Tb was administered to a sub-group of alcohol-fed animals by oral gavage (2g/kg) for 5 days/week for 4 weeks to assess its effects. Serum and liver tissue samples were analyzed for endo-toxemia, hepatic steatosis, inflammation and injury. Results: Tb attenuated the ethanol-induced gut barrier dysfunction,

as shown by the significant reduction in endotoxemia. Histological analysis by H&E staining and choline esterase (CAE) staining showed a significant decrease in ethanol-induced hepatic steatosis and neutrophil accumulation in Tb-treated animals. Moreover, Tb administration attenuated the ethanol induced hepatic expression of the critical inflammatory cytokine, TNFα. Tb also prevented the ethanol-induced down-regulation of CPT1 α, a key enzyme in free fatty acid β-oxidation, with a resultant decrease in hepatic PI3K inhibitor triglycerides. Finally, Tb also significantly attenuated liver injury as seen by a decrease in ALT levels. Conclusion: The present work demonstrates that Tb may be useful in preventing the ethanol-induced alterations in the gut microbiome and barrier function, and may prove to be a useful therapy for the prevention/treatment

of ALD. Disclosures: Craig J. McClain – Consulting: Vertex, Gilead, Baxter, Celgene, Nestle, Danisco, Abbott, Genentech; Grant/Research Support: Ocera, Merck, Glaxo SmithKline; Speaking and Teaching: Roche Shirish Barve – Speaking and Teaching: Abbott The following people have nothing to disclose: Hridgandh Donde, Jingwen Zhang, Smita Ghare, Leila Gobejishvili, Swati Joshi-Barve, Vatsalya Vatsalya

Protease Inhibitor Library high throughput GNA12 Background and aim: Excessive accumulation of triglycer-ide-containing lipid droplets (LDs) within hepatocytes in NAFLD patients is a potentially reversible process, although sustained activation of inflammatory signaling pathways leads to non-alcoholic steatohepatitis (NASH) that can eventually evolve into cirrhosis and HCC. Here we investigated the role of a new EZH2-phosphoSTAT3-miRNAs pathway in the induction of vescicular steatosis and intracellular inflammation in an in vitro cellular model. Methods: DMSO-differentiated human non-transformed hepatocytic HepaRG cells treated with oleic acid were used as a cellular model for the induction of vescicolar steatosis. Results: dHepaRG cells treated with oleic acid show: a) an increased lipid accumulation and intracellular reactive oxygen species (ROS) generation as compared to control cells; b) deregulated lipid metabolism and liver-specific genes, including PDK4, PLIN4, SLC2A1, ALB and ALDOB; c) the activation of an intracellular inflammatory response, as demonstrated by the upregulation of IL6, IL8, OAS1, NFKB and phosphoSTAT3 levels. Oleate treatment also increased the mRNA and protein levels of the EZH2 (Enhancer of Zeste Homolog 2) histone methyl-transferase, the active subunit of the PRC2 transcription repressor complex that catalyzes histone 3 lysine 27 tri-meth-ylation (H3K27me3).

Conclusion: It is critical for the rehabilitation of patients with mild acute pancreatitis to observe and analyze

the causes of serum amylase unfalling and learn more take effective measures to deal with. Key Word(s): 1. acute pancreatitis; 2. serum amylase; 3. analysis; 4. treatment; Presenting Author: CHENWEN JING Additional Authors: TANGGUO DU Corresponding Author: TANGGUO DU Affiliations: guangxi medical university Objective: To investigate the relationship between AOPP and severity of AP by detecting serum levels of AOPP in patients with AP, combination the results of serum interleukin -6(IL-6), indicators which associated with disease severity and clinical datas. Methods: Fifty-eight patients who were diagnosed acute pancreatitis in our hospital from November 2010 to September 2012 were collected[18 cases with severe acute pancreatitis (SAP) and

