Dig Dis Sci. 2008; 53(8): 2258–2267. 2. Lenhart M, Paetzel C, Sackmann M, et al. Superselective arterial embolisation with a liquid polyvinyl alcohol copolymer in patients with acute gastrointestinal haemorrhage. Eur Radiol. 2010; 20:1994–1999. 3. Tian X, Shi Y, Hu Y, et al. Percutaneous transhepatic variceal embolization with cyanoacrylate vs. transjugular intrahepatic portal systemic shunt for esophageal variceal bleeding. Hepatol Int. 2013; 7(2): 636–644. 4. Sun A, Shi YJ, Xu XG, et al. MDCT angiography to evaluate the therapeutic

effect of PTVE for esophageal varices. World J Gastroenterol. INCB024360 2013; 19(10): 1563–1571. EH TSOI,1 CY GOH,1 N PARTHASARATHY,1 KE MARION,3 C MCNAB,1 S GLANCE,1 C LEUNG2 1Department of Gastroenterology, The Northern Hospital, Northern Health, Victoria, Australia,

2University of Melbourne, Doxorubicin clinical trial Melbourne, Victoria, Australia, 3School of Mathematical and Geospatial Sciences College of Science, Engineering and Health, RMIT University, Victoria, Australia Introduction: Current American Association for the Study of Liver Diseases guidelines recommend hepatitis B virus (HBV) screening with hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (antiHBs) and hepatitis B core antibody (antiHBc) in all persons born in high and intermediate endemic areas. Our aim is to audit the screening practices for HBV infection in at-risk patients who attended a metropolitan hospital inflammatory bowel disease clinic. Methods: All patients born in high and intermediate endemic areas with inflammatory bowel disease (IBD) who attended an IBD clinic between January 2012 and January 2014 were identified from clinic records

based on country of birth. Medical records and hospital laboratory results were reviewed; and general practitioners were contacted to determine hepatitis screening practices. Multivariate analysis was used to determine if there were any factors that predicted screening for HBV in these patients. 上海皓元医药股份有限公司 Results: 70 patients who attended IBD clinic between 2012 and 2014 were identified to be from high and intermediate endemic areas. 44% were male with a median age of 55 years. 50% of patients had Crohn’s disease and 50% had ulcerative colitis. The majority of patients were born in Turkey (16%), Italy (13%) and Greece (7%). Only thirty-eight patients (54%) had hepatitis B serology performed and of these, 36 (95%) had HBsAg, 19 (50%) had antiHBs and 20 (53%) had antiHBc tested. Patients with Crohn’s disease were more likely to be tested compared to those with ulcerative colitis (60% vs 45% respectively, p = 0.048). Gender and country of birth did not affect screening practices for HBV infection (p = 0.141 & p = 0.168 respectively).

1). Ceramide is metabolized to sphingosine by ceramidases, which in turn is metabolized by sphingosine kinases to sphingosine-1-phosphate

(S1P). A host of cellular responses have been discovered for these three bioactive sphingolipids (e.g. cell senescence, differentiation, apoptosis and cell cycle arrest for ceramide; apoptosis and cell cycle arrest for sphingosine; and proliferation, mitogenesis, migration, angiogenesis, and protection from apoptosis for S1P). Reviews of sphingolipid metabolism, sphingolipid signaling, and the mechanisms of action of ceramide, sphingosine and S1P emphasize the complex web of interactions that occurs because of the intricately interconnected network of sphingolipid species and enzymes that

are involved.10,11 Lee et al.9 now show that in a mouse strain prone to gallstone formation, feeding a lithogenic diet is associated with GS-1101 cost elevated levels of ceramide in serum and bile. Furthermore, these ceramide levels are decreased by the addition of myoricin, a specific inhibitor of the first and rate-limiting step in the sphingolipid biosynthetic pathway catalyzed by SPT. After 6 weeks on the diets, 65% click here of mice on the lithogenic diet formed gallstones, compared with none in the control chow group and 15% in the lithogenic diet with myoricin group. Serum cholesterol and triglyceride levels were also elevated in the lithogenic diet group; these levels were reduced in the myoricin-treated mice. Gallbladder p38 mitogen-activated protein kinase phosphorylation was

