检索结果-内蒙古大学图书馆

您好，读者！请登录

内蒙古大学图书馆

首页
概况
党建
资源
服务
科研支持
- 论文收录引用证明
- 科技查新
知识产权
档案馆
帮助

咨询与建议

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

您的常用邮箱：*

您的手机号码：*

问题描述：

当前已输入0个字，您还可以输入200个字

全部搜索
期刊论文
图书
学位论文
标准
纸本馆藏
外文资源发现
数据库导航
超星发现

高级检索

时间限定

出版年份：

文献类型

图书期刊文献学位论文多媒体

馆藏选择

电子馆藏纸本馆藏

核心期刊

全部期刊 SCI 收录期刊 SSCI 收录期刊 EI 收录期刊 CSCD 收录期刊 CSSCI 收录期刊

语言

中文英文

文献类型

期刊文献图书学位论文标准纸本馆藏

帮助

文字说明：

T=题名（书名、题名），A=作者（责任者），K=主题词，P=出版物名称，PU=出版社名称，O=机构（作者单位、学位授予单位、专利申请人），L=中图分类号，C=学科分类号，U=全部字段，Y=年（出版发行年、学位年度、标准发布年）

检索规则说明：

AND代表“并且”；OR代表“或者”；NOT代表“不包含”；(注意必须大写,运算符两边需空一格)

检索范例：

范例一：(K=图书馆学 OR K=情报学) AND A=范并思 AND Y=1982-2016
范例二：P=计算机应用与软件 AND (U=C++ OR U=Basic) NOT K=Visual AND Y=2011-2016

分类表

所选分类

>> <<

限定检索结果

文献类型

274 篇 期刊文献
69 篇 会议

馆藏范围

343 篇 电子文献
0 种 纸本馆藏

日期分布

学科分类号

221 篇 医学
- 118 篇 临床医学
- 72 篇 基础医学(可授医学...
- 28 篇 药学(可授医学、理...
- 14 篇 公共卫生与预防医...
- 10 篇 医学技术（可授医学...
- 5 篇 中西医结合
- 2 篇 特种医学
- 1 篇 口腔医学
- 1 篇 中医学
103 篇 理学
- 103 篇 生物学
51 篇 农学
- 43 篇 作物学
- 5 篇 畜牧学
- 3 篇 兽医学
50 篇 工学
- 40 篇 生物工程
- 9 篇 化学工程与技术
- 3 篇 生物医学工程（可授...
- 1 篇 电气工程
11 篇 教育学
- 11 篇 教育学

主题

31 篇 基因表达
23 篇 dna疫苗
19 篇 小鼠
15 篇 临床遗传学
11 篇 肿瘤
10 篇 基因克隆
10 篇 大肠杆菌
9 篇 克隆
9 篇 dna
9 篇 猪囊尾蚴
9 篇 细胞凋亡
8 篇 医学遗传学
8 篇 基因
8 篇 长链非编码rna
7 篇 基因打靶
7 篇 膜联蛋白b1
7 篇 转基因小鼠
7 篇 epigenetics
7 篇 钩端螺旋体
6 篇 癌胚抗原

机构

306 篇 第二军医大学
21 篇 第二军医大学长海...
11 篇 上海第二军医大学
11 篇 上海交通大学
10 篇 海军军医大学
9 篇 第二军医大学长征...
9 篇 河北医科大学
7 篇 中国人民解放军第...
7 篇 第二军医大学附属...
6 篇 复旦大学
5 篇 南京军区福州总医...
4 篇 上海南方模式生物...
4 篇 第二军医大学东方...
4 篇 长海医院
4 篇 承德医学院
4 篇 第二军医大学东方...
3 篇 昆明医学院
3 篇 南京大学临床医学...
3 篇 海军医学研究所舰...
3 篇 郑州大学