40 cases with mild acute pancreatitis (MAP)]. Serum levels of AOPP and IL-6 were dectected by enzymelinked immunosorbent assay (ELISA) within 24 hours. Blood samples were sent to the laboratory to dectect blood routine, liver function, renal function, blood calcium, blood glucose and actate dehydrogenase. APACHE II scores, Ranson scores, CTSI scores, BISAP scores and Glasgow scores were also determined. Results: ① Serum levels of WBC, GLU, LDH in SAP group were higher than MAP group (P < 0.05). ALB and MAPK inhibitor blood calcium in SAP group was lower than MAP group (P < 0.05). ② Serum levels of BUN, Cr, blood amylase were no significant difference between SAP Ibrutinib mouse group and MAP group (P > 0.05). ③ In SAP group and MAP group, APACHE II scores were (5.00 ± 3.67) and (3.39 ± 2.91), Ranson scores were (2.04 ± 1.46) and (1.33 ± 1.21), CTSI scores were (5.87 ± 1.46) and (1.20 ± 1.26), BISAP scores were (1.52 ± 0.80) and (0.86 ± 0.76), Glasgow scores were (2.61 ± 1.20) and (1.24 ± 1.12), respectively, and SAP group was higher than MAP group (P < 0.05). ④ Serum levels of AOPP in

SAP group and MAP group were (38.1156 ± 11.67)ng/ml and (29.40 ± 14.19)ng/ml, respectively, and SAP group was higher than MAP group (P < 0.05). Serum levels of IL-6 in SAP group and MAP group were (211.01 ± 107.98)pg/ml and (129.72 ± 56.53)pg/ml, respectively, and SAP group was higher than MAP group (P < 0.05). ⑤ There are relations between AOPP and WBC, GLU (P < 0.05), but no relations with LDH, blood calcium, ALB, BUN, Cr and blood amylase (P > 0.05). Conclusion: Serum levels of AOPP may be associated with the severity of AP; AOPP may be associated with the process of inflammatory response in the occurrence and development of AP; AOPP and indicators which associated with disease severity may be used as markers to estimate the severity in AP. Key Word(s): 1. acute pancreatitis; 2. AOPP; 3.

Louis, MO) to 1–15 μmol/L. HCC cell viability was determined at 72 hours after addition of 1–15 μmol/L sorafenib or DMSO by WST-8 assay using cell count reagent sulforaphane (Nacalai Tesque, Kyoto, Japan) as previously described.20 The small interfering RNA (siRNA) method was used

to knockdown ADAM9 as previously described.20 At 24 hours after transfection, the cells were analyzed for specific depletion of the messenger RNA (mRNA) of ADAM9 by real-time reverse transcription polymerase chain reaction (RT-PCR) according to the manufacturer’s instructions (Applied Biosystems, Foster City, Panobinostat in vivo CA). The following siRNAs were used: ADAM9, 5′-UGUCCAAACACAUUAAUCCCGCCUG-3′; scramble control, 5′-UGUCGCACAAACACUUAACUCCCUG-3′. HCC cells were cultured with tumor necrosis factor-α protease inhibitor-I (TAPI-I, 50 μmol/L; Calbiochem, San Diego, CA) or sorafenib (1 μmol/mL) for 24 hours and the supernatants were harvested. The supernatants of cultured HCC cells were harvested at 24 hours after transfection with siRNA. The levels of soluble MICA were determined by DuoSet MICA enzyme-linked immunosorbent assay (ELISA) kit (R&D Systems, Minneapolis, MN). For the detection HDAC inhibitor of membrane-bound MICA, cells were incubated with anti-MICA antibody (Ab) (Santa Cruz Biotechnology, Santa Cruz, CA) and stained with phycoerythrin-goat anti-mouse

immunoglobulin (Ig) (Beckman Coulter, Fullerton, CA) as a secondary reagent and then subjected to flow cytometric analysis using a FACScan flow cytometer (Becton Dickinson, San Jose, CA). Total RNA was isolated using the RNeasy Mini Kit (Qiagen K.K., Tokyo, Japan), and was reverse transcribed using SuperScript III First-Strand Synthesis System (Invitrogen, Carlsbad, CA). The mRNA levels were evaluated using ABI-Prism 7900 Sequence Detection System (Applied Biosystems). Ready-to-use assays (Applied Biosystems)

