[6] Most of these findings usually followed reports of genetic predispositions in other autoimmune diseases and the contribution to liver-related autoimmunity remained unclear. Regarding the involvement of environmental triggers, several infections[7-9] and drug exposures were reported to precede the development of AIH, but so far no single causative agent has been identified. In addition, most patients are discovered late in the disease course and therefore infections preceding the diagnosis might not to be causative for the initiation of autoimmunity. It

rather seems as if there is a long lag-period between initiation of autoimmunity and diagnosis of symptomatic disease, as almost 40% present with liver cirrhosis at time of diagnosis. Therefore, the role of environmental triggers also remains unclear. However, the buy Seliciclib search for causative agents was supported by the idea of molecular

BMS-354825 mw mimicry between environmental agents and self-antigens, usually searching for molecular identity.[10] Animal models of AIH are usually restricted to short liver-specific immune responses usually ending in liver-specific tolerance rather than chronic autoimmunity. Although these models were very helpful in studying determinants of liver-specific immune responses, they were insufficient to explain AIH or to develop new therapeutic interventions. We developed a model of chronic AIH by infecting NOD mice with replication deficient adenoviruses expressing the human liver autoantigen formiminotransferase Non-specific serine/threonine protein kinase cyclodeaminase (FTCD), formally known as anti-liver cytosol type 1 (LC-1), which is one of the key antigens in AIH Type 2. The mice were developing a chronic hepatitis that closely resembled the human AIH for the first time. Using this model we could demonstrate that experimental murine AIH (emAIH) is just initiated by a strong inflammatory danger signal. This is just occurring in genetically predisposed individuals, explaining the low prevalence

of AIH in the general population. In addition, we could show that molecular similarity of the autoantigen is as efficient as molecular identity to lose tolerance against endogenous self-antigens. We could demonstrate that a break of humoral and cellular tolerance is required for the development of liver-specific autoimmunity and that CD4+ T cells act as drivers of the disease. Finally, classic immunosuppressive intervention with prednisolone and budesonide were successful in treating the disease. Taken together, we identified several key elements in the initiation of AIH. The model will be helpful to develop and test new therapeutic interventions in the future. Animal care and experiments were done in accordance with institutional and national guidelines.

The history revealed no other YAP-TEAD Inhibitor 1 nmr remarkable features. The examination revealed a palpable spleen. The investigations were normal as per previous case except for ESR >100 mmHg and CRP >200 mg/L. Ultrasound abdomen revealed splenomegaly with irregular hypoechoic regions and CECT of the abdomen confirmed multiple splenic abcesses. Blood cultures

grew Burkholderia pseudomallei. Blood picture was suggestive of bacterial sepsis and fever responded to IV meropenem. Conclusion: In patients with PUO and splenic abscesses in endemic areas, melioidosis should be entertained as a possible differential diagnosis. Key Word(s): 1. PUO Presenting Author: RAVINDRA L SATARASINGHE Additional Authors: SACHITH C WIJESIRIWARDENA, CHAMPIKA GAMAKARANAGE, NARMATHEY THAMBIRAJAH Corresponding Author: RAVINDRA L SATHARASINGHE Affiliations: Sri Jayawardenepura General Hospital, Sri Jayawardenepura General Hospital, Sri Jayawardenepura General Hospital Objective: To report a rare cause for haemoperitoneum. There are many causes resulting in a haemoperitoneum such as blunt or penentrating trauma

to the abdomen, tumour-associated haemorrhage or in blood dyscrasias. Splenic infarctions as a cause of frank hemoperitoneum has not been documented before, to the best of our knowledge. Methods: Case notes of a 54 year old adult Sri Lankan male, CP-673451 nmr who had been diagnosed to have chronic alcoholic cirrhosis, portal hypertension and bronchial Tyrosine-protein kinase BLK asthma, admitted with an acute abdomen and a hypotensive

state were retrospectively analysed. Examination had revealed presence of free fluid with mild tenderness and guarding of the abdomen. His previous abdominal scan revealed no ascites. Results: The investigations revealed the following: On the FBC, Hb was 11.5 g/dl, while other indices and cell lines were normal. CRP was 23 mg/L and the other biochemical and hematological investigations were unremarkable. Ultrasound abdomen showed free fluid. Peritoneal tap was blood stained with a Hb of 11.5 g/dl. Cells were obscured by blood. Clotting screen was normal. The first contrast CT scan abdomen was inconclusive and showed old findings of liver disease and the second paracentesis was dry. Second contrast CT abdomen done the following day revealed a peripheral splenic infarction. The patient had an uneventful recovery. Conclusion: Peripheral splenic infarction should be entertained as a cause for frank hemoperitoneum. Key Word(s): 1. Hemoperitoneum; 2.

