Results: LI-cadherin expression was detected in 39 (55.7%) of the 70 primary HCC tissues, and none of the normal tissues. Postivity for LI-cadherin expression was significantly associated with lymph node metastasis (P = 0.044), venous invasion (P = 0.006) and advanced pTNM stage (P = 0.023) Selleck XAV 939 (both p < 0.05), but no significant association was observed with age, sex, tumor grade, or metastasis (all p > 0.05). Conclusion: LI-cadherin expression may be associated with HCC occurrence, tumor invasion, and metastasis.

Future studies should assess the potential of LI-cadherin expression as a diagnostic biomarker or target of molecular therapy for HCC. Key Word(s): 1. glycoproteins;; 2. liver neoplasms;; 3. microchip; Presenting Author: SHANBU XIE Additional Authors: KUNSHU YAO Corresponding Author: KUNSHU YAO Affiliations: Nanchang University; The Ministry of Health Objective: Matrine, one of the main components extracted from Sophora flavescens, has exhibited potent pharmacological find more effects through autophagy against some tumors. However, the underlying mechanism of autophagy induction by matrine is not clear. Methods: The cultured human hepatocellular carcinoma cell line (HepG2) and Redifferentiation of human hepatoma cells (SMMC-7721) were treated with matrine. The p53 signal transduction in autophagy

activation was detected in HepG2 cells. Results: Matrine stimulated autophagy in human hepatoma cells, which is mammalian 上海皓元 Target of Rapamycin (mTOR)-dependent manner in SMMC-7721 cells, but mTOR-independent manner in HepG2 cells. Next, in HepG2 cells, autophagy induction by matrine is regulated by p53 inactivation through AMP-activated protein kinase (AMPK) signaling transduction, then AMPK suppression switches autophagy to apoptosis. Additionally, the p53 protein isoforms-p53β, p53γ, Δ133p53, and Δ133p53γ, due to alternative

splicing of intron 9, are implicated in the p53-mediated autophagy. Conclusion: These results show that matrine induces autophagy in human hepatoma cells with novel mechanism, that is autophagy modulated by p53 and its variants in matrined-treated HCC cells. Thus target of autophagy is the potential of matrine in liver cancer therapy in potentiating tumor cell death. Key Word(s): 1. autophagy; 2. matrine; 3. p53; 4. p53 isoforms; Presenting Author: QIAN SUN Additional Authors: YAN WANG, JING LUO, RONGHUA WANG, BIN CHENG Corresponding Author: BIN CHENG Affiliations: Dept. of Gastroenterology, Tongji Hospital, Huazhong University of Science and Technology Objective: Hepatitis B virus X protein (HBx) plays a crucial role in the development of hepatocellular carcinoma (HCC). Our prior studies suggest that HBx contribute to the proliferation stimulative and apoptosis inhibitory effects on L02 cells. It is well known that tumorigenesis is related to abnormal proliferation promotion caused by cycle disorders and apoptosis inhibition of cells on molecular levels.

ASMase+/+ PMH pre-treated

with U18666A increased lysosomal cholesterol levels, impaired mitophagy (LAMP-GFP/ mtKeima colocalization) and sensitized to APAP-induced cell death. Conversely, 25-HC reversed the lysosomal cholesterol accumulation induced by U18666A, improved mitophagy and protected against APAP-induced cell death. Moreover, 25-HC abolished the susceptibility of ASMase−/− PMH to APAP exposure. Treatment with Ca-074Me to inhibit cathepsin B did not affect APAP susceptibility of ASMase-/- PMH. Conclusions: Our findings selleck chemicals suggest that the underlying status of the pathway leading to mitophagy may be an important risk factor for APAP hepatotoxicity. The findings may have implications for patients with lysosomal storage diseases who may exhibit susceptibility to APAP-induced liver injury. Disclosures: Neil Kaplowitz – Consulting:

GlaxoSmithKline, JNJ, Merck, Novartis, Hepregen, Takeda, Otsuka, Pfizer, Geron, Daiichi-Sanyo; Independent Contractor: Acetaminophen Litigation The following people have nothing to disclose: Anna Baulies, Susana Nuñez, Vicent Ribas, Sandra Torres, Laura Martinez, Carmen Garcia-Ruiz, Jose Fernan-dez-Checa Background/Aims: Concanavalin A (ConA)-induced Pexidartinib ic50 liver injury is an established model of T cell-mediated hepatitis. CD4 T cells, NKT cells and Kupffer cells all were reported to contribute to ConA-induced hepatitis. We and others have shown that hepatic stellate cells (HSCs) play a major role in hepatic inflammation and immune reactions. We recently developed a novel HSC-depleted

mouse, which is resistant to ischemia/ reperfusion- and endotoxin-induced liver injury. Here, we investigated mechanisms of ConA-induced hepatitis in the HSC-depleted mouse. Methods: HSC-depleted and HSC-sufficient mice (n=6 each) were injected 20 mg/kg ConA or vehicle (PBS) (i.v.) and sacrificed 6h later. H/E-stained liver sections were examined for histopathology and serum ALT measured. mRNA expression of IFNp, TNFα, IL10, CXCL1 and CXCL10 was determined via qRT-PCR. In vitro HSCs were incubated in a medium containing 10 μg/ml ConA or vehicle for 4 and 8h and the 上海皓元医药股份有限公司 medium was transferred to hepatocytes. Viability of hepatocytes was examined by phase-contrast microscopy and TUNEL staining. mRNA expression of INFp, IRF1 and CXCL1 was measured in ConA-stimulated HSCs. Generation of reactive oxygen species (ROS) in HSCs and oxidative stress in hepatocytes was determined via DCFDA fluorescence. Results: ConA treatment caused profound liver injury (primarily in zone 2) accompanied by inflammatory infiltration, sinusoidal congestion, and increased expression of IFN, TNFα, CXCL1 and CXCL10, and JNK1-MAPK activation in HSC-sufficient mice but not in HSC-depleted mice. In contrast, IL10 expression increased in ConA-treated HSC-depleted mice but not in HSC-sufficient mice.

Results: We performed a retrospective study of 41 patients and undergoing 65 endoscopic treatment cases of sigmoid colon volvulus between April 2004 and March 2014. We included a total of 41 patients (men 28, women 13) with a mean age of 78.2 years old. The average session of endoscopic intervention was 1.91 ± 1.55 times. The success rate of endoscopic detortion for sigmoid colon volvulus was 80% (52/65). In 13 unsuccessful endoscopic detortion cases, 4 cases were successful endoscopic detortion (repeated), 6 cases were operated on, 3 cases died. Conclusion: Endoscopic

detortion for sigmoid colon volvulus was effective; however, the principal therapy 3-deazaneplanocin A purchase of this condition is surgery. Only occasionally in patients with advanced age, lack of bowel symptoms and multiple co-morbidities might surgical repair not be considered. Key Word(s): 1. colon volvulus Presenting Author: MOTOHIKO HIROSE Additional Authors: HIRANO NAOKI, SATO SHINJI, DOMON KAORU, UMAKOSHI TOMOKO, IGARASHI YOSHINORI Corresponding RXDX-106 nmr Author: MOTOHIKO HIROSE Affiliations: Toho University Omori Medical Center, Toho University

Omori Medical Center, Toho University Omori Medical Center, Toho University Omori Medical Center, Toho University Omori Medical Center Objective: The volvulus of sigmoid colon is well known as a cause of colorectal obstruction. When the volvulus is not treated, it will result to intestinal strangulations and necrosis, perforation and peritonitis. So it requires emergency treatments. The volvulus is found frequently in patients such as bedridden elderly and neurological patients. Thus, it needs no invasive treatments. It is reported that endoscopic treatments for volvulus and surgical excision are effective. Methods: We studied forty-one patients with sigmoid colon volvulus treated endoscopically from April 2004 to March 2014 in our

hospital. Mean average age was 78.2 ± 11.0, male 28 cases and female 13 cases. Recurrence was 6 cases. Results: Endoscopic treatments for the volvulus of sigmoid colon were 65 times, 52 of all cases were succeessful (80.0%). 13 cases were impossible to endoscopic MCE公司 release for volvulus and intestinal necrosis was seen in 7 cases. Emergency surgical operation was performed on 4 cases. Two of 6 cases without intestinal necrosis required no emergency surgical operation. Conclusion: Endoscopic treatments for the volvulus were effective for sigmoid colon. When it is impossible to release of volvulus, we recommend surgical operation. Key Word(s): 1. sigmoid colon volvulus Presenting Author: SUNG PYO HONG Additional Authors: KWANG HYUN KO, WON HEE KIM Corresponding Author: SUNG PYO HONG Affiliations: Cha Bundang Medical Center, Cha Bundang Medical Center Objective: Radiation proctitis is a common complication of radiation to lower abdomen and pelvis. Different modalities of treatment are available; however, the efficacy is incomplete.

