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

Extracellular adenosine modulates a volume-sensitive-like chloride conductance in immortalized rabbit DC1 cells.

Cl(-) currents induced by cell swelling were characterized in an immortalized cell line (DC1) derived from rabbit distal bright convoluted tubule by the whole cell patch-clamp techniques and by (125)I(-) efflux experiments. Exposure of cells to a hypotonic shock induced outwardly rectifying Cl(-) currents that could be blocked by 0.1 mM 5-nitro-2-(3-phenylpropyl-amino)benzoic acid, 1 mM DIDS, and by 1 mM diphenylamine-2-carboxylate. (125)I(-) efflux experiments showed that exposure of the monolayer to a hypotonic medium increased (125)I(-) loss. Preincubation of cells with LaCl(3) or GdCl(3) prevented the development of the response. The addition of 10 microM adenosine to the bath medium activated outwardly rectifying whole cell currents similar to those recorded after hypotonic shock. This conductance was inhibited by the A(1)-receptor antagonist 8-cyclopentyl-1,3-diproxylxanthine (DPCPX), LaCl(3), or GdCl(3) and was activated by GTPgammaS. The selective A(1)-receptor agonist N(6)-cyclopentyladenosine (CPA) mimicked the effect of hypotonicity on (125)I(-) efflux. The CPA-induced increase of (125)I(-) efflux was inhibited by DPCPX and external application of LaCl(3) or GdCl(3). Adenosine also enhanced Mn(2+) influx across the apical membrane. Overall, the data show that DC1 cells possess swelling- and adenosine-activated Cl(-) conductances that share identical characteristics. The activation of both conductances involved Ca(2+) entry into the cell, probably via mechanosensitive Ca(2+) channels. The effects of adenosine are mediated via A(1) receptors that could mediate the purinergic regulation of the volume-sensitive Cl(-) conductance