21, Fig. 7B,C). Expression of the hepatocyte mitogen HGF also did not change (Fig. 7E). In keeping with human chronic liver disease, increased numbers of LPCs were present in CCl4-injured mice. Three days after BMM delivery, whole tissue mRNA levels of the LPC marker CK-19 were increased by 55% over control recipients (1.55 ± 0.1 versus 1.00 ± 0.2, P = 0.05). By day 7, there was a periportal expansion of PCK and Dlk+ LPCs in BMM recipients. The number of LPCs increased by 40% over control (P < 0.05, Fig. 7B,D).

HER2 inhibitor There was no increase in the level of the cytokines IL-6 and TNF-α which are associated with LPC proliferation10 (Fig. 7F). Donor BMMs used here express high levels of the LPC mitogen TWEAK relative to recipient liver (Fig. 1E).

Three days after BMM therapy, at a time when hepatic macrophage numbers were increased, whole liver TWEAK mRNA levels were significantly elevated to 216% of control (P < 0.05, Fig. 7E). IGF-1 mRNA levels were increased 3 and 7 days after BMM delivery (P < 0.05 and 0.001, respectively, Fig. 7E). CSF-1 protein levels increased to 165% 1 day after BMM delivery (P < 0.01, Fig. 7F) before decreasing over the first week. Vascular endothelial growth factor (VEGF) protein levels increased ATR inhibitor over this period in BMM recipients, reaching 127% of control at day 7 (P < 0.05, Fig. 7F). In addition to the up-regulation of these reparative factors, the increased TWEAK expression and expanded LPC compartment are also implicated in the improved hepatic function in BMM-treated mice. Cell therapy based on a defined, Sclareol homogenous

cell population adds clarity to the cause-effect relationship. Importantly for clinical translation, our data reveal that unfractionated BM had a deleterious effect on liver fibrosis. Interestingly, exogenous macrophage precursors did not significantly improve liver fibrosis. Of note, this population contains Gr-1hi (Ly-6Chi) monocytes15 that have profibrogenic actions during liver injury.23 Following culture in CSF-1 conditioned medium, CSF-1R+ macrophage precursors within BM differentiate into macrophages.15 The BMMs used here are a relatively homogenous population of cells without significant contamination from other cell types such as monocytes, granulocytes, and stem cells. The differentiated macrophages generated by this process are antifibrotic and proregenerative in this model. Unmanipulated BMMs cultured in these nonadherent conditions possess neither the typical classically (M1) nor alternatively activated (M2) profiles. Donor BMM engraftment was transient; however, their effects persisted and were amplified by paracrine signaling to host cell populations. The net effect was a reduction in fibrosis and improved regeneration of the injured liver. BMM therapy caused the recruitment of MMP producing host cells into the hepatic scar.

“
“In patients with chronic hepatitis C, the hepatitis C virus (HCV) RNA level is an important predictor of treatment response. To explore the relationship of HCV http://www.selleckchem.com/products/AZD2281(Olaparib).html RNA with viral and demographic factors, as well as IL28B genotype, we examined viral levels in an ethnically diverse group of injection drug users (IDUs). Between 1998 and 2000, the Urban Health Study (UHS) recruited

IDUs from street settings in San Francisco Bay area neighborhoods. Participants who were positive by HCV enzyme immunoassay were tested for HCV viremia by a branched-chain DNA assay. HCV genotype was determined by sequencing the HCV nonstructural 5B protein region. For a subset of participants, IL28B rs12979860 genotype was determined by Taqman. Among 1,701 participants with HCV viremia, median age was 46 years and median duration of injection drug use was 26 years; 56.0% were African American and 34.0% were of European ancestry

(non-Hispanic). Human immunodeficiency virus type 1 (HIV-1) prevalence was 13.9%. The overall median HCV RNA level was 6.45 log10 copies/mL. In unadjusted analyses, higher levels were found with older age, male gender, African-American ancestry, hepatitis B virus infection, HIV-1 infection, and IL28B rs12979860-CC genotype; compared to participants infected with HCV genotype 1, HCV RNA was lower in participants ABT-263 supplier with genotypes 3 or 4. In an adjusted analysis, age, gender, racial ancestry, HIV-1 infection, HCV genotype, and IL28B rs12979860 genotype were all independently selleck screening library associated with HCV RNA. Conclusion: The level of HCV viremia is influenced by a large number of demographic, viral, and human genetic factors. (HEPATOLOGY 2012;56:86–94) Chronic infection with hepatitis C virus (HCV) is a leading cause of hepatocellular carcinoma, end-stage liver disease, and liver transplantation.1 Successful antiviral treatment (i.e., sustained virological response; SVR) reduces the risk of these outcomes. Higher HCV RNA levels are associated with a lower rate of

