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BACKGROUND: Since high-quality evidence on conservative treatment of acute appendicitis using antibiotics has increased, differentiation of patients with complicated appendicitis (CA) from those with simple appendicitis (SA) has become increasingly important. Previous studies have revealed that male gender, advanced age, comorbid conditions, prehospital delay, fever, and anorexia are risk factors of perforated appendicitis. Elevated serum C-reactive protein (CRP) level and hyponatremia have also been reported as predictive biomarkers of CA. However, confounding between various factors is problematic because most previous studies were limited to univariate analysis. AIM: To evaluate non-laboratory and laboratory predictive factors of CA using logistic regression analyses. METHODS: We performed an exploratory, single-center, retrospective case-control study that evaluated 198 patients (83.9%) with SA and 38 patients (16.1%) with CA. Diagnoses were confirmed by computed tomography images for all cases. We compared age, sex, onset-to-visit interval, epigastric/periumbilical pain, right lower quadrant pain, nausea/vomiting, diarrhea, anorexia, medical history (of previous non-surgically treated appendicitis, diabetes, hypertension, dyslipidemia, liver cirrhosis, hemodialysis, chronic lung diseases, malignant tumors, immunosuppressant use, and antiplatelet use), vital signs, physical findings, and laboratory data to select the explanatory variates for logistic regression. Based on the univariate comparisons, we performed logistic regression for clinical differentiation between CA and SA using only non-laboratory factors and also including both non-laboratory and laboratory factors. RESULTS: The 236 eligible patients consisted of 198 patients (83.9%) with SA and 38 patients (16.1%) with CA. The median ages were 34 years old [interquartile ranges (IR), 24-45 years] in the SA group and 49 years old (IR, 35-63 years) in the CA group (P < 0.001). The median onset-to-visit interval was 1 d (IR, 0-1) and 1 d (IR, 1-2) in the SA and CA groups, respectively (P < 0.001). Heart rate, body temperature, and serum CRP level in the CA group were significantly higher than in the SA group; glomerular filtration rate and serum sodium were significantly lower in the CA group. Anorexia was significantly more prevalent in the CA group. The regression model including age, onset-to-visit interval, anorexia, tachycardia, and fever as non-laboratory predictive factors of CA (Model 1) showed that age ≥ 65 years old, longer onset-to-visit interval, and anorexia had significantly high odds ratios. The logistic regression for prediction of CA including age, onset-to-visit interval, anorexia, serum CRP level, hyponatremia (serum sodium < 135 mEq/L), and glomerular filtration rate < 60 mL/min/1.73 m(2) (Model 2) showed that only elevated CRP levels had significantly high odds ratios. Under the curve values of receiver operating characteristics curves of each regression model were 0.74 for Model 1 and 0.87 for Model 2. CONCLUSION: Our logistic regression analysis on differentiating factors of CA from SA showed that high CRP level was a strong dose-dependent predictor of CA.

BackgroundRecent reports suggest that Helicobacter pylori infection may be related to the onset of certain diseases. However, the H. pylori-related factors that play a role in the etiology of these diseases have not been fully elucidated. This study aimed to elucidate the impact of H. pylori infection on the structure of commensal duodenal microbiota and their biofunctions.MethodsForty-seven (20 male, 27 female) subjects who underwent gastric cancer screening were enrolled. Duodenal fluid samples were aspirated from the descending duodenum and analyzed by 16S rRNA gene sequencing.ResultsThirteen subjects were positive for H. pylori, while thirty-four were negative. We observed 1404 bacterial operational taxonomic units from 23 phyla and 253 genera. In the H. pylori-positive group, we observed higher abundances of Proteobacteria and lower abundances of Actinobacteria and TM7 than that in the H. pylori-negative group. The abundances of 10 genera differed significantly between the H. pylori-positive and -negative groups. Microbiota features in the H. pylori-positive group was significantly influenced by 12 taxa primarily belonging to Gammaproteobacteria. Microbial functional annotation collated using the Kyoto Encyclopedia of Genes and Genomes Orthology database showed that 12 microbial metabolic pathways (Synthesis and degradation of ketone bodies, Tryptophan metabolism, N-glycan biosynthesis, Ether lipid metabolism, Lipoarabinomannan (LAM) biosynthesis, Linoleic acid metabolism, alpha-Linolenic acid metabolism, Biotin metabolism, Carotenoid biosynthesis, Phenylpropanoid biosynthesis, Biosynthesis of siderophore group nonribosomal peptides, Biosynthesis of terpenoids and steroids) were significantly affected by H. pylori infection.ConclusionsH. pylori infection disrupted the normal bacterial communities in the duodenum and changed the biofunctions of the commensal microbiota, primarily by upregulating specific metabolic pathways. This alteration may be related to the onset mechanisms of the diseases suspected of being related to H. pylori infection.

