Methods: Analgesic find more effects of uroguanylin and cGMP were assessed in a rat model of inflammation-induced colonic hypersensitivity. Linaclotide, uroguanylin and cGMP effects on mouse splanchnic colonic nociceptors were measured using in vitro single-unit afferent recordings. GC-C expression in mice was determined by in situ hybridization. Results: During inflammation-induced colonic hypersensitivity, orally administered uroguanylin elicited significant anti-hyperalgesic

effects increasing the pain threshold to colorectal distension. In addition, linaclotide, and uroguanylin in vitro significantly inhibited the mechanical responsiveness of mouse colonic nociceptors, an effect that became particularly pronounced during chronic visceral hypersensitivity. These effects were mimicked by cGMP, suggesting a direct link between activation of the GC-C/cGMP pathway and analgesic effects in this model. Incubation of colonic afferent preparations with the cGMP efflux inhibitor, probenecid, eliminated the inhibitory effect of linaclotide on colonic nociceptors. This suggests that extracellular cGMP, released upon activation of GC-C from intestinal epithelial cells, underlies the anti-hyperalgesic effects of these GC-C agonists. Since we detected high levels PD-0332991 mouse of GC-C expression in the intestine but not dorsal root ganglion neurons this is consistent with a local,

peripheral mechanism linking analgesic effects to activation see more of the GC-C/cGMP pathway. Conclusion: GC-C agonists, such as linaclotide, have pronounced anti-hyperalgesic effects in animal models of abdominal pain. These effects have also translated into the clinic, where in patients with irritable bowel syndrome with constipation, linaclotide treatment improved abdominal pain. These findings suggest that

targeting the GC-C/cGMP pathway is linked to analgesic effects in these patients. Key Word(s): 1. cGMP; 2. GI pain; 3. guanylate cyclase-C; 4. linaclotide; Presenting Author: JUN SU BYUN Additional Authors: JI WON KIM, KOOK LAE LEE, BYEONG GWAN KIM, JAEKYUNG LEE, SEONG-JOON KOH Corresponding Author: JUN SU BYUN Affiliations: Department of Internal Medicine, Seoul Metropolitan Government Boramae Hospital.; Department of Internal Medicine, Seoul Metropolitan Government Boramae Hospital.; Department of Internal Medicine, Seoul Metropolitan Government Boramae Hospital. Objective: Ghrelin and obestatin are produced by cleavage of the ghrelin/obestatin prepropeptide encoded by the same gene. Ghrelin acts as a hunger hormone, increasing food intake and enhancing the motility of the gastrointestinal tract. Obestatin counteracts the induction of food intake by ghrelin. An unclear relationship exists between ghrelin and obestatin levels and functional gastrointestinal disorders (FGIDs) defined by gastrointestinal (GI) symptoms. This study investigates the association between FGIDs and plasma ghrelin, obestatin, and ghrelin/obestatin ratios in elderly patients.

5%). Median follow up was 6.7 years.

Elastin % area was significantly Ulixertinib price associated with the time to a clinical outcome in univariate analysis (p=0.011). We used median elastin % area as a threshold (2.96%) to stratify the cohort and found that those with higher elastin progressed to outcomes more quickly (Fig 1). There was no difference in time to clinical outcomes between those with IS5 and IS6 fibrosis. Quantification of hepatic elastin using immunostaining and automated image analysis is feasible and could be a useful addition to standard histopathological assessment of fibrosis as a tool for stratifying clinical progression in cirrhosis. This could influence intensity of surveillance and timing of referral for transplant. Disclosures: William Irving – Advisory Committees or Review Panels: Novartis, MSD, Janssen

Cilag, Novartis, MSD, Janssen Cilag; Consulting: GlaxoSmithKline, Glaxo-SmithKline; Grant/Research Support: GSK, Pfizer, Janssen Cilag, GSK, Pfizer, Janssen Cilag Indra Neil Guha – Grant/Research Support: Pfizer, Conatus The following people have nothing to disclose: Grace E. Dolman, Jie Shu, Guoping Qiu, Claire Hawkes, Abed Zaitoun, Jonathan Fallowfield Background & Aims: Mac-2BP glycoprotein is involved in the immune defense against a variety of neoplasms and viral infections, modulating the activity of several effectors such as natural killer cells. Wisteria floribunda agglutinin-positive human Mac-2 binding protein (WFA(+)-M2BP) was recently

