Thus, the identification of NAFLD in a child should prompt consideration of cardiovascular health. Therapeutic goals for NAFLD should include GDC-0941 purchase not only the prevention of endstage liver disease but also the prevention of cardiovascular disease and diabetes. We thank Professor John Frederick Osborn from Department of Public Health Sciences, Sapienza University of

Rome, for critical review of the article and for statistical support. “
“The association between functional dyspepsia (FD) and sleep disorders has yet to be studied in detail. The aim of this study is to evaluate the risk factors associated with sleep disorders and the clinical response to nizatidine therapy for sleep disorders in Rome III-based FD patients. We enrolled 94 FD patients and 52 healthy volunteers. We used Rome III criteria to evaluate upper abdominal symptoms, and the Self-Rating Questionnaire for Depression scores to determine depression selleck chemical status. Sleep disorder was evaluated using Pittsburgh Sleep Quality Index (PSQI) scores, and degree of anxiety by the State-Trait Anxiety Inventory. Gastric motility was evaluated. Thirty-four FD patients were treated with nizatidine (300 mg/day) or placebo for 4 weeks in a crossover trial. The primary end point of this study was to determine whether nizatidine could improve clinical

symptoms and sleep disorders in FD patients. The global PSQI score for FD patients was significantly (P < 0.001) higher compared with healthy volunteers. There were significant correlations between

global PSQI scores and total Gastrointestinal Symptom Rating Scale and Self-Rating Questionnaire for Depression scores (P < 0.001, P < 0.0001, respectively) in FD patients than in healthy volunteers. We found significant relationships between subjective sleep quality and both Tmax and T1/2 values in FD patients. Nizatidine significantly improved certain clinical symptoms, gastric emptying, and global PSQI score compared with placebo treatment. Sleep disorders in FD patients correlated significantly Y-27632 2HCl with both clinical symptoms of dyspepsia and depression compared with healthy volunteers. Nizatidine significantly improved gastroesophageal reflux symptoms, gastric emptying, and sleep disorders in FD patients. “
“Understanding patterns of abnormal liver tests can aid in the diagnosis of many causes of liver disease. Serologic liver tests are broadly divided into those that evaluate liver function (prothrombin time, bilirubin, albumin), those that evaluate integrity of hepatocytes (aspartate aminotransferase or AST, alanine aminotransferase or ALT) and those that assess abnormalities of bile ducts and bile flow (bilirubin, alkaline phosphatase or AP, gamma glutamyl transpeptidase or GGT). Patterns of abnormal liver tests include hepatocellular (AST and ALT elevation), cholestatic (bilirubin, AP, GGT) and mixed elevations.

15 The redundancy of these mechanisms in regulating TGF-β signaling underscores the necessity and importance of this pathway in hepatocellular oncogenesis. The tumor necrosis factor (TNF) super family (TNFSF) of cytokines consists of 29 members. In addition to the well-documented pleiotropic roles of TNF-α in the liver, lymphotoxin (LT)α,

along with LTβ and Light (TNFSF 14) have been implicated as drivers of hepatic stellate cell function/wound selleck kinase inhibitor healing,16 liver regeneration,17 and hepatic carcinogenesis.18 These findings have evoked renewed interest in targeting LTβR in an attempt to thwart hepatocellular oncogenesis. Recent work from Haybaeck et al.18 has provided compelling evidence that inflammation resulting from LTαβ signaling is sufficient to drive HCC in the liver-specific AlbLTαβ murine model. Moreover, the authors detail the increase in messenger RNA (mRNA) levels of LTβR ligands in liver samples derived from patients infected with HBV or HCV, as well as samples from patients with HCC, strengthening selleck products the link

between LT signaling and HCC. Although additional studies are needed to confirm the pivotal role of the LTβR in HCC, strategies designed to block signaling by way of LTβR might be beneficial. Activation of individual oncogenes modeling premalignant initiation elicits distinct protective programs including senescence and apoptosis. These processes are dependent on both cell-autonomous and cell-extrinsic mechanisms that function in concert to suppress and/or eliminate cells undergoing oncogenic stress. Senescent cells display characteristic secretomes that commonly include IL-6 and IL-8 to maintain the senescent state and promote immune surveillance of senescent cells. In liver, (oncogene-induced) senescent hepatocytes also secrete CTACK, IL-1α, leptin/leptin R, MCP1, and RANTES.19 Noninitiated bystander cells including immune cells

