23 Therefore, we next compared the transcriptional levels of miR-492 with that of KRT19 and its pseudogene. Upon PLAG1 knockdown, a strong decrease in miR-492 levels was not associated with changes in transcriptional activity of KRT19 (Fig. 1). However, miR-492 induction by PLAG1 overexpression resulted in a moderate induction of KRT19 in HepT1, but not in HUH6 cell clones. Interestingly, PLAG1 modulation was accompanied

by a strong anticorrelation between miR-492 expression and the pseudogene of KRT19. In order to identify BAY 73-4506 nmr the regulatory network and putative direct targets of miR-492 we generated clones that stably express the precursor of miR-492 (pMif-miR-492) and a control vector (pMif-control) in the HUH6 and HepT1 cell lines. pMif-miR-492 clones of both cell lines exhibited enhanced miR-492 expression levels compared to control clones (Fig. 3A) up to 15-fold in HepT1 and up to 4.4-fold in HUH6. Whole genome expression analysis identified 194 genes with significant (adjusted P-value ≤ 0.05) differential expression (Supporting Table 2). Because overexpression of miR-492 must be expected to repress the mRNA targets that are regulated by direct binding interaction of the miR sequence, we prioritized genes being strongly down-regulated and predicted by at least one target prediction program as potential IWR-1 mouse direct targets for quantitative confirmation (Fig. 3B). Significant

down-regulation was confirmed for HSD3B1 (3 beta-hydroxysteroid dehydrogenase), the transcription factor TCF21, the liver-related enzymes ST6GAL1 (ST6 beta-galactosamide alpha-2,6-sialyltranferase 1), BAAT (bile acid coenzyme A: amino acid N-acyltransferase), and GDA (guanine deaminase), the tumor suppressor gene CDKN2A (cyclin-dependent kinase inhibitor 2A), the liver protein ALB (albumin), as well as the proapoptotic gene BID (BH3 interacting domain death agonist) at least in one HB cell line (Fig.

3B). However, Endonuclease NINJ2 (ninjurin 2) expression could not be confirmed to be down-regulated in both miR-492 overexpressing cell lines. Furthermore, we confirmed a strong suppressing effect of miR-492 on the liver tumor-related genes AFP and CASP4 (caspase-4). These genes, however, are not direct targets of miR-492. Annotation and enrichment analyses of functional categories revealed that miR-492 up-regulated genes were most significantly enriched in gene clusters involved in developmental processes, anatomical structure development, and cell communication, whereas suppressed genes were most significantly overrepresented in the functional clusters of metal binding, extracellular space occurrence, and developmental processes (Supporting Table 3). Taken together, these data point to an important influence of miR-492 on a range of genes that are involved in liver metabolism and extracellular structures.

Owing to the greater availability of livestock, particularly cattle, in the peripheral areas as compared with resident livestock, a clear-cut difference in lion diet was evident within and outside protected area. Within the protected area also, including the NP which is located within the Gir PA (Fig. 1), livestock formed a significant Fulvestrant clinical trial part of lion’s diet. Livestock constituted 47% of lion diet within the Gir PA while in the peripheral areas, livestock constituted 76% of the 42 kills. Compensation claim records

of the Forest department also indicated that average livestock loss to predation per month within protected area to be 45 and outside protected area to be 89 (Pathak et al., 2002). Livestock remains were found in 21% of 29 kills collected from NP, 43% of 117 kills of SW and 69% of 32 kills outside protected area (Chellam, 1993). Livestock owners residing within 5 km of Gir PA do not have clear-cut grazing rights and therefore benefit less from proximity to the forest. Yet, more livestock predation occurs outside the protected area because of greater availability of livestock, low density of wild prey (mostly nilgai), and increased lion movement (Soni,

