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1

Van Duijn, B., D. L. Ypey, J. de Goede, A. A. Verveen, and W. Hekkens. "A model study of the regulation of gastric acid secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (July 1, 1989): G157—G168. http://dx.doi.org/10.1152/ajpgi.1989.257.1.g157.

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A computer simulation model is presented of the gastric phase regulation of gastric acid secretion in humans. The model is based on experimental data from the literature and includes terms representing gastric pH and gastric volume-dependent gastrin secretion, gastrin-dependent acid secretion, food storage in the stomach, and gastric emptying. We have explored the predictive value of the model in assessing the relative importance of gastric pH-dependent and gastric volume-dependent acid secretion mechanisms under various conditions. Similarly we have studied the role of gastric acid deregulation in achlorhydria, the Zollinger-Ellison syndrome, and duodenal ulcer, and the influence of the antacid drugs cimetidine and ranitidine under duodenal ulcer conditions. Model analysis of normal gastric acid regulation suggests that gastric volume-controlled acid secretion is of major importance during eating and predicts that pH-dependent gastrin secretion is of major importance in preventing excessively low pH levels between meals and during the night.
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2

Woodtli, W., and C. Owyang. "Duodenal pH governs interdigestive motility in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 268, no. 1 (January 1, 1995): G146—G152. http://dx.doi.org/10.1152/ajpgi.1995.268.1.g146.

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In this study, we examined the potential influence of duodenal pH in regulating the occurrence of the interdigestive migrating myoelectric complex (IMMC). Fasting gastroduodenal motility, duodenal pH, and plasma motilin were studied in 15 healthy subjects. During phase I, duodenal pH remained stable at 7 +/- 0.2. Phase II was accompanied by a lowering of duodenal pH, which fluctuated between 2.0 and 7.5. During late phase II, the duodenal pH increased to 6.9 +/- 0.3 and remained in the alkaline range during phase III. In six of 46 episodes of the IMMC, the occurrence of gastric phase III was delayed. This was associated with a persistently low duodenal pH (< 4) during late phase II. Despite a normal cyclic increase of plasma motilin, no gastric phase III activity was observed until the duodenal pH exceeded 7.0. Further studies showed that lowering of duodenal pH by intraduodenal perfusion of HCl prevented the occurrence of gastric phase III. We concluded that regularity of IMMC is governed by duodenal pH. An alkaline pH is essential for the initiation of gastric phase III; lowering of duodenal pH prevents its occurrence despite normal cyclic increase of plasma motilin.
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3

Nylander, O., G. Flemstrom, D. Delbro, and L. Fandriks. "Vagal influence on gastroduodenal HCO3- secretion in the cat in vivo." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 4 (April 1, 1987): G522—G528. http://dx.doi.org/10.1152/ajpgi.1987.252.4.g522.

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Gastric and duodenal secretions of HCO3- were studied simultaneously in chloralose-anesthetized cats. The adrenals were ligated, and the cervical vagal as well as the abdominal splanchnic nerves were cut. Gastric secretions of H+ and HCO3- were calculated from measurements of the pH and PCO2 in the luminal perfusate. A duodenal segment devoid of Brunner's glands and pancreaticobilary secretions was cannulated in situ and the alkaline secretion determined by continuous titration at luminal pH 7.4. Electrical stimulation in the distal direction for 10–15 min of the cervical vagal nerves resulted in a 6- to 10-fold increase in gastric H+ and in a 20–60% rise in gastric HCO-3 secretion. Duodenal HCO3- secretion increased by 65–155%. Gastric basal secretions of H+ and HCO3- were not affected by atropine or hexamethonium, but both agents inhibited basal duodenal HCO3- secretion. Hexamethonium abolished and atropine reduced the rise in all secretions in response to vagal nerve stimulation. Thus gastroduodenal mucosal HCO3- secretion is stimulated by vagal mechanisms involving action on nicotinic as well as on muscarinic receptors and possibly also noncholinergic neurotransmission.
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4

Meert, Kathleen L., Mary Caverly, Lauren M. Kelm, and Norma A. Metheny. "The pH of Feeding Tube Aspirates From Critically Ill Infants." American Journal of Critical Care 24, no. 5 (September 1, 2015): e72-e77. http://dx.doi.org/10.4037/ajcc2015971.

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Background The extent to which gastric acid inhibitors and feedings affect gastric pH in infants is unclear. Objectives To compare pH values of gastric aspirates from infants according to use or no use of gastric acid inhibitors and feedings. Methods Colorimetric pH tests were used to measure the pH of aspirates from feeding tubes in 54 critically ill infants; 29 of the gastric aspirates were from infants who did not receive acid inhibitors or feedings, 13 were from infants who received acid inhibitors but no feedings, 3 were from infants who received feedings but no acid inhibitors, and 5 were from infants who received both acid inhibitors and feedings. The remaining 4 feeding tubes were in nongastric sites. Results Individual pH readings of 5.5 or less were found in 97% of the gastric aspirates from infants with no recent feedings or acid inhibitors, 77% of the gastric aspirates from infants who received acid inhibitors, and 67% of the gastric aspirates from infants with recent feedings. Among 2 esophageal aspirates and 2 duodenal aspirates, 1 of each type had a pH less than 5.5. A pH cut point of 5.5 or less did not rule out esophageal or duodenal placement. Conclusions The pH of gastric aspirates from critically ill infants is often 5.5 or less, regardless of the use of acid inhibitors, feedings, or both. Most likely a cut point of 5.5 or less would rule out respiratory placement because tracheal pH is typically 6.0 or higher.
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5

Marshall, R. E. K., A. Anggiansah, D. K. Manifold, W. A. Owen, and W. J. Owen. "Effect of omeprazole 20 mg twice daily on duodenogastric and gastro-oesophageal bile reflux in Barrett’s oesophagus." Gut 43, no. 5 (November 1, 1998): 603–6. http://dx.doi.org/10.1136/gut.43.5.603.

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Background—Both acid and duodenal contents are thought to be responsible for the mucosal damage in Barrett’s oesophagus, a condition often treated medically. However, little is known about the effect of omeprazole on duodenogastric reflux (DGR) and duodenogastro-oesophageal reflux (DGOR).Aims—To study the effect of omeprazole 20 mg twice daily on DGR and DGOR, using the technique of ambulatory bilirubin monitoring.Methods—Twenty three patients with Barrett’s oesophagus underwent manometry followed by 24 hour oesophageal and gastric pH monitoring. In conjunction with pH monitoring, 11 patients (group 1) underwent oesophageal bilirubin monitoring and 12 patients (group 2) underwent gastric bilirubin monitoring, both before and during treatment with omeprazole 20 mg twice daily.Results—In both groups there was a significant reduction in oesophageal acid (pH<4) reflux (p<0.005) and a significant increase in the time gastric pH was above 4 (p<0.005). In group 1, median total oesophageal bilirubin exposure was significantly reduced from 28.9% to 2.4% (p<0.005). In group 2, median total gastric bilirubin exposure was significantly reduced from 24.9% to 7.2% (p<0.005). Conclusions—Treatment of Barrett’s oesophagus with omeprazole 20 mg twice daily results in a notable reduction in the exposure of the oesophagus to both acid and duodenal contents. In addition, delivery of duodenal contents to the upper gastric body is reduced.
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6

J, Greffa, Barrionuevo A, Vilcacundo E, and Carrillo W. "GASTROINTESTINAL DIGESTION OF KAHAI PROTEIN CONCENTRATE (CARYODENDRON ORINOCENSE KARST)." Asian Journal of Pharmaceutical and Clinical Research 11, no. 6 (June 7, 2018): 397. http://dx.doi.org/10.22159/ajpcr.2018.v11i6.20374.

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Objective: The aim of this study was to obtain kahai protein concentrate from Caryodendron orinocense karst cultivated in the region Amazonia of Ecuador and characterizes its gastric and duodenal hydrolysates using the sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) electrophoresis method and the reversed-phase ultra-high-performance liquid chromatography (RP-UHPLC) method.Methods: Kahai seeds (C. orinocense karst) were utilized to obtain kahai protein concentrate at pH 5.0 using the isoelectric precipitation method and then subject to gastric hydrolysis with pepsin enzyme (2000 U/mg of protein) at pH 1.2, pH 2.0, and pH 3.2 at 37°C for 2 h with agitation in simulated gastric fluids and then to duodenal hydrolysis with pancreatin (mix enzymes) at pH 7.0 at 37°C for 3 h with agitation in simulated intestinal fluid. Gastric and duodenal hydrolysates from kahai were characterized using the SDS-PAGE electrophoresis method and the RP-UHPLC chromatography method.Results: Proteins obtained from kahai (C. orinocense karst) were hydrolyzed with pepsin, only one protein with molecular weight of 100 kDa presented resistance to hydrolysis with pepsin at all pHs assayed. All proteins from kahai protein concentrate were totally hydrolyzed with pancreatin in in vitro conditions.Conclusion: This study suggests that kahai protein concentrates have a high grade of digestibility in vitro when using the gastroduodenal model of digestion. Kahai protein can be a good source of alternative vegetal proteins to be consumed by animals and humans.
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7

Golubkina, E. V., V. M. Sorokin, A. P. Umerova, and N. V. Kamneva. "Acid formation in gastroenterological patients with colonization of the stomach with virulent and non-virulent strains of helicobacter." Experimental and Clinical Gastroenterology, no. 9 (March 24, 2020): 32–37. http://dx.doi.org/10.31146/1682-8658-ecg-169-9-32-37.

