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加权网格埋伏对策问题研究

兵工自动化 2017年第10期36卷 49-52页

作者：张建军王蔚蔚纪祥鲲海军工程大学理学院中国人民解放军92858部队指挥自动化站

为解决目前埋伏对策模型存在对实际需求适应性不强以及求解效率低等问题,提出一类新的网格埋伏对策模型。考虑埋伏资源的限制,构造局中人的可行策略集合。根据各列的防守程度和价值的不同,赋予各列不同的权值,构造相应的支付函数建立加... 详细信息

为解决目前埋伏对策模型存在对实际需求适应性不强以及求解效率低等问题,提出一类新的网格埋伏对策模型。考虑埋伏资源的限制,构造局中人的可行策略集合。根据各列的防守程度和价值的不同,赋予各列不同的权值,构造相应的支付函数建立加权网格搜索对策模型。将对策论问题转化为约束最优化问题,求解约束问题获得条件极值,转化为模型的对策值,并给出双方的最优策略。军事应用实例结果表明:该模型能较全面地对埋伏问题进行定量描述,具有一定的理论和应用价值。

关键词：埋伏对策网格防守程度价值加权约束最优化问题

Evolution from genetics to phenotype： reinterpretation of NSCLC plasticity, heterogeneity, and drug resistance

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Protein & Cell 2017年第3期8卷 178-190页

作者： Yingjiao Xue Shenda Hou Hongbin ji xiangkun Han Key Laboratory of Systems Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences Shanghai 200031 China Innovation Center for Cell Signaling Network Shanghai Institutes for Biological Sciences Chinese Academy of Sciences_ Shanghai 200031 China CAS Center for Excellence in Molecular Cell Science Institute of Biochemistry and Cell Biology Shanghai Institutes forBiological Sciences Chinese Academy of Sciences Shanghai 200031 China School of Life Science and Technology Shanghai Tech University Shanghai 200120 China Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of SciencesShanghai 200031 China

Lung cancer is the leading cause of cancer-related deaths worldwide. Targeted therapy is beneficial in most cases, but the development of drug resistance stands as an obstacle to good prognosis. Multiple mechanisms were explored such as genetic alterations, activation of bypass signaling, and phenotypic transition. These intrinsic and/or extrinsic dynamic regulations facilitate tumor cell survival in meeting the demands of signaling under different stimulus. This review introduces lung cancer plasticity and heterogeneity and their correlation with drug resistance. While cancer plasticity and heterogeneity play an essential role in the development of drug resistance, the manipulation of them may bring some inspirations to cancer prognosis and treatment. That is to say, lung cancer plasticity and heterogeneity present us with not only challenges but also opportunities.

关键词： lung cancer plasticity heterogeneity drugresistance phenotypic transition

Oxidative stress-triggered Wnt signaling perturbation characterizes the tipping point of lung adeno-to-squamous transdifferentiation

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Signal Transduction and Targeted Therapy 2023年第2期8卷 730-743页

作者： Zhaoyuan Fang xiangkun Han Yueqing Chen Xinyuan Tong Yun Xue Shun Yao Shijie Tang Yunjian Pan Yihua Sun Xue Wang Yujuan jin Haiquan Chen Liang Hu Lijian Hui Lin Li Luonan Chen Hongbin ji State Key Laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell BiologyCAS Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China University of Chinese Academy of Sciences Beijing 100049China Zhejiang University-University of Edinburgh Institute Zhejiang University School of MedicineHaining 314400China Department of Thoracic Surgery Fudan University Shanghai Cancer CenterShanghaiChina Department of Oncology Shanghai Medical CollegeFudan UniversityShanghaiChina School of Life Science and Technology ShanghaiTech UniversityShanghai 200120China State Key Laboratory of Molecular Biology Shanghai Institute of Biochemistry and Cell BiologyCAS Center for Excellence in Molecular Cell ScienceChinese Academy of SciencesShanghai 200031China Key Laboratory of Systems Health Science of Zhejiang Province School of Life ScienceHangzhou Institute for Advanced StudyUniversity of Chinese Academy of SciencesChinese Academy of SciencesHangzhou 310024China

Lkb1 deficiency confers the Kras-mutant lung cancer with strong plasticity and the potential for adeno-to-squamous transdifferentiation(AST).However,it remains largely unknown how Lkb1 deficiency dynamically regulates *** the classical AST mouse model(Kras LSL-G12D/+;Lkb1flox/flox,KL),we here comprehensively analyze the temporal transcriptomic dynamics of lung tumors at different stages by dynamic network biomarker(DNB)and identify the tipping point at which the Wnt signaling is abruptly suppressed by the excessive accumulation of reactive oxygen species(ROS)through its downstream effector *** genetic perturbation of the Wnt pathway using two different Ctnnb1 conditional knockout mouse strains confirms its essential role in the negative regulation of ***,pharmacological activation of the Wnt pathway before but not after the tipping point inhibits squamous transdifferentiation,highlighting the irreversibility of AST after crossing the tipping *** comparative transcriptomic analyses of mouse and human tumors,we find that the lineage-specific transcription factors(TFs)of adenocarcinoma and squamous cell carcinoma form a“Yin-Yang”counteracting ***,inactivation of the Wnt pathway preferentially suppresses the adenomatous lineage TF network and thus disrupts the“Yin-Yang”homeostasis to lean towards the squamous lineage,whereas ectopic expression of NKX2-1,an adenomatous lineage TF,significantly dampens such phenotypic transition accelerated by the Wnt pathway *** negative correlation between the Wnt pathway and AST is further observed in a large cohort of human lung adenosquamous ***,our study identifies the tipping point of AST and highlights an essential role of the ROS-Wnt axis in dynamically orchestrating the homeostasis between adeno-and squamous-specific TF networks at the AST tipping point.

