Of those 175, 16 (M=9, F=7) were included in the NKPS group. The mean age was 64 in both groups. Successful biliary cannulation was achieved in all NKPS patients. PEP was developed in 8 of 159 (5%) in routine group and 2 of 16 (12.5%) in NKPS group (p=0.229). Bleeding was developed in 9 of 159 (5.7%), 1 of 16 (6.3%), respectively (p=1.000).

All the PEP was mild in NKPS group; however, there was a severe PEP in routine group. Mean (SD) serum amylase levels after ERCP were 194.9 (377.5) U/L in routine group and 438.2 (474.6) U/L in NKPS group (p<0.001). All PD stents were dislodged spontaneously within 7 days. Conclusion: Even though NKPS group was high risk for PEP, Pritelivir purchase the incidence of PEP was comparable to the routine group. If biliary cannulation is difficult and incidental PD cannulation is achieved, NKPS would be safe and feasible with a lower rate of post-procedure complications. Key Word(s): 1. post-ERCP pancreatitis; 2. pancreatic stent; 3. precut sphincterotomy; Presenting learn more Author: BIN XU Additional Authors: SUMEI SHA, BIN BAI, XIAOLEI SHI, YONGZHAN NIE, QINGCHUAN ZHAO Corresponding Author: YONGZHAN

NIE, QINGCHUAN ZHAO Affiliations: Fourth Military Medical University Objective: Gastric cancer (GC) is a complex disease resulting from genetic and epigenetic alterations. By using bisulfite-assisted genomic sequencing (BSP) and a novel highthroughput mass spectrometry on matrix-assisted laser desorption/ionization time-of-flight silico-chips (Mass-Array) strategies, we 上海皓元医药股份有限公司 proposed that whether DHRS3, a member of the short-chain dehydrogenases/reductases family, is a potential novel epigenetic target gene. Its biologic function and clinical significance were also investigated in gastric cancer (GC). Methods: BSP and Mass-Array were used to evaluate and quantify the promoter methylation level in 120 primary GC and matched normal mucosa tissue specimens. The mRNA and protein expression were determined by real-time PCR and immunohistochemical staining. The biological function

of DHRS3 was determined by both in vitro and in vivo assays. A two-way hierarchical cluster analysis was used to classify methylation profiles and any correlation between the methylation status of the DHRS3 promoter and clinicopathological characteristics of GC was then assessed. Results: Experiments showed that the promoter of DHRS3 was hypermethylated in GC samples compared with adjacent normal samples (p<0.0001). DHRS3 was silenced or downregulated in GC samples. In contrast, DHRS3 was high expressed in normal gastric mucosa tissues. This down-regulation was closely linked to the promoter methylation of DHRS3 as identified by BSP, Mass-Array and restored by demethylation agent 5-Aza treatment. Up-regulated the expression level of DHRS3 inhibited cell proliferation, reduced colony formation in GC MKN28 cells in vitro and decreased tumor growth in nude mice in vivo; it also induced cell early apoptosis and arrested cells in G1 phase.