作者

228 篇 孙树汉
61 篇 王芳
52 篇 郭瀛军
51 篇 傅继梁
38 篇 张毅
37 篇 颜宏利
27 篇 杨富
26 篇 陈蕊雯
26 篇 胡振林
24 篇 王庆敏
20 篇 戴建新
18 篇 周凤娟
18 篇 章意亮
16 篇 袁继行
16 篇 薛赓
15 篇 黄金凤
15 篇 陈祖欢
14 篇 黎怀星
13 篇 杨湘越
13 篇 胡以平

语言

326 篇 中文
17 篇 英文

检索条件"机构=第二军医大学医学遗传学教研室，上海200433"

共 343 条记录，以下是91-100 订阅

全选清除本页清除全部题录导出标记到"检索档案"

详细简洁

排序：

叶酸通过调节组蛋白甲基化进而抑制肝细胞上皮间质转化及肝癌的发生发展

叶酸通过调节组蛋白甲基化进而抑制肝细胞上皮间质转化及肝癌的发...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：朱晓婷张毅薛赓陈国梁孙树汉第二军医大学基础部医学遗传学教研室上海 200433

目的近年来流行病学调查资料显示,叶酸缺乏与多种肿瘤发生相关,但缺少后续实验支持且作用机制不清.本实验的目的即为探讨补充叶酸对肝癌发生是否有防护作用及作用的具体分子机制,为临床研究提供扎实的理论与实验基础.方法构建肝癌小... 详细信息

目的近年来流行病学调查资料显示,叶酸缺乏与多种肿瘤发生相关,但缺少后续实验支持且作用机制不清.本实验的目的即为探讨补充叶酸对肝癌发生是否有防护作用及作用的具体分子机制,为临床研究提供扎实的理论与实验基础.方法构建肝癌小鼠模型,检测叶酸对肝损伤、肝硬化及肝癌的发生发展情况的影响;realtime-PCR、Western Blot、免疫组化检测叶酸对小鼠肝组织及人肝细胞EMT标志分子的作用.CHIP检测叶酸对组蛋白甲基化水平的影响.结果补充叶酸可显著抑制药物诱发的小鼠肝纤维化、肝硬化及肝癌的发生.补充叶酸可抑制小鼠肝细胞及人肝细胞EMT.进一步的实验表明在人肝细胞及前述小鼠肝组织中,叶酸皆可调节EMT相关基因组蛋白甲基化水平.结论叶酸通过调节组蛋白甲基化水平,调节EMT相关基因的表达,从而抑制肝脏EMT,抑制肝癌的发生发展.证实叶酸对肝癌有着重要的预防作用.

关键词：叶酸组蛋白甲基化上皮间质转化

来源：评论

学校读者我要写书评

暂无评论

受DNA甲基化调控的IncRNA-AY927547在原发性肝癌中作用机制研究

受DNA甲基化调控的IncRNA-AY927547在原发性肝癌中作用机制研究

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：赵晨曦郭瀛军黄金风孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

目的研究在原发性肝癌发生过程中受DNA甲基化调控的lncRNAs对肿瘤形成的影响及其分子机制.方法甲基化相关的lncRNAs芯片数据进行分析,筛选潜在受DNA甲基化调控异常表达的lncRNAs.在多种肝细胞系与肝癌肿瘤样本中通过实时定量PCR技术... 详细信息