increased in the lithogenic diet group, which was reduced with myoricin treatment. The findings reported are preliminary; the mechanisms by which inhibition of the sphingolipid biosynthetic pathway leads to cholesterol gallstone formation remain undefined. Nevertheless, medchemexpress based on the extensive literature that has accumulated with respect to cholesterol gallstone pathogenesis on the one hand, and bioactive sphingolipid biology on the other, one can create a roadmap for future studies that will likely yield mechanistic insights. One potential mechanism involves effects on gallbladder inflammation. Gallstone formation in mouse models involves activation of an inflammatory response.12 Bioactive sphingolipids are known to modulate inflammatory mediators.13 Therefore, one possible mechanism involves downregulation of inflammatory mediators in the gallbladder by inhibition of the de novo sphingolipid biosynthetic pathway. This scenario is supported by the findings of a previous study by the same group.14 A high-cholesterol diet fed to Syrian Golden hamsters induced gallstones in association with sixfold elevations of biliary ceramide and S1P. Levels of gallbladder inducible nitric oxide synthase and phosphorylated signal transducer and activator of transcription 3, which have been linked to inflammation, were increased.

Additional Supporting Information may be found in the online Selleckchem PLX3397 version

of this article. “
“Background and Aim:  Long-term trends of anti-hepatitis C virus (HCV) antibody titer and their associated factors in patients with sustained virological response (SVR) were investigated. Methods:  From May 1999 to July 2005, a total of 166 SVR consecutive patients (M/F: 86/80) were enrolled. Anti-HCV titer, samples to cut-off (S/CO) ratios, were measured with AxSYM HCV version 3.0. Their S/CO ratios were followed every 6 months after SVR and the patterns over time were identified by trajectory analyses. Changes of recombinant immunoblot assay (RIBA) pattern before treatment and end of follow-up were compared (n = 64). Results:  The mean duration of follow-up was 4.7 ± 1.5 years (median 4.3; range 3–9 years). The rates of S/CO

ratios decreased annually (P < 0.001). Two of them (1.2%) achieved seroreversion. Trajectory groups included lower pretreatment S/CO ratios (LAB, n = 83), rapid decrease (RD, n = 62) and slow decrease (SD, n = 21) groups. Comparing LAB to RD group, odds ratio (OR) of increased platelet count per 1 unit and interferon regimen was 1.12 (95% confidence interval [CI] 1.04–1.20) and 2.17 (95% CI 1.04–4.52) respectively. Comparing SD to LAB and RD groups, the OR of advanced fibrotic stage, using mild fibrotic stage as a reference, was 4.33 (95% CI 1.49–12.63). Reaction strength of all four RIBA bands decreased significantly at the end of follow-up. Conclusions:  Anti-HCV titers decreased annually during long-term follow-up after SVR. Higher VX-809 pretreatment platelet count, interferon regimen and mild fibrosis were associated with

decreased anti-HCV titers. However, only a few cases achieved seroreversion. All RIBA bands decreased significantly after long-term follow-up. “
“Background and Aims:  Chronic hepatitis B virus (HBV) infection is a major global health issue, and the prognosis of patients with HBV-associated acute-on-chronic hepatic failure (ACLF) is extremely poor. In this study, MCE the efficacy of lamivudine was investigated in patients with ACLF. The effects of HBV DNA load and its related factors on the prognosis were also further explored. Methods:  A matched retrospective cohort study using data on ACLF patients derived from our hospital database was conducted. One hundred and thirty patients receiving lamivudine were selected into the lamivudine treatment group with another 130 without lamivudine treatment studied as control. They were matched for sex, age and imaging finding with the lamivudine treatment group. All the patients were followed up for 3 months and the survival rates were compared. The influential factors on the mortality were studied by the Cox proportional hazards model. Results:  The cumulative survival rates of patients in the lamivudine group were higher than those of the control group (χ2 = 9.50, P = 0.0021). The mortality of patients in the high virus load group (71/95, 74.

