目的分析糖尿病肾病氧化应激的研究现状、热点和发展趋势。方法检索中国知网、万方数据知识服务平台、维普网及Web of Science核心合集数据库中关于糖尿病肾病氧化应激研究的相关文章,检索时限为2015年9月1日至2025年9月1日;使用CiteSpa...目的分析糖尿病肾病氧化应激的研究现状、热点和发展趋势。方法检索中国知网、万方数据知识服务平台、维普网及Web of Science核心合集数据库中关于糖尿病肾病氧化应激研究的相关文章,检索时限为2015年9月1日至2025年9月1日;使用CiteSpace V6.4.R1软件绘制可视化图谱并对其进行分析。结果共纳入2040篇文献,其中中文文献1004篇,英文文献1036篇。中文文献发文量最多的作者为刘华、刘圣君;英文文献发文量最多的作者为Sun Lin。中文文献发文量最多的机构是山东中医药大学;英文文献发文量最多的机构是Central South University。中英文文献使用频次前3位的关键词均是糖尿病肾病、氧化应激、炎症。关键词聚类分析共得到16个中、英文聚类,关键词突现分析共得到25个中文突现词和25个英文突现词。结论糖尿病肾病氧化应激研究逐渐成熟,对其进行深入探讨有望为糖尿病肾病的诊治提供新策略。展开更多
面向大规模感知与智能应用场景,集中式计算在时延、带宽、能耗与隐私保护的多重约束下逐渐呈现边际效益递减,计算范式因此由单一的“万物上云”模式,逐步转向“就地计算与云边协同”的新形态。在此背景下,本文首先梳理集中化计算路径在...面向大规模感知与智能应用场景,集中式计算在时延、带宽、能耗与隐私保护的多重约束下逐渐呈现边际效益递减,计算范式因此由单一的“万物上云”模式,逐步转向“就地计算与云边协同”的新形态。在此背景下,本文首先梳理集中化计算路径在不同发展阶段所具备的优势及其适用边界,进而界定边缘计算在端-云之间所扮演的关键角色。在此基础上,进一步概述“传感云-边缘-端”协同计算框架,重点分析其中的核心机制,包括数据“必要即上行”的传输原则、面向服务级别协议(SLA)感知的任务分配与双层调度策略,以及边侧即时闭环执行与云侧全局策略治理之间的分工与协同关系。随着计算与智能能力向边缘侧持续下沉,本文进一步讨论边缘智能的发展方向,涵盖模型轻量化与本地学习机制、联邦学习与知识蒸馏的协同范式,以及面向边缘环境的智能运维(AIOps for Edge)与多级降级机制所支撑的自治能力。同时,强调构建以端到端闭环效率、系统韧性与可追责性为导向的综合评价体系的重要性。最后,结合教育等典型应用场景以及产业实践,论证就地计算与云边协同在保障确定性时延、提升系统整体韧性以及实现跨域一致性方面的现实有效性,并据此指出计算范式由边缘计算向云边智能协同演进的必然趋势与发展方向。展开更多
Pharmaceutical formulations derived from Aristolochiaceae herbs, which contain aristolochic acids(AAs), are widely used for medicinal purposes. However, exposure to these plants and isolated AAs is linked to renal tox...Pharmaceutical formulations derived from Aristolochiaceae herbs, which contain aristolochic acids(AAs), are widely used for medicinal purposes. However, exposure to these plants and isolated AAs is linked to renal toxicity, known as AA nephropathy(AAN). Currently, the mechanisms underlying AAN are not fully understood, leading to unsatisfactory treatment strategies. In this study, we explored the protective role of 84-B10(5-[[2-(4-methoxyphenoxy)-5-(trifluoromethyl) phenyl] amino]-5-oxo-3-phenylpentanoic acid) against AAN. RNA-seq analysis revealed that the mitochondrion and peroxisome were the most affected cellular components following 84-B10 treatment in AAN mice. Consistently, 84-B10 treatment preserved mitochondrial ultrastructure, restored mitochondrial respiration, enhanced the expression of key transporters(carnitine palmitoyltransferase 2) and enzymes(acylCoenzyme A dehydrogenase, medium chain) involved in mitochondrial fatty acid β-oxidation, and reduced mitochondrial ROS generation in both aristolochic acid I(AAI)-challenged mice kidneys and cultured proximal tubular epithelial cells. Additionally, 84-B10 treatment increased the expression of key transporters(ATP binding cassette subfamily D) and rate-limiting enzymes(acyl-CoA oxidase 1) involved in peroxisomal fatty acid β-oxidation and restored peroxisomal redox balance. Knocking down LONP1 expression diminished the protective effects of 84-B10 against AAN, suggesting LONP1-dependent protection. In conclusion, our study provides evidence that AAN is associated with significant disturbances in both mitochondrial and peroxisomal functions. The LONP1 activator 84-B10 demonstrates therapeutic potential against AAN, likely by maintaining homeostasis in both mitochondria and peroxisomes.展开更多
