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High Strength-Thermal Conductivity Mg–Ga–Ca–Ce Sheet by Hot-Extrusion and Rolling
Mouxin Wu,Xueqi Jiang,Jihua Chen,Hongge Yan,Weijun Xia,Bin Su,Yifu Deng 대한금속·재료학회 2024 METALS AND MATERIALS International Vol.30 No.1
The thermal conductivity of magnesium alloys is increasingly required for fast heat dissipation in the automotive and electronicfields. However, the methods for mechanical property improvement such as grain refinement and alloying tend to deterioratetheir thermal conductivity. In this work, a novel low-alloy Mg–2Ga–0.6Ca–0.6Ce alloy exhibits a surprisingly goodcombination of high strength and high thermal conductivity compared with the other samples. The wrought alloys are of smallgrain sizes (< 2 μm), have high yield strength (> 272 MPa) and exhibit excellent thermal conductivity (> 143 W·m−1·K−1). The as-extruded alloy exhibits excellent yield strength (272 MPa) and high thermal conductivity (144.6 W·m−1·K−1) atroom temperature. After 30% rolling, the yield strength is further increased to 283 MPa, and the thermal conductivity isslightly reduced to 143.2 W·m−1·K−1. The effects of Ca and Ce addition on mechanical properties and thermal conductivityare analyzed from dislocation density, dynamic recrystallization fraction (fDRX), average grain size (dDRX) and texturecharacteristics. The higher yield strength can be attributed to the combination of grain boundary strengthening, dislocationstrengthening and second phase strengthening. Moreover, the addition of Ca and Ce can obviously reduce solute Ga atomsin α-Mg, which is the key to high thermal conductivity. Therefore, adding two alloying elements, Ca and Ce, significantlyimproves both tensile properties and thermal conductivity.
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Hai-Yan Zhang,Zhen-Xian Du,Bao-Qin Liu,Yan-Yan Gao,Xin Meng,Yifu Guan,Wei-Wei Deng,Hua-Qin Wang 생화학분자생물학회 2009 Experimental and molecular medicine Vol.41 No.5
TNF-related apoptosis-inducing ligand (TRAIL) has been proposed as a promising cancer therapy that preferentially induces apoptosis in cancer cells, but not most normal tissues. However, many cancers are resistant to TRAIL by mechanisms that are poorly understood. In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Of note, tunicamycin did not sensitize the differentiated thyroid epithelial cells to TRAIL-induced apoptosis. Thus, combined treatment with tunicamycin and TRAIL may offer an attractive strategy for safely treating resistant thyroid cancers. TNF-related apoptosis-inducing ligand (TRAIL) has been proposed as a promising cancer therapy that preferentially induces apoptosis in cancer cells, but not most normal tissues. However, many cancers are resistant to TRAIL by mechanisms that are poorly understood. In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin. The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression. Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma. Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin. Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin. Of note, tunicamycin did not sensitize the differentiated thyroid epithelial cells to TRAIL-induced apoptosis. Thus, combined treatment with tunicamycin and TRAIL may offer an attractive strategy for safely treating resistant thyroid cancers.
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