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| 1 | Diagnostic utility of IgG and IgM immunohistochemistry in autoimmune liver disease显示文摘AIM:To assess the role of IgM and IgG immunohistochemistry(IHC) in the evaluation of autoimmune liver conditions-autoimmune hepatitis(AIH),primary biliary cirrhosis(PBC),and primary sclerosing cholangitis(PSC).METHODS:Forty one biopsies from untreated patients diagnosed with autoimmune liver disease(AIH,n = 20;PBC,n = 13;PSC,n = 8) and fourteen biopsies of patients with chronic hepatitis C were selected.IgM and IgG-positive plasma cells were counted in each sample.RESULTS:A predominance of IgG-positive plasma cells was seen in AIH(90% of cases),PSC(75% of cases),and chronic hepatitis C(100% of cases),while IgMpositive plasma cells predominated in PBC(92.8% ofcases).The IgM /IgG ratio(< 1 or ≥ 1) accurately distinguished PBC from AIH in 90.9% of cases(sensitivity = 92.3%,specificity = 90%),and PBC from either AIH or PSC in 87.8% of cases(sensitivity = 92.3%,specificity = 85.7%).CONCLUSION:Plasmacytic infiltrates expressing predominantly IgM are characteristic of PBC,while other forms of liver disease analyzed in this study,including AIH,typically show an IgG-predominant plasma cell infiltrate.Our data indicate that IgM and IgG IHC may be a useful tool when PBC is a diagnostic consideration. | Roger Klein Moreira Frank Revetta Elizabeth Koehler Mary Kay Washington | 2010 | World Journal of Gastroenterology2010，16，4： | 11 |
| 2 | 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 |
| 3 | Regulation of epithelium-specific Ets-like factors ESE-1 and ESE-3 in airway epithelial cells: potential roles in airway inflammation显示文摘航线发炎是许多呼吸障碍的特点,例如气喘和膀胱的纤维变性。在发炎触发的航线基因表示的变化在这些疾病的致病起一个关键作用。基因连接研究建议 ESE-2 和 ESE-3,编码上皮特定的 Ets-domain-containing 抄写因素,是候选人气喘危险性基因。我们这里报导 et 家庭抄写因素 ESE-1 的另一个成员的表示,以及 ESE-3,起来在支气管的上皮的房间线由煽动性的 cytokines interleukin-1beta (IL-1beta ) 和肿瘤坏死 factor-alpha (TNF-alpha ) 调整了。有 IL-1beta 和 TNF-alpha 的这些房间的处理为 ESE-1 和 ESE-3 导致了信使 rna 表示的戏剧的增加。我们证明导致的表示被抄写因素 NF-kappaB 的激活调停。我们描绘了 ESE-1 和 ESE-3 倡导者并且识别了为导致 cytokine 的表达式被要求的 NF-kappaB 有约束力的序列。另外,我们也表明那 ESE-1 在上面调整 ESE-3 表示, down 由 cytokines 调整它的自己的正式就职。最后,我们在 Elf3 显示出那(对人的 ESE-1 相应) 猛烈老鼠,煽动性的 cytokine interleukin-6 (IL-6 ) 的表示是调整的 down。我们的调查结果建议 ESE-1 和 ESE-3 在航线发炎起一个重要作用。 | Jing Wu Rongqi Duan Huibi Cao Deborah Field Catherine M Newnham David R Koehler Noe Zamel Melanie A Pritchard Paul Hertzog Martin Post A Keith Tanswell Jim Hu | 2008 | Cell Research2008，18，6： | 6 |
| 4 | 一种优化关系型溯源信息存储的新方法显示文摘现代数据管理必须处理来源不同、质量各异的数据,因此从系统层面支持数据溯源,让用户了解数据的来源及派生过程成为当前至关重要的一个研究课题.基于标注的方法是支持数据溯源的基本方法之一.这种方法的主要问题是存储空间开销,因为溯源信息可能会超过实际数据的大小.在该文中,作者提出了一个用与查询结构匹配的溯源树来表达和存储溯源信息从而避免数据派生过程中冗余存储的基本框架.基于这个框架,作者提出了一系列针对关系型查询的存储优化方法,选择查询树部分节点来存储溯源信息.这些优化算法对于查询大小是多项式时间,对于溯源信息大小是线性时间,在溯源信息的跟踪和优化方面均不会产生巨大的开销.这一框架是数据溯源研究的一个新思路,有着广泛的应用前景. | 王黎维 鲍芝峰 KOEHLER Henning 周晓方 SADIQ Shazia | 2011 | 计算机学报2011，34，10： | 6 |
| 5 | Utilizing zebrafish and okadaic acid to study Alzheimer's disease显示文摘Despite the many years of extensive research using rodent models to study Alzheimer's disease(AD),no cure or disease halting drug exists.An increasing number of people are suffering from the disease and a therapeutic intervention is needed.Therefore,it is necessary to have complementary models to aid in the drug discovery.The zebrafish animal model is emerging as a valuable model for the investigation of AD and neurodegenerative drug discovery.The main genes involved in human AD have homologous counterparts in zebrafish and have conserved function.The basic brain structure of the zebrafish is also conserved when compared to the mammalian brain.Recently an AD model was established by administering okadaic acid to zebrafish.It was used to test the efficacy of a novel drug,lanthionine ketimine-5-ethyl ester,and to elucidate its mechanism of action.This demonstrated the ability of the okadaic acid-induced AD zebrafish model to be implemented in the drug discovery process for therapeutics against AD. | Daniel Koehler Frederick E.Williams | 2018 | Neural Regeneration Research2018，13，9： | 5 |
