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479篇 您的检索式:作者名="Wiedmann"
    题名 作者 年代 出处 被引量
1Reduced bone mineral density and altered bone turnover markers in patients with non-cirrhotic chronic hepatitis B or C infection显示文摘AIM: Previous studies suggest that loss of bone mineral density (BMD) frequently occurs in patients with chronic viral liver disease, presenting with histologically proven liver cirrhosis. However, little is known about the occurrence of bone disease in non-cirrhotic patients with chronic hepatitis B or C. Therefore, it was the aim of this study to evaluate this particular population for BMD and bone turnover markers.METHODS: Biochemical markers of bone turnover and BMD were measured in 43 consecutive patients with HCV (n = 30)or HBV (n = 13) infection without histological evidence for liver cirrhosis. Mean age was 49 years (range 26-77 years). BMD was measured by dual X-ray absorptiometry in the femoral neck (FN) and the lumbar spine (LS) region. In addition, bone metabolism markers were measured.RESULTS: BMD was lowered in 25 (58%) of the patients with chronic hepatitis B or C (FN: 0.76 (0.53-0.99); LS:0.96 (0.62-1.23) g/cm2). Eight (32%) osteopenic patients were diagnosed with osteoporosis. Bone-specific alkaline phosphatase (P = 0.005) and intact parathyroid hormone (iPTH) (P = 0.001) were significantly elevated in the more advanced stages of fibrosis. Mean 7-score value was lower in patients with chronic hepatitis C as compared to patients suffering from chronic hepatitis B; however, the difference was not statistically significant (P = 0.09).CONCLUSION: There was a significantly reduced BMD in non-cirrhotic patients with chronic hepatitis B or C infection. Alterations of bone metabolism already occurred in advanced liver fibrosis without cirrhosis. According to our results, these secondary effects of chronic viral hepatitis should be further investigated.Ingolf Schiefke Andreas Fach Marcus Wiedmann Andreas V.Aretin Eva Schenker Gudrun Borte Manfred Wiese Joachim Moessner 2005World Journal of Gastroenterology2005,11,12:23
2基于德国大学教育模式的FMS实验室建设显示文摘针对中国高等教育工科专业学生在理论应用能力、独立分析问题和解决问题以及创新能力方面与世界发达国家学生之间存在的问题,围绕引进德国应用科技大学人才培养模式的主题,通过对同济大学中德工程学院背景的介绍,阐述了德国模式的柔性制造系统FMS实验室建设。指出了该实验室的规划设计是依据德国应用科技大学相关实验室模式,遵循接近工业生产系统同时拥有自己功能特色的原则,论述了该实验室建设关键是引进德国先进的高等教育理念,为培养中国自己具有国际竞争力的理论研究、高级工程应用和管理等人才探索一条新路。谢春 Hans Wiedmann 2009实验室研究与探索2009,28,1:8
3Expression of c-kit receptor in human cholangiocarcinoma and in vivo treatment with imatinib mesilate in chimeric mice显示文摘瞄准:与额外的肝的 cholangiocarcinoma (CC ) 从病人在胆道癌症房间线和组织学的节调查 c 工具包表示并且与 imatinib mesilate 评估在试管内和在试管内治疗的功效。方法:在从有额外的肝的 CC 的 19 个病人的人的胆道癌症房间线 Mz-ChA-2 和 EGI-1 和组织学的节的 c 工具包的蛋白质表示被免疫弄污,免疫细胞化学,和免疫组织化学估计。胆道癌症房间线 Mz-ChA-2 和 EGI-1 上的 imatinib mesilate 的 anti-proliferative 效果是由自动化房间数的学习在试管内。另外,免疫缺乏的 NMRI 老鼠(Taconic ) 皮下地与 5x10 (6 ) 被注射房间线 MzChA-2 和 EGI-1 的房间。在到达了 200 mm3 的瘤体积以后,每日的治疗在 50 mg/kg 或生理盐水(NS ) 的剂量以 imatinib mesilate intraperitoneally 被开始。肿瘤体积与游标 caliper 被计算。在 14 d 以后,老鼠被牺牲,肿瘤和决定的肿瘤质量切除了。结果:Immunoblotting 在 EGI-1 房间在 Mz-ChA-2 和缺席揭示了 c 工具包的存在。有 c 工具包抗体的 Immunocytochemistry 在 EGI-1 房间在 Mz-ChA-2 房间和 c 工具包的缺席显示了 cytoplasmatic 和受体蛋白质的膜的本地化。c 工具包在 19 中的 7 个被表示(37%) 额外的肝的人的 CC 织物取样, 2 出现了一中等并且染色的 5 一相当弱的免疫。在 5 micromol/L 的低集中的 Imatinib mesilate 在 c 工具包引起了重要生长抑制积极房间线 Mz-ChA-2 (31%) ,然而并非在 c 工具包 negative,房间衬里 EGI-1 (0%)(P<0.05 ) 。在 10 micromol/L 的中间的集中的 Imatinib mesilate 禁止了两根细胞线(51% 对 57%) 的细胞的生长。在 20 micromol/L 的更高的集中的 Imatinib mesilate 似乎在两根房间线上有一般有毒的效果。IC50 价值分别地是 9.7 micromol/L 和 11 micromol/L。在有 imatinib mesilate 的在试管内处理的 14 d 以后,使用妄想的老鼠模型,积极 Mz-ChA-2 肿瘤有的 c 工具包显著地减少的体积和团作为与 NS 处理(P<0.05 ) 相比。与那相对照,忍受 c 工具包 negative EGI-1 肿瘤的鼠标的处理没作为与 NS 处理相比导致肿瘤体积和质量的任何变化。结论:c 工具包表示是可检测的在一对在胆道癌症的低蛋白质水平中等。Imatinib mesilate 在肿瘤生长在试管内和 c 工具包表示诚实的在试管内依赖者上施加显著效果。Thomas Kamenz Karel Caca Thilo Blüthner Andrea Tannapfel Joachim Mssner Marcus Wiedmann 2006World Journal of Gastroenterology2006,12,10:7
