Anoikis is a specialized form of programmed cell death triggered by the detachment of cells from the extracellular matrix(ECM).Tumor cells that develop resistance to anoikis acquire the ability to detach,migrate,and c...Anoikis is a specialized form of programmed cell death triggered by the detachment of cells from the extracellular matrix(ECM).Tumor cells that develop resistance to anoikis acquire the ability to detach,migrate,and colonize distant sites,ultimately leading to the formation of metastatic tumors.Bit1(Bcl-2 inhibitor of transcription 1),a key effector of anoikis,is released into the cytoplasm upon loss of cell attachment and activates a caspase-independent pathway of apoptosis.Newcastle disease virus(NDV),a pathogen that poses a significant threat to the poultry industry,has also emerged as a promising oncolytic virus capable of selectively targeting and killing tumor cells.However,whether NDV can induce the death of anoikis-resistant tumor cells by activating Bit1 remains unclear.In this study,we utilized physical methods to induce cell suspension as a positive control for anoikis and further examined the expression and cellular localization of Bit1 following NDV infection in tumor cells.The results indicated that both viral infection and cell suspension resulted in partial cell death,accompanied by the translocation of Bit1 from the mitochondria to the cytoplasm and a reduction in its protein levels.Notably,Bit1 expression was found not to significantly affect viral replication.These findings suggest that NDV infection promotes tumor cell death by activating Bit1 translocation,mirroring the effects observed during cell suspension-induced anoikis.In addition,in vivo experiments demonstrated that NDV effectively inhibits the metastasis and growth of melanoma in mice,and that overexpression of Bit1 in tumor cells accelerates this process.This study provides novel insights into NDV-induced tumor cell death and identifies potential targets for understanding the mechanisms of oncolytic virus action.展开更多
目的:探讨BIT1(Bcl-2 inhibitor of transcription1)基因在伴淋巴结转移的食管鳞癌组织中的表达及与食管鳞癌侵袭、转移的关系。方法:采用半定量RT-PCR法检测30例食管鳞癌、30例癌旁不典型增生组织及30例正常食管粘膜组织中BIT1基因的...目的:探讨BIT1(Bcl-2 inhibitor of transcription1)基因在伴淋巴结转移的食管鳞癌组织中的表达及与食管鳞癌侵袭、转移的关系。方法:采用半定量RT-PCR法检测30例食管鳞癌、30例癌旁不典型增生组织及30例正常食管粘膜组织中BIT1基因的相对表达量。结果:BIT1基因的表达在癌组织中均高于不典型增生组织及正常食管粘膜组织(P<0.05),而其在不典型增生及正常食管粘膜中无统计学意义(P>0.05)。BIT1基因的表达水平与患者的年龄、性别及肿瘤浸润深度均无明显相关(P>0.05),但其表达水平与淋巴结转移及临床TNM分期有关。BIT1基因在淋巴结转移组中的表达明显高于无淋巴结转移组(P<0.001);BIT1基因在TNMⅢ/Ⅳ期组中的表达明显高于Ⅰ/Ⅱ期组(P<0.05)。结论:BIT1基因高表达可能与食管鳞癌的侵袭、转移有关。展开更多
设计了一种基于1 bit Sigma-Delta调制技术的数字磁通门磁强计,并利用Matlab Simulink工具对其进行仿真建模与分析,获得了系统在噪声、线性度、动态响应速度以及频率响应等方面的性能参数.在±1000 nT量程范围内,该磁强计系统在1 H...设计了一种基于1 bit Sigma-Delta调制技术的数字磁通门磁强计,并利用Matlab Simulink工具对其进行仿真建模与分析,获得了系统在噪声、线性度、动态响应速度以及频率响应等方面的性能参数.在±1000 nT量程范围内,该磁强计系统在1 Hz处的噪声为0.17 pT·Hz-1/2,最大线性误差为1.04 pT,动态响应速度为1.07×10^(3) nT·s^(-1),频率响应带宽超过30 Hz.仿真结果证实,采用1 bit Sigma-Delta调制技术显著提高了数模转换器(Digital-to-Analog Converter,DAC)的转换精度,有效降低了数字磁强计系统的本底噪声和非线性误差,显著提升了数字磁强计的性能.基于1 bit Sigma-Delta调制技术的数字磁通门磁强计性能指标能够满足高精度磁场探测任务的要求,为空间磁场探测领域提供了一种高精度、高可靠性的探测手段,在深空探测及空间科学领域具有广泛的应用前景.展开更多
设计了一种基于1 bit Sigma-Delta环路调制技术的高精度数字磁通门磁强计,建立了数字磁强计信号处理仿真模型,并利用Matlab的Simulink仿真工具开展了数字磁通门磁强计模型的仿真分析,对数字磁强计系统的噪声、线性度、响应速度和频率响...设计了一种基于1 bit Sigma-Delta环路调制技术的高精度数字磁通门磁强计,建立了数字磁强计信号处理仿真模型,并利用Matlab的Simulink仿真工具开展了数字磁通门磁强计模型的仿真分析,对数字磁强计系统的噪声、线性度、响应速度和频率响应进行了仿真计算。利用本文1 bit Sigma-Delta环路调制技术的数字磁强计在量程超过±10^(5 )nT的情况下,系统在1 Hz处的噪声仅为4.66 pT·Hz^(-1/2),最大线性偏差为0.16 nT,动态响应速度达到2×10^(6) nT·s^(–1),频率响应带宽超过10 Hz。仿真结果表明,基于1 bit Sigma-Delta环路调制技术的数字磁通门磁强计可以有效降低对A/D转换器精度的要求,在保证性能的前提下大幅度降低了电路复杂程度,提高了系统的可靠性,在深空探测、空间磁场测量等领域具有广泛的应用前景。展开更多
基金supported by the National Key Research and Development Program of China(2022YFD1801500)the International Cooperation Project of National Natural Science Foundation of China(32220103012)the Innovation Program of Chinese Academy of Agricultural Sciences(CAAS-CSLPDCP-202402).
