29, 30 We did not attempt to diagnose regenerative or dysplastic nodules in this study. A lesion was diagnosed as HCC on DWI if it showed the following: mild to moderate hyperintensity compared with liver parenchyma on DW images at b 50, restricted diffusion (remained hyperintense) at b 500 and/or b 1,000, with ADC visually lower or equal to that of surrounding liver parenchyma.12 ADC values were not measured in this study. A maximum number of five HCCs per patient was recorded on the basis of the largest size. All data (including

lesion location and size) were transcribed from hard copies to electronic format by a third observer 3 (M.-S. P., 7 years of experience in abdominal MRI), who was responsible for MR-pathologic correlation (see below). The third observer (M.-S. P.) correlated MRI findings as diagnosed by the first two observers ERK inhibitor with the pathologic findings based on the size and segment location of the lesions on explant. All 52 explanted livers were initially sectioned into 5-8

mm contiguous slices in the coronal plane. HCCs were identified grossly as those that were distinct from surrounding regenerative nodules in terms of size, texture, color, or degree of bulging beyond the cut surface of the liver. Livers were photographed, Selleck Epigenetics Compound Library and all lesions other than ordinary regenerative nodules were sampled for histologic examination. Using the diagnostic criteria of the International Working Party’s Terminology of Nodular Hepatocellular Lesions,31 the routine hematoxylin 上海皓元 and eosin–stained slices from the nodules were classified as follows: regenerative nodule; dysplastic nodule, low grade; dysplastic nodule, high grade; small HCC (<2 cm); or HCC (≥2 cm). The HCCs were categorized as well-differentiated, moderately differentiated, and poorly differentiated.

Microvascular invasion was noted. SAS version 9.0 was used for all statistical computations. Generalized estimating equations based on a binary logistic regression model were used to compare the three sets of images. The model included imaging modality and observer as fixed classification factors, and the correlation structure was modeled by assuming observations to be correlated only when derived for the same patient. For the analysis of diagnostic accuracy on a per-subject basis, a patient was classified as positive for HCC if at least one HCC lesion was seen at pathology and was negative for HCC otherwise. Patients were defined as test-positive for HCC whenever an observer diagnosed at least one lesion as HCC using a given imaging modality and test-negative for that given combination of reader and modality otherwise.

The majority of patients with PSC also have inflammatory bowel disease (ulcerative colitis > Crohn’s disease) though the two diseases run their independent courses. As the disease progresses, patients may suffer

from repeated bouts of cholangitis, complications of end-stage liver disease or the dreaded complication of cholangiocarcinoma. Disease progression is very variable and no treatment has been found to be of benefit. Dilatation of dominant strictures may hasten progression of the disease in some. “
“A 73-year-old woman with chronic hepatitis C and hepatocellular carcinoma RO4929097 in vitro (HCC) was hospitalized for radiofrequency ablation (RFA). Laboratory test results showed the following: platelet count, 62,000/mm3; prothrombin time, 12 seconds; albumin, 4.4 g/dL; bilirubin, 0.8 mg/dL; alpha-fetoprotein, 8.5 ng/mL; and des-gamma-carboxy prothrombin, 11 mAU/mL. Gadoxetic acid–enhanced magnetic resonance imaging demonstrated a low-intensity area in the hepatobiliary phase in segment VIII. Contrast-enhanced ultrasonography (CEUS) showed hyperenhancement in the vascular phase with hypoenhancement in the postvascular phase. Aspiration biopsy CB-839 cell line revealed well-differentiated

