Poster Session (pp. 78A–178A)

78A POSTER SESSIONS HEPATOLOGY, October 2003

P O S T E R S E S S I O N S

Poster Session 1

Saturday, October 25 Hyties Corzvrntion Center, Exhibit Hall C

Poster Viewinr: 530 - 8 : 0 0 ~ m

Presenters in Attendance: Even number posters: Odd number posters:

5:30 - 8:OOpm 5:30 - 8:00pm

8 Those posters identified as AASLD Presidential Poster of Distinction by a ribbon icon have received review scores that place them within the top 1OYI of all posters. We encourage you to make them a priority as you visit the poster session.

Cell Transplantation and Stem Cells

fi 259 ENDOTHELIAL PROGENITOR CELLS CONTRIBUTE TO NEOVASCULARIZATION IN LIVER REGENERATION AFTER LIVER INJURY Eitaro Taniguchi, Takuji Torimura, Motoaki Kin, Masaru Harada, Ryukichi Kumashiro, Takato Ueno, Michio Sata, Kurume University School of Medicine, Kurume, Japan

f i 260 TREATMENT OF ACUTE LIVER FAILURE IN THE PIG WITH TRANSPLANTATION OF REVERSIBLY IMMORTALIZED HUMAN HEPATOCYTES Naoya Kobayashi, Tosliinori Totsugawa, Noriaki Tanaka, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan; Philippe Leboulch, Harvard-Massachusetts Institute of Technology Cambridge, MA

# 261 ASSESSMENT OF HUMAN HAEMATOPOIETIC STEM CELLS HOMING AND HEPATIC TRANSDIFFERENTIATION IN A CHIMERIC NOD/SCID MOUSE MODEL Cristiana Di Campli, Anna C Piscaglia, Manuela Nestola, Sergio Rutella, Franco M Vecchio, Paolo Pola, Giuseppe Leone, Giovanni Gasbarrini, Antonio Gasbarrini, Catholic University of Rome, Rome, Italy

# 262 LONGTERM REGULATION OF IMMUNORESISTANT CD8+ T CELL MEDIATED IMMUNE DAMAGE OF LIVER PARENCHYMAL CELLS Keri E Lunsford, Donghong Gao, Anna Hummel, Ginny L Bumgardner, The Ohio State University Medical Center and College of Medicine and Public Health, Columbus, OH

# 263 HEPARANASE INCREASES HEPATOCYTE ENGRAFTMENT AND EARLY ENDOTHELIAL CELL PROLIFERATION AFTER INTRASPLENIC CELL TRANSPLANTATION IN HEPATECTOMIZED RATS Vladislav Tsiperson, Faculty of Medicine, Technion Institute of Technology, Haita, Israel; Orit Goldshmit, Neta Ilan, Rappaport Institution for Research, Haifa, Israel; Gideon Shoshany, Rambam Medical Center, Haifa, Israel; Israel Vlodavsky, Rappaport Institution for Research, Haifa, Israel; Ella Veitzman, Yaacov Baruch, Rambam Medical Center, Haifa, Israel

8 #264

CELL ACTIVATION Aranzazu Sanchez, Peter Nagy, Insa S Schroeder, Valentina M Factor, Snorri S Thorgeirsson, National Cancer Institute, Bethesda, MD

NF-KB AND STAT-3 ARE REQUIRED FOR HEPATIC STEM

8#265 ~~

SYMPATHETIC NERVOUS SYSTEM INHIBITION INCREASES HEPATIC PROGENITORS AND REDUCES LIVER INJURY Jude A Oben, Johns Hopkins University, Baltimore, MD; Tania Roskams, University of Leuven, Leuven, Belgium; Zhiping Li, Michael Torbenson, Johns Hopkins University Baltimore, MD; Nicoletta Sinelli, University of Leuven, Leuven, Belgium; Shiqi Yang, Huizhi Lin, Jiawen Huang, Paul Guarino, Michel Kafrouni, Anna Mae Diehl, Johns Hopkins University, Baltimore, MU

# 266 MOBILIZATION OF PLURIPOTENT HAEMATOPOIETIC STEM CELLS OCCURS IN ALCOHOLIC HEPATITIS AND IS ASSOCIATED WITH AN IMPROVED CLINICAL OUTCOME Evangelos Dalakas, Philip N Newsome, Liu Qing, Rachel Brown, Shonna McCall, Peter C Hayes, David J Harrison, John N Plevris, University of Edinburgh, Edinburgh, UK

# 267 KEY ROLE OF KLF6 IN HEPATOCELLULAR DIFFERENTIATION FROM EMBRYONIC STEM CELLS Nobuyulu Matsumoto, Atsushi Kubo, Huixian Liu, Mount Sinai School of Medicine, New York, NY; Friedrich Laub, Francesco Ramirez, Cornell University, New York, NY; Gordon Keller, Scott L Friedman, Mount Sinai School of Medicine, New York, NY

# 268 SIDE POPULATION (SP) CELLS FROM SPLEEN DIFFERENTIATE INTO HEPATOCYTE IN VIVO Takeshi Nishimura, Toshifumi Azuma, Sayaka Inokuchi, Kengo Tomita, Naoto Kitamura, Hideyuki Okano, Yumi Matsuzaki, Hiroko Kouike, Masaki Kitajima, Go Wakabayashi, Minoru Tanabe, Hidejiro Uragami, Hiromasa Ishii, Keio University School of Medicine, Tokyo, Japan

# 269 FAILURE OF BONE MARROW DERIVED CELLS TO REPLACE INJURED LIVERS Yoshiyulu Kanazawa, Inder M Verma, Salk Institute, La Jolla, CA

# 270 EXPRESSION OF HEPATOBILIARY ORGANIC ANION

IN DIFFERENTIATING MOUSE EMBRYONIC STEM CELLS Yoshinao Kobayashi, Yuji Tanaka, Mie University School of Medicine, Tsu City, Mie, Japan; Masahide Yoshikawa, Nara Medical University, Kashihara-City, Japan; Makoto Kuroda, Toshio Itani, Masahiko Kaito, Mie University School of Medicine, Tsu City, Mie, Japan; Shigeaki Ishizaka, Nara Medical University, Kashihara-City, Japan; Yukihiko Adachi, Mie University School of Medicine, Tsu City, Mie, Japan

TRANSPORTERS AND BILIRUBIN-CONJUGATING ENZYME

8 Denotes AASLD Presidential Poster of Distinction

HEPATOLOGY, Vol. 38, No. 4, suppl. 1,2003 POSTER SESSIONS 79A

# 271 EMBRYONIC HEPATOBLASTS SHARE PATTERNS OF GENE EXPRESSION WITH OTHER STEM CELL POPULATIONS Tammy Ader, Rachel Norel, Charles E Rogler, Leslie E Rogler, Albert Einstein College of Medicine, Bronx, NY

# 278 FETAL LIVER STEM/PROGENITOR CELLS SPECIFIC GENES David Goetz, Erwin Bottinger, David A Shafritz Petko M Petkov, Jiri Zavadil, Petar N Grozdanov, ; Mariana D Dabeva, Albert Einstein College of Medicine, Bronx, NY

# 272 IN VITRO DIFFERENTIATION OF ADULT LIVER STEM CELLS INTO THE HEPATOCYTIC LINEAGE Insa S Schroeder, Valentina M Factor, Aranzazu Sanchez, Ju-Seog Lee, Tanya N Hoang, Snorri S Thorgeirsson, National Cancer Institute, Bethesda, MD

# 273 HEPATOCYTE SPECIFIC METABOLIC ACTIVITY CAN BE INDUCED IN ADULT LIVER STEM CELLS ISOLATED FROM RODENT BONE MARROW Daniel Inderbitzin, Adrian Keogh, Guido Beldi, Markus Gass, Daniel Sidler, Sonja Bisch-Knaden, Bruno Stieger, Deborah M Stroka, Beat Gloor, Daniel Candinas, University Hospital Bern, Bern, Switzerland

# 274

DIFFERENTIATION OF MURINE BONE MARROW CELLS

ENRICHED TRANSCRIPTION FACTORS Yukiko Saji, Shinji Tamura, Yuichi Yoshida, Shinichi Kiso, Ayuko Iizuka, Hitoshi Matsumoto, Takako Kawasaki, Yoshihiro Kamada, Yuji Matsuzawa, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan

BASIC FIBROBLAST GROWTH FACTOR PROMOTES TRANS-

INTO HEPATIC LINAGE CELLS VIA MULTIPLE LIVER-

# 275

ITS RECEPTOR CXCR4 IN HEPATIC REGENERATION FROM OVAL CELLS Philippe Mavier, INSERM U581, Creteil, France; Nadine Martin, HBpital Henri Mondor, Creteil, France; Dominique Couchie, Anne M Preaux, Yannick Laperche, Elie S Zafrani, INSERM U581, Creteil, France

EXPRESSION OF STROMAL-DERIVED FACTOR-1 AND OF

# 276 SIDE POPULATION CELLS DERIVED FROM NON- PARENCHYMAL LIVER CELLS AND SPLENOCYTES ARE CAPABLE OF DIFFERENTIATING INTO HEPATOCYTES IN VITRO Sayaka Inokuchi, Toshifumi Azuma, Takeshi Nishimura, Kengo Tomita, Naoto Kitamura, Go Wakabayashi, Masaki Kitajima, Hiroko Kouike, Yumi Matsuzaki, Hideyuki Okano, Hiromasa Ishii, Keio University School of Medicine, Tokyo, Japan

# 277 EPIMORPHIN, A MESENCHYMAL CELL SURFACE- ASSOCIATED MOLECULE, IS INVOLVED IN DIFFERENTIATION OF HEPATIC STEM-LIKE CELLS THROUGH CELL CONTACT WITH HEPATIC STELLATE CELLS Kouichi Miura, Takashi Goto, Ken-ichiro Mikami, Kunio Nakane, Kazuo Yoneyama, Hirokazu Nagai, Kunihiko Terada, Toshihiro Sugiyama, Katsuyuki Imai, Haruki Senoo, Sumio Watanabe, Akita University, Akita, Japan

# 279 ISOLATION OF MULTIPOTENT STEM CELLS FROM PLACENTA Toshio Miki, Thomas Lehmann, Hongbo Cai, Stephen C Strom, University of Pittsburgh, Pittsburgh, PA

# 280 A NOVEL LIVER SPECIFIC DEVELOPMENTALLY REGULATED SERINE PROTEASE/CONVERTASE Krassimira V Hadjiolova, Petko M Petkov, ; Mariana D Dabeva, Albert Einstein College of Medicine, Bronx, NY

# 281 THE CONTRIBUTION OF THE BONE MARROW TO LIVER REGENERATION DEPENDS UPON THE ENDOGENOUS HEPATOCYTES REPLICATION POTENTIAL Pamela Vig, Howard C Thomas, Malcolm R Alison, Stuart J Forbes, Imperial College, London, UK

Clinical Portal Hypertension: Variceal Hemorrhage

# 282 DIAGNOSTIC VALUE OF FIBROSIS BIOCHEMICAL MARKERS (FIBROTEST) FOR THE PREDICTION OF PORTAL HYPERTENSION IN CHRONIC LIVER DISEASE Dominique Thabut, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Didier Lebrec, HBpital Beaujon, Paris, France; Francoise Imbert-Bismut, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Dominique Cazals-Hatem, Richard Moreau, HBpital Beaujon, Paris, France; Djamila Messous, Vlad Ratziu, Mona Munteanu, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Dominique Valla, Hapita1 Beaujon, Paris, France; Thierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

# 283 PROPHYLACTIC ANTIBIOTIC PREVENTS REBLEEDING IN a 5 PATIENTS WITH ACUTE GASTROESOPHAGEAL VARICEAL "

ru< BLEEDING FOLLOWING ENDOSCOPIC TREATMENT: A RANDOMIZED TRIAL 0 Ming-Chih Hou, Han-Chieh Lin, Fa-Yauh Lee, Full-Young Chang, Shou-Dong Lee, Taipei Veterans General Hospital, Taipei, Taiwan

= P

# 284 DIAGNOSTIC VALUE OF FIBROSIS BIOCHEMICAL MARKERS (FIBROTEST) FOR THE SCREENING OF OESOPHAGEAL VARICES IN PATIENTS WITH CHRONIC LIVER DISEASE Dominique Thabut, Jean Baptiste Trabut, Sophie Le Calvez, Vincent Thibaut, Julien Massard, Cecilia d' Arondel, Joseph Moussalli, Mona Munteanu, Franqoise Imbert-Bismut, Djamila Messous, Yves Benhamou, Vlad Ratziu, Thierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

# 285 INTERIM U.S. MULTICENTER RESULTS OF VIATORR EPTFE TIPS ENDOPROSTHESIS TRIAL Ziv J Haskal, New York Presbyterian Hospital, New York, NY


8 286 PORTAL HYPERTENSIVE GASTROPATHY IS PREVALENT

WITH BRIDGING FIBROSIS AND EARLY CIRRHOSIS:

Robert J Fontana, University of Michigan, Ann Arbor, MI; Arun J Sanyal, Virginia Commonwealth University, Richmond, VA; Elizabeth Wright, NERI, Boston, MA; Adrian Di Bisceglie, Saint Louis University, St. Louis, NH

AMONGST CHRONIC HEPATITIS C NON-RESPONDERS

RESULTS FROM THE HALT-C TRIAL

# 287 PREDICTING SURVIVAL IN PORTAL HYPERTENSION:

Kiran Bambha, Mayo Clinic, Rochester, MN; Alessaiidra Dell’Era, Juan G Abraldes, Juan Tumes, Juan-Carlos Garcia-Pagan, Hospital Clinic, University of Barcelona, Barcelona, Spain; Jeff Thostenson, I’atrick S Kamath, W R k m , Mayo Clinic, Rochester, MN; Jaime Bosch, Hospital Clinic, University of Barcelona, Barcelona, Spain

P‘ 288 HEPATIC VENOUS PRESSURE GRADIENT (HVPG) PREDICTS EARLY RECURRENCE OF VARICES AND REBLEEDING AFTER ENDOSCOPIC BAND LIGATION (EBL) Sonia Alonso, Rafael Baiiares, Hospital General Universitario Gregorio Maraiion, Madrid, Spain; Agustin Albillos, Hospital Ranibn y Cajal, Madrid, Spain; Jose Luis Calleja, Clinica Puerta de Hierro, Madrid, Spain; Diego Rincon, Hospital General Universitario Gregorio Maraiibn, Madrid, Spain; Mbnica Gonzalez, Hospital Ramon y Cajal, Madrid, Spain; Cecilia Gonzalez- Asanza, Hospital General Universitario Gregorio Maraiidn, Madrid, Spain; E Vazquez-Siqueiros, Luis Ruiz-del- Arbol, Hospital Ramon y Cajal, Madrid, Spain; Pedro Menchen, Hospital General Universitario Gregorio Maraiion, Madrid, Spain

HVPG, CHILD-PUGH, OR MELD?

B 289 COMPARISON OF TWO DIFFERENT CYANOACRYLATES WHAT IS THE OPTIMAL CYANOACRYLATE FOR TREATING GASTRIC VARICES? Divyesh V Sejpal, Stephen Caldwell, Elizabeth Hespenheide, University of Virginia, Charlottesville, VA

# 290 BARIUM ESOPHAGOGRAM (BE) VERSUS UPPER ENDOSCOPY (EGD) FOR THE SCREENING OF ESOPHAGEAL VARICES (EV) IN PATIENTS WITH COMPENSATED CIRRHOSIS-A BLINDED PROSPECTIVE STUDY Evgeny Farber, Doron Fisher, Rami Eliakini, Nira Beck-Razi, Ahuva Angel, Ella Veitzmaii, Irit Chermesh, Canial Yassin, Diana Gaitini, Michael Libas, Rambam Medical Center, Haifa, Israel; Soboh Soboh, Porria Hospital, Tiberia, Israel; Yaacov Baruch, Rambam Medical Center, Haifa, Israel

$291

PREDICTION OF CLINICAL EFFICACY IN THE PRIMARY PROPHYLAXIS OF VARICEAL BLEEDING IN PATIENTS WITH CIRRHOSIS C Aracil, JM Lnpez-Balaguer, D Monfort, M Piqueras, B Gonzalez, J Mitiana, X Torras, C Villanueva, J Balanzo, Hospital de Sant Pau, Barcelona, Spain

HEMODYNAMIC RESPONSE TO BETA-BLOCKERS AND

Hepatitis C: Clinical Trials and Therapeutic Developments

gzt292 SYNERGISTIC EFFECTS OF TYPE 1 (INFERGENB) AND TYPE 2 (ACTIMMUNEGI) INTERFERONS IN PRECLINICAL MODELS OF HCV DEMONSTRATION OF POTENTIAL EFFICACY Lawrence M Blatt, Hua ‘Tan, Jin Hong, Jena Derrick, Scott Sei wert, InterMune, Inc., Brisbane, CA; Craig Day, John Morrey, Utah State University, Logan, UT; William M Grosse, Corneliu Sanda, Milton Taylor, Indiana University, Bloomington, IN

8 #293 TARGETING HCV NS3 T O DENDRITIC CELLS (DC) VIA

IMMUNITY I IN VIVO T Curiel, S Landry, C Morris, V Josh, R Berggren, Ch Hawkins, W Zou, A Lackner, M Mohaniadzadeh, Tulane Medical School, New Orleans, LA

DC-BINDING PEPTIDES INDUCES POTENT T CELL

8 #294 SAFETY AND ANTIVIRAL EFFECT OF BILN 2061, A NOVEL HCV SERINE PROTEASE INHIBITOR, AFTER ORAL TREATMENT OVER 2 DAYS IN PATIENTS WITH CHRONIC HEPATITIS C, GENOTYPE 1, AND LIVER CIRRHOSIS Heiner Wedemeyer, Medizinische Hochschule, Hannover, Germany; Andreas Erhardt, Universitatsklinikum Duesseldorf, Duesseldorf, Germany; Wolff Schmiegel, Ruhr-Universitaet Bochum, Bochum, Germany; Holger Hinrichsen, I Medizinische Universitatsklinik Kiel, Kiel, Germany; Ricardo Chaves, Boehringer Ingelheim, Biberach, Germany; Chan-Loi Yong, Boehringer Ingelheini, Ridgefield, CT; Gerhard Nehmiz, Gerhard Steinniann, Boehringer Ingelheini, Biberach, Germany

8 # 295 TREATMENT WITH SOLUBLE TUMOR NECROSIS FACTOR ALPHA (TNFA) RECEPTORS (ETANERCEPT, ETA) RESULTS IN A SYNERGISTIC EFFECT O N T CELL REACTIVITY AFTER EXPOSURE T O PEGYLATED (PEG) INTERFERON (IFN) Nizar N Zein, Tracey Bonefield, Linda R Yen-Lieberman, Mary J Thomassen, The Cleveland Clinic Foundation, Cleveland, OH

8 #296 IMPORTANCE OF RIBAVIRIN DOSAGE ON VIROLOGICAL RESPONSE RATES IN PATIENTS CHRONICALLY INFECTED WITH HEPATITIS C VIRUS AND TREATED WITH

Eva Herrmann, Universitat des Saarlandes, Homburg/Saar, Germany; Thomas Berg, Universitatsklinikum Charite, Campus Vircliow-Klinikum, Humboldt-Universitat, Berlin, Germany; Holger Hinrichsen, Medizinische Universitatsklinik I, Christian-Albrechts-Universitat, Kiel, Germany; Tilman Gerlach, Klinikum Groghadern, Ludwig-Maxiniilians-Universitat, Munchen, Germany; Ulrich Spengler, Medizinische Universitatsklinik, Bonn, Germany; Tobias Goeser. Medizinische Klinik IV, Universitat zu Koln, Kiiln, Germany; Stefan Zeuzem, Universitatsklinikum des Saarlandes, Homburg / Saar, Germany

INTERFERON-BASED COMBINATION THERAPY

8 #297 IMPROVED ADHERENCE T O PEGYLATED INTERFERON ALPHA 28 + RIBAVIRIN IN ACADEMIC CENTERS VS. COMMUNITY-BASED CENTERS: RESULTS FROM A PROSPECTIVE, RANDOMIZED, CONTROLLED, MULTICENTER TRIAL Steven L Flanim, Northwestern University Medical School, Chicago, IL; Jeffrey Goldman, Gastroenterology Associates of Olympia Fields, Hazel Crest, IL; Gregory Nelligan, Rockford Clinic, Rockford, IL; Joel Cahan, Consultants in Gastrolenter- ology, Munster, IN; David Chua, Summit Digestive & Liver Disease Specialists, Oakbrook Terrace, IL; Bradley Shapiro, Northwest Healthcare, Hoffman Estates, IL; Rockford Yapp, Digestive Health Services, S.C., Downers Grove, IL.; Edward Jurkovic, Digestive Diseases Consultants, Kankakee, IL; Thomas Sepe, University Gastroenterology, Providence, RI; Robert Brown, Columbia University Medical Center, New York, NY

8 Denotes AASLD Presidcntial Poster ot Distinction

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1, 2003 POSTER SESSIONS 81A

8 #298 EFFECTS OF RIBAVIRIN AND INTERFERON ALPHA

IMMUNE RESPONSES TO HCV PROTEINS IN PATIENTS CHRONICALLY INFECTED WITH HCV Tony Marion, Inga Warr, Jacquelyn Fleckenstein, Caroline Riely, University of Tennessee Health Science Center, Memphis, TN

8 # 299 A NOVEL GENETIC SCREEN FOR ISOLATION OF

ANTIBODIES Meital Gal-Tanamy, Romy Zemel, Larisa Bachmatov, Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Petach-Tikva, Israel; Yevgeni Berdichevsky, Itai Benhar, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel; Ran Tur-Kaspa, Rabin Medical Center, Petah-Tikva, Israel

COMBINATION THERAPY ON T CELL-DEPENDENT

NEUTRALIZING HCV SERINE PROTEASE SINGLE-CHAIN

8 # 300 SENSITIVITY OF NS3 SERINE PROTEASES FROM VARIOUS HEPATITIS C VIRUS GENOTYPES TO THE ANTIVIRAL COMPOUND BILN 2061 Diane Thibeault, Christiane Bousquet, Rock Gingras, Lisette Lagace, Roger Maurice, Peter W White, Daniel Lamarre, Boehringer Ingelheim (Canada) Ltd, Laval, PQ, Canada

8 4301 TREATMENT AND PERIPHERAL SEROTONERGIC DYSFUNCTION Markus Schwaiger, Maurice Pich, Leonora Franke, Florian van Bommel, Thomas Berg, Martin Schaefer, Charit6 Humboldt- University, Berlin, Germany

CHRONIC HEPATITIS-C INFECTION, INTERFERON-ALPHA

8 #302 UP-REGULATION OF IL-18 IS ONE OF THE KEY FACTORS FOR ANTI-VIRAL EFFECT BY COMBINATION OF IFN/RIBAVIRIN THERAPY Kazumoto Murata, Yukiko Saito, Tomoyuki Kawakita, Kazushi Sugimoto, Katsuya Shiraki, Mie University School of Medicine, Tsu City, Mie, Japan

8 # 303 HIGH ACTIVITY MUTANT OF HCV NS5B POLYMERASE IDENTIFIED IN CHRONICALLY INFECTED CHIMPANZEES Hong Lou, John LaVoy, Youkyung H Choi, Emory University School of Medicine, Atlanta, GA; Marian E Major, CBER/FDA, Bethesda, MD; Curt H Hagedorn, Emory University School of Medicine, Atlanta, GA

8 # 304 DAILY DOSING REGIMEN OF CONSENSUS INTERFERON

CHRONIC HEPATITIS C AND GENOTYPE 1 Stephan Kaiser, Holger G Hass, Michael Gregor, University of Tuebingen, Tuebingen, Germany

AND RIBAVIRIN FOR TREATMENT-NAIVE PATIENTS WITH

# 305 CLINICAL EVALUATION OF A HUMAN MONOCLONAL ANTIBODY AGAINST THE ENVELOPE PROTEIN (E2) OF HCV FOR PREVENTION OF HCV INFECTION Shlomo Dagan, Rachel Eren, XTL Biopharmaceuticals Ltd., Rehovot, Israel; Neil Graham, XTL Biopharmaceuticals Inc., Durham, NC; Ofer Nussbaum, Dov Terkieltaub, XTL Biopharmaceuticals Ltd., Rehovot, Israel; Norah Terrault, University of California San Francisco, San Francisco, CA; Ran Tur-Kaspa, Rabin Medical Center, Petah-Tikva, Israel; Yoav Lurie, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Rifat Safadi, Zvi Akerman, Eithan Galun, Hadassah University Hospital, Jerusalem, Israel

#306 EPOETIN ALFA (EPO) IMPROVES AND MAINTAINS

HCV-INFECTED PATIENTS RECEIVING INTERFERON/ RIBAVIRIN (IFN/RBV): HRQL RESULTS FROM THE PROACTIVE STUDY Nezam H Afdhal, Beth Israel Deaconess Medical Center, Boston, MA; Betty Goon, Kevin Smith, Ortho Biotech Products, L.P., Bridgewater, NJ; Zobair Younossi, Inova Fairfax Hospital, Falls Church, VA

HEALTH-RELATED QUALITY OF LIFE (HRQL) IN ANEMIC

# 307 PEGINTERFERON ALFA-2A (40KD) (PEGASYSB) IN COMBINATION WITH RIBAVIRIN IN AFRICAN AMERICAN AND CAUCASIAN PATIENTS WITH CHRONIC HEPATITIS C VIRUS GENOTYPE 1 INFECTION: ASSESSMENT OF HISTOLOGIC RESPONSE William Cassidy, Louisiana State University Health Sciences Center, Baton Rouge, LA; Lennox S Jeffers, Miami VA Medical Center, Miami, FL; Charles Howell, University of Maryland School of Medicine, Baltimore, MD; K Rajender Reddy, University of Pennsylvania, Philadelphia, PA; Susan Sheridan, Ellen Lentz, George Harb, Sarkis Khouri, Roche Laboratories, Inc., Nutley, NJ

# 308 DELIVERY OF CONSENSUS INTERFERON BY CONTINUOUS INFUSION FOR THE TREATMENT OF CHRONIC HEPATITIS C: A PILOT VIRAL KINETIC STUDY IN NONRESPONDER PATIENTS Myron Tong, Huntington Memorial Hospital Liver Center, Pasadena, CA; Tarek Hassanein, UCSD Medical Center, San Diego, CA; William Van Antwerp, Medtronic MiniMed, Northridge, CA; Elizabeth Olek, Brian Murphy, InterMune, Inc., Brisbane, CA

# 309 QUANTITATIVE TESTS (QLFTS) DETECT IMPAIRED HEPATIC FUNCTION IN A HIGH PROPORTION OF CHRONIC HEPATITIS C PATIENTS WITH FIBROSIS OR COMPENSATED CIRRHOSIS AND MAY PREDICT RISK OF CIRRHOSIS, SPLENOMEGALY, AND VARICES Gregory T Everson, Marcel0 Kugelmas, Jennifer DeSanto, Shannon Lauriski, University of Colorado School of Medicine, Denver, CO; Mitchell L Shiffman, Richard Sterling, Hofmann Charlotte, Virginia Commonwealth University, Richmond, VA; Timothy Morgan, John Hoefs, Nora Milne, William Rietkerk, University of California Irvine, Irvine, CA; David Wagner, Metabolic Solutions, Nashua, NH; Elizabeth Wright, New England Research Institute, Watertown, MA

#310 RIBAVIRIN COUPLED TO HEMOGLOBIN PROTECTS AGAINST VIRAL HEPATITIS INDUCED BY THE

Gary A Levy, Anand Ghanekar, Ian McGilvray, Toronto General Hospital, Toronto, ON, Canada; Nancy F Ng, Hemosol Research Corporation, Mississauga, ON, Canada; Adam Levy, Laisum Fung, M J Phillips, Toronto General Hospital, Toronto, ON, Canada; Pieter Biessels, Caroline Woods, Cord Adamson, David N Bell, Hemosol Research Corporation, Mississauga, ON, Canada

CORONAVIRUS MHV-3 IN MICE


# 311 LONGER TREATMENT DURATION WITH PEGINTERFERON ALFA-LA (40KD) (PEGASYSO) AND RIBAVIRIN (COPEGUSB) IN NAIVE PATIENTS WITH CHRONIC HEPATITIS C AND DETECTABLE HCV RNA BY WEEK 4 OF THERAPY:

J M Sanchez-Tapias, H. Clinic i Provincial, Barcelona, Spain; M Diago, H. General de Valencia, Valencia, Spain; I‘ Escartin, H. Puerta Hierro, Madrid, Spain; J Enriquez, H. Sant Pau, Barcelona, Spain; R Moreno, H. La Princesa, Madrid, Spain; M Romero- Gomez, H. U. de Valme, Sevilla, Spain; R Barcena, H. Ramon y Cajal, Madrid, Spain; J Crespo, H. Marques Valdecilla, Santander, Spain; R Andrade, H. Virgen Victoria, Mdlaga, Spain; R Perez, H. Central de Asturias, Asturias, Spain; M Testillano, H. Cruces, Bilbao, Spain; R Planas, H. Germans Trias i Pujol, Barcelona, Spain; R Sola, H. del Mar, Barcelona, Spain; M Garcia- Bengoechea, N” s” Arinzazu, San Sebastirin, Spain; J Garcia- Samaniego, H. Carlos 111, Madrid, Spain; M Berenguer, H. La Fe, Valencia, Spain; M Montoro, H. General San Jorge, Huesca, Spain; J del Olmo, H. Clinico, Valencia, Spain; G Lopez, H. Clinico San Carlos, Madrid, Spain; S Tome, H. Clinico de Galicia, S. de Compostela, Spain; T Casanovas, H. Bellvitge, Barcelona, Spain; G Castellanos, H. 12 Octubre, Madrid, Spain; A Castro, H. Juan Canalejo, Contfia, Spain; J Salmeron, H. Clin San Cecilio, Granada, Spain; M Muiioz-Shchez, Roche, Madrid, Spain

PRELIMINARY RESULTS OF THE TERAVIC-4 STUDY*

t 312 TREATMENT OF CHRONIC HEPATITIS C WITH ISIS 14803, AN ANTISENSE INHIBITOR OF HCV, GIVEN FOR 12 WEEKS Stuart C Gordon, William Beaumont Hospital, Royal Oak, MI; Bruce R Bacon, Saint Louis University, St. Louis, MO; Ira M Jacobson, Weill Medical College of Cornell University, New York, NY; Mitchell L Shiffman, Medical College of Virginia, Richmond, VA; Nezam H Afdhal, Beth Israel Deaconess Medical Center, Boston, MA; Rosie Z Yu, Isis Pharmaceuticals, Inc., Carlsbad, CA; John G McHutchison, Duke University, Durham, NC; T Jesse Kwoh, Isis Pharmaceuticals, Inc., Carlsbad, CA

8 313 A PHASE 1/2 STUDY TO EVALUATE THE PHARMACOKINETICS, SAFETY, TOLERABILITY, IMMUNOGENICITY, AND PHARMACODYNAMICS OF ALBUFERON(tm) IN TREATMENT EXPERIENCED SUBJECTS WITH CHRONIC HEPATITIS C V Balan, Mayo Clinic, Phoenix, AZ; M Sulkowski, Johns Hopkins University, Baltimore, MD; D Nelson, University of Florida, Gainesville, FL; G Everson, University of Colorado, Denver, CO; T Barnbury, Mayo Clinic, Phoenix, AZ; J Recta, J Zhong, H Mesghali, J Murray, B Osborn, L Novello, W Freimuth, G Subramanian, Human Genome Sciences, Inc., Rockville, MD

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8 314 A PILOT STUDY OF A NOVEL ANTI-INFLAMMATORY AND ANTI-FIBROTIC AGENT, PIRFENIDONE, IN PATIENTS WITH LIVER CIRRHOSIS Juan Armendariz-Borunda, University of Guadalajara, OPD Hospital Civil de Guadalajara, Guadalajara, Jalisco, Mexico; M Cristina Mas-Carbajal, Eduardo Meza, Ana Rosa Rincon, Arnulfo Alvarez, University of Guadalajara, Guadalajara, Jalisco, Mexico; Zachary D Goodman, Armed Forces Institute of Pathology, Washington, DC; ASoledad Sandoval, University of Guadalajara, Guadalajara, Jalisco, Mexico; Amador Covarrubias, Hospital Civil de Guadalajara Juan I Menchaca, Guadalajara, Mexico; Gil Arechiga, University of Guadalajara, Guadalajara, Jalisco, Mexico; Leone1 Garcia, University of Guadalajara, OPD Hospital Civil de Guadalajara, Guadalajara, Jalisco, Mexico

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# 315

IFNlRIBAVIRIN IN HCV/HIV COINFECTED PATIENTS Kenneth E Sherman, Paul S Horn, Susan D Rouster, University of Cincinnati, Cincinnati, OH; Marion G Peters, University of California San Francisco, San Francisco, CA; Margaret J Koziel, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; Raymond T Chung, Massachusetts General Hospital, Boston, MA

MODELING HCV VIRAL KINETIC RESPONSE TO PEG-

~~~

# 316 RACIAL DIFFERENCES IN PATIENTS WITH HEPATITIS C GENOTYPE 1 Steven Belle, University of Pittsburgh, Pittsburgh, PA; Hari S Conjeevaram, University of Michigan, Ann Arbor, MI; Lennox J Jeffers, University of Miami, Miami, FL

# 317 INTERNATIONAL, MULTICENTER, RANDOMIZED, CONTROLLED STUDY COMPARING STANDARD VERSUS DYNAMICALLY INDIVIDUALIZED TREATMENT IN

PROJECT) Stefan Zeuzem, Saarland University Hospital, Homburg / Saar, Germany; Jean-Michel Pawlotsky, HBpital Henri Mondor- Universite Paris XU, Creteil, France; Esther Hagai, Bar-Ilan University, Ramat-Gan, Israel; Michael von Wagner, Saarland University Hospital, Homburg / Saar, Germany; Ioannis Goulis, Aristotle University of Thessaloniki, Thessalonilu, Greece; Yoav Lurie, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Elia Gianfranco, Azienda Ospedaliera di Parma, Parma, Italy; Jan-Maarten Vrolijk, University Hospital Rotterdam Dijkzigt, Rotterdam, Netherlands; Juan I Esteban, Hospital General Val1 d’Hebron, Barcelona, Spain; Cristophe Hezode, HBpital Henri Mondor-Universite Paris XII, Creteil, France; Martin Lagging, University of Goeteborg, Goeteborg, Sweden; Francesco Negro, Hospital University of Geneve, Geneve, Switzerland; Alexandre Soulier, HBpital Henri Mondor-Universite Paris XII, Creteil, France; Elke Verheij-Hart, University Hospital Rotterdam Dijkzigt, Rotterdam, Netherlands; Bettina Hansen, Erasmus University, Rotterdam, Netherlands; Ronen Tal, Bar-Ilan University, Ramat-Gan, Israel; Carlo Ferrari, Azienda Ospedaliera di Parma, Parma, Italy; Solko W Schalm, University Hospital Rotterdam Dijkzigt, Rotterdam, Netherlands; Avidan U Neumann, Bar-Ilan University, Ramat-Gan, Israel

# 318 COMBINATION THERAPY OF INTERFERON INJECTION AND INTERFERON SUPPOSITORY AUGMENS HOSTS’ IMMUNE RESPONSE AGAINST HCV INFECTION Yoshimichi Haruna, Osaka Prefectural General Hospital, Osaka, Japan

PATIENTS WITH CHRONIC HEPATITIS C (DITTO-HCV

# 319

RELAPSERS TO STANDARD INTERFERON + RIBAVIRIN IN CHRONIC HEPATITIS C : EFFICACY AND SAFETY RESULTS FROM A RANDOMIZED MULTICENTRIC FRENCH STUDY Isabelle Portal, Danielle Botta-Fridlund, Hospital Conception, Marseilles, France; Marc Bourliere, Hospital Saint Joseph, Marseilles, France; Michel Rotily, ClinSearch, Bagneux, France; Philippe Halfon, 23 rue de Friedland, Marseille, France; Patrice Couzigou, CHU Groupe Sud, Pessac, France; Karl Barange, Hospital Purpan, Toulouse, France; V Canva, CHR Claude Huriez, Lille Cedex, France; Dominique Larrey, Hospital Saint Eloi, Montpellier cedex 5, France

TREATMENT WITH PEGYLATED-INTERFERON ALFA 28 IN


HEPATOLOGY, Vol. 38, No. 4, Suppl. 1,2003 POSTER SESSlONS 83A

# 320 HEMOGLOBIN INCREASE IS INDEPENDENTLY

QUALITY OF LIFE (HRQL) IN ANEMIC INTERFERON/

INFECTED PATIENTS TREATED WITH EPOETIN ALFA Nezam H Afdhal, Beth Israel Deaconess Medical Center, Boston, MA; Angela Klopfer, Linda Tang, Ortho Biotech Products, L.P., Bridgewater, NJ; Zobair Younossi, Inova Fairfax Hospital, Falls Church, VA

ASSOCIATED WITH INCREASED HEALTH-RELATED

RIBAVIRIN (IFN/RBV)-TREATED HEPATITIS C VIRUS (HCVI-

# 321 THE RENEW TRIAL A NATIONAL, MULTICENTER STUDY OF HIGH-DOSE PEGINTERFERON ALFA-28 + RIBAVIRIN FOR NON-RESPONDERS WITH HEPATITIS C John B Gross, Terry M Therneau, Stephanie M Johnson, Mayo Clinic, Rochester, MN; Paul Y Kwo, Indiana University, Indianapolis, IN; Nezam H Afdhal, Beth Israel Deaconess Medical Center, Boston, MA; Steven L Flamm, Northwestern University, Chicago, IL; RENEW Trial Investigators, National Network, Rochester, MN

# 322 BASELINE PSYCHOSOCIAL CHARACTERISTICS OF

Scott R Smith, University of North Carolina, Chapel Hill, NC; Steven H Belle, University of Pittsburgh, Pittsburgh, PA; Robert S Brown Jr, Columbia University, New York, NY; Dickens Theodore, Michael W Fried, University of North Carolina, Chapel Hill, NC

PARTICIPANTS IN THE VIRAHEP-C STUDY

# 323

CONDITION FOR BETTER RESPONSE IN INTERFERON

Akihiko Okumura, Tetsuya Ishikawa, Minoru Ayada, Ken Sato, Tadashi Maeno, Naoki Hotta, Tsuneaki Tagaya, Yoshitaka Fukuzawa, Shinichi Kakumu, Aichi Medical University School of Medicine, Aichi-ken, Japan

# 324 RESULTS OF A RANDOMIZED CLINICAL TRIAL OF

NUTRITION IS MORE IMPORTANT THAN TH1-DOMINATED

ALPHA-2BIRIBAVIRIN THERAPY

GENOTYPE-4 INFECTED SUBJECTS WHEN TREATED WITH STANDARD OR PEGYLATED INTERFERON ALFA-PB IN COMBINATION WITH RIBAVIRIN Gamal H Esmat, Arm Abouzied, M Abdel-Hamid, M K Mohamed, K Zalata, M S El Raziky, S A Ismael, M Said, A Hasan, M Anwar, A Shaheen, F Abdel-Aziz, N N Mikhail, A Ismail, Tropical Medicine Institute, Cairo, Egypt; Alan Fix, National Institutes of Health, Bethesda, MD; Thomas G Strickland, University of Maryland, Baltimore, MD; Maria H Sjogren, Walter Reed Army Medical Center, Washington, DC

# 325

INTERFERON EFFECT FOR CHRONIC HEPATITIS C Kazuho Imanaka, Shinji Tamura, Koji Fukui, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Nobuyulu Ito, Fukui Medical University, Fukui, Japan; Yuichi Yoshiba, Yoshiyuki Sawai, Akira Wada, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Yasuharu Imai, Ikeda Munici- pal Hospital, Ikeda, Japan; Iwao Yabuuchi, Otemae Hospital, Osaka, Japan; Kouichi Seki, Hyogo Prefectural Nishinomiya Hospital, Nishinomiya, Hyogo, Japan; Masami Inada, Toyonaka Municipal Hospital, Toyonaka, Japan; Takeshi Kashihara, Itami City Hospital, Itami, Japan; Shuzo Noda, Suita Municipal Hospital, Suita, Japan; Shinichi Kiso, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Sumio Kawata, Yamagata University, Yamagata, Japan; Yuji Matsuzawa, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

EXPRESSION OF SOCS-1 IN THE LIVER ATTENUATES

# 326 EARLY PHARMACOKINETICS, PHARMACODYNAMICS AND HEPATITIS C VIRAL KINETICS O N TREATMENT WITH

WITHOUT RIBAVIRIN: CHARACTERIZATION OF THE NULL RESPONDER Adrian M Di Bisceglie, Patricia Osmack, Joyce Hoffman, Janice Strinko, Saint Louis University Health Sciences Center, St. Louis, MO

PEGYLATED INTERFERON (IFN) ALFA-2A WITH OR

~~~

H” 327

VIRAL RNA SEQUENCE IN PATIENTS TREATED WITH INTERFERON AND RIBAVIRIN COMBINATION THERAPY Masamichi Tanaka, Fumio Imazeki, Osamu Yokosuka, Tatsuo Kanda, Hiromitsu Saisho, Chiba University Graduate School of Medicine, Chiba, Japan

CHARACTERIZATION OF FULL-LENGTH HEPATITIS C

# 328 COMPARISON OF 48 OR 72 WEEKS OF TREATMENT WITH

RIBAVIRIN (COPEGUSS) IN TREATMENT-NAIVE PATIENTS WITH CHRONIC HEPATITIS C INFECTED WITH HCV GENOTYPE 1 Thomas Berg, Charite, Campus Virchow-Klinikum, Berlin, Germany; M von Wagner, Universitatsklinikum des Saarlandes, Homburg /Saar, Germany; H Hinrichsen, Christian-Albrecht- Universitat, Kiel, Germany; T Heintges, Heinrich-Heine- University, Dusseldorf, Germany; P Buggisch, Universitatsklinik Eppendorf, Hamburg, Germany; T Goeser, Universitat zu Kdln, Cologne, Germany; J Rasenack, Medizinische Universitatsklinik, Freiburg, Germany; G R Pape, Klinikum Groghadern, Ludwig- Maximilians-Universitat, Munchen, Germany; W E Schmidt, Medizinische Universitatsklinik, St. Josefshospital, Bochum, Germany; B Kallinowski, Universitatsklinik Heidelberg, Heidelberg, Germany; H Klinker, Klinikum der Universitat Wiirzburg, Wiirzburg, Germany; U Spengler, Medizinische Einrichtung der Rh. Fr. Wilhelms Universitat, Bonn, Germany; B Klapperich, Roche, Grenzach, Germany; M Popescu, Roche Diagnostics, Basel, Switzerland; S Zeuzem, Universitatsklinikum des Saarlandes, Homburg/ Saar, Germany

PEGINTERFERON ALFA-2A (40KD) (PEGASYSB) PLUS

tr 329 TREATMENT WITH PEGYLATED INTERFERON ALPHA 2B AND RIBAVIRIN (REBETOL) PRODUCES SIGNIFICANT SUSTAINED VIROLOGIC RESPONSE RATES IN HCV INFECTED PATIENTS WHO FAILED PRIOR THERAPY Paul J Gaglio, David Zimmerman, James Choi, Larry Heller, Robert S Brown Jr, Columbia University College of Physicians and Surgeons, New York, NY

# 330 HEALTH BENEFITS FROM ANTI VIRAL THERAPY FOR MILD

RANDOMISED CONTROLLED TRIAL Mark Wright, Janice Main, Robert D Goldin, Howard C Thomas, Imperial College, London, UK

CHRONIC HEPATITIS C. A UK MULTI-CENTRE

# 331

HCV POLYMERASE INHIBITORS Ming-Qiang Zhang, Laval Chan, Sanjoy K Das, Thumkunta J Reddy, Oswy Z Pereira, Carl Poisson, Melanie Proulx, Liliane Halab, Caroline Roy, Constantin G Yannopoulos, Nghe Nguyen- Ba, Richard Bethell, Maud David, Jean Bkdard, Martine Hamel, Darius Bilimoria, Olivier Nicolas, Nicolas Morin, Philippe Courtemanche-Asselin, Bettina Hamelin, Kelly Dong, Nathalie Rioux, Annie Richard, Shire BioChem Inc., Laval, PQ, Canada; Michael N G James, Meitian Wang, Canadian Institutes for Health Research (CIHR), Edmonton, AB, Canada

THIOPHENE-2-CARBOXYLIC ACIDS: A SERIES OF NOVEL


~ ~~ ~

# 332

COMBINATION WITH RIBAVIRIN IN AFRICAN AMERICAN AND CAUCASIAN PATIENTS WITH CHRONIC HEPATITIS C HCV GENOTYPE 1: SAFETY AND TOLERABILITY Charles Howell, University of Maryland School of Medicine, Baltimore, MD; Lennox S Jeffers, Miami VA Medical Center, Miami, FL; William Cassidy, Louisiana State University Health Sciences Center, Baton Rouge, LA; K Rajender Reddy, University of Pennsylvania, Philadelphia, PA; Susan Sheridan, Irwin Ho, Sarkis Khouri, George Harb, Roche Laboratories, Inc., Nutley, NJ

PEGINTERFERON ALFA-2A (40KD) (PEGASYSB) IN

# 333 CITALOPRAM FOR PREVENTION OF INTERFERON-ALPHA ASSOCIATED DEPRESSION IN PSYCHIATRIC RISK PATIENTS Martin Schaefer, Markus Schwaiger, Thomas Berg, Charite, Humboldt-University, Berlin, Germany

# 334 HC07 ANRS TRIAL-PILOT STUDY OF TRIPLE THERAPY BY RECOMBINANT INTERFERONAZA- RIBAVIRIN- IL-2 FOR TREATMENT OF NONRESPONDER PATIENTS WITH SEVERE LIVER DISEASE INFECTED BY HEPATITIS C VIRUS (HCV) GENOTYPE 1 Laurent L Alric, Jacques Izopet, Sophie Metivier, CHU Purpan, Toulouse, France; Jean Tkaczuck, Bernard Pipy CHU Rangueil, Toulouse, France; Jean-Pierre Vinel, CHU Purpan, Toulouse, France

t 335 INTERIM RESULTS OF A RANDOMIZED TRIAL OF 1.5pG/KG VS. J.OpG/KG PEGYLATED INTERFERON ALFA 2-B PEG-INTRONO (PEG) PLUS RIBAVIRIN (RBV) FOR NAIVE CHRONIC HEPATITIS C PATIENTS AND 3.OpGIKG PEG PLUS

PREVIOUS THERAPY. (THE TARGET TRIAL) Calvin L White, Peter F Malet, Corinne L Wentworth, Veronica L Cantu, Tamara L Alton, William M Lee, University of Texas Southwestern, Dallas, TX

# 336 COMBINATION THERAPY OF INTERFERON-a-2B WITH

POLYUNSATURATED FATTY ACID OF ERYTHROCYTE MEMBRANE PHOSPHOLIPID IN CHRONIC HEPATITIS C PATIENTS Kcisuke Hino, Akira Kitase, Yuh-ichi Hara, Yuhki Yamaguchi, Yamaguchi University School of Medicine, Ube-Yamaguchi, Japan; Yasuko Ota, Ayako Nagai, Takayo Sasagawa, Misako Okita, Okayama Prefectural University, Sohja, Japan; Takakazu Furutani, Ren Fenyu, Michiari Okuda, Kiwamu Okita, Yama- guchi University School of Medicine, Ube-Yamaguchi, Japan

# 337 MXA GENE EXPRESSION AS A SENSITIVE MARKER FOR IFN BIOACTIVITY AND NEUTRALIZING ANTIBODIES IN CHRONIC HEPATITIS C VIRUS INFECTION Carl Joms, Robert T l~ imie , Hans-Christian Spangenberg, Nadine Kersting, Jew Rasenack, Manfred Weidmann, Hubert E Blum, Otto Haller, Ceorg Kochs, University of Freiburg, Freiburg, Germany

RBV FOR NON-RESPONDERS (NR) AND RELAPSERSO T O

RIBAVIRIN DECREASES THE CONTENT OF 20:5N-3

# 338 A PILOT TRIAL OF THYMALFASIN (THYMOSIN ALPHA-1) IN COMBINATION WITH PEGINTERFERON ALPHA-2A (PEG- IFNZA) AND RIBAVIRIN IN HCV NON-RESPONDERS: 12- WEEK INTERIM RESULTS Jorge L Poo, Cif-Biotec, Mexico City, Mexico; Xochil Garcia, Hospital Lopez Mateos ISSSTE, Mexico City, Mexico; Eduardo B Martins, SciClone Pharmaceuticals, San Mateo, CA; David Kershenobich, INCMN Salvador Zubiran, Mexico City Mexico

# 339 INCIDENCE OF HEPATITIS C VIRUS INFECTION AMONG GENERAL POPULATION, RISK POPULATION GROUPS AND PATIENTS WITH CHRONIC RENAL FAILURE, THALASSEMIA AND HEMOPHILIA Chittoor M Habibullah, Deccan College of Medical Sciences, Hyderabad, AndhraPradesh, India

# 340

C (SNMC) FOR THE TREATMENT OF CHRONIC HEPATITIS C: BIOCHEMICAL AND HISTOLOGICAL EFFECTS AFTER 26 WEEKS OF TREATMENT Hans Orlent, Bettina E Hansen, Pieter E Zondervan, Solko W Schalm, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands

GLYCYRRHIZIN GIVEN AS STRONGER NEO-MINOPHAGEN

# 341

PATIENTS WITH CHRONIC HEPATITIS C Kazuko Iwata, Mie University Hospital, Tsu City, Mie, Japan; Motoh Iwasa, Masahiko Kaito, Masaki Takeo, Jiro Ikoma, Yukihiko Adachi, Mie University School of Medicine, Tsu City, Mie, Japan

EFFICACY OF LONG-TERM DIETARY IRON RESTRICTION IN

# 342 TREATMENT OF SEVERE HEPATITIS C (METAVIR FIBROSIS SCORE = 3 OR 4) WITH PEGINTERFERON AND RIBAVIRIN. RESULTS FROM A FRENCH MULTICENTRE RANDOMISED CONTROLLED STUDY Armand Abergel, C Bonny N Martineau, Hotel-Dieu, Clermont Ferrand, France; C Hezode, Hapita1 Heiiri Mondor, Creteil, France; V Leroy, CHRU, Grenoble, France; K Barange, CHRU, Toulouse, France; J P Bronowicki, CHRU, Nancy, France; A Tran, CHRU, Nice, France; C Henquell, CHRU, Clermont Ferrand, France; C Darcha, S Ughetto, P Dechelotte, Hotel-Dieu, Clermont Ferrand, France; H Lafeuille, CHRU, Clermont Ferrand, France; G Bommelaer, Hotel-Dieu, Clermont Ferrand, France

# 343 EFFICACY OF PEG-IFN-ALFA ZA(PEGASYS) VSPEGASYS AND RBV FOR HIV/HCV COINFECTED PATIENTS THAT ARE NONRESPONDERS T O PREVIOUS IFN THERAPY Maribel Rodriguez-Torres, Fundacion de Investigacion de Diego, Santurce, PR; Jose Rodriguez-Orengo, University of Puerto Rico School of Medicine, Rio Piedras, PR

# 344 DEPRESSIVE SYMPTOMS DURING IFN-ALPHA/RIBAVIRIN THERAPY ARE ASSOCIATED WITH REDUCED VIRAL CLEARANCE IN PATIENTS WITH HEPATITIS C Charles L Raison, Sherry D Broadwell, Andrey S Borisov, Amita K Manatunga, Bobbi J Woolwine, Emory University, Atlanta, GA, Ira M Jacobson, Weill Medical College of Cornell University, New York, NY, Charles B Nemeroff, Andiew H Miller, Emory University, Atlanta, GA

# 345 DEPRESSION DURING IFN-ALFA PLUS RIBAVIRIN THERAPY PREVALENCE AND PREDICTION Charles L Raison, Andrey S Borisov, Sherry D Broadwell, Emory University, Atlanta, GA; Amita K Manatunga, Emory University Rollins School of Public Health, Atlanta, GA; Bobbi J Woolwine, Emory University, Atlanta, GA; Ira M Jacobson, Weill Medical College of Cornell University, New York, NY; Charles B Nemeroff, Andrew H Miller, Emory University, Atlanta, CA

8 Denotes AASLD Presidential Poqter of Distinction


# 346 PSYCHOSOCIAL DISCORD UNDERLIES POOR ADHERENCE TO ANTIVIRAL THERAPY IN THE VA POPULATION: RESULTS OF A DEMOGRAPHIC SURVEY OF THE VA POPULATION UNDERGOING HCV THERAPY Steven L Flamm, Northwestern University Medical School, Chicago, IL; Charles Mendenhall, Cincinnati VA Hospital, Cincinnati, OH; David Johnson, Carl T. Hayden VA Hospital, Phoenix, AZ; Maher Azzouz, G.V. "Sonny" Montgomery VA Hospital, Jackson, MS; Lawrence Lumeng, Richard L. Roudebush VA Hospital, Indianapolis, IN; Vivek Huilgol, Overton Brooks VA Medical Center, Shreveport, LA; Helen Wong, Central California VA Hospital, Fresno, CA; Anastasios Mihas, McGuire VA Hospital, Richmond, VA; Frederic Regenstein, New Orleans VA Hospital, New Orleans, LA; Axel Feller, North Chicago VA Hospital, North Chicago, IL; Richard Jaszewski, John D. Dingle VA Hospital, Detroit, MI; Christina M Bromley, Ronald L Bromley, BioStat Solutions, Damascus, MD

# 347 POOR TOLERABILITY TO HIGH DOSE PEG INTERFERON AND RIBAVIRIN IN HIVlHCV COINFECTED PATIENTS; INITIAL RESULTS FROM A RANDOMIZED MULTICENTER TRIAL Ghassan Hammoud, University of Florida at Jacksonville, Jacksonville, FL; Jianjun Li, Eastern Carolina University, Greenville, NC; Kenneth Vega, University of Florida, Jacksonville, FL; Ruth Beggren, Tulane University, New Orleans, LA; Michael Sands, University of Florida, Jacksonville, FL; Barry Rodwick, University of Florida, Safety Harbor, FL; Mitchell Davis, University of Florida, Willington, FL; David Parks, University of Missouri, St. Louis, MO; Daniel Warner, UFL, Daytona Beach, FL; Kathleen Casey, UNJHSC, Neptune, NJ; Uwe Schmidt, UNJHSC, Union, NJ; Rinchen Emgusnov, Costal Medical, Providence, RI; Robert Eng, Tremont, East Orange, NJ; Dennis Israelski, San Mateo Medical Center, San Mateo, CA; David Mayorga, Broward Clinic, Fort Lauderdale, FL; David Lintz, UNJHSC, West Field, NY; Louis Lambiase, University of Florida, Jacksonville, FL

Hepatic Fibrogenesis

8 #348 NOREPINEPHRINE INDUCES HEPATIC FIBROGENESIS IN LEPTIN DEFICIENT OB/OB MICE Jude A Oben, Johns Hopkins, Baltimore, MD; Tania Roskams, Nicoletta Sinelli, University of Leuven, Leuven, Belgium; Michael Torbenson, Shqi Yang, Huizhi Lin, Anna Mae Diehl, Johns Hopkins, Baltimore, MD

8 #349 HEPATIC FIBROGENESIS REQUIRES SYMPATHETIC NEUROTRANSMITTERS Jude A Oben, Johns Hopkins University, Baltimore, MD; Tania Roskams, University of Leuven, Leuven, Belgium; Shiqi Yang, Huizhi Lin, Johns Hopkins University, Baltimore, MD; Nicoletta Sinelli, University of Leuven, Leuven, Belgium; Michael Torbenson, Zhiping Li, Ulrika Smedh, Timothy H Moran, Johns Hopkms University, Baltimore, MD; Steven A Thomas, University of Pennsylvania, Philadelphia, PA; Anna Mae Diehl, Johns Hopkins University, Baltimore, MD

8 # 350 ADIPONECTIN, AN ADIPOCYTOKINE, ATTENUATES

IN MICE Yoshhiro Kamada, Shinji Tamura, Shinichi Kiso, Hitoshi Matsumoto, Yukiko Saji, Yuichi Yoshida, Koji Fukui, Norikazu Maeda, Hitoshi Nishizawa, Hiroyuki Nagaretani, Yoshihisa Okamoto, Shinji Kihara, Jun-ichiro Miyagawa, Tohru Funahashi, Yuji Matsuzawa, Osaka University Graduate School of Medicine, Suita, Osaka, Japan Travel Award Recipient

8 #351 REVERSIBILITY OF CIRRHOSIS IS ASSOCIATED WITH DECREASE OF LIVER RELATED COMPLICATIONS Serpaggi Jeanne, Assistance Publique des HBpitaux de Paris, Paris, France

# 352 LIMITED RESOLUTION OF CIRRHOSIS IN RATS IS ASSOCIATED WITH TISSUE TRANSGLUTAMINASE MEDIATED CROSSLINKING OF THE LIVER EXTRACELLULAR MATRIX Xiaoying Zhou, James Chan, John P Iredale, R Christopher Benyon, Liver Research Group, IIR Division, University of Southampton, Southampton, UK

CARBON-TETRACHLORIDE INDUCED LIVER FIBROSIS

# 353 THE FRIZZLED VARIANT OF THE ENDOSTATIN PRECURSOR COLLAGEN XVIII, A PERICELLULAR MATRIX PROTEIN Orlando Musso, INSERM U456, Rennes, France; Harri Elamaa, Collagen Research Unit, Oulu, Finland; Delphine Quelard, Estelle Robert, INSERM U456, Rennes, France; Roselyne Primault, UFR Medicales et Pharmaceutiques, Rennes, France; Nathalie Thkret, INSERM U456, Rennes, France; Taina Pihlajaniemi, Collagen Research Unit, Oulu, Finland; Bruno Clement, INSERM U456, Rennes, France

# 354 HEPATIC STELLATE CELL SPECIFIC DELIVERY OF MYCOPHENOLIC ACID AS A STRATEGY TO TREAT LIVER FIBROSIS Rick Greupink, Hester Bakker, Anne-Miek van Loenen-Weemaes, Catharina Reker-Smit, Dirk Meijer, Leonie Beljaars, Klaas Poelstra, University of Groningen, Groningen, Netherlands

# 355 BETA 3-SPECIFIC NON-PEPTIDIC INTEGRIN ANTAGONIST EMD409915 BLOCKS PDFG-STIMULATED MIGRATION IN

SFm 8 8 f

HUMAN HEPATIC STELLATE CELLS BUT NOT IN FORESKIN FIBROBLASTS Eleonora Patsenker, Yury Popov, Michael Bauer, University of Erlangen-Nuremberg, Erlangen, Germany; Massimo Pinzani, Universita di Firenze, Firenze, Italy; Simon L Goodman, Merck KGaA, Darmstadt, Germany; Eckhart Hahn, Detlef Schuppan, University of Erlangen-Nuremberg, Erlangen, Germany

# 356 EPITHELIAL TO MESENCHYMAL TRANSITION DURING LIVER FIBROSIS Changqing Yang, Program in Matrix Biology, Division of Gastroenterology and Liver Center, Department of Medicine, Beth Israel Deaconess Medical Center of Harvard Medical School, Boston, MA; Jiyao Wang, Zhongshan Hospital of Fudan University, Shanghai, China; Michael Zeisberg, Mary Soubasakos, Nezam H Afdhal, Raghu Kalluri, Program in Matrix Biology, Division of Gastroenterology and Liver Center, Department of Medicine, Beth Israel Deaconess Medical Center of Harvard Medical School, Boston, MA


f 357 ELEVATED SERUM AND BILIARY MONOCYTE CHEMOTAXIS PROTEIN-1 LEVELS IN CHOLESTATIC LIVER DISEASE: ROLE IN EARLY HEPATIC FIBROGENESIS Sonia A Greco, Anita C Hoskins, Tamara N Pereira, The Queensland Institute of Medical Research, Brisbane, Australia; Bruno Turlin, Hospital Pontchaillou, Rennes, France; Peter J Lewindon, Royal Children's Hospital, Brisbane, Australia; Grant A Ramm, The Queensland Institute of Medical Research, Brisbane, Australia

4 358 POSSIBLE INVOLVEMENT OF RHO-KINASE PATHWAY IN THE TISSUE ANGIOTENSIN SYSTEM OF THE HEPATIC FIBROGENESIS Kumi Kitamura, School of Medicine, Keio University, Tokyo, Japan; Kyoko Toda, Satoshi Tsunematsu, Naoki Kumagai, Kitasato Institution Hospital, Tokyo, Japan; Hitomi Horikawa, Nobuhiro Nakamoto, Hidetsugu Saito, Hiromasa Ishi, School of Medicine, Keio University, Tokyo, Japan

f 359 INSULIN-LIKE GROWTH FACTOR I (IGF-I) THERAPY REDUCES PORTAL PRESSUERE AND BACTERIAL TRANS- LOCATIONIN RATSWITH EXPERIMENTAL CIRRHOSIS Vicente Lorenzo-Zuiiiga, Ramon Bartoli, Ram6n Planas, Hospital Universitari Germans Trias i Pujol, Badalona, Spain; Carlos Rodriguez-Ortigosa, Medical School and Clinica Universitaria, University of Navarra, Pamplona, Spain; Inma Castilla-Cortazar, University of Malaga, Malaga, Spain; Belen ViAado, Isabel qanguren, Miguel Gassull, Hospital Uiiiversitari Germans Trias i Pujol, Badalona, Spain; Jorge Quiroga, Jesus Prieto, Medical School and Clinica Universitaria, University of Navarra, Pamplona, Spain

# 360 THE RAPAMYCIN ANALOGUE EVEROLIMUS REDUCES RAT STELLATE CELL ACTIVATION IN TWO DIFFERENT IN- VITRO MODELS Clare Verrill, Janice Davies, Julia Maltby, University of Southampton, Southampton, UK; Graeme Alexander, Cambridge University, Cambridge, UK; Lars Sundstrom, Nick Sheron, Universitv of Southamuton, Southampton, UK ~

361 CHOLESTERYL ESTER TRANSFER PROTEIN (CETP)ILE405VAL POLYMORPHISM AFFECTS THE RATE OF FIBROSIS DEVELOPMENT IN CHRONIC HEPATITIS C VIRUS INFECTION Mark Wright, Robert D Goldin, Imperial College, London, UK; Adrian V S Hill, Uruversity of Oxford, Oxford, UK, Howard C Thomas, Mark R Thur%z, Imperial College, London, UK

# 362 THE DIRECT ROLE OF HEPATITIS C VIRUS CORE PROTEIN INFLUENCING ON LIVER FIBROGENESIS: IN VITRO STUDY USING CO-CULTURE SYSTEM Seung K Yoon, Ju Y Shin, Chang W Kim, Si H Bae, Jong Y Choi, Se H Cho, Jiii M Yang, Nam I Han, Young S Lee, Kyu W Chung, Hee S Sun, The Catholic University of Korea, Seoul, South Korea

8 363 ACTIVIN SECRETED FROM HEPATOCYTES PLAYS A KEY ROLE IN LIVER FIBROGENESIS Naoto Kitamura, Toshifumi Azuma, Keio University, Tokyo, Japan; YLIZU~U Eto, Ajinonioto, Tokyo, Japan; Kengo Tomita, Sayaka lnokuchi, Takeshi Nishimura, Hiromasa Ishii, Keio University, Tokyo, Japan

'8 Denotes AASLD Presidential Poster of Distinction

# 364 HIGH FAT DIET INDUCES SEVERE HEPATIC FIBROSIS IN

Yi Chen, School of Medicine, Tokai University, I<anagawa, Japan INDUCIBLE NITRIC OXIDE GENE-KNOCKOUT MICE

# 365 ATTENUATED LIVER FIBROSIS IN ANGIOTENSIN TYPE 1 RECEPTOR DEFICIENT MICE Liu Yang, Ramon Bataller, University of North Carolina at Chapel Hill, Chapel Hill, NC; Thomas M Coffman, Duke University and Durham VA Medical Centers, Durham, NC; Richard A Rippe, David A Brenner, University of North Carolina at Chapel Hill, Chapel Hill, NC

# 366

CIRRHOSIS AND IMPROVES HEPATIC ENCEPHALOPATY Juan Armendariz-Borunda, University of Guadalajara, OPD Hospital Civil de Guadalajara, Guadalajara, Jalisco, Mexico; Javier Galvez-Gastelum, Aida Segura-Flores, Carlos Beas-Zara te, Alejandra Miranda, University of Guadalajara, Guadalajara, Jalisco, Mexico

# 367 PPAR-a ACTIVATORS, WY-14,643 AND FENOFIBRATES, INHIBIT HEPATIC FIBROSIS IN EXPERIMENTAL RAT MODEL VIA ANTIOXIDANT EFFECT Tetsuya Toyama, Kyoto Prefectural Umversity of Medicine, Kyoto, Japan; chi Hospital Department of Gastroenterology, Rakuwakai Mamtama, ; Akihito Yamauchi, Yuichi Harano, Hideki Nakamura, Masahito Minami, Yoshifuto Itoh, Takeshi Okanoue, Kyoto Prefectural University of Medicine, Kyoto, Japan

COMBINED HUPA PLUS MMP-8 GENE THERAPY REVERTS

~~

# 368 EVALUATION OF SAMPLING VARIABILITY OF LIVER FIBROSIS IN HEPATITIS C USING VIRTUAL BIOPSIES. HOW LONG THE BIOPSY? Pierre Bedossa, CNRS, HBpital Bicstre, Le Kremlin-Bidtre, France; Delphine Dargere, CNRS, Paris, France; Valerie Paradis, CNRS, HBpital Beaujon, Clichy, France

# 369 MUSASHI-1-POSITIVE CELLS, STEM/PROGENITOR CELLS, DIFFERENTIATE INTO BOTH ALPHA-SMOOTH MUSCLE ACTIN- AND MMP-1-POSITIVE CELLS WHICH APPEAR IN THE RESOLUTION OF LIVER FIBROSIS Tetsu Watanabe, Maki Niioka, Yutaka Inagaki, Yoshihiko Sugioka, Tokai University, Isehara, Kanagawa, Japan; Hideyuki Okano, Keio University, Tokyo, Japan; Isao Okazalu, Tokai University, Isehara, Kanagawa, Japan

# 370

RESPONSIVENESS OF THE ALPHA 2(I) COLLAGEN PROMOTER T O CCL4 IN TRANSGENIC MICE Natalia Nieto, Arthur I Cederbaum, Mount Sinai School of Medicine, New York, NY

S-ADENOSYL-L-METHIONINE REPRESSES THE

# 371

AND REVERSES THE DEVELOPMENT OF CARBON TETRACHLORIDE-INDUCED CIRRHOSIS IN RATS Chinnasamy Thirunavukkarasu, Yongping Yang, University of Pittsburgh, Pittsburgh, PA; Vladimir M Subbotin, Mirus Corporation, Madison, WI; Chandrashekhar R Gaiidh, University of Pittsburgh, Pittsburgh, PA

#372 THE P50 SUBUNIT OF NFKB IS PROTECTIVE IN CHRONIC

Derek A Mann, Fiona Oakley, David Smart, Christothea Constandinou, Xiaoying Zhou, Harry Millward-Sadler, John P Iredale, University of Southampton, Southampton, U K

ENDOTHELIN RECEPTOR ANTAGONIST TAK-044 ARRESTS

CCL4-INDUCED FIBROSIS AND INFLAMMATION

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1,2003 POSTER SESSIONS 87A

# 373 HALOFUGINONE REGULATES PROTEIN TYROSINE PHOSPHATASE OF REGENERATION LIVER -1 (PRL-1): UPREGUALTES THE GENE EXPRESSION AND CAUSES CELLULAR TRANSLOCATION Yulia Gnainsky, Volcani Center, Bet Dagan, Israel; Orna Halevy, Hebrew University of Jerusalem, Rehovot, Israel; Cadi Spira, Technion-Israel Institute of Technology, Haifa, Israel; Rafael Bruck, Wolfson Medical Center, Holon, Israel; Arnon Nagler, Sheba Medical Center, Tel Hashomer, Israel; Mark Pines, Volcani Center, Bet Dagan, Israel

# 374 THROMBIN INHIBITION DECREASES EXPERIMENTAL LIVER FIBROSIS Liliane Dubuisson, Jean Rosenbaum, Jennifer Gillibert- Duplantier, Nathalie Senant, Universite Victor Segalen Bordeaux 2, Bordeaux, France; Genevieve Freyburger, HBpital Pellegrin, Bordeaux, France; Jean-Marc Herbert, Sanofi-Synthelabo, Toulouse, France; Alexis Desmouliere, Universite Victor Segalen Bordeaux 2, Bordeaux, France

# 375 EFFECT OF NUCLEAR HORMONE RECEPTOR LIGANDS ON PROLIFERATION AND ACTIVATION OF HEPATIC STELLATECELLS Alexandra Traister, Noa Ciuraru, Isabel Zvibel, Zaki Kraiem, Ran Oren, Tel Aviv Medical Center, Tel Aviv, Israel

~ ~~ ~

# 376

TISSUE GROWTH FACTOR (CTGF) EXPRESSION IN HEPG2

STRESS Masahiro Konishi, Mikio Kajihara, Shinzo Kato, Sadakazu Aiso, Hiromasa Ishii, Keio University, Tokyo, Japan

5377 THE ECTO-NUCLEOTIDASE NTPDASEP IS SELECTIVELY DOWN-REGULATED IN BILIARY FIBROSIS

ETHANOL UPREGULATES PRO-FIBROTIC CONNECTIVE

CELLS VIA CYTOCHROME P-4502E1-MEDIATED OXIDATIVE

Emma A Kruglov, Joahd Toure, M Nauman Jhandier, Dhanpat Jain, Yale University School of Medicine, New Haven, CT; Jean Sevigny, Universite Laval, Quebec, PQ, Canada; Simon C Robson, Harvard Medical School, Boson, MA; Jonathan A Dranoff, Yale University School of Medicine, New Haven, CT

4'378 A SIGNIFICANT PROPORTION OF MYOFIBROBLASTS IN HUMAN LIVER CIRRHOSIS ARE OF BONE MARROW ORIGIN Stuart J Forbes, Francesco Russo, Imperial College, London, UK; Patrizia Burra, Rugge Massimo, University of Padova, Padova, Italy; Nicholas Wright, Cancer Research UK, London, UK; Malcolm R Alison, Imperial College, London, UK

# 379 ANTIFIBROTIC ACTIVITY OF REFANLIN, A HEPATOCYTE GROWTH FACTOR ANALOGUE IN VITRO AND IN EXPERIMENTAL LIVER FIBROSIS Carlos Alvarez, Mount Sinai School of Medicine, New York, NY; Peter Mento, North Shore University-LIJ Health Science Center, Manhasset, NY; Prakash Narayan, Angion Biomedica Corporation, Manhasset, NY; Itzhak D Goldberg, North Shore University-LIJ Health System, Manhasset, NY; Scott Friedman, Efsevia Albanis, Mount Sinai School of Medicine, New York, NY

Hepatitis C: Pathogenesis I

# 380

POLARIZING ABILITY OF BLOOD DENDRITIC CELL SUBSETS IN CHRONIC HEPATITIS C Tatsuya Kanto, Aki Sato, Michiyo Inoue, Hideki Miyatake, Mitsuru Sakakibara, Takayuki Yakushijin, Chika Oki, Tetsuo Takehara, Norio Hayashi, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

IFN-a OR IL-15 RESTORES THE IMPAIRED HELPER T-CELL

8 # 381 INSERTION OF GREEN FLUORESCENT PROTEIN INTO NONSTRUCTURAL PROTEIN 5A ALLOWS DIRECT VISUALIZATION OF FUNCTIONAL HEPATITIS C VIRUS REPLICATION COMPLEXES IN LIVING CELLS Darius Moradpour, University of Freiburg, Freiburg, Germany; Matthew Evans, Columbia University, New York, NY; Rainer Gosert, University of Freiburg, Freiburg, Germany; Zhenghong Yuan, Rockefeller University, New York, NY; Hubert E Blum, University of Freiburg, Freiburg, Germany; Stephen P Goff, Columbia University, New York, NY; Brett D Lindenbach, Charles M Rice, Rockefeller University, New York, NY

~~ 8 #382 AUTOCRINE IL-15 IS REQUIRED FOR MHC CLASS I- RELATED CHAIN A AND B EXPRESSION ON MONOCYTE- DERIVED DENDRITIC CELLS IN RESPONSE TO INTERFERONdP: IMPAIRMENT OF INTERFERON-INDUCED IL-15 PRODUCTION IN HEPATITIS C VIRUS INFECTION Masahisa Jinushi, Tetsuo Takehara, Tomohide Tatsumi, Takuya Miyagi, Takahiro Suzulu, Tatsuya Kanto, Norio Hay ashi, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

8 # 383 COMPREHENSIVE HCV GENOME-WIDE ANALYSIS OF CD4+ AND CD8+ T CELLS REVEALS HIERARCHY OF IMMUNODOMINANCE Susan Smyk-Pearson, Ian Tester, Anna W Sasaki, Hugo R Rosen, Portland VA Medical Center, Portland, OR

8 #384 CHRONIC HEPATITIC C VIRUS INFECTION AND INSULIN RESISTANCE: HOW DO THEY INTERACT, AND WHAT IS THE EFFECT ON HEPATIC FIBROSIS? Jason M Hui, Archana Sud, Geoffrey C Farrell, Priyanka Bandara, James G Kench, Storr Liver Unit, Westmead Hospital, Westmead, NSW, Australia; Geoffrey W McCaughan, AW Marrow Gastroenterology and Liver Centre, Camperdown NSW, Australia; Jacob George, Storr Liver Unit, Westmead Hospital, Westmead, NSW, Australia

8 #385 PHARMACODYNAMICS AND PHARMACOKINETICS OF

ALFALB IN HUMAN IMMUNODEFICIENCY VIRUS

Preeti Golia, Weill Medical College of Cornell University, New York, NY; Kimberly Powers, Los Alamos National Laboratory, Los Alamos, NM; Gary Dorante, Susanna Cunningham-Rundles, Weill Medical College of Cornell University, New York, NY; Ruy Ribeiro, Los Alanios National Laboratory, Los Alamos, NM; Mohammed T Shata, New York Blood Center, New York, NY; Alan S Perelson, Los Alamos National Laboratory, Los Alamos, NM; Andrew H Talal, Weill Medical College of Cornell University New York, NY

HEPATITIS C VIRUS (HCV) AND PEGYLATED INTERFERON-

(HIV)/HCV CO-INFECTED PATIENTS

Y8A POSTER SESSIONS HEPATOLOGY, October 2003

8 $386 HIGHLY ACTIVE ANTIRETROVIRAL THERAPY IS ASSOCIATED WITH HEPATITIS C QUASISPECIES VARIABILITY IN PATIENTS WITH HEPATITIS C AND HIV COINFECTION Margaret C Shuhart, Daniel G Sullivan, Kirubeal Bekele, Terri L Mathisen, Robert D Harrington, Scott S Emerson, Mari M Kitahata, David R Gretch, University of Washington, Seattle, WA

8 $387 GENE EXPRESSION ARRAY, PHENOTYPIC, AND FUNCTIONAL ASSESSMENT OF HUMAN DENDRITIC CELLS

Anne M Wertheimer, Rachel Leistikow, Hugo R Rosen, Oregon Health and Science University, Portland, OR

ENGULFING HCV-INFECTED APOPTOTIC CELLS

8 $388 RACE, INSULIN RESISTANCE, VISCERAL ADIPOSITY AND HEPATIC STEATOSIS IN GENOTYPE 1 PATIENTS WITH CHRONIC HEPATITIS C Hari S Conjeevaram, University of Michigan, Ann Arbor, MI; David E Kleiner, National Institutes of Health, Bethesda, MD; Nezam Afdhal, Beth Israel Deaconess Medical Center, Boston, MA; Robert S Brown, New York-Presbyterian Medical Center, New York, NY; Michael W Fried, University of North Carolina at Chapel Hill, Chapel Hill, NC; Charles D Howell, University of Maryland, Baltimore, MD; Lennox J Jeffers, University of Miami, Miami, FL; Nora Terrault, University of California San Francisco, San Francisco, CA; Thelma E Wiley, University of Illinois, Chicago, IL; Chris Cherry, Steve Belle, University of Pittsburgh, Pittsburgh, PA; Jay H Hoofnagle, National Institutes of Health, Bethesda, MD

8 # 389

PLASMACYTOID DENDRITIC CELLS AND IMPAIRED THl POLARIZATION BY MYELOID DENDRITIC CELLS IN PATIENTS WITH CHRONIC HEPATITIS C Hidehiro Murakaini, Sk Md Fazle Akbar, Hidetaka Matsui, Norio Horiike, Morikazu Onji, Elume University School of Medicine, Ehime, Japan

LACK OF INTERFERON-ALPHA PRODUCTION BY

8 $390 STEATOSIS AND HEPATITIS C IN A NATIVE AMERICAN POPULATION Steve Livingston, Alaska Native Tribal Health Consortium, Anchorage, AK; Heike Deubner, University of Washington, Seattle, WA; Brian McMahon, Alaska Native Tribal Health Consortium; Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Dana Bruden, Thomas Hennessy, Arctic investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Dan Sullivan, David Gretch, University of Washington School of Medicine, Seattle, WA; Chriss Homan, Josephine Simonetti, Henry Cagle, James Williams, Alaska Native Tribal Health Consortium, Anchorage, AK

8 #391 HCV CORE PROTEIN DIRECTLY MODULATES HEPATIC FATTY ACID METABOLISM THROUGH ENHANCING CARNITINE PALMITOYL TRANSFERASE 1A ACTIVITY TO CAUSE STEATOSIS: RELATION TO COMPENSATORY OVEREXPRESSION OF RESCUE MOLECULES, NUCLEAR RECEPTOR PPARA AND ABC TRANSPORTER MDR3 Atsushi Yamaguchi, Susumu Tazuma, Tomoji Nishioka, Hideyuki Hyogo, Kazuhiko Tsuboi, Minoru Sakomoto, Keishi Kanno, Yoshihiro Numata, Toshiya Kobuke, Daisuke Komichi, Michihiro Nonaka, Yosltaka Nabeshima, Mami Watanabe, Keiko Iwamoto, Motoki Inoue, Waka Oishi, Kazuaki Chayama, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan

8 #392 TWO NOVEL CONSERVED MOTIFS IN THE HEPATITIS C VIRUS NS3 PROTEIN CRITICAL FOR HELICASE ACTION David N Frick, Angela M I Lam, David Keeney, New York Medical College, Valhalla, NY

8 #393 EFFECTS OF HIV TAT ON HEPATITIS C VIRUS REPLICATION Sarah Nangle, Ramesh Prahbu, Srikanta Dash, Robert F Garry, Tulane University Health Sciences Center, New Orleans, LA

# 394 INTERFERON ALPHA INDUCED INTRACELLULAR SIGNALING THROUGH THE JAK-STAT PATHWAY IS INHIBITED IN PATIENTS WITH CHRONIC HEPATITIS C Francois H T Duong, Markus H Heim, University Hospital Basel, Basel, Switzerland

# 395 INTRAHEPATIC CD8+ T CELL FAILURE: T CELL DYSFUNCTION AND VIRAL ESCAPE DURING CHRONIC HCV INFECTION Hans-Christian Spangenberg, Nadine Kersting, University of Freiburg, Freiburg, Germany; Sergei Viazow, Michael Roggendorf, University of Essen, Essen, Germany; Fritz von Weizsacker, Hubert E Blum, Robert Thimme, University of Freiburg, Freiburg, Germany

# 396 EVIDENCE THAT INSULIN RESISTANCE IS NOT THE CONSEQUENCE BUT THE CAUSE OF STEATOSIS AND FIBROSIS PROGRESSION IN PATIENTS WITH CHRONIC HEPATITIS C Lawrence D Serfaty Sr, Laetitia Fartoux, Jerome Guechot, Armelle Poujol-Robert, Raoul Poupon, AP-HP, HBpital Saint- Antoine, Paris, France

# 397 PERINATAL TRANSMISSION OF HCV FROM HCV/HIV COINFECTED MOTHERS TO INFANTS: LIKELY ROLE OF EXTRAHEPATIC REPLICATION AND DELAYED/ABSENT SEROCONVERSION IN CHILDREN Jorge Rakela, Marek Radkowski, Tomasz Laskus, Jeffrey Willunson, Debra Adair, Mayo Clinic, Scottsdale, AZ; Marek Nowicki, Andrea Kovacs, University of Southern California, Los Angeles, CA

# 398 CELLULAR PROLIFERATION AND TRANSCRIPTIONAL CHANGES INDUCED BY EXPRESSION OF HEPATITIS C VIRUS CORE PROTEIN IMPLICATION FOR HEPATIC ONCOGENESIS Shigenobu Kawai, Takayoshi Fukutomi, Jack Wands, Ji Su Li, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

8 Denote5 A ASLD Presidential Poster of Distmction


# 399 HCV INHIBITION OF HIV-INDUCED APOPTOSIS Karen V Kibler, Marek Radkowski, Debra Adair, Juan I Arenas, Jeffrey Wilkinson, Jorge Rakela, Tomasz Laskus, Mayo Clinic Scottsdale, Scottsdale, AZ

#400 LONGITUDINAL FULL GENOME SEQUENCING TO ASSESS THE EXTENT OF CD8+ CTL ESCAPE IN HCV Joerg Timm, Georg M Lauer, Massachusetts General Hospital, Charlestown, MA; Lia L Lewis-Ximenez, Instituto Oswaldo Cruz, Rio de Janeiro, Brazil; Kei Ouchi, Arthur Y Kim, Bruce D Walker, Todd M Allen, Massachusetts General Hospital, Charlestown, MA

# 401

ELEMENT IN THE POLYMERASE GENE: A NEW FEATURE OF THE HCV GENOME WITH IMPLICATIONS FOR DRUG DEVELOPMENT Andrea D Branch, Mount Sinai School of Medicine, New York, NY; Shihyun You, The Rockefeller University, New York, NY; Decherd D Stump, Mount Sinai School of Medicine, New York, NY; Charles Rice, The Rockefeller University, New York, NY

#402 CLINICAL AND DEMOGRAPHIC FEATURES OF HEPATITIS

NORMAL, PERSISTANTLY ELEVATED OR FLUXUATING ALANINE TRANSAMINASE LEVELS Michael Bruce, Dana Bruden, Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Brian McMahon, Alaska Native Tribal Health Consortium; Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Carol Christensen, Chriss Homan, Alaska Native Tribal Health Consortium, Anchorage, AK, Dan Sullivan, University of Washington School of Medicine, Seattle, WA; Heike Dubner, University of Washing- ton, Seattle, WA; Thomas Hennessy, Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; James Williams, Alaska Native Tribal Health Consortium, Anchorage, A K David Gretch, University of Washington School of Medicine, Seattle, WA

HEPATITIS C VIRUS HAS A CIS-ACTING REPLICATION

C-INFECTED ALASKA NATIVES WITH PERSISTENTLY

# 403

HCV INFECTION Georg M Lauer, Massachusetts General Hospital, Charlestown, MA; Michaela Lucas, Oxford University, Oxford, UK; Kei Ouchi, Arthur Y Kim, Cheryl L Day, Deborah R Casson, Massachusetts General Hospital, Charlestown, MA; Isabelle Sheridan, Bernadette Lavender, Oxford University, Oxford, UK; Rajesh T Gandhi, Massachusetts General Hospital, Charlestown, MA; Markus Reiser, Ruhr-Universitaet Bochum, Bochum, Germany; Raymond T Chung, Massachusetts General Hospital, Boston, MA; Bruce D Walker, Massachusetts General Hospital, Charles- town, MA; Paul Klenerman, Oxford University, Oxford, UK

T-CELL RESPONSES DURING EARLY THERAPY FOR

# 404 THE HEPATIC TRANSCRIPTOME IN HEPATITIS C VIRUS (HCV) ASSOCIATED CIRRHOSIS WITH HEPATOCELLULAR CANCER (HCC): IS THERE A PREMALIGNANT PROFILE? Xiao X Huang, Mark D Gorrell, Rohan B H Williams, Devanshi Seth, AW Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital and University of Sydney, Sydney NSW, Australia; Nicholas A Shackel, Medical Center, Duke University, Durham, NC; Geofhey W McCaughan, AW Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital and University of Sydney, Sydney NSW, Australia

P 405 POLYCHROMATIC FLOW CYTOMETRIC AND FUNCTIONAL ANALYSIS OF INTRAHEPATIC LYMPHOCYTES IN CHRONIC HCV INFECTION Jinhui Wang, Ramsey Cheung, Ernst Hansch, Harry B Greenberg, Xiao-Song He, Stanford University, Palo Alto, CA

# 406 CHARACTERIZATION OF THE FUNCTIONAL DOMAIN IN HEPATITIS C VIRUS NS2 PROTEIN THAT MEDIATE REPRESSION OF CELLULAR AND VIRAL GENE TRANSCRIPTIONAL ACTIVITY Annette von dem Bussche, Jack Wands, Ji Su Li, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

# 407

INFECTION Annwyne Houldsworth, Magdalena Metzner, Peninsula Medical School, Plymouth, U K Siegbert Rossol, Riisselsheim Hospital, Russelsheim, Germany; Ed Kaminski, Derriford Hospital, Plymouth, UK; Andy G Demaine, Matthew E Cramp, Peninsula Medical School, Plymouth, UK

IL-12 GENE POLYMORPHISM AND OUTCOME OF HCV

# 408 HEPATITIS C VIRUS CORE PROTEIN INHIBITS

INDUCING OXIDATIVE STRESS Yuh-ichi Hara, Keisuke Hino, Michiari Okuda, Takakazu Furutani, Akira Kitase, Y u h h Yamaguchi, Yamaguchi University, Ube-Yamaguchi, Japan; Kui Li, University of Texas, Galveston, TX; Michael Beard, University of Adelaide, Adelaide, Australia; Steven A Weinman, Stanley M Lemon, University of Texas, Galveston, TX; Kiwamu Okita, Yamaguchi University, Ube- Yamaguchi, Japan

DEOXYCHOLIC ACID-INDUCED APOPTOSIS IN SPITE OF

# 409

AND SPONTANEOUS CLEARANCE OF HEPATITIS C VIRUS INFECTION David E Kaplan, Kazushi Sugimoto, Fusao Ikeda, Jason Stadanlick, Kirti Shetty, K Rajender Reddy, Barbara Rensman, Mary Valiga, Kyong-Mi Chang, University of Pennsylvania, Philadelphia, PA

DIFFERENTIAL MECHANISM OF INTERFERON-INDUCED

f i 410 GENE EXPRESSION PROFILING OF LIVER FIBROSIS IN PATIENTS WITH HEPATITIS C VIRUS CHRONIC INFECTION

Tarik Asselah, Federation d’H6pato-Gastroenterologie et INSERM U481, HBpital Beaujon, Clichy, France; Ivan Bieche, Ingrid Laurendeau, Laboratoire de Genetique Moleculaire, EA 3618, Faculte de Pharmacie, Paris, France; Claude Degott, Service d’ Anatomie Pathologique, HBpital Beaujon, Clichy, France; Doininique Vidaud, Laboratoire de Genetique Moleculaire, EA 3618, Faculte de Pharmacie, et Service de Biochimie, HBpital Beaujon, Clichy, France; Franqoise Degos, Patrick Marcellin, Federation dHepato-Gastroenterologie et INSERM U481, HBpital Beaujon, Clichy, France; Michel Vidaud, Laboratoire de Genetique Moleculaire, EA 3618, Facult6 de Pharmacie, et Service de Biochimie, HBpital Beaujon, Clichy, France

USING A LARGE SCALE REAL-TIME RT-PCR APPROACH

# 411 ACUTE HEPATITIS C INFECTION FOLLOWING PATELLAR TENDON TRANSPLANTATION: IMMUNOLOGIC CORRELATES OF RECOVERY Ian A Tester, Susan Smyk-Pearson, Susan Dean, Hugo R Rosen, Portland VA Medical Center, Portland, OR

90A POSTER SESSIONS HEPATOLCIGY, October 2003

,X 412 HCV AND ALCOHOL INDUCED CYTOTOXICITY INVOLVES SYNERGISTIC REACTIVE OXYGEN SPECIES PRODUCTION AND MITOCHONDRIAL DEPORLARIZATION Kazuhiro Otani, Masaaki Korenaga, Steven A Weinman, University of Texas Medical Branch, Galveston, TX

# 419 HEPATITIS C VIRUS GENOTYPE 3, BUT NOT GENOTYPE 1, IS CYTOPATHIC, STEATOGENIC Christophe Hezode, Franqoise Roudot-Thoraval, Elie-Serge Zafrani, Daniel Dhumeaux, Jean-Michel Pawlotsky, HBpital Henri Mondor, Creteil, France

# 413

RESPONSES ASSOCIATED WITH DIFFERENT OUTCOMES OF HCV INFECTION Monica Malpeli, Amalia Penna, Massimo Pilli, Alessandro Zerbini, Simona Cerioni, Albertina Cavalli, Alessandra Orlandini, Azienda Ospedaliera di Parma, Parma, Italy; Agostino Cividini, IRCCS Policlinico San Matteo, Pavia, Italy; Marco Massari, Azienda Ospedaliera di Reggio Emilia, Reggio Emilia, Italy; Carlo Ferrari, Gabriele Missale, Azienda Ospedaliera di Parma, Parma, Italy

# 414 DIFFERENTIAL DISPLAY AND MICROARRAY ANALYSIS OF GENE EXPRESSION IN CENTRAL NERVOUS SYSTEM IN HEPATITIS C INFECTED PATIENTS Debra M Adair, Marek Radkowski, Jeffrey Wilkinson, Mayo Clinic Scottsdale, Scottsdale, AZ; Marek Nowicki, USC, Los Angeles, CA; Jorge Rakela, Tomasz Laskus, Mayo Clinic Scottsdale, Scottsdale, AZ

# 415

IN A CELL-BASED HCV REPLICATION MODEL USING REPLICATION DEFECTIVE ADENOVIRAL VECTORS OR STABLE CELL LINES EXPRESSING T7 POLYMERASE Yoichi Hiasa, Jason Blackard, Yoshitaka Kamegaya, Massachusetts General Hospital, Boston, MA; Norio Horiike, Morikazu Onji, Ehime University School of Medicine, Ehime, Japan; Emmett V Schmidt, Raymond T Chung, Massachusetts General Hospital, Boston, MA

FUNCTIONAL FEATURES OF HCV-SPECIFIC CD8 MEDIATED

SUSTAINED, INTERFERON-SENSITIVE HCV REPLICATION

~

# 420 STEATOSIS, OXIDATIVE STRESS AND FIBROSIS IN CHRONIC HEPATITIS C Laetitia Fartoux, Lawrence D Serfaty Sr, Guillaume Lefevre, AP-HP, HBpital Saint-Antoine, Paris, France; Marc Conti, AP-HP, HBpital Bicetre, Paris, France; Armelle Poujol-Robert, Jacqueline Capeau, Raoul Poupon, AP-HP, HBpital Saint- Antoine, Paris, France

# 421 NEGATIVE REGULATION OF INTRACELLULAR HEPATITIS C VIRUS REPLICATION BY INTERFERON REGULATORY

Tsuyoshi Yamashiro, Tokyo Medical and Dental University, Tokyo, Japan; Masayuki Kurosaki, Musashio Red Cross Hospital, Tokyo, Japan; Naoya Sakamoto, Nobuyuki Enomoto, Nobuhiko Kanazawa, Yoko Tanabe, Shinya Maekawa, Mina Nakagawa, Cheng-Hsin Chen, Mamoru Watanabe, Tokyo Medical and Dental University, Tokyo, Japan

FACTOR-3

Liver Transplantation

2 #422

SLA ANTIBODIES IN DE NOVO AUTOIMMUNE HEPATITIS AFTER LIVER TRANSPLANTATION Nedim Hadzic, Yun Ma, Ramesh Srinivasan, Paul Cheeseman, Giorgina Mieli-Vergani, Diego Vergani, Institute of Liver Studies, King’s College Hospital, London, UK

POSSIBLE PREDICTIVE AND DIAGNOSTIC ROLE OF ANTI-

rt 416

EXPRESSION ASSOCIATES WITH ADVANCED LIVER DISEASE IN CHRONIC HEPATITIS C: EVIDENCE FOR A

Oscar NLuiez, Hospital Universitario Gregorio Maration, Madrid, Spain; Amalia Femandez-Martinez, Universidad Complutense, Madrid, Spain; Pedro L Majano, Arantxa Apolinario, Hospital Universitario Santa Cristina, Madrid, Spain; Lisardo Bosca, Univer- sidad Complutense, Madrid, Spain; Gerard0 Clemente, Hospital Universitario Gregorio Maraion, Madrid, Spain; Paloma Martin- Sam, Universidad Complutense, Madrid, Spain; Carmelo Garcia- Monzon, Hospital Universitario Santa Cristina, Madrid, Spain

#417 CD4+CD25+ T REGULATORY LYMPHOCYTES MASK VIRUS SPECIFIC TH1 RESPONSES IN CHRONIC HEPATITIS C VIRUS INFECTION Simon M Rushbrook, Esther Unitt, Cambridge University, Cambridge, UK; Shilpa Chokshi, Nikolai Naoumov, University College London, London, UK; Graeme J M Alexander, Cambridge University, Cambridge, UK

3‘418

PLASMACYTOID DENDRITIC CELLS IN ACUTE VIRAL HEPATITIS B AND C Axel Ulsenheimer, Institute of Immunology, Munich, Germany; Norbert H Gruener, Maria-Christina Jung, Tilman J Gerlach, Reinhart Zachoval, Klinikum Groghadern, Munich, Germany; Winnfried Schraut, Institute of Immunology, Munich, Germany; Albrecht C Schirren, Gerd R Pape, Helmut M Diepolder, Klinikum GroGhadern, Munich, Germany

INCREASED INTRAHEPATIC CYCLOOXYGENASE-2

VIRUS-INDUCED GENE UPREGULATION

REDUCED INTERFERON-ALPHA PRODUCTION BY

8#423 LIVER TRANSPLANTATION FOR OBESITY RELATED CRYPTOGENIC CIRRHOSIS. HOW DOES WEIGHT AFFECT

Masaru Tsuchiya, Sammy Saab, Douglas G Farmer, Bob Saggi, Sherlin A Gordon, Garrett M Hisatake, John F Lenz, Mark R Ghobrial, Hassan Yersis, Ronald W Busuttil, David Geffen School of Medicine at UCLA, Los Angeles, CA

8 #424 IMPACT OF LIVER TRANSPLANTATION ON SURVIVAL IN PUGH B ALCOHOLIC CIRRHOTIC PATIENTS: A MULTICENTER RANDOMIZED TRIAL Jean-Philippe Miguet, Claire Vanlemmens, Unit of Liver Transplantation, Besanqon, France; C Milan, Centre d’Epidemiologie de Population EPI 106, Dijon, France; Michel Messner, HBpital Pontchaillou, Rennes, France; Anne Minello, Le Bocage, Dijon, France; Christophe Duvoux, Henri Mondor, Creteil, France; Vincent Di Martino, GH Piti&Salp@triPre, Paris, France; J-M Perarnau, Bon Secours, Metz, France; Marie A Piquet, CHU, Caen, France; Georges-Philippe Pageaux, Saint- Eloi, Montpellier, France; %bastien Dharancy, Claude Huriez, Lille, France; Christine Sylvain, Jean Bernard, Poitiers, France; Sophie Hillaire, Beaujon Hospital, Clichy, France; Gerard Thieffin, Robert Debre, Reims, France; Jean-Pierre Vinel, Purpan, Toulouse, France; Patrick Hillon, Le Bocage, Dijon, France; Estelle Naudet-Collin, Georges Mantion, Solange Bresson-Hadni, Unit of Liver Transplantation, Besanqon, France

POST-OPERATIVE SURVIVAL?