5D). This resulted in an equal staging by blinded Ishak scoring (Fig. 5E) and in comparable sizes of hepatic infiltrates (data not shown). Moreover, T-cell responses against mFTCD were comparable in Ad-mFTCD mice (Fig. 5F) as compared to Ad-hFTCD mice (Fig. 4C). Taken together, molecular similarity was as effective as molecular identity in triggering emAIH. We next wanted to test if the newly developed model PCI32765 of emAIH was not only suited to investigate the pathophysiology of the disease but if it could also be used to develop new therapeutic strategies. To this end it was important to show that the disease can be successfully

treated with our current immunosuppressive standard therapies. Indeed, a single 8-week course of oral therapy with prednisolone was sufficient to substantially improve the hepatitis and 70% of investigated mice showed complete histological remission (Fig. 6). Recently, a prospective randomized trial has established budesonide as an alternative to prednisolone for induction of remission.[16] In fact budesonide was superior to prednisolone in inducing remission and patients treated with budesonide

had fewer steroid-related side effects. It was therefore reassuring that budesonide was as effective as prednisolone in treating murine hepatitis. As both standard immunosuppressive therapies PLX-4720 nmr were also effective in treating emAIH, we suggest that our model might also be suited to develop and test new therapeutic regimens for treatment MCE of AIH. We developed a model of

experimental murine autoimmune hepatitis closely resembling the human disease. Semi-blinded pathological analysis showed features suggestive of AIH such as lymphoplasmacellular infiltrates, interface hepatitis, and lobular inflammation. The disease was chronically evolving after initial priming, which is in sharp contrast to all animal models using liver-specific expression of a model antigen paired with T cells from T-cell receptor transgenic animals.[14, 17-19] In all such models hepatitis is rather short-lived and the outcome of the initial immune attack is usually tolerance. Even in double transgenic models suggesting a chronic hepatitis the liver-specific CD8+ T cells were rather hyporeactive and anergic.[14, 18] Nonetheless, some approaches result in massive lymphoid infiltrations as reasoned by the high precursor frequency of transgenic effector cells.[14, 19] Although these models were helpful in understanding tolerance mediated by the liver, they were not very helpful to study the pathophysiology of AIH or to develop new therapeutic concepts. Models of human disease with a polyspecific T-cell repertoire are, on the other hand, limited to identify exact cellular and molecular mechanisms, as the precursor frequency and affinity of autoreactive is usually low in this setting. AST and ALT were not elevated during the chronic phase of the emAIH.

6/13 (46%) in the placebo group (p<0.0001). Overall and transplant-free survival was similar between study groups; CHRSR was associated with significantly improved survival at Day 90 (p=0.0002). Adverse event (AE) incidence was similar for the 2 groups; serious AEs were reported in 59/97 (63.4%) subjects in the terlipressin group vs. 53/99 (55.8%) subjects in the placebo group. No new or unexpected AEs were reported. Summary: Terlipressin plus

albumin treatment is associated with improved renal function compared to albumin alone in patients with HRS-1; the improvement in renal function correlates with survival. Patients achieving CHRSR with terlipressin had a better outcome compared to those who responded to albumin alone. Conclusion: Terlipressin is effective in improving renal function in HRS-1. Disclosures: Thomas D. Boyer – Consulting: Ikaria; Grant/Research AP24534 Support: Abbvie, Gilead, Merck Arun J. Sanyal – Advisory Committees or Review Panels: Bristol Myers, Gilead, Abbott, Ikaria; Consulting: Salix, Immuron, Exhalenz, Nimbus, Genentech, Echo-sens, Takeda; Grant/Research Support: Salix, Genentech, Genfit, Intercept, Ikaria, Takeda, GalMed, Novartis, Gilead; Independent Contractor: UpToDate, Elsevier Florence Wong – Consulting:

Gore Inc; Grant/Research Support: Grifols R Todd Frederick – Advisory Committees or Review Panels: Vital Therapies; Consulting: Salix, Gilead, 17-AAG price Ocera, Hyperion John R. Lake – Advisory Committees or Review Panels: BMS; Consulting: Vital Therapies, Novartis, HepaHope; Grant/Research Support: Gilead, Salix, Ocera, Essai Jacqueline G. O’Leary – Consulting: Gilead, Jansen Daniel Ganger – Grant/Research Support: merck, gilead, Ocera Terry D. Box – Advisory Committees or Review Panels: Gilead, Genentech, Abb-Vie, Salix, Janssen; 上海皓元医药股份有限公司 Grant/Research Support: Gilead, Merck, BMS, AbbVie, Idenix, Salix, Conatus, Cumberland, Boehringer Ingelheim, Genfit, Vital Therapeutics, Sundise, ikaria; Speaking and Teaching: Gilead, Merck, Genentech, Salix Khurram Jamil – Employment: IKARIA; Stock Shareholder: IKARIA Stephen Chris Pappas – Consulting: Orphan Therapeutics, Abbvie “
“Aim:  This study was conducted

to evaluate the efficacy and safety of radiofrequency ablation (RFA) therapy in elderly patients with hepatocellular carcinoma (HCC). Methods:  Four hundred and sixty-one patients with naïve HCC, including 107 elderly (aged ≥75 years) patients, who were treated with RFA between 2000 and 2007, were enrolled. Baseline characteristics, survival/recurrence rates and complications after RFA were compared between elderly and non-elderly patients. Results:  In the elderly group, the proportion of men, alcohol consumption, serum alanine aminotransferase and γ-glutamyl transpeptidase levels were significantly lower compared with those in the non-elderly group. There were no differences in Child–Pugh grade and tumor characteristics between the two groups.

6/13 (46%) in the placebo group (p<0.0001). Overall and transplant-free survival was similar between study groups; CHRSR was associated with significantly improved survival at Day 90 (p=0.0002). Adverse event (AE) incidence was similar for the 2 groups; serious AEs were reported in 59/97 (63.4%) subjects in the terlipressin group vs. 53/99 (55.8%) subjects in the placebo group. No new or unexpected AEs were reported. Summary: Terlipressin plus

albumin treatment is associated with improved renal function compared to albumin alone in patients with HRS-1; the improvement in renal function correlates with survival. Patients achieving CHRSR with terlipressin had a better outcome compared to those who responded to albumin alone. Conclusion: Terlipressin is effective in improving renal function in HRS-1. Disclosures: Thomas D. Boyer – Consulting: Ikaria; Grant/Research BAY 57-1293 purchase Support: Abbvie, Gilead, Merck Arun J. Sanyal – Advisory Committees or Review Panels: Bristol Myers, Gilead, Abbott, Ikaria; Consulting: Salix, Immuron, Exhalenz, Nimbus, Genentech, Echo-sens, Takeda; Grant/Research Support: Salix, Genentech, Genfit, Intercept, Ikaria, Takeda, GalMed, Novartis, Gilead; Independent Contractor: UpToDate, Elsevier Florence Wong – Consulting:

Gore Inc; Grant/Research Support: Grifols R Todd Frederick – Advisory Committees or Review Panels: Vital Therapies; Consulting: Salix, Gilead, selleck compound Ocera, Hyperion John R. Lake – Advisory Committees or Review Panels: BMS; Consulting: Vital Therapies, Novartis, HepaHope; Grant/Research Support: Gilead, Salix, Ocera, Essai Jacqueline G. O’Leary – Consulting: Gilead, Jansen Daniel Ganger – Grant/Research Support: merck, gilead, Ocera Terry D. Box – Advisory Committees or Review Panels: Gilead, Genentech, Abb-Vie, Salix, Janssen; MCE Grant/Research Support: Gilead, Merck, BMS, AbbVie, Idenix, Salix, Conatus, Cumberland, Boehringer Ingelheim, Genfit, Vital Therapeutics, Sundise, ikaria; Speaking and Teaching: Gilead, Merck, Genentech, Salix Khurram Jamil – Employment: IKARIA; Stock Shareholder: IKARIA Stephen Chris Pappas – Consulting: Orphan Therapeutics, Abbvie “
“Aim:  This study was conducted