Further studies are needed to disclose the detailed mechanism of colorectal carcinogenesis related to 8q24 and diabetes mellitus via diminished expression of IGF2R. We thank Ms. T. Shimooka, Ms. K. Ogata, Ms. M. Kasagi, Ms. Y. Nakagawa, and Ms. T. Kawano for their

technical assistance. This work was supported in part by the following grants and foundations: CREST, Japan Science and Technology Agency (JST); Japan Society for the Promotion of Science (JSPS) Grant-in-Aid for Scientific Research, grant numbers 20390360, 20591547, 20790960, 21591644, 21791295, 21791297, 215921014, and 21679006; the Funding Program for Next Generation World-Leading Researchers (LS094); and NEDO (New Energy and Industrial Technology Development

Organization) Technological Development for Chromosome Analysis. No potential conflict of interest has been declared by the authors. “
“It has been well established selleck chemicals llc that hepatocellular carcinoma (HCC) is one of the most vascular solid tumors, and that angiogenesis plays an important role in both growth and metastasis. It follows find more that angiogenesis could provide a potentially potent therapeutic target for the treatment of HCC. The role of angiogenesis in tumors was first shown over half a century ago.1 Since then, tumor angiogenesis has been intensively studied, and it has become accepted as an important prerequisite for tumor formation in solid malignancies. The growth of a tumor mass requires a sound network of blood vessels that provide oxygen and metabolites, and the angiogenic response

will parallel such growth. Several growth factors are involved in angiogenesis. They include vascular endothelial growth factors (VEGF), angiopoietins, epidermal growth factor medchemexpress (EGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF). Such peptides are released by the neoplastic, hematopoietic, stromal and the endothelial cells. The final status of cancer angiogenesis is determined by the dynamic balance between pro- and anti-angiogenic factors. When the effects of the pro-angiogenic factors are balanced by those of the anti-angiogenic factors, angiogenesis will be switched off, a relative abundance of pro-angiogenic factors will tip the balance in favor of angiogenesis.2,3 Given the characteristically abundant vascularity and production of pro-angiogenic growth factors in HCC, targeting the tumor vasculature is a particularly promising strategy for this most common and highly fatal cancer. Our increased understanding of the balance between angiogenesis and mechanisms of vascular control has led to the development of novel therapeutic agents that influence the process in different ways. For example, work accomplished over the past decade has elucidated the essential role of VEGF in the regulation of biological and pathological angiogenesis.

Materials and Methods:  One hundred AZD4547 twenty nine

helicobacter 16s rRNA gene segments were amplified by PCR and sequenced from ninety-three mammalian, reptilian, avian, or amphibian host species. Prevalence estimates were generated, and univariate logistic regression analyses were used to explore relationships between infection status and the health and characteristics of the 220 individual animals. Results:  One hundred and nineteen novel helicobacter DNA sequences were found. No significant relationship between infection and host health was found; however, multi-infection or infections with particular genotypes were associated with mild clinical signs. Phylogenetic and genetic comparisons of helicobacters suggested prolonged co-adaptation and niche-associated divergence as well as periodic inter-species transmission. Conclusion:  The genus Helicobacter should accordingly be viewed as a collection of hundreds of organisms that have colonized most tetrapod taxa and have the potential to expand into new hosts as contact among animals and between animals and people increases. “
“This review concerned the important pediatric studies published between April 2012 and March 2013. Symptomatology in Helicobacter pylori-positive children is nonspecific,

except for those suffering from peptic ulcer diseases. Investigation of H. pylori status in children and adolescents with sideropenic anemia is recommended, and it is the aim of several studies worldwide. Associations of H. pylori with plasma ghrelin selleck chemicals levels as well as the negative association of H. pylori with atopic disease were interesting objectives for several studies this year. Success rates of sequential therapy tended to be lower in recent studies than in previous trials, which probably reflects the increase in macrolide resistance. A beneficial effect of probiotics was reported although not all trials supported this result in children. Intrafamilial transmission and young age could

