维普中文期刊产品整合服务
27篇 您的检索式:作者名="Christina Klaus"
    题名 作者 年代 出处 被引量
1肠的障碍: 分子的小径和修饰词显示文摘 The gastrointestinal tract is frequently challenged by pathogens/antigens contained in food and water and the intestinal epithelium must be capable of rapid regeneration in the event of tissue damage. Disruption of the intestinal barrier leads to a number of immune-mediated diseases, including inflammatory bowel disease, food allergy, and celiac disease. The intestinal mucosa is composed of different types of epithelial cells in specific barrier functions. Epithelial cells control surfaceassociated bacterial populations without disrupting the intestinal microflora that is crucial for host health. They are also capable of modulating mucosal immune system, and are thus essential in maintaining homeostasis in the gut. Thus, the regulation of intestinal epithelial homeostasis is crucial for the maintenance of the structure of the mucosa and the defensive barrier functions. Recent studies have demonstrated that multiple molecular pathways are involved in the regulation of intestinal epithelial cell polarity. These include the Wnt, Notch, Hippo, transforming growth factor-β(TGF-β)/bone morphogenetic protein(BMP) and Hedgehog pathways, most of which were identified in lower organisms where they play important roles during embryogenesis. These pathways are also used in adult organisms to regulate multiple self-renewing organs. Understanding the interactions between these molecular mechanisms and intestinal barrier function will therefore provide important insight into the pathogenesis of intestinal-based immune-mediated diseases.Min Kyung Jeon Christina Klaus Elke Kaemmerer Nikolaus Gassler 2013World Journal of Gastrointestinal Pathophysiology2013,4,4:10
2Brain changes in diabetes mellitus patients withgastrointestinal symptoms显示文摘Diabetes mellitus is a common disease and its prevalence is increasing worldwide. In various studies up to 30%-70% of patients present dysfunction and complications related to the gut. To date several clinical studies have demonstrated that autonomic nervous system neuropathy and generalized neuropathy of the central nervous system(CNS) may play a major role. This systematic review provides an overview of the neurodegenerative changes that occur as a consequence of diabetes with a focus on the CNS changes and gastrointestinal(GI) dysfunction. Animal models where diabetes was induced experimentally support that the disease induces changes in CNS. Recent investigations with electroencephalography and functional brain imaging in patients with diabetes confirm these structural and functional brain changes. Encephalographic studies demonstrated that altered insular processing of sensory stimuli seems to be a key player in symptom generation. In fact one study indicated that the more GI symptoms the patients experienced, the deeper the insular electrical source was located. The electroencephalography was often used in combination with quantitative sensory testingmainly showing hyposensitivity to stimulation of GI organs. Imaging studies on patients with diabetes and GI symptoms mainly showed microstructural changes,especially in brain areas involved in visceral sensory processing. As the electrophysiological and imaging changes were associated with GI and autonomic symptoms they may represent a future therapeutic target for treating diabetics either pharmacologically or with neuromodulation.Anne M Drewes Eirik Søfteland Georg Dimcevski Adam D Farmer Christina Brock Jens B Frøkjær Klaus Krogh Asbjørn M Drewes 2016World Journal of Diabetes2016,7,2:4