validated DAPT as a liver fibrosis glycobiomarker, which was a unique fibrosis-related glyco-alteration (Kuno A et.al. Scientific reports 201 3). And this novel marker is available for clinically beneficial therapy evaluation through quantification of disease severity. We evaluated the utility of WFA(+)-M2BP to predict the development check details of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C virus (HCV) infection. Methods: A total of 707 patients with chronic HCV infection without the other risks were evaluated for the predictive value of the development of HCC, including age, sex, viral load, genotypes, fibrosis stage, aspartate and alanine aminotransferase levels, bilirubin, albumin, platelet count, alpha-fetoprotein (AFP) and WFA(+)-M2BP at the entry, as well as interferon therapy they received. All patients received the examination of liver biopsy. WFA(+)-M2BP quantification was measured with a fully automated lectin-antibody sandwich immunoassay. Results: Serum WFA(+)-M2BP levels had a significant correlation with the degree of liver fibrosis stage (p < 0.001). The 10-year cumulative risk of the development of HCC was 1.1 % in the patients with WFA(+)-M2BP < 1 cutoff index (COI) at the study entry, 14.8% in the patients with WFA+-M2BP 1-4 COI, and 54.1% in the patients with WFA(+)-M2BP > 4 COI (P < 0.001) . The cumulative incidence of HCC stratified by the fibrosis stage, were significantly higher according to WFA(+)-M2BP level.

5%). Median follow up was 6.7 years.

Elastin % area was significantly http://www.selleckchem.com/products/Everolimus(RAD001).html associated with the time to a clinical outcome in univariate analysis (p=0.011). We used median elastin % area as a threshold (2.96%) to stratify the cohort and found that those with higher elastin progressed to outcomes more quickly (Fig 1). There was no difference in time to clinical outcomes between those with IS5 and IS6 fibrosis. Quantification of hepatic elastin using immunostaining and automated image analysis is feasible and could be a useful addition to standard histopathological assessment of fibrosis as a tool for stratifying clinical progression in cirrhosis. This could influence intensity of surveillance and timing of referral for transplant. Disclosures: William Irving – Advisory Committees or Review Panels: Novartis, MSD, Janssen

Cilag, Novartis, MSD, Janssen Cilag; Consulting: GlaxoSmithKline, Glaxo-SmithKline; Grant/Research Support: GSK, Pfizer, Janssen Cilag, GSK, Pfizer, Janssen Cilag Indra Neil Guha – Grant/Research Support: Pfizer, Conatus The following people have nothing to disclose: Grace E. Dolman, Jie Shu, Guoping Qiu, Claire Hawkes, Abed Zaitoun, Jonathan Fallowfield Background & Aims: Mac-2BP glycoprotein is involved in the immune defense against a variety of neoplasms and viral infections, modulating the activity of several effectors such as natural killer cells. Wisteria floribunda agglutinin-positive human Mac-2 binding protein (WFA(+)-M2BP) was recently

validated INCB024360 cost as a liver fibrosis glycobiomarker, which was a unique fibrosis-related glyco-alteration (Kuno A et.al. Scientific reports 201 3). And this novel marker is available for clinically beneficial therapy evaluation through quantification of disease severity. We evaluated the utility of WFA(+)-M2BP to predict the development this website of hepatocellular carcinoma (HCC) in patients with chronic hepatitis C virus (HCV) infection. Methods: A total of 707 patients with chronic HCV infection without the other risks were evaluated for the predictive value of the development of HCC, including age, sex, viral load, genotypes, fibrosis stage, aspartate and alanine aminotransferase levels, bilirubin, albumin, platelet count, alpha-fetoprotein (AFP) and WFA(+)-M2BP at the entry, as well as interferon therapy they received. All patients received the examination of liver biopsy. WFA(+)-M2BP quantification was measured with a fully automated lectin-antibody sandwich immunoassay. Results: Serum WFA(+)-M2BP levels had a significant correlation with the degree of liver fibrosis stage (p < 0.001). The 10-year cumulative risk of the development of HCC was 1.1 % in the patients with WFA(+)-M2BP < 1 cutoff index (COI) at the study entry, 14.8% in the patients with WFA+-M2BP 1-4 COI, and 54.1% in the patients with WFA(+)-M2BP > 4 COI (P < 0.001) . The cumulative incidence of HCC stratified by the fibrosis stage, were significantly higher according to WFA(+)-M2BP level.