to evaluate the efficacy and safety of radiofrequency ablation (RFA) therapy in elderly patients with hepatocellular carcinoma (HCC). Methods:  Four hundred and sixty-one patients with naïve HCC, including 107 elderly (aged ≥75 years) patients, who were treated with RFA between 2000 and 2007, were enrolled. Baseline characteristics, survival/recurrence rates and complications after RFA were compared between elderly and non-elderly patients. Results:  In the elderly group, the proportion of men, alcohol consumption, serum alanine aminotransferase and γ-glutamyl transpeptidase levels were significantly lower compared with those in the non-elderly group. There were no differences in Child–Pugh grade and tumor characteristics between the two groups.

6/13 (46%) in the placebo group (p<0.0001). Overall and transplant-free survival was similar between study groups; CHRSR was associated with significantly improved survival at Day 90 (p=0.0002). Adverse event (AE) incidence was similar for the 2 groups; serious AEs were reported in 59/97 (63.4%) subjects in the terlipressin group vs. 53/99 (55.8%) subjects in the placebo group. No new or unexpected AEs were reported. Summary: Terlipressin plus

albumin treatment is associated with improved renal function compared to albumin alone in patients with HRS-1; the improvement in renal function correlates with survival. Patients achieving CHRSR with terlipressin had a better outcome compared to those who responded to albumin alone. Conclusion: Terlipressin is effective in improving renal function in HRS-1. Disclosures: Thomas D. Boyer – Consulting: Ikaria; Grant/Research click here Support: Abbvie, Gilead, Merck Arun J. Sanyal – Advisory Committees or Review Panels: Bristol Myers, Gilead, Abbott, Ikaria; Consulting: Salix, Immuron, Exhalenz, Nimbus, Genentech, Echo-sens, Takeda; Grant/Research Support: Salix, Genentech, Genfit, Intercept, Ikaria, Takeda, GalMed, Novartis, Gilead; Independent Contractor: UpToDate, Elsevier Florence Wong – Consulting:

Gore Inc; Grant/Research Support: Grifols R Todd Frederick – Advisory Committees or Review Panels: Vital Therapies; Consulting: Salix, Gilead, PI3K activation Ocera, Hyperion John R. Lake – Advisory Committees or Review Panels: BMS; Consulting: Vital Therapies, Novartis, HepaHope; Grant/Research Support: Gilead, Salix, Ocera, Essai Jacqueline G. O’Leary – Consulting: Gilead, Jansen Daniel Ganger – Grant/Research Support: merck, gilead, Ocera Terry D. Box – Advisory Committees or Review Panels: Gilead, Genentech, Abb-Vie, Salix, Janssen; MCE Grant/Research Support: Gilead, Merck, BMS, AbbVie, Idenix, Salix, Conatus, Cumberland, Boehringer Ingelheim, Genfit, Vital Therapeutics, Sundise, ikaria; Speaking and Teaching: Gilead, Merck, Genentech, Salix Khurram Jamil – Employment: IKARIA; Stock Shareholder: IKARIA Stephen Chris Pappas – Consulting: Orphan Therapeutics, Abbvie “
“Aim:  This study was conducted

to evaluate the efficacy and safety of radiofrequency ablation (RFA) therapy in elderly patients with hepatocellular carcinoma (HCC). Methods:  Four hundred and sixty-one patients with naïve HCC, including 107 elderly (aged ≥75 years) patients, who were treated with RFA between 2000 and 2007, were enrolled. Baseline characteristics, survival/recurrence rates and complications after RFA were compared between elderly and non-elderly patients. Results:  In the elderly group, the proportion of men, alcohol consumption, serum alanine aminotransferase and γ-glutamyl transpeptidase levels were significantly lower compared with those in the non-elderly group. There were no differences in Child–Pugh grade and tumor characteristics between the two groups.

