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Microwave dielectric properties of BaV2O6 ceramics with ultra-low sintering temperature
Cui Jin Pei,Guog Guang Yao,Zhao Yu Ren 한양대학교 세라믹연구소 2016 Journal of Ceramic Processing Research Vol.17 No.7
Microwave dielectric properties of BaV2O6 ceramics were investigated for the first time. The BaV2O6 ceramic was preparedby the solid-state ceramic route. The phase constitution, microstructure, and compatibility with aluminum electrode wereinvestigated using XRD, Raman spectra and SEM. The results confirmed that that pure phase BaV2O6 could be obtained inthe sintering temperature range of 525 oC-600 oC. With an increase in the sintering temperature, the dielectric constant (εr)and quality factor (Qxf) first increase and decrease thereafter, the temperature coefficient of resonant frequency (τf) changesslightly. The BaV2O6 ceramic sintered at 575 oC/4 hr exhibited good microwave dielectric properties of εr = 11.5, τf = 38 ppm/ oC and Qxf = 21 800 GHz (at 10.1 GHz). Moreover, the material had a chemical compatibility with aluminum powders, whichrepresented a promising candidate material for ULTCC applications.
Cui, Xiang‐,Dan,Lee, Mi‐,Jin,Kim, Jong‐,Hyun,Hao, Pei‐,Pei,Liu, Lan,Yu, Goung‐,Ran,Kim, Dae‐,Ghon Wiley Subscription Services, Inc., A Wiley Company 2013 Hepatology Vol.57 No.6
<P><B>Abstract</B></P><P>Eph receptor 2 (EphA2) overexpression is frequently accompanied by the loss of its cognate ligand during tumor progression. However, the molecular mechanism of this ligand‐independent promotion of tumor by EphA2 remains unclear in highly malignant and fatal cholangiocarcinoma (CC). We examined the biological role of EphA2 in tumor growth and metastasis in CC tissues and cells according to the degree of differentiation and we explored the downstream signaling pathways of EphA2. Growth factor‐mediated EphA2 overexpression itself leads to the activation of the mammalian target of rapamycin complex 1 (mTORC1) and extracellular signal‐regulated kinase (ERK) pathways through ligand‐independent activation of EphA2 (phosphorylation of S897). An <I>in vitro</I> soft agar assay and <I>in vivo</I> orthotopic or subcutaneous tumor model showed that EphA2 enhanced colony formation and accelerated tumor growth, and which seemed to be mainly associated with Akt (T308)/mTORC1 activation. Aberrant expression and activation of EphA2 was also associated with poorer differentiation and higher metastatic ability. Enhanced metastatic ability was also observed in an orthotopic tumor model or lung metastasis model, correlating with Pyk2(Y402)/c‐Src/ERK activation in addition to activation of the canonical Raf/MEK/ERK pathway. The mTORC1 and Raf/Pyk2 pathways also appeared to affect each other. These results suggest that growth factor‐mediated EphA2 might be involved in tumor growth and metastasis through activation of the mTORC1 and Raf/Pyk2 pathways. Therapeutic strategies that target EphA2 and its downstream effectors may be useful to control CC. (H<SMALL>EPATOLOGY</SMALL> 2013;57:2248–2260)</P>