were used for the quantification of ADAM9 (Hs00177638_m1), and β-actin (Hs99999903_m1) mRNAs according to the manufacturer’s instructions. β-Actin mRNA from each sample was quantified as an endogenous control of internal RNA. Peptides of 20 amino acid residues buy Staurosporine partially overlapping each other, covering the α3 domain to the C-terminal end of MICA were synthesized by Sigma. Each peptide substrate (30 μM) was incubated with 50 nM of recombinant ADAM9 in a buffer containing 10 mM HEPES (pH 7.2) and 0.0015% Brij (Sigma). After digestion, the samples were passed over a C18 media (ZipTipC18; Millipore, Billerica, MA), eluted with acetonitrile, and analyzed by matrix-assisted laser desorption/ionization–time of flight/mass spectrometry (MALDI-TOF/MS) to determine the masses of the products and thereby the cleavage site recognized by ADAM9. An expression vector of MICA, pcDNA-MICA, was constructed by using specific complementary DNA (cDNA) from the human hepatoma-derived cell line, Huh-7, as described.

COMP-positive cirrhotic patients are see more at an increased risk of progressing

to more severe disease outcome. Serum COMP is a new promising, non-invasive biomarker for risk-assessment and surveillance of patients with chronic liver diseases at risk to develop HCC. Disclosures: Gary L. Norman – Employment: INOVA Diagnostics Zakera Shums – Employment: INOVA DIAGNOSTICS The following people have nothing to disclose: Nikolaos Gatselis, Christos Liaskos, Dimitrios P. Bogdanos, George K. Koukoulis, George N. Dalekos Background The number of non-B or non-C hepatocellular carcinoma (NBNC-HCC) including alcoholic liver diseases, non-alcoholic steatohepatitis (NASH) and cryptogenic has been increasing gradually all over the world. Although inflammation and oxidative stress are suggested to participate to their pathogenesis, clinical characteristics of NBNC-HCC are not fully examined compared with hepatitis virus-related HCC. Recently, advanced glycation end products (AGEs) are known to cause oxidative stress and inflammatory reactions, and play a role in the pathogenesis of a variety of disorders such as

diabetic vascular complications, alcoholic liver injury, and NASH. On the other hand, pigment epithelium derived factor (PEDF) that belongs to the superfamily of serine protease inhibitors has been shown to have anti-oxidative and anti-inflammatory properties that acts restrainingly for AGEs. In the present study, we examined whether serum levels of AGEs and PEDF were elevated in patients with HCC derived learn more from NASH (NASH-HCC) compared with NASH subjects without HCC and further investigated clinical variables to explore the clinical usefulness of AGEs and PEDF as markers of NASH-HCC. Methods Patients with 11 treatment-naïve NASH-HCC and

56 biopsyproven NASH were enrolled. Serum levels of AGEs and PEDF were measured by using the competitive ELISA method. Also, clinical and pathological findings (inflammation, fibrosis) were compared between both groups. Results Type2 diabetes mellitus (DM) was complicated Amobarbital in 64% and 79%, and liver cirrhosis in 27% and 0% in NASH-HCC and NASH without HCC, respectively. NASH-HCC were older in age, and showed significantly advanced fibrosis stage compared with NASH without HCC. Serum levels of AGEs and PEDF in NBNC-HCC were significantly higher than those in NASH without HCC (9.1 vs 5.2 U/ml and 12.8 vs 10.7 μg/ml, respectively, p<0.001, p<0.05). By multivariate analysis, fasting plasma glucose (FPG) and HbA1c were significantly associated with AGEs in NASH without HCC (p<0.05). Matched for age, fibrosis stage, FPG, and HbA1c, AGEs were elevated in NASH-HCC (9.7 vs 5.3 U/ml, p<0.001). By multivariate analysis, gender (p=0.05), homeostasis model assessment-insulin resistance (HOMA-IR) (p=0.07), and the presence of DM (p=0.11) tended to be associated with PEDF in NASH without HCC. Matched for age, gender, fibrosis stage, HOMA-IR, and the presence of DM, PEDF were elevated in NASH-HCC (14.5 vs 10.

