As for O-linked glycosylation, the presence of at least seven O-linked carbohydrate structures glycans in the FVIII B-domain has been reported [3,4]. Unfortunately, no information Trichostatin A cost on their location and precise structure is available, except for the detection of a single di-sialylated T-antigen at position Ser750 in a recombinant B-domainless FVIII preparation

[5]. Interestingly, comparison of pd-FVIII and rFVIII has revealed a number of subtle differences in their glycan structures. First, pd-FVIII but not rFVIII seems to carry blood-group determinants on its biantennary sugar chains [1]. Second, Hironaka et al. detected the presence of Gal(α1-3) Gal structures on rFVIII derived from BHK-cells but not on pd-FVIII. The incorporation of Gal(α1-3) Gal structures requires the presence of α1,3-galactosyltransferase, an enzyme that is mainly expressed in cells of non-primate find more origin, the type of cells used for the production of current rFVIII products. Third, human cells differ from other mammalian cells in that they express a non-functional variant of cytidine monophosphate N-acetylneuraminic acid hydroxylase, which catalyses the conversion

of the sialic acid N-acetyl neuraminic acid (Neu5Ac) into N-Glycolylneuraminic acid (Neu5Gc) [6]. It is possible therefore that rFVIII contains both Neu5Ac and Neu5Gc, whereas pd-FVIII selectively carries the Neu5Ac sialic acid. Of note, the non-human nature of Gal(α1-3)Gal and Neu5Gc structures has been associated with the development of antibodies against these structures, and the presence of, for instance, the Gal(α1-3)Gal moiety on biotherapeutics can cause adverse events [6,7]. Whether these structures contribute to the immune response following treatment with rFVIII is unknown, but so far no evidence in support of this possibility has been provided. Intracellular

processing and routing of FVIII requires the interaction of this molecule with a number of glycan-binding chaperones, including calnexin, calreticulin and the LMAN1(ERGIC53)/MCFD2 complex (for a more detailed review see [8]). Calnexin and calreticulin are resident ER chaperone proteins that interact with mono-glucosylated carbohydrate structures that are present on proteins in the early stage of synthesis, and are part of the quality control system MCE of the cell. The interaction with both chaperones is necessary for optimal protein folding. Once properly folded, trimming of the terminal glucose residue results in dissociation of the protein from both chaperones, allowing the protein to be routed from the ER to the Golgi. With regard to FVIII, it has been shown that the glycans in the B-domain play an important role in the interaction with calreticulin/calnexin [9]. The transition from the ER to the Golgi involves the interaction between FVIII and the LMAN1 (ERGIC-53)/MCFD2 complex.

Methods: Using analytic study design, conducted in outpatient Koja Hospital from June 2013 until July 2013, for all patients with dyspepsia who will be run ramadan fasting. Subjects are divided into 2 groups, one group was given omeprazole during fasting, while others were given a placebo. Before and after 2 weeks of fasting DSSI scores were taken. DSSI scores assessed changes in both groups

were compared using student t test. Results: DSSI LBH589 cell line scores on average before the intervention (pre-test) of the two groups was not significant (p = 0.9). In the omeprazole group obtained without worsening DSSI score from 27.7 ± 14 to 36 ± 14.8 (p = 0.001), whereas the omeprazole group obtained scores from 27.2 ± 9.4 to 30 ± 9.9 (p = 0.08). In the group without omeprazole score worsened by 8.3 ± 7.2 and

in the omeprazole group with only 2.7 ± 5.7 (p = 0.02). Conclusion: Deterioration of DSSI score was significantly occurred in the group without omeprazole therapy. Omeprazole during the month of fasting can reduce exacerbations in patients with dyspeptic complaints. Key Word(s): 1. Dyspepsia; see more 2. DSSI; 3. fasting; 4. Ramadan Presenting Author: WILLIAM TAM Additional Authors: S YEAP, P LEONG, A TIEU, R SINGH, B GEORGE, G NIND Corresponding Author: WILLIAM TAM Affiliations: Lyell Mcewin Hospital, Lyell Mcewin Hospital, Lyell Mcewin Hospital, Lyell Mcewin Hospital, Lyell Mcewin Hospital, Lyell Mcewin Hospital Objective: Surgical management of bariatric complications may be associated with considerable morbidity. Endoscopic

