We hypothesized that ARG might be driving the evolution to ALF, if values JNK inhibitor of ARG were lower than expected in ALF patients, suggesting a muted immune response in this setting. Methods: Serum levels of ARG-1 isotype were measured using a sandwich type ELISA employing HRP-labeled antibody in 107 HBV patients with different phenotypes: HBV-ALF (non-immunosuppressed), acute HBV with

recovery, chronic hep B (with and without flares of activity), and, as controls, 20 acetaminophen-related ALF, 10 chronic hepatitis C and 10 healthy subjects. Results: Healthy controls had median ARG of 5 ng/mL, chronic HBV and HCV ∼25-30 ng/mL (Table), while acute HBV, HBV flares and HBV-ALF median levels were 89.2, 78.4 and 69.5 ng/mL, respectively, markedly lower than APAP median level of 968 ng/mL. HBV-ALF

ARG levels were actually lower than acute or flare HBV despite comparable aminotransferase levels. Particularly low values for ARG were found in those who died of HBV-ALF (median 30.4 ng/ mL; n=5). For chronic HBV phenotypes with relatively low AST values there was poor correlation of AST with ARG (Spearman rho); only flare or APAP patients showed strong correlations (rho >0.75). Summary/Conclusions: Despite massive hepato-cyte necrosis, low ARG levels characterize HBV-ALF and, to a lesser Selleckchem GSK-3 inhibitor extent, acute HBV patients, supporting the postulate of ARG-driven immunomodulation in hepatitis B. A genetically mediated alteration in ARG protein might account for the low levels observed. Further understanding of the significance of ARG levels in these settings will require mechanistic or genomic studies. Median Arginase, AST Results and Correlationby Categories and Etiologies Disclosures: William M. Lee – Consulting: Eli Lilly, Novartis; Grant/Research Support: Gilead, Roche, Vertex, BI, Anadys, BMS, merck; Speaking and Teaching: Merck Background and aims: Some orthotopic liver transplantation (OLT) patients experience HBV recurrence with detectable HBV-DNA despite hepatitis B immune globulin+lamivudine

(HBIg+LAM) prophylaxis. We analyzed changes in the HBV-qua-sispecies in patients with recurrent HBV post-OLT. Methods: Twenty-nine OLT patients included in a previous study(1) to compare LAM vs. LAM+HBIg in preventing HBV recurrence learn more were followed for >10 years (mean, 154.9 months [50-188]). In patients with recurrent HBV after OLT, defined as detectable HBV-DNA by real-time PCR, a region of HBV surface gene (S, codons s92-s200), including the “a” determinant, was studied by ultra-deep pyrosequencing (UDPS, GS-Junior, Roche). Results: Twelve (41%) of 29 patients had detectable HBV-DNA at some timepoint after OLT. In addition, 4 of them were HBsAg positive. Among patients with recurrent HBV, one with, and three without HBsAg had available pre- and post-OLT samples with HBV-DNA above 10E3 IU/mL and were selected for UDPS analysis (table).

BDL, bile duct ligation; BSA, bovine serum albumin; cAMP, cyclic adenosine monophosphate; CCl4, carbon tetrachloride; ERK1/2, extracellular signal-regulated ABT199 kinase; FACS, fluorescence-activated cell sorting; IBDM, intrahepatic bile duct mass; MEK, mitogen-activated protein kinase kinase;