Statistical analysis indicated that the difference is significant (P<0.01).The animal experiments showed that tumors were formed in abdominal cavity in 70% mice of the FATE/BJ-HCC-2 gene-transfected group, but only in 10% mice of mock control group. Furthermore we also find tumor formation in livers of mice of the FATE/BJ-HCC-2 gene-transfected group with naked eyes and under light microscope. There was no tumor cell growth in liver of the mice of mock control group. Conclusion: FATE/BJ-HCC-2 could induce differential expression of a group of genes in tumor cells. It enhances invasion function of tumor cells. Tumor cells with FATE/BJ-HCC-2 expression are easier to form

tumors and tumor’s metastasis. This suggests that FATE/BJ-HCC-2 may be an important factor to promote metastasis of tumor cells. Disclosures: this website The following

people have nothing to disclose: Xiaoang Yang, Lili Ge, Junyan Piao, Yanhui Yin, Yu Zhang Background: Semaphorin7a (sema7a) is a membrane-anchored protein involved in neuronal and immune function regulating axonal growth, immune and inflammatory response. Recent evidences have confirmed an effect of sema7a on the regulation of bleomycin-induced pulmonary fibrosis. Our group have shown the involvement of sema7a in liver fibrogenesis, but no information are currently available on hepatocarcinogene-sis. Aims: to evaluate whether SEMA7A regulate HCC development. Methods: Liver injury was

induced in vivo by diethylnitrosamine (DEN) i.p. injection (25 mg/Kg) in 15 days old wild type and SEMA7A KO mice. Kupffer cells, hepatic stellate cells (HSCs) and hepatocytes GDC0068 were isolated with a nyco-denz-based gradient method from mice livers. Recombinant protein for SEMA7A was used for in vitro experiments in primary hepatocytes and human HepG2 cells. Results: In vivo, mice treated with DEN developed HCC formation after Gefitinib concentration 6 month from the treatment. The number of tumor nodules were significantly lower in SEMA7A KO mice than in WT mice, with an average of 8,2 macroscopic nodules in WT and 3,4 in the SEMA7A KO mice. Morevoer the average of the tumour size was 4.5 mm in WT vs 2 mm in SEMA7A KO. In vitro, we observed an increased expression of SEMA7A mRNA in hepatic stellate cells and in Kupffer cells isolated from fibrotic mouse livers, while a low expression was observed in hepatocytes. Hepatocytes do express one of the main receptor of sema7a: plexin C1, demonstrated by RT PCR. Moreover, primary hepatocytes from WT mice and human HepG2 cells, incubated with sema7a recombinant protein (1nM), show an increase in Ki67 mRNA, PCNA protein expression and a modification in the mRNA levels of carcinogenetic markers: 2.1 folds reduction and 4,1 fold increase respectively in PTEN and osteopontin mRNA expression vs untreated cells. Conclusions: SEMA7A is expressed in the liver and plays a crucial role in the development of HCC.

There is no evidence for a dominant driver mechanism and resulting addiction to it, as can be observed in several childhood malignancies and gastrointestinal stromal tumor. Finally, comprehensive analyses have started and are likely to provide molecular subgrouping of HCC. Initial attempts have been made (e.g., by J. Zucman-Rossi and her group), clearly demonstrating the feasibility of the approach.26 Improvement can be expected from further meta-analyses of existing data and novel comprehensive analyses on well-characterized collectives. There is significant evidence that molecular classification reflects functional aspects

and correlates with prognosis. At least some of the subgroups are CH5424802 datasheet likely to be relevant for therapy and predictive diagnostics, as exemplified by IGF-IR26,35 and mTOR-associated signaling.87 What are the consequences for drug development, clinical trials, and molecular (predictive) diagnostics?1, 88 There is certainly sufficient room and need for further (pathway) targeted approaches. Constitutive activation, for example,

