多孔硅基负极材料因其在硅脱嵌锂过程中能缓解体积膨胀的优势,在电池技术中展现出巨大的应用潜力。但在长期循环使用时,电极在脱嵌锂过程中不可避免的出现容量下降和结构被破坏等问题。随着研究的深入和技术的进步,保证多孔型电极在循...多孔硅基负极材料因其在硅脱嵌锂过程中能缓解体积膨胀的优势,在电池技术中展现出巨大的应用潜力。但在长期循环使用时,电极在脱嵌锂过程中不可避免的出现容量下降和结构被破坏等问题。随着研究的深入和技术的进步,保证多孔型电极在循环过程不发生开裂,并具有更高的比容量和倍率性能,成为了多孔型硅基负极材料的新突破口。本实验分别以葡萄糖和蔗糖为碳的前驱体进行分阶段碳化,使用预氧化的聚乙烯吡咯烷酮(PVP)作为骨架,运用微电子打印技术构建了新型Si@PVP/葡萄糖和Si@PVP/蔗糖多孔碳骨架结构的Si@C复合电极。分析结果表明:Si@PVP/葡萄糖结构电极循环后电极表面开裂明显更小。以0.1 A·g^(–1)的电流密度放电,Si@PVP/葡萄糖结构电极首圈比容量为1655 m A·h·g^(–1),100圈后比容量为1095 m A·h·g^(–1),可逆容量保持为97.4%;Si@PVP/蔗糖结构电极首圈比容量为1455 m A·h·g^(–1),100圈后比容量为970 m A·h·g^(–1),可逆容量保持为91%。展开更多
Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to impr...Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to improve migration and survival of bone marrow–derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest,but the specific mechanisms by which hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown.To this end,we established an in vitro co-culture model of bone marrow–derived mesenchymal stem cells and oxygen–glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis,possibly through inhibition of the MAPK and nuclear factor κB pathways.Subsequently,we transplanted hypoxia-preconditioned bone marrow–derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia.The results showed that hypoxia-preconditioned bone marrow–derived mesenchymal stem cells significantly reduced cardiac arrest–induced neuronal pyroptosis,oxidative stress,and mitochondrial damage,whereas knockdown of the liver isoform of phosphofructokinase in bone marrow–derived mesenchymal stem cells inhibited these effects.To conclude,hypoxia-preconditioned bone marrow–derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest,and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.展开更多
文摘多孔硅基负极材料因其在硅脱嵌锂过程中能缓解体积膨胀的优势,在电池技术中展现出巨大的应用潜力。但在长期循环使用时,电极在脱嵌锂过程中不可避免的出现容量下降和结构被破坏等问题。随着研究的深入和技术的进步,保证多孔型电极在循环过程不发生开裂,并具有更高的比容量和倍率性能,成为了多孔型硅基负极材料的新突破口。本实验分别以葡萄糖和蔗糖为碳的前驱体进行分阶段碳化,使用预氧化的聚乙烯吡咯烷酮(PVP)作为骨架,运用微电子打印技术构建了新型Si@PVP/葡萄糖和Si@PVP/蔗糖多孔碳骨架结构的Si@C复合电极。分析结果表明:Si@PVP/葡萄糖结构电极循环后电极表面开裂明显更小。以0.1 A·g^(–1)的电流密度放电,Si@PVP/葡萄糖结构电极首圈比容量为1655 m A·h·g^(–1),100圈后比容量为1095 m A·h·g^(–1),可逆容量保持为97.4%;Si@PVP/蔗糖结构电极首圈比容量为1455 m A·h·g^(–1),100圈后比容量为970 m A·h·g^(–1),可逆容量保持为91%。
基金supported by the Natural Science Fund of Fujian Province,No.2020J011058(to JK)the Project of Fujian Provincial Hospital for High-level Hospital Construction,No.2020HSJJ12(to JK)+1 种基金the Fujian Provincial Finance Department Special Fund,No.(2021)848(to FC)the Fujian Provincial Major Scientific and Technological Special Projects on Health,No.2022ZD01008(to FC).
文摘Cardiac arrest can lead to severe neurological impairment as a result of inflammation,mitochondrial dysfunction,and post-cardiopulmonary resuscitation neurological damage.Hypoxic preconditioning has been shown to improve migration and survival of bone marrow–derived mesenchymal stem cells and reduce pyroptosis after cardiac arrest,but the specific mechanisms by which hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect against brain injury after cardiac arrest are unknown.To this end,we established an in vitro co-culture model of bone marrow–derived mesenchymal stem cells and oxygen–glucose deprived primary neurons and found that hypoxic preconditioning enhanced the protective effect of bone marrow stromal stem cells against neuronal pyroptosis,possibly through inhibition of the MAPK and nuclear factor κB pathways.Subsequently,we transplanted hypoxia-preconditioned bone marrow–derived mesenchymal stem cells into the lateral ventricle after the return of spontaneous circulation in an 8-minute cardiac arrest rat model induced by asphyxia.The results showed that hypoxia-preconditioned bone marrow–derived mesenchymal stem cells significantly reduced cardiac arrest–induced neuronal pyroptosis,oxidative stress,and mitochondrial damage,whereas knockdown of the liver isoform of phosphofructokinase in bone marrow–derived mesenchymal stem cells inhibited these effects.To conclude,hypoxia-preconditioned bone marrow–derived mesenchymal stem cells offer a promising therapeutic approach for neuronal injury following cardiac arrest,and their beneficial effects are potentially associated with increased expression of the liver isoform of phosphofructokinase following hypoxic preconditioning.