can reinforce this program by also secreting prosenescent cytokines. Apoptotic hepatocytes also release IL-1α, which triggers KCs to orchestrate compensatory proliferation, essential to development of HCC in the diethylnitrosamine (DEN) model.20 Senescence, unlike apoptosis, does not result in cell elimination. Instead, cells that undergo oncogene-induced senescence constitute a quiescent population of initiated premalignancies. Metabolism inhibitor The presence of these senescent cells provides the opportunity for escape or progression to malignancy through accumulated “second hits.” Interestingly, a recent report described an in vivo example of immune-surveillance of such oncogene-induced senescent cells.19 Kang et al.19 demonstrated NrasG12V oncogene-induced senescence in liver by examining senescence marker expression in oncogenic-NrasG12V transposon- and inactivated-Ras (effector loop signaling domain deletion) transposon-transduced livers. Oncogenic NrasG12V induced markers of senescence by 12 days, but by 60 days NrasG12V-expressing cells were undetectable.

Level C (possibly effective, ineffective, or harmful) rating requires at least 2 convincing class III studies. Adapted with permission from Brainin et al. Guidance for the preparation of neurological management guidelines by EFNS scientific task forces—revised recommendations 2004. Eur J Neurol 2004;11:577-581. “
“Migraine is a common primary headache disorder occurring predominantly in a young,

relatively healthy population. There is a growing literature on associations between migraine, especially migraine with aura, and ischemic stroke as well as other vascular events. buy NVP-BGJ398 Migraine as a risk factor for vascular disease and connections between migraine and endothelial, structural, and genetic risk are reviewed. There may be an interaction between endothelial dysfunction and cortical spreading depression affecting risk. Patient education and treatment of modifiable risk factors may decrease future vascular events. “
“(Headache 2011;51:860-868) Migraine is a common, often disabling disorder associated with a significant personal and societal burden. The presence of post-traumatic stress disorder (PTSD) may increase this disability substantially. Migraine and PTSD are both up to 3 times more common in women than in men. The divergence in prevalence rates of migraine and PTSD that occurs between the sexes after puberty suggests that gonadal hormones play an important role. In addition,

the preponderance of PTSD Pexidartinib cost in women may be related to their higher rates of interpersonal trauma, the most common cause of PTSD. However, recent data suggest that although the odds of PTSD are increased in both women and men with episodic migraine, Nabilone this association is stronger in men than women. In this paper, we examine the epidemiology of PTSD and migraine, with an emphasis on the known sex differences. We then discuss the neurobiological changes associated with PTSD, the current hypotheses for the mechanisms relating PTSD and migraine, and the treatment

implications of these findings. “
“Background.— In the absence of biological markers, the diagnosis of primary headache in epidemiological studies rests on clinical findings, as reported through ad-hoc interviews. Objectives.— The aim of this study was to validate a specially designed headache questionnaire to be administered by a physician for the diagnosis of primary headaches or of probable medication overuse headache in the general population according to the 2004 International Classification of Headache Disorders, 2nd edition (ICHD-II). Methods.— The questionnaire comprises 76 questions based on the ICHD-II diagnostic criteria for migraine (codes 1.1, 1.2.1, 1.2.2, 1.2.3, 1.5.1, and 1.6), tension-type headache (codes 2.1, 2.2, 2.3, and 2.4), primary stabbing headache (code 4.1), and probable medication-overuse headache (code 8.2.

Any use of the program content, which includes, but is not limited to oral presentations, audiovisual materials used by speakers, and program handouts, without the written consent of AASLD is prohibited. The CME/CE evaluations are electronic and can be completed using the following options: Upon download, use the meeting app to evaluate the sessions in real-time Using your personal device, link to the CME and/or CE evaluation on The Liver Meeting® website Visit Tech Connect to access the evaluation from any available kiosk CME and CE credit will be awarded upon completion of the electronic evaluation. You will have the ability to download and/or

print a certificate for your records once you have completed the CME and/or CE evaluations. Certificates of Attendance find more are also available. Certificates may be downloaded and/or printed upon completion of The Liver Meeting® evaluation. A follow-up survey

selleck chemical will be sent to all attendees within three months of the conclusion of the meeting to assess the new skills and competencies learned as a result of participating in this live activity. May 16 – 19 Walter E. Washington Convention Center Washington, DC June 27 – 28 The Westin Chicago River North Chicago, Illinois Spring 2015 Location TBD November 13 – 17 Moscone West Convention Center San Francisco, California Managing Liver Disease – From the Clinic to the Community November 14 Moscone West Convention Center San Francisco, California Meeting-at-a-Glance

