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| 1 | Alcohol-induced steatosis in liver cells显示文摘Alcohol-induced fatty liver (steatosis) was believed to result from excessive generation of reducing equivalents from ethanol metabolism, thereby enhancing fat accumulation. Recent findings have revealed a more complex picture in which ethanol oxidation is still required, but specific transcription as well as humoral factors also have important roles. Transcription factors involved include the sterol regulatory element binding protein 1 (SREBP-1) which is activated to induce genes that regulate lipid biosynthesis. Conversely, ethanol consumption causes a general down-regulation of lipid (fatty acid) oxidation, a reflection of inactivation of the peroxisome proliferator- activated receptor-alpha (PPAR-α) that regulates genes involved in fatty acid oxidation. A third transcription factor is the early growth response-1 (Egr-1), which is strongly induced prior to the onset of steatosis. The activities of all these factors are governed by that of the principal regulatory enzyme, AMP kinase. Important humoral factors, including adiponectin, and tumor necrosis factor-α (TNF-α), also regulate alcohol-induced steatosis. Their levels are affected by alcohol consumption and by each other. This review will summarize the actions of these proteins in ethanol-elicited fatty liver. Because steatosis is now regarded as a significant risk factor for advanced liver pathology, an understanding of the molecular mechanisms in its etiology is essential for development of effective therapies. | Terrence M Donohue Jr | 2007 | World Journal of Gastroenterology2007，13，37： | 21 |
| 2 | Autophagy and ethanol-induced liver injury显示文摘The majority of ethanol metabolism occurs in the liver. Consequently, this organ sustains the greatest damage from ethanol abuse. Ethanol consumption disturbs the delicate balance of protein homeostasis in the liver, causing intracellular protein accumulation due to a disruption of hepatic protein catabolism. Evidence indicates that ethanol or its metabolism impairs trafficking events in the liver, including the process of macroautophagy, which is the engulfment and degradation of cytoplasmic constituents by the lysosomal system. Autophagy is an essential, ongoing cellular process that is highly regulated by nutrients, endocrine factors and signaling pathways. A great number of the genes and gene products that govern the autophagic response have been characterized and the major metabolic and signaling pathways that activate or suppress autophagy have been identified. This review describes the process of autophagy, its regulation and the possible mechanisms by which ethanol disrupts the process of autophagic degradation. The implications of autophagic suppression are discussed in relation to the pathogenesis of alcohol-induced liver injury. | Terrence M Donohue Jr | 2009 | World Journal of Gastroenterology2009，15，10： | 11 |
| 3 | Implication of altered proteasome function in alcoholic liverinjury显示文摘The proteasome is a major protein-degrading enzyme, which catalyzes degradation of oxidized and aged proteins, signal transduction factors and cleaves peptides for antigen presentation. Proteasome exists in the equilibrium of 26S and 20S particles. Proteasome function is altered by ethanol metabolism, depending on oxidative stress levels: low oxidative stress induces proteasome activity, while high oxidative stress reduces it. The proposed mechanisms for modulation of proteasome activity are related to oxidative modification of proteasomal proteins with primary and secondary products derived from ethanol oxidation. Decreased proteolysis by the proteasome results in the accumulation of insoluble protein aggregates, which cannot be degraded by proteasome and which further inhibit proteasome function. Mallory bodies, a common signature of alcoholic liver diseases, are formed by liver cells, when proteasome is unable to remove cytokeratins. Proteasome inhibition by ethanol also promotes the accumulation of pro-apoptotic factors in mitochondria of ethanol-metabolizing liver cells that are normally degraded by proteasome. In addition, decreased proteasome function also induces accumulation of the negative regulators of cytokine signaling (I-kB and SOCS), thereby blocking cytokine signal transduction. Finally, ethanol-elicited blockade of interferon type 1 and 2 signaling and decreased proteasome function impairs generation of peptides for MHC class Ⅰ-restricted antigen presentation. | Natalia A Osna Terrence M Donohue Jr | 2007 | World Journal of Gastroenterology2007，13，37： | 10 |
