It is also not associated with adverse reactions, such as thrombocytopenia,

allergic reactions or the development of resistance through antibody formation and thus it is suitable for home treatment. Although, Hyate:C is no longer available, a recombinant factor VIII has been developed as a collaboration between Ipsen, Inspiration and Emory University. This is produced at a facility near Boston in the United States of America. There is a high degree of sequence and functional homology between human and porcine factor VIII. Both human and porcine factor VIII share a common sequence of A1–A2–B–A3–C1–C2 domains and both molecules are cleaved by thrombin to form a dimer composed of a light and heavy chain [24]. BMS-777607 manufacturer OBI-1 is a recombinant B-domain deleted form of porcine factor VIII synthesized in baby hamster kidneys cells grown in a serum-free medium. It does not contain any porcine von Willebrand factor. Phase III clinical trials in patients with acquired haemophilia and congenital haemophilia

A complicated by alloantibodies are underway [25]. A goal of future research will be to attempt to produce a porcine factor VIII molecule, which is even less antigenic than the natural wild type. This could be done by substitution of specific amino acids through genetic engineering, eliminating those that seem to be particularly Sirolimus immunogenic, or creating human/porcine hybrid constructs [26,27]. Such modified molecules could then conceivably be used to treat noninhibitor patients too, or at least as treatment in the early period soon after diagnosis which is known to be the peak risk period MCE for inhibitor development. There is already quite a wealth of information available

on which parts of the porcine and human factor VIII molecules are particularly immunogenic. The antibody response to the individual FVIII domains in haemophilic mice immunized with human or porcine FVIII has provided important information [28].The overall immunogenicity of human and porcine FVIII is similar, but significant differences in domain recognition have been identified. Anti-A2 and anti-C2 antibodies constitute the majority of inhibitors in both the human and porcine FVIII groups, similar to inhibitors that develop in humans. The proportions of anti-A2 or anti-C2 antibodies were not significantly different between the two groups in one study. However, the proportion of anti-C1 antibodies was significantly higher in the human FVIII group, whereas anti-A3 antibodies were more common in the porcine FVIII group. The differential immune response to human and porcine FVIII supports the view that it may be possible to reduce the immunogenicity of porcine (and human) FVIII by mutagenesis at specific sites, within the A2, A3 and C1 domains. In a final twist to this tale, it appears that pigs may be able to provide us with human coagulation proteins like factor VIII and IX [29,30].

pylori infection in the FD group was 49.7% [24]. Another study looking at the

discriminatory value of the Rome III questionnaire in dyspeptic patients found that 136 of 191 (71%) patients had FD, and H. pylori infection was present in 70 (51%) [25]. The pathophysiology of FD is multifactorial. selleckchem Although the role of H. pylori in FD remains controversial, it is possible that immune mechanisms seen in other gut infections could be involved in the pathophysiology of dyspepsia. Li et al. [26] reported increased numbers of enterochromaffin cells and mast cells in the duodenum of patients with postinfectious and nonspecific FD compared with healthy controls, in addition to higher levels of chemicals such as histamine and tryptase derived from these cells. This suggests impaired ability of the immune system to terminate the inflammatory response after infection leading to release of potent chemicals that may be involved in the pathogenesis of postinfectious FD [27]. Suzuki et al. [28] have proposed that H. pylori-associated dyspepsia might be considered an organic disease and, as such, a disease entity separated from FD. While several randomized controlled

trials in Western populations have failed to show a significant advantage of H. pylori eradication in patients with FD, a study suggested that Asian patients benefit from treatment for H. pylori infection with as much as a 13-fold increased chance of symptom CB-839 ic50 resolution following its eradication [29]. The Second Asia Pacific Consensus Guidelines strongly recommended H. pylori eradication in H. pylori-positive patients with FD [30]. A review of current practices in diagnosis and management of functional GI disorders in the Asia-Pacific (AP) region found 58% of doctors who attended the first Asia Pacific Conference in Tokyo in November 2010 checked H. pylori status

in their patients with FD, and when positive, about half (53%) of them opted for eradication therapy [31]. The past few years have seen increased focus on histological assessment and classification of gastritis to provide better correlation with the risk of malignant transformation. The Operative Link on Gastritis 上海皓元 Assessment (OLGA) classification was introduced in 2007 [32], and placed the histological phenotypes of gastritis on a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). OLGA recommends at least five biopsy samples from: (1) the greater and lesser curvatures of the distal antrum (mucus-secreting mucosa), (2) the lesser curvature at the incisura angularis, where the earliest atrophic-metaplastic changes tend to occur, (3) the anterior and posterior walls of the proximal corpus (oxyntic mucosa).An article reviewed the histology reporting of gastritis and provides useful guidance on how to standardize gastritis histology reports in diagnostic practice [33].

