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Gastric Acid Secretion (gastric + acid_secretion)

Distribution by Scientific Domains

Medical Sciences	92%
Life Sciences	7%

Selected Abstracts

MODIFIED ENDOSCOPIC CONGO RED TEST: A RAPID METHOD TO VISUALIZE GASTRIC ACID SECRETION

DIGESTIVE ENDOSCOPY, Issue 1 2003
Ervin Tóth
Background:, The conventional endoscopic Congo red test (CRT) permits visualization of acid-producing mucosa. However, the CRT has not been disseminated into clinical endoscopy, which is partly due to the substantial prolongation of the gastroscopic examination. Methods:, Five healthy volunteers and 551 patients were included in a study designed to develop a more rapid approach based on the CRT. In this modified endoscopic Congo red test (MCRT), 0.2 µg/kg of pentagastrin was given intravenously to stimulate gastric acid production. The technical feasibility, tolerability, reproducibility, and inter- and intra-observer reliability of the MCRT were evaluated. Results:, The MCRT was as effective as the CRT (i.e. 6 µg/kg of pentagastrin was administered intramuscularly) in visualizing the extent of acid-producing gastric mucosa. Moreover, the MCRT significantly reduced the duration of examination by 63% (almost 8 min), compared to the CRT. Conclusions:, This MCRT is a simple, inexpensive, well-tolerated and reproducible method with low inter- and intra-observer variability and is well suited for endoscopy units with high workloads. [source]

Effect of Helicobacter pylori Infection on Gastric Acid Secretion and Meal-Stimulated Serum Gastrin in Children

HELICOBACTER, Issue 2 2004
Seiichi Kato
ABSTRACT Background., Comparative studies of gastric acid secretion in children related to Helicobacter pylori infection are lacking. The purpose of this study was to compare acid secretion and meal-stimulated gastrin in relation to H. pylori infection among pediatric patients. Materials and Methods., Thirty-six children aged 10,17 years (17 with H. pylori infection) undergoing diagnostic endoscopy participated in the study. Diagnoses included gastritis only (n = 23), duodenal ulcer (n = 5) and normal histology (n = 8). Gastric acid output was studied using the endoscopic gastric secretion test before and 2,3 months after H. pylori eradication. Meal-stimulated serum gastrin response was assessed before and 12 months after eradication. Results.,H. pylori gastritis was typically antrum-predominant. Acid secretion was greater in H. pylori- positive patients with duodenal ulcer than in gastritis-only patients or controls [mean ± standard error (SE): 6.56 ± 1.4, 3.11 ± 0.4 and 2.65 ± 0.2 mEq/10 minutes, respectively; p < .001]. Stimulated acid secretion was higher in H. pylori- positive boys than girls (5.0 ± 0.8 vs. 2.51 ± 0.4 mEq/10 minutes, respectively; p < .05). Stimulated acid secretion pre- and post- H. pylori eradication was similar (5.47 ± 0.8 vs. 4.67 ± 0.9 mEq/10 minutes, respectively; p = .21). Increased basal and meal-stimulated gastrin release reversed following H. pylori eradication (e.g. basal from 134 to 46 pg/ml, p < .001 and peak from 544 to 133 pg/ml, p < .05). Conclusions.,H. pylori infection in children is associated with a marked but reversible increase in meal-stimulated serum gastrin release. Gastric acid hypersecretion in duodenal ulcer remains after H. pylori eradication, suggesting that the host factor plays a critical role in outcome of the infection. [source]

Role of the Ventromedial Hypothalamic Orexin-1 Receptors in Regulation of Gastric Acid Secretion in Conscious Rats

JOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2009
A. Eliassi
Orexins play an important role on the central nervous system to modulate gastric acid secretion. The orexin receptors are distributed within the hypothalamus, and expression of orexin-1 receptors (OX1R) is greatest in the anterior hypothalamus and ventromedial nucleus. Therefore, we hypothesised that ventromedial hypothalamic OX1R may be involved in the control of gastric acid secretion. To address this question, we examined the effects of orexin-A and a selective OX1R antagonist, SB-3345867, on gastric acid secretion in pyloric-ligated conscious rats. Intraventromedial injection of orexin-A (0.5,2 ,g/,l) stimulated gastric acid secretion in a dose-dependent manner. This stimulatory effect of orexin-A persisted over 3 h. In some experiments, SB-3345867 (10 mg/kg i.p.) was administered 30 min before orexin-A or saline injections. We found that i.p. injection of SB-334867 suppressed stimulated gastric acid secretion induced by orexin-A (2 ,g/,l). Atropine (5 mg/kg) also inhibited the stimulatory effect of central injection of orexin-A on acid secretion. In conclusion, the present study suggests that endogenous orexin-A acts on the ventromedial hypothalamus to stimulates acid secretion. This stimulatory effect is probably mediated through OX1R. [source]

Rebound Hypersecretion after Inhibition of Gastric Acid Secretion

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 5 2004
Gunnar Qvigstad
However, from clinical experience it seems that symptom relapse is common after withdrawal of these drugs. Experimental as well as clinical studies have demonstrated an increased acid secretion after a period of treatment with either histamine 2 receptor antagonists or proton pump inhibitors. Rebound hypersecretion is likely to reflect the following sequence of events: Long-term inhibition of acid output is accompanied by elevated serum gastrin levels, leading to enterochromaffin-like cell activation and proliferation, resulting in increased amounts of histamine being mobilized from these cells to stimulate the parietal cells. The clinical consequences of rebound hypersecretion have not been settled. [source]

Developments in the inhibition of gastric acid secretion

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2005
J. Mössner
Abstract Understanding the physiology of gastric acid secretion and the pathophysiology of acid-related diseases (e.g. gastrooesophageal reflux and peptic ulcer) has led to the development of numerous ways to decrease acid exposure. Pharmacologically one can try to neutralize secreted acid by antacids, prevent stimulation of the parietal cell, improve mucosal defences and block the functioning of the proton pump. Proton pump inhibitors (PPIs) inhibit the final step of acid secretion, and are currently the most potent acid inhibitors. Major therapeutic improvement within the PPI class appears unlikely, as agents in this class share similar chemistry, mode of action, and pharmacokinetic profiles. New approaches that block acid secretion are now being developed. Gastrin (CCK2) receptor antagonists and potassium-competitive acid blockers (P-CABs) are in clinical development. [source]

Attack and defence in the gastric epithelium , a delicate balance

EXPERIMENTAL PHYSIOLOGY, Issue 4 2007
Rod Dimaline
The gastric epithelium is a complex structure formed into tubular branched gastric glands. The glands contain a wide variety of cell types concerned with the secretion of hydrochloric acid, proteases, mucus and a range of signalling molecules. All cell types originate from stem cells in the neck region of the gland, before migrating and differentiating to assume their characteristic positions and functions. Endocrine and local paracrine mediators are of crucial importance for maintaining structural and functional integrity of the epithelium, in the face of a hostile luminal environment. The first such mediator to be recognized, the hormone gastrin, was identified over a century ago and is now established as the major physiological stimulant of gastric acid secretion. Recent studies, including those using mice that overexpress or lack the gastrin gene, suggest a number of previously unrecognized roles for this hormone in the regulation of cellular proliferation, migration and differentiation. This review focuses on the identification of hitherto unsuspected gastrin-regulated genes and discusses the paracrine cascades that contribute to the maintenance of gastric epithelial architecture and secretory function. Helicobacter infection is also considered in cases where it shares targets and signalling mechanisms with gastrin. [source]

Gastric Acidity in Patients with Follicular Gastritis is Significantly Reduced, but Can be Normalized After Eradication for Helicobacter pylori