4Treatment of biliary tract cancer with NVP-AEW541:Mechanisms of action and resistance显示文摘AIM:To investigate in vitro treatment with NVPAEW541,a small molecule inhibitor of insulin-like growth factor-1 receptor(IGF-1R),in biliary tract cancer (BTC),since this disease is associated with a poor prognosis due to wide resistance to chemotherapeutic agents and radiotherapy.METHODS:Cell growth inhibition by NVP-AEW541 was studied in vitro in 7 human BTC cell lines by automated cell counting.In addition,the anti-tumoral mechanism of NVP-AEW541 was studied by Western blotting,cell cycle analysis and reverse transcription-polymerase chain reaction(RT-PCR).Anti-tumoral drug effect in combination with gemcitabine,5-fluorouracil(5-FU)and Polo-like kinase 1 inhibitor BI2536 was also studied. RESULTS:In vitro treatment with NVP-AEW541 suppressed growth in all human BTC cell lines,however response was lower in gallbladder cancer.Treatment withNVP-AEW541 was associated with dephosphorylation of IGF-1R and AKT.In contrast,phosphorylation of p42/p44 and Stat3 and expression of Bcl-xL were inconsistently downregulated.In addition,treated cells showed cell cycle arrest at the G1/S-checkpoint and an increase in sub-G1 peak.Moreover,IGF-1R and its ligands IGF-1 and IGF-2 were co-expressed in RT-PCR,suggesting an autocrine loop of tumor cell activation.Combined with gemcitabine,NVP-AEW541 exerted synergistic effects, particularly at low concentrations,while effects of combination with 5-FU or BI 2536 were only additive. CONCLUSION:Our findings suggest that NVP-AEW541 is active against BTC in vitro and potentiates the efficacy of gemcitabine.Samuel Wolf Jana Lorenz Joachim Mssner Marcus Wiedmann 2010World Journal of Gastroenterology2010,16,2:5
5Inhibition of histone deacetylase for the treatment of biliary tract cancer:A new effective pharmacological approach显示文摘瞄准:调查在试管内和在活体内治疗学的效果嘘胆道癌症上的一 deacetylase 禁止者 NVP-LAQ824 和 NVP-LBH589。方法:由 NVP-LAQ824 和 NVP-LBH589 的房间生长抑制是在由 MTT 试金的 7 根人的胆道癌症房间线的学习在试管内。另外, NVP-LBH589 的 anti-tumoral 效果在一个妄想的老鼠模型被学习。Anti-tumoral 药机制被为 MIB-1 为 acH4 和 p21 弄污 WAF-1/CIP-1, PARP 试金,房间周期分析, TUNEL 试金,和 immunhistochemistry 的免疫估计。结果:有两混合物的在试管内治疗显著地压制了所有癌症房间线的生长[吝啬的 IC50 ( 3 d ) 0.11 和 0.05 mumol/L ,分别地],并且与 nucleosomal 的 hyperacetylation 被联系嘘一 H4 , p21 WAF-1/CIP-1 的增加的表示, apoptosis ( PARP 劈开)感应,并且房间周期在 G2/M 逮捕检查点。在 28 d 以后, NVP-LBH589 显著地减少了在 66% 集体的肿瘤(胆汁管癌) 并且 87%( 胆囊癌症) 与安慰剂相比的在活体内,并且加强 gemcitabine 的功效。揭示的肿瘤标本的进一步的分析由 TUNEL 试金增加了 apoptosis 并且减少了房间增长(MIB-1 ) 。结论:我们的调查结果建议 NVP-LBH589 和 NVP-LAQ824 对人的胆道癌症是活跃的在试管内。另外, NVP-LBH589 表明了重要在活体内活动并且加强 gemcitabine 的功效。因此,为胆道癌症的治疗的这新药的进一步临床的评估被推荐。Thilo Bluethner Manuel Niederhagen Karel Caca Frederik Serr Helmut Witzigmann Christian Moebius Joachim Mossner Marcus Wiedmann 2007World Journal of Gastroenterology2007,13,35:5
6Allocating ecological footprints to final consumption categories with input–output analysis显示文摘Thomas Wiedmann Jan Minx John Barrett Mathis Wackernagel 2005Ecological Economics2005,,1:2
7A review of recent multi-region input–output models used for consumption-based emission and resource accounting显示文摘Thomas Wiedmann 2009Ecological Economics2009,,2:2
