Indeed, direct binding experiments revealed that FVIII bind to recombinant receptor fragments and that binding was inhibited using competing glycan residues. The authors concluded that CD206 contributes to the uptake of FVIII by BVD-523 molecular weight dendritic cells, thereby contributing to the presentation of FVIII to CD4+ T-cells [76]. As with many physiological interactions, the interaction between FVIII and its receptors is also subject to mechanisms of regulation. This is exemplified for instance by the exposure

of the receptor-binding site within the FVIII A2 domain. The A2 domain region Arg484–Phe509 comprises a binding site for LRP1 and vLDL receptor [53,66]. Interestingly, the isolated FVIII heavy chain (A1-a1-A2-a2-B fragment) binds only poorly to both receptors [33,66,77]. Following thrombin treatment, however, this interactive site becomes exposed. Thus, binding of LRP1 and vLDL receptor to the A2 domain is restricted to FVIIIa.

This may explain why site-directed mutagenesis of this interactive site does not result in improved pharmacokinetic parameters when the mutated FVIII procofactor proteins were tested in mice and rats [78]. Noteworthy, this proteolysis-dependent exposure of the binding site has http://www.selleckchem.com/products/sorafenib.html also been reported for the interaction between FVIII A2 domain and FIXa [79]. With regard to the remaining receptor-binding sites, it appears that their exposure is shielded when FVIII is in complex with

its carrier protein VWF. At least three different sites of interaction have been identified for LRP1within the light chain (residues Lys1804–Phe1838, Lys2065/Lys2092 and one within region Ser2173–Tyr2332). Exposure of these sites is unaffected by proteolysis within FVIII light chain [33,77]. However, the interaction of FVIII light chain with LRP1 is completely inhibited in the presence of VWF [33]. This is also true for binding of FVIII light chain to vLDL receptor and CD206 [66,76]. How VWF inhibits binding to these receptors is not completely clear. Potential mechanisms include direct competition for binding to the C2 domain, steric hindrance and alteration of the FVIII conformation so that the respective binding sites are inappropriately exposed. Of course, Lonafarnib clinical trial proteolytic activation of FVIII coincides with loss of high-affinity VWF binding, thereby indirectly allowing exposure of the receptor-binding sites. One intriguing issue is where FVIII is able to interact with the various receptors and how these interactions affect the life cycle of FVIII. The first possible encounter may be at the cell surface where FVIII is produced, which would result in the re-uptake of FVIII following its secretion. If such scenario would exist, one would expect that blocking these receptors would improve production of FVIII.

We checked

the liver function and blood coagulation function every 3–5 days. Considering the above indicators without improvement, we increased the dose of entecavir to 1.0 mg/day after a week admitted to our hospital. We reexamined liver function, coagulation function, and hepatitis B viral load when the patients discharged, and observed the improvement of laboratory indicators and the outcome of the patient’s conditions. Results: The patient discharged after 37 days, when the serum total bilirubin decreased from 467.9 umol/L to 92.1 umol/L, the prothrombin activity from 23% to 69%, and the hepatitis B viral load from 1.29 × 104 IU/ ml to below the lower limit values. Conclusion: The patient discharged after 37 days, when the serum total bilirubin decreased from 467.9 umol/L to 92.1 umol/L, the prothrombin activity www.selleckchem.com/products/Cilomilast(SB-207499).html from 23% to 69%, and the hepatitis B viral load from 1.29 × 104 IU/ ml to below the lower limit values. Key Word(s): 1. Entecavir; 2. Liver failure; 3. Hepatitis B; 4. Nucleoside analogue; Presenting Author: SUYING LIU Additional Authors:

XIAOLIN GUO, FEI LIU, JINGLAN JIN, QIANQIAN ZHANG, HUIFAN JI Corresponding Author: XIAOLIN GUO Affiliations: the first hospital of jilin university; the first hospital of Jinlin universitiy; the first hospital of university Objective: In clinical work, we found that treatment-naïve check details Fossariinae patients with hepatitis B, who were in the process of the application of peginterferon alfa-2a, the level of quantitation of hepatitis B surface antigen has been changing. So we retrospectively reviewed 20 patients who were HBsAg-positive, HBeAg-positive and HBcAb-positive of our hospital from 2009