3/85.0 for palmitoylcarnitine and m/z 176.1/134.2 for debrisoquine. Using Analyst software (Applied Biosystems), serum palmitoylcarnitine concentrations were determined by calculating the ratio between the peak area of palmitoylcarnitine and

the peak area of debrisoquine and fitting with a calibration curve with a linear range from 10 nM to 1 μM (r = 0.99). Statistical analysis was performed using GraphPad Prism (San Diego, CA). Analysis of variance (ANOVA) with Bonferroni’s multiple comparison test was used to compare the various groups. P < 0.05 was considered significant. Treatment of wildtype MK-2206 purchase mice with APAP for 6 hours results in massive hepatic toxicity as revealed by gross morphology of the liver (Fig. 1A), increased ALT and AST enzyme levels

(Fig. 1B), and faint pericentral and periportal H&E staining of liver parenchyma (Fig. 1C). Pretreatment with Wy-14,643 for 24 hours before APAP treatment results in total protection against APAP toxicity; Wy-14,643 treated mice had no evidence of liver damage. At 24 hours post-APAP treatment, Wy-14,643-treated mice were still protected, as indicated by reduced ALT enzyme levels and normal liver histology (Supporting Fig. 1). In contrast, Ppara-null mice exhibited no Wy-14,643 protection against APAP toxicity (shown by increased ALT and AST activities), indicating selleck chemical that the protection was PPARα-dependent (Fig. 2A). To demonstrate that the effect was not specific to the experimental ligand Wy-14,643 and to mouse PPARα, PPARα-humanized mice (a human PPARα gene introduced in the Ppara-null background) treated 上海皓元 with fenofibrate were also protected (Fig. 2B). However, mice treated with the anti-Fas antibody Jo-2 to stimulate Fas receptor-mediated apoptosis were not protected from Wy-14,643 pretreatment (Supporting Fig. 2). Pretreatment

with Wy-14,643 did not significantly impact APAP metabolism, as demonstrated by serum profiling of APAP and its metabolites (APAP-NAC, APAP-glucuronide, APAP-CYS) 2 hours after APAP administration (Supporting Fig. 3). In order to understand the transcriptional responses associated with toxic doses of APAP-treatment and potential targets whereby PPARα was mediating its protective affects, microarray analysis was carried out on liver mRNA from 6 hours APAP-treated and Wy-14,643-pretreated/APAP-treated mice. A total of 53 genes were up-regulated by APAP and 45 genes up-regulated by Wy-14,643 /APAP; 14 genes were up-regulated by both treatments (greater than 10-fold). Most interesting was the marked induction and suppression of c-fos and c-jun expression upon APAP treatment and Wy-14,643-pretreatment prior to APAP administration, respectively (Fig. 3A). qPCR analysis confirmed that c-fos and c-jun mRNAs were robustly induced by APAP and suppressed by Wy-14,643-pretreatment prior to APAP (Fig. 3B).

1).6, 7 In the presence of inflammation, the analysis of DCs by FACS requires exclusion of autofluorescence, which is normally present in normal liver and is augmented in the setting of inflammation.8 More than that, digestion of the fibrotic tissue results in cell suspension with variable cell doublets and significant Erlotinib order numbers of nonhematopoietic cells that may also express

CD11c (e.g., stellate cells).9 For these reasons, the analysis of the intrahepatic DC population by FACS needs to be carefully validated by a sorting and cytospin approach to confirm that the cells analyzed are corresponding morphologically to DC populations.7, 10 In the article by Connolly et al.,3 the authors investigate in a mouse model of liver fibrosis the composition of hepatic nonparenchymal CD11c+ cells and assess the impact of CD11c+ cells and “DC depletion” on the inflammatory environment. They showed, primarily by using the tool of flow cytometry, that 20%-27% of the nonparenchymal cells during fibrosis progression are CD11c+ “DCs”. These cells express variable levels of costimulatory molecules (CD40 and major histocompatibility complex II [MHC-II]), suggesting their involvement in antigen

