Nude mice inoculated with HepG2-G2 cells developed tumors significantly larger than those developed by control mice (Fig. 8A). A considerable increase in tumor metastasis was observed in draining-tumor lymph nodes of HepG2-G2 mice with respect to controls (Fig. 8B), but no significant metastatic foci were observed in liver or lungs (data not shown). These results suggest a correlation between Gal-1 expression, tumor growth, and metastasis of

HCC. Accumulating evidence indicates that Gal-1 expression is up-regulated in hepatocarcinoma cells, yet the precise role of this lectin in liver pathophysiology is still uncertain. In the present study, we detected endogenous Gal-1 expression in HepG2 cells. Cells overexpressing Gal-1 exhibited a cytoplasmic localization of this lectin, selleck chemicals llc which was found

to be released to the extracellular compartment. Strikingly, if nontransfected cells were cultured continuously in the presence of rGal-1, it was detected intracellularly even after 48 hours of incubation, suggesting internalization of this protein. In fact, it has been demonstrated that Gal-1 is internalized by Jurkat leukemic T cells through receptor-mediated transport in a carbohydrate-dependent manner.22 Hence, Gal-1 secreted from HCC cells might exert its biological functions either by engaging cell surface receptors and transmitting signals inside the selleck chemicals cell or through receptor-mediated internalization and endocytosis. However, because intracellular functions have been described for Gal-1,23 a cell surface receptor-independent mechanism responsible for Gal-1 functions this website cannot be excluded. Depending on the target

cell type and its relative concentrations within local microenvironments, Gal-1 can potentiate or inhibit cell–ECM and cell–cell interactions.5 Here, we show that both soluble and immobilized rGal-1 can promote HepG2 cell adhesion in a dose-dependent manner. Inhibition of rGal-1 effects by TDG or lactose strongly indicates a glycan-dependent mechanism in mediating Gal-1 cell adhesive properties. In fact, cell adhesion to laminin, a basement membrane glycoprotein covered by polylactosamine-enriched glycoconjugates, was also increased following exposure to soluble rGal-1. Concentrations of Gal-1 used ranged between 3.5 and 14 μM, which are in agreement with those reported for human A375 melanoma24 and ovary carcinoma cells.25 Furthermore, lower concentrations were also effective in promoting cell adhesiveness when immobilized rGal-1 was also effective when tested as an ECM protein. Moreover, the enhanced cell adhesion observed in Gal-1–transfected HepG2 cells indicates that HCC cell adhesion might be related to Gal-1 expression levels. Gal-1 can bind and form lattices with different members of the integrin family to control different biological processes, including cell adhesion, migration, proliferation, and survival.

fluorescein Presenting Author: MASAHIRO OKADA Additional Authors: HIROYUKI OSAWA, YOSHIMASA MIURA, YUJI INO, TAKEHITO TAKEZAWA, HIROYUKI SATOH, HIRONORI YAMAMOTO Corresponding Author: MASAHIRO OKADA Affiliations: Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University, Jichi Medical University Objective: Endoscopic diagnosis of early flat gastric cancers is often selleck inhibitor difficult because the subtle changes of surface mucosa are difficult to recognize by standard white-light images. High resolution images or high color contrasted images may improve the

diagnostic accuracy for such cancers. We experienced

a new diagnostic method of blue LASER imaging (BLI) system for early flat gastric cancers. Methods: These new images are generated by two kinds of LASER light source. The illumination of the first source with 410 ± 10 nm wavelength can produce a clear image of superficial microvasculature of digestive mucosa. Another source with 450 ± 10 nm can produce selleck kinase inhibitor a deep vascular image and also excite fluorescence leading to white light images. The combination of these illuminations can characterize as BLI image and BLI-bright image that exhibit both detailed microstructure and microvasculature. BLI-bright images have higher proportion of

white light images than BLI images. Since 2011, we observed a total of five early flat gastric cancer lesions. Results: Without magnification, three lesions were recognized by BLI images but not by LASER white-light images alone. The other two lesions showed distinctively abnormal high-resolution images by LASER white-light. BLI-bright and BLI presented clear images with high color contrast as well as detailed characteristic findings with magnification, leading to the recognition of precise demarcation lines between cancer and surrounding area in all five lesions. Two lesions of 18 mm and 23 mm in diameter respectively showed unstructured areas and irregular microvascular patterns including key frets pattern, suggesting undifferentiated adenocarcinoma supported by find more histopathology of the resected specimens. Three lesions of 12 mm, 4 mm and 14 mm respectively showed irregular microstructural and microvascular patterns, suggesting differentiated adenocarcinoma supported histopathologically. Conclusion: BLI system is useful for detection and detailed examination of early flat gastric cancers exhibiting high color contrasted images and apparent images in both microstructural and microvascular patterns. Key Word(s): 1. Blue laser imaging; 2. gastric cancer; 3.

