RESUMO
With the rapid development of electronic and communication technology for military radars, the demand for microwave-absorbing materials in the low-frequency range with thin layers is growing. In this study, flexible Co3O4/CC (carbon cloth) composites derived from Co-MOFs (metal-organic frameworks) and CC are prepared using hydrothermal and thermal treatment processes. The flexible precursors of the Co-MOFs/CC samples are calcined with different calcination temperatures, for which the material structure, dielectric properties, and microwave absorption performance are changed. With the increases in calcination temperature, the minimum reflection loss of the corresponding Co3O4/CC composites gradually moves to the lower frequency with a thinner thickness. In addition, the Co3O4/CC composites with the 25 wt% filler loading ratio exhibit the minimum reflection loss (RL) of -46.59 dB at 6.24 GHz with a 4.2 mm thickness. When the thickness is 3.70 mm, the effective absorption bandwidth is 3.04 GHz from 5.84 to 8.88 GHz. This study not only proves that the Co3O4/CC composite is an outstanding microwave-absorbing material with better flexibility but also provides useful inspiration for research on wideband microwave absorption materials below 10 GHz.
RESUMO
BACKGROUND Preeclampsia (PE) is a serious complication of pregnancy with no effective therapy. This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia. MATERIAL AND METHODS Human umbilical vein endothelial cells (HUVECs) grown in conditioned medium from hypoxic JEG-3 cells were used to investigate the effects of EGCG on anti-angiogenic state, cell viability, and markers of endothelial dysfunction. To confirm that EGCG exerted its effects via HMGB1, we also examined the impact of EGCG on anti-angiogenic state, cell viability, and endothelial dysfunction following HMGB1 treatment in vitro. RESULTS EGCG inhibited HMGB1 expression in hypoxic trophoblast cells in a dose-dependent manner. In addition, EGCG relieved anti-angiogenic state and endothelial dysfunction in hypoxic trophoblast cells by downregulating HMGB1. Moreover, EGCG dose-dependently promoted cell proliferation by downregulating HMGB1. CONCLUSIONS Taken together, our data show the protective role of EGCG in preeclampsia and revealed EGCG-mediated effects on the production of anti-angiogenic factors, cell viability, and endothelial dysfunction through downregulating HMGB1. These observations suggest that EGCG is a novel therapeutic candidate for preeclampsia.