Another way to implement a model of hepatic damage is the dietary check details depletion of methyl donor groups, such as choline or betaine,2, 3 which leads to nonalcoholic steatohepatitis (NASH). Other studies have reported that supplementation with these kinds of molecules can induce epigenetic changes and regulate the gene expression profile.4 In this sense, we hypothesized that dietary methyl donor supplementation could be able

to reverse the negative effects of a nutritional model of nonalcoholic fatty liver in rats. To confirm this concept, we performed a study with 48 male Wistar rats that were divided into four dietary groups with 12 rats each (Fig. 1): U0126 molecular weight control diet (C), methyl donor–supplemented control (Csupl), a diet high in fat and sugar (HFS), and an HFS diet supplemented with methyl donor groups, including betaine, choline, vitamin B12, and folic acid (HFSsupl). Chow (2014; Harlan Teklad Global Diets) and obesogenic diets (D12451; Research Diets) were provided ad libitum, and food intake was not affected by dietary treatment. The initial and final total fat mass, as well as the final fat content in the liver, were measured by EchoMRi analyzer.5 After 8 weeks of dietary treatment, the animals were sacrificed and tissues and plasma were frozen for later analysis. The obesogenic

model was successfully achieved, showing statistical differences (P < 0.01) between control-fed and HFS-fed rats in different phenotypical

variables such as body and fat depot weights and total fat. The analyses of plasma parameters revealed an increase in the atherogenic index. Moreover, the obesogenic diet induced an increase in liver fat stores when compared to the C group and, and as hypothesized, this damage was partially reversed with methyl donor supplementation (Fig. 1). In conclusion, the HFS diet led to an obese and NAFLD phenotype characterized by an increase in liver lipid accumulation. Nutritional supplementation with a cocktail of methyl donors partially reversed this extra-adipose lipid Buspirone HCl accumulation. These data suggest that methyl donor supplementation might prevent the establishment of NAFLD, a precursor to NASH and cirrhosis, and that different epigenetic changes altering the expression of genes related to liver fat metabolism could be involved. Pául Cordero Ph.D.*, Javier Campion Ph.D.*, Fermín I. Milagro Ph.D.*, J. Alfredo Martínez Ph.D.*, * Department of Nutrition and Food Science, Physiology and Toxicology, University of Navarra, Pamplona, Spain. “
“In the classical form of alpha1-antitrypsin (AT) deficiency, a point mutation in AT alters the folding of a liver-derived secretory glycoprotein and renders it aggregation-prone.

Several pieces of evidence in this study support a close association

between FoxC1 expression and HCC metastasis. First, FoxC1 protein and mRNA levels were correlated with the metastatic potential of the HCC cell lines examined. Second, FoxC1 expression was markedly higher in metastatic lesions, compared with their corresponding primary tumor samples. Third, up-regulation of FoxC1 significantly promoted the invasion and lung metastasis of HCC cells, whereas the knockdown of FoxC1 decreased the invasion and metastasis of HCC cells. EMT plays an important role in HCC invasiveness and metastasis.34, 35 The EMT transition triggered during tumor progression is controlled by several transcription factors, including Twist, Snai1, Slug, Goosecoid, ZEB1, and SIP1.24 In this study, we found that the overexpression of FoxC1 had a significant effect on EMT, as indicated

by the increased Tamoxifen expression of mesenchymal markers (fibronectin and vimentin) and decreased expression of epithelial markers (E-cadherin and ß-catenin). In contrast, knockdown of FoxC1 decreased the expression of mesenchymal markers and increased the expression of epithelial markers. EMT is a key event in tumor invasion and metastasis; epithelial cells lose their epithelial adherence and cell-cell contacts and undergo remarkable cytoskeletal remodeling to facilitate cell motility and invasion.36 Thus, HCC cells overexpressing FoxC1 CP-868596 ic50 most likely become more invasive by undergoing EMT. Disruption of the E-cadherin-mediated adhesion system is a major event in the transition from a noninvasive

