Epitaxial Growth of GaN Nanowires with High Structural Perfection on a Metallic TiN Film.

Vertical GaN nanowires are grown in a self-induced way on a sputtered Ti film by plasma-assisted molecular beam epitaxy. Both in situ electron diffraction and ex situ ellipsometry show that Ti is converted to TiN upon exposure of the surface to the N plasma. In addition, the ellipsometric data demonstrate this TiN film to be metallic. The diffraction data evidence that the GaN nanowires have a strict epitaxial relationship to this film. Photoluminescence spectroscopy of the GaN nanowires shows excitonic transitions virtually identical in spectral position, line width, and decay time to those of state-of-the-art GaN nanowires grown on Si. Therefore, the crystalline quality of the GaN nanowires grown on metallic TiN and on Si is equivalent. The freedom to employ metallic substrates for the epitaxial growth of semiconductor nanowires in high structural quality may enable novel applications that benefit from the associated high thermal and electrical conductivity as well as optical reflectivity.

Correlation between the structural and optical properties of spontaneously formed GaN nanowires: a quantitative evaluation of the impact of nanowire coalescence.

We investigate the structural and optical properties of spontaneously formed GaN nanowires with different degrees of coalescence. This quantity is determined by an analysis of the cross-sectional area and perimeter of the nanowires obtained by plan-view scanning electron microscopy. X-ray diffraction experiments are used to measure the inhomogeneous strain in the nanowire ensembles as well as the orientational distribution of the nanowires. The comparison of the results obtained for GaN nanowire ensembles prepared on bare Si(111) and AlN buffered 6H-SiC(0001) reveals that the main source of the inhomogeneous strain is the random distortions caused by the coalescence of adjacent nanowires. The magnitude of the strain inhomogeneity induced by nanowire coalescence is found not to be determined solely by the coalescence degree, but also by the mutual misorientation of the coalesced nanowires. The linewidth of the donor-bound exciton transition in photoluminescence spectra does not exhibit a monotonic increase with the coalescence degree. In contrast, the comparison of the root mean square strain with the linewidth of the donor-bound exciton transition reveals a clear correlation: the higher the strain inhomogeneity, the larger the linewidth.

Current path in light emitting diodes based on nanowire ensembles.

Light emitting diodes (LEDs) have been fabricated using ensembles of free-standing (In, Ga)N/GaN nanowires (NWs) grown on Si substrates in the self-induced growth mode by molecular beam epitaxy. Electron-beam-induced current analysis, cathodoluminescence as well as biased µ-photoluminescence spectroscopy, transmission electron microscopy, and electrical measurements indicate that the electroluminescence of such LEDs is governed by the differences in the individual current densities of the single-NW LEDs operated in parallel, i.e. by the inhomogeneity of the current path in the ensemble LED. In addition, the optoelectronic characterization leads to the conclusion that these NWs exhibit N-polarity and that the (In, Ga)N quantum well states in the NWs are subject to a non-vanishing quantum confined Stark effect.

Correlation between In content and emission wavelength of In(x)Ga(1-x)N/GaN nanowire heterostructures.

GaN nanowire ensembles with axial In(x)Ga(1-x)N multi-quantum-wells (MQWs) were grown by molecular beam epitaxy. In a series of samples we varied the In content in the MQWs from almost zero to around 20%. Within the nanowire ensemble, the MQWs fluctuate strongly in composition and size. Statistical information about the composition was obtained from x-ray diffraction and Raman spectroscopy. Photoluminescence at room temperature was obtained in the range of 2.2 to 2.5 eV, depending on In content. Contrary to planar MQWs, the intensity increases with increasing In content. We compare the observed emission energies with transition energies obtained from a one-dimensional model, and conclude that several mechanisms for carrier localization affect the luminescence of these three-dimensional structures.

Involvement of cytochrome P-450IIIA in metabolism of potassium canrenoate to an epoxide: mechanism of inhibition of the epoxide formation by spironolactone and its sulfur-containing metabolite.

In vitro metabolism studies of potassium canrenoate (PC) were conducted to examine whether spironolactone (SP) and/or its sulfur-containing metabolites inhibit the PC metabolic pathways to mutagenic metabolites and to elucidate the mechanism for any observed inhibitory effect. The mechanistic study was conducted using liver microsomes prepared from male and female rats with and without pretreatment of a cytochrome (Cyt) P-450IIIA inducer [pregnenolone-16 alpha-carbonitrile (PCN) or dexamethasone (DEX)] and with and without a Cyt P-450IIIA inhibitor, triacetyloleandomycin (TAO). The present study demonstrates that SP and its sulfur-containing metabolite 7 alpha-thio-spirolactone substantially inhibited the formation of promutagen 6 beta, 7 beta-epoxycanrenone (6 beta, 7 beta-epoxy-CAN) from PC. The sulfur-containing metabolite of SP that inhibit promutagen formation were not formed from PC, although a glutathione conjugate of PC was formed. The formation rate of 6 beta, 7 beta-epoxy-CAN was greater in liver microsomes prepared from rats pretreated with a Cyt P-450IIIA inducer (PCN or DEX) than in liver microsomes prepared from the untreated rats. The formation rate of the epoxide metabolite was lower after in vitro addition of TAO. Pretreatment of animals with TAO 4 hr before sacrifice produced similar results. Erythromycin, which is N-demethylated by Cyt P-450IIIA, also reduced the formation rate of 6 beta, 7 beta-epoxy-CAN. Inhibition of PC metabolism to 6 beta, 7 beta-epoxy-CAN by TAO and erythromycin, and its induction by DEX and PCN, suggest involvement of Cyt P-450IIIA, which is in turn inhibited by SP and 7 alpha-thio-spirolactone.

Difference in metabolic profile of potassium canrenoate and spironolactone in the rat: mutagenic metabolites unique to potassium canrenoate.

The metabolic fates of potassium canrenoate (PC) and spironolactone (SP) were compared for the rat in vivo and in vitro. Approximately 18% of an in vivo dose of SP was metabolized to canrenone (CAN) and related compounds in the rat. In vitro, 20-30% of SP was dethioacetylated to CAN and its metabolites by rat liver 9000 g supernatant (S9). Thus, the major route of SP metabolism is via pathways that retain the sulfur moiety in the molecule. PC was metabolized by rat hepatic S9 to 6 alpha, 7 alpha- and 6 beta, 7 beta-epoxy-CAN. The beta-epoxide was further metabolized to its 3 alpha- and 3 beta-hydroxy derivatives as well as its glutathione (GSH) conjugate. Both 3 alpha- and 3 beta-hydroxy-6 beta, 7 beta-epoxy-CAN were shown to be direct acting mutagens in the mouse lymphoma assay, whereas 6 alpha, 7 alpha- and 6 beta, 7 beta-epoxy-CAN were not. These mutagenic metabolites, their precursor epoxides and their GSH conjugates were not formed from SP under identical conditions. The above findings appear to be due to inhibition of metabolism of CAN formed from SP by SP and/or its S-containing metabolites, since the in vitro metabolism of PC by rat hepatic microsomes was appreciably reduced in the presence of SP. The hypothesized mechanism(s) for this inhibition is that SP and its S-containing metabolites specifically inhibit an isozyme of hepatic cytochrome P-450 or SP is a preferred substrate over PC/CAN for the metabolizing enzymes. Absence of the CAN epoxide pathway in the metabolism of SP provides a possible explanation for the observed differences in the toxicological profiles of the two compounds.