PCNA, proliferating cell nuclear antigen; PCR, polymerase chain reation; PKA, protein kinase A; SEM, standard error of the mean; SR, secretin receptor; WT, wild-type. Reagents were purchased from Sigma Chemical Co. (St. Louis, MO) unless otherwise stated. The nuclear dye 4′,6-diamidino-2-phenylindole was obtained from Molecular Probes, Inc. (Eugene, OR). Porcine secretin was purchased from Peninsula Laboratories (Belmont, CA). The polyclonal SR antibody (Santa Cruz Biotechnology, Santa Cruz, CA) was raised against a peptide mapping at the C terminus of SR of human origin and cross-reacts with mouse.20 The antibody

against proliferating cell nuclear antigen (PCNA) was purchased from Santa NVP-LDE225 supplier Cruz Biotechnology. The mouse anti–cytokeratin-19 antibody was purchased from Caltag Laboratories Inc. (Burlingame, CA). Goat phosphorylated ERK1/2 and total ERK1/2 (44-42 kDa) polyclonal affinity purified antibodies were purchased from Santa Cruz Biotechnology. The RIA kits for the determination of intracellular cAMP levels in cholangiocytes were purchased from Perkin Elmer (Shelton, CT). All animal experiments (Table 1) were performed in accordance with a protocol approved by the Scott & White and Texas A&M Health Science Center Institutional Animal Care and Use Committee and conformed to the Guide for the Care and Use of Laboratory Animals published

by the National Institutes of Health (Publication No. 85-23, revised 1996). Our SR+/+ (wild-type [WT]) or SR knockout (SR−/−)21 mice were maintained in a temperature-controlled environment (20-22°C) with a 12:12-hour light/dark cycle. We used adult male WT and SR−/− mice (approximately 25-30 g) of the N5 generation: (1) as normal treated with saline (0.9% NaCl) or secretin selleck kinase inhibitor (2.5 nmol/kg/day, a dose similar to that used by us for another gastrointestinal hormone, gastrin, in rodents)18 by way of intraperitoneally implanted Alzet osmotic minipumps (Alzet, CA) for 7 days; or (2) for sham operation or BDL (for 3 and 7 days).5, 20, 22 Because our previous studies21 showed that SR−/− mice have a renal defect in water reabsorption and associated polyuria and polydipsia, experiments were performed to determine whether the response of SR−/− mice to BDL was due to the lack of SR rather than severe dehydration. Thus, we evaluated changes in body weight and mortality rate in the experimental groups of Table 1. In addition, both WT and SR−/− mice (after BDL or administration of secretin) received oral hydration therapy, consisting of up to 1 ml of normal saline subcutaneously up to twice daily along with water in gel form on the ground and food supplements.

6 mm versus 21 mm). Representative cases are illustrated in Fig. 1. There were nine cases (24%; cases 2, 13, 17, 22, 27, 29, 30, 33, 45) showing disagreement between routine histological analysis and combined RXDX-106 supplier histological analysis. Immunohistochemistry was in agreement with the final diagnosis of surgical specimens in six cases (67%) by correctly reclassifying five HCAs that were initially considered unclassified on routine histological analysis into three telangiectatic/inflammatory and two steatotic LFABP-negative. Data are provided in Table 1. Subtyping of hemorrhagic HCAs was possible in all cases. The diagnostic results

of the two radiologists, routine and combined histological analysis by HCA subtype are set out in Table 2. Representative cases are illustrated in Figs. 2-4. The distribution of patients having MR features suggestive of either steatotic LFABP-negative HCAs or telangiectatic/inflammatory HCAs are shown in Figs. 5 and 6. In addition, there were no statistical differences in correct subtyping between HCA

<5 cm and those >5 cm (imaging: 80% versus 87.5% P = 0.45, routine biopsy: 66.7% versus 81.3%, P = 0.27, and combined biopsy analysis 75% versus 84.6%, (P = 0.48). Agreement between the evaluation of MRI findings by the senior radiologist and routine histological Ulixertinib chemical structure analysis was 74.5% (CI: 59%-87%) corresponding to a kappa value of 0.54 (CI: 0.34-0.74). There was disagreement in 12 cases (cases 6, 9, 17, 22, 30, 31, 32, 33, 36, 37, 41, 47). Correct classification was obtained at MRI and biopsy in seven and three cases, respectively. In 2/12 cases (17%) the lesions were misclassified by both. Agreement between assessment of MRI findings by the senior radiologist and the combined histological analysis was 63.2% (CI: 45%-79%) (kappa = 0.36,