intervention has been increasingly used to manage these complications. However, data on its safety and efficacy are lacking. Methods: A retrospective review of endoscopic intervention from 2009 to 2014 was undertaken in 11 patients (M : F = 2:9, mean age 39.5 years, mean BMI:48.3) with significant bariatric complications requiring hospital admission. All bariatric surgery – vertical banded gastroplasty (VBG), laparoscopic sleeve gastrectomy (LSG) or laparascopic gastric banding (LGB) were performed by the same experienced surgeon. Results: Complications included leaks, sinus/fistulae, stricture formation and migrated silastic ring. 63.6% of the complications occurred early (<30 days) post-bariatric surgery. medchemexpress In 5 patients (45.5%) the bariatric complications were successfully managed with endoscopic intervention alone. The remaining 6 (54.5%) patients had both surgical and endoscopic interventions. Endoscopic techniques used to treat stenosis included through-the-scope (TTS) balloon dilatation (n = 4), wire-guided dilatation (n = 1) and fully-covered stent insertion (n = 2). Post-operative leaks, fistulae and sinuses were managed with fibrin glue injection, clips (TTS and/or over-the-scope clips) and/or insertion of fully-covered stents.

The pertinent question concerns the primary locus of an exercise-mediated benefit in NAFLD, because this has direct implications for exercise prescription. For example,

if exercise exerts the bulk of its benefit via lowering visceral adiposity, selleck compound therapies known to effect visceral adipose tissue reduction (including weight loss) would be best advocated in NAFLD. Yet, if enhancement of cardiorespiratory fitness or insulin sensitivity confers substantial hepatic improvements, there are methods of achieving this which are not contingent upon high energy expenditure and/or weight loss. For instance, progressive resistance training is a stimulus for whole-body insulin sensitization43 and carries less time cost than current aerobic exercise guidelines. BAY 57-1293 solubility dmso In this regard, Zelber-Sagi et al. recently noted an inverse relationship between resistance training and NAFLD, which persisted after adjustment for BMI.24 Data from experimental studies involving young, lean cohorts clearly show that exercise training involving repeated (5-8 times) short bursts of cycling exercise (10-30 seconds) increases maximal aerobic power and muscle oxidative enzymes

and lowers plasma triglycerides to an equivalent level to that seen with traditional aerobic exercise training regimes, despite a 70%-90% reduction in energy expenditure and weekly time commitment.57 上海皓元医药股份有限公司 Such studies are clearly warranted, because lack of time is the principal reason for drop-out from structured exercise programs and the most commonly cited barrier to initiating exercise.27 At present, there is an overall paucity of evidence concerning the benefits of PA as treatment for NAFLD. What is available shows a conclusive benefit of PA when coupled with energy restriction when weight loss is achieved, and it is encouraging for an independent benefit

in the absence of weight loss. Although weight loss remains fundamental, patients should be counseled on the spectrum of benefits conferred by regular PA. Management should include assessment of cardiorespiratory fitness and PA levels, and the setting of lifestyle goals based on adoption of regular exercise, with a focus on the attainment of sustainable PA habits. The dose (intensity and volume) of PA required to reduce liver fat remains unclear. Furthermore, from the present evidence, it is difficult to discern the relative importance of structured exercise and fitness versus less structured PA. This conundrum is borne out in data from cross-sectional research, which shows that both high PA and cardiorespiratory fitness correlate negatively with fatty liver (Tables 2 and 3).

The pertinent question concerns the primary locus of an exercise-mediated benefit in NAFLD, because this has direct implications for exercise prescription. For example,

if exercise exerts the bulk of its benefit via lowering visceral adiposity, Y-27632 nmr therapies known to effect visceral adipose tissue reduction (including weight loss) would be best advocated in NAFLD. Yet, if enhancement of cardiorespiratory fitness or insulin sensitivity confers substantial hepatic improvements, there are methods of achieving this which are not contingent upon high energy expenditure and/or weight loss. For instance, progressive resistance training is a stimulus for whole-body insulin sensitization43 and carries less time cost than current aerobic exercise guidelines. LY2157299 In this regard, Zelber-Sagi et al. recently noted an inverse relationship between resistance training and NAFLD, which persisted after adjustment for BMI.24 Data from experimental studies involving young, lean cohorts clearly show that exercise training involving repeated (5-8 times) short bursts of cycling exercise (10-30 seconds) increases maximal aerobic power and muscle oxidative enzymes

