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| 1 | Pathogenesis of alcoholic liver disease:Role of oxidative metabolism显示文摘Alcohol consumption is a predominant etiological factor in the pathogenesis of chronic liver diseases,resulting in fatty liver,alcoholic hepatitis,fibrosis/cirrhosis,and hepatocellular carcinoma(HCC).Although the pathogenesis of alcoholic liver disease(ALD)involves complex and still unclear biological processes,the oxidative metabolites of ethanol such as acetaldehyde and reactive oxygen species(ROS)play a preeminent role in the clinical and pathological spectrum of ALD.Ethanol oxidative metabolism influences intracellular signaling pathways and deranges the transcriptional control of several genes,leading to fat accumulation,fibrogenesis and activation of innate and adaptive immunity.Acetaldehyde is known to be toxic to the liver and alters lipid homeostasis,decreasing peroxisome proliferator-activated receptors and increasing sterol regulatory element binding protein activity via an AMP-activated protein kinase(AMPK)-dependent mechanism.AMPK activation by ROS modulates autophagy,which has an important role in removing lipid droplets.Acetaldehyde and aldehydes generated from lipid peroxidation induce collagensynthesis by their ability to form protein adducts that activate transforming-growth-factor-β-dependent and independent profibrogenic pathways in activated hepatic stellate cells(HSCs).Furthermore,activation of innate and adaptive immunity in response to ethanol metabolism plays a key role in the development and progression of ALD.Acetaldehyde alters the intestinal barrier and promote lipopolysaccharide(LPS)translocation by disrupting tight and adherent junctions in human colonic mucosa.Acetaldehyde and LPS induce Kupffer cells to release ROS and proinflammatory cytokines and chemokines that contribute to neutrophils infiltration.In addition,alcohol consumption inhibits natural killer cells that are cytotoxic to HSCs and thus have an important antifibrotic function in the liver.Ethanol metabolism may also interfere with cell-mediated adaptive immunity by impairing proteasome function in macrophages and dendritic cells,and consequently alters allogenic antigen presentation.Finally,acetaldehyde and ROS have a role in alcohol-related carcinogenesis because they can form DNA adducts that are prone to mutagenesis,and they interfere with methylation,synthesis and repair of DNA,thereby increasing HCC susceptibility. | Elisabetta Ceni Tommaso Mello Andrea Galli | 2014 | World Journal of Gastroenterology2014，20，47： | 72 |
| 2 | Antidiabetic thiazolidinediones induce ductal differentiation but not apoptosis in pancreatic cancer cells显示文摘AIM: Thiazolidinediones (TZD) are a new class of oral antidiabetic drugs that have been shown to inhibit growth of same epithelial cancer cells. Although TZD were found to be ligands for peroxisome proliferator-activated receptor γ (PPARγ), the mechanism by which TZD exert their anticancer effect is presently unclear. In this study,we analyzed the mechanism by which TZD inhibit growth of human pancreatic carcinoma cell lines in order to evaluate the potential therapeutic use of these drugs in pancreatic adenocarcinoma.METHODS: The effects of TZD in pancreatic cancer cells were assessed in anchorage-independent growth assay.Expression of PPARγ was measured by reverse-transcription polymerase chain reaction and confirmed by Western blot analysis. PPARγ activity was evaluated by transient reporter gene assay. Flow cytometry and DNA fragmentationassay were used to determine the effect of TZD on cell cycle progression and apoptosis respectively. The effect of TZD on ductal differentiation markers was performed by Western blot.RESULTS: Exposure to TZD inhibited colony formation in a PPARγ-dependent manner. Growth inhibition was linked to G1 phase cell cycle arrest through induction of the ductal differentiation program without any increase of the apoptotic rate.CONCLUSION: TZD treatment in pancreatic cancer cells has potent inhibitory effects on growth by a PPAR-dependent induction of pacreatic ductal differentiation. | Elisabetta Ceni Tommaso Mello Mirko Tarocchi David W Crabb Anna Caldini Pietro Invernizzi Calogero Surrenti Stefano Milani Andrea Galli | 2005 | World Journal of Gastroenterology2005，11，8： | 15 |
