RESUMO
SiO2 and TiO2, as conventional dielectric shells of ferromagnetic/dielectric composite particles, can protect ferromagnetic particles from aggregation and oxidation, but contribute little to electromagnetic loss. In this work, we designed nano-assembled CoFe-CoFe2O4@C composite particles, in which ferrites with high permeability were dielectric elements and carbon was introduced as protective layers, aiming for high-efficiency microwave absorption. These assembled particles with different CoFe contents were prepared through solvothermal methods and subsequent hydrogen-thermal reduction. CoFe nanoparticles were dispersed on a CoFe2O4 matrix via an in situ reduction transformation from CoFe2O4 to CoFe. The microstructure evolution of composite particles and corresponding electromagnetic properties tailoring were investigated. The content and size of CoFe as well as the porosity of composite particles increase gradually as the annealing temperature increases. A maximum reflection loss (RL max) of -71.73 dB is observed at 4.78 GHz in 3.4 mm thick coating using particles annealed at 500 °C as fillers. The coating presents double-band absorbing characteristics, as broad effective absorption bandwidth with RL > 5 (ERL 5) and high RL max are observed in both S-C and X-Ku bands. The tunability as well as the assembled characteristic of the electromagnetic property that endued from the composite structure contributes to the excellent electromagnetic wave absorbing performances.
RESUMO
The poor dispersity and oxidation resistance of ferromagnetic metal nanoparticles can induce serious deterioration in electromagnetic properties, which then significantly limits the application of this catalog of materials. In this work, sandwich-like Co/rGo/Co composites were in situ constructed, in which monodispersed Co nanoparticles with diameters of 20-60â¯nm were densely dispersed on both sides of rGO nanosheets. A connecting network between the densely-packed Co nanoparticles can be formed, where Co nanoparticles are abutted or bridged to each other through a neck of Co. These sandwich-like composites evidently contributed to improved permittivity and permeability, which was ascribed to the enhanced interface polarization and exchange coupling in this Co nanoparticles densely-packed structure. A maximum reflection loss (RLmax) of -61â¯dB (at 11.1â¯GHz) together with an efficient absorbing bandwidth (RLâ¯<â¯-10â¯dB, ERL10) of 4â¯GHz was obtained at a very thin matching thickness of 2â¯mm. The coating also presented a potential double-band absorbing performance, at SC band and Ku band, respectively. The excellent electromagnetic absorbing performances were ascribed to the synergistic effect of multiple dielectric losses and ferromagnetic losses. The sandwich-like Co/rGO/Co composites proposed an alternative way for broadband and high-efficiency absorption and provided a typical structure to analyze the loss mechanisms.
RESUMO
Oral submucous fibrosis (OSF) induced by chewing of the areca nut has been considered to be a precancerous lesion with a high probability of developing oral squamous cell carcinoma. Tanshinone (TSN) is the main component extracted from Salvia miltiorrhiza, a traditional Chinese medicine, which was found to have diverse pharmacological effects, such as anti-inflammatory and antitumor. In the current study, we aimed to identify the inhibitory effects and the underlying mechanism of TSN on OSF progress. We found that treatment with TSN inhibited the arecoline-mediated proliferation of primary human oral mucosal fibroblasts and reversed the promotive effects of arecoline on the EMT process. By RNA deep sequencing, we screened two possible targets for TSN: LSD1 and p53. We confirmed that p53 is much lower in OSF than in normal mucous tissues. In addition, p53 and its downstream molecules were decreased by arecoline treatment in oral mucosal fibroblasts, which was reversed by treatment with TSN in a dose-dependent manner. Our results also revealed that arecoline stimulation resulted in hypermethylation of the promoter of TP53 and subsequent downregulation of p53 levels, which was reversed by TSN. Furthermore, we identified that LSD1 could epigenetically activate TP53 by recruiting H3K27me1 and H3K4m2 to its promoter. Our findings provide new insights into the mechanism by which TSN influences arecoline-induced OSF and rationale for the development of clinical intervention strategies for OSF and even oral squamous cell carcinoma.