The expression of Fuc-Hpx in cancer tissue was not different from that in non-cancerous tissue. Conclusion:  Fuc-Hpx is

a valuable biomarker for HCC but it might be a marker for hypercarcinogenic liver rather than a marker for tumor-bearing liver. “
“Non-alcoholic steatohepatitis (NASH) is a common liver disease that may progress Talazoparib clinical trial to cirrhosis and hepatocellular carcinoma. There is currently no approved pharmacological treatment for NASH. Phyllanthus urinaria is a commonly used hepatoprotective herb that ameliorates NASH in animal studies. We aimed to test the hypothesis that Phyllanthus was superior to placebo in improving histological non-alcoholic fatty liver disease (NAFLD) activity score. This was a placebo-controlled parallel-group double-blind randomized controlled trial. Patients with histology-proven NASH were randomized to receive Phyllanthus or placebo for 24 weeks. The primary endpoint was change in NAFLD activity score from baseline to week 24. Secondary check details endpoints included changes in individual histological parameters, liver biochemistry and metabolic profile. We enrolled 60 patients (40 received Phyllanthus and 20 received placebo). The change in NAFLD activity score was −0.8 ± 1.4 in the Phyllanthus group and −0.3 ± 1.3 in the placebo group (P = 0.24). The change in steatosis, lobular inflammation, ballooning and fibrosis was also similar between the two groups.

Within the Phyllanthus group, although there was reduction in hepatic steatosis (−0.2 ± 0.7; P = 0.039) and ballooning grades (−0.4 ± 0.5; P < 0.001), the change was small and of limited clinical significance. Furthermore, there was no

significant difference in the changes in alanine aminotransferase, aspartate aminotransferase, fasting glucose and lipid profile between the two groups. Phyllanthus is not superior to placebo in improving NAFLD activity score in NASH patients. “
“Acid-sensing pathways, which trigger mucosal defense mechanisms in response to luminal acid, 上海皓元 involve the rapid afferent-mediated “capsaicin pathway” and the sustained “prostaglandin (PG) pathway.” Luminal acid quickly increases protective PG synthesis and release from epithelia, although the mechanism by which luminal acid induces PG synthesis is still mostly unknown. Acid exposure augments purinergic ATP-P2Y signaling by inhibition of intestinal alkaline phosphatase activity. Since P2Y activation increases intracellular Ca2+, we further hypothesized that ATP-P2Y signals increase the generation of H2O2 derived from dual oxidase, a member of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family activated by Ca2+. Our recent studies suggest that acid exposure increases H2O2 output, followed by phospholipase A2 and cyclooxygenase activation, increasing PG synthesis. Released prostaglandin E2 augments protective HCO3− and mucus secretion via EP4 receptor activation.

Adenovirus-mediated overexpression of RORα (Ad-RORα) or treatment with the RORα activator, SR1078, reduced aerobic glycolysis and down-regulated biosynthetic pathways in hepatoma cells. Ad-RORα and SR1078 reduced the expression

of pyruvate dehydrogenase kinase 2 (PDK2) and inhibited the phosphorylation of PDHe1α, subsequently shifted pyruvate to complete oxidation. The RORα-mediated decrease in PDK2 levels was caused by up-regulation of p21 rather than p53. Furthermore, RORα inhibited hepatoma growth both in vitro and in a xenograft model in vivo. We also found that suppression of PDK2 inhibited hepatoma growth in a xenograft model. These findings mimic the altered glucose utilization and GDC-973 hepatoma growth caused by glutamine deprivation. Finally, tumor tissue from 187 hepatocellular carcinoma patients expressed lower levels of RORα than adjacent non-tumor tissue, supporting a potential beneficial effect of RORα activation in the treatment of liver cancer. Conclusion: The data reported herein show that RORα mediates reprogramming of glucose metabolism in hepatoma cells in response to glutamine deficiency. The relationships established here between glutamine AZD2281 ic50 metabolism, RORα expression and signaling, and aerobic glycolysis have

implications for therapeutic targeting of liver cancer metabolism. (Hepatology 2014) “
“Background and Aim:  Gastric fundus perforation is a serious complication of endoscopic mucosal resection and endoscopic submucosal dissection performed for the removal of early gastric cancers or subepithelial tumors. The novel over-the-scope MCE公司 clip (OTSC) has recently been found to be effective for closing gastrointestinal-tract perforations and accesses for natural orifice transluminal endoscopic surgery. However, feasibility studies of OTSCs in gastric fundus perforation are still lacking. The aim of this study was therefore to demonstrate the feasibility of endoscopic closure of gastric fundus perforation using the OTSC system in a dog model. Methods:  Gastric fundus