Background The bioactivities of commensal duodenal microbiota greatly influence the biofunction of hosts. We investigated the role of Helicobacter pylori infection in extra-gastroduodenal diseases by determining the impact of H. pylori infection on the duodenal microbiota. We sequenced 16 S rRNA genes in samples aspirated from the descending duodenum of 47 (male, 20; female, 27) individuals who were screened for gastric cancer. Samples were analysed using 16 S rRNA gene amplicon sequencing, and the LEFSe and Kyoto Encyclopaedia of Genes and Genomes methods were used to determine whether the duodenal microflora and microbial biofunctions were affected using H. pylori infection. Results Thirteen and 34 participants tested positive and negative for H. pylori, respectively. We identified 1,404 bacterial operational taxonomic units from 23 phyla and 253 genera. H. pylori infection changed the relative mean abundance of three phyla (Proteobacteria, Actinobacteria, and TM7) and ten genera (Neisseria, Rothia, TM7-3, Leptotrichia, Lachnospiraceae, Megasphaera, F16, Moryella, Filifactor, and Paludibacter). Microbiota features were significantly influenced in H. pylori-positive participants by 12 taxa mostly classified as Gammaproteobacteria. Microbial functional annotation revealed that H. pylori significantly affected 12 microbial metabolic pathways. Conclusions H. pylori disrupted normal bacterial communities in the duodenum and changed the biofunctions of commensal microbiota primarily by upregulating specific metabolic pathways. Such upregulation may be involved in the onset of diseases associated with H. pylori infection.

Original Article, Background: Recent reports indicate that bile acid malabsorption is present in about 30% of patients with chronic diarrhea and a diagnosis of diarrhea-predominant irritable bowel syndrome (IBS-D) and that treatment with bile acid-binding resin is effective. We investigated the effects of colestimide on refractory chronic diarrhea in IBS-D. Methods: Twenty-eight patients with refractory IBS-D or chronic diarrhea were enrolled and treated with colestimide. Fifteen had no past history of gastrointestinal surgery and 13 had undergone such surgery. Small intestinal bacterial overgrowth (SIBO) was also evaluated by lactulose breath testing in 21 patients. All patients were given 1500 mg of colestimide twice a day for 2 weeks, after which the effects of colestimide treatment were evaluated. Results: Of the 21 patients examined for SIBO, 8 (38.1%) had a positive result. Prevalence of SIBO was not associated with past surgical history (p=0.472). In 21 (75.0%) of the 28 patients, colestimide improved diarrhea and bowel habits (p=0.008). The effectiveness of colestimide was not associated with past surgical history or presence of SIBO. Conclusions: Colestimide treatment had a satisfactory effect for chronic diarrhea potentially attributable to bile acid malabsorption. The effectiveness of empirical administration of colestimide for patients with refractory chronic diarrhea and IBS-D should be assessed in a future study.

Chronic alcohol consumption can cause dysbiosis, but it is difficult to determine the effect of alcohol on the structure and activity of gastrointestinal tract microbiota. We therefore designed a noninvasive hydrogen breath test (HBT) to investigate the alteration in the chemical profile of gut microbiota in ethanol-fed rats. Thirteen F344/DuCri rats were fed on a commercial mash food with 16% ethanol solution drinking fluid from 4 weeks of age. HBTs were carried out on six 8-week-old and seven 24-week-old ethanol-fed rats. As controls, HBTs were carried out on sixteen 8-week-old, six 24-week-old, and five 48-week-old male rats. Six 24-week- old male rats were examined twice at 1-week intervals. HBTs were performed after fasting for 24 hr. Rats were orally administrated 4 mL/kg of 65% lactulose solution and housed in an animal chamber. The expired air was collected in a breath-sampling bag at 10-min intervals for 180 min. The hydrogen (H2) and methane (CH4) levels in the breath sample were measured using a breath analyzer and were expressed.as parts- per million (ppm). Elevated H2 and CH4 levels were more frequent in male rats. Maximal values of H2 and CH4 were highest in 8-week- old rats, followed by 48-week-old and 24-week-old rats. No ethanol-fed rat exhaled more than 2 ppm of H2 or CH4 until 180 min after the oral administration of lactulose, unlike the controls. This alteration was more obvious than that of aging or gender differentiation. We conclude that there is a close association between chronic ethanol consumption and H2 and CH4 production. An asymptomatic heavy drinker might have dysbiosis that involves gut microbiota with lower fermentation performance.

