Data were analyzed with FlowJo software (Tree Star, Ashland, OR, USA). BALF cells were placed on glass slides by cytospin (Cytospin 3, SHANDON, Waltham, MA, USA). After

air-drying for 20 min, slides were fixed with 1% PFA/PBS for 10 min. After washing with 0.1% Tween-20/PBS, slides were blocked with 3% BSA/0.1% Tween-20/PBS for 1 h at room temperature, then incubated with polyclonal rabbit anti-mouse arginase 1 Ab (Santa Cruz) and Rat anti-mouse F4/80 Ab (AbD Serotec, Oxford, UK) at 4°C overnight, followed by incubation MAPK Inhibitor Library datasheet with Alexa Fluor 594-conjugated anti-rabbit Ab (Molecular Probes) and Alexa Fluor 488-conjugated anti-rat Ab (Molecular Probes, Japan, K.K. Tokyo, Japan), respectively. Fluorescent images were observed by confocal microscopy (Bio-Rad Radiance 2100, Bio-Rad). We observed more than 300 F4/80+ cells and then calculated the percentage of arginase 1+ cells in the F4/80+ cells. BM cells obtained from naïve female C57BL/6 mice were used for in vitro assays. BM cells were harvested from femurs and tibias, treated with RBC lysis solution, and then sorted for CD117+ cells using a Everolimus c-kit isolation kit (Miltenyi Biotec, Bergisch Gladbach, Germany) according to the manufacturer’s

protocol. The purity of CD117+ cells was>60% in our experiments. Harvested cells were cultured with Gal-9 (3 and 30 nM) in the presence or absence of T. asahii for 5 days. Very stringent gating Carnitine dehydrogenase conditions were used for sorting experiments (FACSAria, Becton Dickinson), with purity checked by

flow cytometry: CD11b+Ly-6C+Ly-6G− cells and CD11b+Ly-6C−Ly-6G+ cells were>95%. Harvested cell pellets were dissolved in SDS lysis buffer, boiled, fractionated on an SDS-polyacrylamide gel, and transferred to a nitrocellulose membrane. After blocking with PBS plus 0.1% Tween-20 containing 5% skim milk for 1 h at room temperature, the membrane was incubated with antibodies against NOS2 (Abcam, Cambridge, MA, USA) and arginase1 (Santa Cruz, CA, USA) overnight at 4°C. After washing with PBS plus 0.1% Tween-20, the membrane was incubated with anti-HRP-linked Ab for 1 h at room temperature and visualized with Western lightning chemiluminescence reagent (PerkinElmer, Waltham, MA, USA) according to the manufacturer’s protocol. Extracts from mouse liver and whole lung tissue were used as positive controls for NOS2 and arginase 1, respectively. T-cell proliferation was evaluated using splenic CD4+ T cells and BALF cells obtained from PBS-treated mice or Gal-9-treated mice.

Improvements from baseline to end-point were also recorded for grip strength in the dominant hand (treatment difference 10·9 kPa; P = 0·0008) and the non-dominant LEE011 molecular weight hand (8·6 kPa; P = 0·005). Results were similar during the second cross-over period. During the extension phase, participants who continued to receive IVIG had

a longer time to relapse than did patients treated with placebo (P = 0·011). This is the first study that demonstrates clearly the long-term efficacy and tolerability of IVIG in CIDP. Another recent, multi-centre, randomized, double-blind, placebo controlled, parallel-group study in 45 patients with CIDP compared the efficacy and tolerability of IVIG (0·5 g/kg/day for 4 consecutive days) to intravenous methylprednisolone (0·5 g/day for 4 consecutive days) given every month for 6 months [37]. After therapy discontinuation, patients were followed-up for 6 months to

assess relapses. The primary outcome was the number of patients discontinuing either therapy owing to inefficacy or intolerance. Talazoparib in vitro Secondary end-points included the proportion of patients experiencing adverse events or worsening after therapy discontinuation. More patients stopped methylprednisolone (52%) than IVIG (13%) (P = 0·0085). The reasons for discontinuation were lack of efficacy, adverse events or voluntary withdrawal. After therapy discontinuation, more patients on IVIG worsened and required further therapy (38%) than did those on methylprednisolone (none) (P = 0·0317). Thus, treatment of CIDP with IVIG for 6 months was discontinued less frequently because of inefficacy, adverse events or intolerance than treatment with intravenous methylprednisolone. Another recent prospective, multi-centre, single-arm, open-label Phase III study [Privigen® Impact on Mobility and Autonomy