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Objective. To prove that increased acid production in patients with gastric ulcer and duodenal ulcer is associated with the impact of the virulent strains of Helicobacter pylori but due not to the persistence of non-virulent strains.Materials and methods. Patients with active gastroduodenal ulcer and patients with active chronic pancreatitis accompanied by the gastritis were compared in the respect of the level of pH in the antrum and corpus gastricum, as well as Helicobacter pylori virulence according to the presence cagA gene, especially in combination with vacA allele s1 / m1 (if any of the strains were found in gastric biopsy specimen).Results. In patients with gastric ulcer the average values of pH were significantly lower, both in the antrum and corpus gastricum, than in patients with chronic pancreatitis accompanied by gastritis. Helicobacter pylori strains were found only in half of the patients, either in the gastric ulcer group or in the group of chronic pancreatitis accompanied by the gastritis. Significant difference was revealed after virulent genes identification: virulent strains prevailed in patients with gastric ulcer and in contrast to the prevalence of non-virulent strains in patients with chronic pancreatitis accompanied by the gastritis (Mann-Whitney test, p = 0.001). Since there is no available data that Helicobacter has an affinity for a highly acidic medium in comparison with moderately acidic medium, it is concluded that just primary colonization of the stomach with virulent strains results in hyperacidity (as the consequence of cytotoxicity) and that persistence of non-virulent strains hardly effects hyperacidity.
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8

Al-Judaibi, B., N. Chande, G. K. Dresser, N. Sultan, and J. C. Gregor. "Gastric Acid-Related Diseases: Focus on Esomeprazole." Clinical Medicine Insights: Therapeutics 2 (January 2010): CMT.S4500. http://dx.doi.org/10.4137/cmt.s4500.

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Esomeprazole (S-omeprazole) is a single optical enantiomer proton-pump inhibitor (PPI) approved for the management of gastro-oesophageal reflux disease, the prevention and treatment of Non-Steroidal Anti-Inflammatory Drugs (NSAID) associated gastric ulcer disease, treatment of duodenal ulcer disease associated with Helicobacter pylori infection, and the treatment of Zollinger-Ellison syndrome. Esomeprazole has been shown to be safe and effective during pregnancy and was introduced to the market in 2001. PPI therapy may interact with clopidogrel by cytocrome 2C19. Clopidogrel is a prodrug which is partially activated by cytochrome 2C19 and esomeprazole is a competitive inhibitor of 2C19. Esomeprazole is more effective than other PPIs in controlling esophageal and gastric pH, but efficacy in symptom relief is less clear.
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9

Faruwu, Ardilon Raxel, Riami Riami, and Fitri Handajani. "Pengaruh Ekstrak Anggur Laut terhadap pH Lambung dan duodenum pada Rattus norvegicus Jantan yang Diinduksi Indometasin." Jurnal Ilmiah Kedokteran Wijaya Kusuma 9, no. 2 (October 1, 2020): 170. http://dx.doi.org/10.30742/jikw.v9i2.884.

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Indomethacin is a nonsteroidal anti-inflammatory drugs (NSAIDs) that act to inhibit COX-1. The inhibition of COX-1 leads to inhibition of prostaglandin production. Prostaglandin is a regulator of gastric acid buffer secretion. Inhibition of prostaglandin decrease gastric and duodenum pH and damage the gastric and duodenum. Sea grapes (Caulerpa racemose var. cylindracea) are marcoalgae that contain flavonoids as antioxidants and anti-inflammatory. The aim of this study was to determine the effect of sea grapes on gastric and duodenum pH in rattus norvegicus induced by indomethacin. 32 male Rattus norvegicus were divided into 4 groups. Group K (-) without treatment. Group K (+) was induced by 30 mg/Kg BW indomethacin for 7 days. Group P1 was induced by 30mg/Kg BW indomethacin for 7 days followed by administration of 1g/100g BW sea grape extract for 14 days. Group P2 was induced by 30mg/Kg BW indomethacin for 7 days followed by administration of 2g/100g BW sea grape extract for 14 days. On the 29th day, rats were terminated, gastric and duodenal were isolated then the fluid pH was measured. One-way Anova test obtained p = 0,023. Post hoc test pH Gaster significantly different between group K (-) and K (+) (p= 0,005) and between group K (-) with P2 (p= 0,020). While in group K (+) with P1 and P2 there was no significant difference in pH. Post hoc test of pH duodenum showed no differences in all group. The administration of sea grape extract did not show a differences of the gastric and duodenal pH significantly between rats induced by indomethacin.
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10

HADJILOUKA, AGNI, PARASKEVAS GKOLFAKIS, APOSTOLIA PATLAKA, ATHENA GROUNTA, GEORGIA VOURLI, SPIROS PARAMITHIOTIS, GIOTA TOULOUMI, KONSTANTINOS TRIANTAFYLLOU, and ELEFTHERIOS H. DROSINOS. "In Vitro Gene Transcription of Listeria monocytogenes After Exposure to Human Gastric and Duodenal Aspirates." Journal of Food Protection 83, no. 1 (December 19, 2019): 89–100. http://dx.doi.org/10.4315/0362-028x.jfp-19-210.

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ABSTRACT The aim of the present study was to assess, for the first time to our knowledge, Listeria monocytogenes CFU changes, as well as to determine the transcription of key virulence genes, namely, sigB, prfA, hly, plcA, plcB,inlA, inlB, inlC, inlJ, inlP, and lmo2672 after in vitro exposure to human gastric and duodenal aspirates. Furthermore, investigations of the potential correlation between CFU changes and gene regulation with factors influencing gastric (proton pump inhibitor intake and presence of gastric atrophy) and duodenal pH were the secondary study aims. Gastric and duodenal fluids that were collected from 25 individuals undergoing upper gastrointestinal endoscopy were inoculated with L. monocytogenes serotype 4b strain LQC 15257 at 9 log CFU·mL−1 and incubated at 37°C for 100 min and 2 h, respectively, with the time corresponding to the actual exposure time to gastric and duodenal fluids in the human gastrointestinal tract. Sampling was performed upon gastric fluid inoculation, after incubation of the inoculated gastric fluids, upon pathogen resuspension in duodenal fluids and after incubation of the inoculated duodenal fluids. L. monocytogenes CFU changes were assessed by colony counting, as well as reverse transcription quantitative PCR by using inlB as a target. Gene transcription was assessed by reverse transcription quantitative PCR. In 56% of the cases, reduction of the pathogen CFU occurred immediately after exposure to gastric aspirate. Upregulation of hly and inlC was observed in 52 and 58% of the cases, respectively. On the contrary, no upregulation or downregulation was noticed regarding sigB, prfA, plcA, plcB, inlA, inlB, inlJ,inlP, and lmo2672. In addition, sigB and plcA transcription was positively and negatively associated, respectively, with an increase of the pH value, and inlA transcription was negatively associated with the presence of gastric atrophy. Finally, a positive correlation between the transcriptomic responses of plcB, inlA, inlB, inlC, inlJ, inlP, and lmo2672 was detected. This study revealed that the CFU of the pathogen was negatively affected after exposure to human gastroduodenal aspirates, as well as significant correlations between the characteristics of the aspirates with the virulence potential of the pathogen.
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11

Geus, W. P., E. H. Eddes, H. A. J. Gielkens, C. B. H. W. Lamers, and A. A. M. Masclee. "Intraluminal gastric and duodenal pH in chronic pancreatitis." Gastroenterology 114 (April 1998): A461. http://dx.doi.org/10.1016/s0016-5085(98)81865-9.

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12

EDDES, E., W. GEUS, H. GIELKENS, C. LAMERS, and A. MASCLEE. "Intraluminal gastric and duodenal pH in chronic pancreatitis." Netherlands Journal of Medicine 48, no. 1 (January 1996): A5. http://dx.doi.org/10.1016/0300-2977(96)89559-3.

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13

Lee, Kwang-Jae, Rita Vos, Jozef Janssens, and Jan Tack. "Influence of duodenal acidification on the sensorimotor function of the proximal stomach in humans." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 2 (February 2004): G278—G284. http://dx.doi.org/10.1152/ajpgi.00086.2003.