HCC. We performed CEUS-guided RFA with a 2-cm Cool-tip RFA system (Radionics, Burlington, MA) through an intercostal space. No abnormalities in the chest wall were found before RFA and the patient had no complaints, except for mild

pain during ablation. Increased thickness of the chest wall was found during RFA. Immediately after ablation, we performed CEUS with perflubutane and identified linear extravasation of microbubbles along the needle tract in the vascular phase (Fig. 1A). After 5 and 10 minutes, we reinjected perflubutane and could find no extravasations of microbubbles (Fig. 1B). Enhanced computed tomography (CT) demonstrated a hemorrhage in the chest wall (Fig. 1C) and a small amount of intraperitoneal MCE hemorrhage on the hepatic surface (Fig. 1D), but no active bleeding. We speculated that an intercostal vessel had been injured by the electrode, with spontaneous resolution of the hemorrhage. CEUS, contrast-enhanced ultrasonography; CT, computed tomography; HCC, hepatocellular carcinoma; RFA, radiofrequency ablation. US, ultrasonic. Hemorrhages resulting from RFA occur in 0.5% of cases.1 In our case, bleeding from an intercostal vessel into the chest wall was clearly detected on CEUS. CEUS is reported to show 100% sensitivity and 100% specificity for the detection of active bleeding.2 We could repeatedly and in real time confirm continued hemorrhaging, even in the pooling of contrast agent, using high-power flashes. Briefly, a high-power flash ultrasonic (US) beam (mechanical index: 1.27) destroys the majority of microbubbles in the US plane and, consequently, allows a resetting of transient perfusion.

The majority of patients with PSC also have inflammatory bowel disease (ulcerative colitis > Crohn’s disease) though the two diseases run their independent courses. As the disease progresses, patients may suffer

from repeated bouts of cholangitis, complications of end-stage liver disease or the dreaded complication of cholangiocarcinoma. Disease progression is very variable and no treatment has been found to be of benefit. Dilatation of dominant strictures may hasten progression of the disease in some. “
“A 73-year-old woman with chronic hepatitis C and hepatocellular carcinoma GS-1101 cell line (HCC) was hospitalized for radiofrequency ablation (RFA). Laboratory test results showed the following: platelet count, 62,000/mm3; prothrombin time, 12 seconds; albumin, 4.4 g/dL; bilirubin, 0.8 mg/dL; alpha-fetoprotein, 8.5 ng/mL; and des-gamma-carboxy prothrombin, 11 mAU/mL. Gadoxetic acid–enhanced magnetic resonance imaging demonstrated a low-intensity area in the hepatobiliary phase in segment VIII. Contrast-enhanced ultrasonography (CEUS) showed hyperenhancement in the vascular phase with hypoenhancement in the postvascular phase. Aspiration biopsy Sirtuin inhibitor revealed well-differentiated

HCC. We performed CEUS-guided RFA with a 2-cm Cool-tip RFA system (Radionics, Burlington, MA) through an intercostal space. No abnormalities in the chest wall were found before RFA and the patient had no complaints, except for mild

pain during ablation. Increased thickness of the chest wall was found during RFA. Immediately after ablation, we performed CEUS with perflubutane and identified linear extravasation of microbubbles along the needle tract in the vascular phase (Fig. 1A). After 5 and 10 minutes, we reinjected perflubutane and could find no extravasations of microbubbles (Fig. 1B). Enhanced computed tomography (CT) demonstrated a hemorrhage in the chest wall (Fig. 1C) and a small amount of intraperitoneal 上海皓元医药股份有限公司 hemorrhage on the hepatic surface (Fig. 1D), but no active bleeding. We speculated that an intercostal vessel had been injured by the electrode, with spontaneous resolution of the hemorrhage. CEUS, contrast-enhanced ultrasonography; CT, computed tomography; HCC, hepatocellular carcinoma; RFA, radiofrequency ablation. US, ultrasonic. Hemorrhages resulting from RFA occur in 0.5% of cases.1 In our case, bleeding from an intercostal vessel into the chest wall was clearly detected on CEUS. CEUS is reported to show 100% sensitivity and 100% specificity for the detection of active bleeding.2 We could repeatedly and in real time confirm continued hemorrhaging, even in the pooling of contrast agent, using high-power flashes. Briefly, a high-power flash ultrasonic (US) beam (mechanical index: 1.27) destroys the majority of microbubbles in the US plane and, consequently, allows a resetting of transient perfusion.