HELICOBACTER, Issue 3 2005
Tomohiko Shimatani
ABSTRACT Background., Follicular gastritis is thought to be caused by Helicobacter pylori infection. However, the pathophysiology of it remains unclear. Materials and methods., We assessed gastric acidity in 15 patients with follicular gastritis, aged 20,37 years, using a 24-hour intragastric pH-metry, as well as by histologic and serologic evaluations; and compared it with that in other age-matched groups: 18 cases of H. pylori -positive antrum-predominant gastritis, 12 of pangastritis, and 24 H. pylori -negative normals. In eight cases with follicular gastritis, it was re-assessed 6 months after the eradication therapy for H. pylori. Results., During nighttime, the percentage of time with intragastric pH above 3.0 in follicular gastritis was significantly higher than that in normals (p < .0001), and in antrum-predominant gastritis (p < .001), but was comparable with that in pangastritis. In the daytime period, this parameter in follicular gastritis was significantly higher than that in normal (p < .001), in antrum-predominant gastritis (p < .001), and in pangastritis (p < .05). Marked mononuclear cell and neutrophil infiltration but no apparent glandular atrophy were observed in both the antrum and corpus. Serum pepsinogen I/II ratio was significantly lower in follicular gastritis than that in normals (p < .0001) and in antrum-predominant gastritis (p < .001), whereas serum gastrin was significantly higher than that in normals (p < .0001), in antrum-predominant gastritis (p < .01) and in pangastritis (p < .05). After eradication for H. pylori, all of the parameters in follicular gastritis were altered to the same ranges as those in normals. Conclusions., In follicular gastritis, gastric acidity is significantly reduced, but can be normalized by eradication of H. pylori. It can thus be speculated that inflammatory cytokines or H. pylori -infection,induced prostaglandins might strongly inhibit gastric acid secretion in follicular gastritis. [source]

Effect of Helicobacter pylori Infection on Gastric Acid Secretion and Meal-Stimulated Serum Gastrin in Children

Clinical trial: Inhibitory effect of revaprazan on gastric acid secretion in healthy male subjects

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2010
Hyung-Keun Kim
Abstract Background and Aim:, Revaprazan is a novel acid pump antagonist. The aim of this study was to investigate the inhibitory effect of revaprazan on gastric acid secretion in healthy male subjects. Methods:, In a double-blind, three-way cross-over study, 30 healthy male volunteers were randomized to 100, 150 or 200 mg of oral revaprazan daily for 7 days. Serum gastrin concentration was measured, and 24-h intragastric pH was recorded at baseline and on days 1 and 7 of each administration period. Serial blood samples were processed for pharmacokinetics. Results:, Median intragastric pH over 24 h and mean percentage time that pH was > 4 increased in a dose-dependent manner and were significantly higher on days 1 and 7 compared with baseline in all groups (P < 0.05). The antisecretory effect of revaprazan was rapid and nearly maximal on day 1 in all groups. Serum gastrin levels were rapidly normalized by 100 and 150 mg/day of revaprazan on days 1 and 7, but were significantly higher in the 200 mg/day revaprazan group. The pharmacokinetic effect was rapidly absorbed and eliminated on days 1 and 7 in all groups. Conclusions:, Revaprazan rapidly and effectively inhibits gastric acid secretion in healthy male subjects. Therefore, revaprazan can be used as an effective drug for acid-related disease. [source]

Role of the Ventromedial Hypothalamic Orexin-1 Receptors in Regulation of Gastric Acid Secretion in Conscious Rats

Effect of hyperprolactinaemia as induced by pituitary homografts under kidney capsule on gastric and duodenal ulcers in rats

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 11 2001
Mohammed Asad
The effect of hyperprolactinaemia, induced by two or four pituitary homografts under the kidney capsule, on gastric and duodenal ulcers has been studied. The acute gastric ulcer models used were pylorus ligation, indometacin-induced and ethanol-induced gastric ulcers. Chronic gastric ulcers were induced using acetic acid and duodenal ulcers by mercaptamine hydrochloride. After pylorus ligation, there was an approximate 30,40% increase in gastric secretion, a significant increase in total acidity (P < 0.01) and in the ulcer index (P < 0.01) in rats bearing pituitary homografts under the kidney capsule when compared with the sham-operated control. Hyperprolactinaemia did not affect the formation of ethanol-induced gastric ulcers but showed a 40% reduction in the development of indometacin-induced gastric ulcers. It also produced a 20% increase in the ulcer index in acetic acid-induced chronic gastric ulcers and a 30% increase in ulcer area in mercaptamine-induced duodenal ulcers. Our results showed that hyperprolactinaemia induced gastric acid secretion and thereby aggravated gastric and duodenal ulcers in rats. Hyperprolactinaemia did not affect gastric cytoprotection. [source]

