We then compared the age and hematological parameters (WBC, CRP, Hb, BUN, Cre, Che, Alb and Tcho) between cases of early mortality and long-term survival. All readings were taken on the day before the PEG procedure. Results: Che and Tcho levels were found to

be significantly lower in cases of early mortality than in cases of long-term survival. Conclusion: PEG must be implemented only when the prognosis and estimated risk factors of the patients condition are understood. It is important to establish a good balance between the patients chance of long-term survival, and improvement in GSK1120212 solubility dmso QOL. Key Word(s): 1. PEG risk Presenting Author: BING HU Additional Authors: HONG ZE ZENG Corresponding Author: HUI LIU Affiliations: West China Hospital, Sichuan University Objective: In recent years, laparoscopic and endoscopic cooperative surgery (LECS) has become increasingly

frequently used for gastrointestinal stromal tumors (GISTs). The aim of our study is to hold a preliminary discussion to the choice between laparoscope-assisted Ku-0059436 clinical trial endoscopic technique (LAET) and endoscope-assisted laparoscopic technique (EALT). Methods: From January 2006 to December 2011, a total of 72 patients received LECS in our hospital. All the patients underwent preoperative endoscopy, endoscopic ultrasonography (EUS) and upper abdominal CT scan. For endogenous tumors with neither serosal invasion nor surrounding organs or lymph nodes metastases, LAET was chosen if preoperative evaluation showed risks of massive bleeding or perforation and difficulties in simple endoscopic resection. For tumors located at cardia or pylorus, LAET was chosen if possible. For exogenous tumors or endogenous tumors with serosal invasion, EALT was chosen. Results: 32 medchemexpress cases were treated by LAET. 40 cases were treated by EALT, of which, 10 cases were indicated for LAET initially but turned to EALT during surgeries. Among the 10 cases, perforation occurred

in 6 cases during endoscopic dissection and high chance of serosal invasion was found in the other 4 cases with tumors located near cardia or pylorus during endoscopic surgeries. All the tumors were completely resected and none of the cases were converted to open surgery. During a median follow-up of 35 months, none of the patients suffered metastasis or recurrence. Conclusion: LECS is safe and effective for gastric GISTs. For endogenous tumors without serosal invasion which can be fully removed by endoscopy, LAET should be considered. Even if an endogenous tumor can be resected simply by endoscopy, LAET is safer. For exogenous tumors or endogenous tumors with invasion beyond the stomach wall, EALT should be chosen. Key Word(s): 1. gastrointestinal stromal tumor; 2.

2 mm) along with a loss of normal five-layer pattern (Fig. 1). The proximal uninvolved esophagus revealed a normal 5-layered wall pattern (Fig. 2). Triamcinolone

acetonide (40 mg/mL diluted 1:1 with saline solution; 0.5 mL at each site) was injected at the proximal margin as well as in the strictured segment. Thereafter, endoscopic dilatation was performed and the patient has since been asymptomatic. Corrosive click here injury of the gastrointestinal tract (GIT) is an important health problem, especially in developing countries. The injury and inflammation of the GIT caused by corrosives can cause hemorrhaging and perforation in an acute setting and strictures in the delayed phase. Corrosive induced GIT strictures are difficult to manage as they require more endoscopic dilatation sessions and are more likely to recur. The factors responsible for this clinical course are unclear but the intense fibrosis and consequent esophageal wall thickening may be responsible for it. EUS could provide more detailed information compared with conventional endoscopy as it images the full thickness of the GIT wall. It has been shown in an acute setting that the involvement of muscularis propria on EUS predicts stricture formation

with an accuracy of 100%. Theoretically, EUS may also be helpful in the management of patients with corrosive strictures but its role needs to be studied. One may predict the response to dilatation by measuring the wall selleck inhibitor thickness on EUS (Fig. 1)