perforations were created by needle-knife electrocautery in seven dogs. The perforations were then closed using the OTSC clipping system. Stomach distension was maintained by maximum insufflation with air and methylene blue solution (500 mL) was instilled to submerge the closed perforation. Leaks were detected laparoscopically. Results:  Perforations were closed in all seven cases with a mean time of 18.5 ± 6.4 min (11–28 min). Twin Grasper assistance failed to release the OTSCs in two of the seven cases (2/7, 28.6%) because of difficulties associated with the J-maneuver (retroflexion of endoscope) required for the gastric fundus procedure, and OTCS were forced into place by suction. Minor leakage was observed in one case (1/7, 14.3%). No damages related to the clip system were found during postmortem examinations.

The second limitation is the ethnic homogeneity of the Japanese population. Because the baseline incidence of HCC development differs among population groups, longer-term longitudinal studies in larger cohorts with various population subgroups are required to verify the generality of our results. With the development of potent direct-acting antiviral agents combinations, IFN-free therapy is likely to be approved in the near future. This raises the question of whether posttreatment ALT and/or AFP levels will remain a significant predictor of HCC risk. Moreover, it

is uncertain whether the suppressive effect of viral eradication by IFN-free regimens on hepatocarcinogenesis will be identical to that obtained by IFN-based regimens. Therefore, it is extremely interesting to prove these issues in future studies. In conclusion, buy HM781-36B post-IFN treatment ALT and AFP levels are strictly associated with hepatocarcinogenesis risk in patients with CHC. Measurement of these values is useful for predicting future HCC risk in IFN-treated patients. Suppression of these values after IFN therapy reduces HCC risk even in patients without HCV eradication, while SVRs with increased ALT and/or AFP levels are at risk for HCC development. The present results have potentially important clinical implications for physicians and may influence their decisions regarding this website treatment strategy and HCC surveillance

for individual patients. Additional Supporting Information may be found in the online version of this article. “
“Background and Aims:  The effects of an EP4 agonist/antagonist on the healing of lesions produced by indomethacin in the small intestine were examined in rats, especially in relation to the expression of vascular endothelial growth factor (VEGF) and angiogenesis. Methods:  Animals were given indomethacin (10 mg/kg s.c.) and killed at various

time points. To impair the healing of these lesions, a small dose of indomethacin (2 mg/kg p.o.) or AE3-208 (EP4 antagonist: 3 mg/kg i.p.) was given once daily for 6 days after the ulceration was induced, with or without medchemexpress the co-administration of AE1-329 (EP4 agonist: 0.1 mg/kg i.p.). Results:  Indomethacin (10 mg/kg) caused severe damage in the small intestine, but the lesions healed rapidly decreasing to approximately one-fifth of their initial size within 7 days. The healing process was significantly impaired by indomethacin (2 mg/kg) given once daily for 6 days after the ulceration. This effect of indomethacin was mimicked by the EP4 antagonist and reversed by co-administration of the EP4 agonist. Mucosal VEGF expression was upregulated after the ulceration, reaching a peak on day 3 followed by a decrease. The changes in VEGF expression paralleled those in mucosal cyclooxygenase-2 expression, as well as prostaglandin E2 (PGE2) content.

The second limitation is the ethnic homogeneity of the Japanese population. Because the baseline incidence of HCC development differs among population groups, longer-term longitudinal studies in larger cohorts with various population subgroups are required to verify the generality of our results. With the development of potent direct-acting antiviral agents combinations, IFN-free therapy is likely to be approved in the near future. This raises the question of whether posttreatment ALT and/or AFP levels will remain a significant predictor of HCC risk. Moreover, it

is uncertain whether the suppressive effect of viral eradication by IFN-free regimens on hepatocarcinogenesis will be identical to that obtained by IFN-based regimens. Therefore, it is extremely interesting to prove these issues in future studies. In conclusion, Small molecule library cost post-IFN treatment ALT and AFP levels are strictly associated with hepatocarcinogenesis risk in patients with CHC. Measurement of these values is useful for predicting future HCC risk in IFN-treated patients. Suppression of these values after IFN therapy reduces HCC risk even in patients without HCV eradication, while SVRs with increased ALT and/or AFP levels are at risk for HCC development. The present results have potentially important clinical implications for physicians and may influence their decisions regarding learn more treatment strategy and HCC surveillance