Therefore, the better sedation methods

and ultra-thin scopes have been developed. However, the field of pediatric gastrointestinal endoscopy as a subspeciality has not been commonly established in Japan. The aim of this study is to understand the current status of pediatric gastrointestinal endoscopy in our hospital. Methods: Pediatric gastrointestinal endoscopy (The http://www.selleckchem.com/products/r428.html count at the first time of testing if you have enforcement pursuant to the provisions first visit age of our hospital pediatrics, repeat the inspection) was defined as a gastrointestinal endoscopy for patients less than 15 year old. The medical records of 55 patients, who underwent pediatric gastrointestinal endoscopy in our hospital from November 2009 to September 2012, were reviewed to assess their chief complaint endoscopic and findings. Results: Among all, 29 esophagogastroduodenoscopy (EGD) and 38 total colonoscopy (TCS) were carried out. Abdominal pain and/or discomfort are found in 20 of patients with EGD and 15 of those with TCS. Biopsy was taken from 51 of total 67 cases even in

cases without and endoscopic findings in particular. No any histological abnormalities were diagnosed. Conclusion: Major complaint was abdominal pain PD0325901 datasheet and discomfort, and biopsy was performed from many patients, even in patients without any endoscopic findings, in order to assess immunological diseases. Key Word(s): 1. pediatrics; 2. endoscopy; Presenting Author: GUOQI ZHENG Additional Authors: HUI SONG, YUEFENG CHEN, SICHEN WEI Corresponding Author: GUOQI ZHENG Affiliations: Cangzhou Central Hospital; Department of Magnetic Resonance Imaging Objective: Malignant peritoneal mesothelioma (MPM) is a rare aggressive

tumor of the peritoneum, which is poorly described and the knowledge of its natural history is very limited. The aim of this study was to summarize CT imaging characteristics and discuss the possible mechanism. this website Methods: The history, clinical manifestations, and imaging appearance of 53 patients with histopathologically proved MPM were retrospectively analyzed. The imaging data was reviewed for the presence and location of ascites, peritoneal, mesenteric, and omental involvement, enlarged lymph nodes, solid abdominal viscera infiltration and metastases, and for the thoracic changes. Our patients consisted of 36 women and 17 men, with an average age of 60 years (age range 45–75 years). Results: There was a definite history of significant asbestos exposure in 50 patients. Abdominal distention (45 of 53) was the most common presenting symptom.

Conclusion: We have isolated an epithelial cell population from primary mouse gallbladder with stem cell characteristics and found it to be unique, compared to IHBD cells. (HEPATOLOGY 2011) Understanding the resident stem cell populations of the biliary system has great importance for basic biology and biliary diseases. The biliary tree is divided into the intra- and extrahepatic biliary systems. The latter consists of the gallbladder, cystic duct, and the common bile duct.1 The biliary system Vismodegib molecular weight is a conduit for bile to be transported from the liver to the intestine. The gallbladder, in

turn, stores the bile and regulates its content and concentration, playing an important role in the digestive process.2, 3 Though there has been a lot of recent interest in the liver stem cell field,4 there is still a paucity of data regarding gallbladder stem cells. The biliary system, hepatocytes, and ventral pancreas develop from the ventral foregut endoderm.5, 6 Histological evidence suggesting that both intra- and extrahepatic systems originate from the hepatic diverticulum has led to the hypothesis that they ICG-001 mw descend from the same progenitor cell. However, the cell-intrinsic factors that result in their specification have heretofore been unclear. Recently, it has been shown that the progenitor cells that give rise to each system separate out during development.7 Using

a Pdx1-Cre mouse, Spence et al.7 demonstrated that hepatocytes and intrahepatic bile duct (IHBD) cells derive from Pdx1- cells, whereas the extrahepatic bile duct (EHBD) cells and ventral pancreas derive from Pdx1+ cells. Sox17 controls the specification selleck kinase inhibitor of the EHBD and pancreatic cells.

Sox17 loss-of-function embryos exhibit gallbladder agenesis and the presence of ectopic pancreatic tissue in the extrahepatic bile duct. Conversely, Sox17 gain of function results in ectopic ductal tissue in the developing pancreas. In both cases, the intrahepatic system is not affected. It appears that the IHBD and EHBD cells descend from separate progenitor cells governed by separate transcriptional cascades. It is, therefore, possible that adult IHBD and EHBD cells could be distinct, as well. The aims of this study were to isolate and characterize stem cells from the adult mouse gallbladder and compare their phenotypic and expression profiles with IHBD cells. In addition to basic biology, an understanding of gallbladder stem cells would be vital to the study of gallbladder carcinoma, a rare, but poorly understood, malignancy8 and congenital diseases involving biliary dysmorphogenesis, such as biliary atresia.9 It would also elucidate the ontogeny of cells in the biliary system. Stem cells are defined as undifferentiated cells that can self-renew at the single-cell level and form lineage-committed progeny.