SVR to current standard pegylated interferon (Peg-IFN)/ribavirin (RBV) therapy2 and, possibly, higher rates of maternal-fetal transmission.3 In previous studies, a number of factors have been shown to be associated with higher HCV RNA levels, including demographic, viral, and human genetic factors,4-7 but, to our knowledge, no previous study has looked at all of these elements simultaneously. The incidence and prevalence of HCV infection among injection drug users (IDUs) are high. The Urban Health Study (UHS) was an epidemiological and interventional research project that enrolled a multiethnic population of IDUs in the San Francisco Bay area. Between 1998 and 2000, we collected data and specimens from these persons for studies of demographic, viral, and host determinants of infection with viruses that may cause cancer.

Consequently, the FVIII–VWF complex serves critical roles in mediating primary haemostasis, and coagulation. The FVIII mRNA and protein have been identified in many human tissues including the spleen, lung and kidney; however the liver is likely to constitute the primary source of FVIII

synthesis in vivo [4–9]. The cell type(s) within the liver principally responsible for the synthesis and secretion of FVIII have not been clearly delineated. Although hepatocytes have been shown to synthesize FVIII, increasing evidence suggests that hepatic sinusoidal endothelial cells (EC) may be of prime importance. FVIII mRNA and protein has been demonstrated in both human and murine liver sinusoidal EC [5–7]; transplantation of Daporinad clinical trial Staurosporine order normal murine sinusoidal EC into a mouse model of haemophilia A has recently been shown to effectively restore normal haemostasis [10]. In vivo biosynthesis of VWF is restricted to EC and megakaryocytes [11,12], though quantitative expression of VWF varies significantly between different vascular beds. Histological studies of animal tissue have shown that VWF expression is significantly higher in venous as compared with arterial EC, and also that secretion is increased in larger vessels [7,13,14]. Highest VWF levels were reported in the lung and brain, with very low levels of expression in the liver [14]. Despite the association of FVIII

and VWF in the peripheral circulation, there is no direct evidence to suggest that VWF and FVIII are actually synthesized together in any particular Teicoplanin cell type

in vivo. Nevertheless expression studies have shown that FVIII and VWF can be co-synthesized, transported to storage granules and released by endothelial cell lineages and megakaryocytes [15–17]. Numerous indicators suggest that limited co-expression may exist in vivo, it is well recognized that the administration of vasopressin or its pharmaceutical analogue desmopressin (DDAVP) results in a transient increase in VWF and FVIII levels. This ability has led to the widespread use of DDAVP in the treatment of patients with VWD and mild haemophilia A patients. Interestingly, recent studies have demonstrated that whilst liver transplantation cures haemophilia A, subsequent infusion of DDAVP in these patients produced a transient increase in plasma VWF levels, but did not further increase plasma FVIII levels [18], whereas non-haemophilic liver transplant recipients demonstrate responses in both VWF and FVIII following DDAVP. Furthermore DDAVP administration does not significantly increase plasma FVIII levels in patients with type 3 VWD [19]. Cumulatively, these data further support the hypothesis that a co-synthesized, releasable pool of FVIII–VWF may indeed exist in vivo [19]. The FVIII binds to VWF with high affinity (Kd approximately 0.2–0.5nm) [20,21].

Symptoms of any coexistent FGID were highly prevalent, even in those with currently-inactive IBD (57%). Conclusions:  Symptoms consistent with FGID are highly prevalent Ulixertinib in IBD and correlate with greater psychological comorbidity and poorer HRQoL in a “load-dependent” fashion. Therapy directed either at symptom load or psychological comorbidity might independently improve HRQoL in IBD. “
“To date, intergenotypic recombinant hepatitis C viruses (HCVs) and their treatment outcomes have not been