(PRIMA) trial] evaluated the efficacy and safety of IVIG in 28 patients with CIDP [38]. Patients received one induction dose of IVIG (2 g/kg body weight) and up to seven maintenance doses (1 g/kg body weight) at 3-week intervals. The overall responder rate defined as an improvement of ≥1 point on the INCAT disability scale at completion triclocarban was 60·7%. IVIG-pretreated patients demonstrated a higher responder rate than IVIG-naive patients (76·9 versus 46·7%). The INCAT score, the maximum grip strength and the Medical Research Council sum score all improved significantly at completion compared to baseline. Thus, these recent trials provide evidence for the long-term efficacy of IVIG in patients with CIDP. Adverse effects, frequent: headache, hypertension, allergic/anaphylactic reactions [especially in immunoglobulin (Ig)A-deficient patients], dermatitis; infrequent: infection (HIV or viral hepatitis) by contaminated blood product, pulmonary oedema from fluid overload, due to the high colloid oncotic pressure of IVIG, venous thrombosis, aseptic meningitis and haemolysis.

Our data classify IL-17A and IL-17F as cytokines produced transiently in response to the local microenvironment, thus showing that IL-17 expression does Selinexor molecular weight not define an end-stage T helper cell subset. Since the finding that IL-23 and not IL-12 is necessary for active induction of EAE 1, 2, the previously common dogma for the pathogenesis of the disease has changed. Th17 cells,

which were soon thereafter shown to depend on IL-23 3, 4, are now regarded as major initiators of pathogenesis in a number of disease models and human conditions. Th17 achieve their pathogenic phenotype by secreting cytokines which in turn induces the surrounding tissue to secrete chemokines and other cytokines important for the immigration of potentially pathogenic leukocytes such as granulocytes and lymphocytes 5. In a previous landmark EAE study, Th17 cells that were expanded in the presence of IL-23 were shown to be extremely efficient in inducing passive EAE 4. Low amounts of transferred cells (150 000) were able to induce EAE in SJL/J animals. This finding together with the full resistance of IL-23-deficient animals in response to active EAE induction 2 cemented the idea of Th17 cells as a major pathogenic cell population in EAE. This was further supported by the discovery that Th17 can be

find protocol very efficiently generated in vitro when naïve CD4+ T cells are activated in the presence of TGF-β and IL-6 6–8 and that IL-6 is necessary for EAE induction 9–12. Furthermore, aminophylline transgenic expression of TGF-β in T cells enhanced EAE severity 6. Another milestone for this hypothesis was the finding that RORγt deficiency led to a major lack of Th17 cells and to a near complete resistance against active EAE, even in the presence of extensive CNS infiltration

13. Other transfer studies in the SJL/J mouse using IL-23 expanded encephalitogenic cells found an enhanced infiltration of granulocytes concomitant with EAE development compared to transfer of IL-12 expanded T cells 5, 14, further supporting a specific role for Th17 cells in autoimmunity. Given the previous lack of suitable Th17 reporter strains, these studies relied on transfer of in vitro generated Th17 cells of a heterogenous nature, rather than a pure Th17 population. Recently, the encephalitogenicity of Th17 cells was challenged by O’Connor et al., who showed that transferring myelin oligodendrocyte glycoprotein (MOG)-specific Th17 cells derived from a polyclonal C57BL/6 T-cell repertoire were not able to passively transfer EAE, in contrast to strong EAE induced by transfer of MOG-specific polyclonal Th1 cells 15. Also in this report, polarized TCR transgenic Th17 cells were transferred to either B10.PL or lymphopenic B10.PL animals. Under these conditions, some animals became sick, but surprisingly upon reanalysis many cells were found to express IFN-γ.