by mutation or ligand based stimulation of growth factor signaling pathways, is a common theme most likely relevant in every case of HCC.74 On the other side, many different pathways can be affected, and their functional consequences in regard to proliferation, motility, antiapoptosis, and angiogenesis significantly overlap. Thus, response to specific tyrosine kinase–directed approaches may be limited and can be expected only in subgroups of HCCs, and secondary resistance is likely to occur this website soon, because

there is little if any evidence for a specific pathway addiction in HCC. From a mechanistic point of view, approaches to inhibit tyrosine kinase/growth factor signaling pathways should be as broad as possible and should consider complementary PLEKHB2 and combinatorial settings up front. Identification of patients who may benefit (more) from these approaches requires comprehensive biomarker analyses accompanying the clinical trails. This is state-of-the-art in most other malignancies, but has not been thoroughly respected in HCC, probably due to the fact that HCC is the only relevant tumor entity that does not necessarily require tissue-based diagnosis prior to therapy. Because molecular definition of responsive subgroups is not possible without tissue access, this difference may cause more trial failures than expected or necessary and may turn out to be a negative aspect of HCC in comparison with other tumor entities. The fact that protumorigenic alterations in relevant pathways in HCCs may occur at different (nodal) points may limit the application of specific inhibitors and has to be respected in predictive diagnostic approaches as well as drug and subsequent trial design.88 A question that must always be addressed is the size of the responsive patient collective and whether it justifies the clinical and commercial effort.

278, 95%CI 1.002–1.629). There was no

significance finding between the selected 8 tag-SNPs and UC. Conclusion: For the first time, our results revealed that polymorphisms of IL-33 had an effect on the development of some extra-intestinal manifestation and clinical phenotypes of CD in Chinese population, which further confirmed a critical role of IL-33 in the pathogenesis of IBD. Key Word(s): 1. IL-33; 2. IBD; 3. SNP; 4. clinical phenotypes; Presenting Author: TAKESHI SATO Additional Authors: EIKI NOMURA, YU SASAKI, NANA KANNO, MAKOTO YAGI, KAZUYA YOSHIZAWA, DAISUKE IWANO, YASUHIKO ABE, SYOICHI NISHISE, YOSHIYUKI UENO Corresponding Author: TAKESHI SATO Affiliations: Yamagata University, faculty of medicine, department of gastroenterology

Objective: In Japan, Infliximab Nutlin-3a ic50 (IFX) was adopted middle to severe ulcerative colitis that indicated adequate effect by selleck chemicals llc current treatment in 2012. We have begun to apply IFX for Ulcerative colitis from July, 2010. We reported our experience of IFX, and its effectiveness. Methods: In our hospital, IFX is applied to severe and intractable case of steroid resistance, and steroid dependent. Patients intake diphenhydramine 10 mg, and injected hydrocortisone sodium succinate before intravenous drip injection IFX 5 mg/kg. Participants in this study were Dimethyl sulfoxide eleven cases of ulcerative colitis induced IFX in our hospital

from 2010 to 2012. We defined effectiveness of IFX by Clinical activity index (CAI). Remission was that CAI decreased lower than 4, improve was that CAI was lower than 10 and decrease over three points from started injection. Results: Mean age of participants was 37 years old, male were six cases, and mean disease time was 9.5 years. Pan colitis were nine cases (82%), left side colitis were two cases. All were middle ulcerative colitis. Steroid resistance ware three cases and steroid dependent were seven cases. All cases take 5-aminosalicylic acid, ten cases treated with steroid, and two cases use immunomodulatory drugs. The effective cases divided into three types of after response. (1) maintenance effectiveness, (2) attenuated effectiveness (couldn’t keep effectiveness for eight weeks), (3) lose effectiveness. Steroid required again or to increase dose in two cases, in type (1). Finally they were stopped steroid. Three cases were attenuated effectiveness, two of three were shortened injection period of IFX, but had no adequate result in type (2). Lose effectiveness cases mostly became clear at fourteen to twenty two weeks. Conclusion: In this study, we reported our experience of IFX, and its effectiveness to ulcerative colitis. We want to evaluate with more cases to superior treatment. Key Word(s): 1. ulcerative colitis; 2.