as well as more precisely injecting intralesional steroids in the thickest GIT wall under EUS guidance. However, this hypothesis needs to be tested in prospective studies. Contributed by “
“A surgeon needs to address MCE four issues on surgical evaluation for a liver transplant candidate. These are: (1) necessity; (2) suitability; (3) strategy; and (4) informed consent. A surgeon’s “eye-ball” test is sometimes more important than consulting many specialists. A creative strategy is key, especially if you practice in extreme organ shortage areas. “
“Sabio G, Cavanagh-Kyros J, Ko HJ, Jung DY, Gray S, Jun JY, et al. Prevention of steatosis by hepatic JNK1. Cell Metab 2009;10:491-498. (Reprinted with permission.) Nonalcoholic steatosis (fatty liver) is a major cause of liver dysfunction that is associated with insulin resistance and metabolic syndrome. The cJun NH2-terminal kinase 1 (JNK1) signaling pathway is implicated in the pathogenesis of hepatic steatosis and drugs that target JNK1 may be useful for treatment of this disease. Indeed, mice with defects in JNK1 expression in adipose tissue are protected against hepatic steatosis. Here we report that mice with specific ablation of Jnk1 in hepatocytes exhibit glucose intolerance, insulin resistance, and hepatic steatosis. JNK1 therefore serves opposing actions in liver and adipose tissue to both promote and prevent hepatic steatosis.

2 mm) along with a loss of normal five-layer pattern (Fig. 1). The proximal uninvolved esophagus revealed a normal 5-layered wall pattern (Fig. 2). Triamcinolone

acetonide (40 mg/mL diluted 1:1 with saline solution; 0.5 mL at each site) was injected at the proximal margin as well as in the strictured segment. Thereafter, endoscopic dilatation was performed and the patient has since been asymptomatic. Corrosive this website injury of the gastrointestinal tract (GIT) is an important health problem, especially in developing countries. The injury and inflammation of the GIT caused by corrosives can cause hemorrhaging and perforation in an acute setting and strictures in the delayed phase. Corrosive induced GIT strictures are difficult to manage as they require more endoscopic dilatation sessions and are more likely to recur. The factors responsible for this clinical course are unclear but the intense fibrosis and consequent esophageal wall thickening may be responsible for it. EUS could provide more detailed information compared with conventional endoscopy as it images the full thickness of the GIT wall. It has been shown in an acute setting that the involvement of muscularis propria on EUS predicts stricture formation

with an accuracy of 100%. Theoretically, EUS may also be helpful in the management of patients with corrosive strictures but its role needs to be studied. One may predict the response to dilatation by measuring the wall Torin 1 supplier thickness on EUS (Fig. 1)

as well as more precisely injecting intralesional steroids in the thickest GIT wall under EUS guidance. However, this hypothesis needs to be tested in prospective studies. Contributed by “
“A surgeon needs to address 上海皓元医药股份有限公司 four issues on surgical evaluation for a liver transplant candidate. These are: (1) necessity; (2) suitability; (3) strategy; and (4) informed consent. A surgeon’s “eye-ball” test is sometimes more important than consulting many specialists. A creative strategy is key, especially if you practice in extreme organ shortage areas. “
“Sabio G, Cavanagh-Kyros J, Ko HJ, Jung DY, Gray S, Jun JY, et al. Prevention of steatosis by hepatic JNK1. Cell Metab 2009;10:491-498. (Reprinted with permission.) Nonalcoholic steatosis (fatty liver) is a major cause of liver dysfunction that is associated with insulin resistance and metabolic syndrome. The cJun NH2-terminal kinase 1 (JNK1) signaling pathway is implicated in the pathogenesis of hepatic steatosis and drugs that target JNK1 may be useful for treatment of this disease. Indeed, mice with defects in JNK1 expression in adipose tissue are protected against hepatic steatosis. Here we report that mice with specific ablation of Jnk1 in hepatocytes exhibit glucose intolerance, insulin resistance, and hepatic steatosis. JNK1 therefore serves opposing actions in liver and adipose tissue to both promote and prevent hepatic steatosis.

RANTES can also directly target HSCs to promote their proliferation and migration, and mice deficient for RANTES or its receptors chemokine (C-C) motif Fulvestrant receptor 1 (CCR1) and CCR5 display substantially reduced fibrosis.30 Here, we show that deficiency of c-Rel is associated with substantially reduced baseline and injury-induced expression of RANTES, which may therefore help explain the reduced numbers of recruited neutrophils, lower numbers of α-SMA+ HSCs, and the attenuated

fibrogenic response. However, using the culture model of HSC transdifferentiation, we also discovered inherent defects in c-rel−/− HSCs, specifically reduced expression of collagen I and α-SMA transcripts. NF-κB is a regulator of HSC survival and their expression of inflammatory regulators intercellular cell adhesion molecule-1 and interleukin-6.31 Pharmacological blockade of NF-κB can promote HSC apoptosis and regression of liver fibrosis.32, 33 However, the precise contribution of the individual NF-κB subunits toward the fate and function of HSCs has not been investigated. Our previous report that the p50 subunit is a suppressor of the inflammatory properties of HSC-derived myofibroblasts,13 taken together with the potential for c-Rel

