However, there are few reports on their effect on the Asian population. We enrolled 104 Japanese genotype 1 CHC individuals treated with PEG-IFN/RBV and 45 with PEG-IFN/RBV/telaprevir, and evaluated the impact of pretreatment serum IP-10

concentrations on their virological see more responses. The pretreatment serum IP-10 concentrations were not correlated with IL28B genotype. The receiver–operator curve analysis determined the cut-off value of IP-10 for predicting a sustained virological response (SVR) as 300 pg/mL. In multivariate analysis, the IL28B favorable genotype and IP-10 concentration of less than 300 pg/mL were independent factors for predicting SVR. In a subgroup of patients with the IL28B favorable genotype, the SVR rate was higher in the patients with IP-10 of less than 300 than in those with 300 pg/mL or more, whereas no patient with the IL28B unfavorable genotype and IP-10 of 300 pg/mL or more achieved SVR. Among the patients treated with INK 128 purchase PEG-IFN/RBV/telaprevir, low pretreatment concentrations of serum IP-10 were associated with a very rapid virological response,

defined as undetectable HCV RNA at week 2 after the start of therapy. Pretreatment serum IP-10 concentrations are associated with treatment efficacy in PEG-IFN/RBV and with early viral kinetics of hepatitis C virus in PEG-IFN/RBV/telaprevir therapy. “
“Aim:  Non-alcoholic steatohepatitis (NASH) is considered a hepatic manifestation of metabolic syndrome. However,

effective drug therapy for NASH has not been established yet. In the present study, we evaluated the efficacy of 6 months of ezetimibe treatment for NASH patients with dyslipidemia for the comparison of improvement of the clinical parameters and histological alterations. Methods:  We prospectively evaluated 10 consecutive NASH patients with dyslipidemia who agreed to participate in this study. The patients were given ezetimibe (10 mg/day) for 6 months, and clinical parameters and histological alterations were comparatively evaluated before and after O-methylated flavonoid treatment. All the patients were given standard calorie diet (30 kcal/kg per day, carbohydrate 50–60%, fat 20–30%, protein 15–20%) and exercise counseling from 3 months before the ezetimibe treatment. Results:  The serum aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transpeptidase, low-density lipoprotein cholesterol, high-sensitivity C-reactive protein and type IV collagen 7 s levels were significantly improved by the treatment with ezetimibe for 6 months. In histological observations, follow-up liver biopsies revealed that the NAS score and steatosis grade were also significantly improved. The fibrosis stage did not change significantly, but six of the 10 patients exhibited an improvement in their fibrosis stage.

However, there are few reports on their effect on the Asian population. We enrolled 104 Japanese genotype 1 CHC individuals treated with PEG-IFN/RBV and 45 with PEG-IFN/RBV/telaprevir, and evaluated the impact of pretreatment serum IP-10

concentrations on their virological SCH772984 datasheet responses. The pretreatment serum IP-10 concentrations were not correlated with IL28B genotype. The receiver–operator curve analysis determined the cut-off value of IP-10 for predicting a sustained virological response (SVR) as 300 pg/mL. In multivariate analysis, the IL28B favorable genotype and IP-10 concentration of less than 300 pg/mL were independent factors for predicting SVR. In a subgroup of patients with the IL28B favorable genotype, the SVR rate was higher in the patients with IP-10 of less than 300 than in those with 300 pg/mL or more, whereas no patient with the IL28B unfavorable genotype and IP-10 of 300 pg/mL or more achieved SVR. Among the patients treated with Selleck Saracatinib PEG-IFN/RBV/telaprevir, low pretreatment concentrations of serum IP-10 were associated with a very rapid virological response,

defined as undetectable HCV RNA at week 2 after the start of therapy. Pretreatment serum IP-10 concentrations are associated with treatment efficacy in PEG-IFN/RBV and with early viral kinetics of hepatitis C virus in PEG-IFN/RBV/telaprevir therapy. “
“Aim:  Non-alcoholic steatohepatitis (NASH) is considered a hepatic manifestation of metabolic syndrome. However,