Routine empirical antimicrobial therapy for patients with infectious diarrhea is not recommended in general practice. Conversely, prescription of empirical antibiotics for hospitalized patients remains controversial due to a lack of studies providing evidence for its benefits. Thus, this study aimed to examine whether empirical antimicrobial therapy would shorten the hospitalization duration for infectious diarrhea patients.This single-center, retrospective cohort study was performed at the Department of General Medicine and Emergency Care, Toho University Medical Center Omori Hospital, using medical records. Adult patients (aged ≥16 years) hospitalized for infectious diarrhea from 2012 to 2015 were enrolled. The primary outcome was the duration of hospitalization. Risk factors examined in parallel to antibiotic therapy included age, sex, relevant medical history, probiotics use, vital signs, leukocyte count, liver and renal functions, and microbiological data.We enrolled 138 and 50 patients treated with and without antimicrobial therapy, respectively. The median hospitalization periods were 6.0 days (interquartile range, 4.0-7.0 days) and 5.0 days (interquartile range, 3.25-6.0 days) for patients treated with and without antibiotics, respectively (p = 0.007). Multiple regression showed that empiric antimicrobial therapy (p = 0.017), advanced age (p = 0.003), hematochezia (p = 0.008), elevated serum creatinine (p 0.001), and elevated serum C-reactive protein (p = 0.002) were significant risk factors of longer hospitalization duration.Empirical antimicrobial therapy was found to relate to a longer hospitalization duration for infectious diarrhea patients. Although its effects on the patients' symptoms were not evaluated, our results suggest that empirical antimicrobial therapy should be administered cautiously to not only outpatients, but also hospitalized patients.

A 77‐year‐old man who had been taking Chinese herbal drugs containing gardenia fruit for a long time visited our hospital following a positive fecal occult blood test. A computed tomography scan showed multiple linear calcifications distributed on the right‐side mesenteric veins, which is a typical finding of idiopathic mesenteric phlebosclerosis (IMP).

It has been suggested that there could be three possible mechanisms of gastric dysfunction in patients with FD: (i) delayed gastric emptying, (ii) impaired gastric accommodation of food intake, and (iii) hypersensitivity to gastric distention. Postprandial fullness seems to be the most severe symptom in patients who report aggravation of their symptoms after meals. Therefore, it has been assumed that delayed gastric emptying and consequent prolonged antral distension could reduce hunger, increase satiety, and even cause gastric discomfort, all of which would pose a significant barrier to adequate nutrition. We previously reported that postprandial water intake inhibits gastric antral motility along with an increase of cholecystokinin (CCK) in normal subjects. We assumed that the rapid increase of CCK after water intake was initiated by a feedback mechanism related to the inflow of fatty chyme into the duodenum that inhibits gastric antral activity. This duodeno-gastric interaction is known as the "duodenal break." We also reported that total gastric emptying was more rapid after the intake of a high-viscosity liquid meal than after a low-viscosity meal, because the low-viscosity liquid meal inhibits gastric emptying after rapid initial inflow into the duodenum. Considering these results, we hypothesized that rapid gastric emptying, rather than delayed gastric emptying, could be a cause of FD. In some patients with postprandial distress syndrome (PDS), we have found a significant correspondence between PDS-related dyspepsia and accelerated gastric emptying in the early postprandial period. It is worth emphasizing that the duodenum and the duodeno-gastric interaction (duodenal break) could have an important role in the pathophysiology of FD. We consider that rapid gastric emptying might be a more important factor than delayed gastric emptying in patients with FD.