well characterized. This study characterized 12 novel HCV recombinant strains and their response to sofosbuvir in combination with ribavirin (SOF/RBV) treatment. Across the phase II/III studies of SOF, HCV samples were genotyped using both the Siemens VERSANT HCV Genotype INNO-LiPA 2.0 Assay (Innogenetics, Ghent, Belgium) and nonstructural (NS)5B sequencing. Among these patient samples, genotype assignment discordance between the two methods was found in 0.5% of all cases DAPT nmr (12 of 2,363), of which all were identified as genotype 2 by INNO-LiPA (12 of 487; 2.5%). HCV full-genome sequences were obtained for these 12 samples by a sequence-independent amplification method coupled with next-generation sequencing. HCV full-genome sequencing revealed

that these viruses were recombinant HCV strains, with the 5′ part corresponding to genotype 2 and the 3′ part corresponding to genotype 1. The recombination breakpoint between genotypes 2 and 1 was consistently located within 80 amino acids of the NS2/NS3 junction. Interestingly, one of the recombinant viruses had a 34-amino-acid duplication at the location of the recombination breakpoint. Eleven of these twelve patients were treated with a regimen for genotype 2 HCV infection, but responded as if they had genotype 1 infection; 1 patient had received

placebo. Conclusion: Twelve new HCV intergenotypic recombinant genotype 2/1 viruses have been characterized. The antiviral response to a 12- to 16-week course of SOF/RBV treatment in these patients was more similar to responses among genotype 1 patients than genotype 2 patients, consistent with their genotype 1 NS5B gene (Hepatology 2014) “
“The benefit of extending treatment duration with peginterferon (PEG-IFN) and ribavirin (RBV) Ribonuclease T1 from 48 weeks to 72 weeks for patients with chronic hepatitis C genotype 1 infection has not been well established. In this prospective, international, open-label, randomized, multicenter study, 1,428 treatment-naïve patients from 133 centers were treated with PEG-IFN alfa-2b (1.5 μg/kg/week) plus RBV (800-1,400 mg/day). Patients with detectable hepatitis C virus (HCV) RNA and a ≥2-log10 drop in HCV RNA levels at week 12 (slow responders) were randomized 1:1 to receive 48 weeks (n = 86) or 72 weeks (n = 73) of treatment.

027).58 This is the first study to suggest that therapy may actually impact the natural history of the disease. More recently, Gluck et

al. described a 20 year experience with endoscopic therapy for 84 symptomatic patients with PSC.59 Similar to the Baluyut study, observed patient survival was higher than expected by the Mayo Risk Score.59 All therapeutic endoscopy comes with risk. In the two largest reported series of patients with long follow-up, the risk of complications was 7.3%–20%. The complications were mild without need for surgical intervention.58, 59 The most common complications were pancreatitis, cholangitis, biliary tract perforation and hemorrhage. Focal PF-01367338 order biliary tract obstruction, whether benign or malignant, has been the primary indication for the nontransplant surgical management of PSC. Despite limitations of the accuracy of current diagnostic modalities for malignancy in PD0325901 datasheet PSC, diagnostic laparotomy has little clinical value. The rationale for surgical management in PSC is bypass of an obstruction caused by a dominant stricture. Non-transplant surgical approaches include biliary bypass by cholangio-enterostomy or resection of the extrahepatic biliary stricture and Roux

Y hepaticojejunostomy.60, 61 Biliary bypass alone has been employed infrequently because dominant strictures are typically hilar. Moreover, the intrahepatic ducts are variably involved which limits the access and quality of these ducts for bypass.60 17-DMAG (Alvespimycin) HCl Biliary bypass has no role in PSC patients with cirrhosis. Extrahepatic

bile duct resection and Roux Y hepaticojejunostomy with or without stenting for dominant strictures is controversial.53, 61 Current evidence suggests that selected patients with non-cirrhotic stage PSC have an overall survival of 83% at 5 years and 60% at 10 years and a readmission free rate from cholangitis of 57% at 3 years for such an approach.62 Bilirubin levels > 2 mg/dL and cirrhosis are associated with decreased survival. No data regarding surgical management have shown that either bypass or resection of a dominant stricture affect natural history or disease progression. Most patients, who have not had biliary tree instrumented, have negative microbial bile cultures.63, 64 However, dominant strictures can induce stagnation of bile resulting in bacterial colonization and secondary cholangitis. This can be the first presentation of the disease occurring in 6.1% of PSC patients in one recent study.65 Furthermore, severe recurrent cholangitis may play a role in the progression of the disease. The relevance of a bile duct stricture was demonstrated by documenting bacterial infection of the bile in 15 out of 37 PSC patients (40.5%) with a dominant stricture but not in the absence of such stenosis; short-course antibiotic treatment proved not very effective in eradicating bacteria from the bile ducts of patients with dominant strictures.