effective drug therapy for NASH has not been established yet. In the present study, we evaluated the efficacy of 6 months of ezetimibe treatment for NASH patients with dyslipidemia for the comparison of improvement of the clinical parameters and histological alterations. Methods:  We prospectively evaluated 10 consecutive NASH patients with dyslipidemia who agreed to participate in this study. The patients were given ezetimibe (10 mg/day) for 6 months, and clinical parameters and histological alterations were comparatively evaluated before and after Chlormezanone treatment. All the patients were given standard calorie diet (30 kcal/kg per day, carbohydrate 50–60%, fat 20–30%, protein 15–20%) and exercise counseling from 3 months before the ezetimibe treatment. Results:  The serum aspartate aminotransferase, alanine aminotransferase, γ-glutamyl transpeptidase, low-density lipoprotein cholesterol, high-sensitivity C-reactive protein and type IV collagen 7 s levels were significantly improved by the treatment with ezetimibe for 6 months. In histological observations, follow-up liver biopsies revealed that the NAS score and steatosis grade were also significantly improved. The fibrosis stage did not change significantly, but six of the 10 patients exhibited an improvement in their fibrosis stage.

However, despite profound therapeutic implications the prognostic relevance of CSCs and their cellular localization CT99021 mouse within the tumor formation remain controversial. Methods: Expression levels and localization of established CSC markers were assessed in 30 HCCs using qRT-PCR, imunohistochemistry and Western-Blotting. Whole

transcriptome analyses of different tumor regions as well as tumor-surrounding liver (SL) were performed to identify associated signaling pathways and integrated with our existing HCC database. Results: Expression patterns of established CSC markers were surprisingly heterogeneous. Activation of CSCs was predominantly observed in SL and continuously decreased to the tumor core. Consistently, tran-scriptome profiles between SL and different tumor regions were quite distinct. A generated gene expression-signature showed activation of pathways related to proliferation as well as apop-tosis in the tumor tissue, while the invasive tumor margin (TM) was characterized by inflammatory and EMT-related gene sets as well as activation of pro-survival signaling such as ERK and FOS. Consistently, integration of the different signatures with our database of find more 53 HCC revealed that the TM signature was associated with the survival of

HCC patients. Conclusion: CSCs in HCC are heterogeneous. The CSC phenotype is predominantly determined by the permissive tumor microenvironment. However, pro-oncogenic properties might originate in the TM. The activation of key oncogenic features as well as immune-response signaling indicates that

the cross-talk between tumor and microenvironment might be a promising therapeutic and/ or preventive target. Disclosures: Marcus A. Woerns – Advisory Committees or Review Panels: Bayer, Bayer Peter R. Galle – Advisory Committees or Review however Panels: Bayer, BMS, Lilly, Daiichi, Jennerex; Consulting: Medimmune; Grant/Research Support: Roche, Lilly; Speaking and Teaching: Bayer, BMS The following people have nothing to disclose: Michael Fischer, Stefan Heinrich, Jesper B. Andersen, Martin F. Sprinzl, Ines Gockel, Snorri S. Thorgeirsson, Hauke Lang, Jens U. Marquardt BACKGROUND & AIMS: Oral supplementation with branched-chain amino acids (BCAA; leucine, isoleucine, and valine) in patients with liver cirrhosis potentially suppresses incidence of hepatocellular carcinoma and improves event-free survival. However, the detailed mechanisms by which BCAA act on hepatic fibrosis have not been fully elucidated. METHODS: BCAA were administered to atherogenic and high-fat (Ath & HF) diet-induced nonalcoholic steatohepatitis (NASH) model mice and platelet-derived growth factor C transgenic mice (Pdgf-c Tg). Liver histology, tumor incidence, and gene expression profiles were evaluated. RESULTS: Ath & HF diet mice developed hepatic tumors at a high frequency at 68 weeks.

“
“The development of vaccination and

novel therapy for hepatitis C virus (HCV) has been hampered by the lack of suitable small-animal models. GB virus B (GBV-B), closely related to HCV, causes viral hepatitis in common marmosets (Callithrix jacchue jacchus) and might represent an attractive surrogate model for HCV infection. However, differences Roscovitine mw exist between GBV-B and HCV in spite of a short genetic distance between the two viruses. Here we report common marmosets infected with two HCV/GBV-B chimeras containing HCV structural genes coding for either whole core and envelope proteins (CE1E2p7) or full envelope proteins (E1E2p7) substituted for the counterpart elements of GBV-B. Naïve animals intrahepatically selleck kinase inhibitor injected with chimeric RNA transcripts or intravenously injected with sera from primary infected animals produced high levels of circulating infectious chimeric viruses and they developed chronic infection. Tacrolimus-treated marmosets inoculated with a CE1E2p7 chimera had higher viral loads and long-term persistent infection. A moderate elevation of serum aspartate aminotransferase (AST) levels was observed in parallel with viral replication. Chimeras recovered from liver samples revealed 1/958 adaptive viral mutations. Histopathological changes typical of viral hepatitis were observed