3Modulating effects of acyl-CoA synthetase 5-derived mitochondrial Wnt2B palmitoylation on intestinal Wnt activity显示文摘AIM:To investigate the role of acyl-CoA synthetase 5(ACSL5)activity in Wnt signaling in intestinal surface epithelia.METHODS:Several cell lines were used to investigate the ACSL5-dependent expression and synthesis of Wnt2B,a mitochondrially expressed protein of the Wnt signaling family.Wnt activity was functionally assessed with a luciferase reporter assay.ACSL5-related biochemical Wnt2B modifications were investigatedwith a modified acyl-exchange assay.The findings from the cell culture models were verified using an Apcmin/+mouse model as well as normal and neoplastic diseased human intestinal tissues.RESULTS:In the presence of ACSL5,Wnt2B was unable to translocate into the nucleus and was enriched in mitochondria,which was paralleled by a significant decrease in Wnt activity.ACSL5-dependent S-palmitoylation of Wnt2B was identified as a molecular reason for mitochondrial Wnt2B accumulation.In cell culture systems,a strong relation of ACSL5 expression,Wnt2B palmitoylation,and degree of malignancy were found.Using normal mucosa,the association of ACSL5 and Wnt2B was seen,but in intestinal neoplasias the mechanism was only rudimentarily observed.CONCLUSION:ACSL5 mediates antiproliferative activities via Wnt2B palmitoylation with diminished Wnt activity.The molecular pathway is probably relevant for intestinal homeostasis,overwhelmed by other pathways in carcinogenesis.Christina Klaus Ursula Schneider Christian Hedberg Anke K Schütz Jürgen Bernhagen Herbert Waldmann Nikolaus Gassler Elke Kaemmerer 2014World Journal of Gastroenterology2014,20,40:4
4The Interaction of the Arabidopsis Response Regulator ARR18 with bZIP63 Mediates the Regulation of PROLINE DEHYDROGENASE Expression显示文摘作为第一并且脯氨酸降级的限制率的酶,脯氨酸 DEHYDROGENASE1 (PDH1 ) 紧在植物压力回答期间被调整,包括在 hypoosmolarity 下面的正式就职和在 waterdeficit 下面的压抑。植物受体 histidine kinases AHK,在 Arabidopsis thaliana 的二部件的系统(TCS ) 的元素,被建议由调整不同压力应答的基因在水压力回答工作。然而,有关 AHK 可得到的小 informationis 调停 phosphorelay 的下游的发信号。这里,我们证明 Arabidopsis type-B 反应管理者(ARR18 ) 当在 Arabidopsis 的一个积极渗透的压力反应管理者播种并且影响 PDH1 倡导者的活动, 18 工作,知道被 Cgroup bZIP 抄写因素控制。而且, ARR18 withbZIP63 的直接物理的相互作用被识别并且出现依赖于在 ARR18 receiverdomain 的保存 aspartate 残余的 phosphorylation。我们进一步证明 bZIP63 本身在渗透的应力之上作为种子萌芽的一个否定管理者工作。在原物的 Usingreporter 基因试金,我们证明那个 ARR18 相互作用否定地在 PDH1 倡导者上防碍 bZIP63 的 transcriptionalactivity。我们的调查结果作为基因 expressionin Arabidopsis 的对抗管理者提供新卓见进 ARR18 和 bZIP63 的功能。Manikandan Veerabagu Tobias Kirchler Kirstin Elgass Bettina Stadelhofer Mark Stahl Klaus Harter Virtudes Mira-Rodado Christina Chaban 2014Molecular Plant2014,7,10:3
5Beta-7 integrin controls enterocyte migration in the small intestine显示文摘AIM:To hypothesize that beta-7 integrin affects cellularmigration of both,lymphocytes and enterocytes.METHODS:The nucleoside analog Brd U was ip injected in beta-7-deficient mice(C57BL/6-Itgbtmlcgn/J)of male gender and age-matched male C57BL/J J mice(wild type)4,20,or 40 h before analysis.The total small intestine was isolated,dissected,and used for morphometrical studies.Brd U-positive epithelial cells were numbered in at least 15 hemi-crypts per duodenum,jejunum,and ileum of each animal.The outer most Brd U-positive cell(cellmax)was determined per hemi-crypt,numerically documented,and statistically analysed.RESULTS:Integrins containing the beta-7-chain were exclusively expressed on leukocytes.In the small intestinal mucosa of beta-7 integrin-deficient mice the number of intraepithelial lymphocytes was drastically decreased.Moreover,the Peyer’s patches of beta-7integrin-deficient mice appeared hypoplastic.In beta-7integrin-deficient mice the location of cellmax was found in a higher position than it was the case for the controls.The difference was already detected at 4 h after