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Decreased acid clearance and increased exposure to acid of the duodenum have been reported in a subset of functional dyspepsia patients. However, the mechanism by which increased duodenal acid exposure may affect symptoms is unclear. The aim of the present study was to investigate the effects of duodenal acidification on proximal gastric tone and mechanosensitivity in humans. An infusion tube with a pH electrode attached was positioned in the second part of the duodenum, and a barostat bag was located in the gastric fundus. In 12 healthy subjects, fundic tone and sensitivity to distensions were assessed before and during duodenal infusion of 0.1 N hydrochloric acid or saline in a randomized, double-blind design. In 10 healthy subjects, meal-induced accommodation was measured during duodenal infusion of acid or saline. Acid infusion in the duodenum significantly increased fundic compliance and decreased fasting fundic tone. This was accompanied by a significant decrease in the pressures and the corresponding wall tensions at the thresholds for discomfort. During infusion of acid, significantly higher perception and symptom scores were obtained for the same distending pressures. The meal-induced fundic relaxation was significantly smaller during acid infusion compared with saline infusion. In conclusion, duodenal acidification induces proximal gastric relaxation, increases sensitivity to gastric distension, and inhibits gastric accommodation to a meal. Through these mechanisms, increased duodenal acid exposure may be involved in the pathogenesis of dyspeptic symptoms.
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14

Guinotte, F., J. Gautron, Y. Nys, and A. Soumarmon. "Calcium solubilization and retention in the gastrointestinal tract in chicks (Gallus domesticus) as a function of gastric acid secretion inhibition and of calcium carbonate particle size." British Journal of Nutrition 73, no. 1 (January 1995): 125–39. http://dx.doi.org/10.1079/bjn19950014.

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In chicks, immature pullets and laying hens, the inhibition of gastric acid secretion by omeprazole, an H+,K+-transporting ATPase (EC 3.6.1.36) inhibitor, greatly increased proventricular and gizzard pH values. Consequently, gizzard soluble Ca concentration deceased and the insoluble Ca fraction increased. Inhibition of acid secretion increased duodenal pH values in immature pullets and laying hens but not in chicks. Duodenal soluble and ionic Ca concentrations were lowered by gastric acid inhibition in chicks and to a larger extent in immature pullets and laying hens. The use of Ca of coarse particle size increased the gizzard insoluble Ca fraction in chicks and pullets. However, it did not influence its soluble Ca fraction in chicks but tended to reinforce the negative effect of omeprazole on soluble Ca in the gizzard and duodenum of chicks and laying hens. Coarse particles of Ca led to an increase in gizzard and duodenal soluble Ca at the end of eggshell calcification in laying hens. An enhancement in the level of Ca in the diet from 10 to 36 g/kg increased gizzard soluble Ca and duodenal soluble and ionic Ca concentrations in immature and adult hens. Intestinal Ca retention and bone mineralization was unaffected by gastric acid inhibition in chicks but were largely diminished by the use of coarse particles of Ca. Gastric acid inhibition was associated in laying hens with decreased Ca retention to a small extent and with reduced eggshell quality. These observations confirm that gastric acid secretion is of importance for CaCO, solubilization but question its role as a prerequisite for intestinal Ca retention in chicks and even in hens fed on a high Ca diet.
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15

Rashid, Hytham, Nathan McKinney, Grant Jernigan, Alexander Rhodes, Emily Nix, and Charles Morrissette. "PMON40 A Rare Etiology of Chronic Diarrhea: Zollinger-Ellison Syndrome." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A552—A553. http://dx.doi.org/10.1210/jendso/bvac150.1148.

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Abstract Introduction Zollinger-Ellison Syndrome (ZES) is a rare etiology of chronic diarrhea caused by a gastrin-secreting neuroendocrine tumor. Early suspicion can prevent multiple readmissions for recurrent diarrhea thus improving clinical outcomes through prompt diagnosis and treatment, as the following case highlights. Case presentation A 74-year-old African-American female with hypertension and chronic atrial fibrillation presented to the ED complaining of watery, non-bloody diarrhea for the past 3 weeks. She reports her symptoms worsened after completing a course of amoxicillin for pharyngitis one week prior. On further questioning, she reported intermittent diarrhea for over 20 years lasting approximately two days per episode. She denied recent travel, sick contacts, pet reptiles, and recent ingestion of undercooked meat. On arrival, she was afebrile and hemodynamically stable. She was admitted for an acute kidney injury with an elevated creatinine of 3.23 mg/dL (N: 0.6-1.1 mg/dL) due to dehydration. Her renal function improved with fluids, but she developed bloody diarrhea for which gastroenterology was consulted. Stool studies were negative for Shiga-toxin, C. difficile, lactoferrin, and parasites. Computed Tomography of the abdomen showed enteritis with fluid noted throughout the colon consistent with colitis. Unprepped colonoscopy revealed blood throughout the length of the colon, suggestive of an upper gastrointestinal bleed. Esophagogastroduodenoscopy (EGD) revealed multiple bleeding duodenal ulcers controlled with hemostasis. Her symptoms improved and she was discharged home on oral pantoprazole, and told to follow up outpatient. Two weeks later, she denied any new episodes of diarrhea, and a random serum gastrin level was elevated at 413 pg/mL (N: &lt;180 pg/mL). Repeat gastrin level off pantoprazole for 7 days was also elevated at 678 pg/mL, and a serum Chromogranin A level was elevated at 629 pg/mL (N: &lt;390 pg/mL). Repeat EGD found her Gastric pH to be 1 with multiple non-bleeding duodenal ulcers. Somatostatin receptor scintigraphy revealed a high intensity signal consistent with a duodenal gastrinoma causing ZES. She elected for surgical resection, and was discharged home on high dose pantoprazole. Three months later, she stated that her diarrhea had completely resolved. Conclusion This case confirms ZES as a rare cause of chronic diarrhea in the setting of multiple duodenal ulcers refractory to proton pump inhibitors. Diagnosis can be made with a fasting serum gastrin level &gt;1000 pg/mL or &gt;400 pg/mL with a gastric pH &lt;1. A Secretin Stimulation Testing can also be used. Treatment starts with high dose proton pump inhibitors, octreotide for hormonal regulation, and surgical resection if necessary. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.
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16

Eriksen, Ellen K., Halvor Holm, Einar Jensen, Ragnhild Aaboe, Tove G. Devold, Morten Jacobsen, and Gerd E. Vegarud. "Different digestion of caprine whey proteins by human and porcine gastrointestinal enzymes." British Journal of Nutrition 104, no. 3 (March 22, 2010): 374–81. http://dx.doi.org/10.1017/s0007114510000577.

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The objective of the present study was twofold: first to compare the degradation patterns of caprine whey proteins digested with either human digestive juices (gastric or duodenal) or commercial porcine enzymes (pepsin or pancreatic enzymes) and second to observe the effect of gastric pH on digestion. An in vitro two-step assay was performed at 37°C to simulate digestion in the stomach (pH 2, 4 or 6) and the duodenum (pH 8). The whey proteins were degraded more efficiently by porcine pepsin than by human gastric juice at all pH values. Irrespective of the enzyme source, gastric digestion at pH 2 followed by duodenal digestion resulted in the most efficient degradation. Lactoferrin, serum albumin and the Ig heavy chains were highly degraded with less than 6 % remaining after digestion. About 15, 56 and 50 % Ig light chains, β-lactoglobulin (β-LG) and α-lactalbumin remained intact, respectively, when digested with porcine enzymes compared with 25, 74 and 81 % with human digestive juices. For comparison, purified bovine β-LG was digested and the peptide profiles obtained were compared with those of the caprine β-LG in the digested whey. The bovine β-LG seemed to be more extensively cleaved than the caprine β-LG in the whey. Commercial enzymes appear to digest whey proteins more efficiently compared with human digestive juices when used at similar enzyme activities. This could lead to conflicting results when comparing human in vivo protein digestion with digestion using purified enzymes of non-human species. Consequently the use of human digestive juices might be preferred.
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17

Roberts, I. M. "Rat lingual lipase: effect of proteases, bile, and pH on enzyme stability." American Journal of Physiology-Gastrointestinal and Liver Physiology 249, no. 4 (October 1, 1985): G496—G500. http://dx.doi.org/10.1152/ajpgi.1985.249.4.g496.

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In addition to initiating fat digestion in the stomach, lingual lipase may play a significant digestive role in the upper small intestine. By in vitro incubation techniques, the stability of rat lingual lipase at various physiological pH values, as well as the effects of pure proteases, rat gastric juice, bile, pancreatic juice, and mixed duodenal contents, on enzyme activity was explored. There were no changes in base-line activity of porcine pepsin, bovine carboxypeptidase-treated lipase, or heat-denatured proteases compared with controls after incubation at pH 2-6 at 37 degrees C for up to 1 h. In contrast, porcine trypsin-treated lipase demonstrated a significant loss from base-line activity to 59 +/- 12% (mean +/- SE) at pH 4, 34 +/- 11% at pH 6, and 41 +/- 4% at pH 8, and bovine chymotrypsin caused a loss in lipase activity to 11 +/- 7% at pH 8. Rat gastric juice containing 5,000 U pepsin reduced lipase activity to 17 +/- 5% of initial activity at pH 2 and to 45 +/- 3% at pH 4. Rat bile alone diminished activity only 35%, but rat pancreatic juice or mixed duodenal juice reduced lingual lipase activity to 1-12% of initial activity after 60 min at pH 6. Lingual lipase is particularly important in fat digestion in the stomach; however, its role in quantitative fat digestion under small intestinal conditions may be limited.
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18

Busygina, M. S., and Ya M. Vakhrushev. "Characteristics of the course of gastric and duodenal ulcer disease concurrent with duodenal insufficiency." Terapevticheskii arkhiv 89, no. 12 (December 15, 2017): 76–80. http://dx.doi.org/10.17116/terarkh2017891276-80.

