Limited literature surrounds the use of high dose, rapid vaccination regimens in cirrhotic patients. The aims of this study were therefore Trichostatin A mw to 1) assess the effectiveness of high dose, rapid vs. standard dose HAV and HBV regimens in a mixed aetiology and disease severity cirrhotic population and 2) determine clinical associations with response to vaccination. Methods: Prospective, non-randomized controlled trial. Standard HAV schedule was; intramuscular Havrix® 720 μg at 0, 1 and 6 months with a 1440 μg booster if non-immune after 3 doses. High dose HAV schedule was; 1440 μg at 0, 1 and 2 months with the schedule repeated as a booster if non-immune after 3 doses. Standard HBV schedule

was; intramuscular Engerix®-B 20 μg at 0, 1 and 6 months with a 40 μg booster if non-immune after 3 doses. High dose HBV schedule was; 40 μg at 0, 1 and 2 months (120 mcg) with the schedule repeated as a booster

(120 mcg) if non-immune after 3 doses. Differences Metformin manufacturer in response rates between standard and high dose regimens were compared using Fishers exact or chi-square test. The following variables (age, gender, aetiology, MELD score, Child Pugh score, INR, albumin, creatinine, bilirubin, smoking status, drinking status, presence of renal dysfunction) were tested for association with response using stepwise logistic regression. Results: For HAV schedules 62 and 37 patients

received standard and high dose regimens, respectively. The overall clinical characteristics selleckchem of this population were; mean age 56 years, male 63%, alcohol liver disease 46%, mean MELD score 10.2, with similar clinical characteristics for standard and high dose groups. The response rates were 87.1% and 97.3% for standard and high dose regimens, respectively (p = 0.15). The only factor that was independently associated with response was age (OR 0.94, 95%C1 0.88–1.0, p = 0.005). For HBV schedules 81 and 48 patients received standard and high dose regimens, respectively. The overall clinical characteristics of this population were; mean age 58 years, 65% male, 56% hepatitis C, mean MELD score 11.1 with similar clinical characteristics for standard and high dose groups. The response rates were 60.5% and 70.8% for standard and high dose regimens, respectively (p = 0.24). Factors independently associated with response included; female gender (OR 3.1, 95%C1 1.04–9.15, p = 0.042) and non-alcoholic fatty liver disease vs. hepatitis C as aetiology (OR 0.13, 95%C1 0.03–0.56, p = 0.006). The mean increase in per patient cost was $50 and $44 for high dose hepatitis A and B vaccination, respectively. Conclusions: In cirrhotic patients an approximately 10% improvement in HAV and HBV responses can be obtained using high dose, rapid vaccination regimens, relative to standard regimens.

11 Interestingly, a connection between PPARα and APAP toxicity was established when it was discovered that pretreatment

with clofibrate, a PPARα activator, learn more protected mice against APAP-induced hepatotoxicity12, 13 and that this protection was PPARα-dependent.14 Furthermore, it was recently reported that toxic doses of APAP inhibit fatty acid β-oxidation and that these effects were significantly reduced in mice lacking the major enzyme responsible for the bioactivation of APAP, CYP2E1, due, in part, to enhanced and persistent activation of PPARα and its target genes.15 Wildtype mice treated with APAP, however, showed suppressed PPARα activity. Thus, PPARα may function to protect mitochondria from ROS that occurs during APAP metabolism and as a natural consequence during fatty acid catabolism. In the present study the protective effects of PPARα activation during APAP-induced hepatotoxicity were further investigated and a role for the PPARα target gene UCP2 in mediating these protective effects explored. ALT, alanine aminotransferase;

APAP, acetaminophen; PLX-4720 in vivo AST aspartate aminotransferase; GSH, glutathione; NAPQI, N-acetyl-p-benzoquinone imine; PPARα, peroxisome proliferator-activated receptor alpha; ROS, reactive oxygen species; UCP2, uncoupling protein 2. Wildtype (C57Bl/6J) and ucp2-null (B6.129-Ucp2tm1Low1/J) mice were obtained from the Jackson Laboratories (Bar Harbor, ME). Ppara-null mice and wildtype counterparts on the 129/Sv background were described previously.16 The PPARα-humanized mouse was described previously.17 All animal experiments were carried out in accordance with the Institute of Laboratory Animal Resources guidelines and approved by the National Cancer Institute Animal Care and Use