Collectively, our findings

support the concept that the use of Cox inhibitors can counteract the goal of vaccines, by inhibiting the generation of plasma cells which produce antibodies, important for fighting infections. Human B lymphocytes learn more isolated from peripheral blood mononuclear cells (PBMC) were cultured in RPMI-1640 (GIBCO/Invitrogen, North Andover, MA) supplemented with 10% fetal bovine serum, 2 mm l-glutamine, 5 × 105 m 2-mercaptoethanol, 10 mm HEPES and 50 μg/ml gentamicin. CpG oligodeoxynucleotide (ODN) 2395 5′-TCGTCGTTTTCGGCGCGCGCCG-3′ was purchased from the Coley Pharmaceutical Group (Wellesley, MA) and used to stimulate B cells at a concentration of 1 μg/ml. Stimulation of BCR was performed using a rabbit anti-human F(ab′)2 anti-IgM antibody fragment (Jackson ImmunoResearch Laboratories, West Grove, PA) at 2 μg/ml. Arachidonic acid (Nu-Chek Prep, Elysian, MN) dissolved in ethanol was supplemented in culture at a concentration of 10 μm. Mitomycin

C (Sigma-Aldrich, St Louis, MO) was added to cell cultures to prevent cell division, acting as a control for carboxyfluorescein Selleck RG7422 succinimidyl ester (CFSE) analysis. SC-58125 and NS-398, (Cayman Chemical, Ann Arbor, MI) small molecule Cox-2 selective inhibitors, were dissolved in dimethyl sulphoxide (DMSO), and used at concentrations of 5, 10 and 20 μm. Cox-2 inhibitors were added on days 0, 3 and 5 of culture unless otherwise stated. Units of peripheral blood were obtained from healthy donors [not taking any non-steroidal anti-inflammatory

drugs (NSAIDs) or other medications] under ethical permission provided by the Research Subjects Review Board at the University of Rochester. B cells were isolated as described previously.11,12 Briefly, PBMC were isolated using Ficoll–Paque (Amersham Biosciences, Piscataway, NJ) gradient centrifugation. The B cells were labelled with CD19 Dynabeads (Invitrogen) and CD19 Dynabead-cell rosettes were disrupted using CD19 Detachabead (Invitrogen). Cells obtained by this method of isolation were > 98% CD19+. B cells were purified from Cox-2-deficient mice (B6.129P2-Ptgs2tm1Unc) and wild-type control splenocytes (Taconic Farms Inc., Hudson, NY) using a CD19 magnetic antibody cell sorter (MACS) separation protocol (Miltenyi Methocarbamol Biotec, Auburn, CA). Purified CD19+ B cells were cultured with lipopolysaccharide (LPS; 10 μg/ml) for 72 hr. Positively isolated CD19+ human B cells (5 × 105 cells/ml) were cultured in 96-well round-bottom plates for 7 days in the presence of CpG ODN 2395, anti-IgM and arachidonic acid (10 μm). Vehicle control or Cox-2 selective inhibitors, SC-58125 or NS-398, were added at onset of culture and on days 3 and 5. Levels of IgM and IgG in the supernatants were assessed by enzyme-linked immunosorbent assay (ELISA; Bethyl Laboratories, Montgomery, TX) on day 7 as described previously.