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Aim. To comprehensively study the course of gastric ulcer disease (GUD) and duodenal ulcer disease (DUD) concurrent with chronic duodenal insufficiency (CDI). Materials and methods. Ulcer disease (UD) was verified on the basis of the results of clinical and fibrogastroduodenoscopic examinations. The data of contrast duodenography and cavitary manometry were used to identify CDI. Gastroduodenal motor activity was investigated using the peripheral electrogastrograph EGG-4M. The results of pH measurements were employed to assess the state of gastric acid secretion and duodenal pH values. Results. A comprehensive examination was made in 106 patients with UD concurrent with CDI (a study group) and 30 UD patients without CDI (a comparison group). Epigastric pain was noted in the patients with GUD in the study and comparison groups (91.5 and 84.6%, respectively), but the pain was mainly aching in the patients with concomitant CDI and more intense (77.8%) in those without this condition. In the study group, heartburn was more common in patients with GUD and DUD (75.3 and 71.4%, respectively) than in those with UD in the comparison group (28.5 and 37.5%, respectively). Helicobacter pylori tests were positive in 23.8% of the patients in the study group and in 57.2% in the comparison group. Electrogastrography indicated that the patients with GUD and CDI had bradygastria and hypokinesis on an empty stomach; the electrical activity was reduced after eating. In the comparison group, tachygastria and hyperkinesis were detected on an empty stomach; these postprandial indicators were elevated. H. pylori tests were positive in 34.7% of the patients with DUD and CDI and in 63.6% of those with DUD without CDI. The postprandial electrical activity increased in patients with DUD and decreased in the comparison group. The specific features of changes in gastric and duodenal pH values in GUD and DUD concurrent with CDI in comparison with the isolated course of UD. Conclusion. The immediate and long-term follow-ups show that GUD and DUD concurrent with CDI run a more persistent course; the time of ulcer healing increases and the periods of remission decrease.
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Hu, Jiani, Rui Liu, Xiaochen Yu, Zhen Li, Xinran Liu, Yuntao Hao, Na Zhu, Jiawei Kang, and Yong Li. "Protective Effects of Small-Molecule Oligopeptides Isolated from Tilapia Fish Scale on Ethanol-Induced Gastroduodenal Injury in Rats." Nutrients 13, no. 6 (June 17, 2021): 2078. http://dx.doi.org/10.3390/nu13062078.

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Peptic ulcer has a serious impact on people’s health around the world, and traditional medicines can cause adverse reactions. This study investigated the protective effects of tilapia collagen oligopeptides (TCOPs) on gastroduodenal injury. Seventy-two specific pathogen-free (SPF) male Sprague Dawley (SD) rats were randomly divided into six groups according to body weight: normal control group, ethanol group, whey protein group (500 mg/kg BW), and three TCOPs dose groups (250, 500, 1000 mg/kg BW). After intragastric administration for 30 days, the acute gastroduodenal injury was induced by anhydrous ethanol (5 mL/kg, intragastrically) in all groups except the normal control group. Biomarkers in gastric and duodenal tissue and serum were measured. Furthermore, western blot was used to detect the expression of apoptosis-related proteins. The results showed that the administration with TCOPs significantly reduced gastric and duodenal ulcer index, increased gastric juice pH, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, along with the reduction of malondialdehyde (MDA) contents. TCOPs decreased tumor Necrosis Factor-α (TNF-α), interleukin-1β (IL-1β), and myeloperoxidase (MPO) levels, while interleukin– 10 (IL-10) levels were increased. Furthermore, pepsinogens 1 (PG1), pepsinogens 2 (PG2), gastrin (GAS), and the pepsinogen ratio (PGR) were decreased, the prostaglandin E2 (PGE2) and NO contents were increased after TCOPs intervention. Moreover, TCOPs up-regulated the expression of Bcl-2 and inhibited the expression of Bax and Caspase-3. In conclusion, TCOPs have protective effects on ethanol-induced gastroduodenal injury through gastrointestinal mucosal microcirculation promotion, antioxidation, anti-inflammation, and anti-apoptosis mechanisms.
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Mohan, Raj, and Revathi A. Gupta. "Design, Development and Evaluation of Gastroretentive Drug Delivery System of Antacids." Journal of Drug Delivery and Therapeutics 12, no. 6-S (December 15, 2022): 55–64. http://dx.doi.org/10.22270/jddt.v12i6-s.5706.

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Magaldrate is an antacid have been widely used in the treatment of various gastric and duodenal disorders such as heartburn, reflux esophagitis, acid indigestion, gastritis, sour stomach, upset stomach, irritable stomach, gastric and duodenal ulcers. The conventional antacids dosage forms have a short duration of action which is about 2-3 hours due to gastric emptying process. A gastroretentive dosage form of antacid is needed since the healing of gastric ulcers occurs when gastric pH is kept above 3-4 during 24 hours. The present study was aimed at developing Gastro retentive bilayer drug delivery systems containing Magaldrate to minimize the side effect, improve the prolongation of action, to reduce the frequency of drug administration. A wet granulation technique was used to formulate 9 batches. Superdisintegrants like Polyplasdone XL-10, Ac-Di-Sol, and sodium starch glycolate was used for immediate release layer and HPMC K4 M, Ac-Di-Sol and lactose like polymers were used in floating layer. Preformulation studies were carried out to optimize the ratios required for various grades of polymers. The prepared floating tablets were evaluated for hardness, weight variation, thickness, friability, drug content uniformity, buoyancy lag time, total floating time, water uptake (swelling index), and in vitro dissolution studies. Successful formulation was developed having floating lag time as low as 30 sec and drug release was sustained up to 12 hrs. A biphasic drug release can be obtained by using bilayer tableting technology which involved compression of immediate and sustained release layer together. Bilayered floating tablets with release characteristics offer critical advantages such as, site specificity with improved absorption and efficacy. This technology can be inculcated to various medicaments which have stomach as the major site of absorption. Keywords: Magaldrate, Antacid, Gastroretentive dosage form, Bilayer floating tab, Superdisintegrant
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Severynovska, O. V., O. O. Galinskij, A. I. Rudenko, O. B. Mursin, V. V. Babicheva, and L. D. Skubytska. "Особливості періодичної активності шлунка за умов дисбалансу NO-ергічної системи." Visnyk of Dnipropetrovsk University. Biology, medicine 5, no. 1 (April 14, 2014): 71–78. http://dx.doi.org/10.15421/021415.

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Nitric oxide is the main inhibitory mediator of the gastrointestinal smooth muscles’ relaxation which stimulates duodenal mucus and bicarbonate secretion. More recent studies have demonstrated that NO also protected the gastrointestinal tract by inhibiting gastric acid secretion. In this study we investigated gastric secretory and motor activity considering the NO imbalance condition. The experiments were carried out on male white laboratory rats (200–230 g). The control group was treated with 0.9% NaCl solution. The injections of NO donator (1.5 mg/kg of 0.1% (Sigma-Aldrich) sodium nitroprusside solution) were made in the second and the third groups during 6 and 12 days. The fourth and the fifth group were treated with NO synthesis inhibitor (40 mg/kg of 1% solution (Sigma-Aldrich) Nω-nitro-L-arginine) during 6 and 12 days respectively. Recording of gastric myoelectric activity (GMA) and gastric juice collection were carried out under anesthesia (ketamine, 110 mg/kg). Next, its volume, pH, glycoprotein and pepsin were measured. Within 6-days stimulation of NO excess decreased gastric juice volume by 47% and increased pH compared to control samples. Pepsin level increased by 62% and glycoprotein level decreased by 68% compared to the checkpoint. After 6 days of L-NNA injections we observed the increase of gastric juice secretion volume (78%) and pH level, however, pepsin concentration remained unchanged. Glycoprotein level increased by 21% compared to control samples. After 12 day NO synthesis inhibitor injections gastric secretion volume increased by 85%. Gastric juice pH level was 200% higher than the control value and exceeded gastric juice pH level (62%) in the third group. In addition, pepsin level tended to decrease when NO deficiency simulation was prolonged. Glycoprotein level decreased by 41% compared to control samples and by 51% compared to the third group. Pepsin level decreased after 12 day NO-inhibitor injections as gastric juice pH level increased. After 12 day Na-nitroprusside treatment, gastric myoelectric index decreased by 42% compared to the checkpoint. The type of contractions is typical to the I phase of the basic electrical rhythm (BER). Also, retrograde entrainment of duodenal rhythm took place. After 6 day L-NNA injections, GMA was the same as the period between II and III phase of BER. Late second and early third phases predominated, while the I phase wasn’t detected during the recording. In case of long-lasting disorder of NO-system, motor index value significantly differed from the control group samples and depended on the duration of NO-synthase blocking. On the 6th day of L-NNA treatment, the level of motor index increased 1.5 times. GMA phases could be identified only on the basis of motor index values. Stomach’s own rhythms disappeared and duodenogastric reflux resulted in domination of duodenal rhythms. After 12 day L-NNA injections, duration of the II and III phases increased while the I phase of gastric BER disappeared; gastric motor index decreased by 27%. After considering the results of the current investigation, it can be stated that NO system imbalance leads to desynchronization of gastric active phases and, perhaps, reassigns the influence of different compensatory-adaptive mechanisms. The longer is the L-NNA treatment, the more gastric functions are imbalanced and the stronger is the process of destruction.
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&NA;. "Simultaneously measured duodenal and gastric pH in with cystic fibrosis." European Journal of Gastroenterology & Hepatology 11, no. 12 (December 1999): A15. http://dx.doi.org/10.1097/00042737-199912000-00051.

