PT-symmetric Solutions of Schrodinger Equation with position-dependent mass via Point Canonical Transformation

PT-symmetric solutions of Schrodinger equation are obtained for the Scarf and generalized harmonic oscillator potentials with the position-dependent mass. A general point canonical transformation is applied by using a free parameter. Three different forms of mass distributions are used. A set of the energy eigenvalues of the bound states and corresponding wave functions for target potentials are obtained as a function of the free parameter.Comment: 13 page

Complete measurement of three-body photodisintegration of 3He for photon energies between 0.35 and 1.55 GeV

The three-body photodisintegration of 3He has been measured with the CLAS detector at Jefferson Lab, using tagged photons of energies between 0.35 GeV and 1.55 GeV. The large acceptance of the spectrometer allowed us for the first time to cover a wide momentum and angular range for the two outgoing protons. Three kinematic regions dominated by either two- or three-body contributions have been distinguished and analyzed. The measured cross sections have been compared with results of a theoretical model, which, in certain kinematic ranges, have been found to be in reasonable agreement with the data.Comment: 22 pages, 25 eps figures, 2 tables, submitted to PRC. Modifications: removed 2 figures, improvements on others, a few minor modifications to the tex

A Kinematically Complete Measurement of the Proton Structure Function F2 in the Resonance Region and Evaluation of Its Moments

We measured the inclusive electron-proton cross section in the nucleon resonance region (W < 2.5 GeV) at momentum transfers Q**2 below 4.5 (GeV/c)**2 with the CLAS detector. The large acceptance of CLAS allowed for the first time the measurement of the cross section in a large, contiguous two-dimensional range of Q**2 and x, making it possible to perform an integration of the data at fixed Q**2 over the whole significant x-interval. From these data we extracted the structure function F2 and, by including other world data, we studied the Q**2 evolution of its moments, Mn(Q**2), in order to estimate higher twist contributions. The small statistical and systematic uncertainties of the CLAS data allow a precise extraction of the higher twists and demand significant improvements in theoretical predictions for a meaningful comparison with new experimental results.Comment: revtex4 18 pp., 12 figure

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

Exclusive ρ0\rho^0 meson electroproduction from hydrogen at CLAS

The longitudinal and transverse components of the cross section for the $e p\to e^\prime p \rho^0$ reaction were measured in Hall B at Jefferson Laboratory using the CLAS detector. The data were taken with a 4.247 GeV electron beam and were analyzed in a range of $x_B$ from 0.2 to 0.6 and of $Q^2$ from 1.5 to 3.0 GeV$^2$. The data are compared to a Regge model based on effective hadronic degrees of freedom and to a calculation based on Generalized Parton Distributions. It is found that the transverse part of the cross section is well described by the former approach while the longitudinal part can be reproduced by the latter.Comment: 6 pages, 4 figure

Insights into Autism Spectrum Disorder Genomic Architecture and Biology from 71 Risk Loci

Analysis of de novo CNVs (dnCNVs) from the full Simons Simplex Collection (SSC) (N = 2,591 families) replicates prior findings of strong association with autism spectrum disorders (ASDs) and confirms six risk loci (1q21.1, 3q29, 7q11.23, 16p11.2, 15q11.2-13, and 22q11.2). The addition of published CNV data from the Autism Genome Project (AGP) and exome sequencing data from the SSC and the Autism Sequencing Consortium (ASC) shows that genes within small de novo deletions, but not within large dnCNVs, significantly overlap the high-effect risk genes identified by sequencing. Alternatively, large dnCNVs are found likely to contain multiple modest-effect risk genes. Overall, we find strong evidence that de novo mutations are associated with ASD apart from the risk for intellectual disability. Extending the transmission and de novo association test (TADA) to include small de novo deletions reveals 71 ASD risk loci, including 6 CNV regions (noted above) and 65 risk genes (FDR ≤ 0.1). Through analysis of de novo mutations in autism spectrum disorder (ASD), Sanders et al. find that small deletions, but not large deletions/duplications, contain one critical gene. Combining CNV and sequencing data, they identify 6 loci and 65 genes associated with ASD. © 2015 Elsevier Inc