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| 1 | Inflammatory status in human hepatic cirrhosis显示文摘This review focuses on new findings about the inflammatory status involved in the development of human liver cirrhosis induced by the two main causes, hepatitis C virus(HCV) infection and chronic alcohol abuse, avoiding results obtained from animal models. When liver is faced to a persistent and/or intense local damage the maintained inflammatory response gives rise to a progressive replacement of normal hepatic tissue by non-functional fibrotic scar. The imbalance between tissue regeneration and fibrosis will determine the outcome toward health recovery or hepatic cirrhosis. In all cases progression toward liver cirrhosis is caused by a dysregulation of mechanisms that govern the balance between activation/homeostasis of the immune system. Detecting differences between the inflammatory status in HCV-induced vs alcoholinduced cirrhosis could be useful to identify specific targets for preventive and therapeutic intervention in each case. Thus, although survival of patients with alcoholic cirrhosis seems to be similar to that of patients with HCV-related cirrhosis(HCV-C), there are important differences in the altered cellular and molecular mechanisms implicated in the progression toward human liver cirrhosis. The predominant features of HCV-C are more related with those that allow viral evasion of the immune defenses, especially although not exclusively, inhibition of interferons secretion, natural killer cells activation and T cell-mediated cytotoxicity. On the contrary, the inflammatory status of alcohol-induced cirrhosis is determined by the combined effect of direct hepatotoxicity of ethanol metabolites and increases of the intestinal permeability, allowing bacteria and bacterial products translocation, into the portal circulation, mesenteric lymph nodes and peritoneal cavity. This phenomenon generates a stronger pro-inflammatory response compared withHCV-related cirrhosis. Hence, therapeutic intervention in HCV-related cirrhosis must be mainly focused to counteract HCV-immune system evasion, while in the case of alcohol-induced cirrhosis it must try to break the inflammatory loop established at the gutmesenteric lymph nodes-peritoneal-systemic axis. | María Martínez-Esparza María Tristán-Manzano Antonio J Ruiz-Alcaraz Pilar García-Penarrubia | 2015 | World Journal of Gastroenterology2015，21，41： | 10 |
| 2 | The Causal Texture of Organizational Environments显示文摘 | EMERY F E TRIST E | 1965 | Human Relations1965，18，1： | 1 |
| 3 | Monoclonal antibodies and synthetic peptides define the active site of FcεRⅠ and a potential receptor antagonist显示文摘 | Rigby LJ Trist H Snider J | 2000 | Allergy2000，55，7： | 1 |
| 4 | Influence of Noise Correlation in Multiple-coil Statistical Models with Sum of Squares Reconstruction显示文摘 | Aja-Fernández S Tristán-Vega A | 2012 | Magnetic Resonance in Medicine2012，67，2： | 1 |
| 5 | The continuing evolution of the drug discovery process in the pharmaceutical industry 显示文摘 | Trist D | 2001 | Pure Appl Chem2001，73，1： | 1 |
| 6 | Referent Organizations and the Development of Inter-organizational Domains显示文摘 | TRIST E | 1983 | Human Relations1983，36，3： | 1 |
| 7 | Some Social and Psychological Consequences of the Long wall Method of Coal-Getting显示文摘 | TRIST E L BAMFORTH K W | 1951 | Human Relations1951，4，： | 1 |
| 8 | The interaction of Fc alpha RI with IgA and its implications for ligand binding by immunoreceptors of the leukocyte receptor clusters显示文摘 | Wines BD Sardjono CT Trist HT | 2001 | J Immunol2001，163，： | 1 |
| 9 | Structural basis for evasion of IgA immunity by Staphylococcus aureus revealed in the complex of SSL7with Fc of human IgA1显示文摘 | Ramsland PA Willoughby N Trist HM | 2007 | Proce Nat Acad Sci USA2007，104，15： | 1 |
| 10 | The Causal Texture of Organizational Environments 显示文摘 | Emery F E Trist E L | 1965 | Human Relations1965，18，： | 1 |
| 11 | Assessing terrestrial ecosystem sustainability: Usefulness of regional carbon and nitrogen models显示文摘 | MOHAN K WALI FATIH EVRENDILEK TRIST RAM OWATTS | 1999 | Nature & Resources1999，35，4： | 1 |
| 12 | The Causal Texture of Organizational Environments 显示文摘 | Emery F E Trist E L | 1965 | Human Rela- tions1965，18，1： | 1 |
| 13 | An experiment in autonomous working in an American underground coal mine 显示文摘 | TRIST E L | 1977 | 1977，，： | 1 |
| 14 | The causal texture of organizationalenvironments显示文摘 | Emery F Trist E | 1965 | Human Relations1965，18，1： | 1 |
| 15 | Bamforth: Some Social and Psychological Consequences of the Longwall Method of Coal - Getting 显示文摘 | TRIST E L | 1951 | Human Relations1951，，4： | 1 |
| 16 | Adapting to a Changing World显示文摘 | Trist E | 1978 | Labor Gazette1978，，： | 1 |
| 17 | The Causal Texture of Organizational Environments显示文摘 | EMERY F E TRIST E L | 1965 | Human Relations1965，18，1： | 1 |
| 18 | Evaluation of ni- grostriata] neurodegeneration and neuroinilammation fol- lowing repeated intranasal 1 -methyl-4-phenyl- 1,2,3,6-tet- rahydropyridine (MPTP) administration in mice, an ex- perimental model of Parkinson ' s disease 显示文摘 | Trist~o FS Amar M Latrous I | 2014 | Neurotox Res2014，25，1： | 1 |
| 19 | Excitatory amino acid agonists and antagonists:pharmacology and therapeutic applications显示文摘 | Trist DG | 2000 | Pharm Acta Helv2000，74，23： | 1 |
| 20 | Randomized controlled community-based nutrition and exercise intervention improves glycemia and cardiovascular risk factors in type 2 diabetic patients in rural Costa Rica显示文摘 | Goldhaber-Fiebert JD Goldhaber-Fiebert SN Tristán ML | | 0，，01： | 1 |
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