be major risk factors associated with reinfection in children. Several studies were performed to identify Helicobacter pylori virulence factors that could be related to the evolution of disease. High positivity of virulence genes was found in dyspeptic or asymptomatic children [1-3]. Acute exposure to VacA MCE initially triggers host autophagy to mitigate the effects of the toxin in epithelial cells. Moreover, chronic exposure leads to the formation of defective autophagosomes. Raju et al. [4] identified a host autophagy gene (ATG16L1), susceptible for H. pylori infection and defined the mechanism by which the autophagy pathway is affected after H. pylori infection. Altman et al. [5] found 11 isolates that expressed type 1 Leb blood-group antigen (22%) among 50 Greek H. pylori isolates from symptomatic children, a feature relatively uncommon in H. pylori isolates from adults.

1). Ceramide is metabolized to sphingosine by ceramidases, which in turn is metabolized by sphingosine kinases to sphingosine-1-phosphate

(S1P). A host of cellular responses have been discovered for these three bioactive sphingolipids (e.g. cell senescence, differentiation, apoptosis and cell cycle arrest for ceramide; apoptosis and cell cycle arrest for sphingosine; and proliferation, mitogenesis, migration, angiogenesis, and protection from apoptosis for S1P). Reviews of sphingolipid metabolism, sphingolipid signaling, and the mechanisms of action of ceramide, sphingosine and S1P emphasize the complex web of interactions that occurs because of the intricately interconnected network of sphingolipid species and enzymes that

are involved.10,11 Lee et al.9 now show that in a mouse strain prone to gallstone formation, feeding a lithogenic diet is associated with Palbociclib in vitro elevated levels of ceramide in serum and bile. Furthermore, these ceramide levels are decreased by the addition of myoricin, a specific inhibitor of the first and rate-limiting step in the sphingolipid biosynthetic pathway catalyzed by SPT. After 6 weeks on the diets, 65% Selleckchem Cilomilast of mice on the lithogenic diet formed gallstones, compared with none in the control chow group and 15% in the lithogenic diet with myoricin group. Serum cholesterol and triglyceride levels were also elevated in the lithogenic diet group; these levels were reduced in the myoricin-treated mice. Gallbladder p38 mitogen-activated protein kinase phosphorylation was

increased in the lithogenic diet group, which was reduced with myoricin treatment. The findings reported are preliminary; the mechanisms by which inhibition of the sphingolipid biosynthetic pathway leads to cholesterol gallstone formation remain undefined. Nevertheless, MCE公司 based on the extensive literature that has accumulated with respect to cholesterol gallstone pathogenesis on the one hand, and bioactive sphingolipid biology on the other, one can create a roadmap for future studies that will likely yield mechanistic insights. One potential mechanism involves effects on gallbladder inflammation. Gallstone formation in mouse models involves activation of an inflammatory response.12 Bioactive sphingolipids are known to modulate inflammatory mediators.13 Therefore, one possible mechanism involves downregulation of inflammatory mediators in the gallbladder by inhibition of the de novo sphingolipid biosynthetic pathway. This scenario is supported by the findings of a previous study by the same group.14 A high-cholesterol diet fed to Syrian Golden hamsters induced gallstones in association with sixfold elevations of biliary ceramide and S1P. Levels of gallbladder inducible nitric oxide synthase and phosphorylated signal transducer and activator of transcription 3, which have been linked to inflammation, were increased.

7 These HLA associations appear to be specific to PSC. For PSC, just as for the majority of HLA-associated

diseases, significant associations have been demonstrated outside the HLA complex with a gene present on chromosome 13q31. However, this gene is not specific to PSC because significant associations at this locus have been found for ulcerative colitis and multiple sclerosis. This suggests that the gene may be involved in the pathogenesis of inflammation rather ATM/ATR inhibitor cancer than specific disease susceptibility. Further significant associations that were also previously established as ulcerative colitis susceptibility loci were detected on chromosomes 2q35 and 3p21.7 The authors suggested G-protein–coupled bile acid receptor 1 and macrophage stimulating 1 (MST1), respectively, as the likely genes involved in the disease process. In the latest study,8 the same group repeated and extended the GWAS by increasing the size of the Scandinavian and German study population and the replication cohort to 715 and 1025 PSC patients, respectively, although the numbers of patients included in the study are still relatively