Traditionally, many modes of β-catenin activation have been reported in HCC. 14 It is unclear, however, whether various mechanisms of β-catenin activation in HCC will have similar and robust growth-promoting effects on tumor cells. Contrary to expectations, a study found that β-catenin/TCF activation was not equivalent when β-catenin stabilization was a consequence of CTNNB1

versus AXIN1 mutations. 15 It would have been useful to determine the cause of β-catenin activation in patients examined in the current Selleck Vemurafenib study. Would β-catenin activation due to the AR/CCRK axis be even more pronounced regardless of preexisting mutations in CTNNB1? Similar studies in vitro examining the effect of AR/CCRK on tumor cells expressing β-catenin with point mutations affecting key serine and threonine residues in exon-3 would be relevant in the future, because such mutations may be predicted to be autonomous of any upstream feed-forward regulation. In other words, mutations in CTNNB1 that are observed in 20%-40% of all HCC patients may

be free of GSK3β-dependent β-catenin phosphorylation and degradation click here and may in fact introduce a break in the proposed positive regulatory circuit. The authors elegantly unveil one of the mechanisms of sex-related disparity of HCC and extend the existing findings that AR and testosterone contribute to HCC predominance in males. The major conclusion drawn from the study is that the presence of androgens in males engages the AR to stimulate 上海皓元医药股份有限公司 the CCRK expression, which activates β-catenin signaling, which in turn would enhance expression of EGFR and cyclin-D1 (thus promoting cell proliferation) and at the same time would up-regulate AR expression and activity and thus establish a positive regulatory cycle (Fig. 1). CCRK belongs to the mammalian cyclin-dependent kinase (CDK) family and although it has been shown to be up-regulated in several cancers, its role and regulation are not fully understood. In fact, it has been reported elsewhere that CCRK does not have an

intrinsic CDK-activating kinase (CAK) activity, but that it does enhance cell proliferation. 16 It is likely that through additional, as yet uncharacterized interactions, CCRK may be influencing Thr390 phosphorylation of GSK3β. Significant studies will be necessary to extrapolate these interactions, especially because p38 mitogen-activated protein kinase (MAPK) is known to induce GSK3β inactivation through this specific event. 17 AR signaling has been attributed to induction of cellular oxidative stress both in vivo and in vitro. Intriguingly, β-catenin has been shown to also regulate the redox state of the cell. In fact, recent studies have shown that β-catenin can switch from binding to TCF4 to other transcription factors like hypoxia-inducible factor 1α (HIF1α) or FOXO and can mount an antioxidant response.

Traditionally, many modes of β-catenin activation have been reported in HCC. 14 It is unclear, however, whether various mechanisms of β-catenin activation in HCC will have similar and robust growth-promoting effects on tumor cells. Contrary to expectations, a study found that β-catenin/TCF activation was not equivalent when β-catenin stabilization was a consequence of CTNNB1

versus AXIN1 mutations. 15 It would have been useful to determine the cause of β-catenin activation in patients examined in the current LBH589 cost study. Would β-catenin activation due to the AR/CCRK axis be even more pronounced regardless of preexisting mutations in CTNNB1? Similar studies in vitro examining the effect of AR/CCRK on tumor cells expressing β-catenin with point mutations affecting key serine and threonine residues in exon-3 would be relevant in the future, because such mutations may be predicted to be autonomous of any upstream feed-forward regulation. In other words, mutations in CTNNB1 that are observed in 20%-40% of all HCC patients may