to regulate expression of collagen I, α-SMA, and RANTES suggests the need for detailed studies of the functions of the NF-κB subunits in HSCs and fibrosis. Nonparenchymal cells, including HSCs, can influence liver regeneration through paracrine stimulation of hepatocyte proliferation.34 Defective function of the inflammatory and Selleck GSK126 fibrogenic compartments may therefore contribute to the attenuated DNA synthesis and mitosis of hepatocytes observed 上海皓元 in injured and PHx livers of c-rel−/− mice. However, we propose that c-Rel also plays a more direct role as a regulator of hepatocyte DNA replication. B cells deficient in c-Rel display deficiencies in cyclin

D3 and cyclin E expression, cyclin-dependent kinase activity, Rb phosphorylation, and E2F activity and fail to progress through the cell cycle in response to B cell receptor stimulation.35 Because ChIP analysis confirmed recruitment of c-Rel to the FoxM1 promoter following PHx, we suggest that c-Rel regulates hepatocyte proliferation via transcriptional control of the cell cycle regulator FoxM1, which following PHx, was not induced at the appropriate time or level of expression in c-Rel–deficient livers. FoxM1 regulates proliferation of many cell types and in the developing liver and heart is essential for normal mitosis.36 Expression profiling identified a cluster of FoxM1-regulated genes including G2/M-specific genes such as cyclin B1 and CENP-F (centromere protein F).37 In particular, transcriptional activation of cyclin B1 by FoxM1 is crucial for timely mitosis.37 Induction of cyclin B1 was delayed in the regenerating c-Rel–deficient liver.

RANTES can also directly target HSCs to promote their proliferation and migration, and mice deficient for RANTES or its receptors chemokine (C-C) motif EPZ015666 mw receptor 1 (CCR1) and CCR5 display substantially reduced fibrosis.30 Here, we show that deficiency of c-Rel is associated with substantially reduced baseline and injury-induced expression of RANTES, which may therefore help explain the reduced numbers of recruited neutrophils, lower numbers of α-SMA+ HSCs, and the attenuated

fibrogenic response. However, using the culture model of HSC transdifferentiation, we also discovered inherent defects in c-rel−/− HSCs, specifically reduced expression of collagen I and α-SMA transcripts. NF-κB is a regulator of HSC survival and their expression of inflammatory regulators intercellular cell adhesion molecule-1 and interleukin-6.31 Pharmacological blockade of NF-κB can promote HSC apoptosis and regression of liver fibrosis.32, 33 However, the precise contribution of the individual NF-κB subunits toward the fate and function of HSCs has not been investigated. Our previous report that the p50 subunit is a suppressor of the inflammatory properties of HSC-derived myofibroblasts,13 taken together with the potential for c-Rel

to regulate expression of collagen I, α-SMA, and RANTES suggests the need for detailed studies of the functions of the NF-κB subunits in HSCs and fibrosis. Nonparenchymal cells, including HSCs, can influence liver regeneration through paracrine stimulation of hepatocyte proliferation.34 Defective function of the inflammatory and selleck inhibitor fibrogenic compartments may therefore contribute to the attenuated DNA synthesis and mitosis of hepatocytes observed medchemexpress in injured and PHx livers of c-rel−/− mice. However, we propose that c-Rel also plays a more direct role as a regulator of hepatocyte DNA replication. B cells deficient in c-Rel display deficiencies in cyclin

D3 and cyclin E expression, cyclin-dependent kinase activity, Rb phosphorylation, and E2F activity and fail to progress through the cell cycle in response to B cell receptor stimulation.35 Because ChIP analysis confirmed recruitment of c-Rel to the FoxM1 promoter following PHx, we suggest that c-Rel regulates hepatocyte proliferation via transcriptional control of the cell cycle regulator FoxM1, which following PHx, was not induced at the appropriate time or level of expression in c-Rel–deficient livers. FoxM1 regulates proliferation of many cell types and in the developing liver and heart is essential for normal mitosis.36 Expression profiling identified a cluster of FoxM1-regulated genes including G2/M-specific genes such as cyclin B1 and CENP-F (centromere protein F).37 In particular, transcriptional activation of cyclin B1 by FoxM1 is crucial for timely mitosis.37 Induction of cyclin B1 was delayed in the regenerating c-Rel–deficient liver.