2000; Pathak et al., 2002; Meena, 2010). Thus, focal areas https://www.selleckchem.com/products/ly2835219.html of interventions have to be outside the protected area. Abundance, size and temporal and spatial distribution of prey influence hunting strategy, activity and daily movement of lions (Schaller, 1972; Eloff, 1973; Stander, 1991; Patterson et al., 2004). Gir has high biomass of resident wild prey available throughout the year in addition to availability of relatively more vulnerable domestic livestock prey base. Felids require large prey and African lions Panthera leo leo preferentially prey upon species of an average weight of 350 kg, range 190–550 kg (Hayward & Kerley, 2005). Our study also indicates greater consumption of large-sized prey in adult age class (Fig. 2). Although, incidental observations of kills tend to be biased

towards large bodied prey because of easier detectibility, our kill data represented by SPTLC1 62% large bodied wild prey are yet comparable to findings from scat analysis. Monitoring lions with the help of radio-telemetry confirmed that 80% of kills (n=10) were of adult prey. Overall, in terms of relative number of individuals consumed, domestic prey occurred in low proportions (20%) yet in terms of biomass contribution, they accounted for 36% (Table 1). In the wild, lions have to hunt to meet their daily requirement of 5–7 kg (Schaller, 1972). In captivity, Asiatic lions (average body mass 100 kg) consume 6% of their total body mass as buffalo meat in a day (Mukherjee & Goyal, 2004) while in the wild, they consume 7–10% of their body weight (Mukherjee & Goyal, 2004).

Therefore, we conducted a prospective cohort study in a clinical setting to assess bleeding risk attributable to gastric biopsy in patients taking antiplatelet agents and the validity of performing endoscopic biopsy with small cup biopsy forceps. Methods: The study was performed during

the 1-year for 5374 scheduled esophagogastroduodenoscopy performed. 1128 patients, Idasanutlin manufacturer including 65 patients taking antiplatelet agents underwent gastric biopsy with small cup biopsy forceps, and 2025 biopsy specimens were obtained from each part of the stomach. Clinical bleeding was investigated during and after endoscopy. Two pathologists assessed the presence of muscularis mucosae in biopsy specimens in addition to the suitability of specimens for histological diagnosis. Results: Ratio of appropriate

specimens obtained with small cup biopsy forceps was 99.3% (2010/2025) and muscularis mucosae was detected ERK inhibitor in 27.8% (538/1394) of specimens. After endoscopy, 1 patient of 1049 patients who took no antithrombotic agents experienced major bleeding (0.095%); however, 65 patients receiving antiplatelet treatment experienced no bleeding. Conclusion: Endoscopic forceps with a small cup is useful and the absolute risk attributable to gastric biopsy in patients taking antiplatelet agents seems to be low. Key Word(s): 1. endoscopic biopsy; 2. antiplatelet agent; 3. bleeding; 4. biopsy forceps; 5. antithrombotic agent Presenting Author: KUNIO IWATSUKA Additional Authors: TAKUJI GOTODA, SHIN KONO, SHO SUZUKI, NAOKO YAGI, CHIKA KUSANO, MASAKATSU FUKUZAWA, TAKASHI KAWAI, FUMINORI MORIYASU Corresponding Author: KUNIO IWATSUKA Affiliations:

Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University, Tokyo Medical University Hospital, Tokyo Medical University Objective: Despite improvements in pharmacological Tenofovir price and endoscopic hemostasis, gastrointestinal bleeding (GIB) remains fatal clinical event in the elderly patients. With increasing numbers of the elderly population, endoscopists might face such kind of serious cases. The aims of this study are to research treatment outcomes and clinical features of GIB in elderly patients. Methods: Medical records of 185 patients (mean age 68.2 years, range 10–99 years, male/female 123/62) with GIB who underwent esophagogastroduodenoscopy or colonoscopy from April 2012 to March 2014 were reviewed. Clinical outcomes and clinicopathological features including pre-existing co-morbidities, prescribed drugs (antiplatelet agent, anticoagulant, NSAIDs, corticosteroid) were compared between younger <70 years old) and elderly groups (≤70 years old). Results: Following features were specifically found in elderly patients (N = 100) compared to non-elderly patients (N = 85): presence of co-morbid diseases (90.0% vs. 62.4%: p < 0.001), low hemoglobin level (9.0 vs. 10.6 g/dl: p < 0.

