No abstract

Stacking faults (SFs) within silicon carbide (SiC) are desired because these faults can enhance the electromagnetic (EM) absorption properties of the material. However, most reported SiC materials are prepared using expensive precursors possessing limited SFs. Herein, we report a facile and economical method to fabricate SiC sheets with a record-high SF density of over fourfold enhancement compared with previously reported SiC materials. The use of paper as a carbon source resulted in a 19-fold decrease in fabrication cost. The microstructure, defect structure, and EM wave absorption performance of the synthesized SiC sheets were investigated in detail. Enhancement of the SF content of the SiC sheets enabled significant interfacial dipole polarization, thereby imparting the sheets with superior EM wave absorption. SiC sheets with the maximum SF content obtained in this work revealed a minimum reflection loss of −22 dB and an effective EM wave absorption band (R L < −10 dB) covering the frequency range of 12.8−18 GHz at a thickness of only 2.2 mm. Our research shows that paper-derived SiC can be used as an efficient EM wave absorption material and provides guidelines for synthesizing highly defected SiC sheets.

Hemangiomas (HAs) are benign neoplasms of the vasculature. MicroRNA-4458 (miR-4458) has been reported to function as a tumor suppressor in multiple malignancies, but its biological function in HAs remains unknown. In the present study, the potential role of miR-4458 in HA-derived endothelial cells (HDECs) was investigated. Firstly, reverse-transcription-quantitative PCR analysis was used to confirm the expression of miR-4458 in HDECs following transfection with miR-4458 mimics or inhibitor. Subsequently, MTT and EdU assays were performed and subsequently determined that miR-4458 overexpression significantly inhibited proliferation, and knockdown promoted cell proliferation in HDECs. Flow cytometry analysis revealed that miR-4458 overexpression induced cell cycle arrest, whereas knockdown reversed G0/G1 phase arrest and apoptosis. Furthermore, insulin-like growth factor 1 receptor (IGF1R) was identified as a target of miR-4458. IGF1R knockdown enhanced the effects of miR-4458 on cell proliferation, cell cycle G0/G1 phase arrest and apoptosis in HDECs. Taken together, the results revealed that miR-4458 targeting of IGF1R may serve as a novel therapeutic strategy for treating patients with HAs.

No abstract

No abstract