Background: Free glutamate activates taste receptors on nerves in the oral cavity to elicit a unique taste known as umami .R ecently, umami taste receptors were also found in the gastric mucosa. Although reports suggest that mucosal receptors may respond to free glutamate to modulate gastric function, no evidence of any effect on gastric emptying has been documented. Objective: We hypothesized that glutamate may act as a modulator of gastric function. We studied the effects of L-glutamate enrichment of a protein-rich liquid meal, and similar enrichment of an equicaloric carbohydrate meal or noncaloric water, on gastric emptying. Design: Ten healthy men were enrolled. Nine of the 10 subjects included in the study ingested all test meals with and without monosodium L-glutamate (MSG), and the remaining subject ingested only the protein-rich meals with and without MSG. All experimental and control liquid meals included [1- 13 C]sodium acetate as a tracer. After a test meal or water was ingested, 13 C breath tests were performed to estimate gastric emptying. Results: MSG enrichment not only resulted in a significant decrease in the mathematically simulated half-excretion (emptying) time of a protein-rich meal, but also increased the area under the curve (%dose/h) significantly. In contrast, MSG had no significant effect on the gastric emptying of a carbohydrate meal or a noncaloric water meal. Conclusions: Enrichment with MSG facilitated gastric emptying of a protein-rich meal exclusively, which suggests that free glutamate is important for protein digestion and may be helpful in the management of delayed gastric emptying. Am J Clin Nutr 2009;89:431‐5.

It has been reported that proton pump inhibitors are more effective than H2 receptor antagonists in patients with functional dyspepsia. Dyspeptic symptoms that respond to proton pump inhibitors are classified as acid-related dyspepsia. A new questionnaire for assessing gastroesophageal reflux disease (GERD), the Frequency Scale for Symptoms of GERD, covers the 12 most common symptoms of GERD patients. A quantitative assessment of the changes of reflux symptoms and acid-related dyspepsia was made in GERD patients receiving proton pump inhibitor therapy. Sixty-eight GERD patients receiving proton pump inhibitor therapy completed the questionnaire before and after treatment for 8 weeks. There is a significant positive correlation between reflux symptoms and acid-related dyspepsia before and after therapy (r = 0.569 and r = 0.569; both P's < 0.001) and acid-related dyspepsia in patients with both nonerosive and erosive GERD. We conclude that GERD patients suffer not only from reflux symptoms, but also from acid-related dyspepsia, and proton pump inhibitors improve both types of symptoms.

Background Acotiamide is a first-in-class drug that is used to treat functional dyspepsia (FD). It is considered that acotiamide acts as an antagonist on muscarinic autoreceptors in the enteric nervous system and inhibits acetylcholinesterase activity. We examined the effect of acotiamide on gastric emptying in healthy adult humans. Materials and methods Twelve healthy adult males were enrolled in this double-blind crossover study. Acotiamide or placebo was administered orally in the 12 subjects 30 min before ingestion of a nutritional liquid meal (400 Kcal/400 mL). Six of the 12 participants took 100 mg of acotiamide or placebo, and six of the 12 participants took 300 mg of acotiamide or placebo in a double-blind crossover fashion. All subjects underwent measurement of gastric emptying by the 13C breath test. Results After the meal with placebo was ingested, the %dose/h curve ascended. The %dose/h curve after a meal with 100 or 300 mg of acotiamide ascended in an identical manner compared with the results with placebo. No significant differences were observed at any studied time point, and there were no significant changes in gastric emptying parameters (gastric emptying coefficient, t-1/2ex and t-lag ex). Conclusions A single administration of 100 or 300 mg of acotiamide did not affect gastric emptying after a liquid meal in healthy adult humans. Acotiamide has profound effects on restoring delayed gastric emptying and impaired accommodation in patients with FD but may have no effect on gastric emptying in healthy subjects. Such pharmacological actions have not been observed in previous gastroprokinetic studies.

In vitro studies on pacemaker-deficient W-mutants have revealed a disappearance of rhythmic contraction in their gastrointestinal tracts. Their contractile force has not been diminished, however. In contrast, W-mutants often present dysmoility-like symptoms with distension of the gastrointestinal tract in vivo. Gastrointestinal motility of W-mutant rats was examined in vivo by an extraluminal strain-gauge force transducer method. We examined a normal gastrointestinal motor pattern in the rats with two distinct motor phases, digestive and interdigestive. Moreover, we detected a failure to form an interdigestive contractile complex in pacemaker-deficient rats. The interdigestive motor activity of the gastrointestinal tract is important for cleaning gastrointestinal tract in preparation for the next meal. The impairment of the interdigestive contractile complex may be related to the dysmoility-like symptoms of W-mutant rats in vivo.