5–2 h (cold ischaemia time) before being implanted into the recipient. The recipients were also anaesthetized with ekviticine and placed on a heated operating table. The left kidney was removed, and the pancreatic-duodenal Selumetinib molecular weight graft was anastomosed to the renal

blood vessels by a non-suturing cuff technique as previously described [17]. The graft duodenum was sutured end-to-side to a loop of the colon of the recipient with 7–0 silk. After closure of the abdominal wound, the animals were injected subcutaneously with 10 mg doxycycline (Idocyclin™; AB Leo, Malmö, Sweden) and were observed until fully recovered from anaesthesia. The animals were surgically prepared for blood flow measurements as given above, 2 days after transplantation. The blood flow values to the endogenous and transplanted pancreases, the islets in both glands and the endogenous and transplanted duodenum were measured with the microsphere technique referred to above. Histological examinations.  After blood flow measurements samples from

both the endogenous and transplanted pancreases were fixed in 4% buffered (pH 7.3) formalin with 1% cetylpyridinium chloride (Sigma). These samples were then dehydrated, embedded in paraffin, sectioned (4 μm thick) and stained with haematoxylin and eosin. The slides selleck products were then examined by an observer unaware of the origin of the samples especially for the presence of interstitial oedema, infiltrating cells and vacuoles within acinar or endocrine cells. In the non-transplanted animals, the endogenous pancreas was removed and studied similarly. Assay of HA and determination of water content.  Samples from Dimethyl sulfoxide both the endogenous and transplanted pancreases and duodenum (approximately 25–35 mg each) were taken from the caudal portions of the glands, or the peri-ampullar region of the intestines. In non-transplanted animals, samples were only taken from the caudal part of the endogenous pancreas. The specimens were put on filter paper and weighed 3 min later to obtain the wet weight. The samples were then lyophilized and weighed again to obtain the dry weight. The

specimens were ground, and HA were extracted for 16 h with 0.5 m sodium chloride. Supernatants, obtained after centrifugation at 2000 g for 15 min, were analysed for HA content with a radiometric assay (Pharmacia & Upjohn Diagnostics, Uppsala, Sweden) as previously described in detail [18]. Standard curves were constructed from samples with known amounts of HA, and double analyses were performed on all samples. The variability was <10%. The relative water content, expressed as per cent water of the total weight of the tissue, was calculated as 100 × (wet weight – dry weight)/wet weight. An initial study was performed in which the measurements were made in transplanted animals on day 2, 4 or 7 post-transplantation. Based on these findings, blood flow measurements and analyses of HA and water contents were performed day 2 post-transplantation.

In this review we focus upon recent advances in our understanding of the tissues and organs involved in host defence in C. elegans, as well as the virulence mechanisms employed by some pathogens to defeat those defences. A major advantage of C. elegans as a model system is its relatively simple anatomy. The C. elegans body plan is tubular, with the mouth at the

anterior end of the head and the anus at the posterior near the tail. The head contains the pharynx, a muscular organ that contracts rhythmically to pump food into the grinder, a chitinous rigid organ that crushes ingested material before it is pumped through the pharyngeal–intestinal valve into the lumen of the intestine [5]. The intestine proper, which takes up approximately one-third of the midbody transversal EPZ-6438 manufacturer section, is a simple organ formed by just 20 non-renewable polarized GDC-0973 research buy epithelial cells, organized in nine rings of directly apposed pairs of cells (except for the first ring, which is formed by four cells). These intestinal epithelial cells exhibit many ultrastructural similarities with mammalian intestinal epithelial cells, most conspicuously an apical brush border of microvilli protruding into the intestinal lumen. The microvilli are formed of actin bundles anchored in an intermediate filament terminal web. The intestine is metabolically

highly active, with similar functions to the fat body in flies and the liver in mammals [5]. Other major organs include the gonads, which fill up most of the transversal section Phospholipase D1 of the animal and generate oocytes that are fertilized