be free of GSK3β-dependent β-catenin phosphorylation and degradation Gamma-secretase inhibitor and may in fact introduce a break in the proposed positive regulatory circuit. The authors elegantly unveil one of the mechanisms of sex-related disparity of HCC and extend the existing findings that AR and testosterone contribute to HCC predominance in males. The major conclusion drawn from the study is that the presence of androgens in males engages the AR to stimulate MCE the CCRK expression, which activates β-catenin signaling, which in turn would enhance expression of EGFR and cyclin-D1 (thus promoting cell proliferation) and at the same time would up-regulate AR expression and activity and thus establish a positive regulatory cycle (Fig. 1). CCRK belongs to the mammalian cyclin-dependent kinase (CDK) family and although it has been shown to be up-regulated in several cancers, its role and regulation are not fully understood. In fact, it has been reported elsewhere that CCRK does not have an

intrinsic CDK-activating kinase (CAK) activity, but that it does enhance cell proliferation. 16 It is likely that through additional, as yet uncharacterized interactions, CCRK may be influencing Thr390 phosphorylation of GSK3β. Significant studies will be necessary to extrapolate these interactions, especially because p38 mitogen-activated protein kinase (MAPK) is known to induce GSK3β inactivation through this specific event. 17 AR signaling has been attributed to induction of cellular oxidative stress both in vivo and in vitro. Intriguingly, β-catenin has been shown to also regulate the redox state of the cell. In fact, recent studies have shown that β-catenin can switch from binding to TCF4 to other transcription factors like hypoxia-inducible factor 1α (HIF1α) or FOXO and can mount an antioxidant response.

Electron microscopy demonstrated that GLP-2 treatment increased number and length of Microvillus of the epithelial cells. The

expression of PCNA in GLP-2 treatment group is obviously higher than transplantation group in intestinal villous and crypt. What’s more, the expression of PCNA in crypts is more apparent. Conclusion: GLP-2 supplementation can stimulate the proliferation and promote ultrastructure recovery of Intestine mucosal cell following congestion–reperfusion injury. Our studies promote the current level of understanding of the molecular determinants of GLP-2 and the patients of LT can get benefits from this research results. Supported by the National Nature Science Foundation of China Decitabine ic50 No. 81370583, No. 30801127; Liaoning BaiQianWan Talents Program No. 2013921053; Liaoning Provincial Natural Science Foundation of China INK128 NO.2014. Key Word(s): 1. liver transplantation; 2. glucagon-like peptide-2; 3. congestion-reperfusion injury; 4. electron microscopy; 5. PCNA Presenting Author: ZULKHAIRI

ZULKHAIRI Additional Authors: HERRY ADLIN, TARIGAN ELIAS, HAKIM ZAIN LUKMAN Corresponding Author: ZULKHAIRI ZULKHAIRI Affiliations: Adam Malik General Hospital Medan, Adam Malik General Hospital Medan, Adam Malik General Hospital Medan Objective: Liver biopsy is the recognized gold standard for liver fibrosis staging but t his procedure is invasive, and has known adverse events and limitations. A great interest has been dedicated to the development

of noninvasive predictive models in recent years to liver biopsy. The aspartate aminotransferase to platelet ratio index (APRI) has been proposed as a noninvasive and readily available tool for the assessment of liver fibrosis in chronic hepatitis C and medchemexpress B (CHC & B). This study aimed to evaluate the diagnostic usefulness of APRI in CHC & B, in a North Sumatera provinsional general hospital setting. Methods: Cross sectional study in 71 patients confirmed with Hepatitis B and C in Adam Malik General Hospital Medan Indonesia had liver biopsy from January 2011 to September 2013. Fibrosis was staged according to the METAVIR scale. Examination of AST and Platelet was done to fulfill the APRI score. Predictive value and AUROC were constructed to assess the accuracy of APRI compared with METAVIR scale. Results: Predictive value for APRI index (cut off > 1,5) to METAVIR scale in diagnose severe fibrosis is: sensitivity 42,4%, Specifity 73,7%, positive predictive value (PPV) 58,3%, negative predictive value (NPP) 59,6%, LR (+) 1,61 and LR (-) 0,78. Accuracy diagnostic is 59,1%, AUROC 0,581 (95% CI:0,446-0,715) with p < 0,005. Conclusion: APRI can be used to assess the degree of fibrosis in chronic hepatitis C and B patients. Key Word(s): 1. APRI; 2.