| 6 | Targeting cell death signaling in colorectal cancer:Current strategies and future perspectives显示文摘The evasion from controlled cell death induction has been considered as one of the hallmarks of cancer cells.Defects in cell death signaling are a fundamental phenomenon in colorectal cancer.Nearly any non-invasive cancer treatment finally aims to induce cell death.However,apoptosis resistance is the major cause for insufficient therapeutic success and disease relapse in gastrointestinal oncology.Various compounds have been developed and evaluated with the aim to meet with this obstacle by triggering cell death in cancer cells.The aim of this review is to illustrate current approaches and future directions in targeting cell death signaling in colorectal cancer.The complex signaling network of apoptosis will be demonstrated and the'druggability'of targets will be identified.In detail,proteins regulating mitochondrial cell death in colorectal cancer,such as Bcl-2 and survivin,will be discussed with respect to potential therapeutic exploitation.Death receptor signaling and targeting in colorectal cancer will be outlined.Encouraging clinical trials including cell death based targeted therapies for colorectal cancer are under way and will be demonstrated.Our conceptual understanding of cell death in cancer is rapidly emerging and new types of controlled cellular death have been identified.To meet this progress in cell death research,the implication of autophagy and necroptosis for colorectal carcinogenesis and therapeutic approaches will also be depicted.The main focus of this topic highlight will be on the revelation of the complex cell death concepts in colorectal cancer and the bridging from basic research to clinical use. | Bruno Christian Koehler Dirk Jger Henning Schulze-Bergkamen | 2014 | World Journal of Gastroenterology2014，20，8： | 4 |
| 7 | External Validation of the Fatty Liver Index for Identifying Nonalcoholic Fatty Liver Disease in a Population-based Study显示文摘 | Edith M. Koehler Jeoffrey N.L. Schouten Bettina E. Hansen Albert Hofman Bruno H. Stricker Harry L.A. Janssen | 2013 | Clinical Gastroenterology and Hepatology2013，，： | 4 |
| 8 | CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes显示文摘AIM:To analyze the role of CYLD for receptor-mediated cell death of murine hepatocytes in acute liver injury models.METHODS:Hepatocyte cell death in CYLD knockout mice(CYLD-/-)was analyzed by application of liver injury models for CD95-(Jo2)and tumor necrosis factor(TNF)-α-[D-Gal N/lipopolysaccharide(LPS)]induced apoptosis.Liver injury was assessed by measurement of serum transaminases and histological analysis.Apoptosis induction was quantified by cleaved PARP staining and Western blotting of activated caspases.Nuclear factor(NF)-κB,ERK,Akt and jun amino-terminal kinases signaling were assessed.Primary Hepatocytes were isolated by two step-collagenase perfusion and treated with recombinant TNF-αand with the CD95-ligand Jo2.Cell viability was analyzed by MTT-assay.RESULTS:Livers of CYLD-/-mice showed increased anti-apoptotic NF-κB signaling.In both applied liver injury models CYLD-/-mice showed a significantly reduced apoptosis sensitivity.After D-Gal N/LPS treatment CYLD-/-mice exhibited significantly lower levels of alanine aminotransferase(ALT)(295 U/L vs 859 U/L,P<0.05)and aspartate aminotransferase(AST)(560 U/L vs 1025 U/L,P<0.01).After Jo injection CYLD-/-mice showed 2-fold lower ALT(50 U/L vs 110 U/L,P<0.01)and lower AST(250 U/L vs 435 U/L,P<0.01)serumlevels compared to WT mice.In addition,isolated CYLD-/-primary murine hepatocytes(PMH)were less sensitive towards death receptor-mediated apoptosis and showed increased levels of Bcl-2,XIAP,c IAP1/2,survivin and c-FLIP expression upon TNF-and CD95-receptor triggering,respectively.Inhibition of NF-κB activation by the inhibitor of NF-κB phosphorylation inhibitor BAY 11-7085 inhibited the expression of antiapoptotic proteins and re-sensitized CYLD-/-PMH towards TNF-and CD95-receptor mediated cell death.CONCLUSION:CYLD is a central regulator of apoptotic cell death in murine hepatocytes by controlling NF-κB dependent anti-apoptotic signaling. | Toni Urbanik Bruno Christian Koehler Laura Wolpert Christin Elbner Anna-Lena Scherr Thomas Longerich Nicole Kautz Stefan Welte Nadine Hovelmeyer Dirk Jager Ari Waisman Henning Schulze-Bergkamen | 2014 | World Journal of Gastroenterology2014，20，45： | 3 |