目的研究在原发性肝癌发生过程中受DNA甲基化调控的lncRNAs对肿瘤形成的影响及其分子机制.方法甲基化相关的lncRNAs芯片数据进行分析,筛选潜在受DNA甲基化调控异常表达的lncRNAs.在多种肝细胞系与肝癌肿瘤样本中通过实时定量PCR技术检测这些lncRNAs的表达量改变;亚硫酸氢盐修饰与甲基化测序技术检测甲基化水平改变.进而通过siRNA干扰及全长载体质粒的构建在细胞水平对lncRNAs进行干扰及过表达后分析肿瘤表型：利用CCK-8法检测细胞的增殖能力;Transwell小室检测细胞的迁移、侵袭能力;Annexin-FITC荧光法检测细胞凋亡.利用UCSC基因组数据库分析lncRNAs的全长序列、结构位置、启动子区CpG岛、DNA甲基化相关转录因子等信息,继而通过双荧光素酶报告技术检测目的基因与转录因子的相互关系及结合方式.利用RNA pull-down技术筛选与lncRNAs相结合的靶蛋白分子,分析其与lncRNAs的作用方式.结果筛选出了lncRNA-AY927547,其在肝癌细胞系及肝癌组织中的表达量较之正常肝细胞系及癌旁组织呈明显下调,且甲基化程度明显增高.干扰lncRNA-AY927547后,肿瘤细胞增殖能力受到促进,迁移及侵袭能力受到明显促进,凋亡差异不明显.过表达IncRNA-AY927547后,肿瘤细胞增殖能力受到抑制,迁移及侵袭能力受到明显抑制,凋亡差异不明显.结构位置分析显示lncRNA-AY927547位于基因LMTK3的反义链上,在干扰及过表达IncRNA-AY927547后,其表达量水平与基因LMTK3呈明显负相关,提示两者之间的相互抑制,且与lncRNA-AY927547正义链及反义链相结合的蛋白谱呈明显差异.生物信息学分析提示lncRNA-AY927547的甲基化改变与转录因子Sp1、MEF-2有关.结论 IncRNA-AY927547能够受到与转录因子相关的DNA甲基化的调控,在原发性肝癌的发生及转移过程中通过其反义链基因LMTK3及其他结合蛋白发挥抑癌基因的作用,为发展表观遗传学药物治疗原发性肝癌提供了新的思路和靶向.

关键词：表观遗传学原发性肝癌 DNA甲基化长链非编码RNA

来源：评论

学校读者我要写书评

暂无评论

靶向抗肿瘤药物AnxB1-MLT的基因构建及诱导表达条件优化

靶向抗肿瘤药物AnxB1-MLT的基因构建及诱导表达条件优化

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：王玉招颜宏利唐冠楠林恒荣章意亮孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

背景靶向药物治疗(targeted drug therapy)逐渐成为是目前肿瘤治疗的重要手段.近年来的研究发现,磷脂酰丝氨酸(Phosphatidylserine,PS)是抗肿瘤治疗的重要靶点之一.膜联蛋白B1(annexin B1)是孙树汉教授克隆的一个新的膜联蛋白(Annexins... 详细信息

背景靶向药物治疗(targeted drug therapy)逐渐成为是目前肿瘤治疗的重要手段.近年来的研究发现,磷脂酰丝氨酸(Phosphatidylserine,PS)是抗肿瘤治疗的重要靶点之一.膜联蛋白B1(annexin B1)是孙树汉教授克隆的一个新的膜联蛋白(Annexins)亚家族成员,对PS的结合具有很高的亲和力和特异性.蜂毒肽(melittin,MLT)是蜂毒的主要成分,具有很强的抗肿瘤作用.目的以肿瘤内皮细胞暴露的磷脂酰丝氨酸为"靶",以AnxB1为"导向分子",以蜂毒素为"抗肿瘤分子",构建基因工程靶向抗肿瘤药物mAnxB1-MLT.方法利用PCR重叠区延伸法连接AnxB1-MLT,融合基因克隆至pGEX5T融合表达载体和pET-28a表达载体,转染大肠杆菌,分别就IPTG浓度、利福平、表达温度等条件进行优化.结果融合蛋白AnxB1-MLT在pET-28a表达载体中无明显表达条带.37℃条件下,pGEX-5T表达质粒中高效表达,表达产物占菌体总蛋白的40％以上;IPTG、利福平对表达影响较小,但表达产物均为包涵体,不利于纯化.在22-25℃条件下诱导表达,虽然大肠杆菌生长较慢,但表达产物均为可溶性表达,且占菌体蛋白30％以上.利用GST亲和层析柱纯化,蛋白纯度大于90％.结论成功构建了融合表达蛋白AnxB1-MLT的表达质粒,优化了诱导表达条件,获得了重组蛋白,为进一步通过动物模型研究其靶向抗肿瘤活性奠定了基础.

