Using the mesoscale eddy trajectory atlas product derived from satellite altimeter data from 1993 to 2016,this study analyzes statistical characteristics and seasonal variability of mesoscale eddies in the Banda Sea o...Using the mesoscale eddy trajectory atlas product derived from satellite altimeter data from 1993 to 2016,this study analyzes statistical characteristics and seasonal variability of mesoscale eddies in the Banda Sea of the Indonesian seas.The results show that there were 147 mesoscale eddies that occurred in the Banda Sea,of which 137 eddies were locally generated and 10 originated from outside.The total numbers of cyclonic eddies(CEs,clockwise)and anticyclonic eddies(AEs,anticlockwise)are 76 and 71,respectively.Seasonally,the number of CEs(AEs)is twice larger than the number of AEs(CEs)in winter(summer).In winter,CEs are distributed in the southern and AEs in the northern basins,respectively,but the opposite thing occurs in summer,i.e.,the polarities of mesoscale eddies observed at the same location reverse seasonally.The mechanisms of polarity distribution reversal(PDR)of mesoscale eddies are examined with reanalysis data of ocean currents and winds.The results indicate that the basin-scale vorticity,wind stress curl,and the meridional shear of zonal current reverse seasonally,which are favorable to the PDR of mesoscale eddies.The possible generation mechanisms of mesoscale eddies include direct wind forcing,barotropic and baroclinic instabilities,of which the direct wind forcing should play the dominant role.展开更多
目的:探究多聚胞嘧啶结合蛋白2[poly(C)-binding protein 2,PCBP2]如何通过调节铁死亡参与大别班达病毒(Dabie Banda virus,DBV)感染后的致病过程及其作用机制。方法:以人单核细胞系THP-1为模型,采用qRT-PCR和Western blot技术检测DBV...目的:探究多聚胞嘧啶结合蛋白2[poly(C)-binding protein 2,PCBP2]如何通过调节铁死亡参与大别班达病毒(Dabie Banda virus,DBV)感染后的致病过程及其作用机制。方法:以人单核细胞系THP-1为模型,采用qRT-PCR和Western blot技术检测DBV感染的THP-1细胞中PCBP2的mRNA及蛋白表达水平。通过透射电镜观察病毒感染下的线粒体结构变化,在THP-1细胞中构建了慢病毒介导的PCBP2过表达和敲低稳转细胞系。FerroOrange荧光探针检测Fe^(2+)水平,2,7-二氯荧光素二乙酸酯(2,7-dichlorofluorescein diacetate,DCFH-DA)探针测定活性氧(reactive oxygen species,ROS)水平,Western blot检测铁死亡相关溶质载体家族7成员11(solute carrier family 7 member 11,SLC7A11)和谷胱甘肽过氧化物酶4(glutathione peroxidase 4,GPX4)蛋白表达,以评估PCBP2调控对铁死亡的影响。使用铁死亡诱导剂(RSL3、erastin)和抑制剂(Fer-1、Lip-1)处理细胞,qRT-PCR和免疫荧光检测病毒复制水平变化,探索PCBP2是否可以通过调控铁死亡影响DBV复制。结果:在DBV感染的细胞模型中,PCBP2的mRNA和蛋白表达水平显著下调,DBV感染诱导典型铁死亡特征(线粒体嵴减少、肿胀)。通过qRT-PCR和Western blot验证,PCBP2敲低和过表达的THP-1细胞系构建成功,PCBP2敲低下调了铁死亡相关基因SLC7A11和GPX4的表达,导致ROS和Fe^(2+)水平升高;相反,PCBP2过表达使得SLC7A11和GPX4的表达水平升高,ROS和Fe^(2+)的水平降低。半数组织培养感染剂量与蛋白水平的检测进一步证实:铁死亡诱导剂可部分抵消PCBP2过表达促病毒复制的效应,铁死亡抑制剂可部分逆转PCBP2敲低抑制病毒复制的效应。结论:研究发现PCBP2可以通过维持SLC7A11/GPX4系统功能抑制铁死亡,从而限制DBV复制。这不仅阐明了PCBP2在DBV感染中的调控作用,为发热伴血小板减少综合征(severe fever with thrombocytope-nia syndrome,SFTS)的发病机制提供了新见解,同时靶向PCBP2-铁死亡通路可能成为SFTS治疗的潜在策略,为抗病毒药物的研发提供新思路。展开更多
