目的探讨已糖激酶2(hexokinase 2,HK2)、转录激活因子3(signal transducer and activator of transcription 3,STAT3)在病毒性肝炎诱发肝癌中的机制。方法应用组织芯片技术和免疫组织化学方法检测在肝炎病毒感染、肝癌和肝纤维化组织中...目的探讨已糖激酶2(hexokinase 2,HK2)、转录激活因子3(signal transducer and activator of transcription 3,STAT3)在病毒性肝炎诱发肝癌中的机制。方法应用组织芯片技术和免疫组织化学方法检测在肝炎病毒感染、肝癌和肝纤维化组织中HK2和STAT3的表达,并对二者的表达进行相关性分析,同时我们还根据肝癌细胞的分化对HK2和STAT3的表达和分布进行了统计学相关分析研究。结果通过计数细胞阳性率,发现乙肝病毒感染的肝癌组织中HK2的表达强度与STAT3的表达强度一致(P=0.141)。乙肝病毒感染的肝癌组织中HK2表达上调(约50%),显著高于肝癌(30%)、丙肝(10%)、肝纤维化(乙肝病毒感染)(30%)以及正常组织(20%)(P<0.05)。STAT3在乙肝病毒感染肝癌组织中主要分布于细胞浆和胞核(90%),显著高于肝癌(65%)、丙肝(40%)、肝纤维化(乙肝病毒感染)(30%)以及正常组织(30%)(P<0.05)。HK2与STAT3表达的相关性分析结果显示,在同一乙肝病毒感染的肝癌组织中STAT3的表达强度与HK2的表达强度一致;肝癌、丙肝、肝纤维化组织中STAT3的表达强度与HK2的表达强度差异具有统计学意义(P<0.05)。HK2的高表达与肝癌的分化无显著相关性。结论 HK2和STAT3的活化与乙肝病毒感染的肝癌发生和发展相关,在乙肝促肝癌的过程中HK2起到了重要作用,而STAT3被活化后定位于细胞核中,极有可能促进了HK2的表达。本研究提示HK2和STAT3在肝癌和乙肝病毒感染肝细胞的恶性转化过程中可能发挥重要作用,为肝癌的发生机制提出新的理论和作用靶位。展开更多
Due to variable symbol length of digital pulse interval modulation(DPIM),it is difficult to analyze the error performances of Turbo coded DPIM.To solve this problem,a fixed-length digital pulse interval modulation(FDP...Due to variable symbol length of digital pulse interval modulation(DPIM),it is difficult to analyze the error performances of Turbo coded DPIM.To solve this problem,a fixed-length digital pulse interval modulation(FDPIM) method is provided.The FDPIM modulation structure is introduced.The packet error rates of uncoded FDPIM are analyzed and compared with that of DPIM.Bit error rates of Turbo coded FDPIM are simulated based on three kinds of analytical models under weak turbulence channel.The results show that packet error rate of uncoded FDPIM is inferior to that of uncoded DPIM.However,FDPIM is easy to be implemented and easy to be combined.with Turbo code for soft-decision because of its fixed length.Besides,the introduction of Turbo code in this modulation can decrease the average power about 10 dBm,which means that it can improve the error performance of the system effectively.展开更多
文摘目的探讨已糖激酶2(hexokinase 2,HK2)、转录激活因子3(signal transducer and activator of transcription 3,STAT3)在病毒性肝炎诱发肝癌中的机制。方法应用组织芯片技术和免疫组织化学方法检测在肝炎病毒感染、肝癌和肝纤维化组织中HK2和STAT3的表达,并对二者的表达进行相关性分析,同时我们还根据肝癌细胞的分化对HK2和STAT3的表达和分布进行了统计学相关分析研究。结果通过计数细胞阳性率,发现乙肝病毒感染的肝癌组织中HK2的表达强度与STAT3的表达强度一致(P=0.141)。乙肝病毒感染的肝癌组织中HK2表达上调(约50%),显著高于肝癌(30%)、丙肝(10%)、肝纤维化(乙肝病毒感染)(30%)以及正常组织(20%)(P<0.05)。STAT3在乙肝病毒感染肝癌组织中主要分布于细胞浆和胞核(90%),显著高于肝癌(65%)、丙肝(40%)、肝纤维化(乙肝病毒感染)(30%)以及正常组织(30%)(P<0.05)。HK2与STAT3表达的相关性分析结果显示,在同一乙肝病毒感染的肝癌组织中STAT3的表达强度与HK2的表达强度一致;肝癌、丙肝、肝纤维化组织中STAT3的表达强度与HK2的表达强度差异具有统计学意义(P<0.05)。HK2的高表达与肝癌的分化无显著相关性。结论 HK2和STAT3的活化与乙肝病毒感染的肝癌发生和发展相关,在乙肝促肝癌的过程中HK2起到了重要作用,而STAT3被活化后定位于细胞核中,极有可能促进了HK2的表达。本研究提示HK2和STAT3在肝癌和乙肝病毒感染肝细胞的恶性转化过程中可能发挥重要作用,为肝癌的发生机制提出新的理论和作用靶位。
文摘Due to variable symbol length of digital pulse interval modulation(DPIM),it is difficult to analyze the error performances of Turbo coded DPIM.To solve this problem,a fixed-length digital pulse interval modulation(FDPIM) method is provided.The FDPIM modulation structure is introduced.The packet error rates of uncoded FDPIM are analyzed and compared with that of DPIM.Bit error rates of Turbo coded FDPIM are simulated based on three kinds of analytical models under weak turbulence channel.The results show that packet error rate of uncoded FDPIM is inferior to that of uncoded DPIM.However,FDPIM is easy to be implemented and easy to be combined.with Turbo code for soft-decision because of its fixed length.Besides,the introduction of Turbo code in this modulation can decrease the average power about 10 dBm,which means that it can improve the error performance of the system effectively.