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中国免疫学会第五届全国代表大会暨学术会议

作者： Zhou Gang, He Yu-ling, He Li, Xie Luo-kun , Xiong Jie, Lei Hao, Wei Li, Hu Chun-song, Liu Jun-yan, Jian Ming-shen, Jin You-xin, Gong Fei-li, Jin Bo-quan, Tan Jin-quan Departments of Immunology Parasitology, Institute of Allergy and Immune-related Diseases Laboratories of Neuroscience Allergy and Clinical Immunology, center for medical research, Wuhan University School of Medicine, Wuhan The State Key Laboratory of molecular biology and Neuroscience, Institute of biochemistry and Cell biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Science, Shanghai The State Key Laboratory of Magnetic Resonance and Atomic and molecular Physics, Institute of Physics and Mathematics, Chinese Academy of Sciences, Wuhan Key Laboratory of Colloid, Interface Science and Chemical Thermodynamics, Institute of Chemistry, Chinese Academy of Sciences, Beijing Department of Immunology, college of Basic medical Sciences, Anhui medical University, Hefei Department of Immunology, Tongji medical college, Huazhong University of Science and Technology, Wuhan Department of Immunology, Fourth Military medical University, Xian, P. R. china

What mechanism to determine microglia accomplishing destructive or constructive role in CNS remains nebulous. We report here that intracranial priming and re-challenging with T. gondii in mice elicit neurotoxic CCR9+ Irg1+(immunoresponsive gene 1) microglia, which are resistant to apoptosis and produce high level of TNF-α;priming and re-challenging with LCMV (lymphocytic choriomeningitis virus) elicit neurosupportive CX-CR3+ Irg1- microglia, which are sensitive to apoptosis and produce high level of IL-10 and TGF-β. Administration of CCR9 or/and Irgl siRNAs alters the frequency and functional profiles of neurotoxic CCR9+ Irg1+ and neurosupportive CXCR3 +Irg1- microglia in vivo. Moreover, by using a series of different neurotropic pathogens including intracellular parasites, chronic virus, bacteria, toxic substances, and CNS injury to intracranially prime and subsequent re-challenge mice, the bi-directional elicitation of microglia has been confirmed as neurotoxic CCR9+ Irg1+ and neurosupportive CXCR3+ Irg1- cells in these mouse models. These data suggest that there exist two different types of microglia, providing with a novel insight into microglial involvement in neurodegenerative and neuroinflam-matory pathogenesis such as Alzheimer s disease and AIDS dementia.

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Aberrant expression of the IFN regulatory factor 4-binding protein (IBP) in human colorectal cancer

Aberrant expression of the IFN regulatory factor 4-binding p...

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第九届西南三省一市生物化学与分子生物学学术交流会

作者： Chuanmin Hu Zhujun Zhang Peng Li Qingliang Wang Yu Zhou Tao Fu Shuhui Li Weijing Yi Xinjun Li Yang Zhang Mingzhen Yang Xiuwu Bian Ji Ming Wang Guoguang Ying An Chen (a Department of Clinical biochemistry Laboratory Science,Third Military medical University,Chongqing 400038,PR china b Institute of Pathology,Southwest Hospital,Third Military medical University,Chongqing 400038,PR china c Laboratory of molecular Immunoregulation,Cancer and Inflammation Program,center for Cancer research,National Cancer Institute at Frederick,Building 560,Room 31-76,Frederick,MD 21702-1201,USA d Tianjin medical University Cancer Institute and Hospital,Tianjin 300060,PR.china)

Recent studies shown that the IFN regulatory factor 4-binding protein (IBP) plays multiple biological roles in the activation,proliferation and differentiation of immun *** order to explore the potential role of IBP in human diseases,The murine hybridoma 2A2 specific for human IBP was obtained epitope *** found that IBP is not only expressed in immun cells as relevant to its functional studies so far executed,but also in human colon cancer cell lines by immunoblotting and *** strain mAb does not react with native IBP in immunocytochemistry (ICH) or immunohistochemistry (IHC).To further evaluate the significance of IBP expression in human colorectal cancer,we generated polyclonal antibodies with high specificity and sensitivity against human IBP through affinity *** systematic assay revealed that 42 cases were IBP-positive in 63 colorectal cancer tissues,while IBP expression was not detectable in control normal tissues with the same origin (p<0.001).Moreover,IBP expression is related to the differentiation of colorectal cancer cells (p<0.05).Taken together,with the Abs generated in this report,future works related to IBP functional characterization,and its potential role in colorectal cancer development would be greatly facilitated.