Digestive tract motility patterns are closely related to the pathophysiology of functional gastrointestinal diseases (FGID), and these patterns differ markedly between the interdigestive period and the postprandial period. The characteristic motility pattern in the interdigestive period is so-called interdigestive migrating contraction (IMC). IMCs have a housekeeping role in the intestinal tract, and could also be related to FGID. IMCs arising from the stomach are called gastrointestinal IMCs (GI-IMC), while IMCs arising from the duodenum without associated gastric contractions are called intestinal IMCs (I-IMC). It is thought that I-IMCs are abnormal in FGID. Transport of food residue to the duodenum via gastric emptying is one of the most important postprandial functions of the stomach. In patients with functional dyspepsia (FD), abnormal gastric emptying is a possible mechanism of gastric dysfunction. Accordingly, delayed gastric emptying has attracted attention, with prokinetic agents and herbal medicines often being administered in Japan to accelerate gastric emptying in patients who have anorexia associated with dyspepsia. Recently, we found that addition of monosodium L-glutamate (MSG) to a high-calorie liquid diet rich in casein promoted gastric emptying in healthy men. Therefore, another potential method of improving delayed gastric emptying could be activation of chemosensors that stimulate the autonomic nervous system of the gastrointestinal tract, suggesting a role for MSG in the management of delayed gastric emptying in patients with FD.

Summary Background Monosodium l-glutamate (MSG) is known to influence the endocrine system and gastrointestinal (GI) motility. The mechanism of postprandial glycemic control by food in the GI tract is mostly unknown and of great interest. Aim To investigate the effect of MSG on glucose homeostasis, incretin secretion and gastric emptying in humans after a lipid-containing meal. Methods Thirteen healthy male volunteers (mean age, 25.5 years) and with no Helicobcter pylori infection were enrolled. A 400 mL (520 kcal) liquid meal with MSG (2 g, 0.5% wt:vol) or NaCl (control) was ingested in a single-blind placebo-controlled cross-over study. Blood glucose, serum insulin, plasma glucagon, plasma glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide were measured. Gastric emptying was monitored by a 13C acetate breath test. Postprandial symptoms were assessed on a visual analogue scale. Results The 30-min postprandial glucose concentration was significantly reduced by adding MSG to the test meal. The area under the glucose concentration vs. time curve (0–60 min) was also significantly reduced by adding MSG (40.6 ± 3.51 mg·1 hr/dL with MSG vs. 49.2 ± 3.86 mg·1 hr/dL with NaCl, P = 0.047), whereas, the 30-min postprandial plasma GLP-1 level was significantly increased (58.1 ± 15.8 pmol/L with MSG vs. 13.4 ± 15.8 pmol/L with NaCl, P = 0.035). MSG did not affect the half gastric emptying time or postprandial symptoms. Conclusions Monosodium l-glutamate improved early postprandial glycaemia after a lipid-containing liquid meal. This effect was not associated with a change in gastric emptying, but was possibly related to stimulation of glucagon-like peptide-1 secretion.

Glutamate is a non-essential amino acid that confers umami taste. Recently, several taste receptors for umami taste have been identified in the oral cavity as well as in the gastrointestinal tract. Gustatory stimulation of the tongue by glutamate activates vagal gastric, pancreatic, and hepatic efferent nerves. In the gastrointestinal tract, glutamate excites afferent fibers of the abdominal vagus nerve. Recent data suggest the possibility that a chemosensory system similar to that found in the mouth is also present in the stomach and small intestine and that this system aids in regulating gastrointestinal functions. In this review, we have summarized the known effects of dietary free glutamate on gastrointestinal functions such as gastric secretion and gastrointestinal motility, and we explore the possibility of application of glutamate as a medical food supplement. Fortification of protein or amino acid rich diets with free glutamate enhances gastric secretion and promotes gastric emptying. Current results indicate that free glutamate modulates gastrointestinal functions, especially gastric digestion, via cephalic or gastrointestinal phase responses. Dietary supplementation of enteral nutrition with free glutamate could help to prevent complications of these diets, especially diarrhea.