for individual patients. Additional Supporting Information may be found in the online version of this article. “
“Background and Aims:  The effects of an EP4 agonist/antagonist on the healing of lesions produced by indomethacin in the small intestine were examined in rats, especially in relation to the expression of vascular endothelial growth factor (VEGF) and angiogenesis. Methods:  Animals were given indomethacin (10 mg/kg s.c.) and killed at various

time points. To impair the healing of these lesions, a small dose of indomethacin (2 mg/kg p.o.) or AE3-208 (EP4 antagonist: 3 mg/kg i.p.) was given once daily for 6 days after the ulceration was induced, with or without MCE公司 the co-administration of AE1-329 (EP4 agonist: 0.1 mg/kg i.p.). Results:  Indomethacin (10 mg/kg) caused severe damage in the small intestine, but the lesions healed rapidly decreasing to approximately one-fifth of their initial size within 7 days. The healing process was significantly impaired by indomethacin (2 mg/kg) given once daily for 6 days after the ulceration. This effect of indomethacin was mimicked by the EP4 antagonist and reversed by co-administration of the EP4 agonist. Mucosal VEGF expression was upregulated after the ulceration, reaching a peak on day 3 followed by a decrease. The changes in VEGF expression paralleled those in mucosal cyclooxygenase-2 expression, as well as prostaglandin E2 (PGE2) content.

The second limitation is the ethnic homogeneity of the Japanese population. Because the baseline incidence of HCC development differs among population groups, longer-term longitudinal studies in larger cohorts with various population subgroups are required to verify the generality of our results. With the development of potent direct-acting antiviral agents combinations, IFN-free therapy is likely to be approved in the near future. This raises the question of whether posttreatment ALT and/or AFP levels will remain a significant predictor of HCC risk. Moreover, it

is uncertain whether the suppressive effect of viral eradication by IFN-free regimens on hepatocarcinogenesis will be identical to that obtained by IFN-based regimens. Therefore, it is extremely interesting to prove these issues in future studies. In conclusion, Rapamycin nmr post-IFN treatment ALT and AFP levels are strictly associated with hepatocarcinogenesis risk in patients with CHC. Measurement of these values is useful for predicting future HCC risk in IFN-treated patients. Suppression of these values after IFN therapy reduces HCC risk even in patients without HCV eradication, while SVRs with increased ALT and/or AFP levels are at risk for HCC development. The present results have potentially important clinical implications for physicians and may influence their decisions regarding selleck kinase inhibitor treatment strategy and HCC surveillance

for individual patients. Additional Supporting Information may be found in the online version of this article. “
“Background and Aims:  The effects of an EP4 agonist/antagonist on the healing of lesions produced by indomethacin in the small intestine were examined in rats, especially in relation to the expression of vascular endothelial growth factor (VEGF) and angiogenesis. Methods:  Animals were given indomethacin (10 mg/kg s.c.) and killed at various

time points. To impair the healing of these lesions, a small dose of indomethacin (2 mg/kg p.o.) or AE3-208 (EP4 antagonist: 3 mg/kg i.p.) was given once daily for 6 days after the ulceration was induced, with or without medchemexpress the co-administration of AE1-329 (EP4 agonist: 0.1 mg/kg i.p.). Results:  Indomethacin (10 mg/kg) caused severe damage in the small intestine, but the lesions healed rapidly decreasing to approximately one-fifth of their initial size within 7 days. The healing process was significantly impaired by indomethacin (2 mg/kg) given once daily for 6 days after the ulceration. This effect of indomethacin was mimicked by the EP4 antagonist and reversed by co-administration of the EP4 agonist. Mucosal VEGF expression was upregulated after the ulceration, reaching a peak on day 3 followed by a decrease. The changes in VEGF expression paralleled those in mucosal cyclooxygenase-2 expression, as well as prostaglandin E2 (PGE2) content.

1, P < 0.001). We therefore fitted a ME-GLM. Firstly, the SEVM retained eight eigenvectors to remove spatial autocorrelation. Once these eight eigenvectors were added as independent variables, the residuals of the selleck kinase inhibitor ME-GLM were no longer spatially autocorrelated (Moran’s I = 0.84, P = 0.2). An analysis of deviance between the GLM and the ME-GLM showed that adding these spatial eigenvectors did provide significantly more information about the variance between core and non-core areas (χ 2 8 = 214.5, P < 0.0001) (Table 3).

