通过在Cu-Mg合金中添加Cu-Ce合金制备Cu-0.4Mg-xCe(x=0,0.1,0.2,0.3)合金。采用扫描电子显微镜(scanning electron microscope,SEM)、透射电子显微镜(transmission electron microscope,TEM)、维氏硬度计、拉伸试验机和导电率测试仪等...通过在Cu-Mg合金中添加Cu-Ce合金制备Cu-0.4Mg-xCe(x=0,0.1,0.2,0.3)合金。采用扫描电子显微镜(scanning electron microscope,SEM)、透射电子显微镜(transmission electron microscope,TEM)、维氏硬度计、拉伸试验机和导电率测试仪等设备对Cu-0.4Mg-xCe合金进行表征。结果表明,Ce能明显降低Cu-0.4Mg-xCe合金的晶粒尺寸,净化Cu基体。Ce的质量分数超过0.2%后,会出现Ce的化合物,Cu-0.4Mg-xCe合金的塑性和导电率降低。Ce的质量分数为0.2%时,合金的综合性能最优。Cu-0.4Mg-0.2Ce合金退火处理后,其维氏硬度、抗拉强度、导电率、软化温度分别为213,548 MPa,75.6%IACS,430℃.展开更多
We described the synthesis and luminescence of Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ phosphor for light emitting diode （LED）. The crystal-linity, morphology, structure, and luminescence spectra were examined by X-ray diffr...We described the synthesis and luminescence of Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ phosphor for light emitting diode （LED）. The crystal-linity, morphology, structure, and luminescence spectra were examined by X-ray diffraction, field emission-scanning electron microscopy and photoluminescence spectroscopy. The results showed that Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ phase was a dominating phase with little impurity phase peaks of Y2O3 when the sintered temperature reached to 1400 oC. Field emission scanning electron microscopy （FE-SEM） images showed the particle size of the phosphor was about 3 μm. Meanwhile, the excitation and emission spectra indicated that the as-prepared phosphors could be effectively excited by blue （460 nm） light and the excitation spectrum showed a broad band extending from 400-500 nm, while emission spectrum showed a broad yellow band peaking at 534 nm. The decay curve at the emission peak consisted of fast and slow components. The Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ should be a promising yellow phosphor for near blue-based white-light-emitting diodes （LEDs）.展开更多
Hepatic ischemia-reperfusion injury(HIRI)has been considered as an inevitable process of liver transplantation.Hepatocyte ferroptosis is a key factor in HIRI development,yet precise mechanism and potential therapies a...Hepatic ischemia-reperfusion injury(HIRI)has been considered as an inevitable process of liver transplantation.Hepatocyte ferroptosis is a key factor in HIRI development,yet precise mechanism and potential therapies are still unclear.Here,we demonstrated a strong correlation between hepatocyte ferroptosis and the downregulation of poly(rC)-binding protein(PCBP2),which compromised the stability of antiporter system Xce(consisted of SL3A2/SLC7A11).Besides,inhibiting PCBP2 contributed to facilitating cofactor p300 to enhance the transcriptional activity of HIF1a,leading to the expression and secretion of HMGB1.Then,released HMGB1 from ferroptotic hepatocytes worsened M1 macrophage recruitment and immune response during HIRI.Additionally,acteoside(ACT)was shown to assist PCBP2 in stabilizing the mRNA stability of Slc3a2 and Slc7a11,as well as enhance the binding affinity of PCBP2esystem Xce.Beyond that,ACT also supported PCBP2 to limit HMGB1-induced M1 macrophage recruitment through imposing restrictions on p300 and HIF1a.Furthermore,specific knockdown of PCBP2 in hepatocytes directly interposed the therapeutic efficacy of ACT on HIRI mice.In conclusion,ACT alleviated hepatocyte ferroptosis and HIRI via promoting PCBP2 to maintain the stability of system Xce and limit HIF1a/p300-HMGB1 signaling.These findings highlight the therapeutic benefits of ACT in treating HIRI and offer insights into innovative therapeutic strategies.展开更多
文摘通过在Cu-Mg合金中添加Cu-Ce合金制备Cu-0.4Mg-xCe(x=0,0.1,0.2,0.3)合金。采用扫描电子显微镜(scanning electron microscope,SEM)、透射电子显微镜(transmission electron microscope,TEM)、维氏硬度计、拉伸试验机和导电率测试仪等设备对Cu-0.4Mg-xCe合金进行表征。结果表明,Ce能明显降低Cu-0.4Mg-xCe合金的晶粒尺寸,净化Cu基体。Ce的质量分数超过0.2%后,会出现Ce的化合物,Cu-0.4Mg-xCe合金的塑性和导电率降低。Ce的质量分数为0.2%时,合金的综合性能最优。Cu-0.4Mg-0.2Ce合金退火处理后,其维氏硬度、抗拉强度、导电率、软化温度分别为213,548 MPa,75.6%IACS,430℃.