The analysis was conducted on 54 of 111 miRNAs for which information on target mRNA was available in mirBase. Strikingly, we found that the majority of ALF-specific miRNAs (74%) target B-lineage-associated genes, including: i) several Ig genes; ii) TNFRSF17/BCMA

and FCRL5, which R788 order promote B-cell maturation and proliferation, respectively; iii) POU2AF1 and PRDM1, two master regulators of germinal center formation and terminal B-cell differentiation. Moreover, we found that most B-cell genes are simultaneously targeted by several miRNAs, including miR-150, 155, 146a, 182 and 181b, which are known to regulate germinal centers, B-cell differentiation and activation. Several miRNAs expressed in ALF are upregulated in B-cell lymphomas. In contrast, only a very small number of miRNA were identified that target T-cell genes, in agreement with the limited T-cell signature detected in ALF and with the absence of IFN-γ and its inducible chemokines

both amongst liver mRNAs and serum proteins. Conclusions: This is the first genome-wide integrated analysis of mRNA and miRNA expression in HBV ALF. Our results reveal selleck chemicals llc a dominant B-cell-driven disease signature consistent with a major role of B-cell immunity in the pathogenesis of ALF. Disclosures: The following people have nothing to disclose: Patrizia Farci, Fausto Zamboni, Ashley B. Tice, Zhaochun Chen, Ronald E. Engle, Giacomo Diaz Background/Aims: Multiple in vitro studies have been conducted characterizing the innate antiviral effects of IFNλ. However to date there are limited data regarding the impact of peginterferon Lambda-1a (Lambda),

which has shown anti-HBV activity both in vitro and in vivo, on host immune responses in vivo. In this study we aimed to longitudinally assess the effect of Lambda on innate and adaptive immunity when administered in combination check details with Entecavir (ETV) employing a sequential dosing approach in treatment-naive HBeAg(+) chronic hepatitis B (CHB) patients. Methods: NK-cell frequency, phenotype, expression of inhibitory/activating signatures and function by IFNγ production and cytotoxicity were measured by FACS. Expression of immunoinhibitory receptors on HBV-specific CD4+/CD8+ T-cells were measured by FACS. Ex-vivo frequency of HBV-specific CD4+/CD8+ T-cells producing IFNγ and IL-10 to genotype-specific HBcAg/HBsAg peptide pools were quantified by Elispot assays and intracellular cytokine staining. Levels of circulating T-regulatory cells were also assessed. Immunological analyses were performed at 9 time-points(TP) through the study period including Baseline, TW4, TW8, TW12 TW16,TW24,TW36 and 2 subsequent follow up visits (TW60, TW84). Virological and clinical parameters were also measured at each TP and correlated with immunological assessments. Results: In this study, a total of 13 subjects received combination Lambda plus ETV. The population was of mean age 31.2 years, 77% male and 92% Asian.

The analysis was conducted on 54 of 111 miRNAs for which information on target mRNA was available in mirBase. Strikingly, we found that the majority of ALF-specific miRNAs (74%) target B-lineage-associated genes, including: i) several Ig genes; ii) TNFRSF17/BCMA

and FCRL5, which Selleckchem TSA HDAC promote B-cell maturation and proliferation, respectively; iii) POU2AF1 and PRDM1, two master regulators of germinal center formation and terminal B-cell differentiation. Moreover, we found that most B-cell genes are simultaneously targeted by several miRNAs, including miR-150, 155, 146a, 182 and 181b, which are known to regulate germinal centers, B-cell differentiation and activation. Several miRNAs expressed in ALF are upregulated in B-cell lymphomas. In contrast, only a very small number of miRNA were identified that target T-cell genes, in agreement with the limited T-cell signature detected in ALF and with the absence of IFN-γ and its inducible chemokines