CI: 0.13-0.60). There was disagreement in 14 cases (cases 2, 6, 9, 13, 22, 27, 29, 32, 33, 36, 37, 41, 45, 47). Correct classification was obtained at MRI and immunohistochemistry in seven and seven cases, respectively. Diagnostic values and likelihood ratios when MRI and routine histological analysis agreed were further assessed according to HCA subtypes. MRI and routine histological analysis were in agreement and correct in classifying 25 of the 34 cases of telangiectatic/inflammatory HCA (sensitivity 73.5%; CI: 55%-88%). check details None of the HCAs were incorrectly classified as telangiectatic/inflammatory (specificity 100%; CI: 75%-100%). When there was agreement for a diagnosis of telangiectatic/inflammatory subtype, the LR was 20.4 (CI: 1.3-313). MRI and routine histological analysis were in agreement and correct in classifying 7 of the 11 cases of steatotic LFABP-negative HCAs (sensitivity 63.6%; CI: 30%-90%). Only one HCA was incorrectly labeled steatotic (specificity 97,2%; CI: 85%-100%). When they agreed on the diagnosis of steatotic, the LR was 22.9 (CI: 3.1-167).

On the other hand, hepatocytes derived from iPS cells do appear to be true to their nature as shown by “proof of concept” experiments from Sullivan et al.22 Their assessment of P450 components cytochrome P450 1A2 (CYP1A2) and CYP3A4 are convincing

among each iPS cell–derived line. Also notable is their test of iPS cells RG7204 from both genders and different races. Their finding that race and gender are not factors for generating functional hepatocytes from iPS cells adds an exclamation point onto their findings. A number of unique highlights are also found in the work from Stephen Duncan’s laboratory. Most notable is the explicit attention in establishing a protocol for generating specific endodermal cell types including definitive endoderm, specified hepatic cells, hepatoblasts, and hepatocytes. Existing protocols for generating hepatocytes from hESCs and adult stem cells have generally included steps where ill-defined components are added to the culture medium. Here, Si-Tayeb et al.23 describe how they eliminate the use of serum, the feeder cell layer, the formation of embryoid bodies, and undefined reagents. Such detail enables anyone with an interest in this field

a simple, straightforward approach for Acalabrutinib concentration generating hepatocytes. Also highlighted is their evidence demonstrating the evolutionary importance of this differentiation process; results from both mouse and human iPS cells aptly parallel each other. However, MCE probably their most impressive feature is the approach used to test the efficacy of the hepatocytes derived from iPS cells. By using tetraploid complementation in a mouse model, they demonstrate that iPS cells could follow the hepatocyte developmental pathway in vivo, and all liver cell types were represented in the iPS cell–derived embryos.

Although the tetraploid complementation approach has been used by a number of investigators to circumvent embryonic lethality in knockout mouse models,24, 25 this was one of the first studies to utilize it as a functional assay showing the fate of a certain cell type (i.e., iPS cells). In essence, Duncan’s group cemented the fact that iPS cells can be used in every respect to ESCs for liver regeneration and for studying pathogens as the cause of hepatocyte and liver dysfunction. Looking ahead, the showing development of hepatocytes from iPS cells could potentially revolutionize hepatology with respect to the study of hepatitis B and C viruses, alcohol-induced cirrhosis, and congenital liver diseases. In vivo, iPS cell–derived hepatocytes will most likely advance the concept of tissue therapies particularly with respect to the autologous nature of these cells.