文摘目的分析糖尿病肾病氧化应激的研究现状、热点和发展趋势。方法检索中国知网、万方数据知识服务平台、维普网及Web of Science核心合集数据库中关于糖尿病肾病氧化应激研究的相关文章,检索时限为2015年9月1日至2025年9月1日;使用CiteSpace V6.4.R1软件绘制可视化图谱并对其进行分析。结果共纳入2040篇文献,其中中文文献1004篇,英文文献1036篇。中文文献发文量最多的作者为刘华、刘圣君;英文文献发文量最多的作者为Sun Lin。中文文献发文量最多的机构是山东中医药大学;英文文献发文量最多的机构是Central South University。中英文文献使用频次前3位的关键词均是糖尿病肾病、氧化应激、炎症。关键词聚类分析共得到16个中、英文聚类,关键词突现分析共得到25个中文突现词和25个英文突现词。结论糖尿病肾病氧化应激研究逐渐成熟,对其进行深入探讨有望为糖尿病肾病的诊治提供新策略。
文摘面向大规模感知与智能应用场景,集中式计算在时延、带宽、能耗与隐私保护的多重约束下逐渐呈现边际效益递减,计算范式因此由单一的“万物上云”模式,逐步转向“就地计算与云边协同”的新形态。在此背景下,本文首先梳理集中化计算路径在不同发展阶段所具备的优势及其适用边界,进而界定边缘计算在端-云之间所扮演的关键角色。在此基础上,进一步概述“传感云-边缘-端”协同计算框架,重点分析其中的核心机制,包括数据“必要即上行”的传输原则、面向服务级别协议(SLA)感知的任务分配与双层调度策略,以及边侧即时闭环执行与云侧全局策略治理之间的分工与协同关系。随着计算与智能能力向边缘侧持续下沉,本文进一步讨论边缘智能的发展方向,涵盖模型轻量化与本地学习机制、联邦学习与知识蒸馏的协同范式,以及面向边缘环境的智能运维(AIOps for Edge)与多级降级机制所支撑的自治能力。同时,强调构建以端到端闭环效率、系统韧性与可追责性为导向的综合评价体系的重要性。最后,结合教育等典型应用场景以及产业实践,论证就地计算与云边协同在保障确定性时延、提升系统整体韧性以及实现跨域一致性方面的现实有效性,并据此指出计算范式由边缘计算向云边智能协同演进的必然趋势与发展方向。
基金supported by the National Key Research and Development Program of China (Nos. 2019YFA0802-702-1, 2022YFC2705100, 2022YFC2705105)the National Natural Science Foundation of China (Nos. 82070701, 82090022, and 8183-0020)+4 种基金the Natural Science Foundation of Jiangsu Province (No. BK20231130)the Social Development Foundation of Jiangsu Province(No. BE2021607)the “333” Talent Plan of Jiangsu Province (No.333-2022001)the Medical Research Project from Jiangsu Health and Health Commission (No. Z2022071)the Outstanding Youth Project from Nanjing Health and Health Commission (No.JQX22010)。
文摘Pharmaceutical formulations derived from Aristolochiaceae herbs, which contain aristolochic acids(AAs), are widely used for medicinal purposes. However, exposure to these plants and isolated AAs is linked to renal toxicity, known as AA nephropathy(AAN). Currently, the mechanisms underlying AAN are not fully understood, leading to unsatisfactory treatment strategies. In this study, we explored the protective role of 84-B10(5-[[2-(4-methoxyphenoxy)-5-(trifluoromethyl) phenyl] amino]-5-oxo-3-phenylpentanoic acid) against AAN. RNA-seq analysis revealed that the mitochondrion and peroxisome were the most affected cellular components following 84-B10 treatment in AAN mice. Consistently, 84-B10 treatment preserved mitochondrial ultrastructure, restored mitochondrial respiration, enhanced the expression of key transporters(carnitine palmitoyltransferase 2) and enzymes(acylCoenzyme A dehydrogenase, medium chain) involved in mitochondrial fatty acid β-oxidation, and reduced mitochondrial ROS generation in both aristolochic acid I(AAI)-challenged mice kidneys and cultured proximal tubular epithelial cells. Additionally, 84-B10 treatment increased the expression of key transporters(ATP binding cassette subfamily D) and rate-limiting enzymes(acyl-CoA oxidase 1) involved in peroxisomal fatty acid β-oxidation and restored peroxisomal redox balance. Knocking down LONP1 expression diminished the protective effects of 84-B10 against AAN, suggesting LONP1-dependent protection. In conclusion, our study provides evidence that AAN is associated with significant disturbances in both mitochondrial and peroxisomal functions. The LONP1 activator 84-B10 demonstrates therapeutic potential against AAN, likely by maintaining homeostasis in both mitochondria and peroxisomes.