Committee. Groups of 6 to 8-week-old male mice were fed Wy-14,643 (0.1%) diet for 24 hours before an intraperitoneal injection of APAP (400 mg/kg) dissolved in saline. All mice were euthanized by CO2 asphyxiation 2 hours, 6 hours, or 24 hours after the APAP dose. Livers were harvested and stored at −80°C before analysis. To MYO10 assess liver damage, tissue was briefly washed with phosphate-buffered saline (PBS) and fixed in 10% neutral buffered formalin. Necrosis was scored by hematoxylin and eosin (H&E) staining. APAP-induced liver injury was determined by measuring aspartate aminotransferase (AST) and alanine aminotransferase (ALT) catalytic activities in serum using a commercial AST or ALT assay kit (Catachem, Bridgeport, CT). Reduced glutathione (GSH) levels in liver were measured by a glutathione assay kit (Sigma-Aldrich, St. Louis, MO) and liver hydrogen peroxide (H2O2) levels were determined by use of the Peroxidetect kit (Sigma-Aldrich).

Two-tailed Student’s t test was used to determine significant differences between data

groups. All analyses were performed using one-way analysis of variance (ANOVA). P < 0.05 (*) was considered statistically significant. Two loxP sequences flank exons 4, 5, and 6 of the murine FXR allele (FXR Fl/Fl). FXR Fl/Fl mice were crossed with the albumin-cre or villin-cre mice to delete FXR gene specifically in liver or intestine, respectively. After correct genotyping, western blotting to measure FXR protein was performed using total protein extracted from liver and ileum. The results indicated no FXR expression in the liver of ΔL-FXR mice. However, liver FXR protein levels were comparable between the FXR Fl/Fl and ΔIN-FXR mice (Fig. 1A). Similarly, no ileum FXR expression was detected in the ΔIN-FXR mice (Fig. 1B). We previously showed that FXR in liver was Adriamycin manufacturer required for promoting liver regeneration.

To confirm the previous observation that hepatic FXR is required to promote liver regeneration, we compared the liver regeneration after 70% PH in FXR Fl/Fl, ΔL-FXR, and FXR KO mice. As expected, a significant delay in hepatocyte proliferation was observed in ΔL-FXR animals compared Lenvatinib supplier to FXR Fl/Fl mice at 24 hours, 36 hours, and 72 hours after surgery. Fewer BrdU-positive hepatocytes were present in ΔL-FXR mice than in FXR Fl/Fl mice (Fig. 2A). In FXR Fl/Fl mice, the hepatocyte Fossariinae proliferation peaked at 36 hours after 70% PH, but this peak was strongly reduced in ΔL-FXR mice compared to the FXR Fl/Fl mice (Fig. 2A). These results suggest that hepatic FXR is required to promote liver regeneration. However, to our surprise, compared to ΔL-FXR mice, FXR KO mice showed significantly decreased BrdU incorporation in the liver at 36 hours and 72 hours (Fig. 2A), suggesting that FXR in other tissues may also contribute to a maximum effect on promoting liver regeneration. We also compared the serum bile acid levels in FXR Fl/Fl, ΔL-FXR,

and FXR KO mice. As expected, serum bile acid levels were significantly higher in the FXR KO and ΔL-FXR mice compared to the FXR Fl/Fl mice at 24 hours and 36 hours after 70% PH. On day 3, serum bile acid levels in ΔL-FXR mice returned to a comparable level compared to the control mice. However, bile acid levels were still significantly higher in FXR KO mice at day 3 (Fig. 2B). This suggests that, although hepatic FXR plays a role in suppressing bile acid levels after 70% PH, FXR in other tissues such as intestine may be required to suppress bile acid levels at later stages after 70% PH. Consistently, the gene encoding the rate-limiting enzyme of bile acids synthesis, CYP7a1, was suppressed in all three groups of mice after 70% PH, but CYP7a1 messenger RNA (mRNA) levels were much higher in ΔL-FXR and FXR KO mice compared to the FXR Fl/Fl mice (Fig. 2C). FXR was shown previously to directly activate the Foxm1b gene after 70% PH.