Methods: A retrospective histological evaluation of 75 patients with AIH was performed to define emperipolesis and related histological features. Confocal staining of cellular markers of immune cellls (CD4, CD8, CD19, CD56, CD163, and CD11b), hepatocytes (CK8/18) and Caspase 3 was performed to illustrate the cellular types of

emperipolesis. Caspase 3 was added into confocal staining to show the consequence of cell-in-cell structure. Results: Emperipolesis was observed in 57.3% (43/75) of the patients with autoimmune hepatitis in H&E staining, which was significantly higher than in the patients with primary biliary cirrhosis (18.9%), chronic hepatitis B (19.6%) and drug-induced liver injury (25.6%). Among AIH patients, the patients with emperipolesis had significantly higher serum ALT/AST levels than those without it. In histology, the existence of emperipolesis was associated Proteases inhibitor with more severe inflammatory and necrotic features and more advanced fibrosis stages. The immune cells inside hepatocytes were identified as CD8 T cells in the process of emperipolesis in patients with autoimmune hepatitis.

Emperipolesis of CD8 T cells induced Caspase 3 expression of infiltrated hepatocytes. Conclusion: Emperipolesis is a relatively specific histological feature of autoimmune hepatitis. Apoptosis of hepatocytes infiltrated by CD8 T cells may reflect another mechanism of immune-mediated liver injury in autoimmune hepatitis. Key Word(s): 1. Autoimmune hepatitis; 2. histology; 3. cell-in-cell; 4. entosis; Presenting Author: PEI WANG Additional Authors: XIAOLI PAN, JIN YE Corresponding Author: PEI WANG Affiliations: Objective: To determine the prevalence PD0325901 order Metalloexopeptidase and the clinical, serological, and histological characters of IgG4-associated

AIH. Methods: According to the liver biopsy, the clinical features and laboratory findings of 14 patients with AIH, 12 patients with AIH-PBC overlap syndrome, 9 patients with primary biliary cirrhosis (PBC) and 9 chronic hepatitis patients with hepatitis B virus (HBV) infection were retrospectively analyzed in our hospital among 2007 and 2012. Liver biopsy tissues from these patients were stained by hematoxylin-eosin to evaluate the histological features, and by immunohistochemistry to mark the IgG4 positive plasma cells. Results: Three of the 14 liver specimens from patients with AIH and one of the 12 liver specimens from patients with AIH-PBC overlap syndrome showed positive staining for IgG4, whereas none of the samples from patients with PBC and patients with HBV hepatitis was positive. The IgG4-associated AIH patients had significantly higher total serum IgG levels and AIH scores as compared with the IgG4 Conclusion: IgG4-associated AIH was found in over 21.4% of Chinese patients with type 1 AIH in our cohort. AIH may be classified into either an IgG4-associated type or an IgG4 non-associated type, which is useful for guiding the clinical practice. Key Word(s): 1. Autoimmune hepatitis; 2.

6C). The liver is a major organ for HGF synthesis, but the decrease in the mature form of HGF in the hepsin−/− mice was not caused by decreased synthesis of pro-HGF, because western blotting analysis of liver lysates revealed that there was no significant difference in the level of pro-HGF in WT and hepsin−/− mice (Fig. 6D). Hepsin−/− mouse livers may therefore be defective in converting pro-HGF produced in the liver into mature HGF that is released into the serum after processing; such a decreased level of mature HGF would be expected to cause diminished

