We observed a transition from film to vertically well-aligned nanorods for ZnO grown on sapphire (0001) substrates by metalorganic chemical vapor deposition. A growth mechanism was proposed to explain such a transition. Vertically well-aligned homogeneous nanorods with average diameters of ∼30, 45, 60, and 70nm were grown with the c-axis orientation. Raman scattering showed that the E2 (high) mode shifted to high frequency with the decrease of nanorod diameters, which revealed the dependence of nanorod diameters on the stress state. This dependence suggests a stress-driven diameter-controlled mechanism for ZnO nanorod arrays grown on sapphire (0001) substrates.
Background/Aims: The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overexpressed in numerous cancers. However, whether MALAT1 is regulated and the related mechanisms in gastric cancer remain unclear. Methods: Immunohistochemistry and qRT-PCR analyses were used to detect the expression levels of UPF1 and MALAT1 in gastric cancer and adjacent normal tissues. MTT, cell cycle, apoptosis and transwell assays were performed to examine the effects of UPF1 on cell cycle progression, cell proliferation, apoptosis, migration and invasion. Additionally, sodium bisulfate sequencing was used to test the promoter hypermethylation on UPF1 in gastric tumor tissues. Finally, RNA immunoprecipitation and luciferase reporter analyses demonstrated that UPF1 directly bound with MALAT1. Results: The expression of UPF1 was significantly downregulated in gastric cancer and negatively correlated with MALAT1 expression. Patients with lower expression of UPF1 had poorer prognosis than those with higher expression. Overexpression of UPF1 inhibited cell proliferation, cell cycle progression, cell migration and invasion, and promoted cell apoptosis in gastric cancer cells. Moreover, the UPF1-mediated inhibition of gastric cancer progression was reversed by overexpression of MALAT1. A profound downregulation of UPF1 in gastric tumor tissues was due to promoter hypermethylation. Overexpression of UPF1 increased nonsense-mediated mRNA decay (NMD) efficiency and thus led to downregulation of MALAT1. Conclusion: Our results demonstrate that UPF1 is a potential modulator of MALAT1 and that UPF1/MALAT1 pathway could be a therapeutic target for gastric cancer.
A sample of the β-Ga2O3/wurtzite GaN heterostructure has been grown by dry thermal oxidation of GaN on a sapphire substrate. X-ray diffraction measurements show that the β-Ga2O3 layer was formed epitaxially on GaN. The valence band offset of the β-Ga2O3/wurtzite GaN heterostructure is measured by X-ray photoelectron spectroscopy. It is demonstrated that the valence band of the β-Ga2O3/GaN structure is 1.40 ± 0.08 eV.
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