Hiki et al.18 reported on 305 patients who underwent pylorus preserving gastrectomy and none of them had tumor recurrence. Kinami et al.19 reported the relationship between the frequency of the lymphatic basin within the right gastric artery and the distance from the pylorus to the distal margin of the tumor. Some patients with the distance less than 8 cm had lymphatic basin within the lymphatic compartment of the right gastric artery area. Thus, the pylorus preserving gastrectomy is the good operation for enrolling to the study of sentinel nodes. In conclusion, the present study shows that HEMS-guided abdominal surgery is feasible under room light. Submucosal injection of 0.5 mL × 4

of 50 µg/mL ICG on the day before operation is the adequate administration for detecting sentinel nodes using HEMS in the gastric cancer surgery. No potential Doxorubicin chemical structure conflict of interest has been declared by the authors. “
“Approximately 75% to 80% of hepatocellular carcinomas (HCC) worldwide are attributed to chronic hepatitis B virus (HBV) and chronic hepatitis C virus (HCV) infection. Thus, effective prevention of HBV and HCV infection selleck inhibitor and progression from acute HBV and HCV infection to chronic hepatitis, cirrhosis and HCC might prevent as many as 450 000 deaths from HCC each year. The most effective approach to preventing HCC is to prevent HBV and HCV infection through

vaccination. Indeed HBV vaccine is the first vaccine demonstrated to prevent cancers. However, a vaccine for HCV is not available and for persons who are chronically infected with HBV or HCV, antiviral therapy is the only option for preventing HCC.

Direct evidence supporting a benefit of antiviral therapy on the prevention of HCC has been shown in a few randomized controlled trials. There is abundant evidence that antiviral therapy, in patients with long-term virological response, can improve liver histology, providing indirect support that antiviral therapy may prevent HCC by slowing progression N-acetylglucosamine-1-phosphate transferase of liver disease and possibly even reversing liver damage. Nevertheless, the risk of HCC remains in patients with chronic HBV or chronic HCV infection if treatment is initiated after cirrhosis is established. These data indicate that treatment might be of greater benefit if instituted earlier in the course of chronic hepatitis B or C. Safer, more effective, and more affordable antiviral therapies are needed for both hepatitis B and hepatitis C so more patients can benefit from treatment and more HCCs can be prevented. “
“Resistance rates of H. pylori to clarithromycin, metronidazole and quinolone are over 30% in S. Korea. Aim of this prospective study was to evaluate the ultimate eradication rate of H. pylori after 1st, 2nd or 3rd line therapy in Korea. A cohort of 2,202 patients with H. pylori was treated with proton pump inhibitor (PPI)-based triple therapy for 7 days.

An impression was taken with a metal strip and silicone-based materials. In the laboratory, a stone die was generated from the impression, and a custom-made cast dowel with ball attachment was constructed. It was then cemented with glass ionomer cement and connected to the denture with the direct method. The alternative procedure described in this clinical report was successful for the removal of the fractured abutment screw and use of the existing denture. “
“Purpose: To evaluate the effect of airborne-particle abrasion and mechanico-thermal cycling on the flexural strength Sirolimus clinical trial of a ceramic fused to cobalt–chromium

alloy or gold alloy. Materials and Methods: Metallic bars (n = 120) were made (25 small molecule library screening mm × 3 mm × 0.5 mm): 60 with gold alloy and 60 with Co–Cr. At the central area of the bars (8 mm × 3 mm), a layer of opaque ceramic and then two layers of glass ceramic (Vita VM13, Vita Zahnfabrick) were fired onto it (thickness: 1 mm). Ten specimens from each alloy group were randomly allocated to a surface treatment [(tungsten bur or air-particle abrasion (APA) with Al2O3 at 10 mm or 20 mm

away)] and mechanico-thermal cycling (no cycling or mechanically loaded 20,000 cycles; 10 N distilled water at 37°C and then thermocycled 3000 cycles; 5°C to 55°C, dwell time 30 seconds) combination. Those specimens that did not undergo mechanico-thermal cycling were stored in water (37°C) for 24 hours. Bond strength was measured using a unless three-point bend test, according to ISO 9693. After the flexural strength test, failure types were noted. The data were analyzed using three factor-ANOVA and Tukey’s test (α= 0.05). Results: There were no significant differences between the flexural bond strength of gold and Co–Cr groups (42.64 ± 8.25 and 43.39 ± 10.89 MPa, respectively). APA 10 and 20 mm away surface treatment (45.86 ± 9.31 and 46.38 ± 8.89 MPa, respectively) had similar mean flexural strength values, and both had significantly higher bond strength than tungsten bur treatment (36.81 ± 7.60 MPa). Mechanico-thermal cycling decreased the mean flexural strength values significantly for all six alloy-surface treatment

combinations tested when compared to the control groups. The failure type was adhesive in the metal/ceramic interface for specimens surface treated only with the tungsten bur, and mixed for specimens surface treated with APA 10 and 20 mm. Conclusions: Considering the levels adopted in this study, the alloy did not affect the bond strength; APA with Al2O3 at 10 and 20 mm improved the flexural bond strength between ceramics and alloys used, and the mechanico-thermal cycling of metal-ceramic specimens resulted in a decrease of bond strength. “
“The purpose of this study was to evaluate the impact of occlusal relief of dies on internal adaptation of metal-ceramic casting copings. Standardized preparations were made on 80 extracted third molar teeth.