as they pass through the spermathecae near the ventral uterus. Fertilized eggs remain inside the animal until early embryogenesis, at which point they are laid through the ventral vulval opening. The hypodermis (epidermis) and body wall muscle sheathe the intestine, the gonads and the body cavity (pseudocoelom). The body wall muscle contracts to generate the characteristic sinusoidal movements that allow locomotion and behaviour, co-ordinated by an intricate nervous system that links environmental sensory perception with movement, endocrine signalling and behaviour. The hypodermis, among other functions, deposits the highly impermeable cuticle, the collagenous exoskeleton of the worm. C. elegans lacks a circulatory system, professional immune cells and macrophage-like phagocytes. Being an invertebrate, it lacks antibody-generating adaptive immunity and relies on epithelial-based innate immunity for defence. Nevertheless, C. elegans mounts a sophisticated immune response, as measured by transcriptional regulation of host defence genes upon infection. In contrast to what is known about flies and mammals, the C. elegans immune response is mostly independent of Toll-like receptor (TLR) signalling [6,7].

13: ≥8.8 kPa for FM≥2 and ≥14.6 kPa for FM4, and those specifically calculated for CHC in the meta-analysis of Stebbing et al.14: ≥8.5 kPa for FM≥2 and ≥16.2 kPa for FM4. As there were various causes of chronic liver disease in our study population, we also tested the cutoff published in the Opaganib meta-analysis of Friedrich-Rust et al.15: ≥7.7 kPa for FM≥2 and ≥13.1 kPa for FM4. By using the diagnostic cutoffs, LSE median was categorized into estimated FFS stages according to the most probable Metavir F stage(s). This approach provided the following LSE classification: LSE result

variables, they were expressed as median with 1st and 3rd quartiles in brackets. Diagnostic accuracy was mainly expressed as area under the receiver operating characteristic (AUROC) (for binary diagnoses of significant fibrosis, severe fibrosis, or cirrhosis) or the rate of well-classified patients by the LSE classification. AUROCs were compared according to

Delong et al.16 for paired groups, and Hanley and McNeil17 for unpaired groups. To identify the factors influencing LSE accuracy, we determined the variables independently associated with the following diagnostic target: significant fibrosis, severe fibrosis, or cirrhosis Talazoparib molecular weight by stepwise forward binary logistic regression. Indeed, by definition, each variable selected by a multivariate analysis is an independent predictor of the diagnostic target studied. In other words, when selected with LSE median, PLEKHM2 an independent predictor influences the outcome (diagnostic target) for each fixed level of liver stiffness. Consequently, the multivariate analysis allowed for the identification of the predictor influencing LSE accuracy. The dependent variable, LSE median, was tested

with the following independent variables: age, sex, body mass index, cause of chronic liver disease (CHC versus other), ≥10 LSE valid measurements, LSE success rate, IQR/M, and biopsy length as a putative confounding variable. Statistical analyses were performed using SPSS v. 18.0 software (IBM, Armonk, NY) and SAS 9.1 (SAS Institute, Cary, NC). The main characteristics of the 1,165 patients included in the study are presented in Table 1. The cause of chronic liver disease was CHC in 68.5% of patients, hepatitis B monoinfection: 5.7%, alcohol: 12.4%, nonalcoholic fatty liver disease (NAFLD): 3.3%, and other: 10.1%. Overweight status (body mass index ≥25.0 kg/m2) was present in 44.0% of patients. Liver biopsies were considered reliable in 92.0% of the cases. The prevalence of significant fibrosis, severe fibrosis, and cirrhosis was, respectively, 63.3%, 38.9%, and 21.0%. The AUROCs (±standard deviation [SD]) of LSE for the diagnosis of significant fibrosis, severe fibrosis, and cirrhosis were, respectively, 0.822 ± 0.012, 0.872 ± 0.010, and 0.910 ± 0.011 (Table 2).