关键词： squamous homeostasis lung

Targeting HSPA1A in ARID2-deficient lung adenocarcinoma

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National Science Review 2021年第10期8卷 89-100页

作者： Xue Wang Yuetong Wang Zhaoyuan Fang Hua Wang jian Zhang Longfu Zhang Hsinyi Huang Zhonglin jiang Yujuan jin xiangkun Han Shenda Hou Bin Zhou Feilong Meng Luonan Chen Kwok-Kin Wong jinfeng Liu Zhiqi Zhang Xin Zhang Haiquan Chen Yihua Sun Liang Hu Hongbin ji State Key Laboratory of Cell Biology Shanghai Institute of Biochemistry and Cell Biology Center for Excellence in Molecular Cell Science Chinese Academy of Sciences University of Chinese Academy of Sciences Department of Pulmonary Medicine Zhong Shan Hospital Fudan University Division of Hematology and Medical Oncology Laura and Isaac Perlmutter Cancer Center New York University Langone Medical Center College of Life Sciences Qufu Normal University Shanghai University of Medicine and Health Sciences Shanghai Sixth People's Hospital East Campus Department of General Surgery Shanghai Jiao Tong University Affiliated Sixth People's Hospital Department of Thoracic Surgery Fudan University Shanghai Cancer Center School of Life Science and Technology Shanghai Tech University School of Life Science Hangzhou Institute for Advanced Study University of Chinese Academy of Sciences

Somatic mutations of the chromatin remodeling gene ARID2 are observed in ～7% of human lung adenocarcinomas(LUADs). However, the role of ARID2 in the pathogenesis of LUADs remains largely unknown. Here we find that ARID2 expression is decreased during the malignant progression of both human and mice LUADs. Using two KrasG12 D-based genetically engineered murine models, we demonstrate that ARID2 knockout significantly promotes lung cancer malignant progression and shortens overall survival. Consistently, ARID2 knockdown significantly promotes cell proliferation in human and mice lung cancer cells. Through integrative analyses of Ch IP-Seq and RNA-Seq data, we find that Hspa1 a is up-regulated by Arid2 loss. Knockdown of Hspa1 a specifically inhibits malignant progression of Arid2-deficient but not Arid2-wt lung cancers in both cell lines as well as animal models. Treatment with an HSPA1 A inhibitor could significantly inhibit the malignant progression of lung cancer with ARID2 deficiency. Together, our findings establish ARID2 as an important tumor suppressor in LUADs with novel mechanistic insights, and further identify HSPA1 A as a potential therapeutic target in ARID2-deficient LUADs.

关键词： lung adenocarcinoma tumor suppressor ARID2 HSPA1A

Transdifferentiation of lung adenocarcinoma with LKB1 deficiency to squamous cell carcinoma in mice

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Transdifferentiation of lung adenocarcinoma with LKB1 defici...

细胞—生命的基础——中国细胞生物学学会2013年全国学术大会·武汉

作者： xiangkun Han Fuming Li Zhaoyuan Fang Yijun Gao Shun Yao Li Li Yingyong Hou Hongbin ji State Key Laboratory of Cell Biology Institute of Biochemistry and Cell BiologyShanghai Institutes for Biological SciencesChinese Academy of Sciences Department of Pathology Zhongshan HospitalFudan University

Lineage transition in different subtypes of non-small cell lung cancer(NSCLC),as implicated by clinical observation of mixed adenocarcinoma(ADC) and squamous cell carcinoma(SCC) pathologies in adenosquamous cell carcinoma(Ad-SCC),remains as a fundamental yet unsolved *** we provide first in vivo evidences showing the ADC-to-SCC transition in mice:LKB1-deficient lung ADC

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剩余电流动作保护电器的分类和选用若干问题

建筑电气 2010年第12期29卷 9-12页

作者：季慧玉贺湘琨上海电器科学研究所(集团)有限公司上海市200063 中机中电设计研究院北京市100048

论述剩余电流动作保护电器(RCD)的分类和选用中的若干技术问题。认为电磁式剩余电流动作保护电器和电子式剩余电流动作保护电器在技术上各有优势,不宜任意限制某一种型式产品的使用。只要符合相应的国家标准的要求,两种型式的剩余电流... 详细信息

