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| 1 | GS-9620, an Oral Agonist of Toll-Like Receptor-7, Induces Prolonged Suppression of Hepatitis B Virus in Chronically Infected Chimpanzees显示文摘 | Robert E. Lanford Bernadette Guerra Deborah Chavez Luis Giavedoni Vida L. Hodara Kathleen M. Brasky Abigail Fosdick Christian R. Frey Jim Zheng Grushenka Wolfgang Randall L. Halcomb Daniel B. Tumas | 2013 | Gastroenterology2013，，7： | 5 |
| 2 | Relationship between oxidative stress and hepatic glutathione levels in ethanol-mediated apoptosis of polarized hepatic cells显示文摘AIM:To investigate the role of reactive oxygen species(ROS) in ethanol-mediated cell death of polarized hepatic(WIF-B) cells.METHODS:In this work,WIF-B cultures were treated with pyrazole(inducer of cytochrome P4502E1,CYP2E1) and/or L-buthionine sulfoximine(BSO),a known inhibitor of hepatic glutathione(GSH),followed by evaluation of ROS production,antioxidant levels,and measures of cell injury(apoptosis and necrosis).RESULTS:The results revealed that ethanol treatment alone caused a significant two-fold increase in the activation of caspase-3 as well as a similar doubling in ROS.When the activity of the CYP2E1 was increased by pyrazole pretreatment,an additional two-fold elevation in ROS was detected.However,the CYP2E1-related ROS elevation was not accompanied with a correlative increase in apoptotic cell injury,but rather was found to be associated with an increase in necrotic cell death.Interestingly,when the thiol status of the cells was manipulated using BSO,the ethanol-induced activation of caspase-3 was abrogated.Additionally,ethanol-treated cells displayed enhanced susceptibility to Fas-mediated apoptosis that was blocked by GSH depletion as a result of diminished caspase-8 activity.CONCLUSION:Apoptotic cell death induced as a consequence of ethanol metabolism is not completely dependent upon ROS status but is dependent on sustained GSH levels. | Benita L McVicker Pamela L Tuma Kusum K Kharbanda Serene ML Lee Dean J Tuma | 2009 | World Journal of Gastroenterology2009，15，21： | 5 |
| 3 | Alcohol-induced protein hyperacetylation: Mechanisms and consequences显示文摘Although the clinical manifestations of alcoholic liver disease are well-described, little is known about the molecular basis of liver injury. Recent studies have indicated that ethanol exposure induces global protein hyperacetylation. This reversible, posttranslational modification on the ε-amino groups of lysine residues has been shown to modulate multiple, diverse cellular processes ranging from transcriptional activation to microtubule stability. Thus, alcoholinduced protein hyperacetylation likely leads to major physiological consequences that contribute to alcohol-induced hepatotoxicity. Lysine acetylation is controlled by the activities of two opposing enzymes, histone acetyltransferases and histone deacetylases. Currently, efforts are aimed at determining which enzymes are responsible for the increased acetylation of specifi c substrates. However, the greater challenge will be to determine the physiological ramifications of protein hyperacetylation and how they might contribute to the progression of liver disease. In this review, we will fi rst list and discuss the proteins known to be hyperacetylated in the presence of ethanol. We will then describe what is known about the mechanisms leading to increased protein acetylation and how hyperacetylation may perturb hepatic function. | Blythe D Shepard Pamela L Tuma | 2009 | World Journal of Gastroenterology2009，15，10： | 3 |
| 4 | Alcohol Consumption Decreases Rat Hepatic Creatine Biosynthesis Via Altered Guanidinoacetate Methyltransferase Activity显示文摘 | Kusum K. Kharbanda Sandra L. Todero Jordan C. Moats Ryan M. Harris Natalia A. Osna Paul G. Thomes Dean J. Tuma | 2014 | Alcohol Clin Exp Res2014，，3： | 2 |