关键词： IFN regulatory factor 4-binding protein (IBP) Monoclonal antibody Polyclonal antibodies Colorectal cancer

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“瘤苗”——细胞因子转导人肿瘤细胞

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生物工程进展 1999年第4期19卷 17-22页

作者：陈诗书上海第二医科大学生化教研室

Ⅰ基因治疗的现状自１９９０年９月美国国立卫生研究院（ＮＩＨ）及食品药物管理局（ＦＤＡ）批准第一个腺苷酸脱氨酶缺乏－严重联合免疫缺陷症（ＡＤＡ－ＳＣＩＤ）临床基因治疗草案至今正好１０年。从美国ＪｏｈｎＷｉｌｅｙ＆Ｓｏｎ... 详细信息

Ⅰ基因治疗的现状自１９９０年９月美国国立卫生研究院（ＮＩＨ）及食品药物管理局（ＦＤＡ）批准第一个腺苷酸脱氨酶缺乏－严重联合免疫缺陷症（ＡＤＡ－ＳＣＩＤ）临床基因治疗草案至今正好１０年。从美国ＪｏｈｎＷｉｌｅｙ＆Ｓｏｎｓ出版社网站１９９９年６月发布的一...

关键词：瘤苗细胞因子转导基因疗法肿瘤

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A Glimpse of Stem Cell research in china

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生物化学与生物物理进展 2011年第11期38卷 1011-1014页

作者： CHEN Zhi-Guo ZHANG Y. Alex Cell Therapy center Xuanwu Hospital Capital Medical University Key Laboratory of Neurodegeneration Ministry of Education Beijing 100053 China

2010 has seen rapid progress in stem cell research in china. Not only the major funding agencies had provided extensive funding to stem cell research, the publications by Chinese stem cell biologists also flourished in top-notch scientific journals. In this special review, we highlighted some recent studies that had been published in Science china Life Sciences and Cell research, two key SCI journals based in china. Not surprisingly, these studies mainly focused on some of the highly pursued stem cell types: embryonic stem cells (ES cells), induced pluripotent stem cells (iPSCs), neural stem cells (NSCs) and mesenchymal stem cells (MSCs). 1 research on embryonic stem cells ES cells are derived from the inner cell mass of blastocysts and are capable of infinite self-renewal and differentiation into various cell lineages within the three germ layers. A fundamental question in stem cell biology is what are the molecular mechanisms underlying lineage specifications along the developmental process. To study the transition of cell fate from A to B, it is important to use a system that can monitor the cell identity in an accurate and timely manner. Ho et al. found that, compared with protein markers and gene expression profiling, a change in the cell signaling network more sensitively reflects cell fate transition during the early differentiation of mouse ES cells[1]. In this study, the authors compared the mouse ES cells with the 2-day embryoid bodies (EBs) in terms of expression of stem cell markers (Oct4, Sox2 and Nanog etc.) as well as the cell signaling networks in response to extracellular stimuli, leukemia inhibitory factor (LIF) and fibroblast growth factor 8 (FGF8). mRNA levels of Oct4, Sox2 and Nanog and protein levels of Oct4 were not significantly different between mouse ES cells and up to 4-day EBs. Using phospho-specific antibody arrays and Western blot, the authors examined the activity of 8 signaling nodes (Erk1/2, p38, Akt1/2, Gsk3α/β, Stat3, β-catenin, S

关键词：英文摘要内容介绍编辑工作期刊

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Expression of ezrin and phosphorylated ezrin （pEzrin） in pancreatic ductal adenocarcinoma

Expression of ezrin and phosphorylated ezrin （pEzrin） in p...

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山东生物化学与分子生物学会2009年学术会议

作者： Yazhou Cui 1,Tianliang Li 1,Denglu Zhang 1,Jinxiang Han 1*. Shandong Medicinal Biotechnology center,Shandong Academy of medical Sciences,Key Laboratory of Ministry of Health for Biotech-Drug,Key Laboratory for Modern Medicine and Technology of Shandong Province.Jinan,china Ph.D.