关键词：膜联蛋白B1 蜂毒素靶向抗肿瘤药物

来源：评论

学校读者我要写书评

暂无评论

Long noncoding RNA-H19promotes proliferation and Epithelial-Mesenchymal transition through a myc-related feedback loop during liver regeneration in mice

Long noncoding RNA-H19promotes proliferation and Epithelial-...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：王芳杨富徐丹袁继行张铃孙树汉第二军医大学医学遗传学教研室上海200433

Liver regeneration driven by hepatocyte proliferation is necessary for tissue repair and survival after acute liver injury,liver transplantation,and chronic hepatic *** a partial hepatectomy(PHx)in mice,a rapid induction of proliferative factors activates quiescent hepatocytes and primes their subsequent *** this process,many transcription factors are activated and up-regulate a large number of proliferation-related target genes to repair the liver.c-Myc is a central transcription factor and is essential for total liver *** up-regulation of c-myc mRNA occurs 30 minutes after PHx and sharply increases after several ***,the mechanism of the fast up-regulation of c-myc in early liver regeneration remains *** this study,we reported for the first time that a c-myc-related positive feedback loop contributed to this phenomenon.A long noncoding RNA(lncRNA),H19,stabilized the c-myc mRNA by forming a H19-hnRNP U-myc complex and was transcriptionally up-regulated by c-myc in liver *** many microRNAs,which are a type of noncoding RNA,have been reported to control liver regeneration,H19 is the first lncRNA that is involved in liver *** also found that H19 promotes an epithelial-to-mesenchymal transition(EMT)in liver cells during ***:lncRNA-H19 promotes hepatocyte proliferation and EMT by stabilizing c-myc mRNA in early liver ***,the existence of a c-myc-related positive feedback loop augmented the effect of c-myc for a short time period during early liver regeneration.

关键词： long noncoding RNA hnRNP U partial hepatectomy RNA-protein complex epithelial-mesenchymal transition

来源：评论

学校读者我要写书评

暂无评论

The"c-Myc/miR-15-16/FGF2"axis plays an important role in hypoxia-induced distant tumor metastasis

The"c-Myc/miR-15-16/FGF2"axis plays an important role in hyp...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：薛赓颜宏利张毅单石孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

Previous studies have established the link between aberrant microRNA(miRNA)level and hypoxia in various ***,how these aberrant miRNAs induced by hypoxia modulate tumor progression is still *** this study,the miRNA patterns of colorectal carcinoma(CRC)cells in hypoxia were screened by a high-resolution miRNA microarray and the hypoxia-induced repression of miR-15-16 was *** repression was associated with higher tumor stage and poor prognosis in *** was further disclosed that the hypoxia-induced repression of miR-15-16 promoted angiogenesis and metastasis by the loss of post-transcriptional inhibition of fibroblast growth factor-2(FGF2),Moreover,the promoter of the host gene (deleted in lymphocytic leukemia 2,DLEU2)of the miR-15-16 cluster was mapped and three Myc/Max binding sites responding in hypoxia were ***,the transcriptional repression of c-Myc to miR-15-16 via these Myc/Max binding sites in hypoxia was ***,we verified that the functional "c-Myc/miR-15-16/FGF2"pathway would play an important role in hypoxia-induced distant tumor *** a word,c-Myc-mediated repression of the miR-15-16 cluster in hypoxia promotes tumor angiogenesis and distant metastasis by upregulating *** study provides a better understanding of the coping mechanisms of microRNAs in response to hypoxia and may be helpful in developing more effective prognostic markers or treatment targets for solid tumors.

