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| 1 | Different effects of a CD14 gene polymorphism on disease outcome in patients with alcoholic liver disease and chronic hepatitis C infection显示文摘AIM: Clinical and experimental data suggest that gut-derived endotoxins are an important pathogenic factors for progression of chronic liver disease. Recently, a C-T (-159)polymorphism in the promoter region of the CD14 gene was detected and found to confer increased CD14 expression and to be associated with advanced alcoholic liver damage. Here, we investigated this polymorphism in patients with less advanced alcoholic liver disease (ALD)and chronic hepatitis C virus (HCV) infection.METHODS: CD14 genotyping was performed by PCR-RFLP analysis in (a) 121 HCV patients, (b) 62 patients with alcohol-associated cirrhosis (Alc-Ci), (c) 118 individuals with heavy alcohol abuse without evidence of advanced liver damage (Alc-w/o Ci), and (d) 247 healthy controls.Furthermore, serum levels of soluble CD14 (sCD14) and transaminases were determined.RESULTS: The TT genotype was significantly more frequent in Alc-Ci compared to Alc-w/o Ci or controls (40.3% vs 23.7% or 24.0%, respectively). In Alc-w/o Ci,serum levels of transaminases did not differ significantly between patients with different CD14 genotypes. In HCV patients, TT-homozygotes had significantly higher sCD14 levels and sCD14 serum levels were significantly higher in patients with advanced fibrosis or cirrhosis. However,no association was found between CD14 genotypes and histological staging or grading.CONCLUSION: Considering serum transaminases as surrogate markers for alcoholic liver damage, the CD14 polymorphism seems to exhibit different effects during the course of ALD. Differences in genotype distribution between cirrhotic HCV patients and alcoholics and the known functional impact of this polymorphism on CD14 expression levels further indicate differences in the pathophysiological role of CD14 and CD14-mediated lipopolysaccharides signal transduction with regard to the stage as well as the type of the underlying liver disease. | C Meiler M Mühlbauer M Johann A Hartmann B Schnabl N Wodarz G Schmitz J Schlmerich C Hellerbrand | 2005 | World Journal of Gastroenterology2005，11，38： | 3 |
| 2 | The ALDH gene superfamily of Arabidopsis显示文摘 | Kirch H H Bartels D Wei Y Schnable P S Wood A J | | 0，，： | 1 |
| 3 | Dexrazoxane (ICRF-187) protects cardiac myocytes against doxorubicin by preventing damage to mitochondria显示文摘 | HASINOFF B B SCHNABL K L MARUSAK R A | 2003 | Cardiovascular Toxicology2003，3，2： | 1 |
| 4 | Interactions Between The Intestinal Microbiome AndLiver Diseases 显示文摘 | Schnabl B Brenner D A | 2014 | Gastroenterology2014，146，6： | 1 |
| 5 | TAK1/JNK and p38 have opposite effects on rat hepatic stellate cells显示文摘 | Schnabl B Bradham C A Bennett B L | 2001 | Hepatology2001，34，5： | 1 |
| 6 | Active middle ear implantation in elderly people: a retrospective study显示文摘 | Wolf-Magele A Schnabl J Woellner T | 2011 | Otoi Neurotol2011，32，5： | 1 |
| 7 | Monetary P0licy,Vagabonding Liquidity and Bursting Bubbles in New and Emerging Markets:An Overinvestment View显示文摘 | Hoffman A and G Schnabl | 2008 | World Economy2008，31，9： | 1 |
| 8 | The B73 maize genome:Complexity,diversity,and dynamics显示文摘 | Schnable P S Ware D Fulton R S Stein J C Wei F Pasternak S Liang C Zhang J Fulton L Graves T A Minx P Reily A D Courtney L Kruchowski S S Tomlinson C Strong C Delehaunty K Fronick C Courtney B Rock S M Belter E Du F Kim K Abbott R M Cotton M Levy A Marche | | 0，，5956： | 1 |
| 9 | Imputed interindustry technology flows- a comparative SMFA analysis 显示文摘 | SCHNABL H | 2000 | Economic Systems Research2000，12，3： | 1 |
| 10 | TAK1/JNK and p38 have opposite effects on rat hepatic stellate cells 显示文摘 | Schnabl B Bradham C A Bennett B L | 2001 | Hepatology2001，34，5： | 1 |
| 11 | Dexrazoxane (ICRF-187) Protects Cardiac Myocytes Against Doxorubicin by Preventing Damage to Mitochondria 显示文摘 | Hasinoff B B Schnabl K L Marusak R A | 2003 | Cardiovasc Toxicol2003，3，： | 1 |
| 12 | The B73 maize genome:complexity,diversity,and dynamics显示文摘 | Schnable P.S Ware D Fulton R.S Stein J.C Wei F Pasternak S Liang C Zhang J Fulton L Graves T.A Minx P Reily A.D Courtney L Kruchowski S.C Tomlinson C Strong C Delehaunty K Fronick C Courtney B Rock S.M Belter E Du F Kim K Abbott R.M Cotton M Levy A Marche | | 0，，： | 1 |
| 13 | Immortal activated human hepatic stellate cells generated by ectopic telomerase expression 显示文摘 | Schnabl B Choi Y H Olsen J C Hagedorn C H Brenner D A | 2002 | Lab Invest2002，82，： | 1 |
| 14 | Seeuritization without risk transfer显示文摘 | Viral V Schnabl A P Suarez G | 2010 | Journal of Financial Economics2010，，： | 1 |
| 15 | Replicative senescence of activaled human hepatic stellate cells is accompanied by a pronouced inflammatory but less fibrogenic phenotype显示文摘 | Schnabl B Purbeck C A Choi Y H Haqedorn C H Brenner D | 2003 | Hepatology2003，37，： | 1 |
| 16 | Antineutrophil cytoplas- mic antibodies in systemic lupus erythematosus; Prevalence's peci- ficifies, and clinical significance 显示文摘 | Schnable A Csemo KE Isenberg DA | 1995 | Arthritis Rheum1995，38，： | 1 |
| 17 | Reduced nicotinamide adenine dinucleotide phosphate oxidase mediates fibrotic and inflammatory effects of leptin on he patic stellate cells显示文摘 | De Minids S Seki E Oesterreicher C Schnabl B Schwabe R F Brenner D A | 2008 | Hepatology2008，48，： | 1 |
| 18 | Imputed Interindustry Technology Flows-A Comparative SMFA Analysis显示文摘 | During A Schnabl H | 2000 | Economic Systems Research2000，，3： | 1 |
| 19 | Parent-of-origin effects on gene expression and DNA methylation in the maize endosperm显示文摘 | Waters A J Makarevitch I Eichten S R Swanson-Wagner R A Yeh C-T Xu W Schnable P S Vaughn M W Gehring M Springer N M | 2011 | The Plant Cell2011，23，12： | 1 |
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