presentation. U0126 nmr Further in the article, the CD11c+ cell population from fibrotic livers was isolated by CD11c immunomagnetic beads and was assessed in terms of the level of cytokine production; with or without toll-like receptor stimulation, this cell population has a high capacity to produce TNF-α and interleukin-6 (IL-6). Ex vivo depletion of CD11c+ cells isolated from fibrotic liver results in attenuated cytokine production. When a transgenic mouse model of conditional depletion of CD11c+ cells was used, cytokine production in the liver was diminished during the inflammatory process upon transitory “DC depletion”. Additionally, the authors showed that CD11c+ cells (labeled as “DCs”) isolated from the fibrotic livers are able to stimulate NK cells

in vivo and in vitro, can be loaded by specific peptides, and induced a significant cytotoxic T lymphocyte response and T cell proliferative response. All these antigen-presentation properties of CD11c+ cells were confirmed in a model of tumor growth challenge; immunization 上海皓元 of mice with CD11c+ cells loaded with ovalbumin peptide resulted in protection from tumor development by a cell line that expressed the peptide. Although the main focus of the experiments is the modulation of the inflammatory process by the CD11c+ cell population during fibrosis progression, a possible link between this population and hepatic stellate cell function during fibrosis is provided by direct coculture experiments showing the augmentation of cytokine production and increased proliferative responses of hepatic stellate cells.

1).6, 7 In the presence of inflammation, the analysis of DCs by FACS requires exclusion of autofluorescence, which is normally present in normal liver and is augmented in the setting of inflammation.8 More than that, digestion of the fibrotic tissue results in cell suspension with variable cell doublets and significant GDC-0199 research buy numbers of nonhematopoietic cells that may also express

CD11c (e.g., stellate cells).9 For these reasons, the analysis of the intrahepatic DC population by FACS needs to be carefully validated by a sorting and cytospin approach to confirm that the cells analyzed are corresponding morphologically to DC populations.7, 10 In the article by Connolly et al.,3 the authors investigate in a mouse model of liver fibrosis the composition of hepatic nonparenchymal CD11c+ cells and assess the impact of CD11c+ cells and “DC depletion” on the inflammatory environment. They showed, primarily by using the tool of flow cytometry, that 20%-27% of the nonparenchymal cells during fibrosis progression are CD11c+ “DCs”. These cells express variable levels of costimulatory molecules (CD40 and major histocompatibility complex II [MHC-II]), suggesting their involvement in antigen

presentation. BAY 80-6946 Further in the article, the CD11c+ cell population from fibrotic livers was isolated by CD11c immunomagnetic beads and was assessed in terms of the level of cytokine production; with or without toll-like receptor stimulation, this cell population has a high capacity to produce TNF-α and interleukin-6 (IL-6). Ex vivo depletion of CD11c+ cells isolated from fibrotic liver results in attenuated cytokine production. When a transgenic mouse model of conditional depletion of CD11c+ cells was used, cytokine production in the liver was diminished during the inflammatory process upon transitory “DC depletion”. Additionally, the authors showed that CD11c+ cells (labeled as “DCs”) isolated from the fibrotic livers are able to stimulate NK cells

in vivo and in vitro, can be loaded by specific peptides, and induced a significant cytotoxic T lymphocyte response and T cell proliferative response. All these antigen-presentation properties of CD11c+ cells were confirmed in a model of tumor growth challenge; immunization medchemexpress of mice with CD11c+ cells loaded with ovalbumin peptide resulted in protection from tumor development by a cell line that expressed the peptide. Although the main focus of the experiments is the modulation of the inflammatory process by the CD11c+ cell population during fibrosis progression, a possible link between this population and hepatic stellate cell function during fibrosis is provided by direct coculture experiments showing the augmentation of cytokine production and increased proliferative responses of hepatic stellate cells.

