Studies using combinations of DAA agents with PEG-IFN/RBV have been initiated, and these studies will multiply. Whether or not RBV (and TBV) can be eliminated altogether remains to be determined. Particularly for those patients with unfavorable treatment characteristics, RBV may remain a part of our therapeutic armamentarium for years to come; if so, TBV could be an option with

the potential to limit toxicity and potentially reduce costs. The ideal study may combine TBV with a DAA agent and PEG-IFN and compare this to RBV to determine if SVR rates can be preserved or improved by the minimization of dose reductions and the reduction of the emergence of resistance. Because of the long wait between the approval of PEG-IFN and RBV and the yet-to-come approval of DAA agents, we should not discount the potential Roscovitine research buy contribution of TBV. Many promising agents have already been stopped

in development because of a lack of efficacy or toxicity.22, MG-132 nmr 23 Thus, if TBV can be shown to preserve or improve efficacy rates in combination with DAAs and PEG-IFN and bring lower rates of anemia, the use of TBV in these clinical settings would be a welcome addition to the HCV armamentarium as we begin to expand the HCV populations that we treat.1 “
“Peritoneovenous shunt (PVS) is accepted as a treatment for refractory ascites due to liver cirrhosis. Infection is a well-known complication of shunting. However, the effects of PVS in terms of complications for renal disease are unclear. We encountered a case involving a 52-year-old man with alcoholic liver cirrhosis and complications of nephrotic syndrome that were worsened by PVS. He received PVS for refractory ascites due to alcoholic liver cirrhosis

before coming to our hospital for evaluation for liver transplantation. Nephrotic syndrome was then identified due to cirrhosis-related membranoproliferative SPTLC1 glomerulonephritis (MPGN). Prednisolone was administrated at 60 mg/day for MPGN. On day 5, he showed grade IV hepatic encephalopathy (West Haven criteria). Tapering prednisolone and intestinal cleansing with lactulose treatment improved hepatic encephalopathy, but hyperammonemia persisted and the PVS was removed. After shunt removal, urinary protein levels decreased from 4–6 g/day to 0.3–0.5 g/day and ammonia levels decreased. PVS may increase the excretion of urinary protein and increase ammonia levels in patients with complications of glomerulonephritis. “
“Lipocalin-2 (Lcn2) is preferentially expressed in hepatocellular carcinoma (HCC). However, the functional role of Lcn2 in HCC progression is still poorly understood, particularly with respect to its involvement in invasion and metastasis.

Among the families enrolled in MIBS, approximately 70% were found to be concordant in which either all or none of the siblings had a history of inhibitors Erlotinib order [6]. The con- and discordancies in each subgroup of mutation are shown in Fig. 1. The concordance in the families with inhibitors was approximately 40%. The corresponding figures for the families with intron 22 inversions were 63% and 40%, respectively. In two families with large gene deletions, none of the siblings had an inhibitor history, and although only a small proportion of the families with missense mutations, small deletions/insertions and splice site mutations experienced inhibitors,

all siblings in some of these families had high-responding inhibitors. The family data clearly indicate that additional inherited genetic determinants, other than the type of causative fVIII mutation, will be of major U0126 nmr importance in predicting the immunological outcome of replacement therapy. The HLA class

I alleles A3, B7 and C7, as well as the class II alleles DQA0102, DQB0602, DR15 have all been associated with higher risk for inhibitor development in unrelated patients [relative risk (RR) of 1.9–4.0], whereas the HLA C2, DQA0103, DQB0603 and DR13 alleles seem to be protective [7,8]. The reported associations were, however, weak and not statistically consistent. In the MIBS study, these alleles were equally distributed between the two patient groups [10].