2A General Meeting Information 5A Limited License 7A Disclosure Index 8A Oral Sessions   Friday, November 7 32A Saturday, November 8 39A Sunday, November 9 43A Monday, November 10 65A Tuesday, November 11 85A Poster Sessions   Saturday, November 8 92A Sunday, November 9 119A Monday, November 10 146A Tuesday, November 11 169A Abstracts 197A Author Index 1206A Category Index 1256A selleckchem The Scientific Program Committee has created an exciting and diverse scientific program that highlights new technology, current clinical issues and hot topics facing the hepatology community. Members include: Adrian M. Di Bisceglie, MD, FACP, Co-Chair Gary L. Davis, MD, Co-Chair Carla W. Brady, MD Kenneth D. Chavin, MD, PhD Mark J. Czaja, MD Marc G. Ghany, MD Saul J. Karpen, MD, PhD Keith D. Lindor, MD Gyongyi Szabo, MD, PhD Rebecca T. Wells, MD “
“We congratulate Berzigotti et al.1 for performing an excellent study that raises more questions, just as many post hoc analyses of observational studies do. It is intriguing that obesity may predict future decompensation in patients with compensated cirrhosis and portal hypertension. The potential mechanism is unexplained. The presence of a proinflammatory and proangiogenic state driven by extrahepatic adipose tissue may accelerate existing liver disease. Furthermore, hemodynamic changes linked to metabolic syndrome may affect the development of portal hypertension.

TZD have been recently shown to activate AMPK, a cellular sensor of energy CDK inhibitor status.37 AMPK may suppress tumorigenesis regulating cell growth via inhibition of mammalian target of rapamycin (mTOR) signaling and p53 activation, and it is indicated as a beneficial target for cancer treatment.38 We showed that TZD induced AMPK activation in PPARγ-deficient hepatocytes and that inhibition of AMPK activity completely prevented the TZD-induced growth arrest and NPM expression. These results are in agreement with the observation that TZD specifically inhibit IGF-I tumor-promoting activity

in mouse skin through activation of AMPK and subsequent inhibition of mTOR pathway.20 In addition, AMPK activation was demonstrated to induce p53 phosphorylation and p53-dependent apoptotic cell death in response to energetic stress.39 Although there is no evidence for a direct involvement of NPM in the regulation of the apoptotic machinery, NPM might function as an antiapoptotic protein through indirect mechanisms. Interaction with p53 might be an important step by which NPM inhibits programmed cell death. In fact, NPM overexpression protects mouse embryonic fibroblast against hypoxic cell death, but this effect is not observed in cell that lacks p53.40 We showed that in cultured PPARγ-deficient hepatocytes, ectopic expression of wild-type NPM significantly blocked TZD inhibition whereas

a mutant click here variant lacking the p53-interacting domain did not prevent TZD antiproliferative and proapoptotic actions. Similarly, in malignant haematopoietic cells, the same NPM mutant does not prevent apoptosis in response to stress stimuli, unlike the overexpression of wild-type NPM.41 NPM-p53 interaction inhibits p53 phosphorylation at the serine 15, and subsequently represses p53 target genes expression such as the cell cycle inhibitor p21. However, in hepatic cells TZD may promote p53 phosphorylation by inhibiting NPM gene expression. Interestingly, NPM has also been shown to interact with p53 in hypoxic cells and to inhibit hypoxia-induced p53 phosphorylation on the same residue.42 Besides, regulation N-acetylglucosamine-1-phosphate transferase of p53 expression and activity by TZD has been

also demonstrated in human cholangiocarcinoma cells.43 In consideration that the ability of AMPK to induce cell cycle arrest is dependent on p53 phosphorylation at Ser15,39 it might be conceivable that TZD modify p53 phosphorylation status and activity by an AMPK-mediated down-regulation of NPM. In conclusion, we have shown that chronic administration of TZD inhibits hepatic tumor formation in mice with a PPARγ-independent mechanism. Furthermore, we found that the anticancer activity of these drugs in the liver was mediated, at least in part, by inhibition of NPM expression and p53 activation. Collectively, these observations provide new insight into the molecular mechanisms of hepatic carcinogenesis and emphasize relevant clinical implication.