Governmental regulations, institutional restrictions and fear of potential

lawsuits may be factors restricting development of advanced EUS interventions in the West. Key selleck products Word(s): 1. Endoscopic ultrasound; 2. interventions; 3. USA; 4. Europe; 5. Asia-Pacific Presenting Author: AMOL BAPAYE Additional Authors: NACHIKET A. DUBALE Corresponding Author: AMOL BAPAYE Affiliations: Deenanath Mangeshkar Hospital and Research Center Objective: Endoscopic sub-mucosal dissection (ESD) is fast replacing endoscopic mucosal resection (EMR) for mucosal and sub-mucosal lesions. We evaluate the learning curve for ESD from a non-endemic region for GI cancers. Methods: Patients with mucosal/sub-mucosal lesions diagnosed on endoscopy http://www.selleckchem.com/products/mitomycin-c.html and radial EUS underwent ESD. The procedure was converted to EMR when necessary. Follow up endoscopy at 1, 3, 6 months. Results: Duration: Aug 10 to Mar 13, N = 33, M: F = 25:8, mean age: 61.2 years (19–83). Locations of lesions: stomach – 9, rectum – 8, colon – 10, esophagus – 2, duodenum – 4. Pathology: villous adenoma (VA) – 19 (CA in situ – 4),

hamartomatous polyps – 2, hyperplastic polyp – 1, carcinoid – 4, SMT – 7. Enbloc resection was achieved in 72.7%. Patients were divided in 2 groups (initial 20 and subsequent 13). Both groups were comparable for location, nature and mean size of lesions. In Gr. I, enbloc resection was successful in 65% patients vs 85% in Gr. II. Mean procedure time

was comparable in both groups – 81 min (30–150) and 82 min (25–150). Two in Gr. I had perforations, treated by clipping in one and surgery in other. Two underwent EFTR in Gr II, none in Gr I. Recurrence occurred in 20% in Gr. 1 vs 8%, Gr. II – all post EPMR. Conclusion: Sessile adenomas and SM lesions present opportunities to perform ESD in centers with low volumes of early cancers. We suggest a learning curve of minimum 20 ESD procedures in a low volume center to achieve reasonable 上海皓元 proficiency. Key Word(s): 1. Endoscopic submucosal dissection; 2. ESD; 3. submucosal tumor; 4. early cancer; 5. adenoma; 6. polyp; 7. training; 8. learning curve Presenting Author: DAN FENG CHEN Additional Authors: CHAI YAN, XIANYANG SU, LISHU ZHANG Corresponding Author: DANFENG CHEN Affiliations: Jilin Tumor Hospital, Jilin Tumor Hospital, Liver and Gall Disease Hospital of Jilin Province Objective: Exploring the photosensitizer dose, the beginning time and the illumination time of photodynamic therapy used for digestive tract malignant tumor, aiming to get the best treatment effect. Methods: The homemade big-power 630 nm gas laser and domestic photosensitizer hematoporphyrin was used to the patients with malignant digestive tumor, using photodynamic therapy.

The analysis was conducted using a fixed-effects or random-effects model. Results: Twenty studies meeting the inclusion criteria were included in this meta-analysis. No significant heterogeneity was found across them. It was shown that higher level or positive ATIs is a significant predictor for loss of Infliximab treatment response (OR = 0.22, 95%CI = 0.09–0.54), and which is a slight but not significant predictor PI3K inhibitor for clinical remission (OR = 0.71, 95%CI = 0.35–1.43). In addition, closely connection was found between ATIs development and treatment strategies (OR = 3.38, 95%CI = 1.42–8.05), concomitant immunosuppressant (OR = 0.38,

95%CI = 0.29–0.48). Presence of ATIs often accompanied with higher risk of infusion reaction (OR = 2.35, 95%CI = 1.60–3.45). Conclusion: This meta-analysis indicated that higher level or positive of ATIs predicts loss of response to infliximab and a higher rate of infusion reaction. Meanwhile scheduled Infliximab click here treatment and immunomodulator administering concomitantly, can be taken to reduce ATIs formation. Key Word(s): 1. Infliximab; 2. ATIs; 3. IBD; 4. meta-analysis; Presenting Author: HUI WU Additional

Authors: XIAOLAN ZHANG Corresponding Author: XIAOLAN ZHANG Affiliations: The Second Hospital of Hebei Medical University Objective: The aberrant immunological MCE公司 reaction is considered an important cause of ulcerative colitis (UC), especially the imbalance of T helper (Th)1 and Th17.1,25-dihydroxyvitamin D3 (1,25 (OH)2D3) was proved an primary regulator of the immune system. The study investigated the influence of 1,25 (OH)2D3 in the spleen immune, the most important peripheral immune organ, by the chronic experimental colitis mice induced by dextran sodium sulfate (DSS). Methods: There are three groups in the study: Control group (receive distilled water), DSS and DSS+VD group (received DSS water). The DSS+VD group received 1,25 (OH)2D3 from the 14th day. Severity