In support of Y-27632 mw this hypothesis, we demonstrate that STA-21 treatment induces

significant disorganization of the MT network in Huh-7.5 cells (Fig. 6A). α-Tubulin displayed a dispersed punctate pattern in STA-21 treated cells, which was not observed in control treated cells, that displayed an organized MT network with long intact MTs radiating from the MT-organizing center (MTOC). If the STAT3/STMN1 interaction plays a role in HCV replication then the siRNA mediated knockdown of STMN1 should restore HCV replication in the presence of STA-21. To establish if this observation was dependent on STMN1, investigation of α-tubulin cellular distribution was performed in the presence of an siRNA knockdown of STMN1 (Fig. 6C) and STA-21 treatment (Fig. 6B). As predicted, siRNA knockdown of STMN1

rescued the effect of MT disorganization induced by STA-21. We therefore monitored JFH-1 RNA in the presence of STMN1 knockdown and STA-21 treatment and showed that under these conditions a significant but partial rebound selleck chemicals llc in HCV RNA levels occurred (Fig. 6D). This partial rescue was most likely attributed to some residual STMN1 expression and the likelihood that STAT3 impacts HCV replication through multiple mechanisms. These results indicate that STAT3 may play an important role in mediating MT dynamics to create a cellular environment favorable for HCV replication. The number of host factors that impact the HCV life cycle continues to grow. These factors have been shown to play roles in multiple facets of the HCV life

cycle, including entry, RNA replication, and egress.[24] Early work using the HCV replicon model and more recently using a genome-wide siRNA screen have implicated STAT3 as a candidate host factor playing a role in HCV replication.[1, 2] However, to date the role of STAT3 in the HCV life cycle has been observational and this raises the 3-oxoacyl-(acyl-carrier-protein) reductase question of how STAT3 exerts its effect on HCV replication, whether it is in an indirect or a direct manner. The highly pleiotropic nature of STAT3 due in part to its ability to be activated by such a large variety of growth factors and cytokines suggests that STAT3′s impact on HCV replication will be multifactorial. It is likely that in the liver, during an active HCV infection, STAT3 activation may occur by way of multiple pathways including virally induced oxidative stress, IL-6, LIF, and EGF. To this end we have shown in vitro that LIF treatment of Huh-7.5 cells markedly increases HCV RNA replication. Oxidative stress is a known activator of STAT3 and as such it is not surprising that HCV replication is capable of activating STAT3.[2] Our study extends the work of Waris et al.

The most commonly used prior treatments were interferon (76%) and lamivudine (59%). The majority of demographic and clinical characteristics did not differ between patients who were from Poland, the country with the greatest number of enrolled patients (n = 74), compared with the other countries (n = 32). Differences were observed only in the distribution of race (all patients from Poland were white, whereas white

patients comprised 75% of the population from all other countries), HBV DNA genotype, and prior treatment. Furthermore, except for the distribution of race, MK0683 cost all characteristics were similar between the site that enrolled the largest number of patients (n = 23) and all other sites (n = 84). Overall adherence to the study drug was measured by pill count and was summarized by treatment and age group. The Trametinib chemical structure mean adherence was high and similar in the tenofovir DF and placebo groups (99% and 98%, respectively) and across all age groups. In the tenofovir DF group, the primary endpoint of HBV DNA <400 copies/mL was achieved by 89% (46/52) of patients by week 72. By comparison, no patients in the placebo group achieved this

endpoint by week 72 (P < 0.001) (Fig. 2A). Among patients treated with tenofovir DF, HBV DNA <169 copies/mL (below the LLOQ) was achieved by 85% (44/52) of patients by week 72. The difference between the tenofovir DF and placebo groups in the proportion of patients achieving either of these levels of viral suppression was statistically significant (P ≤ 0.001). Mean HBV DNA at baseline was approximately 8 log10 copies/mL in both study groups (Table 1). Mean HBV DNA concentrations rapidly declined in the tenofovir DF group while remaining near baseline levels in the placebo group (Fig. 2B). As early as week 4, mean HBV DNA in the tenofovir DF group had decreased more than 3 log10 copies/mL to approximately 5 log10 copies/mL. By week 40, mean HBV DNA in the tenofovir DF group had decreased 5.6 log10 copies/mL to approximately the LLOQ (2.2 log10 copies/mL), where it remained