Objective Gastroptosis is recognized by its characteristic appearance on barium studies. The present prospective study assessed the relationship between gastroptosis and dyspeptic symptoms. Methods Japanese subjects underwent health screening, and gastroptosis was diagnosed by barium studies. Consecutive subjects (500 women and 167 men) with gastroptosis were identified and the same number of age-matched subjects without gastroptosis were selected as controls. Dyspepsia was classified as reflux-like (heartburn and belching), dysmotility-like (bloating and fullness), or ulcer-like dyspepsia (epigastralgia) based on the Rome II criteria. Results Body mass index was significantly lower in women with gastroptosis than in controls [19.7±1.83 (SD) vs. 23.4±3.70, p

It has been suggested that there could be three possible mechanisms of gastric dysfunction in patients with FD: (i) delayed gastric emptying, (ii) impaired gastric accommodation of food intake, and (iii) hypersensitivity to gastric distention. Postprandial fullness seems to be the most severe symptom in patients who report aggravation of their symptoms after meals. Therefore, it has been assumed that delayed gastric emptying and consequent prolonged antral distension could reduce hunger, increase satiety, and even cause gastric discomfort, all of which would pose a significant barrier to adequate nutrition. We previously reported that postprandial water intake inhibits gastric antral motility along with an increase of cholecystokinin (CCK) in normal subjects. We assumed that the rapid increase of CCK after water intake was initiated by a feedback mechanism related to the inflow of fatty chyme into the duodenum that inhibits gastric antral activity. This duodeno-gastric interaction is known as the "duodenal break." We also reported that total gastric emptying was more rapid after the intake of a high-viscosity liquid meal than after a low-viscosity meal, because the low-viscosity liquid meal inhibits gastric emptying after rapid initial inflow into the duodenum. Considering these results, we hypothesized that rapid gastric emptying, rather than delayed gastric emptying, could be a cause of FD. In some patients with postprandial distress syndrome (PDS), we have found a significant correspondence between PDS-related dyspepsia and accelerated gastric emptying in the early postprandial period. It is worth emphasizing that the duodenum and the duodeno-gastric interaction (duodenal break) could have an important role in the pathophysiology of FD. We consider that rapid gastric emptying might be a more important factor than delayed gastric emptying in patients with FD.

Schwannomas are tumors originating from any nerve that has a Schwann cell sheath. Gastrointestinal (GI) schwannomas represent only 3% of all GI mesenchymal tumors. The stomach is the most common site of GI schwannomas, and schwannomas account for 0.2% of all gastric neoplasms. This report presents two cases of gastric schwannomas showing increased [18F]fluorodeoxyglucose (FDG) uptake on positron emission tomography (PET; maximum standardized uptake value 7.10 and 6.05). Additional immunohistochemical staining of glucose transporter type 1 (GLUT1) and the autocrine motility factor (AMF) was conducted after the tumors were resected, to identify the mechanism that increased FDG uptake on PET. Immunohistochemical expression of AMF was positive in both cases, whereas GLUT1 was negative. Autocrine motility factor is also known as phosphoglucose isomerase. However, the mechanism by which FDG is accumulated in schwannoma cells is uncertain, and may be related to intracellular glycolytic activity.

Monosodium l-glutamate (MSG) is a substance known to produce the umami taste. Recent studies indicate that MSG also stimulates a variety of activities in the gastrointestinal tract through its receptor in the gut, but no study has reported the activity in conscious large experimental animals. The aim of our study was to investigate whether direct intragastric MSG stimulates gut motility and to identify the mechanism in conscious dogs. Contractile response to intraluminal injection of MSG was studied in the fed and fasted states by means of chronically implanted force transducers. MSG (5, 15, 45, and 90 mM/kg) dissolved in water was injected into the stomach and duodenum in normal and vagotomized dogs. MSG solution was administered into the stomach before feeding, and gastric emptying was evaluated. Several inhibitors of gastrointestinal motility (atropine, hexamethonium, and granisetron) were injected intravenously before MSG administration to the stomach. The effect of MSG was investigated in Pavlov (vagally innervated corpus pouch), Heidenhain (vagally denervated corpus pouch), and antral pouch (vagally innervated) dogs. Upper gut motility was significantly increased by intragastric MSG but not significantly stimulated by intraduodenal MSG. Intragastric MSG (45 mM/kg) stimulated postprandial motility and accelerated gastric emptying. MSG-induced contractions were inhibited by truncal vagotomy, atropine, hexamethonium, and granisetron. Gut motility was increased by intrapouch injection of MSG in the Pavlov pouch, but it was not affected in the Heidenhain or antral pouch dogs. We conclude that intragastric MSG stimulates upper gut motility and accelerates gastric emptying. The sensory structure of MSG is present in the gastric corpus, and the signal is mediated by the vagus nerve.

