding approach for the supersurfaces with the number of Grassmann directions being less than the half of that for the target superspace are considered on example of Type II superstrings. Focus is on n=(1,1) superworldsheet embedded into D=10 Type II superspace that is of the interest for establishing a relation with the NSR string.Comment: 26 pages, LaTeX, JHEP.cls and JHEP.bst style files are used; v2: misprints corrected, comments, acknowledgments, references adde

Q7-branes and their coupling to IIB supergravity

We show how, by making use of a new basis of the IIB supergravity axion-dilaton coset, SL(2,R)/SO(2), 7-branes that belong to different conjugacy classes of the duality group SL(2,R) naturally couple to IIB supergravity with appropriate source terms characterized by an SL(2,R) charge matrix Q. The conjugacy classes are determined by the value of the determinant of Q. The (p,q) 7-branes are the branes in the conjugacy class detQ = 0. The 7-branes in the conjugacy class detQ > 0 are labelled by three numbers (p,q,r) which parameterize the matrix Q and will be called Q7-branes. We construct the full bosonic Wess--Zumino term for the Q7-branes. In order to realize a gauge invariant coupling of the Q7-brane to the gauge fields of IIB supergravity it is necessary to introduce an SL(2,R) doublet of two distinct Born--Infeld fields on the Q7-brane world-volume.Comment: 31 pages, Latex fil

Review of AdS/CFT Integrability, Chapter V.2: Dual Superconformal Symmetry

Scattering amplitudes in planar N=4 super Yang-Mills theory reveal a remarkable symmetry structure. In addition to the superconformal symmetry of the Lagrangian of the theory, the planar amplitudes exhibit a dual superconformal symmetry. The presence of this additional symmetry imposes strong restrictions on the amplitudes and is connected to a duality relating scattering amplitudes to Wilson loops defined on polygonal light-like contours. The combination of the superconformal and dual superconformal symmetries gives rise to a Yangian, an algebraic structure which is known to be related to the appearance of integrability in other regimes of the theory. We discuss two dual formulations of the symmetry and address the classification of its invariants.Comment: 22 pages, see also overview article arXiv:1012.3982, v2: references to other chapters updated, v3 added references, typos fixe

Genetic drivers of kidney defects in the digeorge syndrome

BACKGROUND The DiGeorge syndrome, the most common of the microdeletion syndromes, affects multiple organs, including the heart, the nervous system, and the kidney. It is caused by deletions on chromosome 22q11.2; the genetic driver of the kidney defects is unknown. METHODS We conducted a genomewide search for structural variants in two cohorts: 2080 patients with congenital kidney and urinary tract anomalies and 22,094 controls. We performed exome and targeted resequencing in samples obtained from 586 additional patients with congenital kidney anomalies. We also carried out functional studies using zebrafish and mice. RESULTS We identified heterozygous deletions of 22q11.2 in 1.1% of the patients with congenital kidney anomalies and in 0.01% of population controls (odds ratio, 81.5; P = 4.5×1014). We localized the main drivers of renal disease in the DiGeorge syndrome to a 370-kb region containing nine genes. In zebrafish embryos, an induced loss of function in snap29, aifm3, and crkl resulted in renal defects; the loss of crkl alone was sufficient to induce defects. Five of 586 patients with congenital urinary anomalies had newly identified, heterozygous protein-Altering variants, including a premature termination codon, in CRKL. The inactivation of Crkl in the mouse model induced developmental defects similar to those observed in patients with congenital urinary anomalies. CONCLUSIONS We identified a recurrent 370-kb deletion at the 22q11.2 locus as a driver of kidney defects in the DiGeorge syndrome and in sporadic congenital kidney and urinary tract anomalies. Of the nine genes at this locus, SNAP29, AIFM3, and CRKL appear to be critical to the phenotype, with haploinsufficiency of CRKL emerging as the main genetic driver

The Spitzer Microlensing Program As A Probe For Globular Cluster Planets: Analysis Of Ogle-2015-BLG-0448

The microlensing event OGLE-2015-BLG-0448 was observed by Spitzer and lay within the tidal radius of the globular cluster NGC 6558. The event had moderate magnification and was intensively observed, hence it had the potential to probe the distribution of planets in globular clusters. We measure the proper motion of NGC 6558 (${{\boldsymbol{\mu }}}_{\mathrm{cl}}(N,E)=(+0.36\pm 0.10,+1.42\pm 0.10)\;{\rm{mas}}\;{{\rm{yr}}}^{-1}$) as well as the source and show that the lens is not a cluster member. Even though this particular event does not probe the distribution of planets in globular clusters, other potential cluster lens events can be verified using our methodology. Additionally, we find that microlens parallax measured using Optical Gravitational Lens Experiment (OGLE) photometry is consistent with the value found based on the light curve displacement between the Earth and Spitzer

Retinal function and morphology in two zebrafish models of oculo-renal syndromes.

We characterized visual system defects in two recessive zebrafish mutants oval and elipsa. These mutants share the syndromic phenotype of outer retinal dystrophy in conjunction with cystic renal disorder. We tested the function of the larval visual system in a behavioural assay, eliciting optokinetic eye movements by high-contrast motion stimulation while recording eye movements in parallel. Visual stimulation did not elicit eye movements in mutant larvae, while spontaneous eye movements could be observed. The retina proved to be unresponsive to light using electroretinography, indicative of a defect in the outer retina. Histological analysis of mutant retinas revealed progressive degeneration of photoreceptors, initiated in central retinal locations and spreading to more peripheral regions with increasing age. The inner retina remains unaffected by the mutation. Photoreceptors display cell type-specific immunoreactivity prior to apoptotic cell death, arguing for a dystrophic defect. Genomic mapping employing simple sequence-length polymorphisms located both mutations on different regions of zebrafish linkage group 9. These mutants may serve as accessible animal models of human outer retinal dystrophies, including oculo-renal diseases, and show the general usefulness of a behavioural genetic approach to study visual system development in the model vertebrate zebrafish