and lowers plasma triglycerides to an equivalent level to that seen with traditional aerobic exercise training regimes, despite a 70%-90% reduction in energy expenditure and weekly time commitment.57 上海皓元医药股份有限公司 Such studies are clearly warranted, because lack of time is the principal reason for drop-out from structured exercise programs and the most commonly cited barrier to initiating exercise.27 At present, there is an overall paucity of evidence concerning the benefits of PA as treatment for NAFLD. What is available shows a conclusive benefit of PA when coupled with energy restriction when weight loss is achieved, and it is encouraging for an independent benefit

in the absence of weight loss. Although weight loss remains fundamental, patients should be counseled on the spectrum of benefits conferred by regular PA. Management should include assessment of cardiorespiratory fitness and PA levels, and the setting of lifestyle goals based on adoption of regular exercise, with a focus on the attainment of sustainable PA habits. The dose (intensity and volume) of PA required to reduce liver fat remains unclear. Furthermore, from the present evidence, it is difficult to discern the relative importance of structured exercise and fitness versus less structured PA. This conundrum is borne out in data from cross-sectional research, which shows that both high PA and cardiorespiratory fitness correlate negatively with fatty liver (Tables 2 and 3).

The

study was a prospective investigation of the changes in immunoregulatory markers in the blood, bone marrow, and liver allograft in recipients converted from TAC monotherapy to SRL monotherapy for clinical indications (e.g., TAC toxicity). Inclusion criteria were as follows: age ≥18 years; ≥6 months post-LT; TAC monotherapy ≥1 month before SRL monotherapy conversion for nephrotoxicity (glomular filtration rate [GFR] 30-60 cc/min by modified diet in renal disease [MDRD]) or other indication; ≥6 months without a rejection episode; Target Selective Inhibitor Library price no lymphocyte depletion therapy for ≥1 year; normal liver-function tests; and no rejection or fibrosis on preconversion liver biopsy. Exclusion criteria were as follows: previous liver or multiorgan transplant; previous immune or viral liver disease unless hepatitis C virus (HCV) RNA was undetectable; proteinuria (≥0.5 g/day); estimated glomerular filtration rate (eGFR) ≤30 cc/min; ≥2 rejections

post-LT; history of hepatic artery thrombosis; hematological abnormalities or severe hypertriglyceridemia; active infection or malignancy; and inadequacy for follow-up. All patients signed informed consent and were followed for 7 months after SRL conversion. The protocol conformed to the Declaration of Helsinki guidelines and was approved by the Northwestern Institutional buy Afatinib Review Board (Northwestern University Feinberg School of Medicine, Chicago, IL). History and physical exams, complete blood counts, comprehensive metabolic panels, fasting lipids, hemoglobin A1C tests (HgA1C), and spot urine protein:creatinine ratios were performed before and 3 and 6 months after conversion. Bone marrow aspirations and percutaneous liver biopsies were performed once before and 6 months after conversion. For conversion, SRL at 2 or 3 mg (< or ≥100 kg body weight) daily was initiated with subsequent weekly SRL trough-level monitoring. When these reached ≥5 ng/mL, TAC was discontinued followed by weekly laboratory tests and SRL trough levels (goal, 5-8 ng/mL) for 1 month,

then monthly. Prospective liver- and renal-function tests, lipid levels, urine protein:creatinine 上海皓元 ratios, and any new SRL toxicities were recorded. Treg immunophenotyping (twice before conversion and 3, 4, 6, and 7 months after conversion): Peripheral blood mononuclear cells (PBMCs) were isolated from heparinized samples on Ficoll-Hypaque gradients. Tregs were enumerated utilizing extracellular immunofluorescent staining with CD3-FITC (fluorescein isothiocyanate), CD4-PerCP (peridinin-chlorophyll protein complex), CD8-PerCP, CD25-APC, and CD127-FITC (BD Biosciences, San Diego, CA). After fixation and permeabilization, the cells were washed and incubated with anti-human FOXP3-PE (phycoerythrin) or rat immunoglobulin G2a-PE isotype control (eBioscience, San Diego, CA) (21, 22).