8 Denote5 AASLD Presidential Poster of Distinct~on


8 #425 A COMPARISON OF IMMUNOSUPPRESSIVE REGIMENS IN LIVER TRANSPLANTATION: PRIMARY SIROLIMUS VS. COMBINATION CALCINEURIN INHBITORS- SIROLIMUS VS. PRIMARY CALCINEURIN INHIBITORS Hassan Zaghla, Robert R Selby, Jeffrey A Kahn, Emily Ramicone, John A Donovan, Nicholas Jabbour, Yuri Genyk, Rodrigo Mateo, Singh Gagandeep, Linda S Sher, Linda Chan, Tse-Ling Fong, University of Southern California, Los Angeles, CA

8 # 426 CLINICAL INVESTIGATION OF USING MOLECULAR ADSORBENT RECIRCULAING SYSTEM(MARS) IN PERIOPERATIVE PERIOD WITH LIVER TRANSPLANTATION Qi-Fa Ye, Jin-Zhong Yuan, Yin-Zi Ming, Kun Wu, Sai-Hong Zhu, Bo Shao, Zu-Fa Huang, Xiangya Transplantation Medical Academy, Central South University, Changsha, China; Min-Min Wang, Therapeutic Blood Purification Research Center, University of Rostock, Shanghai, China

8 #427 IMPACT OF THE MELD SCORE ON RESOURCE UTILIZATION FOLLOWING LIVER TRANSPLANTATION Kirti Shetty, Seema Sonnad, Kim M Olthoff, Abraham Shaked, Rajender K Reddy, University of Pennsylvania, Philadelphia, PA

PRESERVATION OF CANALS OF HERING MITIGATES BILE DUCT LOSS IN LIVER GRAFT REJECTION Marius C van den Heuvel, Koert P de Jong, Marcel Boot, Maarten J H Slooff, Sibrand Poppema, Annette S H Gouw, University Hospital Groningen, Groningen, Netherlands

Bff429 HCV ETIOLOGY OF LIVER DISEASE IS STRONGLY ASSOCIATED WITH EARLY ACUTE REJECTION FOLLOWING LIVER TRANSPLANTATION Ryan A McTaggart, Alan Bostrom, Andrew J Vardanian, Norah A Terrault, Sandy Feng, University of California San Francisco, San Francisco, CA

8 #430 RESULTS OF LIVER TRANSPLANTATION FOR HEPATOCELLULAR CANCER (HCC) UNDER THE MELDlPELD SYSTEM FOR LIVER ALLOCATION Richard B Freeman Jr, Abigail Mithoefer, Michael Angelis, Jeffery Cooper, Tufts-New England Medical Center, Boston, MA; AM Harper, Erick Edwards, United Network for Organ Sharing, Richmond, VA; Russell Wiesner, Mayo Clinic, Rochester, MN

#431 RECIPIENT SELECTION CRITERIA FOR THE IMPLANTATION OF MARGINAL LIVER GRAFTS Charles J Imber, Mesut Atli, Koray Tekin, John A C Buckels, Simon R Bramhall, David Mayer, Paul McMaster, Darius F Mirza, Queen Elizabeth Hospital, Birmingham, UK

#432

PRESENTING CELLS MAY EXPLAIN REJECTION AND GRAFT

FORMATION WITH THYMOGLOBULIN IN PEDIATRIC LIVER TRANSPLANTATION Rakesh Sindhi, Amy Magill, Adrianna Zeevi, University of Pittsburgh, Pittsburgh, PA

# 433 LIVER TRANSPLANTATION FOR HEPATOCELLULAR CARCINOMA BEFORE AND AFTER THE MELD SYSTEM FOR ORGAN ALLOCATION: A PROSPECTIVE ANALYSIS USING AN INTENTION TO TREAT PRINCIPLE Francis Y Yao, Nathan M Bass, Nancy L Ascher, John P Roberts, University of California San Francisco, San Francisco, CA

T-CELL ANERGY AND RELATIVE SPARING OF ANTIGEN-

ADAPTATION BY REGULATORY-SUPPRESSOR CELL

# 434 EARLY STEROID WITHDRAWL AFTER LIVER TRANSPLANTATION : A PLACEBO CONTROLLED STUDY Georges P Pageaux Sr, Olivier Boillot, Yvon Calmus, Christian Ducerf, Claire Vanlemmens, Karim Boudjema, Didier Samuel, CHU Saint Eloi, Montpellier, France

# 435 DOES THE MODEL FOR END-STAGE LIVER DISEASE (MELD) PREDICT POST LIVER TRANSPLANT GRAFT SURVIVAL? Russell H Wiesner, Mayo Clinic, Rochester, MN; Erick Edwards, UNOS, Richmond, VA; Richard Freeman, New England Medical Center, Boston, MA; Ann Harper, UNOS, Richmond, VA

# 436

HEPATITIS IN PEDIATRIC LIVER TRANSPLANT RECIPIENTS Shikha S Sundaram, Brian Stahulak, Joan M Lokar, Peter F Whitington, Estella M Alonso, Northwestern University, Chicago, IL

LONG TERM FOLLOW-UP OF DE-NOVO AUTOIMMUNE

# 437 ABSENCE OF REJECTION AFTER HUMAN LIVER ORTHOTOPIC LIVER TRANSPLANTATION (OLT) IS ASSOCIATED WITH LEUKOCYTE APOPTOSIS, INCREASED LYMPHOCYTE ACTIVATION AND HIGHER DONOR CELL CHIMERISM Andrew Clouston, Daina M Vanags, Wenyi Gu, Elizabeth E Powell, Julie R Jonsson, University of Queensland, Brisbane, Australia

# 438 LIVER TRANSPLANTATION UNDER A TOLEROGENIC REGIMEN OF PRECONDITIONING WITH ALEMTUZUMAB

Bijan Eghtesad, Amadeo Marcos, Bridget Flynn, Paulo Fontes, Thomas Cacciarelli, Wallis Marsh, Michael DeVera, Obaid Shakil, Noriko Murase, Anthony Demetris, John Fung, Thomas E Starzl, University of Pittsburgh, Pittsburgh, PA

AND POST-TRANSPLANT TACROLIMUS

# 439 LIVER TRANSPLANTATION FOR SARCOIDOSIS Evan J Lipson, Kevin M Korenblat, Sander Florman, Mount Sinai Medical Center, New York, NY; Leona Kim Schluger, Westchester Medical Center, Valhalla, NY

# 440

TRANSPLANTATION James D Eason, Ari J Cohen, Satheesh Nair, George Loss, Ochsner Clinic Foundation, New Orleans, LA

EARLY SIROLIMUS CONVERSION IN STEROID-FREE LIVER

# 441

ULTRASTRUCTURAL CHANGES IN THE LIVER ALLOGRAFT Adeyemi A Lawal, Sandy Florman, Isabel Fiel, Ronald Gordon, Myron Schwartz, Charles Miller, Thomas D Schiano, The Mount Sinai Medical Center, New York, NY

# 442 MELD: IMPACT OF HEPATOCELLULAR CARCINOMA ON THE ADULT LIVER TRANSPLANT WAITING LIST Kenneth Washburn, K V Speeg, Juan Guerrero, Russell Havranek, Robert Esterl, Greg Abrahamian, Francisco Cigarroa, Glenn Halff, University of Texas HSC, San Antonio, TX

PRIMARY NON-FUNCTION IS ASSOCIATED WITH

#443 WEIGHT GAIN AND OBESITY AFTER LIVER TRANSPLANTATION James Neuberger, James A Richards, Bridget K Gunson, Jill Johnson, Queen Elizabeth Hospital, Birmingham, UK

Y2A POSTER SESSIONS HEPATOLOGY, October 2003

,t 444 COMPARISON OF SERUM CA 19-9, CEA AND AFP LEVELS IN PATIENTS WITH END STAGE LIVER DISEASE (ESLD) WITH

RETROSPECTIVE STUDY Chhaya Hasyagar, Savant Mehta, UMass Memorial Healthcare, Worcester, MA

OR WITHOUT ASCITES VS HEALTHY CONTROLS- A

# 451 TARGETED PROPHYLAXIS: EFFICACY IN PREVENTING INVASIVE FUNGAL INFECTION IN ORTHOTOPIC LIVER TRANSPLANTATION Rebecca L Jones, Bristol Royal Infirmary, Bristol, UK; Rhys W Vaughan, Antonia Marzec, Peter W Angus, Paul J Cow, Austin and Repatriation Medical Centre, Melbourne, Australia

# 445 SEVERE MITOCHONDRIAL TOXICITY AFTER LIVER TRANSPLANTATION IN HIV-HCV COINFECTED PATIENTS Jean-Charles Duclos-Vallee, Paul Brousse Hospital, Villejuif, France; Claude Jardel, La Pitie Salpetriere, Paris, France; Daniel Vittecoq, Elina Teicher, Bruno Roche, Cyrille Feray, Michelle Gigou, Philippe lchai, Faouzi Saliba, Ren6 Adam, Daniel Azoulay, Catherine Guettier, Denis Castaing, Henri Bismuth, Didier Samuel, Paul Brousse Hospital, Villejuif, France; Anne Lombes, INSERM UR 582, Paris, France

# 452 PREDICTIVE FACTORS FOR THE ABSENCE OF CELLULAR REJECTION AFTER LIVER TRANSPLANTATION IN A PROTOCOL BIOPSY POPULATION Laura Cecilioni, Rosa Stigliano, Royal Free and University College Medical School, London, UK; Gioacchino Leandro, IRCCS, Bari, Italy; Albert0 Quaglia, Amar Paul Dhillon, Keith Rolles, Brian Davidson, Nancy Rolando, David Patch, Andrew Burroughs, Andrew Burroughs, Royal Free and University College Medical School, London, UK

# 446 BENEFICIAL EFFECTS OF TOPICAL TESTOSTERONE REPLACEMENT IN PATIENTS WITH END STAGE LIVER DISEASE Guy W Neff, Kamran Safdar, Michael Karl, Christopher OBrien, Antonette Demanno, Stephanie Kahn, Jose Nery, Doug Meyer, Teresa Bueno, Halim Mush, Seigo Nishida, Eugene R Schiff, Andreas G Tzakis, University of Miami, Miami, FL

# 447 EVALUATION OF PERCUTANEOUS ABLATION TREATMENTS OF HEPATOCELLULAR CARCINOMA (HCC) AS A RISK FACTOR FOR NEOPLASTIC RECURRENCE IN PATIENTS WHO UNDERWENT LIVER TRANSPLANT (LT) V G Mirante, M Pompili, Catholic University of Sacred Heart, Rome, Italy; G Rondinara, D Forti, Niguarda Hospital, Milan, Italy; G Rossi, L R Fassati, Maggiore Hospital, Milan, Italy; S Agnes, M Castagneto, G Pelecca, G Casbarrini, G L Rapaccini, Catholic University of Sacred Heart, Rome, Italy

# 448 FAVORABLE OUTCOMES AFTER SELECTIVE USE OF TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNTS FOLLOWING LIVER TRANSPLANTATION Marwan S Abouljoud, Atsushi Yoshida, Dilip Moonka, Daniel Croteau, David McVinnie, Rajinder Sharma, Kimberly Brown, Henry Ford Hospital, Detroit, MI

# 449 MICROBIOLOGY OF BILE IN PATIENT IN THE LONG-TERM COURSE AFTER LIVER TRANSPLANTATION Thomas Buratti, Gunda Millonig, Ivo W Graziadei, Hubert Schwaighofer, Alfred Koenigsrainer, Raimund Margreiter, Dorothea Orth, Wolfgang Vogel, University of Innsbruck, Innsbruck, Austria

# 450 VALIDATION AND USE OF A NEW MODEL T O MAXIMISE THE UTILITY OF LIVER ALLOGRAFTS Geoffrey H Haydon, The Queen Elizabeth Hospital, Birmingham, UK; Yrjo Hiltunen, Raahe Institute of Computer Engineering and Buisiness, Raahe, Finland; Michael R Lucey, Vanessa Rein, Thomas Chin, University of Wisconsin-Madison, Madison, WI; Peter G Nightingale, Bridget Gunson, Nick Murphy James Neuberger, The Queen Elizabeth Hospital, Birmingham, UK

# 453 EVALUATION OF CYCLOSPORINE PEAK LEVEL C2) TARGET RANGE IN STABLE PAEDIATRIC LIVER TRANSPLANT RECIPIENTS Subramanian B K Mahedevan, Indra D M van Mourik, Patrick J McKiernan, Susan V Beath, Deirdre A Kelly, Birmingham Children’s Hospital, Birmingham, UK

# 454 ADOLESCENT HEALTH RELATED QUALITY OF LIFE AFTER LIVER TRANSPLANTATION Shikha S Sundaram, Katie Neighbors, Lisa Amaruso, James Sinacore, Estella M Alonso, Northwestern University, Chicago, IL

Organic Anion and Bile Acid Transport: Lipid Metabolism

# 455 Withdrawn

#456 FARNESOID X RECEPTOR (FXR) TRANSACTIVATES MOUSE ORGANIC ANION TRANSPORTING POLYPEPTIDE 4 ( OATP4,

EVIDENCE Natarajan Balasubramaniyan, Muhammad F Mirza, The Mount Sinai Medical Center, New York, NY; Christopher J Sinal, Frank J Gonzalez, NCI, NIH, Bethesda, MD; Frederick J Suchy, Meenakshisundaram Ananthanarayanan, The Mount Sinai Medical Center, New York, NY

SLCZlA10, LST-I) PROMOTER : IN VITRO AND IN VIVO

it 457 IDENTIFICATION OF SODIUM/PHOSPHATE COTRA- NSPORTER TYPE IIB (NAPI-IIB) IN THE CANALICULAR PLASMA MEMBRANE OF RAT HEPATOCYTES Pascal Frei, Bruno Stieger, Bruno Hagenbucli, Peter J Meier, University Hospital Zurich, Zurich, Switzerland; Jiirg Biber, Heini Murer, Institute of Physiology, University of Ziirich, Zurich, Switzerland

# 458 THE HUMAN ORGANIC ANION TRANSPORTING POLYPEPTIDE 8 GENE (OATP8) IS TRANSACTIVATED BY THE XENOBIOTICS RIFAMPICIN AND PHENOBARBITAL

Diana Jung, May-Britt Becker, Michael Fried, Peter J Meier, Gerd A Kullak-Ublick, University Hospital, Zurich, Switzerland

THROUGH AN FXR-MEDIATED MECHANISM



# 459 EFFECTS OF HUMAN MRP2 MUTATIONS ON ITS TRANSPORT AND ATPASE ACTIVITIES AND ACTIVATION BY URSODIOL Phillip M Gerk, Yu Yang, University of Kentucky, Lexington, KY; kchard H Ho, Vanderbilt University Medical School, Nashville, TN; Wei Li, University of Kentucky, Lexington, KY; Richard B Kim, Vanderbilt University Medical School, Nashville, TN; Mary E Vore, University of Kentucky, Lexington, KY

ti460 THE BIOPHYSICAL PROPERTIES OF HEPATOCYTE PLASMA MEMBRANE DOMAINS INFLUENCE WATER TRANSPORT:

Raul A Marinelli, Instituto de Fisiologia Experimental, Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Santa Fe, Argentina; Pamela S Tietz, Ariel J Caride, Bing Q Huang, Mayo Medical School, Clinic and Foundation, Rochester, MN; Sergio A Gradilone, Instituto de Fisiologia Experimental, Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Santa Fe, Argentina; Nicholas F LaRusso, Mayo Medical School, Clinic and Foundation, Rochester, MN

THE CANALICULAR MEMBRANE IS RATE-LIMITING

# 461 TRANSCRIPTIONAL REGULATION OF THE HUMAN, MOUSE AND RAT NTCPlNTCP GENES ROLE OF LIVER ENRICHED TRANSCRIPTION FACTORS Diana Jung, Bruno Hagenbuch, Peter J Meier, Gerd A Kullak- Ublick, University Hospital, Zurich, Switzerland

#462 THE ROLE OF ELEVATED SERUM BILIRUBIN LEVELS ON CAROTID ATHEROSCLEROSIS Libor Vitek, Ladislav Novotnf, Jiri Spiicil, Martin Sperl, Roman Holaj, 1st Faculty of Medicine, Charles University, Praha 2, Czech Republic

# 463 CRITICAL ROLE OF CYSTEINE RESIDUES IN HUMAN UGTlAl IN BILIRUBIN GLUCURONIDATION Siddhartha S Ghosh, Sung W Lee, Jayanta Roy-Chowdhury, Namita Roy-Chowdhury, Albert Einstein College of Medicine, Bronx, NY

~ ~~ ~

# 464 LIVER DELIVERY OF ADEFOVIR BY HETEROLOGOUS EXPRESSION OF ORGANIC ANION TRANSPORTER OAT1 Yoshimichi Sai, Hitomi Hashitani, Kanazawa University, Kanazawa, Japan; Ikumi Tamai, Tokyo University of Science, Noda, Japan; Akira Tsuji, Kanazawa University, Kanazawa, Japan

# 465

HORMONE RECEPTORS AND CORRESPONDING HEPATIC TRANSPORTER GENES IN MICE Andreas Geier, Christoph G Dietrich, Sebastian Voigt, Frank Lammert, Siegfried Matem, Carsten Gartung, Aachen University, Aachen, Germany

CYTOKINE-DEPENDENT REGULATION OF NUCLEAR

# 466

EXPRESSION Brett R Jones, Wei Li, Jingsong Cao, Mary Vore, University of Kentucky, Lexington, KY

POST-TRANSCRIPTIONAL REGULATION OF MRP2

~~

#467 PROTEOMICS OF OATPl Yansen Xiao, Ruth H Angeletti, George A Orr, Allan W Wolkoff, Albert Einstein College of Medicine, Bronx, NY

# 468

NAL MRP2 IN RATS AND HUMANS AND INCREASES ORAL

Christoph G Dietrich, Andreas Geier, Nina Salein, Frank Lammert, Elke Roeb, Aachen University, Aachen, Germany; Ronald P J Oude Elferink, Academic Medical Center, Amsterdam, Netherlands; Siegfried Matern, Carsten Gartung, Aachen University, Aachen, Germany

CHOLESTASIS LEADS TO DOWNREGULATION OF INTESTI-

BIOAVAILABILITY OF A FOOD-DERIVED CARCINOGEN

# 469

MODULATION OF RXRa FUNCTION IS AN EARLY EVENT DURING LIVER REGENERATION Sundararajah Thevananther, Hongdan Sun, Samir S Awad, Saul J Karpen, Baylor College of Medicine, Houston, TX

# 470

MICE ELICIT PHENOTYPIC DIFFERENCES IN GALLBLADDER BILE AND GALLSTONE FORMATION Zhixin Wei, fichard M Green, Northwestern University, Chicago, IL

# 471 THE MOLECULAR MECHANISM OF BILIARY CHOLESTEROL SECRETION Astrid Kosters, Cindy Kunne, Norbert Looije, Academic Medical Center, Amsterdam, Netherlands; Folkert Kuipers, University Hospital Groningen, Groningen, Netherlands; Shailesh B Patel, Medical University of South Carolina, Charleston, SC; Ronald P J Oude Elferink, Albert K Groen, Academic Medical Center, Amsterdam, Netherlands

POST-TRANSLATIONAL MODIFICATION AND

TRANSTHYRETIN-ABCB11 (TTR-ABCBll) TRANSGENIC

# 472

HYPERSECRETION DEPENDS ON THE PRESENCE OF ABCG8 Astrid Kosters, Cindy Kunne, Norbert Looije, Academic Medical Center, Amsterdam, Netherlands; Fokert Kuipers, University Hospital Groningen, Groningen, Netherlands; Shailesh B Patel, Medical University of South Carolina, Charleston, SC; Albert K Groen, Academic Medical Center, Amsterdam, Netherlands

# 473 QUANTITATIVE TRAIT LOCUS MAPPING IN AN INTERCROSS OF PERA/EI AND DBA/2J INBRED MICE IDENTIFICATION OF NEW CHOLESTEROL GALLSTONE SUSCEPTIBILITY (LITH) LOCI AND CONFIRMATION OF LITH LOCI FROM PREVIOUS CROSSES Henning Wittenburg, University of Leipzig, Leipzig, Germany; Malcolm A Lyons, Renhua Li, Gary A Churchill, The Jackson Laboratory, Bar Harbor, ME; Joachim Mossner, University of Leipzig, Leipzig, Germany; Martin C Carey, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA; Beverly Paigen, The Jackson Laboratory, Bar Harbor, ME

# 474 RISK FACTORS FOR CHOLESTEROL GALLSTONE FORMA- TION ARE ASSOCIATED WITH COMMON POLYMORPHISMS OF ABCG5IABCG8, THE GENES ENCODING THE BILIARY

MEXICAN GALLSTONE PATIENTS Nahum Mendez-Sanchez, Medica Sur Clinic and Foundation, Mexico City, Mexico; Nadia Rahbar-Tabrizi, Aachen University (RWTH), Aachen, Germany; Ana C King-Martinez, Medica Sur Clinic and Foundation, Mexico City, Mexico; Henning Wittenburg, University of Leipzig, Leipzig, Germany; Hildegard Keppeler, Ramin Schirin-Sokhan, Alexa Werth, Hermann E Wasmuth, Aachen University (RWTH), Aachen, Germany; Misael Uribe, Medica Sur Clinic and Foundation, Mexico City, Mexico; Siegfried Matern, Frank Lammert, Aachen University (RWTH), Aachen, Germany

DIOSGENIN-INDUCED BILIARY CHOLESTEROL

CHOLESTEROL HALF-TRANSPORTERS, IN GERMAN AND

9 I A POSTER SESSIONS HEPATOLOGY, October 2003

475 BILE ACID TRANSPORT ACTIVITY AND INTRACELLULAR DISTRIBUTION OF PFICZ MUTANTS IN MDCKII CELLS COEXPRESSING NTCP AND BSEP Tatehiro Kagawa, Kaori Mochizuki, Tokai University School of Medicine, Isehara, Japan; Matthew J Harris, Tufts University School of Medicine, Boston, MA; Norhito Watanabe, Tetsuya Minc, Shohei Matsuzaki, Tokai University School of Medicine, Isehara, Japan; Irwin M Arias, NIH, Bethesda, MD

f 476 ISOLATION AND CHARACTERIZATION OF SPECIALIZED MICRODOMAINS OF HEPATOCYTE PLASMA MEMBRANES: POTENTIAL ROLE IN CANALICULAR BILE FORMATION Pamela S Tietz, Mayo Medical School, Clinic and Foundation, Rochester, MN, John R Jefferson, Luther College, Decorah, IA, Richard E Pagmo, Nicholas F LaRusso, Mayo Medical School, Clinic and Foundation, Rochester, MN

3 477 IMMUNOHISTOCHEMICALLY RECOGNISED BILE SALT EXPORT PROTEIN IS UNREMARKABLY EXPRESSED AT THE CANALICULUS IN PERSONS WITH ATP8B1 DISEASE A S Knisely King’s College Hosyi tal, London, UK; Y Meier, B Stieger, University Hospital, Zurich, Switzerland; B C Portmann, A C Rayner, S S Strautnieks, R J Thoiiipson, King’s College Hospital, London, UK; R H J Houwen, L W J Homp, University Medical Center, Utrecht, Netherlands; L N Bull, University of California San Francisco, San Francisco, CA

* 478 MECHANISM OF PXR RFGULATION OF BILE ACID METABOLISM John Chiang, Aiindam Chakrabarti, Tiangang Li, Erika Owsley, Sandra Zolla, Northrastern Ohio University’s College of Medicine, Rootstown, OH

0 479 HEPATIC STEATOSIS AND HYPERSECRETION OF BILIARY CHOLESTEROL DUE TO TRANSGENIC COMPLEMENTA- TION OF GLUT4 IN SKELETAL MUSCLE Sure5h K Yadav, X i u Quan Du, Maureen J Charron, David E Cohen, Albert Einstein College of Medicine, Bronx, NY

8 $480

CYTOPLASMIC TRANSLOCATION OF RXRa INVOLVES JNK Tracy L Zimmerman, Ronii Chose, Sundararajah Thevananther, Saul J Karpen, Baylor College of Medicine, Houston, TX

IL-I p MEDIATED MODIFICATION AND NUCLEO-

Oxidative Stress, Antioxidants

88481 HCV CORE PROTEIN INHIBITS MITOCHONDRIAL COMPLEX I FUNCTION AND SENSITIZES MITOCHONDRIA TO OXIDATIVE DAMAGE Masaaki Korenaga, Kazuhiro Otani, Steven A Weinman, Univervty of Texas Medical Branch, Galveston, TX

8 8482 PEROXYNITRITE MODULATES IN VITRO ACTIVITY OF PROTEASOME FROM LIVER AND IN CULTURED HEPATOMA CELLS Natalia A Osna, James Haorah, Todd Wyatt, Terrence M Donohue Tr, UNMC, Omaha, NE

# 483 ALTERATIONS IN HEPATIC STRUCTURE AND FUNCTION IN

Priscilla Ivester, Tracey A Young, Cynthia J Lees, Wake Forest University School of Medicine, Winston-Salem, NC; L Jackson Roberts 11, Vanderbilt University, Nashville, TN; Peter J Pierre, Kathleen A Grant, Carol C Cunningham, Wake Forest University School of Medicine, Winston-Salem, NC

MACACA FASCICULARIS SELF-ADMINISTERING ETHANOL

P 484 CHRONIC ETHANOL CONSUMPTION INCREASES THE

WITH THE MITOCHONDRIAL HYDROXY METHYL GLUTARYL COA SYNTHASE IN LIVER Vinood B Patel, Christina H Spencer, Carol C Cunningham, Wake Forest University School of Medicine, Winston-Salem, NC

CONCENTRATION OF A 4-HYDROXYNONENAL ADDUCT

# 485 RESUSCITATION OF ASPHYXIATED PIGLETS WITH 21% OXYGEN RATHER THAN 100% CAUSES LESS HEPATIC OXIDATIVE STRESS WITHOUT INCREASING HISTOLOGIC DAMAGE Jonathan Stevens, University of Alberta, Edmonton, AB, Canada; Karien Fokkelman, University of Utrecht, Utrecht, Netherlands; Henry Idiluo, Erika Haase, David Bigam, Po-Yin Cheung, University of Alberta, Edmonton, AB, Canada

~~~~ ~ ~ ~ _ _ _ _

# 486

INJURY WITH THE ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITOR CAPTOPRIL Luping Guo, Lindsay M Tucker, Gavin E Arteel, University of Louisville, Louisville, KY

# 487 GLOBAL HYPOXIA SENSITIZES LIVER TO SUBSEQUENT

Lindsay M Tucker, University of Louisville, Louisville, KY; Akira Konno, Juntendo University School of Medicine, Tokyo, Japan; Gavin E Arteel, University of Louisville, Louisville, KY

PREVENTION OF HEPATIC ISCHEMIA-REPERFUSION

LIPOPOLYSACCHARIDE: A NEW 2-HIT MODEL?

# 488 DECREASE IN HEPATIC PROTEASOME ACTIVITY IS ASSOCIATED WITH PATHOLOGICAL SEVERITY AND OXIDATIVE STRESS IN EXPERIMENTAL ALCOHOLIC LIVER DISEASE Terrence M Donohue Jr, Kusum K Kharbanda, Carol A Casey, Omaha VA Medical Center, Omaha, NE; Amin A Nanji, University of Pennsylvania School of Medicine, Philadelphia, PA

# 489 HEPATOCYTE OXIDATIVE STRESS AND LIVER FATTY ACID BINDING PROTEIN GuQi Wang, Yuewen Gong, Dongfeng Sun, Gerald Minuk, Frank J Burczynski, University of Manitoba, Winnipeg, MB, Canada

8 Ilenotei AASLD Prcsidential Poster of Distinction


Poster Session 2

Sundav. October 26 H!yies Conveiztiori Center, Exlzibif Hall C

Poster Viewing: 8:OOam - 5:OOpm


12:30 - 1:45pm 1:45 - 3:OOpm

8 Those posters identified as AASLD Presidential Poster of Distinction by a ribbon icon have received review scores that place them within the top 10% of all posters. We encourage you to make them a priority as you visit the poster session.

Cell Biology of Hepatic Blood Flow and Portal Hypertension

#490 THE ROLE OF AKT IN REGULATION OF SMOOTH MUSCLE

Songling Liu, Don C Rockey, Duke University, Durham, NC ALPHA-ACTIN PROTEIN EXPRESSION IN INJURED LIVER

#491 ESTROGEN UPREGULATES NITRIC OXIDE PRODUCTION VIA ESTROGEN RECEPTOR ALPHA OF HEPATIC SINUSOIDAL ENDOTHELIAL CELLS IN CIRRHOSIS Masaharu Sakamoto, Toru Nakamura, Takuji Torimura, Ryuichiro Sakata, Osamu Hashimoto, Takato Ueno, Michio Sata, Kurume University School of Medicine, Kurume, Japan

# 492 A FUNCTIONAL LINK BETWEEN ENDOTHELIN B RECEPTORS AND ENOS MAINTAINS TISSUE OXYGENATION IN NORMAL LIVER Markus Paxian, University of North Carolina at Charlotte, Charlotte, NC; Steve Keller, Toan T Huynh, Carolinas Medical Center, Charlotte, NC; Mark G Clemens, University of North Carolina at Charlotte, Charlotte, NC

#493 NITROTYROSINE AND NITRIC OXIDE SYNTHASE IN THE BRAIN OF RATS WITH AMMONIA-INDUCED BRAIN EDEMA Javier Vaquero, Michael E Cahill, Chuhan Chung, Andres T Blei, Lakeside VA Medical Center and Northwestern University, Chicago, IL

# 494 AUGMENTED TNFALPHA (TNF) EXPRESSION BY ACTIVATED MONOCYTES AND ALTERED T-CELL HOMEOSTASIS IN ASCITIC CIRRHOSIS: AMELIORATION WITH NORFLOXACIN Agustin Albillos, Hospital Ramon y Cajal, CIB-CSIC, Universidad Alcala, Madrid, Spain; Antonio De-la-Hera, Eduardo Reyes, Jorge Monserrat, Leticia Muiioz, Monica Nieto, CIB-CSIC, Universidad Alcala, Madrid, Spain; Luis Ruiz-del- Arbol, Hospital Ramon y Cajal, Universidad Alcala, Madrid, Spain; Eva Sam, CIB-CSIC, Universidad Alcala, Madrid, Spain; Melchor Alvarez-Mon, Hospital Principe Asturias, CIB-CSIC, Universidad Alcala, Madrid, Spain

# 495 INTRAPULMONARY VASCULAR DILATATION AND NITRIC OXIDE IN HYPOXEMIC RATS WITH CHRONIC BILE DUCT LIGATION Xue-Jun Zhang, Yasumi Katsuta, Toshio Akimoto, Masaru Ohsuga, Yoshihito Kato, Takamichi Nagato, Shuji Shimizu, Hirokazu Komeichi, Katsuaki Satomura, Takumi Aramaki, Nippon Medical School, Tokyo, Japan

# 496 ENHANCED ETB RECEPTOR MEDIATED VASODILATATION

FROM ANIMALS WITH PREHEPATIC PORTAL HYPERTENSION AND EXPERIMENTAL HPS Daisheng Song, David Ku, University of Alabama at Birmingham, Birmingham, AL; Michael B Fallon, University of Alabama at Birmingham and Birmingham VA Medical Center, Birmingham, AL

IN RESPONSE TO ET-1 IN PULMONARY ARTERY SEGMENTS

HCC and Cholangiocarcinoma: Experimental

g #497 TRANSACTIVATION-DEFICIENT ONCOGENIC DELTATAmP73 AND DN-P73 PROTEINS ARE OVEREXPRESSED IN HCCS Emanuele Palescandolo, Stefania Vossio, Antonio Costanzo, Marcella Fulco, Massimo Levrero, Fondazione Andrea Cesalpino, Rome, Italy; Clara Balsano, University of L'Aquila, L'Aquila, Italy

8 #498 ANTIDIABETIC THIAZOLIDINEDIONES INHIBIT HEPATIC TUMOR FORMATION IN HBV TRANSGENIC MOUSE MODEL Elisabetta Ceni, University of Florence, Firenze, Italy; David W Crabb, Indiana University, Indianapolis, IN; Tommaso Mello, University of Florence, Firenze, Italy; Erica Villa, Filippo Schepis, University of Modena, Modena, Italy; Marco Tarocchi, Maria R Biagini, Chiara Corrado, Alessandro Casini, Stefan0 Milani, Calogero Surrenti, Galli Andrea, University of Florence, Firenze, Italy

# 499 RHO-KINASE INHIBITOR SUPPRESSES TUMOR GROWTH AND INTRAHEPATIC METASTASES OF HEPATOCELLULAR

Feng Xue, Terumi Takahara, Kazunobu Nonome, Yutaka Yata, Eiji Shinno, Akiharu Watanabe, Toyama Medical and Pharma- ceutical University, Toyama City, Japan

# 500 THE ROLE OF THE EXTRACELLULAR MATRIX IN THE DEVELOPMENT OF COLORECTAL CANCER LIVER METASTASES John A Conti, Chris Benyon, University of Southampton, Southampton, UK; John N Primrose, University of Southampton, Southampton, UK; John P Iredale, University of Southampton, Southampton, UK

CARCINOMA-IN VITRO AND IN VIVO STUDY

0

O C l u

# 501 :; B $

CYCLOOXYGENASE-2 PROMOTES HEPATOCELLULAR CARCINOMA CELL GROWTH THROUGH AKT ACTIVATION EVIDENCE FOR AKT INHIBITION IN CELECOXIB-INDUCED APOPTOSIS Jing Leng, Chang Han, Anthony J Demetris, George K Michalopoulos, Tong Wu, University of Pittsburgh, Pittsburgh, PA

Q)

# 502

THROUGH SUPPRESSION OF APOPTOSIS Yoshi taka Kamegaya, Yoichi Hiasa, Lawrence Zukerberg, Nina Fowler, Jason Blackard, Wenyu Lin, Emmett Schmidt, Raymond T Cliung, Massachusetts General Hospital, Boston, MA fiavrl Azuard Recipie17 t

HCV CORE-El-EL ACTS AS AN HCC TUMOR ACCELERATOR

POSTER SESSIONS HEPATOLOGY, October 2003 96A

ji 503 EXPRESSION PROFILING IN MULTISTAGE HEPATOCARCINOGENESIS: IDENTIFICATION OF HSP70 AS A MOLECULAR MARKER OF EARLY HEPATOCELLULAR CARCINOMA Makoto Chuma, National Cancer Center Research Institute, Tokyo, Japan; Hokkaido University, Sapporo, Japan, ; Michiie Sakamoto, Keio University Tokyo, Japan; Shuhei Hige, Masahiro Asaka, Hokkaido University, Sapporo, Japan; Setsuo Hirohashi, National Cancer Center Research Institute, Tokyo, Japan

# 504 HEPATIC INVALIDATION OF THE TUMOR SUPPRESSOR GENE APC Sabine Colnot, Thomas Decaens, Institut Cochn, U567 INSERM, Paris, France; Michiko Niwa-Kawakita, CEPH, U431 INSERM, Paris, France; Ghislaine Hamard, Cecile Godard, Servane Le Plenier, Institut Cochin, U567 INSERM, Paris, France; Marco Giovannini, CEPH, U431 INSERM, Paris, France; Christine Perret, Institut Cochin, U567 INSERM, Paris, France

n‘ 505 ANTIANGIOGENIC PROPERTY OF PIGMENT EPITHELIUM DERIVED FACTOR IN HEPATOCELLULAR CARCINOMA Kojiro Matsumoto, Nagasaki University School of Medicine, Nagasaki, Japan

# 506

IN A HUMAN CHOLANGIOCARCINOMA CELL LINE lung-Hwan Yoon, Seoul National University College of Medicine, Seoul, South Korea; Ali E Canbay, Nathan W Werneburg, Gregory J Gores, Mayo Medical School, Clinic and Foundation, Rochester, MN

OXYSTEROL INDUCES CYCLOOXYGENASE-2 EXPRESSION

1: 507 DETECTION OF DNA COPY NUMBER ALTERATION IN HEPATOMA CELL LINES USING CDNA MICROARRAYS: THE DIRECT ROLE OF DNA COPY NUMBER IN THE TRANSCRIPTIONAL PROGRAM OF HEPATOCELLULAR CARCINOMA (HCC) Kazunori Kawaguchi, Masao Honda, Taro Yamashita, Yukihiro Shirota, Shuichi Kaneko, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan

B 508 INVOLVEMENT OF TRAILlTRAIL RECEPTOR PATHWAY IN THE ANTI-TUMOR EFFECT OF 5-FLUOROURACIL AND INTERFERON-ALPHA THERAPY FOR HEPATOCELLULAR CARCINOMA Tameyoshi Yamamoto, Hiroaki Nagano, Masato Sakon, Bazarragchaa Damdinsuren, Hideo Ota, Masato Nakamura, Hisashi Wada, Shigeru Marubashi, Atsushi Miyamoto, Koji Umeshita, Shouji Nakamori, Graduate School of Medicine, Osaka University, Osaka, Japan; Hideo Yagita, Juntendo University School of Medicine, Tokyo, Japan; Morito Monden, Graduate School of Medicine, Osaka University, Osaka, Japan

4 509

CELL ANTIGEN IN HUMAN HEPATOCELLULAR CARCINOMA David H Adams, Elizabeth Torr, Jane Steele, University of Birmingham, Birmingham, UK; Maarten van Lohuizen, The Netherlands Cancer Institute, Amsterdam, Netherlands; Gary M Reynolds, Stefan G Hubscher, University of Birmingham, Birmingham, UK; 1,awrence S Young, CRUK Institute of Cancer Studies, Birmingham, LJK

THE POLYCOMB GROUP PROTEIN BMI-1 IS A NOVEL T

# 510

GROWTH OF HUMAN HEPATOCELLULAR CARCINOMA IMPLANTS IN VIVO Michael Andre Kern, Mirja Mareike Schoneweiss, Dina Sahi, Maryam Bahlo, AnkeMaria Haugg, Hans Peter Dienes, Institute of Pathology, University of Cologne, Cologne, Germany; Herbert Kaferstein, Institute of Forensic Medicine, University of Cologne, Cologne, Germany; Kai Breuhahn, Institute of Pathology, University of Cologne, Cologne, Germany; Peter Schirmacher, Institute of Pathology and Center of Molecular hledicine (ZMMK), University of Cologne, Cologne, Germany

# 511

PROTECTS AGAINST COLON CANCER METASTASISIN A BALB/C MOUSE MODEL Carina Riediger, Dept. of Internal Medicine IV, Heidelberg, Germany; Gerhard Wingeuder, Percy Knolle, ZMBH Heidelberg, Heidelberg, Germany; Wolfgang Stremmel, Jens Encke, Dept. of Internal Medicine IV, HeidelberE, Germany

INHIBITION OF CYCLOOXYGENASE-2 SUPPRESSES THE

ADENOVIRUS-MEDIATED FLT3L-GENE THERAPY

# 512 INTERFERON ALPHA 8 AND 2 SHOW DIFFERENTIAL ACTIVATION OF APOPTOSIS PATHWAY AND GROWTH FACTOR PATHWAY IN HUMAN HEPATOMA CELL LINES Akinobu Takaki, Kazuko Koike, Hidenori Shiraha, Yoshiaki Iwasaki, Kohsaku Sakaguchi, Okayama University, Okayama, Japan; Nirou Inaba, Kiichi Kubota, Japan Genome Solutions, Inc., Hachioji City, Japan; Yasushi Shratori, Okayama University, Okayama, Japan

# 513

HEPATOCELLULAR CARCINOMA Takuji Torimura, Takato Ueno, Eitaro Taniguchi, Osamu Hashimoto, Masaharu Sakamoto, Ryukichi Kumashiro, Michio Sata, H Yano, Masamichi Kojiro, K u x m e University School of Medicine, Kurume, Japan

# 514 A HIGHLY EFFECTIVE BIFUNCTIONAL CHIMERIC SUICIDE GENE ERADICATES SYNGENEIC HEPATOMAS IN A RAT MODEL Florian Graepler, Wolfgang A Wybranietz, Marie-Luise Lemken, Ulrike Schmidt, Irina Smirnow, Christine D Gross, Martin Spiegel, Andrea Schenk, Hansjoerg Graf, Ulrike A Lauer, Michael Gregor, Sorin Armeanu, Michael Bitzer, Ulrich M Lauer, UKT, Tuebingen, Germany

GENE TRANSFER OF K1-5 SUPPRESSES THE GROWTH OF

# 515

MARKER FOR HEPATOCELLULAR CARCINOMA John M Luk, Bonnie W Y Wong, University of Hong Kong, Pokfulam, Hong Kong; Mei Y Hu, Fudan University Shanghai, China; Sheung T Fan, University of Hong Kong, F’okfulam, Hong Kong

# 516 IDENTIFICATION OF POTENTIAL BIOMARKERS FOR AN ENHANCED RISK OF DEVELOPMENT OF HCC IN CIRRHOTIC HCV PATIENTS USING A FUNCTIONAL GENOMICS APPROACH Juergen Jobst, MatriGene GmbH, Reutlingen, Germany; Holger G Hass, Michael Gregor, Stephan Kaiser, University of Tuebingen, Tuebingen, Germany

LIVER-INTESTINE CADHERIN: A POTENTIAL DISEASE

3- Denutes AASLD Presidential Poster of Distinction


#517

WITH THE PRESENCE OF INFLAMMATORY CELLS IN HUMAN PRIMARY HEPATOCELLULAR CARCINOMA A POSSIBLE ROLE IN TUMOR PROMOTION AND ANGIOGENESIS Melchiorre Cervello, CNR, Palermo, Italy; Ada M Florena, University, Palermo, Italy; Daniela FoderB, CNR, Palermo, Italy; Lydia Giannitrapani, Monica Notarbartolo, Natale DAlessandro, Vito Franco, Giuseppe Montalto, University, Palermo, Italy

#518 THE INCREASED AND PROLONGED EPIDERMAL GROWTH FACTOR RECEPTOR (EGFR) ACTIVATION AND THE EFFECT OF EGFR INHIBITION ON CELLULAR PROLIFERATION IN A HUMAN CHOLANGIOCARCINOMA CELL LINE Jung-Hwan Yoon, Geum-Youn Gwak, Kyung-Suk Suh, Hyo-Suk Lee, Seoul National University College of Medicine, Seoul, South Korea; Steven F Bronk, Nathan W Werneburg, Gregory J Gores, Mayo Medical School, Clinic and Foundation, Rochester, MN

CORRELATION OF CYCLOOXYGENASE-2 EXPRESSION

# 519 THE DIFFERENCES OF THE SIGNALING AND RESPONSE TO TYPE I INTERFERONS IN HEPATOCELLULAR CARCINOMA CELL LINES Bazarragchaa Damdinsuren, Hiroaki Nagano, Masato Sakon, Tameyosh Yamamoto, Hideo Ota, Masato Nakamura, Shigeru Marubashi, Atsushi Miyamoto, Koji Umeshita, Keizo Dono, Shoji Nakamori, Morito Monden, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan

# 520 MAGNETIC RESONANCE IMAGING OF A MURINE MODEL FOR HEPATOCELLULAR CARCINOMA Spiros P Hiotis, N W School of Medicine, New York, NY; Youssef Z Wadghiri, NYU School of Medicine, Skirball Institute of Biomolecular Medicine, New York, NY; Herman Yee, Wei Luan, NYU School of Medicine, New York, NY; Steven J Burakoff, NYU School of Medicine, NYU Cancer Institute, Skirball Institute of Biomolecular Medicine, New York, NY

# 521

DURING THE EARLY STAGES OF ONCOGENESIS IN AN ANIMAL MODEL OF HEPATOCELLULAR CARCINOMA John K Olynyk, kchard A Davies, University of Western Australia, Fremantle, Australia; George C Yeoh, University of Western Australia, Perth, Australia

A COX-2 INHIBITOR REDUCES OVAL CELL PROLIFERATION

# 522 CYTOCHROME P450 2E1, BUT NOT NADPH OXIDASE IS

UPREGULATION OF DNA REPAIR GENES IN MOUSE LIVER Ivan Rusyn, University of North Carolina, Chapel Hill, NC; Hiroshi Kono, Yamanashi University, Tamaho, Nakakoma, Yamanashi, Japan; Oksana Kosyk, Blair U Bradford, University of North Carolina, Chapel Hill, NC

# 523 THE COMBINATION OF FURA AND CDDP INCREASES THE APOPTOSIS OF HUMAN HCC VIA FAS/FASL AND ITS TRANSDUCTION Takayuki Kogure, Yoshiyuki Ueno, Noriatsu Kanno, Koji Fukushima, Kana Nishioka, Emiko Mikami, Takao Iwasaki, Tooru Shimosegawa, Tohoku University School of Medicine, Sendai, Japan

REQUIRED FOR ETHANOL-INDUCED DNA DAMAGE AND

# 524 MB07133: A HEPDIRECTTM PRODRUG OF CYTARABINE MONOPHOSPHATE FOR USE IN HEPATOCELLULAR CARCINOMA Deidre A MacKenna, Serge H Boyer, Annika C Montag, Barbara Treash-Osio, Paul A Rolzin, David L Linemeyer, Mark D Erion, Metabasis Therapeutics, Inc., San Diego, CA

# 525 MUTANT BETA CATENIN PROMOTES HEPATOCYTE PROLIFERATION AND INHIBITS APOPTOSIS XianZhang Shang, Haizhen Zhu, Karrie Lin, ; Chen Liu, University of Florida, Gainesville, FL

# 526 INCREASED LIQUOR, PLASMA AND TUMOR TISSUE NOCICEPTIN IN RATS WITH EXPERIMENTALLY INDUCED HEPATOCELLULAR CARCINOMA Ferenc Szalay, Andrea Horvath, Aniko Folhoffer, Peter L Lakatos, Attila Zalatnai, Monika B Hantos, Komelia Tekes, Semmelweis university, Budapest, Hungary

# 527 THE MEANING OF PROTOCADHERIN LKC EXPRESSION IN HEPATOCELLULAR CARCINOMA Hideo Ota, Hiroaki Nagano, Masato Sakon, Motoi Kondo, Tameyoshi Yamamoto, Bazarragchaa Damdinsuren, Masato Nakamura, Shigeru Marubashi, Atsushi Miyamoto, Keizo Dono, Koji Umeshita, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Kenichi Wakasa, Osaka City University, Osaka, Japan; Shoji Nakamori, Morito Monden, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

Portal Hypertension: Experimental

# 528

ASSAY IN INFECTED CIRRHOTIC PATIENTS Andrea Zambruni, Ulrich Thalheimer, Jason Coppell, Anne Riddell, Andrea Mancuso, Gioacchino Leandro, David Perry, Andrew K Burroughs, Royal Free Hospital, London, UK

ENDOGENOUS HEPARIN ACTIVITY DETECTED BY ANTI-XA

# 529 DETERMINATION OF REGIONAL LIVER BLOOD FLOW USING INTRAVASCULAR PET TRACERS: MICROVASCULAR THEORY AND EXPERIMENTAL VALIDATION FOR PIG LIVERS Susanne Keiding, Ole L Munk, Aarhus University Hospital, Aarhus, Denmark; Ludvik Bass, University of Queensland, Brisbane, Australia

# 530

RELATED PULMONARY ARTERIAL HYPERTENSION Raymond L Benza, Jose A Tallaj, Barry K Raybum, Brian A Foley, Robert C Bourge, University of Alabama at Birmingham, Birmingham, AL; Robert Roscigno, United Therapeutics, Research Triangle Park, NC

SAFETY AND EFFICACY OF TREPROSTINIL IN CIRRHOSIS-

# 531 HEPATIC INFLAMMATION IS AN IMPORTANT MODULATOR OF THE CIRCULATORY DISTURBANCES IN CIRRHOSIS Rajeshwar P Mookerjee, Sambit Sen, Stephen J Hodges, Nathan A Davies, Lisa M Cheshire, Roger Williams, Rajiv Jalan, University College London, London, UK


532 HETEROGENEITY OF INTRAHEPATIC ARTERIO-PORTAL BLOOD MIXING STUDIED BY 13N-AMMONIA PET OF INTACT PIG LIVER Susanne Keiding, Ole L Murk, Hendrik Vilstmp, Aarhus University Hospital, Aarhus, Denmark; Ludvik Bass, University of Queensland, Aarhus, Australia

3 533 FACTOR V LEIDEN (FVL) MUTATION IN CHILDREN WITH PORTAL VEIN THROMBOSIS Hanaa El-Karaksy, Mortada Al-Shabrawi, Nehal El-Koofy, Manal El-Hawary, Azza Mostafa, Marwa Safy, Mona Aziz, Manal Wilson, Hala Ah, Afaf El-Guizery, Cairo University, Cairo, Egypt; Hassan H A-Kader, University of Arizona, Tucson, AZ

# 539 ACCELERATED PLATELET TURNOVER IN PATIENTS WITH LIVER CIRRHOSIS Mikio Kajihara, Shinzo Kato, Yuka Okazaki, Yutaka Kawakami, Yasuo Ikeda, Hiromasa Ishii, Masataka Kuwana, Keio University School of Medicine, Tokyo, Japan

# 540 ESTIMATION OF GLOMERULAR FILTRATION RATE IN PATIENTS WITH END-STAGE LIVER DISEASE: A NEW MODEL SUPERIOR TO COCKROFT-GAULT Kiran M Bambha, W Ray Kim, Joanne T Benson, Patrick S Kamath, E Rolland Dickson, Mayo Clinic and Foundation, Rochester, MN; Goran B G Klintmalm, Baylor Institute of Transplantation Sciences, Dallas, TX

~~~

8 534 LONG TERM SURVIVAL AFTER PORTOSYSTEMIC SHUNTING FOR BUDD-CHIARI SYNDROME. SHUNT PATENCY IS DETERMINANT Jean-Baptiste Bachet, Bertrand Condat, Beaujon Hospital, Clichy, France; Hewe Hagege, Centre Hospitalier Intercommunal de Cr&eif, Creteil, France; Aurelie Plessier, Jacques Belghiti, Dominique Valla, Beaujon Hospital, Clichy, France

# 541 DRIVING PERFORMANCE IN PATIENTS WITH CHRONIC LIVER DISEASE Tarek I Hassanein, University of California San Diego, San Diego, CA; Robin C Hilsabeck, Texas Tech University Health Sciences Center, Lubbock, TX; Tom D Marcott, Meghan D Carlson, William Perry, University of California San Diego, San Diego, CA

-” 535 MECHANISM OF THROMBOCYTOPENIA IN PATIENTS WITH CIRRHOSIS: THE ROLE OF FUCTIONAL SPLEEN

PLATELETS ANTIBODIES Eli Zuckerman, Gila Bouskila, Bnai Zion Medical Center, Haifa, Israel; Tsila Zuckerman, Lilach Bonstein, Rambam Medical Center, Haifa, Israel; Naomi Lanir, Aourora Toubi, Elias Toubi, Daniel Yeshu run, David Groshar, Bnai Zion Medical Center, Haifa, Israel

2 536 EVIDENCE FOR ALTERED RENAL BLOOD FLOW AUTOREGULATION IN CIRRHOSIS RajiL. Jalan, Rajeshwar P Mookerjee, University College London, London, UK; Peter C Hayes, Doris N Redhead, Royal Infirmary, Edinburgh, UK; Kevin P Moore, Royal Free Hospital, London, UK; Roger Williams, University College London, London, UK

VOLUME, SERUM THROMBOPOIETIN LEVELSAND ANTI-

P 537 PORTAL-PRESSURE GRADIENT REDUCTION BY K-CANRENOATE IS NOT PARALLELLED BY SYMPATHO- INHIBITION IN POSTVIRAL PREASCITIC CHILD A CIRRHOSIS WITH SMALL OESOPHAGEAL VARICES Massimo Pozzi, Clinica Medica, Azienda Ospedaliera San Gerardo, Universita degli Studi Milano-Bicocca, Monza, Italy; Guido Grassi, Laura Ratti, Clinica Medica, Monza, Italy; Giorgio Favini, Radiologia, Monza, Italy; Elena Redaelli, Fosca Quarti Trwano, Francesca .4renare, Alessandro Redaelli, Giancarla Poli, Giuseppe Mancia, Clinica Medica, Monza, Italy

4 538 EFFECTS OF CANDOXATRILAT, A NEUTRAL ENDOPEPTIDASE INHIBITOR, ON SODIUM AND FREE

INDUCED CIRRHOSIS WITH ASCITES Giovanni Sansoe, Gradenigo Hospital, Torino, Italy; Manuela Aragno, Raffaella Mastrocola, University of Torino, Torino, Italy; Stefano Silvano, Giulio Mengozzi, Giovanni Touscoz, Molinette Hospital, Torino, Italy; Floriano Rosina, Gradenigo Hospital, Torino, Italy; Antonina Smedile, Molinette Hospital, Torino, Italy; Oliviero Danni, University of Torino, Torino, Italy; Mario Rizzetto, Molinette Hospital, Torino, Italy

WATER URINARY EXCRETION IN THE RAT MODEL OF CCL.4-

tf 542 STATISTICAL PARAMETRIC MAPPING ANALYSIS IN CIRRHOTIC PATIENTS WITH AND WITHOUT MINIMAL ENCEPHALOPATHY Motoli Iwasa, Mika Yamamoto, Yuri Nakagawa, Kaname Matsumura, Masaki Takeo, Masahiko Kaito, Yukihiko Adachi, Mie University School of Medicine, Tsu City, Mie, Japan

# 543 MULTICENTER, RANDOMIZED, CONTROLLED, DOUBLE- BLIND TRIAL COMPARING ALBUMIN WITH POLYGELINE FOR INTRAVASCULAR FLUID LOADING IN PATIENTS WITH CIRRHOSIS AND ASCITES Richard Moreau, Service d’Hepatologie and INSERM U-481, HBpital Beaujon, Clichy, France; Doniinique C Valla, Service d’H6patologie and INSERM U-481, Clichy, France; Isabelle Durand-Zaleski, Sant6 Publique, Creteil, France; Dominique Golly, Zera Tellier, Laboratoire Francais du Fractionnement et des Biotechnologies, Courtaboeuf, France

# 544 EFFECTS OF SELECTIVE ENDOTHELIN RECEPTOR ANTAGONISTS ON THE MOLECULAR AND PHYSIOLOGIC ALTERATIONS IN EXPERIMENTAL HPS IN VIVO Yiqun Ling, Junlan Zhang, Liping Tang, Bao LUO, Michael B Fallon, University of Alabama at Birmingham and Birmingham VA Medical Center, Birmingham, AL

# 545 HEPATIC BLOOD FLOW MEASUREMENT WITH ARTERIAL AND PORTAL BLOOD FLOW BY XENON COMPUTED TOMOGRAPHY QUANTITATIVE ANALYSIS OF CORRELATION WITH HEPATIC FIBROSIS IN CHRONIC HEPATITIS C Michihiro Suzuki, Hiroki Ikeda, Hideaki Takahashi, Noriaki Okuse, Yutaro Kobayashi, Yasuhito Takahashi, Hiroshi Yotuyanagi, Funiio Itoh, Shiro Maeyama, Saint Marianna Univer- sity, Kawasaki-shi, Japan; Shiro Iino, Kiyokawa Hospital, Tokyo, Japan; Shigeru Sase, Anzai Medical Co., Ltd., Tokyo, Japan



Hepatitis C: Epidemiology and Natural History

8 #546 INFECTION OF PRIMARY HUMAN MACROPHAGES WITH HEPATITIS C VIRUS IN VITRO: INDUCTION OF TUMOR NECROSIS FACTOR ALPHA AND INTERLEUKIN 8 Tomasz Laskus, Marek Radkowski, Mayo Clinic Scottsdale, Scottsdale, AZ; Marek Nowicki, University of Southern California, Los Angeles, CA; Jeffrey Wilkinson, Debra M Adair, Mayo Clinic Scottsdale, Scottsdale, AZ; Andrzej Horban, Municipal Hospital of Infectious Diseases, Warsaw, Poland; Jorge Rakela, Mayo Clinic Scottsdale, Scottsdale, AZ

88547 HOST-VIRUS INTERACTIONS IN ACUTE HEPATITIS C Kazushi Sugimoto, David E Kaplan, Fusao rkeda, Jason Stadanlick, Gina Suh, University of Pennsylvania and Philadelphia VA Medical Center, Philadelphia, PA; Ayse Aytaman, Brooklyn VA Medical Center, Brooklyn, NY; Michael Lucey, University of Wisconsin, Milwaukee, WI; Stuart Ray, Johns Hopkins University, Baltimore, MD; Frederick Nunes, Pennsylvania Hospital, Philadelphia, PA; K Rajender Reddy, University of Pennsylvania, Philadelphia, PA; Kyong-Mi Chang, University of Pennsylvania and Philadelphia VA Medical Center, Philadelphia, PA ~~ ~~~~~ ~

# 548 USE OF NUCLEOTIDE SEQUENCE ANALYSIS OF THE NS5B REGION FOR ROUTINE GENOTYPING OF HEPATITIS C VIRUS : IDENTIFICATION OF NUMEROUS VARIANTS NOT CLASSIFIABLE INTO THE KNOWN HCV GENOTYPES Donald Murphy, INSPQ-Laboratoire de Sante Publique du Quebec, Montreal, P Q Canada; Bernard Willems, CHUM-HGpital Saint-Luc, Montreal, PQ, Canada; Marc Deschhes, CUSM-HBpital Royal Victoria, Montreal, PQ Canada; Nir Hilzenrat, HGpital General Juif, Montreal, PQ Canada; Roger Mousseau, H6pital Maisonneuve-Rosemont, Montreal, PQ, Canada

# 549 HEPATITIS C IN 2,410 PATIENTS 65 YEARS OR OLDER. A SEVERE AND NEGLECTED CURABLE DISEASE? Dominique Thabut, Sophie Le Calvez, Vincent Thibault, Julien Massard, Cecilia d’ Arondel, Joseph Moussalli, Mona Munteanu, Vincent Di Martino, Yves Benhamou, Wad Ratziu, Thierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

# 550 HEMOPHILIC SIBLINGS WITH CHRONIC HEPATITIS C: EVIDENCE OF A GENETIC ASSOCIATION WITH DISEASE PROGRESSION Michael W Fried, University of North Carolina, Chapel Hill, NC; Barbara L Kroner, Liliana R Preiss, Research Triangle Institute, Rockville, MD; Dickens Theodore, University of North Carolina, Chapel Hill, NC; James J Goedert, National Cancer Institute, Rockville, MD

# 551 PROJECTING THE PROGNOSIS OF HEPATIC FIBROSIS IN

John B Wong, Barbara McGovern, Tufts-New England Medical Center, Boston, MA; Mark S Sulkowski, Johns Hopkim University, Baltimore, MD; Douglas T Dieterich, Mount Sinai Medical Center, New York, NY; Thierry Poynard, Groupe Hospitalier Pitie Salpetriere, Paris, France

# 552 COMPARING THE PUBLIC HEALTH BURDEN OF CHRONIC HEPATITIS C AND HIV INFECTION IN UNITED STATES Sylvie Deuffic-Burban, INSERM U444, Paris, France; John B Wong, Tufts-New England Medical Center, Boston, MA; Thierry Poynard, Groupe Hospitalier Pitie Salpetriere, Paris, France

~

HIV-HCV CO-INFECTION

# 553 HISTOLOGIC-HEMODYNAMIC CORRELATIONS IN HEPATITIS C AND OTHER CHRONIC LIVER DISEASES-IS THERE A HISTOLOGICALLY MILD AND SEVERE CIRRHOSIS? Satish Nagula, Dhanpat Jain, Yale University School of Medicine, New Haven, CT; Roberto J Groszmann, Guadalupe Garcia-Tsao, Yale University School of Medicine, CT-VA Healthcare System, New Haven-West Haven, CT

# 554 THE USEFULNESS OF A NEW IMMUNO-RADIOMETRIC ASSAY TO DETECT HEPATITIS C CORE ANTIGEN IN A

Kazunori Kusumoto, Katsuhiro Hayashi, Hirohumi Uto, Satoru Hasuike, Keiko Toyama, Kenji Nagata, Takeshi Hori, Akihiko Okayama, Hirohito Tsubouchi, Miyazaki Medical College, Miyazalu, Japan; Sherri 0 Stuver, Boston University School of Public Health, Boston, MA

COMMUNITY-BASED POPULATION

# 555 IMPROVED DETECTION OF ACTIVE HEPATITIS C VIRUS INFECTION IN CADAVER DONORS USING TRANSCRIPTION MEDIATED AMPLIFICATION ASSAY Claudia Chinchilla, Livier A Corado, Sali Aswad, National Institute of Transplantation, Los Angeles, CA; Tom Moone, One Legacy, Los Angeles, CA; Robert Mendez, Rafael Mendez, Nasreen S Khan, National Institute of Transplantation, Los Angeles, CA

# 556 ENVIRONMENTAL STABILITY OF HEPATITIS C VIRUS (HCV): VIABILITY OF DRIED/STORED HCV IN CHIMPANZEE INFECTIVITY STUDIES Kris Krawczynski, Miriam J Alter, Betty H Robertson, Ling Lu, John E Spelbring, Karen A McCaustland, Centers for Disease Control and Prevention, Atlanta, GA

# 557 ABSOLUTE CD4 T-CELL SUBSETS ARE DECREASED IN HIV- SERONEGATIVE PATIENTS WITH CIRRHOSIS Barbara McGovern, Marvin Lopez, Yoav Golan, Angela Lawton, Grayson Moore, Daniel Pratt, Mark Epstein, Tamsin Knox, New England Medical Center, Boston, MA

. .-

# 558 PREVALENCE ESTIMATES AND RISK FACTORS FOR HEPATITIS C VIRUS RNA POSITIVITY IN A LARGE

Dana Bruden, Thomas Hennessy, Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Carol Christensen, Alaska Native Tribal Health Consortium, Anchorage, A K Dan Sullivan, University of Washington School of Medicine, Seattle, WA; Chriss Homan, Alaska Native Tribal Health Consortium, Anchorage, AK; Heike Dubner, University of Washington School of Medicine, Seattle, WA; Michael Bruce, Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Steve Livingston, James Williams, Alaska Native Tribal Health Consortium, Anchorage, AK; David Gretch, University of Washington School of Medicine, Anchorage, AK; Brian McMahon, Alaska Native Tribal Health Consortium; Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK

POPULATION-BASED COHORT

I OOA POSTER SESSIONS HEPATOLOGY, October 2003

~~

559 AN OVERVIEW OF BIOCHEMICAL MARKERS (FIBROTEST- ACTITEST) DIAGNOSTIC VALUE IN CHRONIC LIVER

BIOPSY Thierry Poynard, Franqoise Imbert-Bismut, Vlad Ratziu, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Sylvie Naveau, HBpital Antoine Bklhre, Clamart, France; Dominique Thabut, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Didier Lebrec, HBpital Beaujon, Clichy, France; Philippe Halfon, RBML, Marseille, France; Fabien Zoulim, HBpital de l'HGtel Dieu, Lyon, France; Marc Bourliere, HBpital Saint Joseph, Marseille, France; Djamila Messous, Vincent Thibaut, Mona Munteanu, Groupe Hospitalier Pitie-Salpetriere, Paris, France

DISEASES: A NON-INVASIVE ALTERNATIVE TO LIVER

H" 560 MONITORING HCV CORE ANTIGEN DURING ANTIVIRAL THERAPY Adrian M Di Bisceglie, Janice Strinko, Patricia Osmack, Saint Louis University Health Sciences Center, St. Louis, MO

f 561 PIDEMIOLOGY OF ACUTE HCV INFECTION IN A LONDON COHORT OF HIV POSITIVE HOMOSEXUAL MALES Marh Danta, David Brown, Michael Jacobs, Geoffrey Dusheiko, Sanjay Bhagani, Royal Free Hospital, London, UK

2 562 LONG-TERM FOLLOW-UP OF CHRONIC HEPATITIS C PATIENTS-RESPONSE TO THERAPY AND INCIDENCE OF LIVER-RELATED COMPLICATIONS Pierre Pradat, Hotel-Dieu, Lyon, France; Hans L Tillmann, Medizinische Hochschule, Hannover, Germany; Jean-Henrik Uraconier, Universit): Hospital of Lund, Lund, Sweden; Giorgio Saracco, Azienda Ospedaliera San Giovanni Battista, Torino, Italy; Silvia Sauleda, Hospital General Vall d'Hebron, Barcelona, Spain; Mark Thursz, St. Mary's Hospital, London, UK; Paule Merle, Hotel-Dieu, Lyon, France; Salvatore Badalamenti, Scliering-Plough Research Institute, Kenilworth, NJ; Alfred0 Alberti, Universita di Padova, Padova, Italy; Juan-Ignacio Esteban, Hospital General Vall d'Hebron, Barcelona, Spain; Stephanos Hadziyannis, Hippokration Hospital, Athens, Greece; Mario Rizzetto, Azienda Ospedaliera San Giovanni Battista, Torino, Italy; Howard Thomas, St. Mary's Hospital, London, UK; Michael Manns, Medizinische Hochschule, Hannover, Germany; Christian Trepo, Hotel-Dieu, Lyon, France

7563 NEW COMBINATION TEST FOR HEPATITIS C VIRUS GENOTYPE AND AMPLICOR GT HCV MONITOR TEST V 2.0 Motokazu Mukaide, SRL, Inc., Tokyo, Japan; Yasuhito Tanaka, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Kentaro Yoshioka, Nagoya University, Nagoya, Japan; Hirokazu Kakuda, SRL, Inc., Tokyo, Japan; Kiyotaka Fujise, Jikei University School of Medicine, Chiba, Japan; Kazumasa Hiiji, SRL, Inc., Tokyo, Japan; Masashi Mizokami, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

X 564 LIMITATIONS OF THE CORE ANTIGEN ASSAY AS A SECOND LINE SUPPLEMENT TEST IN THE DIAGNOSIS OF ACTIVE HCV INFECTION Me1 Krajden, Rjshrna Sbivji, Kingsley Gunadasa, Annie Mak, Gail McNabb, BC Centre tor Disease Control, Vancouver, BC, Canada; Michel Friesenhahn, David Hendricks, Bayer Diagnostics, Berkeley, CA; Lorraine Comanor, Independent Research Consultant, Palo Alto, CA

# 565

Joseph Sebastian, Carolyn Turnmire, Hawazin Faruki, Laboratory Corporation of America, Research Triangle Park, NC; Deborah Burris, Nang Htun, Marc Short, Elana Swartman, Fawn Wang, Michael Zoccoli, Jianli Cao, Celera Diagnostics, Alameda, CA

HCV GENOTYPING USING REAL-TIME PCR ASSAY

~~

ft 566 FIBROSIS IN CHRONIC HEPATITIS C IS ASSOCIATED WITH HEPATIC PROGENITOR CELL PROLIFERATION AND A PERIPORTAL DUCTULAR REACTION, WHICH IS EXACERBATED BY STEATOSIS: A NEW MODEL FOR DISEASE PROGRESSION Andrew D Clouston, Julie R Jonsson, University of Queensland, Brisbane, Australia; Bernadette Letizia, Sullivan Nicolaides Pathology, Brisbane, Australia; Michelle M Richardson, Daina M Vanags, Meagan Walsh, University of Queensland, Brisbane, Australia; Anthony J Demetris, University of Pittsburgh, Pittsburgh, PA; Elizabeth E Powell, University of Queensland, Brisbane, Australia

# 567 SERUM ALPHA-FETOPROTEIN (AFP) LEVELS IN PATIENTS WITH ADVANCED HEPATITIS C-ASSOCIATED LIVER DISEASE WITHOUT HEPATOCELLULAR CARCINOMA:

Adrian M Di Bisceglie, Saint Louis University Health Sciences Center, St. Louis, MO; Jules Dienstag, Massachusetts General Hospital, Boston, MA; Herbert Bonkovsky, University of Connecticut Health Center, Farmington, CT; Richard Sterling, Medical College of Virginia, Richmond, VA; Raymond Chung, Massachusetts General Hospital, Boston, MA; Jay Everhart, National Institutes of Health, Bethesda, MD; Elizabeth Wright, New England Research Institute, Watertown, MA

# 568 NATURAL HISTORY OF PATIENTS WITH CHRONIC HEPATITIS C AND PERSISTENTLY NORMAL ALANINE AMINOTRANSFERASE LEVELS: DATA FROM THE MULTINATIONAL PEGASYSB STUDY (NR 16071) Mitchell Shiffman, VCU Health System, Richmond, VA; Moisks Diago, Hospital General de Valencia, Valencia, Spain; Albert Tran, HBpital de I'Archet, Nice, France; Paul Pockros, The Scripps Clinic, La Jolla, CA; Robert Reindollar, Carolinas Center for Liver Disease, Charlotte, NC; Daniele Prati, IRCCS Maggiore Hospital, Milan, Italy; Franqois Lamour, Pilar Lardelli, Roche Diagnostics, Basel, Switzerland; Stefan Zeuzem, Saarland University Hospital, Homburg / Saar, Germany

P 569

RESULTS FROM THE HALT-C TRIAL

QUANTITATION OF HCV POSITIVE- AND NEGATIVE- STRAND RNA IN LIVER TISSUE BY STRAND-SPECIFIC TAQMAN REAL-TIME PCR ASSAYS Lan Lin, Marc Van Ranst, Jos Van Pelt, Frederik Nevens, Johan Fevery, Chris Verslype, UZ Gasthuisberg, Leuven, Belgium

.# 570 STAGING OF LIVER FIBROSIS ESTIMATED BY HISTOLOGIC ANALYSIS OF LIVER TISSUE VS COMPUTER ANALYSIS OF DIGITALIZED LIVER IMAGES IN PATIENTS WITH CHRONIC HEPATITIS C Araby A Nacul, UPF/UFRGS, Passo Fundo, Brazil; Hugo Cheinquer, UFRGS/ FFFCMPA, Porto Alegre, Brazil; Carlos T Cersky, UFRGS, Porto Alegre, Brazil; Vinicius Duval, PUCRS, Porto Alegre, Brazil

8 Denotes AASLD Prcsidential Poster of Distinction

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1, 2003 POSTER SESSIONS lOlA

# 571 NEW HEPATITIS C VIRUS GENOTYPING ASSAY AS A ROUTINE METHOD BY NOVEL RESTRICTION FRAGMENT MASS POLYMORPHISM Jong Eun Yeon, Kyoung Oh Kim, Hyoung Joon Lim, Yun Jung Chang, Jin Yong Kim, Jong-Jae Park, Jae Seon Kim, Young-Tae Bak, Korea University College of Medicine, Seoul, South Korea; Hyun Jae Chung, Sukjoon Kim, Sun Pyo Hong, Soo-Ok Kim, Wangdon Yoo, Cancer Research Institute, Seoul National University College of Medicine, Seoul, South Korea; Kwan So0 Byun, Chang Hong Lee, Korea University College of Medicine, Seoul, South Korea

# 572 VIRUS-SPECIFIC CD4+ T CELL RESPONSES IN HEPATITIS C VIRUS-INFECTED PATIENTS WITH DIFFERENT GENOTYPES Heidemarie Hokmann, Judith H Aberle, Institute of Virology, University of Vienna, Vienna, Austria; Petra Steindl-Munda, Elisabeth Forman, Wolfgang Jessner, Harald Hofer, Peter Ferenci, University of Vienna, Vienna, Austria; Therese Popow-Kraupp, Institute of Virology, University of Vienna, Vienna, Austria

# 573 LONG-TERM OUTCOME OF HEPATITIS C INFECTION AFTER BONE MARROW TRANSPLANTATION Tank Asselah, Federation d’H6pato-Gastroenterologie et INSERM U481, HBpital Beaujon, Clichy, France; Regis Peffault De LaTour, Service dHematologie, HBpital Saint Louis, France; Vincent Levy, HBpital Saint-Louis, France; Patrick Marcellin, Federation dH6pato-Gastroenterologie et INSERM U481, HBpital Beaujon, Clichy, France; Catherine Scieux, Service de Virologie, HBpital Saint-Louis, France; Lionel Ades, Service d’Hematologie, HBpital Saint-Louis, France; Richard Traineau, Service dHemobiologie, HBpital Saint-Louis, France; Agnes Devergie, Patricia Ribaud, Helilne Esperou, Eliane Gluckman, Service dHematologie, HBpital Saint-Louis, France; Dominique Valla, Federation &Hepato-Gastroenterologie et INSERM U481, HBpital Beaujon, Clichy, France; Gerard Socie, Service d’Hematologie-Greffe de Mwlle et INSERM ERM-0220, HBpital Saint-Louis, France ~~

#574 STEATOSIS IS COMMON IN ADVANCED HEPATITIS C AND RELATED TO BMI, HYPERTRIGLYCERIDEMIA, AND GENOTYPE 3 Anna S Lok, University of Michigan, AM Arbor, MI; James E Everhart, NIDDK, Bethesda, MD; Elizabeth Wright, NERI, Watertown, MA; Raymond Chung, Massachusetts General Hospital, Boston, MA; Joel K Greenson, University of Michigan, Ann Arbor, MI

# 575 ONINVASIVE PREDICTION OF FIBROSIS BY A NOVEL SERUM MARKER IN PATIENTS WITH CHRONIC HEPATITIS C Yukiko Saitou, Katsuya Shiraki, Tomoyuki Kawakita, Hidekazu Inoue, Hiroshi Okano, Norihiko Yamamoto, Kazushi Sugimoto, Kazumoto Muraki, Takeshi Nakano, First Internal Medicine, Mie University Tsu, Japan

# 576 LIVER ELASTICITY MEASUREMENT BY ULTRASONIC

METHOD FOR ASSESSMENT OF LIVER FIBROSIS IN CHRONIC VIRAL HEPATITIS Michel Beaugrand, Marianne Ziol, CHU Jean Verdier, Bondy, France; Laurent Sandrin, Celine Fournier, Echosens, Paris, France; Annonciade Biaggi-Frassati, Bruno Poulet, Jean-Claude Trinchet, CHU Jean Verdier, Bondy, France; Frederic Mal, Christos Christidis, Institut Mutualiste Montsouris, Paris, France; Farhad Kazemi, Veronique Grando, Nathalie Ganne, CHU Jean Verdier, Bondy, France; Robert Palau, Institut Mutualiste Montsouris, Paris, France

TRANSIENT ELASTOGRAPHY: A NEW NON-INVASIVE

# 577 A LOOKBACK PROGRAM TO NOTIFY PERSONS WHO RECEIVED BLOOD PRODUCTS IN A NEONATAL INTENSIVE CARE UNIT BEFORE JULY 1992 OF THEIR RISK FOR HEPATITIS C VIRUS (HCV) INFECTION: RESULTS FOR THOSE WITH MANAGED CARE PROVIDERS VERSUS PRIVATE SECTOR PROVIDERS Henry Cagle, James Williams, Alaska Native Tribal Health Consortium, Anchorage, AK; Jack Jacob, Alaska Neonatology Associates, Anchorage, AK; Brian McMahon, Chriss Homan, Carol Christensen, Leslie Fox-Leyva, Mary Snowball, Richard Koller, Susan Negus, Alaska Native Tribal Health Consortium, Anchorage, AK; Elizabeth Cornett, Alaska Native Medical Center, Anchorage, AK; Therese Veker, Josephine Simonetti, Steve Livingston, Alaska Native Tribal Health Consortium, Anchorage, AK

# 578 COMPARISON OF RT-PCR AND TMA-BASED ASSAYS FOR DETECTION OF HCV RNA IN FORMALIN FIXED PARAFFIN- EMBEDDED LIVER TISSUE SAMPLES Wolf P Hofmann, Saarland University, Homburg /Saar, Germany; Votker Dries, University of Cologne, Cologne, Germany; Eva Herrmann, Barbara Gartner, Stefan Zeuzem, Christoph Sarrazin, Saarland University, Homburg/ Saar, Germany

# 579 IMPACT OF VARIATIONS OF ASSAY COMPONENTS ON FIBROTEST AND ACTITEST RESULTS. TRANSFERABILITY OF ASSAY RESULTS ON DIFFERENT AUTOMATS IN THE SAME LABORATORY Franqoise Imbert-Bismut, Djamila Messous, Asma Srairi, Rachel Morra, Mona Munteanu, Anne S Guibert, Dominique Thabut, Vincent Thibaut, Annie Piton, Bernard Hainque, Thierry Povnard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

# 580 IRON AND CHRONIC HEPATITIS C : CLINICAL, BIOLOGICAL, HISTOLOGICAL CORRELATIONS AND IMPACT ON FIBROSIS PROGRESSION Dominique Guyader, Liver Unit and INSERM U522, Rennes, France; Nafissa Rakba, INSERM U522, Rennes, France; Anne- Sophie Thirouard, CHU HBpital Pontchaillou, Rennes, France; Sylvie Jacquelinet, Helene Danielou, Liver Unit and INSERM U522, Rennes, France; Michele Perrin, Liver Unit, Rennes, France; Anne-Marie Jouanolle, Molecular Genetic Laboratory, Rennes, France; Pierre Brissot, Liver Unit and INSERM U522,

Rennes, France; Yves Deugnier, Liver Unit and Clinical

0 l m

g 6 Investigation Center, Rennes, France i? Rennes, France; Veronique David, Molecular Genetic Laboratory, 0 c

# 581 0 EFFECTS OF RIBAVIRIN COMBINED WITH INTERFERON

WEEKS OF TREATMENT IN PATIENTS WITH HEPATITIS C VIRUS GENOTYPE 1 AND HIGH BASELINE VIRAL LOADS Masaru Enomoto, Shuhei Nishiguchi, Madoka Kohmoto, Akihiro Tamori, Daiki Habu, Tadashi Takeda, Shuichi Seki, Susumu Shiomi, Osaka City University Medical School, Osaka, Japan

ALPHA-2B ON VIRAL KINETICS DURING THE FIRST 12

# 582

BETWEEN BIOCHEMICAL MARKERS AND BIOPSY IN PATIENTS WITH CHRONIC HEPATIS C (CHC) Mona Munteanu, Franqoise Imbert-Bismut, Frederic Charlotte, Djamila Messous, Dominique Thabut, Vincent Thibaut, Yves Benhamou, Vlad Ratziu, Thierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

A PROSPECTIVE FOLLOW-UP OF DISCORDANCES


5” 583 LONG-TERM FOLLOW-UP OF CHRONIC HEPATITIS C PATIENTS NON-RESPONDERS TO ANTIVIRAL TREATMENT Jose Antonio Galeras, Isabel Cirera, Susanna Coll, Carmen Marquez, Maria Dolors Gimenez, Felipe Bory, Ricard Sola, Hospital del Mar, Barcelona, Spain

# 584 PROTEOMICS TO PREDICT HEPATITIS C FIBROSIS Glenn R Gourley, Libang Yang, Larry L David, Christopher L Corless, Anne M Wertheimer, Hugo R Rosen, OHSU, Portland, OR

# 585

CONVENTIONAL HELICAL CT OF THE LIVER COULD PREDICT LIVER FIBROSIS STAGING IN PATIENTS WITH CHRONIC HEPATITIS C Endio Gbmez-Gonztilez, ESI-University of Seville, Sevilla, Spain; Manuel Romero-G6mez, Hepatology Unit, Hospital Universitario de Valme, Sevilla, Spain; Marina Vera-Valencia, ESI-University of Seville, Sevilla, Spain; Raquel Corpas, Hepatology Unit, Hospital Universitario de Valme, Sevilla, Spain; Maria J Santamaria-Burgos, ESI-University of Seville, Sevilla, Spain; Jorge Luque, Radiology Unit. Hospital Universitario de Valme, Sevilla, Spain; Victor M Castellano- Megias, Patology Unit. Hospital Universitario de Valme, Sevilla, Spain; Laura Sanchez, Hepatology Unit, Hospital Universitario de Valme, Sevilla, Spain; Rafael Aznar, Manuel Fernandez-L6pez, Radiology Unit. Hospital Universitario de Valme, Sevilla, Spain

COMPUTER-PERFORMED OPTICAL ANALYSIS OF

8 586 DIVERSITY OF HEPATITIS C VIRUS HYPERVARIABLE

POSITIVE HOST POPULATIONS Livier A Corado, Claudia Chinchilla, Sali Aswad, Hamid Shidban, Robert Mendez, Nasreen Khan, National Institute of Transplantation, Los Angeles, CA

REGION-1 MUTATIONS VARIES IN DIFFERENT HCV

587 RETROSPECTIVE STUDY CORRELATING THE PROMETHEUS LIVER FIBROSIS PANEL WITH FINDINGS OF FIBROSIS ON PERCUTANEOUS LIVER BIOPSY SPECIMENS IN ALASKA NATIVES WITH HEPATITIS C Carol Christensen, Steve Livingston, Chriss Homan, Alaska Native Tribal Health Consortium, Anchorage, AK; Heike Dubner, University of Washington, Seattle, WA; Dana Bruden, Eitel Dunaway, Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Katie Smith, Jason Do, Esther Oh, Prometheus Laboratories Inc., San Diego, CA; Brian McMahon, Alaska Native Tribal Health Consortium; Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK

3 588 MEASUREMENT OF HUMAN INTERCELLULAR ADHESION

THE OCCURRENCE OF HEPATOCELLULAR CARCINOMA FROM CHRONIC HEPATITIS C Mitsuhiko Moriyama, Hiroshi Matsumura, Hiroshi Aoki, Yasuyuki Arakawa, Nihon University School of Medicine, Tokyo, Japan

MOLECULE-1 IN THE BLOOD IS USEFUL FOR PREDICTING

# 589 HEPATIC STEATOSIS IN PATIENTS WITH CHRONIC HEPATITIS C: A MULTICENTER STUDY OF US VETERANS Ke-Qin Hu, Loma Linda University Medical Center and Loma Linda VA Medical Center, Loma Linda, CA; Ramsey C Cheung, Palo Alto VA Medical Center, Palo Alto, CA; Sue Currie, San Francisco VA Medical Center, San Francisco, CA; Edmund J Bini, New York Harbor VAMC, New York, NY; Hui Shen, University of California San Francisco, San Francisco, CA; Bhupinder Anand, Houston VA Med Center, Houston, TX; Lennox J Jeffers, Miami VA Medical Center, Miami, FL; Samuel B Ho, Minneapolis VA Medical Center, Minneapolis, MN; Norbert Brau, Bronx VAMC, Bronx, NY; Warren N Schmidt, Iowa VAMC, Iowa City, IA; John McCracken, Loma Linda University Medical Center and Loma Linda VA Medical Center, Loma Linda, CA; Stephen J Rossi, Teresa L Wright, San Francisco VA Medical Center, San Francisco, CA

# 590 TRACING THE PANDEMIC BEHAVIOR OF HEPATITIS C

WIDESPREAD INJECTION TREATMENT FOR SCHISTOSOMIASIS Yasihito Tanaka, Takanobu Kato, Etsuro Orito, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Yasuhiro Akahane, Yamanashi Medical University, Yamanashi, Japan; Hiroshi Yoshizawa, Kazuaki Chayama, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan; Tatsuya Ide, Michio Sata, Kurume University School of Medicine, Kurume, Japan; Nobuo Ohta, Masashi Mizokami, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

tt 591 PERFORMANCE EVALUATION OF A NEW ROUTINE HCV

POSITIVE SAMPLES Pierpaolo Valcavi, Maria Cristina Medici, Francesca Casula, Maria Crsitina Arcangeletti, Flora De Conto, Adriana Calderaro, Carlo Chezzi, Giuseppe Dettori, University of Parma, Parma, Italy

8 592 DIFFERENT TRANSLATION EFFICIENCIES OF S‘UTR HEPATITIS C VIRUS VARIANTS BEFORE AND AFTER LIVER TRANSPLANTATION Juan I Arenas, Karen V Kibler, Tomasz Laskus, Jeffrey Willunson, Juan F Gallegos, Debra Adair, Hugo Vargas, Jorge Rakela, Mayo Clinic, Scottsdale, AZ