Brd U application,but significantly increased with time(40 h after Brd U injection)in all small intestinal segments investigated,i.e.,duodenum,jejunum,and ileum.Migration of small intestinal enterocytes was different between the experimental groups measured by cellmax locations.CONCLUSION:The E-cadherin beta-7 integrin pathway probably controls migration of enterocytes within the small intestinal surface lining epithelial layer.Elke Kaemmerer Paula Kuhn Ursula Schneider Thomas Clahsen Min Kyung Jeon Christina Klaus Julia Andruszkow Michael Hrer Sabine Ernst Angela Schippers Norbert Wagner Nikolaus Gassler 2015World Journal of Gastroenterology2015,21,6:3
6Molecular classification of colorectal carcinomas:The genotype-to-phenotype relation显示文摘Colorectal carcinomas(CRCs)are frequently found in industrialized countries and lead to a high incidence of malignancy-related mortality.Defined by histomorphological features,CRCs and their pre-invasive lesions are quite heterogeneous.The underlying molecular mechanisms include genomic instability,genomic mutation of tumor suppressor genes or oncogenes,epigenetic changes,and the microRNA network.The molecular mechanisms are guided by repeated clonal selections.The genotype-to-phenotype relation is assumed to be the great challenge of cancer research and the development of effective targeted therapies.At present a strong genotype-to-phenotype relation is characterized only for a minority of CRCs.Consequently,the molecular characterization of CRCs is essential to interpret histological patterns and to identify prognostic groups as well as patients for targeted therapy.Elke Kaemmerer Christina Klaus Min Kyung Jeon Nikolaus Gassler 2013World Journal of Gastroenterology2013,19,45:2
7Intestinal acyl-CoA synthetase 5: Activation of long chain fatty acids and behind显示文摘The intestinal mucosa is characterized by a high complexity in terms of structure and functions and allows for a controlled demarcation towards the gut lumen.On the one hand it is responsible for pulping and selective absorption of alimentary substances ensuring the immunological tolerance,on the other hand it prevents the penetration of micro-organisms as well as bacterial outgrowth.The continuous regeneration of surface epithelia along the crypt-villus-axis in the small intestine is crucial to assuring these various functions.The core phenomena of intestinal epithelia regeneration comprise cell proliferation,migration,differentiation,and apoptosis.These partly contrarily oriented processes are molecularly balanced through numerous interacting signaling pathways like Wnt/β-catenin,Notch and Hedgehog,and regulated by various modifying factors.One of these modifiers is acyl-CoA synthetase 5(ACSL5).It plays a key role in de novo lipid synthesis,fatty acid degradation and membrane modifications,and regulates several intestinal processes,primarily through different variants of protein lipidation,e.g.,palmitoylation.ACSL5 was shown to interact with proapoptotic molecules,and besides seems to inhibit proliferation along the crypt-villus-axis.Because of its proapoptotic and antiproliferative characteristics it could be of significant relevance for intestinal homeostasis,cellular disorder and tumor development.Christina Klaus Min Kyung Jeon Elke Kaemmerer Nikolaus Gassler 2013World Journal of Gastroenterology2013,19,42:2
8Are urban green spaces optimally distributed to act as places for social integration? Results of a geographical information system (GIS) approach for urban forestry research显示文摘Christina G C Klaus S 2004Forest Policy and Economics2004,6,:1
9Stakeholder Analysis and Social Network Analysis in Natural Resource Management 显示文摘Christina Prell Klaus Hubacek Mark Reed 2009Society & Natural Resources2009,22,6:1
