In this study,ferric nitrate modified carbon nanotube composites (FCNT) were prepared by isovolumetric impregnation using carbon nanotubes (CNTs) as the carrier and ferric nitrates the active agent.The batch experimen...In this study,ferric nitrate modified carbon nanotube composites (FCNT) were prepared by isovolumetric impregnation using carbon nanotubes (CNTs) as the carrier and ferric nitrates the active agent.The batch experiments showed that FCNT could effectively oxidize As(III) to As(V) and react with it to form stable iron arsenate precipitates.When the dosage of FCNT was 0.1 g·L^(–1),pH value was 5–6,reaction temperature was 35℃ and reaction time was 2 h,the best arsenic removal effect could be achieved,and the removal rate of As(V) could reach 99.1%,which was always higher than 90%under acidic conditions.The adsorption results of FCNT were found to be consistent with Langmuir adsorption by static adsorption isotherm fitting,and the maximum adsorption capacity reached 118.3 mg·g^(-1).The material phase and property analysis by scanning electron microscopy,Brunauer–Emmett–Teller,Fourier transform infrared spectoscopy,X-ray photoelectron spectroscopy and other characterization methods,as well as adsorption isotherm modeling,were used to explore the adsorption mechanism of FCNT on arsenic.It was found that FCNT has microporous structure and nanostructure,and iron nanoparticles are loosely distributed on CNTs,which makes the material have good oxidation,adsorption and magnetic separation properties.Arsenic migrates on the surface of FCNT composites is mainly removed by forming insoluble compounds and co-precipitation.All the results show that FCNT treats arsenic at low cost with high adsorption efficiency,and the results also provide the experimental data basis and theoretical basis for arsenic contamination in groundwater.展开更多
目的:探讨罗汉果皂苷V(MV)对铁死亡诱导剂RAS选择性致死分子3(RSL3)诱导的人神经母细胞瘤SH-SY5Y细胞铁死亡的抑制作用及可能机制。方法:用RSL3诱导SH-SY5Y细胞建立铁死亡模型。MTT法检测细胞活力;倒置显微镜观察细胞形态;亚铁离子荧光...目的:探讨罗汉果皂苷V(MV)对铁死亡诱导剂RAS选择性致死分子3(RSL3)诱导的人神经母细胞瘤SH-SY5Y细胞铁死亡的抑制作用及可能机制。方法:用RSL3诱导SH-SY5Y细胞建立铁死亡模型。MTT法检测细胞活力;倒置显微镜观察细胞形态;亚铁离子荧光探针FerroFarRed检测细胞内亚铁离子含量;线粒体红色荧光探针MitoTracker Red CMXRos检测线粒体膜电位(MMP);超氧化物阴离子荧光探针二氢乙啶和线粒体超氧化物红色荧光探针MitoSoX Red分别检测细胞内和线粒体内活性氧(ROS)。微板法检测细胞谷胱甘肽(GSH)和丙二醛(MDA)水平。Western blot检测脂酰辅酶A合成酶长链家族成员4(ACSL4)、环加氧酶2(COX-2、)谷胱甘肽过氧化物酶4(GPX4)和溶质载体家族7成员11(SLC7A11)蛋白表达水平。分子对接技术预测MV与ACSL4、COX-2、GPX4和SLC7A11的靶向关系。结果:与control组相比,RSL3组SH-SY5Y细胞活力显著降低(P<0.01),细胞内亚铁离子含量、细胞内和线粒体内ROS水平及MDA水平显著升高(P<0.05或P<0.01),MMP和GSH水平显著降低(P<0.01),ACSL4和COX-2蛋白表达水平显著升高,而GPX4和SLC7A11蛋白表达水平显著降低(P<0.01),提示成功建立了细胞铁死亡模型。MV处理使细胞活力显著升高(P<0.05),细胞内亚铁离子含量、细胞内和线粒体内ROS水平及MDA水平显著降低(P<0.01),MMP和GSH水平显著升高(P<0.05或P<0.01);ACSL4和COX-2蛋白水平显著降低,而GPX4和SLC7A11蛋白水平显著升高(P<0.05或P<0.01)。分子对接结果显示,MV与铁死亡核心蛋白ACSL4、COX-2、GPX4和SLC7A11存在结合位点。结论:MV可抑制RSL3诱导的SH-SY5Y细胞铁死亡的发生,其机制可能与激活SLC7A11/GPX4和抑制ACSL4/COX-2有关。展开更多
RISC-V指令集架构(Instruction Set Architecture,ISA)作为一种新兴的精简ISA,因免费、开源、自由等特点而得到快速发展.由于国内外对RISC-V的研究主要集中在硬件开发,软件生态相较于成熟ISA还很薄弱,实现一套RISC-V指令集高性能基础数...RISC-V指令集架构(Instruction Set Architecture,ISA)作为一种新兴的精简ISA,因免费、开源、自由等特点而得到快速发展.由于国内外对RISC-V的研究主要集中在硬件开发,软件生态相较于成熟ISA还很薄弱,实现一套RISC-V指令集高性能基础数学库可以进一步丰富RISC-V软件生态.本文基于自动化移植技术实现申威数学库到RISC-V的移植,为RISC-V指令架构提供首个使用向量指令优化的基础数学库系统.本文提出向量寄存器自动分支查表法与路径标记插入法,重点解决不同架构间寄存器映射过程中的寄存器复用问题,实现寄存器正确高效映射,并依据不同指令等价转换策略自动化移植数学函数69个.测试结果表明,RISC-V基础数学库函数可实现正确计算,最大误差为1.90ULP,函数性能平均为157.03节拍.展开更多