Furthermore, to gain insight into the biological function of miR-152 overexpression in HCC cells, the 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) assay, flow cytometric analysis, and the Transwell invasion assay were performed in the constructed cell lines

(data shown in the supporting information). Ectopic miR-152 expression in HCC cells caused an inhibition of cell migration and invasion and BGB324 supplier induced cell apoptosis. However, we did not find any signification role for it in cell proliferation (Supporting Fig. 1). These results indicate that the enhanced expression of miR-152 by gene transfer could reverse the malignant phenotypes of HCC cell lines, and they suggest a tumor-suppressive role and a potential therapeutic target of miR-152. We also believe that these finding have potentially relevant therapeutic implications. The results of this study provide a strong rationale for developing epigenetic therapies that use synthetic miR-152, alone or with other treatments, to reexpress the methylation-silenced TSGs and normalize aberrant patterns of methylation in HBV-related HCC. “
“Background and Aim:  Hepatic excessive iron may

play a role in the pathogenesis of non-alcoholic steatohepatitis (NASH). Nrf2 is a master regulator of antioxidative responses. However, the role of Nrf2 in lipid and iron homeostasis remains unclear. Accordingly, it was examined how Nrf2 regulates lipid-related and

iron-regulatory genes after feeding a high-fat diet (HFD) with iron. Methods:  Wild-type and Nrf2-null mice were fed the following diets: Selumetinib research buy (i) control diet (4% soybean oil) for 12 weeks, (ii) control diet for 8 weeks followed by control diet containing 0.5% carbonyl iron for 4 weeks, (iii) HFD (4% soybean oil and 16% lard) for 12 weeks, (iv) HFD for 8 weeks followed by HFD containing 0.5% carbonyl iron for 4 weeks. Blood and livers were removed after 12 weeks. Results:  Nrf2-null control mice exhibited a tendency towards higher hepatic triglycerides compared to wild-type control mice. Hepatic malondialdehyde was higher and hepatic iron levels Bupivacaine tended to be higher in Nrf2-null mice than wild-type counterparts while on a HFD. The HFD with iron synergistically induced mRNA expression of Pparα targets, including Acox and Cpt1 in wild-type mice, yet the induction was diminished in Nrf2-null mice. Hepatic hepcidin and ferroportin 1 mRNA expression were increased in wild-type mice after feeding a HFD with iron, but were unchanged in any group of Nrf2-null mice. Conclusions:  Nrf2 deletion dysregulates hepatic mRNA expression of β-oxidation enzymes and iron-related genes, possibly causing a trend for increased hepatic triglyceride and iron concentrations. Nrf2 may have roles in the progression of NASH. “
“Genome-wide array studies have associated the patatin-like phospholipase domain-containing 3 (PNPLA3) gene polymorphisms with hepatic steatosis.

A consecutive case series of patients with incident BCS who were diagnosed in the Affiliated Hospital of Xuzhou

Medical College (Jiangsu, China) were enrolled from September 2010 to December 2011. All of the patients had continuous follow-ups to record the symptoms, body features, laboratory and radiology findings, and treatment methods through May 2012. A total of 145 incident cases of BCS were identified. BCS was caused by hepatic venous obstruction in 31% of the patients, inferior vena cava obstruction in 6% of the patients, and 63% suffered from a combination of the two conditions. At least one etiological factor was present in 82% of the patients, with the most common being membranous obstruction (61%). Only 5% of the patients had myeloproliferative neoplasms with a JAK2 see more AZD1208 mouse V617F mutation, and none of the patients had a factor V Leiden mutation. Eighteen months after a percutaneous transluminal angioplasty was performed, the survival rate and the asymptomatic survival rate were 99% (95% confidence interval, 95–100%) and 93% (95% confidence interval, 89–98%), respectively. The most prevalent etiological factor for BCS in China is membranous obstruction. Moreover, most Chinese

patients with chronic BCS are treated with percutaneous transluminal angioplasty and have an excellent clinical outcome. “
“Liver macrophages play integral roles in both the progression and resolution of hepatic inflammation and fibrosis, comprising opposing functions that largely coincide with the activation state of nearby