Stimulatory Effect of N -Methyltyramine, a Congener of Beer, on Pancreatic Secretion in Conscious Rats

ALCOHOLISM, Issue 2010
Eri Tsutsumi
Background:, Alcoholic beverages stimulate gastric acid secretion and increase the appetite. Although ingested ethanol stimulates pancreatic secretion, alcoholic beverages contain several congeners. N -methyltyramine (NMT) was isolated from beer as a factor in stimulating gastric acid secretion. In this study, we examined NMT to determine whether the congener stimulated pancreatic secretion in conscious rats. Methods:, Cannulae were inserted into male Wistar rats to separately drain bile and pancreatic secretions: 2 duodenal cannulae, a gastric cannula, and an external jugular vein cannula. The rats were placed in modified Bollman-type restraint cages. After a 4-day recovery period, experiments were conducted on unanesthetized rats. Different concentrations of NMT (5, 25, and 50 ,g/kg) solutions were infused into the stomach. To examine the mechanism, the effects of the proton pump inhibitor, cholecystokinin (CCK-BR) antagonist (YM022), CCK-AR antagonist (CR1505), and atropine were administered prior to the NMT (25 ,g/kg) infusion. The effect of intravenous infusion of NMT (7.5 ,g/kg) was then determined. Moreover, dispersed acini were prepared, and the effect of different concentrations of NMT on amylase release was determined. Results:, Intragastric administration of NMT significantly increased pancreatic exocrine secretion in a dose-dependent manner. Atropine eliminated the stimulatory effect of NMT, but the infusion of the proton pump inhibitor, YM022, and CR1505 did not. Intravenous infusion of NMT did not affect pancreatic secretion, and NMT did not stimulate amylase release in vitro. Conclusions:,N -methyltyramine stimulates pancreatic secretion via the cholinergic gastro-pancreatic reflex. The NMT content in beer was 2 mg/l, so that if a person weighing 60 kg consumes a 750 ml of beer, 25 ,g/kg NMT will be ingested. Therefore, the stimulatory effect of beer on pancreatic secretion was produced not only by ethanol but also by the congener, NMT. [source]

Effect of proton pump inhibition on the gastric volume: assessed by magnetic resonance imaging

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2009
A. BABAEI
Summary Background Proton pump inhibitor (PPI) therapy is known to suppress gastric acid secretion. Thus PPI therapy may decrease gastric volume and gastric contents available for gastro-oesophageal reflux by decreasing acid secretion. Aim To determine the effect of PPI therapy on the gastric volume after a standard meal. Methods A total of nine healthy subjects were studied using magnetic resonance imaging, before and after a standard liquid meal mixed with a paramagnetic contrast to help demarcate the gastric region. Images were acquired for a total of 90 min after the meal. Studies were conducted before and following esomeprazole twice daily for 7 days. Images were analysed to determine the gastric liquid volume. Results Gastric volume, 15 min after the meal peaked to 611 ± 37 mL on the control day and 539 ± 30 mL following the PPI administration (P < 0.001). Average gastric volume remained significantly lower (56 ± 9 mL, P < 0.05) on the PPI therapy from 5 to 75 min after the meal. Conclusions Proton pump inhibitor therapy causes a significant reduction in the gastric contents volume during first 75 min after the meal. In addition to increasing the gastric pH, PPI therapy may decrease the frequency of gastro-oesophageal reflux by decreasing the volume of gastric contents. [source]

Effect of concomitant dosing of famotidine with lansoprazole on gastric acid secretion in relation to CYP2C19 genotype status