VIRUS GENOTYPE 1B IN JAPAN-ASSOCIATION WITH THE

CORE AG ASSAY FOR VIRAEMIA DETECTION IN ANTI-HCV

# 593 INCIDENCE AND RISK FACTORS OF HCV AND HIV INFECTIONS IN A COHORT OF INTRAVENOUS DRUG USERS IN THE NORTH AND EAST OF FRANCE Damien Lucidarme, HApital Saint Philibert, Lomme cedex, France; Amdie Bruandet, Institut de Veille Sanitaire, Saint Maurice, France; Daniele Ilef, Cellule InterRegionale d’Epidkmiologie, Lille, France; Jean Harbonnier, Centre Boris Vian, Lille, France; Claude Jacob, Centre Baudelaire, Metr, France; Anne Decoste, HApital Saint Philibert, Lomme cedex, France; Catherine Delarnare, Centre Hospitalier, Ihionville, France; Christian Cyran, Le Square, Lens, France; Anne Franqoise Van Hoenacker, Cedre Bleu, Lille, France; Didier Fremaux, Didier Fremaux, Drogue 80, Amiens, France; Pascal Josse, UFATT, Nancy, France; Julien Emmanuelli, Yves Le Strat, Jean Claude Desenclos, Institut de Veille Sanitaire, Saint Maurice, France; Bernard Filoche, HApital Saint Philibert, Lomme cedex, France



# 594 INFLUENCE OF CYTOKINE GENE POLYMORPHISM IN THE PATIENTS INFECTED BY HCV Katsutoshi Tokushige, Noriko Tsuchiya, Kiyoshi Hasegawa, Etsuko Hashimoto, Katsumi Yaniauchi, Keiko Shiratori, Tokyo Women’s Medical University, Tokyo, Japan

# 595 ACUTE HEPATITIS C (HCV) IN INCARCERATED PATIENTS WITH HISTORY OF INTRAVENOUS DRUG USE (IDU) Alysse Wurcel, Lemuel Shattuck Hospital, Jamaica Plain, MA; Ioana Bica, New England Medical Center, Boston, MA; Rajesh Gandhi, Massachusetts General Hospital, Boston, MA; Meg Bradley, Susan Galvin, Lemuel Shattuck Hospital, Jamaica Plain, MA; Arthur Kim, New England Medical Center, Boston, MA; Colleen Corcoran, Joerg Timm, Massachusetts General Hospital, Boston, MA; Barbara McGovern, Lemuel Shattuck Hospital, Jamaica Plain, MA

# 596 DEVELOPMENT OF HEPATIC FAILURE WAS FOUND LESS FREQUENTLY THAN THAT OF HEPATOCELLULAR CARCINOMA IN JAPANESE PATIENTS WITH CHRONIC HEPATITIS C Fumio Imazeki, Osamu Yokosuka, Hironiitsu Saisho, Chiba University, Chiba, Japan

tr 597 OUTBREAK OF GENOTYPE 2 HEPATITIS C VIRUS INFECTION AFTER SCLEROTHERAPY OF VARICOSE VEINS : PHYLOGENETIC ANALYSIS Victor de Ledinghen, University Hospital, Pessac, France; Pascale Trimoulet, University Hospital, Bordeaux, France; Geraldine Cazajous, University Hospital, Pessac, France; Pierre-Henri Bernard, Marie-Helene Schrive, University Hospital, Bordeaux, France; Juliette Foucher, Laurent Castera, Julien Vergniol, University Hospital, Pessac, France; Hewe Fleury, University Hospital, Bordeaux, France; Patrice Couzigou, University Hospital, Pessac, France

# 598 HEPATITIS C VIRAL LOAD IS INCREASED AND RELATED TO GENOTYPE 1 IN HVC+/HIV+ CO-INFECTION COMPARED WITH HCV+ NON-COINFECTED PATIENTS Fernando Bessone, University of Rosario Medical School, Rosario, Argentina; Jorge Daruich, Hospital de Clinicas, Buenos Aires, Argentina; Sergio Lupo, Marcela Agostini, University of Rosario Medical School, Rosario, Argentina; Estela Manero, Juan Sordi, Hospital de Clinicas, Buenos Aires, Argentina; Jorge Palazzi, University of Rosario Medical School, Rosario, Argentina; Maria Nakatsuno, Gustavo Reboredo, Hospital de Clinicas, Buenos Aires, Argentina; Maria V Reggiardo, Alicia Godoy, Maria E Passamonti, Julio Vorobioff, University of Rosario Medical School, Rosario, Argentina; Jorge Findor, Hospital de Clinicas, Buenos Aires, Argentina; Hugo Tanno, University of Rosario Medical School, Rosario, Argentina

# 599 NEWLY-DIAGNOSED HEPATITIS C AND ALCOHOL USE: FINDINGS OF POPULATION-BASED SENTINEL SURVEILLANCE IN THE UNITED STATES Beth P Bell, Centers for Disease Control and Prevention, Atlanta, GA; Andre N Sofair, Connecticut Emerging Infections Program and Yale University School of Medicine, New Haven, CT; Michele M Manos, The Permanente Medical Group, Oakland, CA; Atif Zaman, Oregon Emerging Infections Program and Oregon Health Sciences University, Portland, OR; Ann Thomas, Oregon Emerging Infections Program, Portland, OR; Rose C Murphy, Wendy A Leyden, The Permanente Medical Group, Oakland, CA; Thomas E St. Louis, Amanda Durante, Nicole Hulten, Michelle Tacariello, Connecticut Emerging Infections Program and Yale University School of Medicine, New Haven, CT; Heather L Wurtzel, William Bower, Centers for Disease Control and Prevention, Atlanta, GA; Victor J Navarro, Thomas Jefferson University Hospital, Philadelphia, PA; Norah Terrault, University of California, San Francisco, CA

# 600 EVALUATION OF A PREDICTIVE MODEL FOR SEVERE HEPATIC FIBROSIS OR CIRRHOSIS IN CHRONIC HEPATITIS C Agostino Colli, Ospedale A. Manzoni, Lecco, Italy; Alice Colucci, Silvia Paggi, Mirella Fraquelli, Postgraduate School of Gastroenterology, Milan, Italy; Sara Massironi, Marco Andreoletti, Enrico Zuccoli, Ospedale A. Manzoni, Lecco, Italy; Dario Conte, Postgraduate School of Gastroenterology, Milan, Italy

# 601

RESPONSE TO HIGHLY ACTIVE ANTIRETROVIRAL THERAPY

Giorgio Antonucci, INMI L. Spallanzani, Rome, Italy; Alessandro Cozzi Lepri, Royal Free and University College, London, UK; Enrico Girardi, Maria Rosaria Capobianchi, Mariacarmela Solmone, Fabrizio Carletti, INMI L. Spallanzani, Rome, Italy; Antonella d’Arminio Monforte, University of Milan, Milan, Italy

# 602 LIVER RELATED MORBIDITY AND MORTALITY IN PATIENTS WITH HEPATITIS C VIRUS (HCV) INFECTION: AN INTERIM ANALYSIS OF THE IMPACT OF HIV COINFECTION David Nunes, Catherine Fleming, Demian Christiansen, Boston University, Boston, MA; Timothy Heeren, Boston Unversity, Boston, MA; Philippe Zamor, Boston University, Boston, MA; Cammy Graham, Margaret Koziel, Beth Israel Deaconess Medical Center, Boston, MA; Donald Craven, Lahey Clinic, Burlington, MA; Robert Horsburgh, Boston Unversity, Boston, MA

THE ROLE OF HCV VIREMIA AND GBV-C VIREMIA IN THE

(HAART) IN A COHORT OF HIV-INFECTED SUBJECTS


# 603 EPIDEMIOLOGY OF HEPATITIS C INFECTION AND ELIGIBILITY FOR ANTIVIRAL THERAPY AMONG U.S. VETERANS Edmund J Bini, VA Medical Center, New York, NY; Norbert Brau, VA Medical Center, Bronx, NY; Sue Currie, Hui Shen, VA Medical Center, San Francisco, CA; Bhupinder Anand, VA Medical Center, Houston, TX; Ke-Qin Hu, VA Medical Center, Loma Linda, CA; Lennox Jeffers, VA Medical Center, Miami, FL; Samuel B Ho, VA Medical Center, Minneapolis, MN; David Johnson, VA Medical Center, Bay Pines, FL; Warren Schmidt, VA Medical Center, Iowa City, IA; Paul King, VA Medical Center, Columbia, MO; Ramsey Cheung, VA Medical Center, Palo Alto, CA; Timothy Morgan, VA Medical Center, Long Beach, CA; Joseph Awad, VA Medical Center, Nashville, TN; Marcos Pedrosa, VA Medical Center, Boston, MA; Kyong-Mi Chang, VA Medical Center, Philadelphia, PA; Ayse Aytaman, VA Medical Center, Brooklyn, NY; Fraiu Simon, VA Medical Center, Denver, CO; Curt Hagedorn, VA Medical Center, Atlanta, GA; Richard Moseley, VA Medical Center, Ann Arbor, MI; Jawad Ahmad, VA Medical Center, Pittsburgh, PA; Charles Mendenhall, VA Medical Center, Cincinnati, OH; Stephen Rossi, Teresa Wright, VA Medical Center, San Francisco, CA

4 604

PATIENTS IS STRONGLY RELATED WITH AGE: AN EUROPEAN COLLABORATIVE STUDY LUZ Martin-Carbonero, Javier Garcia-Samaniego, Hospital Carlos 111, Madrid, Spain; Yves Benhamou, HBpital La Pitie-SalpGtri&re, Paris, France; Miriam Romero, Hospital Carlos 111, Madrid, Spain; Massiino Puoti, Spedale Civile, Brescia, Italy; Josep Mallolas, Hospital Clinic, Barcelona, Spain; Juan Berenguer, Hospital General Universitario Gregorio MaraAdn, Madrid, Spain; Jiirgen Rockstroh, University Hospital Bonn, Bonn, Germany; Carmen Quereda, Hospital Ramdn y Cajal, Madrid, Spain; Victor Asensi, Hospital Central de Asturias, Oviedo, Spain; Ana Arizcorreta, Hospital Puerta del Mar, CAdiz, Spain; Martin Vogel, University Hospital Bonn, Bonn, Germany; Vicente Soriano, Hospital Carlos 111, Madrid, Spain

FIBROSIS PROGRESSION IN 914 HIV-HCV CO-INFECTED

# 605 VIRAL STEATOSIS IS NOT RELATED T O FIBROSIS SEVERITY IN PATIENTS WITH CHRONIC HEPATITIS C Christophe Hezode, Sami Boudabbous, Francoise Roudot- Thoraval, Elie-Serge Zafrani, Jean-Michel Pawlotsky, Daniel Dhumeaux, HBpital Henri Mondor, Creteil, France

# 606 IMPAIRED QUALITY OF LIFE IN PATIENTS WITH CHRONIC HEPATITIS C AND PERSISTENTLY NORMAL AMINOTRANSFERASE LEVELS Michael von Wagner, Universitatsklinikum des Saarlandes, Hoiiiburg/Saar, Germany; Jung-Hun Lee, Raphael Friedl, Johann Wolfgang C;oethe-UniversitBt, Frankfurt /Main, Germany; Bernd Kronenberger, Christoph Sarrazin, Stefan Zeuzem, Universitiitsklinikum des Saarlandes, Homburg /Saar, Germany

607 CYTOKINE GENE POLYMORPHISMS AND THE SUSCEPTIBILITY T O LIVER CIRRHOSIS IN PATIENTS WITH CHRONIC HEPATITIS C Matthias J Bahi, Mohamed El Menuawy, Klaus H W Boeker, Petra 8 Mu\holt, Michael P Manns, Ralf Lichtinghagen, Medizini~che Hochschule, Hannover, Germany

Hepatitis C: Pathogenesis II

# 608 REGULATION OF INTRACELLULAR HEPATITIS C VIRUS

Nobuhiko Kanazawa, Tokyo Medical and Dental University, Bunkyo-ku, Japan; Masayuki Kurosaki, Musasluno Red Cross Hospital, Musashino-shi, Japan; Naoya Sakamoto, Nobuyuki Enomoto, Tsuyoshi Yamashiro, Yoko Tanabe, Shinya Maekawa, Mina Nakagawa, Cheng-Hsin Chen, Mamoru Watanabe, Tokyo Medical and Dental University, Bunkyo-ku, Japan

REPLICATION BY INTERFERON REGULATORY FACTOR-1

# 609 ACTIVATED STAT3 INITIATES ANTIVIRAL ACTIVITY AGAINST HEPATITIS C VIRAL RNA REPLICATION Haizhen Zhu, Xiadhang Shang, Naohiro Terada, ; James M

Crawford, Chen Liu, University of Florida, Gainesville, FL

# 610 PATTERN RECOGNITION OF HCV CORE AND NS3 PROTEINS BY INNATE IMMUNE CELLS: ROLE FOR TLR2 BUT NOT FOR TLR4 Angela Dolganiuc, Karen Kodys, Andrea Kopasz, Shilpa Oak, Pranoti Mandrekar, Evelyn Kurt-Jones, Douglas Golenbock, Gyongyi Szabo, University of Massachusetts Medical School, Worcester, MA

# 611

APOPTOTIC RESPONSE IN HEPATOCYTES Aurelie Andre, Chantal Ethier, Marc Bilodeau, CHUM-HBpital Saint-Luc, Montreal, PQ, Canada

# 612 INSULIN RESISTANCE THROUGH DOWN REGULATION OF

PATIENTS WITH CHRONIC HEPATITIS C VIRUS INFECTION Takumi Kawaguchi, Masaru Harada, Takafumi Yoshida, Eitaro Taniguchi, Hiroto Kumemura, Shinichiro Hanada, Shinji Baba, Michiko Maeyama, Hironori Koga, Ryukichi Kumashiro, Takato Ueno, Kurume University School of Medicine, Kurume, Japan; Kyuichi Tanikawa, International Institute of Liver Research, Kurume, Japan; Michio Sata, Kurume University School of Medicine, Kurume, Japan

HCV INFECTION IS ASSOCIATED WITH A POTENT ANTI-

INSULIN RECEPTOR SUBSTRATE (1RS)-1 AND IRS-2 IN

B 613 DIFFERENTIAL INDUCTION OF EPITOPE-SPECIFIC IMMUNE RESPONSES BY HEPATITIS C VIRUS (HCV)-DERIVED LIPOPEPTIDES Bettina Renate Langhans, Susann Schweitzer, Hans Dieter Nischalke, Ingrid Braunschweiger, Tilman Sauerbruch, Ulrich Spengler, University of Bonn, Bonn, Germany

# 614 ASSOCIATION OF GENETIC VARIANTS OF THE

OF TREATMENT OF PERSISTANT HCV INFECTION Simon Hellier, Addenbrooke’s Hospital, Cambridge, UK; Angela J Frodsham, Branwen J Hennig, The Wellcome Trust Centre for Human Genetics, Oxford, UK; Suzanne Knapp, Mark Wright, Imperial College, London, UK; Lyna Zhang, The Wellcome Trust Centre for Human Genetics, Oxford, UK; Howard C Thomas, Mark Thursz, Imperial College, London, UK; Adrian V S Hill, The Wellcome Trust Centre for Human Genetics, Oxford, UK

# 615 HEPATITIS VIRUS C INFECTION UPREGULATES THE EXPRESSION OF TRANSFERRIN RECEPTOR 2 AT TRANSCRIPTIONAL LEVEL Masaki Takeo, Naoki Fujita, Jiro Ikoma, Hideaki Tanaka, Shinichiro Horiike, Motoh Iwasa, Masahiko Kaito, Yukihiko Adachi, Mie University School of Medicine, Tsu City, Mie, Japan

INTERFERON ALPHA RECEPTOR-2 GENE WITH OUTCOME

8 Denotes AASLD Presidential T’oster of Distinction


# 616 PERIPHERAL NATURAL KILLER (NK) CELLS ARE DEPLETED AND FUNCTIONALLY IMPAIRED IN CHRONIC HCV INFECTION Lucy M Golden-Mason, St. Vincent’s UniversityHospital, Dublin, Ireland; Hameda Asrafel, NU1 Maynooth, Maynooth, Ireland; Hugo Rosen, OHSU, Portland, OR; Laura Madrigal-Estebas, Derek G Doherty, NU1 Maynooth, Maynooth, Ireland; John Hegarty, Cliona OFarrelly Conway Institute, Dublin, Ireland

# 617 PROCREATION MEDICALLY ASSISTED (PMA) AND TRANSMISSION OF HEPATITIS C VIRUS (HCV): ABSENCE OF HCV RNA IN PURIFIED SPERM FRACTION IN HCV PATIENTS WITH PRESENCE OF VIRAL RNA IN SEMEN P Halfon, Alphabio Laboratory, Marseille, France; C Georgetti, V Chabert-Orsoni, J M Chincholle, IMR Marseille, Marseille, France; H Khiri, J M Feryn, Alphabio Laboratory, Marseille, France; P Terriou, IMR Marseille, Marseille, France; L Cravello, Hopital de la Conception, Marseille, France; F Franquebalme, R Roulier, IMR Marseille, Marseille, France; M Bourliere, HBpital Saint Joseph, Marseille, France

# 618 INTRODUCTION OF NS5A MUTATIONS ENABLES SUBGENOMIC HCV-REPLICON DERIVED FROM CHIMPANZEE-INFECTIOUS HC-J4 ISOLATE TO REPLICATE EFFICIENTLY IN HUH-7 CELLS Shinya Maekawa, Nobuyuki Enomoto, Naoya Sakamoto, Masayuki Kurosaki, Eri Ueda, Takahiro Kohashi, Hideki Watanabe, Cheng-Hsin Chen, Tsuyoshi Yamashiro, Yoko Tanabe, Nobuhiko Kanazawa, Mina Nakagawa, Mamoru Watanabe, Tokyo Medical and Dental University, Tokyo, Japan

# 619 SERIAL PHENOTYPIC PROFILING OF INTRAHEPATIC LYMPHOCYTES IN PATIENTS WITH CHRONIC HEPATITIS C

AND RIBAVIRIN THERAPY Satoshi Yamagiwa, Niigata University, Niigata, Japan; Takafumi Ichida, Niigata University Hospital, Niigata, Japan; Shogo Okoshi, Xiu Hua Yang, Yuiko Ishimoto, Takuya Genda, Yasunobu Matsuda, Toru Abo, Yutaka Aoyagi, Niigata University, Niigata, Japan; Hisami Watanabe, University of the Ryukyus, Naha, Japan

# 620 CORRELATION BETWEEN TRANSLATION EFFICIENCY AND OUTCOME OF COMBINATION THERAPY IN CHRONIC HEPATITIS C GENOTYPE 3 PATIENTS Anila Yasmeen, Saeed S Hamid, The Aga Khan University, Karachi, Pakistan; Fredrik N Granath, Hannah Lindstrom, Karolinska Institute, Stockholm, Sweden; Richard M Elliot, University of Glasgow, Glasgow, UK; Anwar A Siddiqui, The Aga Khan University, Karachi, Pakistan; Mats A A Persson, Karolinska Institute, Stockholm, Sweden

BEFORE AND AFTER COMBINATION INTERFERON a-2B

# 621

PERIPHERAL BLOOD MONONUCLEAR CELLS IN RESPONSE

Susan Behan, Vincent Leroy, Margaret OBrien, Conor OBrien, John Hegarty, Cliona OFarrelly, St. Vincent’s University Hospital, Dublin, Ireland

INTERFERON-ALPHA INDUCIBLE GENE EXPRESSION IN

TO STIMULATION WITH INTERFERON-ALPHA

# 622 INTRA-HEPATIC CD8 T-CELL RESPONSES TOWARDS HCV IN SUBJECTS CO-INFECTED WITH HEPATITIS C VIRUS (HCV) AND HUMAN IMMUNODEFICIENCY VIRUS (HIV)

Nadia Alatrakchi, Camilla Graham, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA; Kenneth E Sherman, University of Cincinnati, Cincinnati, OH; Margaret J Koziel, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA

BEFORE THE ANTI-HCV TREATMENT

# 623 HEPATITIS C VIRUS (HCV) ISOLATES INTERACT WITH

Jason P Gardner, Robert J Durso, Robert R Arrigale, Gerald P Donovan, Paul J Maddon, Progenics Pharmaceuticals, Inc., Tarrytown, NY; Tatjana Dragic, Albert Einstein College of Medecine, Bronx, NY; William C Olson, Progenics Pharmaceuticals, Inc., Tarrytown, NY

# 624 CULTURE AND IMMORTALIZATION OF HEPATITIS C VIRAL POSITIVE HUMAN HEPATOCYTES Chen Liu, University of Florida, Gainesville, FL

L-SIGN, A LIVER-SPECIFIC CAPTURE RECEPTOR

# 625 PERIPHERAL BLOOD AND INTRAHEPATIC CD4/CD8 DOUBLE POSITIVE CELLS IN HEPATITIS C VIRUS INFECTION Michelina Nascimbeni, Eui-Cheol Shin, National Institutes of Health, Bethesda, MD; Luis Chiriboga, New York University School of Medicine, New York, NY; David E Kleiner, Barbara Rehermann, National Institutes of Health, Bethesda, MD

# 626 CD4+ CD25+ REGULATORY T LYMPHOCYTES RESPOND DIRECTLY TO HCVANTIGENSVIA CYTOKINE RELEASE AND

Roniel Cabrera, Zhengkun Tu, Roberto J Firpi, Yiling Xu, David R Nelson, Section of Hepatobiliary Diseases, University of Florida, Gainesville, FL

SUPPRESS HCV-SPECIFIC T CELL RESPONSES

# 627 INVOLVEMENT OF CD4+CD25+ REGULATORY T CELLS AS IMMUNE MODULATORS IN CHRONIC HEPATITIS C VIRUS (HCV) INFECTION Akihiko Okumura, Tetsuya Ishikawa, Taeko Yamauchi, Tadashi Maeno, Ken Sato, Minoru Ayada, Naoki Hotta, Tsuneaki Tagaya,

University School of Medicine, Aichi-ken, Japan

THE ROLE OF REGULATORY T CELLS IN HCV PERSISTENCE Fusao Ikeda, Kazushi Sugimoto, David Kaplan, Jason Stadanlick, Mary Valiga, Jin Ding, Kyong-Mi Chang, University of Pennsylvania, Philadelphia, PA

# 629

CO-INFECTED PERSONS INITIATING ANTIRETROVIRAL THERAPY Jason T Blackard, Massachusetts General Hospital, Boston, MA

0

Yoshitaka Fukuzawa, Shinichi Kakumu, Aichi Medical :! $6 # 628 z?

HEPATITIS C VIRUS (HCV) DIVERSITY IN HIV-HCV


2 630 HEPATOCYTE PROLIFERATION IN HEPATITIS C: CORRELATION WITH DEGREE OF LIVER INJURY AND

P Wilfred0 Canchis, L.ydia Petrovic, Furqaan Ahmed, Jennifer Davila, Weill Medical College of Cornell University, New York, NY; M Isabel Fiel, Mount Sinai School of Medicine, New York, NY; Sang Kim, Alex Teixeira, New York Hospital Medical Center of Queens, Queens, NY; Luis Chiriboga, Herman Yee, Bellevue Hospital Medical Center, New York, NY; Brian R Edlin, Andrew M Talal, Ira M Jacobson, Weill Medical College of Cornell University, New York, NY

T 631

BY HEPATITIS C VIRUS CORE PROTEIN Roiiiy Zemel, Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Petach-Tikva, Israel; Nir Barak, Rabin Medical Center, Petah-Tikva, Israel; Larisa Bachmatove, Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Petach-Tikva, Israel; Rafit Drori, Molecular Hepatology Lab., Felsenstein Medical Research Center, Sackler Faculty of Medicine, Tel-Aviv University, Petach-Tikva, Israel; Yaron Rotman, Ran Tur-Kaspa, Rabin Medical Center, Petah-Tikva, Israel

SERUM ALPHA-FETOPROTEIN

AUGMENTATION OF PPAR-ALPHA EXPRESSION INDUCED

632 HEPATITIS C VIRUS INFECTION IN A JUVENILE PRISON: HIGH PREVALENCE OF HCV AMONG IMMIGRANTS FROM THE FORMER SOVIET UNION TO GERMANY Manuela F Meyer, Heiner Wedemeyer, Medizinische Hochschule, Hannover, Germany; Johannes Dreesman, Niedersachsisches Landesgesundheitsamt, Hannover, Germany; Michael P Manns, Medizinische Hochschule, Hannover, Germany; Armin Baillot, Niedersachsisches Landesgesundheitsamt, Hannover, Germany; Marc Lehmann, Jugendanstalt Hameln, Hameln, Germany

P 633 ENHANCED EXPRESSION OF CD94/NKG2A ON CD8+ T

Jacob Nattermann, Hans Dieter Nischalke, Georg Feldmann, Tilman Sauerbruch, Lrlrich Spengler, University of Bonn, Bonn, Germany

LYMPHOCYTES FROM HCV-POSITIVE PATIENTS

r: 634

GENE IN HCV INFECTION Jacob Nattermann, Golo Ahlenstiel, Georg Feldmann, Hans Dieter Nischalke, Martin Vogel, University of Bonn, Bonn, Germany; Thomas Berg, Humboldt-University, Berlin, Germany; Jurgen Rockstroh, Rainer Woitas, Tilman Sauerbruch, Ulrich Spengler, University of Bonn, BOM, Germany

THE TANDEM-REPEAT POLYMORPHISM OF THE DC-SIGNR

f 635 CD4+CD25+ T-REGULATORY LYMPHOCYTES CONTROL EXPANSION OF HEPATITIS VIRUS SPECIFIC CD8+ T CELLS Simon M Rushbrook, Cambridge University, Cambridge, UK; Scott Ward, Nuffield Department of Medicine, Oxford, UK; Esther Unitt, Cambridge University, Cambridge, UK; Paul Klenerman, Oxford University, Oxford, UK; Graeme J M Alemndcr, Cambriclgc University, Cambridge, UK

# 636 HOST IMMUNE RESPONSES DO NOT CORRELATE WITH HISTOLOGIC INJURY: BASELINE ANALYSIS OF THE HALT-C TRIAL IN ADVANCED HEPATITIS C DISEASE Alan L Rothman, University of Massachusetts Medical School, Worcester, MA; Chihiro Morishima, University of Washington, Seattle, WA; Ranjit Ray, Sant Louis University, St. Louis, MO; Ming Chang, University of Washington, Seattle, WA; Herbert L Bonkovsky, University of Connecticut Health Center, Farmington, CT; Adrian Di Bisceglie, Sant Louis University, St. Louis, MO; William M Lee, University of Texas Southwestern Medical Center, Dallas, TX; Karen L Lindsay, University of Southern California, Los Angeles, CA; David R Gretch, Daniel G Sullivan, Steve J Polyak, University of Washington, Seattle, WA; Elizabeth C Wright, New England Research Institute, Watertown, MA; Margaret J Koziel, Beth Israel Deaconess Medical Center, Boston, MA

# 637

OF CHRONIC LIVER DISEASE FROM HEPATITIS TO CANCER Marina Bortolami, Harry Waldner, Carla Venturi, Romilda Cardin, Chiara Carlotto, Remo Naccarato, Fabio Farinati, University of Padua, Padua, Italy

FASlFASL SYSTEM AND IL-lP IN THE NATURAL HISTORY

~ ~~

i7 638 ANALYSIS OF THE INVOLVEMENT OF PKR PROTEIN IN RESISTANCE TO THERAPY FOR CHRONIC HEPATITIS C VIRUS INFECTION Gerry C MacQuillan, University Hospital Birmingham, Birmingham, UK; Paul Caterina, W Bastiaan de Boer, Michael Platten, Pathcentre, Nedlands, Australia; William D Reed, Hollywood Private Hospital, Nedlands, Australia; Gary P Jeffrey, University of Western Australia / Sir Charles Gairdner Hospital, Nedlands, Australia

# 639 THE HCV CORE AG/ HCV RNA RATIO PREDICTS THE COURSE OF HCV REPLICATION IN TREATED AN UNTREATED LIVER TRANSPLANTED PATIENTS Cyrille Feray, Paul Brousse Hospital, Villejuif, France; Pascale Berthillon, Hotel-Dieu Hospital, Lyon, France; Delphine Ducoulombier, Paul Brousse Hospital, Villejuif, France; Marianne Maynard, Liana Codes, Hotel-Dieu Hospital, Lyon, France; Michelle Gigou, Paul Brousse Hospital, Villejuif, France; Thierry Bizollon, Hotel-Dieu Hospital, Lyon, France; Didier Samuel, Paul Brousse Hospital, Villejuif, France; Christian Trepo, Hotel-Dieu Hospital, Lyon, France

# 640 HCV ALTERNATE READING FRAME PROTEINS (ARFPS) MAY BE VIRULENCE FACTORS THAT HELP THE VIRUS SURVIVE ADVERSE CONDITIONS Andrea D Branch, J L Walewski, J A Gutierrez, E J Fernandez, G Y Im, D T Dieterich, T D Schiano, S H Sigal, M L Schilsky, M E Schwartz, Mount Sinai School of Medicine, New York, NY; C R Kyrk, A S Muerhoff, T P Leary, J A Stewart, G J Dawson, S M Desai, Abbott Laboratories, Abbott Park, IL

~~

# 641 EFFICIENT REPLICATION OF HEPATITIS C VIRUS GENOTYPE 2A SUBGENOMIC REPLICON ISOLATED FROM FULMINANT HEPATITIS PATIENTS Takanobu Kato, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan, Tomoko Date, Michiko Miyamoto, Takaji Waluta, Tokyo Metropolitan Institute for Neuroscience, Tokyo, Japan


# 642 OUTBREAK OF HEPATITIS C VIRUS INFECTION THROUGH

TRACING THE SOURCE BY MOLECULAR EVOLUTIONARY ANALYSIS Izumi Hasegawa, Yasuhito Tanaka, Takanobu Kato, Etsuro Orito, Tomoyoshi Ohno, Ryuzo Ueda, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Yuzo Miyakawa, Miyakawa Memorial Resarch Foundation, Tokyo, Japan; Shiro Iino, Saint Marianna University School of Medicine, Kawasaki-shi, Japan; Masashi Mizokami, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

# 643 HEPATIC GENE EXPRESSIONS ASSOCIATED WITH FIBROSIS PROGRESSION AND HEPATOCARCINOGENESIS IN HEPATITIS C Run-Xuan Shao, Yujin Hoshida, Motoyuki Otsuka, Naoya Kato, Hiroyoshi Taniguchi, Masaru Moriyama, Ryosuke Tateishi, Shuntaro Obi, Shuichiro Shiina, Takao Kawabe, Masao Omata, University of Tokyo, Tokyo, Japan

CONTAMINATED FIBRINOGEN CONCENTRATES IN JAPAN-

# 644 PSEUDOTYPE HEPATITIS C VIRUS INFECTS IMMATURE MYELOID DENDRITIC CELLS THROUGH THE INTERACTION WITH LECTIN Aki Sato, Tatsuya Kanto, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Chang K Limn, Yasumasa Komoda, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan; Chika Oki, Michiyo Inoue, Hideki Miyatake, Mitsuru Sakakibara, Takayuki Yakushijin, Tetsuo Takehara, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Yoshiharu Matsuura, Research Institute for Microbial Diseases, Osaka University Osaka, Japan; Norio Hayashi, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

# 645 GENE EXPRESSION PROFILE OF T CELL-SPECIFIC CHEMOKINES IN HEPATITIS C VIRUS-TRANSFECTED HUMAN HEPATOCYTE-DERIVED CELL LINES Arantxa Apolinario, Pedro L Majano, Raquel Lorente, Hospital Universitario Santa Cristina, Madrid, Spain; Gerard0 Clemente, Hospital Universitario Gregorio Maraiion, Madrid, Spain; Carmelo Garcia-Monzon, Hospital Universitario Santa Cristina, Madrid, Spain

# 646 ANALYSIS OF PERMISSIVE CELL LINES FOR HCV REPLICON Cheng-Hsin Chen, Nobuyuki Enomoto, Shinya Maekawa, Yoko Tanabe, Nobuhiko Kanazawa, Mina Nakagawa, Tsuyoshi Yamashiro, Naoya Sakamoto, Masayuki Kurosaki, Mamoru Watanabe, Tokyo Medical and Dental University, Tokyo, Japan

# 647 HEPATITIS C VIRUS CORE PROTEIN INDUCES INTRACELLULAR LIPID ACCUMULATION IN HELA CELLS

Kui Li, University of Texas Medical Branch, Galveston, TX; John McLauchlan, University of Glasgow, Glasgow, UK; Stanley M Lemon, University of Texas Medical Branch, Galveston, TX

# 648 CELL CYCLE ARREST IN CHRONIC HEPATITIS C VIRUS INFECTION LEADS TO APOPTOSIS: A CYTOPATHIC MECHANISM FOR HCV INDUCED LIVER DAMAGE? Saeed S Hamid, Saira Sarfraz, Snawar Hussain, Shahid Parvez, Anwar A Siddiqui, The Aga Khan University, Karachi, Pakistan

VIA AN MTP-INDEPENDENT PATHWAY

# 649 SERUM COMPARTMENTALIZATION OF HEPATITS C VIRUS (HCV) QUASISPECIES Michael G Hughes Jr, Tae W Chong, Robert L Smith 11, Heather L Evans, Jeremy R Camden, Robert G Sawyer, Christine K Rudy Timothy L Pruett, University of Virginia, Charlottesville, VA

Hepatobiliary Surgery: Clinical and Experimental

8 # 6 5 0

HEPATIC ISCHEMIA REPERFUSION INJURY Narci C Teoh, Jacqueline Field, Geoffrey C Farrell, Westmead Millennium Institute, Sydney, Australia

# 651 CHARACTERIZATION OF THE MOLECULAR MACHINES INVOLVED IN ACTIN REMODELLING UPON ISCHEMIA AND REPERFUSION IN HUMAN LIVER Anouk Emadali, Tarek Boutros, Beatrice Muscatelli-Groux, Georges Tzimas, Sarah Jenna, Caroline Rochon, Duc Thang Nguyen, Marie-Elaine Caruso, Eric Chevet, Peter Metrakos, McGill University, Montreal, P Q Canada

INTERLEUKIN-6 MEDIATES PRECONDITIONING IN

# 652 REMOTE ISCHAEMIC PRECONDITIONING OF THE HIND LIMB IMPROVES SYSTEMIC HAEMODYNAMICS AND REDUCES REPERFUSION INJURY TO THE LIVER AND LUNGS Sanjeev Kanoria, Royal Free Hospital, London, UK; Rajiv Jalan, University College London, London, UK; Alex Seifalian, Royal Free Hospital, London, UK; Roger Williams, University College London, London, UK; Brian Davidson, Royal Free Hospital, London, UK

# 653 RELATIONSHIP AMONG COMPLEMENT ACTIVATION, SUPEROXIDE GENERATION AND CYTOKINE EXPRESSION

Ian N Hines, Hirohisa Harada, Matthew B Grisham, LSU Health Sciences Center, Shreveport, LA

# 654 DIFFERENT PATHOPHYSIOLOGICAL MECHANISMS OF

DURATION OF ISCHEMIA Ian N Hines, Sulaiman Bharwani, Laura Gray, Matthew B Grisham, LSU Health Sciences Center, Shreveport, LA

IN POST-ISCHEMIC LIVER INJURY

POST-ISCHEMIC LIVER INJURY DEPENDING UPON

# 655 RECOVERY OF ENERGY STORES AND MITOCHONDRIAL FUNCTION OF HYPOTHERMIC MACHINE PERFUSION

Charles Y Lee, Heather M Duncan, Shailendra Jain, Jian X Zhang, University of North Carolina at Charlotte, Charlotte, NC; Jon W Jones Jr, Carolinas Medical Center, Charlotte, NC; James H Southard, University of Wisconsin Medical School, Madison, WI; Mark G Clemens, University of North Carolina at Charlotte, Charlotte, NC

PRESERVED NON-HEART-BEATING DONOR RAT LIVERS

# 656 LOCAL HEMODYNAMIC IMPAIRMENT AND ASSOCIATED POOR FUNCTION OF SMALL LIVER GRAFTS TRANSPLANTED INTO ANIMALS WITH FULMINANT HEPATIC FAILURE Vassilios Smyrniotis, Nikolaos Arkadopoulos, Georgia Kostopanagiotou, Ioannis Tierris, Kassianh Theodoraki, John Kontis, John Vassiliou, Panagiotis Dimakakos, University of Athens Medical School, Athens, Greece

I W A POSTER SESSIONS HEPATOLOGY, October 2003

X 657 GLUTATHIONE TREATMENT INCREASES THE TOLERANCE

THE RAT Thomas Priifer, Rolf Schauer, Alexander Gerbes, Manfred Bilzer, Klinikum GroRhadern, LMU Munich, Munich, Germany

B 658

LIVER GRAFTS IS ASSOCIATED WITH INHIBITION OF CYCLIN D1 EXPRESSION: REVERSAL BY PLANT POLYPHENOLS Zhi Zhong, Robert F Schwabe, Matthias Froh, Liu Yang, David A Brenner, Hartwig Bunzendahl, John J LeMasters, University of North Carolincj, Chapel Hill, NC

# 659

APOPTOSIS FOLLOWING COLD PRESERVATION INVOLVES BAX TRANSLOCATION Christopher D Anderson, Janene Pierce, Andrey Belous, Ian B Nicoud, Clayton Knox, Aya Wakata, Charles W Pinson, Ravi S Chari, Vanderbilt University Medical Center, Nashville, TN

OF FATTY LIVER T O ISCHEMIA-REPERFUSION INJURY IN

SUPRESSION OF REGENERATION IN SMALL-FOR-SIZE

MITOCHONDRIAL CALCIUM OVERLOAD-ASSOCIATED

8 660 INTERMITTENT CLAMPING AND ISCHEMIC PRECONDITIONING IMPROVE LIVER MICROCIRCULATION

PROTECTION Katharina Vajdova, Stefan Heinrich, Yinhua Tian, Rolf Graf, Pierre-Alain Clavien, University Hospital of Zurich, Zurich, Switzerland

ft 661 ISCHEMIC PRECONDITIONING PROMOTES LIVER REGENERATION AFTER PARTIAL HEPATECTOMY BY STIMULATION OF ADENOSINE A2 RECEPTOR PATHWAY Masahiro Arai, Kazuaki Tejima, Hitoshi Ikeda, Tonioaki Tomiya, Mikio Yanase, Yukiko [noue, Kayo Nagashima, Masao Oniata, University of Tokyo, Tokyo, Japan; Kenji Fujiwara, Saitama Medical School, Saitama, Japan

u‘ 662 TPEN ATTENUATES HEPATIC ISCHEMIA/REPERFUSION INJURY AND REMOTE CARDIAC DYSFUNCTION IN ISOLATED RAT LIVER Ziv Ben-Ari, Rahin Medical Center, Petah-Tikva, Israel; Bernardo Vidne, Felsenstein Medical Research Center, Petacli-Tikva, Israel; Orit Pappo, Rabin Medical Center, Petah-Tikva, Israel; Edit Hochhauser, Felsenstein Medical Research Center, Petach-Tikva, Israel

AND KUPFFER CELL FUNCTION- A NOVEL PATHWAY OF

H 663 5-AMINOISOQUINOLINONE, A NOVEL INHIBITOR OF POLY(ADPRIB0SE)POLYMERASE: IMPACT O N MICRO- VASCULAR INJURY AND SURVIVAL AFTER HEPATIC

Andrel Khandoga, Gcorg Ender5, Peter Biberthaler, Fritz Kiombach, Uni \ eryity of Munich, Mumch, Germany

c* 664 PERFUSION OF ISOLATED RAT LIVERS WITH RED BLOOD

APOPTOSIS OF SINUSOIDAL ENDOTHELIAL CELLS (SECS) Pierre-Michel Huet, Marie-Pierre Bralet, Makeda Seniret, Antoine Brault, Centre de Recherche-Centre Hospitaher de I’Umversite de Montreal-H6pital 5alnt-Luc, Montreal, PQ, Canada

ISCHEMIA-REPERFUSION

CELL (RBC)-FREE PERFUSATE RAPIDLY LEADS T O

8 Denotes AASLD Preside11 tial Poster of Distinction

8 # 665

LAPAROSCOPIC CHOLECYSTECTOMY BILE DUCT INJURIES Vijayaragavan Muralidharan, Michael Silva, Simon R Bramhall, David Mayer, John A C Buckels, Paul McMaster, Darius F Mirza, University Hospital Birmingham, Birmingham, UK

EARLY BILIARY RECONSTRUCTION FOR POST-

# 666 ISCHEMIC PRECONDITIONING ATTENUATES LIVER INJURY DURING HEPATECTOMIES PERFORMED UNDER SELECTIVE VASCULAR EXCLUSION Nikolaos Arkadopoulos, Vassilios Smymiotis, John Kontis, Georgia Kostopanagiotou, Kassianh Theodoraki, John Vassiliou, Agathi Pafith, Panagiotis Dimakakos, University of Athens Medical School, Athens, Greece

# 667 RECOMBINANT FACTOR VIIA (RFVIIA) AS A SAFE AND EFFECTIVE THERAPEUTIC OPTION FOR THE CORRECTION OF MODERATE TO SEVERE HEPATIC COAGULOPATHY Mohammad A Wehbi, Kamil Obideen, Enrique Martinez, Alexander Duncan, Emory University School of Medicine, Atlanta, GA

# 668 MOBILIZED BONE MARROW CELLS CONTRIBUTE TO SINUSOIDAL ENDOTHELIAL STRUCTURING OF THE REGENERATING LIVER AFTER PARTIAL HEPATECTOMY IN MICE Satoshi Ogata, Yonson Ku, Takumi Fukumoto, Masahro Tominaga, Takeshi Iwasaki, Masahiro Kido, Masanori Takahashi, Yoslukazu Kuroda, Kobe University Graduate School of Medicine, Kobe, Japan

# 669 SURGICAL INTERVENTION OUTCOMES IN FICl (ATP8B1) AND BSEP (ABCBl1) DISEASE Ludmilla Pawlikowska, UCSF, San Francisco, CA; Sandra S Strautnieks, Institute of Liver Studies, King’s College Hospital, London, UK; Piotr Czubkowski, Children’s Memorial Hospital, Warsaw, Poland; Anthony Antoniou, Jane Byme, Institute of Liver Studies, King’s College Hospital, London, UK; Billy Bourke, University College, Dublin, UK; Sami Wali, Riyadh Armed Forces Hospital, Riyadh, Saudi Arabia; Ben Shneider, Mount Sinai Medical Center, New York, NY; S Lobritto, Columbia-Presbyterian Medical Center, New York, NY; Im Nielsen, University Institute of Medical Biochemistry and Genetics, Copenhagen, Denmark; S Blanchard, Rainbow Babies and Children’s Hospital, Cleveland, OH; Patricia McClean, St. James’s University Hospital, Leeds, UK; H Sharp, University of Minnesota, Minneapolis, MN; Phil Rosenthal, The Children’s Hospital of Philadelphia, Philadelphia, PA; Emmanuel Jacquemin, Michelle Hadchouel, HBpital Bicetre, Paris, France; Giorgina Mieli-Vergani, Institute of Liver Studies, King’s College Hospital, London, UK; Antal Nemeth, Bjohn Fischler, Uppsala University Children’s Hospital, Uppsala, Sweden; Peter Whitington, Children’s Memorial Hospital, Chicago, IL; Alex Knisely, Institute of Liver Studies, King’s College Hospital, London, UK; Irene Jankowska, Joanna Pawlowska, Children’s Memorial Hospital, Warsaw, Poland; Laura Bull, UCSF, San Francisco, CA; Richard J Thompson, Institute o f Liver Studies, King’s College Hospital, London, UK

P 670 EFFECT OF PORTAL HEMODYNAMICS ON LIVER REGENERATION, STUDIED IN A NOVEL PORTOHEPATIC SHUNT RAT MODEL Shigeru Marubashi, Masato Sakon, Hiroaki Nagano, Atsushi Miyanioto, Keizo Dono, Shoji Nakamori, Koji Umeshita, Morito Monden, Osaka University Graduate School of Medicine, Suita, Osaka, Japan


Liver Immunobiology: Autoimmune Liver and Biliary Tract Disease

8 #671 HOW IS THE LOSS OF TOLERANCE TO MITOCHONDRIAL AUTOANTIGENS SUSTAINED IN PRIMARY BILIARY CIRRHOSIS? Shinji Shimoda, Takashi Kamihira, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan; Hiromi Ishibashi, Minoru Nakamura, Nagasaki Medical Center, Nagasaki, Japan; M Eric Gershwin, University of California Davis, Davis, CA

# 672 ESTABLISHMENT OF A NOVEL MOUSE MODEL FOR AIH TYPE 2 Akihiko Okumura, Tetsuya Ishikawa, Ken Sato, Minoru Ayada, Tadashi Maeno, Naoki Hotta, Tsuneaki Tagaya, Yoshitaka Fukuzawa, Shinichi Kakumu, Aichi Medical University School of Medicine, Aichi-ken, Japan

# 673 THE NEWLY CHARACTERIZED CD4+CD25+ REGULATORY T CELLS ARE DEFECTIVE IN AUTOIMMUNE HEPATITIS Maria Serena Longhi, Yun Ma, Giorgina Mieli-Vergani, Diego Vergani, King’s College Hospital, London, UK

# 674 EXAMINATION OF AUTOANTIBODY PROFILES IN A NOVEL CONGENIC MOUSE STRAIN WITH BILIARY TRACT DISEASE, THE NOD.IDD3/10/17/18/9 MOUSE David A Sass, Syuichi Koarada, Yue Hong Wu, Noreen Fertig, Michael Nalesnik, University of Pittsburgh Medical Center, Pittsburgh, PA; John A Todd, Paul A Lyons, Cambridge University Cambridge, UK; Judith Fenyk-Melody, Linda S Wicker, Laurence B Peterson, Merck Research Laboratories, Rahway, NJ; William M Ridgway, University of Pittsburgh Medical Center, Pittsburgh, PA

# 675 AUTOIMMUNE HEPATITIS AND PREGNANCY COURSE OF DISEASE AND OUTCOME OF PREGNANCIES Christoph Schramm, Stephan Kanzler, University of Mainz, Maim, Germany; Hans Weidenbach, University of Ulm, Ulm, Germany; Peter R Galle, Ansgar W Lohse, University of Mainz, Maim, Germany

# 676 DIAGNOSING AUTOIMMUNE HEPATITIS IN CHILDREN: IS THE INTERNATIONAL AUTOIMMUNE HEPATITIS GROUP SCORING SYSTEM USEFUL? Regan L Ebbeson, Richard A Schreiber, University of British Columbia, BC Children’s Hospital, Vancouver, BC, Canada

# 677 ASSOCIATION OF FIBROSIS WITH INFLAMMATORY ACTIVITY IN AUTOIMMUNE HEPATITIS: REVERSAL DURING CORTICOSTEROID THERAPY Albert J Czaja, Herschel A Carpenter, Mayo Clinic, Rochester, MN

# 678 AUTOIMMUNE HEPATITIS IN THE AFRICAN AMERICAN POPULATION Enrique A Valdivia, Henry Ford Hospital, Detroit, MI; Julia Greer, Wayne State University School of Medicine, Detroit, MI; Ivan P Cubas, Henry Ford Hospital, Detroit, MI; Milt Mutchnick, Wayne State University School of Medicine, Detroit, MI; Kimberly Brown, Dilip Moonka, Henry Ford Hospital, Detroit, MI

# 679 IDENTIFICATION OF LIVER CYTOSOLIC PROTEINS

(MAA) ADDUCTED LIVER CYTOSOL INDUCED AUTOIMMUNE HEPATITIS Geoffrey M Thiele, Thomas L Freeman, University of Nebraska Medical Center, Omaha, NE; Monte S Willis, University of Texas Southwestern Medical Center, Dallas, TX; Carlos D Hunter, University of Nebraska Medical Center, Omaha, NE; Dean J Tuma, Lynell W Klassen, Veterans Administration Medical Center, Omaha, NE

# 680 THE IMMUNOLOGICAL MECHANISM OF LIVER INJURY INDUCED BY IMMUNIZATION OF MICE WITH DENDRITIC CELLS LOADED WITH WELL DIFFERENTIATED HEPATOMA

Shigeo Tamaki, Hiroki Takahashi, Sadamu Honma, Mikio Zeniya, Gotaro Toda, Jikei University School of Medicine, Tokyo, Japan

ASSOCIATED WITH MALONDIALDEHYDE-ACETALDEHYDE

CELLS AND FOLLOWING IL-12 ADMINISTRATION

# 681 IDENTIFICATION OF NEW AUTOANTIBODY IN PATIENTS WITH CHRONIC HEPATITIS Yasunobu Fukuda, Hiroshi Yotsuyanagi, Michihiro Suzuki, Fumio Itoh, St. Marianna University Kawasaki, Japan; Kusuki Nishioka, Tomohiro Kato, Institute of Medical Science, St. Marianna University, Kawasaki, Japan ~~

# 682 UTILITY OF THIOPURINE METHYLTRANSFERASE GENOTYPING AND PHENOTYPING AND MEASUREMENT

OF AUTOIMMUNE HEPATITIS Michael A Heneghan, Michael L Allan, Jeffrey D Bomstein, Andrew J Muir, David A Tendler, Duke University Medical Center, Durham, NC

OF 6-THIOGUANINE METABOLITES IN THE MANAGEMENT

# 683 MYCOPHENOLATE MOFETIL IMPROVES LIVER TESTS IN PATIENTS WITH AUTOIMMUNE HEPATITIS (AIH) Atoya Adams, Robert Gish, Ed Wakil, Natalie Bzowej, Ed Doo, Maurizio Bonacini, California Pacific Medical Center, San Francisco, CA

# 684

PROGNOSIS OF AUTOIMMUNE HEPATITIS (AIH) / PRIMARY SCLEROSING CHOLANGITIS (PSC) OVERLAP-SYNDROME 3 Stefan Luth, Stephan Kanzler, Anna Vieth, University Hospital of Mainz, Mainz, Germany; Hans P Dienes, University Hospital of Cologne, Mainz, Germany; Peter R Galle, Ansgar W Lohse,

0 CLINICAL CHARACTERISTICS AND LONG-TERM

University Hospital of Mainz, Mainz, Germany Q,

# 685 ADOPTIVE TRANSFER OF NKT CELLS ALLEVIATES GRAFT VERSUS HOST DISEASE AND IMPROVES SURVIVAL IN A

TRANSPLANTATION: THE ROLE OF THE LIVER IN TOLERANCE INDUCTION Maya Margalit, Hadassah Hebrew University Medical Center, Jerusalem, Israel; Amon Nagler, Chaim Sheba Medical Center, Tel Hashomer, Israel; Meir Ohana, Rifat Safadi, Ruslana Alper, Yoav Sherman, Victoria Doviner, Hadassah Hebrew University Medical Center, Jerusalem, Israel; Elazar Rabbani, Dean L Engelhardt, Enzo Biochem Inc., Framingdale, NY; Yaron Ilan, Hadassah Hebrew University Medical Center, Jerusalem, Israel

MURINE MODEL OF SEMI-ALLOGENEIC BONE MARROW

I10A POSTER SESSIONS HEPATOLOGY, October 2003

# 686 MEMBRANE OVALBUMIN MODEL OF LIVER INFLAMMATION DEMONSTRATES AN EARLY ROBUST CYTOTOXIC T CELL RESPONSE James Buxbaum, UCSF, San Francisco, CA, Paul M Allen, Washington University School of Medicine, St Louis, MO, Marion C Peters UCSF, San Franciwo, CA

687 FUNCTIONAL POLARIZATION OF LYMPHOCYTES TARGETS THE HEPATOBILIARY SYSTEM IN A MURINE MODEL OF BILIARY ATRESIA Pranavkuniar Shivakumar, Gregg Sabla, Monica McNeal, Richard Ward, Jorge A Bezerra, Children’s Hospital Medical Center, Cincinnati, OH

# 688

AND LYMPHOID (CD123+) DENDRITIC CELLS AND THEIR ROLES IN AUTOIMMUNE LIVER DISEASES AND LIVER VIRAL HEPATITIS Zhengbin Lu, Sean Albei, Audra Ziegeiifuss, Donna B Stolz, Simon Watkins, Lma Lu, Anthony J Demetris, University of Pitt+urgh Medical Center, Pltt5burgh, PA

IDENTIFICATION OF HUMAN LIVER MYELOID (CDllC+)

~~

2 689 THE VALIDITY OF A POLYMERASE CHAIN REACTION ASSAYIN THE DETECTION OF MYCOBACTERIUM TUBERCULOSISIN LIVER BIOPSY SPECIMENS OF CHILDREN Josie Grace V Causing, University of the Philippines, Manila, Philippines; Liezel Cornista, Filipinas Natividad, St. Luke‘s Medical Center, Quezon City, Philippines; Germana V Gregorio, University of the Philippines, Manila, Philippines

$690 INTERLEUKIN-1J3 INDUCES MACROPHAGE INFLAMMATORY PROTEIN-1O EXPRESSION IN HUMAN HEPATOCYTES Ting Zhang, Chang J Guo, Yuan Li, Steven D Douglas, Xiao-Xue Qi, Li Song, Wen Z Ho, The Children’s Hospital of Philadelphia, Philadelphia, PA

2 691 IMMUNOLOGICAL AND PATHOLOGICAL FEATURES OF TRANSGENIC MICE EXPRESSING OSTEOPONTIN IN HEPATOCYTES: A POSSIBLE MODEL OF AUTOIMMUNE HEPATITIS Sumie Mirnura, Satoshi Mochida, HeaSaeng Koh, Eiko Saitoh, Mie Inao, Kayoko Nailu, Atsushi Matsiii, Sumiko Nagoshi, Akihiko Ohno, Third Department of Internal Medicine, Saitama Medical School, Sai tama, Japan; Shuichi Kayano, Saitaina Medical School, Saitama, Japan; Takayuki Yoshimoto, Intractable Disease Research Center, Tokyo Medical University, Tokyo, Japan; Kenji Fujiwara, Third Department of Internal Medicine, Saitama Medical School, Saitama, Japan

NASH: Experimental

692 ADOPTIVE TRANSFER OF REGULATORY NKT LYMPHOCYTES AMELIORATES STEATOHEPATITIS AND

Eran Elinav, Orit I’appo, Miriam Sklair-Levy, Moshe Gomori, Oren Shibolet, Hadassah Hebrew University Medical Center, Jerusalem, Israel; Barbara Thalenfeld, Dean Engelhardt, Elazar Iiabbani, Enm Biochem Inc., Farmingdale, NY; Yaron Ilan, Hadassah Hebrew University Medical Center, Jerusalem, lsrael

GLUCOSE INTOLERANCE IN LEPTIN-DEFICIENT MICE

# 693

ACTIVATED RECEPTORS GAMMA AND UNCOUPLING PROTEIN 2 IN LIVER OF RATS WITH NONALCOHOLIC STEATOHEPATITIS Jian-Gao Fan, Xiao-Dong Ding, Guo-Lian Wang, Xiao-Ying Zheng, Zeng-Jie Xu, Li-Yan Tian, Shanghai First People’s Hospital, Shanghai, China

OVEREXPRESSION OF PEROXISOME PROLIFERATOR-

# 694 LONG TERM EXPOSURE T O LOW LEVELS OF BACTERIAL DERIVED CELL WALL PRODUCTS ACTIVATES MURINE HEPATIC STELLATE CELLS Paola Brun, Ignazio Castagliuolo, University of Padua, Padua, Italy; Massiino Pinzani, University of Florence, Florence, Italy; Giorgio Palii, Diego Martines, University of Padua, Padua, Italy

# 695 LIPOPHILIC BUT NOT HYDROPHILIC ANTIOXIDANTS IN COMBINATION WITH URSODEOXYCHOLIC ACID PROTECT MOUSE HEPATOCYTES AGAINST AMIODARONE TOXICITY Amine Ouazzani-Chahdi, Allal Chabli, Aziz Elimadi, University of Montreal, Montreal, PQ Canada; Patrick Collin, Axcaii Pharma, Mont Saint-Hilaire, PQ, Canada; Pierre S Haddad, University of Montreal, Montreal, P Q Canada

# 696

ALCOHOLIC STEATOHEPATITIS IN RATS INDUCED BY

Jian-Gao Fan, Xiao-Ying Zheng, Yan Qian, Xiao-Dong Ding, Zeng-Jie Zheng, Shanghai First People’s Hospital, Shanghai, China

ROTECTIVE EFFECTS OF PENTOXIFYLINE IN NON-

FAT-RICH DIET

4‘ 697 PRECLINICAL ACTIVITY OF PIRFENIDONE (§-METHYL- lPHENYL-2(IH)-PYRIDONE) IN CELL-BASED MODELS OF NONALCOHOLIC STEATOHEPATITIS Osman N Ozes, Sarah Stevens, Tony Wang, Tim Tran, Lawrence M Blatt, InterMune, Inc., Brisbane, CA

# 698

STEATOHEPATITIS GENERATED USING A SENSITISED ENU MUTAGENESIS SCREEN Quentin M Anstee, Imperial College School o f Nledicine, London, UK; Michelle Goldsworthy, Alison Haynes, Alison Hugill, MRC Harwell, Harwell, Oxfordshire, UK; Rob Goldin, Mark Thursz, Imperial College School of Medicine, London, UK; Roger D Cox, MRC Harwell, Harwell, Oxfordshire, UK; Howard Thomas, Imperial College School of Medicine, London, UK

A NOVEL MURINE MODEL OF NON-ALCOHOLIC

699 LIVER PEROXISOMES ARE AN OBLIGATORY SOURCE OF

FROM PROLIFERATED RAT LIVER PEROXISOMES Reiner Fritz, Internal Medicine IV, Heidelberg, Germany; Alfred Volkl, Cell Biology and Anatomy, Heidelberg, Germany; Wolfgang Stremmel, Sebastian Mueller, Internal Medicine IV, Heidelberg, Germany

OXIDATIVE STRESS: DIRECT EVIDENCE OF H202-RELEASE

P 700 STEATOHEPATITIS AND LIVER FIBROSIS ASSOCl ATED WITH UPREGULATED OSTEOPONTIN EXPRESSION IN

METHIONINE AND CHOLINE DEFICIENT DIET Atul Sahai, Padmini Malladi, Richard M Green, Peter F Whi tington, Northwestern University, Chicago, IL

DIABETIC/INSULIN-RESISTANT DB/DB MICE FED A

~ ~

# 701 STEATOHEPATITIS IN MICE IMMOBILIZED BY HINDLIMB UNLOADING: ROLE OF ENDOTOXIN M Hossein Tcharmtclii, C Wayne Smith, Chantal A Rivera, Baylor College of Medicine, Houston, TX

8 Denotri AASLD Presidential Poster of Distinction

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1,2003 POSTER SESSIONS l l l A

# 702

BY CYP2E1 INHIBITION: IMPLICATIONS FOR THE ROLE OF

Nghi Phung, Geoffrey C Farrell, Krishanthi Gunaratnam, Jayshree Sesha, Pauline Hall, Jacob George, Storr Liver Unit, Westmead Millennium Institute, Sydney, Australia

# 703

OBESE,INSULIN RESISTANT AND DEVELOP HEPATIC STEATOSIS Mary E Rinella, Richard M Green, Northwestem University, Chicago, IL

AMELIORATION OF MCD-ASSOCIATED STEATOHEPATITIS

EXTRA-MITOCHONDRIAL SOURCE OF PRO-OXIDANTS

TTR-ABCBl1 TRANSGENIC MICE FED A HIGH FAT DIET ARE

# 704 TUMOR NECROSIS FACTOR ALPHA PROMOTER

(NASH) ASSOCIATED WITH OBESITY Karina C Trujillo, Faculty of Medicine, UANL, Monterrey, Mexico; Irma Calderbn, University Hospital Dr. Jos6 E. Gonzllez, UANL, Monterrey, Mexico; Pablo Zorrilla, Ricardo Salinas, none, Monterrey, Mexico; Albert0 Niderhauser, Juan P Flores, Univer- sity Hospital Dr. Jose E. Gonzllez, UANL, Monterrey, Mexico; Hugo A Barrera, Herminia G Martinez, Faculty of Medicine, UANL, Monterrey, Mexico; Francisco J Bosques, University Hospital Dr. Jose E. Gonzllez, UANL, Monterrey, Mexico

POLYMORPHISMS IN NON-ALCOHOLIC STEATOHEPATITIS

~

# 705 CHANGES OF KUPFFER CELL ACTIVITY IN THE PROCESS OF INDUCING THE RAT MODEL OF NONALCOHOLIC STE ATOHEPATITIS Jian-Gao Fan, Zeng-Jie Xu, Xiao-Dong Ding, Xiao-Ying Zheng, Li-Yan Tian, Shanghai First People’s Hospital, Shanghai, China

# 706 MOLECULAR EVIDENCE FOR A TOXIC MEMORY EFFECT IN STEATOHEPATITIS Conny Stumptner, Karin Wagner, Helmut Denk, Kurt Zatloukal, University of Graz, Graz, Austria

# 707

DEVELOPMENT OF STEATOHEPATITIS ON A METHIONINE CHOLINE DEFICIENT DIET Sean W P Koppe, Richard M Green, Northwestern University, Chicago, IL

CD 14(-/-) KNOCK-OUT MICE ARE NOT RESISTANT TO THE

# 708 ALTERED BILE SECRETORY FUNCTION IN EXPERIMENTAL

Amoldo Riquelme, Paula Vial, Margarita Pizarro, Nancy Solis, Luigi Accatino, Marco A Arrese, Universidad Catolica de Chile, Santiago, Chile

NON-ALCOHOLIC FATTY LIVER DISEASE

# 709 THE ROLE OF KERATIN IN STEATOHEPATITIS Kurt Zatloukal, Conny Stumptner, Andrea Fuchsbichler, Peter Fickert, Michael Trauner, Helmut Denk, University of Graz, Graz, Austria

~

# 710

ALCOHOLIC STEAOHEPATITIS (NASH) DEVELOP IN MALE MICE FED A NUTRITIONALLY COMLETE HIGH FAT DIET Kengathevy Morgan, Lin Mao, VA Medical Center, Long Beach, CA; Samuel W French, Harbor UCLA Medical Center REI, Torrance, CA; Timothy R Morgan, VA Medical Center, Long Beach, CA

FATTY LIVER AND HISTOLOGIC FEATURES OF NON-

# 711 PREVENTIE EFFECTS OF METFORMIN ON RATS WITH NONALCOHOLIC STEATOHEPATITIS Jian-Gao Fan, Xiao-Dong Ding, Zeng-Jie Xu, Xiao-Ying Zheng, Li-Yan Tian, Shanghai First People’s Hospital, Shanghai, China

~

# 712 REDUCED EXPRESSION OF PEROXISOMAL PROLIFERATOR ACTIVATED RECEPTOR ALPHA IN THE EARLY STAGE OF NONALCOHOLIC FATTY LIVER DISEASE Jong Eun Yeon, Kyoung Oh Kim, Hyoung Joon Lim, Ki Ho Park, Kyung Mook Choi, Sei Hyun Baik, Jin Yong Kim, Jong-Jae Park, Jae Seon Kim, Young-Tae Bak, Kwan So0 Byun, Chang Hong Lee, Korea University, Seoul, South Korea

# 713 A LIPOGENIC DIET DEFICIENT IN METHIONINE AND CHOLINE (MCD) SUPPRESSES HEPATIC STEAROYL-COA DESATURASE-1: A POSSIBLE ROLE FOR LIPOTOXICITY IN THE PATHOGENESIS OF MCD-INDUCED STEATOHEPATITIS Gizem Rizki, University of California San Francisco, San Francisco, CA; Lorenzo Arnaboldi, Bianca Gabrielli, Gladstone Institute of Cardiovascular Disease, San Francisco, CA; Gene Lee, University of California San Francisco, San Francisco, CA; Robert E Pitas, Gladstone Institute of Cardiovascular Disease, San Francisco, CA; Jacquelyn J Maher, University of California San Francisco, San Francisco, CA

NASH: Clinical # 714 PREVALENCE OF AUTOANTIBODIES AND AUTOIMMUNE HEPATITIS IN NONALCOHOLIC FATTY LIVER DISEASE Leon A Adams, Jill Keach, Keith D Lindor, Paul Angulo, Mayo Clinic, Rochester, MN ~ ~ ~ ~~ ~

# 715 HYALURONIC ACID, AN ACCURATE SERUM MARKER FOR ADVANCED FIBROSIS AMONG NONALCOHOLIC STEATOHEPATITIS Ayako Suzuki, Paul Angulo, James Lymp, Mayo Clinic, Rochester, MN; Dave Li, Wako Pure Chemical Industries, Ktd., Osaka, Japan; Shinji Satomura, Wako Pure Chemical Industries, Ltd., Osaka, Japan; Keith Lindor, Mayo Clinic, Rochester, MN

BENEFIT OF SUSTAINED WEIGHT LOSS AND EXERCISE IN OVERWEIGHT PATIENTS WITH LIVER DISEASE- INDICATORS FOR SUCCESS Ingrid J Hickman, Julie R Jonsson, Johannes B Prins, University of Queensland, Brisbane, Australia; Susan Ash, Princess

Queensland Institute of Medical Research, Brisbane, Australia; Andrew D Clouston, Elizabeth E Powell, University of Queensland, Brisbane, Australia

# 716 0 U,

8 5 ;$ IQD

Q, Alexandra Hospital, Brisbane, Australia; David M Purdie,

# 717 THE SPECTRUM OF NONALCOHOLIC FATTY LIVER DISEASE IN PATIENTS WITH HYPOTHALAMIC AND PITUITARY DYSFUNCTION Leon A Adams, Ariel Feldstein, Keith D Lindor, Paul Angulo, Mayo Clinic, Rochester, MN

L124 POSTER SESSIONS HEPATOLOGY, October 2003

t 718 NEUTROPHIL MYELOPEROXIDASE AND OXIDIZED

LIVER DISEASE: A POTENTIAL SOURCE OF OXIDATIVE STRESS IN STEATOTIC LIVERS Yoshihiro Ikura, Masahiko Ohsawa, Eishu Hai, Soichiro Kayo, Noriko Yoshimi, Nobuyuki Shirai, Yoshimi Sugama, Hiroko Fujino, Osaka City University Graduate School of Medicine, Osaka, Japan; Takeshi Inoue, Osaka City General Hospital, Osaka, Japan; Hisato Jomura, Wakakohkai Hospital, Osaka, Japan; Hiroyuki ltabe, Faculty of Pharmaceutical Sciences, Teikyo University, Sagamiko-chou, Japan; Makiko Ueda, Osaka City University Graduate School of Medicine, Osaka, Japan

f 719 REFINEMENT OF A CLINICOPATHOLOGICAL TYPING

(NAFLD): CLINICAL, BIOCHEMICAL, AND PATHOLOGICAL FEATURES IN 98 PATIENTS WITH NAFLD Metin Basaranoglu, Gulsen Ozbay, Cerrahpasa Medical School, Istanbul, Turkcy; Stephen H Caldwell, University of Virginia Health System, Charlottesville, VA; Abdullah Sonsuz, Cerrahpasa Medical School, Istanbul, Turkey

PHOSPHATIDYLCHOLINE IN NON-ALCOHOLIC FATTY

SYSTEM FOR NON-ALCOHOLIC FATTY LIVER DISEASE

# 720 OXIDATIVE STRESS IS AN INDEPENDENT RISK FACTOR

LIVER DISEASE (NAFLD) T O ADVANCED FIBROSIS Emanuelc Albano, Elisa Mottaran, Matteo Vidali, Emanuela Reale, Univcrsity of East Piedmont, Novara, Italy; Sushma Saksena, University of Newcastle, School of Clinical Medical Sciences, Ncwcastle-upon-Tyne, UK; Giuseppa Occhino, University of East Piedmont, Novara, Italy; Alastair D Burt, Christopher P Day, University of Newcastle, School of Clinical Medical Sciences, Newcastle-upon-Tyne, UK

xi 721 PREVALENCE AND CLINICAL FEATURES ASSOCIATED WITH AUTOANTIBODIES IN NONALCOHOLIC STEATOHEPATITIS (NASH) Kiran Kanji, Shriram Jakate, Ali Keshavarzian, Donald M Jensen, Scott J Cotler, Rush-Presbyterian-St. Luke's Medical Center, Chicago, JL

FOR THE PROGRESSION OF NON-ALCOHOLIC FATTY

X 722 LOCALIZATION OF OXIDIZED PHOSPHATIDYLCHOLINE IN STEATOTIC LIVERS; ITS RELATION T O OXIDATIVE INJURY IN FATTY LIVER DISORDERS Yoshihiro Ikura, Masahiko Ohsawa, Yoshihiko Ogawa, Kazuhisa Kaneda, Eishu Hai, Soichiro Kayo, Noriko Yoshimi, Nobuyuki Shirai, Yoshimi Sugama, Hiroko Fujino, Osaka City University Graduate School of Medicine, Osaka, Japan; Hiroyulu Itabe, Faculty of Pharmaceutical Sciences, Teikyo University, Sagamiko- chou, Japan; Makiko Ueda, Osaka City University Graduate School of Medicine, Osaka, Japan

# 723 DIFFERENTIAL GENE EXPRESSION IN THE LIVER OF TYPE 2 DIABETIC PATIENTS: FEATURES OF ATHEROSCLEROSIS AND NASH Toshinari Takamura, Masao Honda, Masaru Sakurai, Tsuguhito Ota, Shuichi Kaneko, Kanazawa University Graduate School of Medicine, Kanazawa, Japan

n 724 CONTINUOUS GLUCOSE MONITORING AND METABOLIC EVIDENCE OF SUBCLINICAL GLUCOSE INTOLERANCE IN NAFLD: LOOKING BEYOND THE TIP OF THE INSULIN RESISTANCE ICEBERG Barbara Rosado-Carrion, Keith Lindor, Jayant Talwalkar, John Miles, Robert Rizza, Brian Gorman, Michael Charlton, Mayo Clinic, Rochester, MN


# 725 VARIANTS OF ADIPOCYTE GENES AFFECTING FREE FATTY ACID FLUX IN PATIENTS WITH NON ALCOHOLIC FATTY LIVER DISEASE Raphael B Merriman, Bradley E Aouizerat, Molly Yankovich, Medha V Kulkarni, Mary J Malloy, John P Kane, Nathan M Bass, University of California San Francisco, San Francisco, CA

# 726

(NASH): ANALYSIS OF PROTEIN EXPRESSION PROFILES

Katherine Miller, Timothy Born, George Mason University, Manassas, VA; Janus P Ong, Abraham Younoszai, Hazem Elariny, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA; Karen Schlauch, Vikas Chandhoke, George Mason University, Manassas, VA; Zachary Goodman, Armed Forces Institute of Pathology, Washington, DC; Zobair M Younossi, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA

PROTEOMICS OF NON-ALCOHOLIC STEATOHEPATITIS

USING SELDI-TOF MASS SPECTROMETRY

f 727 OXIDATIVE STRESS IN NAFLD OF MORBID OBESITY PATIENTS Claudia P M Oliveira, Alessandra Raskovisk, Carlos K Funiya, Joel Faintuch, Maria do Socorro C B Bastos, Bianca I Della Nina, Mitisunori Matsuda, Denise P Vezozo, Bruno Zilberstein, Luiz Carlos C Gayotto, Alfredo Halpern, Flair J Carrilho, Joaquim G Rodrigues, School of Medicine of University of Sao Paulo, Sao Paulo, Brazil; Dulciiieia S P Abdalla, School of Pharmaceutical Sciences of University of Sao Paulo, Sao Paulo, Brazil

# 728 BIOCHEMICAL RELAPSE AND CONTINUED WEIGHT GAIN IN SUBJECTS WITH NONALCOHOLIC STEATOHEPATITIS (NASH) AFTER DISCONTINUATION OF PIOGLITAZONE Glen A Lutchman, Kittichai Promrat, Alejandro Soza, Theo Heller, Lijun Mi, Marc Ghany, Yoon Park, Renee Freedman, Jack Yanovsky, David Kleiner, T Jake Liang, Jay Hoofnagle, National Institutes of Health, Bethesda, MD

# 729 DIAGNOSTIC VALUE OF BIOCHEMICAL MARKERS (FIBROTEST) FOR THE PREDICTION OF LIVER FIBROSIS

DISEASE (NAFLD) Vlad Ratziu, Sophie Le Calvez, Frantpise Imbert-Bismut, Djamila Messous, Frederic Charlotte, Luminita Bonyhay, Mona Munteanu, Thierry Poynard, Groupe Hospitalier Pitie- Salpetriere, Paris, France

IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER

# 730 N A S H CLINICAL ASSESSMENT OF 501 PATIENTS FROM TWO SEPARATE ACADEMIC MEDICAL CENTERS WITH VALIDATION OF A CLINICAL SCORING SYSTEM FOR ADVANCED HEPATIC FIBROSIS Stephen A Harrison, Dana A Oliver, Saint Louis University, St. Louis, MO; Sigurd Torgerson, Brooke Army Medical Center, San Antonio, TX; Hayashi Paul, University of Colorado, Denver, CO; Brent A Neuschwander-Tetri, Saint Louis University, St. Louis, MO

# 731 LIPID PROFILES IN NONALCOHOLIC FATTY LIVER DISEASE Leon A Adams, Jill Keach, Keith D Lindor, Paul Angulo, Mayo Clinic, Rochester, MN

113A HEPATOLOGY, Vol. 38, No. 4, Suppl. 1, 2003 POSTER SESSIONS

# 732 GENDER DIFFERENCES IN HEPATIC GENE EXPRESSION OF

(NASH) Francesco Gorreta, Luca Del Giacco, Karen Schlauch, Amy VanMeter, Geraldine Grant, Alan Christensen, Vikas Chandhoke, George Mason University, Manassas, VA; Zachary Goodman, Armed Forces Institute of Pathology, Washington, DC; Abraham Younoszai, Hazem Elariny, Janus P Ong, Zobair M Younossi, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA

# 733 A BEHAVIORAL ANALYSIS OF NONALCOHOLIC FATTY LIVER DISEASE: IMPLICATIONS FOR THE CLINICIAN Deborah L Haller, Carol Sargeant, Velimir A Luketic, Melissa J Contos, Richard Sterling, Mitchell L Shiffman, Richard T Stravitz, Arun J Sanyal, Virginia Commonwealth University, Richmond, VA

PATIENTS WITH NON-ALCOHOLIC STEATOHEPATITIS

~~ ~

# 734 DIETARY COMPOSITION AND FATTY LIVER DISEASE Amir R A Al-Khuraishi, Steven F Solga, Jeanne M Clark, Michael Torbenson, Ashli Cohen, Anna Mae Diehl, Thomas H Magnuson, Johns Hopkins University, Baltimore, MD

# 735 SERUM LEPTIN LEVELS IN NONALCOHOLIC FATTY LIVER DISEASE: RESULTS FROM THE THIRD NATIONAL HEALTH AND NUTRITION EXAMINATION SURVEY (NHANES 111) Suthat Liangpunsakul, Naga Chalasani, Indiana University School of Medicine, Indianapolis, IN

# 736 THE UTILITY OF IMMUNOSTAINING FOR MALLORY

(NAFLD) Anupamjit Mehrotra, Zachary Goodman, Armed Forces Institute of Pathology, Washington, DC; Hazem Elariny, Janus P Ong, Abraham Younoszai, Navdeep Boparai, Jennifer Assmann, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA; Vikas Chandhoke, George Mason University, Manassas, VA; Zobair M Younossi, Center for Liver Diseases, Inova Fairfax Hospital, Falls Church, VA

BODIES IN NON-ALCOHOLIC FATTY LIVER DISEASE

~

# 737 DIAGNOSIS OF NASH USING KUPFFER IMAGING OF CONTRAST ENHANCED ULTRASOUND Hiroko Iijima, Fuminori Moriyasu, Tokyo Medical University, Tokyo, Japan; Kaoru Tsuchiya, Musashino Red Cross Hospital, Tokyo, Japan; Shunichi Sasaki, Shiro Suzulu, Toshiya Horibe, Tokyo Medical University, Tokyo, Japan

PBC/PSC and Complications of Cholestasis

# 738 HIGH PREVALENCE OF PROTEIN C DEFICIENCY IN PRIMARY SCLEROSING CHOLANGITIS Bertrand Condat, HBpital Beaujon, Clichy, France; Olivier Chazouill&es, HBpital Saint Antoine, Paris, France; Dermot OToole, Marie-Helhe Denninger, Camille Barreau, Marie-Pierre Vuillerme, Marie-Pierre Ripault, HBpital Beaujon, Clichy, France; Zair Hassani, HBpital Saint Louis, Paris, France; Annie Robert, HBpitaI Saint Antoine, Paris, France; Pierre Ruffat, Annie Bezeaud, Yann Consigny, HBpital Beaujon, Clichy, France; Yann Ngo, HGpital Saint Camille, B y sur Mame, France; Nathalie Goutte, HBpital Beaujon, Clichy, France; Marc Leman, HBpital Saint Louis, Paris, France; Philippe Ruszniewski, Dominique Valla, HGpital Beaujon, Clichy, France

# 739 PROTEASOME IS REQUIRED FOR CLASS I-RESTRICTED PRESENTATION BY FC GAMMA RECEPTOR-MEDIATED ENDOCYTOSIS IN PRIMARY BILIARY CIRRHOSIS Hiroto Kita, University of California Davis, Davis, CA; Aftab A Ansari, Emory University School of Medicine, Atlanta, GA; Xiao-Song He, Zhe-Xiong Lian, Judy Van de Water, University of California Davis, Davis, CA; Ross L Coppel, Monash University, Melbourne, Australia; Velimir Luketic, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA; Marshall M Kaplan, New England Medical Center, Boston, MA; Hideaki Inamori, Norio Isoda, Kentaro Sugano, Jichi Medical School, Yakushiji, Japan; Michio Imawari, Omiya Medical Center, Jichi Medical School, Saitama, Japan; M Eric Gershwin, University of California Davis, Davis, CA

# 740

SUPPLEMENTATION ON BONE MINERAL DENSITY IN PRIMARY BILIARY CIRRHOSIS(PBC) Dermot Gleeson, Sheffield Teaching Hospitals, Sheffield, UK; Stephen Hodges, University of Sheffield, Sheffield, UK; Elizabeth Rigney, Sheffield Teaching Hospitals, Sheffield, UK; Aubrey Blumsohn, Rosemary Hannon, Nicola F A Peel, Richard Eastell, University of Sheffield, Sheffield, UK

PLACEBO-CONTROLLED TRIAL OF VITAMIN K

# 741 AUTOANTIBODIES TO LIPOIC ACID AND TO CONJUGATED LIPOATE ARE UNIQUELY FOUND IN PRIMARY BILIARY CIRRHOSIS Sylvaine F A Bruggraber, Patrick S C Leung, Katsushi Amano, Chao Quan, Mark J Kurth, Michael H Nantz, University of California Davis, Davis, CA; Gordon D Benson, Robert Wood Johnson Medical School, Camden, NJ; Judy Van de Water, University of California Davis, Davis, CA; Velimir A Luketic, Medical College of Virginia, Richmond, VA; Aftab A Ansari, Emory University School of Medicine, Atlanta, GA; Ross L Coppel, Monash University, Melbourne, Australia; M Eric Gershwin, University of California Davis, Davis, CA

# 742 EXPRESSION OF CD40 LIGAND (CD154) IS SPECIFICALLY UPREGULATED IN THE LIVER OF PATIENTS WITH PRIMARY BILIARY CIRRHOSIS Marlyn J Mayo, Burton Combes, Smina Khilnani, Maha Al- Halimi, Rohan Jeyarajah, University of Texas Southwestern Medical Center, Dallas, TX; Peter E Lipsky National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD

# 743 BSEP AND MDR3 SEQUENCE DIVERSITY AND HAPLOTYPE STRUCTURE IN PRIMARY SCLEROSING CHOLANGITIS AND PRIMARY BILIARY CIRRHOSIS Christiane Pauli-Magnus, Karin E Fattinger, Peter J Meier, Clinical Pharmacology and Toxicology, University of Ztirich, Zurich, Switzerland; Gerd A Kullak-Ublick, Gastroenterology and Hepatology, University Zurich, Switzerland; Reinhold Kerb, Thomas Lang, Epidauros AG, Bernried, Germany; Ulrich Beuers, Klinikum Groghadern, University Munich, Munich, Germany

# 744 FENOFIBRATE FOR PATIENTS WITH ASYMPTOMATIC PRIMARY BILIARY CIRRHOSIS Kazufumi Dohmen, Clinical Research Center, National Nagasaki Medical Center, Omura, Japan; Toshihiko Mizuta, Saga Medical School, Saga, Japan; Makoto Nakamuta, Kyushu University, Fukuoka, Japan; Naoya Shimohashi, Fukuoka City Hospital, Fukuoka, Japan; Hiromi Ishibashi, Clinical Research Center, National Nagasaki Medical Center, Omura, Japan; Kyosuke Yamamoto, Saga Medical School, Saga, Japan

POSTER SESSIONS HEPATOLOGY, October 2003 11314

t 745 EPIDEMIOLOGY OF PRIMARY BILIARY CIRRHOSIS (PBC) IN VICTORIA, AUSTRALIA. HIGH PREVALENCE IN MIGRANT POPULATIONS Paul J Gow, Siddharth Sood, John M Christie, Peter W Angus, Austin Hospital, Melbourne, Australia

if 746 THE IMPACT OF URSODEOXYCHOLIC ACID (UDCA) THERAPY WITH OR WITHOUT LIVER TRANSPLANTATION

CIRRHOSIS Christoplie Corpechot, Fabrice Carrat, Abbas Bahr, Renee E Poupon, Raoul Poupon, H8pital Saint Antoine, Paris, France

(OLT) ON LONG-TERM SURVIVAL IN PRIMARY BILIARY

8 747 CYTOKINE PRODUCTION AND BONE MINERAL DENSITY IN PATIENTS WITH PRlMARY BILIARY CIRRHOSIS Cynthia Levy, Paul Angulo, Mayo Clinic, Rochester, MN; Manuela Neuman, Sunnybrook Health Science Center, Ontario, ON, Canada; Keith D Lindor, Mayo Clinic, Rochester, MN

d 748 EVIDENCE THAT AN E. COLI REPLICATION PRIMASE PEPTIDE, HIGHLY HOMOLOGOUS TO THE MAJOR SPlOO

REACTIVITY IN PRIMARY BILIARY CIRRHOSIS Dimitrios-Petrou Bogdanos, King’s College Hospital, London, UK; Harold Baum, King’s College, London, UK; Patrice Butler, Royal Free Hospital, London, UK; Eirini I Rigopoulou, Academic Liver Unit, Larisa Medical School, University of Thessaly, Larisa, Greece; Yun Ma, King’s College Hospital, London, UK; Andrew K Burroughs, Royal Free Hospital, London, UK; Diego Vergani, King‘s College Hospital, London, UK

EPITOPE, IS A POSSIBLE TRIGGER OF ANTI-SP100

~ ~

;7 749 ANTI-MITOCHONDRIAL ANTIBODIES IN A GENETICALLY HOMOGENOUS POPULATION OF PATIENTS WITH PRIMARY BILIARY CIRRHOSIS AND RELATIVES: THE CASE OF ICELAND Sigu rdur Olafsson, Hallgriniur Gudjonsson, University Hospital, Reykjavik, Iceland; Carlo Selmi, Katsushi Amano, University of California Davis, Davis, CA; Pietro Invernizzi, Mauro Podda, University of Milan, Milan, Italy; M Eric Gershwin, University of California Davis, Davis, CA

G 750 IS PDC-EJBP (PROTEIN X) A T-CELL AUTOANTIGEN IN PRIMARY BILIARY CIRRHOSIS? Anna McHugh, Jeremy M Palmer, Steve J Yeaman, David E J Jonc5, Univer\it\ ot Newcade, Newcastle-upon-Tyne, UK

2 751 MODELLING ADVENT OF COMPLICATIONS IN PRIMARY BILIARY CIRRHOSIS Chun-Wing Chan, Royal Free Hospital and School of Medicine, London, UK, James R Carpenter, London School of Hygiene and Tropical Medicine, London, UK, Maria Mela, David W Patch, A K Burroughs, Royal Free Hospital and School of Medicine, London, UK

d 752 INFECTION BY CHLAMYDIA PNEUMONIAE IN THE PATHOGENESIS OF PRIMARY BILIARY CIRRHOSIS Marco Cayanni, Maria R Biagini, Orsini Barbara, Alessandro Tozzi, Maria C Benini, Raffaele Manta, Nadia Lazzerini, Andrea Galli, Calogero Surrenti, Stefano Milani, University of Florence, Florence, Italy

8 Denote; AASLD Presidential Poster of Distinction

8 8753 SEQUENCE ANALYSIS OF BSEP AND MDR3 IN PATIENTS WITH INTRAHEPATIC CHOLESTASIS OF PREGNANCY Cliristiane Pauli-Magnus, Yvonne Meier, University of Zurich, Zurich, Switzerland; Reinhold Kerb, Epidauros AG, Bernried, Germany; Tuia Zodan-Marin, University of Zurich, Ziirich, Switzerland; Thomas Lang, Epidauros AG, Bemried, Germany; Beat Mullhaupt, Rolf Zimmermann, Peter J Meier, Gerd A Kullak-Ublick, University of Zurich, Zurich, Switzerland

# 754 THE ONTOGENY OF CDlO EXPRESSION BY HEPATOCYTES AND ITS CLINICAL IMPLICATIONS FOR PLASMA NEUTRAL ENDOPEPTIDASE ACTIVITY AS A MARKER OF CHOLESTASIS N J Meara, J A Byrne, A C Rayner, R J Thompson, A S Knisely, kng’s College Hospital, London, UK

# 755 DEVELOPMENTAL OUTCOME OF EXTRAHEPATIC BILIARY ATRESIA INFANTS WITH FAILED AND WORKING KASAI PORTOENTEROSTOMIES Michael Balthazor, Vicky Lee Ng, Lina Barkas, Eve A Roberts, Hospital for Sick Children, Toronto, ON, Canada

# 756 BILIARY ATRESIA SPLENIC MALFORMATION SYNDROME; A SINGLE CENTER EXPERIENCE OVER 25 YEARS Sarah Tizzard, Nedim Hadzic, lnstitute of Liver Studies, King’s College Hospital, London, UK; Mark Davenport, Dept of Paediatric Surgery, London, UK; Edward R Howard, lnstitute of Liver Studies, London, UK; Anil Dhawan, Alastair J Baker, Giorgina Mieli-Vergani, Institute of Liver Studies, King’s College Hospital, London, UK

P 757 BILIARY OBSTRUCTION IMPAIRS RED CELL OXIDATIVE CAPACITY Ibrahim El Sayed, Ibrahim El Kady Genetic Engineering Institute, Menoufiya University, Shebeen El-Kom, Egypt; Gamal Badra, Imam Waked, National Liver Institute, Shebeen El-Kom, Egypt

# 758 UPREGULATION OF A TH1 INFLAMMATORY CYTOKINE OSTEOPONTIN IN PATIENTS WITH BILIARY ATRESIA: DIFFERENTIAL LOCALIZATION AT DIAGNOSIS AND AT TRANSPLANT Peter F Whitington, Padmini Malladi, Hector Melin-Aldana, Northwestern University, Chicago, IL; Cara L Mack, University of Colorado, Denver, CO; Atul Sahai, Northwestern University Chicago, IL

Viral Hepatitis and Liver Transplantation

8 # 759 OUTCOME OF LIVER TRANSPLANTATION FOR HEPATITIS B IN THE U S W Ray Kim, John J Poterucha, Michael B Ishitani, E Rolland Dickson, Mayo Clinic and Foundation, Rochester, MN

8 # 760 FATAL CRYPTOGENIC LIVER DISEASE AFTER SUSTAINED ERADICATION OF RECURRENT HEPATITIC C IN LIVER TRANSPLANTATION Sandeep Mukherjee, Richard K Gilroy, Joyce Rogge, Lynne Weaver, Timothy M McCashland, Daniel F Scliafer, University of Nebraska Medical Center, Omaha, NE


# 761 EXPANDING THE DONOR POOL BY TRANSPLANTING CADAVERIC LIVERS FROM OLDER DONORS: AN ANALYSIS OF PATIENT AND GRAFT SURVIVAL BY DONOR AGE FROM THE UNITED NETWORK FOR ORGAN SHARING DATABASE Mark W Russo, Joseph A Galanko, Kimberly Beavers, Steven L Zacks, Michael W Fried, Roshan Shrestha, University of North Carolina, Chapel Hill, NC

# 762

RIBAVIRIN FOR RECURRENT HEPATITIS C AFTER LIVER TRANSPLANTATION: A PRELIMINARY ANALYSIS Reem H Ghalib, Methodist Hospital of Dallas, Dallas, TX; Cheryl D Levine, University of Texas, Houston, TX; Blaine Hollinger, Rise Stribling, Baylor College of Medicine, Houston, TX; Tricia McClelland, Methodist Hospital of Dallas, Dallas, TX; Terry D Box, William R Hutson, University of Utah, Salt Lake City, UT; Anthony B Post, University Hospitals of Cleveland, Cleveland, OH; Fredric G Regenstein, Shobha Goshi, Tulane University, New Orleans, LA; Jeffrey Weinstein, Methodist Hospital of Dallas, Dallas, TX; Philip Seu, John Goss, Baylor College of Medicine, Houston, TX; Steven Cheng, Methodist Hospital of Dallas, Dallas, TX

SAFETY AND EFFICACY OF PEG IFN ALFA-28 PLUS

# 763

WITH SEVERE HEPATITIS C VIRUS INFECTION Jian-Qing He, University of British Columbia McDonald Research Laboratories, Vancouver, BC, Canada; Karen Nelson, Puget Sound Blood Center, Seattle, WA; Robert L Carithers Jr, University of Washington School of Medicine, Seattle, WA; lakshmi K Gaur, WA National Primate Research Center, Seattle, WA

# 764 PRELIMINARY ANALYSIS: GRAFT LOSS FROM RECURRENT HEPATITIS C IS NOT INCREASED IN PATIENTS RECEIVING SIROLIMUS AS PRIMARY IMMUNOSUPPRESSION Michael J Osgood, Lisa Forman, Marcel0 Kugelmas, Gregory Everson, Thomas Bak, Michael Wachs, Igal Kam, James Trotter, University of Colorado, Denver, CO

ASSOCIATION OF HLA-DRB1 AND DQBl POLYMORPHISMS

# 765 EARLY HEPATITIS C RECURRENCE FOLLOWING LIVER TRANSPLANTATION IS INFLUENCED BY OPERATIVE AND

Rafik M Ghobrial, Ian Carmody, Yue Ming Huang, Sammy Saab, Jeffrey A Gombein, Randolph Steadman, Steven-Huy Han, Francisco A Durazo, Douglas G Farmer, Hasan Yersiz, Curtis D Holt, Leonard Goldstein, Ronald W Busuttil, David Geffen School of Medicine at UCLA, Los Angeles, CA

PERI-TRANSPLANT VARIABLES

# 766 EARLY LOBULAR NECROSIS AND LIVING DONOR LIVER TRANSPLANTATION ARE STRONG PREDICTORS OF SEVERE HCV RECURRENCE AFTER LIVER TRANSPLANTATION Montserrat Garcia-Retortillo, Xavier Forns, Josep M Llovet, Miquel Navasa, Juan Turnes, Juan Carlos Garcia-Pagan, Jaume Bosch, Josep Fuster, Juan Carlos Garcia-Valdecasas, Antoni Rimola, Hospital Clinic, Barcelona, Spain

# 767 TREATMENT OF PATIENTS WITH RECURRENT HEPATITIS C AFTER LIVER TRANSPLANTATION WITH PEGYLATED INTERFERON AND RIBAVIRIN Didier Samuel, Paul Brousse Hospital, Villejuif, France

# 768 TREATMENT OF RECURRENT HEPATITIS C AFTER LIVER

RIB AVIRIN Ulf P Neumann, Jan M Langrehr, Thomas Berg, Peter Neuhaus, Charit6, Virchow Clinic, Berlin, Germany

TRANSPLANTATION WITH PEGINTERFERON ALFA-PB AND

# 769 REJECTION TREATMENT MODIFIES HCV QUASISPECIES EVOLUTION AFTER LIVER TRANSPLANTATION Juan I Arenas, Tomasz Laskus, Jeff Wilkinson, Juan F Gallegos, Mayo Clinic, Scottsdale, AZ; Carlos G Fasola, St. John Hospital, Detroit, MI; Debra Adair, Marek Radowski, Karen V Kibler, David Douglas, James Williams, Mayo Clinic, Scottsdale, AZ; George Netto, Baylor University Medical Center, Dallas, TX; David Mulligan, Mayo Clinic, Scottsdale, AZ; Goran Klintmalm, Baylor University Medical Center, Dallas, TX; Jorge Rakela, Hugo E Vargas, Mayo Clinic, Scottsdale, AZ

# 770 IMPACT OF HEPATITIS C VIRAL (HCV) INFECTION IN PRIMARY CADAVERIC LIVER ALLOGRAFT VfS PRIMARILY LIVING LIVER ALLOGRAFT IN 100 CONSECUTIVE LIVER TRANSPLANT PATIENTS? Adel Bozorgzadeh, Ashokkumar B Jain, John Daller, URMC, Rochester, NY; Charlotte Ryan, URMC Pathology, Rochester, NY; Uma Sundrum, URMC Medicine, Rochester, NY; Kerrie Lansing, URMC, Rochester, NY; David Kaufman, Critical Care and Anesthesiology, Rochester, NY; Daniel Ornt, Martin Zand, Robert Betts, URMC Medicine, Rochester, NY; Mark Orloff, URMC, Rochester, NY

# 771 PROSPECTIVE AND RIGOROUS TESTING OF THE ABILITY T O DISTINGUISH BETWEEN RECURRENT HEPATITIS C AND ACUTE AND CHRONIC REJECTION DURING A TOLERANCE INDUCTION TRIAL Anthony J Demetris, Bijan Eghtesad, Amadeo Marcos, Mike Nalesnik, Paulo Fontes, Tom Caccairelli, Parmjeet Randhawa, Tong Wu, Alyssa Krasinskas, John Fung, Thomas Starzl, UPMC, Pittsburgh, PA

# 772 HEPATITIS C AFTER LIVER TRANSPLANTATION- IMPORTANCE OF LOBULAR ACIDOPHIL BODIES IN PREDICTING RECURRENCE Matthew M Yeh, Shari L Taylor, Anne M Larson, Hao A Do, Nancy McCaulley, Jame P Perkins, Robert L Carithers Jr, University of Washington, Seattle, WA

# 773 PREDICTORS OF DEATH OR RETRANSPLANTATION IN PATIENTS WITH HEPATITIS C FOLLOWING LIVER TRANSPLANTATION Steven L Condron, Michael A Heneghan, Keyur Patel, Anouk Dev, John G McHutchison, Andrew J Muir, Duke University, Durham, NC

# 774 INTERFERON-BASED TREATMENT FOR RECURRENT HCV INFECTION DOES NOT INFLUENCE THE PROGRESSION OF HEPATIC FIBROSIS IN LIVER TRANSPLANT RECIPIENTS Daniel Gan, M Isabel Fiel, The Mount Sinai Medical Center, New York, NY; Veronika Dubrovskaya, Beth Israel Medical Center, New York, NY; Arief Suriawinata, The Mount Sinai Medical Center, New York, NY; P Wilfred0 Canchis, Weill Medical College of Cornell University New York, NY; Prodromos Hytiroglou, University of Thessaloniki, Thessaloniki, Greece; Swan N Thung, Thomas D Schiano, The Mount Sinai Medical Center, New York, NY


$77S TREATMENT OF RECURRENT HEPATITIS C AFTER LIVER TRANSPLANTATION : A PILOT STUDY OF PEGINTERFERON

Jerome Dumortier, Jean-Yves Scoazec, HBpital Edouard Herriot, Lyon, France; Philippe Chevallier, Domaine Rockefeller, Lyon, France; Olivier Boillot, HBpital Edouard Herriot, Lyoi~, France

8 776 CHANGES IN HEMOGLOBIN DURING THERAPY WITH PEG

RECURRENT HEPATITIS C AFTER LIVER TRANSPLANTATION Reem H Ghalib, Methodist Hospital of Dallas, Dallas, TX; Cheryl D Levine, University of Texas MD Anderson Cancer Center, F'iouston, PX; Blaine Hollinger, Rise Stribling, Baylor College of hledicine, Houston, TX; Tricia McClelland, Methodist Hospital of Dallas, Dallas, TX; Terry D Box, William R Hutson, University of Utah, Salt Lake City, UT; Anthony B Post, University Hospitals of Cleveland, Cleveland, OH; Fredric G Regenstein, Shobha Goshi, Tulane University, New Orleans, LA; Jeffrey Weinstein, Fay Simon, Methodist Hospital of Dallas, Dallas, TX; Philip Seu, John Goss, Baylor College of Medicine, Houston, TX; Steven Cheng, Methodist Hospital of Dallas, Dallas, TX

ALFA-2B AND RIBAVIRIN COMBINATION

IFN ALFA-2B PLUS RIBAVIRIN IN PATIENTS WITH

: 777 CYTOKINE GENE POLYMORPHISMS ARE ASSOCIATED WITH HEPATITIS C VIRUS INDUCED END-STAGE LIVER DISEASE Jian-Qing He, University of British Columbia McDonald Research Laboratories, Vancouver, BC, Canada; Robert L Carithers Jr, University of Washington School of Medicine, Seattle, WA; Lakshmi K Gaur, WA National Primate Research Center, Seattle, WA

F# 778

LIVER TRANSPLANTATION IS INEFFECTIVE, EVEN

Mario Angelico, Daniele Di Paolo, Claudia Telesca, Ilaria Lenci, Ralfaella Lionetti, Alessandra Petrolati, Settimio Zazza, Giuseppe Tisone, University of Rome Tor Vergata, Rome, Italy

EXTENDED DOUBLE-DOSAGE HBV VACCINATION AFTER

WITHOUT LAMIVUDINE AND PRIOR HBIG WASH-OUT

# 779 IMPACT OF LAMIVUDINE RESISTANT MUTANTS IN HEPATITIS B VIRUS RELATED LIVER DISEASES AFTER LIVER TRANSPLANTATION Henry L Y Chan, Albert K K Chui, Wan-Yee Lau, Francis K L Chan, Alex Y Hui, Nitin Rao, John Wong, Eric C H Lai, Joseph J Y Sung, Chinese University of Hong Kong, Hong Kong, Hong Kong ~~ ~~ ~ ~

# 780

TERM RESPONSE T O LAMIVUDINE WITHOUT SELECTION FOR YMDD MUTANTS IN LIVER TRANSPLANT RECIPIENTS Hans L Tillmann, Kersten Borchert, Thomas C Bock, Andrea Finger, Elmar Jaeckel, Jens Rosenau, Isabella Glomb, Klaus H W Boker, Bjorn Nashan, Jiirgen Klempnauer, Christian Trautwein, Michael P Manns, Hannover Medical School, Hannover, Germany

COMPLETE HBEAG-SEROCONVERSION PREDICTS LONG-

t 781 PREVENTION OF HEPATITIS B AFTER LIVER TRANSPLANTATION Nam-Joon Yi, Kyung-Suk Suh, Seong-Hwan Chang, Seok Ho Choi, Choon Hyuck Kwon, Kuhii Uk Lee, Seoul National University Hospital, Seoul, South Korea



Poster Session 3

Monday, October 27 Hynes Convention Center, Exhibit Hall C

Poster Viewing: 8:OOam - 5:OOpm

Presenters in Attendance: Even number posters: 12:30 - 1:45pm Odd number posters: 1:45 - 3:OOpm

8 Those posters identified as AASLD Presidential Poster of Distinction by a ribbon icon have received review scores that place them within the top 10% of all posters. We encourage you to make them a priority as you visit the poster session.

