ABSTRACT
The rapid emergence of graphene has attracted numerous efforts to explore other two-dimensional materials. Here, we combine first-principles calculations and Boltzmann theory to investigate the structural, electronic, and thermoelectric transport properties of monolayer C3N, which exhibits a honeycomb structure very similar to graphene. It is found that the system is both dynamically and thermally stable even at high temperature. Unlike graphene, the monolayer has an indirect band gap of 0.38 eV and much lower lattice thermal conductivity. Moreover, the system exhibits obviously larger electrical conductivity and Seebeck coefficients for the hole carriers. Consequently, theZTvalue ofp-type C3N can reach 1.4 at 1200 K when a constant relaxation time is predicted by the simple deformation potential theory. However, such a largerZTis reduced to 0.6 if we fully consider the electron-phonon coupling. Even so, the thermoelectric performance of monolayer C3N is still significantly enhanced compared with that of graphene, and is surprisingly good for low-dimensional thermoelectric materials consisting of very light elements.
ABSTRACT
OBJECTIVE: To elucidate the role of miRNA-409-5p in the pathogenesis of child chronic myeloid leukemia (CML) and its potential mechanism. PATIENTS AND METHODS: Expression levels of miRNA-409-5p and NUP43 in peripheral blood of CML children and healthy controls were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell counting kit-8 (CCK-8) and flow cytometry were conducted to evaluate the regulatory effect of miRNA-409-5p on proliferative potential and cell cycle progression of CML cells. Protein levels of PCNA, c-Myc, and cyclin D1 in CML were examined by Western blot. Dual-luciferase reporter gene assay verified the binding of target gene NUP43 to miRNA-409-5p. Finally, the potential effect of miRNA-409-5p on Imatinib resistance in CML was elucidated. RESULTS: Compared with healthy children, miRNA-409-5p expression in peripheral blood of CML children markedly decreased. Similarly, miRNA-409-5p expression was lower in CML cells. Contrary to the expression pattern of miRNA-409-5p, NUP43 was highly expressed in CML. The miRNA-409-5p overexpression remarkably inhibited proliferative potential and arrested cell cycle in the G0/G1 phase. Protein levels of PCNA, c-Myc, and cyclin D1 were downregulated in CML cells overexpressing miRNA-409-5p. The knockdown of miRNA-409-5p obtained the opposite trends. NUP43 was proved to be the target gene of miRNA-409-5p and negatively regulated by miRNA-409-5p. After overexpression of miRNA-409-5p, Imatinib treatment elevated proliferation inhibition and cell cycle arrest of K562 and KG-1a cells. CONCLUSIONS: MiRNA-409-5p is lowly expressed in child CML, which inhibits proliferative potential and cell cycle progression by upregulating NUP43 expression. In addition, miRNA-409-5p overexpression enhances Imatinib resistance in CML.