Interestingly, a second CRP determination obtained ∼6 weeks later in the validation cohort, and therefore post-TACE in most cases, retained the

predictive value. The mean CRP levels increased with increasing Barcelona Clinic Liver Cancer (BCLC) stage. CRP levels also stratified patients within the same BCLC stage into long- and short-term survivors. Within BCLC stage B and C, patients with elevated CRP had a shorter survival than patients with low CRP. Within the BCLC C stage, Child B patients with a normal CRP had a survival comparable to Child A patients with an elevated CRP (median survival 15 and 14 months, respectively). Peck-Radosavljevic and co-workers further considered the Selleck NVP-BGJ398 presence/absence

of clinically evident infection. When unrelated PS-341 clinical trial to infection, elevated CRP levels correlated directly with tumor characteristics, in particular with tumor burden. This suggests that elevation of CRP might be tumor-related. The authors also compared the proportion of patients with CRP elevation from unknown origin and from infectious origin, in their cohort as well as in a group of 104 non-HCC patients undergoing a transjugular intrahepatic portosystemic shunt (TIPS) placement. Elevated CRP was more frequently of unknown origin in HCC patients than in non-HCC patients (38% versus 17%). Nevertheless, elevated CRP in both groups was associated with poor prognosis. Similarly, Cervoni et al.12 recently reported a benefit of CRP determination in predicting short-term mortality in patients with advanced cirrhosis. What pathophysiological mechanisms trigger CRP elevation in HCC? Low-grade inflammation promotes tumor development. Mdr2−/− mice show defective biliary secretion of phospholipids, spontaneous cholangitis, and eventually develop HCC.13 Transgenic mice that express lymphotoxin α:β develop a chronic parenchymal inflammation with the production of cytokines and eventually HCC.14 IL-6, which is the principal regulator of CRP production, is produced by Kupffer

cells. In the diethylnitrosamine (DEN) rodent model for HCC, IL-6 rises in response to IL-1a, which is released from necrotic hepatocytes.15 This IL-6 production is gender-specific and may partly 上海皓元 explain the male predominance of HCC.16 In fact, IL-6 expression is elevated in patients with cirrhosis and HCC.17 Moreover IL-6 levels were reported to correlate with the development of HCC.18, 19 This suggests that the hepatocellular signaling pathway of IL-6 might be a therapeutic target. The transcription factor STAT3 mediates the IL-6 effects. STAT3 was found to be activated in the majority of HCCs and seems to identify more aggressive tumors.20 Inactivation of the negative feedback loop of the JAK/STAT pathway by methylation of the SCOCS genes is frequent in HCC.

5B). Finally, we assessed the phosphorylated levels of these

signaling molecules in mouse livers posthepatic ATP infusion as described above. The phosphorylation of these signaling components in both untreated and ATP-stimulated Cd39-null livers nearly exactly recapitulates the same pattern observed in cells (Fig. 5C). These data indicate that Cd39 deletion results in persistent activation of oncogenic pathways with an increased incidence of autochthonous tumor formation in the liver. We further sought to delineate the role of mTOR by addition of rapamycin to these model systems. Stem Cells antagonist First, hepatocyte proliferation was significantly inhibited by rapamycin in both ATP-stimulated DNA Damage inhibitor and nonstimulated cells (Fig. 6A). Furthermore, ATP-stimulated proliferative responses

could be almost completely blocked by this approach (Fig. 6A). However, Cd39-null cells exhibited a higher proliferation rate than WT cells, regardless of the treatment strategy (Fig. 6A). Second, we evaluated the effect of rapamycin on hepatocyte autophagy. This fully restored the previously noted ATP-induced inhibition of autophagy in WT cells at the level of LC3 degradation (Fig. 6B). Third, we analyzed mitochondrial gene/regulator mRNA expression post-rapamycin treatment. The dysregulation of mitochondrial genes (LDH-A, cytochrome B, UCP2, Cox1, Cox2, NADHsub1, and NADHsub2) and regulators (PGC-1β, TFAM, NRF, and glucagon) in Cd39-null cells could be reversed by mTOR inhibition (Fig. 6C; Fig. S5). We also noted that rapamycin exhibited comparable effects on WT cell signaling responses, albeit with variable potency (Table S3). Fourth, we examined the impacts of rapamycin on lactate production by hepatocytes. Accumulated lactate levels in both WT and null cells were significantly inhibited by this approach (Fig. S6). No significant 上海皓元医药股份有限公司 differences between WT and