10 Primary antibodies were mouse monoclonal anti-PCNA (1:1000) or anti-cyclin D1 (1:500) www.selleckchem.com/products/Everolimus(RAD001).html and secondary antibody was peroxidase-conjugated goat anti-mouse IgG antibody (1:5000), all from Santa Cruz Biotechnology. Proteins were visualized by an enhanced chemiluminescence assay kit (ECL Plus; GE Healthcare). Signals were quantified

using ImageJ. Quantification relative to β-actin (mouse monoclonal 1:100,000; Sigma) was performed on 8-10 animals/group. Total RNA was extracted using RNeasy Mini kit (Qiagen). Real-time polymerase chain reaction (RT-PCR) was carried out on a LightCycler (Roche), using Quantitech SYBR Green PCR kit (Qiagen), with oligonucleotide primers from MWG Biotech (see Supporting Material). The PCR-amplified products were analyzed on a 2% agarose gel and sequenced. Data are from 6-10 animals/group. Hepatic myofibroblasts were obtained selleck chemicals llc by outgrowth of explants prepared from surgical specimens of

human normal liver, as described.23 This procedure was performed in accordance with ethical regulations imposed by the French legislation. Experiments were performed on confluent cells that were made quiescent by 48 hours incubation in serum-free medium. Bone-marrow–derived macrophages (BMDM) were isolated from bone marrow obtained from posterior leg bones of WT mice, following differentiation in Hank’s balanced salt solution completed with supernatant from L-cells for 5 days. BMDM were collected, allowed to adhere on six-well dishes and further treated with 5 μM JWH-133 for 7 hours. The purity of BMDM was > 95%. Results are the mean of triplicate determinations

on five wells/condition. Proteins (50 μg) from liver homogenates were obtained as described23 and separated on a 10% polyacrylamide gel containing 1 mg/mL of bovine skin gelatin (Sigma). After washing for 2 hours in 2.5% Triton X-100, gels were incubated for 18 hours at 37°C in 50 mM Tris pH 7.8 containing 5 mM CaCl2, stained Celecoxib with Coomassie blue, destained in methanol 25%/acitic acid 10%, and fixed in methanol 10%/glycerol 5%. Values represent means ± standard error of the mean. Results were analyzed by either Mann-Whitney test or one-way or two-way analysis of variance followed by multiple comparison test, as appropriate. P < 0.05 was taken as the minimum level of significance. Administration of CCl4 was associated with a 10-fold induction of CB2 messenger RNA (mRNA) expression at 24 hours that was maintained after 48 hours (Fig. 1A). CB2 receptors were not detected in hepatocytes isolated from either control or CCl4-treated animals (Fig. 1B). In contrast, nonparenchymal cells showed basal expression of CB2 receptors and marked induction following CCl4 administration (Fig. 1B). Toxic damage induced by CCl4 is associated with activation of Kupffer cells and hepatic myofibroblasts, and promotes infiltration of the liver by inflammatory cells (monocytes/macrophages and neutrophils) all of which express CB2 receptors.

10 Primary antibodies were mouse monoclonal anti-PCNA (1:1000) or anti-cyclin D1 (1:500) find more and secondary antibody was peroxidase-conjugated goat anti-mouse IgG antibody (1:5000), all from Santa Cruz Biotechnology. Proteins were visualized by an enhanced chemiluminescence assay kit (ECL Plus; GE Healthcare). Signals were quantified

using ImageJ. Quantification relative to β-actin (mouse monoclonal 1:100,000; Sigma) was performed on 8-10 animals/group. Total RNA was extracted using RNeasy Mini kit (Qiagen). Real-time polymerase chain reaction (RT-PCR) was carried out on a LightCycler (Roche), using Quantitech SYBR Green PCR kit (Qiagen), with oligonucleotide primers from MWG Biotech (see Supporting Material). The PCR-amplified products were analyzed on a 2% agarose gel and sequenced. Data are from 6-10 animals/group. Hepatic myofibroblasts were obtained PF-01367338 research buy by outgrowth of explants prepared from surgical specimens of