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2005
T. FURUTA
Background :,Famotidine increases Helicobacter pylori -eradication rates by a triple lansoprazole/amoxicillin/clarithromycin therapy in patients with the rapid extensive metabolizer genotype of CYP2C19. Aim :,To determine the effect of famotidine on the gastric acid inhibition by lansoprazole in relation to CYP2C19 genotypes. Methods :,Twenty healthy volunteers with different CYP2C19 genotypes , consisting of six rapid extensive metabolizers, nine intermediate metabolizers and five poor metabolizers , underwent three 7-day courses with placebo, lansoprazole 30 mg twice daily, and lansoprazole 30 mg twice plus famotidine 20 mg twice daily. Lansoprazole was dosed after breakfast and dinner. Famotidine was dosed after lunch and at bedtime. Intragastric pH monitoring was performed for 24 h on day 7 of each course. Results :,With placebo, no difference was observed in intragastric pH profiles among the three CYP2C19 genotype groups. With lansoprazole 30 mg twice daily, the median of 24-h intragastric pH in poor metabolizers (6.1) was significantly higher than those of rapid extensive metabolizers (4.5) and intermediate metabolizers (5.0), respectively (P = 0.0176 and 0.0388), whereas with lansoprazole 30 mg twice and famotidine 20 mg twice daily, the medians were 5.4, 5.7, and 6.1, respectively (not significant). Conclusion :,Acid inhibition by lansoprazole was influenced by CYP2C19 genotype status. This influence was offset by the concomitant use of famotidine. [source]

Cisapride inhibits meal-stimulated gastric acid secretion and post-prandial gastric acidity in subjects with gastro-oesophageal reflux disease

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2002
J. D. Gardner
Summary Background and aims : KCNQ1 potassium channels in human gastric parietal cells are thought to be involved in gastric acid secretion. As cisapride can inhibit similar channels in other tissues and is an effective treatment for nocturnal heartburn, we examined the effects of cisapride on gastric and oesophageal acidity, gastric emptying and heartburn severity in subjects with gastro-oesophageal reflux disease. Methods : Subjects (n=11) had suffered from heartburn four times or more per week for at least 6 months. Gastric pH and oesophageal pH were measured before, during and after a standard meal ingested over 15 min. Each subject received placebo or 10 mg cisapride orally, 30 min before the beginning of the meal. Meal-stimulated gastric acid secretion was calculated from the amount of HCl required to titrate the homogenized standard meal to pH 2 in vitro and the time required for the pH of the ingested meal to decrease to pH 2 in vivo. Heartburn severity was assessed at 15-min intervals beginning at the end of the meal. Gastric emptying of solids was measured using a [13C]-octanoic acid breath test. Results : Cisapride significantly decreased meal-stimulated gastric acid secretion by 20%, decreased integrated gastric and oesophageal acidity by 50,60% and transiently increased the expiration of 13CO2. Cisapride did not significantly alter heartburn severity. Conclusions : The cisapride-induced decreases in meal-stimulated gastric acid secretion, gastric acidity and oesophageal acidity in subjects with gastro-oesophageal reflux disease can account for its beneficial clinical effects. These results also raise the possibility that gastric KCNQ1 potassium channels are important in meal-stimulated gastric acid secretion and possibly in the pathophysiology of gastro-oesophageal reflux disease. [source]

Oxyntic lesions may be provoked in the rat both by the process of acid secretion and also by gastric acidity

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2000
Waldum
Background: Gastric ischaemia appears to be a common pathogenetic factor for stress ulcers. These ulcers occur predominantly in the oxyntic mucosa, suggesting that the acid secretory process or its stimulation is involved in the pathogenesis. Methods: We examined separately the role of the acid secretory process and gastric luminal acidity in the pathogenesis of gastric lesions using the isolated vascularly perfused acid-secreting rat stomach. Results: Pentagastrin-stimulated acid secretion induced submucosal bleeding in the oxyntic mucosa whether accompanied by perfusion of the gastric lumen with saline or a phosphate buffer at pH 7.0. On the other hand, acidity, whether endogenous or introduced by luminal perfusion, induced erosions in both the oxyntic and antral mucosa. Conclusion: It is concluded that the acid secretory process itself contributes to the particular vulnerability of the oxyntic mucosa to ischaemia. Histamine released upon stimulation of gastric acid secretion or shortage of energy due to the requirements for acid secretion may both contribute to this vulnerability. Furthermore, these findings suggest that inhibition of gastric acid secretion should be superior to antacids in preventing stress ulcers. [source]