关键词： c-Myc fibroblast growth factor-2 hypoxia metastasis miR-15-1

来源：评论

学校读者我要写书评

暂无评论

DNA Methylomes in CpG Island Methylator Phenotype(CIMP)Colon Cancer:new screening marks proposal

DNA Methylomes in CpG Island Methylator Phenotype(CIMP)Colon...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：颜宏利唐冠楠章意亮王玉招孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

DNA methylation is essential for normal development and is frequently altered in *** Island Methylator Phenotype(CIMP)is a subset of colorectal cancers was postulated to have a higher propensity for DNA ***,the validity of CIMP,its molecular basis,and its prognostic values are highly *** aims of this study were to(1)compare and characterize the unique features of DNA methylomes of CIMP with Non-CIMP colonrectal cancers;(2)propose a new panel of valuable markers for CIMP *** we utilized MBD-isolated Genome Sequencing(MiGS)to map the DNA methylomes of three sets of normal colon,non-CIMP colon cancers,and CIMP colon *** regions only robust hypermethylated in CIMP tumors were evaluated in 120 colorectal tumors by Bisulfite genomic sequencing or Methylation Specific PCR(MSP).We found 4,800 sites were hypermethylated in both non-CIMP and CIMP colon cancers when compared with normal *** those sites,318 sites were robust hypermethylated in CIMP tumors *** of these CpG islands regulates 122 key genes in tumorgenesis and progress.A panel of 5 new markers was proposed for CIMP screening in 120 consecutive colon samples,13.3%(16/120)were methylated in all 5 markers and 87.5%(14/16)were *** the markers described by Weisenberger et al.,22.5%(27/120)were methylated in all 5 markers and only 51.8%(14/27)were MSI *** are a subset of colorectal cancer has unique features in DNA *** genes only hypermethylated in CIMP tumors shed lights on exploration the mechanism of CIMP tumorgenesis and provide new targets for cancer *** new panel of markers facilitates CIMP screening in sporadic colorectal cancers.

关键词： colorectal cancer CpG island methylator phenotype MBD-isolated genome sequencing DNA methylome

来源：评论

学校读者我要写书评

暂无评论

DNA methylation activates CTCF-mediated silencing of GAD1in colon and liver cancer by perturbing chromatin-loop formation

DNA methylation activates CTCF-mediated silencing of GAD1in ...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：颜宏利唐冠楠章意亮王玉招孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

It is widely accepted that aberrant DNA methylation at promoter regions commonly occurs in cancer cells and has been implicated in the epigenetic silencing of tumor suppressor *** we demonstrate that the human GAD1 promoter were hypermethylated both in cancer cells and in clinical samples that expressed high amounts of *** of DNA methyltransferases decreased GAD1 mRNA levels,suggesting that hypermethylation plays a positive role in GAD1 *** further mapped the key region regulate GAD1 expression to an intragenic CpG island and found that the chromatin loop between 5-UTR and the intron 3 mediated by transcription factor CTCF was abolished by DNA *** findings indicated that DNA methylation could activate GAD1 expression by preventing CTCF-mediated *** DNA methylation at gene promoter often linked to silence tumor suppressor genes in cancer,recent genome-wide methylation studies have markedly changed the conception of DNA methylation negatively regulate gene expression in the mammalian *** demonstrated here that hypermethylation prevents CTCF-mediated silencing of GAD 1 by perturbing chromatin-loop *** is the first time,to my knowledge,to elucidate the mechanism underlying GAD1 transcription activation in *** results also provide a graphic example of aberrant DNA methylation in cancer should not always be considered as a "silencing marker"for tumor suppressor genes,as it can also serve to promote expression of oncogenes.