Much of the pattern absorbed by the eigenvectors was correlation along a south-north axis (Fig. 3a–d). The last eigenvectors point towards processes taking place at a smaller spatial scale, particularly highlighting areas that were more similar than the rest of the home range (Fig. 3e–h). Spider monkeys in the Santa Rosa sector used core areas containing higher habitat quality than the rest

of their home range. Thus, our study provides quantitative evidence supporting the view that core areas contain critical resources for an animal population (Leuthold, 1977; Samuel et al., 1985). This study also corroborates check details findings in other species in which core areas have more biologically relevant features than non-core areas, such as decayed logs for voles (Thompson et al., 2009) and large trees for woolly spider monkeys (da Silva Júnior et al., 2009). Our results are in agreement with previous findings

that spider monkeys prefer mature forest or forest with the latest successional stage of regeneration (Chapman, 1988; De Gama-Blanchet & Fedigan, 2006; Chaves et al., 2011). Indeed, we demonstrated that spider monkeys have preferences for areas including even more profitable habitat than the rest of their home range: spider monkeys’ MCE公司 core areas contained a higher density and diversity of food trees, more mature forest and a higher density of sleeping trees. Preference for higher quality areas within a matrix of high-quality habitat may explain why spider monkeys are especially vulnerable species when facing habitat fragmentation and disturbance (Ramos-Fernández & Wallace, 2008; Di Fiore et al., 2010). Habitat fragmentation forces spider monkeys to travel between distant high-quality core areas in order to meet their dietary requirements. In addition, given their highly arboreal lifestyle (van Roosmalen & Klein, 1988; Campbell et al., 2005), fragmentation can also eliminate critical arboreal routes to move between core areas (Laurance, 1994; Lindenmayer, Cunningham & Dunnelly, 1994).

5%) moderate (F2), 29

(24.2%) severe (F3), and 24 (20.0%) had liver cirrhosis (F4). Conclusions: In this study, a high proportion of HIV-HCV co-infected patients Erlotinib mw have chronic HCV infection. HCV GT 1 was found in 40% of patients, the favorable IL28B CC genotype is most common, and 67% of patients have a liver fibrosis indicating the need for treatment. Disclosures: Nicolas Durier – Grant/Research Support: ViiV Healthcare Kiat Ruxrungtham – Advisory Committees or Review Panels, Merck, TIBOTEC, Merck, TIBOTEC, Merck, TIBOTEC, Merck, TIBOTEC; Grant/Research Support: Boehringer Ingelheim, Gilead, Roche, TIBOTEC, Boehringer Ingelheim, Gilead, Roche, TIBOTEC, Boehringer Ingelheim, Gilead, Roche, TIBOTEC, Boehringer Ingelheim, Gilead, Roche, TIBOTEC; Speaking and Teaching: Abbott, Bristol-Myers Squibb,

GlaxoSmithKline, J&J, Abbott, Bristol-Myers Squibb, GlaxoSmithKline, J&J, Abbott, Bristol-Myers Squibb, GlaxoSmithKline, J&J, Abbott, Bristol-Myers Squibb, GlaxoSmithKline, J&J Gail Matthews – Advisory Committees or Review Panels: gilead; Consulting: Viiv; Grant/Research Support: Gilead Sciences, janssen; Speaking and Teaching: BMS, MSD The selleck chemicals following people have nothing to disclose: Anchalee Avihingsanon, Kinh Nguyen Van, Bui Vu Huy, Evy Yunihastuti, Andri S. Sulaiman, Sharifah Faridah binti Syed Omar, Ilias Adam Yee, Patricia Morgan, David Boettiger Introduction: 25-hydroxyvitamin D [25(OH)D] level has been associated with advanced liver fibrosis in chronic hepatitis