Instead, significant associations were identified for two of the other class I alleles, i.e. HLA A26 and B44, but after correction for multiple comparisons no significant differences remained. IL-10 is an important anti-inflammatory cytokine exerting a broad spectrum of activities. IL-10 also enhances the in vitro production of all types of immunoglobulins by peripheral blood mononuclear cells in patients with autoimmune diseases and the serum concentration of IL-10 has been correlated to the disease activity in these patients [12,13]. The most interesting Buspirone HCl polymorphism with a functional implication described in the IL-10 gene is a 134 bp long variant of a CA microsatellite in the promoter region (IL-10.G) [14–16]. In the MIBS study, the allele 134 bp was identified in 44 of all 164 patients with haemophilia A (26.8%) [9]. Thirty-two of these 44 patients (72.7%) developed inhibitors compared with 45 of the 120 patients (37.5%) without the allele. Among all 77 patients with a history of inhibitors, allele 134 was found in 32 patients (41.6%) compared with 12 of the 87 inhibitor negative patients (13.8%; P < 0.001). This corresponds to an odds ratio (OR) of 4.4 with a 95% confidence interval (CI) of 2.1–9.5. A significant association between the allele and the development of inhibitors was also found in a subgroup analysis of patients with severe haemophilia A, i.e.

Among the families enrolled in MIBS, approximately 70% were found to be concordant in which either all or none of the siblings had a history of inhibitors p38 MAPK inhibitor [6]. The con- and discordancies in each subgroup of mutation are shown in Fig. 1. The concordance in the families with inhibitors was approximately 40%. The corresponding figures for the families with intron 22 inversions were 63% and 40%, respectively. In two families with large gene deletions, none of the siblings had an inhibitor history, and although only a small proportion of the families with missense mutations, small deletions/insertions and splice site mutations experienced inhibitors,

all siblings in some of these families had high-responding inhibitors. The family data clearly indicate that additional inherited genetic determinants, other than the type of causative fVIII mutation, will be of major GDC-0199 ic50 importance in predicting the immunological outcome of replacement therapy. The HLA class

I alleles A3, B7 and C7, as well as the class II alleles DQA0102, DQB0602, DR15 have all been associated with higher risk for inhibitor development in unrelated patients [relative risk (RR) of 1.9–4.0], whereas the HLA C2, DQA0103, DQB0603 and DR13 alleles seem to be protective [7,8]. The reported associations were, however, weak and not statistically consistent. In the MIBS study, these alleles were equally distributed between the two patient groups [10].

Instead, significant associations were identified for two of the other class I alleles, i.e. HLA A26 and B44, but after correction for multiple comparisons no significant differences remained. IL-10 is an important anti-inflammatory cytokine exerting a broad spectrum of activities. IL-10 also enhances the in vitro production of all types of immunoglobulins by peripheral blood mononuclear cells in patients with autoimmune diseases and the serum concentration of IL-10 has been correlated to the disease activity in these patients [12,13]. The most interesting Succinyl-CoA polymorphism with a functional implication described in the IL-10 gene is a 134 bp long variant of a CA microsatellite in the promoter region (IL-10.G) [14–16]. In the MIBS study, the allele 134 bp was identified in 44 of all 164 patients with haemophilia A (26.8%) [9]. Thirty-two of these 44 patients (72.7%) developed inhibitors compared with 45 of the 120 patients (37.5%) without the allele. Among all 77 patients with a history of inhibitors, allele 134 was found in 32 patients (41.6%) compared with 12 of the 87 inhibitor negative patients (13.8%; P < 0.001). This corresponds to an odds ratio (OR) of 4.4 with a 95% confidence interval (CI) of 2.1–9.5. A significant association between the allele and the development of inhibitors was also found in a subgroup analysis of patients with severe haemophilia A, i.e.

However, in addition to side effects common to immunomodulatory therapy, FTY720 was reported to cause cardiovascular complications, macular edema, and brain inflammation,4 presumably the result of interactions with more than one S1P-receptor subtype.8 Previously, we demonstrated that FTY720 induces learn more apoptosis in HCC cells through the reactive oxygen species (ROS)-dependent activation of protein kinase C (PKC)δ.7 Dissociation of the apoptosis-inducing activity of FTY720 from its S1P receptor agonist activity provides a basis for its pharmacological