10Are urban green spaces optimally distributed to act as places for social integration? Results of a geographical information system (GIS) approach for urban forestry research显示文摘CHRISTINA G C KLAUS S 2004Forest Policy and Economics2004,,6:1
11Membrane connexin 43 acts as an independent prognostic marker in oralsquamous cell carcinoma显示文摘Phillipp Brockmeyer Klaus Jung Christina Perske Henning Schliephake Bernhard Hemmerlein 2014International Journal of Oncology2014,,1:1
12Pharmacotherapeutic in- tervention in impulsive preschool children:the need for a comprehensive therapeutic approach显示文摘Christina S Margarete B Klaus S 2011Child Adolesc Psy- chiatry Ment Heahh2011,5,1:1
13The Effect of Xenon on Isoflurane Protection Against Experimental Myocardial Infarction显示文摘Jan H. Baumert Marc Hein Christina Gerets Thomas Baltus Klaus E. Hecker Rolf Rossaint 2009Journal of Cardiothoracic and Vascular Anesthesia2009,,5:1
14Pharmacotherapeutic inter- vention in impulsive preschool children: The need for a compre- hensive therapeutieapproach 显示文摘Christina S Margarete B Klaus S 2011Child Adol Psychi Ment Heal2011,5,11:1
15Diverse expression patterns of the EMT suppressor grainyhead‐like 2 ( GRHL 2) in normal and tumour tissues显示文摘Sabine Riethdorf Sabrina Frey Sonja Santjer Malgorzata Stoupiec Benjamin Otto Lutz Riethdorf Christina Koop Waldemar Wilczak Ronald Simon Guido Sauter Klaus Pantel Volker Assmann 2016Int. J. Cancer2016,,:1
16Effects of Phytoestrogen Extracts Isolated from Pumpkin Seeds on Estradiol Production and ER/PR Expression in Breast Cancer and Trophoblast Tumor Cells显示文摘Dagmar Richter Sibylle Abarzua Mareike Chrobak Thomas Vrekoussis Tobias Weissenbacher Christina Kuhn Sandra Schulze MarkusS. Kupka Klaus Friese Volker Briese Birgit Piechulla Antonis Makrigiannakis Udo Jeschke Darius Dian 2013Nutrition and Cancer2013,,5:1
17In vitro analysis of multipotent mesenchymal stromal cells as potential cellular therapeutics in neurometabolic diseases in pediatric patients显示文摘Ingo Müller Birgit Kustermann-Kuhn Christina Holzwarth Gesa Isensee Martin Vaegler Klaus Harzer Ingeborg Kr?geloh-Mann Rupert Handgretinger Gernot Bruchelt 2006Experimental Hematology2006,,10:1
18Mid- to long-term results after bipolar radial head arthroplasty显示文摘Klaus Josef Burkhart Stefan G. Mattyasovszky Martin Runkel Christina Schwarz Raphael Küchle Martin H. Hessmann Pol M. Rommens Lars P. Müller 2010Journal of Shoulder and Elbow Surgery2010,,7:1
19Ligand stimulation of CD95 induces activation of PIk3 followed by phosphorylation of caspase-8显示文摘在有它的 ligand 的 CD95 受体的相互作用之上,适配器分子 FADD (MORT1 ) 的顺序的协会, caspases-8/10,和 caspase-8/10 管理者 c 扭动支持形式导致导致死亡的发信号建筑群的形成。这里,我们识别像马球的 kinase (Plk ) 3 死亡受体 CD95 作为一个新相互作用合伙。Plk3 的酶的活动与它的 ligand 增加 CD95 受体的后面的相互作用。大美人(击倒) 或 caspase-8, CD95 或 FADD 击倒在 CD95 刺激之上阻止 Plk3 的激活,为 Plk3 激活建议一个功能的磁盘的一个要求。而且,我们为 Plk3 作为新底层识别 caspase-8。Phosphorylation 在 T273 上发生并且导致 caspase-8 proapoptotic 功能的刺激。在在一个营救实验或在 CRISPR/Cas9 产生的 Plk3 击倒房间表示 non-phosphorylatable caspase-8-T273A 异种的房间的 CD95 的刺激减少显著地处理 caspase-8。低 T273 phosphorylation 在 95 个肛门肿瘤病人的一个队与低 Plk3 表示显著地相关。我们的数据在 Plk 家庭以内建议 kinase 激活的新奇机制并且与高 Plk3 在肿瘤为外来的死亡小径的刺激建议一个新模型表示。Christina Helmke Monika Raab Franz Rodel Yves Matthess Thomas Oellerich Ranadip Mandal Mourad Sanhaji Henning Urlaub Claus Rodel Sven Becker Klaus Strebhardt 2016Cell Research2016,26,8:1
20Effects of a new postnatal stress model on monoaminergic neurotransmitters in rat brains显示文摘Christina J. Huppertz-Kessler Johannes Poeschl Richard Hertel Klaus Unsicker Johannes Schenkel 2011Brain and Development2011,,4:1
返回顶部 每页显示:
共2页 首页 上一页 第1页 下一页 末页 /2 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