small in comparison with the much larger numbers included in GWASs of inflammatory bowel disease. In agreement with the original study, the strongest associations were detected in the HLA complex. An analysis revealed a complex association signal in the class II region and confirmed the strong association with the HLA-B*08 locus in the class I region. This suggests multiple causative Palbociclib ic50 loci within the region. Clear differences were found in the HLA complex in comparison with ulcerative colitis (for which the association signal is less extensive), and associated single-nucleotide polymorphisms (SNPs) were observed

near the HLA class II region. This is a potentially important observation that requires further MCE公司 study in the search for the elusive PSC susceptibility gene or genes in this region. Outside the HLA complex, the findings of the first study were confirmed and extended. Multiple SNPs in strong linkage equilibrium at chromosome 3p21 were associated at a genome-wide significance level.8 Further analysis using the replication cohort demonstrated the most prominent association at MST1. The amino acid change at this locus, which is now associated with PSC and was previously demonstrated in patients with ulcerative colitis and Crohn’s disease,9 has been proposed to affect the MST1 receptor interaction. MST1 is known to encode macrophage stimulating protein, which regulates innate immune responses to bacterial ligands. The variant (rs3197999, R689C) identified in this study and previously in patients with inflammatory bowel disease9 has been predicted to interfere with the binding of macrophage stimulating protein to its receptor.

There are, for example, major differences between the six genotypes of HCV in response rate to therapy and evidence for some genotype-associated variability in the rate of disease progression and associated

selleck compound library liver pathology.2, 3 HCV replication is additionally associated with high mutation rates; this confers on HCV, in common with human immunodeficiency virus 1 (HIV-1), considerable adaptive capacity to escape from immunological or drug-treatment pressure. The effectiveness of newly developed protease and polymerase inhibitors for HCV, at least as monotherapy, is indeed likely to be substantially impaired through the acquisition or selection for preexisting amino acid mutations that confer antiviral resistance. Genetic heterogeneity between HCV genotypes translates into significant molecular and clinical differences. For example, individuals infected with genotype 1 or 4 show lower response rates to the current standard of care of IFN/RBV combination treatment than those infected with genotype 2 or 3.4-6 Furthermore, substantial differences were also reported in the susceptibility of the individual genotypes towards the different antivirals currently in clinical trials.7 The first widely used protease inhibitor (PI), BILN 2061, was developed based

on the structure of the NS3 protease of genotype 1. In early clinical trials

it was found to selleck be substantially less effective in individuals infected with genotype 2 or 3.8-11 Similarly, VX-950 (telaprevir), another PI, showed MCE公司 potent activity against HCV genotypes 1 and 2,12 but almost no efficacy against genotypes 3 and 4.13, 14 Genotype 1-infected individuals have been almost exclusively targeted for antiviral therapy in current, ongoing clinical trials, partly because of the lack of information about the true effectiveness of PIs against nontype 1 genotypes and because the response rate of type 1 to conventional IFN/RBV therapy is problematically low (40%-50% clearance) compared to genotypes 2 and 3 (˜80%).4 Genotype 1 is highly prevalent in the USA, Europe, and the Far East15 and therefore represents a treatment priority. This generic focus, although understandable, does, however, ignore growing problems with clinical management and therapy of other genotypes, particularly genotypes 4 and 6, which frequently respond poorly to IFN/RBV and which are extensively distributed and rapidly spreading throughout Southern Europe, the Middle East, and South East Asia.2 Assessment of the efficacy of PIs against different genotypes has been greatly hampered by the lack of a convenient animal model or a method for in vitro culture of HCV other than the type 1/2-based replicons and the infectious genotype 2a clone, JFH1.

After 10ds continuous medication, P selectin, TXB2 and P450 enzyme activity were detected to observe the anti-platelet efficacy of Asp and Clo. Results: P selectin in blank group (111.20 ng/ml) was much higher than that in control (61.0 ng/ml), Ome (79.2 ng/ml), Lan (78.7 ng/ml), Eso (71.9 ng/ml), Pan (77.5 ng/ml) and Rab (78.2 ng/ml), all

