The authors demonstrate the heteroepitaxial and homoepitaxial growth of single crystalline β-Ga2O3 by plasma-assisted molecular beam epitaxy. Phase-pure (2¯01) and (100) β-Ga2O3 thin films were grown on c-plane sapphire and (100) β-Ga2O3 substrates, respectively. Based on the homoepitaxial results, detailed information is reported on the dependence between the β-Ga2O3 film quality and various growth parameters. At an optimized growth temperature of 700 °C, a growth relationship between growth rates and increasing gallium fluxes was established at a fixed oxygen pressure. A three-dimensional columnar growth with a relatively high growth rate was measured at a low gallium flux while a terrace surface morphology with a reduced growth rate was observed as the gallium flux increased. The gallium flux played an important role on both surface morphology and growth rate. We associated the decreasing growth rate with increasing gallium flux with the formation of gallium suboxides monitored by quadrupole mass spectrometry. The formation and desorption of volatile gallium suboxides limited the resulting growth rate of β-Ga2O3 growth.

By antimony doping tin oxide, SnO2:Sb (ATO), below 1.0% Sb concentration, controllable n-type doping was realized. Plasma-assisted molecular beam epitaxy has been used to grow high quality single crystalline epitaxial thin films of unintentionally doped (UID) and Sb-doped SnO2 on r-plane sapphire substrates. A UID thickness series showed an electron concentration of 7.9×1018cm−3 for a 26nm film, which decreased to 2.7×1017cm−3 for a 1570nm film, whereas the mobility increased from 15to103cm2∕Vs, respectively. This series illustrated the importance of a buffer layer to separate unintentional heterointerface effects from the effect of low Sb doping. Unambiguous bulk electron doping was established by keeping the Sb concentration constant but changing the Sb-doped layer thickness. A separate doping series correlated Sb concentration and bulk electron doping. Films containing between 9.8×1017 and 2.8×1020 Sb atoms/cm3 generated an electron concentration of 1.1×1018–2.6×1020cm−3. As the atomic Sb concentration increased, the mobility and resistivity decreased from 110to36cm2∕Vs and 5.1×10−2to6.7×10−4Ωcm, respectively. The Sb concentration was determined by secondary ion mass spectrometry. X-ray diffraction and atomic force microscopy measurements showed no detrimental effects arising from the highest levels of Sb incorporation. Temperature dependent Hall measurements established a lower limit for the Sb electron activation energy of 13.2meV and found that films with greater than 4.9×1019electrons∕cm3 were degenerately doped. Within experimental uncertainties, 100% donor efficiency was determined for Sb-doped SnO2 in the range studied.

Plasma-assisted molecular beam epitaxy has been shown to be a viable and practical method for producing high quality tin oxide, SnO2. Phase-pure epitaxial single crystalline SnO2 (101) thin films of 1μm in thickness were reproducibly grown on r-plane sapphire Al2O3 (101¯2) substrates. The SnO2 epitaxy progressed in the Volmer–Weber growth mode. A minimum on-axis ω-scan full width at half maximum of 0.22° for the SnO2 (101) peak was measured indicating relatively low film mosaic. An epitaxial relationship of [010]SnO2∥[1¯21¯0]sapphire and [1¯01]SnO2∥[1¯011]sapphire was determined between the film and substrate. A SnO2 film tilt of 1.3° around the [010]SnO2 toward [0001]sapphire was measured. A dislocation density of 8×109cm−2 was measured. Hall effect measurements quantified an unintentionally doped electron concentration for different samples in a range (0.3–3.0)×1017cm−3 with a corresponding electron mobility range of 20–100cm2∕Vs. The SnO2 growth behavior was determined to be in one of the two distinct growth regimes. An oxygen-rich regime was characterized by a linear increase in the film growth rate with increasing Sn flux; whereas, the films grown entirely in the Sn-rich regime showed a decrease in the growth rate with increased Sn flux.

The surface roughness of In2O3(001) films is a roadblock to potential semiconductor applications of this material. Using plasma-assisted molecular beam epitaxy we found that In2O3(001) films grow rough by the formation of {111} facets and In2O3(111) films grow smooth without facetting due to the conventionally used (oxygen-rich) conditions. This behavior indicates that the (111) surface is thermodynamically prefered over the (001) surface. We demonstrate that under indium-rich growth conditions these thermodynamics are changed allowing In2O3(001) films to grow smoothly without facetting. Surface indium plays a key role by acting as an auto surfactant that lowers the surface free energy difference between the (001) and the (111) surface.

Hypoxia-inducible factor (HIF) 1α and HIF2α and the inhibitor of apoptosis survivin represent prominent markers of many human cancers. They are also widely expressed in various embryonic tissues, including the central nervous system; however, little is known about their functions in embryos. Here, we show that zebrafish HIF2α protects neural progenitor cells and neural differentiation processes by upregulating the survivin orthologues birc5a and birc5b during embryogenesis. Morpholino-mediated knockdown of hif2α reduced the transcription of birc5a and birc5b, induced p53-independent apoptosis and abrogated neural cell differentiation. Depletion of birc5a and birc5b recaptured the neural development defects that were observed in the hif2α morphants. The phenotypes induced by HIF2α depletion were largely rescued by ectopic birc5a and birc5b mRNAs, indicating that Birc5a and Birc5b act downstream of HIF2α. Chromatin immunoprecipitation assay revealed that HIF2α binds to birc5a and birc5b promoters directly to modulate their transcriptions. Knockdown of hif2α, birc5a or birc5b reduced the expression of the cdk inhibitors p27/cdkn1b and p57/cdkn1c and increased ccnd1/cyclin D1 transcription in the surviving neural progenitor cells. The reduction in elavl3/HuC expression and enhanced pcna, nestin, ascl1b and sox3 expression indicate that the surviving neural progenitor cells in hif2α morphants maintain a high proliferation rate without terminally differentiating. We propose that a subset of developmental defects attributed to HIF2α depletion is due in part to the loss of survivin activity.