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Kaur, Simran, Oxana Norkina, Donna Ziemer, Linda C. Samuelson, and Robert C. De Lisle. "Acidic duodenal pH alters gene expression in the cystic fibrosis mouse pancreas." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 2 (August 2004): G480—G490. http://dx.doi.org/10.1152/ajpgi.00035.2004.

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The duodenum is abnormally acidic in cystic fibrosis (CF) due to decreased bicarbonate ion secretion that is dependent on the CF gene product CFTR. In the CFTR null mouse, the acidic duodenum results in increased signaling from the intestine to the exocrine pancreas in an attempt to stimulate pancreatic bicarbonate ion secretion. Excess stimulation is proposed to add to the stress/inflammation of the pancreas in CF. DNA microarray analysis of the CF mouse revealed altered pancreatic gene expression characteristic of stress/inflammation. When the duodenal pH was corrected genetically (crossing CFTR null with gastrin null mice) or pharmacologically (use of the proton pump inhibitor omeprazole), expression levels of genes measured by quantitative RT-PCR were significantly normalized. It is concluded that the acidic duodenal pH in CF contributes to the stress on the exocrine pancreas and that normalizing duodenal pH reduces this stress.
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O'May, Graeme A., Nigel Reynolds, and George T. Macfarlane. "Effect of pH on an In Vitro Model of Gastric Microbiota in Enteral Nutrition Patients." Applied and Environmental Microbiology 71, no. 8 (August 2005): 4777–83. http://dx.doi.org/10.1128/aem.71.8.4777-4783.2005.

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ABSTRACT Patients with dysphagia due to oropharyngeal disease or cerebrovascular accident require long-term nutritional support via enteral feeding, which often results in microbial overgrowth in the upper gastrointestinal (GI) tract. Gastric acid is the primary innate defense mechanism in the stomach and has been assumed to provide an effective barrier to microbial colonization at pH values of <4. To evaluate the efficacy of gastric acid as a barrier to overgrowth, the microbiota of gastric and duodenal aspirates was assessed by culturing methods. Additionally, a fermentor-based model incorporating enteral nutrition tubing of the gastric microbiota of enteral nutrition (EN) patients was constructed to assess the effect of pH on the microbiota. Results showed that gastric acidity had a relatively small effect on the numbers of microorganisms recovered from intestinal aspirates but did influence microbiota composition. Similarly, at pH 3 in the fermentor, a complex microbiota developed in the planktonic phase and in biofilms. The effect of pH on microbiota composition was similar in aspirates and in the fermentors. Candidas and lactobacilli were aciduric, while recoveries of Escherichia coli and Klebsiella pneumoniae decreased as pH was reduced, although both were still present in significant numbers at pH 3. Only Staphylococcus aureus and Bifidobacterium adolescentis persisted at higher pH values both in vitro and in vivo. Lactate and acetate were the main organic acids detected in both aspirates and fermentors. These data show that the simulator used in this investigation was capable of modeling the effects of environmental influences on the upper GI microbiota of EN patients and that gastric pH of <4 is not sufficient to prevent microbial overgrowth in these individuals.
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Jones, Michael P., Christine C. Ebert, Laura Bianchi, John Pandolfino, and Peter J. Kahrilas. "EVALUATION OF DUODENAL AND GASTRIC ACID EXPOSURE USING RADIOTELEMETRY PH MONITORING." American Journal of Gastroenterology 98 (September 2003): S48. http://dx.doi.org/10.1111/j.1572-0241.2003.07874.x.

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Shetty, Bhuvan, and Mrinal Kumar Vishwanath. "An expert opinion on antacids: A review of its pharmacological properties and therapeutic efficacy." F1000Research 11 (September 15, 2022): 1057. http://dx.doi.org/10.12688/f1000research.124024.1.

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Acidity caused by common gastric conditions such as non-ulcer dyspepsia, duodenal ulcer, gastric ulcer, stress gastritis, gastroesophageal reflux disease (GERD), pancreatic insufficiency, bile acid-mediated diarrhea, biliary reflux, and constipation can be treated by administration of potent and efficacious acid suppressant (anti-secretory) agents such as antacids, histamine H2 receptor blockers, and proton pump inhibitors (PPIs). Antacids provide symptomatic relief from hyperacidity as well as other associated conditions by neutralizing the gastric acid directly, thereby raising the gastric pH, attenuating the pepsin activity, restoring acid-base balance, and increasing prostaglandin and bicarbonate secretion. The effectiveness of antacids is determined by its acid neutralizing capacity (ANC) and buffering capacity. Antacids containing a combination of aluminum hydroxide, magnesium hydroxide, and other ingredients such as those present in Digene showed better therapeutic efficacy even at low dosage with fewer side effects, persistent increase in gastric pH, faster and longer duration of pain relief, and fast relief from gas. Various clinical studies suggest that to obtain fast symptomatic relief, the treating physician can utilize antacids with the highest neutralizing capacities like Digene.
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Savarino, V., G. S. Mela, P. Zentilin, M. R. Mele, G. Bisso, M. Pivari, C. Mansi, et al. "24-hour gastric pH and duodenal gastric metaplasia one year after eradication of Helicobacter pylori infection in duodenal ulcer patients." Gastroenterology 114 (April 1998): A278. http://dx.doi.org/10.1016/s0016-5085(98)81131-1.

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Yamamoto, O., Y. Matsunaga, N. Haga, and Z. Itoh. "Vagovagal inhibition of motilin-induced phase III contractions by antral acidification in dog stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 267, no. 1 (July 1, 1994): G129—G134. http://dx.doi.org/10.1152/ajpgi.1994.267.1.g129.

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Gastric acidification at pH 1.0 strongly inhibits the spontaneously occurring and motilin-induced phase III contractions in canine and human stomach. In this study, we examined inhibition by gastric acidification in dogs following gastrojejunostomy, truncal vagotomy, and antrectomy. As a result, gastric acidification with 0.1 N HCl solution at pH 1.0 for 30 min at a rate of 1.0 ml/min significantly inhibited motilin-induced phase III activity to 23.5 +/- 5.9% of the control in the normal intact dogs and to 17.2 +/- 3.4% in the gastrojejunostomized dogs. In the antrectomized dogs, gastric acidification did not significantly inhibit the action of motilin (81.7 +/- 10%), but, in the vagotomized dogs, gastric acidification inhibited the action of motilin to 72.0 +/- 4.9%; the inhibition was much weaker than in the intact and gastrojejunostomized dogs but was significant. The duodenal acidification had no effect at all on the action of motilin (94.6 +/- 12.5%) in the gastrojejunostomized dogs. These findings strongly suggest the existence of a vagovagal reflex in the inhibition of motilin-induced phase III contractions by gastric antral acidification, although the involvement of sympathetic regulation cannot be completely ruled out.
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Sori, Ravi K., Balaji O., Shalini Adiga, and Huban Thomas. "Evaluation of the antipeptic ulcer activity of the seed extract of sesame (Sesamum indicum) in stress induced peptic ulcers in rats." International Journal of Basic & Clinical Pharmacology 7, no. 6 (May 22, 2018): 1131. http://dx.doi.org/10.18203/2319-2003.ijbcp20182094.

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Background: The peptic ulcers can be developed inside the inner lining of the stomach (gastric ulcer) or the small intestine (duodenal ulcer). Around 10% population of the world is suffering from the peptic ulcer disease. From the ancient times there is a reference about herbal extracts like Sesame indicum for the treatment of various diseases. The aim of the study is Evaluation of the anti-peptic ulcer activity of the seed extract of sesame (Sesamum indicum) in stress induced peptic ulcers in rats.Methods: The study was carried out by stress-induced ulcer model in wistar rats. The antiulcer activity of S. indicum (0.5, 1mg/kg p.o. for 7 days) was compared with standard drugs (pantoprazole). The studied parameters were mucin content, gastric volume, pH, total acidity, free acidity, ulcer index, size and number.Results: The low and high dose of S. indicum extract significantly reduced gastric mucosal lesion, mucin content, volume of gastric juice, gastric pH, free and total acidity when compared to positive control group. The high dose of S. indicum extract showed comparable results in parameters like effect on mucin content, gastric volume, pH, free acidity and total acidity with standard group. The statistical significant changes noted only in ulcer size, number and index.Conclusions: Although the high dose S. indicum (1mg/kg) group showed significant gastric protection against ulcer induced by cold restraint method. However, no clear inference can be drawn at this stage and hence there is a need for further extensive research.
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Savarino, V., GS Mela, P. Zentilin, G. Lapertosa, P. Ceppa, S. Vigneri, MR Mele, et al. "24-hour gastric pH and extent of duodenal gastric metaplasia in Helicobacter pylori-positive patients." Gastroenterology 113, no. 3 (September 1997): 741–45. http://dx.doi.org/10.1016/s0016-5085(97)70166-5.