Adding pectin to an elemental formula increases its viscosity through gelatinization, thus presumably preventing gastro-oesophageal reflux and aspiration pneumonia. We investigated the influence of the viscosity of an elemental formula on gastric emptying. Eleven healthy volunteers underwent three tests at intervals of >1 week. After fasting for >8 h, each subject received a test meal (enteral nutrition solution, enteral solution plus pectin, or water). Then gastric emptying (continuous (13)C breath test), gastro-oesophageal intraluminal pressures, oesophageal pH, and blood levels of glucose, insulin and gastrin were all measured simultaneously. The gastric emptying coefficient was significantly increased by adding pectin to enteral nutrition (3.01 +/- 0.10 vs 2.78 +/- 0.10, mean +/- SE, P < 0.05). The antral motility index was also significantly higher with pectin than without at 45-60 min and 60-75 min after the test meal (526 +/- 237 vs 6.5 +/- 4.6 mmHg s(-1) and 448 +/- 173 vs 2.3 +/- 2.3 mmHg s(-1) respectively; P < 0.05). Plasma glucose was significantly higher with pectin than without it at 60 min after ingestion (141.5 +/- 6.03 vs 125.8 +/- 4.69 microM mL(-1), P < 0.05). In healthy individuals, pectin increased the viscosity of enteral nutrition and accelerated gastric emptying.

Background and aim An early and accurate evaluation by a general practitioner is needed to screen out non-gastroesophageal reflux disease (GERD) patients. A recent questionnaire (QUEST) highlighted problems with specificity and complexity, so the aim of the present study was to design a simplified questionnaire. Methods When admitted to hospital to undergo an upper gastrointestinal endoscopy for suspected GERD, 333 patients completed a 50-item questionnaire requiring 'yes/no' answers to different combinations of questions relating to symptoms of upper gastrointestinal tract conditions (e.g. GERD, ulcers and functional dyspepsia) and psychosomatic symptoms. The endoscopic diagnosis was then correlated with the rate of positive answers to each question. Results Based on the analysis of the 50 items, the 8-10 questions most often answered affirmatively by each of the GERD and non-GERD groups were chosen for the simplified questionnaire. Three draft questionnaires were compiled. After calculating the sensitivity, specificity and accuracy in relation to the diagnosis of GERD and other conditions, it was found that questionnaire B (selection of persons answering 'yes' to at least one of questions 1-5 and exclusion of persons answering 'yes' to at least three of questions 7-10) had a high sensitivity, high specificity and low false positive rate. Conclusion A novel questionnaire was developed. It was designed to detect the symptoms of GERD while simultaneously excluding non-GERD patients. This simplified nine-item simplified questionnaire had a sensitivity of 79.8%, a specificity of 53.6% and an accuracy of 63.4%.

The aim of this study was to produce a simplified questionnaire for evaluation of the symptoms of gastroesophageal reflux disease (GERD).A total of 124 patients with an endoscopic diagnosis of GERD completed a 50-part questionnaire, requiring only "yes" or "no" answers, that covered various symptoms related to the upper gastrointestinal tract, as well as psychosomatic symptoms. The 12 questions to which patients most often answered "yes" were selected, and were assigned scores (never = 0; occasionally = 1; sometimes = 2; often = 3; and always = 4) to produce a frequency scale for symptoms of GERD (FSSG). Sensitivity, specificity, and accuracy of the FSSG questionnaire were evaluated in another group of patients with GERD and non-GERD. The usefulness of this questionnaire was evaluated in 26 other GERD patients who were treated with proton pump inhibitors for 8 weeks.When the cutoff score was set at 8 points, the FSSG showed a sensitivity of 62%, a specificity of 59%, and an accuracy of 60%, whereas a cutoff score of 10 points altered these values to 55%, 69%, and 63%. The score obtained using the questionnaire correlated well with the extent of endoscopic improvement in patients with mild or severe GERD.This new questionnaire is useful for the objective evaluation of symptoms in GERD patients.