Acute Liver Failure

8 # 782 ANTI-APOPTOTIC FUNCTION OF GELSOLIN IN FAS-ANTIBODY INDUCED ACUTE LIVER FAILURE Ludger Leifeld, Klaus Fink, Magdalene Fielenbach, Tilman Sauerbruch, Ulrich Spengler, University of BOM, Bonn, Germany Travel Award Recipient

8 # 7 8 3 INFLUENCE OF TNF GENE POLYMORPHISM IN PATIENTS WITH ACUTE AND FULMINNANT HEPATITIS Noriko Tsuchiya, Katsutoshi Tokushige, Kiyoshi Hasegawa, Etsuko Hashimoto, Katsumi Yamauchi, Keiko Shiratori, Tokyo Women's Medical University, Tokyo, Japan

8 # 784 SERUM ACETAMINOPHEN ADDUCTS RELIABLY DISTINGUISH ACETAMINOPHEN TOXICITY FROM OTHER CAUSES OF ACUTE LIVER FAILURE Timothy J Davern 11, University of California San Francisco, San Francisco, CA; Laura P James, University of Arkansas for Medical Sciences, Little Rock, AR; Robert J Fontana, University of Michigan, AM Arbor, MI; Anne M Larson, University of Washington, Seattle, WA; Julie Polson, Ezmina Lalani, University of Texas Southwestern Medical Center, Dallas, TX; Jack A Hinson, University of Arkansas for Medical Sciences, Little Rock, AR; William M Lee, University of Texas Southwestern Medical Center, Dallas, TX

8 # 785 HEPATOCYTE GROWTH FACTOR ACCELERATES

ACETYLAMINOFLUORENE/PARTIAL HEPATECTOMY MODEL IN RAT Satoru Hasuike, Hirofumi Uto, Chihiro Nakanishi, Kazunori Kusumoto, Shojiro Yamamoto, Takeshi Hori, Katsuhiro Hayashi, Hirohito Tsubouchi, Miyazaki Medical College, Miyazaki, Japan; Yoshiko Nagata, Akihiro Moriuchi, Akio Ido, Kyoto University Hospital Translational Research Center, Kyoto, Japan

DIFFERENTIATION OF HEPATIC OVAL CELLS IN A 2-

8 # 786 ALBUMIN DIALYSIS REDUCES BRAIN WATER AND INTRACRANIAL PRESSURE IN ACUTE LIVER FAILURE: A RANDOMISED CONTROLLED STUDY IN A PIG MODEL Sambit Sen, University College London, London, UK; Christopher Rose, Max-Delbriick Center for Molecular Medicine, Berlin, Germany; Lars M Ytreba, University Hospital Northern Norway, Tromsa, Norway; Nathan A Davies, University College London, London, UK; Geir I Nedredal, Synnove S Drevland, Marianne Kjonno, University Hospital Northern Norway, Tromsa, Norway; Roger Williams, University College London, London, UK; Roger F Butterworth, HBpital Saint-Luc, Centre Hospitalier de l'llniversite de Montreal, Montreal, PQ, Canada; Arthur Revhaug, University Hospital Northern Norway, Tromsa, Norway; Rajiv Jalan, University College London, London, UK

# 787 WORSENING OF CEREBRAL HYPEREMIA IN ACUTE LIVER FAILURE WITH SEVERE HEPATIC ENCEPHALOPATHY FOLLOWING TERLIPRESSIN? Debbie L Shawcross, Nathan A Davies, Rajeshwar P Mookejee, University College London, London, UK; Peter C Hayes, Alistair Lee, Scottish Liver Transplantation Unit, Royal Infirmary of Edinburgh, Edinburgh, UK; Roger Williams, Rajiv Jalan, University College London, London, UK

# 788 TREATMENT WITH AN ENDOCANNABINOID ANTAGONIST IMPROVES NEUROLOGICAL FUNCTION AND SURVIVAL IN AN ANIMAL MODEL OF FULMINANT HEPATIC FAILURE Ezra Gabbay, Hadassah Hebrew University Medical Center, Ein Karem, Jerusalem, Israel; Yosefa Avraham, Elliot M Berry, Hadassah Hebrew University Medical School, Jerusalem, Israel; Yaron Ilan, Hadassah Hebrew University Medical Center, Ein Karem, Jerusalem, Israel; Olga Zolotrev, Avital Okun, Hadassah Hebrew University Medical School, Jerusalem, Israel; Eran Yisraeli, Hadassah Hebrew University Medical Center, Ein Karem, Jerusalem, Israel

# 789 EXPRESSION OF CALPASTATIN AND ANNEXIN I IN NEWLY DIVIDED HEPATOCYTES: MECHANISM BEHIND RESISTANCE FROM ACUTE LIVER FAILURE Pallavi B Limaye, Udayan M Apte, Prajakta S Palkar, The University of Louisiana at Monroe, Monroe, LA; John C Latendresse, Pathology Associates International, NCTR-A Charles River Company, Jefferson, AR; Harihara M Mehendale, The University of Louisiana at Monroe, Monroe, LA

# 790 ACETAMINOPHEN OVERDOSE: RELATIONSHIP OF GLUCURONYLTRANSFERASE UGTl A1 PROMOTER VARIANTS TO SUBSEQUENT ACUTE LIVER FAILURE Jemimah E Adams, Phillip J Murphy, William Bernal, Julia A Wendon, J Michael Tredger, King's College Hospital, London, LJK ~~

# 791 CONTRACTILE RESPONSE OF FEMORAL ARTERIES IN PIGS WITH ACUTE LIVER FAILURE Lars M Ytreba, Sveinung Eke, University Hospital Northern Norway, Tromser, Norway; Sambit Sen, University College London, London, UK; Christopher Rose, Max-Delbriick Center for Molecular Medicine, Berlin, Germany; Ole M Fuskeviig, Geir I Nedredal, University Hospital Northern Norway, Tromss, Norway; Rajiv Jalan, University College London, London, UK; Arthur Revhaug, University Hospital Northern Norway, Tromsa, Norway

l l8A POSTER SESSIONS HEPATOLOGY, October 2003

$792 PROGNOSTIC IMPORTANCE OF SOLUBLE CD163 IN PATIENTS WITH FULMINANT HEPATITIS Atsushi Hiraoka, Norio Horiike, Sk Md Fazle Akbar, Ehime University School of Medicine, Elunie, Japan; Takami Matsu yama, Kagoshima University School of Medicine, Kagoshima, Japan; Morikazu Onji, Ehime University School of Medicine, Ehime, Japan

k 793 EDARAVONE, A NOVEL FREE RADICAL SCAVENGER, PREVENTS LIVER INJURY AND MORTALITY IN RATS ADMINISTERED ENDOTOXIN Hiroshi Kono, Masami Asakawa, Hideki Fujii, Akira Maki, Hidetake Aniemiya, Yu Hirai, University of Yamanashi, Yamanashi, Japan; Masayuki Yamanioto, Shinko Byoin Hospital, Hyogo, Liberia

# 794 ROLE OF ACETAMINOPHEN IN ACUTE LIVER FAILURE DUE TO VIRAL HEPATITIS Julie E Polson, Ponsiano Ocama, University of Texas Southwestern Medical Center, Dallas, TX; Anne M Larson, University of Washington Medical Center, Seattle, WA; Linda Hynan, Ezniina K Lalani, University of Texas Southwestern Medical Center, Dallas, TX; M E Harrison, Mayo Clinic Scottsdale, Scotsdale, AZ; William M Lee, University of Texas Southwestern Medical Center, Dallas, TX

~~

f 795 PROSPECTIVE ANALYSIS OF POTENTIAL FATTY ACID OXIDATION (FAO) DEFECTS IN CHILDREN WITH ACUTE LIVER FAILURE USING ELECTROSPRAY TANDEM MASS SPECTROMETRY (ETMS) OF BILE Benjamin L Sluieider, Mount Sinai School of Medicine, New York, NY; Piero Rinaldo, Mayo Clinic, Rochester, MN; Robert H Squires, University of Texas Southwestern Medical Center, Dallas, TX; John Bucuvalas, University of Cincinnati, Cincinnati, OH; Michael R Narkewicz, University of Colorado, Denver, CO; Sukru Emre, Mount Sinai School of Medicine, New York, NY

# 796 HISTAMINE TREATMENT ACCELERATES LIVER REGENERATION FOLLOWING PARTIAL HEPATECTOMY BY

LIPOPOLYSACCHARIDE Edward B Little, Stephen C Hornyak, Adrian Radi, Kurt R Gehlsen, Tapio Haaparanta, Maxim Pharmaceuticals, Inc., San Diego, CA

UP-REGULATING TGF-P DESPITE PRETREATMENT WITH

3 797 STAGING SEVERITY OF ILLNESS FOR ACUTE LIVER FAlLURE IN CHILDREN Edwm Liu, Emily L Dobyns, Chirag R Parikh, Todd MacKenzie, Frederick M Karrer, Michael R Narkewicz, Ronald J Sokol, Univeisity of Colorado, Denver, CO

# 798 THE IMMUNOPARALYSIS OF ACUTE LIVER FAILURE (ALF) IS REVERSED BY ORTHOTOPIC LIVER TRANSPLANTATION (OLT) Charalambos G G Antoniades, Institute of Liver Studies, King’s College Hospital, London, UK; Edward T Davies, Department of Clinical Immunology, London, UK; Diego Vergani, Julia Wendon, Institute of Liver Studies, King’s College Hospital, London, UK

P 799 THE EFFECT OF ERYTHROPOIETIN ON SURVIVAL IN A NOVEL SMALL FOR SIZE LIVER REMNANT MOUSE MODEL G~iido Beldi, Daniel Inderbitzin, Adrian Keogh, Sonja Bisch- Knaden, Beat Gloor, Deborah M Stroka, Daniel Candinas, University Hospital Bern, Bern, Switzerland

# 800 DO SERUM PHOSPHATE AND LACTATE LEVELS PREDICT PATIENT OUTCOME IN FULMINANT HEPATLC FAILURE Moataz Seyam, Gerry C MacQuillan, Nick Murphy, James Neuberger, University Hospital Birmingham, Birmingham, UK

t 801

CYTOKINES IN PATIENTS WITH ACUTE LIVER FAILURE AND UNCONTROLLED INTRACRANIAL HYPERTENSION: EVIDENCE OF DISRUPTED BLOOD BRAIN BARRIER? Rajiv Jalan, University College London, London, UK; Steven W M Olde Daniink, Academic Hospital Maastricht, Maastricht, UK; Alistair Lee, Peter C Hayes, Scottish Liver Transplantation Unit, Edinburgh, UK; Roger Williams, University College London, London, UK

BRAIN PRODUCTION OF PRO-INFLAMMATORY

t 802 IMPAIRED BLOOD CLEARANCE OF MACROMOLECULES IN A PORCINE ACUTE LIVER FAILURE MODEL, WITH OR WITHOUT TREATMENT WITH MOLECULAR ADSORBENTS RECIRCULATING SYSTEM (MARS), SUGGESTING FUNCTIONAL ABSENCE OF LIVER SINUSOIDAL ENDOTHELIAL CELLS (LSEC) Geir I Nedredal, University Hospital of Northern Norway, Tromso, Norway; Kjetil H Elvevold, University of Tromso, Tromso, Norway; Lars M Ytreber, University Hospital of Northern Norway Tromso, Norway; Sambit Sen, University College London, London, UK; Christopher Rose, Max-Delbriick Center for Molecular Medicine, Berlin, Gemiany; Bard Smedsrod, University of Tromso, Tromso, Norway; Arthur Revhaug, University Hospital of Northern Norway, Tromso, Norway

~

# 803 INHIBITED NF-KB TRANSCRIPTIONAL REGULATION MAY

INDUCED ACUTE LIVER FAILURE IN TYPE I DIABETIC RATS Sachin S Devi, Harihara M Mehendale, The University of Louisiana at Monroe, Monroe, LA

# 804 APOPTOTIC HEPATOCYTES ACCELERATE BLOOD COAGULATION Yasuhiro Miyamoto, Yastlhiro Takikawa, Akira Ushio, Ryujin Endo, Kazuyuki Suzuki, Iwate Medical University, Morioka, Japan; Tadashi Kawakami, Esashi Hospital, Esashi, Japan

EXPLAIN FAILED TISSUE REPAIR IN THIOACETAMIDE-

~

# 805 ACTIVATION, PROLIFERATION AND DIFFERENTIATION OF

GALACTOSAMINE AND BILIARY DUCT LIGATION Qing Xie, Yumin Xu, Chungen Yan, Huijuan Zhou, Jiacheng Xiao, Xiaqiu Zhou, Hong Yu, Qing Guo, Shanghai Ruijin Hospital, Shanghai Second Medical University, Shanghai, China

PROGENITOR CELLS IN THE RAT MODEL WITH D-

# 806 THE EFFECT OF RECOMBINANT FACTOR VIIA AND FRESH FROZEN PLASMA O N THE INR IN PATIENTS WITH ACUTE AND CHRONIC LIVER FAILURE David J Quan, Nathan M Bass, Ryutaro Hirosc, University of California San Francisco, San Francisco, CA

# 807 CEREBRAL AMINO ACIDS AND INTRACRANIAL PRESSURE IN PATIENTS WITH FULMINANT HEPATIC FAILURE: A MICRODIALYSIS STUDY Flemming Tofteng, John Hauerberg, Peter Ott, Bent A Hansen, Jens Kondrup, Fin Stolze Larsen, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark



# 808 TRANSJUGULAR BIOPSY FOR BONE MARROW TRANSPLANT PATIENTS WITH HEPATOPATHY SAFE AND USEFUL? Peter Buggisch, Barbara Seegers, Andreas Koops, Susanne Petri, Nikolaus Kroger, Gerrit Kmpski, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany

~

# 809 IMPROVEMENT IN CEREBRAL LACTATE, GLUTAMATE AND ENERGY METABOLISM WITH ALBUMIN DIALYSIS IN A LARGE ANIMAL MODEL OF ACUTE LIVER FAILURE A MICRODIALYSIS STUDY Christopher Rose, Max-Delbriick Center for Molecular Medicine, Berlin, Germany; Sambit Sen, University College London, London, UK; Lars M Ytreba, University Hospital Northern Norway, Tromss, Norway; Nathan A Davies, University College London, London, UK; Geir I Nedredal, University Hospital Northern Norway, Tromss, Norway; Roger Williams, University College London, London, UK; Roger F Butterworth, Universite de Montreal, Hopital Saint-Luc, Montreal, PQ, Canada; Arthur Revhaug, University Hospital Northern Norway, Tromsa, Norway; Rajiv Jalan, University College London, London, UK

# 810 AUTOIMMUNE HEPATITIS IS AN IMPORTANT CAUSE OF ACUTE LIVER FAILURE IN CHILDREN Robert H Squires, University of Texas Southwestern Medical Center, Dallas, TX; Benjamin Shneider, Mount Sinai Medical Center, New York, NY; Ronald J Sokol, University of Colorado and The Children’s Hospital, Denver, CO; Michael R Narkewicz, The University of Colorado and the Children’s Hospital, Denver, CO; Anil Dhawan, King’s College Hospital, London, UK; Maureen Jonas, Children’s Hospital, Boston, MA; John Bucuvalas, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH; Nancy Simonds, University of Texas Southwestern Medical Center, Dallas, TX

# 811 HYPERGLYCEMIA AND BRAIN EDEMA IN PORTACAVAL- SHUNTED RATS RECEIVING AN AMMONIA INFUSION Javier Vaquero, Lakeside VA Medical Center and Northwestern University, Chicago, IL; Claudia Zwingmann, University of Bremen, Bremen, Germany; Dieter Leibfritz, Andres T Blei, Lakeside VA Medical Center and Northwestern University, Chicago, IL

# 812 APPLICABILITY OF MELD SCORING SYSTEM TO PREDICT PROGNOSIS IN PATIENTS WITH ACUTE LIVER FAILURE Cengiz Aydin, Brian Berk, John J Fung, AObaid Shakil, University of Pittsburgh, Pittsburgh, PA

#813

PATIENTS WITH ACUTE LIVER FAILURE Isao Sakaida, Teruaki Kimura, Kaoru Omori, Shuji Terai, Kiwamu Okita, Yamaguchi University, Ube-Yamaguchi, Japan

CYTOCHROME-C IS THE POSSIBLE NEW MARKER FOR THE

# 814 LACTULOSE THERAPY IN ACUTE LIVER FAILURE J Eileen Hay, Paul Angulo, Mayo Clinic, Rochester, MN; Brendan McGuire, University of Alabama at Birmingham, Birmingham, AL; Lorenzo Rossaro, University of California Davis Medical Center, Sacramento, CA; Ray Chung, Massachusetts General Hospital, Boston, MA; Santiago M~~iioz, Albert Einstein Medical Center, Philadelphia, PA; William Lee, University of Texas, Dallas, TX

# 815

RELATED ACUTE LIVER FAILURE IN THE UNITED STATES: A MULTICENTER CASE CONTROL STUDY Chun-Tao Wai, Robert J Fontana, University of Michigan, Ann Arbor, MI; Michael Schilsky, Mount Sinai Medical Center, New York, NY; Timothy McCashland, University of Nebraska, Omaha, NE; Steven Han, UCLA, Los Angeles, CA; Julie Polson, University of Texas Southwestern, Dallas, TX; Munira Hussain, University of Michigan, Ann Arbor, M1; William Lee, University of Texas Southwestern, Dallas, TX; Anna S Lok, University of Michigan, Ann Arbor, MI

MOLECULAR EPIDEMIOLOGY OF HEPATITIS B VIRUS-

H” 816 PROSTAGLANDIN 12-ANALOGUE, BERAPROST SODIUM, PREVENTS CONCANAVALIN A-INDUCED LIVER INJURY THROUGH IMPROVEMENT OF HEPATIC BLOOD CIRCULATION AND SUPPRESSION OF CYTOKINE PI‘,ODUCTION IN MICE Satoshi Ohta, Marie Fukushima, Masami Kuniyosi, Shusuke Morizono, Kyushu University, Fukuoka, Japan; Rie Sugimoto, Hara-Sansin Hospital, Fukuoka, Japan; Munechika Enjoji, Makoto Nakamuta, Kyushu University, Fukuoka, Japan

Cell Biology and Signal Transduction

8 #817

IS REQUIRED FOR MITOCHONDRIAL TARGETING IN HEPATOCYTES Kelly R Pitts, Mark A McNiven, Yisang Yoon, Mayo Clinic, Rochester, MN

THE C-TERMINUS OF THE DYNAMIN-LIKE PROTEIN DLPl

25 #818 FUNCTIONAL ANALYSIS OF THE CYTOSKELETAL PROTEIN

EXPRESSED IN LIVER Costa Schmitz, Zhanhai Su, Susanne Strand, Peter R Galle, Johannes Gutenberg University, Mainz, Germany; Dennis Strand, 1. Dept. of Internal Medicine, Mainz, Germany

HUGL-2, A TUMOR SUPPRESSOR-HOMOLOGUE HIGHLY

8 47819 CONDITIONAL ABLATION OF C-MET REVEALS AN ESSENTIAL ROLE IN LIVER REPAIR AFTER INJURY Valentina M Factor, Chang-Goo Huh, Aranzazu Sanchez, Koichi Uchida, Elizabeth A Comer, Snorri S Thorgeirsson, National Cancer Institute, Bethesda, MD

8 $820 KERATIN 8 Y53H AND G61C MUTATIONS ARE NO GENETIC RISK FACTORS FOR DEVELOPING CRYPTOGENIC OR NONCRYPTOGENIC LIVER DISEASE

Charite, Humboldt-University, Berlin, Germany; Olfert Landt, TIB MOLBIOL, Berlin, Germany; Bertram Wiedenmann, Werner Luck, Heiko Witt, Charite, Humboldt-University, Berlin, Germany

DYNAMIN MEDIATES MICROTUBULE-CENTROSOME \I

Juliane Halangk, Thomas Berg, Gero Puhl, Tobias Mueller, 0 1 3 0 s

g # 821 ;% ORGANIZATION IN HEPATOCYTES Heather M Thompson, Mark A McNiven, Mayo Clinic, Rochester, MN

8 $822

EARLY AND LATE ENDOSOMES IS MEDIATED BY DISTINCT MOTOR PROTEINS Eustratios Bananis, John W Murray, Richard J Stockert, Peter Satir, Allan W Wolkoff, Albert Einstein College of Medicine, Bronx, NY

MICROTUBULE-BASED BI-DIRECTIONAL MOTILITY OF


Y 823

DNA SYNTHESIS AND CELL PROLIFERATION IN RAT LIVER AFTER PARTIAL HEPATECTOMY Peter Starkel, Christine Sempoux, Christine Desaeger, St. Luc University Hospital, Brussels, Belgium; Eric Legrand, Universite Catholique de Louvain, Brussels, Belgium; Yves Horsmans, St. Luc University Hospital, Brussels, Belgium

THE CDK2 INHIBITOR CYC202 (R-ROSCOVITINE) INHIBITS 8 #832

FIBROBLAST GROWTH FACTOR (FGF) AND HEPATOCYTE GROWTH FACTOR (HGF) SIGNALING IN HUMAN HEPATOCELLULAR CARCINOMA Jin-Ping Lai, Jeremy R Chien, Julie K Staub, Ileana Aderca, Damian P Montoya, Tori A Matthews, David I Smith, Eddie L Greene, Viji Shridhar, Lewis R Roberts, Mayo Clinic, Rochester, MN

A NOVEL SULFATASE, HSULFI, DOWN-REGULATES

# 824 MULTIPLE KINASES REGULATE ADAPTOR PROTEIN COMPLEXING WITH THE ASIALOGLYCOPROTEIN RECEPTOR CYTOPLASMIC DOMAIN Tianmin Huang, Allan W Wolkoff, Richard J Stockert, Albert Einstein College of Medicine, Bronx, NY

# 825

OF ENDOCYTOSED ASIALOGLYCOPROTEIN IN LIVING HEPATOCYTES FOLLOWING DISRUPTION OF ENDOSOMAL PH Sangeeta Nath, Eustratios Bananis, Allan W Wolkoff, John W Murray, Albert Einstein College of Medicine, Bronx, NY

# 826 UCP2 EXPRESSION IN MOUSE HEPATOCYTES IS REGULATED BY INTRACELLULAR ATP AND IS ASSOCIATED WITH CELL PROLIFERATION Gang Cheng, Carmen C Polito, Julia K Haines, Xin Zhou, Michael Schmidt, Kenneth D Chavin, Medical University of South Carolina, Charleston, SC

PERTURBATION OF MICROTUBULE-BASED TRAFFICKING

tt 827 POLARIZED TRANSPORT DIFFERENTIATION OF SMALL HEPTOCYTES IN CULTURE Marguerite-Anne Sidler, University Hospital, Zurich, Switzerland; Mathias Hochli, University of Zurich, Zurich, Switzerland; Daniel Inderbitzin, Insel Hospital, Bern, Switzerland; Peter J Meier, Bruno Stieger, University Hospital, Zurich, Switzerland

X 828 PROINFLAMMATORY CYTOKINES STIMULATE IMMORTALIZED BILIARY EPITHELIAL CELLS (IBECS) T O CHEMOATTRACT T CELLS Haimei Wang, Marius Braun, Cedars-Sinai Medical Center, Los Angeles, CA; Oliver Hartley, Centre Medicale Universitaire, Geneve, Switzerland; john M Vierling, Cedars-Sinai Medical Center, Los Angeles, CA

# 829

HEPATOCYTES IN CULTURE Yutaka Uniehara, Thomas Hui, Marjorie R Chelly, Takeshi Aoki, Arthur H Cohen, Achilles A Demetriou, Jacek Rozga, Cedars- Sinai Medical Center, Los Angeles, CA

P 830

SUPPRESSES CELL GROWTH AND COLLAGEN PRODUCTION IN RAT HEPATIC STELLATE CELLS Marie Fukushima, Satoshi Olita, Masami Kuniyoshi, Munechika Enjoji, Makoto Nakamuta, Kyushu University, Fukuoka, Japan

t 831 DEVELOPMENT OF A GC/MS ASSAY FOR THE CHARACTERIZATION OF LEAN, STEATOTIC AND CERULENIN TREATED LIVERS Ryan Fiorini, Stephen Shafizadeh, Michael Schmidt, Kenneth D Chavin, Medical University of South Carolina, Charleston, SC

FREEZE-DRIED LIVER POWDER (FDLP) SUPPORTSRAT

HYDROXYFASUDIL, A RHO-KINASE (ROCK) INHIBITOR,

8 Denotes AASLD I’residential Poster of Distinction

8 #833 BILE ACID MEDIATED ACTIVATION OF JNK REQUIRES THE BILE ACID NUCLEAR RECEPTOR FXR Amethyst C Kurbegov, Sundararajah Thevananther, Andrew M Perry Saul J Karpen, Baylor College of Medicine, Houston, TX

8 #834 FUNCTIONAL CONSEQUENCES OF FRIZZLED-7 RECEPTOR OVER-EXPRESSION IN HUMAN HEPATOCELLULAR CARCINOMA Philippe Merle, Suzanne de la Monte, Marc Herrmann, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI; Shinji Tanaka, Kyushu University, Fukuoka, Japan; Miran Kim, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI; Christian Trkpo, Hotel U271, Hotel-Dieu, Lyon, France; Jack Wands, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

8 #835

IN HUMAN HCC CELLS Tomomi Kogiso, Hikaru Nagahara, Keiko Shiratori, Tokyo Women’s Medical University, Tokyo, Japan Travel Award Recipient

P21CIPl SIRNA ENHANCED TGF-P-MEDIATED APOPTOSIS

8 #836 HYPOTHALAMIC VASOPRESSIN RELEASE AND HEPATOCYTE CA2+ SIGNALING DURING LIVER REGENERATION: AN INTERPLAY STIMULATING LIVER GROWTH AND BILE FLOW Alexandra Nicou, Valerie Serriere, Sylvie Prigent, Sylviane Boucherie, Laurent Combettes, INSERM, Orsay, France; Gilles Guillon, INSERM, Montpellier, France; Gerard Alonso, CNRS, Montpellier, France; Thierry Tordjmann, INSERM, Orsay France

8 #837 TRANSFORMING GROWTH FACTOR BETA 1-INDUCED HEPATOCYTE APOPTOSIS IS MEDIATED BY SMAD3- DEPENDENT ACUTE GENERATION OF REACTIVE OXYGEN SPECIES Dalliah Black, Suzanne Lyman, Ting Qian, John J LeMasters, Richard Rippe, Kevin E Behrns, University of North Carolina at Chapel Hill, Chapel Hill, NC Travel Award Recipient

8 #838

IN VIVO AND PROTECT FROM LIVER INJURY Tom Luedde, Ulrike Assmus, Torsten Wuestefeld, Medical School of Hannover, Hannover, Germany; Manolis Pasparakis, EMBL Monterotondo, Monterotondo (Rome), Italy; Michael P Manns, Christian Trautwein, Medical School of Hannover, Hannover, Germany Rai.4 Auwd Recipient

8 #839 ERK1/2 MAPK SIGNALING PROMOTED ASSEMBLY FORMATION OF P27KIP1 WITH CYCE:CDK2 LEADING T O G1

Hikaru Nagahara, Tomomi Kogiso, Keiko Shiratori, Tokyo Women’s Medical University, Tokyo, Japan

IKK-BETA INDEPENDENT PATHWAYS CAN ACTIVATE NF-KB

CELL CYCLE ARREST IN HGF-TREATED HEPG2 CELLS


8 # 840 DNP73 REGULATES NFKB-DEPENDENT PROLIFERATION AND COUNTERACTS P53 AND TAP73-INDUCED GROWTH ARREST OF HEPATOCYTES Stefania Vossio, Emanuele Palescandolo, Francesca Moretti, Marcella Fulco, Antonio Costanzo, Fondazione Andrea Cesalpino, Rome, Italy; Clara Balsano, University of L'Aquila, L' Aquila, Italy; Massimo Levrero, Fondazione Andrea Cesalpino, Rome, Italy

8 # 841 INTEGRIN-STIMULATED CELL SCATTERING IS REGULATED BY EXTRACELLULAR SIGNAL-REGULATED KINASE (ERK) PATHWAYS IN HIGHLY METASTATIC HEPATOCELLULAR CARCINOMA CELLS Nobuyuki Honma, Takuya Genda, Yasunobu Matsuda, Takafumi Ichida, Yutaka Aoyagi, Niigata University Graduate School of Medical and Dental Sciences, Niigata City, Japan

8 #842

CYTOKINE REGULATION Yvonne Drechsler, Laszlo Romics Jr, Weibo Li, Gyongyi Szabo, University of Massachusetts Medical School, Worcester, MA

# 843 IKBA AND IKBB POSSESS INJURY CONTEXT SPECIFIC

INDUCTION AND INFLAMMATION TO ENDOTOXIN AND ISCHEMIA/REPERFUSION Chenguang Fan, Qiang Li, Yulong Zhang, Xiaoming Liu, Weihong Zhou, John F Engelhardt, University of Iowa, Iowa City, IA

ROLE OF HEME OXYGENASE-1 IN ALCOHOL MEDIATED

FUNCTIONS THAT UNIQUELY INFLUENCE HEPATIC NF-KB

# 844 PROTECTION OF TRANSFORMING FACTOR-BETAl- INDUCED APOPTOSIS BY BETAl-INTEGRIN IN HUMAN HEPATOMA CELLS Iwata Ozaki, Hao Zhang, Toshihiko Mizuta, Tom Yoshimura, Saga Medical School, Saga, Japan; Sachiko Matsuhashi, Towa University, Fukuoka, Japan; Yuichiro Eguchi, Tsutomu Yasutake, Akitaka Hisatomi, Kyosuke Yamamoto, Saga Medical School, Saga, Japan

# 845 HIGH MORTALITY AND DELAYED ONSET OF PROLIFERATION AFTER PARTIAL HEPATECTOMY IN TRANSGENIC MICE EXPRESSING DOMINANT NEGATIVE MORTllFADD IN HEPATOCYTES Marcus Schuchmann, Felix Ruckert, Andrea Karg, Jurgen Burg, Wolfgang Schreiber, University of Mainz, Mainz, Germany; David Wallach, The Weizmann Institute of Science, Rehovot, Israel; Ansgar W Lohse, Peter R Galle, University of Mainz, Mainz, Germany Travel Award Recipient

# 846 LEUCINE STIMULATES HGF PRODUCTION BY HEPATIC

SIGNALING PATHWAY Tomoaki Tomiya, Yukiko Inoue, University of Tokyo, Tokyo, Japan; Miho Yamaoka, Saitama Medical School, Saitama, Japan; Mikio Yanase, Masahiro Arai, Hitoshi Ikeda, Kazuaki Tejima, Kayo Nagashima, Takako Nishikawa, Naoko Watanabe, Masao Omata, University of Tokyo, Tokyo, Japan; Kenji Fujiwara, Saitama Medical School, Saitama, Japan

STELLATE CELLS THROUGH AN MTOR-DEPENDENT

# 847 HYPOOSMOTIC SWELLING INCREASES PROTEIN TYROSINE NITRATION IN CULTURED RAT ASTROCYTES Freimut Schliess, Natalie Foster, Boris Gorg, Roland Reinehr, Dieter Haussinger, Heinrich-Heine-University, Diisseldorf, Germany

# 848

RESTORATION OF QUIESCENCE IN THE REGENERATING LIVER AND OF THE LIVER MASS: BODY WEIGHT RATIO AFTER PARTIAL HEPATECTOMY Judith Romero-Gallo, Anna Chytil, William Russell, Mark Magnuson, Shiva Gautam, Harold Moses, William M Grady, Vanderbilt University Medical School, Nashville, TN

TGF-P SIGNAL PATHWAY ACTIVATION REGULATES

# 849

CD95/EGF RECEPTOR ASSOCIATION AND TYROSINE PHOSPHORYLATION OF CD95 AS PREREQUISITES FOR CD95 MEMBRANE TRAFFICKING AND DISC FORMATION Roland Reinehr, Freimut Schliess, Dieter Haussinger, Universitatsklinikum Diisseldorf, Duesseldorf, Germany

CD95-LIGAND AND HYPEROSMOLARITY TRIGGER

# 850 INHIBITON OF HEPATOCELLULAR CARCINOMA (HCC)

Diarmuid M Moran, UNC at Charlotte, Charlotte, NC; Teressa A Zimmers, Leonidas G Koniaris, University of Miami, Miami, FL; Iain H McKillop, UNC at Charlotte, Charlotte, NC

CELL GROWTH BY INTERLEUKIN-6

# 851

HEPATOCELLULAR CARCINOMA (HCC) GROWTH Julie A Price, Stephen J Kovach, Nicholas G Theodorakis, University of Rochester Medical Center, Rochester, NY; Iain H McKillop, UNC at Charlotte, Charlotte, NC

STIMULATORY G-PROTEIN (GS) INHIBITION OF

# 852 CHRONIC ETHANOL EXPOSURE WITH FOLATE DEFICIENCY PROMOTES HEPATOCELLULAR APOPTOSIS SIGNALS IN THE MICROPIG Farah Esfandiari, Donna H Wong, Charles H Halsted, University of California Davis, Davis, CA

# 853 P38 MAPK INDUCED G1 CELL CYCLE ARREST THROUGH UP-REGULATION OF PZlCIPl IN TGF-P -TREATED HUMAN HCCS Tomomi Kogiso, Hikaru Nagahara, Keiko Shiratori, Tokyo Women's Medical University, Tokyo, Japan

# 854 BACTERIAL DNA ACTIVATES TYPE I IMMUNE RESPONSE IN PERITONEAL MACROPHAGES FROM PATIENTS WITH CIRRHOSIS AND ASCITES Ruben Frances, Carlos Muiioz, Pedro Zapater, Sonia Pascual, Miguel Perez-Mateo, Jose Such, Hospital General Universitario, Alicante, Spain

# 855 DEFICIENT STAT3 DNA-BINDING AND INCREASED PIASJ, BCL-2 AND BCL-X EXPRESSION IN ALD AND HCV LIVER CIRRHOSIS Peter Starkel, Christine Desaeger, Valerie Lebrun, St. Luc University Hospital, Brussels, Belgium; Alastair J Strain, University of Birmingham, Birmingham, U K Yves Horsmans, St. Luc University Hospital, Brussels, Belgium


X 856

SYSTEM IN THE GROWTH OF HEPATOMA CELL LINES IN VlTRO Hidelu Fujii, Yoshito Itoh, Kanji Yamaguchi, Norihito Yamauchi, Koujirou Mori, Masahito Minami, Tomoki Nakajima, Takeshi Okanoue, Kyoto Prefectural University, Graduate School of Medicine, Kyoto, Japan

INVOLVEMENT OF CHEMOKINE-CHEMOKINE RECEPTOR

f i 857 FN-T/STATl ACTS AS A PRO-INFLAMMATORY SIGNAL IN T CELL-MEDIATED HEPATITIS VIA INDUCTION OF MULTIPLE CHEMOKINES AND ADHESION MOLECULES: A CRITICAL

Barbara Jamga, Won-Ho Kim, Feng Hong, Bin Gao, NIHINIAAA, Rockville, MU

ROLE OF IRF-1

f 858

Erika L Lawson, Nikia Laurie, Brown University, Providence, RI; Helen Callanan, Debra Britt, Douglas C Hixson, Rhode Island Hospital, Providence, RI

# 859 UNEXPECTED IDENTIFICATION OF THE B LYMPHOCYTE TRANSCRIPTION FACTOR PAX5 IN MOUSE IMMORTALIZED BILIARY EPITHELIAL CELLS (IBECS) STIMULATED WITH LIPOPOLYSACCHARIDE OR PROINFLAMMATORY CYTOKINES Haimei Wang, Cedars-Sinai Medical Center, Encino, CA; Marius Braun, John M Vierling, Cedars-Sinai Medical Center, Los Angeles, CA

THE EFFECTS OF CEACAMlB-4S ON TUMORIGENICITY

Cell Death

8 # 860 EXPRESSION OF THE NF-KAPPAB TARGET GENE IEX-IS ENHANCES TNF-ALPHA INDUCED HEPATOCYTE APOPTOSIS BY INHIBITING AKT ACTIVATION Yosuke Osawa, Masahito Nagaki, Gifu University School of Medicine, Gifu City, Japan; David A Brenner, University of North Carolina, Chapel Hill, NC; Hisataka Moriwaki, Gifu University School of Medicine, Gifu City, Japan

8 # 861 TISSUE REPAIR: A KEY PLAYER IN INCREASED CARBON

DIABETIC RATS Sharmilee P Sawant, hnkur V Dnyanmote, The University of Louisiana at Monroe, Monroe, LA; John R Latendresse, Pathology Associates International, NCTR-A Charles River Company, Jetferson, AR; Harihara M Mehendale, The University of Louisiana at Monroe, Monroe, LA

P 862

ENHANCES CD95/FAS MEDIATED APOPTOSIS AND INDUCES G2/M CELL CYCLE ARREST IN LIVER CELLS Christian Kuntzen, Alexander L Gerbes, Soeren T Eichhorst, LMU Munich Grosshadern, Munich, Germany Travel Award Recipient

TETRACHLORIDE-HEPATOTOXICITY IN TYPE 2

INHIBITION OF JUN-N-TERMINAL KINASE 1/2 (JNK1/2)

P 863

INDUCED APOPTOSIS OF MURINE HEPATOCYTES BY PREVENTION OF SIGNALING PATHWAY AT MITOCHONDRIA Toinohiro Shiotani, Iw'io lkai, Etsuro Hatano, Kyoto University, Kyoto, Japan

PHOSPHOCREATINE ACCUMULATION INHIBITS TNF-a

# 864

PROTECTS MICE FROM CHOLESTATIC LIVER INJURY Peter Fickert, Michael Trauner, Andrea Fuchsbichler, Gernot Zollner, Martin Wagner, Karl-Franzens University, Graz, Austria; Rainer Zenz, Research Insitute of Molecular Pathology, Vienna, Austria; Zsuzsanna Zsengeller, Csaba Szabo, Inotek Pharmaceuticals Corporation, Beverly, MA; Helmut Denk, Karl-Franzens University, Graz, Austria

INHIBITION OF POLY(ADP-RIBOSE) POLYMERASE (PARP)

# 865 BILE ACID FEEDING PROTECTS CHOLANGIOCYTES FROM

STIMULATING CHOLANGIOCYTE VEGF SECRETION THROUGH A PI3K/AKT DEPENDENT MECHANISM Shannon Glaser, Heather Francis, Silvia Taffetani, Jo Lynne Phinizy, Scott and White Hospital, Temple, TX; Domenico Alvaro, Eugenio Gaudio, University of Rome La Sapienza, Rome, Italy; Trenton Horst, Scott and White Hospital, Temple, TX; Marco Marzioni, University of Ancona, Ancona, Italy; Gene LeSage, The University of Texas Houston Medical School, Houston, TX; Brandy Bauniann, Julie Venter, Giammarco Fava, The Texas A & M University System HSC COM, Temple, TX; Yoshiyuki Ueno, Tohoku University School of Medicine, Sendai, Japan; Giaiifranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

$866 REACTIVE OXYGEN SPECIES INDUCE HEPATOCYTE CELL DEATH VIA DIFFERENT MECHANISMS: A BALANCE BETWEEN APOPTOSIS AND NECROSIS Laura Conde de la Rosa, Marieke H Schoemaker, Manon Homan, Peter L M Jansen, Han Moshage, University Hospital Groningen, Groningen, Netherlands

HEPATIC ARTERY LIGATION-INDUCED APOPTOSIS BY

P 867 CHEMOKINES PROTECT AGAINST PARACETAMOL HEPATOTOXICITY IN IN VITRO MODEL SYSTEMS Carylyn J Marek, University of Aberdeen, Aberdeen, UK; John Frew, University of Edinburgh, Edinburgh, UK; Ken J Simpson, Scottish Liver Transplantation Unit, Edinburgh, UK; Matthew C Wright, University of Aberdeen, Aberdeen, UK

P 868 LITHIUM CHLORIDE INDUCES NFKB AND JNK ACTIVATION AND CELL DEATH IN HUMAN HEPATOMA

CYTOTOXICITY Leila Gobejishvili, University of Louisville, Louisville, KY

CELLS AND SENSITIZES THEM TO TNF-ALPHA

4 869 THE BILE ACID TAUROCHOLIC ACID PROTECTS AGAINST

BILE DUCT LIGATED (BDL) RATS BY ACTIVATION OF THE PI3K/AKT-DEPENDENT PATHWAY Silvia Taffetani, Shannon Glaser, Heather Francis, Scott and White Hospital, Temple, TX; Yoshiyuki Ueno, Tohoku University School of Medicine, Sendai, Japan; Tushar Patel, Scott and White Hospital and The Texas A&M University System HSC COM, Temple, TX; Jo Lynne Phinizy, Scott and White Hospital, Temple, TX; Marco Marzioni, Antonio Benedetti, University of Ancona, Ancona, Italy; Giammarco Fava, Brandy Baumann, Julie Venter, The Texas A & M University System HSC COM, Temple, TX; Giantranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

TNF-ALPHA INDUCED CHOLANGIOCYTE APOPTOSIS IN



# 870 MITOCHONDRIAL GLUTATHIONE UNFOLDS THE

ALPHA (TNF) Montserrat Mari, Anna Colell, Carmen Garcia-Ruiz, Jose Carlos Femfindez-Checa, Hospital Clinic, IDIBAPS, CSIC, Barcelona, Spain

f; 871

INHIBITOR: PRECLINICAL EFFICACY AND SAFETY Niel C Hoglen, Craig D Fisher, Brad P Hirakawa, Karen L Valentino, David A Shapiro, Patricia C Contreras, Idun Pharmaceuticals, Inc., San Diego, CA

# 872

APOPTOTIC POTENTIAL OF TUMOR NECROSIS FACTOR-

IDN-6556, THE FIRST ANTI-APOPTOTIC CASPASE

TUMOR NECROSIS FACTOR (TNF)- ALFA MEDIATED APOPTOSIS IN ANTI-TUBERCULAR DRUG INDUCED HEPATOTOXICITY Abhijit Chowdhury, Institute of Post Graduate Medical Education and Research, Kolkata, India

# 873

PROTECT HEPATOCYTES FROM APOPTOSIS INDUCED BY

Sumiko Nagoshi, Saitama Medical School, Saitama, Japan; Takayuki Yoshimoto, Tokyo Medical University, Tokyo, Japan; Satoshi Mochida, Kenji Fujiwara, Saitama Medical School, Saitama, Tapan

INHIBITOR OF APOPTOSIS PROTEIN-1 AND -2 MAY

TUMOR NECROSIS FACTOR-ALPHA IN MICE

# 874

INHIBITOR IN CLINICAL TRIALS: TISSUE DISTRIBUTION AND PHARMACOKINETICS Long-Shiuh Chen, Niel C Hoglen, Craig D Fisher, Karen L Valentino, Patricia C Contreras, Idun Pharmaceuticals, Inc., San Diego, CA

# 875 Withdrawn

IDN-6556, THE FIRST ANTI-APOPTOTIC CASPASE

Gene Expression and Therapy

8 # 876 EXPRESSION OF A SHORT CYCLIN E l SPLICE VARIANT INVERSELY CORRELATES WITH CELL CYCLE PROGRESSION OF HEPATOCYTES Nils-Holger Zschemisch, Christian Liedtke, Torsten Wustefeld, Medical School of Hannover, Hannover, Germany; Roman Halter, Juergen Borlack, Fraunhofer Institute of Toxicology and Experimental Medicine, Hanover, Germany; Michael P Manns, Christian Trautwein, Medical School of Hannover, Hannover, Germany

8 #877

OF COLON CANCER DIFFERENCE IN GENERATION OF INNATE AND ADAPTIVE IMMUNE RESPONSES Chihiro Ohnishi, Tetsuo Takehara, Takahiro Suzuki, Masahisa Jinushi, Takuya Miyagi, Tomohide Tatsumi, Naoki Hiramatsu, Tatsuya Kanto, Norio Hayashi, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

IL-12 AND IFNa GENE THERAPY FOR HEPATIC METASTASIS

8 # 878 HEPATIC OVEREXPRESSION OF TGF-BETA 1 DURING LIVER INJURY LEADS TO MASSIVELY INCREASED IL-6 LEVELS AND HIGH MORTALITY RATES Florian R Thieringer, Jose F Garcia-Lazaro, Piotr Czochra, Diana Friebe, Erik Meyer, Stefan Liith, Marcus Schuchmann, Peter R Galle, Ansgar W Lohse, Stephan Kanzler, Johannes Gutenberg University, Mainz, Germany

8 # 879

GLUCOSE AND HEME Sridevi Kolluri, University of Connecticut Health Center, Farmington, CT; Timothy J Sadlon, Child Health Research Institute, North Adelaide, Australia; Brian K May, University of Adelaide, Adelaide, Australia; Herbert L Bonkovsky, University of Connecticut Health Center, Farmington, CT

REGULATION OF 5-AMINOLEVULINATE SYNTHASE-1 BY

s#sso CASPASE-8 TRANSCRIPTION CAN RAPIDLY BE UPREGULATED UPON INTERFERON a STIMULATION VIA A STAT1 DEPENDENT MECHANISM IN HUMAN HEPATOMA CELLS Christian Liedtke, Michael P Manns, Christian Trautwein, Medical School of Hannover, Hannover, Germany

8 #881 REGULATION OF FERROCHELATASE GENE EXPRESSION BY HYPOXIA IN HUMAN CELL LINES Yunying L Liu, Douglas A Weigent, University of Alabama at Birmingham, Birmingham, AL; Sonny 0 Ang, Josef T Prchal, Baylor College of Medicine, Houston, TX; Joseph R Bloomer, University of Alabama at Birmingham, Birmingham, AL

FAMILIAL INTRAHEPATIC CHOLESTASIS MUTATION DETECTION IN THE SAUDI ARABIAN AND ISRAELI POPULATIONS Anthony Antoniou, Sandra Strautnieks, Institute of Liver Studies, King’s College Hospital, London, UK; Laura Bull, Julie Vargus, Ludmilla Pawlikowska, UCSF Liver Center Laboratory, San Francisco, CA; Jane Byrne, Institute of Liver Studies, King’s College Hospital, London, UK; Cathy Hartman, Meyer Children’s Hospital, Haifa, Israel; H Hebby, A Bassas, Riyadh Armed Forces Hospital, Riyadh, Saudi Arabia; A Kagalwalla, Naperville, Naperville, IL; Nigel Heaton, Giorgina Mieli-Vergani, Institute of Liver Studies, King’s College Hospital, London, UK; R Shamir, Meyer Children’s Hospital, Haifa, Israel; Sami Wali, Ryadh Armed Forces Hospital, Riyadh, Saudi Arabia; Richard Thompson, Institute of Liver Studies, King’s College Hospital, London, UK

8 # 8 8 3 THE IMPACT OF TELOMERE SHORTENING ON LIVER

HEPATOCARCINOGENESIS A Satyanarayana, S Wiemann, A C Kabbasch, M P Manns, Karl L Rudolph, Medical School of Hannover, Hannover, Germany

REGENERATION, DNA-DAMAGE-RESPONSE AND

8 # 884 URSODEOXYCHOLIC ACID MODULATES THE RB/EZF-l APOPTOTIC PATHWAY IN RAT HEPATOCYTES AS DETERMINED BY MICROARRAY ANALYSIS Rui E Castro, Susana Sola, University of Lisbon, Faculty of Pharmacy, Lisbon, Portugal; Betsy T Kren, Clifford J Steer, University of Minnesota Medical School, Minneapolis, MN; Cecilia M P Rodrigues, University of Lisbon, Faculty of Pharmacy, Lisbon, Portugal Travel Award Recipient

123.A POSTER SESSIONS HEPATOLOGY, October 2003

If 885 METALLOPROTEINASE-8 GENE DELIVERY UP-REGULATES MMP-2, MMP-3 AND INDUCES CELL PROLIFERATION IN EXPERIMENTAL LIVER CIRRHOSIS Juan Armendariz-Borunda, Fernando Siller-Lopez, Jesus Garcia, Ana Sandoval, Silvia Salgado, Adriana Salazar, University of Guadalajara, Guadalajara, Jalisco, Mexico; Estuardo Aguilar- Cordova, Advantagene, Inc., San Diego, CA