4, 5 Chronic HCV infection is the leading indication for liver transplantation in the U.S., and the disease is estimated to cause ∼5,000 to 10,000 deaths each year.6, 7 Between 1999 and 2007 HCV-associated mortality increased significantly and, in 2007, the number of HCV-related deaths surpassed the number of HIV-related deaths for the first time.8 Progression of liver fibrosis does not occur at a constant rate.9 Rather, disease progression is highly variable and is accelerated by, among other factors, alcohol consumption, obesity, and metabolic syndrome.

MG-132 clinical trial Current treatment guidelines suggest clinicians consider withholding treatment in patients with mild fibrosis because of the low likelihood of disease progression and complications, and because of the high cost of treatment.10 However, once advanced fibrosis develops, the rate of liver-related disease progression is high: it is estimated that, each year, 10% of patients with bridging fibrosis progress to cirrhosis, and 5% of patients with SB203580 supplier cirrhosis die or undergo liver

transplantation.11 Treatment of chronic hepatitis C (CHC) is associated with significant costs and delaying or forgoing treatment incurs additional costs associated with caring for patients with advanced HCV-related liver disease. HCV infection increases healthcare costs overall,9, 12, 13 and treatment of HCC and liver transplantation are undoubtedly associated with very high healthcare costs,14 but the specific impact of the progression of liver disease on healthcare costs has not been well studied. 上海皓元 The purpose of this study was to analyze the demographic characteristics, healthcare utilization, and healthcare costs of patients with HCV in a large U.S. private insurance database as

stratified by liver disease severity: noncirrhotic liver disease (NCD), compensated cirrhosis (CC), and ESLD. CC, compensated cirrhosis; CHC, chronic hepatitis C; ESLD, endstage liver disease; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; NCD, noncirrhotic liver disease; OLT, orthotopic liver transplantation; PPPM, per-patient-per-month. Medical and pharmacy claims data, enrollment information, and linked laboratory results and mortality information from commercial health plan enrollees for the period January 1, 2002 to August 31, 2010 were analyzed. Patients eligible for this analysis were commercial health plan members with both pharmacy and medical benefits who had evidence of chronic HCV infection during the patient identification period (January 1, 2003 to August 31, 2010). Specifically, to be included in the analysis patients were required to have an HCV diagnosis code based on the presence of International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9 CM) codes during the patient identification period and at least one nondiagnostic code for HCV during the study period (in order to exclude patients who only had rule-out codes for HCV).

26 We now show that FGF21 expression is increased in MED1ΔLiv mouse liver after PPARγ overexpression (Fig. 6B). This might suggest that FGF21-regulated inhibition of SREBP-1 and Y 27632 of other adipogenesis-related genes, such as adipsin, adiponectin, caveolin-1, and SMAF1, contribute to the attenuation of hepatic steatosis in MED1ΔLiv mouse following PPARγ overexpression (Fig. 6B). However, it is unclear as to how FGF21 levels are increased in

MED1ΔLiv mouse liver following PPARγ overexpression. FGF21 is regulated by both PPARγ and PPARα and because this regulation requires MED1 it is conceivable that other mechanism(s) also exist to maintain high FGF21 levels in MED1 null livers. In this study, we also report that other coactivators, namely SRC-1, PRIC285, PRIP, and PIMT, are not essential for PPARγ-induced adipogenic steatosis (Supporting Fig. 3). PPARγ stimulated hepatic steatosis in these

coactivator null mouse livers, indicating the redundancy of these coactivators in PPARγ function in vivo. Disruption of genes encoding for p160/SRC-1 family members (SRC-1, SRC-2, and SRC-3) singly, has been shown to be redundant for PPARα-regulated gene expression in mouse liver.17, 32 PRIC285, a component of PRIC complex, has been shown to interact with PPARα, PPARγ, TRβ1, ERα, and RXRα.33 PRIC285−/− mice showed no differences in the magnitude of pleiotropic responses when challenged with PPARα ligands, such as Wy-14,643 or ciprofibrate, implying Cabozantinib that PRIC285 is not essential for PPARα function.34 We now demonstrate that PRIC285 is also unnecessary for PPARγ function in liver. Coactivator PRIP (NCoA6) and its associated protein PIMT (NCoA6IP), function as linkers between the two major multiprotein complexes