HSCs are liver pericytes that reside in the space between parenchymal cells and sinusoidal endothelial cells of the liver.[2] HSCs are rich in vitamin A and store nearly 80% of retinoids of the whole body in its lipid droplets in the cytoplasm.[3, 4] Interestingly, recent studies[5-15] suggest that HSCs participate in the liver immunity. In this paper, we review the recent development in HSC-mediated

immunity and the significance of these new observations. HCV represents one of the major causes of liver fibrosis. The rate of progression of liver fibrosis varies widely in the chronic HCV infection, and progresses to cirrhosis within 20 years in an estimated 20–30% of individuals with chronic HCV infection.[16] The role of HSCs in this website HCV-mediated liver fibrosis has been well documented. HCV-infected hepatocytes release transforming growth factor-β1 (TGF-β1) and other profibrogenic factors that differentially modulate HSC expression of Atezolizumab in vitro several key genes involved in liver fibrosis.[17] HCV infection-induced hepatocyte

apoptosis is a common feature in chronic HCV infection.[18, 19] Apoptosis results in the generation of apoptotic bodies (ABs), which are subsequently cleared by phagocytosis. Several studies showed that HSCs have the ability to engulf ABs through phagocytosis, which can trigger a profibrogenic response.[20, 21] It was reported that ABs derived from HCV-infected Huh7 cells exhibited a more pronounced effect on profibrotic genes expression in HSCs than HCV-negative ABs.[22] Besides the indirect effects of HCV on HSCs function through infected

hepatocytes, several studies[23-26] Selleckchem Etoposide indicated that there is also a direct contact between HCV and HSCs. The potential interaction between HSCs and HCV is suggested by the observation that HSCs express high levels of CD81 protein,[23] a key entry coreceptor for HCV.[24] It has been demonstrated that the HCV E2 protein can directly bind to CD81 on HSC surface, inducing fibrogenic effects on HSCs.[25] In addition to HCV envelope protein, HCV core and nonstructural proteins have also been shown to affect HSC functions.[26] Recombinant HCV core and NS3 proteins could increase intracellular calcium concentration and reactive oxygen species production in activated HSCs.[26] HCV core protein could increase HSC proliferation, and NS3-NS5 protein preferentially induced pro-inflammatory cytokines in HSCs. The roles of HSCs in HCV infection-mediated liver fibrosis are summarized in Table 1. HSCs have recently been implicated to play a novel role in the liver immunity. It was reported that HSCs could induce vigorous natural killer T (NKT) cell responses in vitro and in vivo, and promote homeostatic proliferation of NKT cells.[13] In addition, HSCs could elicit antigen-specific T cells and inhibit bacterial infection in a Listeria monocytogenes infection model.

(HEPATOLOGY 2013) Hepatitis C virus (HCV) infection is a

major global health issue. Nutlin-3a purchase Previous global burden of disease estimates published by the World Health Organization (WHO) include only burden from acute HCV infection.1 Available estimates indicate that worldwide there were 54,000 deaths and 955,000 disability adjusted life-years associated with acute HCV infection. The major burden from HCV infection comes from sequelae from chronic infection.2 Estimates indicate that three to four million persons are newly infected each year, 170 million people are chronically infected and at risk of developing liver disease including cirrhosis and liver cancer, and 350,000 deaths occur each year due to all HCV-related causes.2 Antibodies to HCV check details (anti-HCV) are a commonly available marker of HCV infection. The prevalence of anti-HCV from population-based studies is used to compare HCV infection levels globally. Historically, countries in Africa and Asia have the highest reported anti-HCV prevalence, whereas industrialized countries in North America, Western Europe, and Australia are known to have lower prevalence.3-6 Without an effective vaccine, primary prevention against hepatitis C focuses on reducing risks of infection through safe injections and blood safety. With new and promising drugs

