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

1,161 篇 期刊文献
91 篇 会议

馆藏范围

1,252 篇 电子文献
0 种 纸本馆藏

日期分布

学科分类号

995 篇 医学
- 563 篇 临床医学
- 254 篇 基础医学(可授医学...
- 174 篇 药学(可授医学、理...
- 79 篇 中西医结合
- 74 篇 公共卫生与预防医...
- 35 篇 中药学(可授医学、...
- 29 篇 医学技术（可授医学...
- 6 篇 中医学
- 4 篇 口腔医学
- 3 篇 护理学（可授医学、...
- 2 篇 特种医学
258 篇 理学
- 243 篇 生物学
- 6 篇 统计学（可授理学、...
- 5 篇 数学
- 4 篇 化学
- 3 篇 海洋科学
194 篇 工学
- 109 篇 生物工程
- 65 篇 化学工程与技术
- 20 篇 生物医学工程（可授...
- 16 篇 材料科学与工程（可...
- 5 篇 电气工程
127 篇 农学
- 119 篇 作物学
- 3 篇 兽医学
- 2 篇 农业资源与环境
29 篇 教育学
- 28 篇 教育学
- 1 篇 心理学(可授教育学...
14 篇 管理学
- 13 篇 公共管理
6 篇 经济学
- 6 篇 应用经济学
1 篇 法学
- 1 篇 社会学
1 篇 文学
- 1 篇 外国语言文学

主题

66 篇 基因表达
50 篇 大鼠
40 篇 基因治疗
36 篇 肝肿瘤
31 篇 线粒体
30 篇 受体
27 篇 糖皮质激素
27 篇 小鼠
25 篇 克隆
24 篇 dna
24 篇 细胞凋亡
24 篇 脊髓损伤
23 篇 肿瘤
23 篇 mrna
21 篇 乙型肝炎病毒
20 篇 聚合酶链反应
19 篇 转基因小鼠
18 篇 大肠杆菌
17 篇 dna疫苗
16 篇 肿瘤坏死因子

机构

1,095 篇 第二军医大学
200 篇 第二军医大学长海...
109 篇 第二军医大学长征...
33 篇 长海医院
32 篇 第二军医大学东方...
26 篇 长征医院
20 篇 复旦大学
18 篇 中国人民解放军第...
15 篇 华东理工大学
14 篇 上海第二军医大学
12 篇 基础医学部生物化...
12 篇 第二军医大学附属...
11 篇 上海交通大学
10 篇 基础医学部微生物...
9 篇 郑州大学
9 篇 基础医学部神经生...
8 篇 第三军医大学
8 篇 中国水产科学研究...
7 篇 第二军医大学附属...
7 篇 首都医科大学附属...

作者

117 篇 焦炳华
112 篇 孙树汉
69 篇 胡以平
61 篇 戚中田
53 篇 路长林
52 篇 缪明永
42 篇 李建秀
36 篇 王学敏
35 篇 王梁华
33 篇 刘厚奇
32 篇 王成海
30 篇 潘卫
29 篇 蔡在龙
29 篇 毛积芳
28 篇 颜宏利
27 篇 冯伟华
27 篇 袁文俊
27 篇 王新民
27 篇 祝国强
26 篇 黄才国

语言

1,240 篇 中文
12 篇 英文

检索条件"机构=第二军医大学基础医学部医学遗传教研室"

共 1252 条记录，以下是101-110 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：

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

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

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：黄金凤郭瀛军王坡赵晨曦唐冠楠王越刘音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

Liver cancer is the fifth most common cancer in the world and the third most common cause of cancer-related ***,50% to 55% of cases of primary liver cancer are attributable to persistent hepatitis B virus(HBV)*** the pathogenesis of liver cancer is not very clear at *** the in-depth understanding of cancer,it is recognized that epigenetic modifications play crucial roles in the initiation and development of human *** is as much an epigenetic disease as it is a genetic disease,which together lead to the malignant transformation of cells caused by the activation of oncogene and the inactivation of tumor suppressor genes.

关键词： epigenetics hepatocellular carcinoma hepatitis B virus X protein long non-coding RNA vimentin

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

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

Evi-1is a critical regulator of the HBx-induced aberrant transcription of long non-coding RNAs

Evi-1is a critical regulator of the HBx-induced aberrant tra...

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：郭瀛军王越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

The role of long non-coding RNAs(lncRNAs)in tumorigenesis is gradually being elucidated largely due to an increasing number of ***,the regulatory mechanism for lncRNA expression remains *** this study,we employed a systemic approach to analyze the key regulator of aberrantly expressed lncRNAs in HBV X protein(HBx)-transgenic mice,which is a well-proven mouse tumorigenesis model for hepatitis B virus-related hepatocellular *** a bioinformatics analysis of microarray data,ecotropic viral integration site 1(Evi-1)was identified as a key regulatory transcriptional factor contributing to the aberrant expression of lncRNAs in the livers of HBx-transgenic *** a consequence of the up-regulation of Evi-1,we also identified that an Evi-1-regulated lncRNA AK015487 contributed to hepatocyte proliferative activity and *** findings highlight a novel mechanism for hepatocellular carcinoma tumorigenesis through Evi-1 and its target *** addition,our study also provides a good model for investigation of the regulatory mechanism for lncRNA expression using a systemic approach.

