We investigated the change in HBsAg level and MELD score for predicting prognosis during lamivudine treatment for patients with hepatitis B

e antigen (HBeAg) negative ACLF. Methods: Fifty-seven patients with HBeAg-negative ACLF were treated with 100 mg of lamivudine daily. Serum levels of HBsAg, PLX3397 in vitro HBV DNA and biochemical items were detected at baseline, before death (patients died within 12 weeks), week 12 (patients survived) meanwhile MELD score was calculated. Dynamic of these items and 12-week mortality were analyzed. Results: Thirty-two patients were pretreatment HBsAg levels above 4000 COI, whose HBsAg, HBV DNA and MELD scores were 8096 ± 2535 COI, 5.02 ± 1.38 lg copies/mL and 26.03 ± 5.61 respectively at baseline but were 7509 ± 378 COI, 2.84 ± 1.15 lg copies/mL and 19.85 ± 7.54 in sequence after treatment. Twenty-five patients were pretreatment HBsAg levels below 4000 COI, whose HBsAg, HBV DNA and MELD scores were 3173 ± 2026 COI, 5.17 ± 2.20 lg copies/mL and 24.56 ± 4.58 respectively at baseline but were 2015 ± 1069 COI, 3.13 ± 1.17 lg copies/mL and 26.93 ± 10.13 in CT99021 sequence after treatment. There weren’t significant differences in HBV DNA levels and pretreatment

MELD scores between two groups (all P > 0.05). Significant differences were found in HBsAg levels and post-treatment MELD scores (all P < 0.05). The 12-week mortality of patients with pretreatment HBsAg levels above 4000 COI was significantly lower than that of below 4000 COI (34.3% (11/32) vs 64.0% (16/25), χ2 = 4.941, P = 0.026). Conclusion: In HBeAg-negative ACLF, the patient with higher pretreatment HBsAg levels and early decrease in MELD score has lower 12-week mortality than the one without it. Key Word(s): 1. ACLF; 2. HBsAg level; 3. MELD score; 4. lamivudine; Presenting Author: PRABODH RISAL Additional Authors: YEONJUN

JEONG Corresponding Author: PRABODH RISAL Objective: Peptidyl-prolyl isomerase, Pin1, a member of parvulin family of PPIase enzyme plays a crucial role in the regulation of post phosphorylation reaction, which governs important role in the cell signalling mechanism. Studies have shown the role of Pin1 in normal as well as in pathological conditions. Here we examined the role of Pin1 in acute and chronic liver injuries. Methods: A single dose of carbon tetrachloride (CCl4) was injected FER to induce acute liver injury and apoptosis of hepatocytes in mice. Similarly, 0.1%DDC diet was fed for three weeks to induce chronic liver injury and induction of hepatic progenitor cell in mice. Results: Hepaotycte apoptosis was increased when Pin1 was inhibited by Juglone. Further, over-expression of Pin1 reduced hepatocyte apoptosis both invitro and invivo. Pin1 increased in the liver after three weeks of DDC diet along with the expansion of hepatic progenitor cell, which was confirmed by the expression of CD44 and A6. Cultured hepatic progenitor cell expressed high level of Pin1 along with other markers like EP-CAM, CK-19 and AFP.