hepatic stellate cells (HSC). While cross-talk between HSC and macrophages may be essential at various stages of inflammation and fibrogenesis, many facets of this interaction have yet to be thoroughly explored. Here, we examine the potential roles of HSC-derived signaling molecules as mediators of liver macrophage differentiation. Human peripheral blood mononuclear cells (PBMC) were differentiated to macrophages in selleck kinase inhibitor the presence or absence of cultured HSC-derived conditioned media. The phenotype of resulting macrophages was characterized by examination of cell surface marker expression, antigen-presenting capabilities and cytokine secretion. Conditioned media from activated human HSC promoted the differentiation of a unique set of macrophages that differed in morphology and function from both classical (M1) and alternative (M2) macrophages, expressing increased levels of CD14 and CD16, as well as a distinct interleukin (IL)-6high/IL-10low/transforming growth factor (TGF)-βhigh expression profile. These macrophages expressed high levels of CD206, CD209, CD80 and human leukocyte antigen DR, though no significant increases in antigen presentation were apparent. HSC-derived macrophages exhibited specific activation of p38 mitogen-activated protein kinase, and inhibition of this activation by p38 inhibitors during differentiation effectively reversed increases in IL-6 and TGF-β.

Immunodeficient Alb-uPA mice reconstituted with human hepatocytes, have been demonstrated to be susceptible to productive infections with both HBV and HCV3, 4 and this

model has been used for a variety of investigations, including drug metabolism studies,5 the assessment of antiviral compounds,6 the demonstration of viral neutralization,7 Selleckchem Apitolisib and the analysis of mechanisms of control of viral replication.8 However, because of a number of technical challenges associated with this model, wide adoption of this system has not occurred, with its use essentially limited to a few specialized centers. The breeding of homozygous Alb-uPA immunodeficient mice is hampered by infertility; in addition, there is relatively high perinatal mortality in this lineage.4 Furthermore, this lineage has a bleeding diathesis, consistent with the development of Alb-uPA mice as a model for exploring coagulation, that can be associated with the death of transplanted animals from diffuse hemorrhaging.3 Hepatocyte transplantation in this model must be carried out at an early age, BAY 73-4506 and there is a short window of opportunity for successful repopulation, with the optimal age range for this procedure being 5 to 14 days.4 Somatic mutations leading to deletion of the uPA transgene can also develop and lead to the presence of wild-type mouse hepatocytes

that can compete with transplanted xenogeneic hepatocytes; this limits the success of repopulation with human hepatocytes in those animals in which this occurs. Animals successfully repopulated with human hepatocytes have also been reported to remain somewhat unhealthy,9 and renal disease has been observed in this model.5 In order to develop

a more robust chimeric human liver mouse model, two groups have recently harnessed the fumaryl acetoacetate hydrolase (FAH) knockout mouse lineage. This enzyme is the terminal factor in the tyrosine catabolism pathway, and the accumulation of toxic tyrosine Endonuclease metabolites resulting from its deficiency leads to fulminant hepatic failure in FAH-deficient mice. However, the administration of 2-(2-nitro-4-trifluoro-methylbenzoyl)-1,3-cyclohexanedione (NTBC) blocks the activity of an enzyme upstream of FAH and thus abrogates the accumulation of toxic metabolites that mediate hepatotoxicity. Thus, the timing of the toxic insult applied to native murine hepatocytes to provide a selective advantage to transferred human hepatocytes in the repopulation of the liver can be manipulated by the administration and withdrawal of NTBC. Grompe and colleagues10 crossed FAH knockout mice with recombination activating gene 2 knockout/interleukin-2R gamma chain knockout mice deficient in T, B, and natural killer cells; this triple knockout model has been termed the FRG lineage.

However, no

provision CB-839 ic50 has been made for situations where there is significant potency disagreement within one assay method. A proposal to establish an IS for recombinant FIX with unitage traceable to the current 4th IS for FIX Concentrate has been made and the use of such a standard would substantially reduce or eliminate assay discrepancies for the recombinant FIX. For the LrFIX, the results from the collaborative study support product-specific reference standard calibrated against the IS, but the method and reagent used would need to be specified. However, the direction for potency labelling of these new generation products requires further discussions and agreement amongst the regulators and manufacturers. Assay discrepancies for FVIII are well-known and have been investigated for decades. Nonetheless, the magnitude of the discrepancies especially for the new long-acting products remains unclear. A similar comparability study for FVIII has now been initiated and it is hoped that the results will help to identify options Neratinib chemical structure that will reduce assay discrepancies. During the 1980s, biotechnology has brought access to recombinant FVIII and FIX for the treatment of haemophilia A and B. The first generation of recombinant products has been designed to provide exact copies of their natural, plasma-derived counterparts. Deviating from the natural