8Experimental treatment of pancreatic cancer with two novel histone deacetylase inhibitors显示文摘AIM:To investigate in vitro and in vivo treatment with histone deacetylase inhibitors NVP-LAQ824 and NVP-LBH589 in pancreatic cancer. METHODS:Cell-growth inhibition by NVP-LAQ824 and NVP-LBH589 was studied in vitro in 8 human pancreatic cancer cell lines using the 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide(MTT) assay. In addition,the anti-tumoral effect of NVP-LBH589 was studied in a chimeric mouse model. Anti-tumoral activity of the drugs was assessed by immunoblotting for p21WAF-1,acH4,cell cycle analysis,TUNEL assay,and immunohistochemistry for MIB-1. RESULTS:In vitro treatment with both compounds significantly suppressed the growth of all cancer cell lines and was associated with hyperacetylation of nucleosomal histone H4,increased expression of p21WAF-1,cell cycle arrest at G2/M-checkpoint,and increased apoptosis. In vivo,NVP-LBH589 alone significantly reduced tumor mass and potentiated the efficacy of gemcitabine. Further analysis of the tumor specimens revealed slightly increased apoptosis and no significant reduction of cell proliferation.CONCLUSION:Our findings suggest that NVP-LBH589 and NVP-LAQ824 are active against human pancreatic cancer,although the precise mechanism of in vivo drug action is not yet completely understood. Therefore,further preclinical and clinical studies for the treatment of pancreatic cancer are recommended.Martin Haefner Thilo Bluethner Manuel Niederhagen Christian Moebius Christian Wittekind Joachim Mossner Karel Caca Marcus Wiedmann 2008World Journal of Gastroenterology2008,14,23:2
9Integrating Ecological, Carbon and Water footprint into a “Footprint Family” of indicators: Definition and role in tracking human pressure on the planet显示文摘Alessandro Galli Thomas Wiedmann Ertug Ercin Doris Knoblauch Brad Ewing Stefan Giljum 2011Ecological Indicators2011,,:2
10Examining the global environmental impact of regional consumption activities — Part 2: Review of input–output models for the assessment of environmental impacts embodied in trade显示文摘Thomas Wiedmann Manfred Lenzen Karen Turner John Barrett 2006Ecological Economics2006,,1:2
11Editorial~ Carbon Footprint and Input-output Analysis- an Introduction显示文摘Wiedmann T 2009Economic Sys- tems Research2009,21,3:1
12Cdk5-mediated inhibition of the protective effects of transcription factor MEF2 in neurotoxicityinduced apoptosis显示文摘Gong X Tang X Wiedmann M 0,,01:1
13A first empirical comparison of energy Footprints embodied in trade--MRIO versus PLUM 显示文摘WIEDMANN T 2009Ecological economics2009,68,7:1
14Drivers and outcomes of brand heritage: Consumers ’ perceptionof heritage brands in the automotive industry 显示文摘Wiedmann K-P Hennigs N Schmidt S Wuestefeld T 2011Journal of Marketing Theory and Practice2011,19,2:1
15Photodynamic therapy in patients with non-resectable hilar cholangiocareinoma: 5-year follow-up of a prnspective phase 1I study显示文摘Wiedmann M Berr F Schiefke I 2004Gastrointest Endosc2004,60,1:1
16Sigma B contributes to Listeria monocytogenes gastrointestinal infection but not to systemic spread in the guinea pig infection model显示文摘Garner MR Njaa BL Wiedmann M 2006Infect Immun2006,74,2:1
17Biotin supplement ation ceanses inereased expression of genes eneoding interferon -3' , interleukin -y , and 3- methylerotony 1-CoA earboxylase,and ceanses decereased expression of the gene eneoding interleu-kin-4in human peripheral blood mononuclear cells显示文摘Wiedmann 5 Eudy J D ZemPleni J 2003J of Nutr2003,133,71:1
18Constitutive over-expression of the insulin receptor substrate-1 causes functional up regulation of Fas receptor 显示文摘Wiedmann M Tamaki S Silberrnan R 2003J Hepatol2003,38,6:1
19Allocating ecological footprints to final consumption categories with input–output analysis显示文摘Thomas Wiedmann Jan Minx John Barrett Mathis Wackernagel 2005Ecological Economics2005,,1:1
20Humanity's unsustainable environmental footprint显示文摘Hoekstra A Y Wiedmann T O 2014Science2014,344,6188:1
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