in liver tissues from all types of HCV chimeras-infected marmosets. HCV core and E2 proteins were detected in liver tissues from infected animals by immunohistochemical staining. Fluctuations of chimeric virus replication in marmosets with spontaneous and sporadic viral clearance might be related to specific antibody and T-cell response to HCV proteins in vivo. Replication of CE1E2p7 chimera was observed in primary hepatocyte cultures by immunofluorescent staining in vitro. Conclusion: Infectious HCV chimeras causing chronic hepatitis in marmosets might constitute a small

primate model suitable for evaluation of virus-cell interaction, vaccination, and antiviral therapy against HCV infection. (Hepatology 2014;59:789–802) “
“Yusa K, Rashid ST, Strick-Marchand H, Varela I, Liu PQ, Paschon DE, et al. Targeted gene correction of α1-antitrypsin many deficiency in induced pluripotent stem cells. Nature 2011;478:391-394. www.nature.com (Reprinted with permission) Human induced pluripotent stem cells (iPSCs) represent a unique opportunity for regenerative medicine because they offer the prospect of generating unlimited quantities of cells for autologous transplantation, with potential application in treatments for a broad range of disorders. However, the use of human iPSCs in the context of genetically inherited human disease will require the correction of disease-causing mutations in a manner that is fully compatible with clinical applications.

“
“The development of vaccination and

novel therapy for hepatitis C virus (HCV) has been hampered by the lack of suitable small-animal models. GB virus B (GBV-B), closely related to HCV, causes viral hepatitis in common marmosets (Callithrix jacchue jacchus) and might represent an attractive surrogate model for HCV infection. However, differences http://www.selleckchem.com/products/Bortezomib.html exist between GBV-B and HCV in spite of a short genetic distance between the two viruses. Here we report common marmosets infected with two HCV/GBV-B chimeras containing HCV structural genes coding for either whole core and envelope proteins (CE1E2p7) or full envelope proteins (E1E2p7) substituted for the counterpart elements of GBV-B. Naïve animals intrahepatically Apitolisib supplier injected with chimeric RNA transcripts or intravenously injected with sera from primary infected animals produced high levels of circulating infectious chimeric viruses and they developed chronic infection. Tacrolimus-treated marmosets inoculated with a CE1E2p7 chimera had higher viral loads and long-term persistent infection. A moderate elevation of serum aspartate aminotransferase (AST) levels was observed in parallel with viral replication. Chimeras recovered from liver samples revealed 1/958 adaptive viral mutations. Histopathological changes typical of viral hepatitis were observed

in liver tissues from all types of HCV chimeras-infected marmosets. HCV core and E2 proteins were detected in liver tissues from infected animals by immunohistochemical staining. Fluctuations of chimeric virus replication in marmosets with spontaneous and sporadic viral clearance might be related to specific antibody and T-cell response to HCV proteins in vivo. Replication of CE1E2p7 chimera was observed in primary hepatocyte cultures by immunofluorescent staining in vitro. Conclusion: Infectious HCV chimeras causing chronic hepatitis in marmosets might constitute a small

primate model suitable for evaluation of virus-cell interaction, vaccination, and antiviral therapy against HCV infection. (Hepatology 2014;59:789–802) “
“Yusa K, Rashid ST, Strick-Marchand H, Varela I, Liu PQ, Paschon DE, et al. Targeted gene correction of α1-antitrypsin Oxalosuccinic acid deficiency in induced pluripotent stem cells. Nature 2011;478:391-394. www.nature.com (Reprinted with permission) Human induced pluripotent stem cells (iPSCs) represent a unique opportunity for regenerative medicine because they offer the prospect of generating unlimited quantities of cells for autologous transplantation, with potential application in treatments for a broad range of disorders. However, the use of human iPSCs in the context of genetically inherited human disease will require the correction of disease-causing mutations in a manner that is fully compatible with clinical applications.