0% in the control group. Xiang et al. described a similar trend in subjects affected by Crohn’s disease, who were positive at biopsy in 27.1% of cases, much less than in the control group (47.9%), with CDK activity no particular difference in the extension of the disease [32]. Looking more closely, the prevalence of this infection appears to have declined over the last decade. Indeed Triantafillidis et al. estimated the prevalence of this infection at 35.5% in 2002, and 24% in 2012 in the IBD group [33]. Finally, Hansen et al. [34] investigated microaerophilic microbiota in the colon of a pediatric population affected by IBD at the onset, showing that Campylobacter appears to be surprisingly common (around

8% of pediatric colonic biopsies), while Helicobacter species are relatively rare. It has been hypothesized that H. pylori could exert an immunomodulatory action on the intestinal mucosa [35], thus protecting against IBD but, at the moment, there is only a speculative observation that H. pylori infection has a relative risk for IBD of 0.43–0.59 [36]. Therefore, in the absence of strong evidence, the most reasonable BI 6727 mw explanation is that this trend could be attributed to previous antibiotic treatments, very frequent in subjects suffering from IBD [33]. It is a debated topic whether H. pylori might induce direct damage on the intestinal mucosa. Kim et al. reported multiple small bowel ulcerative lesions associated with H. pylori in an 11-year-old girl without any

systemic disease [37]. Authors justified this event due to a weak mucosal defense mechanism against the bacterium for a structural deformity of the duodenal bulb caused by a previous gastrotomy. Even though a clear relationship

could not be found, basic research demonstrated that H. pylori can use its pathogenic action against colonic cells, when they produce a gastric mucin (MUC5AC) [38]. Finally, secretory antibodies can modulate the progress of H. pylori infection, particularly in the duodenum, as shown by Gorrell et al.: Knockout mice for polymeric immunoglobulin receptors had a very intense colonization of the duodenum [39]. Competing interests: The authors have no competing interests. “
“Background: Helicobacter pylori infection has been proved to be of great relevance to public health in unindustrialized countries, especially in low socioeconomic groups. Poor 上海皓元 hygiene, deficient sanitation, and crowded conditions have been reported as risk factors for this infection. In this work, we investigated whether social and demographic characteristics were associated with anti-H. pylori IgG antibodies in 1104 children aged 4–11 years old from Salvador, a large city located in northeastern Brazil. Methods:  Standardized questionnaires were used to obtain social, demographic, and environmental data for the studied population in two periods of time (from 1997 to 2003 and in 2005). Anti-H. pylori IgG antibodies were assessed by indirect enzyme-linked immunosorbent assay in 2005. Results:  Anti-H.

CONCLUSION: Our results reveal that the SphK1-S1P axis has a pivotal role in liver injury and suggests that it deserves consideration as a therapeutic target for acute liver failure. Disclosures: Arun J. Sanyal – Advisory Committees or Review Panels: Gore, Gilead, Abbott, Ikaria; Consulting: Salix, Immuron, Exhalenz, Bayer-Onyx, Genentech, Norgine, GalMed, Novartis,

Echosens, Takeda; Grant/Research Support: Salix, Genentech, Genfit, Intercept, Ikaria, Takeda, Gilead; Independent Contractor: UpToDate The following people have nothing to disclose: Dorit Avni, Wei-Ching Huang, Jeremy Allegood, Sarah Spiegel Alcoholic liver disease (ALD) is Talazoparib associated with a spectrum of liver injury ranging from steatosis and steatohepatitis to fibrosis and cirrhosis. In Ceritinib mw response to gut-derived lipopolysaccharide (LPS), activation of Kupffer cells plays a key role in the development and progression of ALD by secreting a variety of proinflammatory

cytokines. Consequently, inhibition of macrophage-activation would have therapeutic benefits for alleviating the progression of ALD. Salidroside (Sal), one of main bioactive components isolated from Rhodiola Sachalinensis, has been reported to suppress LPS-induced inflammatory response, but the underlying mechanisms in macrophages remain poorly understood. In this study, we investigate the anti-inflammatory effects of Salidroside and the possible mechanisms in LPS-stimulated phrobol 12-myristate 13-acetate (PMA)-differentiated

