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| 1 | Hepatocytic differentiation of mesenchymal stem cells in cocultures with fetal liver cells显示文摘瞄准:为了与胎儿的肝细胞(FLC ) 和可能性在合作文化调查间充质的干细胞(MSC ) 的 hepatocytic 区别膨胀,区分了 hepatocytic 房间。方法:MSC 被制动火箭与绿荧光灯的蛋白质(GFP ) 标记病毒的基因转导变异。同种细胞的显著 MSC 在用与干细胞补充的fibronectin涂的培养皿和媒介刺激条件的肝下面是也有教养的因素( SCF ), hepatocyte 生长因素( HGF ),表皮的生长因素( EGF ),和成纤维细胞生长因素 4 ( FGF-4 )独自一个,或在刚孤立的 FLC 的存在。在合作文化的房间被收获,并且 GFP+ 或 GFP- 房间用荧光被分开激活的房间排序。为肝 specific 标记 cytokeratin-18 (CK-18 ) 的反向的抄写聚合酶链反应(RT-PCR )( 法新社) ,白朊,和 alpha-fetoprotein 在不同房间人口被执行。结果:在指定文化条件下面,与 FLC co 有教养的老鼠 MSC 超过二个星期表示了白朊, CK-18,和 AFP-RNA。在 wk 3, MSC 失去了 hepatocytic 基因表示,可能由于 cocultured FLC 的增生。FLC 也在合作文化和一个很高的生长潜力显示出稳定的肝 specific 基因表情。结论:从骨髓的老鼠 MSC 能面对 FLC 在试管内区分 hepatocytic 房间,在合作文化的 MSC 的存在也为 FLC 的扩大和区别提供有益的环境。 | Claudia Lange Helge Bruns Dietrich Kluth Axel R Zander Henning C Fiegel | 2006 | World Journal of Gastroenterology2006，12，15： | 23 |
| 2 | Genetics of hepatocellular carcinoma显示文摘The completely assembled human genome has made it possible for modern medicine to step into an era rich in genetic information and high-throughput genomic analysis. These novel and readily available genetic resources and analytical tools may be the key to unravel the molecular basis of hepatocellular carcinoma (HCC). Moreover, since an efficient treatment for this disease is lacking, further understanding of the genetic background of HCC will be crucial in order to develop new therapies aimed at selected targets. We report on the current status and recent developments in HCC genetics. Special emphasis is given to the genetics and regulation of major signalling pathways involved in HCC such as p53, Wnt- signalling, TGFβ, Ras, and Rb pathways. Furthermore, we describe the influence of chromosomal aberrations as well as of DNA methylation. Finally, we report on the rapidly developing field of genomic expression profiling in HCC, mainly by microarray analysis. | Andreas Teufel Frank Staib Stephan Kanzler Arndt Weinmann Henning Schulze-Bergkamen Peter R Galle | 2007 | World Journal of Gastroenterology2007，13，16： | 21 |
| 3 | TRAIL-induced apoptosis of hepatocellular carcinoma cells is augmented by targeted therapies显示文摘AIM:To analyze the effect of chemotherapeutic drugs and specific kinase inhibitors,in combination with the death receptor ligand tumor necrosis factor-related apoptosis inducing ligand(TRAIL),on overcoming TRAIL resistance in hepatocellular carcinoma(HCC)and to study the efficacy of agonistic TRAIL antibodies,as well as the commitment of antiapoptotic BCL-2 proteins, in TRAIL-induced apoptosis. METHODS:Surface expression of TRAIL receptors (TRAIL-R1-4)and expression levels of the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL were analyzed by flow cytometry and Western blotting,respectively. Knock-down of MCL-1 and BCL-xL was performed by transfecting specific small interfering RNAs.HCC cellswere treated with kinase inhibitors and chemotherapeutic drugs.Apoptosis induction and cell viability were analyzed via flow cytometry and 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS:TRAIL-R1 and-R2 were profoundly expressed on the HCC cell lines Huh7 and Hep-G2. However,treatment of Huh7 and Hep-G2 with TRAIL and agonistic antibodies only induced minor apoptosis rates.Apoptosis