, unpublished results), and in previous studies10, 22 indicate the relevance of this strategy to hereditary liver disease in general. We thank Rina Wichers and Gözde Isik for assistance. Additional Supporting Information may be found in the online version of this article. “
“Epidemiological data associate coffee consumption with a lower prevalence of chronic liver disease and a reduced risk of elevated liver enzyme levels (γ glutamyl transpeptidase and alanine aminotransferase), advanced liver disease and its complications, and hepatocellular carcinoma. Knowledge of the mechanisms MG132 underlying these

effects and the coffee components responsible for these properties is still lacking. In this study, 1.5 mL/day of decaffeinated coffee or its polyphenols or melanoidins (corresponding to approximately 2 cups of filtered coffee or 6 cups of espresso coffee for a 70-kg person) were added for 8 weeks to the drinking water of rats who were being fed a high-fat, high-calorie solid diet (HFD) for the previous 4 weeks. At week 12, HFD + water

rats showed a clinical picture typical of advanced nonalcoholic steatohepatitis compared with control rats (normal diet + water). In comparison, HFD + coffee rats showed: (1) reduced hepatic fat and collagen, as well as reduced serum alanine aminotransferase and triglycerides; (2) a two-fold reduced/oxidized glutathione ratio in both serum and liver; (3) reduced serum malondialdehyde (lipid peroxidation) and increased selleck ferric reducing antioxidant power (reducing activity); (4) reduced expression of tumor necrosis factor α (TNF-α), tissue transglutaminase, and transforming growth factor β and increased expression before of adiponectin receptor and peroxisome proliferator-activated receptor α in liver tissue; and (5) reduced hepatic concentrations of proinflammatory TNF-α and interferon-γ and increased anti-inflammatory interleukin-4 and interleukin-10.

Conclusion: Our data demonstrate that coffee consumption protects the liver from damage caused by a high-fat diet. This effect was mediated by a reduction in hepatic fat accumulation (through increased fatty acid β-oxidation); systemic and liver oxidative stress (through the glutathione system); liver inflammation (through modulation of genes); and expression and concentrations of proteins and cytokines related to inflammation. (HEPATOLOGY 2010;52:1652-1661) Nonalcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of the metabolic syndrome and is associated with its clinical features, including visceral obesity, dislipidemia, and type 2 diabetes.1 NAFLD has high prevalence in the general population, and it can evolve into nonalcoholic steatohepatitis (NASH), cirrhosis, and complications such as liver failure and hepatocellular carcinoma.

An Egy-Score of 3.67 or more was superior to APRI, FIB-4 and Forns’ index for detecting cirrhosis with a sensitivity of 82% and specificity of 87%. Forns’ index was superior to Egy-Score, FIB-4 and APRI for detecting significant fibrosis. The Egy-Score is a promising, accurate, easily calculated, cost-effective score in the prediction of hepatic

fibrosis in chronic HCV patients with superiority over APRI, FIB-4 and Forns’ index in advanced hepatic fibrosis and cirrhosis. “
“Background and Aim:  To estimate the sero-prevalence of Helicobacter Pylori infection in the Australian adult population and identify determinants. Methods:  We analyzed serum samples and questionnaire data Silmitasertib mw from 1355 community controls who participated in a nationwide case-control study of esophageal cancer in Australia between 2002 and 2005. We estimated the prevalence ratio and 95% confidence interval using log binomial regression models. Results:  The age and sex standardized sero-prevalence of H. pylori was 15.5%. The prevalence of infection varied significantly with age, ranging from 5% selleck products (< 40 years) to 32% (≥ 70 years). H. pylori infection was significantly higher among those born overseas (prevalence ratio [PR] 1.63; 95% confidence interval [CI] 1.34–1.98) compared with those born in Australia or New Zealand. H. pylori sero-prevalence

was 23% higher among participants living in the lowest quartile of socio-economic areas (PR 0.77; 95%CI 0.59–0.99 for Q4 compared with Q1). H pylori serostatus was