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Venkatesh, P., and M. Durga srinivasrao. "FORMULATION AND INVITRO EVALUATION OF PRAZOSIN HYDROCHLORIDE UNFOLDING TYPE GASTRO RETENTIVE FILM." YMER Digital 21, no. 07 (July 10, 2022): 460–82. http://dx.doi.org/10.37896/ymer21.07/36.

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The present work is based on the formulation and In-vitro evaluation of a gastroretentive mucoadhesvie based drug delivery system containing prazosin hydrochloride for controlled release. It consists of a drug loaded polymeric film folded into a hard gelatin capsule. After administration film unfolds and its swelling and bioadhesion to the gastric mucosa. Prazosin hydrochloride, a histamine H2 receptor antagonist used for gastroesophageal reflux disease (GERD), duodenal ulcer and gastric ulcer. Prazosin hydrochloride absorbed only in the initial part of gastro intestinal tract (GIT) and has less bioavailability. Thus by retaining the drug in the gastric region improves its bioavailability. Films were prepared by solventcasting method using HPMC K4M, and Carbopol 971P NF as polymers and PEG 400 as the plasticizer. The prepared film were evaluated for various parameters such as film thickness, folding endurance, uniformity of weight, surface pH, determination of drug content, moisture content, swelling index, In-vitro mucoadhesive study retention time, In-vitro unfolding behavior and In-vitro drug release studies and drug release kinetics. Differential scanning calorimetry revealed there were no polymorphic changes in drug as well as polymers during the formulation of polymeric film. Optimized formulation showed 99.02 % drug release at the end of 12 hrs and it follows the Korsmeyer-peppas kinetics model of drug release. Keywords: Gastroretentive mucoadhesive film, Solvent casting method, Prazosin hydrochloride
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Lin, H. C., J. E. Doty, T. J. Reedy, and J. H. Meyer. "Inhibition of gastric emptying by acids depends on pH, titratable acidity, and length of intestine exposed to acid." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 6 (December 1, 1990): G1025—G1030. http://dx.doi.org/10.1152/ajpgi.1990.259.6.g1025.

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Exposure of the small intestine to acid inhibits gastric emptying in a dose-related fashion that depends on titratable acidity and pH. Little information is available on the location of this inhibitory mechanism or on the relative contribution of titratable acidity and pH to this feedback control. We hypothesized that the dependence on titratable acidity is related to the length of the intestine exposed to acid and that the dependence on pH is related to the region of the intestine exposed to acid. To test these ideas, we studied 11 dogs with duodenal and jejunal fistulas. The inhibitory effects were tested when different lengths of the small intestine were exposed to test solutions of 0.03, 0.06, and 0.12 meq/ml titratable acidities. pH as an independent covariable was separated from titratable acidity by comparing the inhibition of gastric emptying of lactic acid (pH fixed to 2.4) to HCl (pH 0.96-1.6). Maximal inhibition of gastric emptying by both acids depended on acid exposure of a length of small intestine that was greater than 65 but less than or equal to 150 cm long. When acid was confined to the proximal 15 cm, increasing concentration of HCl (decreasing pH) resulted in increasing inhibition, but this effect was absent with increasing concentration of lactic acid (fixed pH). Inhibition was absent when 0.06 meq/ml HCl was infused into the intestine beyond the midintestine.(ABSTRACT TRUNCATED AT 250 WORDS)
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Marangella, Martino, Cristiana Bagnis, Francesca Bermond, Silvia Berutti, Laura Fabbrini, Paolo Gabella, Cristina Marcuccio, Giorgio Soragna, Alberto Tricerri, and Corrado Vitale. "Update sulla calcolosi renale." Giornale di Clinica Nefrologica e Dialisi 25, no. 4 (September 1, 2014): 299–303. http://dx.doi.org/10.33393/gcnd.2013.1061.

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Molti lavori recenti analizzano l'associazione fra calcolosi renale e altre patologie non trasmissibili tipiche dei paesi industrializzati. I dati epidemiologici, su casistiche ampie, indicano un aumento di incidenza della calcolosi in pazienti con sindrome metabolica, obesità e ipertensione. Viene anche descritto un aumento del rischio di infarto miocardico e di ictus nei litiasici. Si ipotizza che il denominatore comune in queste patologie sia l'aumento della resistenza all'insulina. Questo causa alterazioni della biochimica urinaria, pH più acido e riduzione della citraturia, tali da aumentare il rischio litogeno. Nel ratto diabetico è stata descritta una steatosi renale che riduce l'ammoniogenesi e che è reversibile con una terapia con PPARγ. Il pioglitazone è stato efficace nel ridurre il danno renale indotto nel ratto da etilen glicole. Altra associazione nota è quella fra calcolosi renale e gotta. Due recenti studi documentano un'incidenza della calcolosi calcica e non solo urica nella gotta, con anomalie metaboliche in parte simili a quelle dei pazienti non gottosi. L'indagine TC mostra che l'incidenza di calcolosi è sottostimata nella gotta e, inoltre, la calcolosi, in alcuni pazienti, precede anche di molti anni l'attacco gottoso. Un altro argomento analizza il potenziale effetto che favorisce la calcolosi nelle donne trattate con calcio e vitamina D. Emergono un modesto ma significativo aumento del rischio litogeno indipendente da altre covariabili e un conseguente invito all'attenta valutazione del rapporto rischio/beneficio. La chirurgia bariatrica per la correzione della grave obesità era, in passato, gravata da un elevato rischio di calcolosi renale iperossalurica con quadri anche di ossalosi severa. Negli ultimi anni si sono diffuse tecniche meno litogene come il bendaggio gastrico e il bypass gastrico alla Roux. Iperossaluria e ipocitraturia conseguono a questi interventi e il rischio di calcolosi è di gran lunga inferiore, ma restano segnalazioni in letteratura di casi di ossalosi renale specialmente dopo bypass gastrico alla Roux.
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Rosenblum, J. L., C. L. Irwin, and D. H. Alpers. "Starch and glucose oligosaccharides protect salivary-type amylase activity at acid pH." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 5 (May 1, 1988): G775—G780. http://dx.doi.org/10.1152/ajpgi.1988.254.5.g775.

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Salivary-type amylase may significantly contribute to duodenal starch hydrolysis in exocrine pancreatic insufficiency, provided that gastric inactivation does not occur. We investigated the effect of starch and its hydrolytic products, therefore, on salivary amylase activity in vitro at low pH. When incubated at pH 3 in the presence of 1% starch, 56% of the initial activity of amylase purified from saliva remained after 60 min at 37 degrees C compared with only 6% without starch. Similar protection of amylolytic activity was observed using human milk, which also contains a salivary-type amylase. In addition, partially hydrolyzed starch protected salivary amylase activity at pH 3, and purified glucose oligomers ranging in length from two to seven glucose molecules protected amylase in a concentration-dependent manner. Lactose, sucrose, and glucose, however, were ineffective in sparing amylase. Starch protected amylase activity even in the presence of pepsin, and maltotriose conferred striking protection below pH 3. These studies indicate that salivary-type isoamylases are protected in a simulated gastric environment by substrates of amylase as well as its end products of hydrolysis.
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JONES, M. "Evaluation of duodenal and gastric acid exposure using radiotelemetry pH monitoring*1." American Journal of Gastroenterology 98, no. 9 (September 2003): S48. http://dx.doi.org/10.1016/s0002-9270(03)00907-9.

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Quigley, E. M. M., and L. A. Turnberg. "pH of the microclimate lining human gastric and duodenal mucosa in vivo." Gastroenterology 92, no. 6 (June 1987): 1876–84. http://dx.doi.org/10.1016/0016-5085(87)90619-6.

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Bendtsen, F., and S. J. Rune. "Effect of a Single Dose of Antacid on Gastric and Duodenal Bulb pH in Duodenal Ulcer Patients." Scandinavian Journal of Gastroenterology 23, no. 8 (January 1988): 935–40. http://dx.doi.org/10.3109/00365528809090150.

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Petersen, Karl-Uwe. "Pepsin and Its Importance for Functional Dyspepsia: Relic, Regulator or Remedy?" Digestive Diseases 36, no. 2 (October 5, 2017): 98–105. http://dx.doi.org/10.1159/000481399.