tumor to invasive malignant carcinoma and is a key biomarker for EMT.23 E-cadherin is directly repressed by Snai1, which, in turn, induces mesenchymal phenotype acquisition in epithelial tumor cells.37, 38 FoxC1 increases cell migration and invasion in mammary epithelial cells by inhibiting E-cadherin expression.18 However, the molecular mechanism by which FoxC1 inhibits E-cadherin expression remains unknown. This study was the first to demonstrate that FoxC1 transactivates Snai1 expression by directly binding to its promoter, thus leading to the inhibition of E-cadherin transcription by its repressor, Snai1. Inhibition of Snai1 expression significantly suppressed FoxC1-enhanced invasion and lung metastasis. In addition, in a cohort of 406 this website human HCC tissues, we found that FoxC1 expression was positively correlated with Snai1 expression, but inversely correlated with E-cadherin expression. More important, patients exhibiting FoxC1(+)/Snai1(+) coexpression had the highest recurrence rates and lowest OS among the four subgroups, whereas patients exhibiting FoxC1(+)/E-cadherin(−) expression had shorter OS times and higher recurrence rates. Thus, both experimental and clinical evidence indicate that the FoxC1/Snai1/E-cadherin pathway may play an important role in promoting HCC metastasis and producing a poor clinical outcome.

Several pieces of evidence in this study support a close association

between FoxC1 expression and HCC metastasis. First, FoxC1 protein and mRNA levels were correlated with the metastatic potential of the HCC cell lines examined. Second, FoxC1 expression was markedly higher in metastatic lesions, compared with their corresponding primary tumor samples. Third, up-regulation of FoxC1 significantly promoted the invasion and lung metastasis of HCC cells, whereas the knockdown of FoxC1 decreased the invasion and metastasis of HCC cells. EMT plays an important role in HCC invasiveness and metastasis.34, 35 The EMT transition triggered during tumor progression is controlled by several transcription factors, including Twist, Snai1, Slug, Goosecoid, ZEB1, and SIP1.24 In this study, we found that the overexpression of FoxC1 had a significant effect on EMT, as indicated

by the increased Napabucasin clinical trial expression of mesenchymal markers (fibronectin and vimentin) and decreased expression of epithelial markers (E-cadherin and ß-catenin). In contrast, knockdown of FoxC1 decreased the expression of mesenchymal markers and increased the expression of epithelial markers. EMT is a key event in tumor invasion and metastasis; epithelial cells lose their epithelial adherence and cell-cell contacts and undergo remarkable cytoskeletal remodeling to facilitate cell motility and invasion.36 Thus, HCC cells overexpressing FoxC1 selleck chemical most likely become more invasive by undergoing EMT. Disruption of the E-cadherin-mediated adhesion system is a major event in the transition from a noninvasive

tumor to invasive malignant carcinoma and is a key biomarker for EMT.23 E-cadherin is directly repressed by Snai1, which, in turn, induces mesenchymal phenotype acquisition in epithelial tumor cells.37, 38 FoxC1 increases cell migration and invasion in mammary epithelial cells by inhibiting E-cadherin expression.18 However, the molecular mechanism by which FoxC1 inhibits E-cadherin expression remains unknown. This study was the first to demonstrate that FoxC1 transactivates Snai1 expression by directly binding to its promoter, thus leading to the inhibition of E-cadherin transcription by its repressor, Snai1. Inhibition of Snai1 expression significantly suppressed FoxC1-enhanced invasion and lung metastasis. In addition, in a cohort of 406 Niclosamide human HCC tissues, we found that FoxC1 expression was positively correlated with Snai1 expression, but inversely correlated with E-cadherin expression. More important, patients exhibiting FoxC1(+)/Snai1(+) coexpression had the highest recurrence rates and lowest OS among the four subgroups, whereas patients exhibiting FoxC1(+)/E-cadherin(−) expression had shorter OS times and higher recurrence rates. Thus, both experimental and clinical evidence indicate that the FoxC1/Snai1/E-cadherin pathway may play an important role in promoting HCC metastasis and producing a poor clinical outcome.