exploitation to develop a novel class of antitumor agents. Here, we report the development of a nonimmunosuppressive FTY720 analogue, OSU-2S [(S)-2-amino-2-(4-[(6-methylheptyl)-oxy]phenethyl)pentan-1-ol], which exhibits higher in vitro and in vivo potency than FTY720 in suppressing HCC cell

growth through PKCδ signaling. CA-Akt, constitutively active Akt; DAPI, 4,6-diamidino-2-phenylindole; DCFDA (5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein diacetate); DMEM, Dulbecco’s modified Eagle medium; DMS, N,N-dimethylsphingosine; PD-0332991 ic50 DPI, diphenyleneiodonium; FBS, fetal bovine serum; GST-π, glutathione S-transferase-π; HA, hemagglutinin; HCC, hepatocellular carcinoma; Hep3B-luc, luciferase-expressing Hep3B; i.p., intraperitoneal; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide; PARP, poly (ADP-ribose) polymerase; p-FTY720, phosphorylated FTY720; PKCδ, protein kinase Cδ; PP2A, protein phosphatase 2A; ROS, reactive oxygen species; S1P, sphingosine-1-phosphate; siRNA, small interfering RNA; shRNA, short hairpin RNA; SphK2, sphingosine kinase 2; TLC, thin-layer chromatography; TMA, tissue Cytidine deaminase microarray. Details about reagents, their commercial sources, and experimental procedures are provided in the Supporting Information. The HCC cell lines, Hep3B, PLC5 and Huh7, and primary nonmalignant human hepatocytes were used in this study. FTY720 was synthesized as described,9 and p-FTY720 was purchased from Cayman Chemical (Ann Arbor, MI). Synthesis of OSU-2S and phosphorylated OSU-2S (p-OSU-2S) will be described elsewhere. Various polyclonal and monoclonal antibodies were used for western

blotting, immunocytochemical, and flow cytometric analyses. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assays as previously reported.10 For assessment of apoptosis, treated cells were stained with Annexin V-Alexa Fluor 488 and propidium iodide according to the vendor’s protocols. For caspase-3 activity, cells were incubated with the fluorogenic caspase-3 substrate (Ac-DMQD)2-Rh110 for 20 minutes. ROS production was detected using the fluorescence probe 5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (DCFDA) as described.7 Data were analyzed by ModFitLT V3.0 software program. Immunoblotting of biomarkers in cell lysates and tumor tissue homogenates was performed as reported.

However, in addition to side effects common to immunomodulatory therapy, FTY720 was reported to cause cardiovascular complications, macular edema, and brain inflammation,4 presumably the result of interactions with more than one S1P-receptor subtype.8 Previously, we demonstrated that FTY720 induces Angiogenesis inhibitor apoptosis in HCC cells through the reactive oxygen species (ROS)-dependent activation of protein kinase C (PKC)δ.7 Dissociation of the apoptosis-inducing activity of FTY720 from its S1P receptor agonist activity provides a basis for its pharmacological

exploitation to develop a novel class of antitumor agents. Here, we report the development of a nonimmunosuppressive FTY720 analogue, OSU-2S [(S)-2-amino-2-(4-[(6-methylheptyl)-oxy]phenethyl)pentan-1-ol], which exhibits higher in vitro and in vivo potency than FTY720 in suppressing HCC cell

growth through PKCδ signaling. CA-Akt, constitutively active Akt; DAPI, 4,6-diamidino-2-phenylindole; DCFDA (5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein diacetate); DMEM, Dulbecco’s modified Eagle medium; DMS, N,N-dimethylsphingosine; selleck kinase inhibitor DPI, diphenyleneiodonium; FBS, fetal bovine serum; GST-π, glutathione S-transferase-π; HA, hemagglutinin; HCC, hepatocellular carcinoma; Hep3B-luc, luciferase-expressing Hep3B; i.p., intraperitoneal; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide; PARP, poly (ADP-ribose) polymerase; p-FTY720, phosphorylated FTY720; PKCδ, protein kinase Cδ; PP2A, protein phosphatase 2A; ROS, reactive oxygen species; S1P, sphingosine-1-phosphate; siRNA, small interfering RNA; shRNA, short hairpin RNA; SphK2, sphingosine kinase 2; TLC, thin-layer chromatography; TMA, tissue Nintedanib (BIBF 1120) microarray. Details about reagents, their commercial sources, and experimental procedures are provided in the Supporting Information. The HCC cell lines, Hep3B, PLC5 and Huh7, and primary nonmalignant human hepatocytes were used in this study. FTY720 was synthesized as described,9 and p-FTY720 was purchased from Cayman Chemical (Ann Arbor, MI). Synthesis of OSU-2S and phosphorylated OSU-2S (p-OSU-2S) will be described elsewhere. Various polyclonal and monoclonal antibodies were used for western