anchored by CBP/p300 and MED1.35 PIMT interacts with coactivators CBP, p300, MED1, and PRIP in vivo and in vitro.35 PRIP-deficient mouse embryonic fibroblasts are refractory to PPARγ-stimulated 上海皓元 adipogenic conversion and fail to express adipogenic marker aP2, a PPARγ-responsive gene.36 However, surprisingly, our in vivo observations indicated the development of severe fatty liver in PRIPΔLiv and PIMTΔLiv mice following PPARγ overexpression. These results suggest that under in vivo conditions, MED1 absence results in a dominant phenotype as compared to PRIP deletion. The nonessential role of PRIP and PIMT in the PPARγ pathway may be due to the compensation between PRIP and PIMT in vivo. In conclusion, this study provides evidence that MED1 is required for high-fat diet–induced and PPARγ-induced hepatic steatosis and that loss of MED1 protects against fatty liver under these conditions. It is possible that expression levels of MED1 in liver might also play a significant role in the progression of fatty liver disease by modulating lipotoxicity and influencing steatohepatitis and endoplasmic reticulum stress.

Disease-associated capillarization of LSEC in vivo and dedifferentiation of LSEC in vitro indicate the importance of the hepatic microenvironment. To identify the LSEC-specific molecular differentiation program in the rat we used a two-sided gene expression profiling approach comparing LSEC freshly isolated ex vivo with both lung microvascular this website endothelial cells (LMEC) and with LSEC cultured for 42 hours. The LSEC

signature consisted of 48 genes both down-regulated in LMEC and in LSEC upon culture (fold change >7 in at least one comparison); quantitative reverse-transcription polymerase chain reaction confirmation of these genes included numerous family members and signaling pathway-associated molecules. The LSEC differentiation program comprised click here distinct sets of growth (Wnt2, Fzd4, 5, 9, Wls, vascular endothelial growth factors [VEGFR] 1, 2, 3, Nrp2) and transcription factors (Gata4, Lmo3, Tcfec, Maf) as well as endocytosis-related (Stabilin-1/2, Lyve1, and Ehd3) and cytoskeleton-associated molecules (Rnd3/RhoE). Specific gene induction in cultured LSEC versus

freshly isolated LSEC as well as LMEC (Esm-1, Aatf) and up-regulation of gene expression to LMEC levels (CXCR4, Apelin) confirmed true transdifferentiation of LSEC in vitro. In addition, our analysis identified a novel 26-kDa single-pass transmembrane protein, liver endothelial differentiation-associated protein (Leda)-1, that was selectively expressed in all liver endothelial cells and preferentially localized to the abluminal cell surface. Upon forced overexpression in MDCK cells, Leda-1 was sorted basolaterally to E-cadherin-positive adherens junctions, suggesting functional involvement in cell adhesion and 上海皓元 polarity. Conclusion: Comparative microvascular analysis in rat identified a hepatic microenvironment-dependent LSEC-specific differentiation program including the novel junctional molecule Leda-1. HEPATOLOGY 2010 Endothelial cells (ECs) display marked heterogeneity in different organs and in different segments of the vascular tree. Liver sinusoidal endothelial cells

(LSECs) are a prime example of uniquely differentiated microvascular EC that exert highly specialized functions as professional endocytes1 and participate in induction of hepatic immune tolerance.2 For endocytosis, LSEC express a broad range of different scavenger receptors including Stabilin-1 and Stabilin-2, two members of a novel scavenger receptor gene family selectively expressed in sinusoidal ECs that have been identified and thoroughly characterized by us.3 Stabilin-2 is the major hyaluronan scavenger receptor of the liver, whereas Stabilin-1 mediates endocytosis of acLDL (low density lipoprotein) and SPARC. Stabilin-1 and -2 use the constitutive clathrin-mediated endocytic pathway in LSEC (4); in addition, Stabilin-1 fulfills a second role as an intracellular cargo carrier.

