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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 | Reducing transfusion requirements in liver transplantation显示文摘Liver transplantation(LT) was historically associated with massive blood loss and transfusion. Over the past two decades transfusion requirements have reduced dramatically and increasingly transfusionfree transplantation is a reality. Both bleeding and transfusion are associated with adverse outcomes in LT. Minimising bleeding and reducing unnecessary transfusions are therefore key goals in the perioperative period. As the understanding of the causes of bleeding has evolved so too have techniques to minimize or reduce the impact of blood loss. Surgical 'piggyback' techniques, anaesthetic low central venous pressure and haemodilution strategies and the use of autologous cell salvage, point of care monitoring and targeted correction of coagulopathy, particularly through use of factor concentrates, have all contributed to declining reliance on allogenic blood products. Pre-emptive management of preoperative anaemia and adoption of more restrictive transfusion thresholds is increasingly common as patient blood management(PBM) gains momentum. Despite progress, increasing use of marginal grafts and transplantation of sicker recipients will continue to present new challenges in bleeding and transfusion management. Variation in practice across different centres and within the literature demonstrates the current lack of clear transfusion guidance. In this article we summarise the causes and predictors of bleeding and present the evidence for a variety of PBM strategies in LT. | Ciara I Donohue Susan V Mallett | 2015 | World Journal of Transplantation2015，5，4： | 4 |
| 6 | Metastatic Nonfunctioning Pancreatic Neuroendocrine Carcinoma to Liver: Surgical Treatment and Outcomes显示文摘 | Daniel Cusati Lizhi Zhang William S. Harmsen Amy Hu Michael B. Farnell David M. Nagorney John H. Donohue Florencia G. Que Kaye M. Reid-Lombardo Michael L. Kendrick | 2012 | Journal of the American College of Surgeons2012，，1： | 3 |
| 7 | Hepatic resection of hepatocellular carcinoma in patients with cirrhosis: Model of end-stage liver disease (MELD) score predicts perioperative mortality显示文摘 | Swee H. Teh John Christein John Donohue Florencia Que Michael Kendrick Michael Farnell Stephen Cha Patrick Kamath Raymond Kim David M. Nagorney | 2005 | Journal of Gastrointestinal Surgery2005，，9： | 2 |
| 8 | Breast Cancer: Presentation and Intervention in Women With Gastrointestinal Metastasis and Carcinomatosis显示文摘 | Elisabeth C. McLemore Barbara A. Pockaj Carol Reynolds Richard J. Gray Jose L. Hernandez Clive S. Grant John H. Donohue | 2005 | Annals of Surgical Oncology2005，，11： | 2 |
| 9 | Global review and synthesis of trends in observed terrestrial near-surface wind speeds: Implications for evaporation显示文摘 | Tim R. McVicar Michael L. Roderick Randall J. Donohue Ling Tao Li Thomas G. Van Niel Axel Thomas Jürgen Grieser Deepak Jhajharia Youcef Himri Natalie M. Mahowald Anna V. Mescherskaya Andries C. Kruger Shafiqur Rehman Yagob Dinpashoh | 2011 | Journal of Hydrology2011，，： | 2 |
| 10 | Hepatic resection of hepatocellular carcinoma in patients with cirrhosis: Model of end-stage liver disease (MELD) score predicts perioperative mortality显示文摘 | Swee H. Teh M.D. John Christein M.D. John Donohue M.D. Florencia Que M.D. Michael Kendrick M.D. Michael Farnell M.D. Stephen Cha Patrick Kamath M.D. Raymond Kim M.D. David M. Nagorney M.D | 2005 | Journal of Gastrointestinal Surgery2005，，9： | 2 |
| 11 | Is There a Role for Endoscopic Therapy as a Definitive Treatment for Post-Laparoscopic Bile Duct Injuries?显示文摘 | Javairiah Fatima Joshua G. Barton Travis E. Grotz Zhimin Geng William S. Harmsen Marianne Huebner Todd H. Baron Michael L. Kendrick John H. Donohue Florencia G. Que David M. Nagorney Michael B. Farnell | 2010 | Journal of the American College of Surgeons2010，，4： | 2 |
| 12 | Diagnosis and Surgical Management of Gallbladder Cancer: A Review显示文摘 | Kaye M. Reid Antonio Ramos-De la Medina John H. Donohue | 2007 | Journal of Gastrointestinal Surgery2007，，5： | 2 |
| 13 | Functions of autophagy in normal and diseased liver显示文摘 | Mark J. Czaja Wen-Xing Ding Terrence M. Donohue Scott L. Friedman Jae-Sung Kim Masaaki Komatsu John J. Lemasters Antoinette Lemoine Jiandie D. Lin Jing-hsiung James Ou David H. Perlmutter Glenn Randall Ratna B. Ray Allan Tsung Xiao-Ming Yin | 2013 | Autophagy2013，，8： | 2 |
| 14 | The relative impact of attribute, severity, and timing of psychological contract breach on behavioral and attitudinal outcomes显示文摘 | Stephanie Eckerd James Hill Kenneth K. Boyer Karen Donohue Peter T. Ward | 2013 | Journal of Operations Management2013，，： | 2 |
| 15 | Team-based stepped care in integrated delivery settings显示文摘Fragmented health care delivery is recognized as increasingly problematic.Integrated care has been advanced as a reform that will improve quality of care and lower costs.Despite the application of integrated care systems in the United States,there has been a limited amount of empirical work explicating the most effective health care pathways.Stepped care has been proposed as a framework by which to implement coordinated team-based care and has gained preliminary empirical support.In this manuscript a rationale for team-based stepped care is presented,tools for implementation are provided,and future research directions are suggested. | Cassandra Snipes Alexandros Maragakis William O’Donohue | 2015 | Family Medicine and Community Health2015，3，1： | 2 |
| 16 | Role of Bachl and Nrf2 in up-regulation of the heme oxygenase- 1 gene by cobalt protoporphyrin 显示文摘 | Shan Y Lambrecht RW Donohue SE | 2006 | FASEB J2006，20，14： | 1 |
| 17 | Transurethral prostate re- section and bleeding:a randomized, placebo controlled trial of role of finasteride for decreasing operative blood loss显示文摘 | Donohue JF Sharma H Abraham R | 2002 | J Urol2002，168，5： | 1 |
| 18 | Surgical treatment of gallbladder cancer显示文摘 | Taner CB Nagorney DM Donohue JH | 2004 | JOGS2004，8，： | 1 |
| 19 | Wnt signaling mediates reorientation of outer hair cell stereociliary bundles in the mammalian cochlea显示文摘 | Dabdoub A Donohue MJ Brennan A | 2003 | Development2003，130，： | 1 |
| 20 | Induction of myocardial insulin-like growth factor-1 gene expression in left ventricular hypertrophy 显示文摘 | Donohue TJ Dworkin LD Lango MN | 1994 | Circulation1994，89，： | 1 |
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