significantly inversely associated with university education (PR 0.56; 95%CI 0.38–0.83), frequent reflux symptoms (PR 0.62; 95%CI 0.42–0.91), use of proton pump inhibitor (PR 0.69; 95%CI 0.48–0.98) and use of medications for gut spasms (PR 0.48; 95%CI 0.25–0.93). H. pylori serostatus was not associated Phosphatidylinositol diacylglycerol-lyase with body mass index, smoking, alcohol or physical activity. Conclusions:  The prevalence of H. pylori infection in Australian adults is lower than other developed countries. H. pylori infection is most common among those living in the areas of socio-economic disadvantage or who were born overseas. “
“AASLD/ASGE Endoscopy Course Friday, November 1 7:55 AM – 3:00 PM Room 146A Endoscopy in Patients with Hepatobiliary Disorders: Evolving Concepts, Technologies and Techniques COURSE DIRECTORS: Subhas Banerjee, MD Barham K. Abu Dayyeh, MD 6.5 CME Credits The overall goal of this activity is to educate the target audience in state-of-the-art best practices pertaining to diagnostic and therapeutic endoscopy in patients with hepatobiliary disease. This should result in a significant improvement in their understanding of the relative benefits and risks of these modalities, in optimizing patient selection for different endoscopic interventions and in the performance of these endoscopic interventions.

6 cases of anastomotic stenosis distal PSV was significantly increased (PSV: 250 ± 102 cm/s), P < 0.01, Hepatic artery left tributary speed increased in some cases, mainly for the envelope is not see more smooth, the resistance index (RI) reduce (RI < 0.5), P < 0.01. Two false-positive cases mainly for lower RI < 0.5, The reason is moderate aortic stenosis after further examination; one missed cases without clear images of anastomotic, the left branch of the hepatic artery RI is normal, after further examination, we found the moderate aortic regurgitation caused sonographer

miscarriage of justice. Conclusion: Hepatic Hemodynamic checks help to find early hepatic artery complications after liver transplantation, but there are still some deficiencies, especially extrahepatic factors interfereing with the hemodynamic

parameters should caught clinicians attention. Key Word(s): 1. liver transplantation; 2. anastomotic stenosis; 3. hemodynamic; 4. resistance index; Presenting Author: YANG BAI Additional Authors: YINGQIAO ZHU, YANYAN FAN Corresponding Author: YINGQIAO ZHU Affiliations: 1st Hospital of Jilin University, 1st Hospital of Jilin University Objective: To investigate the value of contrast-enhanced ultrasound for mesenteric artery stenosis Methods: 68 cases suspected of superior mesenteric artery stenosis by color Doppler sonography underwent CEUS examination, all the patients underwent CT angiography (CTA) examination or digital subtraction angiography (DSA), as a reference 3-deazaneplanocin A in vivo standards. Under supine resting state, ID-8 on the right elbow shallow intravenous bolus injection of ultrasound contrast agent (SonoVue) 1.5 ml, Siemens s2000, 4s-1 probe, scan mode at angiography, recording the whole process of enhanced and playback analysis arterial contrast agent arrival time, the superior mesenteric contrast agent filling process. Diameter stenosis is defined as: mild stenosis <50%; moderate stenosis of 50% to 75%; severe stenosis >75%. Moderate and severe stenosis is defined

as a clinically significant stenosis of the superior mesenteric artery. Results: CTA or DSA diagnose 52 cases of clinically significant stenosis. CEUS diagnose clinically significant stenosis 51 cases (17 cases with severe stenosis, moderate stenosis 34 cases), color Doppler ultrasound diagnosis of mesenteric artery stenosis diagnostic specificity and accuracy were 100%, 98.1%, respectively. CEUS diagnostic specificity and accuracy of arterial stenosis of the superior mesenteric artery were 75.0% and 75,0%, respectively. Conclusion: CEUS is a non-invasive, accurate method to diagnose superior mesenteric artery stenosis, which provides important reference information for clinical treatment. Key Word(s): 1. CEUS; 2. superior mesenteric artery; 3.