| 4 | Involvement of autophagy in alcoholic liver injury and hepatitis C pathogenesis显示文摘This review describes the principal pathways of macroautophagy (i.e. autophagy), microautophagy and chaperone-mediated autophagy as they are currently known to occur in mammalian cells. Because of its crucial role as an accessory digestive organ, the liver has a particularly robust autophagic activity that is sensitive to changes in plasma and dietary components. Ethanol consumption causes major changes in hepatic protein and lipid metabolism and both are regulated by autophagy, which is significantly affected by hepatic ethanol metabolism. Ethanol exposure enhances autophagosome formation in liver cells, but suppresses lysosome function. Excessive ethanol consumption synergizes with hepatitis C virus (HCV) to exacerbate liver injury, as alcohol-consuming HCV patients frequently have a longer course of infection and more severe manifestations of chronic hepatitis than abstinent HCV patients. Alcohol-elicited exacerbation of HCV infection pathogenesis is related to modulation by ethanol metabolism of HCV replication. Additionally, as part of this mechanism, autophagic proteins have been shown to regulate viral (HCV) replication and their intracel-lular accumulation. Because ethanol induces autophagosome expression, enhanced levels of autophagic proteins may enhance HCV infectivity in liver cells of alcoholics and heavy drinkers. | Natalia A Osna Paul G Thomes Terrence M Donohue | 2011 | World Journal of Gastroenterology2011，17，20： | 5 |
| 5 | Immunity to influenza A H9N2 viruses induced by infection and vaccination显示文摘 | Xiuhua Lu Mary Renshaw Terrence M | 2001 | J of Virology2001，75，10： | 1 |
| 6 | The efficiency of enhanced biological phosphorus removal from real wastewater affected by different ratio of acetic to propionic acid显示文摘 | Yinguang Chen Andrew A R Terrence M | 2004 | Water Research2004，38，1： | 1 |
| 7 | Maximum-likelihood estimation, the cramer-rao bound, and the method of scoring with parameter constraints 显示文摘 | Terrence J Moore Brian M Sadler Richard J Kozick | 2008 | IEEE Transaction on Signal Processing2008，56，3： | 1 |
| 8 | A constraint manager to support virtual maintainability显示文摘 | LUIS M NORMAN M TERRENCE F | 2003 | Computers & Graphics2003，27，： | 1 |
| 9 | Protection against H1, HS, H6 and H9 influenza A infection with liposomal matrix 2 epitope vaccines显示文摘 | Ernst W A Kim H J Terrence M | 2006 | Vaccine2006，24，24： | 1 |
| 10 | CoMFA and HQSAR of Acylhydrazide Cruzain Inhibitors 显示文摘 | Carlos R Terrence M | 2002 | Bioorganic and Medicinal Chemistry Letters2002，12，： | 1 |
| 11 | Tumpey ocular tropism of respiratory viruses显示文摘 | Belser JA Rota PA Terrence M | 2013 | Microbiol Mol Biol Rev2013，77，1： | 1 |
| 12 | Design and Realizationof a Digital Modulator for Fractional- Frequency Synthesis显示文摘 | Terrence P Kenny Thomas A D Riley Norman M Filiol Miles A Copeland | 1999 | IEEE TRANSACTIONS ON VEHICULAR TECHNOLOGY1999，48，2： | 1 |
| 13 | The psychological impact of maxillofacial trauma: An overview of reactions to trauma显示文摘 | Alastair M H Terrence L Patrieia M F | 2003 | Oral Surgery Oral Medicine Oral Pathology Oral Radiology & Endodontics2003，95，4： | 1 |
| 14 | Ocular tropism of respiratory viruses 显示文摘 | Jessica A B Paul A R Terrence M T | 2013 | Microbiol Mol Biol Rev2013，77，3： | 1 |
| 15 | A new monoterpene glycoside of paeonia lactiflora显示文摘 | Lang HY Li SZ Terrence M | 1984 | Planta Medica1984，50，60： | 1 |
| 16 | UV communications channel modeling incorporating multiple scattering interactions 显示文摘 | Robert J Drost Terrence J Moore Brian M Sadler | 2011 | Optical Society of America2011，28，4： | 1 |
| 17 | Depression and Functional Recovery After a Disabling Hospitalization in Older Persons显示文摘 | Lisa C Barry Terrence E Murphy and Thomas M Gill | 2011 | J Am Geriatr Soc2011，59，： | 1 |
| 18 | The efficiency of enhanced biological phosphorus removal from real wastewater affected by different ratio of acetic to propionic acid 显示文摘 | Chen Y G Andrew A R Terrence M C | 2004 | Water Research2004，38，1： | 1 |
| 19 | A model of duopoly and meeting or beating competition显示文摘 | Belton Terrence M | 1987 | International Journal of Industrial Organization1987，，5： | 1 |
| 20 | Decreased proteasome activity is associated with increased everity of liver pathology and oxidative stress in experimental alcoholic liver disease显示文摘 | Terrence M Donohue Jr | 2004 | Alcoholism2004，28，8： | 1 |
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