4C-i-k). Pretreating BM-MSCs CM with IL1Ra neutralization Ab significantly masked BM-MSCs CM inhibition on CCL2, CXCL1, and CXCL2, suggesting that BM-MSCs exerted anti-inflammatory actions through IL1Ra inhibiting IL1 signaling to abolish the elevation of CCL2,

CXCL1, and CXCL2 blocking macrophage infiltration (Fig. 4D-l-n). Together, results (from Fig. 4) concluded that KO of AR in BM-MSCs led to more secreted IL1Ra that resulted in suppression of macrophage infiltration (anti-inflammation) and HSCs activation (anti-fibrosis) and then yielded better transplantation therapeutic efficacy to treat liver cirrhosis. To apply these findings in clinical application by targeting AR in BM-MSCs (mimicking genetic ARKO BM-MSC effects in treating liver cirrhosis), we applied the currently available agents, such as AR-siRNA and ASC-J9®, that

could degrade AR in selective cells with little side effects.34 We found ARKO with lentiviral AR-siRNA infection in primary WT BM-MSCs (or C3H10T1/2 B-Raf inhibitor clinical trial and D1 Enzalutamide chemical structure cells) led to increased cell migration and proliferation (Fig. 5A-a-c,B). Similar results were also obtained when we replaced AR-siRNA with ASC-J9®. Results showed that ASC-J9® treatment in WT BM-MSCs caused elevated migration into regular media or to hepatocytes (Fig. 5C-d-f). ASC-J9® was also applied to WT BM-MSCs to determine its effect on WT BM-MSC self-renewal and proliferation potential, and results from the bromodeoxyuridine (BrdU) assay proved that ASC-J9® treatment led to enhanced self-renewal and proliferation in WT BM-MSCs (Fig. 5D). Zymographic analysis also showed that AR-siRNA or ASC-J9® treatment increased MMP-9 activity (Fig. 5E,F). Together, results (from Fig. 5A-F) conclude that targeting AR in BM-MSCs with either AR-siRNA or ASC-J9® yielded similar effects, when compared with BM-MSC effects isolated from ARKO mice, showing

better anti-inflammation and anti-fibrosis effects. With consistent in vitro results obtained (Fig. 5), it see more was essential to test whether concordant outcomes could be reached in the in vivo mouse liver cirrhosis model. As expected, we found that lentiviral AR-siRNA infected BM-MSCs have better transplantation therapeutic effects in treating liver cirrhotic mice induced with CCl4 or TAA than scramble control BM-MSCs, when demonstrated using collagen deposition staining and expressions of fibronectin and α-SMA (Fig. 6A-a-c and Supporting Fig. 12A,B). This conclusion was further supported in liver functional assays in CCl4-induced liver cirrhosis mice (Fig. 6B-d-f). Similar results were also obtained in the TAA-induced liver cirrhosis mouse model (Supporting Fig. 12C). Consistent therapeutic outcomes in cirrhotic liver mice were obtained from ASC-J9®-treated WT BM-MSCs. Expression of fibrosis markers confirmed that WT BM-MSCs treated with the ASC-J9® suppressed liver cirrhosis better than vehicle-treated WT BM-MSCs (Fig. 6C-g-i and Supporting Fig. 12D,E). Liver functional assays showed similar results in the CCl4 (Fig.