C virus (HCV) infection. Liver stiffness measurement (LSM) via transient elastography is well validated for assessing fibrosis in chronic HCV. Therefore we assessed any association between LSM and 25(OH)D level and identified predictors medchemexpress of 25(OH) D level in a prospective cohort of patients with chronic HCV infection. Methods: 209 consecutive HCV PCR positive patients attending a dedicated hepatitis C clinic at a tertiary referral center between October 2011 and October 2013 were formally interviewed. Data on duration of infection, alcohol and recreational drug use was prospectively collected, and routine blood tests including 25(OH)D levels obtained. LSM by Fibroscan® was obtained as part of routine care. Predictors of LSM and 25(OH)D level were identified. Results: Mean age of the cohort was 46 ± 10 years with 121 (58%) male. Mode of infection was injecting drug use in 73%, while duration of infection was >20 years in 60%. HCV genotype distribution was: G1 57.4%, G2 4.3%, G3 35.9%, and 2.4% other. Mean 25(OH)D level was 69.7 ± 33.5 nmol/L with vitamin D deficiency (<50 nmol/L) present in 30%. Predictors of 25(OH) D level on multivariate analysis included season (P<0.0001), gender (P<0.0001), INR (P=0.001), and vitamin D supplementation (P=0.04). Median LSM was 6.2 kPa, with 38.7% and 16.5% having an LSM >7.65 kPa and >13.0 kPa respectively. 9.6% of patients used vitamin D supplementation and 34.9% were assessed during Summer/Autumn months.

), with or without bismuth, in the same prescription order, with a treatment duration of 7-14 days (Supporting Table 2). The information on medications was retrieved from the pharmacy prescription database, a subpart of the NHIRD containing details of every prescription including dosage, frequency, starting and ending days, total number of pills, and administration routes. Reliability of the retrieved GDC-0068 price information was verified

independently by two statisticians. Because death usually results from the underlying illness that may also affect the risk of PUB, its occurrence leads to informative censoring in estimating the rebleeding incidence. Therefore, death occurring prior to recurrent bleeding was considered a competing risk event in analysis. The death-adjusted cumulative incidences of recurrent PUB

were calculated using a two-step process and were tested for equality between the two cohorts.19, 20 After confirming the assumption of proportional hazards (Supporting Fig. 1), we applied the modified Cox proportional hazard model in the presence of competing risk event to examine the independent association between cirrhosis and peptic ulcer rebleeding.21, 22 The influence of cirrhosis on PUB recurrence was further explored in different strata according to age, sex, comorbidity, therapeutic agents, and H. pylori status. We defined users of a certain medication SCH727965 manufacturer if the drug duration

was longer than 10% of the observation period. Moreover, we analyzed whether alcoholic etiology or prior episode of AVH confounded the rebleeding risk in patients with cirrhosis. SAS version 9.2 (SAS Institute., Cary, NC) was applied for data management, and R software with package cmprsk_2.1-4 (by Robert J. Gray; http://biowww.dfci.harvard.edu/∼gray/) was used to calculate the cumulative incidence and hazard ratio (HR) in the competing risk analysis. Calculated results were expressed with the estimated number together with the 95% confidence interval (CI). All statistical tests were two-sided, with significance set at P < 0.05. We identified a total of 9,711 patients with liver cirrhosis among 271,030 patients who were hospitalized for the first 上海皓元 time with a primary diagnosis of PUB between 1997 and 2006. This cohort was matched with 38,844 PUB patients without cirrhosis in terms of age, sex, and use of antisecretory agents. Demographic data, H. pylori status, drugs that might protect or induce peptic ulcers, propranolol, major comorbidities, and follow-up duration of the two cohorts are summarized in Table 1. Using the Kaplan–Meier approach without accounting for competing risk events, the 10-year cumulative incidences of recurrent bleeding were 43.7% (95% CI, 41.0-46.3%) and 31.4% (95% CI, 30.6-32.2%), respectively, in patients with cirrhosis and matched controls (P < 0.0001) (Fig. 1A).

She did not have any adverse events during or after the therapy, nor did she feel any epigastralgia, and 2 months later, the urea breath test was negative (0.2 per mil for delta value). Histology and bacterial culture of endoscopic biopsy samples taken from the antrum and corpus 1 year later were negative for H. pylori

infection. The optimal third therapy for patients who failed to eradicate H. pylori infection with the standard first and second therapies containing a PPI and antibiotics has not been established. selleck products Although the patient already had multiple-antibiotic-resistant strains, we had some experiences of successful treatment with a prolonged duration of the same drugs even if the patient had resistant strains,7 so we increased the duration Selleck Buparlisib of treatment with an increased dose of CAM followed by MNZ supplement, which might be called a modified sequential therapy,8 to avoid creating a new antibiotic-resistant stain of the bacteria. However, it was confirmed that the prolonged duration with increased doses of the same drugs did not succeed in eradicating the infection in this patient. Further examination of bacterial culture and

