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| 1 | Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection显示文摘It has been known that,the novel coronavirus,2019-nCoV,which is considered similar to SARS-CoV,invades human cells via the receptor angiotensin converting enzyme II(ACE2).Moreover,lung cells that have ACE2 expression may be the main target cells during 2019-nCoV infection.However,some patients also exhibit non-respiratory symptoms,such as kidney failure,implying that 2019-nCoV could also invade other organs.To construct a risk map of different human organs,we analyzed the single-cell RNA sequencing(scRNA-seq)datasets derived from major human physiological systems,including the respiratory,cardiovascular,digestive,and urinary systems.Through scRNA-seq data analyses,we identified the organs at risk,such as lung,heart,esophagus,kidney,bladder,and ileum,and located specific cell types(i.e.,type II alveolar cells(AT2),myocardial cells,proximal tubule cells of the kidney,ileum and esophagus epithelial cells,and bladder urothelial cells),which are vulnerable to 2019-nCoV infection.Based on the findings,we constructed a risk map indicating the vulnerability of different organs to 2019-nCoV infection.This study may provide potential clues for further investigation of the pathogenesis and route of 2019-nCoV infection. | Xin Zou Ke Chen Jiawei Zou Peiyi Han Jie Hao Zeguang Han | 2020 | Frontiers of Medicine2020，14，2： | 193 |
| 2 | Recent progress in 8igenomic research of liver cancer显示文摘Along the course of occurrence and development of liver cancer,the corresponding somatic cells accumulate some important genetic variations.These variations may be divided into two categories.For the genetic changes closely related to etiology of liver cancer,the well-known cases include insertion and integration of the hepatitis B virus(HBV) DNA after infection,and mutations at site 249 of the tumor suppressor gene p53 induced by exposure to aflatoxin B1.The secondary genetic changes include amplification and deletion of certain chromosome regions,mutations in p53 at the sites other than 249,as well as the mutational activation of the Wnt/β-catenin signal pathway.The tumor cells with these genetic variations may gradually become the dominant clones under evolutionary selection.Besides,identification of genetic susceptible against risk of liver malignancy is also an important aspect of research in this field. | HAN ZeGuang Shanghai-MOST Key Laboratory for Disease and Health Genomics,Chinese National Human Genome Center at Shanghai,Shanghai 201203,China | 2009 | Science China(Life Sciences)2009，52，1： | 7 |
| 3 | siRNA mediated the type 1 insulin-like growth factor receptor and epidermal growth factor receptor silencing induces chemosensitization of liver cancer cells显示文摘 | Jian Niu Xiang-nong Li Haixin Qian Zeguang Han | 2008 | Journal of Cancer Research and Clinical Oncology2008，，4： | 1 |
| 4 | 靶向IGF1R的siRNA抑制人肝癌细胞SMMC7721裸鼠移植瘤的实验研究(英文)显示文摘调查像胰岛素的生长因素 1 受体(IGF1R ) 的效果的目的在裸体老鼠的人的肝癌症 SMMC7721 房间异种皮移植的生长上的小介入 RNA (siRNA ) 。指向 IGF1R 的方法 siRNA 被设计,并且原生质标志 SMMC7721-IGF1R-siRNA 被构造并且 transfected 进 SMMC7721 房间(SMMC7721-IGF1R-siRNA 房间) ;有 SMMC7721-IGF1R-mutation (SMMC7721-IGF1R-mutation 房间) 的房间 transfected 作为空控制被用作否定控制,和 untransfected 房间。稳定的房间克隆被 G418 屏蔽,并且移植了进裸体老鼠建立癌症异种皮移植。肿瘤生长被监视。肿瘤形态学被观察与他染色。在肿瘤纸巾的 IGF1R 蛋白质的表示被西方的污点检测。在肿瘤纸巾的 Microvessel 密度(MVD ) 被 SP 免疫组织化学检测。房间 apoptosis 被终端 deoxynucleotidyl 检测调停 transferase 的 dUTP 刻痕标记结束(TUNEL ) 试金。结果肿瘤体积比在 SMMC7721-IGF1R-mutation 和 SMMC7721 组在 SMMC7721-IGF1R-siRNA 组是显著地更小的(P <
0.05 ) 。坏死和房间 apoptosis 在 SMMC7721-IGF1R-siRNA 组被发现。IGF1R 蛋白质的表示比在 SMMC7721-IGF1R-mutation 和 SMMC7721 组在 SMMC7721-IGF-1R-siRNA 组是显著地更低的(P <
0.05 ) 。MVD 比在 SMMC7721-IGF1R-mutation 和 SMMC7721 组在 SMMC7721-IGF1R-siRNA 组是显著地更低的(11.3 ± 4.4 对 36.7 ± 7.6 和 28.4 ± 6.5, P <
0.05 ) 。肿瘤房间的 apoptosis 率比在 SMMC7721-IGF1R-mutation 和 SMMC7721 组在 SMMC7721-IGF1R-siRNA 组是显著地更高的[(50.2 ± 6.4 )% 对(5.4 ± 1.0 )% 或(6.0 ± 2.1 )% , P <
0.05 ] 。结论 IGF1R siRNA 能在裸体老鼠禁止 SMMC7721 细胞异种皮移植的生长。 | Jian Niu Haixin Qian Xiangnong Li Zeguang Han | 2008 | The Chinese-German Journal of Clinical Oncology2008，7，5： | 0 |
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