p < 0.01. And the differences between all PPIs and control group were also significant, all p < 0.05, but no difference was found among all kinds of PPIs, all p > 0.05. TXB2 levels in all PPIs groups were significant higher than that in control this website and brank groups, all p < 0.05, but no difference was found among different kinds of PPIs, all p > 0.05. The Crizotinib chemical structure activity of liver drug enzyme CYP3A4 in blank group and control groups were much higher than that in all PPI groups, in which the activity of CYP3A4 in Ome group was the lowest, but no significant difference was found among all PPIs groups. Compared with blank and control groups, the CYP2C19 enzyme activity in all PPIs groups were obviously decreased, all p < 0.01, in which those in Ome, Lan and Eso groups were relatively lower than that in Pan and Rab groups, but no significant

difference was found, all p > 0.05. Conclusion: PPIs may affect the anti-platelet efficacy of Asp and Clo by reducing the activity of liver drug metabolizing 上海皓元 enzyme CYP2C19 and CYP3A4. This may led to the probability of cardiovascular events occurrence. Key Word(s): 1. PPIs; 2. Dual Anti-platelet; 3. clopidogrel; 4. Mechanisms; Presenting Author: PEDROBOAL CARVALHO Additional Authors: BRUNO ROSA, MARIAJOÃO MOREIRA, JOSÉ COTTER Corresponding Author: PEDROBOAL CARVALHO, BRUNO ROSA, MARIAJOÃO MOREIRA, JOSÉ COTTER Affiliations: Centro Hospitalar

do Alto Ave Objective: Capsule enteroscopy (CE) plays a decisive role in the obscure gastrointestinal bleeding (OGIB) diagnosis. Antiplatelet and anticoagulant drugs may result in an increased digestive bleeding risk, both in patients with pre-existent lesions as well as through mucosal aggression. Our aim was to analyze and correlate these drugs with potential bleeding lesions found in CE. Methods: Unicentric retrospective study including 219 consecutive and complete CE performed in 5 years for OGIB diagnosis. The lesions observed during the CE were classified as P0 (no potential for bleeding), P1 (uncertain potential for bleeding) and P2 (high potential for bleeding). We also assessed antiplatelet and anticoagulant drug usage during the 30 days previous to the CE. Statistical analysis was performed with SPSS 17.0. Results: OGIB had a visible presentation in 17,4% of the patients. Approximately one quarter of the patients was taking antithrombotics (21,5% were on antiplatelet and 6,4% on anticoagulant drugs).

However, we are not assured if it is meaningful for them to receive CRC screening, especially colonoscopy as a second-stage examination considering

their remaining life expectancy. The purpose of this study was to evaluate Wnt inhibitor the efficacy of colonoscopy for advanced aged people performed as a detailed examination for CRC screening as compared with people of non-advanced age. Methods: A total of 804 persons (403 men and 401 women, mean age 70.3 years), who underwent the entire colonoscopy because of positive FOBT between 2008 and 2013, were divided into two groups: group A aged 80 or older–176 persons, and group B aged under 80–628 persons. The detection rates of total CRC, invasive CRC, and premalignant lesion (adenoma) were determined and compared between the two groups. Results: CRC was detected in 18 persons (10.2%) in group A and in 43 (6.8%) in group B (p = 0.147). The detection rate of invasive CRC,

the depth of which is deeper than the mucosal layer, was significantly higher in group A (14 persons, 8.0%) than in group B (18, 2.9%), (p = 0.013). The detection rates of adenoma showed no significant difference between the two groups. Conclusion: Invasive CRC showed a higher detection rate in advanced aged people than in those aged under 80. We conclude that it will be meaningful for advanced aged Opaganib ic50 people to receive detailed 上海皓元医药股份有限公司 colonoscopy because of the high detection rate of invasive CRC which will soon become life-threatening and shorten

their limited expected life span even further. Key Word(s): 1. Colorectal cancer; 2. screening; 3. colonoscopy; 4. aged people Presenting Author: YUJI INO Additional Authors: TOMONORI YANO, YOSHIKAZU HAYASHI, HIROTSUGU SAKAMOTO, HIROYUKI OSAWA, KEIJIRO SUNADA, HIROYUKI SATO, YOSHIMASA MIURA, HAKUEI SHINHATA, TAKAHITO TAKEZAWA, HIRONORI YAMAMOTO Corresponding Author: YUJI INO Affiliations: Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University Objective: Capsule endoscopy (CE) relies on an intact swallowing mechanism and unimpeded passage of the capsule through the pylorus. A new method for endoscopic placement of the capsule is described. Methods: A transparent hood (MH–464, Olympus, Japan), with the inside wall lined with vinyl tape, is attached to the tip of the endoscope.