structure was generally considered undesirable in view of the potential risk of immunogenicity and inhibitor formation. This paradigm, however, started shifting during the past decade, and bioengineered variants

with improvements over the natural, wild-type coagulation factors attracted increasing interest. Mutagenesis, chemical modification or the construction of hybrid proteins became no longer a priori undesirable, and several potential ‘improvements on nature’ are currently being explored for their potential 3-oxoacyl-(acyl-carrier-protein) reductase merit [[39, 40] and references therein]. Coagulation factors have been designed that display supranormal-specific activity or resistance against inactivation. Half-life extension is another target for improvement, because this holds the promise of reducing treatment frequency and product usage. One obvious implication of engineering FVIII or FIX is that this may affect biological activity, both in vivo and in vitro. Because the International Unit of FVIII and IX is activity-based, one should anticipate complications in product potency assessment, as well as therapy monitoring. Such activity changes may be assay- and reagent-dependent, which raises analytical problems as reviewed above by Drs. Kitchen and Gray. Even for the current generation of products, assay discrepancies have proven difficult to eliminate. For the new bioengineered variants this may become even more problematic.

This method can be easily applied and can predict clinical outcomes in biliary atresia and extra-hepatic PHT patients. Key Word(s): 1. Spleen

stiffness; 2. Method; 3. Clinical application; 4. Fibroscan; Presenting Author: YANYING ZHAO Corresponding Author: YANYING ZHAO Affiliations: the Fourth Hospital of Jilin University Objective: To construct a short hairpin (sh) RNA targeting the gene encoding the MDM2 oncoprotein in order to investigate its role in human hepatocellular carcinoma (HCC) and its potential for use as a gene therapy strategy to inhibit HCC growth in vivo. Methods: Small interfering (si) RNAs were designed targeting the MDM2 gene (siMDM2-1 and siMDM2-2) and unrelated sequences (negative control) and cloned into the expression plasmid pGCSilencer-U6-neo-GFP. GSK2126458 ic50 A HCC mouse model was established by subcutaneous inoculation of HepG2 cells (2 × 106 in 0.2 mL) into 20 nude mice. The inoculated mice were divided into four equal groups for tumor-localized Dabrafenib in vitro injections of saline, negative control siRNA plasmid, siMDM2-1 plasmid, and siMDM2-2 plasmid.

Tumor growth was observed daily (by caliper measurement) for one month, when mice were sacrificed by cervical dislocation. The tumor mass was resected for analysis of tumor inhibition rate (% = [(average tumor weight of control group – average tumor weight of treatment group) / average tumor weight of control group × 100]) and effects on MDM2 and

p53 mRNA and protein PAK5 expression (by reverse transcription-PCR and western blotting, both normalized to β-actin). Significance of between-group differences was assessed by one-way ANOVA or LSD test; pairwise comparisons were made by the Chi-squared test. Results: Both siMDM2-1 and siMDM2-2 suppressed the xenografted tumor growth remarkably (60.6% and 54.6% inhibition rates, respectively), significantly reduced the expression of MDM2 gene (62.8% and 61.6%) and protein (60.7% and 59.5%), and significantly increased p53 gene (47.1% and 45.6%) and protein (45.9% and 44.3%) (all, P < 0.05). Conclusion: shRNA-mediated silencing of the MDM2 gene effectively inhibits HCC tumorigenesis of subcutaneously xenografted HepG2 cells in nude mice, and the mechanism may involve p53. Key Word(s): 1. carcinoma; 2. MDM2; 3. p53; 4. siRNA; Presenting Author: FENFEN WANG Corresponding Author: FENFEN WANG Affiliations: The Second Affiliated Hospital of Nanchang University Objective: To observe the expressions of DNp73 and GADD45 beta genes and their effects on the proliferation and apoptosis of SMMC-7721 cells that have been transfected with XPD gene. Methods: SMMC-7721 hepatoma cells were cultured in PRIM-1640 supplemented with 10% fetal calf serum at 37°C and 5% CO2. pEGFP-N2-XPD and pEGFP-N2 were transfected into SMMC-7721 cells by Lipofectamine2000, respectively.