# 886 IDENTIFICATION OF KEY ELEMENTS THAT ARE RESPONSIBLE FOR HEME-MEDIATED INDUCTION ON THE HEME OXYGENASE-1 GENE Ying Shnn, Richard W Lambrecht, Herbert L Bonkovsky, University of Connecticut Health Center, Farmington, CT

~~~~~~~~~ ~ ~~

# 887 PROTEOMIC ANALYSIS OF DIFFERENTIALLY EXPRESSED PROTEINS IN HEPATOCELLULAR CARCINOMA DEVELOPED IN PATIENTS WITH CHRONIC VIRAL HEPATITIS C Jean-Frederic Blaiic, INSERM EM1 0362 Universite Bordeaux 2, Bordeaux, France; Celine Lalanne, Christophe Plomion, INM- Pierroton, Cestas, France; Jean-Marie Schmitter, Uiiiversite Bordeaux 1, Pessac, France; Paulette Bioulac-Sage, Charles Balabaud, INSERM EM1 0362 Universite Bordeaux 2, Bordeaux, France; Marc Bonneu, Universite Bordeaux 2, Bordeaux, France; Jean Rosenbaurn, INSEIM EM1 0362 Universite Bordeaux 2, Bordeaux, France

f 888

EXPRESSION IN HEPATIC STELLATE CELLS VIA UPREGULATION OF SMAD7 Harun M Said, Peter Mertens, Abdelaziz Ennia, Axel M Gressner, Steven Dooley, University Hospital, RWTH, Aachen, Germany

THE Y-BOX PROTEIN YB-1 SUPPRESSES COLLAGEN

X 889 ROLE OF C-JUN N-TERMINAL KINASE PATHWAY FOR MATRIX METALLOPROTEINASE-1 EXPRESSION IN HEPATOCELLULAR CARTINOMA Yoshihiko Sugioka, Tetsu Watanabe, Yutaka Inagaki, Maki Niioka, Hitoslu Endo, Reiichi Higashiyama, Miwa Kushda, Isao Okazaki, Tokai University, Isehara, Kanagawa, Japan

~~

i: 890 THE MOLECULAR MECHANISMS OF VITAMIN K2 AS A PROMISING CHEMOPREVENTIVE DRUG IN THE MANAGEMENT OF HEPATOCELLULAR CARCINOMA Motoyuki Otsuka, Yukihiro Koike, Naoya Kato, Run-Xuan Shao, Yuujin Hoshida, Masaru Moriyama, Taniguchi Hiroyoshi, Takayuki Kawakami, Hideaki Ijichi, Keisuke Tateishi, Yasushi Shiratori, Takao Kawabe, Masao Omata, Graduate School of Medicine, University of Tokyo, Tokyo, Japan

# 891

GENESIS OF HUMAN HEPATOCELLULAR CARCINOMA Philippe Merle, Suzanne de la Monte, Marc Herrmann, Liver Research Center, RI Hospital and Brown Medical School, Providcnce, R1; Shinji Tanaka, Kyushu University, Fukuoka, Japan; Michael Kew, Witwatersrand University Medical School, Johannesburg, South Africa; Christian Treppo, INSERM U271, IHotel Dieu, Lyon, France; Jack Wands, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

THE ROLE OF FRIZZLED 7 EXPRESSION IN THE PATHO-

t 892 UP-REGULATION OF MONOUNSATURATED FATTY ACID SYNTHESISIS IS ASSOCIATED WITH THE DEVELOPMENT OF HUMAN HEPATOCELLULAR CARCINOMA Taro Yamashita, Masao Honda, Shuichi Kaneko, Kanazawa Univcr\ity Graduate School of Medical Science, Kanazawa, Japan

8 Denote5 AASLD Piesidential Poster of Distinction

# 893 LTRS IN A RETROVIRUS VECTOR EQUIPPED WITH THE SEQUENCE FROM HBV ENHANCER I1 DEMONSTRATE

TRANGENES IN VITRO AND IN VIVO Kanji Yamaguchi, Yoshito Itoh, Naoki Ohnishi, Takeshi Okanoue, Kyoto Prefectural University, Graduate School of Medicine, Kyoto, Japan; Katsuhiko Itoh, Jun Fujita, Faculty of Medicine, Kyoto University, Kyoto, Japan

HIGHER AND HEPATOCYTE-SPECIFIC EXPRESSION OF

# 894 EXPRESSION OF PARACELLULAR JUNCTION GENES IN

John P Bilello, Harriet C Isom, The Penn State University, Hershey, PA

IRON-LOADED HEPATOCYTES

~

# 895

IN RESPONSE T O HYPOXIA AND CYTOKINE STIMULATION Melanie Baker, Daniel Candinas, Deborah M Stroka, University Hospital Bern, Bern, Switzerland

ACTIVATION OF HIF-1 IN PRIMARY HUMAN HEPATOCYTES

# 896 THE NFKB INHIBITOR SULFASALAZINE ENHANCES RECOVERY FROM CCL4 INDUCED FIBROSIS: THERAPEUTIC IMPLICATIONS Derek A Mann, Fiona Oakley, University of Southampton, Southampton, UK; Caralyn Marek, University of Aberdeen, Aberdeen, UK; Murial Meso, Harry Millward-Sadler, University of Southampton, Southampton, UK; Matthew Wright, University of Aberdeen, Aberdeen, UK

i: 897 HOMOZYGOUS DELETION ON CHROMOSOME 1P36.2 AND HYPERMETHYLATION OF RIZl GENE IN HEPATOCELLULAR CARCINOMA Hiu Ming Li, Choong-Tsek Liew, Cui Juan Zhang, Lai Mu Yau, Lai Mu Yau, Paul Bo San Lai, Lin Yee Hin, Kin Wah Suen, Chinese University of Hong Kong, Hong Kong, China; Joseph Wan Yee Lau, Chinese University of Hong Kong, Shatin, Hong Kong, China

&f 898 LIVER CELL THERAPY FOR CORRECTING HEMOPHILIA A IN A MOUSE MODEL Vinay Kuniaran, Daniel Benten, Brigid Joseph, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY; Rita Sarkar, University of Pennsylvania School of Medicine, Philadelphia, PA; Sanjeev Gupta, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY

# 899 INVESTIGATION OF THE TRANSCRIPTIONAL REGULATION OF THE HUMAN BILE SALT EXPORT PUMP GENE Jane A Byme, Sandra S Strautnieks, Giorgina Mieli-Vergani, Richard J Thompson, Institute of Liver Studies, King's College Hospital, London, UK

# 900 ACYCLIC RETINOID INHIBITS THE GROWTH OF HUMAN HEPATOMA CELLS BY SUPPRESSING FGF SIGNALING PATH WAYS Run-Xuan Shao, Motoyuki Otsuka, Naoya Kato, Hiroyoshi Taniguchi, Yuujin Hoshida, Masaru Moriyama, Takao Kawabe, Masao Omata, Graduate School of Medicine, University of Tokyo, Tokyo, Japan


# 901 DNA METHYLTRANSFERASE (DNMT) 1 PROTEIN EXPRESSION IS SIGNIFICANTLY INCREASED IN HUMAN HEPATOCELLULAR CARCINOMAS WITH MALIGNANT POTENTIAL AND MAY BE A BIOLOGICAL PREDICTOR OF PROGNOSIS IN HEPATOCELLULAR CARCINOMA PATIENTS Yoshimasa Saito, Keio University School of Medicine, Tokyo, Japan; Yae Kanai, Tohru Nakagawa, Michiie Sakamoto, National Cancer Center Research Institute, Tokyo, Japan; Hidetsugu Saito, Hiromasa Ishii, Keio University School of Medicine, Tokyo, Japan; Setsuo Hirohashi, National Cancer Center Research Institute, Tokyo, Japan

# 902 Withdrawn

# 903 IDENTIFICATION OF HEPATIC GENE ISLANDS ON THE HUMAN CHROMOSOMES BY TRANSCRIPTOME MAPPING Taro Yamashita, Masao Honda, Hajime Takatori, Ryuhei Nishino, Shuichi Kaneko, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan

# 904

INCREASED MORTALITY AND ALTERED LIVER ARCHITECTURE Stefan Luth, Tanja Iakovleva, Johannes Herkel, Paco Garcia, Jurgen Burg, Kurt Reifenberg, Christian Frenzel, Stephan Kanzler, Markus Neurath, Peter R Galle, Ansgar W Lohse, University Hospital of Mainz, Mainz, Germany

# 905

LIVER-SPECIFIC IL-18-TRANSGENIC MICE DISPLAY

NITROSATIVE STRESS ENHANCES CD95-MEDIATED APOPTOSIS BUT LONG TERM EXPOSURE SELECTS FOR NO- AND APOPTOSIS-RESISTANCE Zhanhai Su, Gosta Schmitz, Peter R Galle, Dennis Strand, Susanne Strand, I. Medizin Uniklinik Mainz, Mainz, Germany

# 906 ROLE OF THE CCAAT/ENHANCER BINDING PROTEIN BETA (C/EBPB) ISOFORMS LAP AND LIP IN LIVER REGENERATION Moritz Duderstadt, Tom Luedde, Konrad L Streetz, Torsten Wuestefeld, Frank Tacke, Michael P Manns, Christian Trautwein, Medical School of Hannover, Hannover, Germany

# 907 Withdrawn

# 908 MOLECULAR MECHANISMS OF HEPATIC DIFFERENTIATION

Aaron W Bell, George K Michalopoulos, University of Pittsburgh, Pittsburgh, PA

IN- VITR 0

# 909

DEACETYLASE INHIBITION USING CDNA MICROARRAY AND ASSOCIATION BETWEEN GENE EXPRESSION AND EPIGENETIC ALTERATIONS ON HEPATOMA CELLS Tetsuhiro Chiba, Osamu Yokosuka, Makoto Arai, Motohisa Tada, Kenichi Fukai, Fumio Imazeki, Masaki Kato, Naohiko Seki, Hiromitsu Saisho, Graduate School of Medicine, Chiba University, Chiba, Japan

IDENTIFICATION OF UP-REGULATED GENES BY HISTONE

6910 STRUCTURAL AND FUNCTIONAL CHARACTERIZATION OF HUMAN HEPATIC STIMULATOR SUBSTANCE (HHSS) GENE PROMOTER Wei An, Xin-nan Wang, Zhi-gang Song, Li Chen, Yuan Wu, Capital University of Medical Sciences, Beijing, China

# 911 IRON AND INSULIN RESISTANCE: EFFECT OF IRON MANIPULATION ON INSULIN RECEPTOR IN HEPG2 CELLS Paola Dongiovanni, Luca Valenti, Lorenzo Carmagnola, Filomena Di Caterino, Anna Ludovica Fracanzani, Silvia Fargion, Universith degli Studi, Milano, Milan, Italy

#912 INVOLVEMENT OF P21WAFl/CIP1, P27KIP1, CDKP, CDK4, CDCZ, CYCLIN A AND CYCLIN B1 AND MAP KINASE SIGNAL PATHWAY IN GROWTH INHIBITION AND CELL CYCLE ARREST BY A SELECTIVE CYCLOOXYGENASE 2 INHIBITOR, ETODOLAC, IN HUMAN HEPATOCELLULAR CARCINOMA CELL LINES Jidong Cheng, Hiroyasu Imanishi, Weidong Liu, Arata Iwasaki, Hideji Nakamura, Junichi Yamanaka, Jiro Fujimoto, Toshikazu Hada, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan

# 913 FAMILIAL LIVER ADENOMATOSIS ASSOCIATED WITH HEPATOCYTE NUCLEAR FACTOR 1 ALPHA INACTIVATION Yannick Bacq, HBpital Trousseau, Tours, France; Emmanuel Jacquemin, HBpital de BicGtre, Le Kremlin Bicetre, France; Charles Balabaud, HBpital de Bordeaux, Bordeaux, France; Emmanuelle Jeannot, INSERM U434, CEPH-Fondation Jean Dausset, Paris, France; Beatrice Scotto, HBpital Trousseau, Tours, France; Sophie Branchereau, HBpital de Bicetre, Le Kremlin Bicetre, France; Christophe Lament, HBpital de Bordeaux, Bordeaux, France; Pascal Bourlier, HGpital Trousseau, Tours, France; Daniel Pariente, HBpital de Bicetre, Le Kremlin Bidtre, France; Anne de Muret, HBpital Trousseau, Tours, France; Monique Fabre, HBpital de BicGtre, Le Kremlin Bicetre, France; Paulette Bioulac-Sage, HBpital de Bordeaux, Bordeaux, France; Jessica Zucman-Rossi, INSERM U434, CEPH-Fondation Jean Dausset, Paris, France

# 914 HEPARANASE EXPRESSION DURING NORMAL LIVER DEVELOPMENT AND LIVER REGENERATION FOLLOWING PARTIAL HEPATECTOMY Orit Goldshmidt, Rita Yeikilis, Melia Paizi, Israel Vlodavsky, Gadi Spira, Technion-Israel Institute of Technology, Haifa, Israel

# 915

LIGAND IN HUMAN HEPATOCELLULAR CARCINOMA Katsuya Shiraki, Takenari Yamanaka, Hiroslu Okano, Tomoyuki Kawakita, Yukiko Saitou, Yumi Yamaguchi, Kazushi Sugimoto, Kazumoto Murata, Takeshi Nakano, 1st Medicine, Mie University, Tsu, Japan

#916 SYSTEMIC ADMINISTRATION OF AN ADENOVIRUS ENCODING A TRUNCATED, SOLUBLE DOMINANT

TUMOR MODEL FOR LIVER METASTASIS OF COLORECTAL CANCER Volker Schmitz, Tobias Hilbert, Christian Dzienisowicz, Esther Raskopf, Christian Rabe, Tilman Sauerbruch, Wolfgang H Caselmann, University Hospital Bonn, Bonn, Germany

EXPRESSION OF TNF-RELATED APOPTOSIS INDUCING

NEGATIVE VEGF (FLK-1/KDR) RECEPTOR IN A MURINE

12hA POSTER SESSIONS HEPATOLOGY, October 2003

i 917 Withdrawn

d 918

INHIBITS THE GROWTH OF LIVER CANCER CELL LINES IN VITRO AND IN VIVO Hirohisa Yano, Tom Hisaka, Seiya Momosaki, Sachiko Ogasawara, Naoyo Nishida, Yumi Takemoto, Sakiko Kojiro, Eriko Nitta, Masamichi Kojiro, Kurume University School of Medicine, Kurume, Japan

CONSENSUS INTERFERON (INTERFERON-ALPHACONl)

# 919 PROINFLAMMATORY CYTOKINES IFNr AND TNFa INDUCE GENE EXPRESSION IN MOUSE IMMORTALIZED BILIARY EPITHELIAL CELLS (IBECS) THAT INCREASES SUSCEPTIBILITY T O IMMUNOLOGIC DESTRUCTION BY T CELLS Marius Braun, Haimei Wang, Ning Ning Chai, Charles Wang, John M Vierling, Cedars-Sinai Medical Center, Los Angeles, CA

Hepatic lnflamation

8 #920 NORMAL LIVER REGENERATION AND LIVER CELL APOPTOSIS AFTER PARTIAL HEPATECTOMY IN TUMOR

Hideki Hayashi, Masahito Nagaki, Motoaki Imose, Yosuke Osawa, Takafumi Naiki, Shinichi Satake, Motohiro Imao, Kiminori Kimura, Hisataka Moriwaki, G i h University School of Medicine, Gifu City, Japan

NECROSIS FACTOR-DEFICIENT MICE

# 921 ROLE OF ADENOSINE RECEPTORS IN THE PROTECTIVE EFFECT OF ETHANOL O N GUT ISCHEMIA / REPERFUSION INDUCED HEPATOCELLULAR INJURY IN RATS Yoshiyuki Yamagishi, Yoshinori Horie, Mikio Kajihara, Masahiro Konishi, Shuka Mori, Hironao Tamai, Shinzo Kato, Hiromasa Ishii, Keio University, Tokyo, Japan

# 922 RECOMBINANT G-CSF-INDUCED FACILITATION OF BOTH LIVER REGENATION AND DOWN-REGULATION OF IL-12 PRODUCTION AFTER PARTIAL HEPATECTOMY Koichi Oishi, Keiske Hayamizu, Xeuhelati Aihaiti, Ichiro Ohmori, Toshiyuki Itamoto, Toshimasa Asahara, Hiroshima University, Hiroshima, Japan

ti 923 CLONING AND PARTIAL CHARACTERIZATION OF

REGULATOR OF NEGATIVE ACUTE PHASE PROTEINS Xiangdang Liu, Richard Whalen, Thomas D Boyer, University of Arizona, TLICSO~I, AZ

PUTATIVE RAT ILGDEX-NP, A TRANSCRIPTIONAL

8 924 PROTECTION FROM T CELL-MEDIATED HEPATITIS IN CXCR3-DEFICIENT MICE Ilaria I’etrai, Persio Dello Sbarba, Francesco Annunziato, Sara Aleffi, University of Florence, Florence, Italy; Bao Lu, Craig Gerard, Children’s Hospital and Harvard Medical School, Boston, MA; Fabio Marra, University of Florence, Florence, Italy

8 925 A CRITICAL INVOLVEMENT OF OXIDATIVE STRESS IN

PRODUCTION Zhanxiang Zhou, Lipeng Wang, Zhenyuan Song, Jason C Lambert, Craig J McClain, Y James Kang, University of Louisville, Louisville, KY

ACUTE ALCOHOL-INDUCED HEPATIC TNF-ALPHA

# 926 INFLUENCE OF ADHESION MOLECULE DELETION ON HEPATIC LISTERIOSIS IN MICE Chantal A Rivera, Waleska E Arias, M Hossein Tcharmtchi, C Wayne Smith, Baylor College of Medicine, Houston, TX

4 927

INJURY IN MICE Masahito Nagaki, Motoaki Imose, Kiminori Kimura, Takafumi Naiki, Yosuke Osawa, Atsushi Suetsugu, Takahiko Asano, Shinji Takai, Hideki Hayashi, Tomohiro Kato, Hisataka Moriwaki, Gifu University School of Medicine, Gifu City, Japan

LEFLUNOMIDE PROTECTS FROM T CELL-MEDIATED LIVER

# 928

PATIENTS WITH ADVANCED LIVER CIRRHOSIS. RESULTS

PILOT STUDY Mariam Conchillo, Clinica Universitaria and Medical School, University of Navarra, Pamplona, Spain; Robert de Knegt, University Hospital, Groningen, Netherlands; Marina Payeras, Jorge Quiroga, Bruno Sangro, Ignacio Herrero, Clinica Universitaria and Medical School, University of Navarra, Pamplona, Spain; Carl Yoshizawa, Chiron Corporation, Emeryville, CA; Peter Jansen, University Hospital, Groningen, Netherlands; Bruce Scharschmidt, Chiron Corporation, Emeryville, CA; Jesus Prieto, Clinica Universitaria and Medical School, University of Navarra, Pamplona, Spain

A 929 PROPRANOLOL BLOCKS THE URINARY ALCOHOL CYCLE OF THE INTRAGASTRIC FEEDING MODEL OF ALCOHOLIC LIVER DISEASE Jun Li, Barbara A French, Samuel W French, Harbor UCLA Medical Center REI, Torrance, CA

INSULIN-LIKE GROWTH FACTOR-I (IGF-I) THERAPY IN

OF A RANDOMIZED DOUBLE-BLIND, CONTROLLED

# 930 DIVERSE REGULATION OF NFKAPPAB ACTIVATION AND

ALCOHOL TREATMENT IN HUMAN MONOCYTES Pranoti Mandrekar, Gary Bellerose, Donna Catalano, Gyongyi Szabo, University of Massachusetts Medical Center, Worcester, MA

TNF-ALPHA PRODUCTION AFTER ACUTE AND CHRONIC

Hepatitis B Natural History and Pathogenesis

8 #931 CORRELATES OF ISOLATED HEPATITIS B CORE ANTIBODY

AND HEPATITIS C VIREMIA Diana L Sylvestre, University of California, San Francisco, Oakland, CA; Suzanne Lester, University of California, San Francisco, San Francisco, CA; Barry J Clements, O.A.S.I.S., Oakland, CA

IN INJECTION DRUG USERS: AFRICAN-AMERICAN RACE



8 #932 LONG-TERM PRODUCTIVE REPLICATION OF HEPATITIS B VIRUS (HBV) IN THE LIVER BY SINGLE INTRAVENOUS INJECTION OF NAKED HBV DNA IN IMMUNOCOMPROMISED MICE Takahiro Suzuki, Tetsuo Takehara, Kazuyoshi Ohkawa, Hisashi Ishida, Chihiro Ohnishi, Masahisa Jinushi, Takuya Miyagi, Norio Hayashi, Osaka University Graduate School of Medicine, Osaka, Japan

LONGITUDINAL ANALYSIS OF HEPATITIS B VIRUS GENOTYPE IN CHILDREN WITH CHRONIC INFECTION AND HEPATOCELLULAR CARCINOMA Yen-Hsuan Ni, Mei-Hwei Chang, National Taiwan University Hospital, Taipei, Taiwan

ASSOCIATION BETWEEN CHRONIC HEPATITIS B VIRUS

8 $933

8 #934

INFECTION AND INTERLEUKIN-10 (IL-lo), TUMOR NECROSIS FACTOR-cx (TNF-CX) GENE PROMOTER POLYMORPHISMS Jaeyoun Cheong, Sohee Hong, Kimyung Lee, Ajou University Medical College, Suwon, South Korea; Seungkew Yoon, Catholic University of Korea, Seoul, South Korea; Dohyun Kim, Eunhee Lee, Hyunjoo Song, Byungmoo Yoo, Kibaik Hahm, Jinhong Kim, Sungwon Cho, Ajou University Medical College, Suwon, South Korea

# 935 DEDIFFERENTIATION OF HEPATOCYTE MAY PROCEED AND PRIME THE LIVER FOR HYPERCARCINOGENIC STAGE IN THE HBX TRANSGENIC MOUSE Shogo Okoshi, Yasuo Takeda, Masahiko Yano, Kenta Suzuki, Yutaka Aoyagi, Niigata University School of Medicine, Niigata, Japan

# 936 DISTINCT INTRAHEPATIC IMMUNOLOGICAL ENVIRON- MENT IN CHRONIC VIRAL HEPATITIS ANALYSED BY FLOW

Dave Sprengers, Renate G van der Molen, Johannes G Kusters, Jaap Kwekkeboom, Luc J W van der Laan, Solko W Schalm, Harry LA Janssen, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands

CYTOMETRY OF FINE-NEEDLE-ASPIRATION-BIOPSIES

# 937 A PROSPECTIVE STUDY OF ABNORMAL SERUM AMINOTRANSFERASE LEVELS IN A POPULATION-BASED COHORT OF 1057 PERSONS CHRONICALLY INFECTED WITH HEPATITIS B VIRUS Brian McMahon, Alaska Native Tribal Health Consortium; Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK; Steve Livingston, Josephine Simonetti, Mary Snowball, Alaska Native Tribal Health Consortium, Anchorage, AK; Lisa Bulkow, Arctic Investigations Program, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Anchorage, AK Chriss Homan, Kathy Hurlburt, James Williams, Alaska Native Tribal Health Consortium, Anchorage, AK

# 938 IDENTIFICATION OF NATURALLY OCCURRING MUTATIONS IN THE S DOMAIN OF HEPATITIS B VIRUS ENVELOPE PROTIENS THAT MARKEDLY ENHANCE VIRION SECRETION Nasser Khan, Michael Guarnieri, Sang Hoon A h , Yonghong Zhou, Ji Su Li, Jack Wands, Shuping Tong, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

# 939 PREDICTING LIVER DISEASE SEVERITY IN E ANTIGEN NEGATIVE CHRONIC HEPATITIS B Jordan J Feld, Dalia El-Ashri, University of Toronto, UHN- TWH, Toronto, ON, Canada; Melissa Ayers, Tony Mazulli, Raymond Tellier, University of Toronto, Toronto, ON, Canada; E Jenny Heathcote, University of Toronto, UHN-TWH, Toronto, ON, Canada

# 940 HBV REPLICATION INCREASES STEADY STATE MRNA LEVEL OF SELECTED LIPID BIOSYNTHESIS GENES IN HBV TRANSGENIC MOUSE LIVER Mustapha Hajjou, Raquel Norel, Robert Carver, Albert Einstein College of Medicine, Bronx, NY; Patricia Marion, Stanford University, Palo Alto, CA; John Cullen, North Carolina State University, Raleigh, NC; Leslie E Rogler, Charles E Rogler, Albert Einstein College of Medicine, Bronx, NY

!# 941 REVERSE TRANSCRIPTION OF A NON-VIRAL RNA TEM- PLATE BY THE HUMAN HEPATITIS B-VIRUS POLYMERASE Peter Hafkemeyer, Fritz von Weizsacker, Josef Kock, Michael Nassal, University of Freiburg, Freiburg, Germany; Ira R Pastan, National Institutes of Health, Bethesda, MD; Hubert E Blum, University of Freiburg, Freiburg, Germany

# 942 HBV GENOTYPES AND PRECORE/CORE PROMOTER MUTA- TIONS IN PATIENTS WITH CHRONIC HBV INFECTION Evangelini Dimou, Henry Dunant Hospital, Athens, Greece; Andreas Laras, George V Papatheodoridis, Athens University School of Medicine, Athens, Greece; Stefanos J H a d z i y d s , Henry Dunant Hospital, Athens, Greece

# 943 NATURAL OCCURING MUTATIONS AFFECTING THE INTRAMOLECULAR DISULFIDE BOND BUT NOT SIGNAL PEPTIDASE CLEAVAGE SITE GREATLY IMPAIR HBEAG FORMATION Genie Bang, Michael Guarnieri, Ji Su Li, Yonghong Zhou, Jack Wands, Shuping Tong, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

# 944 HBX INTERACTS WITH THE PCAF ACETYLTRANSFERASE AND IT IS RECRUITED ON THE HBV CCCDNA TO INDUCE A TRANSCRIPTIONALLY ACTIVE HBV MINICHROMOSOME AND TO ACTIVATE REPLICATION Teresa Pollicino, University of Messina, Messina, Italy; Monica Di Padova, Regina Elena Cancer Institute, Rome, Italy; Natalia Pediconi, Fondazione Andrea Cesalpino, Rome, Italy; Giuseppina Raffa, Giovanni Squadrito, University of Messina, Messina, Italy; Maurizio Fanciulli, Regina Elena Cancer Institute, Rome, Italy; Giovanni Raimondo, University of Messina, Messina, Italy; Massimo Levrero, Fondazione Andrea Cesalpino, Rome, Italy

# 945 CENTRAL ROLE OF THE HEPATITIS B VIRUS X PROTEIN FOR THE INITIATION OF INFECTION IN PRIMARY HEPATOCYTE S Josef Kock, Thomas F Baumert, University of Freiburg, Freiburg, Germany; Ulrike Protzer, University of Cologne, Cologne, Germany; Hubert E Blum, Fritz von Weizsacker, University of Freiburg, Freiburg, Germany

13x.A POSTER SESSIONS HEPATOLOCY, October 2003

2 946 ASSOCIATION BETWEEN CCR5 PROMOTER POLYMORPHISM AND HEPATITIS B VIRUS INFECTION H ye-Young Chang, Yonsei University College of Medicine, BK 21 Project for Medical Science, 21C Frontier Functional Hunian Genomjc Project, Seoul, South Korea; Sang Hoon Ahn, Yonsei University College of Medicine, BK 21 Project for Medical Science, Seoul, South Korea; J i Eun Sin, Si Nae Hong, Yonsei University College of Medicine, 21C Frontier Functional Hunian Genomic Project, Seoul, South Korea; Young Myoung Moon, Chae Yoon Chon, Yonsei University College of Medicine, Seoul, South Korea; Kwang-Hyub Han, Yonsei University College of Medicine, BK 21 Project for Medical Science, 21C Frontier Functional Human Genoniic Project, Seoul, South Korea

f i 947 PRECORE AND CORE PROMOTER MUTATIONS OR SERUM HBV DNA LEVELS DO NOT ALLOW T O DISTINGUISH TRUE INACTIVE HBSAG CARRIERS FROM HBEAG NEGATIVE CHRONIC HEPATITIS B WITH FLUCTUATING ALT Michelle Martinot Peignoux, INSERM U481, Clichy, France; Nathalie Buyer, Service d’H+atologie, HBpital Beaujon, Clichy, France; Bacli-Nga Pham, Service d’H6matologie-lmmunologie Biologiques, HBpital Beaujon, Clichy, France; Vanessa Esnault, Canan Kumas, INSERM U481, Clichy, France; Patrick Marcellin, Service d’HPpatoIogie, Clichy, France

# 948 HEPATITIS B VIRUS (HBV) INFECTION, PHENOTYPE AND FUNCTION OF MYELOID AND PLASMACYTOID DENDRITIC CELLS IN PATIENTS WITH CHRONIC HEPATITIS B Sohcila Tavakoli, Denis Strand, Silke Schniitt, University Hospital, Mainz, Germany; Mona Ali, University Hospital, Freiburg, Germany; Sandra Weyer, University Hospital, Mainz, Gerniany; Michael Ceissler, University Hospital, Freiburg, Germany; Peter R Galle, Wulf 0 Boecher, University Hospital, Mainz, Germany

R 949 LOW HBV REPLICATION AND LIVER FIBROSIS: THE IMPACT OF RACE IN A STUDY OF 552 CHRONIC HEPATITIS B PATIENTS Vlad Ratziu, Vincent Thibault, Yves Benhamou, Marie-Helene Tainturier, Sophie Le Calvez, Frederic Charlotte, Thierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

ti 950 EVIDENCE FOR A REDUCED FITNESS OF THE HBV IMMUNE ESCAPE MUTANT G145R Martina Sterneck, University Hospital Hamburg-Eppendorf, Hamburg, Germany; Hans Will, Anna ku-Garcia, Heinrich Pette Institut, Hamburg, Germany; Lutz Fischer, University Hospital Hamburg-Eppcndorf, Hamburg, Germany; Tatyana Kalinina, Heinrich Pette Institut, Hamburg, Germany

k 951 EXPRESSION OF FASL AND PERFORIN/GRANZYME B MRNAIN CHRONIC HEPATITIS B Ja Young Lee, Kyung Ho Kim, Joon Yong Park, Jin Heon Lee, Hak Yang Kim, Jae Young Yoo, Hallym University College o f Medicine, Seoul, South Korea

# 952

(HBV) VARIANTS IS HIGHLY PREVALENT IN PATIENTS WITH LIVER DISEASE AND SIGNIFICANTLY ASSOCIATES WITH HEPATOCELLULAR CARCINOMA. IDENTIFICATION

MOLECULAR APPROACHES Lucy Costantino, Santa Brancatelli, Gaia Caccamo, Irene Cacaola, Giovanni Squadrito, Teresa Pollmno, Giovaruii Raimondo, University of Messina, Messina, Italy

INFECTION BY PRES2-DEFECTIVE HEPATITIS B VIRUS

OF THE PRE-S2 VARIANTS BY NON-SEQUENCING

# 953 EPIDEMIOLOGICAL DATA OF HEPATITIS B INFECTION IN FRANCE: RESULTS OF NATIONWIDE SURVEY Jean-Franqois Cadranel Sr, Centre Hospitalier Laennec de Creil, Creil, France; Bruno Lesgourgues, Centre Hospitalier du Raincy- Montfermeil, Montfermeil, France; Xavier Causse, Centre Hospitalier d’Orleans, Orl&ans, France; Pierre Lahmek, Centre Hospitalier du Raincy-Montfermeil, Montfermeil, France; Guy Bellai’che, HBpital Robert Ballanger, Aulnay sous Bois, France; Louis Bettan, Centre Hospitalier de Villeneuve Saint Georges, Villeneuve Saint Ceorges, France; Thierry Fontanges, Centre Rospitalier de Bourgoin-Jallieu, Bourgoin-Jallieu, France; Ariiaud Pauwells, Centre Hospitalier de Gonesse, Gonesse, France; Jean Henrion, Centre Hospitalier de Jolimont, Jolimont, Belgium; Michel Chousterman, Centre Hospitalier Intercommunal de Creteil, Creteil, France; Bertrand Condat, HBpital de Bry sur Manie, Bry sur Marne, France; Claude Eugene, Centre Hospitalier de Poissy, Poissy, France; Pascale Hervio, Centre Hospitalier de Pontoise, Pontoise, France; Pierre Periac, Centre Hospitalier de Saint Denis, Saint Denis, France; Henri Moindrot, Centre Hospitalier de Valence, Valence, France; Denis Grasset, Centre Hospitalier de Montauban, Montauban, France; Olivier Nouel, Centre Hospitalier de Saint Brieuc, Saint Brieuc, France; Jacques Denis, Centre Hospitalier de Corbeil-Evry, Corbeil-Evry, France

P 954 CD4tCD25+ T-REGULATORY LYMPHOCYTES SUPPORT PERSISTENT HEPATITIS B VIRUS INFECTION Simon M Rushbrook, Cambridge University, Cambridge, UK; Shilpa Chokshi, Institute of Hepatology, UCL, London, UK; Esther Uiitt, Cambridge University, Cambridge, UK; Nikolai Naoumov, Institute of Hepatology, UCL, London, UK; Graenie J M Alexander, Cambridge Universitv, Cambridne, UK

# 955 THE PREDICTIVE VALUE OF INTRAHEPATIC CD8 T-LYMPHOCYTES AND HBV CORE EXPRESSION IN RELATION TO RESPONSE TO ANTIVIRAL THERAPY FOR CHRONIC HEPATITIS B PATIENTS Thjon J Tang, Robert A de Man, Johaimes G Kusters, Jaap Kwekkeboom, Renate G van der Molen, Solko W Schalm, Harry L A Janssen, Erasnius MC, Uiiiverslty Medical Center Rotterdam, Rotterdam, Netherlands

# 956 MOLECULAR INTERACTIONS OF HEPATITlS B VIRUS NUCLEOCAPSID AND ENVELOPE PEPTIDES WITH HLA- DR1, -DR3, -DR7 AND -DR13 GLYCOPROTEINS Andrew J Godkm, Univer5ity Hospital of Wales, Cardiff, UK, Miles Davenport, Weatherall Institute of Molecular Medicine, Oxford, UK; Mark Thursz, Imperial College of Science, Technology and Medicine, London, UK, Adrian V S Hill, Weatherall Institute of Molecular Medicine, Oxtord, UK

8 Denotes AASLD I’residential Poster of Distinction


# 957 EFFECT OF CHRONIC HEPATITIS B INFECTION ON DENDRITIC CELL (DC) FUNCTION: IMPAIRED ANTIGEN

PRODUCTION BY PLASMACYTOID DC Renate G van der Molen, Dave Sprengers, Rekha S Binda, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands; Esther C de Jong, Academic Medical Center, Amsterdam, Netherlands; Johannes G Kusters, Jaap Kwekkeboom, Harry L A Janssen, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands

PRESENTATION BY MYELOID DC AND REDUCED IFN-CY.

# 958

PATIENTS: GEOGRAPHIC DISTRIBUTION AND RELATION TO VIRAL REPLICATION AND FIBROSIS Jesse T Sameel, Hubert G M Niesters, Robert A de Man, Solko W Schalm, Harry L A Janssen, Erasmus Medical Center, Rotterdam, Netherlands

# 959 COMPARISON OF HISTOLOGICAL AND CLINICAL CHANGES BETWEEN BEFORE AND AFTER SPONTANEOUS LOSS OF HEPATITIS B SURFACE ANTIGEN Sang Hoon Ahn, Yonsei University College of Medicine, BK 21 Project for Medical Science, Seoul, South Korea; Chae Yoon Chon, Yonsei University College of Medicine, Seoul, South Korea; Young Nyun Park, Hye-Young Chang, Yonsei University College of Medicine, BK 21 Project for Medical Science, Seoul, South Korea; Jun Yong Park, Yonsei University College of Medicine, Seoul, South Korea; Kwang-Hyub Han, Yonsei University College of Medicine, BK 21 Project for Medical Science, Seoul, South Korea; Chanil Park, Young Myoung Moon, Yonsei University College of Medicine, Seoul, South Korea

HEPATITIS B VIRUS GENOTYPES IN HBEAG-POSITIVE

# 960

FOR HEPATITIS B VIRUS SURFACE ANTIGEN EXPRESSION IS CONTROLLED BY CREB AND PKA Frank Tacke, Sarah Bocklage, Christina Gehrke, Christian Klein, Michael P Manns, Christian Trautwein, Medical School of Hannover, Hannover, Germany

BASAL PRESZ/S-PROMOTER ACTIVITY AND INDUCIBILITY

# 961 DISTRIBUTION OF HBVGENOTYPES AND MUTATION IN THE CORE PROMOTER AND PRECORE REGION IN ACUTE FORMS OF LIVER DISEASE IN JAPAN Takaaki Imamura, Osamu Yokosuka, Hajime Sumi, Tatso Kanda, Kenichi Fukai, Fumio Imazeki, Graduate School of Medicine, Chiba University, Chiba, Japan; Naoya Kato, Fumihiko Kanai, Masao Omata, Graduate School of Medicine, Tokyo University, Tokyo, Japan

8 962 INFLUENCE OF HBV GENOTYPE AND BASAL CORE

Tatsuo Kanda, Osamu Yokosuka, Fumio Imazeki, Hiromitsu Saisho, Keiichi Nagao, Graduate School of Medicine, Chiba University, Chiba, Japan

PROMOTER MUTATIONS TO PX-INDUCED APOPTOSIS

~~ ~

# 963

RELATED HEPATOCELLULAR CARCINOMA Yoshiki Murakami, National Tsuruga Hospital, Tsuruga, Fukui, Japan; Kenichi Saigo, Chiba University, Chiba, Japan; Masahito Minami, Kyoto Prefectural University of Medicine, Kyoto, Japan; Christian Brechot, INSERM, Paris, France; Patrizia Paterlini- Brechot, INSERM U370, Paris, France; Takeshi Okanoue, Kyoto Prefectural University of Medicine, Kyoto, Japan

ANALYSIS OF THE HBVDNA INTEGRATION IN HBV-

# 964 HBV OCCULT INFECTION IN PATIENTS WITH CHRONIC HEPATITIS C:A MULTICENTRIC PROSPECTIVE STUDY Evangelista Sagnelli, Nicola Coppola, Cecilia Marrocco, Michele Imparato, Carlo Scolastico, Second University of Naples, NapIes, Italy; Guido Piai, San Sebastian Hospital, Caserta, Italy; Lucia Cimmino, University of Federico 11, Naples, Italy; Antonio Giorgio, A.O. Cotugno, Naples, Italy; Armando Marone, Catenna Sagnelli, Pietro Filippini, Felice Piccinino, Second University of Naples, Naples, Italy

# 965 HBV GENOTYPE F AND PRECORE STOP CODON MUTATION PREDOMINATE IN AN ARGENTINIAN BLOOD DONOR POPULATION Paulo H C Franqa, UFRJ, Rio de Janeiro, Brazil; Jorge E Gonzilez, Silvina Munn6, Dr C. G. Malbrin, National Reference Lab / INEI ANLIS, Buenos Aires, Argentina; Larissa H BrandZo, IDMT, Rio de Janeiro, Brazil; Vera Gouvea, UFRJ, Rio de Janeiro, Brazil; Erwin Sablon, Bart 0 M Vanderborght, Innogenetics NV, Gent, Belgium

# 966

INFECTED PATIENTS CORRELATES WITH SERUM HBV DNA LEVELS BUT NOT HIV RNA LEVELS OR CD4 COUNTS Alejandro Soza, Lijun Mi, David E Kleiner, Judith Falloon, Douglas Brust, Jay H Hoofnagle, Jake Liang, The0 Heller, National Institutes of Health, Bethesda, MD

HEPATITIS B CORE ANTIGEN STAINING IN HIV-HBV CO-

# 967 VIROLOGICAL AND CLINICAL IMPACT OF OCCULT HBV INFECTION IN PATIENTS WITH HIV REPLICATION. PRELIMINARY DATA OF A PROSPECTIVE STUDY Pietro Filippini, Nicola Coppola, Second University of Naples, Naples, Italy; Cesare Nacca, San Sebastian Hospital, Caserta, Italy; Raffaella Pisapia, Cecilia Marrocco, Martina Battaglia, Patrizia Franca Bellomo, Annamaria Lettieri, Felice Piccinino, Second University of Naples, Naples, Italy; Umberto Di Luzio Paparatti, Abbott SPA, Campoverde (Latina), Italy; Evangelista Samelli, Second University of Naples, Naples, Italy

# 968

FERASE LEVELS PREDICT HEPATIC FIBROSIS IN CHRONIC HEPATITIS B OVER 3 YEARS? Nancy W Y Leung, The Chinese University of Hong Kong, Hong Kong, Hong Kong; Desmond C H Yiu, Alice Ho Miu Ling Taipo Nethersole Hospital, Hong Kong, Hong Kong; Vincent W S Wong, Alex Y Hui, The Chinese University of Hong Kong, Hong Kong, Hong Kong

# 969 DETERMINANTS FOR THE OCCURRENCE OF ACUTE EXACERBATION AFTER HBEAG SEROCLEARANCE IN CHINESE PATIENTS

Sum, The University of Hong Kong, Hong Kong, Hong Kong; Joke Doutreloigne, Erwin Sablon, Innogenetics NV, Ghent, Belgium; Ching-Lung Lai, The University of Hong Kong, Hong Kong, Hong Kong

DO CUMMULATIVE SERIAL ALANINE AMINOTRANS-

0 q 3 om8 Y

He-Jun Yuan, Man-Fung Yuen, Danny Ka-Ho Wong, Siu-Man Pi0 ;O $


t 970 MOLECULAR CHARACTERIZATION OF HEPATITIS B VIRUS SURFACE ANTIGEN NEGATIVITY CAUSED BY SPONTANEOUS LOSS OR ANTIVIRAL THERAPY Hye-Young Chang, Kyun-Hwan Kim, Yonsei University College of Medicine, BK 21 Project for Medical Science, 21C Frontier Functional Human Genomic Project, Seoul, South Korea; Chae Yoon Chon, Yonsei University College of Medicine, Seoul, South Korea; Sang Hoon Ahn, Yonsei University College of Medicine, BK 21 Project for Medical Science, Seoul, South Korea; Jun Yong Park, Yonsei University College of Medicine, Seoul, South Korea; Ja Kyung Kim, Yonsei University College of Medicine, BK 21 Project for Medical Science, Seoul, South Korea; Young Myoung Moon, Yonsei University College of Medicine, Seoul, South Korea; Kwang-Hyub Han, Yonsei University College of Medicine, BK 21 Project for Medical Science, 21C Frontier Functional Human Genomic Project, Seoul, South Korea

Hepatitis C: Therapy I

8 #971 LONG TERM FOLLOW UP OF SUSTAINED RESPONDERS T O

ANALYSIS ASSESSING TRUE CLINICAL ENDPOINTS Bart J Veldt, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands; Giorgio Saracco, Ospedale Molinette, Torino, Italy; Bettina E Hansen, Solko W Schalm, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands

8 $972

HEPATITIS C NS3=4A PROTEASE AND A POTENTIAL HEPTITIS C VIRUS THERAPEUTIC Robert B Perni, Gurudatt Chandorkar, Pravin R Chaturvedi, Lawrence F Courtney, Caroline J Decker, Cynthia A Gates, Scott L Harbeson, Ann D Kwong, Chao Lin, Yu-Ping Luong, William Markland, Govinda Rao, Roger D Tung, John A Thomson, Vertex Pharmaceuticals Inc., Cambridge, MA

INTERFERON ALPHA IN CHRONIC HEPATITIS C: A META-

VX-950: THE DISCOVERY OF AN INHIBITOR OF THE

88973 INHIBITION OF HCV NTPASE/HELICASE BY RING EXPANDED NUCLEOSIDES (RENS): A NEW CLASS OF ANTIVIRAL AGENTS Peter Borowski, Bernhard-Nocht-Institute for Tropical Medicine, Hamburg, Germany; Julian C R Schulze zur Wiesch, Partners AIDS Research Institute, Charlestown, MA; Herbert Schmitz, Beri~ard-Noclit-Institute for Tropical Medicine, Hamburg, Germany; Ramachandra S Hosmane, University of Maryland, Baltimore, MD

8 $974 IFN-A 28 INHIBITS INTERNAL RIBOSOME ENTRY SITE MEDIATED TRANSLATION OF GREEN FLUORESCENCE PROTEIN FROM SIX DIFFERENT HCV GENOTYPES Alfredo Panebra, Krishna Shah, Ramesh Prabhu, Frank Bastian, Robert F Carry, Virenda ra Joshi, Salima Haque, Fredric G Regenstein, Tulane University Health Sciences Center, New Orleans, LA; Richard Elliott, University of Glasgow, Glasgow, UK; Srikanta Dash, Tulane University Health Sciences Center, New Orleans, LA

8#975 SALIVARY GLANDS IMPAIRMENT IN PATIENTS WITH

RIBAVIRIN TREATMENT Alessio M Aghemo, Maria G Rumi, IRCCS Maggiore Hospital, University of Milan, Milano, Italy; Valeria Cuccarini, Massimo Paglia, Francesco Ottaviani, IV Clinica ORL, Azienda Ospedaliera Luigi Sacco Milano, Universita degli Studi di Milano, Milano, Italy; Ersilio Del Ninno, Massimo Colombo, IRCCS Maggiore Hospital, University of Milan, Milano, Italy

CHRONIC HEPATITIS C UNDERGOING PEG-INTERFERON/

# 976 TOTAL HCV CORE ANTIGEN CORRELATES WITH HCV RNA, AND PREDICTS RESPONSE TO PEGINTERFERON ALFA 2-A (PEG-IFN) AND RIBAVIRIN (RIB) THERAPY IN CHRONIC HEPATITIS C Eduardo Padilla, Ramon Planas, Vicky Gonzalez, Hospital Germans Trias i Pujol, Badalona, Spain; Celia Perez, Hospital General de Valencia, Badalona, Spain; Dolors Gimenez, Hospital del Mar, Barcelona, Spain; Lourdes Matas, Rosa Maria Morillas, Eduard Cabre, Hospital Germans Trias i Pujol, Badalona, Spain; Ricard Sola, Hospital del Mar, Barcelona, Spain; Mois6s Diago, Hospital General de Valencia, Valencia, Spain; Vicens Ausina, Hospital Germans Trias i Pujol, Badalona, Spain

# 977 THE PRESENCE OF SEVERE STEATOSIS OR STEATOHEPATITIS IMPAIRS RESPONSE T O ANTIVIRAL THERAPY IN PATIENTS WITH CHRONIC HEPATITIS C Stephen A Harrison, Elizabeth M Brunt, Dana A Oliver, Brent A Neuschwander-Tetri, Adrian M Di Bisceglie, Bruce R Bacon, Saint Louis University, St. Louis, MO

# 978 DEVELOPMENT OF SIRNA AS A THERAPEUTIC FOR HEPATITIS C David V Morrissey, Kristi Jensen, Shawn Ziniien, Brent Dickinson, Kim Hartsough, Cindy Shaw, James A McSwiggen, Chaiidra Vargeese, Keith Bowman, Chris S Shaffer, Barry Polisky, Jennifer A Lockridge, Sirna Therapeutics, Inc., Boulder, CO

# 979 SEQUENCE CHARACTERISTICS OF HCV (GENOTYPE 1) E2 HYPERVARIABLE REGION 1: POSSIBLE CORRELATION WITH RESPONSE TO COMBINATION THERAPY Swapna Menon, Mi Zhou, Yan Cui, Jacquelyn Fleckenstein, Michael Whitt, Vicki Park, University of Tennessee Health Science Center, Memphis, TN

# 980 INHIBITION OF HEPATITIS C VIRUS RNA TRANSLATION WITH ANTISENSE TAUROCHOLATE CONJUGATED

NUCLEOTIDES (ODN) IN CELL CULTURE Maria Quasdorff, Maria A Gonzalez-Carmona, Anja Tamke, Per Hoffmann, University of Bonn, Bonn, Germany; Thomas Lehmann, Joachim W Engels, University of Frankfurt / Main, Frankfurt / Main, Germany; Gerd A Kullak-Lklick, University Hospital of Zurich, Zurich, Switzerland; Tilman Sauerbnich, Wolfgang H Caselmann, University of Bonn, BOM, Germany

PHOSPHOROTHIOATE MODIFIED OLIGODEOXY-

# 981 ANTIDEPRESSANT PRESCRIBING IN MEDICAID PATIENTS

DIAGNOSIS AND PRIOR T O THE INITIATION OF INTERFERON THERAPY Jeffrey S Markowitz, Elane M Gutterman, Health Data Analytics, Princeton Junction, NJ

WITH HEPATITIS-C VIRUS (HCV) BEFORE AND AFTER HCV

Z L A A S L D Presidenhal Poster of Distinction


# 982

WITH RIBAVIRIN FOR THE TREATMENT OF CHRONIC HEPATITISC GENOTYPE 4 Fuad Hasan, Haifa Asker, Jamila AI-Khaldi, Iqbal Siddique, Salim F Owaid, Misfer Al-Ajmi, Basil Al-Nakib, Kuwait University, Kuwait, Kuwait

PEGYLATED INTERFERON ALFA-2B IN COMBINATION # 988 PERIPHERAL DENDRITIC CELLS AND TETRAMER+ T CELLS DURING INTERFERON/RIBAVIRIN COMBINATION THERAPY Masaaki Shiina, Sendai National Hospital, Sendai, Japan; Koju Kobayashi, Yasuteru Kondo, Yoshiyuki Ueno, Tooru Shimosegawa, Tohoku University, Sendai, Japan

# 983 STEATOSIS IS A COFACTOR FOR FIBROSIS AND RESPONSE TO THERAPY IN GENOTYPE 1B CHRONIC HEPATITIS C (CHC) Calogero CammB, IBIM, CNR; Cattedra e Unit& Operativa di Gastroenterologia University of Palermo, Palermo, Italy; Vito Di Marco, Cattedra e Unita Operativa di Gastroenterologia University of Palermo, Palermo, Italy; Mario Camozzi, Azienda Ospedaliera Niguarda Milano, Milano, Italy; Savino Bruno, IBS S. Paolo Milano, Milano, Italy; Danilo Di Bona, Cattedra e Unita Operativa di Gastroenterologia University of Palermo, Palermo, Italy; Mariagrazia Rumi, Ospedale Maggiore, Milano, Italy; Maria Vinci, Azienda Ospedaliera Niguarda Milano, Milano, Italy; Mario U Mondelli, Malattie Infettive, IRCCS S. Matteo Pavia, Pavia, Italy; Massimo Colombo, Ospedale Maggiore, Milano, Italy; Giovanbattista Pinzello, Azienda Ospedaliera Niguarda Milano, Milano, Italy; Antonio Craxi, Cattedra e Unit& Operativa di Gastroenterologia University of Palermo, Palermo, Italy

# 984 MOLECULAR PROFILES OF DRUG RESPONSE IN HCV INFECTED PATIENTS DURING THE FIRST 4 WEEKS OF THERAPY FOR CHRONIC HEPATITIS C VIRUS WITH PEGYLATED INTERFERON CONTAINING REGIMENS OR ALBUFERONTM V Balan, Mayo Clinic, Phoenix, AZ; D Nelson, University of Florida, Gainesville, FL; M Sulkowski, Johns Hopkins University, Baltimore, MD; M Rosati, Mayo Clinic, Phoenix, AZ; C Birse, J Praestgaard, B Osbom, H Mesghali, L Novello, 0 Pickeral, W Freimuth, G Subramanian, Human Genome Sciences, Inc., Rockville, MD

# 985 INCREASE IN CD4 LYMPHOCYTE COUNT FOLLOWING HEPATITIS C VIRAL CLEARANCE IN A COHORT OF HIVlHCV INFECTED INDIVIDUALS Alison J Uriel, Julio A Gutierrez, Avi Reichenberg, Douglas T Dieterich, Mount Sinai School of Medicine, New York, NY

# 986 PRE-TREATMENT PREDICTION OF RESPONSE TO INTERFERON BY CDNA MICROARRAY WITH HIGH ACCURACY VALIDATED BY CROSS-OVER STUDY Shuichi Kaneko, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan; Takeshi Tanaka, Tokyo Metropolitan Komagome Hospital, Tokyo, Japan; Michinori Kohara, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan; Akito Daiba, Satoru Ito, Kiichi Kubota, Japan Genome Solutions, Inc, Tokyo, Japan

# 987 PEGINTERFERON ALFA-2A (40KD) (PEGASYSB) AND RIBAVIRIN (COPEGUSB) IN PATIENTS WITH HIV/HCV COINFECTION INTERIM RESULTS OF A RANDOMIZED, MULTICENTER STUDY FROM SPAIN Jose Hernandez-Quero, Hospital Clinico San Cecilio, Granada, Spain; Rafael Granados, Hospital Dr. Negrin, Las Palmas, Spain; Eugenio P6rez-GuzmAn, Hospital Puerta del Mar, CAdiz, Spain; Fernando Lozano, Hospital de Valme, Sevilla, Spain; Jorge Parra, Hospital Clinico San Cecilio, Granada, Spain; Maria del Mar Alonso, Hospital Universitario de Canarias, Tenerife, Spain

# 989 GENETIC VARIATIONS OF INTERFERON ACTIVATION HAVE NO EFFECT ON RESPONSE TO ANTIVIRAL THERAPY IN

Christoph H Oesterreicher, Harald Hofer, Elisabeth Formann, Wolfgang Jessner, University of Vienna, Vienna, Austria; Michael Gschwantler, Krankenhaus Rudolfstiftung, Vienna, Austria; Heidemarie Holzmann, Peter Ferenci, University of Vienna, Vienna, Austria

CHRONIC HEPATITIS C-GENOTYPE 1

!# 990 HEPATITIS C VIRUS GENOMIC AND SUB-GENOMIC CLONES ACTIVATE INTERFERON-STIMULATED RESPONSE ELEMENT IN HUH-7 CELLS Alfredo Panebra, Krishna Shah, Ramesh Prabhu, Frank Bastian, Robert F Garry, Virendra Joshi, Salima Haque, Fredric G Regenstein, Tulane University Health Sciences Center, New Orleans, LA; Steve Goodbourn, University of London, London, UK; Srikanta Dash, Tulane University Health Sciences Center, New Orleans, LA

# 991 DEVELOPMENT OF A HOMOGENEOUS SCINTILLATION PROXIMITY ASSAY (SPA) FOR DETERMINING ACTIVITY OF HCV POLYMERASE AND SCREENING FOR ENZYME INHIBITORS Derek Latour, Kevin Fung, Emil Michelotti, Jeffrey Pouliot, Lillian Lou, Martin D Kirk, Genelabs Technologies, Redwood City, CA

# 992 IN VITRO STUDIES TO ASSESS PREDICTIVE BIOMARKERS OF INTERFERON INDUCED DEPRESSION Wei Cai, Vladimir I Khaoustov, Qing Xie, Tianhong Pan, Weidong Le, Boris Yoffe, Baylor College of Medicine, Houston, TX

# 993 TYPE 1 INTERFERON AUGMENTS DNA-BASED VACCINA- TION AGAINST HEPATITIS C VIRUS CORE PROTEIN Stephan Gehring, Noriyoshi Kuzushita, Stephen Gregory, Jack Wands, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI # 994 COMBINATION THERAPY FOR HEPATITIS C POSITIVE SELECTION PRESSURE AT BASELINE IS ASSOCIATED WITH VIROLOGIC RESPONSE TO THERAPY Vicki Park, Swapna Menon, Barbara Mason, Rongling Li, Julia Krushkal, Caroline Riely, Jaquelyn Fleckenstein, University of Tennessee Health Science Center, Memphis, TN

# 995 A DYNAMIC MODEL TO PREDICT SUSTAINED VIROLOGI- CAL RESPONSE TO COMBINATION PEGINTERFERON

THERAPY IN PATIENTS WITH CHRONIC HEPATITIS C Peter Ferenci, University of Vienna, Vienna, Austria; Michael W Fried, University of North Carolina, Chapel Hill, NC; Monique Chaneac, Roche Diagnostics, Basel, Switzerland

ALFA-2A (40KD) (PEGASYSO) AND RIBAVIRIN (COPEGUSB)

I32A POSTER SESSIONS HEPATOLOGY, October 2003

0 996

(40KD) (PEGASYSB) AND RIBAVIRIN (COPEGUSB) SIGNIFICANTLY ENHANCE SUSTAINED VIROLOGICAL AND BIOCHEMICAL RESPONSE RATE IN CHRONIC HEPATITIS C GENOTYPE 4 PATIENTS IN SAUDI ARABIA 0 A Shobokshi, Kmg Faisal Specialist Hospital, Riyadh, Saudi Arabia; F E Serebour, L Skakni, N Al-Jasser, Central Lab/Blood Bank (MOH), Riyadh, Saudi Arabia; A 0 Tantawi, A Sabah, Riyadh Medical Complex (MOH), Riyadh, Saudi Arabia; T Dinish, King Fahad General Hospital (MOH), Al-Baha, Saudi Arabia; M Al-Quaiz, K Qahtani, King Faisal Specialist Hospital, Riyadh, Saudi Arabia; A Sandokji, A Al-Blowi, M Al-Karawi, Armed Forces Hospital, Riyadh, Saudi Arabia; B Al-Kayyal, Prince Salman Hospital (MOH), Riyadh, Saudi Arabia; S Al- Momen, Central Hospital (MOH), Dammam, Saudi Arabia; H Akbar, King Abdulaziz University Hospital, Jeddah, Saudi Arabia; A Ayoola, M El-Hazmi, King Fahad General Hospital (MOH), Gizan, Saudi Arabia; A Humaida, I El-Hazmi, King Fahad General Hospital (MOH), Qunfudah, Saudi Arabia; H Eissa, Qatif General Hospital (MOH), Qatif, Saudi Arabia; F Khawajah, King Fahad General Hospital (MOH), Madinah, Saudi Arabia; M Al-Khalifa, Regional Laboratory, Dammam, Saudi Arabia

COMBINATION THERAPY OF PEGINTERFERON ALFAQA

# 997 TRIPLE THERAPY COMPARED TO STANDARD PEGYLATED INTERFERON ALFA 28 + WEIGHT BASED RIBAVIRIN FOR

TRIAL]: FINAL RESULTS Eric J Lawitz, Norma S Cantu, Brooke Army Medical Center, San Antonio, TX; Mitchell Davis, South Florida Center of Gastroenterology, West Palm Beach, FL; Nezam Afdhal, Michael Curry, Beth Israel Deaconess Medical Center, Boston, MA; Mark Mailliard, University of Nebraska Medical Center, Omaha, NE; Frank Adams, Austin Consultants in Gastroenterology, Austin, TX; Naoky Tsai, St. Francis Medical Center, Honolulu, HI; Andrei Gasic, Longview Gastroentrology Clinic, Longview, TX; Tarun Kothari, Private Practice, Rochester, NY; K P Ganeshappa, Digestive Disease Center of South Texas, San Antonio, TX; James Cox, Texas Digestive Disease Consultants, Lewisville, TX; Bruce Silverman, Gastroenterology Associates, Olympia, WA; Shailesh C Kadakia, Institute of Liver and Gastrointestinal Diseases, San Antonio, TX

X 998 DIRECT INHIBITION OF INTRACELLULAR HEPATITIS C VIRUS REPLICATION BY RIBAVIRIN AND ITS SYNERGISTIC ACTION USED IN COMBINATION WITH

Yoko Tanabe, Naoya Sakanioto, Nobuyuki Enomoto, Masayuki Kurosaki, Eri Ueda, Shinya Maekawa, Tuyoshu Yamashiro, Mina Nakagawa, Cheng-Hsin Chen, Nobuhiko Kanazawa, Mamoru Watanabe, Tokyo Medical and Dental University, Tokyo, Japan

TREATMENT NAIVE CHRONIC HEPATITIS C [TRI-STAR

INTERFERON-ALPHA

d 999 META-ANALYSIS OF ISDR MUTATIONS AND INTERFERON- ALPHA (IFNA) SENSITIVITY IN PATIENTS WITH CHRONIC HEPATITIS C VIRUS (HCV) GENOTYPE l B INFECTION Maria E Pascu, Campus Virchow, Charite, Berlin, Germany; Peter Martus, Institute of Medical Informatics, Biometry and Epidemiology, Berlin, Germany; Marina Hoehne, Robert Koch Institut, Berlin, Germany; Bertram Wiedenmann, Uwe Hopf, Campus Virchow, Charite, Berlin, Germany; Eckart Schreier, Robert Koch Instihit, Berlin, Germany; Thomas Berg, Campus Virchow, Chnri te, Berlin, Germany

# 1000 VX-950, A HCV PROTEASE INHIBITOR, RETAINS POTENCY AGAINST BILN-2061 RESISTANT REPLICON CELLS Chao Lin, Kai Lin, Cynthia A Gates, Sue Ma, Debra Brennan, John Fulghum, Hsun-Mei Hsiao, Govinda Rao, Yunyi Wei, John Alford, Robert B Perni, AM D Kwong, Vertex Pharmaceuticals Inc., Cambridge, MA

# 1001 RELATIONSHIP BETWEEN HEPATIC IRON CONTENT AND HISTOLOGICAL RESPONSE IN CHRONIC HEPATITIS C Stephen J Rulyak, Sue C Eng, University of Washington, Seattle, WA; Keyur Patel, John McHutchison, Duke University, Durham, NC; Stuart C Gordon, William Beaumont Hospital, Royal Oak, MI; Kris V Kowdley, University of Washington, Seattle, WA

# 1002 BREAK-EVEN REEMBURSEMENT OF PRACTICE-BASED HEPATITIS C TREATMENT IS HIGHLY DEPENDENT ON GENOTYPE, TREATMENT MODEL, AND PHYSICIAN EXTENDER GENOTYPE 1, LITTLE TO NO PHYSICIAN CONTACT, AND EXTENSIVE REGISTERED NURSE CARE MAY BE THE MOST COST EFFICIENT MODEL Victor R Araya, Juan Acosta, Jorge Uribe, Kenneth D Rothstein, Albert Einstein Medical Center, Philadelphia, PA

~~

# 1003 A PROSPECTIVE ASSESEMENT OF "A LA CARTE" REGIMEN OF PEG INTERFERON ALPHA 2B AND RIBAVIRIN COMBINATION IN PATIENTS WITH CHRONIC HEPATITIS C (CHC) Cecilia d' Arondel, Joseph Moussalli, Vincent Thibaut, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Sylvie Naveau, HBpital Antoine Bkclgre, Clamart, France; Anne Simon, Mona Munteanu, Franqoise Imbert-Bismut, Djamila Messous, Rachel Morra, Cecile Blot, Yves Benhamou, Vlad Ratziu, l'hierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Park, France

X 1004 A SIMPLE MODEL CAN PREDICT RESPONSE TO

HEPATITIS C Eva Martinez-Bauer, Xavier Forns, Josep M Barrera, Josep Costa, Jose M Sanchez-Tapias, Hospital Clinic, Barcelona, Spain

INTERFERON-RIBAVIRIN IN GENOTYPE 1 CHRONIC

# 1005 ESTIMATING THE BENEFIT OF INTERFERON THERAPY FOR INDIVIDUAL PATIENTS WITH CHRONIC HEPATITIS C Haruhiko Yoshida, Ryosuke Tateishi, University of Tokyo, Tokyo, Japan; Yasuyuki Arakawa, Nilion University, Tokyo, Japan; Michio Sata, Kurume University, Kurume, Japan; Shuhei Nisluguchi, Osaka City University Osaka, Japan; Hirorni Ishibashi, Nagasaki Medical Center, Nagasaki, Japan; Shigetoshi Fujiyama, Kumamoto University, Kumamoto, Japan; Gotaro Yamada, Kawasaki University Kawasaki Hospital, Okayama, Japan; Osamu Yokosuka, Chiba University, Chiba, Japan; Yasushi Shiratori, Okayama University, Okayama, Japan; Masao Omata, University of Tokyo, Tokyo, Japan

# 1006 VIRAL KINETICS IN CHRONICALLY HCV INFECTED PATIENTS WITH PERSISTENTLY NORMAL OR ELEVATED ALT LEVELS Bernd Kronenberger, h e r e Medizin 11, Homburg/ Saar, Germany; Eva Herrmann, Fachbereicli Mathematik, Darmstadt, Germany; Stefan Zeuzem, Innere Medizin 11, Homburg/Saar, Germany

8 Denote5 AASILD Presiilcntial Poster o f Distinction

HEI’ATOLOGY, Vol. 38, No. 4, Suppl. 1, 2003 POSTER SESSIONS 133A

# 1007 SUCCESSFUL TREATMENT OF ACUTE HEPATITIS C WITH

ANALYSIS Teresa Santantonio, Emanuele Sinisi, Fabio Signorile, Angela Guastadisegni, Caterina Casalino, University of Bari, Ban, Italy; Michele Mazzola, Ruggiero Francavilla, Bisceglie Hospital, Bisceglie, Italy; Giuseppe Pastore, University of Bari, Bari, Italy

li 1008

TREATMENT NAIVE AFRICAN AMERICAN PATIENTS INFECTED WITH HCV GENOTYPE 1 David F Stein, Sandra D McKenzie, Saint Barnabas Hospital, Bronx, NY

ft 1009 TREATMENT OF CHRONIC HEPATITIS C WITH

ALPHA 2B PEG-INTERFERON MONOTHERAPY AN INTERIM

PEG-INTERFERON ALFA-2B AND RIBAVIRIN IN

INTERFERON ALFA-2B AND RIBAVIRIN IN THE COMMUNITY-BASED PRACTICE. A PROSPECTIVE STUDY OF 813 U.S. VETERANS Norbert Brau, Veterans Affairs Medical Center, Bronx, NY; Edmund J Bini, VA Medical Center, New York, NY; Sue Currie, VA Medical Center, Sail Francisco, CA; Hui Shen, University of California, Sail Francisco, CA; Bhupinder S Anand, VA Medical Center, Houston, TX; Ke-Qin Hu, VA Medical Center, Loma Linda, CA; Samuel B Ho, VA Medical Center, Minneapolis, MN; David Johnson, VA Medical Center, Bay Pines, FL; Warren N Schmidt, VA Medical Center, Iowa City, IA; Paul D King, VA Medical Center, Columbia, MO; Ramsey C Cheung, VA Medical Center, Palo Alto, CA; Stephen J Rossi, VA Medical Center, San Francisco, CA; Lennox J Jeffers, VA Medical Center, Miami, FL; Teresa L Wright, VA Medical Center, San Francisco, CA

4 1010 ROFECOXIB PREVENTS THE REDUCTION IN PLATELETS EXPERIENCED AS A RESULT OF PEGASYS THERAPY OF CHRONIC HEPATITIS C: A SHORT TERM PILOT STUDY David H Van Thiel, Magdalene M George, Mehdi Baluch, Sonu Dhillon, Nancy Leone, Loretta Murphy, Loyola University Medical Center, Maywood, IL

# 1011 OCCURRENCE OF INFECTIONS DURING COMBINATION TREATMENT WITH INTERFERONS AND RIBAVIRIN FOR CHRONIC HEPATITIS C ROLE OF NEUTROPENIA AND OF INTERFERON PEGYLATION Massimo Puoti, Maria G Antonini, Clinica Malattie Infettive, Brescia, Italy; Sergio Babudieri, Ivana Maida, L Fenu, Maria S Mura, S Sassu, Clinica Malattie Infettive, Sassari, Italy; Chiara Baiguera, Katiela Prestini, Paola Pagani, Lucian0 Biasi, Giampiero Carosi, Clinica Malattie Infettive, Brescia, Italy

# 1012 CONSENSUS INTERFERON AND RIBAVIRIN RETREATMENT OF CHRONIC HCV PATIENTS WITH NON-RESPONSE OR RELAPSE AFTER PREVIOUS ALPHA-INTERFERON THERAPY Wulf 0 Boecher, Martin Sprinzl, Jonas Mudter, Heribert Hillenbrand, Holger Brociunann, Peter R Galle, H a m s F Loehr, University Hospital, Maim, Germany

# 1013 INTERFERON TREATMENT OUTCOMES IN PATIENTS WITH DECOMPENSATED HCV + CIRRHOSIS William Alvarez, Shilun D Li, Nikunj Shah, David H Van Thiel, Loyola University (Chicago), Stritch School of Medicine, Maywood, IL

# 1014 EVALUATION AND OUTCOMES OF COMBINATION THERAPY WITH INTERFERON OR PEGINTERFERON PLUS RIBAVIRIN IN 67 SOUTHEAST ASIAN PATIENTS WITH HEPATITIS C GENOTYPES 6,7,8, AND 9 Mindie H Nguyen, Stanford University, Palo Alto, CA; Huy N Trinh, Rue1 T Garcia, Jing Ning, Liver and Digestive Health Medical Clinic, San Jose, CA; Emmet B Keeffe, Stanford University, Palo Alto, CA

3 # 1015 DISCONTINUATION OF PEGYLATED INTERFERON PLUS RIBAVIRIN IN PATIENTS WHO ARE NOT RESPONDING TO

Graham R Foster, Raymond F C D’Souza, QMLJL, Barts and The London, London, UK; Janice Main, Mary Crossey, Imperial College Faculty of Medicine, London, UK; William Rosenberg, University of Southamptom, Southamptom, UK; Iain M Murray- Lyon, Chelsea and Westminster Hospital, London, UK; Colin Hayward, Roche Products Ltd, Welwyn Garden City, UK

THERAPY-IS IT WORTHWHILE?

Kupffer Cell Endothelial Cell Biology

8 # 1016 DISORDERED ANGIOGENESIS AND LIVER REGENERATION

Xiaofeng Sun, Andres Cardenas, Keiichi Enjyoji, Yan Wu, Simon C Robson, Harvard University, Boston, MA

IN CD39/NTPDASEl-NULL MICE

# 1017 NRAMPl MUTATION CAUSES ENHANCED IRON

EXPRESSION IN MACROPHAGES Shigang Xiong, Hongyun She, Jiaohong Wang, Hidekazu Tsukamoto, Keck School of Medicine of the University of Southern California, Los Angeles, CA

SIGNALING FOR NF-KB ACTIVATION AND TNF-ALPHA

# 1018 VASCULAR ADHESION PROTEIN-1 LIGATION AND ENZYME ACTIVITY LEAD T O PI-3 KINASE DEPENDENT ACTIVATION OF NF-KB IN HEPATIC SINUSOIDAL ENDOTHELIAL CELLS Phoebe J Sun, Patricia F Lalor, Michael J 0 Wakelam, David H Adams, University of Birmingham, Birmingham, UK

# 1019 LIPOPOLYSACCHARIDE AS A CO-FACTOR FOR MALONDIALDEHYDE-ACETALDEHYDE (MAA) MODIFIED PROTEINS T O INDUCE PRO-INFLAMMATORY RESPONSES BY KUPFFER AND LIVER ENDOTHELIAL CELLS Geoffrey M Thiele, Thomas L Freeman, Michael J Duryee, University of Nebraska Medical Center, Omaha, NE; Monte S Willis, University of Texas Southwestern Medical Center, Dallas, TX; Dean J Tuma, Lynell W Klassen, Veterans Administration Medical Center, Omaha, NE

# 1020 MUCOSAL CELL ADHESION MOLECULE (MADCAM-1) EXPRESSION IN CHRONIC LIVER DISEASE AND DEVELOPMENT OF AN IN VITRO MODEL T O INVESTIGATE THERAPEUTIC MODULATION Aftab Ala, David Brown, Mark Stubbs, Ruth Jacobs, Humphrey Hodgson, Royal Free and University College Medical School, London, UK

# 1021 INHIBITION OF LPS-INDUCED -ALPHA PROMOTER ACTIVITY BY S-ADENLSYLMETHIONINE AND 5’- METHYLTHIOADENOSINE Nary Veal, Shigang Xiong, Chili-Lin Hsieh, Shelly Lu, Hidekazu Tsukamoto, Keck School of Medicine of the University of Southern California, Los Angeles, CA


ff 1022 INDUCTION OF F4/80HIGH+ MAC-1HIGH+ NONPARENCHYMAL ADHERENT LIVER CELL SUPPRESSOR

INJURY: INVOLVEMENT OF NITRIC OXIDE? Ayako Mabuclu, University of Otago, Dunedin, New Zealand; Tomokazu Nagao, Osamu Koshio, Kazuo Suzuki, National Institute of Infectious Diseases, Tokyo, Japan; Antony M Wheatley, University of Otago, Dunedin, New Zealand

FUNCTION IN T CELL-MEDIATED MURINE HEPATIC

# 1023 PARACRINE AND AUTOCRINE REGULATION OF RAT SINUSOIDAL ENDOTHELIAL CELL PHENOTYPE Laurie D DeLeve, Xiangdong Wang, Liping Hu, University of Southern California, Los Angeles, CA; Margaret K McCuskey, Robert S McCuskey, University of Arizona, Tucson, AZ

# 1024

OVERLOAD Wouter H Lamers, Roben G Gieling, Jan Ruijter, Adri Maas, Marius Van Den Bergh Weerman, Koert Dingemans, University of Amsterdam, Amsterdam, Netherlands

HEPATIC RESPONSE TO RIGHT-VENTRICULAR PRESSURE

Living Donor Liver Transplantaion

8 X 1025 RECIPIENT-DERIVED HEPATOCYTES IN SEX-MISMATCHED LIVING-RELATED PARTIAL LIVER TRANSPLANTS Ramazan Idilman, Esra Erden, Isinsu Kuzu, Sadik Ersoz, Kaan Karayalcin, Mehmet A Yerdel, Ajlan Tukum, Ankara University School of Medicine, Ankara, Turkey; Gulen Akyol, Gazi University School of Medicine, Ankara, Turkey; Hakan Bozkaya, Cihan Yurdaydin, Selim Karayalcin, Ankara University School of Medicine, Ankara, Turkey

8 X 1026 HISTOLOGIC FINDINGS IN POTENTIAL LIVING LIVER DONOR BIOPSIES Mohammad Kamal, Charles R Lassman, Rafik M Ghobrial, Sammy Saab, Karyn Marks, Ronald Busuttil, UCLA, Los Angeles, CA

8 # 1027 INCIDENCE OF HEPATITIS C RECURRENCE AND SURVIVAL AFTER LIVER TRANSPLANTATION: SPLIT VS CADAVERIC LIVER TRANSPLANTATION Adeyemi A Lawal, The Mount Sinai Medical Center, New York, NY; Rafik Ghobrial, University of California Los Angeles, Los Angeles, CA; Helen Te. University of Chicago, Chicago, IL; Lucy Artinian, University of California Los Angeles, Los Angeles, CA; Andrea Branch, Myron Schwartz, Thomas D Schiano, The Mount Sinai Medical Center, New York, NY

# 1028 TREATMENT OF ACUTE CELLULAR REJECTION WITH

BASELINE IMMUNOSUPPRESSION, IS ASSOCIATED WITH SEVERE HCV RECURRENCE IN BOTH LIVING AND DECEASED DONOR LIVER TRANSPLANT RECIPIENTS Paul J Gaglio, Jaqueline J Park, Jay Lefkowitch, Jean C Emond, Robert S Brown Jr, Columbia University College of Physicians and Surgeons, New York, NY

HIGH-DOSE STEROIDS, BUT NOT MODULATION OF

# 1029 COMPARISON OF HISTOLOGICAL PROGRESSION OF RECURRENT HCV INFECTION IN LIVE DONOR (LDLT) VERSUS CADAVERIC LIVER TRANSPLANTATION (CLT) RECIPIENTS Hassan Zaghla, Gary C Kanel, John A Donovan, Jeffrey A Kahn, Yuri Genyk, Emily Ramicone, Robert R Selby, Tse-Ling Fong, University of Southern California, Los Angeles, CA

# 1030

DONOR LIVER TRANSPLANTATION Kirti Shetty, Kim M Olthoff, Rajender K Reddy, Abraham Shaked, University of Pennsylvania, Philadelphia, PA

COST-COMPARISON BETWEEN CADAVERIC AND LIVING-

# 1031 PEDIATRIC LIVER TRANSPLANTATION WITH SEGMENTAL GRAFTS: OUTCOME ANALYSIS OF LIVING DONOR VS CADAVERIC SPLIT GRAFTS Sukru H Emre, Tarik Artis, Gabriel Gondolesi, Sander Florman, Sasan Roayaie, Myron Schwartz, Nancy Krieger, Charles Miller, Benjamin Shneider, Mount Sinai School of Medicine, New York, NY

# 1032 RADIOGRAPHIC EVALUATION OF 146 DONORS PRIOR T O RIGHT LOBE DONATION FOR LIVE DONOR ADULT LIVER

TIVE AND INTRAOPERATIVE FINDINGS: THE LAHEY CLINIC EXPERIENCE Christoph Wald, Mary Ann Simpson, Elizabeth A Pomfret, Nazli Erbay, Lahey Clinic Medical Center, Burlington, MA; Vassilios Raptopoulos, Beth Israel Deaconess Medical Center, Boston, MA; Roger L Jenkins, Lahey Clinic Medical Center, Burlington, MA

TRANSPLANTATION WITH CORRELATION OF PREOPERA-

# 1033 RIGHT LOBE LIVER DONORS: ASSOCIATION BETWEEN HEPATIC ARTERIAL, PORTAL VENOUS, AND BILIARY ANATOMIC VARIANTS Jennifer P Cha, Vivian S Lee, Glenn A Krinsky, Devon John, Thomas Diflo, Lewis Teperman, Glyn R Morgan, NYU School of Medicine, New York, NY

# 1034 DOES THE USE OF PARTIAL GRAFTS IN ADULT LIVER TRANSPLANTATION MODIFY EARLY PATIENT SURVIVAL ? Olivier Boillot Sr, Emmanuelle Pianta, Yannick Le Derf, Mustapha Adham, Pierre Sagnard, Jerome Bumortier, Edouard Herriot Hospital, Lyon, France

# 1035 DOES HARVESTING THE MEDIAN HEPATIC VEIN IN RIGHT

TATION INCREASE THE RISK FOR THE DONORS ? Olivier Scatton, Federica Dondero, Diane Goere, Reza Kianmanesh, Daniele Sommacale, Marylene Plasse, Alain Sauvanet, Franqois Durand, Olivier Farges, Jacques Belghiti, Hospital Beaujon, Clichy, France

# 1036 PRETRANSPLANT MELD SCORE AND POSTTRANSPLANT SURVIVAL IN ADULT PATIENTS UNDERGOING LIVE DONOR LIVER TRANSPLANTATION Zeki Karasu, Murat Akyildiz, Murat Kdic, Yildiray Yuzer, Ulus Akarca, Yaman Tokat, Arzu Celebi, Galip Ersoz, Yucel Batur, Fulya Gunsar, Ege University Medical School, Izmir, Turkey

HEPATECTOMY FOR LIVING-DONOR LIVER TRANSPLAN-

8 Denotei AASLD Prewlential I’oster of Distmction


# 1037 MRI DOES NOT ACCURATELY PREDICT FAT IN EVALUATION FOR LIVING DONOR LIVER TRANSPLANTATION Tram T Tran, Steven Colquhoun, Nicholas Nissen, Paul Martin, Rola Saouaf, Linda Hwa, Chanikam Changsri, Fred Poordad, Stephen A Geller, John M Vierling, Christopher Shackleton, Cedars-Sinai Medical Center, Los Angeles, CA

# 1038 SPLIT LIVER TRANSPLANTATION: SINGLE CENTER EXPERIENCE Sukru H Emre, Tarik Artis, Gabriel Gondolesi, Sander Florman, Sasan Roayaie, Krieger Nancy, Benjamin Shneider, Thomas Fishbein, Myron Schwartz, Charles Miller, Mount Sinai School of Medicine, New York, NY

# 1039 DONOR QUALITY OF LIFE AFTER LIVE DONOR ADULT LIVER TRANSPLANTATION (LDALT) Mary Ann Simpson, James J Pomposelli, Fredric D Gordon, W David Lewis, Roger L Jenkins, Alyson M Nixon, Eric Richman, Elizabeth A Pomfret, Lahey Clinic Medical Center, Burlington, MA

# 1040 LIVER REGENERATION OF DONORS AFTER MODIFIED EXTENDED RIGHT HEPATECTOMY COMPARED WITH CONVENTIONAL RIGHT HEPATECTOMY IN LIVING DONOR LIVER TRANSPLANTATION Nam-Joon Yi, Kyung-Suk Suh, Seong-Hwan Chang, Seok Ho Choi, Choon Hyuck Kwon, Kuhn Uk Lee, Seoul National University Hospital, Seoul, South Korea

Metabolic Liver Diseases

8 # 1041 GENE THERAPY OF WILSON DISEASE WITH LENTIVIRAL VECTORS IN A RAT MODEL Uta Merle, Jens Encke, University of Heidelberg, Heidelberg, Germany; Luigi Naldini, Institute for Cancer Research and Treatment (IRCC), Candiolo (TO), Italy; Wolfgang Stremmel, University of Heidelberg, Heidelberg, Germany

# 1042 MITOCHONDRIAL SUPEROXIDE DISMUTASE ALA9VAL POLYMORPHISM AND PHENOTYPIC EXPRESSION OF HEREDITARY HEMOCHROMATOSIS Luca Valenti, Paola Dongiovanni, Elena Mangano, Anna Ludovica Fracanzani, Erika Fatta, Cristina Bertelli, Gennaro Santorelli, Silvia Fargion, Universith degli Studi, Milano, Milan, Italy

# 1043 TIN MESOPORPHYRIN POTENTIATION OF HEME THERAPY:

K E Anderson, C Kormos-Hallberg, N G Egger, D E Goeger, C Lee, University of Texas Medical Branch, Galveston, TX

# 1044 A COMPARISON OF THE HEPATIC EXTRACTION OF TRANSFERRIN-BOUND AND NON-TRANSFERRIN BOUND IRON IN AN ANIMAL MODEL OF HEMOLYTIC ANEMIA Linda Fletcher, Princess Alexandra Hospital, Woolloongabba, Australia; Kim Bridle, University of Queensland, Woolloongabba, Australia; Therese Murphy, Margaret Walters, Princess Alexandra Hospital, Woolloongabba, Australia; Daniel Hung, Ping Chang, Gerhard Siebert, Michael Roberts, University of Queensland, Woolloongabba, Australia; Darrell Crawford, Princess Alexandra Hospital, Woolloongabba, Australia

A DOSE-RANGING STUDY IN ASYMPTOMATIC PORPHYRIA

# 1045 EFFECT OF COPPER ON PROTEIN EXPRESSION IN AN IN VITRO MODEL OF WILSON DISEASE: A PROTEOMICS APPROACH Han Roelofsen, Reshma Balgobind, Roe1 J Vonk, University Hospital Groningen, Groningen, Netherlands

# 1046 MITOCHONDRIA IN WILSON DISEASE (WD): FUNCTIONAL AND STRUCTURAL ABNORMALITIES IN THE TOXIC MILK

Eve A Roberts, Michelle Sabean, Suyun Yang, Brian H Robinson, Hospital for Sick Children, Toronto, ON, Canada

(TX-J) MOUSE

# 1047 GLUCOCEREBROSIDE INDUCES ALTERED ANTI HEPATITIS C IMMUNITY IN PATIENTS WITH GAUCHER'S DISEASE Maya Margalit, Lydia Zolotarov, Nilla Hemed, Hadassah Hebrew University Medical Center, Jerusalem, Israel; Deborah Elstein, Ari Zimran, Shaare Zedek Medical Center, Jerusalem, Israel; Yaron Ilan, Hadassah Hebrew University Medical Center, Jerusalem, Israel

# 1048 CLINICAL AND GENETIC STUDIES OF THE BANGALORE WILSON'S DISEASE PHENOTYPE: RAPID PROGRESSION TO

D-PENICILLAMINE/ZINC SULPHATE (DP/ZN) COMBINATION THERAPY IN 220 PATIENTS Srinivas Seela, Yale University, New Haven, CT; H S Swamy, KIT, Bangalore, India; Pramod K Mistry, Yale University New Haven, CT

# 1049 HEPATIC IRON CONCENTRATION AND TOTAL BODY IRON STORES IN GENETIC HEMOCHROMATOSIS AND THALASSEMIA MAJOR Sylvie Jacquelinet, University Hospital and INSERM U-522 Pontchaillou, Rennes, France; Gary M Brittenham, Columbia University College of Physicians and Surgeons, New York, NY; Emanuele Angelucci, University Hospital, Cagliari, Italy; Christine E McLaren, College of Medicine, University of Colombia, Irvine, CA; Pierre Brissot, University Hospital Pontchaillou and INSERM U-522, Rennes, France

NEUROLOGICAL DISEASE AND RESPONSE TO LOW-DOSE

# 1050 HEPCIDIN EXPRESSION IS DOWN-REGULATED IN ALCOHOL-FED RATS: A POSSIBLE PATHOGENIC FACTOR IN ALCOHOL RELATED HEPATIC SIDEROSIS Ting Kin Cheung, Linda Fletcher, Princess Alexandra Hospital, Woolloongabba, Australia; Kim Bridle, University of Queensland, Woolloongabba, Australia; Therese Murphy, Darrell Crawford, Princess Alexandra Hospital, Woolloongabba, Australia

# 1051 LABILE PLASMA IRON IN C282Y/C282Y HEMOCHROMATOSIS: A REALITY OF POTENTIAL PATHOPHYSIOLOGICAL AND CLINICAL IMPORTANCE Caroline Le Lan, University Hospital Pontchaillou and INSERM U-522, Rennes, France; Tally Cohen, Institute of Life Sciences, Jerusalem, Israel; Martine Ropert, University Hospital Pontchaillou, Rennes, France; Hava Glickstein, Institute of Life Sciences, Jerusalem, Israel; Michel Pouchard, Centre dExamens de Sante CPAM, Rennes, France; Andre Le Treut, Laboratoire de Biochime Generale et Enzymologie, University Hospital Pontchaillou, Rennes, France; Yves Deugnier, Olivier Loreal, University Hospital Pontchaillou and INSERM U-522, Rennes, France; William Breuer, Ioav Cabantchik, Institute of Life Sciences, Jerusalem, Israel; Pierre Brissot, University Hospital Pontchaillou and INSERM U-522, Rennes, France

POSTER SESSIONS HEPATOLOGY, October 2003 13hA

f 1052 DECREASED E-CADHERIN EXPRESSION IN AN IN VIVO MODEL OF CHRONIC IRON OVERLOAD Stephanie A Stoehr, John P Bilello, Harriet C Isom, Pennsylvania State University College of Medicine, Hershey, PA

4 1053

FREQUENCIES AS AN INHERITED RISK FACTOR FOR THE DEVELOPMENT OF CHRONIC LIVER DISEASE OF DIFFERENT ETIOLOGIES Thomas Berg, Medizinische Klinik mit Schwerpunkt Hepatologie und Castroenterologie, Universitaetsklinikum Charit6, Campus Virchow-Klinikum, Humboldt-Universitaet, Berlin, Germany; Juliane Halangk, Klinik fuer Paediatrie, Universitaetsklinikum Charitb, Campus Virchow-Klinikum, Humboldt-Universitaet, Berlin, Germany; Gero Puhl, Klinik h e r Allgemein-, Viszeral- und Transplanta tionschirurgie, Universitaetsklinikum Charit6, Campus Virchow-Klinikum, Humboldt-Universitaet, Berlin, Germany; Tobias Mueller, Medizinische Klinik mit Schwerpunkt Hepatologie und Gastroenterologie, Universitaetsklinikum Charite, Campus Virchow-Klinikum, Humboldt-Universitaet, Berlin, Germany; Olfert Landt, TIB MOLBIOL, Berlin, Germany; Peter Neuhaus, Klinik fuer Allgemein-, Viszeral- und Transplanta- tionschirurgie, Universitaetsklinikuni Charit6, Campus Virchow- Klinikum, Huniboldt-Universitaet, Berlin, Germany; Bertram Wiedenmann, Uwe Hopf, Medizinische Klinik mit Schwerpunkt Hepatologie L i d Gastroenterologie, Universitaetsklinikum Charite, Campus Virchow-Klinikum, Huinboldt-Universitaet, Berlin, Germany; Werner Luck, Heiko Witt, Klinik h e r Paediatrie, Univt.rsitaetsklinikuiri Charit@, Campus Virchow-Klinikum, Humboldt-Uni\wsitaet, Berlin, Germany

3 1054 FERROPORTIN AND DMTl GENE EXPRESSION IS DIFFERENTIALLY REGULATED IN THE MONOCYTES OF GENETIC HEMOCHROMATOSIS (GH)I'ATIENTS: IMPLICATIONS FOR RETICULOENDOTHELIAL IRON HOMEOSTASIS IN GH D ~ y g ~ i Dee Harrison-Findik, University of Nebraska Medical Center, Omaha, NE; George Hatzinikolas, University of Adelaide, Adelaide, Australia; John Gollan, University of Nebraska Medical Center, Omaha, NE

EVALUATION OF ALPHA-I-ANTITRYPSIN ALLELE

P 1055

HEREDITARY HEMOCHROMATOSIS Jayant Talwalkar, Heidi Torgerson, Michael Malinchoc, David Brandhagcn, Mayo Clinic and Foundation, Rochester, MN

HEALTH-RELATED QUALITY OF LIFE ASSESSMENT IN

-* 1056 RATES OF IRON ACCUMULATION IN UNTREATED SUBJECTS HOMOZYGOUS FOR THE C282Y HEMOCHROMATOSIS MUTATION: RELEVANCE TO DISEASE I'ENETRANCE Lawrie W Powell, Jeannette L Dixon, The Queensland Institute of Medical Research, Brisbane, Australia; David G Hewett, The Royal Brisbane and Women's Hospital, Brisbane, Australia; David M Purdie, Grant A Ramm, Greg J Anderson, Nathan Subramaniam, The Queensland Institute of Medical Research, Brisbane, Australia; Linda M Fletcher, Darrell H Crawford, Princess Alexandra Hospital, Brisbane, Australia; Juleen A Cavanaugh, Mark L Bassett, The Canberra Hospital, Canberra, Australia

# 1057 HEPATIC AND SPLENIC IRON OVERLOAD WITHOUT HEMOCHROMATOSIS GENE MUTATIONS IN DIVERSE ETHNIC GROUPS DEMONSTRATED BY MAGNETIC RESONANCE IMAGING Tusar K Desai, William Beaumont Hospital, Bloomfield Hills, MI; S Lingham, K Bis, A Shetty, William Beaumont Hospital, Royal Oak, MI

# 1058

WITH WILSON DISEASE (WD) Peter Ferenci, University of Vienna, Wien, Austria; Mark Sch8er, University of Heidelberg, Heidelberg, Germany; Ferenc Szalay, Semmelweis University, Budapest, Hungary; Viera Kupcova, Comenius University, Bratislava, Slovakia; Karel Caca, University of Leipzig, Leipzig, Germany; Kara Demir, University of Istanbul, Istanbul, Turkey; Wolfgang Vogel, University of Innsbruck, Innsbruck, Austria; Christian Datz, St. Johann Spital, Salzburg, Austria; Johan Fevery, University of Leuven, Leuven, Belgium; Cihan Yurdaydin, University of Ankara, Ankara, Turkey; Claudia Willheim, University of Vienna, Wien, Austria

PHENOTYPE-GENOTYPE CORRELATIONS IN PATIENTS

# 1059 THE CLINICAL RELEVANCE OF COMPOUND HETEROZY GOSITY FOR THE HEMOCHROMATOSIS MUTATIONS (C282Y/H63D) David G Hewett, The Royal Brisbane and Women's Hospital, Brisbane, Australia; Jeannette L Dixon, David M Purdie, Grant A Ramm, Greg J Anderson, Nathan Subramaniam, The Queensland Institute of Medical Research, Brisbane, Australia; Linda M Fletcher, Darrell H Crawford, Princess Alexandra Hospital, Brisbane, Australia; Juleen A Cavanaugh, Mark L Bassett, The Canberra Hospital, Canberra, Australia; Lawrie W Powell, The Queensland Institute of Medical Research, Brisbane, Australia

# 1060

IMPLICATIONS FOR THE USE AND VALUE OF PHLEBOTOMY IN THE TREATMENT OF HEREDITARY HAEMOCHROMATOSIS Eleanor Ryan, Sharon Barrett, Barbara Coughlan, Barry Kelleher, Ferga Gleeson, John Crowe, Mater Misericordiae University Hospital, Dublin, Ireland

IRON RE-ACCUMULATION FOLLOWING PHLEBOTOMY

# 1061 HEPATIC SIDEROSIS IS ASSOCIATED WITH ACCELERATED DECOMPENSATION AND DECREASED SURVIVAL IN PATIENTS WITH CIRRHOSIS Zeid Kayali, USC, Pasedena, CA; Farshad Elmi, Rostislav Ranguelov, Frank Mitros, Stephen Rayhill, Warren Schmidt, Kyle Brown, University of Iowa, Iowa City, IA

Viral Hepatitis, Other

8 # 1062 THE HEPATITIS E VIRUS ORF3 PROTEIN INTERACTS WITH HUMAN AMBP AND ENHANCES THE EXPORT OF ITS

LIVER CELLS Sunil K Lal, International Centre for Genetic Engineering and Biotechnology, New Delhi, India

PROCESSED PROTEIN ALPHA 1-MICROGLOBULIN FROM

8 Denotes AASLC Presidential Poster of Distinction


8 # 1063 QUANTITATIVE ANALYSIS OF HEPATITIS B VIRUS REPLICATIVE INTERMEDIATES IN THE LIVER A COMPARISON OF PREGENOMIC RNA VS CCCDNA DETECTION Andreas Laras, Athens University School of Medicine, Athens, Greece; Evangelini Dimou, Henry Dunant Hospital, Athens, Greece; Agelilu Kostamena, John Koskinas, Athens University School of Medicine, Athens, Greece; Stephanos J Hadziyannis, Henry Dunant Hospital, Athens, Greece

8 #lo64 INVOLVEMENT OF HEPATITIS E VIRUS INFECTION IN NON-ABC ACUTE HEPATITIS IN JAPAN Koji Yano, Yoko Tamada, Hiroshi Yatsuhashi, Manabu Daikoku, National Nagasaki Medical Center, Nagasaki, Japan; Michiaki Koga, National Ureshino Hospital, Ureshino, Japan; Hiromi Ishibashi, Michitami Yano, National Nagasaki Medical Center, Nagasaki, Japan

# 1065 SEN VIRUS INFECTION INFLUENCE THE PATHOLOGICAL FINDINGS IN LIVER, BUT NOT AFFECT THE INCIDENCE OF CAR C I N 0 MA Miki Kaneko, Mitsuhiko Moriyama, Hiroshi Matsumura, Hitomi Nakamura, Shyu Oshiro, Hiroshi Aoki, Atsuo Shioda, Yasuyuki Arakawa, School of Medicine, Nihon University, Tokyo, Japan

# 1066 GB VIRUS-C CLEARANCE IS FREQUENT IN HIV/HCV

RIBAVIRIN TREATMENT BUT DOES NOT ADVERSELY

STUDY GROUP Carolynne Zander, Massachusetts General Hospital, Boston, MA; J Andersen, Harvard School of Public Health, Boston, MA; Jason Blackard, Wenyu Lin, Massachusetts General Hospital, Boston, MA; D Zdunek, G Hess, Roche Diagnostics, Basel, Switzerland; M Peters, University of California San Francisco, San Francisco, CA; M Koziel, Beth Israel Deaconess Medical Center, Boston, MA; Kenneth E Sherman, University of Cincinnati College of Medicine, Cincinnati, OH; G K Robbins, Massachusetts General Hospital, Boston, MA; Raymond T Chung, Massachusetts General Hospital, Harvard Medical School, Boston, MA

CO-INFECTED PATIENTS RECEIVING INTERFERON AND

AFFECT HIV-1 VIREMIA THE ADULT ACTG A5071

# 1067 ACUTE HEPATITIS E : A STUDY OF 17 CONSECUTIVE

PERIOD Helene Poirson, Jean Marie Peron, Laurent Alric, Christophe Bureau, Sophie Metivier, Emmanuel Dupuis, Jacques Izopet, Jean-Pierre Vinel, CHU Purpan, Toulouse, France

tt 1068 SYNERGISTIC THERAPEUTIC EFFECT OF COMBINATION OF

THE EARLY VIREMIC PHASE IN A MURINE MODEL OF FULMINANT HEPATIC FAILURE Uichiro Fuchizaki, Yasunari Nakamoto, Kanazawa University, Kanazawa, Japan; Yoshihiro Sugiyama, Kenichi Imagawa, Mikio Kikuchi, Otsuka Pharmaceutical, Tokushma, Japan; Shuichi Kaneko, Kanazawa University, Kanazawa, Japan

# 1069 ASSOCIATION OF HCV PARTICLES WITH LDL/VLDL: ANALYSIS USING ISOTONIC IODIXANOL GRADIENT CENTRIFUGATION & REAL TIME PCR Soren U Nielson, Alastair D Burt, C Martin, Margaret F Bassendine, Geoffrey L Toms, The Medical School, University of Newcastle, Newcastle upon Tyne, UK

# 1070 EFFECTS OF THE PROTEASE DOMAIN OF HEPATITIS C VIRUS NS3 PROTEIN O N ITS HELICASE ACTIVITY Ryan S Rypma, Angela M I Lam, David N Frick, New York Medical College, Valhalla, NY

# 1071 HBV GENOTYPE & PRECOREl PRECORE PROMOTOR STATUS IN A SYDNEY POPULATION Evelyn B Crewe, Gemma Sandico, Dhara Patel, Chris Liddle, Westmead Hospital, Sydney, Australia; Erwin Sablon, Innogenetics NV, Ghent, Belgium; Jacob George, Westmead Hospital, Sydney, Australia

PATIENTS IN SOUTH-WEST FRANCE OVER A 13 MONTH

INTERFERON-ALPHA AND INTERFERON-GAMMA DURING

# 1072

INFECTION WITH HBV AND HCV Francesca Agnelli, Maria F Donato, Eliana Arosio, Valentina Monti, Angelo Sangiovanni, Pietro Lampertico, Maria G Rumi, Giovanna Lunghi, Ersilio Del Ninno, Massimo Colombo, Ospedale Maggiore IRCCS Policlinico, University of Milan, Milano, Italy

A FIVE-YEAR COHORT STUDY OF PATIENTS WITH DUAL


Poster Session 4

Tuesday, October 28 Hyrirs Cormviliori Center, Exhibit Hull C

Poster Viewinc 8:00am - 12:30um


1O:OO - 11:15am 1O:OO - 11:15am

8 Those posters identified as AASLD Presidential Poster of Distinction by a ribbon icon have received review scores that place them within the top 10%) of all posters. We encourage you to make them a priority as you visit the poster session.

Alcoholic Liver Disease

# 1073 REPRODUCIBILITY OF ALCOHOL CONSUMPTION HISTORIES IN PATIENTS WITH CHRONIC LIVER DISEASE Steven Herrine, Andra Greenberg, Deborah Moretti, Jonathan Fenkel, Kimberly Campbell, Glenda Wrenn Davis, Mina Oh, Mahesh Swaminathan, Victor Navarro, Thomas Jefferson University, Philadelphia, PA

$1074 SAMPLING ERROR AND RELIABILITY OF LIVER BIOPSY

DISEASE (NAFLD) Patricia Mendez, Arie Regev, Enrique Molina, Mariana Berho, Pablo Bejarano, Marco Ladino, Eugene Schiff, University of Miami, Miami, FI,

IN PATIENTS WITH NON-ALCOHOLIC FATTY LIVER

~~

rt 1075 DIAGNOSTIC VALUE OF BIOCHEMICAL MARKERS (FIBROTEST) FOR THE PREDICTION OF LIVER FIBROSIS IN PATIENTS WITH CHRONIC ALCOHOLIC LIVER DISEASE (ALD) Sylvie Naveau, Bruno Raynard, HBpital Antoine Becli.re, Clamart, France; Vlad Ratziu, Groupe Hospitalier Pitie- Salpetriere, Paris, France; Annie Abella, H6pital Antoine Beckre, Clamart, France; Franqoise Irnbert-Bismut, Djamila Messous, Groupe Hospitalier Pitie-Salpetriere, Paris, France; Fabienne Beuzen, Frederique Capron, Jean C Chaput, HBpital Antoine Beclere, Clamart, France; Thierry Poynard, Groupe Hospitalier Pitie-Salpetriere, Paris, France

P 1076

PROTECTS HEAVY DRINKERS FROM ALCOHOLIC LIVER DISEASE Bijay K Baburajan, Faculty of Medicine, University of Newcastle, Newcastle Upon Tyne, UK; Mark Wright, Imperial College, London, UK; Ann K Daly, J B Leathart, Faculty of Medicine, University of Newcastle, Newcastle Upon Tyne, UK; M Thursz, Imperial College, London, UK; Christopher P Day, Faculty of Medicine, University of Newcastle, Newcastle Upon Tyne, UK

A "LOSS- OF- FUNCTION " POLYMORPHISM IN ICAM-1

tt 1077 RESPONSE T O CORTICOSTEROID TREATMENT FOR ACUTE ALCOHOLIC HEPATITIS IS INDICATED BY AN EARLY FALL IN BILIRUBIN Judith M Morris, Ewan H Forrest, Victoria Infirmary, Glaqgow, UK

8 ti 1078

PIOGLITAZONE IMPROVED ALCOHOLIC FATTY LIVER IN RATS Kengo Tomita, Toshifumi Azuma, Naoto Kitamura, Sayaka Inokuchi, Takeshi Nishimura, Shinzo Kato, Hiromasa Ishii, Keio University School of Medicine, Tokyo, Japan

HGF/C-MET SIGNALING ACTIVATION INDUCED BY

# 1079

GLUTAMYLTRANSFERASE IN ALCOHOLIC LIVER DISEASE Makoto Irie, Norihisa Suzuki, Teturo Sohda, Akira Anan, Kaoru Iwata, Makoto Yoshikane, Hidetoshi Nakane, Hiroshi Watanabe, Fukuoka University School of Medicine, Fukuoka, Japan; Peter Fischer, Jurgen E Sherberich, Center of Internal h/ledicine, Hospital of the J. W. Goethe-University, Frankfurt, Germany; Shotaro Sakisaka, Fukuoka University School of Medicine, Fukuoka, Japan

INTRAHEPATIC LOCALIZATION OF GAMMA-

~~ ~

# 1080 PIOGLITAZONE WITH ALNINE SUPPLEMENTATION

Toshifumi Azuma, Kengo Tomita, Naoto Kitamura, Sayaka Inokuchi, Takeshi Nishimura, Hiromasa Ishii, Keio University School of Medicine, Tokyo, Japan

PREVENTS ALCOHOL-INDUCED FATTY LIVER

# 1081 HIGH PREVALENCE OF THE VAL/VAL POLYMORPHISM OF SOD2 IN NORTHEAST OF MEXICO: A COUNTRY WITH HIGH INCIDENCE OF ALD Diana E Flores, University Hospital, Monterrey, Mexico; Mireya Landeta, Rocio Ortiz, Augusto Rojas, Faculty of Medicine, UANL, Monterrey, Mexico; Hector J Maldonado, University Hospital, Monterrey, Mexico; Francisco J Bosques, University Hospital Dr. Jose E. Gonzilez, UANL, Monterrey, Mexico

Artificial Liver Support

8 # 1082 DESIGNER CELLS FOR A BIOARTIFICIAL LIVER- RESTORING ORNITHINE CARBAMYL TRANSFERASE (OTC)

DIMENSIONAL CULTURE RESTORES UREA SYNTHESIS T O IN VIVO LEVELS Clare Selden, Sam Coward, Catherine Jones, Marianne Khalil, Demetra Mavri, Humphrey J F Hodgson, Royal Free and University College Medical School, London, UK

# 1083 MARS TREATMENT IMPROVES RENAL FUNCTION INDEPENDENT OF SYSTEMIC HAEMODYNAMICS IN ACUTE LIVER FAILURE: A RANDOMIZED CONTROLLED STUDY IN A PIG MODEL Lars M Ytreba, University Hospital Northern Norway, Tromso, Norway; Sambit Sen, University College London, London, UK; Christopher Rose, Max-Delbruck Center for Molecular Medicine, Berlin, Germany; Geir I Nedredal, University Hospital Northern Norway, Tromsn, Norway; Nathan A Davies, Roger Williams, University College London, London, UK; Arthur Revhaug, University Hospital Northern Norway, Tromso, Norway; Rajiv Jalan, University College London, London, UK

# 1084 CYTOCHROME P450 ISOFORM DYSFUNCTION IN ALCOHOLIC HEPATITIS CAN BE REVERSED BY ALBUMIN DIALYSIS (MARS) Jan Stange, University of California San Diego, San Diego, CA; M Siekmoller, University of Rostock, Rostock, Germany; Deanna L Oliver, D P Chauhan, Tarek Hassanein, University of California San Diego, San Diego, CA

ACTIVITY TO HEP G2 CELLS BY TRANSFECTION AND 3-



# 1085 BIAOARTIFICIAL LVIER THERAPY IN MONKEYS USING REVESIBLY IMMORTALIZED HUMAN HEPATOCYTES Naoya Kobayashi, Okayama Graduate School of Medicine and Dentistry, Okayama, Japan; Shuhei Nakaji, Kuraray Medical Co., Kurashilu, Japan; Makoto Kodama, Tissue Engineering Research Center, Tsukuba, Japan; Philippe Leboulch, Harvard- Massachusetts Institute of Technology, Cambridge, MA; Noriaki Tanaka, Okayama Graduate School of Medicine and Dentistry, Okayama, Japan

# 1086

ELEVATED EXPRESSION OF GENES ASSOCIATED WITH

CULTURED IN ALGINATE CAN PROVIDE THE CELLULAR COMPONENT OF A BIOARTIFICIAL LIVER Leonard Damelin, Sarah Choudhury, Sam Coward, Royal Free and University College Medical School, London, UK; Mike Hubank, Institute of Child Health, UCL, London, UK; Humphrey Hodgson, Clare Selden, Royal Free and University College Medical School, London, UK

HEPG2 CELLS IN 3-DIMENSIONAL CULTURE EXHIBIT

LIPID METABOLISM-FURTHER EVIDENCE THAT CELLS

# 1087 IMPROVEMENT OF THE HAEMODYNAMIC DERANGEMENT IN HEPATORENAL SYNDROME WITH ALBUMIN DIALYSIS Stewart H Lambie, Derby City General Hospital, Derby, UK; Terry Bennett, Centre for Integrated Systems Biology and Medicine, Nottingham, UK; Christopher W McIntyre, Jan G Freeman, Derby City General Hospital, Derby, UK

Cholangiocyte Biology and Experimental Cholestasis

# 1088 THE a-2 ADRENERGIC RECEPTOR AGONIST, UK14,304,

BILE DUCT LIGATED (BDL) RATS BY ACTIVATION OF THE G-PROTEIN Gal Heather Francis, Shannon Glaser, Scott and White Hospital, Temple, TX; Domenico Alvaro, University of Rome La Sapienza, Rome, Italy; Silvia Taffetani, Scott and White Hospital, Temple, TX; Luca Marucci, Antonio Benedetti, University of Ancona, Ancona, Italy; Yoshiyuki Ueno, Tohoku University School of Medicine, Sendai, Japan; Marco Marzioni, University of Ancona, Ancona, Italy; Gene LeSage, The University of Texas Houston Medical School, Houston, TX; Julie Venter, Brandy Baumann, The Texas A & M University System HSC COM, Temple, TX; Jo Lynne Phinizy, Scott and White Hospital, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

INHIBITS SECRETIN-STIMULATED DUCTAL SECRETION OF

tt 1089 ACTIVATION OF THE MEKS/ERK5 CASCADE IN BILIARY EPITHELIUM OF POLYCYSTIC KIDNEY RAT, AN ANIMAL MODEL OF CAROLI'S DISEASE Yasunori Sato, Kenichi Harada, Yasuni Nakanuma, Kanazawa University Graduate School of Medicine, Kanazawa, Japan

# 1090 GAMMA-AMINOBUTYRIC ACID (GABA) INHIBITS CHOLANGIOCARCINOMA GROWTH BY CAMP-DEPENDENT INHIBITION OF THE PKA/SRC/MEK/ERKl/P PATHWAY Giammarco Fava, The Texas A & M University System HSC COM, Temple, TX; Jo Lynne Phinizy, Shannon Glaser, Heather Francis, Scott and White Hospital, Temple, TX; Luca Marucci, Antonio Benedetti, University of Ancona, Ancona, Italy; Brandy Baumann, The Texas A & M University System HSC COM, Temple, TX; Silvia Taffetani, Scott and White Hospital, Temple, TX; Julie Venter, The Texas A & M University System HSC COM, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

# 1091

CHOLANGIOCYTE APICAL BILE ACID TRANSPORTER (ASBT) REGULATES TRANSPORT ACTIVITY IN CHOLANGIOCYTES Xuefeng Xia, Marlon Roundtree, Xiaohui Lu, Shujun Shentu, Azmeena Najam, Afkhamossadat Meriklu, Gene D LeSage, University of Texas, Houston, TX

PROTEASOME-DEPENDENT DEGRADATION OF THE

# 1092

CYTE APOPTOSIS IS PREVENTED BY TAUROCHOLATE Marco Marzioni, University of Ancona, Ancona, Italy; Silvia Taffetani, Shannon Glaser, Heather Francis, Scott and White Hospital, Temple, TX; Yoshiyuki Ueno, Tohoku University School of Medicine, Sendai, Japan; Jo Lynne Phinizy, Scott and White Hospital, Temple, TX; Brandy Baumann, Giammarco Fava, Julie Venter, The Texas A & M University System HSC COM, Temple, TX; Antonio Benedetti, University of Ancona, Ancona, Italy; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

# 1093

ESTROGENS COOPERATE IN MODULATING THE PROLIFERATION OF RAT CHOLANGIOCYTES BY ACTING

Domenico Alvaro, Veronica Drudi-Metalli, Barbara Barbaro, Antonio Augello, Vincenzo Cardinale, Roberto Tari, Maria Grazia Mancino, Adolfo Francesco Attili, University of Rome, Rome, Italy; Shannon Glaser, Jo Lynne Phinizy, Silvia Taffetani, Heather Francis, Scott and White Hospital, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

CA2+-MEDIATED, SEROTONIN-INDUCED CHOLANGIO-

INSULIN LIKE GROWTH FACTOR 1 (IGF-1) AND

AT BOTH RECEPTOR AND POST-RECEPTOR LEVELS

# 1094 ESTROGEN ADMINISTRATION PROTECTS FROM BILE

DIVERSION IN THE BDL RAT Gianluca Svegliati-Baroni, Roberto Ghiselli, Marco Marzioni, Universith Politecnica delle Marche, Ancona, Italy; Domenico Alvaro, Universita La Sapienza di Roma, Roma, Italy; Federico Mocchegiani, Stefania Saccomanno, Valerio Sisti, Laura Ugili, Fiorenza Orlando, Vittorio Saba, Universith Politecnica delle Marche, Ancona, Italy; Gianfranco Alpini, Texas A & M University

DUCT VANISHING INDUCED BY BILIARY-DIGESTIVE

HSC and Central Texas Veterans HCS, Ancona, Italy; Antonio Benedetti, Universita Politecnica delle Marche, Ancona, Italy

0 12 a N 9 m 0

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g 1095 HISTAMINE STIMULATES PROLIFERATION OF NORMAL CHOLANGIOCYTES BY CAZ+/PKC-DEPENDENT MODULATION OF THE CAMP-DEPENDENT PKA/SRC/MEK/ERKl/Z PATHWAY Heather Francis, Shannon Glaser, Silvia Taffetani, Scott and White Hospital, Temple, TX; Julie Venter, The Texas A & M University System HSC COM, Temple, TX; Jo Lynne Phinizy, Scott and Wlute Hospital, Temple, TX; Brandy Baumann, Giammarco Fava, The Texas A & M University System HSC COM, Temple, TX; Ramona Reichenbach, Central Texas Veterans HCS, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

8 1096 THE PITUITARY HORMONE, PROLACTIN STIMULATES NORMAL CHOLANGIOCYTE PROLIFERATION BY A CA2+ AND PKC MEDIATED MECHANISM Silivia Taffetani, Heather Francis, Shannon Glaser, Jo Lynne Phinizy, Scott and White Hospital, Temple, TX; Luca Marucci, Antonio Benedetti, University of Ancona, Ancona, Italy; Brandy Baumann, The Texas A & M University System HSC COM, Temple, TX; Ramona Reichenbach, Central Texas Veterans HCS, Temple, TX; Julie Venter, The Texas A & M University System HSC COM, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

# 1097 THYROID HORMONE INHIBITS CAMP DEPENDENT PROLIFERATION OF CHOLANGIOCYTES FROM BILE DUCT

MECHANISM Giammarco Fava, The Texas A & M University System HSC COM, Temple, TX; Shannon Glaser, Jo Lynne Phinizy, Heather Francis, Scott and White Hospital, Temple, TX; Luca Marucci, Antonio Benedetti, University of Ancona, Ancona, Italy; Silvia Tafettani, Scott and White Hospital, Temple, TX; Julie Venter, Brandy Baumann, The Texas A & M University System HSC CO.M, Temple, TX; Ramona Reichenbach, Central Texas Veterans HCS, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

$1098

REGULATED BY FXR AND RXR ALPHA NUCLEAR RECEPTORS IN THE HUMAN GALLBLADDER EPITHELIUM Nicolas Chignard, Martine Mergey, Vhronique Barbu, Annick Paul, Chantal Housset, INSERM U402, Paris, France

i; 1099 TANNIC ACID INHIBITS CHOLANGIOCYTE PROLIFERATION IN BILE DUCT LIGATED RATS BY A SRC DEPENDENT PATHWAY Silvia Taffetani, Scott and White Hospital, Temple, TX; Giaiifranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX; Heather Francis, Shannon Glaser, Jo Lynne Phinizy, Scott and White Hospital, Temple, TX; Julie Venter, Brandy Baumann, The Texas A & M University System HSC COM, Temple, TX; Tushar Patel, Scott and White Hospital and The Texas A&M University System HSC COM, Temple, 'TX

LIGATED RATS BY A IP3/CAZ+/PKC-DEPENDENT

THE VIP RECEPTOR VPAC-1 IN HIGHLY EXPRESSED AND

# 1100 CROSS-TALK BETWEEN THE CAMP AND CALCIUM DEPENDENT SIGNALING PATHWAYS REGULATES VEGF-A- STIMULATED NORMAL RAT CHOLANGIOCYTE PROLIFERATION Shannon Glaser, Heather Francis, Jo Lynne Phinizy, Silvia Taffetani, Scott and White Hospital, Temple, TX; Julie Venter, Brandy Baumann, The Texas A & M University System HSC COM, Temple, TX; Domenico Alvaro, University of Rome La Sapienza, Rome, Italy; Marco Marzioiii, University of Ancona, Ancona, Italy; Giammarco Fava, The Texas A & M University System HSC COM, Temple, TX; Ramona Reichenbach, Central Texas Veterans HCS, Temple, TX; Gianfranco Alpini, The Texas A & M University System HSC COM and Central Texas Veterans HCS, Temple, TX

# 1101 PORTAL FIBROBLASTS ATTENUATE PROLIFERATION OF BILE DUCT EPITHELIA THROUGH BLOCKADE OF PURINERGIC STIMULATION OF MAP KINASES M Nauman Jhandier, Emma A Kruglov, Jonathan A Dranoff, Yale University School of Medicine, New Haven, CT

# 1102 SUSCEPTIBILITY T O ESTROGEN INDUCED CHOLESTASIS IN THE FEMALE IS ASSOCIATED WITH LOSS OF RADIXIN, AN MRP2 TETHERING PROTEIN, FROM THE CANALICULAR MEMBRANE Carol J Soroka, Albert Mennone, James L Boyer, Yale University School of Medicine, New Haven, CT

# 1103 EXPRESSION AND REGULATION OF ADENYLYL CYCLASE ISOFORMS (ACS) IN RAT CHOLANGIOCYTES;

NAPHTHYLISOTHIOCYANATE (ANIT) TREATMENT Saida Melero, Mario Strazzabosco, Carlo Spirli, Roniina Fiorotto, Ospedali Riuniti di Bergamo, Bergamo, Italy; Shannon Glaser, Heather Francis, Scott and White Hospital, Temple, TX; Gianfranco Alpini, Central Texas Veterans HSC, Temple, TX

EFFECTS OF LIPOPOLYSACCARIDE (LPS) AND U-

# 1104 NEUTROPHIL EXTRAVASATION AND ACUTE LIVER INJURY IN BILE DUCT-LIGATED MICE IS DEPENDENT ON INTERCELLULAR ADHESION MOLECULE-1 (ICAM-1) Jaspreet S Gujral, University of Arizona, Tucson, AZ; Anwar Farhood, University of Texas Health Science Center, Houston, TX; Hartmut Jaeschke, University of Arizona, Tucson, AZ

# 1105 TAUROURSODEOXYCHOLIC ACID INSERTS THE BILE SALT EXPORT PUMP INTO CANALICULAR MEMBRANES IN CHOLESTATIC RAT LIVER Frank Dombrowski, University of Magdeburg, Magdeburg, Germany; Bruno Stieger, University Hospital Zurich, Zurich, Switzerland; Ulrich Beuers, Ludwig-Maximilians-University, Munich, Germany

# 1106 HEPATIC AND RENAL ABC TRANSPORTER EXPRESSION AS CRITICAL DETERMINANTS OF URSODEOXYCHOLIC ACID- INDUCED BILE INFARCTS IN BILE DUCT-LIGATED MICE Martin Wagner, Peter Fickert, Andrea Fuchsbichler, Dagmar Silbert, Judith Guniliold, Gernot Zollner, Kurt Zatloukal, Karl- Franzens University, Graz, Austria; Hanns-Ulrich Marschall, Karolinska Institute, Stoc!&olni, Sweden; John D Schuetz, St. Jude Children's Research Hospital, Memphis, TN; Frank J Gonzalez, National Cancer Institute, Bethesda, MD; Helmut Denk, Michael Trauner, Karl-Franzens University, Graz, Austria



# 1107

ASSOCIATED PROTEINS 2 AND 3 (MRP2, MRP3) BY CHOLIC ACID (CA) AND URSODEOXYCHOLIC ACID (UDCA) IN MICE Gemot Zollner, Peter Fickert, Martin Wagner, Andrea Fuchsbichler, Dagmar Silbert, Judith Gumhold, Kurt Zatloukal, Helmut Denk, Michael Trauner, Karl-Franzens University, Graz, Austria

INDUCTION OF INTESTINAL MULTIDRUG RESISTANCE-

# 1108 GP130 DEPENDENT SIGNALLING IS PROTECTIVE AFTER BILE DUCT LIGATION IN MICE Torsten Wuestefeld, Christian Klein, Medical School of Hannover, Hannover, Germany; Gregory J Gores, Mayo Medical School, Rochester, MN; Jiirgen Schoelmerich, University of Regensburg, Regensburg, Germany; Michael P Manns, Christian Trautwein, Medical School of Hannover, Hannover, Germany

# 1109 BILE DUCT INJURY AND REPAIR FOLLOWING ARTERIAL ISCHEMIA IN THE RAT LIVER Marc Beaussier, Anesthesiologie, HBpital Saint-Antoine, Paris, France; Dominique Wendum, Anatomie Pathologique, HBpital Saint-Antoine, Paris, France; Olivier Rosmorduc, Colette Rey, Veronique Barbu, INSERM U402, Paris, France; Elisabeth Lasnier, Biochimie, HBpital Saint-Antoine, Paris, France; Andre Lienhart, Anesthesiologie, HBpital Saint-Antoine, Paris, France; Chantal Housset, INSERM U402, Paris, France

# 1110 ALPHA-V/BETA-6 INTEGRIN AND BILIARY FIBROSIS D Montgomery Bissell, Bruce Wang, Noriko Kikuchi, Nina Lysenko, University of California, San Francisco, CA; Brian Dolinski, Diane Leone, Ken Simon, Shelia Violette, Biogen, Inc., Cambridge, MA

Chronic Liver Disease: Clinical and Epidemiology # 1111 LIVER BIOPSY FOR SERONEGATIVE ALT LESS THAN TWICE NORMAL: FINDINGS IN 249 PATIENTS Stephen D Ryder, Guruprasad Aithal, Peter D James, Queens Medical Centre, Nottingham, UK

# 1112 RECIPIENT CHARACTERISTICS AND POST-LIVER TRANPLANTATION (LT) OUTCOMES BEFORE AND AFTER MELD Fasiha Kanwal, David Geffen School of Medicine at UCLA, Los Angeles, CA; Gareth S Dulai, David Geffen School of Medicine at UCLA, VA Greater Los Angeles Healthcare System, Los Angeles, CA; Jeffrey Gombein, David Geffen School of Medicine at UCLA, Los Angeles, CA; Ian M Gralnek, David Geffen School of Medicine at UCLA, VA Greater Los Angeles Healthcare System, Los Angeles, CA

# 1113 HCV INFECTION IS AN INDEPENDENT RISK FACTOR FOR

RESULTS FROM THE THIRD NATIONAL HEALTH AND NUTRITION EXAMINATION SURVEY (NHANES 111) Suthat Liangpunsakul, Prashant Pandya, Paul Y Kwo, Naga Chalasani, Indiana University School of Medicine, Indianapolis, IN

INSULIN RESISTANCE IN NON-DIABETIC SUBJECTS:

# 1114 SERUM ALANINE AMINOTRANSFERASE (ALT) LEVELS IN

IMPLICATION TO THE PATHOGENESIS OF NON ALCOHOLIC FATTY LIVER DISEASE Revital Kariv, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Moshe Leshno, Tel Aviv University, Tel Aviv, Israel; Varda Shalev, Maccabi Health Care Services, Tel Aviv, Israel; Ran Oren, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Anat Beth-Or, Maccabi Health Care Services, Tel Aviv, Israel; Shira Zelber-Sagi, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Martin Bialik, Maccabi Health Care Services, Tel Aviv, Israel; Zamir Halpern, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel

TYPE 1 AND TYPE 2 DIABETES MELLITUS PATIENTS-

# 1115 RISK FACTORS FOR HEPATOCELLULAR CARCINOMA IN HEPATITIS B SURFACE ANTIGEN POSITIVE CARRIERS Chang Mo Moon, Kwang-Hyub Han, Ki Jun Song, Sang Hoon Ahn, Jong Won Choi, Yong Han Paik, Dong Kee Kim, Sung Min Myung, Chae Yoon Chon, Young Myoung Moon, Yonsei University College of Medicine, Seoul, South Korea

# 1116 INFORMED CONSENT AND CLINICAL TRIALS FOR CHRONIC HEPATITIS B IN ASIA: DO PATIENTS UNDERSTAND THE CONCEPTS? Belinda Mak, Chun-Tao Wai, Mei-Hua Chen, Seng-Gee Lim, National University Hospital, Singapore, Singapore

# 1117

INCARCERATED POPULATIONS Dickens Theodore, Karen A Dougherty, The University of North Carolina at Chapel Hill, Chapel Hill, NC; Paula Smith, Rosemary Jackson, North Carolina Department of Correction, Raleigh, NC; Steven Zacks, Joseph Galanko, Mark Russo, The University of North Carolina at Chapel Hill, Chapel Hill, NC; Georgia Stephens, North Carolina Department of Correction, Raleigh, NC; Michael W Fried, The University of North Carolina at Chapel Hill, Chapel Hill, NC

INCREASING LIVER-RELATED MORTALITY IN

# 1118 THE EFFECT OF HIV CO-INFECTION ON THE RISK OF CIRRHOSIS AND HEPATOCELLULAR CARCINOMA IN HCV- INFECTED PATIENTS Jennifer R Kramer, Thomas P Giordano, Julianne Souchek, Peter Richardson, Hashem El-Serag, Houston VA Med Center, Houston, TX

# 1119 BONE LOSS IS RELATED TO SERUM TRANSAMINASES LEVELS IN CHRONIC HEPATITIS C Eduardo Redondo-Cerezo, Hospital Universitario Virgen de las Nieves, Granada, Spain; Jorge Luis Gonzalez-Calvin, Hospital Universitario San Cecilio, Granada, Spain; Rafael Martin-Vivaldi, Flor Nogueras-L6pez, Hospital Universitario Virgen de las Nieves, Granada, Spain; Rosaura Ferngndez-Pascual, Universidad de Jaen, Granada, Spain; Fernando Escobar- Jimenez, Hospital Universitario San Cecilio, Granada, Spain

# 1120 0 $ 2

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HEPATITIS C TREATMENT PRACTICE PATTERNS IN THE UNITED STATES: A NATIONAL SURVEY Sean Hurley, Eric J Lawitz, Brooke Army Medical Center, San Antonio, TX

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J 1’A POSTER SESSIONS HEPATOLOGY, October 2003

= 1121 A RELIABLE METHOD FOR MONITORING ALCOHOL CONSUMPTION IN A NON-INVASIVE WAY IN PATIENTS WITH LIVER DISEASE Michael Zilly, Peter Langmann, Verena Satzinger, Ralf Winzer, Andreas Benesic, Ulrike Lenker, Diana Schirmer, Hartwig Klinker, University of Wdrzburg, Wurzburg, Germany

Drug Metabolism and Toxicity

8 1122 SEVERE HEPATIC SINUSOIDAL OBSTRUCTION ASSOCIATED WITH OXALIPLATIN-BASED CHEMOTHERAPY FOR METASTATIC COLORECTAL CANCER Laura Rubbia-Brandt, Division of Clinical Pathology, Geneva, SwitLerland; Virginie Audard, Service d’ Anatomie Pathologique, HBpital Cochin, Paris, France; Pascal Sartoretti, Division of Clinical Patliology Geneva, Switzerland; Arnaud D Roth, Oncosurgery Geneva, Switzerland; Catherine Brezault, Monique I..echarpentier, Service d Anatomie Pathologique, Paris, France; Bertrand Dousset, HApital Cochn, Paris, France; Phdippe Morel, Surgery, Geneva, Switzerland; Olivier Soubrane, HBpital Cochin, Paris, France; Stanislas Chaussade, gastroenterology, Paris, France; Gillcs Mcntha, Surgery, Geneva, Switzerland; Benoit Terris, Service d’ Anatomie Pathologique, HBpital Cochin, Paris, France

i 1123 HEPATOTOXICITY AND ANTIRETROVIRAL DRUGS IN HIV-HCV PATIENTS WITH CONGENITAL COAGULOPATHIES FOLLOWED AT AN HAEMOPHILIA UNIT DURING A DECADE Victor Vargas, Hospital Val1 d‘Hebron, Barcelona, Spain; Silvia Sauleda, CTBT-Val1 d’Hebron, Barcelona, Spain; Marta Martorell, Juan I Esteban, Hospital Val1 d’Hebron, Barcelona, Spain; Cristina Tiiral, Hospital Germans Trias i Pujol, Badalona, Spain; Isabel Ruiz, Hospital Val1 dHebron, Barcelona, Spain; Monica Tejeda, Lluis Puig, CTBT-Val1 d’Hebron, Barcelona, Spain; Rafael Esteban, laime Cuardia, Hospital Val1 d’Hebron, Barcelona, Spain

r1124 DO HYPERLIPIDEMIC PATIENTS WITH ELEVATED BASELINE LIVER ENZYMES HAVE A HIGHER RISK OF

INHIBITORS (STATINS)? Naga Chalasani, Suthat Liangpunsakul, Indiana University School of Medicine, Indianapolis, IN; Michael Murray, Joseph Kesterson, Regenstrief Institute for Health Care, Indianapolis, IN; Stephen D Nall, Indiana University School of Medicine, Indianapolis, 1N

HEPATOTOXICITY FROM HMG CO-A REDUCTASE

1125 HEPATOTOXICITY ASSOCIATED WITH THE ANTIRETROVIRAL THERAPY (ART) CONTAINING PROTEASE INHIBITORS (PIS) WITH OR WITHOUT PHARMACOKINETIC BOOSTING BY LOW-DOSE RITONAVIR (RTV) Mark S Sulkomrski, David L Thomas, Johns Hopkins School of Medicine, Baltimore, MD; Shruti H Mehta, Johns Hopkins School of Public Health, Baltimore, MD; Richard E Chaisson, Richard D Moore, Joluis Hopkins School of Medicine, Baltimore, MD

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i 1126 USE OF VECTOR ANALYSIS OF LIVER FUNCTION TESTS TO DETECT AN EARLY SIGNAL OF HEPATOTOXICITY OF A DRUG IN EARLY CLINICAL TRIALS Donald C Trost, I’fizer lnc, Groton, CT; James W Freston, Unnwsity of Connecticut Health Center, Farmington, CT

# 1127 D O OVER-THE-COUNTER ANALGESICS CONTRIBUTE T O DECOMPENSATION OF CIRRHOSIS?-A PROSPECTIVE STUDY Sakib K Khalid, Yale University, Hepatitis C Resource Center CT- VA Healthcare System, New Haven-West Haven, CT; Jill Addesa, Victor J Navarro, Yale University, New Haven, CT; Guadalupe Garcia-Tsao, Yale University, CT-VA Healthcare System, New Haven-West Haven, CT

# 1128 EFFECT OF ALCOHOL CONSUMPTION ON CYP2E1 AND CYP3A ACTIVITIES IN HUMANS: INSIGHT INTO ACETAMINOPHEN HEPATOTOXICITY IN ALCOHOLICS Suthat Liangpunsakul, Christopher J Gorski, David W Crabb, Stephen D Hall, Naga Chalasani, Indiana University School of Medicine, Indianapolis, IN

# 1129 AN EARLY OCCURRENCE OF IGA RESPONSES AGAINST

CONSUMERS Onni J Niemela, Jaana Latvala, Petra Anttila, Kirnmo Jarvi, El’ Central Hospital, Seinajoki, Finland

ACETALDEHYDE-MODIFIED PROTEINS IN ALCOHOL

# 1130 PHARMACOLOGICAL INHIBITION OF ACID CERAMIDASE SELECTIVELY SENSITIZES HUMAN LIVER TUMOR CELLS

Albert Morales, Raquel Paris, Jos6 Carlos Fernitndez-Checa, Hospital Clinic, IDIBAPS, CSIC, Barcelona, Spain

TO ANTI-CANCER DRUGS

# 1131 EFFECTIVENESS OF ASPARTATE OF ADENOSINE AS

COMPARED WITH THE PARENTAL ADENOSINE Roland0 Hernandez-Mufioz Sr, Instituto de Fisiologia Celular, UNAM, Mexico, Mexico

HEPATOPROTECTIVE AND ANTI-FIBROTIC AGENT AS

~ ~~

# 1132

FICITY FOR DETECTING RARE SERIOUS LIVER DISEASE John R Senior, Food and Drug Administration, Rockville, MD; Robert W Tipping, Merck Research Laboratories, Bluebell, PA

# 1133 CYPPEl ACTIVITY IN CIRRHOSIS Jean-Pierre Villeneuve, Claire Fournier, Soumeya Brachemi, Louise Trudel, HBpital Saint-Luc, Centre Hospitalier de I’Universite de Montreal, Montreal, PQ, Canada

SERUM TRANSAMINASE ELEVATIONS ALONE LACK SPECI-

# 1134 HIGH THROUGHPUT SCREENING FOR DRUG INDUCED

TOXICOLOGY Norman L Sussman, James H Kelly, Amphioxus Cell Technologies, Houston, TX

# 1135 IMMUNOHISTOCHEMICAL ANALYSIS OF LIVER TISSUE USING ANTIBODIES T O ACETALDEHYDE ADDUCTS, IGA

RELATED LIVER DISEASE (ALD) J Koskinas, Hippokration General Hospital, Athens, Greece; L Ramsay, A Warn, S Howard, N Coleman, Addenbrooke’s Hos- pital, Cambridge, UK; G Kenna, St. Mary’s Hospital, London, UK; G Alexander, Addenbrooke’s Hospital, Cambridge, UK

# 1136 REGULATION OF METHIONINE CYCLE ENZYMES IN THE MICROPIG MODEL OF ALCOHOLIC LIVER DISEASE Jesus A Villanueva, Charles H Halsted, University of California Davis, Davis, CA

LIVER DISEASE-INVESTIGATIVE AND PREEMPTIVE

AND INTERLEUKIN-8 IN PATIENTS WITH ALCOHOL



# 1137 ASSESSMENT OF THE DIAGNOSTIC SCALE FOR DRUG INDUCED LIVER INJURY (DILI) BY THE INTERNATIONAL CONSENSUS MEETING (ICM) AND A PROPOSAL OF ITS MODIFICATIONS Yoriyuki Takamori, Hajime Takikawa, Teikyo University School of Medicine, Tokyo, Japan; Tem Kumagi, Morikazu Onji, Ehime University School of Medicine, Ehime, Japan; Masaaki Watanabe, Akitaka Shibata, Kitasato University East Hospital, Kanagawa, Japan; Akiko Hisamochi, Ryukichi Kumashiro, Kumme University School of Medicine, Kurume, Japan; Tadashi Ito, Yasuhide Mitsumoto, JR-West Osaka Hospital, Osaka, Japan; Astushi Nakamura, Takashi Sakaguchi, Yokohama City University School of Medicine, Kanagawa, Japan

#1138 HEPATIC CYTOCHROME P450 DECREASES THROUGH CONTINUOUS INFUSIONS OF ORGANIC NITRATES Yukiko Minamiyama, Graduate School of Medicine and Dentistry, Okayama University, Okayama, Japan; Shigekazu Takemura, Keiichi Yamasaki, Seikan Hai, Graduate School of Medicine, Osaka City University, Osaka, Japan; Satoshi Yamamoto, Graduate School of Medicine, Osaka City University, Okayama, Japan; Michitaka Ozaki, S l g e r u Okada, Graduate School of Medicine and Dentistry, Okayama University, Okayama, Japan

Hepatitis B: Treatment

# 1139 CHARACTERISATION AND FUNCTIONAL ANALYSIS OF HEPATITIS B VIRUS MUTANTS SELECTED IN PATIENTS WITH SEVERE HEPATITIS DURING LONG TERM LAMIVUDINE THERAPY: ROLE OF COMPENSATORY MUTATIONS IN DISEASE PROGRESSION Nadia Warner, Stephen A Locarnini, Anna Ayres, Geoff Thompson, Ros Edwards, Vitina Sozzi, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia; Nancy W Y Leung, Prince of Wales Hospital, Hong Kong, SAR, China; Ben Tehan, David Chalmers, Victorian College of Pharmacy, Parkville, Vic, Australia; Angeline Bartholomeusz, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia

# 1140

INCREASING IN PERIPHERAL BLOOD DURING LAMIVUDINE THERAPY Yasuteru Kondo, Tohoku University School of Medicine, Sendai, Japan; Shinnichi Asabe, Jichi Medical School, Kamikawachi, Japan; Koju Kobayashi, Koju Kobayashi, Tohoku University School of Health Science, Sendai, Japan; Masaaki Shiina, National Sendai Hospital, Sendai, Japan; Yoshiyuki Ueno, Noriatsu Kanno, Koji Fukushima, Toom Shimosegawa, Tohoku University School of Medicine, Sendai, Japan

ANALYSIS OF HBV-SPECIFIC CYTOTOXIC T LYMPHOCYTES

# 1141 COMPLETE GENOTYPIC AND PHENOTYPIC ANALYSES OF

CHRONIC HEPATITIS B PATIENTS RECEIVING 96 WEEKS OF ADEFOVIR DIPIVOXIL (ADV) Huiling Yang, Christopher Westland, William E Delaney IV, Gilead Sciences, Inc., Foster City, CA; Peter W Angus, Austin Hospital, Melbourne, Australia; Stephen A Locamini, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia; George Kitis, Georgios Papanikolaou Hospital, Thessaloniki, Greece; Michael Wulfsohn, Craig S Gibbs, Michael D Miller, Carol L Brosgart, Shelly Xiong, Gilead Sciences, Inc., Foster City, CA

HBV MUTATIONS IDENTIFIED IN HBEAG-NEGATIVE

# 1142 PROPHYLACTIC AND THERAPEUTIC EFFICACY OF A DENDRITIC CELL-BASED VACCINE FOR IMMUNOSUPPRESSED NORMAL AND CHRONIC HEPATITIS B VIRUS CARRIER MOUSE Shinya Furukawa, Sk Md Fazle Akbar, Aki Hasebe, Norio Horiike, Morikazu Onji, Ehime University School of Medicine, Ehime, Japan

# 1143 MB6866 (HEPAVIR B), A HEPDIRECTTM PRODRUG OF ADEFOVIR MECHANISM OF ACTIVATION AND LIVER TARGETING Paul D van Poelje, Timothy J Colby, James M Fujitaki, K Raja Reddy, Michael C Matelich, Kathy A Senekeo, David L Linemeyer, Mark D Erion, Metabasis Therapeutics, Inc., San Diego, CA

# 1144 A PHASE 2 CLINICAL STUDY EVALUATING SAFETY AND

MONOCLONAL ANTIBODIES TO HBSAG IN COMBINATION WITH LAMIVUDINE IN CHRONIC HBV PATIENTS Eithan Galun, Rifat Safadi, Alla Milchem, Zvi Akerman, Yaffa Ashur, Idit Mathot, Hadassah University Hospital, Jerusalem, Israel; Zobair M Younossi, Inova Fairfax Hospital, Falls Church, VA; Gerald Y Minuk, Health Sciences Centre, Winnipeg, MB, Canada; Ofer Nussbaum, Dov Terkieltaub, XTL Biopharmaceuticals Ltd., Rehovot, Israel; Neil Graham, XTL Biopharmaceuticals Inc., Durham, NC; Rachel Eren, Shlomo Dagan, XTL Biopharmaceuticals Ltd., Rehovot, Israel

EFFICACY OF HEPEX-B, A MIXTURE OF TWO HUMAN

# 1145 LAMIVUDINE TREATMENT DURING PREGNANCY TO PREVENT PERINATAL TRANSMISSION OF HEPATITIS B VIRUS INFECTION Monika van Zonneveld, Andeltje B van Nunen, Hubert G M Niesters, Robert A de Man, Solko W Schalm, Harry LA Janssen, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands

# 1146

AND REDUCES THE RISK OF HEPATOCELLULAR CARCINOMA IN CHRONIC HEPATITIS B Monika van Zonneveld, Hubert G M Niesters, Robert A de Man, Solko W Schalm, Harry L A Janssen, Erasmus MC, University Medical Center Rotterdam, Rotterdam, Netherlands

RESPONSE TO ALPHA-INTERFERON PROLONGS SURVIVAL

# 1147 5-YEAR FOLLOW-UP OF 998 CHRONIC HEPATITS B PATIENTS TO DETERMINE LONG-TERM SAFETY OF LAMIVUDINE AND CLINICAL CONSEQUENCES OF

Anna S Lok, University of Michigan, AM Arbor, MI; Ching-Lung Lai, University of Hong Kong, Hong Kong, Hong Kong; Nancy Leung, Prince of Wales Hospital, Hong Kong, Hong Kong; Guang-Bi Yao, Jiangan-Qu Central Hospital, Shanghai, China; Zhen-Yu Cui, Ditan Hospital, Beijing, China; Eugene R Schiff, University of Miami, Miami, FL; Jules L Dienstag, Massachusetts General Hospital, Boston, MA; Jenny Heathcote, University of Toronto, Toronto, ON, Canada; Nancy R Little, Dorothea A Griffiths, Stephen D Gardner, Mary Castiglia, GSK, Research Triangle Park, NC

LAMIVUDINE-RESISTANT MUTATIONS


# 1148 VIRAL DYNAMICS MODELING INDICATES THAT THE

HEPATITIS B VIRUS IS ACCELERATION OF THE FREE VIRUS CLEARANCE Avidan U Neumann, Idit Feldberg, Bar-Ilan University, Ramat- Gan, Israel; Rachel Eren, Shlomo Dagan, XTL Biopharmaceuticals Ltd., Rehovot, Israel

f 1149 CELLULAR IMMUNE RESPONSES TO THE HEPATITIS B VIRUS POLYMERASE DECREASE DURING LONGTERM ANTIVIRAL THERAPY Eishiro Mizukoshi, National Institutes of Health, Bethesda, MD; John Sidney, La Jolla Institute for Allergy and Immunology, San Diego, CA; Brian Livingston, Epimmune Inc., San Diego, CA; Marc Ghany, Jay H Hoofnagle, National Institutes of Health, Bethesda, MD; Alessandro Sette, La Jolla Institute for Allergy and Immunology, San Diego, CA; Barbara Rehermann, National Institutes of Health, Bethesda, MD

MAJOR MECHANISM OF ACTION OF HEPEX-B AGAINST

~ ~

# 1150 DYNAMICS AND EARLY DIAGNOSIS OF HBV RESISTANCE TO LAMIVUDINE: A THOROUGH QUASISPECIES ANALYSIS Coralie Pallier, HBpital Henri Mondor and Hopital de Bicetre, Creteil & Le Kremlin-Bicetre, France; Laurent Castera, Alexandre Soulier, Bertrand Pellegrin, Rozenn Brillet, Jean-Michel Metreau, Daniel Dhumeaux, Jean-Michel Pawlotsky, HBpital Henri Mondor, Creteil, France

# 1151

CHILDREN WITH CHRONIC HEPATITIS B (CHB) WHO HAVE COMPLETED PREVIOUS LAMIVUDINE STUDIES Etienne M Sokal, Clinques Universitaires St. Luc, Brussels, Belgium; Jacek Mizerski, John Paul I1 Hospital, Krakow, Poland; Marek Woynarowski, Child’s Health Memorial Institute, Warsaw, Poland; Wojciech Sluzewski, Institute of Paediatrics, Poznan, Poland; Isabel B Badia, Hospital de Ninos Ricardo Gutierrez, Buenos Aires, Argentina; Deirdre A Kelly, Birmingham Children’s Hospital, Birmingham, UK; Kathleen B Schwarz, Johns Hopkins University, Baltimore, MD; Jorge A Areias, Hospital General de Santo Antonio, Porto, Portugal; Nancy Little, Stephen Gardner, Maiy Castiglia, GlaxoSmithKline, Research Triangle Park, NC; Maureen M Jonas, Children’s Hospital, Boston, MA

B11.52 A PHASE I1 STUDY IN CHINA OF THE SAFETY & ANTIVIRAL ACTIVITY OF ENTECAVIR IN ADULTS WITH CHRONIC HEPATITIS B INFECTION Guang-Bi Yao, Shanghai Jingan Hospital, Shanghai, China; Daozhen Xu, Beijing Ditan Hospital, Beijing, China; Baoen Wang, Beijing Friendship Hospital, Beijing, China; Xiaqiu Zhou, Shanghai Ruijin Hospital, Shanghai, China; Bingjun Lei, No. 1 Affiliated Hospital to Huaxi Medical University, Chengdu, China; Dingfeng Zhang, No. 2 Affiliated Hospital to Chongqing Medical University, Chongqing, China; Dong Xu, Bristol-Myers Squibb Company, Wallingford, CT; Jessica Liu, Bristol-Myers Squibb Company, Beijing, China; Laurie MacDonald, Bristol- Myers Squibb Company, Wallingford, CT

B 1153

AN EXTENDED, STRATIFIED, FOLLOW-ON STUDY IN

THE IMPACT OF INTERFERON-ALFA (IFNA) THERAPY ON LIVER HISTOLOGY IN PATIENTS WITH HBEAG-NEGATIVE CHRONIC HEPATITIS B [HBEAG(-)CHBl George V Papatheodoridis, Evangelos Cholongitas, Efi Kanta, Kalliopi Petraki, Ioannis Ketikoglou, Emanuel K Manesis, Hippokration Hospital, Athens, Greece

# 1154 INFLUENCE OF ETHNICITY AND HBSAG STATUS ON THE SLECTION OF LAMIVUDINE RESISTANCE Paul V Desmond, Sally Bell, St. Vincent’s Hospital, Fitzroy, Victoria, Australia; Anna Ayers, Angeline Bartholomeusz, Lucy Yue, Steven Locarnini, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Australia

# 1155 EFFICACY OF TENOFOVIR DISOPROXIL FUMARATE (TDF) FOR HEPATITIS B VIRUS (HBV) IN HUMAN IMMUNODEFICIENCY VIRUS (HIV) INFECTED PATIENTS Y Benhamou, Groupe Hospitalier Pitie Salpetriere, Paris, France; C Piketty, HBpital Georges Pompidou, Paris, France; C Katlama, Groupe Hospitalier Pitie Salpetriere, Paris, France; W Rozembaum, HBpital Tenon, Paris, France; D Neau, HBpital Pellegrin, Bordeaux, France; A Lafeuillade, Hopital Chalucet, Toulon, France; D Rey, HBpital Universitaire, Strasbourg, France; Y Yazdanpanah, HBpital de Tourcoing, Tourcoing, France; P Trimoulet, H Fleury, HBpital Pellegrin, Bordeaux, France

# 1156 48 WEEKS OF ADEFOVIR DIPIVOXIL (ADV) RESULTS IN A CONSISTENT AND SIGNIFICANT IMPROVEMENT IN LIVER HISTOLOGY AND VIROLOGICAL STATUS REGARDLESS OF BASELINE KNODELL FIBROSIS SCORE IN PATIENTS WITH

Patrick Marcellin, HBpital Beaujon, Clichy, France; Stefanos Hadziyannis, Henry Dunant Hospital, Athens, Greece; Nickolas Tassopoulos, Western Attica Hospital, Athens, Greece; Elizabeth Heathcote, Toronto Western Hospital, Toronto, ON, Canada; Ting-Tsung Chang, National Cheng Kung Hospital, Taiwan, Taiwan; George Kitis, Georgios Papanikolaou Hospital, Thessaloniki, Greece; Mario Rizzetto, Azienda Ospedaliera San Giovanni Battista, Torino, Italy; Zackery Goodman. Armed Forces Institute of Pathology, Washington, DC; Shan-Shan Chen, Michael Wulfsohn, Michael Wollman, Craig James, Carol Brosgart, Gilead Sciences, Inc., Foster City, CA

HBEAG- CHRONIC HEPATITIS B

# 1157

ANTIVIRAL ACTIVITY AGAINST BOTH WILD TYPE AND LAMIVUDINE RESISTANT HEPATITIS B VIRUS IN VITRO RESULTS OF ASSAYS USING THE RECOMBINANT BACULOVIRUS SYSTEM Stephen A Locarnini, Vitina Sozzi, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia; H Zhang, B Oberg, Medivir AB, Huddinge, Sweden; Tim Shaw, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia

# 1158 LONG TERM TREATMENT WITH ADEFOVIR DIPIVOXIL (ADV) FOR THREE YEARS IN PATIENTS WITH

INFECTION RESULTS IN SIGNIFICANT AND SUSTAINED CLINICAL IMPROVEMENT Yves Benhamou, Vincent Thibault, Pamela Vig, Marc Antoine Valantin, Patricia Guyon, Christine Katlama, Biau Lu, Groupe Hospitalier Pitie Salpetriere, Paris, France; Graeme Currie, Carol Brosgart, Gilead Sciences, Inc., Foster City, CA; Thierry Poynard, Groupe Hospitalier Pitie Salpetriere, Paris, France

2’,3’-DIDEOXY-3’-FLUOROGUANOSINE (FLG) HAS

LAMIVUDINE-RESISTANT (LAM-R) HBV AND HIV CO-



# 1159 LACK OF ETHNIC DIFFERENCES IN RESPONSE TO

PATIENTS WITH CHRONIC HEPATITIS B Seng-Gee Lim, National University Hospital, Singapore, Singapore; Patrick Marcellin, HBpital Beaujon, Paris, France; Nickolas Tassopoulos, Western Attica General Hospital, Athens, Greece; Stefanos Hadziyannis, Henry Dunant Hospital, Athens, Greece; Ting -Tsung Chang, National Cheng Kung University Hospital, Hong Kong, Hong Kong; Myron Tong, Huntington Memorial Hospital, Pasadena, CA; William Sievert, Monash Medical Centre, Victoria, Australia; P Hu, Peking Union Medical College Hospital, Peking, China; Graeme Currie, Craig James, Gavin S Choy, Brian Kearney Shan-Shan Chen, Carol L Brosgart, Gilead Sciences, Inc., Foster City, CA

ADEFOVIR DIPIVOXIL THERAPY IN HBEAG+ AND HBEAG-

# 1166

DNA 3.0 ASSAY: ASSESSMENT OF ANALYTICAL AND CLINICAL PERFORMANCE Joseph D C Yao, Mayo Clinic, Rochester, MN; Marcel G H M Beld, Academic Medical Center, Amsterdam, Netherlands; Lynette L E Oon, Singapore General Hospital, Singapore, Singapore; Christopher H Sherlock, University of British Columbia, Vancouver, BC, Canada; Jeffrey Germer, Mayo Clinic, Rochester, MN; Sandra Menting, Academic Medical Center, Amsterdam, Netherlands; Su Yun Se Thoe, Singapore General Hospital, Singapore, Singapore; Linda Merrick, University of British Columbia, Vancouver, BC, Canada; Rainer Ziermann, Johan Surtihadi, H James Hnatyszyn, Bayer Healthcare, Berkeley, CA

MULTI-CENTER EVALUATION OF THE VERSANTO HBV

# 1160

REACTIVITY IN RELATION TO HBEAG SEROCONVERSION DURING THE FIRST 12 WEEKS OF ANTIVIRAL THERAPY FOR CHRONIC HEPATITIS B George K K Lau, Queen Mary Hospital, Hong Kong, Hong Kong; Helen Cooksley University College London, London, UK; Elsa Mondou, Carol L Brosgart, Gilead Sciences, Inc., Foster City, CA; Sharon Lewin, Alan A Perelson, Scott Bowden, Kimberly A Powers, Ruy M Ribeiro, Stephen Locarnini, University of Melbourne, Parkville, Victoria, Australia; Nikolai V Naoumov, University College London, London, UK

# 1161

VIRAL VECTOR DELIVERED HAMMERHEAD RIBOZYMES Kathryn L Nash, Graeme J M Alexander, Andrew M L Lever, University of Cambridge, Cambridge, UK

ANALYSIS OF EARLY VIRAL KINETICS AND T-CELL

SPECIFIC INHIBITION OF HEPATITIS B VIRUS BY LENTI-

# 1162

ANALOGUE, INHIBITS PACKAGING AND REPLICATION OF HBV GENOME IN VITRO Tim Shaw, Danni Colledge, Vitina Sozzi, Stephen A Locarnini, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia

LY582563 (MCC-478), A 2-AMINOPURINE NUCLEOTIDE

# 1163 THE EFFICACY OF OLIGONUCLEOTIDE CHIP DETECTING

TREATED PATIENTS Jeong Heo, Mong Cho, Gwang Ha I m , Dae Hwan Kang, Geun Am Song, Ung Suk Yang, Pusan National University, College of Medicine, Busan, South Korea; Hyun Jung Jang, Pusan National University, College of Natural Science, Busan, South Korea; Hee Kyung Park, Cheol Min Kim, Hyung Hoi IOm, Byung Mann Cho, Pusan National University, College of Medicine, Busan, South Korea; Woo Won Shin, Donga University, College of Medicine, Busan, South Korea

# 1164

YMDD MUTANTS OF HEPATITIS B VIRUS IN LAMIWDINE-

IN VITRO SUSCEPTIBILITY OF WILD-TYPE AND LAMIVUDINE-RESISTANT HEPATITIS B VIRUS TO TENOFOVIR AND ADEFOVIR Olivier Lada, Yves Benhamou, Marc Antoine Valantin, Christine Katlama, Thierry Poynard, Annie Cahour, Vincent Thibault, GH Pitie-Salp@tri@re, Paris, France

# 1165 COMBINATION THERAPY OF LAMIVUDINE AND HB VACCINE FOR THE TREATMENT OF CHRONIC HEPATITIS B Tetsuya Ishikawa, Akihiko Okumura, Tadashi Maeno, Ken Sato, Minoru Ayada, Naoki Hotta, Tsuneaki Tagaya, Yoshikata Fukuzawa, Shinichi Kakumu, Aichi Medical University School of Medicine, Aichi-ken, Japan

# 1167

HEPATITIS B VIRUS Kathryn L Nash, Graeme J M Alexander, Andrew M L Lever, University of Cambridge, Cambridge, UK

SENSE AND ANTISENSE RNA-MEDIATED INHIBITION OF

# 1168 INHIBITORY EFFECT OF ADEFOVIR AND LAMIVUDINE ON THE INITIATION OF HEPATITIS B VIRUS INFECTION IN PRIMARY TUPAIA HEPATOCYTES Josef Kock, Thomas F Baumert, Hubert E Blum, Fritz von Weizsacker, University of Freiburg, Freiburg, Germany

# 1169 CASE-CONTROL STUDY OF LAMIVUDINE TREATMENT IN

CARCINOMA Shin-ichi Fujioka, Okayama University School of Medicine and Dentistry, Okayama, Japan

PATIENTS WITH HBV-RELATED HEPATOCELLULAR

# 1170 KINETICS OF VIRAL RESISTANCE AND SERUM HBV DNA IN PATIENTS UNDERLAMIVUDINE THERAPY Michelle Martinot Peignoux, INSERM U481, Clichy, France; Anne Gervais, Service dHepatologie, Clichy, France; Corinne Castelnau, Nathalie Boyer, Michele Pouteau, Service d’H@patologie, HGpital Beaujon, Clichy France; Bach-Nga Pham, Service d’Hematologie-Immunologie Biologiques, HGpital Beaujon, Clichy, France; Patrick Marcellin, Service d’Hkpatologie, HGpital Beaujon, Clichy, France

# 1171 MOLECULAR EPIDEMIOLOGY OF HEPATITIS B VIRUS IN

CHRONIC HEPATITIS B FROM DIFFERENT GEOGRAPHICAL PATIENTS WITH HBEAG-NEGATIVEIANTI-HBE-POSITIVE

AREAS. DATA FROM THE PEGASYSB STUDY IN HBE- ANTIGEN-NEGATIVE CHB Maurizia Brunetto, AnnaMaria Maina, Filippo Oliveri, Azienda Ospedaliera Pisana, Pisa, Italy; Ferruccio Bonino, IRCCS Maggiore Hospital, Milan, Italy; Giuseppe Colucci, Roche Molecular Diagnostics, Rotkreuz, Switzerland; Patrick Marcellin, Hapita1 Beaujon, Clichy, France; George K K Lau, The University of Hong Kong, Hong Kong, China; Patrizia Farci, University of Cagliari, Cagliari, Italy; Stefanos Hadziyannis, Henry Dunant Hospital, Athens, Greece; Nigel Pluck, Roche Products Ltd, Welwyn, UK

146A POSTER SESSIONS HEPATOLOC;Y, October 2003

# 1172 MULTIFACTORIAL ANALYSIS OF HOST AND VIRUS RELATED RISK FACTORS FOR THE DEVELOPMENT OF

TREATMENT OF HBV INFECTION Florian van Biimmel, Charite, Campus Virchow-Klinikum, Berlin, Germany; Ulrike Mihm, Universitatsklinikum des Saarlandes, Homburg, Germany; Christina Maria Jung, Ludwig- Maximillian-Universitat, Klinikum der Universitat-Groghadern, Munchen, Germany; Christoph Sarrazin, Universitatsklinikum des Saarlandes, Homburg, Germany; Thomas Gerlach, Ludwig- Maximillian-Universitat, Klinikum der Universitat-GroBhadern, Miinchen, Germany; Alexandra Bergk, Uwe Hopf, Bertram Wiedenmann, Thomas Berg, Charit6, Campus Virchow- Klinikum, Berlin, Germany

VIRAL RESISTANCE DURING LONG-TERM LAMIVUDINE

# 1173 COMBINATION THERAPY USING INTERFERON AND LAMIVUDINE IN PEDIATRIC PATIENTS WITH HEPATITIS B Steven J Lobritto, Patricia Harren, Yvette Sims, Robert S Brown Jr, New York Presbyterian Hospital-Columbia, New York, NY

rt 1174 DETECTION OF HEPATITIS B VIRUS VARIANTS ASSOCIATED WITH LAMIVUDINE RESISTANCE USING MASS SPECTROMETRIC ANALYSIS Seong-Gyu Hwang, Nam Keun Kim, Jin Hee Han, Kyu Sung Rim, Bundang CHA Hospital, Pochon CHA University College of Medicine, Sungnam, Kyunggi-Do, South Korea; Wang Dong Yoo, So0 Ok Kim, Sun Pyo Hong, Gene Matrix, Seoul, South Korea

# 1175 EVALUATION OF CHRONIC ACTIVE HEPATITIS B (CAHB) TREATMENT EFFICACY P Tsekoura, A Ioannidis, E Vasiliadou, P Mamasi, D Chrysagis, Infectious Diseases Hospital, Thessaloniki, Greece

d 1176 A SENSITIVE, QUANTITATIVE REAL-TIME PCR ASSAY TO DETECT LAMIVUDINE RESISTANCE-ASSOCIATED MUTATIONS IN HEPATITIS B VIRUS (HBV) Sharon Lewin, Alfred Hospital, Prahran, Vic, Australia; Fiona Whiteman, Monash University, Clayton, Vic, Australia; Scott Bowden, Anna Ayres, Tomas Walters, Stephen Locarnini, Victorian Infectious Diseases Reference Laboratory, North Melbourne, Vic, Australia; Daryl Lau, University of Texas, Calveston, TX

A+ 1177 PREDICTING RELAPSE AFTER CESSATION OF LAMIVUDINE MONOTHERAPY FOR CHRONIC HEPATITIS B VIRUS

REAL-TIME DETECTION DIRECT TEST Kiyoaki Ito, Yasuliito Tanaka, Eturo Orito, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Noboru Hirashima, Chukyo Hospital, Nagoya, Japan; Motokazu Mukaide, SRL, Inc., Hachiouji, Japan; Tatsuya Ide, Michio Sata, Kurume University School of Medicine, Kurunie, Japan; Ryuzo Ueda, Masashi Mizokami, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

INFECTION-APPLICATION OF NEWLY DEVELOPED HBV

# 1178 EFFECT OF THE PRECORE MUTATIONS ON THE HBEAG LOSS AND VIRAL BREAKTHROUGH DURING LAMIVUDINE

Sun Suk Kim, Yu Jin Hwang, Kwang An Kwon, Moon Gi Jung, Dong Kyun Park, Oh Sang Kwon, So Young Kwon, Yeon Suk Kim, Yang Suh Koo, Yu Kyung Kim, Deok Ju Choi, Ju Hyun Kim, Gachon Medical School, Gil Medical Center, Incheon, South Korea

THERAPY IN HBEAG-POSITIVE CHRONIC HEPATITIS B

# 1179 HEPATITIS B VIRUS GENOTYPES B AND C DO NOT AFFECT

Man-Fung Yuen, Danny Ka-Ho Wong, The University of Hong Kong, Queen Mary Hospital, Hong Kong, Hong Kong; Erwin Sablon, Innogenetics NV, Ghent, Belgium; He-Jun Yuan, Siu-Man Sum, Chee-Kin Hui, Benjamin Chun-Yu Wong, Ching-Lung Lai, The University of Hong Kong, Queen Mary Hospital, Hong Kong, Hong Kong

THE ANTI-VIRAL RESPONSE TO LAMIVUDINE

# 1180 ALT FLARES IN PATIENTS WITH HBEAG-POSITIVE CHRONIC HEPATITIS B AND TREATED WITH EITHER CONVENTIONAL INTERFERON ALFA-PA OR PEGINTERFERON ALFA-2A (40KD) (PEGASYSO) ARE NOT NECESSARY FOR A SIGNIFICANT RESPONSE TO THERAPY W Graham E Cooksley, Royal Brisbane Hospital, Herston, Australia; Ming-Yang Lai, National Taiwan University, Taipei, Taiwan; Teerha Piratvisuth, Songklanakarin Hospital, Songkla, Thailand; Yuan-Jen Wang, Taipei Veterans General Hospital, Taipei, Taiwan; Varocha Mahachai, Chulalongkom Hospital, Bangkok, Thailand; You-Chen Chao, Tri-Services General Hospital, Taipei, Taiwan; Tawesak Tanwandee, Siriraj Hospital, Bangkok, Thailand; Anuchit Chutaputti, Pramongkutklao Hospital, Bangkok, Thailand; Wen-Yu Chang, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; Friederike E Zahm, Roche Diagnostics, Basel, Switzerland; Nigel Pluck, Roche Products Ltd, Welwyn, UK

# 1181

ATING THE EFFICACY AND SAFETY OF PEGINTERFERON

WITH LAMIVUDINE VS LAMIVUDINE IN 546 PATIENTS

HEPATITIS B Patrick Marcellin, HBpital Beaujon, Clichy, France; George K K Lau, The University of Hong Kong, Hong Kong, China; Ferruccio Bonino, IRCCS Maggiore Hospital, Milan, Italy; Patrizia Farci, University of Cagliari, Cagliari, Italy; Stefanos Hadziyannis, Henry Dunant Hospital, Athens, Greece; Rui Jin, Beijing You An Hospital, Beijing, China; Zhi-Meng Lu, Ruijin Hospital, Shanghai, China; Teerha Piratvisuth, Songklanakarin Hospital, Songkla, Thailand; Georgios Germanidis, Papageorgiou General Hospital, Thessalonika, Greece; Cihan Yurdaydin, University of Ankara, Ankara, Turkey; Moises Diago, Hospital General Universitario de Valencia, Valencia, Spain; Selim Gurel, University of Uludag, Bursa, Turkey; Ming-Yang Lai, National Taiwan University, Taipei, Taiwan; Peter Button, Roche, Dee Why, Australia; Nigel Pluck, Roche Products Ltd, Welwyn, UK

A PHASE 111, PARTIALLY DOUBLE-BLINDED STUDY EVALU-

ALFA-2A (40KD) (PEGASYSB) ALONE OR IN COMBINATION

WITH HBEAG-NEGATIVE/ANTI-HBE-POSITIVE CHRONIC

P 1182 IMPROVEMENT OF MULTIPLE ORGAN FUNCTIONS IN CHRONIC SEVERE VIRAL HEPATITIS B WITH THE MOLECULAR ADSORBENT RECIRCULATING SYSTEM AND IT'S PROGNOSIS ASSESSMENT BY MELD SCORE Yi-Jun Yang, Li-Rong Wang, Ning Zhang, Ping Huang, Gui-Xia Meng, Xiao-Dong Gai, Nanjing No. 2 People's Hospital, South- East University Medical College, Nanjing, China; Min-Min Wang, Therapeutic Blood Purification Research Center, University of Rostock, Shanghai, China



~ ~~

# 1183 CLINICAL EVALUATION OF A NEW ENZYME

ANTIGEN; A MARKER DISTINCT FROM VIRAL DNA FOR MONITORING LAMIVUDINE TREATMENT Akinori Rokuhara, Shinshu University School of Medicine, Matsumoto, Nagano, Japan; Tatsuji Kimura, Advanced Life Science Institute, Inc., Wako, Saitama, Japan; Akihiro Matsumoto, Eiji Tanaka, Shinshu University School of Medicine, Matsumoto, Nagano, Japan; Noboru Maki, Advanced Life Science Institute, Inc., Wako, Saitama, Japan; Kendo Kiyosawa, Shinshu University School of Medicine, Matsumoto, Nagano, Japan

IMMUNOASSAY FOR HEPATITIS B VIRUS CORE-RELATED

~ ~~

# 1184 INHIBITION OF HEPATITIS B VIRUS REPLICATION BY SMALL INTERFERING RNAS Motokazu Mukaide, SRL, Inc., Tokyo, Japan; Yasuhito Tanaka, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; Kazumasa Hikiji, SRL, Inc., Tokyo, Japan; Masashi Mizokami, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

Hepatitis C: Therapy I I # 1185 FIRST PHASE HCV KINETICS IN INTERFERON AND RIBAVIRIN COMBINATION THERAPY IS AN USEFUL PREDICTOR OF TREATMENT RESPONSE IN CHRONIC HEPATITIS C PATIENTS Akiko Makiyama, Yoshito Itoh, Tomoaki Nakajima, Atsushi Umemura, Youuichi Harano, Kouji Kunimoto, Mika Okita, Mika Nakayama, Koujirou Mori, Junk0 Yamaoka, Hideki Fujii, Kanji Yanaguchi, Norihito Yamauchi, Masahito Minami, Takeshi Okanoue, Kyoto Prefectural University, Graduate School of Medicine, Kyoto, Japan

# 1186

(AMA) OR RIBAVIRIN (REV) IN NAIVE PATIENTS WITH CHRONIC HEPATITIS C (CHC) Gaetano Ideo, S. Giuseppe Hospital, Milano, Italy; Giorgio Antonucci, Spallanzani Institute, Roma, Italy; Adolfo F Attili, Policlinico Umberto I Hospital, Roma, Italy; Sergio Babudieri, University of Sassari, Sassari, Italy; Antonio Chirianni, Cotugno Hospital, Napoli, Italy; Antonio Craxi, University of Palermo, Palermo, Italy; Giovanni Di Perri, Amedeo Di Savoia Hospital, Torino, Italy; Antonio Francavilla, University of Bari, Bari, Italy; Alessandra Mangia, Casa Sollievo Della Sofferenza Hospital, S. Giovanni Rotondo, Italy; Antonino Picciotto, University of Genova, Genova, Italy; Mario Rizzetto, Molinette Hospital, Torino, Italy; Giuseppe Ruggiero, University of Napoli, Napoli, Italy; Fredy Suter, Spedali Riuniti Hospital, Bergamo, Italy; Salvatore Tripi, University of Palermo, Palerrno, Italy; Massimo Sarracino, Roche S.p.A., Monza, Italy

PEG-IFN ALFA-PA (40KD) (PEGASYSB) PLUS AMANTADINE

# 1187 THE PREDICTIVE VALUE OF CORE AG TESTING IN THE MANAGEMENT OF PATIENTS RECEIVING PEG- IFN/RIBAVIRIN TREATMENT-RELEVANCE FOR THE EARLY IDENTIFICATION OF NON-RESPONDERS AND RELAPSERS Pierre Pradat, Marianne Maynard, Hotel-Dieu, Lyon, France; Pascale Berthillon, INSERM U271, Lyon, France; Gaston Picchio, Ortho Clinical Diagnostics, Raritan, NJ; Hans Tillmann, Johannes Wiegand, Medizinische Hochschule, Hannover, Germany; Nicolas Voirin, Hotel-Dieu, Lyon, France; Michael Manns, Medizinische Hochschule, Hannover, Germany; Maria Buti, Juan-Ignacio Esteban, Hospital General Val1 d’Hebron, Barcelona, Spain; Michele Martinot, Patrick Marcellin, INSERM U483, Paris, France; Christian Trepo, INSERM U271, Hotel Dieu, Lyon, France

# 1188 SITE OF PEGYLATION AND PEG MOLECULE SIZE DIRECTLY

ACTIVITY THROUGH THE JAWSTAT SIGNALING PATHWAY Michael J Grace, Susan Cannon-Carlson, Sheri Bradshaw, Constance Cullen, Jeffrey Chapman, Jeffrey Spond, Seoju Lee, David Wylie, Stephen R Indelicato, Marcio Voloch, Ronald W Bordens, Schering-Plough Research Institute, Union, NJ

ATTENUATE INTERFERON-ALPHA ANTI-VIRAL SPECIFIC

# 1189 MECHANISMS OF RIBAVIRIN EARLY ANTIVIRAL EFFECT IN CHRONIC HEPATITIS C : IS IT RELATED TO RIBAVIRIN MUTAGENIC PROPERTIES INDUCING ?ERROR CATASTROPHE? Jean-Michel Pawlotsky, Rozenn Brillet, Christophe Hezode, Daniel Dhumeaux, HBpital Henri Mondor-Universite Paris XII, Creteil, France

# 1190 DIABETES MELLITUS OF NEW ONSET DURING PEGYLATED INTERFERON AND RIBAVIRIN THERAPY FOR CHRONIC

Furqaan Ahmed, Ira M Jacobson, Weill Medical College of Cornell University, New York, NY; Thomas Hargrave, Eastbay Center for Digestive Health, Oakland, CA; Eric Lawitz, Brooke Army Medical Center, San Antonio, TX; Barry Migicovsky, Gastroenterology Consultants, Pembroke Pines, FL; Vishnu Reddy, Internal Medicine Specialists, Orlando, FL; Norah Terrault, University of California San Francisco, San Francisco, CA; Robert S Brown Jr, Columbia-Presbyterian Medical Center, New York, NY; Clifford Brass, Schering-Plough Research Institute, Kenilworth, NJ

# 1191

COMBINATION THERAPY FOR THE TREATMENT OF HEPATITIS C IN PATIENTS WITH PERSISTENTLY NORMAL ALT LEVELS Edmund J Bini, Saurabh Mehandru, VA Medical Center, New York, NY

# 1192 TREATMENT RATES FOR CHRONIC HEPATITIS C AFTER LIVER BIOPSY Tamer N Sargios, Radhakrishna Kalakuntla, Gopal Narasimhan, Veronika Dubrovskaya, Peter Homel, David J Clain, Henry C Bodenheimer Jr, Albert D Min, Beth Israel Medical Center, New York, NY

HEPATITIS C: OBSERVATIONS FROM THE WIN-R TRIAL

EFFICACY OF INTERFERON ALFA-PB AND RIBAVIRIN

# 1193 ABSORPTION, METABOLISM AND EXCRETION OF [14C]HEPAVIR B AND [14ClHEPSERA IN RATS AND MONKEYS Chin-Chung Lin, Li-Tain Yeh, Christine Xu, Yifei Liu, Nanqun Zhu, Ribapharm, Inc., Costa Mesa, CA

# 1194 END OF TREATMENT AND SUSTAINED RESPONSE TO

RIBAVIRIN (RBV) (COPEGUS) AND AMANTADINE (AMA), AND TO INDUCTION THERAPY WITH INTERFERON (IFN)

NONRESPONDERS WITH CHRONIC HEPATITIS C (CHC) Silvia Fargion, Universith degli Studi, Milano, Milan, Italy; Mauro Borzio, Ospedale Predabissi, Melegnano, Italy; Antonietta Carpel, Ospedale Sacco, Milan, Italy

PEGINTERFERON ALFA-PA (40KD) (PEGASYS) PLUS

ALFA-PA (ROFERON-A) PLUS REV AND AMA IN IFN/RBV

I-I-HA POSTER SESSIONS HEPATOLOGY, October 2003

3 1195 SEIZURES DURING PEGYLATED INTERFERON AND RIBAVIRIN THERAPY FOR CHRONIC HEPATITIS C IN THE

Furqaan Ahnied, Deborah Rovner, Ira M Jacobson, Weill Medical College of Cornell University, New York, NY; Clive Albert, DeKalb Gastroenterology and Associates, Decator, GA; Myron Brand, Connecticut Gastroenterology Consultants, New Haven, CT; Michael E Cox, Mercy Medical Center, Baltimore, MD; Alan M Fixelle, Gastroenterology Consultants, Atlanta, GA; Jorge Herrera, University of South Alabama, Mobile, AL; Vinod Rustgi, Metropolitan Liver Diseases, Fairfax, VA; Ronald B Wasserman, lnfectious Disease Doctors Medical Group, Walnut Creek, CA; Robert S Brown Jr, Columbia-Presbyterian Medical Center, New York, NY; Clifford Brass, Schering-Plough Research Institute, Kenilworth, NJ

WIN-R TRIAL

P 1196 SERIOUS OPHTHALMOLOGIC EVENTS DURING PEGYLATED INTERFERON AND RIBAVIRIN THERAPY FOR CHRONIC

Furqaan Ahmed, Ira M Jacobson, Weill Medical College of Cornell University, New York, NY; Steve T Chen, Lancaster Gastroenterology, Lancaster, PA; Simon Cofrancesco, Gastroenterology Associates, McComb, MS; Jeffrey Cooley, Caritas-St. Elizabeth‘s Medical Center, Brighton, MA; Michael Demicco, Associated Gastroenterology Medical Group, Anaheim, CA; Bradley Freilich, Baptist Medical Center, Kansas City, MO; Brian Hudes, Advanced Gastroenterology Associates, Duluth, GA; Jonathan Jensen, Front Range Gastroenterology, Longmont, CO; Arnold Levin, Eastside Gastroenterology Consultants, Kirkland, WA; Kip Lyche, Private Practice, Ventura, CA; Jonathan McCone, Mount Vernon Endoscopy Center, Alexandria, VA; Howard P Monsour, Liver Specialists of Texas, Houston, TX; Craig Peine, Hennepin County Medical Center, Minneapolis, MN; Neville Pimstone, University of California, Davis Medical Center, Sacramento, CA; Thomas Rosenfield, Medical Specialists at the Palm Beaches, Atlantis, FL; Robert Strauss, Northwest Georgia Gastroenterology, Marietta, GA; Kusum Stokes, Eureka Liver Center, Eureka, CA; Norah Terrault, University of California San Francisco, Sail Francisco, CA; Naoky Tsai, St. Francis Medical Center, Honolulu, HI; Ronald B Wasserman, Intectious Disease Doctors Medical Group, Walnut Creek, CA; Graham M Woolf, Cedars-Sinai Medical Center, Los Angeles, CA; Robert S Brown Jr, Columbia-Presbyterian Medical Center, New York, NY; Clifford Brass, Schering-Plough Research Institutc, Kenilworth, NJ

HEPATITIS C: OBSERVATIONS FROM THE WIN-R TRIAL

31197 INCIDENCE, RISK FACTORS AND TREATMENT OF MOOD DISORDERS ASSOCIATED WITH PEGINTERFERON AND RIBAVIRIN THERAPY IN PATIENTS WITH CHRONIC HEPATITIS C : RESULTS OF A PROSPECTIVE STUDY Laurent Castcra, Hnpital Haut Leveque, Pessac, France; Aymery Constant, UniversitC Victor Segalen Bordeaux 2, Bordeaux, France; Chantal Henry HBpital Charles Perrens, Bordeaux, France; Patrick Champbenoit, Guillaume Sauve, Victor de Ledinghen, HBpital Haut Lkveque, Pessac, France; Pierre-Henri Bernard, HBpital Saint Andre, Bordeaux, France; Juliette Foucher, Jacques Demotes-Mainard, Patrice Couzigou, HBpital Haut Lev@que, Pessac, France

# 1198 TUMOR ABLATION PLUS INTERFERON THERAPY FOR

META-ANALYSIS OF RANDOMIZED CONTROLLED TRIALS Hisashi Moriguchi, Research Center for Advanced Science and Technology, University of Tokyo, Tokyo, Japan; Raymond T Chung, Massachusetts General Hospital, Harvard Medical School, Boston, MA; Makoto Kobayashi, Crecon Research and Consulting, Inc, Tokyo, Japan; Chifumi Sato, Tokyo Medical and Dental University, Tokyo, Japan

HCV-RELATED EARLY HEPATOCELLULAR CARCINOMA A

# 1199 LACK OF INCREASED FREQUENCY OF THE CC CHEMOKINE

Annarosa Floreani, Anna Maria Tommasi, Anna Baragiotta, Vincenzo Baldo, University of Padova, Padova, Italy; Giulia Tositti, S. Bortolo Hospital, Vicenza, Italy; Carla Venturi, University of Padova, Padova, Italy; Maria Teresa Giordani, Paolo Fabris, S. Bortolo Hospital, Vicenza, Italy

RECEPTOR 5-DELTA32/DELTA32 GENOTYPE IN HEPATITIS C

P 1200 HIGH-DOSE VITAMIN E SUPPLEMENTATION DOES NOT DIMINISH RIBAVIRIN-ASSOCIATED HEMOLYSIS IN CHRONIC HEPATITIS C Jasmohan S Bajaj, Kia Saeian, Jose Franco, Rajiv Varma, Josh Knox, Jack Daniel, Medical College of Wisconsin, Milwaukee, WI; Samuel B Ho, Veterans Affairs Medical Center, Minneapolis, MN; Craig Peine, Hennepin County Medical Center, Minne- apolis, MN; Daniel Mckee, St. Luke’s Hospital, Duluth, MN

# 1201 PEG-INTERFERON-ALPHA-2B AND RIBAVIRIN TREATMENT IN CHILDREN AND ADOLESCENTS WITH CHRONIC HEPATITIS C Stefan Wirth, Children’s Department, Helios Klinikum, Wuppertal, Germany; Ulrike Kullmer, Children’s Hospital, University of Mainz, Mainz, Germany; Thomas Lang, Children’s Hospital, University of Munich, Munich, Germany; Heidrun Pieper-Boustani, Philip Wintermeyer, Patrick Gerner, Children’s Department, Helios Klinikum, Wuppertal, Germany

# 1202 COMPARISON OF LOW DOSE WITH STANDARD DOSE PEG-INTERFERON ALFA-2B PLUS RIBAVIRIN FOR INITIAL TREATMENT OF CHRONIC HEPATITS C Edward L Krawitt, University of Vermont, Burlington, VT; Norman D Grace, Faulkner and Brigham & Women’s Hospitals, Boston, MA; Stuart R Gordon, Hans Fromm, Dartmouth Hitchcock Medical Center, Lebanon, NH; Melissa Palmer, Liver Center of Long Island, Plainview, NY; Joseph C Yarze, Gastroenterology Associates of Northern NY, Glens Falls, NY; Alan Sheinbaum, Robert D Thomson, Concord Gastroenterology, Concord, NH; Sam Moskowitz, Liviu Schapira, Gastro-Biliary Association, Forest Hills, NY; James G Corsanti, Digestive Health Physicians, Cheektowaga, NY; John Polio, Connecticut GI Associates, Hartford, CT; Robert E Smith, Cheshire Medical Center, Keene, NH; Robert A Levine, SUNY Upstate Medical University, Syracus, NY; Leslie Bank, United Medical Associates, Binghampton, NY; Alan E Kilby, Portland Gastroenterology Associates, Portland, ME; Martin B Fried, Gastroenterology Consultants, Kingston, PA; Louis V Antignano, Rochester GI Consultants, Rochester, NY; Kenneth R Kohagen, Digestive Health Care, Raleigh, NC; Nicholas Ferrentino, Steven D Lidofsky, University of Vermont, South Burlington, VT; Douglas R LaBrecque, University of Iowa Hospitals and Clinics, Iowa City VT



# 1203 TREATMENT OF INTERFERON-NAIVE PATIENTS WITH HCV GENOTYPE 5 WITH INTERFERON (OR PEG-INTERFERON) PLUS RIBAVIRIN RESULTS IN A VERY HIGH SUSTAINED VIROLOGICAL RESPONSE Corinne Bonny, Christine Roche, Karine Randl, Sylvie Ughetto, Cecile Henquell, Nathalie Martineau, CHRU Clermont, Clermont Ferrand, France; Helene Fontaine, Stanislas Pol, HBpital Necker, Paris, France; Helilne Lafeuille, Gilles Bommelaer, Armand Abergel, CHRU Clermont, Clerniont Ferrand, France

# 1204 EARLYHCV KINETCS IN IMMUNOSUPPRESSED PATIENTS

COINFECTED VS. NORMAL PATIENTS Markus Peck-Radosavljevic, Armin Rieger, Monika Schmid, Wolfgang Jessner, Peter Ferenci, Susanne Rasoul-Rockenschaub, Hanns Hofmann, Medical University of Vienna, Vienna, Austria

UNDERGOING ANTIVIRAL THERAPY: OLT VS. HIV-HCV

# 1205

CHRONIC HEPATITIS C Ola Weiland, Anna Hollander, Karin Frisell, Staffan Sandell, Karolinska Institute, Stockholm, Sweden

COST-EFFECTIVE THERAPY FOR GENOTYPE 2 AND 3

# 1206 SUSTAINED VIRAL RESPONSE DURING HCV TREATMENT IS ASSOCIATED WITH HIGHER DEPRESSION SCALE SCORES Jennifer L G Moss, Lauren Senkbeil, Paul Gaglio, Silvia Hafliger, Lorna Dove, Steven Lobritto, New York Presbyterian Hospital, New York, NY; Ira Jacobsen, New York Weill Cornell Medical Center, New York, NY; Robert S Brown Jr, New York Presbyterian Hospital, New York, NY

# 1207

AND RIBAVIRIN (COPEGUSB) IN PATIENTS INFECTED WITH HEPATITIS C VIRUS (HCV) GENOTYPE 1 WHO FAILED TO RESPOND TO INTERFERON ALFA AND RIBAVIRIN M Diago, H. General de Valencia, Valencia, Spain; M Romero- Gomez, H. U. de Valme, Sevilla, Spain; J Crespo, H. Marques Valdecilla, Santander, Spain; A Olveira, H. La Paz, Madrid, Spain; R Perez, H. Central de Asturias, Asturias, Spain; R BBrcena, H. Ramon y Cajal, Madrid, Spain; J M SBnchez-Tapias, H. Clinic i Provincial, Barcelona, Spain; M Mufioz-SBnchez, Roche, Madrid, Spain

# 1208 ADHERENCE TO COMBINATION THERAPY INCREASES SUSTAINED RESPONSE IN PATIENTS WITH CHRONIC HEPATITIS C Jose Antonio Galeras, Isabel Cirera, Susanna Coll, Carmen Marquez, Maria Dolors Gimenez, Maria Carme Vila, Ricard Sola, Hospital del Mar, Barcelona, Spain

HIGH-DOSE PEGINTERFERON ALFA-2A (40KD) (PEGASYSB)

# 1209 TRIPLE THERAPY COMPARED TO STANDARD PEGYLATED INTERFERON ALFA 28 + WEIGHT BASED RIBAVIRIN FOR PREVIOUS NONRESPONDERS AND RELAPSERS WITH CHRONIC HEPATITIS C Eric J Lawitz, Norma S Cantu, Brooke Army Medical Center, San Antonio, TX; Mitchell Davis, South Florida Center of Gastroenterology, West Palm Beach, FL; Nezam Afdhal, Michael Curry, Beth Israel Deaconess Medical Center, Boston, MA; Mark Mailliard, University of Nebraska Medical Center, Omaha, NE; Frank Adams, Austin Consultants in Gastroenterology, Austin, TX; Naoky Tsai, St. Francis Medical Center, Honolulu, HI; Andrei Gasic, Longview Gastroentrology Clinic, Longview, TX; Tarun Kothari, Private Practice, Rochester, NY; K P Ganeshappa, Digestive Disease Center of South Texas, San Antonio, TX; James Cox, Texas Digestive Disease Consultants, Lewisville, TX; Bruce Silverman, Gastroenterology Associates, Olympia, WA; Shailesh C Kadakia, Institute of Liver and Gastrointestinal Diseases, San Antonio, TX

# 1210 EFFECT OF PEG INTERFERON ALPHA-2B AND RIBAVIRIN DOSE ON THE HISTOLOGICAL CHANGES IN VIROLOGIC NON-RESPONDERS TO THE COMBINATION OF STANDARD INTERFERON ALPHA-2B AND RIBAVIRIN A RANDOMIZED CONTROLLED STUDY Tarek I Hassanein, Fatma M Barakat, Wendy Y Myers, Meghan D Carlson, Eileen R Chatfield, Khaled M Selim, Cynthia Behling, University of California San Diego, San Diego, CA