A case for primary gastrointestinal stromal tumor (GIST) is described with reference to its ultrastructural characteristics and mutation within the exon 11 of c-kit gene. A forty-seven years old woman complaining of dysphasia was examined by endoscopy, which depicted a submucosal tumor (70 mm in diameter) with ulcerations at the fundus of the stomach. Histopathologically, the tumor cells had large nuclei and eosinophilic cytoplasm and were frequently during mitosis phase. The tumor cells were immunopositive for KIT, CD 34 and vimentin, suggesting their fibroblast-like characteristics. In contrast, desmin and S-100, a smooth muscle and an enteroglial marker, were not immunopositive within the cells. At least 30 % of the tumor cells possessed MIB-I and 20 % of them possessed p53, which are compatible with fast development of the tumor. By electron microscopy, the tumor cells possessed large oval nuclei, abundant mitochondria, caveolae and smooth endoplasmic reticulums, while no gap junctions were seen on the cells: The tumor cells thus possessed interstitial cells-like characteristics at least in part. DNA mutation search for the tumor cells however realized no gain-of-function mutation within the exon 11 of the c-kit gene, suggesting existence of other mechanism for neoplasmic growth of the tumor cells classified as gastrointestinal stromal tumors.

In this study, we examined the mechanism by which constant intravenous infusion of physiological doses of PYY affects gastric secretion and motility in the vagally innervated (Pavlov) and denervated (Heidenhain) corpus pouch. As a result, only in the Heidenhain pouch, PYY at a dose of 100 pmol/kg-h significantly inhibited gastric secretion in the interdigestive and postprandial states. A dose of 300 pmol/kg-h inhibited the gastric secretion in both types of pouch, but inhibition in the Pavlov pouch was less than in the Heidenhain pouch. The inhibitory effect of PYY on phase III contractile activity was dose-dependent and significant, except in the Heidenhain pouch, and no dose of PYY had any effect on postprandial gastric motility. After all, vagal denervation enhanced the inhibitory effect of PYY on gastric secretion, but abolished the inhibitory effect on phase III contractile activity. Our findings strongly suggest that the inhibitory effect of PYY on gastric secretion is in part mediated by a non-vagal pathway and the inhibitory effect of PYY on gastric motor activities is completely dependent on vagal innervation, but the vagus nerve acts as an inhibitory modulator of the inhibitory effect of PYY on gastric secretion.

Background Gastro-esophageal reflux disease (GERD)-related chronic cough (CC) may have multifactorial causes. To clarify the characteristics of esophagopharyngeal reflux (EPR) events in CC patients whose cough was apparently influenced by gastro-esophageal reflux (GER), we studied patients with CC clearly responding to full-dose proton pump inhibitor (PPI) therapy (CC patients). Methods Ten CC patients, 10 GERD patients, and 10 healthy controls underwent 24-h ambulatory pharyngo-esophageal impedance and pH monitoring. Weakly acidic reflux was defined as a decrease of pH by >1 unit with a nadir pH >4. In six CC patients, monitoring was repeated after 8 weeks of PPI therapy. The number of each EPR event and the symptom association probability (SAP) were calculated. Symptoms were evaluated by a validated GERD symptom questionnaire. Key Results Weakly acidic gas EPR and swallowing-induced acidic/weakly acidic EPR only occurred in CC patients, and the numbers of such events was significantly higher in the CC group than in the other two groups (P

Free glutamate activates the taste receptors in the oral cavity and excites taste nerves to elicit a unique taste eumami. Recently the receptors sensitive to free glutamate were also found in the upper gastrointestinal (GI) tract. These reports suggest that glutamate acts as a modulator of gastric function. Therefore, we examined its effect on gastric emptying and the postprandial sensation for protein-rich meal in healthy volunteers. The base liquid meal (400 kcal/400 ml) consisted of 12.5% dextrin and 12.5% casein-calcium. To enrich free glutamate, monosodium L -glutamate (0.5% w/v) was supplemented. The following two studies comparing glutamate-enriched meal with control one were performed separately. Gastric emptying was measured by 13C breath test. The intensities of postprandial sensations were assessed at 15 min intervals for 4 h using a questionnaire with visual analogue scales (VAS). Glutamate significantly reduced gastric half-emptying time (153+34.6 /212.7+102.6 min, glutamate +/−, mean+S.D., n =10, p p =0.202) of the subjects older than 45 years old ( n =14). These data suggest that glutamate may affect the subject with declined GI function by aging.