both amongst liver mRNAs and serum proteins. Conclusions: This is the first genome-wide integrated analysis of mRNA and miRNA expression in HBV ALF. Our results reveal VX-809 order a dominant B-cell-driven disease signature consistent with a major role of B-cell immunity in the pathogenesis of ALF. Disclosures: The following people have nothing to disclose: Patrizia Farci, Fausto Zamboni, Ashley B. Tice, Zhaochun Chen, Ronald E. Engle, Giacomo Diaz Background/Aims: Multiple in vitro studies have been conducted characterizing the innate antiviral effects of IFNλ. However to date there are limited data regarding the impact of peginterferon Lambda-1a (Lambda),

which has shown anti-HBV activity both in vitro and in vivo, on host immune responses in vivo. In this study we aimed to longitudinally assess the effect of Lambda on innate and adaptive immunity when administered in combination this website with Entecavir (ETV) employing a sequential dosing approach in treatment-naive HBeAg(+) chronic hepatitis B (CHB) patients. Methods: NK-cell frequency, phenotype, expression of inhibitory/activating signatures and function by IFNγ production and cytotoxicity were measured by FACS. Expression of immunoinhibitory receptors on HBV-specific CD4+/CD8+ T-cells were measured by FACS. Ex-vivo frequency of HBV-specific CD4+/CD8+ T-cells producing IFNγ and IL-10 to genotype-specific HBcAg/HBsAg peptide pools were quantified by Elispot assays and intracellular cytokine staining. Levels of circulating T-regulatory cells were also assessed. Immunological analyses were performed at 9 time-points(TP) through the study period including Baseline, TW4, TW8, TW12 TW16,TW24,TW36 and 2 subsequent follow up visits (TW60, TW84). Virological and clinical parameters were also measured at each TP and correlated with immunological assessments. Results: In this study, a total of 13 subjects received combination Lambda plus ETV. The population was of mean age 31.2 years, 77% male and 92% Asian.

We recommend that headache medicine specialists and other physicians who evaluate and treat headache disorders should use this list when discussing care with patients. In 2012, the American Board

of Internal Medicine (ABIM) Foundation launched a campaign called Choosing Wisely. The goal of the project was to encourage discussion about medical care that might be unnecessary or even harmful.[1] Project leaders invited physician specialty societies to submit lists of five things that “physicians and patients should question” MK0683 nmr in order to make “wise decisions about the most appropriate care based on the individual situation.” The head of the ABIM Foundation, Dr. Christine Cassel, remarked that these lists were “intended to start a national conversation about eliminating waste and unnecessary tests and Ixazomib datasheet procedures that don’t benefit the patient and can even cause harm.”[2] The first set of lists by nine societies was released in April 2012. The announcement generated substantial attention in the lay press as well as the medical community.[3] The second set of lists by 16 societies was released in early 2013 and generated a similar amount of attention. The American Headache

Society (AHS) has joined roughly 30 other specialty societies that are participating in the creation of the third set of lists. This paper describes

the AHS list development process and provides the rationale and supporting evidence for each recommendation. The ABIM requested that each participating specialty society identify commonly used tests, medications, or other treatments in their specialty for which harms often outweigh benefits, or which are known to be misused or overused. Participating societies were free to develop their own methods for list creation as long as the process was documented and described. The AHS president appointed an ad hoc AHS “Choosing Wisely” committee click here of eight headache specialists. The committee was intended to be broadly representative of the AHS membership, and included trainee members, members in private practice, as well as academic headache specialists with expertise in evidence appraisal and synthesis. Committee members were: Elizabeth Loder, AHS President and Chair; Stephen Silberstein, Chair of the AHS Guidelines and Position Statement Committee; Benjamin Frishberg; Randolph W. Evans; Jessica Ailani; Scott Litin; Josif Stakic; and Donald Dworek. The committee sent an electronic survey to AHS members in order to generate a list of candidate items for the list.

Methods: 1. We measured the expession of miR-148a using the technology of real-time qRT-PCR in pancreatic cancer cell lines PANC-1 and BXPC-3. After over-expressing miR-148a of the cells, MTT assays were used to determine the proliferation of the cancer cells, and migration assays were done using a modified transwell chamber system. 2. The putative downstream target gene of miR148a was found through bio-informatics analysis. Both panceratic cancer cell lines were transfected with the ErbB3 3′-UTR reporter plasmid. Then the activity of renilla and firefly luciferase

was assessed using the selleck dual-luciferase reporter assay system, Taqman PCR assay was used to assess miR-148a expression. The expression of ErbB3 was detected using western blot analysis. 3. Both panceratic cancer cell lines were transfected with ErbB3 RNAi by using Lipofectamine2000.