0001). Specifically, concomitant regimen eradicated 7/10, 70% of dual resistant strains as first-line treatment and 5/12, 42% as second-line treatment. Multivariate analysis showed that dual resistance was the only independent significant predictor of treatment failure. The 10-days “concomitant” regimen is effective and safe first-line H. pylori treatment, in a high clarithromycin resistance

area, although dual antibiotic resistance may compromise its effectiveness. “
“Sequential therapy is a two-step therapy achieving a promising eradication rate for Helicobacter pylori infection. The rationale of sequential method has been proposed that amoxicillin weakens bacterial cell walls in the initial phase of treatment,

preventing the development of drug efflux channels for clarithromycin and metronidazole Temozolomide price used in the second phase. The aim of this prospective, randomized, controlled study was to investigate whether the efficacy of reverse sequential therapy was noninferior to sequential therapy in the treatment of H. pylori infection. From January 2009 to December 2010, consecutive H. pylori-infected patients were randomly assigned to receive either sequential therapy (a 5-day dual therapy with pantoprazole plus amoxicillin, followed by a 5-day triple therapy with pantoprazole plus clarithromycin and metronidazole) or reverse sequential therapy (a 5-day triple therapy with pantoprazole plus clarithromycin and Palbociclib mw metronidazole, followed by a 5-day dual therapy with pantoprazole plus amoxicillin). H. pylori status was MCE examined 6 weeks after the end of treatment by rapid urease and histology or urea breath

test. One hundred and twenty-two H. pylori-infected participants were randomized to receive sequential (n = 60) or reverse sequential therapy (n = 62). The eradication rates, by intention-to-treat analysis, were similar: 91.9% (95% confidence interval (CI): 85.1–98.7%) for sequential therapy and 96.7% (95% CI: 92.2–101.2%) for reverse sequential therapy (p = .44). Per-protocol analysis also showed similar results: 91.8% (95% CI: 84.9–98.7%) for sequential group and 96.7% (95% CI: 92.2–101.2%) for reverse sequential therapy (p = .43). The two treatments exhibited comparable frequencies of adverse events (11.3% vs 6.7%, respectively) and drug compliance (98.4% vs 100%, respectively). The overall resistance rates of antibiotics were clarithromycin 10.5%, amoxicillin 0%, and metronidazole 44.2% of patients, respectively. The dual resistance rate of clarithromycin and metronidazole was 4.2%. Both therapies achieved a high eradication rate for clarithromycin-resistant strains (100% vs 100%, respectively) and metronidazole-resistant strains (81.8% vs 95%, respectively) by intention-to-treat analysis. Ten-day reverse sequential therapy and standard sequential therapy are equally effective for H. Pylori eradication.

We define this endocytic motif by site-directed mutagenesis as a canonical tyrosine-based motif 1310YYKLV1314 (YxxØ). When expressed in HEK293T cells, TacCterm is constitutively internalized via a dynamin- and clathrin-dependent pathway. Mutation of the Y1310Y1311 amino acids in TacCterm and in full-length human BSEP blocks the internalization. Subsequent sequence analysis reveals this motif to be highly conserved between the closely related ABCB subfamily members that

mediate ATP-dependent transport of broad substrate specificity. Conclusion: Ibrutinib in vivo Our results indicate that constitutive internalization of BSEP is clathrin-mediated and dependent on RG-7388 research buy the tyrosine-based endocytic motif at the C-terminal end of BSEP. (HEPATOLOGY 2012;55:1901–1911) The bile salt export pump (BSEP, ABCB11) is an adenosine triphosphate (ATP)-dependent

bile salt pump that functions at the liver canalicular membrane. Mutations in BSEP that result in defective trafficking can cause cholestatic disorders including progressive familial intrahepatic cholestasis type 2 (PFIC2), benign recurrent intrahepatic cholestasis, and cholestasis of pregnancy.1-3 The amount of BSEP on the canalicular membrane is regulated by postprandial demand for the enterohepatic circulation of bile salts.4 Pulse-chase experiments revealed a large intracellular pool of Bsep in rat liver that is

mobilized for targeting and recycling of Bsep to and from the canalicular membrane.5 Furthermore, Bsep constitutively recycles between the canalicular membrane and Rab11a-positive 上海皓元医药股份有限公司 endosomes in WIF-B9 cells.6 Thus, the maintenance and retrieval of BSEP on the apical membrane is crucial for its function.4, 6 The retrieval of Bsep also plays an important role in the pathophysiology of rat cholestatic models. Bsep protein is internalized in isolated perfused rat liver and rat hepatocyte couplets after estradiol 17β-D-glucuronide administration, a process blocked by protein kinase inhibitors or dibutyrl cyclic adenosine monophosphate (cAMP).7, 8 Cholestasis due to lipopolysaccharide administration, as well as oxidative stress in rats, results in internalization of Bsep.9 However, the mechanism by which Bsep is retrieved from the canalicular membrane remains largely unknown. In Madin-Darby canine kidney (MDCK) cells, dominant-negative expression of Eps15 increases the apical membrane expression of rat Bsep, suggesting that a clathrin-dependent mechanism may play a role in regulating cell surface Bsep expression.10 Clathrin has been shown to be involved in apical endocytosis in rat hepatocytes.11 Targeting and trafficking of membrane proteins depends on sequence motifs and protein–protein interactions with various forms of trafficking machinery.