Several pieces of evidence in this study support a close association

between FoxC1 expression and HCC metastasis. First, FoxC1 protein and mRNA levels were correlated with the metastatic potential of the HCC cell lines examined. Second, FoxC1 expression was markedly higher in metastatic lesions, compared with their corresponding primary tumor samples. Third, up-regulation of FoxC1 significantly promoted the invasion and lung metastasis of HCC cells, whereas the knockdown of FoxC1 decreased the invasion and metastasis of HCC cells. EMT plays an important role in HCC invasiveness and metastasis.34, 35 The EMT transition triggered during tumor progression is controlled by several transcription factors, including Twist, Snai1, Slug, Goosecoid, ZEB1, and SIP1.24 In this study, we found that the overexpression of FoxC1 had a significant effect on EMT, as indicated

by the increased Daporinad clinical trial expression of mesenchymal markers (fibronectin and vimentin) and decreased expression of epithelial markers (E-cadherin and ß-catenin). In contrast, knockdown of FoxC1 decreased the expression of mesenchymal markers and increased the expression of epithelial markers. EMT is a key event in tumor invasion and metastasis; epithelial cells lose their epithelial adherence and cell-cell contacts and undergo remarkable cytoskeletal remodeling to facilitate cell motility and invasion.36 Thus, HCC cells overexpressing FoxC1 Hydroxychloroquine nmr most likely become more invasive by undergoing EMT. Disruption of the E-cadherin-mediated adhesion system is a major event in the transition from a noninvasive

tumor to invasive malignant carcinoma and is a key biomarker for EMT.23 E-cadherin is directly repressed by Snai1, which, in turn, induces mesenchymal phenotype acquisition in epithelial tumor cells.37, 38 FoxC1 increases cell migration and invasion in mammary epithelial cells by inhibiting E-cadherin expression.18 However, the molecular mechanism by which FoxC1 inhibits E-cadherin expression remains unknown. This study was the first to demonstrate that FoxC1 transactivates Snai1 expression by directly binding to its promoter, thus leading to the inhibition of E-cadherin transcription by its repressor, Snai1. Inhibition of Snai1 expression significantly suppressed FoxC1-enhanced invasion and lung metastasis. In addition, in a cohort of 406 new human HCC tissues, we found that FoxC1 expression was positively correlated with Snai1 expression, but inversely correlated with E-cadherin expression. More important, patients exhibiting FoxC1(+)/Snai1(+) coexpression had the highest recurrence rates and lowest OS among the four subgroups, whereas patients exhibiting FoxC1(+)/E-cadherin(−) expression had shorter OS times and higher recurrence rates. Thus, both experimental and clinical evidence indicate that the FoxC1/Snai1/E-cadherin pathway may play an important role in promoting HCC metastasis and producing a poor clinical outcome.

34 Bile salt reabsorption was reduced by 30% in both models. Although bile salt reabsorption was not fully impaired, Fgf15 expression levels were not detectable in the ilea of sequestrant-treated wild-type mice. It is possible that bile salt sequestration decreases the cellular content of bile salts below a certain threshold value necessary to activate FXR in enterocytes, as observed in an in vivo study in rabbits.35 Interestingly, hepatic TG contents of colesevelam-treated lean and db/db mice were enhanced, Napabucasin chemical structure which appeared to be mediated by an increased de novo synthesis of hepatic fatty acids and chain elongation. In contrast to our data, other studies addressing the effects of bile salt sequestration

on lipid metabolism showed that bile salt sequestration prevented TG accumulation in the liver.36, 37 It should be realized that those studies were performed in Carfilzomib order high-fat diet–fed mice in which the beneficial effects of bile salt sequestration are likely partly attributable to sequestrant-induced malabsorption of lipids. In addition, strain-specific responses to sequestrant treatment cannot be ruled out. At a molecular level, the interrelationship between bile salt and lipid metabolism is generally accepted to be mediated

by FXR. Nevertheless, data to explain the exact mechanisms of this relationship are still very inconsistent. Pharmacological activation of FXR has been shown to reduce free fatty acid levels in insulin-resistant rodents.15, 38 Absence of FXR signaling in Fxr−/− mice leads to increased very low-density lipoprotein–TG levels in plasma of these mice,39 suggestive of a role for FXR in control of very low-density lipoprotein

assembly. Colesevelam treatment induced hepatic expression levels of the lipogenic gene Srebp1c in lean and db/db mice. Hepatic expression levels of the lipogenic gene Srebp1c were reduced in Fxr−/− mice compared with controls.39, 40 Conversely, FXR Tideglusib activation was also shown to repress the expression of Srebp1c in a pathway involving SHP.17, 40 Expression levels of the FXR target gene Shp were unaffected and decreased in colesevelam-treated lean and db/db mice, respectively. These results are suggestive of SHP-independent regulation of Srebp1c upon sequestrant treatment. Supportive of SHP-independent regulation of lipogenic gene expression by FXR was the observation that FXR regulates the transcription of the lipogenic gene Fas through direct binding to the Fas promoter.41 Because expression levels of well-known FXR target genes were differentially affected in lean and db/db mice, we studied the role of FXR in the lipogenic response of sequestrant treatment in Fxr−/− mice and found that in contrast to wild-type mice littermates, lipogenic gene expression levels were barely affected. Srebp1c, is strongly regulated by the oxysterol receptor LXRα.