resistance towards TRAIL could be considerably reduced by adding the chemotherapeutic drugs 5-fluorouracil and doxorubicin as well as the kinase inhibitors LY294002[inhibition of phosphoinositol- 3-kinase(PI3K)],AG1478(epidermal growth factor receptor kinase),PD98059(MEK1),rapamycin(mam- malian target of rapamycin)and the multi-kinase inhibitor Sorafenib.Furthermore,the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL play a major role in TRAIL resistance:knock-down by RNA interference increased TRAIL-induced apoptosis of HCC cells.Additionally, knock-down of MCL-1 and BCL-xL led to a significant sensitization of HCC cells towards inhibition of both c-Jun N-terminal kinase and PI3K.CONCLUSION:Our data identify the blockage of survival kinases,combination with chemotherapeutic drugs and targeting of antiapoptotic BCL-2 proteins as promising ways to overcome TRAIL resistance in HCC. | Bruno Christian Koehler Toni Urbanik Binje Vick Regina Johanna Boger Steffen Heeger Peter R Galle Marcus Schuchmann Henning Schulze-Bergkamen | 2009 | World Journal of Gastroenterology2009，15，47： | 9 |
| 4 | Bcl-x_L and Myeloid cell leukaemia-1 contribute to apoptosis resistance of colorectal cancer cells显示文摘AIM: To explore the role of Bcl-xL and Myeloid cell leukaemia (Mcl)-1 for the apoptosis resistance of colorectal carcinoma (CRC) cells towards current treat-ment modalities. METHODS: Bcl-xL and Mcl-1 mRNA and protein ex-pression were analyzed in CRC cell lines as well as human CRC tissue by Western blot,quantitative PCRand immunohistochemistry. Bcl-xL and Mcl-1 protein expression was knocked down or increased in CRC cell lines by applying specific siRNAs or expression plas-mids,respectively. After modulation of protein expres-sion,CRC cells were treated with chemotherapeutic agents,an antagonistic epidermal growth factor recep-tor (EGFR1) antibody,an EGFR1 tyrosine kinase inhibi-tor,or with the death receptor ligand TRAIL. Apoptosis induction and cell viability were analyzed. RESULTS: Here we show that in human CRC tis-sue and various CRC cell lines both Bcl-xL and Mcl-1 are expressed. Bcl-xL expression was higher in CRC tissue than in surrounding non-malignant tissue,both on protein and mRNA level. Mcl-1 mRNA expression was significantly lower in ma-lignant tissues. However,protein expression was slightly higher. Viability rates of CRC cells were significantly decreased after knock down of Bcl-xL expression,and,to a lower extent,after knock down of Mcl-1 expression. Furthermore,cells with reduced Bcl-xL or Mcl-1 expression was more sensitive towards oxaliplatin-and irinotecan-induced apoptosis,and in the case of Bcl-xL also towards 5-FU-induced apoptosis. On the other hand,upregulation of Bcl-xL by transfec-tion of an expression plasmid decreased chemothera-peutic drug-induced apoptosis. EGF treatment clearly induced Bcl-xL and Mcl-1 expression in CRC cells. Apop-tosis induction upon EGFR1 blockage by cetuximab or PD168393 was increased by inhibiting Mcl-1 and Bcl-xL expression. More strikingly,CD95-and TRAIL-induced apoptosis was increased by Bcl-xL knock down. CONCLUSION: Our data suggest that Bcl-xL and,to a lower extent,Mcl-1,are important anti-apoptotic factors in CRC. Specific downregulation of Bcl-xL is a promising approach to sensitize CRC cells towards chemotherapy and targeted therapy. | Henning Schulze-Bergkamen Roland Ehrenberg Lothar Hickmann Binje Vick Toni Urbanik Christoph C Schimanski Martin R Berger Arno Schad Achim Weber Steffen Heeger Peter R Galle Markus Moehler | 2008 | World Journal of Gastroenterology2008，14，24： | 4 |