Disease-associated capillarization of LSEC in vivo and dedifferentiation of LSEC in vitro indicate the importance of the hepatic microenvironment. To identify the LSEC-specific molecular differentiation program in the rat we used a two-sided gene expression profiling approach comparing LSEC freshly isolated ex vivo with both lung microvascular click here endothelial cells (LMEC) and with LSEC cultured for 42 hours. The LSEC

signature consisted of 48 genes both down-regulated in LMEC and in LSEC upon culture (fold change >7 in at least one comparison); quantitative reverse-transcription polymerase chain reaction confirmation of these genes included numerous family members and signaling pathway-associated molecules. The LSEC differentiation program comprised Pritelivir distinct sets of growth (Wnt2, Fzd4, 5, 9, Wls, vascular endothelial growth factors [VEGFR] 1, 2, 3, Nrp2) and transcription factors (Gata4, Lmo3, Tcfec, Maf) as well as endocytosis-related (Stabilin-1/2, Lyve1, and Ehd3) and cytoskeleton-associated molecules (Rnd3/RhoE). Specific gene induction in cultured LSEC versus

freshly isolated LSEC as well as LMEC (Esm-1, Aatf) and up-regulation of gene expression to LMEC levels (CXCR4, Apelin) confirmed true transdifferentiation of LSEC in vitro. In addition, our analysis identified a novel 26-kDa single-pass transmembrane protein, liver endothelial differentiation-associated protein (Leda)-1, that was selectively expressed in all liver endothelial cells and preferentially localized to the abluminal cell surface. Upon forced overexpression in MDCK cells, Leda-1 was sorted basolaterally to E-cadherin-positive adherens junctions, suggesting functional involvement in cell adhesion and MCE公司 polarity. Conclusion: Comparative microvascular analysis in rat identified a hepatic microenvironment-dependent LSEC-specific differentiation program including the novel junctional molecule Leda-1. HEPATOLOGY 2010 Endothelial cells (ECs) display marked heterogeneity in different organs and in different segments of the vascular tree. Liver sinusoidal endothelial cells

(LSECs) are a prime example of uniquely differentiated microvascular EC that exert highly specialized functions as professional endocytes1 and participate in induction of hepatic immune tolerance.2 For endocytosis, LSEC express a broad range of different scavenger receptors including Stabilin-1 and Stabilin-2, two members of a novel scavenger receptor gene family selectively expressed in sinusoidal ECs that have been identified and thoroughly characterized by us.3 Stabilin-2 is the major hyaluronan scavenger receptor of the liver, whereas Stabilin-1 mediates endocytosis of acLDL (low density lipoprotein) and SPARC. Stabilin-1 and -2 use the constitutive clathrin-mediated endocytic pathway in LSEC (4); in addition, Stabilin-1 fulfills a second role as an intracellular cargo carrier.

Key Word(s): 1. miR-155; 2. EMT; 3. ERK1

pathway; 4. HSC; Presenting Author: SHIRAN SHETTY Additional Authors: KRISHNAVENI JANARATHANAN, LEELAVENKATAKRISHNAN VENKATAKRISHNAN Corresponding Author: SHIRAN SHETTY Affiliations: PSGIMSR Objective: Bacterial infections are the common cause of morbidity and mortality in chronic liver disease patients. Infections in patients with liver disease have a different clinical presentation and early identification is important for good outcome. Increasing prevalence and antibiotic resistance are on the rise. we aimed selleck chemicals to evaluate the recent changes in microorganisms causing clinical/ sub-clinical infections in cirrhotic patients and their antibiotic resistance pattern. Methods: In this retrospective study, 150 patients of chronic liver disease admitted in department of gastroenterology PSG medical college hospital, Coimbatore india were

included in this study over one year. Institutional Ethics Committee approval was obtained regarding inclusion and exclusion criteria, prior to commencement of study. Results: Of the 150 patients, 58 (38.7%) were found to have culture positive infection. While the most common bacteria isolated from our study was E coli, we also noticed an increasing trend of Gram positive organisms like Staphylococcus. click here Our study showed nearly 50% of organism being resistant to 3rd generation Cephalosporins and fluoroquinolones, unlike previous studies. Conclusion: Appropriate usage of antibiotics and strict adherence