Our results showed that ∼90% of the ETV-treated patients had sustained viral suppression at year 1, and that drug resistance was minimal (0.8%) during the median follow-up period of 3.2 years. We found that the effect of ETV treatment in reducing the risk of HCC was more prominent among high-risk patients. This phenomenon

was observed by examining the combination of parameters associated with the recently developed risk scores (Fig. 4). The published risk scores were developed mainly to create easy-to-use nomograms based on clinical characteristics to predict the risk of HCC in patients with HBV. These scales have been validated, and can accurately estimate the risk of HCC up to 10 years. The cutoff scores used in these studies were based on their sensitivity to detect HCC derived and validated with nontreated HBV cohorts. The importance of our study using these risk scales in our cohorts was to see the change in risk IWR-1 purchase with the initiation of therapy. We found that the ETV treatment effect to reduce the risk of HCC was more prominent

FK228 solubility dmso among cirrhosis and high-risk patients despite the lack of interactions between ETV treatment and preexisting cirrhosis or risk factors. The lower treatment effect among lower-risk patients was somewhat not surprising. HCC development among low-risk patients is generally rare, and therefore, the treatment effect may not have occurred in large enough numbers during the treatment period allotted in our study to be able to detect a difference. In addition, HCC development Acyl CoA dehydrogenase differs greatly by cirrhotic status and risk factors in the control group. The treatment effect of ETV to reduce HCC is probably more likely reflected among cirrhosis or high-risk patients. A study with a longer observation period and higher patient numbers might be necessary to examine this ETV treatment effect among low-risk patients. The development of a scoring system to predict treatment effect

of HBV patients with different risk levels will be useful in determining the most appropriate timing of treatment initiation in clinical settings. There were several limitations to our study. First, because our patients were recruited from one hospital, they might not have been representative of the general Japanese HBV population. Second, our control group included historically observed patients who entered the cohort long before the ETV group, resulting in treatment differences during the time gap. However, we used PS matching and a similar follow-up period between the two cohorts to minimize this bias. Third, our study was an observational study with patients having large demographic differences. Although we used a PS to match ETV-treated and control groups, our sample size did not take into account other unobserved confounding factors such as HCC family history, stage of cirrhosis, and comorbidities when determining associating factors for carcinogenesis in HBV.

Our results showed that ∼90% of the ETV-treated patients had sustained viral suppression at year 1, and that drug resistance was minimal (0.8%) during the median follow-up period of 3.2 years. We found that the effect of ETV treatment in reducing the risk of HCC was more prominent among high-risk patients. This phenomenon

was observed by examining the combination of parameters associated with the recently developed risk scores (Fig. 4). The published risk scores were developed mainly to create easy-to-use nomograms based on clinical characteristics to predict the risk of HCC in patients with HBV. These scales have been validated, and can accurately estimate the risk of HCC up to 10 years. The cutoff scores used in these studies were based on their sensitivity to detect HCC derived and validated with nontreated HBV cohorts. The importance of our study using these risk scales in our cohorts was to see the change in risk Bcl-2 inhibitor with the initiation of therapy. We found that the ETV treatment effect to reduce the risk of HCC was more prominent

LEE011 among cirrhosis and high-risk patients despite the lack of interactions between ETV treatment and preexisting cirrhosis or risk factors. The lower treatment effect among lower-risk patients was somewhat not surprising. HCC development among low-risk patients is generally rare, and therefore, the treatment effect may not have occurred in large enough numbers during the treatment period allotted in our study to be able to detect a difference. In addition, HCC development Cyclooxygenase (COX) differs greatly by cirrhotic status and risk factors in the control group. The treatment effect of ETV to reduce HCC is probably more likely reflected among cirrhosis or high-risk patients. A study with a longer observation period and higher patient numbers might be necessary to examine this ETV treatment effect among low-risk patients. The development of a scoring system to predict treatment effect

of HBV patients with different risk levels will be useful in determining the most appropriate timing of treatment initiation in clinical settings. There were several limitations to our study. First, because our patients were recruited from one hospital, they might not have been representative of the general Japanese HBV population. Second, our control group included historically observed patients who entered the cohort long before the ETV group, resulting in treatment differences during the time gap. However, we used PS matching and a similar follow-up period between the two cohorts to minimize this bias. Third, our study was an observational study with patients having large demographic differences. Although we used a PS to match ETV-treated and control groups, our sample size did not take into account other unobserved confounding factors such as HCC family history, stage of cirrhosis, and comorbidities when determining associating factors for carcinogenesis in HBV.