through week 72. The same degree of viral load reduction was observed irrespective of the presence (n = 6) or absence (n = 46) of baseline lamivudine-resistant mutations. Virologic breakthrough was defined as HBV DNA measurements of ≥400 Branched chain aminotransferase copies/mL or a 10-fold increase in HBV DNA levels over the patient’s HBV DNA nadir. At week 72, among patients treated with tenofovir DF, four patients had virologic breakthrough, and one patient never achieved an HBV DNA level of <400 copies/mL (i.e., no breakthrough). All four instances of virologic breakthrough were associated with tenofovir DF plasma levels below the limit of detection, suggesting nonadherence with tenofovir DF dosing. Consistent with this observation, sequence analysis of the HBV pol/RT and subsequent phenotypic analysis of patient isolates from week 72 samples did not identify any tenofovir DF resistance–associated mutations in the HBV pol/RT of any patients evaluated.

, MBChB, PhD (Abstract Reviewer) Nothing to disclose Horne, Patrick, MSN, ARNP (Education Committee, Hepatology Associates Committee) Advisory Board: Gilead Grants/Research Support: Bayer Horslen, Simon, MD (Abstract Reviewer) Nothing to disclose Howell, Charles D., MD (Education Committee) Grants/Research Support: Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Leadership in a Related Society: National Medical Association https://www.selleckchem.com/products/azd4547.html Hepatitis C Task Force Ioannou, George, MD (Clinical Research Committee) Nothing to disclose Jalan, Rajiv, MD, PhD (Abstract Reviewer)

Consulting: Ocera, Conatus Grants/Research Support: Grifols, Gambro Janssen, Harry L.A., MD, PhD (Program Evaluation Committee, Abstract Reviewer) Consulting: Santaris, Roche, Novartis, Medtronic, Merck, Gilead, Debio, Abbott, Bristol-Myers Squibb Grants/Research Support: Anadys, Bristol-Myers Squibb, Gilead, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris Jeong, Won-ll, DVM, PhD (Abstract Reviewer) Nothing to disclose Jonas, Maureen M., MD (Abstract Reviewer) Consulting: Eisai Grants/Research

Support: Bristol-Myers Squibb, Roche, Merck Advisory Board: Gilead Kaestner, Klaus H., PhD (Abstract Reviewer) Nothing to disclose Kamath, Patrick S., MD (Abstract Reviewer) Advisory Board: Sequana Medical Kaplowitz, Neil, MD (Abstract Reviewer) Consulting: GlaxoSmithKline, JNJ, Merck,

Novartis, Hepregen, Takeda, Otsuka, Pfizer, RG7422 price Geron, Daiichi-Sanyo Independent Contractor: Acetaminophen Litigation Karpen, Saul J., MD, PhD (Scientific Program Committee, Abstract Reviewer) Nothing to disclose Keaveny, Andrew, MD (Education Committee) Expert Testimony: UpToDate, Inc. Kim, Arthur Y., this website MD (Abstract Reviewer) Grants/Research Support: Gilead, Bristol-Myers Squibb Consulting: AbbVie, Gilead Kisseleva, Tatiana, MD, PhD (Abstract Reviewer) Nothing to disclose Klett, Janeil (Staff) Stock: Merck, Pfizer Klintmalm, Goran, MD, PhD (Abstract Reviewer) Grants/Research Support: Astellas, Novartis, Opson, Quark Advisory Board: Novartis Kneteman, Norman M., MD (Abstract Reviewer) Nothing to disclose Knisely, Alexander S., MD (Abstract Reviewer) Nothing to disclose Kohli, Rohit, MD (Clinical Research Committee, Abstract Reviewer) Grants/Research Support: Synageva Biopharma, Johnson and Johnson Independent Contractor: Lumena Pharmaceuticals, Galectin Therapeutics Korenblat, Kevin M., MD (Abstract Reviewer) Grants/Research Support: Merck Advisory Board: Vertex Koteish, Ayman A., MD (Program Evaluation Committee) Nothing to disclose Kowdley, Kris V.