| 9 | 教育:青年与青年奥运会显示文摘有人把体育运动中的兴奋剂归咎于参赛运动员违背了体育运动精神的价值取向,从不太严格的意义上讲,体育精神可以这样来描述,即运动员通过努力的训练及顽强的意志(而不是使用违禁物质与方法),来实现对体育运动的热爱、卓越的追求,并由此获取相应的物质回报。另一方面,运动员是否以为他(她)的对手在使用兴奋剂也会影响他们的态度,因为他们往往会为了取得同等的竞争条件而做同样的事情;另外一些影响运动员是否使用兴奋剂的因素来自于他(她)的同伴、支持者、赞助商、媒体、公众舆论等,这些因素都有可能左右他(她)们的决定,即在比赛当中是否应使用提高运动成绩的违禁药物或措施。 | Rob KOEHLER | 2008 | 体育科研2008，29，5： | 3 |
| 10 | Modulation of Longevity and Tissue Homeostasis by the Drosophila PGC-1 Homolog显示文摘 | Michael Rera Sepehr Bahadorani Jaehyoung Cho Christopher L. Koehler Matthew Ulgherait Jae H. Hur William S. Ansari Thomas Lo D. Leanne Jones David W. Walker | 2011 | Cell Metabolism2011，，5： | 2 |
| 11 | Prevalence and risk factors of non-alcoholic fatty liver disease in the elderly: Results from the Rotterdam study显示文摘 | Edith M. Koehler Jeoffrey N.L. Schouten Bettina E. Hansen Frank J.A. van Rooij Albert Hofman Bruno H. Stricker Harry L.A. Janssen | 2012 | Journal of Hepatology2012，，6： | 2 |
| 12 | 欧洲钢铁工业并购的全球化的几点教训显示文摘全球钢铁工业当前蒸蒸日上,主要是由于中国的快速发展,欧洲是世界上最有竞争力的地区之一,提供技术精良的产品。从20世纪70年代中期到90年代初,欧洲钢铁工业经历了众多危机和严重的损失;当前,钢铁业的繁荣除了全球经济增长因素以外,主要有以下3个原因:(1)整合与生产效率提高;(2)产品优化和质量提高,和(3)价值链为基础的更紧密合作。但是,这一变化的基本前提为:再私有化与对补贴的严格控制,致使政府干预减少。 | Karl-Ulrich Koehler | 2006 | 中国钢铁业2006，，5： | 2 |
| 13 | Methylene blue-aided chromoendoscopy for the detection of intraepithelial neoplasia and colon cancer in ulcerative colitis显示文摘 | Ralf Kiesslich Johannes Fritsch Martin Holtmann Heinz H. Koehler Manfred Stolte Stephan Kanzler Bernhard Nafe Michael Jung Peter R. Galle Markus F. Neurath | 2003 | Gastroenterology2003，，4： | 2 |
| 14 | Cost-Efficiency and Outcomes in the Treatment of Perforated Peptic Ulcer Disease: Laparoscopic Versus Open Approach显示文摘 | G. Paul Wright Alan T. Davis Tracy J. Koehler David E. Scheeres | 2014 | Surgery2014，，： | 2 |
| 15 | Procalcitonin (PCT)-guided algorithm reduces length of antibiotic treatment in surgical intensive care patients with severe sepsis: results of a prospective randomized study显示文摘 | S. Schroeder M. Hochreiter T. Koehler A.-M. Schweiger B. Bein F. S. Keck T. Spiegel | 2009 | Langenbeck’s Archives of Surgery2009，，2： | 2 |
| 16 | Integration of Chinese Medicine and Western Medicine in Clinical Practice(Patient Care):Past,Present,and A Proposed Model for the Future显示文摘Historic Background Chinese medicine(CM) has over 2,000 years of history in China and was the only health care system providing care for Chinese prior to the introduction of Western medicine(WM) into China.WM was slowly introduced into China by missionaries from the middle 17th century to the beginning of the 19th century. By 1840,WM began to take root in China.Western hospitals,clinics,medical schools and nursing | Ian Tsang Simon Huang Barry Koehler | 2013 | Chinese Journal of Integrative Medicine2013，19，2： | 2 |
| 17 | Drainage of single plateau borders: direct observation of rigid and mobile interfaces 显示文摘 | KOEHLER S A HILGENFELDT S WEEKS E R | 2002 | Physical Review E2002，66，04： | 1 |
| 18 | Novel extraction of German cockroach fecal pellets enhances efficacy of spray formulation insecticides 显示文摘 | Miller DM Koehler PG | 2000 | Ann Entomol Soc Am2000，93，： | 1 |
| 19 | Tracing the development of teacher knowledge in a design seminar:Integrating content, pedagogy and technology 显示文摘 | Koehler M J Mishra P Yahya K | 2007 | Computers & Education2007，49，3： | 1 |
| 20 | Stopping criteria for finite length genetic algorithms显示文摘 | KOEHLER H A G J | 1996 | Informs Journal on Computer1996，8，2： | 1 |
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