Role of defects in ultra-high gain in fast planar tin gallium oxide UV-C photodetector by MBE

We report ultra-high responsivity of epitaxial (SnxGa1-x)2O3 (TGO) Schottky UV-C photodetectors and experimentally identified the source of gain as deep-level defects, supported by first principles calculations. Epitaxial TGO films were grown by plasma-assisted molecular beam epitaxy on (-201) oriented n-type β-Ga2O3 substrates. Fabricated vertical Schottky devices exhibited peak responsivities as high as 3.5×104 A/W at -5V applied bias under 250nm illumination with sharp cutoff shorter than 280nm and fast rise/fall time in milliseconds order. Hyperspectral imaging cathodoluminescence (CL) spectra were examined to find the mid-bandgap defects, the source of this high gain. Irrespective of different tin mole fractions, the TGO epilayer exhibited extra CL peaks at the green band (2.20 eV) not seen in β-Ga2O3 along with enhancement of the blue emission-band (2.64 eV) and suppression of the UV emission-band. Based on hybrid functional calculations of the optical emission expected for defects involving Sn in β-Ga2O3, VGa–Sn complexes are proposed as potential defect origins of the observed green and blue emission-bands. Such complexes behave as acceptors that can efficiently trap photogenerated holes and are predicted to be predominantly responsible for the ultra-high photoconductive gain in the Sn-alloyed Ga2O3 devices by means of thermionic emission and electron tunneling. Regenerating the VGa–Sn defect complexes by optimizing the growth techniques, we have demonstrated a planar Schottky UV-C photodetector of the highest peak responsivity

Continuous Si doping in (010) and (001) β-Ga2O3 films by plasma-assisted molecular beam epitaxy

We report the continuous Si doping in β-Ga2O3 epitaxial films grown by plasma-assisted molecular beam epitaxy through the use of a valved effusion cell for the Si source. Secondary ion mass spectroscopy results exhibit that the Si doping profiles in β-Ga2O3 are flat and have sharp turn-on/off depth profiles. The Si doping concentration was able to be controlled by either varying the cell temperatures or changing the aperture of the valve of the Si effusion cell. High crystal quality and smooth surface morphologies were confirmed on Si-doped β-Ga2O3 epitaxial films grown on (010) and (001) substrates. The electronic properties of Si-doped (001) β-Ga2O3 epitaxial film showed an electron mobility of 67 cm2/Vs at the Hall concentration of 3 × 1018 cm−3

Phenotypically distinct subsets of CD4+ T cells induce or protect from chronic intestinal inflammation in C. B-17 scid mice.

CD4+ T cells in the mouse can be subdivided into two fractions based on the level of expression of the CD45RB determinant. Previous studies have shown that these subsets are functionally distinct. We have further characterized the properties of these subpopulations in vivo by injecting them into C. B-17 scid mice. The animals restored with the CD45RBhighCD4+ T cell population developed a lethal wasting disease with severe mononuclear cell infiltrates into the colon and elevated levels of IFN-gamma mRNA. In contrast, animals restored with the reciprocal CD45RBlow subset or with unfractionated CD4+ T cells did not develop the wasting or colitis. Importantly, the co-transfer of the CD45RBlow population with the CD45RBhigh population prevented the wasting disease and colitis. These data indicate that important regulatory interactions occur between the CD45RBhigh and CD45RBlowCD4+ T cell subsets and that disruption of this mechanism has fatal consequences

A critical role for transforming growth factor-beta but not interleukin 4 in the suppression of T helper type 1-mediated colitis by CD45RB(low) CD4+ T cells.

A T helper type 1 (Th1)-mediated colitis with similarities to inflammatory bowel disease in humans developed in severe combined immunodeficiency mice reconstituted with CD45RB(high) CD4+ splenic T cells and could be prevented by cotransfer of CD45RB(low) CD4+ T cells. Inhibition of this Th1 response by the CD45RB(low) T cell population could be reversed in vivo by an anti-transforming growth factor (TGF) beta antibody. Interleukin (IL) 4 was not required for either the differentiation of function of protective cells as CD45RB(low) CD4+ cells from IL-4-deficient mice were fully effective. These results identify a subpopulation of peripheral CD4+ cells and TGF-beta as critical components of the natural immune regulatory mechanism, which prevents the development of pathogenic Th1 responses in the gut, and suggests that this immunoregulatory population is distinct from Th2 cells

Inhibition of Th1 responses prevents inflammatory bowel disease in scid mice reconstituted with CD45RBhi CD4+ T cells.

We have described a murine model of IBD that was induced in C.B-17 scid mice by transfer of the CD45RBhi subpopulation of CD4+ T cells from normal BALB/c mice and could be prevented by cotransfer of the CD45RBlo CD4+ T cell subset. Here we have dissected the mechanism of pathogenesis of IBD in this model and used this information for rational immunotherapy of the disease. CD4+ cells from diseased mice displayed a highly polarized Th1 pattern of cytokine synthesis upon polyclonal stimulation in vitro. The administration of anti-IFN gamma MAb to mice soon after T cell transfer prevented development of colitis for up to 12 weeks. Continual neutralization of TNF with anti-TNF MAbs reduced the incidence of severe disease; however, neutralization of TNF during only the first 3-4 weeks had no effect. Severe colitis was completely abrogated in mice treated systemically with rIL-10, but not with rIL-4