Conclusion: 

IL-17 plays an important role in H. pylori-related gastritis and in the reduction of Helicobacter infection in mice following immunization. “
“Background:  Small molecule library Lafutidine is an H2-receptor antagonist with gastroprotective action through capsaicin-sensitive afferent neurons and relatively inexpensive compare to proton-pump inhibitors (PPIs). A 7-day course of PPIs–amoxicillin–metronidazole is recommended as standard second-line Helicobacter pylori therapy and is covered by national health insurance in Japan. The aim of this study was to determine the efficacy and safety of second-line eradication using the H2-receptor antagonist lafutidine as a substitute for a PPI. Materials and Methods:  Fifty-two patients who failed in first-line eradication using PPI–amoxicillin–clarithromycin were randomly assigned to a 7-day course of rabeprazole at 10 mg b.i.d., amoxicillin at 750 mg b.i.d., and metronidazole at 250 mg b.i.d. (RPZ-AM) or a 7-day course of lafutidine at 10 mg t.i.d., amoxicillin at 750 mg b.i.d., and metronidazole at 250 mg b.i.d. (LFT-AM) as second-line therapy. Eradication was assessed by the 13C urea breath test. A drug susceptibility test was performed before the second-line therapy. Results:  Prior to second-line H. pylori eradication, the rate of resistance to clarithromycin was 86.5% and the rate of resistance

to metronidazole was 3.8%. The eradication rates Selleck 3-MA for both LFT-AM and RPZ-AM groups were 96% (95%CI = 88.6–100%). There were no severe adverse events in either group. Conclusions:  Lafutidine plus metronidazole–amoxicillin as second-line therapy provided a high mafosfamide eradication rate and safe treatment similar to a PPI-based regimen. Lafutidine-based

eradication therapy is therefore considered to be a promising alternative and is also expected to reduce health care costs in H. pylori eradication. “
“Background: Helicobacter pylori infection can lead to the development of gastritis, peptic ulcers and gastric cancer, which makes this bacterium an important concern for human health. Despite evoking a strong immune response in the host, H. pylori persists, requiring complex antibiotic therapy for eradication. Here we have studied the impact of a patient’s immune serum on H. pylori in relation to macrophage uptake, phagosome maturation, and bacterial killing. Materials and Methods:  Primary human macrophages were infected in vitro with both immune serum-treated and control H. pylori. The ability of primary human macrophages to kill H. pylori was characterized at various time points after infection. H. pylori phagosome maturation was analyzed by confocal immune fluorescence microscopy using markers specific for H. pylori, early endosomes (EEA1), late endosomes (CD63) and lysosomes (LAMP-1). Results:  Immune serum enhanced H. pylori uptake into macrophages when compared to control bacteria.

It remains uncertain if proton pump inhibitors (PPI)should be stopped prior to functional tests. Aim: To compare the diagnostic yield of all ambulatory studies performed to date in subjects off and on PPI therapy. Methods: Systematic review of all studies published between 1996 and 2012. Data were extracted for patient demographics, acid exposure times and symptom index (SI). Prevalence of abnormal AET and symptom marker based SI was compared using chi-square and student t-test. Results: A total of 31 studies involving 2768 patients (1059 Male, mean (SD) age

50.6 ± 10.3 years) were identified. Studies included 490 subjects (24 hour pH study), 65 subjects (pH-bilitec) and 2213 subjects (MII-pH). Elevated esophageal AET occurred in 381 of 1068 (35.7%)patients and 198 of 943 (21% patients) selleck products who were studied off and on MAPK inhibitor PPI respectively (p < 0.05). A positive SI for AR occurred in 49.3% and 14.5% of patients off and on PPI respectively (p < 0.05). A positive SI for NAR occurred in 17.5% and 34.2% of patients off and on PPI respectively (p < 0.05). Improved diagnostic yield was observed when patients were studied for AR events off PPI therapy and for NAR events on PPI. Conclusion: MII-pH

monitoring performed on PPI therapy improves diagnosis of NAR. Whilst this may help direct appropriate therapy, further outcome studies are required. Key Word(s): 1. NERD; 2. Impedance-pH; 3. Reflux; 4. symptom index; Presenting Author: YU-QING ZHAO Additional Authors: LI-PING DUAN, YING GE Corresponding Author: LI-PING DUAN Affiliations: Peking University Third Hospital Objective: Air swallow is a normal physiological phenomenon in health. Some researchers believed that patients with gastroesophageal reflux disease (GERD) swallowed air more, but there PtdIns(3,4)P2 were some contradictory reports. We aimed to investigate the relationship between air swallow and GERD by using the 24 h multichannel esophageal pH-impedance monitoring. Methods: GERD patients and health volunteers (controls) underwent 24 h multichannel intraluminal impedance and pH monitoring.