to 2010. And all of the patients had received the treatment of peginterferon alfa-2a. Methods: We divided 20 patients who had accepted the treatment of peginterferon alfa-2a into 2 groups. Qne group achieved sustained virological response and the other did not. There were no significant differences in the 2 groups in gender, age, genotype, serum HBV – DNA and surface antigen quantitative. Results: 6 patients achieved sustained virological response (24 weeks after the treatment of peginterferon alfa-2a, the quantitative of hepatitis B virus was still under 500 IU/ml), whose quantitative of hepatitis B virus was undetectable at the 24th week of application of peginterferon alfa-2a (the quantitative of hepatitis B virus was under 500 IU/ml), and serological conversion occured at 48th week. The 6 patients’quantitative of hepatitis B surface antigen continued to decline during treatment of peginterferon alfa-2a, quantitative of hepatitis B surface antigen less than 1500 IU/mL at 24th week, which declined 1 log10 IU/ml compared with baseline.

However, studies concerning the association between them have been rare. The aims of this study were to evaluate whether colorectal adenoma increases the risk of GB polyps and analyze the risk factors of GB polyp. Methods: Health examinees who underwent both hepatobiliary sonography and colonoscopy in Yeungnam University Hospital health promotion center from January 2010 to

December 2013 were included. The clinical characteristics, colonoscopy and ultrasonographic findings of the subjects were reviewed and analyzed retrospectively. Results: Among 4327 subjects, colorectal adenoma was detected in 1431 (33.1%) and colorectal cancer in 11 (0.3%). GB polyp was noted in 358 (8.3%) cases. Subjects with colorectal adenoma only or with concomitant colorectal cancer had significantly more GB polyp than those without (143 (10.0%) vs 215 (7.4%), (p = 0.004)). Although mean age of the subjects was selleck products not significantly different CH5424802 order depending on the presence of GB polyp, male was more common in subjects with GB polyp. Five (0.1%) subjects underwent operation of GB polyp and diagnosed as cholesterol polyp and/or adenoma. By multivariate analysis, gender, presence of GB stone, and presence of colorectal adenoma were significantly associated with

presence of GB polyp. Conclusion: Colorectal adenoma is associated with risk of GB polyp. Meticulous examination with ultrasonography of GB should be considered especially in cases with male, presence of GB stone, and colorectal adenoma. Further studies concerning the common pathogenesis associated with both of them are warranted. Key Word(s): 1. gallbladder polyp colorectal adenoma Presenting Author: JI YEONG KWAK Additional Authors: SANG GOON SHIM, KIL JONG YU, DAE HYEON CHO, JI EUN OH, Idelalisib clinical trial CHANG UK JEONG, HYUN CHIN CHO, KWANG MIN KIM, HAE JIN YANG Corresponding Author: JI YEONG KWAK Affiliations: Samsung Changwon Hospital, Samsung Changwon Hospital, Samsung Changwon Hospital, Samsung Changwon Hospital, Samsung Changwon Hospital, Samsung Changwon Hospital, Samsung Changwon Hospital, Hanheart

Hospital Objective: The prevalance of colorectal adenomatous polyps is rapidly increasing in average-risk population in Korea. But, there were few available data about colorectal adenoma in young adults under 40 years of age. We aimed to investigate the prevalence and risk factor of colorectal adenoma in Korean young adulthood 20 to 39 years of age. Methods: A cross-sectional study was conducted and the study participants were composed of asymptomatic young adulthood 20 to 39 years of age who underwent their colonoscopy screening for the first time as part of employer-provided health wellness program at the Health Promotion Center, Samsung Changwon Hospital, Korea, from January 2011 to December 2013.

Here we show that an unusual phosphatidyl-choline species with two saturated 12 carbon fatty acid acyl side chains (dilauroyl phosphatidylcholine

(DLPC)) is an LRH-1 agonist ligand in vitro. DLPC treatment induces bile acid biosynthetic enzymes in mouse liver, increases bile acid levels, and lowers hepatic triglycerides and serum glucose. DLPC treatment also decreases hepatic steatosis and improves glucose homeostasis in two mouse models of insulin resistance. Both the antidiabetic and lipotropic effects are lost in liver-specific Lrh-1 knockouts. These findings identify an LRH-1 dependent phosphatidylcholine signalling pathway that regulates bile acid metabolism and glucose AP24534 purchase homeostasis. The orphan nuclear receptor liver receptor homolog-1 (LRH-1, NR5A2) is regarded as a central regulator of bile salt biosynthesis and bile salts are increasingly recognized as modulators