~~~~

# 1211 ADVANCED AGE AND SERUM RIBAVIRIN LEVEL AFFECT THE DEGREE OF HEMOLYTIC ANEMIA DURING THE

RIBAVIRIN FOR CHRONIC HEPATITIS C Yoshiyasu Karino, Jouji Toyota, Tomohiro Arakawa, Yasualu Kuwata, Jm Akaike, Takumi Ohmura, Takahiro Sato, Sapporo Kosei General Hospital, Sapporo, Japan; Takashi Matsushima, Hakodate Munincipal Hospital, Hakodate, Japan

# 1212 COST ANALYSIS OF UNTREATED ANEMIA IN HEPATITIS C VIRUS (HCV)- INFECTED PATIENTS: AN EMPLOYERS PERSPECTIVE Mei-Sheng Duh, Analysis Group, Boston, MA; Erick Moyneur, Sharon Buteau, Groupe d’Analyse, Montreal, PQ, Canada; Vaibhavi Desai, Samir H Mody, Ortho Biotech Products, L.P., Bridgewater, NJ

COMBINATION THERAPY OF IFN-ALPHA 2B AND

# 1213 ERYTHROPOIETIN MAINTAINS RIBAVIRIN DOSE AND SUSTAINED VIROLOGIC RESPONSE DURING HCV TREATMENT Lauren E Senkbeil, Jennifer G Moss, Paul J Gaglio, Lorna M Dove, Steven J Lobritto, Ira M Jacobson, Robert S Brown Jr, New York-Presbyterian, New York, NY

# 1214 RIBAVIRIN MONOTHERAPY PROMOTES SIGNALING FOR APOPTOSIS ENHANCING CASPASE ACTIVITY IN PATIENTS WITH CHRONIC HEPATITIS C Manuela Neuman, University of Toronto, Toronto, ON, Canada; Cyril Bonaventure, Marianne Maynard-Muet, Christian Trepo, INSERM 271 & Service d’Hepatologie, Lyon, France

150A POSTER SESSIONS HEPATOLOCY, October 2003

5 1215 MULTIVARIATE MODELS PREDICT OUTCOME T O HEPATITIS C VIRUS THERAPY AT BASELINE AND AT WEEKS 4 AND 8 Michele Martinot Peignoux, INSERM U481, Clichy, France; Lorraine Comanor, Independent Research Consultant, Palo Alto, CA; James Minor, Independent Research Consultant, Los Altos, CA, CA; Marie Pierre Ripault, Natalie Boyer, INSERM U481, Clichy, France, France; Corinne Castelnau, INSERM U481, Clichy, France, France; Nathalie Guily, INSERM U481, Clichy, France, France; David Hendricks, Bayer Diagnostics, Berkeley, CA; Patrick Marcellin, INSERM U481, Clichy, France

$1216 DISPOSITION AND METABOLIC PROFILE IN MONKEY LIVER FOLLOWING SINGLE AND MULTIPLE ORAL DOSING OF [14ClRIBAVIRIN AND [lQCIVIRAMIDINE Li-Tain Yeh, David Lourenco, Chin-Chung Lin, Ribapharm, Inc., Costa Mesa, CA

P 1217 COMBINATION THERAPY FOR HCV AFFECTS THE HIV VIRAL LOAD IN PATIENTS RECEIVING HIGHLY ACTIVE ANTIRETROVIRAL THERAPY(HAART) Joel Kertznus, Enrique G Molina, Arie Regev, Eugene R Schiff, University of Miami, Miami, FL

~~ ~~ ~ ~

# 1218 A PROSPECTIVE, CONTROLLED STUDY ASSESSING THE TREATMENT OF CHRONIC HEPATITIS C IN PATIENTS O N METHADONE MAINTENANCE Stefan Mauss, Florian Berger, Guenther Schmutz, Center for HIV and Hepatogastroenterology, Duesseldorf, Germany; Bemhard Jacob, Municipal Methadone Outpatient Clinic, Duesseldorf, Germany; Joerg Goelz, Medical Practice Center Kaiserdamm, Berlin, Germany

# 1219 INSULIN RESISTANCE IMPAIRS SUSTAINED RESPONSE RATE T O ANTIVIRAL THERAPY IN PATIENTS WITH CHRONIC HEPATITIS C Manuel Romero-G6mez, Raquel Corpas, Lourdes Grande, Victor M Castellano-Megias, Hepatology Unit, Hospital Universitario de Valme, Sevilla, Spain; Marina Cruz, Biochemistry Unit, Hospital Universitario de Valme, Sevilla, Spain; Diego Sanchez- Mufioz, Hepatology Unit, Hospital Universitario de Valme, Sevilla, Spain; Felipe Garcia-Pesquera, Hospital Universitario Virgen del Rocio, Sevilla, Spain; Ricardo Vazquez-Albertino, Hospital Universitario de Valme, Sevilla, Spain

# 1220 POTENTIAL EARLY BIOMARKERS OF A RESPONSE T O INTERFERON THERAPY IhT INDIVIDUALS WITH CHRONIC HEPATITIS C TREATED WITH PEGASYS David H Van Thiel, Magdalene M George, Sonu Dhillon, Mehdi Balucli, Loretta Murphy, Nancy Leone, Loyola University Medical Center, Maywood, IL

P 1221 RATE OF SUSTAINED VIROLOGIC RESPONSE WITH 24 VS 48 WEEKS OF INTERFERON PLUS RIBAVIRIN IN HCV CIRRHOTICS WITH GENOTYPE 2,3 Hugo Cheinquer, UFRGS/ FFFCMPA, Porto Alegre, Brazil; Silvia Coelho-Borges, Nelson Cheinquer, UFRGS, Porto Alegre, Brazil


# 1222 ABSENCE OF SUSTAINED VIROLOGIC RESPONSE TO INTERFERON PLUS RIBAVIRIN IN GENOTYPE 213 CHRONIC HEPATITIS C PATIENTS WITH ELEVATED SERUM FERRITIN AND H63D OR C282Y HFE GENE MUTATIONS Hugo Cheinquer, UFRGS / FFFCMPA, Porto Alegre, Brazil; Silvia Coelho-Borges, Nelson Cheinquer, UFRGS, Porto Alegre, Brazil; Luciano Krug, Patricia Ashton-Prolla, Amplicon Laboratories, Porto Alegre, Brazil

# 1223

RESPONSE T O PEGYLATED INTERFERON/RIBAVIRIN IN

CHRONIC HEPATITIS C Ana Moreno, Carmen Quereda, Leonor Moreno, Rafael Barcena, M Luisa Mateos, Silvia Garcia-Garzon, M Jesus Perez-Elias, Jose L Casado, Alfonso Muriel, Santiago Moreno, Hospital Ram6n y Cajal, Madrid, Spain

VIRAL KINETICS AND EARLY PREDICTION OF NON-

HIV INFECTED PATIENTS WITH GENOTYPES 1/4- RELATED

# 1224 EVALUATION OF HEPATITIS C GENOTYPE TESTING IN NEWLY DIAGNOSED HEPATITIS C MANAGED CARE PATIENTS Trong K Le, Jenifer Wogen, TIER, Bridgewater, NJ

# 1225

INTERFERON ALFA AND RIBAVIRIN FOR CHRONIC HEPATITIS C Paul Y Kwo, Indiana University School of Medicine, Indianapolis, IN; Brett R Neustater, 16855 NE 2 Avenue #202, N. Miami Beach, FL; Frederic A Stelzer, 451 Chew Street, Allentown, PA; Brian K Hudes, Advanced Gastro Associates, LLC, Duluth, GA; David C Pound, Indianapolis Gastro and Hepatology, Indianapolis, IN; John J Santoro, Atlantic Gastroenterology Associates, Egg Harbor Township, NJ; Richard S Aycock, Memphis Gastro Group, P.C., Memphis, TN; Eugenio R Grunvald, 953 Stevens Drive, Richland, WA; Beverly Musick, George Eckert, Indiana University School of Medicine, Indianapolis, IN

# 1226 INTERFERON COMBINED WITH CYCLOSPORIN A IS A POTENT ANTIVIRAL AND CHEMOPREVENTIVE TREATMENT Kazuaki Inoue, Makoto Yoshiba, Hiroshi Yasuda, Showa University Fujigaoka Hospital, Yokohama, Japan

ANTI-DEPRESSANT USE IN PATIENTS RECEIVING

# 1227 DELAYED RECOVERY OF PEGYLATED INTERFERON AND RIBAVIRIN INDUCED ANEMIA Helen Azzam, Furqaan Ahmed, Brent Peterson, Deborah Rovner, Nicole Taylor, Ira M Jacobson, Weill Medical College of Cornell University, New York, NY

Hepatocellular Carcinoma and Cholangiocarcinoma: Clinical

8 # 1228 STRATIFICATION ABILITY OF THE NEW PROGNOSTIC STAGING SYSTEM, JAPAN INTEGRATED STAGING SCORE (JIS SCORE) FOR HEPATOCELLULAR CARCINOMA: COMPARISON WITH CLIP SCORE Hobyung Chung, Masatoshi Kudo, Kinh University School of Medicine, Osaka, Japan; Yukio Osaki, Osaka Red Cross Hospital, Osaka, Japan; Seiji Haji, Yasunori Minami, Chikara Ogawa, Toyokazu Fukunaga, Masayuki Kitano, Toshihiko Kawasaki, Kink University School of Medicine, Osaka, Japan

HEPATOLOGY, Vol. 38, No. 4, Supyl. I , 2003 POSTER SESSIONS 151A

8 # 1229 IDENTIFICATION OF A NEW MARKER OF HEPATOCELLULAR CARCINOMA (HCC) BY SERUM PROTEIN PROFILING OF CIRRHOTIC PATIENTS USING

Valerie Paradis, CNRS, HApital Beaujon, Clichy France; Franqoise Degos, HGpital Beaujon, Clichy, France; Delphine Dargere, CNRS, Paris, France; Nanou Pham, Jacques Belghiti, Claude Degott, HApital Beaujon, Clichy, France; Jean-Louis Janeau, CNRS, Paris, France; Dominique Delforge, Myriame Cubizole, Ciphergen, Cergy, France; Pierre Bedossa, CNRS, Le Kremlin-Bicetre, France

8 # 1230

CARCINOMA SUSCEPTIBILITY GENES IN PATIENTS WITH HEPATITIS C VIRUS INFECTION Naoya Kato, University of Tokyo, Tokyo, Japan; Guijin Ji, HuBit Genoniics Inc., Tokyo, Japan; Yujin Hoshida, Yue Wang, Motoyuh Otsuka, Hiroyoshi Taniguchi, Masaru Moriyama, Tadashi Goto, University of Tokyo, Tokyo, Japan; Tadashi Matsuura, Keisuke Ishii, HuBit Genomics Inc., Tokyo, Japan; Shuichiro Shiina, Takao Kawabe, University of Tokyo, Tokyo, Japan; Masaaki Muramatsu, HuBit Genomics Inc., Tokyo, Japan; Masao Omata, University of Tokyo, Tokyo, Japan

# 1231

SELDI-TOF PROTEINCHIP

LARGE-SCALE SEARCH OF SNPS FOR HEPATOCELLULAR

SOLUBLE GLYPICAN-3 (SGPC3), IDENTIFIED BY GENOME- WIDE ANALYSIS OF GENE-EXPRESSION PROFILES USING OLIGONUCLEOTIDE MICROARRAY, IS A CANDIDATE OF BIOMARKER FOR WELL T O MODERATELY DIFFERENTIATED HEPATOCELLULAR CARCINOMA Kiyotaka Watanabe, Yutaka Midorikawa, Hiroslii Kanamori, Yoshitaka Hippo, Akira Watanabe, Shin Ohnishi, Tatsuhiko Kodama, Masatoshi Makuuchi, Hiroyuki Aburatani, University of Tokyo, Tokyo, Japan

# 1232 VALIDATION STUDY OF THE NEW PROGNOSTIC STAGING SYSTEM, THE JAPAN INTEGRATED STAGING SCORE (JIS SCORE) FOR HEPATOCELLULAR CARCINOMA IN 3,934 JAPANESE PATIENTS: A MULTICENTER COLLABORATIVE STUDY Masatoshi Kudo, Hobyung Chung, Kinki University School of Medicine, Osaka, Japan; Yukio Osaki, Osaka Red Cross Hospital, Osaka, Japan; Hiroko Oka, Osaka City General Medical Center, Osaka, Japan; Hiroshi Kasugai, Yo Sasaki, Osaka Medical Center for Cancer and CVD, Osaka, Japan; Toshihito Seki, Kansai Medical University, Osaka, Japan; Seiji Haji, Kink University School of Medicine, Osaka, Japan

# 1233 T-REGULATORY LYMPHOCYTES IN HEPATOCELLULAR CARCINOMA Esther Unitt, Simon Rushbrook, Aileen Marshall, Susan Davis, Addenbrooke’s Hospital, Cambridge, UK; Lesley Morris, Nicholas Coleman, MRC / Hutchinson Research Centre, Cambridge, UK; Graeme Alexander, Addenbrooke’s Hospital, Cambridge, UK

# 1234 LIVER TRANSPLANTATION FOR PRIMARY SCLEROSING CHOLANGITIS; PREDICTORS AND CONSEQUENCES OF HEPATOBILIARY MALIGNANCY Bjorn J Brandsaeter, Rikshospitalet, Oslo, Norway; Helena Isoniemi, University Hospital Helsinki, Helsinki, Finland; Ulrika Broome, Huddinge University Hospital, Stockholm, Sweden; Michael Olausson, Lars Backman, Sahlgrenska Hospital, Gothenburg, Sweden; Bent Hansen, Rigshospitalet, Copenhagen, Denmark; Erik Schrumpf, Rikshospitalet, Oslo, Norway; Antti Oksanen, Bo-Goran Ericzon, Huddinge University Hospital, Stockholm, Sweden; Krister Hockerstedt, Heikki Makisalo, University Hospital Helsinki, Helsinki, Finland; Preben Kirkegaard, Rigshospitalet, Copenhagen, Denmark; Styrbjorn Friman, Sahlgrenska Hospital, Gothenburg, Sweden; Kristian Bjero, Rikshospitalet, Oslo, Norway

# 1235 ADJUVANT CHEMOTHERAPY DOES NOT AFFECT SURVIVAL IN INCIDENTAL HEPATOCELLULAR CARCINOMA Walid Ayoub, John Vierling, Emanuel Cavazzoni, Melissa Meehan, Nicholas Nissen, Paul Martin, Tram Tran, Fred Poordad, Christopher Shackleton, Stephen Geller, Steven Colquhoun, Cedars-Sinai Medical Center, Los Angeles, CA

tt 1236 PROGNOSTIC EVALUATION OF HEPATOCELLULAR CARICNOMA: A COMPARATIVE ANALYSIS OF FOUR

WITH LIVER CIRRHOSIS Edoardo Giannini, Federica Botta, Paola Romagnoli, Federica Malfatti, Alessandra Fumagalli, Emanuela Testa, Elena Podesta, Bruno Chiarbonello, Simone Polegato, Roberto Testa, Gastro- enterology Unit and Postgraduate School of Gastroenterology, Genoa, Italy

DIFFERENT STAGING SYSTEMS IN ANTI-HCV PATIENTS

# 1237 PROTON THERAPY FOR HEPATOCELLULAR CARCINOMA LARGEST REPORTED U.S. EXPERIENCE TO DATE Donald J Hillebrand, David A Bush, Ke-Qin Hu, Patti Radovich, Jerry D Slater, James A Slater, Lonia Linda University Medical Center, Loma Linda, CA

# 1238 EXPANDING THE SELECTION CRITERIA FOR TRANSPLANT PATIENTS WITH HEPATOCELLULAR CARCINOMA: A WORD OF CAUTION Bashar A Aqel, Mayo Clinic, Jacksonville, FL; Gregory Gores, Mayo Clinic, Rochester, MN; Jeffery Steers, Mayo Clinic, Jacksonville, FL; Charles Rosen, Mayo Clinic, Rochester, MN; Victor Machcao, Denise Harnois, Mayo Clinic, Jacksonville, FL

# 1239 MELD SCORE IS A BETTER PREDICTOR OF MORTALITY THAN TUMOR CHARACTERISTICS IN INOPERABLE HEPATOCELLULAR CARCINOMA IN THE UNITED STATES Jorge A Marrero, Robert J Fontana, Grace L Su, Hari S Conjeevaram, Sherry Fu, Anna S Lok, University of Michigan, Ann Arbor, MI

# 1240 0- i COMPARISON OF POSTTREATMENT PROGNOSIS BETWEEN ABLATION AND RESECTION FOR EARLY-STAGE m u , HEPATOCELLULAR CARCINOMA STANDARDIZED m 0 ANALYSIS OF 737 PATIENTS BY STRATIFICATION METHOD BASED ON JIS SCORING SYSTEM Masatoshi Kudo, Hobyung Chung, kink^ University School of Medicine, Osaka, Japan

0

$ a,


$1241

HEPATOCELLULAR CARCINOMA RESULTS IN A SURVIVAL DISADVANTAGE Emanuel Cavazzoni, Melissa D Meehan, Christopher Shackleton, Cedars-Sinai Medical Center, Los Angeles, CA; Linda Sher, University of Southern California, Los Angeles, CA; John Vierling, Nicholas Nissen, Paul Martin, Fred Poordad, Tram Tran, Walid Ayoub, Steven Colquhoun, Cedars-Sinai Medical Center, Los Angeles, CA

PRE-TRANSPLANT ADJUVANT THERAPY FOR

# 1242 PERCUTANEOUS ACETIC ACID VERSUS ETHANOL IN THE TREATMENT OF HEPATOCELLULAR CARCINOMA A PROSPECTIVE RANDOMIZED TRIAL Eman Rewisha, Adel El Mallah, Imam Waked, Saleh Mahmoud Saleh, National Liver Institute, Shebeen El-Kom, Egypt

# 1243 OCTREOTIDE TREATMENT IN PATIENTS WITH ADVANCED HEPATOCELLULAR CARCINOMA FIRST RESULTS OF THE

HECTOR TRIAL Hans-Peter Allgaier, HELIOS-Klinik, Titisee-Neustadt, Germany; Gerhild Becker, Manfred Olschewski, Andreas Zahringer, Hubert E Blum, University Hospital of Freiburg, Freiburg, Germany

RANDOMIZED PLACEBO-CONTROLLED DOUBLE-BLIND

t; 1244 IMMUNOCYTOCHEMICAL DETECTION OF HEPATOCELLULAR CARCINOMA MICROMETASTASES

UNDERGOING LIVER TRANSPLANTATION Robert P Sutcliffe, Dona1 D Maguire, Bernard Portmann, Mohamed Rela, King's College Hospital, London, UK; Gerald C O'Sullivan, Mercy Hospital, Cork, Ireland; Ghulam J Mufti, Nigel D Heaton, King's College Hospital, London, UK

USING HEP PAR-1 MONOCLONAL ANTIBODY IN PATIENTS

# 1245

INVASION IN HEPATOCELLULAR CARCINOMA Yoshiyuki Sawai, Shinji Tamura, Koji Fukui, Osaka University Graduate School of Medicine, Suita, Osaka, Japan; Nobuyuki Ito, Fukui Medical University, Fukui, Japan; Kazuho Imanaka, Ayuko Saeki, Shigeru Sakuda, Shinichi Kiso, Yuji Matsuzawa, Osaka University Graduate School of Medicine, Suita, Osaka, Japan

EPHRIN-B1 PROMOTES NEOVASCULARIZATION AND

# 1246 INDUCTION OF APOPTOSIS IN HUMAN HEPATOCELLULAR CARCINOMA BY PHOTODYNAMIC THERAPY IS ASSOCIATED WITH THE ACTIVATION OF CASPASE 2 AND

Tetsuya Yoshikawa, Koichi Nariai, Hideko Uga, Yoko Yumoto, Masataka Date, Hiroshi Takahashi, Institute of Clinical Medicine and Research, Jikei University School of Medicine, Kashiwa, Japan

# I247 OPTIMAL TREATMENT STRATEGY FOR ELDERLY PATIENTS WITH HEPATOCELLULAR CARCINOMA Kazufumi Dohmen, National Nagasaki Medical Center, Omura, Japan; Hirohisa Shigematsu, Koji Irie, Saga Prefectual Hospital, Saga, Japan; Hiromi Ishibashi, National Nagasaki Medical Center, Omura, Japan

# 1248 A NOVEL TREATMENT TECHNIQUE FOR SYMPTOMATIC HUGE LIVER CYST: INTRACYSTIC INJECTION THERAPY OF MONOETHANOLAMINE OLEATE IN 12 CASES WITH 15 LIVER CYSTS Ryosuke Nakaoka, Emi Ishikawa, Shigenaga Matsui, Nobuhiro Fukuta, Youichirou Suetomi, Yasunori Minami, Hobyung Chung, Masayuki Kitano, Toshihiko Kawasaki, Mikio Shiomi, Masatoshi Kudo, Kinki University School of Medicine, Osaka, Japan

DEAMIDATION OF BCL-XL


# 1249 SEVERE COMPLICATIONS OF RADIOFREQUENCY ABLATION THERAPY FOR HEPATOCELLULAR CARCINOMA: ANALYSIS OF 3,891 ABLATIONS IN 2,614 PATIENTS Hiroshi Kasugai, Osaka Medical Center for Cancer and CVD, Osaka, Japan; Yukio Osaki, Osaka Red Cross Hospital, Osaka, Japan; Hiroko Oka, Osaka City General Medical Center, Osaka, Japan; Toshihito Seki, Masatoshi Kudo, Kinki University School of Medicine, Osaka, Japan

# 1250

WITH HEPATOCELLULAR CARCINOMA CANDIDATES FOR LIVER TRASNPLANTATION Josep M Llovet, Margarita Sala, Josep Fuster, Miquel Navasa, Fernando Pons, Manel Sole, Carmen Ayuso, Antoni Rimola, Juan Carlos Garcia-Valdecasas, Jordi Bruix, BCLC Group, Liver Unit; Surgery Department, Digestive Disease Institute; Pathology Department, Radiology Department; IDIBAPS Hospital Clinic, Barcelona, Spain

PREDICTORS OF DROP-OUT AND SURVIVAL OF PATIENTS

f 1251 TREATMENT OF HUMAN HEPATOCELULAR CARCINOMA

LOCALIZING PHOTOSENSITIZER Koichi Nariai, Tetsuya Yoshikawa, Hiroshi Takahashi, Institute of Clinical Medicine and Research, Jikei University School of Medicine, Kashiwa, Japan

BY INTRAHEPATIC LASER IRRADIATION USING A TUMOR-

# 1252 HOMOZYGOSITY FOR THE ALCOHOLDEHYDROGENASE 3*1 ALLELE IS ASSOCIATED WITH HEPATOCELLULAR

Felix Stickel, University of Erlangen-Nuremberg, Erlangen, Germany; Nils Homann, University of Liibeck, Lubeck, Germany; Monika Benesova, Salem Medical Center, Heidelberg, Germany; h a Zuber, University of Freiburg, Freiburg, Germany; Susanne Richter, University of Erlangen-Nuremberg, Erlangen, Germany; Claus Hellerbrand, University of Regensburg, Regensburg, Germany; Hubert E Blum, University of Freiburg, Freiburg, Germany; Christoph Herold, Detlef Schuppan, University of Erlangen-Nuremberg, Erlangen, Germany; Helmut K Seitz, Salem Medical Center, Heidelberg, Germany

CARCINOMA IN ALCOHOL-INDUCED CIRRHOSIS

# 1253 SURVIVAL IN HEPATOCELLULAR CARCINOMA (HCC): IMPACT OF SCREENING AND AETIOLOGY OF LIVER DISEASE William W M Kemp, Stephen Pianko, Shara Nguyen, Michael S Bailey, Stuart K Roberts, The Alfred Hospital, Melbourne, Australia

# 1254 EFFECTIVITY OF A COMBINATION OF THE ANTI- ESTROGEN TAMOXIFEN AND 9CIS-RETINOIC ACID IN A RAT HCC MODEL Marion Ganslmayer, Christopher Herold, Matthias Ocker, Eckhart G Hahn, Detlef Schuppan, University of Erlangen, Erlangen, Germany

tr 1255 HIGH SENSITIVITY AND SPECIFICITY OF COMBINATIONAL USAGE OF DES-G AMMA-CARBOXY PROTHROMBIN AND ALPHA-FETOPROTEIN FOR DETECTING HEPATOCELLULAR CARCINOMAS Shinichiro Nakamura, Kohsaku Sakaguchi, Hiroyuki Shimomura, Yoshiaki Iwasaki, Yoshiyuki Kobayashi, Nobuyuki Toshikuni, Hironori Tanaka, Eiji Matsumoto, Yasushi Shiratori, Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan; Yasuyuki Araki, Kazuhiro Nouso, Mitsuhiko Kawaguchi, Hiroshi Ikeda, Keiji Kita, Okayama Hepatocellular Carcinoma Group, Okayama, Japan


# 1256

IN COMPLETE RESPONSE IN 14 CASES OUT OF 64 WITH ADVANCED HEPATOCELLULAR CARCINOMA AND PORTAL VEIN INVASION Shuntaro Obi, Shuichiro Shiina, Takuma Teratani, Shmpei Sato, Yukihiro Koike, Masatoshi Akamatu, Tomonori Fujishima, Ryosuke Tateishi, Miho Kanda, Takash Ishikawa, Haruhiko Yoshida, Takashi Kawabe, Masao Omata, Tokyo University, Tokyo, Japan

COMBINATION THERAPY WITH IFN-cx AND 5-FU RESULT

# 1257 PLASMA LEVELS OF GROWTH FACTORS (HGH, IGF-1 AND IGFBP-3) IN CIRRHOTIC PATIENTS WITH OR WITHOUT HEPATOCELLULAR CARCINOMA (HCC) Jean-Louis Legoux, Agnes Georges, Bordeaux University Hospital, Pessac, France; Rene Thibeault, Victor Segalen Bordeaux 2 University, Bordeaux, France; Aude Lepoutre, David Laharie, Sophie Cazorla, Johan Dubuc, Laurence Bordenave, Michel Amouretti, Victor de Ledinghen, Patrice Couzigou, Bordeaux University Hospital, Pessac, France

# 1258

OUTCOME OF HEPATOCELLULAR CARCINOMA Esther Unitt, Aileen Marshall, Simon Rushbrook, Susan Davis, Addenbrooke’s Hospital, Cambridge, UK; Sarah Vowler, University of Cambridge, Cambridge, UK; Lesley Morris, Nicholas Coleman, MRC / Hutchinson Research Centre, Cambridge, UK; Graeme Alexander, Addenbrooke’s Hospital, Cambridge, UK

# 1259 HEPATIC ARTERY CHEMOEMBOLIZATION FOR

TRANSPLANT ANALYSIS Michael Osgood, Paul H Hayashi, Michael Ludkowski, Steven Johnson, Durham Janet, Timothy Brackett, Tracy Steinberg, Lisa Forman, Marcelo Kugelmas, James Trotter, Thomas Bak, Michael Wachs, Igal Kam, Gregory Everson, University of Colorado Health Sciences Center, Denver, CO

T-CELL TUMOUR IMMUNITY IS IMPORTANT IN THE

HEPATOCELLULAR CARCINOMA AN INTENTION-TO-

# 1260 HEPATOCYTE MEMBRANE POTENTIALS AND GABAERGICACTIVITY IN HUMAN HEPATOCELLULAR CARCINOMA. NEW INSIGHTS INTO PATHOGENESIS AND POTENTIAL DIAGNOSTIC AND/OR THERAPEUTIC OPPORTUNITIES Dongfeng Sun, Manna Zhang, Yuewen Gong, University of Manitoba, Winnipeg, MB, Canada; Hans Dienes, University of Cologne, Cologne, Germany; Michael Kew, University of Wittwaterstrand, Johannesburg, Germany; Gerald Y Minuk, University of Manitoba, Winnipeg, MB, Canada

# 1261 GP73, A RESIDENT GOLGI MEMBRANE PROTEIN, APPEARS IN SERA OF PATIENTS WITH VIRAL LIVER DISEASE AND HEPATOCELLULAR CANCER Patrick R Romano, Olga V Nikolaeva, Laura Steel, Jefferson Center for Biomedical Research, Doylestown, PA; Claus J Fimmel, Saint Louis University Health Sciences Center, St. Louis, MO; Jorge Marrero, University of Michigan Medical Center, Ann Arbor, MI; Alison A Evans, Fox Chase Cancer Center, Phila- delphia, PA; Mary A Communale, Jefferson Center for Biomedical Research, Doylestown, PA; Anna Lok, University of Michigan Medical Center, Ann Arbor, MI; W T London, Fox Chase Cancer Center, Philadelphia, PA; Adrian Di Bisceglie, Saint Louis University Health Sciences Center, St. Louis, MO; Timothy M Block, Jefferson Center for Biomedical Research, Doylestown, PA

# 1262 SAFETY OF THE PHASE I11 RANDOMIZED STUDY OF HYMITAQB VS. DOXORUBICIN IN UNRESECTABLE HEPATOCELLULAR CARCINOMA (HCC): ETHECC(C) TRIAL (EVALUATION OF THYMITAQO IN HCC) VS. SAFETY OF THE PHASE I1 PROGRAM WITH THYMITAQR Robert Gish, California Pacific Medical Center, San Francisco, CA

# 1263 EVALUATION OF ABLATED AREA OF PERCUTANEOUS RADIOFREQUENCY ABLATION, USING LEVEEN NEEDLE ELECTRODE, OF SMALL HEPATOCELLULAR CARCINOMA WITH CT IMAGING Shinsuke Kira, Shuji Date, Saiseikai Hiroshima Hospital, Hiroshima, Japan; Yoshihmi Yamashita, Yoshida General Hospi- tal, Hiroshima, Japan; Tsuyoshi Kawakami, Koji Sumii, Yukmobu Sumida, Saiseikai Hiroshima Hospital, Hiroshima, Japan

# 1264 CHANGES OF LENS CULINARIS AGGLUTININ-REACTIVE ALPHA-FETOPROTEIN (AFP-L3 FRACTION) AFTER COMPLETE RADIOFREQUENCY ABLATION FOR HEPATO- CELLULAR CARCINOMA ANALYSIS OF 186 PATIENTS Chikara Ogawa, Yasunori Minami, Hobyung Chung, Ryosuke Nakaoka, Shigenaga Matsui, Toyokazu Fukunaga, Masayuki b tano , Toshihiko Kawasaki, Mikio Shiomi, Masatoshi Kudo, Kink University School of Medicine, Osaka, Japan

# 1265 SERUM AND BILIARY CYTOKERATIN FRAGMENT CYFRA

CHOLANGIOCARCINOMA Gamal Badra, National Liver Institute, Shebeen El-Kom, Egypt; Hosam Ghanem, Mansoura University School of Medicine, Mansoura, Egypt; Hosam Taha, National Liver Institute, Shebeen El-Kom, Egypt; Seham Seif, Mansoura University School of Medicine, Mansoura, Egypt; Imam Waked, National Liver Institute, Shebeen El-Kom, Egypt

# 1266 PROGENITOR CELL FEATURES IN HEPATOCELLULAR CARCINOMA Anne M T Durnez, Chris Verslype, Raymond Aerts, Jacques Pirenne, Tania Roskams, KUL Leuven, Leuven, Belgium

# 1267

HEPATOCELLULAR CARCINOMA AN ASSESSMENT OF CURRENT STAGING SYSTEMS AND INDIVIDUAL PARAMETERS Emanuel Cavazzoni, Melissa D Meehan, Christopher Shackleton, Cedars-Sinai Medical Center, Los Angeles, CA; Linda Sher, University of Southern California, Los Angeles, CA; Nicholas Nissen, John Vierling, Paul Martin, Fred Poordad, Tram Tran, Walid Ayoub, Steven Colquhoun, Cedars-Sinai Medical Center, Los Angeles, CA

8 # 1268

CELLS SELECTIVELY ACTIVATES HEPATIC NATURAL

MANNER AND INDUCES THE ACTIVATION OF ACQUIRED

21-1, CEA, AND CA 19.9 AS TUMOR MARKERS FOR

PREDICTING POST-TRANSPLANT SURVIVAL WITH

CDID-MEDIATED STIMULATION OF NATURAL KILLER T

KILLER CELLS IN INTERFERON-GAMMA INDEPENDENT 0

IMMUNITY AGAINST MURINE HEPATOCELLULAR 1:

;?