基金Project supported by National Natural Science Foundation of China (51172165)Key Foundation of Zhejiang Province Natural Science Foundation(Z4110347)+2 种基金Zhejiang Province Key Technology Innovation Team (2009R50010)Wenzhou Municipal Science and Technology Bureau Key Program (G20090082)Huzhou Municipal Natural Science Foundation (2011YZ02)
文摘We described the synthesis and luminescence of Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ phosphor for light emitting diode （LED）. The crystal-linity, morphology, structure, and luminescence spectra were examined by X-ray diffraction, field emission-scanning electron microscopy and photoluminescence spectroscopy. The results showed that Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ phase was a dominating phase with little impurity phase peaks of Y2O3 when the sintered temperature reached to 1400 oC. Field emission scanning electron microscopy （FE-SEM） images showed the particle size of the phosphor was about 3 μm. Meanwhile, the excitation and emission spectra indicated that the as-prepared phosphors could be effectively excited by blue （460 nm） light and the excitation spectrum showed a broad band extending from 400-500 nm, while emission spectrum showed a broad yellow band peaking at 534 nm. The decay curve at the emission peak consisted of fast and slow components. The Ca1.5Y1.5Al3.5Si1.5O12：Ce^3＋ should be a promising yellow phosphor for near blue-based white-light-emitting diodes （LEDs）.
基金supported by the National Natural Science Foundation of China(Grant No.82274186 to Xiaojiaoyang Li)National Key Research and Development Program on Modernization of Traditional Chinese Medicine(No.2022YFC3502100 to Xiaojiaoyang Li,China)+2 种基金National High-Level Talents Special Support Program(China)to Xiaojiaoyang LiFundamental Research Funds for the Central Universities(Grant No.2023-JYBJBZD-046 to Xiaojiaoyang Li,China)High-level traditional Chinese medicine key subjects construction project of National Administration of Traditional Chinese Medicine-Beijing University of Chinese Medicine,Chinese Medicine Epidemic Disease(Grant No.zyyzdxk-2023264,China).
文摘Hepatic ischemia-reperfusion injury(HIRI)has been considered as an inevitable process of liver transplantation.Hepatocyte ferroptosis is a key factor in HIRI development,yet precise mechanism and potential therapies are still unclear.Here,we demonstrated a strong correlation between hepatocyte ferroptosis and the downregulation of poly(rC)-binding protein(PCBP2),which compromised the stability of antiporter system Xce(consisted of SL3A2/SLC7A11).Besides,inhibiting PCBP2 contributed to facilitating cofactor p300 to enhance the transcriptional activity of HIF1a,leading to the expression and secretion of HMGB1.Then,released HMGB1 from ferroptotic hepatocytes worsened M1 macrophage recruitment and immune response during HIRI.Additionally,acteoside(ACT)was shown to assist PCBP2 in stabilizing the mRNA stability of Slc3a2 and Slc7a11,as well as enhance the binding affinity of PCBP2esystem Xce.Beyond that,ACT also supported PCBP2 to limit HMGB1-induced M1 macrophage recruitment through imposing restrictions on p300 and HIF1a.Furthermore,specific knockdown of PCBP2 in hepatocytes directly interposed the therapeutic efficacy of ACT on HIRI mice.In conclusion,ACT alleviated hepatocyte ferroptosis and HIRI via promoting PCBP2 to maintain the stability of system Xce and limit HIF1a/p300-HMGB1 signaling.These findings highlight the therapeutic benefits of ACT in treating HIRI and offer insights into innovative therapeutic strategies.