＜正＞It has been suggested that ezrin activation plays a key role in the regulation of cancer *** this study,we immunohistochemically investigated the expression patterns of total ezrin and its two phosphorylated forms,pEzrin-Thr567 and pEzrin-Tyr353,in 66 samples of invasive pancreatic carcinomas and 11 samples of normal pancreas *** expressions of ezrin and pEzrin-Thr567 were detected in most PDAC tissues,significantly higher than that of ***,over-expression of pEzrin-Tyr353 in pancreatic cancers was associated with positive lymphnode metastasis,less differentiation,pAkt over-expression and shorter survival ***-Tyr353 may be a potent prognosis predictor for pancreatic cancer.

关键词： pancreatic cancer phosphorsylation ezrin metastasis prognosis

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胚胎干细胞对急性髓系白血病细胞KG-1a的影响

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中国实验血液学杂志 2018年第2期26卷 389-394页

作者：刘洁霍本念张婷刘梦楠王薛冯涛重庆医科大学分子医学与肿瘤研究中心重庆市生物化学与分子药理学重点实验室重庆400016

目的:研究人胚胎干细胞H9在体外对人急性髓系白血病细胞KG-1a增殖、凋亡的影响,并探讨其作用机制。方法:体外将人胚胎干细胞H9和白血病细胞KG-1a进行接触式共培养,用CCK8检测KG-1a的增殖情况;用流式细胞术检测共培养后细胞的凋亡以及周... 详细信息

目的:研究人胚胎干细胞H9在体外对人急性髓系白血病细胞KG-1a增殖、凋亡的影响,并探讨其作用机制。方法:体外将人胚胎干细胞H9和白血病细胞KG-1a进行接触式共培养,用CCK8检测KG-1a的增殖情况;用流式细胞术检测共培养后细胞的凋亡以及周期改变;荧光定量PCR检测BAX、BCL-2、caspase-3的m RNA表达;Western blot分析BAX、BCL-2、caspase-3的蛋白表达。结果:H9能明显抑制KG-1a细胞的增殖,将细胞阻滞于G2/M期,共培养后的KG-1a细胞的凋亡率高于对照组。BAX、Caspse-3的m RNA和蛋白表达均上调,BCL-2的m RNA和蛋白表达下调。结论:胚胎干细胞能抑制KG-1a细胞的增殖,促进其凋亡,其机制可能与BCL-2表达下调和BAX、Caspse-3表达上调有关。

关键词：胚胎干细胞急性髓系白血病细胞共培养

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血浆D-二聚体及纤维蛋白原在AECOPD患者中的变化及利伐沙班干预疗效评价

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药物评价研究 2018年第8期41卷 1463-1467页

作者：周芳赵杰贾晓民徐州医科大学研究生院江苏徐州221000 徐州医科大学第二附属医院呼吸内科江苏徐州221006

目的探索血浆D-二聚体及纤维蛋白原在慢性阻塞性肺疾病急性加重期(AECOPD)患者中的变化以及利伐沙班对其干预的疗效评价。方法选择2016年1月—2018年4月在徐州医科大学第二附属医院呼吸内科就诊的确诊慢性阻塞性肺疾病(COPD)患者120例,A... 详细信息

目的探索血浆D-二聚体及纤维蛋白原在慢性阻塞性肺疾病急性加重期(AECOPD)患者中的变化以及利伐沙班对其干预的疗效评价。方法选择2016年1月—2018年4月在徐州医科大学第二附属医院呼吸内科就诊的确诊慢性阻塞性肺疾病(COPD)患者120例,AECOPD组与COPD稳定期对照组各60例,选择同期在此院健康体检者62例作为对照,均于早晨空腹静脉采血,比较3组研究对象的D-二聚体及纤维蛋白原水平;将AECOPD患者随机分为两组,即利伐沙班组和低分子肝素组,每组30例,分别在常规治疗的基础上口服利伐沙班药物及皮下注射低分子肝素,比较两组的疗效。结果AECOPD组患者的血浆D-二聚体及纤维蛋白原水平高于稳定期对照组及健康体检组,差异具有统计学意义(P2均较治疗前有所上升,p CO2均治疗前有所降低,血气分析指标明显改善(P<0.05),但两组间差异均无统计学意义;低分子肝素组治疗AECOPD患者总有效率(73.33%)略低于利伐沙班组(80.00%),但差异无统计学意义。结论 AECOPD患者的血浆D-二聚体及纤维蛋白原水平高于稳定期患者及健康者,血液处于高凝状态。利伐沙班与低分子肝素两种药物的疗效接近,但利伐沙班克服了低分子肝素与传统口服抗凝药的局限,在临床治疗AECOPD患者中具有更好的应用价值。

