维普中文期刊产品整合服务
164篇 您的检索式:作者名="DENIZOT"
    题名 作者 年代 出处 被引量
1Quantitative analysis using ELISA of vascular endothelial growth factor and basic fibroblast growth factor in human colorectal cancer,liver metastasis of colorectal cancer and hepatocellular carcinoma显示文摘TO THE EDITOR Angiogenesis consists of the sprouting of capillaries from pre-existing vessels . It is well-known that tumor growth is angiogenesis-dependent. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) stimulated vascular endothelial cell proliferation and are involved in the neoplastic angiogenesis of several types of tumors including those of the intestinal tract.Authors usually investigated VEGF and bFGF protein expressions using immunohistochemistry or Western blotting and VEGF and bFGF transcripts using reverse transcriptase polymerase chain reaction (RT-PCR). We recently reported in a previous issue of the World Journal of Gastroenterology that cirrhotic liver tissue levels of these twoMuriel Mathonnet Bernard Descottes Denis Valleix Francois Labrousse Véronique Truffinet Yves Denizot 2006World Journal of Gastroenterology2006,12,23:27
2Platelet-activating factor in cirrhotic liver and hepatocellular carcinoma显示文摘瞄准:激活血小板的因素(PAF ) 是一个支持 inflammatory 和 angiogenic 类脂化合物调停人。这里,我们试图调查 PAF 的层次, lyso-PAF ( PAF 先锋),磷脂酶 A ( 2 )( PLA ( 2 ),产生 lyso-PAF 的酶的活动), acetylhydrolase 活动(啊哈, PAF 降级的酶)并且在硬变肝和肝细胞癌( HCC )的 PAF 受体( PAF-R )抄本。方法:有 HCC 的 29 个病人在这研究被注册。肝硬化在十四个病人是在场的,七没有肝疾病。织物 PAF 层次被血小板聚集试金调查。Lyso-PAF 在它的化学乙酰化作用以后被估计进 PAF。啊哈被降级决定[(3 ) H ]-PAF。PLA (2 ) 层次被 EIA 估计。PAF-R 抄本用 RT-PCR 被调查。结果:PAF 和 PAF-R 抄本的提高的数量(白血球类型) 1 作为与非肝脏硬化症的相比在肝脏硬化症的纸巾被发现。PAF 和 PAF-R 抄本的更高的数量(织物类型) 1 和 2 作为与非肿瘤纸巾相比在 HCC 纸巾被发现。PLA (2 ) , lyso-PAF 和啊哈层次没在肝脏硬化症的纸巾和 HCC 被改变。结论:当 PAF 的角色在肝生理学当前是未知的时,这研究在在 HCC 期间在硬变肝并且在 angiogenic 反应发现的煽动性的网络建议它的潜在的参与。Muriel Mathonnet Bernard Descottes Denis Valleix Véronique Truffinet Franois Labrousse Yves Denizot 2006World Journal of Gastroenterology2006,12,17:7
3IgD class switch recombination is not controlled through the immunoglobulin heavy chain 3′ regulatory region super-enhancer显示文摘In secondary lymphoid organs,mature B cells express membrane immunoglobulin(Ig)of M and D isotypes(IgM and IgD,respectively)of the same specificity through alternative splicing of a pre-mRNA encompassing the VDJ variable region and Cμand Cδheavy chain constant exons.1 After encountering antigen,B cells undergo class switch recombination(CSR)by which the Cμgene is substituted with Cγ,Cεor Cα,thereby generating IgG,IgE and IgA antibodies of the same antigenic specificity but with new effector functions.CSR requires the DNA-editing enzyme activation-induced deaminase(AID).Hussein Issaoui Nour Ghazzaui Alexis Saintamand Yves Denizot François Boyer 2017Cellular & Molecular Immunology2017,14,10:6
4VEGF in hepatocellular carcinoma and surrounding cirrhotic liver tissues显示文摘TO THE EDITORWe read with a great interest the recent work of Deli andcolleagues. in the World Journal of Gastroenterology reportingvascular endothelial growth factor (VEGF) expressionin hepatocellular carcinoma (HCC) and cirrhotic livertissues. This well-documented work shows that VEGFwas significantly higher in surrounding cirrhotic livertissues than in HCC. Authors assessed VEGF expressionusing immunohistochemistry.TheMuriel Mathonnet Bernard Descottes Denis Valleix Francois Labrousse Yves Denizot 2006World Journal of Gastroenterology2006,12,5:5
5Hallmarks in colorectal cancer:Angiogenesis and cancer stem-like cells显示文摘Carcinogenesis is a multistep process that requires the accumulation of various genetic and epigenetic aberrations to drive the progressive malignant transformation of normal human cells.Two major hallmarks of carcinogenesis that have been described are angiogenesis and the stem cell characteristic of limitless replicative potential.These properties have been targeted over the past decade in the development of therapeutic treatments for colorectal cancer(CRC),one of the most commonly diagnosed and lethal cancers worldwide.The treatment of solid tumor cancers such as CRC has been challenging due to the