blotting, immunocytochemical, and flow cytometric analyses. Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assays as previously reported.10 For assessment of apoptosis, treated cells were stained with Annexin V-Alexa Fluor 488 and propidium iodide according to the vendor’s protocols. For caspase-3 activity, cells were incubated with the fluorogenic caspase-3 substrate (Ac-DMQD)2-Rh110 for 20 minutes. ROS production was detected using the fluorescence probe 5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (DCFDA) as described.7 Data were analyzed by ModFitLT V3.0 software program. Immunoblotting of biomarkers in cell lysates and tumor tissue homogenates was performed as reported.

IL-28B polymorphisms and amino acid substitution in the HCV core region predicted SVR to telaprevir, MG-132 molecular weight pegylated interferon, and ribavirin.7 Mehta et al.8 reported an SVR rate of 21% in treated patients in an urban HIV clinic but only 0.7% in the full cohort; the latter was due to a low referral rate. New treatment strategies are needed for HCV-infected and HIV/HCV-coinfected patients in urban settings because of the low rates of SVR, particularly in genotype 1 HIV–infected non-Caucasian men.

If a larger series corroborates these results, maintaining the current standard of care in this subpopulation of HCV-infected individuals should be questioned. Using IL-28B genotyping to assist with treatment decisions and SB203580 deferring therapy until new targeted therapies are available should be considered. Clinicians are faced with the dilemma of recommending immediate treatment or warehousing patients (i.e., foregoing

standard-of-care treatment) in anticipation of novel therapies. Finally, when clinicians discuss the possible benefits and risks of hepatitis C therapy, the sobering, real-world treatment results should be made available to their patients. “
“Dill et al. demonstrated how aberrant activation of Notch2 signaling in albumin-expressing cells of AlbCre/N2ICD mice resulted in hepatocellular carcinomas (HCCs) associated with proliferation and expansion of immature biliary epithelial cells (BECs).[1] HCC formation was enhanced by treatment Rolziracetam with diethylnitrosamine (DEN), which induced the appearance of combined HCC-cholangiocarcinoma (CCC) and of CCC with immature BEC features.[1] Expansion of the BEC compartment in AlbCre/N2ICD mice mimics activation of hepatic stem cells (HpSCs) in human diseases characterized by Notch2 up-regulation.[2] Moreover, aberrant Notch2 signaling induces the formation of human liver cancers with HpSC features.[3] Thus, the HpSC compartment is the most likely candidate for oncogenic events in AlbCre/N2ICD mice, supporting the concept that a spectrum of liver cancers could originate from activation of HpSCs. Alternatively, it was proposed that CCCs might originate

from dedifferentiation of hepatocytes.[4, 5] This provocative assumption is based on observations by genetic tracing studies that CCCs arose from albumin- or transthyretin-expressing cells.[4, 5] However, albumin and transthyretin are expressed in cells undergoing liver differentiation from embryoid bodies[6] and in hepatic and biliary tree stem/progenitors in intrahepatic (canals of Hering) and/or extrahepatic (peribiliary glands) niches.[7, 8] In the studies by Dill et al.,[1] biliary hyperplasia and large biliary cyst formation were induced, even though the albumin gene promoter was targeted to induce selective hepatic N2ICD overexpression. Therefore, albumin-expressing cells in different anatomical sites could have been targeted.