关键词： D-二聚体纤维蛋白原 AECOPD 利伐沙班

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抗肿瘤药物：PBK/TOPK抑制剂的研究进展

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生命的化学 2018年第1期38卷 150-155页

作者：曾晨曦袁萍孙军华中科技大学同济医学院武汉430030 华中科技大学同济医学院基础医学院生物化学与分子生物学系武汉430030

PBK/TOPK是一种丝-苏氨酸蛋白激酶,正常生理情况下,TOPK仅在睾丸和胸腺中表达。近年来研究表明,TOPK在多种恶性肿瘤细胞中呈高表达,调控肿瘤细胞的细胞周期,与肿瘤细胞的增殖、侵袭、转移、抗凋亡过程相关。因此,TOPK成为肿瘤治疗的一... 详细信息

PBK/TOPK是一种丝-苏氨酸蛋白激酶,正常生理情况下,TOPK仅在睾丸和胸腺中表达。近年来研究表明,TOPK在多种恶性肿瘤细胞中呈高表达,调控肿瘤细胞的细胞周期,与肿瘤细胞的增殖、侵袭、转移、抗凋亡过程相关。因此,TOPK成为肿瘤治疗的一个靶标,其特异性抑制剂正在研究当中。目前,使用最多的TOPK抑制剂均能与TOPK分子活性中心结合,直接抑制TOPK的功能,从而达到抑制效果。本文综述了TOPK的结构和功能,以及现用于研究的TOPK抑制剂的抗肿瘤作用。

关键词： TOPK/PBK 抑制剂抗肿瘤药物

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Responsible genes in children with primary vesicoureteral reflux: findings from the Chinese Children Genetic Kidney Disease Database

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World Journal of Pediatrics 2021年第4期17卷 409-418页

作者： Jia-Lu Liu Qian Shen Ming-Yan Wu Guang-Hua Zhu Yu-Feng Li Xiao-Wen Wang Xiao-Shan Tang Yun-Li Bi Yi-Nv Gong Jing Chen Xiao-Yan Fang Yi-Hui Zhai Bing-Bing Wu Guo-Min Li Yu Bo Sun Xiao-Jie Gao Cui-Hua Liu Xiao-Yun Jiang Sheng Hao Yu-Lin Kang Ying-Liang Gong Li-Ping Rong Di Li Si Wang Duan Ma Jia Rao Hong Xu Chinese Children Genetic Kidney Disease Database(CCGKDD) “Internet Plus”Nephrology Alliance of the National center for Children’s Care Department of Nephrology Children’s Hospital of Fudan UniversityNational Children’s Medical Center399 Wan Yuan RoadShanghai201102People’s Republic of China Shanghai Kidney Development and Pediatric Kidney Disease research center ShanghaiChina Department of Nephrology Shanghai Children’s HospitalShanghaiChina Department of Pediatric Nephrology Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of MedicineShanghaiChina Wuhan Children’s Hospital Tongji Medical CollegeHuazhong University of Science and TechnologyWuhanChina Department of Urology Children’s Hospital of Fudan UniversityNational Children’s Medical CenterShanghaiChina Department of Rheumatology Children’s Hospital of Fudan UniversityNational Children’s Medical CenterShanghaiChina Clinical Genetic center Children’s Hospital of Fudan UniversityNational Children’s Medical CenterShanghaiChina Department of Nephrology Shenzhen Children’s HospitalShenzhenGuangdongChina Department of Nephrology and Rheumatology Children’s Hospital Affiliated to Zhengzhou UniversityZhengzhou Key Laboratory of Pediatric Kidney Disease ResearchZhengzhouChina The First Affiliated Hospital of Zhongshan University GuangzhouChina Key Laboratory of Metabolism and molecular Medicine Ministry of EducationDepartment of Biochemistry and Molecular BiologyInstitutes of Biomedical SciencesSchool of Basic Medical SciencesFudan UniversityShanghaiChina 不详