of the disease was assessed by body weight (BW), disease activity index (DAI), splenic morphology, weight, length, the spleen index (SI) and histopathology. The levels of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin (IL)-17 and IL-6 were also detected. Results: BW was significantly decreased in the DSS group than that in the Control group, and restored rapidly in the DSS+VD group. The DSS group developed higher DAI, splenomegaly, the spleen weight, length and the SI were remarkably increased than that in the Control group, while lessened in the DSS+VD group than that in the DSS group. The number of mononuclearcells, also the percentage of the macrophages and the dentritic cells in the DSS group were significantly increased, and decreased in the DSS+VD group.

5 All cases of FNH and HCA that were included in our present study were categorized according SB525334 chemical structure to their immunophenotypes. Although our study was focused on the possible role of the angiopoietins in the development of the vascular lesions of FNH and HCA and not on the classification of the lesions, our findings of increased Ang-1 in FNH and HCA are in line with the aforementioned studies. The most characteristic vascular features of FNH are the thick-walled vessels with myointimal hyperplasia located in the central scar

and in the radiating septa, and they exist next to the periseptal sinusoidal enhanced α-SMA and CD34 expression, which is indicative of sinusoidal capillarization and vascular remodeling.20, 21 The increased

expression of Ang-1 and Tie-2 without a concurrent increase in Ang-2 expression creates a condition that can facilitate Ang-1/Tie-2 signaling. Among other things, this can lead to recruitment of SMCs and promotion of differentiation of mesenchymal cells into vascular SMCs.22, 23 Gain-of-function studies have shown that prolonged expression or overexpression of Ang-1 results in various vascular abnormalities, including larger, more numerous, and highly branched vessels in the skin, vascular enlargement in hepatic microvascular remodeling, and cardiac allograft vasculopathy, which are all dysmorphic MAPK Inhibitor Library vascular changes that resemble the vascular features found in FNH and HCA.14, 15, 24, 25 In cardiac graft vasculopathy, inflammation and arterial injury initiate subsequent myointimal proliferation. Transgenic overexpression of both Ang-1 and Ang-2 decrease inflammation, whereas induced Ang-1 expression (not Ang-2) stimulates activation of vascular SMCs, which results in myointimal growth and development of cardiac vasculopathy.25 It is conceivable that in FNH, overexpression of Ang-1 and a relative lack of Ang-2 lead to a similar course of action. Within the context of the assumed primary vascular injury, the dominant Ang-1 overexpression in FNH, which is emphasized by the significantly enhanced Ang-1/Ang-2

ratio, might stimulate excessive recruitment of vascular 上海皓元 SMCs and elicit myointimal hyperplasia. As a result, the dystrophic vessels characteristic of FNH can form. The subsequent compromised vascular supply may underlie local hemodynamic changes leading to regenerative parenchymal hyperplasia; this finding is similar to the FNH-like nodules in mouse livers under the influence of overexpression of Ang-1.14 Also, the occurrence of other vascular abnormalities found in HCA and FNH is supportive of the concept that they are related to excessive Ang-1 activity. In the studies of transgenic expression of Ang-1 in hepatocytes, a spectrum of hepatic vascular changes were documented, and they consisted of arterial sprouting, loss of portal triads, peliotic changes, and vessel dilatation.

Induction of effective cell-mediated immunity will be key for the development of a vaccine, and new work

published analyzed the relevance and contribution of CD4 T helper cell subsets to the immune reaction. Th17 cells, which are also induced during natural infection, were shown to be DMXAA particularly important for vaccination. Cost-efficiency of vaccination was re-assessed and confirmed. Thus, induction and shaping of the effector roles of such protective Th populations will be a target of the newly described vaccine antigens, formulations, and modes of application that we also review here. Helicobacter pylori remains one of the most prevalent pathogens worldwide, infecting every second human being. Infection causes gastritis that in most infected people remains check details clinically asymptomatic for decades. However, H. pylori is the etiologic agent of a majority of gastric and duodenal ulcer diseases and can lead to gastric adenocarcinoma and mucosa-associated lymphoid tissue (MALT) B-cell lymphoma [1]. The factors that determine these diverse clinical outcomes are subject to continuous investigations, but it has become clear that variant

pathogen virulence factors, host genetics [2] and environmental variables, such as co-infections [3], contribute to the course of the disease triggered or promoted by the infection. Here, we review selected literature that has advanced our understanding of the innate and adaptive immune responses to infection as well as advancing efforts to develop a vaccine against this medically important pathogen.