HGF signal transduction in the livers of hepsin−/− mice. Correspondingly, see more we observed that the level of c-Met phosphorylation (HGF activation site, residues Y1234 and Y1235, in the tyrosine kinase domain) was significantly decreased in hepsin−/− livers, as compared to WT livers, whereas the total c-Met level appeared unchanged (Fig. 6E). Furthermore, when both WT

and hepsin−/− mice were treated with an antibody against hepsin, only WT mice exhibited a decrease in HGF and phosphorylated c-Met (Supporting Fig. 17). All of these results indicate that the c-Met-signaling pathway was down-regulated in the hepsin−/− mouse liver because of the defect in pro-HGF Selleckchem R428 activation in the liver. It has been shown that HGF down-regulates the level of connexin expression in vitro.23 In addition, we observed increased connexin expression and decreased HGF/c-Met signaling in hepsin−/− mouse livers. Therefore, we hypothesized that

the decreased HGF level in hepsin−/− mice caused an increase in both the expression of connexins and hepatocyte size in the liver. To test this, we first analyzed the level of connexin expression in WT and hepsin−/− mouse livers treated with HGF or an antagonist of the HGF receptor, NK4. HGF treatment decreased the expression of connexins in hepsin−/− mice (Fig. 7A), whereas NK4 increased the expression of connexins in WT mice (Fig. 7B). Consistently, hepsin−/− mice had significantly enlarged liver sinusoids after HGF treatment (Fig. 8A), and WT mice had significantly narrowed liver sinusoids after NK4 treatment Erastin (Fig. 8B). A dose-dependent increase in the level of phosphorylated c-Met was also detected after HGF treatment (Supporting Fig. 18). Overall, these results suggest that hepsin regulates the liver architecture through the HGF/c-Met/connexin-signaling axis. The identification of novel phenotypes in our hepsin−/− mice establishes a strong connection in vivo between hepsin and the maintenance of liver architecture. We propose that hepsin deficiency reduces HGF maturation and downstream c-Met phosphorylation that is required for expressing proper levels of connexins, which are, in turn, critical for the maintenance of normal hepatocyte size and, ultimately, normal sinusoidal diameter (Supporting Fig. 19).

61], P = .68). AZD5363 mw These findings are consistent with glutamatergic differences in migraine patients during the interictal period compared with healthy controls. We hypothesize that an increased Glu/Gln ratio could arise from neuronal–glial coupling of glutamatergic metabolism differences or an increased neuron/astrocyte

ratio in the OC. “
“(Headache 2012;52:785-791) Background.— Although both pharmacological and behavioral interventions may relieve tension-type headache, data are lacking regarding treatment preference, long-term patient compliance, and feasibility of behavioral intervention in a standard neurological outpatient clinic setting. Objective.— To describe patient choice, long-term compliance, and clinical outcome in a neurological clinic setting where patients are given the choice of the approach they wish to pursue. Design.— Patients presenting to the headache clinic with a diagnosis of tension-type headache that justified prophylactic therapy (frequent episodic tension-type headache or chronic tension-type headache) were given the choice of amitriptyline (AMT) treatment or hypnotic relaxation (HR), and

were treated accordingly. Patients were given the option click here to cross-over to the other treatment group at each visit. HR was performed during standard length neurology clinic appointments by a neurologist trained to perform hypnosis (Y.E.). Follow-up interviews were performed between 6 and 12 months following treatment initiation to evaluate patient compliance, changes in headache frequency or severity, and quality-of-life parameters. Results.— Ninety-eight patients were enrolled, 92 agreed to receive prophylactic therapy of some kind. Fifty-three (57.6%) patients chose HR of which 36 (67.9%) actually initiated this treatment, while 39 (42.4%) chose pharmacological therapy with AMT of which 25 (64.1%) patients actually initiated therapy. Patients with greater analgesic use were more likely to opt for AMT (P = .0002). Eleven of the patients initially choosing

AMT and 2 of the patients initially choosing HR crossed over to the other group. Seventy-four percent of the patients in the HR group and 58% of patients in the AMT group had a 50% SPTLC1 reduction in the frequency of headaches (P = .16). Long-term adherence to treatment with HR exceeded that of AMT. At the end of the study period, 26 of 47 patients who tried HR compared with 10 of 27 who tried AMT continued receiving their initial treatment. Conclusions.— HR treatment was a more popular choice among patients. Patients choosing HR reported greater symptom relief than those choosing AMT and were found to have greater treatment compliance. Patients receiving HR were less likely to change treatments. HR practiced by a neurologist is feasible in a standard neurological outpatient clinic setting; HR training should be considered for neurologists involved in headache treatment.