recently available and more in the pipeline, hepatitis C is now considered curable in up to 70% of treated patients. Although therapy for hepatitis C can be instrumental in the prevention of advanced liver disease, lack of knowledge and of skill to deliver treatment among providers, and the high costs of HCV genotyping and drugs, make access to treatment a major global problem.7 Secondary prevention of advanced liver disease from chronic HCV infection through screening for early Bupivacaine detection and promoting and aiding cessation of alcohol intake remain key public health strategies.7-9 Proper planning and public health investments are necessary to ensure that preventive measures can be implemented. To facilitate

evidence-based policymaking and prudent resource allocation, it is essential to estimate the burden of HCV infection globally, regionally, and nationally. Additional epidemiological measures typically included in a generic disease model, such as incidence and excess mortality, are difficult to obtain because HCV infections are rarely clinically apparent. Limitations of available assays to distinguish acute and chronic infections6 and poor surveillance systems worldwide for HCV infection further impede efforts to usefully quantify HCV burden. However, recent developments in modeling allow the seroprevalence of anti-HCV to be used to estimate the burden of disease for HCV infections.

The role of PKC-delta was evaluated using a PKC activator (PMA, 100 nM), PKC inhibitors KU 57788 (5 uM chelethryine, 100 uM H-7 or 0.5 uM calphostin), siRNA to PKC delta, and wild type (WT) or constitutively active (CA) PKC delta plasmid constructs. Activation of PKC

delta was monitored by immunoblotting for Thr 505 phosphorylation (HUH7Ntcp) or for total PKC delta in the mitochondria (rat hepatocytes). Phosphorylation of JNK and Akt and the amount of total BIM were determined by immunoblotting. RESULTS: GCDC treatment increased total PKC delta expression in rat hepatocyte mitochondria by 1.70 +/- 0.22 fold and induced a 5.71 +/-1.2 fold increase in the phosphorylation of PKC delta in HUH7-Ntcp cells. Within 2 hrs GCDC induced apoptosis in 16% +/- 4.5 % of rat hepatocytes and 10.5% +/- 2.3% of HUH7-Ntcp cells and resulted XL184 price in cleavage of caspase 3.Treatment of hepatocytes or HUH7-Ntcp cells with PMA decreased GCDC apoptosis by 71% +/-3.4% and 92% +/1 6.7%, respectively. In rat hepatocytes, PKC inhibitors increased GCDC induced apoptosis from 24% to 92%. Knock down of PKC delta increased GCDC apoptosis by 2.7 +/-0.98

fold, while WT- and CA-PKC-delta decreased apoptosis by 35% +/2.5% and 54% +/- 5.6%, respectively. Knock down of PKC delta increased pro-apoptotic JNK phosphorylation and total BIM levels by 2.4 and 2.3 times, respectively and decreased anti-apoptotic Akt phosphorylation by 52% +/-6.7%. GCDC apoptosis was accompanied by mitochondrial translocation of BIM and knock down

of BIM decreased GCDC induced apoptosis in HUH7-Ntcp cells by 51% +/- Exoribonuclease 3.6%. CONCLUSION: Taken together, these results suggest that activation of PKC-delta by GCDC induces a cytoprotective pathway that results in inhibition of JNK activation, activation of Akt and down-regulation of BIM. Disclosures: The following people have nothing to disclose: Cynthia R. Webster, Mohammed S. Anwer “
“Background and Aim:  Gallstone formation is characterized by the abnormal regulation of cholesterol trafficking and solubilization. The prevalence of gallstone disease (GSD) differs between ethnic groups sharing the common environment. These differences can be explained by a genetic predisposition to gallstone formation. Studies have identified single nucleotide polymorphisms (SNP) D19H and T400K in the cholesterol transporter gene ATP-binding cassette, subfamily G, member 8 (ABCG8) in patients with cholesterol gallstones. The aim of this study was to analyze the relationship between D19H and T400K polymorphisms in the ABCG8 gene and GSD in an Indian population, and the effects of these polymorphisms on cholesterol levels in sera and bile. Methods:  A total of 226 patients with GSD were analyzed for their lipid profile in plasma and bile.