The issue on the natural history of gastroesophageal reflux disease (GERD) is controversial. One pathogenesis model emphasizes the potential progression of GERD over time, other state demonstrated Dabrafenib cell line a very limited movement in between the 3 phenotypic presentations of GERD (Hershcovici

T., 2010, Malfertheiner P., 2012). Aim. To study the frequency of transformation of non-erosive reflux disease (NERD), erosive esophagitis and Barrett’s esophagus (BE) in elderly patients based on the results of five-year prospective study. Methods: We performed a prospective five-year observation of 891 elderly GERD patients (569 females, 322 males, median age 78,1 years). GERD was diagnosed on the basis of the Montreal Consensus (Vakil N et al., 2006). The Ku0059436 presence of erosive esophagitis was classified using Los Angeles classification (Lundell LR et al., 1999). During the five-year follow-up clinical examination and endoscopy of the esophagus were performed twice a year. Morphological examinations of the esophagus to determine BE were done in the beginning and the end of study. Results: A five-year prospective study in elderly patients showed an increase in the frequency of erosive esophagitis and BE and reducing of NERD frequency (Table 1). The

main risk factors for progressive course of GERD were obesity (OR = 2,23, CI 1,50–3,29; p < 0,001), hiatal hernia (OR = 5,2, CI 3,2–8,2; p < 0,001) and the lack of maintenance

proton pomp inhibitors therapy (OR = 6,1, CI 4,0–9,2; p < 0,001). Conclusion: The five-year prospective study has demonstrated that GERD is a progressive disease in elderly patients. Key Word(s): 1. GERD; 2. NERD; 3. erosive esophagitis; 4. Barrett's esophagus; Table 1. Five-year dynamics of GERD structure Pathology NERD Erosive esophagitis BE Abs. % Abs. % Abs. % Beginning of the study 472 52,9 357 40,1 61 7,0 In 5 years 335 37,6 471 52,9 85 9,5 OR; Cl; p 1,87; 1,56–2,26; <0,001 0,60; 0,49–0,72; <0,001 0,71; 0,51–1,0; 0,058 Presenting Author: SEOK-MIN PARK Additional Smoothened Authors: BYUNG-WOOK KIM, SEOK-CHEON YEOM, EUN-HEE SHIM, JEE-HEE KIM Corresponding Author: BYUNG-WOOK KIM Affiliations: Incheon St. Mary’s Hospital, The Catholic University of Korea Objective: The lifestyle changes accompanied by economic growth have influenced disease patterns in Korea. The aim of this study was to evaluate the changing patterns of peptic ulcer disease (PUD) over the past two decades in Korea. Methods: Serial multi-center surveys on lifestyles of peptic ulcer patients immediately after esophagogastroduodenoscopy (EGD) were performed in 1988–1989, 1996–1997, and 2011–2012 in 8 institutes affiliated with The Catholic University of Korea (Seoul St. Mary’s Hospital, Yeouido St. Mary’s Hospital, Uijeongbu St. Mary’s Hospital, Bucheon St. Mary’s Hospital, St. Paul’s Hospital, Incheon St.

“
“We read with great interest

the 2009 update of the American Association for the Study of Liver Diseases Practice Guideline.1 Boyer and Haskal did not recommend the prophylactic use of nonabsorbable disaccharides or antibiotics to decrease the episodes of hepatic encephalopathy (HE) in patients with cirrhosis after transjugular intrahepatic portosystemic shunt (TIPS). Probably, the power of abandoning SP600125 in vitro the prophylactic use of this two series of oral drugs in patients after TIPS procedure is not strong enough based on the only research about this subject conducted by Riggio et al.2 The reason is the small sample size (25 per group) which was caused by too high an expected effect (40% versus 10%) of pharmacological treatments in their trial. It is well known that small sample size would lead to a poor representative conclusion easily disturbed

by various errors. In 2009, Sharma et al.3 and Neff et al.4 reported lactulose was effective in preventing recurrence of HE (19.6% versus 46.8%) and rifaximin was effective in reducing the HE-related hospitalizations (16% versus 26%), respectively. The main Cell Cycle inhibitor difference between patients with HE who had or had not undergone TIPS procedure is a newly created shunt which bypasses splanchnic blood from portal vein to systemic circulation in HE patients with TIPS. However, the neurotoxins derived from gut, such as ammonia, affect patients with HE both with and without TIPS