Purity of OC and hepatocyte fractions was determined by morphology analysis, histologic analysis of hematoxylin and eosin (H&E)-stained cytospins and expression analysis by quantitative polymerase chain reaction (qPCR). All images were acquired on a Leica DMLB microscope and processed using Photoshop CS5 (Adobe, Munich, Germany). Error bars represent standard deviation (SD) except where indicated. Pairwise comparisons between continuous data were done using unpaired two-tailed Student t test. AGEs advanced glycation

endproducts ALT alanine aminotransferase AST aspartate transaminase BMOL bipotential murine oval liver CDE choline deficient ethionine-supplemented diet CML N-carboxymethyllysine DEN diethylnitrosamine dKO Mdr2−/− Nutlin3a Rage−/− HCC hepatocellular carcinoma HMGB1 high mobility learn more group box 1 Mdr2 multidrug resistance protein 2 OC oval cells RAGE receptor for advanced glycation endproducts sRAGE soluble RAGE To define the role of RAGE in inflammation-driven tumor development, we crossed Rage−/− mice with the Mdr2−/− mouse strain.23, 25 Mdr2−/− Rage−/− double knockout (dKO) mice were viable and produced offspring in a Mendelian ratio. At 15 months of age, control, Rage,−/− Mdr2−/−, and dKO mice (n = 10 for each group) were sacrificed and livers were subjected to histological analysis. Control and Rage−/− livers

did not present any focal lesion, while Mdr2−/− mice had enlarged livers that developed multiple HCCs and dysplastic nodules (Fig.

1A, and data not shown). Pathological grading of tumors from Mdr2−/− mice ranged from well differentiated (G1), moderately (G2), up to poorly differentiated (G3), according to the Armed Forces Institute of Pathology grading system. In contrast, dKO mice developed mainly dysplastic nodules (Fig. Sinomenine 1A,B) and only two dKO mice exhibited a single HCC classified as moderately differentiated (G2). Interestingly, while the percentage of mice without any detectable lesion was comparable between Mdr2−/− (28%) and dKO (30%) mice, most Mdr2−/− mice (61%) developed HCCs, whereas the majority of dKO mice (50%) exhibited only premalignant dysplastic nodules (Fig. 1B). In particular, dKO mice showed fewer and smaller liver lesions that did not exceed 12 mm in diameter, whereas lesions in Mdr2−/− mice were bigger in size (up to 20 mm in diameter) and in number (Fig. 1C). Furthermore, dKO mice showed significantly less multifocal tumorigenesis compared to Mdr2−/− mice (Fig. 1D). In contrast, when mice were treated with DEN, which is an alkylating agent causing DNA strand breaks promoting mutations and subsequent HCC formation in a cirrhosis-free manner,28–30 we could not detect any significant difference in tumor number, size, and multiplicity between wildtype (WT) and Rage−/− mice at 12 months after injection (Supporting Fig. 1).