human normal liver, as described.23 This procedure was performed in accordance with ethical regulations imposed by the French legislation. Experiments were performed on confluent cells that were made quiescent by 48 hours incubation in serum-free medium. Bone-marrow–derived macrophages (BMDM) were isolated from bone marrow obtained from posterior leg bones of WT mice, following differentiation in Hank’s balanced salt solution completed with supernatant from L-cells for 5 days. BMDM were collected, allowed to adhere on six-well dishes and further treated with 5 μM JWH-133 for 7 hours. The purity of BMDM was > 95%. Results are the mean of triplicate determinations

on five wells/condition. Proteins (50 μg) from liver homogenates were obtained as described23 and separated on a 10% polyacrylamide gel containing 1 mg/mL of bovine skin gelatin (Sigma). After washing for 2 hours in 2.5% Triton X-100, gels were incubated for 18 hours at 37°C in 50 mM Tris pH 7.8 containing 5 mM CaCl2, stained Resminostat with Coomassie blue, destained in methanol 25%/acitic acid 10%, and fixed in methanol 10%/glycerol 5%. Values represent means ± standard error of the mean. Results were analyzed by either Mann-Whitney test or one-way or two-way analysis of variance followed by multiple comparison test, as appropriate. P < 0.05 was taken as the minimum level of significance. Administration of CCl4 was associated with a 10-fold induction of CB2 messenger RNA (mRNA) expression at 24 hours that was maintained after 48 hours (Fig. 1A). CB2 receptors were not detected in hepatocytes isolated from either control or CCl4-treated animals (Fig. 1B). In contrast, nonparenchymal cells showed basal expression of CB2 receptors and marked induction following CCl4 administration (Fig. 1B). Toxic damage induced by CCl4 is associated with activation of Kupffer cells and hepatic myofibroblasts, and promotes infiltration of the liver by inflammatory cells (monocytes/macrophages and neutrophils) all of which express CB2 receptors.

3 pg/ml (range, 43.0-5556.3 pg/ ml). Serum

DKK-1 levels did not correlate with those of AFP or des-γ-carboxy prothrombin (DCP). When cut off value of 450 pg/ml was used, sensitivity Angiogenesis inhibitor and specificity of DKK-1 for HCC were 26.8% and 88.9%, respectively. HpSC-HCCs showed poor prognosis with high serum DKK-1 levels compared with MH-HCCs who received surgery, and HCC patients showed elevation of DKK-1 (DKK-1 high HCC) showed a significantly high frequency of portal vein invasion (p < 0.001). Among Barcelona Clinic Liver Cancer (BCLC) stage C patients treated with sorafenib or hepatic arterial infusion chemotherapy using interferon-α/5-FU/cisplatin, DKK-1high HCCs showed a significantly poor prognosis compared with DKK-1 low HCCs (median overall survival 10.6 vs. 13.2 months: p=0.03, and 4.1 vs. 26.7 months: p=0.01, respectively). The expression of DKK1 was correlated to the EpCAM expression, in vitro. Furthermore, anti-DKK1 antibody administration suppressed tumor formation ability of EpCAM-positive HCC cells,

in vivo(p=0.044). Conclusions Serum DKK-1 is elevated in HCC with stem cell features. The poor response of DKK-1 high HCCs to sorafenib or cytotoxic reagents warrants the needs for the development of a novel treatment strategy against this deadly HCC subtype. Disclosures: ��-catenin signaling Shuichi Kaneko – Grant/Research Support: MDS, Co., Inc, Chugai Pharma., Co., Inc, Toray Co., Inc, Daiichi Sankyo., Co., Inc, Dainippon Sumitomo, Co., Inc, Ajinomoto Co., Inc, MDS, Co., Inc, Chugai Pharma., Co., Inc, Toray Co., Inc, Daiichi Sankyo., Co., Inc, Dainippon Sumitomo, Co., Inc, Ajinomoto Co., Inc, Bayer Japan The following people have nothing to disclose: Hajime Sunagozaka, Taro Yamashita, Naoki Oishi, Takehiro Hayashi, Hajime Takatori, Tetsuro Shimakami, Kazuya Kitamura,