CARCINOMA om m 0

a,

mur Takuya Miyagi, Tetsuo Takehara, Takahiro Suzulu, Masahisa Jinushi, Chihiro Ohnishi, Tomohide Tatsumi, Naoki Hiramatsu, Tatsuya Kanto, Norio Hayashi, Osaka University Graduate School of Medicine, Suita, Osaka, Japan


5 1269 MECHANISM OF HEPATOCELLULAR CARCINOMA RECURRENCE AFTER LIVER TRANSPLANTATION: ROLE OF

Robert P Sutcliffe, Ragai R Mitry, King’s College Hospital, London, UK; Elodie Mordelet, Pippa Hillyer, Open University Milton Keynes, UK; Anil Dhawan, Nigel D Heaton, Adam T Llnke, King’s College Hospital, London, UK

TUMOR NECROSIS FACTOR-ALPHA

Stellate Cell Biology

g k 1270 CONNECTIVE TISSUE GROWTH FACTOR (CTGF) INDUCES ADHESION OF RAT ACTIVATED HEPATIC STELLATE CELLS VIA INTEGRIN ALPHA V BETA 3 AND HEPARAN SULFATE

DOMAIN R~iiipiiig Gao, David R Brigstock, Children’s Research Inshtute, Columbus, OH

PROTEOGLYCANS THROUGH ITS CARBOXYL-TERMINAL

LEPTIN PREVENTS GLIOTOXIN-INDUCED APOPTOSIS IN ISOLATED HEPATIC STELLATE CELLS: INVOLVEMENT OF

Tie Lang, Kenichi Ikelima, Shunhei Yamashma, Nobuyulu Enomoto, Tsuneo Kitamura, Yoshiyuh Takei, Nobuhro Sato, Juntendo University School of Medicine, Tokyo, Japan

THE PHOSPHATIDYLINOSITOL 3-KINASEIAKT PATHWAY

: 1272 SERUM AMYLOID A ACTIVATES PROINFLAMMATORY SIGNALING PATHWAYS AND ENHANCES CHEMOKINE SECRETION IN ACTIVATED HUMAN HEPATIC STELLATE CELLS Robert F Schwabe, Columbia University College of Physicians and Surgeons, New York, NY; Ramon Bataller, University of North Carolina, Chapel Hill, NC; David A Brenner, Columbia University College of Physicians and Surgeons, New York, NY; Humberto B Jijon, University of Calgary, Calgary, AB, Canada

L 1273

INTERNALIZATION VARIES BETWEEN QUIESCENT AND ACTIVATED HEPATIC STELLATE CELLS Marianna D A Gaca, University of Pennsylvania School of Mcdicme, Philadelphia, PA; Chenghai Liu, Shanghai Institute of Traditional Chinese Medicine, Shanghai, China; Rebecca G Wells, University of Pennsylvania School of Medicine, Philadelphia, PA

TGF-fi RECEPTOR CELL SURFACE EXPRESSION AND

2 1274 MEF2 REGULATES HEPATIC STELLATE CELL ACTIVATION AND GROWTH Xuemin Wang, Xiaoli Tang, Xiaoming Gong, Jack Wands, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI; Scott Friedman, Mount Sinai School of Medicine, New York, NY; Zixu Mao, Liver Research Center, RI Hospital and Brown Medical School, Providence, RI

# 1275 PRESENCE AND FUNCTION OF MYRISTOYLATED

IN ACTIVATED HUMAN LIVER HEPATIC STELLATE CELLS (HHSC) Krista Rombouts, Benedetta Lottiii, Alessandra Caligiuri, Vinicio Carloni, Massimo Pinzani, University of Florence, Florence, Italy

X 1276 ACTIVATED HEPATIC STELLATE CELLS EXPRESS A

IS REQUIRED FOR MIGRATION Shojiro Kikuchi, Shao-Shean Wang, Courtney Griffin, D Montgomerv Bissell, University of California, San Francisco, CA

ALANINE-RICH PROTEIN KINASE C SUBSTRATE (MARCKS)

VARIANT HYALURONIC ACID RECEPTOR, CD44-V6, THAT

8 Denotes AASLD T’reridential Poster of Distinction

# 1277 PDGF-BB INDUCES THROMBOSPONDIN-1 EXPRESSION IN A SRC-DEPENDENT MANNER LEADING TO ACTIVATION OF LATENT TGF-P IN HEPATIC STELLATE CELLS Katja Breitkopf, Iris Sawitza, Axel M Gressner, Institute of Clinical Chemistry, Aachen, Germany

# 1278 TARGETING ANTI-FIBROGENIC THERAPEUTICS TO HEPATIC STELLATE CELLS-GENERATING HUMAN ANTIBODY FRAGMENTS BY PHAGE DISPLAY Lucy J Elrick, Valerie Leel, Carylyn J Marek, N Koruth, Keith A Charlton, Andrew R Porter, Matthew C Wright, University of Aberdeen, Aberdeen, UK

# 1279 ENOS GENE TRANSFER INHIBITS HEPATIC STELLATE CELL PROLIFERATION AND MIGRATION THROUGH A CGMP

MECHANISM: IMPLICATIONS FOR INHIBITION OF TUMOR ANGIOGENESIS IN LIVER June S Lee, Suvro Chatterjee, Vijay Shah, Mayo Clinic, Rochester, MN

INDEPENDENT, S-NITROSYLATION DEPENDENT

# 1280 LEPTIN RECEPTORS ON HUMAN HEPATIC STELLATE CELLS MEDIATE THE EXPRESSION OF PRO-INFLAMMATORY AND PRO-ANGIOGENIC CYTOKINES Sara Aleffi, Ilaria Petrai, Alessandra Caligiuri, Giacomo Laffi, Massimo Pinzani, Paolo Gentilini, Fabio Marra, University of Florence, Florence, Italy

# 1281 MATRIX COMPLIANCE DETERMINES HEPATIC STELLATE CELL PHENOTYPE Marianna D A Gaca, University of Pennsylvania School of Medicine, Philadelphia, PA; Penelope Georges, Paul Janmey, University of Pennsylvania Institute for Medicine and Engineering, Philadelphia, PA; Rebecca G Wells, University of Pennsylvania School of Medicine, Philadelphia, PA

# 1282 FOXFl HAPLOINSUFFICIENCY IN MICE ACCELERATES BILIARY INFARCTION AND HEPATIC APOPTOSIS FOLLOWING BILIARY OBSTRUCTION MinHua Wang, Vladimir Kalinichenko, Robert H Costa, Ai-Xuan L Holterman, University of Illinois at Chicago, Chicago, IL

# 1283 TYPE I COLLAGEN AND IL-1 SERVE AS CO-STIMULATORY SIGNALS FOR MMP-9 INDUCTION AND HEPATIC STELLATE CELL ACTIVATION Yuan-Ping Han, Ling Zhou, Jiaohong Wang, Shigang Xiong, Warren L Garner, Hidekazu Tsukamoto, Keck School of Medicine of the University of Southern California, Los Angeles, CA

# 1284

ACTIVATED HEPATIC STELLATE CELLS AND CONTROL OF THEIR SURVIVAL IN CULTURE Fouad Lafdil-, INSERM U581, Creteil, France; Dominique Couchie, INSERM U581, Creteil, France; Marie N Chobert, INSERM U581, Creteil, France; Anne M Preaux, Liying Li, Elie S Zafrani, INSERM U581, Creteil, France; Philippe Mavier, Yannick Laperche, INSERM U581, Creteil, France

SECRETION OF GROWTH ARREST-SPECIFIC 6 PROTEIN BY

# 1285 ACTIVATED HEPATIC STELLATE CELLS EXPRESS CD39L2/NTPDASE6 AND CD39L3/NTPDASE3 Mika Ogawa, Norihiko Ogawa, Marcia Wink, Keiichi Enjyoji, Eva Csizmadia, Simon C Robson, Harvard University, Boston, MA


# 1286 RAT HEPATIC STELLATE CELLS EXPRESS RELAXIN RECEPTORS, AND RELAXIN TREATMENT CAUSES REDUCED CONTRACTILE RESPONSE TO ENDOTHELIN-1 Robert G Bennett, Katrina J Mahan, Dean J Tuma, VA Medical Center, Omaha, NE

# 1287 N-(METHYLAMIN0)ISOBUTYRIC ACID INHIBITS PROLIFERATION OF CFSC-PG HEPATIC STELLATE CELLS Thomas L Freeman, Geoffrey M Thiele, University of Nebraska Medical Center, Omaha, NE; Lynell W Klassen, Mark E Mailliard, Veterans Administration Medical Center, Omaha, NE

# 1288 ROLE OF REACTIVE OXYGEN SPECIES IN ZINC

STELLATECELLS Akiko Kojima-Yuasa, Tomoko Ohkita, Kanako Umeda, Graduate School of Human Life Science, Osaka City University, Osaka, Japan; David 0 Kennedy, Mailman School of Public Health, Columbia University New York, NY; Shuhei Nishiguchi, Graduate School of Medicine, Osaka City University, Osaka, Japan; Isao Matsui-Yuasa, Graduate School of Human Life Science, Osaka City University, Osaka, Japan

DEFICIENCY-INDUCED ACTIVATION OF HEPATIC

# 1289 FRAGMENTS OF THE LIVER COLLAGENS VI AND XIV SHOW DISTINCT EFFECTS ON DIFFERENTIATION OF ADIPOCYTES AND HEPATIC STELLATE CELLS Martin Ruehl, Anita Zeller, Ma& Loesekann, Gisela Stoltenburg- Diedinger, UKBF, Berlin, Germany; Walburga Dieterich, University of Erlangen-Nuremberg, Erlangen, Germany; Martin Zeitz, UKBF, Berlin, Germany; Detlef Schuppan, University of Erlangen-Nuremberg, Erlangen, Germany; Rajan Somasundaram, UKBF, Berlin, Germany

# 1290 ACTIVATED HEPATIC STELLATE CELLS EXPRESS A

Kyle Brown, Maleah Mathas, Douglas Spitz, University of Iowa, Iowa City, IA

SUPEROXIDE-GENERATING NAD(P)H OXIDASE

# 1291 DEVELOPMENT OF A NOVEL IN VITRO MODEL OF LIVER FIBROSIS USING ORGANOTYPIC LIVER SLICE CULTURE Janice L Davies, Clare Verrill, Harry Millward-Sadler, Lars Sundstrom, Nick Sheron, University of Southampton, Southampton, UK

#1292 HUMAN HEPATIC MYOFIBROBLASTS PRODUCE CHEMOKINES AND ADHESION MOLECULES WHICH PROMOTE THE RETENTION OF LYMPHOCYTES DURING LIVER INJURY AND FIBROSIS Patricia F Lalor, Anthonis Giannakakis, John Curnow, Christopher D Buckley, David H Adams, University of Birmingham, Birmingham, UK

# 1293

LYSOPHOSPHATIDIC ACID IN HEPATIC STELLATE CELLS Mikio Yanase, Hitoshi Ikeda, Eisei Noiri, Tomoaki Tomiya, Masahiro Arai, Yukiko Inoue, Kazuaki Tejima, Kayo Nagashima, Masao Omata, Faculty of Medicine, University of Tokyo, Tokyo, Japan; Kenji Fujiwara, Saitama Medical School, Saitama, Japan

# 1294 IDENTIFICATION AND UPREGULATION OF THE

(IKCA) CHANNEL IN ACTIVATED RAT HEPATIC STELLATE CELLS: SPECIFIC BLOCKAGE BY CHARYBDOTOXIN AND CLOTRIMAZOL RESULTS IN SIGNIFICANT REDUCTION OF PROLIFERATION Rajan Somasundaram, Martin Ruehl, Ralf Koehler, Maik Loesekann, UKBF, Berlin, Germany; Detlef Schuppan, University of Erlangen-Nuremberg, Erlangen, Germany; Martin Zeitz, Joachim Hoyer, UKBF, Berlin, Germany # 1295 A1 ADRENERGIC RECEPTOR ANTAGONIST PRAZOSIN INHIBITS HEPATIC STELLATE CELLS ACTIVATION WHILE IT STIMULATES PROGENITOR CELL REGENERATION Nicoletta Sinelli, David Cassiman, Gert De Hertogh, KU Leuven, Leuven, Belgium; Jude Oben, Johns Hopkins University, Baltimore, MD; Tania Roskams, KU Leuven, Leuven, Belgium

# 1296 HORMONE SENSITIVE LIPASE IS A RETINYL ESTER HYDROLASE IN HEPATIC STELLATE CELLS Sonal P Sanghani, Tommaso Mello, Wilhelmina I Davis, Indiana University School of Medicine, Indianapolis, IN; Hidekazu Tsukamoto, University of Southern California, Los Angeles, CA; Andrea Galli, Alessandro Casini, University of Florence, Florence, Italy; William F Bosron, Indiana University School of Medicine, Indianapolis, IN

# 1297 THE PORCINE ARACHNOCYTE SPECTRUM: PANZONAL POLYMORPHISM OF HEPATIC STELLATE CELL POPULATION AS REVEALED BY EXTENSIVE RECONSTRUCTION OF CONFOCAL OPTICAL IMAGING Gedsuda Pattanapen, Mahidol University, Bangkok, Thailand

RECEPTOR-MEDIATED BIOLOGICAL ACTIVITIES OF

INTERMEDIATE-CONDUCTANCE CA2+-ACTIVATED K+

1 %,A AASLD ABSTRACTS HF PATOI-OGY, Octoher 2003

1 THE CLINICAL COURSE OF ULCERATIVE COLITIS AFTER ORTHOTOPIC LIVER TRANSPLANTATION FOR PRIMARY SCLEROSING CHOLANGITIS. Alexandra ] Seddon, Gwo-Tzer Ho, Wrstcrn Griierrrl Hospital, Eilinburgh, LIK; George Tlzerapondos, Petrr C Hayes, Royal I n f i t ~ ? i a ~ j of Edinburgh, Edinburgh, UK; Jack Satstan@, Western General Hospital, Edinburglz, UK Background Primary sclerosing cholangitis (PSC) is often associated with ulcerative colitis (UC). The effect of orthotopic liver transplantation (OLT) on the course of UC in these patients remains unclear and published studies have given conflicting results. Aims To document the course of UC pre and post OLT in patients with PSC and UC, who underwent OLT in the Scottish Liver Trans- plant Unit between November 1992 and March 2003. Methods Retrospective analysis of the medical records of the 42 OLT patients with PSC identified from the unit database. 29/42 patients had coexisting inflammatory bowel disease (26 UC and 3 Crohn's disease). Only the patients with UC were studied. There were 16 males and 10 females (age 15-62, mean age at OLT= 46.9 years). Five patients were excluded from the study because of death at day 7 post-OLT (1 patient) and pre-OLT colectomy (4 patients). One patient was excluded because UC developed post-OLT. Median follow up pre and post OLT was 11.67 and 4.33 years respectively. Results Relapses: There was a statistically significant increase in relapses per year post OLT compared with pre OLT (1.11 -t 1.0 vs 0.30 2 0.35, p-= 0.002). Of those who relapsed, 56% (9/16) were on prednisolone and 37.5'XB (6/16) were on more than lOmg prednisolone at the time of relapse. Corticosteroid use for UC post-OLT: More oral or IV corticosteroid courses per year were required for treatment of active UC post OLT compared with pre OLT (0.76 t 0.98 vs 0.13 i- 0.27, p=0.007). Corticosteroid deuendence: Only one patient was corticosteroid dependent prior to OLT and remained so until colectomy post OLT. 20"/0 of patients (4/20) became corticosteroid dependent post OLT. Cohectomv post-OLT 35% (7120) patients underwent colectomy post OLT, 4 for severe disease, 1 for adenocarcinoma and 2 for severe dysplasia. Neoplasia 3/20 patients developed Colonic adenocarcinoma (1) or moderate- severe dysplasia (2). Gastro-intestinal lymphoma, and Bowen's disease were also diagnosed in 2 patients of the PSClUC group who had undergone colectomy pre OLT. Conclusions Despite immunosuppression, UC in patients after OLT for PSC/UC has a more aggressive clinical course than before transplant and is associated with a high rate of neoplasia. Disclosures: Peter C Hayes - No relationships to disclose Gwo-Tzer Ho - No relationships to disclose Jack Satstangi - No relationships to disclose Alexandra J Scddon - No relationships to disclose George Thcrapondos - No relationships to disclose

2 LIVER TRANSPLANTATION FOR FAMILIAL AMYLOID POLYNEUROPATHY DOES NOT PREVENT DISEASE PROGRESSION IN A MAJORITY OF PATIENTS. Roman E Perri, D a d Brandhagen, Sterien Zeldenrust, Charles B Rosen, John J Poterucha, Morie A Gertz, Gregory ] Gores, Mayo Clinic, Rochester, MN

Introduction: Familial amyloid polyneuropathy (FAP) is an auto- soma1 dominant hereditary condition in which the liver produces a variant transthyretin protein that accumulates in various organs. Disease manifestations include progressive sensorimotor neuropathy, as well as cardiac and gastrointestinal disorders. Orthotopic liver transplantation (OLT) eliminates further production of the abnormal protein but it is uncertain if it halts disease progression. Aim: To determine the outcome including the status of clinical manifestations in patients transplanted for FAP. Methods: We reviewed the medical records of all patients undergoing OLT for FAP at our institution between 11/96 and 12/02. Information collected included date of birth, sex, FAP mutation, age at diagnosis, pre and post-OLT clinical manifestations, and patient and allograft survival. When available, neurologic involvement was quantified by ulnar nerve conduction velocity obtained by electromyography. Cardiac involvement was assessed by echocar- diography with measurement of the intraventricular septa1 thick- ness (IVST). Results: Our study population consisted of 12 male patients with a mean age of 58 years (range 47-68). Six patients received liver and 6 patients a liver and heart transplant. Amyloid mutations included MET-30 (n=4), ALA-60 (n=4), TYR-77 (N=2), GLY-42 ( n = l ) and LYS-89 (n= l ) . The mean time from onset of symptoms to diagnosis was 3.4 years (0-10) and patients were listed for OLT an average of 10.8 months (0-60) after diagnosis. The mean time from listing to OLT was 8.2 months (1-18). Five patients died after OLT, during a mean follow-up of 3.5 years (4 months - 6 years). One-year patient survival was 100% and three- year patient survival was 92%. One patient required retransplantation for hepatic artery thrombosis. Neurologic symptoms were the initial clinical manifestation in the majority of patients (7/12), followed by cardiopulmonary (4112) and gastrointestinal symptoms (1112). Most patients experienced multiple symptoms. Sub- jective evolution of symptoms as assessed by chart review demonstrated that symptoms referable to amyloidosis worsened after OLT in seven patients, and improved or stabilized in five. Following OLT, neuropathy symptoms improved in four patients, worsened in seven patients and were unchanged in one patient. Pre and post-OLT nerve conduction velocities were available for 5 patients and the post-OLT studies showed progression of disease in 3, improvement in 1 and were unchanged in 1 patient. Prior to OLT, all twelve patients had an increased IVST on echocardio- gram. Post OLT cardiac symptoms improved in six patients (five of whom also had cardiac transplantation), worsened in three patients, and were unchanged in three patients (one of whom also had cardiac transplantation). Pre and post-OLT echocardiograms were available in 4 of 6 patients who had not received a cardiac transplant. Echocardiograms were performed an average of 29.3 months (12-36) post-transplant and demonstrated IVST improvement in one patient, worsening in two, and remained the same in one patient. Conclusions: 1. Disease progression occurs despite OLT in the majority of patients with FAP. 2. Diagnosis of patients and OLT at an earlier stage of disease may be a means of affecting disease progression in a larger number of patients. 3. Further studies are needed to determine if OLT slows disease progression in FAP. Disclosures: David Brandhagen - No relationships to disclose Morie A Gertz - No relationships to disclose Gregory J Gores - No relationships to disclose Roman E Perri - No relationships to disclose John J Poterucha - No relationships to disclose Charles B Rosen - No relationships to disclose Steven Zeldenrust - No relationships to disclose

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1, 2003 AASLD ABSTRACTS 157A

3 THE IMPACT OF EXPANSION OF CONVENTIONAL TUMOR CRITERIA AND PRE-OPERATIVE LOCO-REGIONAL TREATMENTS ON SURVIVAL FOLLOWING LIVER TRANSPLANTATION FOR HEPATOCELLULAR CARCINOMA RESULTS FROM TWO CENTERS. Francis Y Yao, University of California San Francisco, Sun Francisco, CA; Milan Kinkhabwala, New York Presbyterian Hospital, Nezu York, Ny; Jeanne LaBerge, Nathan M Bass, Robert Kerlan, John P Roberts, University of California Sun Francisco, Sun Francisco, CA BACKGROUND: It has been suggested that modest expansion of the conventional criteria used for orthotopic liver transplantation (OLT) for hepatocellular carcinoma (HCC) does not adversely impact survival. In this study, we further evaluated the outcome of OLT according to HCC stage, and reassessed the impact of the expanded criteria based on a combined analysis from two transplant centers. We also hypothesized that pre-operative transarte- rial chemoembolization (TACE) or ablation therapies might have played a role in preserving excellent survival after modest expansion of the tumor size limits. PATIENTS AND METHODS The study cohort included 168 consecutive patients with HCC who underwent OLT from two liver transplant centers with at least 6 months of follow-up. Forty-four patients (26.2%) had incidental HCC. Seventy-six patients (45.2%) received pre-operative TACE alone, including 59 patients who received TACE within 24 hours prior to OLT when a donor became available. Thirteen patients (7.7%) received ablation only, and 14 others (8.3%) received a combination of these treatments. Sixty-five patients (38.7%) received no specific pre-operative treatment. Pathologic tumor staging of the explanted liver revealed pT1 (single tumor under 2 cm) in 27 patients, pT2 (solitary tumor 2 to 5 cm; or 2 to 3 lesions none > 3 cm) in 90 patients, pT3 (1 nodule > 5.0 cm; 2 or 3 nodules, at least one > 3.0 cm) in 36 patients and pT4 (4 or more nodules of any size or gross invasion of the main portal vein) in 15 patients. The 24 patients (14.3%) with pT3 HCC who met the proposed expanded criteria (single lesion not exceeding 6.5 cm, or up to 3 lesions none greater than 4.5 cm with total tumor diameter up to 8 cm) were classified as pT3A. The other 12 patients with pT3 were assigned pT3B. RESULTS Eighteen patients (10.7%) had HCC recurrence after a median of 243 days after OLT (range 32 to 976 days). The 5-year recurrence-free survival rates for patients with pT1, pT2, or pT3A were loo%, 93.8%, and 88.5%, respectively. The differences between the three groups were not statistically significant (p=0.61 by log-rank test between pT2 and pT3A). The recurrence-free survival was significantly reduced for patients with pT3B (59.3% at 5 years, p=0.006 versus pT2) and for pT4 (27.8% at 3 years, p<O.OOOl versus pT2). The strongest predictor for HCC recurrence in the univariate Cox Proportional Hazards model was HCC stage exceeding the proposed T3A criteria (hazard ratio (HR) 15.4, p<O.OOOl). Other significant predictors for recurrence included microvascular invasion (HR 5.8, p=0.0003), poorly differentiated grade (HR 15.0, p=0.006), alpha-fetoprotein > 500 nglml (HR 4.7, P=0.003) and diagnosis of liver disease other than hepatitis C, hepatitis B or alcoholic liver disease (HR 3.1, P=0.04). The analysis of the impact of pre-operative TACE or ablation treatments was stratified according to HCC stage. In the subgroup of pT2 and pT3 combined at intermediate risk for HCC recurrence, the 1 and 5 year- recurrence-free survival rates were 96.4% and 93.8%, respectively, for the 85 patients who received pre-operative treatments, versus 91.5% and 80.6%, respectively, for the 41 patients who did not received pre-operative treatment (p=0.049 by log-rank test). The positive effect of pre-operative treatments appeared to be greater for the pT3 group (p=0.05) than the pT2 group (p=O.12). Treatment was associated with worse outcome in

the pT4 group (p=O.O2). CONCLUSION: Our results continued to support modest expansion of the tumor size limits based on a larger cohort of patients. Pre-operative TACE or ablation may benefit a subgroup of patients with HCC at intermediate risk for recurrence after OLT, and possibly play a role in preserving excellent survival after modest expansion of the tumor size limits. Disclosures: Nathan M Bass - No relationships to disclose Robert Kerlan - No relationships to disclose Milan Kinkhabwala - No relationships to disclose Jeanne LaBerge - No relationships to disclose John P Roberts - No relationships to disclose Francis Y Yao - No relationships to disclose

4 THE SELECTION OF CALCINEURIN INHIBITOR AFFECTS THE RATE OF RECURRENCE OF PRIMARY BILIARY CIRRHOSIS (PBC). James Neuberger, Bridget K Gunson, Queen Elizabeth Hospital, Birmingham, UK; Stefan G Hubscher, University of Birmingham Medical School, Birmingham, UK; Peter Nightingale, Queen Elizabeth Hospital, Birmingham, UK Introduction: it is now generally accepted that PBC recurs after liver transplantation although the effect on graft survival, at least in the medium term, is small. Identification of factors that are associated with disease recurrence may help in the understanding of the pathogenesis of the disease and may allow a tailored approach to post-transplant management. ethods: all patients grafted for PBC in this unit between 1982 and 2002 were evaluated. Post transplant, patients were maintained on immunosuppression with a calcineurin inhibitor (cyclosporine A (CyA) or tacrolimus (Tac)); azathioprine and corticosteroids. Ste- roids were withdrawn at 3 months. Patients underwent protocol liver biopsies at 1 year and initially at annual intervals and, after 1993, at 3 yearly intervals. The diagnosis of recurrent PBC was made on histologic criteria, including the presence of portal gran- ulomas, inflammatory bile duct lesions and bile duct loss, in the absence of other causes of bile duct damage. To analyse risk factors associated with disease recurrence, both donor and recipient factors were analysed in a univariate and multivariate model. Findings: 485 patients were grafted for PBC: at transplant, the median age was 55 years and median serum bilirubin 15lumol/L. The median follow-up time was 79 months. Overall, recurrence was first diagnosed in about 20% at 5 years and in 35% at 10 years. On univariate analysis, immunosuppression was associated with disease recurrence: use of azathioprine beyond one year and type of calcineurin inhibitor (CyA or Tac) were both associated with recurrence. No other recipient or donor factor was associated with recurrence. The median time to recurrence was 93 months if not taking azathioprine beyond one year and 120 months if taking azathioprine after 1 year (p=0.03)). However on multivariate analysis only immunosuppression with either CyA or Tac was significantly associated with recurrence (median time to recurrence 123 months for CyA and 62 months for tacrolimus, p<O.OOl). This difference was not an effect of the year of transplant or the number or timing of biopsies. Conclusions: The only factor identified that was associated with PBC recurrence was the type of immunosuppression. This should be considered when tailoring immunosuppression to the individual patient Disclosures: Bridget K Gunson - No relationships to disclose Stefan G Hubscher - No relationships to disclose James Neuberger - No relationships to disclose Peter Nightingale - No relationships to disclose

158A AASLD ABSTRACTS HEPATClLOGY, October 2003

5 CLASSIFICATION OF OPERATIVE COMPLICATIONS IN LIVE LIVER DONORS. Christopher R Shackleton, Steven D Colqukoun, Nicholas Nissen, John M Vierling, Paul Marfin, Fred Poordad, Tram Tran, Andrea Peterson, Shannon Hogan, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, CA BACKGR0UND:Accurate delineation of the scope and magnitude of peri-operative donor risk is necessary to better allow for informed consent, to maximize the potential for donor safety, for comparative outcome analysis and ultimately to serve as a key determinant of the utility of adult-to-adult living donor liver transplantation (AALDLT). However, at present, there is lack of uniformity regarding what constitutes a complication in this setting. Moreover, a system to stratify adverse events with respect to their life altering (quantity or quality) impact is lacking. AIMS: 1) to define a graded, inclusive classification schema for both early (E) and late (L) adverse operation-related events in live liver donors a n d 2) to apply this system to a retrospective review of events in individuals undergoing partial hepatectomy for live liver donation at our center. PATIENTS and METHODS From 12/07/ 1999 through 05/29/2003, 195 individuals underwent evaluation liver donation at our center. Of these, 31 (22%, MIF = 20/11, mean age 40 yrs, range 21-56 years) underwent partial hepatectomy and their records were reviewed. The proposed definitions of early and late complications are included in the results tables. RE- SULTS: At a median follow-up of 507 days (range 52-1270 days), 6 of 31 (19.4%) patients had developed 8 complications, 6 early and 2 late. Median donor length of stay (LOS) was 8 days (range, 5-20). Two patients (6.5%) suffered cut-surface bile leaks and one (3.2%) a right colon injury (Grade 3E complications). One patient (3.2%) developed a transient bilateral ulnar neuropathy (Grade 2E). Two patients (6.5%) were readmitted within 30 days of operation for nausea and dyspnea respectively (Grade 1E). One patient underwent repair of an incisional hernia 6 months post donation (Grade 2L). One patient suffered positioning-related brachial plexopathy (Grade 3L). CONCLUSIONS: The definition and adoption of a graded, scale-based system of operation-related adverse events in live liver donors will allow for an inclusive, consistent and uni- versally applicable method to collect, analyze and report donor complications. All AALDLT programs must be encouraged to fully review and report their donor related morbidity, ideally through the creation of a national donor registry

Grade 1E 2E 3E

4E 5E Grade 1L 2L 3L 4L JL

Definition (Early, less than or equal to 30 days) Requiring readmission to hospital after discharge

Requiring non-invasive intervention during the initial hospitalization Requiring operative or other invasive intervention during the initial

hospitalization Acute liver failure requiring liver transplantation Death within 30 days attributable to donation

Definition (Late, greater than 30 days) Resulting in psychosoctal or occupational impairment

Requiring non-hepatobiliary invasive intervention Resulting in a chronic non-hepatobiliary disability

Resulting in chronic hepatic, portal andlor biliary disease Death after 30 days attributable to donation

Number (%) 2 (6.5) 1 (3.2) 3 (9.7)

0 (0) 0 (0)

Number (36) 0 (0)

1 (3.2) 1 (3.2)

Disclosures: Steven D Colquhoun - No relationships to disclose Shannon Hogan - No relationships to disclose Paul Martin - No relationships to disclose Nicholas Nissen - No relationships to disclose Andrea Peterson - No relationships to disclose Fred Poordad - No relationships to disclose Christopher R Shackleton - No relationships to disclose Tram Tran - No relationships to disclose John M Vierling - No relationships to disclose

6 DEFINITIONS AND OUTCOMES OF TRANSPLANTS USING EXPANDED CRITERIA DONOR LIVERS. Sandy Feng, University of Cali$oomia Sun Francisco, Sun Francisco, CA; Iennifer L Bragg-Gresham, Dawn M Dykstra, SRTRIURREA, Ann Arbor, MI; Jefiey D Punch, Meelie DebRoy, University of Michigan, Ann Arbor, MI; Stuart M Greenstein, Albert Einstein College of Medicine, Bronx, NY; Robert M Merion, University of Michigun, Ann Arbor, MI Background: Recently, an expanded criteria donor (ECD) kidney was defined based upon four donor factors known to predispose to graft loss. This definition then engendered a new allocation policy designed to diminish discard and improve outcomes of valuable albeit suboptimal organs. A parallel definition of the ECD liver based upon donor characteristics is needed. The definition may then similarly facilitate consideration of alternative allocation strategies to improve the outcome and utilization of suboptimal livers. Methods: We analyzed 12,412 recipients who underwent transplantion between 711997 and 3/2001 with livers from deceased donors 2 18 years of age. Cox regression was used to analyze the risk of graft loss including death (adjusted for donor race and sex and recipient age, race, sex, status, BMI, NYHA functional status, PRA>lO%, cold ischemia time, ventilator use, serum creatinine, and hepatitis C status). Results: Five donor characteristics were significantly and independently associated with the graft failure including recipient death: age, cardiac arrest after neurological event (arrest), cerebrovascular accident (CVA) as cause of death, any serum sodium > 170 mEq/L, and split or partial liver. The ideal donor was defined as an 18 - 39 year old donor without any of these characteristics. The table below iden- tifies donor categories with a relative risk (RR) of graft failure including recipient death exceeding 1.7 compared to the ideal donor reference group (Ref.). Using a RR of > 1.7 to define the ECD liver, ECD livers accounted for 15.9% of all transplanted livers and 28.8% of all discarded livers in the analysis. During the study, 20.9% of recovered ECD livers were not transplanted, compared with 9.9% of non-ECD livers. Conclusions: This study offers a definition of the ECD liver and analyzes associated discard and failure rates for these organs. The results which stratify transplantation risk based upon donor factors may be used in discussions with liver transplant candidates. In addition, the data can be further analyzed, perhaps in conjunction with recipient factors known to impact graft and patient survival, to consider whether alternative allocation policies may improve transplant outcomes and I or organ utilization of ECD livers. Supported by HRSA, Contract # 231-00-0116

~~

Donor Charxeristic (X = ECD Liver = RR > 1.7) 18-39 40.49 50-59 60-69 270 None Ref. X Arrest or CVA or Na>170 x x Arrest and CVA x x x x Spllffpattial; All other combinations x x x x x

Donor Age Categories (years)

Disclosures: Jennifer L Bragg-Gresham - No relationships to disclose Meelie DebRoy - No relationships to disclose Dawn M Dykstra - No relationships to disclose Sandy Feng - No relationships to disclose Stuart M Greenstein - No relationships to disclose Robert M Merion - No relationships to disclose Jeffrey D Punch - No relationships to disclose

7 EFFICACY AND TOLERABILITY OF PREEMPTlVE INTERFERON (IFN) VERSUS IFN PLUS RIBAVIRIN (RBV) TREATMENT IN HEPATITIS C VIRUS (HCV) INFECTED LIVER TRANSPLANT RECIPIENTS. Norah A Terrault, Mandana Khalili, Stephanie Sfraley, Kathy Bollinger, Nathan Bass, John P Roberts, Nancy A Ascher, University of Culifonuu Sun Francisco, Sun Francisco, CA Recurrent and progressive HCV disease is the most common cause of graft loss in HCV-infected liver transplant (LT) recipients. Strategies to prevent or ameliorate recurrent disease are needed.


Initiation of antiviral therapy in the early post-transplant period, prior to overt evidence of HCV recurrence (i.e. preemptive therapy) may enhance rates of HCV eradication. Aims: To determine the efficacy and tolerability of preemptive IFN versus IFNlRBV in anti-HCV positive LT patients. Methods: Consecutive and eligible LT recipients from a single center were enrolled. The goal was to initiate treatment within 6 wks of LT. Patients were randomized to IFN or IFN plus RBV (400mg daily X 2wks, then 800mg daily X 2 wks, then 1.0-1.2g daily based upon body weight 75 kg). Induction therapy with daily IFN was used for the first 8 wks (1.5MU daily X 2wks, then 3MU daily X 6 wks) followed by 3 MU TIW (N=39) or peg-IFN 1.5 uglkglwk (N=10) for 40 wks. Key inclusion criteria were stable clinical status, Cr45,OOO and WBC>3.0. Dose reductions for side effects, especially cytopenias were standardized. Growth factors were given for neutropenia (ANC<1000) and anemia (Hgb<9.0gldL) beginning 7l2001. Virological (VR) and biochemical responses (BR) were evaluated at end-of-treatment (ET) and 6 mos post-treatment (sustained virological (SVR) and biochemical (SBR) responses). Results: Between 12/99 and 6102, 107 LT for HCV were performed; 63 (59%) patients met eligibility criteria and 49 were enrolled (80% males, median age 50 yrs). Treatment was initiated 5.1 wks (median, range 1.7-9.3) post-LT. A total of 24 LT patients were randomized to treatment with IFN (71% genotype 1,48% high viral load, VL) and 25 to IFN plus RBV (68% genotype 1, 46% high VL). Five patients dropped out after randomization but prior to treatment, 19 discontinued treatment due to adverse events, and 25 patients completed 48 wks treatment. Five patients died during the treatment period of non- treatment related causes. Full doses of IFN and RBV were obtained in 84% and 23% respectively; the median dose of RBV was 360 mglday. ET-BR and SBR were obtained in 64% and 53% of treated patients, with higher rates of ET-BR in patients completing 48 wks treatment (74% vs. 38%, p=0.02). ET-VR and SVR were obtained in 12% and 11% (2 ET-VRs still in follow-up). SVR was more frequent in patients with undetectable HCV RNA by quantitative assay (qHCVRNA) pre-treatment (67% vs 4% with mea- surable qHCVRNA, p=O. 0009). Neither time from LT to treatment, age, receipt of full-dose IFN or RBV, genotype, nor treatment group (table below) were associated with response. Histological disease was mild in the majority of patients at treatment end (78% stage 0 fibrosis and 72% grade 1 or less necroinflammatory activity). Conclusions: Preemptive antiviral therapy was applicable to -60% of transplanted patients. Biochemical responses were frequent but SVRs uncommon. Treatment discontinuation and lowering of RBV doses due to side effects likely reduced SVRs and may have limited our ability to detect differences between treatment groups. The only predictor of SVR was a negative qHCVRNA pre-treatment, which implies that patients with low VL early post-LT may be the best candidates for preemptive therapy. Compared to historical reports, the severity of histological disease was very mild at 1-year post-LT in the majority of treated patients, suggesting preemptive antiviral therapy may provide important histological benefits.

Response by Treatment Group IFN IFN + RBV P value

ET BR 12/22 (55%) 16/22 (73%) 0.21 ET VR 1/21 (5%) 4/22(18%) 017 SBR 10/17(63%) 7/15 (47%) 0.38 SVR 111 5 (7%) 2/13(15%) 0.46 Stages0 at 12 mos 15/17 (88%) 10/15(67%) 0.47 Grade< or = 1 at 12 mos 13/17 (76%) 10115 (67%) 0.52

Disclosures: Nancy A Ascher - No relationships to disclose Nathan Bass - No relationships to disclose Kathy Bollinger - No relationships to disclose Mandana Khalili - Schering Plough: Meeting PartiapantlLecturer; Scientific StudylTrial; Roche Pharmaceuticals: Scientific StudylTrial John P Roberts - No relationships to disclose Stephanie Straley - No relationships to disclose Norah A Terrault - Fugisawa Healthcare Inc: Scientific Study/ Trial; Schering Plough: Scientific StudylTrial; Roche Pharmaceu- ticals: ConsultantlAdvisor; Meeting ParticipantlLecturer; Scientific StudylTrial

8 PATIENT AND GRAFT SURVIVAL AFTER ADULT LIVING DONOR LIVER TRANSPLANTATION COMPARED TO CADAVERIC LIVER TRANSPLANTATION IN PATIENTS WITH CHRONIC HEPATITIS C AN ANALYSIS OF THE UNITED NETWORK FOR ORGAN SHARING DATABASE. Mark W Russo, Joseph A Galanko, Kimberly Beavers, Michael W Fried, Steven L Zacks, Roshan Shrestha, University of North Carolina, Chapel Hill, NC Background: - The cadaveric organ shortage has led to the development of alternative strategies for organ transplantation. Living donor liver transplant (LDLT) is one strategy that has offered many individuals transplantation before they die or become too sick for transplant.Chronic hepatitis C (HCV) is the leading indi- cation for liver transplantation. Preliminary results from small single center studies suggest that recurrent HCV is more common after LDLT compared to cadaveric transplant with concern that graft survival may be lower after LDLT. &: To compare patient and graft survival in HCV recipients who undergo LDLT to cadaveric liver transplant recipients. Methods: We analyzed the United Network for Organ Sharing (UNOS) liver transplant database from January, 1999 - December, 2002. Inclusion criteria included liver transplant recipients 218 years old transplanted from 1999- 2002 with the transplant diagnosis of chronic hepatitis C. Exclusion criteria included subjects who were hepatitis B surface antigen positive, history of prior organ transplant, concurrent kidney or heart transplant. The log- rank test was used to compare survival between the two groups. Results: From 1999-2002 6.6% of adult liver transplants were LDLT. 279 LDLT recipients and 3,955 cadaveric recipients transplanted for end stage liver disease from HCV were identified. The results are shown in the Table:

LDLT (11.278) Cadwwk (n=3,955) Aae beus) 51 51 Male(okr Donor age’ Total blllrubln (mgldl)’ ProthromMn tlme (a)‘ Crdnlne (mg/dl)’ Cold Iachemla (houm)’ Patient and Graft Survlvrl(%) I-yoar graft aurvlval >yew graft survlval 1- year patient survlvrl % y W p&ent 6UNhJal

*p<o.oM)1

59 71 37 An

77 82 63 MI 87 87

77 72

A greater proportion of LDLT recipients were female and LDLT recipients were less ill at the time of transplant.1 and 3 year patient and graft survival were not significantly different between the 2 groups, (p=O.11). If only the pre-MELD era is considered (01l99 thru 2/02) 1 year graft survival for LDLT (n=240) and CLT (n=3322) are 78% and 83%, respectively, p=O.lO. Conclusions: Our analysis demonstrates that short-term patient and graft survival are equivalent in LDLT and cadaveric recipients with HCV suggesting recurrent hepatitis C does not adversely affect survival over this time period. LDLT recipients are less ill at transplantation which did not confer a short-term survival advantage. Continued follow-up should determine the impact of less advanced liver disease at the time of transplant and recurrent hepatitis C after transplant on long-term graft and patient survival in LDLT recipients. Disclosures: Kimberly Beavers - No relationships to disclose Michael W Fried - No relationships to disclose Joseph A Galanko - No relationships to disclose Mark W Russo - No relationships to disclose Roshan Shrestha - No relationships to disclose Steven L Zacks - No relationships to disclose

160A AASLD ABSTRACTS HEPATOLOGY. October 2003

9 INCREASED RISK OF CHOLESTATIC HEPATITIS C IN RECIPIENTS OF GRAFTS FROM LIVING VERSUS CADAVERIC LIVER DONORS. Paul ] Gaglio, Srikar Malireddy, Brian A Levitt, Dianne Lapointe-Rudow, Jay Lefkowitch, Milan Kinkhabwala, Mark W Russo, Jean C Ernond, Robert S Brown ]r, Columbia University College of Physicians and Surgeons, Nezu York, m Introduction: Histologic injury due to recurrent HCV has been reported in up to 90% of HCV infected patients who undergo liver transplantation with a cadaveric graft. However, the natural history of HCV following living donor liver transplantation (LDLT) is not as well described. Anecdotal evidence suggests that HCV recurrence may be more severe in LDLT recipients. We hypoth- esize that post-operative liver regeneration in the partial graft procured from living donors may facilitate HCV replication, or increase the vulnerability of hepatocytes to infection. Methods: We performed a retrospective analysis comparing outcomes, and the incidence, timing, and severity of histologic recurrence of HCV following transplantation in patients who underwent living donor liver transplant compared to recipients of cadaveric organs. Between 12/98 and 3/02,68 HCV infected adult patients (age > 18 years old) underwent liver transplantation for HCV associated cirrhosis. 45 patients received a cadaveric graft (CAD) and 23 received a graft from a living donor (LDLT). Mean time of patient follow up was 25 months, with a range of 6 to 39 months. Elevated serum transaminases, positive HCV RNA, and liver biopsy consistent with histologic evidence of HCV defined recurrence. Cholestatic Hepatitis C (CHC) was confirmed if all of the following criteria were met: serum total bilirubin greater than lOmg/dl with no evidence of extra-hepatic biliary obstruction on ultrasound and cholangiography, and histologic features on liver biopsy consisting of portal expansion, ductular proliferation, and bile stasis with or without hepatocyte ballooning. Immunosup- pression, definition and treatment of rejection were standardized for both CAD and LDLT. Results: When comparing CAD to LDLT, both the incidence of HCV recurrence and time to recurrence were not different. The overall incidence of "severe" sequelae of HCV recurrence, either cholestatic hepatitis, grade 111-IV inflammation, and/or HCV induced graft failure requiring re-transplantation was also not different when comparing CAD to LDLT. However, when comparing CAD versus LDLT, no CAD patient developed cholestatic hepatitis C, compared to 17% of LDLT who developed this complication (p = 0.001). Conclusions: In this patient population, the timing and OVERALL incidence of HCV recurrence were not different when comparing CAD versus LDLT, but the incidence of cholestatic hepatitis was significantly greater in patients with HCV who underwent LDLT. Further multicenter studies are warranted to determine the incidence and risk factors for cholestatic hepatitis C following liver transplantation.

ACR HCV Recurrence Cholestatic Hepatltis C CAD 45 pto 28/45 (62%) 31/45 (69%) 0 Pk LDLT 23 pts 14/23 (61%) 18/23 (79%) 4/23(17%)

Disclosures: Robert S Brown Jr - No relationships to disclose Jean C Emond - No relationships to disclose Paul J Gaglio - No relationships to disclose Milan Kinkhabwala - No relationships to disclose Dianne Lapointe-Rudow - No relationships to disclose Jay Lefkowitch - No relationships to disclose Brian A Levitt - No relationships to disclose Srikar Malireddy - No relationships to disclose Mark W Russo - No relationships to disclose

10 RESISTANCE SURVEILLANCE OF LIVER TRANSPLANTATION PATIENTS WITH LAMIVUDINE- RESISTANT HEPATITIS B VIRUS (HBV) AFTER 96 WEEKS OF ADEFOVIR DIPIVOXIL TREATMENT. Christopher E Westland, Gilead Sciences, Inc., Foster City, GI; Jean-Pierre Villeneuve, H6pital Saint-Luc, Centre Hospitalier de I'Universitk de Montrkal, Montreal, PQ, Canada; Norah A Terrault, UCSF, Sun Francisco, CA; Fabien Zoulim, INSERM, Lyon, France; Carol L Brosgart, Michael Wulfsohn, Michael D Miller, Shelly Xiong, Gilead Sciences, Inc., Foster City, CA Background Lamivudine (LAM) resistance occurs in approximately 40% of chronic hepatitis B (CHB) patients after 2 years of LAM monotherapy. In contrast, resistance to adefovir dipivoxil (ADV) occurs infrequently with 1.6% of CHB patients developing the adefovir resistance mutation rtN236T after 2 years of ADV therapy. Pre-existing LAM resistance mutations or concurrent use of immunosuppressive therapy by LT patients may increase the risk of resistance to ADV. Objective: To determine the incidence of ADV resistance in a clinical trial of liver transplantation (pre and post) patients with LAM-resistant HBV treated with ADV for 96 weeks (LAM therapy was maintained in most patients). Meth- ods: The HBV reverse transcriptase domain was sequenced for LT patients with detectable HBV DNA by PCR (>lo00 copieslml) after 96 weeks of ADV therapy (n=114). In vih-o drug susceptibility was determined following transfection of HepG2 cells with patient-derived HBV clones from baseline and week 96 serum samples. Results: The rtN236T mutation wa!j observed in 21114 patients (1.8%) at week 96. LAM had been discontinued at weeks 16 and 28 after initiation of ADV in these two patients respectively. The baseline LAM-resistant YMDD mutation reverted to wildtype prior to week 96 in both patients. Emergence of rtN236T was associated with rebound in serum HBV DNA and ALT elevation in both patients. In vitro phenotypic analysis showed approximately 4-fold reduced susceptibility to adefovir with rtN236T. However, these adefovir-resistant HBV clones were fully susceptible to LAM and entecavir in vitro. LAM therapy was re-initiated, in addition to the ongoing ADV therapy, after emergence of rtN236T in these patients resulting in a > 2.9 loglo copies1mL reduction in serum HBV DNA in both patients. One patient also had a significant reduction (>80%) in ALT within 5 months of LAM treatment. No other mutations potentially associated with adefovir resistance were detected. Conclusions: Emergence of the adefovir resistance mutation rtN236T was observed infrequently after 2 years in liver transplantation patients (1.8%, 2/114) infected with LAM-resistant HBV, similar to observations in treatment naYve non-liver transplantation patients. The ADV-resistant HBV was sensitive to LAM and addition of LAM resulted in clinical stabiliation in both patients. Disclosures: Carol L Brosgart - Gilead Sciences: Employee Michael D Miller - Gilead Sciences: Employee Norah A Terrault - No relationships to disclose Jean-Pierre Villeneuve - No relationships to disclose Christopher E Westland - Gilead Sciences: Employee Michael Wulfsohn - Gilead Sciences: Employee Shelly Xiong - Gilead Sciences: Employee Fabien Zoulim - No relationships to disclose

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1,2003 AASLD ABSTRACTS 161A

11 ADEFOVIR DIPIVOXIL 10 MG (ADV) FOR THE TREATMENT OF CHRONIC HEPATITIS B IN PATIENTS PRE-LIVER TRANSPLANTATION WITH LAMIVUDINE-RESISTANT PATIENTS. Eugene Schiff, University of Miami, Miami, FL; Ching- Lung Lai, Queen Mary Hospital, Hong Kong, Hong Kong Stefanos Hadziyannis, Hen ry Dunant Hospital, Athens, Greece; Peter Neuhaus, Charifi, Campus Virchow-Klinikum, Berlin, Germany; Norah Terrault, University of California Sun Francisco, Sun Francisco, CA; Pietro Lampertico, Universitt? degli Studi Milano e IRCCS, Ospedale Magsore, Milano, Italy; Hans Tillmann, Hannover Medical School, Hannover, Germany; Samuel Didier, Paul Brousse Hospital, Vilfejuif, France; Nicole Lama, Craig lames, Graeme Cum’e, Carol L Brosgart, Gilead Sciences, Inc., Foster City, CA Background The incidence of lamuvidine resistance is 24% at one year increasing to 70% with 4 years of therapy. Lamuvidine resistance is a significant clinical problem in patients pre-orthotopic liver transplantation (OLT) and is associated with disease progression and death. High serum HBV DNA pre-OLT may prevent patients being waitlisted for transplantation; and, for patients who go on to transplantation, may result in re-infection of the new graft. ADV has potent in vivo and in vitro activity against wild-type and lamuvidine resistant HBV. Objective: To evaluate safety and efficacy of ADV and evaluate the impact on waitlist priority in patients receiving ADV 10 mg in an open-label study of pre-OLT patients with lamuvidine-resistant HBV. ADV was added to existing HBV and immunosuppressive therapy. Methods: One-hundred and twenty-eight pre-OLT patients failing lamuvidine enrolled at 75 centers. The median duration on ADV therapy was 18.7 weeks for the pre-OLT patients. The baseline characteristics were as follows: median serum HBV DNA was 7.4 loglo copieslml, median ALT was 1.8 xULN (75 IUIL), 40% were Child-Pugh- Turcotte (CPT) Class A, 40% were Class B and 21% were Class C. The median time on lamivudine therapy until loss of response was 17 months, serum total bilirubin was >ULN in 66%, serum albumin was <LLN in 55%, and prothrombin time was >ULN in 53% of patients. A retrospective analysis was conducted to evaluate the status of the 128 pre-OLT patients while receiving ADV. Physicians completed an additional CRF for 100 of 128 patients (78%) addressing clinical status of waitlisted patients during treatment. The CRF also assessed if ADV treatment allowed transplantation or changed priority on the transplantation waitlist. Results: At week 48 the median change in serum HBV DNA was -4.1 loglo copieslml, ALT normalized in 78%, albumin in 81%, bilirubin in 50%, and prothrombin time in 83% of patients. Ninety-two percent had stable or improved CPT scores, the survival rate was 84% (Kaplan-Meier estimate). Of the 45 (45%) pre-OLT patients who subsequently underwent liver transplantation, physicians indicated treatment with ADV improved the clinical condition in 38 (84%) patients, thus allowing them to undergo liver transplantation. At the time of follow-up, 55 patients had not been transplanted. In 20 of these patients (36%), treatment with ADV resulted in the clinical condition improving sufficiently to allow removal from the transplantation waitlist or allowed downgrading from high priority to low priority status. Conclusion: Treatment with ADV 10 mg resulted in significant clinical and laboratory improvements, and improved survival in pre-OLT patients failing LAM therapy. In addition, the clinical condition improved to allow a reduction in their priority status for requiring transplantation or significantly reduced serum HBV DNA and improved clinical status to allow transplantation. Disclosures: Carol L Brosgart - Gilead Sciences, Inc.: Employee Graeme Currie - Gilead Sciences, Inc.: Employee Samuel Didier - Gilead Sciences, Inc.: Investigator Stefanos Hadziyannis - Gilead Sciences, Inc.: Investigator Craig James - Gilead Sciences, Inc.: Employee Ching-Lung Lai - Gilead Sciences, Inc.: Investigator Nicole Lama - Gilead Sciences, Inc.: Employee Pietro Lampertico - Gilead Sciences, Inc.: Investigator Peter Neuhaus - Gilead Sciences, Inc.: Investigator Eugene Schiff - Gilead Sciences, Inc.: Investigator Norah Terrault - Gilead Sciences, Inc.: Investigator Hans Tillmann - Gilead Sciences, Inc.: Investigator

12 PROGRESSION AND TREATMENT OF RECURRENT HEPATITIS C AFTER LIVER TRANSPLANTATION IN PATIENTS CO-INFECTED WITH HIV. Michael E de Vera, Bijan Eghtesad, Ashokkumar Jain, John J Fung, University of Pittsburgh, Pittsburgh, PA Although liver transplantation in patients with HW infection in the era of highly active antiretroviral therapy (HAART) has been successful, some have reported significant graft loss in patients with hepatitis C due to its aggressive recurrence post transplant. Here we report the clinical outcomes of hepatitis C recurrence and treatment in 15 patients who underwent liver transplantation between March, 1997 to the present. Immunosuppression consisted of FK and steroids. Results: Three patients were excluded because of early deaths (<30 days) from sepsis (2 patients) or primary non-function. The 12 remaining patients had a mean follow-up of 22.1 months (1.4 - 57.3 months). Four patients have died, none from recurrent hepatitis C (hepatocellular carcinoma, chronic rejection, overwhelming fungal sepsis, and bacterial pneumonia). Two of these patients had biopsy-proven hepatitis C including 1 who developed cirrhosis despite interferon-a and ribavirin. Of the 8 patients who are alive, 7 have biopsy-proven recurrent hepatitis C diagnosed at a mean time of 6.7 5 2.4 months after their transplant. Four subjects are currently on treatment, three with Pegylated-interferonkibavirin. Biochemical response was 75% while virological response was 25%. Histologically, the only patient who cleared HCV still progressed to cirrhosis and 2 other patients had stable hepatitis activity indexes and staging. The remaining patient has not had a follow-up biopsy. All 4 patients on treatment required erythropoeitin andlor G-CSF and 1 patient required suspension of peg-interferon because of hema- tologic side effects. All patients have CD4 counts >200 and undetectable HIV viral loads. Conclusion: Liver transplantation in patients co-infected with HIV and HCV is a successful therapeutic option. We have not had any rapid or aggressive courses of recurrent hepatitis C leading to allograft failure. Thus far, these patients have been able to tolerate treatment and they appear to have a similar short-term response as compared to HCV patients without HIV. It remains to be seen whether HIV and immunosuppression will significantly hasten HCV recurrence with longer

Disclosures: Michael E de Vera - No relationships to disclose Bijan Eghtesad - No relationships to disclose John J Fung - No relationships to disclose Ashokkumar Jain - No relationships to disclose

follow-ups.

162A AASLD ABSTRACTS HEPATOLOGY, October 2003

13 BILE DUCT INJURY IN RESPONSE TO EXPRESSION OF ANTIGEN ON THE SURFACE OF BILIARY EPITHELIUM. Yuki Young, James Buxbaum, Ciera Khuu, UCSF, San Francisco, CA; Benjamin Shneider, Mount Sinai School of Medicine, New York, W; Paul M Allen, Washington University School of Medicine, St. Louis, MO; Marion G Peters, UCSF, San Francisco, CA Local liver immune responses are thought to play a major role in chronic autoimmune diseases directed at biliary epithelium.Using the apical sodium dependent bile acid transporter (ASBT) promoter to drive biliary epithelial cell -specific expression of a membrane form of ovalbumin (OVA), we have previously developed OVA-BIL transgenic mice. Because these mice are tolerant to OVA, we use OVA-specific T cells from OT-1 and OT-I1 transgenic mice, restricted by MHC class I and class 11, respectively, with well defined peptide epitopes specific for OVA to induce biliary damage in a dose dependent manner. AIM: 1) To determine the liver mononuclear cell populations (MNC) involved in necroinflammatory disease, and 2) to determine where adoptively transferred cells home and proliferate. METHODS: 10 million OT-I and 2 million OT-I1 naYve T cells were adoptively transferred to OVA-BIL mice by intraperitoneal injection. At days 0, 5, and 7, liver MNC were isolated by collagenase digestion, purified by discontinuous Percoll gradient centrifugation, and analyzed by flow cytometry. Tail bleeds were performed at days 0, 3, 5, and 7 to follow serum ALT. In a subset of experiments, OT-1 cells were labeled with carboxyfluorescein diacetate succinimidyl ester (CFSE) and analyzed on day 3 and 5 by flow cytometry after adoptive transfer with unlabeled OT-I1 T cells into OVA-BIL mice. RESULTS: OVA-BIL mice develop normally without evidence of disease up to 2 years. After adoptive transfer of OVA-specific T cells, there was a marked increase in serum ALT. CD8+ OT-I T cells were required for liver damage and OVA-specific CD4+ T cells markedly augmented this inflammation. Adoptive transfer of OT-I1 CD4 T cells alone did not induce liver injury. There was extensive portal inflammation in every portal triad, centered around the bile ducts with infiltrating lymphocytes in the bile duct epithelia, apoptotic cells, loss of biliary epithelial cells as well as interface hepatitis. Liver MNC were abundant in OVA-BIL mice and increased after adoptive transfer of OVA-specific T cells. Serum ALT peaked at day 5 (mean 263 IUlml), coincident with liver MNC peak. CFSE labeling studies revealed robust homing of adoptively transferred OT-I CD8 cells to the liver, but not to the spleen, of OVA-BIL mice. The OVA-specific CD8 cells, but not CD4, NK1.l, or CD19 cells, underwent cell division. CONCLU- SION: Recognition of biliary epithelial antigen in OVA-BIL mice induces a necroinflammatory response in the liver as assessed by serum ALT, liver MNC numbers and immunohistochemistry. The magnitude of this response correlates with influx of nahe OVA- specific cytotoxic T cells, which are activated and divide in the liver but not in the spleen. T cell recognition of antigen expressed on bile duct epithelium occurs rapidly, causes biliary specific inflammation with interface hepatitis, which may be a model of autoimmune bile duct injury or cholangiopathy. Disclosures: Paul M Allen - No relationships to disclose James Buxbaum - No relationships to disclose Ciera Khuu - No relationships to disclose Marion G Peters - No relationships to disclose Benjamin Shneider - No relationships to disclose Yuki Young - No relationships to disclose

14 DEVELOPMENT OF AN ANIMAL MODEL FOR

TOLERANCE IN THE CYP2D6 HUMANIZED MOUSE BY VIRAL INFECTION. Urs Christen, Anfje Rhode, La Jolla Institute for Allergy and Immunology, Sun Diego, CA; Eric F Johnson, The Scripys Research Institute, La Jofla, CA; Michael P Manns, Hannover Medical School, Hannover, Germany; Matthias G von Herrath, La Jolla Institute for Allergy and Immunology, Sun Viego, CA The etiology of autoimmune hepatitis (AIH) is only poorly under- stood although the major autoantigens, such as cytochrome P450 2D6 (CYP2D6), could be identified and immunodominant epitopes have been mapped. One major reason for this lack of comprehension is the fact that there are currently only few valid animal models for AIH and none of them involves the autoantigen targeted in humans. Thus, we generated an animal model for human AIH using a natural autoantigen (CYP2D6). Self-tolerance in transgenic mice that express human CYP2D6 in the liver was challenged by infecting these CYP2D6-mice with an Adenovirus- CYP2D6 vector (Ad-2D6) in order to deliver large amounts of the critical antigen to the liver and to provide a inflammatory envi- ronment that would favour autoimmunity. Infection with an empty Adenovirus vector resulted in a transient form of focal necrosis 4 days after infection that subsequently disappeared after 2 weeks. In contrast, infection with Ad-2D6 resulted in extended and persistent infiltration of CD4, CD8 lymphocytes as well as macrophages resulting in confluentlbridging necrosis at week 10 post-infection. In addition, the overall morphology of the liver was massively disturbed after Ad-2D6 infection. At week 10 post- infection, the liver was approximately half the size of the control and its lobules were fused together and rounded up. First indica- tions of fibrosis and hyperplasic nodules become apparent. The overall architecture of the liver was disrupted I disorganized and the liver parenchyma was partially collapsed. Furthermore, the- liver of Ad-2D6 infected mice was surrounded by multiple layers of connective tissue as seen in some stages of liver cirrhosis. Additional signs of cirrhosis started to become apparent in the form of nodules that are entrapped in fibrous tissue. In addition, accumulation of infiltrating cells are visible directly under the liver capsule. These observations indicate that the CYP2D6-mouse displays a persistent form of hepatitis after infection with Ad-2D6 that may form the basis for a novel model system which would allow to study mechanisms involved in the initiation, propagation and precipitation of autoimmune processes involved in human autoimmune hepatitis. Disclosures: Urs Christen - No relationships to disclose Eric F Johnson - No relationships to disclose Michael P Manns - No relationships to disclose Antje Rhode - No relationships to disclose Matthias G von Herrath - No relationships to disclose

AUTOIMMUNE HEPATITIS: BREAKING OF SELF-

15 TOLEROGENIC ANTIGEN PRESENTATION IN THE LIVER. ANTIGEN PRESENTING HEPATOCYTES RE- DIFFERENTIATE DENDRITIC CELL-PRIMED PRO- INFLAMMATORY TH1 CD4 T CELLS TO ANTI- INFLAMMATORY TH2 CELLS. Christiane Wiegard, Johannes Herkel, Peter R Galle, Edgar Schmitt, Ansgar W Lohse, Johannes Gutenberg University, Mainz, Germany Background: In clinical hepatitis, hepatocytes express MHC class I1 molecules; we recently reported that MHC I1 expressing hepatocytes can function as antigen presenting cells that stimulate specific CD4 T cells (Hepatology 2003; 37: 1079-85). To understand the relevance of hepatocellular antigen presentation for hepatic immunity, we now examined whether hepatocytes may induce the differentiation of primary CD4 T cells. Because inflammatory CD4 T cells in the liver are most likely primed by dendritic cells of the draining lymph nodes, we also examined whether hepatocytes may also re-differentiate dendritic cell-primed CD4 T cells. Methods: Primary CD4 T cells from Ovalbumin-specific T cell receptor-transgenic mice were stimulated by antigen presenting hepatocytes from hepatocyte-specific CIITA-transgenic mice or


splenic dendritic cells.The response type was determined by measuring secreted interferon-gamma (IFN) and interleukin-4 (IL-4). Results: We found that antigen presenting hepatocytes by default induced differentiation of primary CD4 T cells to TH2 cells (IFN: 200 Ulml; 1L-4: 1800 Ulml). In contrast, primary CD4 T cells stimulated by dendritic cells differentiated to Thl effector cells (IFN: 2400 Ulml; 1L-4 20 Ulml). However, these dendritic cell- primed Thl type cells, when re-stimulated by hepatocytes, had a decreased capacity to produce IFN (580 Ulml vs. 2800 Ulml after dentritic cell stimulation); and after repeated re-stimulation by hepatocytes, the dendritic-cell primed T cells even differentiated into Th2 cells (IFN: 112 Ulml; IL-4: 1270 Ulml). Conclusions: These data show that antigen presenting hepatocytes induce Th2 differentiation of undifferentiated CD4 T cells. Most nota- bly, even dendritic cell-primed CD4 T cells that are committed to Thl differentiation could be reverted by hepatocytes to Th2 type. Thus, hepatocytes seem to have an extraordinary capacity to promote anti- inflammatory hepatic immune responses. It is therefore conceivable that antigen presentation by hepatocytes associated with clinical hepatitis, in the absence of pro-inflammatory stimuli, seems to down- regulate inflammatory infiltrating T cells. Disclosures: Peter R Galle - No relationships to disclose Johannes Herkel - No relationships to disclose Ansgar W Lohse - No relationships to disclose Edgar Schmitt - No relationships to disclose Christiane Wicgard - No relationships to disclose

16 GLUCOCEREBROSIDE TREATMENT AMELIORATES CON-A HEPATITIS BY INHIBITION OF NKT LYMPHOCYTES A NEW IMMUNEMODULATORY TOOL. Maya Margalit, Ruslana Afper, Nilla Hemed, Victoria Doviner, Yoav Sherman, Hadassah Hebrew University Medical Center, Jerusalem, Israel; Barbara E Thalenfeld, Dean L Engelhardt, Elazar Rabbani, Enzo Biochem Inc., Eramingdale, Ny; Yaron Ilan, Hadassah Hebrew University Medical Center, Jerusalem, Israel Background NKT cells are a unique subset of regulatory lymphocytes with important immune modulatory effects. These cells rec- ognize exogenous glycolipids anchored by a ceramide tail to the MHC-like CDld molecule, expressed by various antigen presenting cells. Glycosylceramides, including the marine sponge-derived a-galactosylceramide can activate NKT cells, leading to exacerbation of hepatitis. Concanavalin A induces immune mediated hepatitis in which NKT cells are key participants. Glucoce- rebroside (GC) is a naturally occurring glycolipid. Aims: To determine the immune modulatory effect of GC in a murine model of Con A hepatitis. Methods: Five groups of BalblC mice were studied Group A and B mice were treated with GC (1.0 pg IP) two hours prior to and two hours following administration of 500 pg Con A, respectively; group C mice were treated with Con A alone; group D mice were treated with GC alone; group E mice did not receive any treatment. The degree of liver damage was evaluated by serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, and by liver histology. The immu- nmodulatory effect of GC was determined by FACS analysis of intrahepatic and intrasplenic lymphocytes for NKT markers, and by ELISA measurements of serum IFNy, IL2, IL4, IL10, and IL12. The effect of GC on NKT lymphocyte proliferation was assessed in vitro. Results: Treatment with GC markedly reduced serum AST and ALT levels in group A compared to group C (143 vs. 600 IU in group A and group C, respectively, for AST; 57 vs. 801 IU in group A and group C, respectively, for ALT, p<0.05). Administration of GC alone did not change AST or ALT levels compared to naive controls. Histological sections of livers from group A mice revealed markedly attenuated damage compared to sections from group C livers, in which massive hepatocyte necrosis was present. The beneficial effect of GC on immune mediated hepatitis was associated with a 20% decrease in the intrahepatic NKT lymphocyte number, and with significant lowering of serum IFNy levels (3725 vs. 5620 pglml in groups A and C, respectively, p<0.05); administration of GC alone led to increased serum IL-12 levels (573 pglml vs. 92 pglml in group D vs. group E, respectively, p<0.05). In vitro, administration of GC decreased NKT cell pro-

liferation by 42% in the presence of dendritic cells, but not in their absence. Conclusions: Administration of GC led to significant amelioration of Con A hepatitis that was associated with a dendritic cell-dependent decrease of NKT cell proliferation in vitro, and with decreased intrahepatic NKT lymphocytes and serum IFNy levels in vivo. These results suggest that the effect of GC may be mediated by inhibition of intrahepatic NKT cells, resulting from competitive displacement of activating elements from the CDld molecule on antigen presenting cells. Glucocerebroside, a naturally occurring glycolipid, holds promise as a new immuno- modulatory agent, with a possible role in treatment of autoimmune hepatitis and other immune-mediated liver disorders. Disclosures: Ruslana Alper - No relationships to disclose Victoria Doviner - No relationships to disclose Dean L Engelhardt - ENZO Biochem Inc.: Board MemberlOfficerl Trustee; Employee Nilla Hemed - No relationships to disclose Yaron Ilan - ENZO Biochem Inc.: ConsultantlAdvisor Maya Margalit - No relationships to disclose Elazar Rabbani - ENZO Biochem Inc.: Board MemberlOfficerl Trustee; Employee Yoav Sherman - No relationships to disclose Barbara E Thalenfeld - ENZO Biochem Inc.: Board MemberlOffi- cerlTrustee; Employee

17 FUNCTIONAL IMPAIRMENT OF CD25+CD4+ REGULATORY T CELLS CHARACTERIZES AUTOIMMUNE HEPATITIS TYPE 2. Yun Ma, Maria Serena Longhi, Dimitrios P Bogdanos, Giorgina Mieli-Vergani, Diego Vergani, King's College Hospital, London, UK Background CD4+ cells constitutively expressing CD25 have a regulatory function, their experimental removal leading to spontaneous autoimmune disease in normal rodents. CD4+CD25+ regulatory T cells suppress both TH1 and TH2 responses, com- peting with effector CD4+ cells in recognizing the same peptide antigens. Their ability of expansion is key to the maintenance of tolerance. Autoimmune hepatitis type 2 (AIH-2) is characterized by T cell immune responses against 6 well-defined regions on cytochrome P4502D6, the autoantigen of AIH-2. Aims: To investigate the ability of expansion of CD4+CD25+ after exposure to non-antigen-specific and CYPZD6-specific stimuli in AIH-2. Methods: CD4+CD25+ T cells were analysed by triple colour flow-cytometry of freshlcryopreserved peripheral blood mononuclear cells (PBMCs) befare and after culture in the presence of a T cell expander capable of maintaining the original T cell function (CD3KD28 Dynabeads T cell expander, Dynal Biotech, Norway) and of 28 synthetic CYP2D6 peptides (10 pMol), spanning the 6 antigenic regions known to induce proliferative CD4+ responses in AIH-2. Patients and controls: Nine patients with AIH-2 (7 female, median age 11.4 yrs, range 2.5 to 21 yrs) were investigated, 3 at diagnosis and 6 while on sustained remission. Nine healthy laboratory workers served as normal controls. Results: Before stimulation, the level of CD4+CD25+ T cells was significantly lower in AIH-2 patients (3.59 2 1.08) than in normal controls (6.39 f 0.87; p=O.O2), a difference present both at diagnosis (2.24 ? 0.56, p<0.005) and during remission (4.25 2 0.35, p=O.Ol). Following exposure to the T cell expander, the level of CD4+CD25+ T cells increased 4.5 times (28.6 2 30.8) in normal controls, but only 1.85 times in AM-2 patients (6.62 ? 1.85, p=O.Ol). Upon exposure to cyMD6 peptides, CD4+CD25+ T cells remained numerically unchanged, in contrast to the PBMCs from the same patients giving a strong proliferative response (up to 6.9 times). Summary & Conclusion: Our data show a numerical and functional impairment of regulatory T cells in AM-2. This defect is likely to be key to the initiation and perpetuation of the autoaggressive process in this condition. Disclosures: Dimitrios P Bogdanos - No relationships to disclose Maria Serena Longhi - No relationships to disclose Yun Ma - No relationships to disclose Giorgina Mieli-Vergani - No relationships to disclose Diego Vergani - No relationships to disclose

164A AASLD ABSTRACTS HEPATOLOGY. October 2003

1s CRYPTOSPORIDIUM PARVUM INVADES HUMAN CHOLANGIOCYTES BY ACTIVATING A CDC42 SIGNALING PATHWAY CAUSING ACTIN REMODELING. Xian-Ming Chen, Bing Q Huang, Patrick L Splinter, James I) Orth, Mark A McNiven, Nicholas F LaRusso, Mayo Medical School, Clinic and Foundation, Rochester, MN Cryptosporidium parvum (CP) opportunistically infects intestinal and biliary epithelia causing worldwide morbidity, especially in patients with AIDS. Epithelial invasion by CP involves host cell membrane alterations resulting in a parasitophorous vacuole that envelops the parasite and a dense-band within the host cell underlying the attachment site; both processes require host cell actin remodeling. Since recent studies in other systems have demonstrated that Cdc42, an actin-associated GTP-binding protein, plays a central role in microbial-induced actin remodeling, we tested the HYPOTHESIS that CP activates host cell Cdc42 and its downstream effectors to induce actin rearrangement and microbial invasion. METHODS: We exposed cholangiocytes derived from normal human liver and immortalized by SV40 transforma- tion to freshly excysted CP sporozoites and applied molecular and morphofogical approaches to test our hypothesis. RESULTS By immunofluorescent and immunoelectron microscopy, we found accumulation of Cdc42 in cholangiocytes at the parasite-host cell interface during CP invasion. We confirmed activation of Cdc42 in infected cholangiocytes by immunoprecipitation using an antibody to PAK4, a downstream effector molecule that binds exclu- sively to the activated form of Cdc42. Phosphatidylinositol 3-kinase (PI-3K), a membrane-associated kinase associated with Cdc42 activation, was also recruited to the site of attachment, as were N-WASP, PAK4 and p34-Arc, downstream effectors of Cdc42. Inhibition of PI-3K by wortmannin or LY294002 blocked CP-induced Cdc42 accumulation. While overexpression in cholangiocytes of a constitutively active mutant of Cdc42 promoted CP invasion (up to 50%), overexpression of function-deficient mutants of PI-3K, Cdc42 or of the WA fragment of N-WASP inhibited CP invasion by 60 - 80 %. Moreover, inhibition of host cell Cdc42 activation by dominant negative mutation inhibited CP-induced actin accumulation, and parasitophorous vacuole and dense-band formation at the attachment site. CONCLUSIONS: These combined data suggest that CP invasion of cholangiocytes (and perhaps other target epithelia) results from the organism’s ability to activate a complex host cell Cdc42 signaling pathway that induces host cell actin remodeling at the attachment site. Category: C 0 4 Cholangiocyte Biology Keywords: Epithelium, biology; Signal transduction; Host defense; Actin; Cy- toskeleton Disclosures: Xian-Ming Chen - No relationships to disclose Bing Q Huang - No relationships to disclose Nicholas F LaRusso - No relationships to disclose Mark A McNiven - No relationships to disclose James D Orth - No relationships to disclose Patrick L Splinter - No relationships to disclose

19 HUMAN HEPATOCYTES TRANSPLANTED INTO IMMUNOCOMPETENT RATS ARE SUSCEPTIBLE TO HEPATITIS C VIRAL INFECTION. George Y Wu, Cherie M WaIton, Denise Olive, Masayoshi Konishi, Catherine H Wu, University of Connecticut Health Center, Farmington, CT BACKGROUND: Hepatitis B (HBV) and Hepatitis C (HCV) infections are a world-wide health concern. Studies of these infections have been hampered by a lack of a convenient animal model. We previously have shown that immunocompetent rats tolerized and transplanted with human hepatocytes can support HBV infection for at least 15 weeks. AIM: To demonstrate that the immunocompetent rat which has been tolerized and transplanted with human hepatocytes can be used to sustain and study HCV infection. METHODS: Sprague-Dawley rats were injected in utero at 16-17 days gestation with one hundred thousand Huh 7 cells (human hepatocyte cell line) to tolerized them to human hepatocytes. One week after birth, the tolerized newborns were intrasplenically transplanted with 5 million Huh 7 cells. One week after transplantation, rodents were inoculated with one hundred thousand HCV RNA copies, genotype l b human serum. Animals were sacrificed at 6 and 12 weeks. The presence of human cells was determined by immunofluorescent staining of cryosectioned liver tissue using antibodies to human albumin. PCR and RT-PCR was used to confirm the presence of human albumin in liver tissue. The presence of HCV was assayed using an antibody to NS5A viral protein, and visualized using a rhodamine labeled secondary antibody. HCV infection in the liver was confirmed by the presence of negative strand RNA using nested PCR. RESULTS: Functional Huh7 cells in the chimeric livers were confirmed by the presence of human albumin mRNA and DNA using RT-PCR and PCR. The presence of human albumin protein in the liver was further demonstrated by immunofluorescence of human albumin in frozen liver sections. Eighty-one percent (n=57) of the tolerized, Huh 7 transplanted rodents were positive for human albumin in the livers. Seventy-two percent (n=36) of the chimeric animals infected with HCV were positive for the presence of NS5A HCV protein from immunofluorescence studies. Livers of control rats that were only tolerized and control rats that were tolerized and transplanted with Huh7 cells, but not inoculated with HCV were negative for NS5A (n=12). HCV viral replication could be demonstrated in livers of tolerized, transplanted and HCV infected rats by the presence of HCV RNA bands of the correct size from nested PCR using negative strand specific primers. CONCLUSION Immunocompetent rats tolerized and transplanted with human hepatocytes can be a useful laboratory model to study HCV infection. (This work was supported by grants from American Liver Foun- dationlBlowitz Ridgeway Foundation [CHW]; NIDDK DK-42182 [GYW], and the Herman Lopata Chair in Hepatitis Research [GYW] and Hepaticus, Inc. [CHW & G Y W ) Disclosures: Masayoshi Konishi - No relationships to disclose Denise Olive - No relationships to disclose Cherie M Walton - No relationships to disclose Catherine H Wu - Hepaticus, Inc.: ConsultantlAdvisor George Y Wu - Hepaticus, Inc.: Consultant/Advisor


20 ACCEPTANCE OF IMMUNOGENIC HEPATOCYTE ALLOGRAFTS UNDER COVER OF DONOR SPECIFIC TRANSFUSION AND COSTIMULATORY BLOCKADE WITH ANTI-CD40L MAB REQUIRES HOST CD8+ T CELLS. Keri E Lunsford, Donghong Gao, Ginny L Bumgardner, The Ohio State University Medical Center and College of Medicine and Public Health, Columbus, OH We have previously observed that allogeneic hepatocellular transplants are highly immunogenic and are resistant to immunosuppressive therapy with a variety of agents. Donor specific transfusion in combination with anti-CD40L mAb is highly effective in inducing prolonged survival of skin and myoblasts and inducing indefinite and donor-specific tolerance to heart and islet allografts. The proposed mechanism of action for DST and anti- CD40L mAb suggests peripheral deletion of alloreactive CD8+ T cells and induction of a regulatory CD4+ T cell population. Resis- tance to induction of indefinite acceptance has been attributed to peripheral reappearance of alloreactive CD8+ T cells. In preliminary studies, we observed that DST and anti-CD40L mAb prolonged FVBlN hepatocyte (HC) survival in C57E3L/6 mice to median survival time (MST) of 88 days and induced indefinite acceptance (>90 days) in 43% of mice. HC rejection occurs by CD4-dependent and (CD4-independent) CD8-dependent pathways. This model permits evaluation on these two pathways sep- arately. The current studies address the hypothesis that DST and anti-CD40L mAb induces prolonged HC allograft acceptance by inducing immunoregulation of both alloreactive CD4+ and CD8+ T cells. Methods: FVBlN (hAlAT-FVBIN, H-24) HCs were transplanted into CD4 KO, CD8 KO, and C57BL/6 (all H-2b) mice. Hc survival was monitored by detection of reporter hAlAT protein in serum by ELISA. For comparison, donor-matched islets were transplanted into streptozotocin-induced diabetic CD8 KO (H-2b) mice, and survival was monitored by blood glucose. Recipient mice received peritransplant administration of DST ( 1 0 ~ 1 0 ~ FVBlN splenocytes, day -7) and anti-CD4OL mAb (1.0 mg, ip, d-7, -4, 0, 4). Some CD8 KO hosts were reconstituted CD8+ T cells (2x107 iv, d-10). Results: When the CD8-dependent rejection was studied in isolation (CD4 KO mice), DST and anti-CD4OL mAb prolonged HC survival to MST of 35 days (N=4) compared to 10 days in untreated CD4 KO (N=7); however, this was not significantly different from anti-CD40L mAb alone. When CD4-dependent rejection was studied in isolation (CD8 KO mice), HCs were unexpectedly rejected with MST of 7 days (N=8) despite DST and anti-CD40L mAb treatment. In contrast, islets of the same strain were accepted indefinitely in CD8 KO mice (N=5, MST>70 days). Since this siraiegy effectively controlled HC rejection in C57BL16 mice which have both CD4- and CD8-dependent pathways available, the collective results suggested that perhaps host CD8+ T cells were necessary for the beneficial effects of the DST and anti-CD40L mAb. To determine whether CD8+ T cells were required for induction of longterm HC survival with DST and anti- CD40L mAb, CD8 KO HC recipients were reconstituted with CD8+ T cells prior to DST and anti-CD4OL mAb treatment. CD8- reconstituted CD8 KOs accepted HCs for MST of 56 days. Con- clusion: The effects of DST and anti-CD40L mAb on combined CD4- and CD8-initated HC rejection are more pronounced than on either pathway alone. CD8+ T cells appear to be required for induction of longterm HC survival under cover DST and anti- CD40L mAb, which offers an apparently distinct mechanism compared to the existing paradigm for the mechanism of action of DST and anti-CD40L mAb. Disclosures: Ginny L Bumgardner - No relationships to disclose Donghong Gao - No relationships to disclose Ken E Lunsford - No relationships to disclose

21 HEPATIC STELLATE CELLS (HSC) ARE PERTURBED BY HEPATOCYTE TRANSPLANTATION IN THE LIVER AND HSC PERTURBATION IMPROVES CELL ENGRAFTMENT. Daniel Benten, Vinay Kumaran, Brigid Joseph, Sanjeev Gupta, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, hJY Engraftment of transplanted cells in the liver is affected by cell- cell interactions involving hepatic endothelial cells and Kupffer cells. The proximity of transplanted cells to HSC suggested that HSC could promote cell adhesion and extracellular matrix remodeling during cell engraftment. To investigate cell-cell interactions in the liver, we analyzed HSC activation in DPPN- rats transplanted intrasplenically with F344 hepatocytes. Analysis of tissues by immunostaining from animals 6h, 24h, 3d and 7d after cell transplantation showed appearance of desmin +ve HSC in peri- portal areas, reaching a peak on day 3 (4-10 fold increase in desmin f v e HSC in cell recipients, p<O.OOl). Using combined immunostaining and DPPIV histochemistry, desmin +ve HSC were often observed in the immediate vicinity of transplanted cells. However, a-smooth muscle actin (SMA) was not expressed in HSC perturbed by cell transplantation, whereas CCl&reatment in control animals induced SMA expression in HSC, as shown by tissue immunostaining, as well as western blots of tissue extracts. After cell transplantation, perturbed HSC expressed desmin ex- tensively, especially in areas with cell transplantation-induced ischemia and consequential GGT expression. To examine whether desmin +ve HSC were perturbed following activation of Kupffer cells by cell transplantation, we administered carbon particles to hepatocyte recipients intrasplenically. These studies established that the majority (up to 72%) of desmin +ve HSC were located directly adjacent to carbon containing activated Kupffer cells. As Kupffer cells are activated within 6 hrs after cell transplantation, whereas HSC were perturbed maximally at a later time, we rea- soned that these cell-cell interactions were likely mediated by soluble factors. To demonstrate whether TNF-alpha plays a role in the stellate cell activation process, we transplanted hepatocytes into animals treated with the TNF-alpha-blocker etanercept. However, etanercept did not prevent perturbation of HSC, suggesting that factors other than TNF-alpha must be involved. To eliminate the component of ischemia-mediated cell activations, we treated animals with intrasplenic nitroglycerine infusion before and during cell transplantation, which resulted in marked attenuation of hepatic GGT expression. Interestingly, desmin +ve HSC were now distributed throughout the entire liver lobule, with 3-5 fold greater prevalence, compared to rats treated with cells alone without nitroglycerine, p<O.OOl, suggesting that circulating soluble factors reached HSC more effectively. In contrast, treatment of animals with nitroglycerine alone did not perturb HSC. To determine effects on cell integration, bile canalicular reconsti- tution was analyzed with DPPIV and ATPase co-stainings. Nitro- glycerine pretreatment resulted in superior parenchymal integration of transplanted cells, in proximity with desmin +ve HSC. Conclusions: Transplantation of cells in liver sinusoids activates desmin, but not SMA, expression in HSC. Activated Kupffer cells are likely mediators of HSC perturbation. Improved cell engraftment following perturbation of HSC indicates that extracellular matrix remodeling could facilitate this process. These findings offer ways to further optimize liver repopulation with transplanted cells. Disclosures: Daniel Benten - No relationships to disclose Sanjeev Gupta - No relationships to disclose Brigid Joseph - No relationships to disclose Vinay Kumaran - No relationships to disclose


22 IN VIVO EVALUATION OF SURVIVAL AND FUNCTION OF PORCINE HEPATOCYTES IN RECIPIENT MICE. Ryuta Nishitai, Bruce E Knudsen, Timothy B Hummer, Kim A Buffers, Kiyoshi Ogata, Cody A Koch, Jefiey L Platt, Mayo Clinic, Rochester, M N Background Hepatocyte transplantation has been of much inter- est as a biological liver support. How to treat hepatocytes to achieve optimum function has been uncertain. Cultured, cryopreserved and hypothermically preserved hepatocytes have been employed for clinical hepatocyte transplantation, but the efficacy was rarely compared between those cell sources. Using a xenoge- neic hepatocyte transplantation model, the function of transplanted hepatocytes was quantified in vivo. Methods: Porcine hepatocytes were isolated by a two-step collagenase technique. The hepatocytes were: (1) immediately used; (2) kept in UW solution at 4°C; (3) cultured in supplemented Williams E medium; or (4) cryopreserved in LJW solution with 10% DMSO before use. The viability of hepatocytes was determined by trypan blue exclusion, and 1 x lo6 viable hepatocytes were injected into the spleens of Rag-2-defficient mice. To evaluate the function of transplanted hepatocytes, the porcine albumin level in the recipient plasma was determined by a sandwich ELISA. The number of surviving porcine cells in the recipients' spleen was estimated by a quantification of porcine genomic DNA sequences. Results: The viability of hepatocytes was as follows: freshly isolated hepatocytes, 92.2 2 1.9%; 24 hours, 48 hours, and 72 hours at 4"C, 85.8 t 3.1, 74.3 i 1.9, 71.0 i 3.2%; cryopreserved hepatocytes after thaw, 65.0 2 2.6%; cultured hepatocytes after dissociation, 78.4 t 6.3% (means t SE). After transplanting comparable numbers of viable hepatocytes, the porcine albumin concentration was found to be lower in recipients of hypothermically-stored (Group 2) and cultured hepatocytes (group 3) than recipients of fresh hepatocytes (Group 1). Cryopreserved hepatocytes (group 4) failed to secrete any albumin. Because the half-life of porcine albumin in Rag-2- deficient mice was 13.5 hours, the porcine albumin concentration in the recipient plasma reflected real-time albumin secretion from the transplanted hepatocytes. The porcine genomic DNA in the recipient spleen was quantified 4 weeks after transplantation. Fewer cells were found in the hypothermically preserved hepatocyte-recipients (group 2). Therefore, the lower level of the porcine albumin secretion in the group 2 was mainly attributable to the failure of the transplanted hepatocytes to survive. The amount of porcine genomic DNA was comparable between cultured hepatocyte-recipients and freshly isolated hepatocyte-recipients, although the plasma of cultured hepatocyte-recipients included less porcine albumin. It suggested that the hepatocytes had dediffer- entiated during culture and secreted less albumin thereafter in vivo. The cultured hepatocytes did not seem to differentiate again in murine spleen. Conclusions: Both the survival and differentiation of hepatocytes were important to maintenance of good function in vivo. The hypothermically preserved and cryopreserved hepatocytes did not survive long after transplantation contrary to their good viable look. Cultured hepatocytes showed relatively good survival, although their dedifferentiation was not reversible resulting in poor outcome. Freshly isolated hepatocytes are rec- ommended for cell transplantation. Disclosures: Kim A Butters - No relationships to disclose Bruce E Knudsen - No relationships to disclose Cody A Koch - No relationships to disclose Ryuta Nishitai - No relationships to disclose Kiyoshi Ogata - No relationships to disclose Jeffrey L Platt - No relationships to disclose Timothy B Plummer - No relationships to disclose

23

DIFFERENTIATION AND PROLIFERATION OF BONE MALLOW CELLS INTO HEPATOCYTES. Tsuyoshi Ishikawa, Shuji Terai, Kouji Aoyama, Kaoru Omori, Isao Sakaida, Yamaguchi University School of Medicine, Ube-Yamaguchi, Japan; Hiroshi Nishina, University of Tokyo, Tokyo, Japan; Kiwamu Okita, Yamaguchi University School of Medicine, Ube-Yamaguchi, Japan Obiective; We had developed an in vivo model to monitor the trans-differentiation and proliferation of BMCs into functional hepatocytes via hepatoblast phenotype (GFPICC14 model). In this model, transplanted GFP-positive BMCs via tail vein efficiently migrated to the peri-portal area of liver lobules under CC14- induced chronic liver damage condition. Transplanted BMCs gradually proliferated and spread from the peri-portal area (zone 1) into the central area (zone 2). Under persistent liver damage condition, BMCs trans-differentiated into functional hepatocytes. Previous analysis had shown that inflammatory signals had been important for the trans-differentiatin of BMCs. In this study, we focused on growth factors and analyzed which affected the transdifferentiation and proliferation of BMCs into hepatocytes in GFPl CC14 model. Materials and methods; Immunohistochemical staining and immunofluorescent double staining with antibody of GFP, several growth factors and their receptors were performed in GFPICCl4 model. Hepatocyte growth factor (HGF), epidermal growth factor (EGF), fibroblast growth factor (FGF), vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), and transforming growth factor (TGF) were analyzed. The percentage of stained area was quantified in the sections at thirty random fields (n=6 in each group), and statistical analysis was performed using PLSD test (ANOVA). Results; The most significant result was shown in fibroblast growth factors (FGFI, FGF2) and their receptors (Flg, Bek). In immunohistochemical staining, the stained region migrated and increased from zone1 into zone2 of liver lobules with the time after BMT. In immunofluorescent double staining, co-expressions both GFP and FGFs, FGF-receptors were detected at the same distribution. The percentage of stained area of FGFs and FGF- receptors gradually increased with significant difference (The data was shown in Table 1). Although expressions of other growth factors and their receptors were detected, the significant differences were not shown. Conclusions; FGFs are the most important growth factor to trans- differentiate and proliferate BMCs into hepatocytes. Table 1: The percentage of stained area in GFPICC14 model

FIBROBLAST GROWTH FACTORS ENHANCE THE TRANS-

lweek after BMT 4weeks after BMT FGFI 6.1 t 1 3 7 5 t l T FGF2 5.8 * 1.3 7.1 * 1.T Flg 5.3 f 1.1 6.7 f 1.2 Bek 5.4 f 0.9 6.8 i 0.9' C-Met 55* 1.1 5 .6 t1 .5

Values are given as mean t s.e.m. n=6 in each group. ' showed significant difference compared with the value at lweek (p<O.Ol).