susceptibility testing revealed resistance to LVFX, namely, multiple-antibiotic-resistant H. pylori, although the breakpoint of LVFX for H. pylori therapy had not been determined at that time. Recently, the breakpoint of LVFX was suggested to be 1 µg/mL,17 but even with that breakpoint, the strain would still be evaluated as LVFX-resistant and thus LVFX-containing combination therapy would be ineffective. Therefore, we selected antibiotics according to the profiles in the second

susceptibility testing, which revealed the strain was MINO-sensitive. We selected a MINO-containing combination therapy, the most famous of which is the classical quadruple therapy with PPI, MNZ, bismuth, and MINO.1,4 Because our patient had MNZ-resistant 上海皓元医药股份有限公司 strains, we chose AMPC instead of MNZ for the final therapy because the MIC to AMPC was not too high, although it was not sensitive. Thus we modified the classical quadruple therapy as shown in Table 4. The second factor in the design of the regimen was the doses and cycles of the drugs. PK/PD theory is important in the design of antibiotic regimens.9 Because MINO is time-dependent and has a post-antibiotic effect, we prescribed it twice daily. Because the effect of AMPC depends on the time spent above the MIC, but its clearance time is short,15,18 we increased its cycle to four times daily, although the dose per cycle was less (500 mg) than in the first to third therapies (750 mg). Although the MICs of bismuth salts for H. pylori are high1 and the mechanism of the antibacterial effect is not fully understood, bismuth is reportedly effective in combination with H. pylori therapy in any types of its salts.10–12 Bismuth subnitrate and bismuth subgallate are the only bismuth salts available in Japan, but are not approved for treating H.

She did not have any adverse events during or after the therapy, nor did she feel any epigastralgia, and 2 months later, the urea breath test was negative (0.2 per mil for delta value). Histology and bacterial culture of endoscopic biopsy samples taken from the antrum and corpus 1 year later were negative for H. pylori

infection. The optimal third therapy for patients who failed to eradicate H. pylori infection with the standard first and second therapies containing a PPI and antibiotics has not been established. Proteasomal inhibitor Although the patient already had multiple-antibiotic-resistant strains, we had some experiences of successful treatment with a prolonged duration of the same drugs even if the patient had resistant strains,7 so we increased the duration VDA chemical of treatment with an increased dose of CAM followed by MNZ supplement, which might be called a modified sequential therapy,8 to avoid creating a new antibiotic-resistant stain of the bacteria. However, it was confirmed that the prolonged duration with increased doses of the same drugs did not succeed in eradicating the infection in this patient. Further examination of bacterial culture and

susceptibility testing revealed resistance to LVFX, namely, multiple-antibiotic-resistant H. pylori, although the breakpoint of LVFX for H. pylori therapy had not been determined at that time. Recently, the breakpoint of LVFX was suggested to be 1 µg/mL,17 but even with that breakpoint, the strain would still be evaluated as LVFX-resistant and thus LVFX-containing combination therapy would be ineffective. Therefore, we selected antibiotics according to the profiles in the second

susceptibility testing, which revealed the strain was MINO-sensitive. We selected a MINO-containing combination therapy, the most famous of which is the classical quadruple therapy with PPI, MNZ, bismuth, and MINO.1,4 Because our patient had MNZ-resistant 上海皓元 strains, we chose AMPC instead of MNZ for the final therapy because the MIC to AMPC was not too high, although it was not sensitive. Thus we modified the classical quadruple therapy as shown in Table 4. The second factor in the design of the regimen was the doses and cycles of the drugs. PK/PD theory is important in the design of antibiotic regimens.9 Because MINO is time-dependent and has a post-antibiotic effect, we prescribed it twice daily. Because the effect of AMPC depends on the time spent above the MIC, but its clearance time is short,15,18 we increased its cycle to four times daily, although the dose per cycle was less (500 mg) than in the first to third therapies (750 mg). Although the MICs of bismuth salts for H. pylori are high1 and the mechanism of the antibacterial effect is not fully understood, bismuth is reportedly effective in combination with H. pylori therapy in any types of its salts.10–12 Bismuth subnitrate and bismuth subgallate are the only bismuth salts available in Japan, but are not approved for treating H.