Background Primary vesicoureteral reflux(VUR)is a common congenital anomaly of the kidney and urinary tract(CAKUT)in *** present study identified the possible genetic contributions to primary VUR in *** Patients with primary VUR were enrolled and analysed based on a national multi-center registration network(Chinese Children Genetic Kidney Disease Database,CCGKDD)that covered 23 different provinces/regions in china from 2014 to *** causes were sought using whole-exome sequencing(WES)or targeted-exome *** A total of 379 unrelated patients(male:female 219:160)with primary VUR were ***-four(16.9%)children had extrarenal manifestations,and 165(43.5%)patients showed the coexistence of other CAKUT ***-eight patient(23.2%)exhibited impaired renal function at their last visit,and 18 of them(20.5%)developed ESRD at the median age of 7.0(IQR 0.9–11.4)years.A monogenic cause was identified in 28 patients(7.39%).These genes included PAX2(n=4),TNXB(n=3),GATA3(n=3),SLIT2(n=3),ROBO2(n=2),TBX18(n=2),and the other 11 genes(one gene for each patient).There was a significant difference in the rate of gene mutations between patients with or without extrarenal complications(14.1%vs.6%,P=0.035).The frequency of genetic abnormality was not statistically significant based on the coexistence of another CAKUT(9.6%vs.5.6%,P=0.139,Chi-square test)and the grade of reflux(9.4%vs.6.7%,P=0.429).Kaplan–Meier survival curve showed that the presence of genetic mutations did affect renal survival(Log-rank test,P=0.01).PAX2 mutation carriers(HR 5.1,95%CI 1.3–20.0;P=0.02)and TNXB mutation carriers(HR 20.3,95%CI 2.4–168.7;P=0.01)were associated with increased risk of progression to *** PAX2,TNXB,GATA3 and SLIT2 were the main underlying monogenic causes and accounted for up to 46.4%of monogenic *** complications and renal function were significantly related to the findings of genetic factors in children with p

关键词： Children Congenital anomalies of the kidney and urinary tract Gene mutation Vesicoureteral reflux Whole-exome sequencing

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低糖增强肿瘤对二甲双胍的敏感度

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肿瘤防治研究 2018年第3期45卷 125-130页

作者：张杰丛明华高云简美诚徐嘉溪缪明永石汉平俞伟男徐州医科大学附属淮安医院内分泌科淮安223002 国家癌症中心中国医学科学院北京协和医学院肿瘤医院北京100021 第二军医大学基础医学部生物化学与分子生物学教研室上海200433 首都医科大学附属北京世纪坛医院普外四科/临床营养科北京100038

目的观察不同浓度葡萄糖对二甲双胍抗肿瘤作用的影响并探讨其作用机制。方法在含不同浓度葡萄糖的培养基中加入二甲双胍培养细胞24 h后,检测细胞增殖情况及ATP水平。构建裸鼠皮下移植瘤,随机分成四组:正常饮食(SD)组、SD+二甲双胍(Met)... 详细信息

目的观察不同浓度葡萄糖对二甲双胍抗肿瘤作用的影响并探讨其作用机制。方法在含不同浓度葡萄糖的培养基中加入二甲双胍培养细胞24 h后,检测细胞增殖情况及ATP水平。构建裸鼠皮下移植瘤,随机分成四组:正常饮食(SD)组、SD+二甲双胍(Met)组、生酮饮食(KD)组、KD+Met组,实验干预8周后,检测瘤体体积、重量以及裸鼠血糖水平。结果培养基中葡萄糖水平≥10 mmol/L时,二甲双胍对胰腺癌细胞增殖抑制不明显,但在低糖培养基(≤5 mmol/L)中,10mmol/L二甲双胍能明显抑制胰腺癌细胞增殖。同时,低糖培养基中各细胞ATP水平显著降低(P<0.01)。体内实验中,KD组血糖水平明显降低(P<0.01),肿瘤生长受到显著抑制(P<0.01)。与KD组相比,KD+Met组可进一步抑制移植瘤生长(P<0.05)。结论低糖增强肿瘤对二甲双胍的敏感度,其机制可能与减少机体ATP生成有关。

关键词：二甲双胍生酮饮食肿瘤葡萄糖

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