The proliferation and migration of the cells were oberserved, and the results were compared with those of over-expressing miR-148a. Results:  1. MiR-148a was significantly downregulated in both cell lines, and the expression of miR-148a was correlated with the degree of malignancy. Functional studies indicated overexpression of miR-148a dramatically inhibits proliferation http://www.selleckchem.com/products/crenolanib-cp-868596.html and migration of pancreatic cancer cells. 2. Bio-informatic studies revealed that ErbB3 might be the direct target gene of miR-148a. Overexpression of miR-148a in pancreatic cancer cells could reduce the mRNA and protein levels of ErbB3, whereas miR-148a silencing significantly increased ErbB3 expression. Luciferase assays confirmed that miR-148a could directly bind to the site of 3′untranslated region of ErbB3. 3. Silencing of ErbB3 with RNA interference inhibited the growth of pancreatic cancer cells in vitro. this website While the inhibition

of miR-148a slightly better than direct interference with siRNA in pancreatic cancer cell lines. Conclusion: In conclusion, miR-148a can inhibit cell proliferation and migration by targeting ErbB3. Our present results implicate the potential effects of miR-148a on treatment of pancreatic cancer. Key Word(s): 1. pancreatic cancer; 2. miR-148a; 3. ErbB3; Presenting Author: LIU PI Additional Authors: XIA LIANG, ZHANGWEI LONG, KEHUA JING, SU TAO, CHENYOU -XIANG, LUNONG HUA Corresponding Author: LIU PI Affiliations: Nanchang University Objective: To identify serum miRNAs differentially expressed in acute pancreatitis and evaluate their diagnostic potentials in disease detection and severity prediction. Methods: We first compared the serum miRNA expression profiles between 12 acute pancreatitis patients with various disease severities and three healthy controls. Differentially expressed serum miRNAs were identified and then validated in a larger cohort of patients and controls.

Methods: 1. We measured the expession of miR-148a using the technology of real-time qRT-PCR in pancreatic cancer cell lines PANC-1 and BXPC-3. After over-expressing miR-148a of the cells, MTT assays were used to determine the proliferation of the cancer cells, and migration assays were done using a modified transwell chamber system. 2. The putative downstream target gene of miR148a was found through bio-informatics analysis. Both panceratic cancer cell lines were transfected with the ErbB3 3′-UTR reporter plasmid. Then the activity of renilla and firefly luciferase

was assessed using the ABT-737 dual-luciferase reporter assay system, Taqman PCR assay was used to assess miR-148a expression. The expression of ErbB3 was detected using western blot analysis. 3. Both panceratic cancer cell lines were transfected with ErbB3 RNAi by using Lipofectamine2000.

The proliferation and migration of the cells were oberserved, and the results were compared with those of over-expressing miR-148a. Results:  1. MiR-148a was significantly downregulated in both cell lines, and the expression of miR-148a was correlated with the degree of malignancy. Functional studies indicated overexpression of miR-148a dramatically inhibits proliferation click here and migration of pancreatic cancer cells. 2. Bio-informatic studies revealed that ErbB3 might be the direct target gene of miR-148a. Overexpression of miR-148a in pancreatic cancer cells could reduce the mRNA and protein levels of ErbB3, whereas miR-148a silencing significantly increased ErbB3 expression. Luciferase assays confirmed that miR-148a could directly bind to the site of 3′untranslated region of ErbB3. 3. Silencing of ErbB3 with RNA interference inhibited the growth of pancreatic cancer cells in vitro. selleck chemicals While the inhibition

of miR-148a slightly better than direct interference with siRNA in pancreatic cancer cell lines. Conclusion: In conclusion, miR-148a can inhibit cell proliferation and migration by targeting ErbB3. Our present results implicate the potential effects of miR-148a on treatment of pancreatic cancer. Key Word(s): 1. pancreatic cancer; 2. miR-148a; 3. ErbB3; Presenting Author: LIU PI Additional Authors: XIA LIANG, ZHANGWEI LONG, KEHUA JING, SU TAO, CHENYOU -XIANG, LUNONG HUA Corresponding Author: LIU PI Affiliations: Nanchang University Objective: To identify serum miRNAs differentially expressed in acute pancreatitis and evaluate their diagnostic potentials in disease detection and severity prediction. Methods: We first compared the serum miRNA expression profiles between 12 acute pancreatitis patients with various disease severities and three healthy controls. Differentially expressed serum miRNAs were identified and then validated in a larger cohort of patients and controls.