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| 1 | Long-term antifibrotic action of interferon-γ treatment in patients with chronic hepatitis B virus infection显示文摘BACKGROUND:The first priority in treating fibrosis is to eliminate the causes that result in liver injury,e.g.,hepatitis B and C virus.However,in many liver diseases the cause is either unknown or untreatable.The present study was designed to investigate the long-term antifibrotic effect of interferon-gamma(IFN-γ)treatment in patients chronically infected with hepatitis B virus. METHODS:A total of 42 patients,30 treated with IFN-γand 12 controls,were enrolled from an original clinical trial(Clin Gastroenterol Hepatol 2005;3:819.).Three serial liver biopsies that were obtained at the initiation and end of IFN-γtreatment as well as 4 to 6 years after treatment discontinuation were assessed according to the modified Chevallier scoring system. RESULTS:Twenty-five out of 30 IFN-γ-treated patients were followed up until 4 to 6 years after the treatment was stopped. However,all controls were excluded from follow-up due to death,loss and elevated virus level within 2 years.Twenty-five IFN-γ-treated patients had stable serum liver function and liver fibrosis indices without any further antiviral or anti-fibrotic treatment.Improved inflammatory and fibrotic scores were found after nine months of IFN-γtreatment according to the modified Chevallier scoring system(inflammation:11.8±6.5 at the beginning of IFN-γtreatment vs.9.2±4.1 after 9 months, P<0.05;fibrosis:15.0±7.3 at baseline vs.12.6±6.8 after 9 months, P<0.05).Among them,14 patients accepted a third serial liver biopsy 4 to 6 years after treatment discontinuation,and the fibrotic score was increased(14.2±8.3 vs.11.9±7.6 after 9 months, P<0.05). CONCLUSIONS:Nine-month IFN-γtreatment significantly improves the fibrosis score in patients with chronic HBV infection.The majority of patients demonstrate stable serum biochemical indices and quality of life.However,they do not show a long-term benefit according to histological criteria. Given the limited sample size,long-term IFN-γtreatment regimens should be assessed in further clinical trials. | Peter R Mertens Steven Dooley | 2011 | Hepatobiliary & Pancreatic Diseases International2011，10，2： | 6 |
| 2 | Hepatocyte-Specific Smad7 Expression Attenuates TGF-β–Mediated Fibrogenesis and Protects Against Liver Damage显示文摘 | Steven Dooley Jafar Hamzavi Loredana Ciuclan Patricio Godoy Iryna Ilkavets Sabrina Ehnert Elke Ueberham Rolf Gebhardt Stephan Kanzler Andreas Geier Katja Breitkopf Honglei Weng Peter R. Mertens | 2008 | Gastroenterology2008，，2： | 2 |
| 3 | Multicenter analysis of soluble A xl reveals diagnostic value for very early stage hepatocellular carcinoma显示文摘 | Patrick Reichl Meng Fang Patrick Starlinger Katharina Staufer Rudolf Nenutil Petr Muller Kristina Greplova Dalibor Valik Steven Dooley Christine Brostjan Thomas Gruenberger Jiayun Shen Kwan Man Michael Trauner Jun Yu Chun Fang Gao Wolfgang Mikulits | 2015 | Int. J. Cancer2015，，2： | 2 |
| 4 | Smad7 dependent expression signature highlights BMP2 and HK2 signaling in HSC transdifferentiation显示文摘AIM: To analyse the influence of Smad7, antagonist of transforming growth factor (TGF)-β canonical signaling pathways on hepatic stellate cell (HSC) transdifferentia-tion in detail. METHODS: We systematically analysed genes regulated by TGF-β/Smad7 in activated HSCs by microarray analy-sis and validated the results using real time polymerase chain reaction and Western blotting analysis. RESULTS: We identif ied 100 known and unknown tar-gets underlying the regulation of Smad7 expression and delineated 8 gene ontology groups. Hk2, involved in glycolysis, was one of the most downregulated proteins, while BMP2, activator of the Smad1/5/8 pathway, was extremely upregulated by Smad7. However, BMP2 de-pendent Smad1 activation could be inhibited in vitro by Smad7 overexpression in HSCs. CONCLUSION: We conclude (1) the existence of a tight crosstalk of TGF-β and BMP2 pathways in HSCs and (2) a Smad7 dependently decreased sugar metabolism ameliorates HSC activation probably by energy with-drawal. | Bernd Denecke Lucia Wickert Loredana Ciuclan Steven Dooley Nadja M Meindl-Beinker Yan Liu | 2010 | World Journal of Gastroenterology2010，16，41： | 1 |
| 5 | Pancreaticoduodenectomy for Cancer of the Head of the Pancreas 201 Patients显示文摘 | Charles J. Yeo John L. Cameron Keith D. Lillemoe James V. Sitzmann Ralph H. Hruban Steven N. Goodman William C. Dooley JoAnn Coleman Henry A. Pitt | 1995 | Annals of Surgery1995，，： | 1 |