上海皓元 THP-1 macrophage models. The results showed that Sal markedly decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2(COX2), interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) at both mRNA and protein levels, and there was dose-effect relationship between the three Sal pre-treated groups. Further studies revealed that Sal strongly suppressed NF-κB activation and down-regulated the phosphorylation of ERK, p38 and JNK. Our present study demonstrated that Sal could suppress the production of iNOS, COX2, IL-1 β, IL-6 and TNF-α in LPS-stimulated PMA-differeti-ated THP-1 cells by inhibiting NF-κB activation and MAPK signal pathway phosphorylation. Disclosures: Qin Ning – Advisory Committees or Review Panels: ROCHE, NOVARTIS, BMS, MSD, GSK; Consulting: ROCHE, NOVARTIS, BMS, MSD, GSK; Grant/Research Support: ROCHE, NOVARTIS, BMS; Speaking and Teaching: ROCHE, NOVARTIS, BMS, MSD, GSK The following people have nothing to disclose: Hongwu Wang, Ting Wu, Junying Qi, Yaqi Wang, Xiaoping Luo Background: Liver cell injury in alcoholic hepatitis (AH) is in part, due to macrophage generated proinflammatory cytokines i.e. M1 i, M2a, M2b, and M2c might be involved in ALD. The T cell response to chemokines and cytokines differs not only when M1 and M2 macrophages are compared but even when individual M2 subtypes are profiled.

McGovern – Employment: AbbVie Andrew R. Lloyd – Grant/Research Support: Merck Maria Prins – Speaking and Teaching: msd, roche check details Gregory J. Dore – Board Membership: Bristol-Myers Squibb, Roche, Gilead, Merck, Janssen, Abbvie; Grant/Research Support: Janssen, Bristol-Myers Squibb, Vertex, Roche, Gilead, Merck, Abbvie; Speaking and Teaching: Roche, Merck, Janssen Jason Grebely – Advisory Committees or Review Panels: Merck, Gilead; Grant/ Research Support: Merck, Gilead, Abbvie, BMS The following people have nothing to disclose: Behzad Hajarizadeh, Bart P. Grady, Kimberly Page, Andrea Cox, Thomas M. Rice, Rachel Sacks-Davis, Julie Bruneau, Meghan D. Morris, Janaki

Amin, Janke Schinkel, Tanya L. Applegate,

Lisa Maher, Margaret Hellard Background Vertical transmission of Hepatitis C Virus (HCV) from mother to infant is the most common route of infection among children. Five percent of infants born to mothers with chronic HCV are unable to clear the infection by 18 months and live with chronic Crizotinib manufacturer disease. HCV positive infants and young children are often asymptomatic so screening in the early years of life is crucial for appropriate diagnosis. There are guidelines that require testing of both hepatitis B virus positive pregnant mothers and their infants, but no protocols exist for perinatal HCV. This study demonstrates provider success in appropriately testing infants born to HCV positive mothers in a major US city with a high burden of HCV. Methods HCV antibody and RNA tests reported to the Philadelphia Department of Public Health (PDPH) between 2008 and 2013 were used to identify maternal and infant testing. Additional tests were retrospectively collected from the three largest laboratories serving the pediatric population. Datasets were matched

with 2011-2013 birth certificates to identify infants born to HCV infected mothers and to ascertain reporting of infant testing practices. HCV seropositivity among infants born to HCV positive mothers was compared to the expected rate of 5%. Results PDPH received reports on 8,152 females 上海皓元 who were HCV positive and 12-45 years of age in 2011-2013. Of these, 730 (9%) were found to have delivered at least 1 child, accounting for 816 (1%) of the 74,718 infants born in Philadelphia in the study period. Forty-six of these infants matched to the HCV data (6% overall; 17% from RNA positive mothers), 3 (7%) of whom were RNA-positive. Assuming a rate of 5%, an additional 38 infants would be expected to develop chronic HCV infection. Discussion Repetitive and conclusive testing of pregnant women and infants in their first 18 months is necessary to identify vertical transmission of HCV and initiate infected infants into care.