All of the subjects received gastroendoscopy to exclude abnormalities other than erosive esophagitis or chronic superficial gastritis previously. Impedance data was analyzed to record the numbers of air events and the parameters of gastroesophageal reflux. Correlation between the parameters of air events and gastroesophageal reflux was analyzed. P value less than 0.05 was considered statistically significant. Results: A total of 30 GERD patients (45 ± 13 yrs., m/f = 18/12) and 30 controls (41 ± 13 yrs., m/f = 10/20) was enrolled. The numbers of air swallow in GERD patients were higher than that in controls (22.6 ± 20.8 vs. 16.1 ± 12.7, p < 0.05), especially in female GERD patients (GERD vs. controls: f, 23.4 ± 21.5 vs. 14.3 ± 11.3, p < 0.05; m, 22.1 ± 20.0 vs. 19.9 ± 15.0, p > 0.05). Air swallow happened mainly between meals (GERD vs. controls, female: between meals: 21.

, MD (Parallel Session) Nothing to disclose Harris, Matthew S., MD (Clinical Research Workshop) Consulting: Theravance, PD-0332991 ic50 Drais Pharmaceuticals, Symbiomix, Rhythm Pharmaceuticals, BioMedical Systems Stock Shareholder: Ocera Therapeutics, Avaxia Biologics

Harrison, Stephen A., MD (Meet-the-Professor Luncheon) Advisory Committees or Review Panels: Merck, Nimbus Discovery Grant/Research Support: Merck, Genentech Speaking and Teaching: Merck, Vertex Heimbach, Julie, MD (AASLD/ILTS Transplant Course, Plenary Session, Transplant Surgery Workshop) Nothing to disclose Heller, Theo, MD (Early Morning Workshops, Parallel Session) Nothing to disclose Henderson, Neil C., MBChB, BSc, PhD (Parallel Session) Nothing to disclose Heneghan, Michael A., MD, MRCP (General Hepatology Update) selleck chemicals Speaking and Teaching: Falk Hohmann, Elizabeth L., MD (Clinical Research Workshop) Nothing to disclose Hoofnagle, Jay H., MD (State-of-the-Art Lecture) Nothing to disclose Horne, Patrick M., MSN, APRN, FNP-BC (Hepatology Associates Course) Consulting: Vertex Pharmaceuticals, Gilead Sciences, Kadmon Pharmaceuticals Grant/Research Support: Bayer Pharmaceuticals Idle, Jeffrey, PhD (SIG Program) Nothing to disclose Israni, Ajay, MD, MS (AASLD/ILTS Transplant Course) Advisory Committees or Review Panels: Astellas Grant/Research Support: Novartis, BMS Iwakiri, Yasuko, PhD (SIG Program) Nothing to disclose Jacobson, Ira M., MD (HCV Symposium) Consulting: Abbvie, Achillion, Boehringer

Ingelheim, Bristol Myers Squibb, Gilead, Idenix, Genentech, Merck, Janssen, Vertex Grant/Research Support: Abbvie, Boehringer Ingelheim, Bristol Myers Squibb, Gilead, Novartis, Genentech, Merck, Janssen, Vertex Speaking and Teaching: Bristol Myers Squibb, Gilead, Genentech, Vertex, Janssen

Jalan, Rajiv, MD, PhD (AASLD Postgraduate Course) Consulting: Ocera Therapeutics, Conatus Grant/Research Support: Grifols, Gambro Janssen, Harry L., MD, PhD (Early Morning Workshops, Meet-the-Professor Luncheon, Parallel Session) Consulting: Abbott, Bristol Myers Squibb, Carnitine palmitoyltransferase II Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris Jensen, Donald M., MD (Early Morning Workshops) Grant/Research Support: Abbvie, Boehringer, BMS, Genentech/ Roche, Janssen Kamath, Binita M., MBBChir (Early Morning Workshops, Parallel Session) Nothing to disclose Kamath, Patrick S., MD (AASLD Postgraduate Course, Emerging Trends Symposium, Meet-the-Professor Luncheon) Advisory Committees or Review Panels: Sequana Medical Kanwal, Fasiha, MD (Early Morning Workshops, Parallel Session) Nothing to disclose Kapalko, Angela, MS, PA-C (Hepatology Associates Course) Advisory Committees or Review Panels: Gilead Sciences Karlsen, Tom H., MD, PhD (SIG Program) Nothing to disclose Karp, Seth J., MD (Parallel Session) Nothing to disclose Karpen, Saul J.