73 research outputs found
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
Microstructure and Wear Behavior of Laser-Aided Direct Metal Deposited Co-285 and Co-285 + WC Coatings
Exclusive meson electroproduction from hydrogen at CLAS
The longitudinal and transverse components of the cross section for the 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 from 0.2 to 0.6 and of
from 1.5 to 3.0 GeV. 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
Trajetórias, transições e âncoras de carreiras: um estudo comparativo e de recursos humanos
Seasonal variation in insect abundance among three Australian rain forests, with particular reference to phytophagous types
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