基金The National Natural Science Foundation of China under contract No.41776034the Special Project of Global Change and Air and Sea Interaction under contract Nos GASI-IPOVAI-01-02 and GASI-02-SCS-YGST2-02the Guangdong Province First-Class Discipline Plan under contract Nos CYL231419012 and 231819002
文摘Using the mesoscale eddy trajectory atlas product derived from satellite altimeter data from 1993 to 2016,this study analyzes statistical characteristics and seasonal variability of mesoscale eddies in the Banda Sea of the Indonesian seas.The results show that there were 147 mesoscale eddies that occurred in the Banda Sea,of which 137 eddies were locally generated and 10 originated from outside.The total numbers of cyclonic eddies(CEs,clockwise)and anticyclonic eddies(AEs,anticlockwise)are 76 and 71,respectively.Seasonally,the number of CEs(AEs)is twice larger than the number of AEs(CEs)in winter(summer).In winter,CEs are distributed in the southern and AEs in the northern basins,respectively,but the opposite thing occurs in summer,i.e.,the polarities of mesoscale eddies observed at the same location reverse seasonally.The mechanisms of polarity distribution reversal(PDR)of mesoscale eddies are examined with reanalysis data of ocean currents and winds.The results indicate that the basin-scale vorticity,wind stress curl,and the meridional shear of zonal current reverse seasonally,which are favorable to the PDR of mesoscale eddies.The possible generation mechanisms of mesoscale eddies include direct wind forcing,barotropic and baroclinic instabilities,of which the direct wind forcing should play the dominant role.
文摘目的:探究多聚胞嘧啶结合蛋白2[poly(C)-binding protein 2,PCBP2]如何通过调节铁死亡参与大别班达病毒(Dabie Banda virus,DBV)感染后的致病过程及其作用机制。方法:以人单核细胞系THP-1为模型,采用qRT-PCR和Western blot技术检测DBV感染的THP-1细胞中PCBP2的mRNA及蛋白表达水平。通过透射电镜观察病毒感染下的线粒体结构变化,在THP-1细胞中构建了慢病毒介导的PCBP2过表达和敲低稳转细胞系。FerroOrange荧光探针检测Fe^(2+)水平,2,7-二氯荧光素二乙酸酯(2,7-dichlorofluorescein diacetate,DCFH-DA)探针测定活性氧(reactive oxygen species,ROS)水平,Western blot检测铁死亡相关溶质载体家族7成员11(solute carrier family 7 member 11,SLC7A11)和谷胱甘肽过氧化物酶4(glutathione peroxidase 4,GPX4)蛋白表达,以评估PCBP2调控对铁死亡的影响。使用铁死亡诱导剂(RSL3、erastin)和抑制剂(Fer-1、Lip-1)处理细胞,qRT-PCR和免疫荧光检测病毒复制水平变化,探索PCBP2是否可以通过调控铁死亡影响DBV复制。结果:在DBV感染的细胞模型中,PCBP2的mRNA和蛋白表达水平显著下调,DBV感染诱导典型铁死亡特征(线粒体嵴减少、肿胀)。通过qRT-PCR和Western blot验证,PCBP2敲低和过表达的THP-1细胞系构建成功,PCBP2敲低下调了铁死亡相关基因SLC7A11和GPX4的表达,导致ROS和Fe^(2+)水平升高;相反,PCBP2过表达使得SLC7A11和GPX4的表达水平升高,ROS和Fe^(2+)的水平降低。半数组织培养感染剂量与蛋白水平的检测进一步证实:铁死亡诱导剂可部分抵消PCBP2过表达促病毒复制的效应,铁死亡抑制剂可部分逆转PCBP2敲低抑制病毒复制的效应。结论:研究发现PCBP2可以通过维持SLC7A11/GPX4系统功能抑制铁死亡,从而限制DBV复制。这不仅阐明了PCBP2在DBV感染中的调控作用,为发热伴血小板减少综合征(severe fever with thrombocytope-nia syndrome,SFTS)的发病机制提供了新见解,同时靶向PCBP2-铁死亡通路可能成为SFTS治疗的潜在策略,为抗病毒药物的研发提供新思路。