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Background: Functional dyspepsia is a heterogeneous disorder lacking an established therapeutic strategy. Historical treatment attempts with pepsin products were shrugged off, as a simple calculation shows that quantitative substitution is pointless. However, such attempts might have been right for the wrong reason. Summary: Today, the role of pepsins is primarily seen in the provision of signalling amino acids (especially phenylalanine and tryptophan) and peptides, which initiate processes promoting digestion. Proteolysis benefits from pepsin variants showing, contrary to common belief, activities of up to a pH value of 5.0. Non-clinical and clinical studies support the view that liberated amino acids produce a variety of direct and indirect effects. Signal chains stimulated by (mostly aromatic) amino acids lead to secretion of gastrin and cholecystokinin (CCK), mediated, respectively, by CCK2 (gastrin) and Ca2+-sensing receptors in the parietal cell, and Ca2+-sensing receptors in the antral and duodenal mucosa. Thus, CCK effects such as secretion of pancreatic enzymes and promotion of gastric accommodation are (also) consequential to peptic liberation of amino acids. Key Message: As functional dyspepsia represents a heterogeneous disorder, it may be intriguing to view pepsin as a potential (although still to be proven) treatment modality, distinguished by a diversity of pro-digestive effects.
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Johansson, Berndt, Mathias Holm, Sara Ewert, Anna Casselbrant, Anders Pettersson, and Lars Fändriks. "Angiotensin II type 2 receptor-mediated duodenal mucosal alkaline secretion in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 280, no. 6 (June 1, 2001): G1254—G1260. http://dx.doi.org/10.1152/ajpgi.2001.280.6.g1254.

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The aims of this study were to elucidate the distribution of angiotensin receptors (AT1and AT2) in the duodenal wall and to investigate whether AT2 receptors are involved in the regulation of duodenal mucosal alkaline secretion, which is of importance for the mucosal defense against gastric acid. Immunohistochemistry was used to locate AT1 and AT2 receptors in chloralose-anesthetized rats. Duodenal mucosal alkaline output was measured by use of in situ pH-stat titration. Immunohistochemistry demonstrated a distinct staining for both AT1 and AT2 receptors in the lamina propria of the villi and also for AT1 receptors in the muscularis interna. When angiotensin II was infused in the presence of the AT1receptor antagonist losartan, mucosal alkaline secretion increased by ∼50%. This response was inhibited by the AT2 receptor antagonist PD-123319. The AT2 receptor agonist CGP-42112A increased mucosal alkaline secretion by ∼50%. This increase was absent in the presence of PD-123319 but not in the presence of losartan or the local anesthetic lidocaine. We conclude that angiotensin II stimulates duodenal mucosal alkaline secretion by activation of AT2 receptors located in the duodenal mucosa/submucosa.
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Wilcox, C. M., K. B. Waites, and P. D. Smith. "No relationship between gastric pH, small bowel bacterial colonisation, and diarrhoea in HIV-1 infected patients." Gut 44, no. 1 (January 1, 1999): 101–5. http://dx.doi.org/10.1136/gut.44.1.101.

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Background/AimsConclusive studies of small bowel bacterial overgrowth in patients with HIV-1 infection are limited. The relation was therefore determined between the quantity and species of bacteria in the proximal small intestine of HIV-1 infected patients and the presence of diarrhoea, gastric acidity, severity of immune deficiency, and clinical outcome.MethodsBacteria in the duodenal fluids obtained endoscopically from 32 HIV-1 infected patients, 21 of whom had diarrhoea, and seven control subjects without HIV-1 risk factors were quantified and speciated. Gastric pH was determined at the time of endoscopy. Clinical follow up was performed to assess outcome.ResultsOropharyngeal Gram positive cocci were present in fluids from 28 patients (88%). Gram negative aerobic or facultatively anaerobic bacteria were present in fluids from 12 patients (38%), and strict anaerobes were detected in six patients (19%), but for both groups colony counts infrequently exceeded 104 colony forming units/ml. The number and species of bacteria did not correlate with the presence of diarrhoea, gastric pH, or CD4 lymphocyte count.ConclusionsSmall bowel bacterial overgrowth is not common in HIV-1 infected patients, regardless of the presence of diarrhoea, and is not associated with hypochlorhydria.
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41

Welch, Neil T., Akihiro Yasui, Choong B. Kim, Antony P. Barlow, Ronald A. Hinder, Tom R. DeMeeSter, Paul V. Polishuk, Geoffrey W. B. Clark, and Thomas E. Adrian. "Effect of duodenal switch procedure on gastric acid production, intragastric pH, gastric emptying, and gastrointestinal hormones." American Journal of Surgery 163, no. 1 (January 1992): 37–45. http://dx.doi.org/10.1016/0002-9610(92)90250-u.

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42

Avramenko, Anatoly A. "INFLUENCE OF PECULARITIES OF ANATOMICAL STRUCTURE (SHAPE) OF DUODENAL BULB ON THE MECHANISM OF FORMATION OF “KISSING” ULCERS OF PATIENTS WITH CHRONIC NON-ATROPHIC GASTRITIS." Wiadomości Lekarskie 73, no. 12 (2020): 2568–71. http://dx.doi.org/10.36740/wlek202012102.

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The aim: To determine of the factors influencing the formation of “kissing” duodenal bulb ulcer in patients with chronic non-atrophic gastritis. Materials and methods: The data of a comprehensive examination of 34 patients with chronic non-atrophic gastritis were analyzed, in which the examination revealed “kissing” ulcers of the duodenal bulb (primary group), and 37 patients with chronic non-atrophic gastritis, in which single ulcers were detected in the bulb (control group). Comprehensive examination included: step-by-step intragastric pH-metry, esophagogastroduodenoscopy, helicobacter infection test (НР) (helicobacter urease test and microscopic examination of stained smears), histological investigations of the gastric stump mucous, material for which was taken during endoscopy from 4 topographical zones: from the middle third of the gastric antrum and body of stomach on the big and small curvature. Results: In the course of the examination, the presence of chronic non-atrophic gastritis in 100% of cases was confirmed with a different degree of activity of the inflammatory process on the gastric mucosa, as well as the presence of Helicobacter pylori infection with a high degree of colonization of the gastric mucosa in the absence of a significant difference (p> 0.05) in the stomach zones. It was found that the main difference that can be traced in 100% of cases is the difference in the anatomical structure of the bulb of the duodenum, namely, the shape: in the control group, the shape and lumen of the duodenal bulb are round, while in the patients of the main group the bulb the duodenum, starting from the pylorus, is stretched toward the large and small curvature, which gives the lumen bulb its oval shape. Conclusions: “Kissing” ulcers of the duodenal bulb are formed in patients with chronic non-atrophic gastritis only if the patients have a peculiar anatomical structure of the bulb, in which the lumen has an oval shape.
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43

Sohn, Sang-Kwon, Man-Sik Chang, Wahn-Soo Choi, Kyu-Bong Kim, Tae-Wook Woo, Seok-Bong Lee, and Young-Kuk Chung. "Biochemical and pharmacological characteristics of a newly synthesized H+-K+ ATPase inhibitor, YJA20379-1, 2-amino-4,5-dihydro-8-phenylimidazole [2,1-b]thiazolo[5,4-g]benzothiazole." Canadian Journal of Physiology and Pharmacology 77, no. 5 (June 15, 1999): 330–38. http://dx.doi.org/10.1139/y99-026.

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The biochemical and pharmacological characteristics of a newly synthesized H+-K+ ATPase inhibitor, 2-amino-4,5-dihydro-8-phenylimidazole[2,1-b]thiazolo[5,4-g]benzothiazole (YJA20379-1), were investigated. In the pig gastric microsomes, YJA20379-1 inhibited the gastric H+-K+ ATPase regardless of pH condition, IC50 values being 21 and 24 µM at pH 6.4 and 7.4, respectively. The inhibitory activity of YJA20379-1 was antagonized by dithiothreitol treatment but could not be reversed by dilution and washing of the enzyme preparation. In Sprague-Dawley rats, YJA20379-1, administered i.d., p.o, i.v., or s.c., significantly inhibited basal gastric acid secretion, with ED50 values of 4.7, 20.2, 6.3, and 13.4 mg/kg, respectively. The antisecretory action of YJA20379-1 was short lasting (less than 7 h at an oral dosing of 30 mg/kg). Oral administration of YJA20379-1 also prevented the formation of ethanol, indomethacin, and water immersion stress induced gastric lesions and mepirizole-induced duodenal ulcers in rats. Furthermore, YJA20379-1 accelerated the healing of acetic acid induced chronic gastric ulcers in rats. In conclusion, these results suggest that YJA20379-1 has a potent inhibitory activity on the gastric H+-K+ ATPase but much shorter duration of antisecretory action than omeprazole, thereby exerting its anti-ulcer effects partly with cytoprotective activity.Key words: proton pump inhibitor, acid secretion, anti-ulcer effects, cytoprotective activity.
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44

Gonzalez-Alvarez, Isabel, Marival Bermejo, Yasuhiro Tsume, Alejandro Ruiz-Picazo, Marta Gonzalez-Alvarez, Bart Hens, Alfredo Garcia-Arieta, Greg E. Amidon, and Gordon L. Amidon. "An In Vivo Predictive Dissolution Methodology (iPD Methodology) with a BCS Class IIb Drug Can Predict the In Vivo Bioequivalence Results: Etoricoxib Products." Pharmaceutics 13, no. 4 (April 7, 2021): 507. http://dx.doi.org/10.3390/pharmaceutics13040507.

