An infrared absorption investigation of hydrogen, deuterium, and nitrogen in ZnSe grown by molecular beam epitaxy

Surprising concentrations of hydrogen and deuterium, as high as 5×10 cm, were incorporated into nitrogen‐doped ZnSe grown on GaAs by molecular beam epitaxy. Infrared absorption bands due to local vibration modes were observed at 3193 and 783 cm for ZnSe:N,H samples, and at 2368 cm for ZnSe:N,D samples using Fourier transform infrared spectroscopy. The isotopic shift in the absorption band agrees with predictions of a simple harmonic oscillator approximation for N–H bonding. The variation of the absorption band associated with substitutional nitrogen with nitrogen concentration indicates that not all nitrogen is substitutional, and also exhibited significant changes related to hydrogen incorporation. © 1996 American Institute of Physics

The Effect of Atomic Hydrogen on the Growth of Gallium Nitride by Molecular Beam Epitaxy

GaN was grown by molecular beam epitaxy using an rf plasma source. Growth under gallium‐rich conditions at 730 °C was required to produce high quality layers as indicated by photoluminescence, Hall effect, atomic force microscopy, and x‐ray diffraction measurements. Atomic hydrogen has a significant effect for Ga‐rich growth, increasing growth rates by as much as a factor of 2

Observation Of Singly Ionized Selenium Vacancies In Znse Grown By Molecular Beam Epitaxy

Electron paramagnetic resonance(EPR) has been used to investigate singly ionized selenium vacancy V Se + centers in ZnSe epilayers grown by molecular beam epitaxy(MBE). The study included undoped and nitrogen-doped films. Spectra taken at 8 K and 9.45 GHz, as the magnetic field was rotated in the plane from [100] to [010], showed an isotropic signal at g =2.0027±0.0004 with a linewidth of 5.8 G. In the two samples where this signal was observed, estimates of concentration were approximately 1.1×10 17 and 6.3×10 17 cm −3 . The appearance of the EPR signal correlated with an increase in the Zn/Se beam equivalent pressure ratio (during growth) in undoped films and with an increase in the nitrogen concentration in doped films. We conclude that the singly ionized selenium vacancy may be a dominant point defect in many MBE-grown ZnSe layers and that these defects may play a role in the compensation mechanisms in heavily nitrogen-doped ZnSe thin films

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=4.5×10(-14)). 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. (Funded by the National Institutes of Health and others.)