| 5 | Hydroxyethyl Starch Reduces Coagulation Competence and Increases Blood Loss During Major Surgery: Results From a Randomized Controlled Trial显示文摘 | Kirsten C. Rasmussen P?r I. Johansson Michael H?jskov Irina Kridina Thomas Kistorp Peter Thind Henning B. Nielsen Birgitte Ruhnau Tom Pedersen Niels H. Secher | 2014 | Annals of Surgery2014，，2： | 2 |
| 6 | Anthraquinones in Rheum palmatum and Rumex dentatus (Polygonaceae),and phorbol esters in Jatropha curcas (Euphorbiaceae) with molluscicidal activity against the schistosome vector snails Oncomelania,Biomphalaria and Bulinus显示文摘 | LIU S Y SPORER F WINK M JOURDANE J HENNING R Li Y L RUPPEL A | 1997 | Trop Med Int Health1997，2，2： | 1 |
| 7 | Hippocampal neurogenesis : regulation bystress and antidepressants显示文摘 | Dranovsky A Hen R | 2006 | Biol Psychiatry2006，59，12： | 1 |
| 8 | Air filters from HVAC systems as possible source of volatile organic compounds(VOC)-laboratory and field assays显示文摘 | Hans S Henning R | 1999 | Atmospheric Environment1999，33，28： | 1 |
| 9 | Characteristics of hemicellulose, cellulose and lignin pyrolysis显示文摘 | Yang H Yan R C hen H | 2007 | Fuel2007，86，： | 1 |
| 10 | Labeling human embryonic stem-cell-derived car- diomyocytes for tracking with MR imaging 显示文摘 | CASTANEDA R T BODDINGTON S HENNING T D | 2011 | Pediatric radiology2011，41，11： | 1 |
| 11 | Environ- mental Assessment in The Netherlands: Effectively Governing Environmental Protection? A Discourse A- nalysis 显示文摘 | HENS R FRANK VAN L PETER D | 2012 | Environmental Impact Assessment Re- view In Press Corrected Proof2012，20，： | 1 |
| 12 | Dentate gyms neurogenesis and depression显示文摘 | Sahay A Drew M R Hen R | 2007 | Prog Brain Res2007，163，： | 1 |
| 13 | Chemical methods and phytoremediation of soil contaminated with heavy metals显示文摘 | Hen H M Zheng C R Tu C | 2000 | Chemosphere2000，41，12： | 1 |
| 14 | Magnetic anomalies in the Pacific and sea floor spreading显示文摘 | Pitman W C III Hen'on E M Heirtzler J R | 1968 | Journal of Geophysical Research1968，73，： | 1 |
| 15 | Beat shock proteins and atrial fibrillation显示文摘 | Henning R H van Gelder I C | 2007 | Cell Stress Chaperones2007，12，2： | 1 |
| 16 | Formation mechanism of policyclic aromatic hydrocarbons and fullerenes in premixed benzene flames显示文摘 | HENNING R WILLIAM J G JACK B H | 1999 | Combus Flame1999，119，12： | 1 |
| 17 | A favorable diastereoselective synthesis of N-( 1 -S-ethoxycarbonyl-3-phenylpropy 1 )-S-alanine显示文摘 | Urbach H Henning R | 1984 | Tetrahedron Lett1984，25，11： | 1 |
| 18 | LFTs for automotive appli- cations显示文摘 | Henning F Ernst H Brussel R | 2005 | Reinforced plastics2005，49，2： | 1 |
| 19 | Respiratory tract mucins: structure and expression patterns 显示文摘 | Davies J R Hen'mann A Russell W | 2002 | Novartis Found Symp2002，248，： | 1 |
| 20 | Hippocampal granule neuron number and dentate gyrus volume in antidepressant-treated and untreated major depression显示文摘 | BOLDRINI M SANTIAGO A N HEN R | 2013 | Neuropsychopharmacology2013，38，6： | 1 |
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