For this reason, it should be recommended to perform endoscopic resection for high-grade dysplasia (early mucosal gastric cancer according to the Japanese criteria). To reconcile these discrepant diagnostic criteria between Japan and the West, the term “noninvasive high-grade neoplasia” was adopted in the Vienna classification. Unfortunately, however, this term has not been widely used in either side. Moreover, the term, “intraepithelial neoplasia”

was introduced in the recent World Health Organization classification. In the future, we definitely need a global consensus how to deal with such “neoplastic” lesions, for which recent BMS-354825 nmr technological advancement would be instrumental in promoting mutual understanding. This review article is the results of intensive clinical and research efforts of colleagues in Jichi Medical University. Special thanks to Dr Hiroyuki

Mutoh who contributed to the molecular mechanisms of IM and to Dr Kiichi Satoh for the histological analysis. I also thank Dr Yoshikazu Hayashi in our department and Dr Shunji Hayashi in the department of microbiology, Jichi Medical University who contributed to gastric microbiology. Endoscopic images were kindly provided by Dr Hiroyuki Osawa Carfilzomib cell line in our department. “
“We read with interest the article by Ghouri et al.,1 who reviewed the evidence regarding the link between nonalcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). The authors concluded that the connection between NAFLD and CVD is not well supported by existing data because of the presence of confounders such as age and established cardiovascular risk factors. We agree that the main limitation of these studies is that their results make it difficult to distinguish the contribution of liver fat per se to the risk of CVD. However, we should consider that the liver is the main regulator of insulin sensitivity

and finely tunes insulin-regulated metabolic Ibrutinib pathways such as glucose and lipid homeostasis that are involved in endothelial dysfunction and atherogenesis. Studies in null mice have clearly substantiated this issue. In particular, the disruption of insulin signaling in the liver is more relevant to whole body glucose homeostasis than its disruption in adipose tissue and muscle.2 In addition, hepatic insulin signaling regulates the secretion of very low density lipoprotein and thus lipotoxicity and atherogenesis.3 Therefore, it is impossible to identify the intrahepatic triglyceride level, which precisely reflects liver insulin resistance, as an isolated variable in the generation of CVD risk.

5 ug/kg/week for 24 weeks along with continuation of nucleoside till end of therapy) for 52 weeks. Monitoring included Hepatitis B profile (HbsAg, HbeAg, Anti-Hbe, HBV DNA levels) and safety assessment (hematology, thyroid profile and growth assessment). Results: A total of 33 chronic hepatitis b patients (20 in immunotolerant and 13 in immunoclearance phase) were enrolled in the study. 10 immunotolerant and 5 immunoclearance children agreed to participate in the study

and were given the sequential therapy. Mean age of the children was 10.16 + 4.58 years. Of 11 patients with available genotype data, 8 belonged to genotype D with 2 patients of genotype A and 1 Dabrafenib mouse of genotype B. In Immunoclearance group (3 in lamivudine and 2 in tenofovir RO4929097 purchase group), all 5 patients (100 %) cleared HbeAg after completion of therapy

and 2 out of 5 (in lamivudine group) cleared HbsAg with appearance of anti-Hbs suggestive of cure. In the immunotolerant phase, none out of the 10 patients had HbeAg clearance after 52 weeks of therapy. Side effects included mild cytopenias (4 patients), transient flu-like illness (all patients) and interferon dose reduction in 2 patients. Conclusion: In immunoclearance phase, sequential therapy allows HbeAg seroconversion in all cases and around half of the cases may be amenable

to apparent cure with HbsAg loss. Six months of Pegylated Interferon therapy preceded by nucleoside therapy is not sufficient enough to allow response in immunotolerant phase which may be due to predominance of Genotype D in our population. Overall, therapy was well tolerated by all children Disclosures: The following people have nothing to disclose: Vikrant Sood, Sanjeev K. Verma, Seema Alam, Rajeev Khanna, Dinesh Rawat Data on long-term outcomes after interferon (IFN) based therapy in chronic hepatitis B (CHB) are limited. mRNA expression of PRKD3 interferon-stimulated genes (ISG) in pre-treatment liver biopsy in immunotolerant CHB patients prior to IFN therapy showed that lower mRNA CXCL10 expression in the liver was associated with therapy response, but there was wide variability in mRNA ISG expression results in therapy non-responders. We aimed to assess whether different viral (genotype, precore) factors at baseline and long-term post-therapy responses might contribute to variability in ISG expression and can predict long- term CHB outcome. Patients: 23 patients (8 males, median age 10.2 years) with infancy-acquired CHB, treated for 52 weeks [lead-in LAM (3mg/kg/d) for 9 weeks; add-on IFN-α (5MU/ m2TIW) from week 9] were followed-up 13 years post-stopping therapy.