of glucose and lipid metabolism in mice and men. In their remarkable study, Lee et al.1 identified a ligand for LRH-1, dilauroyl phosphatidylcholine (DLPC), a C12:0/C12:0 phospholipid, which had potent effects on glucose, Talazoparib cost lipid, and bile salt homeostasis in vivo. In a cell-free system, Lee et al. demonstrated by mass spectrometry that DLPC specifically binds to a recombinant LRH-1 ligand-binding domain. Agonism for LRH-1 could be confirmed in an elegant mammalian two-hybrid assay for DLPC and its sister-molecule diundecanoyl phosphatidylcholine (DUPC; C11:0/C11:0). On functional level, DLPC and even more DUPC were strong activators of both human and mouse LRH-1, whereas other nuclear receptors including FXR, CAR, PXR, PPARα and PPARγ were all unaffected in cell culture. DLPC and

DUPC induced transactivation of the native mouse Shp and Oct4 promoters, in line with previous studies on Lrh-1.2, 3 In the human hepatoma cell line HepG2, DLPC induced the expression of CYP8B1. When orally applied to wildtype mice, DLPC and DUPC induced the expression of hepatic Cyp7a1, Cyp8b1, and Sr-b1 but repressed Shp, leading to a modest increase in serum bile salts and total bile salt pool. These findings were consistent with previous observations in why liver-specific Lrh-1 knockouts.4 More strikingly, DUPC- and DLPC-treated mice showed significantly decreased serum glucose, serum nonesterified fatty acids (NEFAs), and hepatic triglycerides. The effects of DLPC were lost in LRH-1 floxed (Lrh-1f/f) mice after administration of adenoviral Cre (Ad-Cre) vector, deleting LRH-1. Comparative oral administration of cholate (100 mg/kg body weight twice daily) improved serum NEFAs and hepatic triglycerides to a similar degree, but did not affect serum glucose. The surprising effects of DLPC on glucose metabolism were further investigated in a diabetic model, utilizing insulin-resistant leptin receptor deficient db/db mice. DLPC improved glucose homeostasis, as assessed by serum insulin, glucose tolerance test (GTT), and insulin tolerance test (ITT).

Further investigation into the societal cost of cognitive dysfunction in cirrhosis is SCH772984 order important to encourage routine diagnosis and therapy of MHE beyond the research setting. “
“See article in J. Gastroenterol. Hepatol. 2010; 25: 1416–1419. Drainage is needed for symptomatic or infected intraabdominal/pelvic fluid collections. The options are surgical, imaging-guided and endoscopic drainage. The surgical approach allows greater access, facilitates more thorough drainage and debridement,

and may address the predisposing condition at the same setting, but at the expense of being more invasive and associated with greater morbidity.1 An imaging-guided approach using computer tomography and ultrasound Selleckchem Saracatinib by the interventional radiologist is less invasive than surgical drainage. However, access for drainage may be limited by interposed organs, blood vessels, nerves and bony structures. There is also the possibility of inadvertent puncture of undetected interposed organs and vessels. Furthermore there is a need to insert an external indwelling drainage catheter for a prolonged period of time which can be uncomfortable for patients; the catheter may also be prone to slippage. Endoscopic transenteric drainage is less invasive than surgery, and may be able to access collections not possible with the imaging-guided approach. In addition, it does away with the need for an indwelling external drainage catheter because an internal

transenteric stent can be inserted, thus improving patient comfort. In the past, before the introduction of endoscopic ultrasound (EUS), endoscopic transenteric drainage was performed by puncturing the endoscopically visible intraluminal bulge caused by the fluid collection, after which guidewire and transenteric

stent insertion were performed under fluoroscopic guidance. Increasingly endoscopic drainage is being performed under real time EUS guidance.1 The difference between EUS and non-EUS guided endoscopic drainage is that during EUS-guided drainage, EUS is used to visualize the fluid collection and guide the initial puncture and guidewire insertion. All subsequent steps such as balloon dilatation of the puncture tract and stent insertion are similar between both approaches, and usually performed with fluoroscopic Chlormezanone monitoring. EUS has made it possible for endoscopic drainage to be performed even in the absence of endoscopic bulging, because the collection can now be visualized directly, thus extending the spectrum of cases that are treatable endoscopically.2,3 With the use of colour Doppler ultrasound during EUS-guided drainage, EUS may potentially decrease the risk of puncturing interposed blood vessels.4 Most published data for EUS-guided drainage are in the context of pancreatic fluid collections, although drainage of liver and subphrenic abscesses has been reported.1,5 There are limited data concerning EUS-guided drainage of pelvic abscesses.