文摘Anoikis is a specialized form of programmed cell death triggered by the detachment of cells from the extracellular matrix(ECM).Tumor cells that develop resistance to anoikis acquire the ability to detach,migrate,and colonize distant sites,ultimately leading to the formation of metastatic tumors.Bit1(Bcl-2 inhibitor of transcription 1),a key effector of anoikis,is released into the cytoplasm upon loss of cell attachment and activates a caspase-independent pathway of apoptosis.Newcastle disease virus(NDV),a pathogen that poses a significant threat to the poultry industry,has also emerged as a promising oncolytic virus capable of selectively targeting and killing tumor cells.However,whether NDV can induce the death of anoikis-resistant tumor cells by activating Bit1 remains unclear.In this study,we utilized physical methods to induce cell suspension as a positive control for anoikis and further examined the expression and cellular localization of Bit1 following NDV infection in tumor cells.The results indicated that both viral infection and cell suspension resulted in partial cell death,accompanied by the translocation of Bit1 from the mitochondria to the cytoplasm and a reduction in its protein levels.Notably,Bit1 expression was found not to significantly affect viral replication.These findings suggest that NDV infection promotes tumor cell death by activating Bit1 translocation,mirroring the effects observed during cell suspension-induced anoikis.In addition,in vivo experiments demonstrated that NDV effectively inhibits the metastasis and growth of melanoma in mice,and that overexpression of Bit1 in tumor cells accelerates this process.This study provides novel insights into NDV-induced tumor cell death and identifies potential targets for understanding the mechanisms of oncolytic virus action.
文摘目的:探讨BIT1(Bcl-2 inhibitor of transcription1)基因在伴淋巴结转移的食管鳞癌组织中的表达及与食管鳞癌侵袭、转移的关系。方法:采用半定量RT-PCR法检测30例食管鳞癌、30例癌旁不典型增生组织及30例正常食管粘膜组织中BIT1基因的相对表达量。结果:BIT1基因的表达在癌组织中均高于不典型增生组织及正常食管粘膜组织(P<0.05),而其在不典型增生及正常食管粘膜中无统计学意义(P>0.05)。BIT1基因的表达水平与患者的年龄、性别及肿瘤浸润深度均无明显相关(P>0.05),但其表达水平与淋巴结转移及临床TNM分期有关。BIT1基因在淋巴结转移组中的表达明显高于无淋巴结转移组(P<0.001);BIT1基因在TNMⅢ/Ⅳ期组中的表达明显高于Ⅰ/Ⅱ期组(P<0.05)。结论:BIT1基因高表达可能与食管鳞癌的侵袭、转移有关。
文摘设计了一种基于1 bit Sigma-Delta调制技术的数字磁通门磁强计,并利用Matlab Simulink工具对其进行仿真建模与分析,获得了系统在噪声、线性度、动态响应速度以及频率响应等方面的性能参数.在±1000 nT量程范围内,该磁强计系统在1 Hz处的噪声为0.17 pT·Hz-1/2,最大线性误差为1.04 pT,动态响应速度为1.07×10^(3) nT·s^(-1),频率响应带宽超过30 Hz.仿真结果证实,采用1 bit Sigma-Delta调制技术显著提高了数模转换器(Digital-to-Analog Converter,DAC)的转换精度,有效降低了数字磁强计系统的本底噪声和非线性误差,显著提升了数字磁强计的性能.基于1 bit Sigma-Delta调制技术的数字磁通门磁强计性能指标能够满足高精度磁场探测任务的要求,为空间磁场探测领域提供了一种高精度、高可靠性的探测手段,在深空探测及空间科学领域具有广泛的应用前景.
文摘设计了一种基于1 bit Sigma-Delta环路调制技术的高精度数字磁通门磁强计,建立了数字磁强计信号处理仿真模型,并利用Matlab的Simulink仿真工具开展了数字磁通门磁强计模型的仿真分析,对数字磁强计系统的噪声、线性度、响应速度和频率响应进行了仿真计算。利用本文1 bit Sigma-Delta环路调制技术的数字磁强计在量程超过±10^(5 )nT的情况下,系统在1 Hz处的噪声仅为4.66 pT·Hz^(-1/2),最大线性偏差为0.16 nT,动态响应速度达到2×10^(6) nT·s^(–1),频率响应带宽超过10 Hz。仿真结果表明,基于1 bit Sigma-Delta环路调制技术的数字磁通门磁强计可以有效降低对A/D转换器精度的要求,在保证性能的前提下大幅度降低了电路复杂程度,提高了系统的可靠性,在深空探测、空间磁场测量等领域具有广泛的应用前景。