Over the last two decades, the concept of recognition of patterns associated with microbes as envisaged by the late Charley Janeway has led to the discovery of a multitude of so-called pattern recognition receptors (PRR) [4,5]. Depending on their subcellular localization, they sense their cognate class of ligands at the cell surface or in intracellular vesicles 上海皓元医药股份有限公司 – such as members of the Toll-like receptor family (TLR) – or in the cytoplasm – e.g. the retinoic acid-inducible gene I (RIG-I)-like or the nucleotide-binding domain and leucine-rich repeat-containing receptors (RLR and NLR, respectively). The latter are multi-domain proteins with an N-terminal effector, a central nucleotide oligomerization (NOD), and the C-terminal leucine-rich repeat domain. These PRR families recognize diverse classes of abundant microbial structures like lipoproteins, LPS; peptidoglycan derivatives (by TLR-2, -4, and NOD-1, respectively) or particular structures and forms of RNA and DNA (e.g. TLR-3, TLR-7 to -9, RIG-1, MDA-5). Functioning as sentinels their role upon ligand recognition is to trigger signaling cascades that start an alarm and immediate defense program that mostly relies on de novo gene expression and has a critical impact on both innate and adaptive immunity.

Results: CK18 levels were higher in theNA^LD activity score (NAS)>5 than NAS<4 (675.1 U/L vs 348.7 U/L; p<0.0001). The receiver operating characteristic curve indicated a cutoff value of 375 U/L, with specificity, 81.5%; Ixazomib sensitivity, 65%; and positive and negative

predictive values, 80.8% and 43.1%, respectively, for the diagnosis NAS>5. The serum CK18 levels correlated with those of ALT (r=0.49, p<0.0001), AST (r=0.47, p<0.0001), ferritin (r=0.42, p<0.0001), TIMP-1 (r=0.44, p<0.0001), and procollagen III peptide (r = 0.31, p<0.0001) and with HOMA-IR (r=0.33, p<0.0001). In addition, the serum CK18 levels were associated with lobular and portal inflammations, hepatocellular ballooning, and Mallory body formation, but not with steatosis. Among the 71 patients who required a second liver biopsy, 19 with fibrosis progression had significantly high mean CK1 8 levels (from 539 to 907 U/L, p<0.01) and the NAS score increased from 5.2 to 6.1 (p<0.05). In contrast, a significant decrease was noted in the mean CK18 levels

(from 637.3 to 468.7 U/L, p<0.001) and NAS score (from 5.8 to 4.1, p<0.0001) in 52 patients with static or improved fibrosis. Conclusion: CK18 levels were significantly elevated in NASH/NAFLD patients with fibrosis progression, but not in patients with static or improved fibrosis. Careful monitoring of serum CK18 AZD9668 purchase levels may be useful in predicting fibrosis progression in NASH. Disclosures: The following people have nothing to disclose: Miwa Kawanaka, Ken Nishino, Jun Nakamura, Takahito Oka, Noriyo Urata, Daisuke Goto, Mitsuhiko Suehiro, Hircfumi Kawamoto, Gotaro Yamada Nonalcoholic fatty liver disease (NAFLD) is rapidly increasing in prevalence and will become the number one cause of liver disease worldwide by 2020. NAFLD is associated with high triglycerides (TG), high low-density lipoprotein cholesterol (LDLC) levels, and low high-density lipoprotein cholesterol (HDL-C) levels. Both

NAFLD and blood lipid levels are genetically influenced and may share a common genetic etiology. Purpose: We aimed to identify genes MCE and pathways enriched for genetic associations with both blood lipids and NAFLD using human genome wide association study (GWAS) data. Methods: We examined whether genome wide, significantly associated lipid SNP sets from publicly available HDL-C, LDL-C and TG GWAS analyses (N=99, 000) were enriched for associations with hepatic steatosis, the hallmark of NAFLD, measured using computed tomography(CT) (N=7, 126, Speliotes, PLoS Gen, 2011). We then used gene set enrichment analysis (GSEA) as implemented in MAGENTA to identify pathways enriched in HDL-C, LDL-C, and TG GWAS analyses.