| 5 | Prolonged feeding with guanidinoacetate, a methyl group consumer, exacerbates ethanol-induced liver injury显示文摘AIM To investigate the hypothesis that exposure to guanidinoacetate(GAA, a potent methyl-group consumer) either alone or combined with ethanol intake for a prolonged period of time would cause more advanced liver pathology thus identifying methylation defects as the initiator and stimulator for progressive liver damage.METHODS Adult male Wistar rats were fed the control or ethanolLieber De Carli diet in the absence or presence of GAA supplementation. At the end of 6 wk of the feeding regimen, various biochemical and histological analyses were conducted. RESULTS Contrary to our expectations, we observed that GAA treatment alone resulted in a histologically normal liver without evidence of hepatosteatosis despite persistence of some abnormal biochemical parameters. This protection could result from the generation of creatine from the ingested GAA. Ethanol treatment for 6 wk exhibited changes in liver methionine metabolism and persistence of histological and biochemical defects as reported before. Further, when the rats were fed the GAA-supplemented ethanol diet, similar histological and biochemical changes as observed after 2 wk of combined treatment, including inflammation, macroand micro-vesicular steatosis and a marked decrease in the methylation index were noted. In addition, rats on the combined treatment exhibited increased liver toxicity and even early fibrotic changes in a subset of animals in this group. The worsening liver pathology could be related to the profound reduction in the hepatic methylation index, an increased accumulation of GAA and the inability of creatine generated to exert its hepato-protective effects in the setting of ethanol.CONCLUSION To conclude, prolonged exposure to a methyl consumer superimposed on chronic ethanol consumption causes persistent and pronounced liver damage. | Natalia A Osna Dan Feng Murali Ganesan Priya F Maillacheruvu David J Orlicky Samuel W French Dean J Tuma Kusum K Kharbanda | 2016 | World Journal of Gastroenterology2016，22，38： | 2 |
| 6 | Alcohol-induced alterations of the hepatocyte cytoskeleton显示文摘The hepatocyte cytoskeleton consists of three fi lamentous networks: microtubules, actin microfi laments and keratin intermediate filaments. Because of the abundance of the proteins that comprise each system and the central role each network plays in a variety of cellular processes, the three fi lament systems have been the focus of a host of studies aimed at understanding the progression of alcohol-induced liver injury. In this review, we will briefly discuss the hepatic organization of each cytoskeletal network and highlight some components of each system. We will also describe what is known about ethanol-induced changes in the dynamics and distributions of each cytoskeletal system and discuss what is known about changes in protein expression levels and post-translational modifi cations. Finally, we will describe the possible consequences of these cytoskeletal alterations on hepatocyte function and how they might contribute to the progression of liver disease. | Blythe D Shepard Pamela L Tuma | 2010 | World Journal of Gastroenterology2010，16，11： | 2 |
| 7 | Effect of ethanol on pro-apoptotic mechanisms in polarizedhepatic cells显示文摘Chronic ethanol consumption is associated with serious and potentially fatal alcohol-related liver injuries such as hepatomegaly, alcoholic hepatitis and cirrhosis. Moreover, it has been documented that the clinical progression of alcohol-induced liver damage may be associated with an increase in hepatocellular death that involves apoptotic mechanisms. Although much information has been learned about the clinical manifestations associated with alcohol-related diseases, the search continues for a better understanding of the molecular and/or cellular mechanisms by which ethanol exerts its deleterious effects such as the induction of pro-apoptotic mechanisms and related cell damaging events. As part of the