Recommendations Treatment is indicated in patients with chronic hepatitis with ALT levels ≥31 U/L and HBV DNA levels ≥4 log copies/mL, regardless of HBeAg status. Even in those cases not meeting the above criteria, if ALT

levels rise slowly or intermittently, or the patient is aged ≥40 with a high HBV DNA levels, platelet count <150 000 /μl and/or family history of HCC, or if advanced fibrosis is suspected by imaging studies, the risk of hepatocarcinogenesis is high and liver biopsy (or noninvasive alternative) should be performed as an optional investigation to determine the extent of fibrosis. Even in patients meeting the definition of an inactive carrier, the combination of positive HBV DNA and Etoposide advanced fibrosis suggests a high risk of hepatocarcinogenesis, and treatment is indicated. The criteria for treatment of chronic hepatitis – ALT and HBV DNA levels – are also considered in patients with cirrhosis. However, more aggressive

Selumetinib therapeutic intervention is normally required and the treatment indications are different, since the risk of progression to hepatic failure and HCC is increased in cirrhotic patients. As Table 8 shows, treatment is indicated in cirrhosis patients with detectable HBV DNA irrespective of HBeAg status, ALT levels or HBV DNA levels, whereas if HBV DNA is below the detectable threshold antiviral treatment is not indicated. Recommendation Treatment is indicated in patients with liver cirrhosis with detectable HBV DNA, regardless of HBeAg status Methocarbamol and ALT or HBV DNA levels. Certain patients on a monitoring regimen with no treatment may yet be at high risk of hepatocarcinogenesis and should be placed under HCC surveillance with regular imaging, particularly those with contributing factors such as age ≥40, male, alcohol consumption, high HBV load, family history of HCC, simultaneous infection with HCV/HDV/HIV, advanced liver fibrosis, low platelet count associated with advanced fibrosis, genotype C, and core promoter mutation. In patients with chronic hepatitis

who become HBsAg negative and anti- HBs antibody positive, if cirrhosis was already present prior to elimination of HBsAg there is a high risk of hepatocarcinogenesis.[46-52] It is important to be aware of the ongoing risk of HCC even where cccDNA has been eliminated, due to HBV genome recombination.[53-55] Recommendations Patients under a monitoring regimen who are at a high risk of hepatocarcinogenesis should be placed under HCC surveillance with regular imaging. It is important to be aware of the risk of HCC in cases of chronic hepatitis in whom HBsAg has disappeared. HBV markers are an indispensable tool for the evaluation of acute hepatitis, chronic hepatitis and cirrhosis caused by HBV.

To create our estimates, we modeled the annual disease burden of HEV genotypes 1 and 2 for 9 of 21 regions defined for the Global Burden of Diseases, Injuries, and Risk Factors Study (the GBD 2010 Study), which represent XL765 71% of the world’s population. We estimated the seroprevalence of anti-HEV antibody and annual incidence of infection for each region using data from 37 published national studies and the DISMOD 3, a generic disease model designed for the GBD Study. We converted incident infections into three mutually exclusive results of infection: (1) asymptomatic episodes, (2) symptomatic disease, and (3) death from HEV.

We also estimated incremental cases of stillbirths among infected pregnant women. For 2005, we estimated 20.1 (95% credible interval [Cr.I.]: 2.8-37.0) million incident HEV infections across the nine GBD Regions, resulting in 3.4 (95% Cr.I.: 0.5-6.5) million symptomatic cases, 70,000 (95% Cr.I.: 12,400-132,732) deaths, and 3,000 (95% Cr.I.: 1,892-4,424) stillbirths. We estimated a probability of symptomatic illness given infection of 0.198 (95% Cr.I.: 0.167-0.229) and a probability of death given symptomatic illness of 0.019 (95% selleck screening library Cr.I.: 0.017-0.021) for nonpregnant

cases and 0.198 (95% Cr.I.: 0.169-0.227) for pregnant cases. Conclusion: The model was most sensitive to estimates of age-specific incidence of HEV disease. (HEPATOLOGY 2012) The hepatitis E virus (HEV) is an enterically transmitted RNA virus that can cause outbreaks or sporadic disease.1 HEV was first postulated as a unique infectious agent following a large outbreak of hepatitis in Kashmir in 1978, and was first isolated in the stool of Soviet military recruits stationed in Afghanistan in 1983.2, 3 HEV outbreaks Olopatadine are thought to result primarily from contamination of water supplies, although some evidence exists for person-to-person transmission.4 The prevalence of HEV infection varies genotypically by global region. HEV has one serotype and four reported