The nt sequence identities of resultant CP- and polyprotein-encoding sequences against the type isolate of the AO strain were >98.5 and >98.8%, respectively, confirming that all the 17 isolates are of the same genetic group. Estimates of nt diversity showed that the EAPV population in Amami-O-shima had low diversity through the genome and all the genes were under negative selection, but the genetic constraints were varied

between different protein-encoding regions. Phylogenetic analyses revealed that EAPV isolates showed a star-like phyl-ogeny based on their CP-encoding regions, and it is suggested that the population in Sumiyo has expanded recently. “
“Reduced flower pigmentation in the legume Swainsona formosa is associated with increased susceptibility to Phytophthora cinnamomi and other soil-borne

pathogens. see more This study aimed to identify the mechanism for these differences in susceptibility. Chemical analyses of stem tissues that had been previously inoculated with P. cinnamomi revealed that neither anthocyanin nor total phenolic content increased with infection. Such results suggested that observed differences in susceptibility, as indicated by flower colour, were related to preformed rather than induced stem chemistry. Acetone extracts from healthy, uninfected stem tissues of a red-flowered line were highly toxic to the fungus, while extracts from a white-flowered line were non-toxic and those from a pink-flowered line were intermediate Torin 1 in toxicity and this was correlated with the total phenolic and proanthocyanidin concentration of the extracts. Precipitation of proanthocyanidins with bovine serum albumen removed the toxicity of the extracts. It was concluded that differences in the proanthocyanidin content of tissues contributed MCE to the differences in disease susceptibility of plants with different flower colours. “
“The castor bean cercospora leaf

spot (Cercospora ricinella Sacc. & Berl.) is a common disease in castor bean crop (Ricinus communis L.), causing defoliation and losses. In spite of this, the evaluation of disease severity is an important decision support for adoption of strategies and tactics for disease control. Therefore the objective of this work was to elaborate and to validate a diagrammatic to evaluate cercospora leaf spot severity in the castor bean. The scale was developed based on six treatments with different irrigation depths plus the control treatment without irrigation. Based on disease incidence analysis, it was possible to select different severity levels per treatment, which were used to define the percentage intervals of foliar diseased area of the diagrammatic scale.

While the use of such a proxy for sun time may be justified for short-term studies close to the equator, where the difference is small, the increase of this difference with increasing duration

and latitude has never been quantified. We thus aimed at characterizing the potential error in recording behaviours with a clock, according to study duration and geographical location. The main goal of this work is to provide a simple tool for correcting the time at which behaviours are recorded when using a clock in order to make it corresponds to solar time. To highlight the importance of this, we first used a simple mathematical model to investigate the potential error of recording behaviours based on ‘clock time’, according to both the location and the duration of the study. BVD-523 clinical trial We used the example of a simulated behaviour set at sunrise for ease of demonstration. We then used a real high throughput screening compounds dataset, from a long-term study of the ecology of African wild dogs, Lycaon pictus, in Zimbabwe, to illustrate how using clock time rather than sun time may result in some artificial noise and thus

to different conclusions regarding the observed behaviours. Moreover, we assessed the frequency of using a clock to record behaviours in published studies. We investigated 100 peer-reviewed papers studying various species and behaviours, lasting for different 上海皓元 periods of time and located in a wide range of latitudes. Finally, we discuss the implication of this factor for the future collection of ethological,

behavioural and demographic data as well as for the analysis of existing data. Determining the time of sunset (-rise) according to the date and latitude (Meeus, 1991; Meeus & Savoie, 1995; Savoie, 2001; and see Appendix S1) enables us to model an event occurring at sunrise (and recorded by clock time). Then, we intend to estimate the loss of information expressed as the noise due to change in sunrise while recording data using clock time. We set a hypothetical behaviour occurring at sunrise. The demonstration holds for other moments of the day, such as zenith or sunset. For the sake of realism, the occurrence of this behaviour is not instantaneous, but rather follows a normal distribution centred on sunrise: (1) The density of probability reaches its maximum at HSrise, meaning the best way to observe the behaviour is to watch the individuals at this time of the day. The probability density decreases symmetrically around its maximum, meaning the further one is from HSrise, the less chance one has to observe the behaviour. If a behaviour is to be observed daily over an N-day period, one can assess the overall distribution of the timing of the behaviour using either sun time or clock time.