effort to enhance our understanding of those particular cellular pathways and mechanisms associated with ethanol toxicity, researchers over the years have utilized a variety of model systems. Recently, work has come forth demonstrating the utility of a hybrid cell line (WIF-B) as a cell culture model system for the study of alcohol-associated alterations in hepatocellular mechanisms. Success with such emerging model systems could aid in the development of potential therapeutic treatments for the prevention of alcohol- induced apoptotic cell death that may ultimately serve as a significant target in delaying the onset and/or progression of clinical symptoms of alcohol-mediated liver disease. This review article summarizes the current understanding of ethanol-mediated modifications in cell survival and thus the promotion of pro-apoptotic events with emphasis on analyses made in various experimental model systems, particularly the more recently characterized WIF-B cell system. | Benita L McVicker Dean J Tuma Carol A Casey | 2007 | World Journal of Gastroenterology2007，13，37： | 2 |
| 8 | Proteomics reveal a concerted upregulation of methionine metabolic pathway enzymes, and downregulation of carbonic anhydrase-III, in betaine supplemented ethanol-fed rats显示文摘 | Kusum K. Kharbanda Vasanthy Vigneswara Benita L. McVicker Anna U. Newlaczyl Kevin Bailey Dean Tuma David E. Ray Wayne G. Carter | 2009 | Biochemical and Biophysical Research Communications2009，，4： | 2 |
| 9 | Accumulation of proteins bearing atypical isoaspartyl residues in livers of alcohol-fed rats is prevented by betaine administration: Effects on protein- l -isoaspartyl methyltransferase activity显示文摘 | Kusum K. Kharbanda Mark E. Mailliard Cheryl R. Baldwin Michael F. Sorrell Dean J. Tuma | 2007 | Journal of Hepatology2007，，6： | 2 |
| 10 | Betaine attenuates alcoholic steatosis by restoring phosphatidylcholine generation via the phosphatidylethanolamine methyltransferase pathway显示文摘 | Kusum K. Kharbanda Mark E. Mailliard Cheryl R. Baldwin Harriet C. Beckenhauer Michael F. Sorrell Dean J. Tuma | 2006 | Journal of Hepatology2006，，2： | 2 |
| 11 | Role of elevated S-adenosylhomocysteine in rat hepatocyte apoptosis: Protection by betaine显示文摘 | Kusum K. Kharbanda David D. Rogers Mark E. Mailliard Gerri L. Siford Anthony J. Barak Harriet C. Beckenhauer Michael F. Sorrell Dean J. Tuma | 2005 | Biochemical Pharmacology2005，，12： | 2 |
| 12 | Betaine administration corrects ethanol-induced defective VLDL secretion显示文摘 | Kusum K. Kharbanda Sandra L. Todero Brian W. Ward John J. Cannella Dean J. Tuma | 2009 | Molecular and Cellular Biochemistry2009，，： | 2 |
| 13 | Influence of marbling and animal age on factors associated with beef quality显示文摘 | Tuma H J Henrickson R L Stephens D F | 1962 | Animal Science1962，21，11： | 1 |
| 14 | Solubility of CO2 in the ionic liquid 显示文摘 | Perez-Salado Kamps A Tuma D Xia J | 2003 | Journal of Chemical & Engineering Data2003，48，3： | 1 |
| 15 | Dosing and switch- ing strategies for quetiapine fumarate显示文摘 | Cutler AJ Goldstein JM Tumas JA | 2002 | Clinical Thera- peutics2002，24，2： | 1 |
| 16 | Retinoids and lung cancer: targeting the right population显示文摘 | Tuma R S | 2002 | J Nail Cancer Inst2002，94，13： | 1 |
| 17 | Evaluation and prediction ofnonpoint pollution in Lthuania显示文摘 | TUMAS R | 2000 | Ecological Engineering2000，14，： | 1 |
| 18 | Management of calyceal diverticular stones with extracorporeal shock wave lithotripsy and percutaneous neph- rolithotomy : long-term outcome显示文摘 | Tuma B Raza A Moussa A | 2007 | BJU lnt2007，1130，1： | 1 |
| 19 | Group-47η61 -pyrrolyl complexes incorporating N, N-Di (pyrrolyl-α-methyl)-N-methylamine 显示文摘 | Li Y H Tumas A Cizewski J T | 2002 | Inorg Chem2002，41，： | 1 |
| 20 | The chemistry and biological effects of malondisldehyde-acetaldehyde adducts 显示文摘 | Thiele GM Worrall S Tuma D | 2001 | Alcohol Clin Exp Red2001，，25： | 1 |
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