1 These were glued to the animal’s fur on the neck behind the head Ixazomib chemical structure with quick-setting epoxy. The tags were configured to attempt Fastloc GPS locations every 10 min provided the seal was at the sea surface. Both seals were captured and tagged in the Molène archipelago, western Brittany, France. During their whole track duration (172 and 204 d, respectively), both seals crossed the English Channel, back and forth, moving directly from one colony

to another. We consider here two such transits of the English Channel from the United Kingdom to known seal haul-out sites. These movements occurred outside the breeding or molting season of gray seals in the French colonies, but there could be breeding in the Isles of Scilly at that time of the year (September). Seal B24 departed from the Isles of Scilly (UK) and arrived at the Isle of Molène (France) after 43.5 h (Fig. 1). B23 crossed

the English Channel (Fig. 2) in 48 h between Porthleven (UK) to the Nature Reserve of Les Sept Iles (France). At total, 158 Fastloc GPS locations were obtained for seal B23 over its crossing the English Channel (mean = 3.3 locations per hour) and 148 for seal B24 (mean = 3.4 locations per hour). Hourly ground track locations were then determined using linear interpolation of the raw track data. In the English Channel, tidal currents dominate current patterns due to wind, wave, and thermohaline effects Serine Protease inhibitor (Sentchev et al. 2009). For this reason, we estimated the currents along the seals’ pathways using a tidal model. We used a 2-D model that estimates currents averaged over the whole water column (TELEMAC software, Hervouet 2007), which has been shown to be very effective for modeling tidal propagation in coastal waters (Nicolle et al. 2009, Davies et al. 2011). The model was initially developed for numerical simulations of tides and storms surges (Chevaillier 2011) and it was validated through extensive Y-27632 solubility dmso comparisons with the sea level and sea current measurements in

the Bay of Biscay and in the English Channel. In this study we define: “Ground Track” (GT) as a series of movement vectors built from the GPS time-stamped location fixes; “bearing” as the direction of a Ground Track vector; and “heading” as the direction a seal is pointing. A seal’s ground track, D, can be represented as a sum of drifting and swimming vectors: D  =  Dd + Ds. We calculated the drift, Dd, as a Lagrangian transport displacement experienced by a passive particle in tidal flows (TELEMAC, Hervouet 2007). The measured surface velocities of the tracked seals were not used for the numerical simulations. These are the result of both the swimming speed of the seal and the current’s speed, and we aimed at modeling the animals’ movements from a data set completely distinct from the “real” seal data before comparison of the model vs. the track of the seals. We compared two navigation rules.

In a univariate analysis using Cox’s proportional hazards model, serum total bilirubin,

the serum level of protein induced by vitamin K absence/antagonist-II (≤100 vs ≥101 mAU/mL), tumor morphology (pattern 1 vs 2) and tumor number (≤3 vs ≥4) showed statistical significance (≤0.05). In a multivariate analysis of these factors, morphology and tumor number showed significance. According to Kaplan–Meier estimation, the cumulative disease-free survival rates were significantly lower in patients click here with four or more lesions than in those with three or less lesions and in patients showing pattern 2 than in those showing pattern 1. Patients with pattern 2 hepatocellular carcinoma and/or four or more lesions may have a relatively high recurrence rate after transarterial chemoembolization. HEPATOCELLULAR CARCINOMA (HCC) is the fifth and seventh most common

cause of cancer-related deaths in men and women, respectively, worldwide.[1] Therefore, establishing an effective treatment strategy is important. Currently, the main treatments for cure include hepatectomy and percutaneous radiofrequency ablation (RFA), and those for palliation in cases of incurable HCC include transarterial chemoembolization (TACE).[2] For advanced HCC, none of these treatments is indicated, but sorafenib, a small-molecule inhibitor of various kinases, has been Epacadostat datasheet reported to be effective.[3] TACE is indicated for moderately advanced HCC when hepatectomy or RFA is unlikely to be effective.[2, 4] The role of TACE in improving patient survival was initially debated; however, many subsequent randomized controlled trials

have proven its effectiveness. Thus, TACE is now commonly used in the clinical setting.[5, 6] However, because a 5-year survival rate of less than 50% is achieved with TACE, improvements in this methodology are definitely warranted.[4] One of the most common setbacks in achieving better HCC treatment outcomes are the high post-treatment recurrence rates. Post-treatment recurrence often requires retreatment, but repeating triclocarban TACE at short intervals is associated with a high risk of low hepatic functional reserve.[4-7] Therefore, identifying factors that contribute to high post-treatment recurrence rates is important for establishing an effective treatment strategy. In HCC, both treatment selection and patient outcomes are determined by tumor progression and hepatic functional reserve.[8-11] Hepatocellular carcinoma is known to demonstrate various morphological appearances.[12] Kanai et al.[13] classified the nodular type of HCC into three categories depending on gross appearance, in accordance with the clinicopathological features: simple nodular (SN) type, simple nodular type with extranodular growth (SNEG) and confluent multinodular (CM) type.