论述剩余电流动作保护电器(RCD)的分类和选用中的若干技术问题。认为电磁式剩余电流动作保护电器和电子式剩余电流动作保护电器在技术上各有优势,不宜任意限制某一种型式产品的使用。只要符合相应的国家标准的要求,两种型式的剩余电流动作保护电器在工作的可靠性方面均是可以满足使用要求的。

关键词：剩余电流动作保护电器 RCD的分类 RCD选用中的若干问题接地故障

景德镇佛手湖商业楼项目结构BIM正向设计应用

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建筑结构 2023年第S2期53卷 2063-2069页

作者：吉久茂孙伟宾彭振峰梁祥锟周浩同济大学建筑设计研究院(集团)有限公司上海200092 中国建筑第四工程局有限公司广州510665

分析BIM正向设计应用于商业楼项目的基本流程、优点以及相关局限性。结合该项目重点说明基础正向设计、主结构正向设计的基本方法,提出基于计算-出图的BIM一体化出图的基本思路,并阐述BIM参数化结构族库的设计、创建和具体应用方法。实... 详细信息

分析BIM正向设计应用于商业楼项目的基本流程、优点以及相关局限性。结合该项目重点说明基础正向设计、主结构正向设计的基本方法,提出基于计算-出图的BIM一体化出图的基本思路,并阐述BIM参数化结构族库的设计、创建和具体应用方法。实现了BIM环境下的正向设计技术落地,进一步分析当下BIM正向设计的优点和局限性,为以后智能设计奠定良好的研究基础。

关键词： BIM三维设计结构设计参数化族数字转型

基于集成式线控液压制动系统的车辆稳定性控制

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汽车安全与节能学报 2017年第2期8卷 170-177页

作者：何祥坤杨恺明季学武武健刘亚辉清华大学汽车安全与节能国家重点实验室

为提高汽车在极限工况下的行驶稳定性,提出了一种基于集成式线控液压制动(IEHB)系统的车辆动力学稳定性控制策略。在多学科领域复杂系统建模仿真平台(AMESim)中建立了IEHB执行机构、15自由度非线性车辆动力学物理仿真模型;采用分层控制... 详细信息

为提高汽车在极限工况下的行驶稳定性,提出了一种基于集成式线控液压制动(IEHB)系统的车辆动力学稳定性控制策略。在多学科领域复杂系统建模仿真平台(AMESim)中建立了IEHB执行机构、15自由度非线性车辆动力学物理仿真模型;采用分层控制构架,运用线性比例控制与非线性补偿控制设计了横摆力矩控制层,设计了制动力矩分配层和执行层以保证被控车辆对参考模型层输出的跟踪品质。结果表明:相比于基于传统车身电子稳定性控制系统(ESC)的动力稳定性控制系统,横摆角速度峰值跟踪误差减少13.6%,收敛时间缩短1.3 s,侧倾角、侧偏角、侧向加速度等也均有明显改善,车辆行驶稳定性显著提高。因而,本控制方法能确保车辆在极限工况下快速、准确地跟踪参考模型输出。

关键词：汽车主动安全集成式线控液压制动(IEHB)系统物理仿真模型动力学稳定性分层控制构架非线性控制

LKB1在非小细胞肺癌可塑性及耐药反应中的重要作用及机制

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中国细胞生物学学报 2015年第7期37卷 919-924页

作者：李福明韩向琨李飞季红斌中国科学院上海生命科学研究院生物化学与细胞生物学研究所系统生物学重点实验室

LKB1(liver kinase B1)调控细胞增殖和细胞代谢。在非小细胞肺癌发病过程中,缺失LKB1的肿瘤细胞如何协调快速增殖和代谢应激这一矛盾目前尚不清楚。在该研究中,利用KrasG12D;Lkb1lox/lox(KL)小鼠模拟缺失LKB1的非小细胞肺癌的发病过程,... 详细信息

LKB1(liver kinase B1)调控细胞增殖和细胞代谢。在非小细胞肺癌发病过程中,缺失LKB1的肿瘤细胞如何协调快速增殖和代谢应激这一矛盾目前尚不清楚。在该研究中,利用KrasG12D;Lkb1lox/lox(KL)小鼠模拟缺失LKB1的非小细胞肺癌的发病过程,发现KL肺腺癌和鳞癌具有不同的氧化还原水平,且活性氧簇(reactive oxygen species,ROS)可以调控肺腺癌向肺鳞癌的转分化过程。进一步的研究发现,肺腺癌中氧化还原态失衡源于戊糖磷酸途径的失调和受AMPK-ACC信号轴调控的脂肪酸氧化通路的失活。有趣的是,类似的肿瘤异质性和氧化还原异质性同样存在于LKB1失活的临床肺癌样本中。在KL小鼠中进行临床前药理学研究发现,一部分肺腺癌可以通过转分化为肺鳞癌逃脱靶向细胞代谢的药物作用并获得耐药性。该研究揭示了氧化还原调控缺失LKB1的非小细胞肺癌可塑性以及药物响应的重要作用。

关键词： LKB1 腺癌鳞癌转分化活性氧簇