null cells were noted. Fifth, to further investigate the signaling pathways impacted by rapamycin, we studied the phosphorylated levels of mTOR-S6K1-S6 and downstream targets of Ras. We noted three key findings. In both rapamycin-treated WT and Cd39-null cells, mTOR phosphorylation was significantly decreased, whereas phosphorylation of the downstream S6K1 and S6 was completely abolished (Fig. 6D). AKT phosphorylation was increased after short-time exposure to rapamycin (Fig. 6E,F). Interestingly, phosphorylation events of downstream components of Ras signaling, e.g., MEK and JNK/SAPK were also enhanced by rapamycin (Fig. 6E), suggesting a possible negative-feedback loop on Ras signaling by mTOR-S6K1 in hepatocytes. However, phosphorylation of NF-κB was not affected by rapamycin (Fig. 6E). Finally, we explored the effect of AKT-PI3K-mTOR pharmacologic inhibitors. As shown in Fig.

5B). Finally, we assessed the phosphorylated levels of these

signaling molecules in mouse livers posthepatic ATP infusion as described above. The phosphorylation of these signaling components in both untreated and ATP-stimulated Cd39-null livers nearly exactly recapitulates the same pattern observed in cells (Fig. 5C). These data indicate that Cd39 deletion results in persistent activation of oncogenic pathways with an increased incidence of autochthonous tumor formation in the liver. We further sought to delineate the role of mTOR by addition of rapamycin to these model systems. Galunisertib order First, hepatocyte proliferation was significantly inhibited by rapamycin in both ATP-stimulated Talazoparib clinical trial and nonstimulated cells (Fig. 6A). Furthermore, ATP-stimulated proliferative responses

could be almost completely blocked by this approach (Fig. 6A). However, Cd39-null cells exhibited a higher proliferation rate than WT cells, regardless of the treatment strategy (Fig. 6A). Second, we evaluated the effect of rapamycin on hepatocyte autophagy. This fully restored the previously noted ATP-induced inhibition of autophagy in WT cells at the level of LC3 degradation (Fig. 6B). Third, we analyzed mitochondrial gene/regulator mRNA expression post-rapamycin treatment. The dysregulation of mitochondrial genes (LDH-A, cytochrome B, UCP2, Cox1, Cox2, NADHsub1, and NADHsub2) and regulators (PGC-1β, TFAM, NRF, and glucagon) in Cd39-null cells could be reversed by mTOR inhibition (Fig. 6C; Fig. S5). We also noted that rapamycin exhibited comparable effects on WT cell signaling responses, albeit with variable potency (Table S3). Fourth, we examined the impacts of rapamycin on lactate production by hepatocytes. Accumulated lactate levels in both WT and null cells were significantly inhibited by this approach (Fig. S6). No significant medchemexpress differences between WT and

null cells were noted. Fifth, to further investigate the signaling pathways impacted by rapamycin, we studied the phosphorylated levels of mTOR-S6K1-S6 and downstream targets of Ras. We noted three key findings. In both rapamycin-treated WT and Cd39-null cells, mTOR phosphorylation was significantly decreased, whereas phosphorylation of the downstream S6K1 and S6 was completely abolished (Fig. 6D). AKT phosphorylation was increased after short-time exposure to rapamycin (Fig. 6E,F). Interestingly, phosphorylation events of downstream components of Ras signaling, e.g., MEK and JNK/SAPK were also enhanced by rapamycin (Fig. 6E), suggesting a possible negative-feedback loop on Ras signaling by mTOR-S6K1 in hepatocytes. However, phosphorylation of NF-κB was not affected by rapamycin (Fig. 6E). Finally, we explored the effect of AKT-PI3K-mTOR pharmacologic inhibitors. As shown in Fig.

Results: Rates of SVR and PR were 20 and 50%, respectively. In multivariate analysis, younger age (< 32 yr, p=0.04, OR=13.15) and lower HBV-DNA titer (< 7.9 LGE/ml, p=0.03, OR=17.98) were significantly associated with PR. To analyze the impacts of Th1/2 ratio for PR, Th1/2 ratios at the commencements of LMV and IFN-α were compared between partial and non-partial responders. The ratios were not different between two groups at the commencement of LMV, however the ratio of partial responder increased during LMV treatment and became significantly higher than those of non-responders (p=0.01). Conclusions: The present study indicated that HBV-DNA and age were predictive factors for

the effectiveness of sequential therapy and an increase of Th1/2 ratio AP24534 caused by HBV suppression with LMV might improve the effect of IFN-α in HBeAg-positive chronic hepatitis B patients. Disclosures: Kazuaki 17-AAG solubility dmso Chayama – Consulting: Abbvie;