| 6 | Hepatocyte-Specific Smad7 Expression Attenuates TGF-β–Mediated Fibrogenesis and Protects Against Liver Damage显示文摘 | Steven Dooley Jafar Hamzavi Loredana Ciuclan Patricio Godoy Iryna Ilkavets Sabrina Ehnert Elke Ueberham Rolf Gebhardt Stephan Kanzler Andreas Geier Katja Breitkopf Honglei Weng Peter R. Mertens | 2008 | Gastroenterology2008，，2： | 1 |
| 7 | Genomic locus and promoter region of rat Smad7, an important antagonist of TGFβ signaling显示文摘 | Marcin Stopa Vladimir Benes Wilhelm Ansorge Axel M. Gressner Steven Dooley | 2000 | Mammalian Genome2000，，2： | 1 |
| 8 | TGF-β in progression of liver disease显示文摘 | Steven Dooley Peter Dijke | 2012 | Cell and Tissue Research2012，，1： | 1 |
| 9 | IFN- γ inhibits liver progenitor cell proliferation in HBV-infected patients and in 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet-fed mice显示文摘 | Hong-lei Weng De-chun Feng Svetlana Radaeva Xiao-ni Kong Lei Wang Yan Liu Qi Li Hong Shen Yun-peng Gao Roman Müllenbach Stefan Munker Tong Huang Jia-lin Chen Vincent Zimmer Frank Lammert Peter R. Mertens Wei-min Cai Steven Dooley Bin Gao | 2013 | Journal of Hepatology2013，，： | 1 |
| 10 | Hepatocyte-Specific Smad7 Expression Attenuates TGF-β–Mediated Fibrogenesis and Protects Against Liver Damage显示文摘 | Steven Dooley Jafar Hamzavi Loredana Ciuclan Patricio Godoy Iryna Ilkavets Sabrina Ehnert Elke Ueberham Rolf Gebhardt Stephan Kanzler Andreas Geier Katja Breitkopf Honglei Weng Peter R. Mertens | 2008 | Gastroenterology2008，，2： | 1 |
| 11 | Transforming growth factor β signal transduction in hepatic stellate cells via Smad2/3 phosphorylation, a pathway that is abrogated during in vitro progression to myofibroblasts显示文摘 | Steven Dooley Bert Delvoux Maike Streckert Linda Bonzel Marcin Stopa Peter ten Dijke Axel M. Gressner | 2001 | FEBS Letters2001，，1： | 1 |
| 12 | Reciprocal regulation by TLR4 and TGF-[Beta] in tumor-initiating stem-like cells显示文摘 | Chen Chia-Lin Tsukamoto Hidekazu Liu Jian-Chang Kashiwabara Claudine Feldman Douglas Sher Linda Dooley Steven French Samuel W Mishra Lopa Petrovic Lydia Jeong Joseph H Machida Keigo | 2013 | Journal of Clinical Investigation2013，，7： | 1 |
| 13 | TGF-β in progression of liver disease显示文摘 | Steven Dooley Peter Dijke | 2012 | Cell and Tissue Research2012，，1： | 1 |
| 14 | Transforming Growth Factor-β (TGF-β)-mediated Connective Tissue Growth Factor (CTGF) Expression in Hepatic Stellate Cells Requires Stat3 Signaling Activation显示文摘 | Yan Liu Heng Liu Christoph Meyer Jun Li Silvio Nadalin Alfred K?nigsrainer Honglei Weng Steven Dooley Peter ten Dijke | 2013 | Journal of Biological Chemistry2013，，42： | 1 |
| 15 | Loss of TGF-β dependent growth control during HSC transdifferentiation显示文摘 | Oliver Purps Birgit Lahme Axel M. Gressner Nadja M. Meindl-Beinker Steven Dooley | 2006 | Biochemical and Biophysical Research Communications2006，，3： | 1 |
| 16 | Transforming growth factor - b and hepatocyte transdifferentiation in liver fibrogenesis 显示文摘 | Nadja M Meindl -Beinker Steven Dooley | 2008 | Journal of Gastroenterology and Hepatology2008，23，： | 1 |
| 17 | TGF-β in progression of liver disease显示文摘 | Steven Dooley Peter Dijke | 2012 | Cell and Tissue Research2012，，1： | 1 |
| 18 | A randomized comparison of continuous vs. intermittent infliximab maintenance regimens over 1 year in the treatment of moderate-to-severe plaque psoriasis显示文摘 | Alan Menter Steven R. Feldman Gerald D. Weinstein Kim Papp Robert Evans Cynthia Guzzo Shu Li Lisa T. Dooley Cynthia Arnold Alice B. Gottlieb | 2007 | Journal of the American Academy of Dermatology2007，，1： | 1 |
| 19 | Acute liver injury induces expression of FGF23 in hepatocytes via orphan nuclear receptor ERRγ signaling显示文摘Fibroblast growth factor 23(FGF23)is an osteocyte-and osteoblast-derived hormone that primarily regulates phosphate and vitamin D metabolism.Circulatory FGF23 levels are abnormally increased in pathological conditions like acute or chronic kidney injury,resulting in disease progression as well as increased rates of morbidity and mortality.^(1) However,FGF23 production in acute liver injury is not fully investigated.In this study. | Yoon Seok Jung Yong-Hoon Kim Kamalakannan Radhakrishnan Jung-Ran Noh Jung Hyeon Choi Hyo-Jin Kim Jae-Ho Jeong Steven Dooley Chul-Ho Lee Hueng-Sik Choi | 2023 | Genes & Diseases2023，10，3： | 0 |
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