Immune tolerance protocols for the eradication of inhibitors require daily delivery of intravenous FVIII. We evaluated the immune responses to serial intravenous administration of FVIII in preimmunized haemophilia A mice. We introduced an implantable venous-access device (iVAD) system into haemophilia A mice to facilitate sequential infusion of FVIII. After preimmunization with FVIII, the haemophilia A mice were subjected to serial intravenous administration of FVIII through the iVAD system. In all mice with serial infusion of FVIII, high titers of anti-FVIII inhibitory antibodies developed at 10 exposure

days (EDs). However, the anti-FVIII IgG titers were decreased after 150 EDs of sequential low-dose infusion of FVIII [0.05 U g−1 body weight (BW) five times per check details week]. Proliferative response to ex vivo FVIII stimulation was significantly suppressed in splenic CD4+ T cells from mice with serial low-dose FVIII infusion compared with those from mice with high-dose FVIII infusion (0.5 U g−1 BW five times per week) or preimmunized mice. Moreover, splenic CD4+ T cells from mice with serial low-dose infusion of FVIII failed to produce interleukin-2 and interferon-γ. These data suggest that serial infusion of FVIII could induce T-cell anergy in haemophilia A mice with inhibitor antibodies. “
“Summary. 

Health economic evaluations provide valuable PF-02341066 in vivo information for healthcare providers, facilitating the treatment decision-making process in a climate where demand for healthcare exceeds the supply. Although an uncommon disease, haemophilia

is a life-long condition that places a considerable burden on patients, healthcare systems and society. This burden is particularly large for patients with haemophilia with inhibitors, who can develop serious bleeding complications unresponsive to standard factor replacement therapies. Hence, bleeding episodes in these patients are treated Methane monooxygenase with bypassing agents such as recombinant activated FVII (rFVIIa) and plasma-derived activated prothrombin complex concentrates (pd-APCC). With the efficacy of these agents now well established, a number of health economic studies have been conducted to compare their cost-effectiveness for the on-demand treatment of bleeding episodes in haemophiliacs with inhibitors. In a cost-utility analysis, which assesses the effects of treatment on quality of life (QoL) and quantity of life, the incremental cost per quality-adjusted life-year (QALY) gained (US $44 834) indicated that rFVIIa was cost-effective. Similarly, eight of 11 other economic modelling evaluations found that rFVIIa was more cost-effective than pd-APCC in the on-demand treatment of bleeding episodes. These findings indicate that treating patients with haemophilia promptly and with the most effective therapy available may result in cost savings.

Immunohistochemical staining were done for Ki67 (hepatocyte replication) & CK19 (HPC & intermediate hepatocytes) for characterization of nature of hepatic regeneration & CD68 (liver tissue macrophages) CD163 (M2 macrophages)

for analysis of macrophages in liver tissue samples from patients with ACLF (n=15), ALF (n=21), CLD, (n=22). Expression CD68 & CD163 macrophages were correlated with hepatocyte replication, HPC activation & maturation. Results RT-PCR analysis documented significant increase in M2 gene markers CD163 CD206 & TGM2 (p=.001, .001 & .002) & decrease in M1 markers iNOS & CD80 (p=.001, .001) in ACLF comparison to CLD. Similarly there was significant

increase in M2 gene markers CD163, CD206 & TGM2 (p=.002, .002 & .002) & decrease in M1 markers iNOS CD80 (p=.002, p=.002) in ACLF comparison to ALF. Immunohistochemical analysis shows increase in Ki67+ hepatocytes selleck screening library in ALF as compared to ACLF & CLD (p=.0001, .0001). Further, the number of CK19+ HPC & its maturational lineages was increased in ACLF than ALF & CLD (p=.0001, .0002). Using spearman rho correlation shows that CD163 positivity & M2/M1 macrophage ratio is significantly associated with extant of HPC differentiation to hepatocyte (p=.0001, .0004). Further Pu1 (yolk sac originated Kupffer Cells) & Myb (bone marrow originated monocyte derived macrophage) expression suggest significant increase in Pu1 expression relative to CD68 in ACLF in comparison to ALF & CLD (p=0.002, 0.001) suggesting majority of M2 macrophage in ACLF are kupffer JQ1 Carnitine palmitoyltransferase II cells.