关键词： hepatocarcinogenesis IncRNA Evi-1 HBx epigenetics

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

ilencing of Grainyhead-like-2(GRHL2)at the tumor edge by DNA methylation facilitates Epithelial-Mesenchymal Transition through targeting Rab25and E-cadherin

ilencing of Grainyhead-like-2(GRHL2)at the tumor edge by DNA...

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：唐冠楠颜宏利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

Epithelial-Mesenchymal Transition(EMT)plays a pivotal role in tumor invasion and *** it is well documented that EMT occurred predominantly at the tumor edge where it is induced by cytokines,the extracellular matrix environment,or hypoxia,the mechanism(s)underlying the tumor microenvironment-induced Epithelial-Mesenchymal Transition remains ***-like-2 (GRHL2)is a new transcription factor involved in embryo development and epithelial *** of GRHL2 has been noted in several tumor types,including breast cancer,colon *** addition,it has been reported that GRHL2 regulated the epithelial apical junctional complex by targeting the tight junction gene claudin 4(Cldn4).These findings imply that GRHL2 might play a key role in Epithelial-Mesenchymal *** systemically analyzed the expression of GRHL2 in colon and liver cancer *** control by querying oncomine database and real time PCR analysis,the resulted showed that GRHL2 was respectively down-regulated in 40% and 76% of colon cancer and liver *** investing the expression of GRHL2 in colon cancer by immunohistochemistry analysis indicated that GRHL2 was loss of expression at the tumor edge and surround fibroblast *** further found that promoter of GRHL2 was embedded in a large CpG island and methylated in tumor cells with a low level of *** by 5-aza-dc treatment significantly enhanced GRHL2 expression in SW480 and SW620 cells,revealed that GRHL2 is epigenetically silenced by DNA *** of GRHL2 in SW480 and SW620 promotes Epithelial-Mesenchymal Transition(MET).Real time PCR,Western blot and Immunoprecipitation (ChIP)assay indicated that over-expression of GRHL2 enhances E-cadherin and Rab25 expression by binding to the promoter of these two *** addition,we also found that overexpression of GRHL2 suppresses CD24 *** conclusion,these data indicated that loss of expression GRHL2 in colon an

关键词： colorectal cancer liver cancer grainyhead-like-2(GRHL2) DNA methylation epithelial-mesenchymal transition(EMT)

来源：评论

学校读者我要写书评

暂无评论

Identification of copy number variations associated lncRNAs analysis reveals IncRNA-PRAL promotes apoptosis through p53in Hepatocellular carcinoma

Identification of copy number variations associated lncRNAs ...

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：周传传王芳孙树汉杨富徐丹张铃袁继行袁声贤毕海珊陶其飞刘峰第二军医大学基础医学部医学遗传学教研室上海200433 第二军医大学东方肝胆外科医院肝外三科上海200433

Recurrent genome copy number aberrations are known to be a common feature of many cancers,including hepatocellular carcinoma(HCC),and their analysis is expected to reveal genes involved in *** copy number variation(CNV)is one of the mechanisms to regulate the expression level of genes which contributes to the development and progression of ***,in many regions with high frequency copy number variations(CNVs),the aberrantly expressed protein-coding genes is unable to make a sense,which suggests that the mechanisms underlying carcinogenesis may be partly contributed to the differently expression of long non-coding RNAs(IncRNAs).We carried out an association analysis of lncRNAs expression microarray and genome copy number variations data in HCC was and identified a set of lncRNAs whose expression levels correlated with common chromosomal *** we examined the relative copy number and expression levels of the related lncRNAs at candidate regions in 42 pairs HBV-related HCC and paired adjacent nontumor tissues via real-time quantitative PCR *** these lncRNA-PRAL(P53 Regulatory Associated LncRNA)is consistently decreased(p<0.001,n=42)with a significant correlation with the copy number variations(R=0.537,p=0.006).We further found that IncRNA-PRAL could promote the tumor cell apoptosis and suppress the progress of carcinogenesis in ***,lncRNA-PRAL can participate in HSP90-p53 protein complex formation to help facilitate the nuclear transportation of p53.A large amount of regions of high frequent copy number variations can be ascribed to the lncRNAs genome *** lncRNA-PRAL can promotes the tumor cell apoptosis through p53 and it presents this functional copy-number variation as a potential therapeutic target for HCC.

关键词： copy number variation long non-coding RNA p53 HSP90 HCC

来源：评论

学校读者我要写书评

暂无评论

Repression of the Long Non-Coding RNA-LET by Histone Deacetylase3Contributes to Hypoxia-Mediated Metastasis

Repression of the Long Non-Coding RNA-LET by Histone Deacety...

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：杨富霍希松袁声贤张铃周伟平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 第二军医大学东方肝胆外科医院肝外三科上海200433

A new class of non-coding RNAs,designated long non-coding RNAs(lncRNAs),was recently found to be frequently deregulated in various *** previous data suggested that lncRNAs are likely to have biological effects,this possibility needs to be confirmed by specific hypothesis-driven *** the precise molecular mechanisms by which lncRNAs function in various diseases will be critical for exploring new potential strategies for early diagnosis and *** the past several years,multiple studies have demonstrated that nearly every step in the life cycle of a gene can be regulated by lncRNAs.

关键词： long non-coding RNA-LET histone deacetylase 3 hypoxia metastasis HCC

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126页 << < 7 8 9 10 11 12 13 14 15 16 > >>

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：