Lake, MD 9:50 – 9:55 AM Discussion 9:55 – 10:15 AM Surviving and Thriving with Value and Excellence From an Administrative Perspective Jennifer

Milton, RN, MSN 10:15 – 10:20 AM Discussion 10:20 -10:30 AM Break Session II: Successes and Challenges in Sustaining Excellence in Private Health Care Systems 10:30 – 10:50 AM Perspectives From A Surgical Program Director William C. Chapman, MD 10:50 – 10:55 AM Discussion 10:55 – 11:15 AM Perspectives From A Medical Program Director-Private Sector James F. Trotter, MD 11:15 – 11:20 AM Discussion 11:20 – 11:40 INCB024360 nmr AM Surviving and Thriving with Value and Excellence Karen Hess, RN, MS, MBA, ACNP 11:40 – 11:45 AM Discussion 11:45 AM – Noon Panel Discussion Meet-the-Professor Luncheon Saturday, November 2 12:15 -1:15 PM Refer to your luncheon ticket for meeting

room location. MTP-1 Use of Statins in Patients with Liver Disease Curtis K. Argo, MD and Naga P. Chalasani, MD MTP-2 Safe Prescribing in Liver Disease James H. Lewis, MD and Timothy J. Davern, MD MTP-3 Herbs and Natural Remedies in Patients with Liver Disease Victor J. Navarro, MD and Leonard B. Seeff, MD MTP-4 HCV: Treat Now or Wait Paul J. Pockros, MD and Christoph Sarrazin, MD MTP-5 HCV: Side Effects of New selleck products Antiviral Agents John F. Reinus, M.D. and Reem H. Ghalib, MD MTP-6 Hepatitis C Management in the Liver Transplant Candidate Catherine T. Frenette, MD and Marina Berenguer, MD MTP-7 The Hepatitis C Drug Pipeline Douglas T. Dieterich, MD and Raymond T. Chung, MD MTP-8 Optimal Management of Hepatic Encephalopathy Norman Gitlin, MD and Kevin D. Mullen, MD MTP-9 Viral Hepatitis and HIV Infection Norbert Brau, MD and Maribel Rodriguez-Torres, MD MTP-10 Viral Hepatitis in Patients Undergoing

Heart, Kidney and Bone Marrow Transplants Michael P. Curry, MD and Maya Gambarin-Gelwan, MD MTP-11 HCC: How to Screen Roniel Cabrera, MD and Jose Franco, MD MTP-12 NAFLD: Who to Biopsy Neeral L. Shah, MD and Nizar N. Zein, MD MTP-13 OLT: Improving Long-term Outcomes Francisco A. Durazo, MD and Jacqueline G. O’Leary, MD MTP-14 Endoscopy Issues in Patients with End-stage Liver Disease Vijay Shah, MD and Bruce A. Luxon, MD, PhD MTP-15 Alcoholic Hepatitis: MCE公司 What Should I do? Philippe Mathurin, MD, PhD and Timothy R. Morgan, MD Poster Session I Saturday, November 2 2: 00 – 7: 30 PM Hall E Refer to page 92A for Poster Presentations Exhibit Hall Opening and Reception Saturday, November 2 5: 00 – 7: 30 PM Hall D Transplant Surgery Workshop Saturday, November 2 3:30 – 7:00 PM Room 146A Management of Rare Liver Tumors COURSE DIRECTORS: Sasan Roayaie, MD Kenneth D. Chavin, MD, PhD 3.5 CME Credits The program will provide the audience with an evidence based review of the current diagnostic and treatment strategies for less commonly encountered liver tumors.