1–3 T2D may cause metabolic fatty liver disease (so-called NAFLD) and, like diabetes,NAFLD is now considered a manifestation of metabolic syndrome (MetS).1 Insulin resistance, the primary pathophysiological disorder leading to T2D and MetS is so often found in NAFLD that this form of liver disease may be regarded as similar to or a complication of ‘pre-diabetes’, thereby indicating the high future risk for onset of diabetes as well as cardiovascular disease.1,3 In several studies, NAFLD diagnosed by

ultrasonography together with unexplained elevation of liver enzymes predicted diabetes risk, independent of obesity signaling pathway and other components of MetS.4–11 Thus, the concept has arisen that NAFLD may signify more than just the presence of a liver disease; it may also be an early mediator of T2D and MetS. RAD001 solubility dmso Although histological examination remains the gold standard for diagnosis of NAFLD, pathological definition is often not

possible in community-based epidemiological studies. Alternatively, in subjects without substantial alcohol consumption or other causes of liver disease, persistent elevation of alanine aminotransferase (ALT) and γ-glutamyltransferase (GGT) is regarded as a surrogate marker of NAFLD.1,12 In 1998, a longitudinal study examined the association of elevated liver enzymes with incident diabetes.4 Since then, high values of ALT and GGT, even within the normal range, have been reported to predict incident diabetes and MetS; some studies demonstrated stronger association between GGT selleck compound and diabetes than ALT, while other studies reported the

opposite.4–6 In a meta-analysis of results from prospective population-based studies fully adjusted for other diabetes risk factors (albeit variably adjusted), 1 U/L increase of loge ALT was associated with 85% increase in diabetes risk, and 1 U/L increase of loge GGT with 92% increase.4 This indicates that elevations in liver enzymes attributable to NAFLD increase incident diabetes rate independently of commonly measured diabetes risk factors. Recently, Adams et al. found subjects with elevated liver enzymes attributed to NAFLD were at increased risk of developing metabolic complications at 11 years follow up; they were threefold more likely to develop diabetes and 50% more likely to develop MetS compared with the age-matched population.5 Multivariate modeling showed that the increased risk of metabolic complications could be explained by associated visceral obesity and subsequent insulin resistance, which almost invariably accompanies patients with NAFLD. In contrast to this high risk of diabetes, only a small minority of subjects with NAFLD develop cirrhosis over 10 years, with an even smaller proportion dying from liver disease during this period of follow up.

7 In 2000, the Journal of Gastroenterology and Hepatology published a review on the subject which commented on the low prevalence of GERD in Asia but also projected that, based on sparse published data available at that time, the disease appeared to be on the increase.8 For that review, references

were difficult to obtain, with few direct prevalence studies available. Since then, there has been a steady increase in published literature on GERD from the Asia-Pacific region. More recent studies with better defined study methodology are now available and have shown that GERD is in fact, not uncommon in Asia. Two Asian Pacific consensus meeting on GERD have been convened selleck and their proceedings published,9,10 and GERD is now considered an important disease in the Asia-Pacific region. The burden of GERD has been measured by determining the frequency of esophagitis

in endoscoped patients as well as the prevalence of GERD symptoms in the community or population. The latter has been thought to be a more accurate indicator of the true burden of GERD in a population, especially with the recognition of non-erosive reflux disease (NERD) as the predominant disease subgroup. In the earlier years studies on GERD were based on the presence of erosive esophagitis at endoscopy. Gastroscopy affords objective visualization of reflux-associated damage to the lower esophagus. The definition of esophagitis used, however, has been variable, and this has led to differences in the rates of esophagitis reported. For example, in the older Savary-Miller classification, find more erythema was considered as already Grade 1 esophagitis, whereas in the more recent and now more widely used Los Angeles classification, a breach in the esophageal mucosa must be evident before a diagnosis of esophagitis can be made. Studies based on reflux symptoms have been thought to be a more reliable indicator of GERD but symptom-based diagnosis has also not been easy. click here Many studies have used predominant symptoms of

heartburn and acid regurgitation as a marker of GERD, but there has been great variability in the definition of GERD based on the frequency, and sometimes on the severity, of symptoms. Reflux disease specific questionnaires have now been constructed, and their application has allowed a more consistent and reliable way of measuring the burden of disease.11,12 A summary of the published reports on esophagitis in Asia is shown in Table 1.1,13–32 The prevalence of erosive esophagitis ranges from < 1.0% to 20.8%. This considerable variability in values could be due to different groups of patients studied: routine health screening patients, patients screened for gastric cancer, patients with dyspepsia or upper gastrointestinal symptoms or all gastroscoped patients.