Patient and disease specific characteristics including severity of chronic liver disease (Child-Pugh class), bleeding severity (Rockall & Glasgow-Blatchford scores; need for transfusion) and outcomes (mortality) were examined in relation to TTE. Results: Of

1766 patients referred, 79 patients with variceal bleed were included in the analysis, after excluding those with 1) endoscopy elsewhere prior to admission (n = 2) 2) bleeding during admission (n = 11) & 3) incomplete or unreliable data (n = 7). Mortality was similar in patients who received endoscopy within 15 hours (8/62) compared to those that did not (1/17) (p = 0.675). Median TTE for patients who died was significantly shorter than for survivors (2.1 vs. 8.23 hours, p = 0.04). There was a moderate inverse correlation between TTE and the full Rockall score (rs = -0.519 p < 0.001), and a weaker inverse correlation Alectinib in vivo with the pre-endoscopy Rockall Score (rs = -0.39, p < 0.001) and Glasgow Blatchford

score (rs = -0.371, p = 0.011, n = 46). When adjusted for age, gender, presentation symptoms of either haematemesis and/or melaena, blood transfusion, pre-endoscopy Rockall score and TTE, mortality was significantly increased only in patients with Child Pugh Class C (OR 12.3, 95% CI 1.21–125.2). Conclusion: Time to endoscopy does not affect mortality in patients with variceal bleeding. However, it is influenced by patient’s condition with Edoxaban patients with more severe disease or bleeding receiving

endoscopy sooner. When adjusted for other factors, Child Pugh Class C was the main risk factor for mortality. Key Word(s): 1. varices; 2. quality; BGJ398 purchase 3. endoscopy; Presenting Author: ROMAN PLAKHOV Additional Authors: SERGEY SHAPOVALYANZ, EVGENY FEDOROV, LUDMILA MICHALEVA, ZALINA GALKOVA, EKATERINA IVANOVA, ANDREY SERGEENKO, DENIS SELESNEV, EVGENYA POLUCHINA Corresponding Author: ROMAN PLAKHOV Affiliations: Moscow University Hospital 31 Objective: Assessment of currently available methods of diagnostics and treatment of patients with bleeding gastrointestinal subepithelial tumours (SET). Methods: From 01.01.1999 till 01.01.2013 243 patients with SET have been treated; the bleeding was revealed in 64 (26,3%) cases. Mean age was 57,2 ± 7,2 years, range from 16 to 89 years; male – 31 (48,4%), female – 33 (51,6%). Preliminary diagnosis was determined by urgent EGD in 48 patients; enteroscopy in 15, colonoscopy in 1; EUS have been used in 43 patients, X-ray in 19, CT-scan in 19, mesentericography in 2. Endoscopic interventions were performed with videogastroscopes EVIS GIF-1T140R, GIF-2T160, GIF-H180, videoenteroscope SIF-Q180, videocolonoscope CF-Q160ZL and various endoscopic instruments; EUS was performed with echo-endoscopes GF-UM160, GF-UM20 and EUS-centers EU-M20, EU-M60 (all – Olympus, Japan). Electrosurgical unit ICC200+APC300 (ERBE, Germany) was used to remove SET.

Results: Immunohistochemical analyses showed that the expression of claudin-4 in RE and BE tissues was increased compared with the NERD. There was a significant

correlation between DeMeester score and the level of the claudin4 expression (r = 0.53, P = 0.04). Bile salt induced claudin-4 and p38 MAPK expression in esophageal squamous cells. SB203580, an antagonist of p38, inhibited expressions of Claudin-4 induced by bile salt in esophageal squamous cells. Conclusion: Our findings suggest that bile salt exposure induce expression of tight junction protein claudin-4 in squamous epithelium in gastroesophageal reflux disease through a mitogen-activated protein kinase-dependent mechanism. Key Word(s): 1. GRED; 2. claudin-4; 3. p38; Presenting selleck chemicals Author: WEI ZHU Additional Authors: XIAOMING XIN Corresponding Author: WEI ZHU Affiliations: nanfang