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The purpose of this study was to predict in vivo performance of three oral products of Etoricoxib (Arcoxia® as reference and two generic formulations in development) by conducting in vivo predictive dissolution with GIS (Gastro Intestinal Simulator) and computational analysis. Those predictions were compared with the results from previous bioequivalence (BE) human studies. Product dissolution studies were performed using a computer-controlled multicompartmental dissolution device (GIS) equipped with three dissolution chambers, representing stomach, duodenum, and jejunum, with integrated transit times and secretion rates. The measured dissolved amounts were modelled in each compartment with a set of differential equations representing transit, dissolution, and precipitation processes. The observed drug concentration by in vitro dissolution studies were directly convoluted with permeability and disposition parameters from literature to generate the predicted plasma concentrations. The GIS was able to detect the dissolution differences among reference and generic formulations in the gastric chamber where the drug solubility is high (pH 2) while the USP 2 standard dissolution test at pH 2 did not show any difference. Therefore, the current study confirms the importance of multicompartmental dissolution testing for weak bases as observed for other case examples but also the impact of excipients on duodenal and jejunal in vivo behavior.
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45

Takeuchi, K., K. Takehara, S. Kato, and K. Yagi. "PACAPs stimulate duodenal bicarbonate secretion at PACAP receptors in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 3 (March 1, 1997): G646—G653. http://dx.doi.org/10.1152/ajpgi.1997.272.3.g646.

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We investigated the effects of pituitary adenylate cyclase-activating polypeptides (PACAPs) on gastroduodenal HCO(3)- secretion in anesthetized rats and characterized their effects by comparison with the effects of vasoactive intestinal polypeptide (VIP). Under urethan anesthesia, a rat proximal duodenal loop or a rat stomach mounted in an ex vivo chamber (in the absence of acid secretion) was perfused with saline, and HCO(3)- secretion was measured at pH 7.0 using a pH-stat method and by addition of 10 mM HCl. Intravenous injection of PACAP-27 stimulated HCO(3)- secretion in a dose-dependent manner in the duodenum, but not in the stomach, although this peptide had no effect on duodenal HCO(3)- secretion after intracisternal administration. The duodenal HCO(3)- stimulatory action was similarly observed after intravenous administration of PACAP-38 and VIP, and the potency of action was in the following order: PACAP-27 > PACAP-38 = VIP. The duodenal HCO(3)- stimulatory action of PACAP-27 was potentiated by pretreatment with 3-isobutyl-1-methylxanthine, similar to that of prostaglandin E2, and was significantly attenuated by PACAP-(6--27) (PACAP antagonist) or Ac-Tyr1,D-Phe2-VIP (VIP antagonist) but was not affected by bilateral vagotomy or prior administration of atropine, verapamil, and indomethacin. Forskolin, the stimulator of adenylate cyclase, also increased HCO(3)- secretion in the duodenum, but not in the stomach. These results suggest that 1) PACAP is a potent stimulator of HCO(3)- secretion in the duodenum, but not in the stomach, and may be involved in the peripheral regulation of duodenal HCO(3)- secretion, 2) this action is mediated by adenosine 3',5'-cyclic monophosphate, probably through PACAP and VIP receptors, and 3) adenosine 3',5'-cyclic monophosphate is a mediator in duodenal, but not in gastric, HCO(3)- secretion.
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46

Singh, Raghuvendra, Anubha Gupta, and Shweta Patel. "Pharmacological Screening Model and Its Treatment of Peptic Ulcer Disease." Journal for Research in Applied Sciences and Biotechnology 1, no. 5 (December 1, 2022): 36–47. http://dx.doi.org/10.55544/jrasb.1.5.4.

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Peptic ulcer is a ceaseless sickness influencing up to 10% of the total population. Peptic ulcer created by the unevenness of gastric juice pH and mucosal protections. Two fundamental components delivered Peptic ulcer. Frist is central point it included bacterial disease, for example, Helicobacter Pylori (H. Pylori) and medicine non-steroidal anti-inflammatory medication and synthetic E.g., HCL, Ethanol. Second is minor factor it included pressure, smoking, fiery food and nourishment lopsidedness. Ordinary treatment of Peptic ulcer, for example, proton siphon inhibitor (PPI) and Histamine-2 (H2) Receptor Antagonist. Also, other Hand therapeutic plant and their concoction compound are valuable in the counteraction and treatment of peptic ulcer infection. Various creature models are utilizing to influenced ulcer to identifying the antiulcer activity of many new existed drugs such as Pylorus ligated (shay) rats, Stress ulcers, Restraint ulcer in rats, Water immersion-induced restraint ulcers, Cold and restraint ulcers, Gastric mucosal damage induced by NSAID in rats, Induced solitary chronic gastric ulcer, Acetic acid induced kissing gastric ulcers in rats Histamine induced gastric ulcer in guinea pig, Duodenal anti-ulcer activity, Gastric cytoprotective action.
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47

Frieri, G., G. De Petris, A. Aggio, D. Santarelli, E. Ligas, R. Rosoni, and R. Caprilli. "Gastric and Duodenal Juxtamucosal pH and Helicobacter pylori." Digestion 56, no. 2 (1995): 107–10. http://dx.doi.org/10.1159/000201229.

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48

Brown, Timothy H., Greg S. Walton, Curt Manning, Hollis A. Thomas, and Gerald M. Larson. "Influence of Food, Posture and Gastric Alkaline Events on 24-Hour Gastric and Duodenal pH in Normals." Digestive Surgery 8, no. 3 (1991): 149–56. http://dx.doi.org/10.1159/000172021.

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49

Lloyd, K. C., H. H. Holzer, T. T. Zittel, and H. E. Raybould. "Duodenal lipid inhibits gastric acid secretion by vagal, capsaicin-sensitive afferent pathways in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no. 4 (April 1, 1993): G659—G663. http://dx.doi.org/10.1152/ajpgi.1993.264.4.g659.

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Neural and endocrine pathways mediate the inhibitory effects of intestinal fat on gastric acid secretion. To study whether vagal and/or spinal afferent nerves contribute to the neural component of the enterogastric reflex, the sensory neurotoxin capsaicin was applied topically either to the vagus nerves bilaterally or to the celiac-superior mesenteric ganglia in rats with chronic gastric and duodenal fistulas. In lightly restrained, awake rats acid secretion was stimulated for 2 h by continuous intragastric perfusion with 8% peptone and was measured by extragastric titration to pH 5.5. Duodenal lipid perfusion (0-20%) during the 2nd h caused inhibition of peptone-stimulated acid output. Acid output was inhibited by 81% during 5% lipid perfusion of the duodenum and was restored after capsaicin treatment of the vagus nerves. In contrast, capsaicin treatment of the celiac ganglion did not alter the acid inhibitory response to any dose of intestinal lipid. Basal and maximum acid outputs were not significantly different among rats treated by either method with capsaicin. The neural component of the enterogastric reflex in awake rats is mediated in part by a capsaicin-sensitive, vagal-afferent neural reflex.
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50

S. Al-Lami, Mohammed. "Formulation and Evaluation of Sustained and Raft Forming Antacid Tablet." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 26, no. 1 (July 8, 2017): 26–31. http://dx.doi.org/10.31351/vol26iss1pp26-31.

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Antacids have been widely used in the treatment of various gastric and duodenal disorders such as heartburn, reflux esophagitis, gastritis, irritable stomach, gastric and duodenal ulcers. A pH-responsive of bi-polymer of sodium alginate and pectin have been studied as raft-forming polymers using sodium bicarbonate and calcium carbonate as gas-generating and calcium ion sources. The aim of study was to formulate and evaluate mono and bilayer tablets of floating and sustained release antacid delivery systems using sodium carboxy methyl cellulose as a gel forming substance, calcium and magnesium carbonate as sources of acid neutralizing and carbon dioxide gas generators agents upon contact with acidic solution. The effect of the formulation contents on the buoyancy has been investigated. In addition to, the antacid activities of intact and pulverized tablets have been studied. The result obtained showed that the buoyance is remarkably affected by the percentages of sodium carboxy methyl cellulose and carbonates salts. All formulas of mono and bilayer tablets revealed sustained action of acid neutralization and raft formation. Besides, bilayer tablets showed a significant and higher level of acid neutralizing capacity than monolayer tablets. Moreover, the pulverized of bilayer tablets exhibited significant and higher acid neutralizing capacity at raft than that at bulk of artificial gastric juice medium. Keywords: Raft forming agent, Antacid, floating drug delivery, Acid neutralizing capacity, Sodium carboxy methyl cellulose.
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