7 In 2000, the Journal of Gastroenterology and Hepatology published a review on the subject which commented on the low prevalence of GERD in Asia but also projected that, based on sparse published data available at that time, the disease appeared to be on the increase.8 For that review, references

were difficult to obtain, with few direct prevalence studies available. Since then, there has been a steady increase in published literature on GERD from the Asia-Pacific region. More recent studies with better defined study methodology are now available and have shown that GERD is in fact, not uncommon in Asia. Two Asian Pacific consensus meeting on GERD have been convened PD98059 datasheet and their proceedings published,9,10 and GERD is now considered an important disease in the Asia-Pacific region. The burden of GERD has been measured by determining the frequency of esophagitis

in endoscoped patients as well as the prevalence of GERD symptoms in the community or population. The latter has been thought to be a more accurate indicator of the true burden of GERD in a population, especially with the recognition of non-erosive reflux disease (NERD) as the predominant disease subgroup. In the earlier years studies on GERD were based on the presence of erosive esophagitis at endoscopy. Gastroscopy affords objective visualization of reflux-associated damage to the lower esophagus. The definition of esophagitis used, however, has been variable, and this has led to differences in the rates of esophagitis reported. For example, in the older Savary-Miller classification, KPT-330 order erythema was considered as already Grade 1 esophagitis, whereas in the more recent and now more widely used Los Angeles classification, a breach in the esophageal mucosa must be evident before a diagnosis of esophagitis can be made. Studies based on reflux symptoms have been thought to be a more reliable indicator of GERD but symptom-based diagnosis has also not been easy. click here Many studies have used predominant symptoms of

heartburn and acid regurgitation as a marker of GERD, but there has been great variability in the definition of GERD based on the frequency, and sometimes on the severity, of symptoms. Reflux disease specific questionnaires have now been constructed, and their application has allowed a more consistent and reliable way of measuring the burden of disease.11,12 A summary of the published reports on esophagitis in Asia is shown in Table 1.1,13–32 The prevalence of erosive esophagitis ranges from < 1.0% to 20.8%. This considerable variability in values could be due to different groups of patients studied: routine health screening patients, patients screened for gastric cancer, patients with dyspepsia or upper gastrointestinal symptoms or all gastroscoped patients.

Native and post-translationally modified HMGB1 were detected in human and in mice with alcoholic liver disease. In liver and in serum from control mice and in serum from healthy volunteers, the lysine residues within the peptides containing nuclear localization signals-1

and 2 were non-acetylated and all cysteine residues were reduced. However, in livers from ethanol-fed mice, in addition to all thiol/non-acetylated isoforms of HMGB1, we observed acetylated nuclear localization signals-1 and 2, a unique phosphorylation site in serine 35 and an increase in oxidation of HMGB1 to the disulfide isoform. In serum from ethanol-fed mice and from patients with alcoholic liver disease there Selleck CHIR-99021 was disulphide bonded hyper-acetylated-HMGB1, disulphide bonded non-acetylated-HMGB1 and HMGB1 phos-phorylated in serine 35. Hepatocytes appeared to be a major source of these HMGB1 isoforms. Conclusion: Hepatocyte HMGB1 participates in the pathogenesis of alcoholic liver disease and undergoes post-translational modifications that could condition its

toxic effects. Disclosures: Andrea D. Branch – Grant/Research Support: Kadmon, Gilead, Janssen The following people have nothing to disclose: Xiaodong Ge, Daniel J. Antoine, Yongke Lu, Elena Arriazu, Tung Ming Leung, Arielle L. Klepper, M. Isabel Fiel, Natalia Nieto Background: Chronic alcohol consumption leads to hepatic ste-atosis. The molecular mechanisms of lipid accumulation have been Selleck SCH727965 selleckchem primarily investigated in hepatocytes, while the roles of neighboring cells in this process have been less explored. Nogo-B (a.k.a., Reticulon 4B) is an endoplasmic reticulum resident protein and plays important roles in pathological conditions in