of hospital antibiotic policy is required to prevent emergence of resistant organism. Key Word(s): 1. cirrhosis; 2. bacteria infection; 3. resistance; 4. Ecoli; Presenting Author: JUAN ZHAO Additional Authors: NAN TANG, KAIMING WU, WEIPING DAI, CHANGHONG YE, JIAN SHI, BEIFANG NING, XIN ZENG, YONG LIN Corresponding Author: XIN ZENG, YONG LIN Affiliations: Shanghai Changzheng Hospital, Second Military Medical University; Department of Gastroenterology, Shanghai Changzheng Hospital Objective: Activation of extracellular signal-regulated kinase 1 (ERK1) signaling pathway in hepatic stellate cell (HSC) and epithelial-mesenchymal transition (EMT) process in hepatocyte are considered as the important contributors to promoting accumulation of activated fibroblasts and exacerbating hepatic fibrosis. Enhancement of microRNA-21 (miR-21) expression has been 上海皓元医药股份有限公司 confirmed in activated HSC and fibrotic liver. The aim of this study was to explore the mechanism of miR-21 participating in the simultaneous regulation of ERK1 pathway and EMT process in both of HSC and hepatocyte during hepatic fibrogenesis. Methods: miR-21 levels were determined in liver tissues or serum from fibrotic models or serum from patients. Luciferase reporter assay was performed to validate whether miR-21 could directly target sprouty2 (Spry2) and hepatocyte nuclear factor 4α (HNF4α) through 3′-untranslated region (3′-UTR) interactions respectively.

2% of controls (p=0.02). This trend was even more pronounced among OAC patients with moderate to severe rejection in 23.3% of narcotic users versus 3.9% of controls (p=0.002). At 6 months post-transplant (t=6m), 27.3% were narcotic users including 25.7% of whites, 30.4% of blacks and 29.8% of others. Among patients alive and on narcotics at t=6m, 91.7% of narcotic users survived to 1 year versus 97.4% of controls (p=0.04). 75% of t=6m narcotic users FK506 supplier survived

to 3 years post-transplant versus 88% of controls (p=0.01). OAC patient group had increased mortality when on narcotics at t=6m with 3 year survival of 81.8% versus 74.3 (p=0.172). In patients with hepatitis C on narcotics 3 year survival was 90.1% versus 76.9% in controls (p=0.76). CONCLUSION Chronic narcotic use in the periliver transplant period significantly decreases long-term survival and increases moderate to severe rejection rates. Pretransplant narcotic use had significant survival disadvantage regardless of etiology. Post-transplant narcotic use was harmful in all patients, and most significantly in those with a history of alcoholic liver disease. Disclosures: Syed-Mohammed R. Jafri – Advisory Committees or Review Panels: Gilead

The following people have nothing to disclose: Mina Pirzadeh, Amir Prushani, Maria C. Segovia Background. Liver transplantation (LT) is the treatment for terminal liver diseases. Long term survival MCE is excellent, however immunosuppressive drugs required for rejection Selleckchem ALK inhibitor prophylaxis are responsible of side effects such as infections, malignancies or renal failure. The modulation of host immune system to induce tolerance is a promising new approach to reduce immunosuppressive treatment. Particularly, the promotion of natural CD4+ CD25+ FoxP3+ regulatory T cells (Tregs) could be crucial for operational tolerance. Tacrolimus is usually included in standard immunosuppression protocols after LT and has been shown to have a deleterious effect on Treg population. In contrast, reports indicate that mTOR inhibitors, like everolimus, may have a positive impact on Tregs

and thus could favor the establishment of operational tolerance. Aim of the study. In this study, Tregs levels were evaluated in 30 liver transplant recipients included in a prospective study comparing tacrolimus-based and everolimus-based immunosuppressive regimens. Patients and methods. All study patients received tacrolimus during the first month after LT, then, were randomized to continue tacrolimus or to be progressively converted to everolimus. Blood samples were obtained before LT, one, three and six months after LT. Flow-cytometry immunophenotyping of Tregs (CD4+ CD25+ CD127- FoxP3+) was performed using freshly isolated PBMC. Tregs were isolated from PBMC using magnetic sorting to assess their immunosuppressive capacities. Results.