genotypes. Genotypes 1 and 2 exclusively infect humans and are often associated with large outbreaks and epidemics in developing countries with poor sanitation conditions. Genotypes 3 and 4 infect humans, pigs, and other animal species and have been responsible for sporadic cases of disease in developed and developing countries.5 Although genotype 3 has been reported to cause chronic hepatitis in persons with chronic liver disease, those infected with human immunodeficiency virus (HIV), or organ transplant recipients, the extent to which genotype 3 and 4 infections result in disease in otherwise healthy patients is unknown and warrants further investigation.6-11 Like hepatitis A virus infection, only a portion of those infected with HEV develop symptoms and the risk of symptomatic illness may depend on age of infection.

Addition of the third method – HME-NBI can increase specificity on 45.95%. Combination of AFI with NBI-HME known as trimodal endoscopy may increase detection rate of early cancer lesions. Key Word(s): 1. autofluorecence; 2. gastric cancer; 3. endoscopy; 4. chromoendoscopy; Presenting Author: JIPENG YIN Additional Authors: XIAOLI HUI, LIPING YAO, MING LI, HAO HU, JING ZHANG, JING Alvelestat price WANG, YONGZHAN NIE, KAICHUN WU Corresponding

Author: JIPENG YIN Affiliations: Xijing Hospital of Digestive Disease; First Affiliated Hospital; Department of Nuclear Medicine, Xijing Hospital Objective: Polymer peptide-based tumor angiogenesis imaging has proven to be a promising method for anticipating tumors and evaluating vascular targeted therapies. The phage display peptide

CGNSNPKSC (GX1) has been confirmed to target the tumor vasculature endothelial cells in previous studies. In the present study, GX1 was PEGylated and labeled with 99mTcO4-. The potential potency of labeled PEGylated GX1 as a radiotracer for SPECT imaging of gastric cancer click here vasculature was evaluated in a SGC 7901 tumor xenografted mouse model. Methods: PEG-(GX1)2 was synthesized and labeled with the radioactive isotope 99mTc. The binding affinity of the 99mTc-PEG-(GX1)2 peptide was evaluated using radioligand binding and receptor competitive inhibition assays. The targeting ability of the peptide was evaluated using SPECT imaging and biodistribution in the nude mice model bearing SGC 7901 tumor Morin Hydrate xenografts. Immunofluorescence staining was used to locate PEG-(GX1)2 in gastric cancer. Results: 99mTc-PEG-(GX1)2 was found to have high labeling efficiency and high in vitro stability. Immunofluorescence staining, the in vitro receptor competitive binding inhibition assay and the multidrop saturating receptor binding assay demonstrated that PEG-(GX1)2 and 99mTc-PEG-(GX1)2

bound specifically to Co-HUVEC with a high affinity. SPECT imaging and biodistribution results showed that 99mTc-PEG-(GX1)2 targeted the tumor tissue with higher radioactivity accumulation than did 99mTc-GX1. Conclusion: PEG-(GX1)2 displayed higher affinity and targeting ability than did GX1. 99mTc-PEG-(GX1)2 is a promising radiotracer for tumor angiogenesis imaging and internal radiotherapy of gastric cancer. Key Word(s): 1. Molecular imaging; 2. PEGylation; 3. Angiogenesis; 4. Tumor targeting; Presenting Author: NAOKI OKANO Additional Authors: YOSHINORI IGARASHI, ITARU KAMATA, TAKAHIKO MIMURA, YUI KISHIMOTO, KEN ITO, TOMIHIRO MIURA, YASUKIYO SUMINO Corresponding Author: NAOKI OKANO Affiliations: Toho University Omori Medical Center Objective: Recently endoscopic snare papillectomy has been performed to treat ampullary tumors. However there is no obvious evidence for its indication. We evaluated preoperative diagnosis and outcome of endoscopic snare papillectomy for ampullary tumors.