Conclusion:  The epidemiology of gastric cancer in the experience of Hospital “José Carrasco Arteaga” corresponds to result of international data published in several studies. It should make new guidelines for asymptomatic patients older than 40 years taking into account genetic factors, educational, food, refrigeration of food, drinking water, and increase the detection rate of early gastric cancer of 7.1% to 50% as it is in Japan. Conducting Cilomilast solubility dmso annual checkups funded by the state and private enterprise in this way private employees and provide certificates updated every one or two years. Determination by histopathology, tumor type, and marker KI67 ploidies

of pre-neoplastic lesions such as polyps, villous tubules, low-grade dysplasia, metaplasia intestinal secretory type II B sulphomucins

to determine the degree of histological damage, and the presence of infection by H. pylori, since in our setting this is present in more than 50% in children under 10 years of age, especially the differentiated histological type. Key Word(s): 1. gastric cancer; 2. histopatology; 3. early cancer; 4. advanced cancer; Presenting Author: SHANJIN ZHANG Corresponding Author: SHANJIN ZHANG Affiliations: people’s hospital of yichun city Objective: To explore the causes of the common complications and its treatment and prevention measures through the retrospective analysis of 203 cases of ERCP examination. BMS-907351 in vitro Methods: Through reviewing and summarizing 203 cases of clinical data from the diagnostic and therapeutic ERCP examinations from April 2007 to April 2007, analyzing the cause of the complications and treatment methods, effective preventive measures were explored. Results: 9 cases of complications were in 203 cases of ERCP examination (4.43%), and the incidence of diagnostic ERCP was 3.84% (5/130), complicating with acute pancreatitis in 4 cases, hemorrhage

in 1 case; the incidence of therapeutic ERCP was 5.47% (4/73), complicated with hemorrhage these in 2 cases, acute pancreatitis in 1 case, debris basket in 1 case. In 9 cases of complications, 5 cases with the medical therapy (55.56%), 4 cases with the surgical treatment (44.44%). Conclusion: Therapeutic ERCP complications were significantly higher than diagnostic ERCP, may due to a long time of operation and many equipments. The most common complications of diagnostic ERCP was acute pancreatitis, which related with reiterative development, difficult intubation, excessive contrast agents and high pressure. The most common complication of therapeutic ERCP was bleeding, relating with technical operation, accompanying with jaundice, and diabetes. Most of complications after the medical therapy were alleviated, and only a few severe complications required surgical treatment. Key Word(s): 1. ERCP complications; 2. treatment; 3.

Cytotoxicity was assessed by alanine and aspar-tate aminotransferase, lactate dehydrogenase, water-soluble tetrazolium salt 1 proliferation and caspase-3 activity assays. Small animal imaging by dynamic

contrast-enhanced-MRI and choline PET was performed. Results. In both cell lines, artesunate dose dependently reduced cell viability and proliferation (from 50 micromolar: p<0.05). This reduction was enhanced by hypoxia (from 12.5 micromolar: p<0.01). Moreover, artesunate downregulated the secretion of VEGF and placental growth factor in vitro (both p<0.05) and in vivo (both p<0.01). In the mouse model for HCC, artesunate decreased vessel density and tumor burden (both p<0.05). No apparent hepatotox-icity or mortality was observed. In vitro and in vivo activation of the PKR-like endoplasmic reticulum kinase pathway (resp. p<0.05 and p<0.01) together with decreased ATP-binding cassette transporter G2 expression (resp. Cabozantinib cost p<0.01 and p<0.05) by artesunate

was demonstrated. Conclusions. These observations exhibit the potential of artesunate as a safe treatment of HCC optionally combined with current hypoxia-inducing therapies such as transarterial embolization or sorafenib. As a low-cost drug, artesunate might be of particular interest for the developing countries with high incidence of HCC. Disclosures: Isabelle Colle – Advisory Committees or Review Panels: MSD, Janssen, MSD, Gilead; Patent Held/Filed: Trombogenics; Speaking and Teaching: BMS, Janssen The following people have nothing to disclose: Yves-Paul Vandewynckel, Debby Laukens, Anja M. Geerts, Louis Libbrecht, Eliene Bogaerts, Roxadustat Lindsey Devisscher, Annelies Paridaens,