D., Brent Neuschwander-Tetri, M.D., Elizabeth M. Brunt, M.D., Debra King, R.N. (Saint Louis University School of Medicine, St. Louis, MO (Contract N01-DK-9-2324); Jules L. Dienstag, M.D., Raymond T. Chung, M.D., Andrea E. Reid, M.D., Atul K. Bhan, M.D., Wallis A. Molchen, David P. Lundmark (Massachusetts General Hospital, Boston, MA; Contract N01-DK-9-2319, Grant M01RR-01066; Grant 1 UL1 RR025758-01, Harvard Clinical and Translational Science Center); Talazoparib purchase Gregory T. Everson, M.D., Thomas Trouillot, M.D., Marcelo Kugelmas, M.D., S. Russell Nash, M.D., Jennifer DeSanto, R.N., Carol McKinley, R.N. (University of Colorado Denver, School of Medicine, Aurora, CO; Contract N01-DK-9-2327, Grant M01RR-00051,

Grant 1 UL1 RR 025780-01); John C. Hoefs, M.D., Choon Park, R.N. (University of California, Irvine, Irvine, CA; Contract N01-DK-9-2320, Grant M01RR-00827); William M. Lee, M.D., Thomas E. Rogers, M.D., Peter F. Malet, M.D., Janel Shelton, Nicole Crowder, L.V.N., Rivka Elbein, R.N., B.S.N., Nancy Liston, M.P.H. (University of Texas Southwestern Medical Center, Dallas, TX; Contract N01-DK-9-2321, Grant M01RR-00633, Grant 1 UL1 RR024982-01, North and Central Texas Clinical and Translational Science Initiative); Karen L. Lindsay, M.D., M.M.M., Sugantha Govindarajan, M.D., Carol Epigenetics Compound Library in vitro B. Jones, R.N., Susan L. Milstein,

R.N. (University of Southern California, Los Angeles, CA; Contract N01-DK-9-2325, Grant M01RR-00043); Robert J. Fontana, M.D., Joel K. Greenson, M.D., Pamela A. Richtmyer, L.P.N., C.C.R.C., R. Tess Bonham, B.S. (University of Michigan

Medical Center, Ann Arbor, MI; Contract N01-DK-9-2323, Grant M01RR-00042, Grant 1 UL1 RR024986, Michigan Center for Clinical and Health Research); Mitchell L. Shiffman, M.D., Richard K. Sterling, M.D., M.Sc., Melissa J. Contos, M.D., A. Scott Mills, M.D., Charlotte Hofmann, R.N., Paula Smith, R.N. (Virginia Commonwealth University Health System, Richmond, VA; Contract N01-DK-9-2322, Grant M01RR-00065); Marc G. Ghany, M.D., T. Jake Liang, M.D., David Kleiner, M.D., Ph.D., Yoon Park, R.N., Elenita Rivera, R.N., Vanessa Haynes-Williams, R.N. (Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD); 上海皓元医药股份有限公司 Leonard B. Seeff, M.D., Patricia R. Robuck, Ph.D., Jay H. Hoofnagle, M.D., Elizabeth C. Wright, Ph.D. (National Institute of Diabetes and Digestive and Kidney Diseases, Division of Digestive Diseases and Nutrition, Bethesda, MD); Chihiro Morishima, M.D., David R. Gretch, M.D., Ph.D., Minjun Chung Apodaca, B.S., A.S.C.P., Rohit Shankar, B.C., A.S.C.P., Natalia Antonov, M. Ed. (University of Washington, Seattle, WA; Contract N01-DK-9-2318); Kristin K. Snow, M.Sc., Sc.D., Anne M. Stoddard, Sc.D., Teresa M. Curto, M.S.W., M.P.H. (New England Research Institutes, Watertown, MA; Contract N01-DK-9-2328); Zachary D. Goodman, M.D., Ph.D.