Several investigators have reported on CLE for the diagnosis and surveillance of many gastrointestinal diseases, such as Barrett’s esophagus,3 gastritis,4 gastric intestinal metaplasia,5

gastric cancer,6 colonic neoplasia and even intestinal spirochaetosis.7,8Acriflavine-guided endomicroscopy was used for the first time to detect H. pylori in a patient in 2005.9 However, the diagnostic efficacy of CLE for H. pylori Selleck GW-572016 infection lacks detailed data. Consequently, we aimed to compare CLE features of H. pylori infection with histology findings and evaluated the use of CLE for in vivo diagnosis of H. pylori infection. Consecutive patients with gastrointestinal symptoms undergoing endoscopy in our endoscopy unit from August 2008 to March 2009 were enrolled. Exclusion criteria were severe

systemic disease, bleeding, advanced adenocarcinoma in the stomach, pregnancy or lactation, use of non-steroidal anti-inflammatory drugs and medications (i.e. bismuth, proton pump inhibitors, or antibiotics) within 6 weeks, history of treatment for eradication H. pylori infection, or gastric surgery. The study protocol was approved by the institutional ethics committee of Qilu Hospital. Informed consent for participation was obtained from all participants. Before embarking on the prospective study, we establish the CLE image criteria for H. pylori infection. The first 20 patients were recruited for a pilot study. Endoscopy procedures were carried out as described in the prospective study. Besides taking biopsy specimens for H. pylori examination, we took a target biopsy sample

from the observed sites in all 20 cases. Targeted biopsies were possible because selleck the working channel Niclosamide and the endomicroscopy window are joined at the distal tip of the endoscope. The biopsy site was located 5 mm to the left of the mucosal erythema created by suction. The CLE recording images and the corresponding histopathology images were openly evaluated by three senior endoscopists (YQL, XMG, TY) and one pathologist (CJZ). All endoscopists have carried out more than 500 confocal procedures prior to patient recruitment. The CLE features of H. pylori were identified by comparing conventional ex vivo histopathology specimens and previously published features.9 Considering that the CLE generates images parallel to the mucosal surface, corresponding to an en face view, target biopsy samples from the pilot study were sectioned in both the horizontal and vertical planes to facilitate CLE image comparison. Diagnostic criteria should be prominent in infected cases and absent in controls. The CLE criteria in images for the subsequent consecutive patients were evaluated blinded. All procedures involved the use of a confocal laser endomicroscope (Pentax EC-3870K, Tokyo, Japan). CLE has a miniature laser scanning microscope integrated into the distal tip of a conventional video endoscope that enables simultaneous white-light endoscopy and confocal microscopy.

Although the body weight significantly decreased in incretin based medicine group (80.0 kg to 78.1 kg, P < 0.01), the body weight did not change

in conventional treatments group (76.4 kg to 77.0 kg, P = 0.68). The cumulative normalization rates of serum ALT level significantly differed between the two groups (P = 0.04); 20.5%, and 35.1% at 250, and 500 days, respectively, in the incretin based medicine group and 15.8%, and 26.7% in the conventional treatments group. Multivariate analysis indicated that administration of incretin based medicine (OR 0.44, P < 0.01), existence of hypertension (OR 1.60, P = 0.048), and comorbidity with dyslipidemia (OR 1.64, P = 0.04) as independent factors which contributed to normalization of serum ALT level. Conclusions: Administration of incretin based medicine led not only SAR245409 cell line good control

of type 2 DM but also reduction of body weight, and rapid improvement of liver inflammation. Disclosures: The following people have nothing to disclose: Takamasa Ohki, Isogawa Akihiro, Mari Yamagami, Tomoharu Yamada, Koki Sato, Yasuhide Yamamoto, Michiharu Seki, Nobuo Toda, Kazumi Tagawa BACKGROUND: Recurrence of non-alcoholic steatohepatitis (NASH) in up to 33% of the liver transplant (LT) recipients has been reported (Bhagat et al 2009). It is not known whether steroid free immunosuppression reduces the risk of NASH after liver transplantation. AIM: We aimed to determine the prevalence of NASH post- Wnt drug transplant in a cohort of patients with NASH cirrhosis and alcoholic cirrhosis (ETOH) who received a steroid free immunosuppression regimen based on one year protocol liver biopsy,