Disclosures: Kouji Aoyama - No relationships to disclose Tsuyoshi Ishikawa - No relationships to disclose Hiroshi Nishina - No relationships to disclose Kiwamu Okita - No relationships to disclose Kaoru Omori - No relationships to disclose Isao Sakaida - No relationships to disclose Shuji Terai - No relationships to disclose


24 PROLONGED SURVIVAL OF PORCINE HEPATOCYTES IN CYNOMOLGUS MONKEYS. H Nagata, R Nishitai, C Shirota, J Zhang, University of Nebraska Medical Center, Omaha, NE; C A Koch, Mayo Clinic, Rochester, MN; J Cai, University of Nebraska Medical Center, Omaha, NE; M Awaad, H J Schuurman, Immerge BioTherapeutics, Inc., Charlestown, MA; U Christians, University of Colorado Health Sciences Center, Denver, CO; J L Platt, Mayo Clinic, Rochester, MN; Ira J Fox, University of Nebraska Medical Center, Omaha, NE Introduction: Porcine hepatocyte xenografts can restore hepatic function in decompensated cirrhotic rats. While hepatocyte xeno- transplants are less invasive than whole liver transplants and resist infection by hepatitis viruses, their survival is thought to be limited by a severe immune response to the graft. Here we report that contrary to that view, porcine hepatocytes can survive and function for many months in non-human primates treated with conventional immune suppression. Materials and Methods: Three 6-7 kg male cynomolgus monkeys underwent intrasplenic transplantation with 1-2 billion CFDA-SE labeled, freshly isolated pig hepatocytes. Immune suppression included induction with 15mglkg IV Thymoglobulin on days -2 and -1, lOOmgld IV methylprednisolone on days 0 and +1, and 5mg basiliximab on days 0 and +4, and maintenance immune suppression with cyclosporine (trough level 200-250ng/ml), RAD 0.1-0.5mglkgld IV, and FTY720 O.3mglkgld IV. Monitoring included anti-pig antibody levels (anti-gal and non-gal specific antibodies) and serum pig albumin (sensitive ELISA). Results: Each recipient exhibited prolonged survival and function of transplanted porcine hepatocytes. In the 1st recipient, pig albumin in the serum reached 9mglL but the recipient expired 25 days after transplantation from disseminated CMV infection. The spleen of this animal contained numerous fluorescence-labeled engrafted pig hepatocytes. To prevent CMY, the 2nd recipient received prophylactic Gancyclovir and maintained serum pig albumin for approximately 90 days. To neutralize high anti-gal antibody levels, the 3rd recipient also received soluble Gal-glyco- conjugate GAS 914 (5mglkgld). In this animal, hepatocyte transplants on days 0, 84, and 111 resulted in persistence of circulating pig albumin to more than 240 days after transplantation. Engraft- ment at 40 days was confirmed by ASGPR-directed nuclear scanning. This animal showed no change in anti-gal antibodies but developed IgG antibodies to non-Gal porcine epitopes. Conclusion: Prolonged survival and enduring function of porcine hepatocytes can be achieved in primate recipients using conventional chronic immune suppression. Generation of an anti-pig antibody response does not apparently lead to graft dysfunction. Disclosures: M Awaad - Immerge BioTherapeutics, Inc.: Employee J Cai - No relationships to disclose U Christians - No relationships to disclose Ira J Fox - Immerge Biotherapeutics, Inc.: Other: Collaborator C A Koch - No relationships to disclose H Nagata - No relationships to disclose R Nishitai - No relationships to disclose J L Platt - No relationships to disclose H J Schuurman - Immerge BioTherapeutics, Inc.: Employee C Shirota - No relationships to disclose J Zhang - No relationships to disclose

25 FIBROCYSTIN, THE ARPKD PROTEIN, IS LOCALIZED TO CHOLANGIOCYTE CILIA AND IS DISRUPTED IN THE ORTHOLOGOUS RAT MODEL, PCK. Tatyana VMasyuk, Bing Q Huang, Anatoliy I Masyuk, Patrick L Splinter, Christopher J Ward, Xiofang Wang, Rachaneekom Punyashthiti, Peter C Ham’s, Vicente E Torres, Nicholas F LaRusso, Mayo Medical School, Clinic and Foundation, Rochester, M N Biliary dysgenesis leading to bile duct dilatation, cyst development and/or congenital hepatic fibrosis is seen alone or in combination with polycystic kidney disease (PKD). Previously, we showed that a rodent orthologous for autosomal recessive PKD (ARPKD), the PCK rat, has a splicing mutation IVS35-2A-T in Pkhdl (the gene coding for fibrocystin) and displayed extensive postnatal remodeling of the biliary tree resembling human ARPKD. Recent studies have indicated a possible role for primary cilia in renal cyst formation, but involvement of these organelles in related liver disease has not been demonstrated. We employed scanning (SEM), transmission (TEM), immonoelectron (IEM) and immunofluorescent (IMF) microscopy to examine the expression of fibrocystin, the protein product of Pkhdl, in cholangiocytes and its role in biliary cyst formation using specific monoclonal and polyclonal antibodies. We also designed small interfering RNAs (siRNAs) targeting nucleotide 6830-6851 of the Pkhdl coding sequence to determine the effect of fibrocystin inactivation on ciliary structure. Experiments were performed on intrahepatic bile duct units (IBDUs) isolated from normal rats and on liver cysts isolated from PCK rats. RESULTS: In normal liver by SEM and TEM, each cholangiocyte possessed a single cilium projecting into the lumen. IMF and IEM microscopy using specific antibodies against fibrocystin and acetylated a-tubulin (a known ciliary component) demonstrated that fibrocystin was localized to cholangiocyte cilia. In the PCK rat, cilia were abnormal-appearing with bulbous exten- sions, shorter than normal (3.8622.16j~m, vs. 6.6821.67prn; p<O.OOl) and very heterogeneous in length (range 0.24 - 6.31j~m). IMF and IEM microscopy showed that cilia in biliary cysts were devoid of fibrocystin. Normal IBDUs treated with siRNA to silence Pkhdl (mRNA level inhibited by 80%) did not express fibrocystin and were significantly decreased in length compared to IBDUs treated with scrambled siRNA (2.4221.51pm vs. 5.9121.32pm; p<O.OOl). CONCLUSIONS: Our results suggest that fibrocystin is required for the maintenance of cholangiocyte cilia under normal conditions. Mutations to Pkhdl, as seen in the PCK rat, result in biliary cystogenesis, abnormalities in ciliary morphology, and diminished fibrocystin expression in cilia. The data support the notion that biliary cystogenesis in the PCK rat, and possibly in human ARPKD, is associated with defects in cholangiocyte cilia. Disclosures: Peter C Harris - No relationships to disclose Bing Q Huang - No relationships to disclose Nicholas F LaRusso - No relationships to disclose Anatoliy I Masyuk - No relationships to disclose Tatyana V Masyuk - No relationships to disclose Rachaneekorn Punyashthiti - No relationships to disclose Patrick L Splinter - No relationships to disclose Vicente E Torres - No relationships to disclose Xiofang Wang - No relationships to disclose Christopher J Ward - No relationships to disclose


26

REGULATION AND FUNCTIONAL IMPAIRMENT OF THE ORGANIC CATION TRANSPORTER 1 (OCT1) IN RAT LIVER. Gerald U Denk, Carol ] Soroka, Albert Mennone, Yale University School of Medicine, Liver Center, New Haven, CT; Hermann Koepsell, Bayensche Julius-Maximilians-Universitat, lnstitut f i r Anatomie und Zellbiologie, Wiirzburg, Germany; Ulrich Beuers, Ludwig-Maximilians- Universitat, Medizinische Klinik 11, Klinikum Grophadern, Munich, Gemany; James L Boyer, Yale University School of Medicine, Liver Center, New Haven, CT Backpound: The liver plays a major role in the biotransformation and elimination of various therapeutic agents and xenobiotics, many of which are organic cations. In 1994 the first organic cation transporter, Octl, was isolated from rat kidney through expression cloning (Grundemann et al., Nature 1994; 372 549-52). Many physiological substances (e.g. choline, thiamine, transmitters) and xenobiotics (e.g. metformin, azidothymidine, cytosinarabinoside, tetraethylammonium (TEA)) are substrates of Octl. Rat Octl is expressed at the basolateral membrane of hepatocytes, proximal renal tubules, and enterocytes. Although cholestasis alters the expression of several basolateral and canalicular transport proteins, nothing is known about the effects of cholestasis on hepatic cation homeostasis and transport. Aim: To investigate the effect of obstructive cholestasis on Octl expression in rat liver and kidney and on organic cation transport. Methods: Male Sprague-Dawley rats were subjected to bile duct ligation (BDL) or sham surgery. Animals were sacrificed after 3, 7, and 14 days and tissues were harvested for Western analysis, real-time RT-PCR, and immunohistochemistry (n=3-5 each group). To assess functional effects of BDL on organic cation transport, the model Octl substrate TEA (0.2 mg [14C]-TEA / kg bw plus 1.1 mg TEA I kg bw), was administered i.v. to male Sprague-Dawley rats 14 days after BDL or sham surgery, respectively (n=4-6 each group). After 1 h the distribution of radioactivity was determined. Results: Western analysis of total membranes revealed a significant decrease of Octl protein expression in cholestatic livers. Three days after BDL hepatic Octl protein levels were 42.1?17.7% of controls (RO.01). After 7 and 14 days of BDL there was a further loss of Octl protein in the liver (15.5?4.7% and 8.6i2.7% of controls, respectively, R 0 . 0 5 ) . In contrast, there were no significant changes of Octl protein expression in kidneys even 14 days after BDL. Real-time RT-PCR demonstrated a decrease of hepatic Octl mRNA levels after BDL to 77.2?12.7%, 40.7i8.1% (P<0.05), and 50.3-C7.5% (R0.05) after 3,7, and 14 days, respectively. In contrast, there was a significant increase of Octl mRNA levels in BDL kidneys (179.4?24.7% of controls (RO.01)) but only after 3 days. Thereaf- ter, kidney Octl mRNA levels returned to normal. Tissue immunofluorescence corroborated the data from Western analysis. Control liver sections showed the typical distribution pattern of Octl in the hepatocytes surrounding the central veins. However, 14 days after BDL only a weak signal was detected. Functional studies confirmed these findings since the hepatic accumulation of [14C]-TEA in 14 day BDL rats was reduced to 29.6?10.9% of controls (P<O.OOl). Conclusion: Obstructive cholestasis results in progressive down-regulation of Octl in rat liver which is associated with a reduced hepatic uptake of the Octl substrate TEA. These findings suggest that the hepatic uptake of therapeutic agents that are small organic cations may be impaired in cholestatic liver diseases. Disclosures: Ulrich Beuers - No relationships to disclose James L Boyer - No relationships to disclose Gerald U Denk - No relationships to disclose Hermann Koepsell - No relationships to disclose Albert Mennone - No relationships to disclose Carol J Soroka - No relationships to disclose

OBSTRUCTIVE CHOLESTASIS RESULTS IN DOWN- 27

VIA CHOLESTEROL 7 a HYDROXYLASE PROMOTER FACTOR (CPF) AND IS HEPATOPROTECTIVE IN OBSTRUCTIVE CHOLESTASIS. Alan Bohan, Wen-Sheng Chen, Lee A Denson, Matthew A Held, James L Boyer, Yale University School of Medicine, New Haven, CT Background. The multidrug resistance associated protein 3(MRP3/Mrp3/ABCCB/Abcc3) is up-regulated in obstructive cholestasis and is thought to convey hepatoprotection by functioning as a basolateral bile salt export pump. We have previously reported the association between Mrp3 and CPF (FTFILrh-1) induction and hepatocyte protection in bile duct ligated (BDL) mice (Hepatology 2002;36(4):241A); and that Mrp3 expression is induced by ligands for nuclear hormone receptors (NHRs) and that one of these, CPF, directly up-regulates MRP3 promoter activity (Hepatology 2002;36(4):323A). We hypothesized that some of the factors responsible for the up-regulation of Mrp3 may include cytokines and may exert their activity via CPF. Methods. We performed sham surgery and bile duct ligation on wildtype C57BL6J (WT) and Tnfa Receptor I knockout (TnfrI-l-) mice. He- patic histology, serum and tissue bile acid levels and Mrp3 and Lrh-1 expression were determined. HepG2 cells were treated with cytokines or bile acids and expression of MRP3 and CPF were assessed. Electrophoretic mobility shift assays were performed using both murine and tissue culture nuclear proteins to determine the degree of CPF binding to the response elements on the Mrp3 promoter. Activity of the 0.5kb MPR3 promoter, containing both intact and mutated adjacent CPF response elements (REs), which had been transfected into HepG2 cells, was determined by luciferase assay after co-transfection with cpf or treatment with Tnfa. Results. Wildtype mice manifested significantly less histological necrosis, higher serum bile acids and lower hepatic bile acids than TnfrI-l- mice. This was associated with hepatic upregulation of Lrh-1 and Mrp3 in WT, a response that appeared absent in TnfrI-l-, mice. CPF and Mrp3 RNA and protein were up-regulated in HepG2 cells after treatment with Tnfa, ILlp or CDCA. EMSA demonstrated significantly increased DNA binding to adjacent CPF response elements (RE) from the Mrp3 promoter in WT BDL compared to TnfrI-/- BDL mice, and in cells treated with Tnfa, ILlp or CDCA. Furthermore, activity of the MRP3 promoter was up-regulated by co-transfection with CPF or treatment with Tnfa in HepG2 cells, while combined mutation of the CPF REs abolished these effects. Conclusion. Up-regulation of Mrp3 appears to be hepatoprotective in obstructive cholestasis. MRP3 expression is up-regulated by cytokines and bile acids. This is associated with an increase in DNA binding to the CPF RE on the MRP3/Mrp3 promoter in mice and HepG2 cells, and upregulation of Mrp3 promoter activity via adjacent CPF elements in transfected HepG2 cells. Tnfa appears to up-regulate Mrp3 via CPF activation, the therapeutic manipulation of which may lead to new treatments for cholestatic liver disease. Disclosures: Alan Bohan - No relationships to disclose James L Boyer - No relationships to disclose Wen-Sheng Chen - No relationships to disclose Lee A Denson - No relationships to disclose Matthew A Held - No relationships to disclose

MRP3/MRP3(ABCC3/ABCC3) IS UP-REGULATED BY TNF (Y


28 TAUROCHOLATE FEEDING PREVENTS THE FUNCTIONAL DAMAGE OF INTRAHEPATIC BILE DUCTS INDUCED BY ADRENERGIC DENERVATION IN A PIJK DEPENDENT MANNER. Marco Marzioni, The Texas A & M University System HSC COM, Temple, TX; Shannon Glaser, Heather Francis, Silvia Taffetani, Scoff and White Hospital, Temple, rX. Luca Marucci, Antonio Benedetti, University of Ancona, Ancona, Italy; Domenico Alvaro, University of Rome La Sapienza, Rome, Italy; Jo Lynne Phinizy, Scoff and White Hospital, Temple, m Brandy Baumann, Julie Venter, The Texas A 6 M University System HSC COM, Temple, rX; Yoshiyuki Ueno, Tohoku University School of Medicine, Sendai, Japan; Gianfranco Alpini, The Texas A b M University System HSC COM and Central Texas Veterans HCS, Temple, TX Cholangiocytes are the target cells of chronic cholestatic liver diseases (i.e., cholangiopathies), characterized by the dysregula- tion of the balance between apoptosis and proliferation that leads to changes in ductal bile secretion. In rats with bile duct ligation (BDL), there is increased cholangiocyte proliferation and enhanced basal and secretin-stimulated ductal secretion. We have shown that both cholinergic (by vagotomy) and adrenergic b y administration of a single intraportal injection of 6-hydroxydopa- mine (60HDA)I denervation impairs the proliferative and secretory responses of intrahepatic bile ducts to BDL through an increase in cholangiocyte apoptosis. We have shown that bile acids and nerves co-ordinately regulate the balance between cholangiocyte apoptosislproliieration in hyperplastic rat livers. In BDL rats, while ursodeoxycholate and tauroursodeoxycholate feeding prevents the loss of bile ducts caused by vagotomy in a CaZ+/PKC-dependent manner, taurocholate feeding prevents vagotomy-induced duct damage in a PI3K dependent manner. No information exists regarding the interaction between bile acids and adrenergic innervation in the regulation of cholangiocyte function. Thus, we tested the hypothesis that taurocholate feeding protects from bile duct damage induced by adrenergic denervation by 6-OHDA. Methods: Immediately after BDL, rats received a single intraportal injection of 6-OHDA (which induces degen- eration of adrenergic terminal fibers, 50 mglKglbody weight) or vehicle, and subsequently were fed 1% taurocholate or control diet in the presence of daily injections of wortmannin (a PI3K inhibitor, 0.7 mgl kg body weight) or a control solution. We used 1 week BDL rats as control animals. Seven days later, we evaluated cholangiocyte apoptosis by : (i) TUNEL assay in liver sections; and (ii) measurement of caspase 3 activity and protein expression for cleaved pro-caspase 3, and the number of purified cholangiocytes positive for annexin-V. Cholangiocyte proliferation was evaluated by measurement of the number of PCNA- and CK-19-positive cholangiocytes in liver sections, and PCNA immu- noblots in pure isolated cholangiocytes. The changes in ductal functional activity were evaluated by measurement of (i) secretin- stimulated cAMP levels and Cl-IHCOS exchanger activity in pure cholangiocytes; and (ii) secretin-stimulated bile flow and bicarbonate secretion in bile fistula rats. Results: Taurocholate feeding prevented the increase in the number of apoptotic cholangiocytes and the enhancement of caspase 3 activity and protein expression for cleaved pro-caspase 3 induced by 6-OHDA. Taurocholate feeding prevented 6-OHDA-induced decrease in the number of PCNA- and CK-19 positive cholangiocytes, and the loss of PCNA protein expression. At the functional level, taurocholate feeding prevented the decrease in secretin-stimulated cAMP levels, C1-l HCO3 exchanger activity and bile and bicarbonate secretion. Con- sistent with the concept that PI3K regulates the interaction of bile acids with adrenergic nerves in cholangiocytes, we found that administration of wortmannin blocks 6-OHDA-induced activation of cholangiocyte apoptosis, and inhibition of cholangiocyte proliferation and ductal secretion. Summarylconclusion: Tauro- cholate feeding prevents the increase in cholangiocyte apoptosis and the loss of cholangiocyte proliferation and ductal functional activity induced by adrenergic denervation by 6-OHDA. Tauro- cholate effects are mediated by the PI3K pathway, since the si- multaneous administration of wortmannin reverses such effects. These novel findings suggest that bile acids play a major role in sustaining the growth and functional activity of the intrahepatic biliary tree following liver transplantation.

Disclosures: Gianfranco Alpini - No relationships to disclose Domenico Alvaro - No relationships to disclose Brandy Baumann - No relationships to disclose Antonio Benedetti - No relationships to disclose Heather Francis - No relationships to disclose Shannon Glaser - No relationships to disclose Luca Marucci - No relationships to disclose Marco Marzioni - No relationships to disclose Jo Lynne Phinizy - No relationships to disclose Silvia Taffetani - No relationships to disclose Yoshiyuki Ueno - No relationships to disclose Julie Venter - No relationships to disclose

29 KUPFFER CELL GENERATED DEATH LIGANDS POTENTIATE CHOLESTATIC LIVER INJURY. Ali Canbay, Ariel E Feldstein, Hajime Higuchi, Nate Wemeburg, Annette Grambihler, Steve F Bronk, Gregory J Gores, Mayo Clinic, Rochester, MN Hepatocyte apoptosis by death receptors is emerging as a critical determinant in the initiation of hepatic inflammation and fibrosis during cholestatic liver diseases. However, the cellular sources of death ligands to activate the death receptors is unknown. We postulated that Kupffer cells, which contribute to hepatic inflammation, may also contribute to hepatocyte apoptosis and liver fibrosis by generating death ligands. Thus, our AIM was to ascer- tain whether Kupffer cells express death ligands and contribute to hepatocyte apoptosis and liver fibrosis in the bile duct ligated mouse, an animal model of cholestasis. METHODS: Mice were subjected to bile duct ligation (BDL) or a sham operation and treated with gadolinium chloride, a Kupffer cell intoxicant, or saline for three days. Hepatocyte apoptosis in liver sections was assessed using the TUNEL assay. Serum ALT values were quan- titated using commercially available kits. Kupffer cells were isolated using arabinogalactan gradient centrifugation. Real time PCR was used to measure expression of death ligands and fibrosis indicators. RESULTS: Hepatocyte TUNEL positive cells, and serum ALT values were 3.3-fold, and 5.2-fold, respectively, greater in 3 day- (BDL) saline-treated vs. gadolinium chloride-treated mice. Kupffer cell expression of the death ligands TNF-alpha and Fas ligand was 14 and 20-fold greater when Kupffer cells were obtained from BDL vs. sham operated mice. The enhanced expression of Fas ligand was verified by immunoblot analysis and TNF-alpha by an ELISA. These data confirm that Kupffer cells generate death ligands and contribute to hepatocyte apoptosis in cholestatic liver injury. Consistent with a role for Kupffer cell- associated hepatocyte apoptosis in liver inflammation, neutrophil infiltration into the BDL liver was abrogated by gadolinium chloride. Hepatic mRNA transcripts for a -smooth muscle actin, and collagen a 1(I), markers for stellate activation were all significantly attenuated gadolinium chloride vs. vehicle-treated animals. Fi- nally, the mechanisms for Kupffer cell activation were explored in cell culture. Isolated Kupffer cells phagocytosed apoptotic bodies, which induced death ligand expression. In contrast, bile acids had no effect on Kupffer cell gene expression. In CONCLUSION, these findings support a model of cholestatic liver injury where Kupffer cells phagocytose apoptic bodies which induces death ligand expression, further mediating hepatocyte apoptosis. Inhib- iting Kupffer cell death ligand expression may be therapeutic in cholestatic liver diseases. Disclosures: Steve F Bronk - No relationships to disclose Ali Canbay - No relationships to disclose Ariel E Feldstein - No relationships to disclose Gregory J Gores - No relationships to disclose Annette Grambihler - No relationships to disclose Hajime Higuchi - No relationships to disclose Nate Werneburg - No relationships to disclose


30 REGULATION OF TREFOIL FACTOR FAMILY EXPRESSION

MEDIATED GP130 STAT3 SIGNALING UNDER STEADY STATE CONDITIONS AND DURING BILIARY TRACT DISEASES. lsao Nozaki, John G Lunz, Tsukasa Ezure, Susan Specht, Noriko Murase, Anthony Demetris, University of Pittsburgh, Pittsburgh, PA BACKGROUND AND AIM: Previous studies from our lab show that interleukin-6 (IL-6) is a complete biliary epithelial cell (BEC) mitogen that is normally produced by BEC at low levels and upregulated by mechanical, infectious, or immunologic biliary tract injury. Bile duct ligation (BDL) in IL-6-deficient (IL-6-/-) mice results in a reproducible phenotype that includes rapidly decom- pensating biliary cirrhosis, which is at least partially attributable to impaired biliary tree integrity. METHODS AND RESULTS: Oligonucleotide array analysis of primary mouse IL-64- and wild type IL-6+/+ BEC cultures was used to search for possible molecular mechanisms that might account for impaired biliary tree integrity in IL-64- mice. The results showed upregulation of Trefoil factor family (TFF) messenger RNA (mRNA) in the IL-6+/+ BEC compared to the IL-64- BEC. TFF are mucin-associated protease-resistant peptides that greatly contribute to barrier and epithelial repair in the gastrointestinal tract. Various molecular analyses in vitro using BEC cultures confirmed that IL-6-mediated gp130 signaling through the signal transducer and activator of transcription 3 (STAT3) importantly contributes to TFF3 mRNA and protein expression. In vivo, TFF3 mRNA and protein was expressed predominantly in the medium and large bile ducts and peribfiary glands in normal mouse liver in IL-6+/+ mice, but weakly present or absent in IL-64- mice. Within several weeks after BDL, TFF3 mRNA and protein levels decreased transiently then increased to near baseline levels by twelve (12) weeks after BDL in the IL-6+/+. In contrast, the IL-64- mice failed to show the secondary recovery of TFF3 by 12 weeks when mRNA and protein levels were significantly lower than IL-6+/+ (Figure). The retarded recovery of TFF3 mRNA and protein in the IL-6-I- mice was reversed by daily treatment of recombinant IL-6. Similar results were obtained in analysis of normal human liver and various biliary tract diseases. CONCLUSIONS: TFF3 is the predominant Trefoil factor expressed in the mouse and human biliary tree; its expression appears to be upregulated by STAT3 signaling and suppressed by the mitogen-activated protein kinases (MAPK) signaling in the BEC. TFF expression in the biliary tree importantly contributes to biliary tree integrity and repair reactions.

IN BILIARY EPITHELIAL CELLS BY INTERLEUKIN-6 (IL-6)-

TFF3 mRNA expression in mouse liver after BDL

Normal 3 w after BDL 7 w a f f a BDL I2 w sffa BDL (1 w treat.) (6 w treat )

Disclosures: Anthony J Demetris - No relationships to disclose Tsukasa Ezure - No relationships to disclose John G Lunz - No relationships to disclose Noriko Murase - No relationships to disclose Isao Nozaki - No relationships to disclose Susan Specht - No relationships to disclose

31 HCV EXPRESSION INHIBITS INTERFERON SIGNALING IN A CELL-BASED HCV REPLICATION MODEL. Wenyu Lin, Yoichi Hiasa, Yoshitaka Kamegaya, Jason Blackard, Carolynne Zander, Massachusetts General Hospital, Harvard Medical School, Boston, MA; Gregory Beck, University of Massachusetts, Boston, MA; Emmett V Schmidt, Raymond T Chung, Massachusetts General Hospital, Harvard Medical School, Boston, MA BackgroundlAims: The innate immune response (type I IFN system) is postulated to play a critical role in control of viral infection.The role of the IFN system in controlling HCV replication has been inferred but not proven. In addition, HCV protein expression has been shown to antag- onize the IFN response in vitro. Until recently, it has been impossible to assess the interaction between HCV and the type I IFN system in vivo without a model that successfully supports viral replication. We have developed a cell-based binary HCV replication model that successfully recapitulates the early stages of the HCV life cycle (PNAS 98 9847,2001). We therefore used this system (1) to assess the role of type I IFN in controlling HCV replication; and (2) to assess the effect of HCV expression or replication on IFN-induced intracellular signaling. Methods: Full-length HCV cDNA corresponding to the pH77 strain previously shown to be infectious in the presence of ?7 was transfected into Huh-T7 cells (a T7 stably-transfected Huh7 be) , as well as mutant m G H human fibroblast cell lines null for the IFN signaling proteins Tyk2 (Ul), IRF9 (U2), Statl (U3), Jakl (U4), and Stat2 (US) respectively. To test the effects of known IFN antagoflists on HCV replication, the IFN signaling antagonist Sendai virus Y2 protein was cotransfected into Huh-T7 cells. In addition, neutralizing antibodies (nAb) to type I IFN were added to selected Huh-TI cells. To study the effect of HCV on IFN signaling, Huh-TI cells were cotransfected with the reporter plasmids pISRE-luc and pRL-TK. IFNa (1000 IU/ml) was added to selected cells after transfection. Reporter gene expression was monitored by the dual-luciferase reporter assay system and measured as relative luciferase activity. HCV core protein was measured using the Trak-C HCV core Ag ELISA. Results IFNa significantly reduced HCV core Ag production from 203.5 pg/ml (pH77+/IFN-) to 41.3 pglml (pH77+/IFN t) (p=O.OOl). In contrast, Y2 protein enhanced HCV core Ag production to 407.6 pglml in pH771Y2 cotransfected cells (p=O.OOOl). Control experiments confirmed that Y2 protein inhibited IFNa-induced ISRE-mediated signaling in Huh-T7 cells; relative luciferase activity was reduced from 653 (pH771

IFNP nAb increased HCV core Ag replication by 42% and 23% compared to no treatment (p=O.O1). The Combination of anti-1FNa nAb and anti-IFNP nAb significantly enhanced HCV core Ag production by 73% (p=O.004). The U3 cell line enhanced HCV core Ag replication by over two-fold compared to the parental m G H and other mutant cell lines. HCV (pH77) transfection suppressed IFN-induced relative luciferase activity by 50% compared to IFN-treated pGEM transfected cells (p= 0.W). Transfection with a replication defective H77 mutant, subgenomic HCV core, or HCV structural protein mutant constructs had effects on suppression of ISRE-luc similar to H77. Conclusions: Using a binary, full length HCV replication model, we found that (I) HCV replication is enhanced in the presence of the IFN antagonist Y2 as well as by IFN neutralizing antibodies, confirming the criticality of the type I IFN system in innate control of HCV replication. (2) Statl null cell lines enhanced HCV replication, indicating that this protein is the critical signaling component in innate antiviral immunity to HCV. (3) HCV expression inhibits IFN signaling. HCV protein expression and specifically HCV core expression appears to be su€ficient to suppress IFN signaling. These findings demonstrate that the innate immune response exerts direct antiviral effects on HCV, and that HCV protein expression subverts type I IFN signaling. Our replication model has the potential to provide new insights into the mechanisms of host control of HCV replication as well as the mechanism of HCV persistence. Disclosures: Gregory Beck - No relationships to disclose Jason Blackard - No relationships to disclose Raymond T Chung - No relationships to disclose Yoichi Hiasa - No relationships to disclose Yoshitaka Kamegaya - No relationships to disclose Wenyu Lin - No relationships to disclose Emmett V Schmidt - No relationships to disclose Carolynne Zander - No relationships to disclose

IFNa) to 21.2 (pH77/ IFNdY2) (p=O.O001). Anti-IFNa nAb and anti-

HEPATOLOGY, Vol. 38, No. 4, Suppl. 1,2003 AASLD ABSTRACTS 171A

32 AN ANALYSIS OF CTLA4 SINGLE NUCLEOTIDE FOLYMORPHISMSAND HAPLOTYPES WITH HEPATITIS C VIRUS OUTCOMES. Chloe L Thio, Timothy Mosbruger, Jacquie Astemborski, Johns Hopkins School of Medicine, Baltimore, MD; James G Goedert, National Cancer Institute, Rockville, MD; Stephen O'Brien, National Cancer Institute, Frederick, MD; David L Thomas, Johns Hopkins School of Medicine, Baltimore, M D Background Cytotoxic T lymphocyte activator 4 downregulates T cell activation by ligating B7. Single nucleotide polymorphisms (SNPs) at positions -318 in the promoter and +49 in exon 1 of the CTLA4 gene have been associated with an increased risk for autoimmune diseases. The +49G allele has also been associated with a greater likelihood of response to interferon-alpha in patients treated for chronic hepatitis C. Since some of the CTLA4 SNPs either individually or linked together (haplotypes) may alter CTLA4 expression or activity, we hypothesized that they may be associated with natural hepatitis C virus (HCV) clearance or persistence. Methods: Utilizing a nested case-control study design from an injection drug using cohort and a hemophiliac cohorts, we matched subjects with HCV clearance (anti-HCV positive and HCV RNA negative on two occasions separated by a minimum of 6 months) to two persistently HCV-infected individuals (HCV RNA positive on two occasions) based on H N status, race, and gender. Five CTLA4 SNPs, which define all common haplotypes, were genotyped using either sequence specific primers or a single base extension method. Conditional logistic regression was used to determine odds ratios and P-values for these SNPs. Haplotypes were constructed using the PHASE program and analyzed using the SNPEM program. Results: Included in this study were 190 and 370 subjects who either cleared or had a persistent infection with HCV, respectively. The study cohort was 47% Black, 46% White, and 7% Other. Blacks who were homozygous for the mutant allele 49G were more likely to experience viral clearance (OR 0.45, P=0.03). This association was not found in White subjects (OR 0.92, P=0.81). Since, HLA-Cw"O4 is associated with viral persistence in these cohorts (Thio et a1 J Virol2002), we stratified the 49G homozygous individuals by C w W . Both Blacks and Whites who did not have CwW4 were more likely to have viral clearance if they were homozygous for 49G (OR 0.45, P=0.13 and OR 0.49, P=O.11, respectively). Stratification by other HLA alleles associated with HCV clearance or persistence did not reveal additional relationships. The 49G formed haplotypes with the wild type alleles at three of the four other SNPs examined, and those haplotypes did not have a stronger association than 49G alone. 49G was found in haplotypes with both the mutant and wild type alleles at the -1722 promoter position, but neither of these haplotypes had a stronger association with clearance. Conclusions: Homozygosity for the CTLA4 49G SNP is associated with clearance of HCV in Blacks regardless of HLA genotype, whereas in Whites, homozygosity at this position trends toward an association with clearance in HLA-Cw*M-negative persons. Since CTLA4 49G has been reported to augment T ceIl activation by decreasing CTLA4 expression, these results point to the importance of T cell activation in HCV clearance. Disclosures: Jacquie Astemborski - No relationships to disclose James G Goedert - No relationships to disclose Timothy Mosbruger - No relationships to disclose Stephen O'Brien - No relationships to disclose Chloe L Thio - No relationships to disclose David L Thomas - No relationships to disclose

33 MICROARRAY ANALYSIS OF INTRAHEPATIC GENE EXPRESSION IN DIFFERENT PATTERNS OF HCV RECURRENCE POST LIVER TRANSPLANT. Amany Zeky , Rohan William, Centenary Institute for Cancer Research and Cell Biology, Sydney, Australia; Geoffrey W McCaughan, Centena y Instztute for Cancer Research and Cell Biology and the AW Morrow Gastroenterology and Liver Centre, Sydney, Australia Recurrence of HCV infection post liver transplant is universal. High levels of viraemia characterize the post transplant course. In this setting, acute rejection in association with HCV re-infection of the graft (AR (HCV)) and recurrent chronic hepatitis (CHI) are recognized clinical entities. We aimed to 1) Determine the intrahepatic gene profile in AR (HCV) and CHI. 2) Examine whether the gene profile in AR (HCV) is different to that of acute rejection in non-HCV infected allografts (AR non-HCV). 3) Examine whether the gene profile of CHI is different to chronic hepatitis C pre-transplant (CH). Methods: GeneChip arrays were utilized to study pooled RNA from 34 liver tissue; 6 patients with AR (HCV), 6 patients with AR (non-HCV), 8 patients with CHI, 8 patients with CH and 6 normal livers. Probe level data was analysed using the Bioconductor affy library and genes with more than 2 fold changes were considered to be upregulated. Results: AR (HCV) us AR (non-HCV): Compared to normal tissue, both groups were similarly characterized by upregulation of several T cell dependent immune activation genes such as the lymphocyte antigen CAMPATH-1, Mac-2 binding protein and IFN related genes. However, compared to AR (non-HCV), AR (HCV) was specifically characterized by upregulation of several IFN-alpha associated genes including 2-50AS, and p27. CHI vs C H Compared to normal, both groups were characterized by upregulation of genes involved in antigen presentation (proteasome subunit 42, MDW), T cell activation (T cell receptor and CTL-17), IFN-gamma inducible genes (IFN- 56KD, IP-10, Humig and class I1 MHC) and IFN-alpha associated genes (p27 and 2-5 OAS). However, the IFN-alpha and gamma genes were more upregulated in CHI compared to CH. Furthermore, compared to CH, the CHI group displayed increased expression of genes involved in cellular proliferation (PCNA, cyclin, beta integrin), apoptosis (cytochrome c, Fas-L, caspase 4), inflammation (macrophage mannose receptor, complement factor H) and fibrosis (angiotensin I1 receptor, pro- teoglycan core protein). Conclusions: At the transcriptome level, the pathological process in HCV infected allografts with acute rejection or recurrent chronic hepatitis is characterized by upregulation of several IFN- alpha and gamma related genes compared to other livers. Moreover, chronic HCV post transplant is further characterized by an increased process of cellular proliferation, apoptosis and fibrosis compared to chronic hepatitis in the pretransplant setting. Collectively the data suggest that the high levels of viraemia which characterize the post transplant setting drive the immune response to act at a higher level. In addition, the upregulation of several interferon related antiviral genes supports the notion that HCV is a strong inducer of intrahepatic interferons, but is relatively resistant to their antiviral activity. Disclosures: Geoffrey W McCaughan - No relationships to disclose Rohan William - No relationships to disclose Amany Zekry - No relationships to disclose


34 CROSSPRIMING OF HEPATITIS C VIRUS SPECIFIC CD8+ T CELLS IN MICE BY IMMUNIZATION WITH DENDRITIC CELLS TRANSFECTED WITH SELF-REPLICATING RNA. Vito Racanelli, National Institutes of Health, Bethesda, MD; Sven Erik Behrens, Fox Chase Cancer Center, Philadelphia, PA; Julio Aliberti; Barbara Rehermann, National institutes of Health, Bethesda, M D Background: Spontaneous resolution of hepatitis C virus (HCV) infection is associated with vigorous, durable CD8+ T cell responses against nonstructural HCV proteins. HCV persistence has been attributed to poor priming of cellular immune responses. One of the factors that contributes to poor priming of cellular immune responses may be the noncytopathic nature of HCV and to the subsequent absence or scarcity of virus-infected apoptotic or dead cells as source of exogenous antigens for crosspresenta- tion. Because crosspriming contributes to the induction of CD8+ T cells in vivo (Nature 1999; 39877-80), we hypothesized that cross-priming with dendritic cells (DCs) containing self-replicating RNA might be useful to induce strong, HCV-specific cellular immune responses. Methods: Choosing HCV NS3 as a model antigen, we generated a recombinant cytopathic pestivirus self-replicating RNA to amplify HCV NS3 in DCs. The principal characteristic of this vector is its ability to replicate in transfected cells which in turn enhances production, processing and presentation of the encoded HCV NS3 antigen. Moreover, the availability of cytopathic and noncytopathic forms of the same replicon enabled us to study the immunologic implications of DC apoptosis and antigen reprocessing, leading to crosspriming in vivo. Results: The murine dendritic cell lines DC2.4 was transfected with cytopathic and noncytopathic recombinant replicon RNA, respectively. HCV NS3 expression was detectable in more than 95% of the transfected cells by immunofluorescence. The time kinetics of apoptosis induction was monitored by flow cytometry using annexin V and propidium iodide staining. In contrast to the noncytopathic replicon, the cytopathic replicon led to DC apoptosis 12 hours after transfection. DC2.4 transfected with the cytopathic recombinant replicon RNA were then used to immunize HLA-A2 transgenic mice subcuta- neously. IFN- positive, proliferative CD4+ T cells and IFN--y positive, cytotoxic CD8+ T cell responses were detectable after a single subcutaneous immunization with replicon-transfected dendritic cells and significantly stronger than after conventional, in- tramuscular DNA immunization, the previous gold standard. Crosspriming was demonstrated when T cells, primed by injection of H-2b+ DCs into the H-2b+ HLA-A2+ mice, were tested with HLA-A2+ antigen-presenting cells. Transfer of cellular material from the vaccine DCs to the endogenous APCs, a phenomenon that underlies crosspriming, was directly visualized in vivo when fragments of CSFE-labeled, injected H2b+ DCs were demonstrated in HLA-A2+ host cells in lymph nodes and spleens by flow cytometry and IF microscopy. Finally, the protective effect and the in vivo function of the induced HCV-specific T cells were evaluated in a surrorgate challenge model with recombinant, HCV NS3 encoding vaccinia virus. Whereas lo4 to lo7 pfu were detected in nonvaccinated control mice, no vaccinia virus was detected in mice vaccinated with replicon-transfected DCs, indicating complete protection. Summary and conclusion: These findings demonstrate and explain the immunologic potential of the proposed vaccination strategy. Moreover, they support the hypothesis that experimental forcing of exogenous antigens into the MHC class I pathway and subsequent promotion of cross-priming is particularly important to generate T cell responses against noncytopathic and tissue tropic viruses such as HCV. Disclosures: Julio Aliberti - No relationships to disclose Sven Erik Behrens - No relationships to disclose Vito Racanelli - No relationships to disclose Barbara Rehermann - No relationships to disclose

35 CHARACTERIZATION OF NOVEL CD4+ T CELL EPITOPES IN ACUTE SELFLIMITED HCV INFECTION. Tilman Gerlach, Klinikum Grophadern, Munich, Germany; Axel Ulsenheimer, Instifute for Immunology, Munich, Germany; Norbert Gruener, Klinikum Grophadern, Munich, Germany; Reinhart Zachoval, Maria-Christina Jung, Medical Department 11, Grosshadem, Munich, Germany; Winnfned Schraut, Institute for Immunology, Munich, Germany; Albercht Schirren, Medical Department 11, Grosshadern, Munich, Germany; Martin Wiichtter, Michael Backmund, Sfiidtisches Krankenhaus Schwabing, Munich, Germany; Gerd R Pape, Helmut Diepolder, Klinikum Grophadern, Munich, Germany Introduction: Hepatitis C virus (HCV) infection leads to chronic liver disease in about 85% of infected individuals while only a minority achieves spontaneous viral elimination in the initial phase of acute hepatitis C. Anti viral mechanisms clearing the infection in these patients, however, could contribute to the gen- era-tion of therapeutic or prophylactic vaccines. The strong association of a broad, HLA restricted, vigorous and long lived anti viral CD4+/ Th1 T-cell response with spontaneously resolving acute hepatitis C has been demonstarted in the past. Only few epitopes recognized by anti HCV specific CD4+ T cells that are associated with spontaneous viral clearance have been characterized so far. The aim of the present study was to identify and characterize HCV specific CD4+ T cell epitopes and their HLA restriction during acute self limited HCV infection andlor viral control. Methods: Proliferative CD4+ T cell responses (3H-thymidin incorporation) against viral proteins (HCV-NS3, -NS4) and against overlapping 20-mer pep-tides covering the entire NS3 and NS4 (aa 1027-1972) region were performed in 25 patients with acute self limited HCV infection and in two patients during temporary viral control (HCV RNA negative). Ten patients with chronic HCV infection served as control group. CD4+ T cell clones were generated by limit-ing dilution of HCV protein specific T cell lines. HCV specific CD4+ T cell clones were further characterized fine specificity was assessed by proliferation assay after stimulation with overlapping peptides of the corresponding protein region, then the minimal epitope was defined with N- and C-terminal truncated peptides for each epitope. HLA restriction was assessed by inhibition experi-ments (anti-DP, -DQ, -DR) and CD25+ expression in the presence of a panel of EBV blasts by flowcytom- etry. Results: We studied 25 patients with acute self limited HCV infection. All pa-tients displayed significant proliferative T cell responses against HCV-NS3 or -NS4 protein, that was strongly associated with self-limited disease and absence of HCV RNA. Proliferative responses against 20-mer peptides showed multiple responses within the NS3 and NS4 region, possibly reflecting multiple epitopes in this region. In contrast no virus specific T cell responses were detectable in a control group of patients with chronic HCV. For further characterization of T cell epitopes HCV specific T cell clones were generated from 6 patients against eight different HCV epitopes located within the NS3 (aa1027-1657, two epi-topes) and NS4alb (aa1658-1972, six epitopes) region. The minimal epitopes consist of 8 to 12 amino acids. All T cell clones were HLA class I1 restricted and could be stimulated by protein or peptide pulsed EBV blasts expressing the cor-responding HLA-DR or -DQ. Conclusion: The HCV NS3 and NS4 proteins contain several immunodominant CD4+ T cell epitopes which are associated with spontaneous viral clearance. The detailed characterization of minimal epitopes and HLA restriction are a pre-requisite for the synthesis of HLA class I1 tetramers and for the development of prophylactic and therapeutic T cell vaccines. Disclosures: Michael Backmund - No relationships to disclose Helmut Diepolder - No relationships to disclose Tilman Gerlach - No relationships to disclose Norbert Gruener - No relationships to disclose Maria-Christina Jung - No relationships to disclose Gerd R Pape - No relationships to disclose Albercht Schirren - No relationships to disclose Winnfried Schraut - No relationships to disclose


Axel Ulsenheimer - No relationships to disclose Martin Wachtler - No relationships to disclose Reinhart Zachoval - No relationships to disclose

36 INDUCTION OF HEPATITIS C VIRUS SPECIFIC T CELLS BY NEEDLE STICK INJURY IN THE ABSENCE OF HCV- VIREMIA. Anne K Kubitschke, Maffhias Bahr, Nuray Aslan, Hannover Medical Sehoof, Hannouer, Germany; Christoph Sarazzin, University of Saarland, Homburg, Germany; Hans L Tillmann, Tim Greten, Manuela Meyer, Johannes Wiegand, Michael P Manns, Heiner Wedemeyer, Hannover Medical School, Hannover, Germany Introduction: Clearance of acute hepatitis C virus (HCV) infection is thought to be mediated by a multispecific immune response. HCV-specific T cells have been described in HCV-seronegative virus-exposed individuals such as i.v.-drug addicts, family members of chronic HCV-patients and lab-personnel. However, it is not known whether these individuals had recovered from previous asymptomatic acute hepatitis C. In this study, we prospectively followed 10 individuals who experienced an injury with an HCV-contaminated needle. Methods: Between January 2001 and March 2003 we collected PBMC from 10 individuals (medical health professionals at our institution; 3 females, 7 males; age 30-45 years) who experienced an injury with an HCV contaminated needle. Blood samples were taken on the day or the day after the event and at different time points during follow-up for up to 12 months. Low levels of HCV- RNA were examined in serum by the highly sensitive transcription-mediated TMA-Assay (detection limit 5-50 IUIML) and in RNA of PBMC. T cell-cytokine secretion (ELISPOT-assays for IFN-gamma and IL-10, flow-cytometry-based IFN-g capture assays), T cell-proliferation (3-thymidin incorporation, CFSE-staining), and T cell-cytotoxicity (51-chromium release assays) were investigated directly ex vivo and in T cell lines. Results: None of the individuals became positive for HCV-RNA in serum (TMA-assay) or PBMC and all of them remained anti-HCV- negative throughout follow-up. At the time of the needle stick injury, HCV-specific CD4+ T cell responses were already detectable in 2 of the individuals and became detectable thereafter in 2 additional persons. HCV-specific CD8+ T cell responses could be investigated in one HLA-A2-positive individual in more detail at several time points. He was negative for HCV-specific interferon gamma- and IL-10-producing cells on the day of the injury as determined by ELISPOT assays. However, after 18 weeks, we detected for Core-178-specific IFN-gamma producing CD8+ T cells. Out of 7 MHC-class I-restricted HCV epitopes tested, one additional peptide (NS3-1406) became positive 8 weeks later. The presence of Core-178 and NS3-1406-specific CD8+ T cells was confirmed by a second flow-cytometry-based assay. HCV-specific INF-gamma positive cells were CD8-dim and HLA-DR-negative. The frequency of NS3-1406 and Core-178-specific CD8+ T cells was about 114500 and 118500 PBMC, respectively, in the ELISPOT assay and remained constant in this subject until month 11 of follow- up. The increase of CD8+ T cell responses was accompanied by the development of an HCV-specific CD4+ response targeting predominantly the HCV-core and HCV-helicase antigens. Conclusions: We here demonstrate in a prospective study the development of HCV-specific T cells in HCV-exposed individuals after needle stick i n j q in the absence of viremia. Surprisingly, these HCV- specific T cells became detectable rather late after the potential exposure. Our data are in line with previous studies demonstrating HCV- specific T cell responses in chimpanzees inoculated with sub- infectious doses of HCV. T cell immunity in medical health professionals against HCV may contribute to the low prevalence of HCV among doctors and nurses since HCV prevalence in medical health personnel has been shown to be equal or even lower as compared to the general population in most studies. This study was funded by the German Viral Hepatitis Network [HEP-NET] (Project 10.2.2) Disclosures: Nuray Aslan - No relationships to disclose Matthias Bahr - No relationships to disclose Tim Greten - No relationships to disclose

Anne K Kubitschke - No relationships to disclose Michael P Manns - No relationships to disclose Manuela Meyer - No relationships to disclose Christoph Sarazzin - No relationships to disclose Hans L Tillmann - No relationships to disclose Heiner Wedemeyer - No relationships to disclose Johannes Wiegand - No relationships to disclose

37 A SINGLE CENTER EXPERIENCE IN THE MANAGEMENT OF 125 IATROGENIC BILE DUCT INJURIES FOLLOWING LAPAROSCOPIC CHOLECYSTECTOMY. Vijayaragavan Muralidharan, Michael Silva, Simon R Bramhall, David Mayer, John A C Buckels, Paul McMaster, Darius F Mirza, University Hospital Birmingham, Birmingham, UK Aims: Laparoscopic cholecystectomy is the treatment of choice for symptomatic gallstone disease at present. Despite its wide spread application in the past decade, the incidence of iatrogenic bile duct injuries related to this procedure has remained unchanged around 0.3-0.6%. We review the investigation, management and outcomes of such injuries referred to a tertiary referral center in the United Kingdom. Methods: Prospectively collected data on iatrogenic bile duct injuries following elective laparoscopic cholecystectomy referred to our center was analyzed. The Strasberg classification was used for defining the types of injury. Results: A series of 125 patients were referred for management of iatrogenic bile duct injuries between January 1991 and June 2003. Median follow up period was 55 months. 87 patients had type E injuries (To%), followed by 20 with type A (16%) 14 with type D (11%) and 2 each of types B (1.6%) and C (1.6%). An uncomplicated primary operation was described in 74 patients (60%). Despite the operation being converted to an open procedure in 27 patients only 18 injuries were recognized at the time of surgery.(l4.4%) Although the median time to recognition of biliary tract injury was 2 days (1-21) the median time to referral increased to 10 days (0-99) for a type A injury, and 16 days (0-2200) for a type E injury. A total of 29 patients underwent surgical intervention prior to referral of which 20 had biliary reconstruction. Nine of these patients required subsequent revision surgery. After referral 15(13%) patients were managed conservatively while 6(5%) had ERCP and biliary stenting and 24(29%) had in- terventional radiology as the main procedure. Surgical intervention was required in 79 patients (53%) at our center following referral. This included T-tube insertion (7), primary common bile duct repair (lo), biliary reconstruction (60) and liver resection (2) with three patients requiring subsequent revision surgery. Major associated vascular injuries were present in eight patients. One patient suffers from recurrent cholangitis while five remain asymptomatic on follow up. Two required liver resection due to severe ischaemic necrosis. Bowel perforations were associated in three patients. Both vascular and bowel injuries occurred in patients with type E bile duct injuries. Nine patients (7%) had recurrent cholangitis following treatment. Three patients developed end-stage liver disease due to secondary biliary cirrhosis with one undergoing orthotopic liver transplantation. There were five deaths related to bile duct injuries. Two had associated vascular injuries and one had bowel perforation. A further two patients with type A injuries died following multi- organ failure due to sepsis. Conclusions: Iatrogenic bile duct injuries are associated with significant morbidity and mortality. Delay in recognition and appro- priate referral remain a continuing problem. A multi disciplinary approach in a specialized institution has a significantly better long term outcome. Disclosures: Simon R Bramhall - No relationships to disclose John A C Buckels - No relationships to disclose David Mayer - No relationships to disclose Paul McMaster - No relationships to disclose Darius F Mirza - No relationships to disclose Vijayaragavan Muralidharan - No relationships to disclose Michael Silva - No relationships to disclose


38 ACTIVATION OF TUMOR SPECIFIC T LYMPHOCYTES

WITH LIVER METASTASES. Thaddaeus Till H Wissniowski Jr, lohannes Haensler, Thomas Bernatik, Detlef Schuppan, E G Hahn, Deike Strobel, Friedrich-Alexander- University Erlangen Nuernberg, Erlangen, Germany Background Radio-frequency ablation (RFA) is widely used as a treatment of inoperable tumor leasons in the liver. Preliminary studies of a VX2 hepatoma model in rabbits showed tumor specific T lymphocytes after RFA treatment and a significantly prolonged survival of these treated animals compared to a control group. Aim: The aim of the study was to assess whether the observed tumor specific T cell response after RFA treatment, found in the VX2 tumor model, is transferable to humans. Methods: 12 Patients were included into a pilot study. 6 Patients had metastases of colonic cancer and 6 patients were suffering from hepatocellular carcinoma (HCC) with underlying cirrhosis. All patients were treated with RFA (Elektrotom Him 106, Berchtold, Germany). Blood samples were taken before and 4 weeks after RFA. An Interferon gamma cytokine secretion assay (Miltenyi, Ger- many) was carried out on whole blood and measured by a flow- cytometer (FACS Calibur, BD Science, Germany). As test antigens served autologous liver tissue and tumor tissue received by biopsy. T cells were doublestained with CD 8 antibody to detect cytotoxic T cells. The basic IFN gamma secretion was also measured unstimulated. The activated/non activated CD8 positive T cell ratio (ANR) was calculated and analysed statistically with SPSS. Only RFA naive were included. Results: Before RFA patients had a mean stimulation of 0,022 ANR (SD=0,001) against liver tissue and 0,027 ANR (SD=0,002) against tumor tissue (see tab.1). 4 weeks after RFA a strong increase of ANR was observed with 0,11 ANR (HCC) and 0,15 ANR (colorectal carcinoma) against tumor tissue. This increase was also detectable 8 weeks after RFA (0,14 ANR (SD=0,003) (HCC) and 0,14 ANR (0,003) (colorectal carcinoma)) (see Fig. 1 and tab.1). The ANR levels were allways low against liver tissue with 0,03 ANR (SD=0,002). Discussion: RFA shows significant tumor specific T-cell stimulation in patients with primary and secondary tumors of the liver. RFA seems to overcome immune tolerance or presents alterated and/or cryptic tumor antigens, and causes a significant tumor specific cytotoxic Tcell response. This effect could be exploided in multimodal antitumoral strategies. Disclosures: Thomas Bernatik - No relationships to disclose Johannes Haensler - No relationships to disclose E G Hahn - No relationships to disclose Detlef Schuppan - No relationships to disclose Deike Strobel - No relationships to disclose Thaddaeus Till H Wissniowski Jr - No relationships to disclose

AFTER RADIO-FREQUENCY ABLATION IN PATIENTS

39 RESECTION PRIOR TO LIVER TRANSPLANTATION FOR HEPATOCELLULAR CARCINOMA. Alexandre Cortes, Franfois Durand, Reza Kianmanesh, Eddie K Abdalla, Daniele Sommacale, Federica Dondero, Alain Sauvanet, Olivier Farges, Jacques Belghiti, Hospital Beaujon, Clichy, France The strategy of primary hepatic resection followed by secondary liver transplantation (SLT)was not evaluated in-term of operative risks and survival. Between 1991-2001, among 88 cirrhotic patients transplanted for HCC with Mazzafero's criteria on analysis of the specimen, 18 had liver resection prior to SLT : for recurrence (n=11), deterioration of liver function (n=4) or high risk for recurrence (n=3) with a mean time between liver resection and listing for LT was 20 months (1-84). The comparison between SLT group and patients who underwent primary liver transplantation (PLT) showed similar median age (55 vs. 53 years), sex and etiology of liver disease (alcohol/viral BIClother). Overall time on LT waiting list of the two groups was

similar (5 vs. 3 months). Pathologic analysis of the specimen revealed similar number (1.7 vs. 1.6) and tumor size (2.3 vs. 2.2 cm). Pen- and post-operative course were not different in terms of operative time (551 vs. 530 min), blood loss (1282 vs. 1191 mL), transfusion (3 vs. 2 units), ICU (10 vs. 9 days) or hospital stay (32 vs. 31 days), morbidity (56% vs. 51%) or 30-day mortality (5.7% vs. 5.6%). During a median follow-up of 32 months (3 to 158 months), 3 patients recurred after PLT and one after SLT. After transplantation, 3 and 5-year overall survivals were not different between groups (82 vs. 82% and 59 vs. 61%). Results of our study showed that liver resection for HCC prior to transplantation did not increased the morbidity or impair long-term survival following LT. Therefore liver resection prior to transplantation can be integrated in the treatment strategy for HCC. Disclosures: Eddie K Abdalla - No relationships to disclose Jacques Belghiti - No relationships to disclose Alexandre Cortes - No relationships to disclose Federica Dondero - No relationships to disclose Francois Durand - No relationships to disclose Olivier Farges - No relationships to disclose Reza Kianmanesh - No relationships to disclose Alain Sauvanet - No relationships to disclose Daniele Sommacale - No relationships to disclose

40

HEPATOPROTECTIVE FACTOR WHICH DEFENDS THE LIVER AGAINST ISCHEMIA-REPERFUSION INJURY. Maria Irliguez, Eduardo Martinez-Ansd, Naiara Beraza, Matilde Bustos, Puri Fortes, @us Prieto, Clinica Universitaria and Medical School, University of Navarra, Pamplona, Spain AIMS: CT-1 is a member of the IL-6 family of cytokines which protects myocardiocytes against thermal and ischemic insults. In this work we analyzed the expression of CT-1 by normal and diseased liver and whether this cytokine might protect the liver against ischemia-reperfusion injury. METHODS: Rat CT-1 cDNA was cloned, recombinat rat CT-1 was produced and used for generation of poly and monoclonal antibodies which were employed in immunochemistry, western blot and ELISA. The recombinant cytokine was assayed for therapeutic use in rat models of ischemia-reperfusion injury. Wistar rats were subjected to 60 min ischemia of 70% of the liver by clamping the corresponding branches of the hepatic and portal vein. After this period the clamp was released and serum and tissue samples were obtained at 6 hours. Rats were divided into three groups: group 1 received 100 mcg CT-1 10 minutes prior to ischemia (n=8), group 2 received saline instead of CT-1 (n=8) and group 3 were sham operated (n=4). RESULTS: Immunohistochemistry of normal livers demonstrated CT-1 expression selectively in hepatocytes of the centrolobular area. Six hours after reperfusion of ischemic livers the values of serum ALT were 10 times higher in group 2 than in group 1 (pCO.01). Severe focal hepatocellular necrosis was found in animals from group 2 while no apparent morpholgical changes were observed in rats from group 1. Serum CT-1 levels were raised after reperfusion in untreated animals as compared with sham operated rats. Western blot of liver samples showed an increase of CT-1 expression in the non-ischemic liver lobule as compared with the damaged part of the liver. CONCLUSIONS: CT-1 is a hepatoprotective cytokine produced by hepatocytes in centrolobular areas. CT-1 synthesis increases after ischemic insults. Administration of recombinant CT-1 protects very efficiently the liver against ischemia-reperfusion injury. CT-1 may be a valuable therapy to attenuate hepatic damage of the donor liver during orthotopic liver transplantation. Disclosures: Naiara Beraza - No relationships to disclose Matilde Bustos - No relationships to disclose Pun Fortes - No relationships to disclose Maria Ifiiguez - No relationships to disclose Eduardo Martinez-Ans6 - No relationships to disclose Jesus Prieto - No relationships to disclose

CARDIOTROPHIN-1 (CT-1) IS A POTENT


41 ISCHEMIC PRECONDITIONING PROTECTS HEPATOCYTES AGAINST WARM ISCHEMINREPERFUSION INJURY VIA OXYGEN RADICALS DERIVED FROM KUPFFER CELLS. Kazuaki Tejima, Masahiro Arai, Hitoshi lkeda, Tomoaki Tomiya, Mikio Yanase, Yukiko Inoue, Kayo Nagashima, Naoko Watanabe, Masao Omata, University of Tokyo, Tokyo, Japan; Kenji Fujiwara, Saituma Medical School, Saitama, japan Background A brief period of tissue ischemia followed by reperfusion renders tissue resistant against subsequent prolonged ischemia and reperfusion, a phenomenon called ischemic preconditioning. Hepatic ischemic preconditioning protects sinusoidal endothelial cells against subsequent cold storagelwarm reperfusion injury and improves graft survival after liver transplantation in rats. Aim Ischemic preconditioning also reduces liver injury after warm ischemia and reperfusion, in which hepatocyte damage and Kupffer cell activation are dominant features. However, it is incompletely elucidated which cell type ischemic preconditioning affects and how it works. Therefore, our aim was to investigate the mechanisms of ischemic preconditioning against warm ischemia and reperfusion injury. Method Male Sprague-Dawley rats were injected intravenously with 20 mglkg gadolinium chloride (GdCls), 10000 Ulkg superoxide dismutase (SOD) or 300 mglkg N-acethyl-L-cyctein (NAC) to suppress Kupffer cells, superoxide formation or oxygen radical formation, respectively. Livers were then preconditioned by clamping the hepatic artery and portal vein to the median and left lobes for 10 min followed by 10 min reperfusion. Subsequently, livers were subjected to warm ischemialreperfusion injury in in vivo experiments and in liver perfusion experiments as follows. In vivo experiments: The blood flow to the median and left lobes was occluded with a vascular clamp for 40 min. One hour after removal of the clamp, blood was collected for determination of ALT activity and hyaluronic acid (HA) concentration. Liver perfusion experiments: Livers were perfused through the portal vein for 10 min with physiological buffer and stored at 37°C in the same buffer. After 40 min, livers were reperfused with the buffer containing 500 ng/mL HA for 60 min in a recirculating system for determination of ALT activity in the perfusate and hepatic HA uptake as a marker of sinusoidal endothelial cell injury. Livers of other non-treated rats were preconditioned by perfusion with the buffer containing H202 instead of ischemic preconditioning, and then subjected to warm ischemialreperfusion similarly. In other experiments, livers were subjected to ischemic preconditioning and perfused with the buffer containing 0.5 mglmL nitro blue tetrazolium (NBT) for 10 min and fixed with formalin. Since NBT reacts with superoxide to form insoluble blue formazan, Kupffer cell superoxide formation was evaluated in histological sections. Results Ischemic preconditioning decreased serum ALT activity compared to control (168 ? 34 [mean 5 SEMI vs 333 ? 52, p < 0.05), but did not change serum HA concentration. Pretreatment with GdC13 reversed the effect of ischemic preconditioning (262 2 41), though GdC13 itself did not change ALT activity after ischemialreperfusion (318 t_ 33). Similar results were obtained in liver perfusion experiments, suggesting that ischemic preconditioning protected hepatocytes, but did not change sinusoidal endothelial cell injury. It is also suggested that Kupffer cells mediate hepatocytes protection by ischemic preconditioning. In rats treated with SOD or NAC, decrease in ALT activity in the perfusate by ischemic preconditioning was reversed (38 2 3.5 [sham] vs 48 * 1.7 [ischemic preconditioning] and 43 ? 4.8 vs 48 * 4.1, respectively). Liver perfusion with 0.1 mM H202 decreased ALT activity after warm ischemialreperfusion compared to control (22 ? 3.4 vs 37 ? 2.8, p < 0.01). Liver perfusion with NBT revealed superoxide formation in Kupffer cells even after 10 min ischemia. Conclusion Ischemic preconditioning reduced warm ischemialreperfusion injury by protection of hepatocyte, not by suppression of sinusoidal endothelial cell injury in contrast with the effect against cold ischemialreperfusion injury. This effect may be mediated by oxygen radical formation in Kupffer cells during ischemic preconditioning. Disclosures: Masahiro Arai - No relationships to disclose Kenji Fujiwara - No relationships to disclose

Hitoshi Ikeda - No relationships to disclose Yukiko Inoue - No relationships to disclose Kayo Nagashima - No relationships to disclose Masao Omata - No relationships to disclose Kazuaki Tejima - No relationships to disclose Tomoaki Tomiya - No relationships to disclose Naoko Watanabe - No relationships to disclose Mikio Yanase - No relationships to disclose

42 A20 CONFERS A PROLIFERATIVE ADVANTAGE TO HEPATOCYTES AND PROMOTES LIVER REGENERATION. Christopher R Longo, Virendra 1 Patel, Maria B Arvelo, Soizic Daniel, Shane T Grey, Christiane Fewan, Beth Israel Deaconess Medical Center, Boston, MA

Background: Living donor liver transplantation (LDLT) and split livers have emerged as a solution to ease the shortage of liver transplants and have achieved remarkable success in pediatric populations. In adults, LDLT is limited by the size of the graft that can be safely harvested and transplanted. Similar limitations apply when extensive liver resections are needed for the treatment of hepatic tumors. We have previously demonstrated that the anti-apoptotic gene A20 is part of the physiologic response of hepatocytes to injury, protecting them from apoptosis and limiting inflammation by inhibiting NF-KB activation. Our objective was to check whether A20 expression would help decrease the minimal liver mass required for mice survival. Methods and Results: Two-thirds partial hepatectomy is well toler- ated and is an accepted model of liver regeneration in rodents. We performed an extended (78%) liver resection (n=12/group) in non-infected (NI) mice (10-12 week BALB/c) and mice infected with recombinant A20 adenovirus (rAd.A20) or a control adenovirus (rAd.P-gal). Surviving mice suffer a delay in regeneration as assessed by the number of proliferation cell nuclear antigen (PCNA) positive nuclei 48 h following resection (5-10 positive cellslHPF in mice with 78% liver resection vs. 60-70 positive cells/ HPF in mice with a 2/3 liver resection). Interestingly, such a delay was not noted in mice expressing A20 (70-80 PCNA positive cells/ HPF were detected 48 h following 78% resection). A20 also prevented the development of coagulopathy as assessed by prothrombin time. We extended our resection to a radical hepatectomy comprising 87% of the liver (n=12lgroup). We observed 100% lethality in NI and rAd.P-gal infected mice. Expression of A20 resulted in the survival of 60% of the animals and correlated with increased PCNA positive hepatocytes as an indicator of increased cell proliferation. A20 mediated increase in hepatocyte proliferation was not merely dependent upon its anti-apoptotic function. Expression of A20 in hepatocyte cultures, in a non- apoptotic milieu, increased their proliferative response to serum and HGF as compared to NI and rAd.P-gal infected cells. Conclusion: These results demonstrate a novel pro-proliferatif function for A20 in hepatocytes and argue for its critical role in accelerating liver regeneration and promoting hepatocyte survival and function, even when facing extreme metabolic demands. Gene therapy with A20 may allow for successful transplantation with smaller LDLT, split liver allografts and even hepatocellular grafts. Additionally, A20 based therapy to the liver may allow for extensive liver resections in the setting of cancer therapy. Disclosures: Maria B Arvelo - No relationships to disclose Soizic Daniel - No relationships to disclose Christiane Ferran - No relationships to disclose Shane T Grey - No relationships to disclose Christopher R Longo - No relationships to disclose Virendra I Patel - No relationships to disclose


43 LOSS OF CEREBRAL AUTOREGULATION IN RATS AFTER PORTACAVAL ANASTOMOSIS. Chuhan Chung, Javier Vaquero, Jeanne Gottstein, Andres T Blei, Lakeside V A Medical Center and Northwestern University, Chicago, IL

BACKGROUND: In experimental and clinical acute liver failure, both a loss of cerebrovascular autoregulation and an increase in cerebral blood flow (CBF) have been implicated in the development of brain edema. It is unclear whether the pathogenesis of these two phenomena are linked. The accumulation of glutamine within astrocytes appears to be a critical first step in the development of cerebral hyperemia, as experimental inhibition of glutamine synthetase with methionine sulfoximine (MSO) attenuates brain edema and corrects cerebral hyperemia. To study cerebrovascular autoregulation without the confounding variable of brain edema, we examined animals one day after portacaval anastomosis (PCA), where a decreased cerebral blood flow has been noted in the setting of a hyperdynamic systemic circulation. MATERIAL AND METHODS: A PCA or sham surgery was performed in male SlD rats (300-400 gm). At 24 hrs, mean arterial pressure (MAP) was measured continuously in anesthetized rats. Noradrenaline was infused at a dose of 1 pglkglmin for 60 minutes. MSO or saline was given as an intraperitoneal injection (150 mglkg) three hours prior to NA infusion. Relative changes in cortical blood flow (CBF) were measured with a laser Doppler probe placed over the parietal cortex. The animals were mechan- ically ventilated and arterial blood gases were monitored throughout the experiment. Three groups of rats were studied (n= 18). RESULTS: The sham group had significantly higher MAP, in accordance with the systemic vasodilatation seen in PCA rats. Adding NA to all groups significantly raised MAP and HR. The sham+NA group did not exhibit an increase in CBF with a rise in MAP. The PCA+NA group had a significant increase in laser Doppler flow (LDF) from baseline that coincided with an increase in MAP. Pretreatment of the PCA animals with MSO prevented the rise in CBF despite a rise in MAP. There were no significant differences in pC02 among the three groups. As expected, arterial ammonia levels were higher in PCA animals and increased further after inhibition of glutamine synthetase in the group that received MSO.

MAP MAP HR HR LDF FinalNH3 GROUP M) e30min t-0 P3Omin %chanaa (vmoln] Sham+NA 102t3’108i3” 394i12 417*16 3*11 68+8 PCA+Saline+NA 84 i 1 98 f 1 358 i 13 396 i 19 70 r 8*” 141 i 5“ PCA+MSO+NA 84i3 9223 365t 13 394* 14 7 i 13 239t 14# ‘p<O.OOl vs other groups: “p<O 05 vs other groups: “’p=O 002 vs other groups, a p<O 0001 vs other groups, “p < 0 0001 vs Sham

CONCLUSIONS: A rise of MAP in rats after PCA results in an increase of CBF, indicating a loss of cerebrovascular autoregulation. The restoration of autoregulation with MSO, despite higher arterial ammonia levels, suggests that accumulation of glutamine within the brain is critical to the pathogenesis of altered cerebrovascular regulation in this model. As similar conclusions can be reached regarding the development of cerebral hyperemia in experimental acute liver failure, it appears that the mechanisms responsible for cerebral hyperemia and failed cerebrovascular autoregulation are linked. Future studies should focus on the nature of the intracerebral signal that is responsible for the loss of cerebral autoregulation in this model. Disclosures: Andres T Blei - No relationships to disclose Chuhan Chung - No relationships to disclose Jeanne Gottstein - No relationships to disclose Javier Vaquero - No relationships to disclose

44 A LIVER-SPECIFIC NITRIC OXIDE DONOR IMPROVES THE INTRA-HEPATIC VASCULAR RESPONSE TO INCREASE PORTAL BLOOD FLOW AND METHOXAMINE IN CIRRHOTIC RATS. Mauricio Loureiro-Silva, Yale University School of Medicine, VA Medical Center, West Haven, CT; Gregory W Cadelina, VA Medical Center, West Haven, CT; Yasuko Iwakiri, Roberto J Groszmann, Yale University School of Medicine, CT-VA Healthcare System, West Haven, CT Background. A decreased intra-hepatic production of nitric oxide (NO) participates on the pathogenesis of portal hypertension in cirrhosis. Although non-specific NO donor substances, such as nitrates, are able to decrease the intra-hepatic vascular resistance to portal blood flow, the use of these vasodilators to treat portal hypertension in cirrhotic patients is limited by the occurrence of side effects (arterial hypotension, headaches etc). Aim. To test the effect of a liver-specific NO donor (NCX-1000), an ursodeoxycholic acid-derived compound, on both systemic and intra-hepatic hemodynamics in portal hypertensive cirrhotic rats. Method. After the development of ascites, cirrhotic rats (CC4-induced) were treated with NCX-1000 (28 mglKg b.w.) or ursodeoxycholic acid (15 mglKg b.w., control group) by gavage once a day for 14 days and, then, used in 1 of 3 studies: 1) in vivo mean arterial pressure (MAP), portal pressure (PP), and superior mesenteric artery (SMA) blood flow measurements before and during progressive blood volume expansion (blood infusion); 2) in situ liver perfusion to obtain doselresponse curves to methoxamine (alpha*-adrenergic agonist) or flowlpressure curves; and 3) cGMP concentration measurement in liver tissue. Results. Both MAP and heart rate were similar in both groups, indicating that NCX-1000 had no effect on systemic hemodynamics. PP was also similar in both groups. During blood infusion, NCX-1000 treated rats and control rats showed similar MAP (p=0.134) and SMA blood flow (p=0.449) increases; however, the PP increase observed in control rats was blunted in NCX-1000 treated rats (p=0.015). Flowlpres- sure curves obtained during liver perfusion were similar in both groups; however, livers from NCX-1000-treated rats showed a decreased response to methoxamine (p=0.016) than controls. The concentration of cGMP in NCX-1000-treated livers was significantly higher (p=0.015; ) than in ursodeoxycholic acid-treated livers (27.65 t 7.95 vs. 11.20 2 6.03 fmollmg of protein). Conclusion. NCX-1000 improves the portal system adaptability to portal blood flow increase and decreases the intra-hepatic hyper-reactivity to methoxamine observed in cirrhotic rat livers without causing systemic side effects. These beneficial effects are probably due to increase in the intra-hepatic NO bioavailability. Disclosures: Gregory W Cadelina - No relationships to disclose Roberto J Groszmann - NICOX ConsultantlAdvisor; Scientific StudylTrial; Other: Partial support Yasuko Iwakiri - No relationships to disclose Mauricio Loureiro-Silva - No relationships to disclose

45 MESENTERIC VASOCONSTRICTION IS RESPONSIBLE FOR THE INITIAL ENOS UPREGULATION IN THE SUPERIOR MESENTERIC ARTERY OF PORTAL HYPERTENSIVE RATS. Ming-Hung Tsai, Chang Guns Memorial Hospital, Taipei, Taiwan; Yasuko lwakiri, Yale University School of Medicine, V A Medical Center, West Haven, CT; Grego ry Cadelina, Veterans Administration Medical Center, West Haven, CT; William C Sessa, Yale University School of Medicine, New Haven, CT; Roberto J Groszrnann, Yale University School of Medicine, VA Medical Center, West Haven, CT Background and Aims: The mechanisms behind the upregulation of endothelial nitric oxide synthase (eNOS) in portal hypertensive animals remain unknown. The aim of this study was to investigate the mechanism that initiates eNOS upregulation in the superior mesenteric artery (SMA) in portal hypertension. It has been shown that the vasoconstriction of the SMA with the consequent increase in the SMA cyclic strain is the earliest event that occurs within hours after portal vein ligation (PVL). Thus, we tested the hypothesis that this early vasoconstriction of the SMA may initiate eNOS upregulation in PVL animals. Methods: Portal hypertension


was induced by partial ligation of the portal vein (n=99). In a separate group of rats, mesenteric vasoconstriction was achieved also by renal artery ligation (RAL, n=26). Corresponding sham-operated rats were used as control groups (n=50). Effects of vasoconstriction of the SMA in PVL and RAL rats were evaluated by measuring perfusion pressure changes in the isolated SMA beds in response to methoxamine, NOS activity and eNOS protein expression. Data were compared to the corresponding sham group. Hemodynamic features were also determined. Mean arterial pressure (MAP), portal pressure (I") and SMA blood flow (Qsma) were measured by catheterization and pulsed Doppler flowmetry. SMA vascular resistance was calculated from MAP, PP and Qsma. Results: There was a significant increase in the SMA vascular resistance in PVL (2.33%0.13 vs 1.2220.03 rnmHgl %flow, K0.05) and RAL rats (23220.18 vs 1.18%0.02 mmHgf%flow, P<0.05) compared to their corresponding sham-operated rats, demonstrating the presence of SMA vasoconstriction in both PVL and RAL groups. The mesenteric vasculature of PVL and RAL animals showed hyporeactivity to methoxamine compared to their respective sham groups (P< 0.01). Whiie PVL rats were portal hypertensive (P<O.Ol), RAL rats were not. The SMA vascular hyporeactivity of PVL and RAL were corrected by L-NMMA and while there was not significant difference in eNOS protein expression NOS enzyme activity was significantly higher in the PVL and RAL rats compared to the corresponding sham-operated groups (see figure). Conclusions: Mesenteric arterial vasoconstriction in itself leads to eNOS upregulation and therefore, plays a triggering role in the initial increase of eNOS cata- lyhc activity in SMA of PVL rats.

Disclosures: Gregory Cadelina - No relationships to disclose Roberto J Groszmann - No relationships to disclose Yasuko Iwakiri - No relationships to disclose William C Sessa - No relationships to disclose Ming-Hung Tsai - No relationships to disclose

46 CAVEOLIN INHIBITS A CONSTITUTIVELY ACTIVATED FORM OF RECOMBINANT ENOS EXPRESSED IN HEPATIC STELLATE CELLS: POSSIBLE MECHANISM FOR DYSFUNCTION OF RECOMBINANT ENOS GENE DELIVERY TO LIVER IN PORTAL HYPERTENSION. Suvro Chatterjee, Helen Hendrickson, Vijay Shah, Mayo Clinic, Rochester, M N Background. Diminished eNOS derived NO production from the hepatic vascular endothelium contributes to hepatic vasoconstriction in cirrhotic portal hypertension. Unfortunately, prior studies aimed at delivering a constitutively active form of eNOS (S1179DeNOS) using an adenoviral vector (AdS1179DeNOS) were unsuccessful in correcting hepatic vasoconstriction in the bile duct ligated (BDL) rat liver. Aim. To better understand the mechanism of S1179DeNOS dysfunction in BDL liver by examining the influence of the eNOS inhibitory protein caveolin on recombinant S1179DeNOS function in transduced hepatic stellate cells, which do not express eNOS endogenously but are a prominent cell target of systemically delivered adenoviral vectors. Methods. Cel- lular localization of caveolin was determined from fixed sham and BDL liver sections by immunogold electron microscopy. In vitro gene transfer was performed in the LX2 HSC line with AdS1179DeNOS and an adenoviral vector encoding caveolin (Ad- Cav). Protein interactions were determined by immunoprecipita-

tion and Western blot analysis. NOS activity was assessed by arginine to citrulline conversion assay. Results. Caveolin immunogold analysis in BDL liver demonstrated prominent expression not only in liver endothelial cells, but also in stellate cells. Western blot analysis from LX2 cell lysates confirmed caveolin protein expression in vitro. In LX2 cells transduced with AdS1179DeNOS, immunoprecipitation of caveolin co-precipitated recombinant S1179DeNOS and conversely, immunoprecipitation of S1179DeNOS coprecipitated caveolin. To examine the influence of excess caveolin protein levels on S1179DeNOS, LX2 cells were co-transduced with AdS1179DeNO.S and AdCav. Co-transduction of AdCav and AdS1179D promotes the enhanced binding between S1179DeNOS and caveolin as well as a decrease in the activity of recombinant S1179DeNOS by 25% (P<0.05; AdS1179DeNOS vs AdS1179DeNOS +Adcav; n=5). Conclusion. These studies demonstrate a functional effect of enhanced caveolin expression and binding with S1179DeNOS in stellate cells and indicate that the lack of function of recombinant S1179DeNOS protein delivered in vivo to cirrhotic liver may be due to inhibition of S1179DeNOS by caveolin-1 in stellate cells. Disclosures: Suvro Chatterjee - No relationships to disclose Helen Hendrickson - No relationships to disclose Vijay Shah - No relationships to disclose

47 RHO MODULATES HEPATIC SINUSOIDAL ENDOTHELIAL FENESTRAE VIA REGULATION OF THE ACTIN CYTOSKELETON. Hiroaki Yokomori, Kitasafo Institute Medical Center, Saitama, Japan; Masaya Oda, Organized Center of Clinical Medicine, Tokyo, Japan; Hiromasa lshii, Keio Unioersity School of Medicine, Tokyo, Japan Background and Aims: The presence of actin-like microfilaments in the neighborhood of sinusoidal endothelial fenestrae (SEF) indicates that the cytoskeleton of sinusoidal endothelial cells (SEC)s plays an important role in the modulation of SEF. We have reported that a potent vasoconstrictor endothelin (ET) causes con- tractions of SEF as well as hepatic stellate cells via the ETA and ETB receptors, leading to the elevations of sinusoidal microvascular resistance supposed to be one the essential factors in the pathogenesis of portal hypertension. Rho has emerged as an important regulator of the actin cytoskeleton, and consequently cell morphology. The present study aimed to examine how a Rho stimulator; lysophophatidic acid (LPA), and a Rho inhibitor; Y-27632 Rho-kinase inhibitor, affect the morphology of SEF in vitro. Methods: Monolayers of cultured SEC were obtained by collagenase infusion of a rat liver and then subjected to primary culture for 24 hours. The cells were separated into three groups; control, LPA-treated (lOpM), and Y-27632-treated (10pM) groups (treatment duration, 30 min). SEF morphology was observed by scanning electron microscopy. Formation of F-actin stress fibers was observed by confocal microscopy. Actin cytoskeleton around SEF was investigated by permealizing cells with streptolysin-0 (1.5 U) for 30 min and examined by transmission electron microscopy. Rho A and phosphorylated myosin light chain kinase were analyzed by Western blotting. Rho activation was measured by Rhotekin binding assay. Results: Following LPA treatment, F-actin stress fiber and active Rho increased concomitant with a decrease in diameter of SEF. However, following Y-27632 treatment, F-actin stress fiber and active Rho were reduced, concomitant with an increase in diameter of SEF. Actin cytoskeleton around SEF increased in LPA-treated cell, but decreased in Y-27632-treated cell. Rho A levels were similar in control, LPA-treated, and Y-27632- treated SECs. Phosphorylated myosin light chain kinase levels were diminished gradually after 5 min in Y-27632-treated SECs and increased after 5 min in LPA-treated cells. LPA treatment increased the amount of active Rho, compared to control and Y-27632 treatment. Conclusion: These results indicate that Rho may play an essential role in the regulation of contraction and dilation of SEF through the actomyosin system. Disclosures: Hiroaki Yokomori - No relationship to disclose Masaya Oda - No relationship to disclose Hiromasa Ishii - No relationship to disclose


48 UNEQUIVOCAL EVIDENCE FOR A ROLE OF NEUROSTEROIDS WITH POSITIVE ALLOSTERIC

IN THE PATHOGENESIS OF HEPATIC ENCEPHALOPATHY. Samir Ahboucha, Nicolas Chatauret, Paul Desjardins, Gilles Pomier- Layrargues, Roger F Butterworth, CHUM-Hapital Saint-Luc, Montrt!al, PQ, Canada Analysis of visual-evoked response patterns suggests that GABAergic tone is increased in brain in liver failure and that this is a major cause of hepatic encephalopathy (Schafer et al., troenterolow 86:540-545,1984). However, the precise mechanisms responsible have eluded researchers in this area for the last two decades. Studies in brain tissue from both human and experimental animals with liver failure have consistently shown that GABA synthesis, GABA receptors and their associated benzodiazepine modulatory sites are intact and that expression of the subunit proteins of the GABA-A receptor complex are unchanged (Zwing- mann et al., Hevatologv 37420-428,2003; Ahboucha et al., Neuro- chem. Int., 2003). On the other hand, there is emerging evidence to suggest that neurosteroids (NS), a novel class of compounds with potent GABA agonist properties are increased in brain in end- stage chronic liver failure in humans (Ahboucha et al., Hepatol- a 36: 318A, 2002). In order to further assess this possibility, NS concentrations were measured using a sensitive radioassay in samples of frontal cortex obtained at autopsy from 15 cirrhotic patients who died in hepatic coma compared to an equal number of controls matched for age, gender, and autopsy delay intervals. Patient material contained up to 12-fold increases of NS and subsequent analysis by gas chromatography-mass spectrometry showed that the major component NS with positive allosteric properties at the GABA-A receptor was allopregnanolone. Patient material did not contain significantly increased concentrations of either GABA or benzodiazepines. In a separate series of experiments, NS concentrations were found elevated up to 2-fold (p<0.02) in brains of rats following end-to-side portacaval anastomosis (PCA) and 5.2-fold (p<O.Ol) in brains of rats following hepatic devascularization (PCA followed by hepatic artery ligation) compared to sham-operated controls. Administration of inhibitors of the NS synthesis enzyme 3-hydroxysteroid dehydrogenase (trilostane or indomethacin) resulted in dose-dependent reductions in brain concentrations of allopregnanolone and a concomitant improvement in locomotor activity scores in PCA rats. Together, these findings offer unequivocal evidence that NS with positive allosteric modulatory properties are generated in brain in both human and experimental liver failure and that these substances contribute to the "increased GABAergic tone" characteristic of hepatic encephalopathy. Pharmacological agents aimed at reduction of NS synthesis or modulation of the NS site on the GABA-A receptor complex could afford effective novel therapeutic strategies in the treatment of hepatic encephalopathy [Funded by CIHR Canada]. Disclosures: Samir Ahboucha - No relationships to disclose Roger F Butterworth - No relationships to disclose Nicolas Chatauret - No relationships to disclose Paul Desjardins - No relationships to disclose Gilles Pomier-Layrargues - No relationships to disclose

MODULATORY PROPERTIES AT THE GABA-A RECEPTOR

49 THE MOUSE FORKHEAD BOX M1B TRANSCRIPTION FACTOR IS REQUIRED FOR DEVELOPMENT OF HEPATOCELLULAR CARCINOMAS. Robed H Costa, Vladimir V Kalinichenko, Xinhe Wang, Joseph Kuechle, Yoder Yoder, Brian Shin, University of Illinois at Chicago, College of Medicine, Chicago, 1L ABSTRACT Primary hepatocellular carcinoma (HCC) is one of the most common malignancies, ranks fi&h in frequency among all cancers worldwide, and causes over 1 million deaths annually. Although a number of oncogenes and alterations in signaling pathways have been identified in HCC, current treatment for this liver tumor is largely ineffective and has poor patient prognosis. One of the potentially curative approaches in HCC therapy is based on interfering with HCC progression by blocking cell division. In regenerating liver, expression of the proliferation-specific Forkhead Box mlb (Foxmlb) transcription factor is reactivated prior to hepatocyte DNA replication and its levels are sustained throughout the period of hepatocyte proliferation. Deletion of the Foxmlb fllfl (LoxP targeted) allele using Albumin promoterlenhancer driven- Cre recombinase (Alb-Cre) transgene resulted in significant reduction in regenerating hepatocyte proliferation, which was associated with diminished expression of cell-cycle promoting Cdc25A and Cdc25B phosphatases and increased nuclear levels of cyclin dependent kinase (Cdk) inhibitor p21Cipl protein. In order to test the hypothesis that Foxmlb is required for the development of HCC, we subjected Alb-Cre Foxmlb -/- mice and Foxmlb fllfl (control) mice to a Diethylnitrosamine (DEN)lPhenobarbital (W) liver tumor induction protocol. Our data demonstrated that Alb-Cre Foxmlb -I- mice are highly resistant to liver tumor formation as evidenced by their failure to develop either hepatic adenomas or HCC following 33 weeks of DENlPB tumor induction protocol. In contrast, at 23 weeks following DEN/PB tumor induction protocol, Foxmlb fllfl livers displayed a large number of adenomas that progressed to HCC by 33 weeks following DEN/PB treatment. The Alb-Cre Foxmlb - I - liver displayed enzyme-altered foci as evidenced by protein expression of the Glutathione- S-Transferase placental isoform. However, Alb-Cre Foxmlb -/- hepatocytes failed to develop hyper-proliferative foci, whereas abundant BrdU labeling was found in hepatic adenomas and HCC of DENlPB treated Foxmlb fllfl mice. This reduced DNA replication of Foxmlb -/- hepatocytes was associated with increased nuclear levels of the Cdk inhibitor p27Kipl protein. Furthermore, Foxmlb fllfl tumors expressed high nuclear levels of M-phase promoting Cdc25B protein, while undetectable nuclear levels of Cdc25B were found in Foxmlb - I - hepatocytes after DEN/PB treatment. The Cdc25B phosphatase is required for mitosis because it activates the M-phase promoting Cyclin B-Cdkl complex, and its increased expression is a prognostic marker for a variety of aggressive tumors. Consistent with this finding, Foxmlb -/- hepatocytes failed to enter mitosis following DENlPH tumor induction protocol and this was associated with accumulation of large polyploid hepatocytes. These studies demonstrate that Foxmlb is required for the proliferative expansion of hepatic tumors, suggesting that Foxmlb can be used as a potential target in treatment of patients with HCC. Disclosures: Robert H Costa - No relationships to disclose Vladimir V Kalinichenko - No relationships to disclose Joseph Kuechle - No relationships to disclose Brian Shin - No relationships to disclose Xinhe Wang - No relationships to disclose Yoder Yoder - No relationships to disclose

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Poster Session (pp. 78A–178A)