基金supported by the National Natural Science Foundation of China (NSFC) on the micro behavior of heavy metal migration and transformation in lead–zinc tailings and its nano micro scale high targeted stabilization mechanism (51968033)the National Key Research and Development Program “long-term solidification of heavy metal tailings pollution/environmental functional materials, technologies and equipment of stabilizers” (2018YFC1801702)。
文摘In this study,ferric nitrate modified carbon nanotube composites (FCNT) were prepared by isovolumetric impregnation using carbon nanotubes (CNTs) as the carrier and ferric nitrates the active agent.The batch experiments showed that FCNT could effectively oxidize As(III) to As(V) and react with it to form stable iron arsenate precipitates.When the dosage of FCNT was 0.1 g·L^(–1),pH value was 5–6,reaction temperature was 35℃ and reaction time was 2 h,the best arsenic removal effect could be achieved,and the removal rate of As(V) could reach 99.1%,which was always higher than 90%under acidic conditions.The adsorption results of FCNT were found to be consistent with Langmuir adsorption by static adsorption isotherm fitting,and the maximum adsorption capacity reached 118.3 mg·g^(-1).The material phase and property analysis by scanning electron microscopy,Brunauer–Emmett–Teller,Fourier transform infrared spectoscopy,X-ray photoelectron spectroscopy and other characterization methods,as well as adsorption isotherm modeling,were used to explore the adsorption mechanism of FCNT on arsenic.It was found that FCNT has microporous structure and nanostructure,and iron nanoparticles are loosely distributed on CNTs,which makes the material have good oxidation,adsorption and magnetic separation properties.Arsenic migrates on the surface of FCNT composites is mainly removed by forming insoluble compounds and co-precipitation.All the results show that FCNT treats arsenic at low cost with high adsorption efficiency,and the results also provide the experimental data basis and theoretical basis for arsenic contamination in groundwater.
文摘目的:探讨罗汉果皂苷V(MV)对铁死亡诱导剂RAS选择性致死分子3(RSL3)诱导的人神经母细胞瘤SH-SY5Y细胞铁死亡的抑制作用及可能机制。方法:用RSL3诱导SH-SY5Y细胞建立铁死亡模型。MTT法检测细胞活力;倒置显微镜观察细胞形态;亚铁离子荧光探针FerroFarRed检测细胞内亚铁离子含量;线粒体红色荧光探针MitoTracker Red CMXRos检测线粒体膜电位(MMP);超氧化物阴离子荧光探针二氢乙啶和线粒体超氧化物红色荧光探针MitoSoX Red分别检测细胞内和线粒体内活性氧(ROS)。微板法检测细胞谷胱甘肽(GSH)和丙二醛(MDA)水平。Western blot检测脂酰辅酶A合成酶长链家族成员4(ACSL4)、环加氧酶2(COX-2、)谷胱甘肽过氧化物酶4(GPX4)和溶质载体家族7成员11(SLC7A11)蛋白表达水平。分子对接技术预测MV与ACSL4、COX-2、GPX4和SLC7A11的靶向关系。结果:与control组相比,RSL3组SH-SY5Y细胞活力显著降低(P<0.01),细胞内亚铁离子含量、细胞内和线粒体内ROS水平及MDA水平显著升高(P<0.05或P<0.01),MMP和GSH水平显著降低(P<0.01),ACSL4和COX-2蛋白表达水平显著升高,而GPX4和SLC7A11蛋白表达水平显著降低(P<0.01),提示成功建立了细胞铁死亡模型。MV处理使细胞活力显著升高(P<0.05),细胞内亚铁离子含量、细胞内和线粒体内ROS水平及MDA水平显著降低(P<0.01),MMP和GSH水平显著升高(P<0.05或P<0.01);ACSL4和COX-2蛋白水平显著降低,而GPX4和SLC7A11蛋白水平显著升高(P<0.05或P<0.01)。分子对接结果显示,MV与铁死亡核心蛋白ACSL4、COX-2、GPX4和SLC7A11存在结合位点。结论:MV可抑制RSL3诱导的SH-SY5Y细胞铁死亡的发生,其机制可能与激活SLC7A11/GPX4和抑制ACSL4/COX-2有关。
文摘RISC-V指令集架构(Instruction Set Architecture,ISA)作为一种新兴的精简ISA,因免费、开源、自由等特点而得到快速发展.由于国内外对RISC-V的研究主要集中在硬件开发,软件生态相较于成熟ISA还很薄弱,实现一套RISC-V指令集高性能基础数学库可以进一步丰富RISC-V软件生态.本文基于自动化移植技术实现申威数学库到RISC-V的移植,为RISC-V指令架构提供首个使用向量指令优化的基础数学库系统.本文提出向量寄存器自动分支查表法与路径标记插入法,重点解决不同架构间寄存器映射过程中的寄存器复用问题,实现寄存器正确高效映射,并依据不同指令等价转换策略自动化移植数学函数69个.测试结果表明,RISC-V基础数学库函数可实现正确计算,最大误差为1.90ULP,函数性能平均为157.03节拍.