Xavier Verhelst, Christian Vanhove, Benedicte Descamps, Sophie Janssens, Bart Lambrecht, Christophe Van Steenkiste, Hans Van Vlier-berghe Background/Aim: Aptamers not are small synthetic oligonu-cleotides that bind to protein targets with high specificity and affinity. AS1411 is the first nucleic acid aptamer in clinical development for cancers. AS1411 binds to the protein nucle-olin, which is over-expressed in the cytoplasm and on the surface of cancer cells. Glypican-3 (GPC3), a cell surface protein that is highly expressed in hepatocellular carcinoma (HCC), has emerged as a candidate therapeutic target. We aimed to investigate the therapeutic potential of aptamers for HCC by evaluating AS1411 effect on HCC cell growth and by confirming the affinity and specificity of GPC3 aptamer in HCC cells. Methods: Human HCC cell lines (Huh-7, SNU 761 cells) and human cholangiocarcinoma (CCA) cell lines (KMBC, Witt cells) were used. Cell growth was assessed using MTS assay and cell death signaling was explored by immunoblot analysis. Fluorescence-activated cell sorting was performed to evaluate the affinity and specificity of GPC3 aptamers in HCC cells.

8 Unfortunately, the methods used by Hu and Colletti preclude the evaluation of the relevant cell death pathways, but might have

led to the misinterpretation of apoptosis as the principal mechanism of APAP hepatotoxicity. First, the authors show that a caspase inhibitor, which was solubilized in dimethylsulfoxide (DMSO), prevented terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining in hepatocytes. TUNEL is an unspecific marker that cannot distinguish between apoptotic and necrotic DNA fragmentation. Moreover, a DMSO control was not presented but is mandatory, because DMSO is a radical scavenger and by itself exerts cytoprotective effects.9 Second, although the authors show that APAP-induced DNA fragmentation was prevented, it remains unclear whether caspase inhibition indeed improves the survival of mice. There are many cases known in which caspase inhibitors prevent apoptotic

Epigenetics Compound Library datasheet alterations but do not affect cell survival. Finally, on the basis of the assessment of proteolytic caspase fragments, the authors suggest that caspase-9 is activated by APAP. However, they do not present data AZD1208 datasheet on the enzymatic caspase activity. Indeed, caspase-9 does not require cleavage to be activated. Moreover, calpains that are activated by APAP can induce proteolytic cleavage of caspase-9.10 These cleavages generate fragments of Selleck Paclitaxel similar size but occur at sites that render the caspase-9 proteolytically inactive. Hence, the mere cleavage of caspase-9 cannot be taken as sufficient evidence for its activation. Altogether, we have serious concerns regarding the interpretation of the results

by Hu and Colletti. Apoptosis is certainly of major importance in many chronic liver diseases. APAP-induced ALF is, however, one of the few examples where necrosis but not apoptosis predominates. An understanding of the cell death processes will be essential for effective interventions in ALF and other liver diseases. Klaus Schulze- Osthoff M.D*, Heike Bantel M.D†, * Interfaculty Institute for Biochemistry, University of Tübingen, Tübingen, Germany, † Department of Gastroenterology, Hepatology, and Endocrinology, Hannover Medical School, Hannover, Germany. “
“An 80 year old woman presented as an emergency with a two week history of progressively worsening diffuse abdominal pain, bilious vomiting and diarrhoea. There was no history of trauma. She was commenced on Warfarin three weeks before this admission for paroxysmal atrial fibrillation. She previously had undergone a right hemicolectomy for poorly differentiated adenocarcinoma in 2008. Her past history was also significant for hypertension, chronic renal failure and breast cancer. Initial examination revealed normal vital signs. The abdomen was soft but diffusely tender, without guarding or rigidity. Normal bowel sounds were present. There was no lymphadenopathy.