heterogeneity of the tumor itself and the chemoresistance of the malignant cells.Furthermore,the same microenvironment that maintains the pool of intestinal stem cells that contribute to the continuous renewal of the intestinal epithelia also provides the necessary conditions for proliferative growth of cancer stem-like cells.These cancer stem-like cells are responsible for the resistance to therapy and cancer recurrence,though they represent less than 2.5%of the tumor mass.The stromal environment surrounding the tumor cells,referred to as the tumor niche,also supports angiogenesis,which supplies the oxygen and nutrients needed for tumor development.Anti-angiogenic therapy,such as with bevacizumab,a monoclonal antibody against vascular-endothelial growth factor,significantly prolongs the survival of metastatic CRC patients.However,such treatments are not completely curative,and a large proportion of patient tumors retain chemoresistance or show recurrence.This article reviews the current knowledge regarding the molecular phenotype of CRC cancer cells,as well as discusses the mechanisms contributing to their maintenance.Future personalized therapeutic approaches that are based on the interaction of the carcinogenic hallmarks,namely angiogenic and proliferative attributes,could improve survival and decrease adverse effects induced by unnecessary chemotherapy.Muriel Mathonnet Aurelie Perraud Niki Christou Hussein Akil Carole Melin Serge Battu Marie-Odile Jauberteau Yves Denizot 2014World Journal of Gastroenterology2014,20,15:5
6The IgH 3′ regulatory region super-enhancer does not control IgA class switch recombination in the B1 lineage显示文摘The bone marrow-derived B2 population represents the vast majority of bone marrow,blood,lymph node and splenic B-cells.Mouse B1 B-cells mostly originate during embryonic life in the liver and represent the main B-cell population in the pleural and peritoneal cavities.1,2,3,4,5 B1 and B2 B-cells differ in their origin,antigen specificity,cell surface markers,tissue distribution and capacity for class switch recombination(CSR).Schematically,B1 B-cells appear earlier than B2 B-cells during fetal development and maintain their self-renewal ability throughout their life.Hussein Issaoui Nour Ghazzaui Alexis Saintamand Claire Carrion Christelle Oblet Yves Denizot 2018Cellular & Molecular Immunology2018,15,3:4
7High-throughput sequencing reveals similar molecular signatures for class switch recombination junctions for theγandαisotypes显示文摘INTRODUCTION After encountering an antigen,B cells undergo class switch recombination(CSR),which substitutes the Cμgene with Cγ,Cε,or Cαto generate IgG,IgE,and IgA antibodies with the same antigenic specificity but new effector functions.1 The DNAediting enzyme activation-induced deaminase(AID)is essential for CSR by targeting switch(S)regions preceding Cμ(namely,the Sμdonor region)and the Cγ,Cε,and Cαgenes(namely,the Sγ,ε,αacceptor regions).1 Cis-and trans-controlled DNA double strand beaks are generated during this process.2–6 Recruitment of DNA repair factors that facilitate the end-joining process is a crucial step of class switch recombination.Two pathways are implicated in this end joining.The classical non-homogenous end joining(c-NHEJ)pathway ligates DNA ends with no or little homology.By contrast,the alternative end joining(A-EJ)pathways is used to ligate DNA ends that have microhomology.ussein Issaoui Nour Ghazzaui Alexis Saintamand Yves Denizot François Boyer 2019Cellular & Molecular Immunology2019,16,1:2
