Albira SI小动物单光子发射断层显像-X线计算机体层成像仪(SPECT-CT)是单光子放射性药物临床前研究的先进影像工具,其质量控制及检测性能是图像质量和实验数据可靠性的基本保障。为评价Albira SI SPECT-CT设备应用的真实性、可靠性,采...Albira SI小动物单光子发射断层显像-X线计算机体层成像仪(SPECT-CT)是单光子放射性药物临床前研究的先进影像工具,其质量控制及检测性能是图像质量和实验数据可靠性的基本保障。为评价Albira SI SPECT-CT设备应用的真实性、可靠性,采用临床常用单光子核素^(99m)Tc对Albira SI小动物SPECT-CT进行季度性质量控制,同时进行测量结果的线性、稳定性、偏差的检测,并初步尝试小动物骨代谢扫描。结果表明,该设备与放射性活度之间线性关系良好,稳定性强,与常用活度测量设备测量结果差异较小。Albira SI小动物SPECT-CT能够准确反映单光子核素^(99m)Tc的放射性活度分布,小鼠骨代谢显像效果好,适用于临床前放射性药物研究。本研究中建立的系统研究SPECT-CT性能的方法可为类似设备的操作提供方法学依据。展开更多
文章以国内某部高性能训练机CESSNA525 M2飞机为研究对象,通过对该型飞机发动机关键部件—燃油控制组件FCU(Fuel Control Unin)典型故障进行统计分析,从系统结构和原理分析故障原因、排故逻辑并得到最终处理措施和建议,可对相同或类似...文章以国内某部高性能训练机CESSNA525 M2飞机为研究对象,通过对该型飞机发动机关键部件—燃油控制组件FCU(Fuel Control Unin)典型故障进行统计分析,从系统结构和原理分析故障原因、排故逻辑并得到最终处理措施和建议,可对相同或类似机型的故障排除提供借鉴和参考。展开更多
Background Liver ischemia/reperfusion(I/R)injury is usually caused by hepatic inflow occlusion during liver surgery,and is frequently observed during war wounds and trauma.Hepatocyte ferroptosis plays a critical role ...Background Liver ischemia/reperfusion(I/R)injury is usually caused by hepatic inflow occlusion during liver surgery,and is frequently observed during war wounds and trauma.Hepatocyte ferroptosis plays a critical role in liver I/R injury,however,it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase(DDX/DHX)family.Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis.Hepatocyte-specific Dhx58 knockout mice were constructed,and a partial liver I/R operation was performed.Single-cell RNA sequencing(scRNA-seq)in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−.The mRNAs and proteins associated with DExH-box helicase 58(DHX58)were screened using RNA immunoprecipitation-sequencing(RIP-seq)and IP-mass spectrometry(IP-MS).Results Excessive production of reactive oxygen species(ROS)decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis,while treatment using IFN-αincreased DHX58 expression and prevented ferroptosis during liver I/R injury.Mechanistically,DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4(GPX4),a central ferroptosis suppressor,and recruits the m6A reader YT521-B homology domain containing 2(YTHDC2)to promote the translation of Gpx4 mRNA in an m6A-dependent manner,thus enhancing GPX4 protein levels and preventing hepatic ferroptosis.Conclusions This study provides mechanistic evidence that IFN-αstimulates DHX58 to promote the translation of m6A-modified Gpx4 mRNA,suggesting the potential clinical application of IFN-αin the prevention of hepatic ferroptosis during liver I/R injury.展开更多
基金National Key Research and Development Program of China(2023YFC2505900)National Natural Science Foundation of China(92269204,82171755,92369106,82171749,82171811,82073184)+1 种基金Military Outstanding Youth Program(2020QN06119,01-SWK JYCJJ07,23SWAQ53)Program of Leading Talents in Shanghai,and Shanghai Shuguang Program(20SG39)。
文摘Background Liver ischemia/reperfusion(I/R)injury is usually caused by hepatic inflow occlusion during liver surgery,and is frequently observed during war wounds and trauma.Hepatocyte ferroptosis plays a critical role in liver I/R injury,however,it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase(DDX/DHX)family.Methods The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis.Hepatocyte-specific Dhx58 knockout mice were constructed,and a partial liver I/R operation was performed.Single-cell RNA sequencing(scRNA-seq)in the liver post I/R suggested enhanced ferroptosis by Dhx58hep−/−.The mRNAs and proteins associated with DExH-box helicase 58(DHX58)were screened using RNA immunoprecipitation-sequencing(RIP-seq)and IP-mass spectrometry(IP-MS).Results Excessive production of reactive oxygen species(ROS)decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis,while treatment using IFN-αincreased DHX58 expression and prevented ferroptosis during liver I/R injury.Mechanistically,DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4(GPX4),a central ferroptosis suppressor,and recruits the m6A reader YT521-B homology domain containing 2(YTHDC2)to promote the translation of Gpx4 mRNA in an m6A-dependent manner,thus enhancing GPX4 protein levels and preventing hepatic ferroptosis.Conclusions This study provides mechanistic evidence that IFN-αstimulates DHX58 to promote the translation of m6A-modified Gpx4 mRNA,suggesting the potential clinical application of IFN-αin the prevention of hepatic ferroptosis during liver I/R injury.