Conclusions Alternatively activated M2 macrophages are major population in ACLF liver which promotes differentiation of HPC to hepatocyte. These M2 macrophages are of kupffer cell origin. Disclosures: The following people have nothing to disclose: Dhananjay Kumar, Sheetalnath Rooge, Smriti Shubham, Adil Bhat, Charvi Syal, Archana Rastogi, Chhagan Bihari, Viniyendra Pamecha, Anupam Kumar, Shiv K. Sarin Background/aim: Patients with HCV/HIV co-infection show faster progression of liver fibrosis, in part associated with miRNA dysregulation and more severe inflammation. The HIV protein gp120 modulates directional migration and expression of pro-fibrogenic cytokines in hepatic stellate cells (HSC), through engagement of the chemokine receptor CCR5. The NALP3 inflammasome is a critical pathway in the generation of pro-inflammatory signals during liver injury. Aim of this study was to evaluate the role miRNAs and inflammasome activation in mediating the effect HSC. Methods: HSC were isolated from normal human liver tissue. Inflammasome complex gene expression was measured by qRT-PCR. Levels of mature IL-1 β were assayed by ELISA. miRNA expression was evaluated via RT-PCR.

On the other hand, serum CagA antibody positive rate was 58.6% (17/29) in male. In fact, serum CagA antibody titer

was significantly higher in female than male (38.6 ± 35.7 vs 18.6 ± 23.2 U/mL, P = 0.003). PG II level was significantly higher in serum CagA antibody positive group than negative group (P = 0.04). PG I level was also higher in serum CagA antibody positive than negative group; however, it was not statistically significant (P = 0.30). There was no difference of PG levels between male and female (data not shown). The correlation between serum CagA antibody titers and PG levels was also examined (Fig. 1). Serum CagA antibody titer was significantly correlated with PG I level (r = 0.30, P = 0.003). In addition, serum CagA antibody titer was also correlated with PG II level (r = 0.30, P = 0.004). There Belnacasan was no correlation between serum CagA antibody titer and PG I/II ratio (P = 0.77). Even when only serum CagA antibody positive group was selected, serum CagA antibody titer was significantly correlated with PG I and PG II (r = 0.40, P = 0.001 for PG I; r = 0.40, P = 0.001 for PG II, respectively). Next, the relationship between serum CagA antibody titer and histological score was examined. There were no significant differences of each score between serum CagA antibody

positive and negative group (Table 2). However, the see more correlation between serum CagA antibody titer and histological score was examined; the inflammation in the corpus was significantly correlated with serum CagA antibody PAK6 titer (r = 0.26, P = 0.01) (Fig. 2). Mucosal activity in the corpus was tended to be correlated with serum CagA antibody titer; however, there was no statistical significance (P = 0.07). These correlations was not found in the antrum (P = 0.47 for the inflammation, P = 0.60 for the activity). On the other hand, there was no association between serum CagA antibody titer and bacterial density both in the antrum and corpus (P = 0.87 and 0.79, respectively; Fig. 2). This suggests that low bacterial density

cannot be a reason for low serum CagA antibody titer. Neither atrophy nor intestinal metaplasia both in the antrum and corpus was correlated with serum CagA antibody titer. PG II was significantly correlated with inflammation and activity in the corpus (P < 0.001, P < 0.001, respectively). These correlations was not found in the antrum (P = 0.20 for the inflammation, P = 0.15 for the activity). Bacterial density in the antrum was significantly correlated with activity and inflammation in the antrum (P = 0.001 and P < 0.001, respectively), whereas bacterial density in the corpus was not correlated with any histological score. Even when only serum CagA antibody positive group was selected, serum CagA antibody titer was significantly correlated with inflammation and activity in the corpus (r = 0.26, P = 0.04 for inflammation, r = 0.24, P = 0.04 for activity, respectively).