procedure. Nolte et al.5 reported that the HE rate declined to the level before TIPS despite the higher arterial ammonia level beyond 3 months, which was explained tentatively by the adaptability of the brain. Although the HE rate was high after TIPS, only about 5% could not tolerate the shunt, resulting in refractory HE.6 This phenomenon somewhat verified the cerebral adaptability theory. Furthermore, the patients who accepted a TIPS procedure in our center in 2008 demonstrated early HE episode (≤40 days), which could be partially explained by cerebral adaptability as well (Table Molecular motor 1). From our point of view, following the two hypotheses derived from this theory would decrease HE risk after TIPS procedure: 1 Decrease post-TIPS portosystemic gradient step by step. The linchpin for this process is an adjustable stent system of which the radius could be adjusted ad libitum. An adjustable stent system will assist clinicians in achieving an accurate post-TIPS portosystemic gradient, which should be lower than 12 mmHg6 or 25%–50% of the pre-TIPS portosystemic gradient.7 In expectation of this, an adjustable stent system should be designed in the near future.

Discolouration of mango tissues was congruent or just behind the advancing hyphae of C. manginecans. Although there were no significant differences in the rate of internal discolouration in opposite directions from the point of inoculation, severity of wood discolouration was significantly higher above the area of inoculation compared to the area below inoculation. Tissues above and below the inoculation point were also examined microscopically. Tissues of inoculated mango seedlings were darkened, implying excessive production of phenolic compounds

and gums as a defence mechanism following infection. In addition, tyloses and fungal mycelium were observed in the xylem of sections of the inoculated seedlings.

This implies tyloses, mycelium movement in the vascular system and tissue discolouration as INCB024360 mechanisms responsible for wilt and death of infected mango trees. “
“Strains of Pseudomonas syringae are effective in controlling postharvest diseases of citrus fruits, and antagonistic activity has been correlated with in vitro production of lipodepsipeptides. Additionally, biocontrol agents can induce a range of defence mechanisms of resistance in citrus tissue that result in a broad spectrum of metabolic modifications, such as systemic acquired resistance, induced systemic resistance and production of reactive oxygen species. The aim of this study was to Torin 1 cell line evaluate the expression of syringomycin (syrB1) and syringopeptin (sypA) synthetase genes from P. syringae pv. syringae biocontrol strains ID-8 in vitro on different culture media and in vivo on citrus fruits (Citrus sinensis cv. Tarocco) during the interaction with Penicillium digitatum by quantitative RT-PCR. Similarly, gene transcript levels of chitinase (CHI1), allene oxide synthase (AOS), glutathione peroxidase

(GPX1) and phenylalanine ammonia-lyase (PAL1) were measured. SyrB1 and sypA genes were more actively expressed when antagonistic Pseudomonas strains were grown on orange peel broth as compared to NB and PDB. Penicillium digitatum resulted to be strongly stimulatory only to syrB1 expression, thus suggesting that syrB1 gene could be involved in biocontrol activity. QRT-PCR showed that both P. s. pv. syringae and P. digitatum strains increase CHI1 transcription in inoculated flavedo tissues relative to the untreated control. Interestingly, CHI1 transcription was markedly induced by co-inoculation of P. s. pv syringae and P. digitatum strains. Pseudomonas syringae pv. syringae, alone or co-inoculated with P. digitatum, was weakly effective in enhancing GPX1, AOS and PAL1 gene expression, whereas P. digitatum alone strongly enhanced GPX1, AOS and PAL1 expression. Moreover, we assume that CHI1 gene is most likely part of the molecular mechanisms involved in pathogen defence responses in citrus fruit.

“
“We tested how the availability of carbon and nitrogen determines both the production of Asparagopsis taxiformis (Delile) V. Trevis. and content of the two major halocarbons, bromoform and dibromoacetic acid. The halogenated secondary metabolites

of Asparagopsis species selleck products are particularly interesting from an applied perspective due to their remarkable antimicrobial activity. Terrestrial ecologists named the relationship between resources and secondary metabolites as the carbon (C)/nutrient balance (CNB) hypothesis. This relationship was tested both in the laboratory, with a factorial analysis using different concentrations of total ammonia (TAN) and dissolved inorganic carbon (DIC), and in an integrated aquaculture system where TAN and GSK458 nmr DIC fluxes of fish effluent were manipulated.