Lack of effect of ranitidine on gastric luminal pH and mucosal PCO2 during the first day in the ICU

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2005
S. M. Jakob
Background:, Histamine2 (H2)-blocking agents can attenuate intragastric CO2 -production by reducing gastric acid secretion and preventing the interaction between H+ and bicarbonate. However, gastric acid production may be impaired in acute circulatory failure due to poor mucosal perfusion, and H2 -blockade could further impair mucosal perfusion. Methods:, Forty patients with acute circulatory and/or respiratory failure, age 61 ± 16 years (mean ± SD), APACHE II score 21 ± 7, and SOFA score 8 ± 3, received randomly either ranitidine, 50 mg (R) or placebo (P) every 8 h. Gastric intraluminal pH (gpH; antimony probe with external reference electrode) and mucosal pCO2 (prCO2, semicontinuous air-tonometry) were measured during 24 h, and blood gases were taken at 6-h intervals. Results:, Gastric intraluminal pH was 4.3 ± 2.4 in P and 5.1 ± 1.6 in R (NS). Mean prCO2 was 6.8 ± 2.7 kPa in P and 7.4 ± 2.1 kPa in R, and mucosal-arterial pCO2 gradient (,pCO2) was 2.2 ± 2.9 kPa and 2.4 ± 2.4 kPa, respectively (NS). Within-patient variabilities of gpH and prCO2 were not influenced by ranitidine. A posthoc analysis revealed that non-survival in R was associated with a low mucosal pHi after 24 h (P = 0.002). This was explained by a low arterial pH but not by differences in gpH or prCO2. Conclusion:, In acute respiratory and circulatory failure, H2 blockade has an inconsistent impact on gpH and does not reduce variabilities of gpH or prCO2. [source]

The peptide hormone xenin induces gallbladder contractions in conscious dogs

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2007
Y. Kamiyama
Abstract, Xenin is a 25-amino acid peptide isolated from human gastric mucosa. The biological activities of xenin include modulating intestinal motility and affecting exocrine pancreatic secretion and gastric acid secretion. The physiological effect of xenin on the gastrointestinal tract, however, is incomplete. The objective of this study is to investigate the effects of xenin on the gastrointestinal tract motility of conscious dogs. Gastrointestinal tract and gallbladder contractions were monitored by chronically implanted force transducers. Synthetic xenin was injected intravenously during the interdigestive state with or without pretreatment with cholinergic blockers. The effects of xenin following cholecystectomy and truncal vagotomy were also investigated. Xenin induced gallbladder and jejunal contractions, although a dose-dependent response was shown only with gallbladder contractions. These effects were inhibited by pretreatment with cholinergic blockers, but were not enhanced by truncal vagotomy. The jejunal contractions were completely inhibited by cholecystectomy. The only direct effect of xenin in terms of gastrointestinal motility was to induce gallbladder contractions in conscious dogs. The neural pathway mediating xenin's action was cholinergic, but not the vagal. This novel finding indicates a new role of xenin. [source]

Use of ferrous fumarate to fortify foods for infants and young children

NUTRITION REVIEWS, Issue 9 2010
Richard Hurrell
Ferrous fumarate is currently recommended for use in the fortification of foods for infants and young children. This recommendation is based on the compound's good sensory properties and on results from isotope studies in adults that reported similar iron absorption values for ferrous fumarate and ferrous sulphate (relative bioavailability [RBV] of ferrous fumarate, 100). However, later isotope studies conducted on both iron-replete and iron-deficient young children found that iron absorption from ferrous fumarate was only about 30% of that achieved from ferrous sulphate (RBV, 30). The reasons for the differences observed in adults compared with children are unclear but could be related to the following factors: lower iron status in children resulting in greater iron absorption via upregulation from ferrous sulphate but not from ferrous fumarate; reduced gastric acid secretion in children leading to retarded dissolution of ferrous fumarate; or an influence of added ascorbic acid on RBV. Ferrous fumarate-fortified complementary foods have been demonstrated to improve iron status in iron-deficient infants and, more recently, to prevent iron deficiency equally as well as ferrous sulphate in iron-replete infants. However, current evidence indicates that iron-deficient infants and young children may absorb iron from ferrous fumarate less well than iron from ferrous sulfate and that, for equivalent efficacy, complementary foods targeted at such infants and young children should contain more iron in the form of fumarate. [source]