8Uracil-DNA glycosylase is not implicated in the choice of the DNA repair pathway during B-cell class switch recombination显示文摘Mature B-cells express membrane IgM and IgD(of same specificity)through alternative splicing of a pre-mRNA encompassing constant(C)μand Cδgenes.After encountering antigen,Bcells undergo class switch recombination(CSR)that substitutes the Cμgene with Cγ,Cε,or Cα,thereby generating IgG,IgE,and IgA antibodies with the same antigenic specificity but new effector functions.DNA-editing enzyme activation-induced deaminase(AID)is essential for CSR by targeting switch(S)regions preceding Cμ(namely,the Sμdonor region)and the Cγ,Cε,and Cαgenes(namely,the Sγ,ε,αacceptor regions).1,2 CSR is controlled in cis by IgH locus super-enhancers3 and in trans by a wide spectrum of enzymes and proteins.1,2 Among them,the role of the uracil DNA glycosylase(UNG)remains controversial.UNG is a key enzyme of base excision repair,which carries out faithful repair.Some authors estimate that during CSR,the UNG enzymatic activity removes the AID-induced dC to dU converted base of singlestrand DNA,generating abasic sites and leading to DNA strand breaks.1 For other authors,the role of UNG is to stabilize the S–S synapse and to recruit DNA repair factors that facilitate the endjoining process.4,5 Thus,the classical non-homogenous end joining pathway would be increased over the alternative end joining(A-EJ)pathway in UNG-deficient mice,4 suggesting an intriguing role of UNG in promoting the A-EJ pathway.Nour Ghazzaui Hussein Issaoui Alexis Saintamand Yves Denizot François Boyer 2019Cellular & Molecular Immunology2019,16,1:2
9Effect of PAF on human T and B cell显示文摘Denizot Y Dupuis F Praloran V 1994Res Immunol1994,145,2:1
10Autophagy is involved in T cell death after binding of HIV-1 envelope proteins to CXCR4显示文摘ESPERT L DENIZOT M GRIMALDI M 0,,:1
11Point mu- tations in FimH adhesin of Crohn's disease- associated ad- herent- invasive Escherichia coli enhance intestinal inflam- matory response 显示文摘Dreux N Denizot J Martinez-Medina M 2013PLoS pathogens2013,9,10:1
12Serum interleukin-8(IL-8) and IL-6 concentrations in patients with hematologic malignances显示文摘 FIX P LIOZON E 1996Blood1996,87,:1
13Comparative biodistribution of thin-coated iron oxide显示文摘Povtet D Denizot B Rump E 2001Drug Development Research2001,54,4:1
14A new member of the immunoglobulin superfamily CTLA-4显示文摘Brunet JF Denizot F Luciani MF 1987Nature1987,328,6127:1
15HIV-1 gp41 fusogenic function triggers autophagy in uninfected cells显示文摘DENIZOT M VARBANOV M ESPERT L 0,,:1
16A new member of the immunoglobulin superfamily-CTLA-4 显示文摘Brunet JF Denizot F Luciani MF 1987Nature1987,328,6127:1
17Umbilical cord blood procalcitonin and C-reactive protein concentrations as marker for early diagnosis of very early onset neonatal infection显示文摘Joran N Boscher C Denizot S 2006Arch Dis Child Fetal Neonatal2006,91,1:1
18Class switch recombination junctions are not affected by the absence of the immunoglobulin heavy chain E_(μ) enhancer显示文摘After encountering antigen,B-cells undergo class switch recombination(CSR)that substitutes the constant(C)μgene with Cγ,Cε,or Cα,thereby generating IgG,IgE,and IgA antibodies with new effector functions but the same antigenic specificity.1 The DNA-editing enzyme activation-induced deaminase(AID)is required for CSR by targeting specific DNA switch(S)regions preceding the C region,except Cδ.2 Sμis the donor region,while Sγ,ε,αare the acceptor regions.CSR is controlled in cis by the immunoglobulin heavy chain(IgH)3’regulatory region(3’RR).3 The 3’RR is essential to poise AID on the S acceptor region.During CSR IgH,intrachromosomal interactions(schematized in Fig.1a)are found between the 3’RR and the intronic Eμenhancer.1,4 Looping allows transcriptional binding activators to enhancers to facilitate CSR.However,CSR is only modestly influenced by Eμdeletion.5–7 During CSR,two different DNA repair pathways take place:the classical nonhomologous end joining(c-NHEJ)and the alternative end joining(A-EJ)pathways.Hussein Issaoui Nour Ghazzaui Mélissa Ferrad François Boyer Yves Denizot 2019Cellular & Molecular Immunology2019,16,7:1
19A new member of the immunoglobulin supeffamily-CTLA-4显示文摘Brunet JF Denizot F Luciani MF 1987Nature1987,328,6127:1
20Morbidity of pro- phylactic lymph node dissection in the central neck area in patients with papillary thyroid carcinoma 显示文摘Henry JF Gramatica L Denizot A 1998Langen- becks Arch Surg1998,383,2:1
返回顶部 每页显示:
共9页 首页 上一页 第1页 下一页 末页 /9 跳转

网站首页 | 关于我们 | 联系我们 | 产品服务 | 客服中心 | 广告服务 | 版权声明 | 网站联盟 | 友情链接 | 售卡网点

版权所有© 渝B2-20050021-1 渝公网安备 50019002500403号 违法和不良信息举报中心

互联网出版许可证 新出网证(渝)字10号 全国400电话 - 免长途话费