| 3 | Hyperhomocysteinemia and hypercoagulability in primary biliary cirrhosis显示文摘瞄准:在有人半胱氨酸(HCY ) 和 haemostatic 系统的各种各样的部件的 PBC 和它的关系估计 hypercoagulability。方法:我们调查了 51 个 PBC 病人(43F/8M;意味着年龄:63+/-13.9 年) 并且 102 个健康题目(86 个 women/16 人;63+/-13 年) ,并且由 PFA-100 由 Sonoclot 分析和血小板功能在全血评估了 haemostatic 过程设备。我们然后测量了 HCY (禁食并且在蛋氨酸装载以后) ,织物因素(TF ) , thrombin-antithrombin 建筑群(梭织) , D 暗淡(D-D ) , thrombomodulin (TM ) , folic,维生素 B6 和 B12 血浆铺平。C677T 5,10-methylenetetrahydrofolate 还原酶(MTHFR ) 多型性被分析。结果:病人的 Sonoclot 率值是显著地(P<0.001 ) 比那些高控制。山峰价值的 Sonoclot 时间和 PFA-100 闭合时间在病人和控制是可比较的。梭织, TF 和 HCY 层次,两个在禁食并且蛋氨酸以后的装载,显著地(P<0.001 ) 在病人更高与比在控制。维生素缺乏在 45/51 病人(88.2%) 被检测。同型结合的 TT677 MTHFR 遗传型的流行比在控制(17.5%)(P<0.05 ) 在病人(31.4%) 是显著地更高的。Sonoclot 率价值与 HCY 层次和 TF 显著地相关。结论:在 PBC, hyper-HCY 与维生素缺少和基因预先安排因素有关。内皮激活的增加的 TF 和 HCY 层次和符号与 hypercoagulability 被联系并且可以在血凝固激活有一个重要角色。 | Maria Rosa Biagini Alessandro Tozzi Rossella Marcucci Rita Paniccia Sandra Fedi Stefano Milani Andrea Galli Elisabetta Ceni Marco Capanni Raffaele Manta Rosanna Abbate Calogero Surrenti | 2006 | World Journal of Gastroenterology2006，12，10： | 6 |
| 4 | Acetaldehyde Inhibits PPARγ via H 2 O 2 -Mediated c-Abl Activation in Human Hepatic Stellate Cells显示文摘 | Elisabetta Ceni David W. Crabb Marco Foschi Tommaso Mello Mirko Tarocchi Valentino Patussi Luca Moraldi Renato Moretti Stefano Milani Calogero Surrenti Andrea Galli | 2006 | Gastroenterology2006，，4： | 2 |
| 5 | Identification of aphid (Homoptera:Aphididae) species and clones by random amplification polymorphic DNA显示文摘 | CENIS J L PEREZ P FERERES A | 1993 | Annals of the Entomological Sciety of America1993，86，5： | 1 |
| 6 | Genetics and specific immune response in allergy to birch pollen and food:edvidence of a strong,positive association between atopy and the HLA class Ⅱ allele HLA-DR7显示文摘 | SNECHAL H CENY S DESVAUX F X | 1999 | J Allergy Clin Immunol1999，104，2： | 1 |
| 7 | Oxidative stress stimulates proliferation and invasiveness of hepatic stellate cells via a MMP2-mediated mechanism显示文摘 | Svegliati-Baroni G Ceni E | 2005 | Hepatology2005，41，： | 1 |
| 8 | Expression of MDR/P-glyprotein in human sarcoma显示文摘 | Veriger B Ceny L G Heny W | 1993 | Br J Cancer1993，68，10： | 1 |
| 9 | Survey of Bernisia tabaci (Hemiptera : Aleyrodidae) biotypes in Italy with the description of a new biotype(T) from Euphorbia characias 显示文摘 | Simon B Cenis JL Demichelis S | 2003 | Bulletin of Entomological Research2003，93，： | 1 |
| 10 | Rapid extraction of fungal DNA for PCR amplification显示文摘 | Cenis J L | 1992 | Nucleic Acids Research1992，20，： | 1 |
| 11 | The p75NTR intracellular domain generated by neurotrophin-induced receptor cleavage potentiates Trk signaling显示文摘 | Ceni C Kommeddi RP | 2010 | Cell Sei2010，123，13： | 1 |
| 12 | A simple 4D chaotic oscillator显示文摘 | Namajunas A Cenys | 1996 | Electronics Letters1996，32，： | 1 |
| 13 | Peroxisome proliferator- activated receptor γ transcriptional regulation is involved in platelet-derived growth factor-induced proliferation in human hepatic stellate cells 显示文摘 | Galli A Crabb D Ceni E | 2000 | Hepatology2000，，： | 1 |
| 14 | Oxidative stress stimulates proliferation and invasiveness of hepatic stellate cells via a MMP2-mediated mechanism 显示文摘 | Galli A Svegliati-Baroni G Ceni E | 2005 | Hepatology2005，41，5： | 1 |
| 15 | Physical synchronizing hyperchaos with one single variable显示文摘 | Tamasevicius A Cenys A | 1997 | Physical Review E1997，55，： | 1 |
| 16 | Acetaldehyde inhibits PPARgamma via H202 -mediated c- Abl activation in hu- man hepatic stellate cells显示文摘 | Ceni E Crabb DW Foschi M | 2006 | Gastroenterology2006，131，： | 1 |
| 17 | Alcohol induced hepatie fibrosis:role of acetaldehyde显示文摘 | Mello T Ceni E Surrenti C | 2008 | Mol Aspects Med2008，29，12： | 1 |
| 18 | Acetaldehyde inhibits PPARgamma via H2 02-mediated c-Abl activation in human hepatic stellate cells 显示文摘 | Ceni E Crabb D W Foschi M | 2006 | Gastroenterology2006，131，4： | 1 |
| 19 | Minimally invasive approach for the resection of spinal neoplasm显示文摘 | Haji FA Cenie A Crevier L | 2011 | Spine (Phila Pa 1976)2011，36，15： | 1 |
| 20 | Hyperchaotic oscillator with gyrators显示文摘 | Cenys S Mykolaitis G | 1996 | Electron Lett1996，33，7： | 1 |
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