We synthesized carbon nanowalls (CNWs) using radical injection plasma-enhanced chemical vapor deposition. The initial growth process of CNWs was investigated with and without O2 gas addition to a C2F6 capacitively coupled plasma with H radical injection. In the case of the CNW synthesis without the addition of O2 gas, scanning electron microscopy (SEM), transmission electron microscopy, x-ray photoelectron spectroscopy (XPS), and Raman spectroscopy revealed that a 10-nm-thick interface layer composed of nanoislands was formed on a Si substrate approximately 1 min prior to CNW formation. In contrast, with O2 gas addition, SEM and XPS revealed that an interface layer was not formed and that CNWs were grown directly from nanoislands. Moreover, Raman spectroscopy suggested that the interface layer was composed of amorphous carbon and that O2 gas addition during CNW growth is effective for achieving a high graphitization of CNWs. Therefore, O2 gas addition has the effect of reducing the amorphicity and disorder of CNWs and controlling CNW nucleation.

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Two-dimensional carbon nanostructures, carbon nanowalls (CNWs), were fabricated on a Si substrate using radical injection plasma-enhanced chemical vapor deposition, employing fluorocarbon (C2F6) and hydrogen (H2) mixtures. The influence of the surface conditions of the chamber wall on CNW growth was investigated in order to determine the optimum conditions for CNW growth with high stability and reproducibility. In order to monitor the surface conditions of the chamber wall, optical emission spectroscopy in the plasma was measured, and the correlation between CNW growth and the surface conditions in the chamber wall was investigated. The growth rate and morphology of grown CNWs were determined to be influenced by the surface conditions of the chamber wall. Furthermore, O2 plasma chamber cleaning followed by predeposition for passivation was found to be effective for maintaining steady conditions to attain CNWs with high reproducibility.

The key issue in GaN growth by radio‐frequency plasma‐assisted molecular beam epitaxy is the low growth rate compared with that obtained using an ammonia source. To reduce the processing time and to improve the crystalline quality of the epilayer, a high‐density radical source (HDRS) with high stability has been developed. The growth rate of the GaN epilayer was improved using the HDRS rather than a conventional radical source. During the growth, a sharp streak pattern obtained by reflection high‐energy electron diffraction was maintained. An atomically smooth surface was confirmed by atomic force microscopy observation (© 2011 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)

Hypothalamic hormones, including dopamine, regulate critical functions of pituitary cells via the cAMP-protein kinase A (PKA) pathway. The PKA-downstream transcription factor cAMP response element (CRE)-binding protein (CREB) is an integrating molecule that is also activated by many other protein kinase pathways. We investigated the involvement of CREB in the regulation of cell proliferation and the PRL promoter of rat lactotrophs in primary cell culture. Recombinant adenoviruses were used for efficient gene delivery into pituitary cells. Bromocriptine, a dopaminergic agonist known to decrease intracellular cAMP concentrations, caused inhibition of PRL promoter activity and lactotroph proliferation, which was accompanied by decreases in CRE-mediated transcription and CREB phosphorylation in lactotrophs. Expression of a dominant-negative form of CREB (MCREB), which was effective in suppressing CRE-mediated transcription induced by the adenylate cyclase activator forskolin, inhibited basal and forskolin-induced PRL promoter activity and PRL mRNA expression. MCREB expression lowered basal proliferative levels and blocked forskolin-induced proliferation of lactotrophs. Insulin-like growth factor I (IGF-I), a potent mitogen in lactotrophs, did not affect intracellular cAMP concentrations but transiently increased lactotroph CREB phosphorylation. MCREB expression also inhibited IGF-I-induced lactotroph proliferation. These results suggest that CREB is involved in the regulation of cell proliferation and the PRL promoter in normal lactotrophs and that dopamine inhibition of these lactotroph functions is at least in part due to inhibition of the cAMP-PKA-CREB pathway.