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Tin dioxide (SnO2) thin films, as a candidate for realizing next-generation electrical and optical devices, were grown on 2-inch diameter m -plane sapphire substrates by mist chemical vapour deposition at atmospheric pressure. The SnO2 thin films were characterized by scanning electron microscope (SEM), atomic force microscope (AFM), X-ray diffraction (XRD) in θ-2θ and φ scanning modes, and electron backscatter diffraction (EBSD). Although the SEM and AFM images showed a relatively rough surface morphology, it was found from the XRD and EBSD measurements that SnO2 films were epitaxially grown on the substrates under optimised growth condition. Epitaxial growth of SnO2 thin film growth at three typical areas on the substrate was confirmed by the EBSD measurements. It is likely that the single crystalline SnO2 (001) thin film was formed across the 2-inch sapphire substrate. Finally, the second SnO2 layer was overgrown on the above single crystalline SnO2 thin film, which functioned as a buffer layer. This method which drastically improved surface roughness of the second SnO2 layer. [ABSTRACT FROM AUTHOR]

Myelosuppression is a major side effect of chemotherapy. Although decreased blood cells are restored with the recovery of bone marrow cells, insufficient recovery of decreased lymphocytes was observed in mice given azacitidine (AZA), a DNA methyltransferase (DNMT) inhibitor, even following the restoration of bone marrow cells. To understand the mechanisms behind this sustained lymphopenia, we examined AZA's impact on the hematopoietic progenitor cells and the expression of Dnmts and differentiation-related genes. An antimetabolite of cytidine analog, cytarabine (Ara-C), was used as a reference compound. Decreases in almost all blood parameters and common lymphoid progenitors (CLPs) and the downregulation of Dnmts and differentiation-related genes in Lineage-Sca-1+c-kit+ (LSK) cells were observed in mice administered AZA or Ara-C for 7 d. In the posttreatment observation, all parameters, except for lymphocytes and monocytes, exhibited recovery within 3 wk after the final dosing in both treated groups. However, no recovery from the decreases in lymphocytes, especially B cells, and monocytes occurred even after 5 wk. The number of CLPs was elevated after 3 wk. There was a tendency toward recovery from the decreased expression of Dnmt1 and differentiation-related genes, but the expression levels of Dnmt3a and Dnmt3b did not fully recover even 5 wk after the final dosing. Taken together, the findings revealed that the mechanism of sustained lymphopenia observed in mice treated with AZA or Ara-C is associated, at least in part, with the abnormal differentiation of CLPs into B cells accompanied by the prolonged suppression of Dnmt3a and Dnmt3b expression on LSK cells., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)