hospital Objective: Heterotopic gastric mucosa (HGM) in duodenum is a rare congenital embryonic residual lesion, and patients always show the symptoms of functional learn more dyspepsia (FD) or chronic gastritis in clinical, so it has a big misdiagnosis rate. In this paper, we analyzed 134 cases of HGM in duodenum to investigate the characteristics ofits diagnosis and treatment. Methods: We performed gastroscopy, endoscopic resection and pathological examinationto patients who have symptoms of FD or chronic gastritis when HGM in duodenum was found. Meanwhile, we also analyzed Helicobacter pylori (Hp) infection and got symptom score before and after treatment using Glasgow score. Results: In all 4650 patients, 135 patients (2.9%) are diagnosed as HGM

in duodenum. The main symptoms of these patients are epigastric discomfort, acid reflux, bloating and so on. According to the Rome III standard classification, 92 cases (69.2%) can be diagnosed as postprandial distress syndrome (PDS) and 43 (31.8%) epigastricpain syndrome (EPS). HGM of the duodenum is mainly located in the duodenal bulb (93.3%) and rare in the descending part (6.7%). The morphology mainly divides into 4 types: the multiple nodular upliftis the most (57%), single polyp or multiple granular uplift (34.1%) are the second, and ulcerative (6.7%) and mess (2.2%) are the least. The last two types are easily oxyclozanide misdiagnosed as peptic ulcer or tumor because of their untypical morphology. It is meaningful to distinguish the atypical HGM using endoscopic ultrasound (EUS). The performance under the EUS is hypoechoic mass in the submucosa with anechoic shadow, but this characteristic is easily misdiagnosed as ectopic pancreas. Conclusion: HGM in duodenum is the reason why the symptoms in part of patients with FD or chronic gastritis attack again and again. And it will be helpful to improve the symptoms by resecting the HGM under the endoscopy. Key Word(s): 1. HGM; 2. Duodenum; 3. Functional dyspepsia; 4.

Results: Immunohistochemical analyses showed that the expression of claudin-4 in RE and BE tissues was increased compared with the NERD. There was a significant

correlation between DeMeester score and the level of the claudin4 expression (r = 0.53, P = 0.04). Bile salt induced claudin-4 and p38 MAPK expression in esophageal squamous cells. SB203580, an antagonist of p38, inhibited expressions of Claudin-4 induced by bile salt in esophageal squamous cells. Conclusion: Our findings suggest that bile salt exposure induce expression of tight junction protein claudin-4 in squamous epithelium in gastroesophageal reflux disease through a mitogen-activated protein kinase-dependent mechanism. Key Word(s): 1. GRED; 2. claudin-4; 3. p38; Presenting SCH727965 mouse Author: WEI ZHU Additional Authors: XIAOMING XIN Corresponding Author: WEI ZHU Affiliations: nanfang

hospital Objective: Heterotopic gastric mucosa (HGM) in duodenum is a rare congenital embryonic residual lesion, and patients always show the symptoms of functional buy ABT-263 dyspepsia (FD) or chronic gastritis in clinical, so it has a big misdiagnosis rate. In this paper, we analyzed 134 cases of HGM in duodenum to investigate the characteristics ofits diagnosis and treatment. Methods: We performed gastroscopy, endoscopic resection and pathological examinationto patients who have symptoms of FD or chronic gastritis when HGM in duodenum was found. Meanwhile, we also analyzed Helicobacter pylori (Hp) infection and got symptom score before and after treatment using Glasgow score. Results: In all 4650 patients, 135 patients (2.9%) are diagnosed as HGM