Grant/Research Support: Dainippon Sumitomo, Chugai, Mitsubishi Tanabe, DAIICHI SANKYO, Toray, BMS, MSD; Speaking and Teaching: Chugai, Mitsubishi Tanabe, DAIICHI SANKYO, KYORIN, Nihon Medi-Physics, BMS, Dainippon Sumitomo, MSD, ASKA, Astellas, AstraZeneca, Eisai, Olympus, GlaxoSmithKline, ZERIA, Bayer, Minophagen, JANSSEN, JIMRO, TSUMURA, Otsuka, Taiho, Nippon Kayaku, Nippon Shinyaku, Takeda, AJINOMOTO, Meiji Seika, Toray The following people have nothing to disclose: Nami Mori, Masataka Tsuge, Yoshiiku Kawakami, Hiroiku Kawakami Background/Aim: Suboptimal virological response to adefovir rescue therapy is often experienced in patients with lamivudine (LAM)-resistant chronic hepatitis B. The aim of this study was to investigate association between efficacy of adefovir (ADV) rescue therapy and the occurrence of hepatocellular carcinoma (HCC). Methods: Electronic medical records of 221 patients with LAM-resistant chronic hepatitis B who received ADV more than 1 2 months with or without LAM from 3 referral centers of Soonchunhyang University, Korea were reviewed retrospectively from

July 2007 to June 2012. Baseline characteristics, outcomes of antiviral therapy, and MCE公司 occurrence of HCC were investigated during ADV rescue therapy. Virological response was defined as undetectable serum HBV DNA levels (< 20 IU/mL). The risk factors for development of HCC were evaluated with Cox-proportional hazard model. Results: Study subjects were followed for median period of 51 (12-1 01) months. Sixty-nine percent (152/221) of patients were treated with ADV-LAM combination during follow-up periods and 26% (59/221) of the patients were assessed as cirrhosis at beginning of rescue therapy. Seventy-six percent of patients HBeAg positive and baseline HBV DNA levels was 5.95 (1.94-8.98) log 10 IU/mL. Cumulative virological response was 22%, 41% and 55% at 1, 3, and 5 years, respectively. ADV resistant mutations with virological breakthrough were confirmed in 7 patients during rescue therapy.

It may be more optimally performed in selected patients at very high risk of rebleeding. This study aims to analyze the clinical and endoscopic factors that contribute to intractable endoscopic hemostasis and to determine the optimal role of second-look endoscopy.

Methods: Prospectively collected UGI bleeding registry data was reviewed and data from 464 patients who underwent UGI endoscopy for acute non-variceal UGI bleeding from 8 hospitals in Korea between February 2011 and December 2013 were analyzed. Significant predictive factors (P < 0.05) of intractable endoscopic hemostasis in univariate analysis were entered in a multivariate logistic regression analysis. Results: Successful hemostasis was achieved in 394 patients selleck kinase inhibitor by using initial endoscopic procedures. Seventy patients at the second-look endoscopy were considered

Selleck Deforolimus intractable or insufficient to the initial endoscopic hemostasis, and they required second endoscopic hemostasis. Univariate analysis significantly related intractable endoscopic hemostasis with large amount of transfusion (≥5 units), Glasgow-Blatchford score, Rockall score, Forrest bleeding type Ia and degree of initial endoscopic hemostasis. Multivariate analysis showed that large amount of transfusion and Rockall score were only predictive factors of secondary endoscopic hemostasis. Conclusion: Large amount of transfusion and Rockall score are identified as independent risk factors associated with intractable initial endoscopic hemostasis in patients with acute non-variceal bleeding. Second-look endoscopy after initial endoscopic hemostasis in these patients MCE is not routinely

indicated and be reserved for selected patients with high risk of rebleeding. Key Word(s): 1. second look endoscopy; 2. acute non-variceal upper gastrointestinal bleeding Presenting Author: HYUN-WOO PARK Additional Authors: SEONG WOO JEON, JUN HEO Corresponding Author: HYUN-WOO PARK Affiliations: Kyungpook National University Medical Center, Kyungpook National University School of Medicine Objective: This study aimed to clarify the features of non-peptic ulcer related bleeding compared with peptic ulcer related bleeding in non-variceal upper gastrointestinal bleeding (NVUGIB) patients.