关键词： DNA methylation glutamate decarboxylase 1 CTCF oncogene

来源：评论

学校读者我要写书评

暂无评论

Hepatitis C-induced upregulation of miR-155promotes hepatocarcinogenesis by activating Wnt signaling

Hepatitis C-induced upregulation of miR-155promotes hepatoca...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：章意亮孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

Hepatitis C virus(HCV)infection induces chronic hepatic inflammation,which usually favors the initiation and progression of *** is also increasing clearly that microRNA-155 (miR-155)plays an important role in regulating both inflammation and ***,little is known about whether and how miR-155 provides the link between inflammation and *** we found that miR-155 levels were markedly increased after HCV infection and in hepatitis ***-155 expression was transcribed by NF-κB,and p300/CBP increased NF-κB-dependent miR-155 *** of miR-155 significantly inhibited hepatocytes apoptosis and promoted cells growth,whereas miR-155 inhibition induced G0/G1 *** miR-155 resulted in nuclear accumulation of β-catenin and a concomitant increase in cyclin D1,c-myc and ***-of-function and loss-of-function studies demonstrated that miR-155 promoted hepatocytes proliferation and tumorigenesis by increasing Wnt signaling in vitro and in vivo,and DKK1(Wnt pathway inhibitor)overexpression inhibited the biological role of miR-155 in ***,adenomatous polyposis coli(APC),which negatively regulates Wnt signaling,was identified as the direct and functional target of ***:Hepatitis C-induced upregulation of miR-155 promotes hepatocytes proliferation and tumorigenesis by activating Wnt *** present study provides a better understanding of the relationship between inflammation and tumor,and thus may be helpful in developing effective diagnosis and treatment strategies against HCV-HCC.

关键词： miR-155 wnt HCV HCC

来源：评论

学校读者我要写书评

暂无评论

LncRNA-LALR accelerates hepatocyte proliferation and cell cycle progression in liver regeneration by Wnt/β-Catenin signaling

LncRNA-LALR accelerates hepatocyte proliferation and cell cy...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：徐丹杨富毕海姗张铃周传传袁继行刘峰王芳孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

来源：评论

学校读者我要写书评

暂无评论

Epigenetic Activation of MiR-200Family Contributes to H19mediated Metastasis Suppression in Hepatocellular Carcinoma

Epigenetic Activation of MiR-200Family Contributes to H19med...

引用

中华医学会2012年医学遗传学年会暨全国第十一次医学遗传学学术会议

作者：张铃杨富孙树汉第二军医大学基础医学部医学遗传学教研室上海200433

Recently,long non-coding RNA is thought to be contained in human genome as important regulatory transcripts in which we can identify far more previously *** serve as scaffolds associating with a protein and genome *** our recent study,we identified non-overlapping signatures of a small number of lncRNAs that are aberrantly expressed in human HBV-related HCC compared to paired pertitumoral tissues and among which lncRNA H19 was found to speculate a potential role in HCC *** from past studies has shown a strong association between H19 and carcinogenesis in several types of cancer including *** expression of H19 usually changes from monoallelic to biallelic in HCC through aberrant DNA methylation.

关键词： epigenetics histone acetylation hepatocellular carcinoma aggressiveness peritumoral tissues epithelial-to-mesenchymal transition

来源：评论

学校读者我要写书评

暂无评论

没有更多数据了...

全选清除本页清除全部题录导出标记到“检索档案”

共35页 << < 6 7 8 9 10 11 12 13 14 15 > >>

检索报告对象比较合并检索0

隐藏清空

合并搜索

回到顶部

执行限定条件

内容：

评分：

请选择保存的检索档案：

请选择收藏分类：

订阅名称：

通借通还

温馨提示：

图书名称：

借书校区：

取书校区：

手机号码：

邮箱地址：

一卡通帐号：

电话和邮箱必须正确填写，我们会与您联系确认。

联系人：

所在院系：

联系邮箱：

联系电话：

内蒙古自治区呼和浩特市赛罕区大学西街235号邮编: 010021

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：