14(0.98-1.33) and 1.19(1.03-1.38)(P-trend=0.02). Conclusion: A common genetic variant in NPC1L1, mimicking the effects of ezetimibe on LDL cholesterol, was associated with increased risk of symptomatic gallstone disease and with a trend towards reduced risk of ischemic vascular disease. These results raise the question whether long-term treatment with ezetimibe might increase the risk of symptomatic INCB024360 price gallstone disease. Disclosures:

The following people have nothing to disclose: Bo K. Lauridsen, Stefan Stender, Ruth Frikke-Schmidt, Bøfrge G. Nordestgaard, Anne Tybjærg-Hansen Background / Aim: The secretion of the intestinal hormone FGF19 is induced by binding of bile acid (BA) to the bile acidnuclear farnesoid X receptor (FXR) in the terminal ileum.

On the other side FGF19 suppresses hepatic bile acid biosynthesis. We hypothesized that patients with Crohn΄s disease (CD) show lower FGF19 levels as compared to patients with ulcerative colitis (UC). Patients and Methods: In total, we recruited 12 CD patients after ileocecal resection (ICR), 12 nonoperated CD patients and 12 UC patients as controls in remission. Serum FGF19 levels were determined by ELISA after 10 hrs of overnight fasting. All individuals received orally 1g fat (Calogen®) per kg body weight, and FGF19 levels were measured after 2, 4 and 6 hrs. Serum concentrations of BA and 7α-OHcholesterol levels, which is a valid marker Everolimus manufacturer of BA biosynthesis, were determined by GC-MS after 2, 4 and 6 hrs. Results: Basal FGF19 levels are significantly lower in CD patients (± ICR) as compared to UC patients. The increase of FGF19 levels 2, 4 und 6 hrs after the oral fat load differs between UC and CD (ICR+) patients, with highest levels after 4 hrs in UC patients (p<0.05). CD (ICR+) patients display the lowest FGF19 levels at all time points. Fasting and postprandial levels of BA are not significantly different between CD and UC patients. However at all time points, serum 7α-OH-cholesterol levels are significantly higher in CD (ICR+) in comparison to UCpatients. In the

whole study cohort basal FGF19 and basal 7 α- O H-cholesterol levels are inversely correlated (r=0.397, p=0.017). Conclusions: Low FGF19 levels in CD (± ICR) patients could be the consequence of persistent inflammation and impaired bile acid signaling in the ileum. MCE公司 CD (ICR+) patients display lowest FGF19 levels, consistent with highest 7α-O H-cholesterol levels and lack of repression of BA synthesis. We speculate that this observation results from insufficient intestinal FXR activity in CD. Disclosures: The following people have nothing to disclose: Dana Friedrich, Dieter Luetjohann, Frank Lammert, Christoph Reichel “
“Liver inflammation is greater in nonalcoholic steatohepatitis (NASH) than steatosis, suggesting that immune responses contribute to nonalcoholic fatty liver disease (NAFLD) progression.

14(0.98-1.33) and 1.19(1.03-1.38)(P-trend=0.02). Conclusion: A common genetic variant in NPC1L1, mimicking the effects of ezetimibe on LDL cholesterol, was associated with increased risk of symptomatic gallstone disease and with a trend towards reduced risk of ischemic vascular disease. These results raise the question whether long-term treatment with ezetimibe might increase the risk of symptomatic Paclitaxel purchase gallstone disease. Disclosures:

The following people have nothing to disclose: Bo K. Lauridsen, Stefan Stender, Ruth Frikke-Schmidt, Bøfrge G. Nordestgaard, Anne Tybjærg-Hansen Background / Aim: The secretion of the intestinal hormone FGF19 is induced by binding of bile acid (BA) to the bile acidnuclear farnesoid X receptor (FXR) in the terminal ileum.