The effect of experimental inhibition of gastric acid secretion on curd formation in abomasum and weight gain of calves

ANIMAL SCIENCE JOURNAL, Issue 1 2010
Keiji OKADA
ABSTRACT Eight Holstein bull calves were divided into two groups; a non-treated control group and a famotidine treated group. Fresh milk was fed twice a day. The experiment was conducted between 7 and 14 days of age. During the experimental period the control group was injected with physiological saline, and the famotidine group was injected with famotidine, a histamine-H2-receptor blocker, into the jugular vein 30 minutes prior to each feeding. The control group showed maximum curd formation 2 h after feeding at both 7 and 14 days of age. Curd scores of 7-day-old and 14-day-old calves were significantly lower in the famotidine than in the control group at 2 and 4 h after feeding. Most fecal samples from the famotidine group exhibited an acidic smell. The famotidine group showed significantly lower values for both average weight gain and the rate of weight gain from 7 to 14 days of age. The inhibition of gastric acid secretion decreased curd formation in the abomasum as well as daily weight gain compared to non-treated control calves. This suggested that curd formation in the abomasum is important for the weight gain of newborn calves. [source]

The Choice of Proton Pump Inhibitor: Does it matter?

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2004
Per M. Hellström
Comparisons of four different proton pump inhibitors: lansoprazole, omeprazole, pantoprazole, and rabeprazole show that they all have similar potency and efficacy. Rabeprazole, however, displays a slightly more rapid onset of acid inhibition than the others; the clinical advantage of this seems limited. The S-isomer of omeprazole, esomeprazole, exhibits a somewhat higher potency than the other proton pump inhibitors. Reports supporting a clinical advantage of this property are not convincing. To conclude, all inhibitors seem comparable as regards inhibition of gastric acid secretion. [source]

Hypermethylation of the somatostatin promoter is a common, early event in human esophageal carcinogenesis

CANCER, Issue 1 2008
Zhe Jin MD
Abstract BACKGROUND. The promoter of somatostatin (SST), a primary inhibitor of gastrin-stimulated gastric acid secretion, is hypermethylated in 80% of human colon cancers. The aim of the current study was to investigate whether and at what stage promoter hypermethylation of SST is involved in human esophageal carcinogenesis. METHODS. SST promoter hypermethylation was examined by real-time methylation-specific polymerase chain reaction (PCR) (MSP) in 260 human esophageal tissue specimens. Real-time reverse-transcriptase PCR and MSP were also performed on esophageal cancer cell lines before and after treatment with 5-aza-2,-deoxycytidine (5-Aza-dC). RESULTS. SST hypermethylation showed highly discriminative receiver-operator characteristic curve profiles, clearly distinguishing esophageal squamous cell carcinomas (ESCC) and esophageal adenocarcinomas (EAC) from normal esophagus (NE) (P < .01). Both SST methylation frequency and normalized methylation value (NMV) were significantly higher in Barrett metaplasia without dysplasia or EAC (BE), low-grade and high-grade (HGD) dysplasia occurring in BE, EAC, and ESCC than in NE (P < .01). SST hypermethylation frequency was significantly lower in NE (9%) than in BE (70%), HGD (71.4%), or EAC (71.6%), whereas 14 (53.8%) of 26 ESCCs exhibited SST hypermethylation. There was a significant relation between SST hypermethylation and BE segment length, a known clinical risk factor for neoplastic progression. Demethylation of KYSE220 ESCC and OE33 EAC cells with 5-Aza-dC reduced SST methylation and increased SST mRNA expression. SST mRNA levels in native unmethylated EACs were significantly higher than in native methylated EACs (P < .05). CONCLUSIONS. SST promoter hypermethylation is a common event in human esophageal carcinomas and is related to early neoplastic progression in Barrett esophagus. Cancer 2008. © 2007 American Cancer Society. [source]