The total C/N content of A. taxiformis biomass cultivated in laboratory was highly significantly linearly related to the content of both halocarbons, as predicted by the CNB hypothesis. A. taxiformis cultivated at low levels of carbon and high levels of nitrogen (N) (lowest C/N ratio) had the lowest content in both halogenated metabolites. Increased availability of CO2 in the medium resulted in a general higher halocarbon content in the biomass, even though the effect was only statistically significant for bromoform at high levels of N. The farm experiments

supported the results of the laboratory experiments. DIC fluxes had the highest effect on the production of both bromoform and biomass, as shown by multiple regression analysis. In A. taxiformis integrated aquaculture, C, rather than N, is the most important factor affecting the production of biomass and of valuable halocarbon secondary metabolites. “
“The brown algal genus Celecoxib Padina (Dictyotales, Phaeophyceae) is distributed worldwide in tropical and temperate seas. Global species diversity and distribution ranges, however, remain largely unknown. Species-level diversity was reassessed using DNA-based, algorithmic species delineation techniques based on cox3 and rbcL sequence data from 221 specimens collected worldwide. This resulted in estimates ranging from 39 to 61 putative species (ESUs), depending on the technique as well as the locus. We discuss the merits, potential pitfalls, and evolutionary and biogeographic significance of algorithmic species delineation. We unveil patterns whereby ESUs are in all but one case restricted to either the Atlantic or Indo-Pacific Ocean. Within ocean basins we find evidence for the vast majority of ESUs to be confined to a single marine realm. Exceptions, whereby ESUs span up to three realms, are located in the Indo-Pacific Ocean.

To investigate the usefulness of the PQ, we compared the insertion time of the PQ cases with that of the AZ cases. Results: The mean insertion time with the PQ was shorter than that of the AZ (7.20 ± 3.93 minutes vs 9.10 ± 5.60, P < 0.01). If we face a difficult-insertion case, colonoscopy using the PQ should be recommended. We should

perform colonoscopy accurately and also reduce the patient’s burden. Conclusion: The selection of the slimmest caliber colonoscope (PCF-PQ260) may improve the quality of inspection, shortening the insertion time for difficult-insertion cases. Key Word(s): 1. colonoscope; 2. PCF-PQ260; Presenting Author: WEI WEI GAO Additional Authors: KUI JIANG, BANG MAO WANG, DONG BO XU Corresponding Author: WEI

WEI GAO, KUI JIANG Affiliations: Department of Gastroenterology; Department of Pathology Objective: We aim to investigate the value of selleckchem endoscopic ultrasonograghy in the diagnosis selleck screening library and treatment of Gastrointestional Neuroendocrine Neoplasm (GI-NEN). Methods: We retrospectively summarized the clinical data of 44 patients with GI-NEN which were found by endoscopy and confirmed by pathology and immunohistochemisty, and analyzed the EUS features and the Follow-up data of patients who received EUS exam and EUS-assisted endoscopic resection, meanwhile reviewed with related literatures. Results: 47 neoplasms in 44 patients (2 patients

with multiple neoplasms). According to 2010 WHO classification of tumours of the digestive system, 87% (41/47) were Neuroendocrine Tumors (NET) confirmed by histological evaluation, which were polypoid or protruded lesions in endoscopy; 13% (6/47) were Neuroendocrine Carcinoma (NEC), which were ulcerative lesions in endoscopy. The clinical symptoms of patients with GI-NEN were non-specific. All patients with NET received EUS exam and EUS-assisted endoscopic resection. EUS showed that lesions depended from mucosal and submucosal layer were respectively 18 and 23, the diagnosis coincidence rate for lesion layer was 100% compared with pathology, all lesions had regular edges, were hypoechoic, and had homogengous echographic patter. All cases underwent follow-up endoscopy and/or EUS at 3∼6 mo, SPTLC1 12 mo after operation, which showed the wounds healing were well, no residual tumors and recurrence confirmed by histological evaluation. Conclusion: EUS may accurately determine the depended wall layer of GI-NEN lesions, size, edge, echo etc., and provide important information for adapting appropriate treatment strategies in order to insure the safety and completeness of endoscopic resection, has highly clinical practice value in the diagnosis and treatment of GI-NEN. Key Word(s): 1. EUS; 2. GI-NEN; 3. Diagnosis; 4.