On the other side FGF19 suppresses hepatic bile acid biosynthesis. We hypothesized that patients with Crohn΄s disease (CD) show lower FGF19 levels as compared to patients with ulcerative colitis (UC). Patients and Methods: In total, we recruited 12 CD patients after ileocecal resection (ICR), 12 nonoperated CD patients and 12 UC patients as controls in remission. Serum FGF19 levels were determined by ELISA after 10 hrs of overnight fasting. All individuals received orally 1g fat (Calogen®) per kg body weight, and FGF19 levels were measured after 2, 4 and 6 hrs. Serum concentrations of BA and 7α-OHcholesterol levels, which is a valid marker check details of BA biosynthesis, were determined by GC-MS after 2, 4 and 6 hrs. Results: Basal FGF19 levels are significantly lower in CD patients (± ICR) as compared to UC patients. The increase of FGF19 levels 2, 4 und 6 hrs after the oral fat load differs between UC and CD (ICR+) patients, with highest levels after 4 hrs in UC patients (p<0.05). CD (ICR+) patients display the lowest FGF19 levels at all time points. Fasting and postprandial levels of BA are not significantly different between CD and UC patients. However at all time points, serum 7α-OH-cholesterol levels are significantly higher in CD (ICR+) in comparison to UCpatients. In the

whole study cohort basal FGF19 and basal 7 α- O H-cholesterol levels are inversely correlated (r=0.397, p=0.017). Conclusions: Low FGF19 levels in CD (± ICR) patients could be the consequence of persistent inflammation and impaired bile acid signaling in the ileum. 上海皓元 CD (ICR+) patients display lowest FGF19 levels, consistent with highest 7α-O H-cholesterol levels and lack of repression of BA synthesis. We speculate that this observation results from insufficient intestinal FXR activity in CD. Disclosures: The following people have nothing to disclose: Dana Friedrich, Dieter Luetjohann, Frank Lammert, Christoph Reichel “
“Liver inflammation is greater in nonalcoholic steatohepatitis (NASH) than steatosis, suggesting that immune responses contribute to nonalcoholic fatty liver disease (NAFLD) progression.

S8). Although these results are not conclusive due to limited cases, they appear consistent with the hypothesis that both NVP-BGJ398 molecular weight type-B and type-C CHC could originate from the same hepatic progenitor cells shared by HCC and CHC tumors. A new histological subtyping of CHC according to the WHO Classification based on the presence of stem-cell features has been proposed.52 Long-term follow-up of larger cohorts is needed to define the

clinical and biological behavior of all CHC cases. Our analysis dissecting the heterogeneous ICC based on the expression of stem cell-like signatures could classify ICC cases into subgroups with more uniform and prognostic phenotypes. In principle, targeting molecular pathways specific to each subpopulation would be more effective for the development of personalized clinical strategies. We suggest that the miR-200c-associated EMT pathway and stem-cell activities may contribute to the development of the HpSC-ICC tumors. The association of EMT with poor prognosis is well known in many cancer types. Moreover, recent studies have demonstrated the critical role of miR200c

in the control of stem/progenitor cell renewal and differentiation. Our findings are consistent with the hypothesis Imatinib supporting the pivotal role of miR-200c in the aggressive progression of stem-like ICC. We thank Drs. Gregory J. Gores for H69 cells, Kathleen C. Flanders and Lalage M. Wakefield for anti-TGF-beta1 antibody, and Li Wang for the miR-200c luciferase reporter. We also thank Dr. Xiaolin Wu and members of the microarray core at the NCI-SAIC for help on microarray analysis and Ms. Karen Yarrick for bibliographic assistance. Additional

Supporting Information may be found in the online version of this article. “
“Background and Aim:  To clarify the usefulness of a newly designed method for measuring intraduodenal pH to examine the relationship between duodenal acidity and upper gastrointestinal symptoms during intragastric acid infusion. Methods:  The study subjects were six healthy volunteers. A Bravo pH capsule with thread fixed to the gastric wall medchemexpress was endoscopically introduced into the second portion of the duodenum, and intraduodenal acidity was measured during intragastric infusion of 300 mL of 0.1 mol/L hydrochloric acid or pure water through an elemental diet tube. The severity of several upper gastrointestinal symptoms were assessed by using a 10-cm visual analogue scale every 2 min for up to 30 min, and the area under the severity scale-time curve (cm × min.) were calculated. Results:  The percentage time during 30 min when the intraduodenal pH was < 4.0 and was significantly greater than during water infusion (61.4 ± 6.1% vs 24.8 ± 6.5%). Several upper gastrointestinal symptoms were observed during acid infusion (acid vs water epigastric heaviness, 29.1 ± 12.0 vs 2.7 ± 1.