Kuniaki Arai, Takashi Kagaya, Yoshio Sakai, Tatsuya Yamashita, Eishiro Mizukoshi, Masao Honda Background: Hepatocellular carcinoma (HCC) is one of the cancer types with poor prognosis. At present, serum tumor markers of HCC such as alpha-fetoprotein (AFP), prothrombin induced by vitamin K absence II (PIVKA II) or alpha-fetoprotein Lens culinaris agglutinin 3 (AFP-L3%) are not adequate to predict survival or recurrence after curative hepatectomy. We reported Fatty Acid Binding Protein 5 (FABP5) was a significant prognostic and recurrence factor SSR128129E for HCC patients by immunohistochemical analysis and showed positive correlation of tumor size, intrahepatic metastasis, and micro/macro vascular invasion (Ohata T, et al. AASLD Liver Meeting 2013). Purposes: To examine a correlation between the expression of FABP5 and malignant behavior of HCC using human HCC cell lines. Methods: Protein expression of FABP5 in HCC cell lines (HLE, HLF, Li7, HepG2 and Hep3B) was assessed by western blot analysis. Lentiviral short-hairpin RNA (shRNA) vectors were used to suppress FABP5 expression in higher expression cells or lentiviral overexpression vectors to express FABP5 in lower expression cells.

, MD (Early Morning Workshops) Advisory Committees or Review Panels: Janssen, Merck, Genentech, BMS, Gilead, Boehinger Ingelheim, AbbVioe Consulting: Genentech, Lumena, Regulus, Beckman Coulter, RMS Grant/Research Support: Novartis, Intercept, Janssen, Genentech, BMS, Gilead, Vertex, MDV3100 order Boehinger Ingelheim, Lumena, Beckman Coulter, AbbVie, RMS, Novartis, Merck Speaking and Teaching: Genentech, BMS, Gilead Podskalny, Judith, PhD (Career Development Workshop) Nothing to disclose Poelstra, Klaas, PhD (Basic Research Workshop) Consulting: BiOrion Technologies BV Grant/Research Support: BiOrion Technologies

BV Stock Shareholder: BiOrion Technologies BV Pomposelli, James, MD, PhD (Parallel Session) Nothing to disclose Poordad, Fred, MD (General Hepatology Update) Advisory Committees or Review Panels: Abbott, Achillion, BMS, Inhibitex, Boeheringer Ingelheim, Pfizer, Genentech, Idenix, Gilead, Merck, Vertex, Rucaparib cost Salix, Janssen, Novartis Grant/Research Support: Abbott, Anadys, Achillion, BMS, Boehringer Ingelheim, Genentech, Idenix, Gilead, Merck, Pharmassett, Vertex, Salix, Tibotec/Janssen, Novartis Porte, Robert J., MD, PhD, FEBS (AASLD/ILTS Transplant Course) Advisory Committees or Review Panels: Organ Assist Quigley, Eamonn M., MD (AASLD Postgraduate Course) Advisory Committees

or Review Panels: Salix, Shire, Almirall, Ironwood/Forest Board Membership: Alimentary Health Consulting: Alimentary Health, Vibrant Grant/Research Support: Ironwood/Forest, Rhythm, Norgine Speaking and Teaching: Procter and Gamble, Janssen, Shire, Almirall Stock Shareholder: Alimentary Health Rafii, Shahin, MD (Basic Research Workshop) Consulting: Angiocrine Bioscience Ramsay, Michael A., MD (Transplant Surgery Workshop) Grant/Research Support: Masimo Inc Reddy, K. Gautham, MD (Competency Training Workshop) Advisory Committees or Review Panels: AASLD Transplant Hepatology Pilot Steering Ergoloid Committee, ACG Training Committee, Program Director’s

Caucus Steering Committee Grant/Research Support: Intercept, Ocera, Merck, Lumena Reddy, K. Rajender, MD (Advances for Practitioners, Meet-the-Professor Luncheon) Advisory Committees or Review Panels: Genentech-Roche, Merck, Janssen, Vertex, Gilead, BMS, Novartis, Abbvie Grant/Research Support: Merck, BMS, Ikaria, Gilead, Janssen, AbbVie Rehermann, Barbara, MD (AASLD Postgraduate Course, Early Morning Workshops, Parallel Session) Nothing to disclose Reich, David J., MD (Plenary Session) Consulting: VTI Grant/Research Support: VTI Speaking and Teaching: neuwave Renz, John F., MD, PhD (AASLD/ILTS Transplant Course) Nothing to disclose Reuben, Adrian, MBBS, FRCP, FACG (Early Morning Workshops, State-of-the-Art Lecture) Nothing to disclose Rex, Douglas K.