in duodenum. The main symptoms of these patients are epigastric discomfort, acid reflux, bloating and so on. According to the Rome III standard classification, 92 cases (69.2%) can be diagnosed as postprandial distress syndrome (PDS) and 43 (31.8%) epigastricpain syndrome (EPS). HGM of the duodenum is mainly located in the duodenal bulb (93.3%) and rare in the descending part (6.7%). The morphology mainly divides into 4 types: the multiple nodular upliftis the most (57%), single polyp or multiple granular uplift (34.1%) are the second, and ulcerative (6.7%) and mess (2.2%) are the least. The last two types are easily 3-mercaptopyruvate sulfurtransferase misdiagnosed as peptic ulcer or tumor because of their untypical morphology. It is meaningful to distinguish the atypical HGM using endoscopic ultrasound (EUS). The performance under the EUS is hypoechoic mass in the submucosa with anechoic shadow, but this characteristic is easily misdiagnosed as ectopic pancreas. Conclusion: HGM in duodenum is the reason why the symptoms in part of patients with FD or chronic gastritis attack again and again. And it will be helpful to improve the symptoms by resecting the HGM under the endoscopy. Key Word(s): 1. HGM; 2. Duodenum; 3. Functional dyspepsia; 4.

Nagorney, MD Session II: Adenoma 3:50 – 4:10 PM Imaging Characteristics of Adenomas BachirTaouli, MD 4:10 – 4:30 PM How Molecular and Immunohistochemical Analyses Can Help Us Guide Therapy For Hepatic Adenomas and FNH Jessica Zucman-Rossi, MD, PhD 4:30 – 4:50

PM Resection, Transplantation and Local Regional Therapies For Adenomas Jacques Belghiti, MD 4:50 – 5:10 PM Break Session III: Neuroendocrine Tumors 5:10 – 5:30 PM Imaging Characteristics of Neuroendocrine Tumors Bachir Taouli, MD GW 572016 5:30 – 5:50 PM Current NANETS and ENETS Guidelines for Management Of Neuroendocrine Tumors Diane Reidy, MD 5:50 – 6:10 PM Liver Transplantation for Neuroendocrine Tumors Vincenzo Mazzaferro, MD 6:10 – 6:30 PM Liver Resection and Local Regional Therapies for Neuroendocrine Tumors Timothy M. Pawlik, MD, PhD 6:30 – 6:40 PM Debate: Patients with Neuroendocrine Tumors Will Do Well No Matter What We Do – So Why Treat Them? Vincenzo Mazzaferro, MD 6:40 – 6:50

PM Debate: Patients with Neuroendocrine Tumor Will Do Better With Aggressive Treatment Timothy M. Pawlik, MD, PhD 6:50 – 7:00 PM Closing Remarks AASLD BUSINESS MEETING (MEMBERS ONLY) Saturday, see more November 2 5:15 – 6:15 PM Hall E – General Session Room J. Gregory Fiz, MD, presiding Early Morning Workshops Sunday, November 3 6:45 – 7:45 AM Refer to your luncheon ticket for meeting room location. Sunday Basic Early Morning Workshops Goals and Objectives: Bring together investigators in a specific area of research to discuss their ongoing work. Focus of discussions is on new work and not a review of previous studies. Allow ample time for questions from the audience. EMW-1 Artificial Liver Support Systems Jayanta Roy-Chowdhury, MD and Vicente Arroyo, EMW-2 HCV Replication Andrew H. Talal, MD and Raymond T.

Chung, MD EMW-3 Triggers of Fibrosis in NASH Ariel E. Feldstein, MD and Detlef Schuppan, MD, PhD EMW-4 Cholangiocyte Pathobiology Gianfranco Alpini, PhD and Marco Marzioni, MD EMW-5 Microbiome and the Liver Bernd Schnabl, MD and David Brenner, MD EMW-6 Animal Models of NAFLD Rohit Kohli, MD and Michael R. Charlton, MD anti-PD-1 antibody inhibitor Sunday Clinical Early Morning Workshops Goals and Objectives: Discuss difficult management issues utilizing acknowledged experts in the area. Provide an overview of the current state-of-the-art in each area. Allow ample time for questions from the audience. EMW-7 Imaging of Liver Tumors Claude B. Sirlin, MD and Laura M. Kulik, MD EMW-8 Liver Transplantation for Hepatitis C Xavier Forns, MD and Norah Terrault, MD EMW-9 New Anti-Tumor Agents in Development for HCC Jorge A. Marrero, MD and Josep M.