This suggests that obtaining larger samples may improve estimates of lipid concentrations. Our initial results indicate that remote biopsy darts may not be suitable for quantifying lipid content, but we recommend future studies examine the potential for using wider and longer biopsy heads (Gauthier et al. 1997), rinsing samples in distilled water as soon as they are recovered, and, for comparisons with other studies, targeting the same area of the body from which samples are taken from immobilized polar bears (i.e., the rump). We found the painted orange PD darts easy to recover on land despite being smaller than the other darts we tested. Both the silver PC darts and green PC darts were difficult to spot and

recover on land, but the green

PC PF-01367338 supplier darts were generally easy to spot and recover on the sea ice. The red PX darts were the easiest to spot and recover on land given their bright color and large size. Dye marking prevented accidentally resampling 96% check details of the bears. Although we did not resample any bears in autumn 2010 when we did not dye mark bears, we struggled to keep track of which bears had been sampled when darting bears in groups and avoided sampling some bears because we were unsure whether they had already been sampled. In addition, our on-shore survey methodology (progressively flying from east to west) made it unlikely that we would have encountered the same individuals more than once. In the spring, we randomly searched the sea ice, so we had a higher probability of re-encountering previously sampled individuals. We resighted three bears that had been previously

sampled and marked earlier in the spring, and we resampled one individual whose mark was either undetectable or overlooked. We resampled a total of four bears in autumn 2011. Three of these occurred in August when we were marking with a Nyanzol dye. 17-DMAG (Alvespimycin) HCl This was likely in part because the Nyanzol dye marks looked similar to the mud or dirt marks on polar bears during the autumn. In addition, bears may have been molting (Kolenosky 1987) and bears frequently entered the water shortly after being darted, which may have reduced the intensity of marks. Bears marked with livestock solution or tree marking paint in September appeared to quickly lose their marks upon entering the water. The only bear resampled in September 2011 had been darted in the water and marked with tree marking paint, indicating that the paint is not effective at marking when bears are in the water. Neither the solution nor paint appeared to be suitable if marks are desired to last more than several minutes. We have subsequently tested five different dye/paint combinations of various colors, but these did not improve mark longevity (USGS, unpublished data). Further study should focus on finding appropriately colored, fast-fixing dye. The PC marking darts provided a larger and darker mark on bears than the PX darts (Fig. 5).

P-values <0.05 were taken as statistically significant. Values in impedance–pH monitoring are presented as medians and in the 25th–75th percentiles. An analysis using a generalized linear mixed model was done for comparisons between patients Selleck Pritelivir with pathological acid exposure and patients with pathological bolus exposure.

The characteristics of the patients are shown in Table 1. Typical esophageal symptoms, such as heartburn or acid regurgitation, were observed in 41 patients (54.6%). Sixteen patients (21.3%) had reflux esophagitis, as determined by UGI endoscopy. Esophageal manometry identified 37 patients (49.3%) with esophageal dysmotility. This included nutcracker esophagus in 17 patients, ineffective esophageal motility in 12, non-specific esophageal motility disorder in five, and other findings in three patients. PPI medication improved the symptoms in 50 selleck inhibitor of 54 patients (92.6%), regardless of the presence of GERD. The results of MII–pH metering in patients with NCCP are summarized in Table 2. The impedance test determined a longer bolus exposure in the postprandial period than in the fasting period (P = 0.003). In addition, reflux episodes predominantly involved the distal esophagus. The composition of GERD-related NCCP changed in the postprandial period (Fig. 1). A total

of 48 patients (64%) were compatible with a diagnosis of GERD-related NCCP in the postprandial period. Sixteen patients (21.3%) had GERD-related NCCP upon pH metering.

In contrast, 40 patients (53.3%) also proved to have GERD-related NCCP, according to the impedance test; this included 13 patients (17.3%) who showed pathological bolus exposure and pathological acid exposure at the same acetylcholine time. In this study, pathological bolus exposure upon MII was increased during meals, because more patients in the postprandial period had pathological bolus exposure than in the fasting period (40 patients [53.3%]vs 18 patients [24.0%], respectively). Patients with NCCP were classified as having pathological acid exposure or pathological bolus exposure, according to the results of MII–pH metering. When the patients were classified based on MII–pH metering, 16 (21.3%) showed pathological acid exposure, and 40 (53.3%) showed pathological bolus exposure, respectively (Table 3). There was no significant difference in age, sex, typical esophageal symptoms, presence of esophageal erosion, esophageal dysmotility, improvement with PPI medication, symptom index ≥50%, percentage of time clearance pH below 4 ≥4%, and all reflux time ≥1.4% in the fasting period between the two groups. Although the median values of both patients with pathological acid exposure and patients with pathological bolus exposure were within normal limits, the DeMeester score of patients with pathological acid exposure was higher than that of patients with pathological bolus exposure (P = 0.002). The patients were divided into two groups, according to the presence of GERD (Table 4).