various tissues. In the liver, Nogo-B is expressed in non-parenchymal cells including Kupffer cells, but not in hepatocytes, and promotes liver fibrosis. Given that Kupffer cells play a role in hepatic steatosis in a paracrine manner, we hypothesize that Nogo-B may contribute to ethanol-in-duced steatosis by modulating Kupffer cell function. Methods: Wild-type (WT) or Nogo-B knockout (KO) mice were fed with control or Lieber-DeCarli ethanol liquid diets (5% ethanol) for 6 weeks. Lipopolysaccharide (LPS) was injected intraperito-neally 9 hours before sample collection. For in vitro studies, Kupffer cells were isolated from WT and KO mice and treated with 0 or 100 mM ethanol in the presence or absence of LPS. Results: Lipid accumulation was significantly reduced in livers of Nogo-B KO mice fed with ethanol diet, compared to WT mice (hepatic triglyceride levels: 10+/−2 vs. 28+/−4 mg/g liver, p<0.01; steatosis score: 0.8+/−0.1 vs. 2.0+/−0.3, p<0.05). A histological score showed a trend toward reduced inflammation in KO livers, compared to WT livers (p=0.07), and was associated with decreased infiltration of neutrophils (p<0.

Standard thromboprophylaxis should be used in patients in whom VWF levels are normalized. Over the past decade, it has become clear that in severe forms of VWD, long-term prophylaxis is beneficial [21-23]. As mucosal surfaces are rich in fibrinolytic activity [9], blocking fibrinolysis is a useful adjunctive measure to stop bleeding. Epsilon-aminocaproic acid (at a dose

of 50–60 mg kg−1 every 4–6 h) or tranexamic acid (at a dose of 10–15 mg kg−1 every 8–12 h) may be administered orally, intravenously, or topically [9]. Oestrogen–progesteron preparations render the endometrium less susceptible to bleeding, and may be very useful in managing CHIR-99021 in vitro menorrhagia in VWD patients [8, 9]. As there are no population-based data, the prevalence of inherited platelet disorders, which encompass both functional disorders and thrombocytopenia (Table 3), remains unknown. In studies of SCH727965 price patients presenting with mucocutaneous bleeding, platelet abnormalities are at least as common as VWD. Severe disorders are often recognized in childhood, but mild disorders may go undiagnosed unless there is a family history that prompts testing, or until a haemostatic challenge results in significant bleeding. Algorithms have been developed to aid with the investigation

of inherited platelet function disorders [24] (available at: www.ahcdc.ca/index.php/research/rare-inherited-bleeding-disorders) [25], and thrombocytopenias [26]. Validated bleeding assessment tools (BATs) are useful

in standardizing information obtained learn more from the patient history and accurately recording the severity and frequency of bleeding symptoms [27]. The high negative predictive value of some of these tools may make it possible to use them as a screen prior to laboratory testing. However, existing tools have low specificity and will not provide a definitive diagnosis [27, 28]. There is no ideal simple, inexpensive, sensitive screening test that reliably identifies patients requiring specialized testing of platelet function. Although both bleeding times and PFA-100/200® closure times have been used for this purpose, these tests are not adequately sensitive to rule out the need for further testing [29], and should be considered optional. A validated BAT may be more useful in assessing a patient’s bleeding propensity and determining whether further specialized laboratory investigations are warranted. The most widely used method for assessing platelet function is light transmission aggregometry (LTA), in which the change in optical density of a stirred sample of citrated platelet-rich plasma is measured by a photometer following the addition of agonists. Although many pre-analytical and analytical variables affect the results, and international surveys have shown that there is wide variation in methodology, LTA remains the gold standard platelet function test. Recommendations for standardization have recently been published [30].

05), and correlated with the degree of fibrosis. PA-induced lipoapoptosis in primary hepatocytes in vitro lead to mtDNA release into the supernatant, and mice with HFD-induced fatty liver were predisposed to greater increases in serum mtDNA in response to thioacetamide-induced liver injury. Intravenous administration of purified mtDNA at physiological doses (10μg/mouse) induced robust upregulation of a-SMA expression in HSC in mice primed with short-term MCD feeding, as determined by in situ immunostaining and immunoblotting of liver lysates 24h post-mtDNA (p<0.05). Activation of HSC was following by 2-3-fold increases in pro-fibrogenic gene expression (TGFp1, procollagen a1(I) and

TIMP-1) 48 hours after mtDNA administration (p<0.05). In vitro, addition of mtDNA (1-5μg/ml) induced significant upregulation of a-SMA expression in primary HSC cultures and pro-inflammatory cytokine Selleck Obeticholic Acid TNFα secretion by murine macrophages in a dose-dependent fashion (p<0.05) CONCLUSIONS: In murine NASH models, mtDNA is released from injured fat-laden hepatocytes, circulates in serum and

correlates with fibrosis progression. Administration selleck compound of purified mtDNA induces pro-inflammatory and pro-fibrogenic responses in liver cells in vivo and in vitro. Our results suggest hepatocyte-derived mtDNA acts as a “danger signal”, promotes progression of NAFLD/NASH and is a potential disease biomarker. Disclosures: Yury Popov – Consulting: Gilead Sciences, Inc; Grant/Research Support: Gilead Sciences, Inc, Takeda The following people have nothing to disclose: Naoki