and determine risk factors for recurrence and outcomes for these patients. METHODS: We performed a retrospective review for all patients who underwent LT for NASH or ETOH who had protocol liver biopsy at one year follow up at our center from April 2006 to April 2012. Comparison was made between ETOH and NASH groups as well as those who developed steatohepatitis (SH group) and those who did not develop steatohepatitis (non-SH group). RESULTS: The study included 40 recipients (M/F: 20/20) in the NASH group and 47(M/F: 40/7) in the ETOH group. Recurrence/development of NASH in recipients of LT with cirrhosis secondary to NASH is significantly SSR128129E higher compared to recipients secondary to ETOH [16 of 40(40%) vs.8 of 47(17%); P= 0.017]. Multivariate analysis failed to identify any single predictive variable for predicting recurrence/development of steatohepatitis in both NASH and ETOH groups. Atherosclerotic cardiovascular events, defined as acute myocardial infraction, cerebrovascular accident, need for percutaneous coronary intervention and coronary artery bypass graft was noted in six recipients, 5(12.5%) from the NASH group, and 1(2.1%) from the ETOH group (P=0.09). Presence of steatohepatitis did not predict cardiovascular events (R=-0.68, P=0.54, OR 0.50) or death (R=0.73, P=0.37, OR 0.

Although the body weight significantly decreased in incretin based medicine group (80.0 kg to 78.1 kg, P < 0.01), the body weight did not change

in conventional treatments group (76.4 kg to 77.0 kg, P = 0.68). The cumulative normalization rates of serum ALT level significantly differed between the two groups (P = 0.04); 20.5%, and 35.1% at 250, and 500 days, respectively, in the incretin based medicine group and 15.8%, and 26.7% in the conventional treatments group. Multivariate analysis indicated that administration of incretin based medicine (OR 0.44, P < 0.01), existence of hypertension (OR 1.60, P = 0.048), and comorbidity with dyslipidemia (OR 1.64, P = 0.04) as independent factors which contributed to normalization of serum ALT level. Conclusions: Administration of incretin based medicine led not only BAY 80-6946 ic50 good control

of type 2 DM but also reduction of body weight, and rapid improvement of liver inflammation. Disclosures: The following people have nothing to disclose: Takamasa Ohki, Isogawa Akihiro, Mari Yamagami, Tomoharu Yamada, Koki Sato, Yasuhide Yamamoto, Michiharu Seki, Nobuo Toda, Kazumi Tagawa BACKGROUND: Recurrence of non-alcoholic steatohepatitis (NASH) in up to 33% of the liver transplant (LT) recipients has been reported (Bhagat et al 2009). It is not known whether steroid free immunosuppression reduces the risk of NASH after liver transplantation. AIM: We aimed to determine the prevalence of NASH post- this website transplant in a cohort of patients with NASH cirrhosis and alcoholic cirrhosis (ETOH) who received a steroid free immunosuppression regimen based on one year protocol liver biopsy,

and determine risk factors for recurrence and outcomes for these patients. METHODS: We performed a retrospective review for all patients who underwent LT for NASH or ETOH who had protocol liver biopsy at one year follow up at our center from April 2006 to April 2012. Comparison was made between ETOH and NASH groups as well as those who developed steatohepatitis (SH group) and those who did not develop steatohepatitis (non-SH group). RESULTS: The study included 40 recipients (M/F: 20/20) in the NASH group and 47(M/F: 40/7) in the ETOH group. Recurrence/development of NASH in recipients of LT with cirrhosis secondary to NASH is significantly Ribonucleotide reductase higher compared to recipients secondary to ETOH [16 of 40(40%) vs.8 of 47(17%); P= 0.017]. Multivariate analysis failed to identify any single predictive variable for predicting recurrence/development of steatohepatitis in both NASH and ETOH groups. Atherosclerotic cardiovascular events, defined as acute myocardial infraction, cerebrovascular accident, need for percutaneous coronary intervention and coronary artery bypass graft was noted in six recipients, 5(12.5%) from the NASH group, and 1(2.1%) from the ETOH group (P=0.09). Presence of steatohepatitis did not predict cardiovascular events (R=-0.68, P=0.54, OR 0.50) or death (R=0.73, P=0.37, OR 0.