Ikenaga, Makoto Miyamoto, Susan B. Liu, Zhen-Wei Peng, Shuhei Yoshida, Konstantin Khrapko, Henry Koziel BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease and can progress to cirrhosis and hepatocellular cancer (HCC). NAFLD is characterized by steatosis, inflammation, ballooning and pericellular fibrosis. It is also associated with obesity, insulin resistance, hyperglycemia and dyslipidemia. While numerous mouse models of NASH have been described, they do not mimic human disease and do not develop HCC reliably without genetic manipulation. selleck screening library AIMS: To characterize a mouse model of NAFLD that is associated with obesity/insulin resistance and develops increasing fibrosis and HCC. METHODS: A unique isogenic mouse strain derived from a C57Bl/6J and 129Sl/ SvlmJ background was created and maintained with inbreeding. Mice were fed one of four diets: (1) chow diet (Harlan TD.7012), (2) high-fat diet (HFD) with 42% Kcal from fat (Harlan TD.88137) (3) HFD + high fructose-glucose solution (HFS, 23.1g/l d-fructose + 18.9 g/l d-glucose), and (4) chow diet + HFS. Normal tap water was provided ad lib to groups 1 and 2. Histology was assessed from hematoxylin+eosin and trichrome stains.

pylori)

are proton pump inhibitor, amoxacillin, and clarithromycin. Considering the convenience of the patient, it is more helpful to take the drugs at once postprandial compared to take the drugs dividing by preprandial and postprandial. But, proton pump inhibitor is more effective when taking preprandial. The aim of this study was to determine the difference in eradication rates according to the method of treatment of H.pylori. Methods: Between January 2008 and December 2012, a total 160 patients with positive by rapid urease test at our hospital were reviewed, retrospectively. We divided into two groups in accordance with the prescribed methods of H.pylori. PF-562271 One group of people were prescribed the drugs at once postprandial (group A). Another group of people were prescribed proton pump inhibitor at preprandial with amoxicillin and clarithromycin at postprandial (group B). After 4 weeks, urea breath test was performed to validate eradication of H.pylori. Results: The rate of eradication of group A was 75% (60/80) and the rate of eradication

of group B was 72.5% (58/80). There was no Doramapimod mw significant difference between two groups (p = 0.719). Conclusion: To take the regimens for treatment of H.pylori at once postprandial or dividing by preprandial and postprandial was no significant difference in eradication rates of H.pylori. Therefore, to prescribe at once postprandial

maybe the better way, considering the convenience of the patient. Key Word(s): 1. PPI; 2. Pre-prandial; 3. H.Pyolori;   Group A Group B p-value Male: Female ratio 50:30 59:21 0.127 Mean age 51.45 53.34 0.334 Eradication rate of H.pylori 75% (60/80) 72.5% (58/80) 0.719 Presenting Author: KYU KEUN KANG Additional Authors: DONG HO LEE, DONG HYUN OH, NAYOUNG KIM, YOUNG SOO PARK, CHEOL MIN SHIN, HYUK YOON, JIN HYEOK HWANG Corresponding Author: DONG HO LEE Affiliations: this website Seoul National University Bundang Hospital Objective: There was a controversy the efficacy of eradication with moxifloxacin based triple therapy as second line treatment for Helicobacter pylori infection. And most of published papers focused on patients failed to treat with standard triple therapy. So, we investigated the efficacy of moxifloxacin as second line therapy and the eradication rates of that according to previous first-line regimen. Methods: A total of 298 patients who were failed to eradicate with first line treatment received 14 days moxifloxacin containing triple therapy (moxifloxacin 400 mg q.d, amoxicillin 1000 mg b.i.d, rabeprazole 20 mg b.i.d). As first line treatment, they were prescribed 7day-standard triple therapy (n = 184), 7day-bisthmus containing quadruple therapy (n = 29), 7day-concomitant therapy (n = 39) and 14day-sequential therapy (n = 46).