Gastric Lumen (gastric + lumen)

Distribution by Scientific Domains


Selected Abstracts


A case of gastric cancer with high pepsinogen II levels in both serum and ascites

DIGESTIVE ENDOSCOPY, Issue 1 2000
Manabu Muto
The first case of gastric cancer in which pepsinogen (PG) II levels were found to be extremely high not only in the serum but also in the ascites, with values of 603 ng/mL and 1910 ng/mL, respectively, is reported. Pepsinogen I and PG II are normally secreted into the gastric lumen and only 1% of the amount secreted enters the circulation. Although gastric cancer cells are found to produce PG II more often than PG I, elevated PG values in serum are extremely rare, and only one case has ever been reported. That patient had extremely high serum levels of PG I and PG II at the time of gastric cancer relapse. Pepsinogen has never been reported in the ascites, and thus nothing is known about the mechanism of entry into the ascites. In this case report, we postulate two mechanisms to explain the increased PG II in the ascites: (i) a high level of serum PG II infiltrated the ascites and caused elevation of PG II in the ascites; or (ii) disseminated cancer cells directly produced PG II and it elevated PG II levels in the ascites. [source]


The Effect of Ascorbic Acid on Helicobacter pylori Induced Cyclooxygenase 2 Expression and Prostaglandin E2 Production by Gastric Epithelial Cells in vitro

HELICOBACTER, Issue 1 2005
Geoff V. Smith
ABSTRACT Background., Cyclooxygenase 2 (COX-2) is induced by the presence of Helicobacter pylori (H. pylori) on the gastric mucosa as part of the inflammatory response; this results in the synthesis of prostaglandins that amplify the local inflammatory response. The presence of H. pylori inhibits the secretion of ascorbate into the gastric lumen. Interestingly, ascorbate inhibits the growth of H. pylori and low dietary levels are associated with an increased risk of gastric adenocarcinoma. We therefore investigated the effect of ascorbate on H. pylori mediated COX-2 induction and prostaglandin production in vitro. Methods.,H. pylori was cocultured with gastric epithelial cells in the presence of ascorbate at physiological concentrations. The expression of COX-2 was assessed by Western blotting and prostaglandin E2 (PGE2) was assessed by ELISA. Results., Ascorbate inhibited gastric cell PGE2 synthesis but not in COX-2 expression in response to H. pylori. In the absence of the organism, ascorbate also reduced PGE2 expression in cells that constitutively express COX-2, again with no reduction of COX-2 protein expression. Conclusions., Physiological concentrations of ascorbate inhibit PGE2 but not COX-2 expression in response to H. pylori in gastric epithelial cells. [source]


Helicobacter pylori eradication therapy modulates acidity and interleukin-1, mRNA levels in un-operated stomach and in remnant stomach after gastrectomy in gastric cancer patients

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2006
S. KATO
Summary Background A number of studies have indicated that Helicobacter pylori eradication therapy helps prevent secondary cancers in the stomach. Aim To investigate the risk of secondary cancer in the residual stomach after gastrectomy by comparing molecular biomarkers from stomach mucosa biopsies and the pH of gastric juice between H. pylori patients with and without gastrectomy. Methods Conventional H. pylori eradication therapy was administered to 22 patients who had undergone gastrectomy and to 37 un-operated patients. We measured pH levels of gastric juice, and collected stomach mucosa biopsy specimens by gastrointestinal fiberscopy. The mRNA expression levels of interleukin-1,, interleukin-8 and cyclo-oxygenase 2 in the biopsy tissues were measured by real-time polymerase chain reaction. Results Interleukin-1, levels in the antrum of un-operated H. pylori -positive patients showed a reverse correlation with pH levels in the gastric lumen (correlation coefficient: ,0.50, P = 0.007). After eradication, pH levels were strongly associated with interleukin-1, mRNA levels, r = 0.83, P = 0.01, which, in the remnant stomach mucosa, decreased from 22.5 to 4.6 in the anastomosis and from 3.1 to 2.4 in the upper corpus, with a simultaneous and statistically significant decrease in pH. Conclusions Interleukin-1, mRNA levels correlated with pH levels in the remnant stomach. This indicates that eradication therapy may contribute not only to a reduction in these cancer-associated cytokines, but also to an improvement in the internal environment of the remnant stomach. [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]


Morphological Features of the Stomach of Malayan Pangolin, Manis javanica

ANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2010
C. Nisa'
With 6 figures Summary The morphology of the stomach of Malayan pangolin, Manis javanica was studied at macroscopic, light microscopic, and scanning electron microscopic levels. The stomach of M. javanica was C-shaped with short lesser curvature. At the oesophageal junction, the inner smooth muscle was thickened in the greater curvature side. The entire stomach was lined by a thick cornified stratified squamous epithelium, except at the duct orifices of glands and in the pyloric gland region. The wall of the fundus was thin and devoid of glands. The gastric glands consisted of mucous, oxyntic, and pyloric glands. The mucous glands were observed in the lesser curvature (Mg-L), in the greater curvature (Mg-G), and in the pyloric canal (Mg-C) respectively. The oxyntic glands were organized into gland mass, making an oval mound elevated to the gastric lumen, in the middle of the greater curvature. The oxyntic gland mass has a single common duct with opening directed to the pyloric side. This duct was surrounded by mucus gland (Mg-G). The pyloric glands were located caudal to the pylorus. There was no sphincter at the pyloric-duodenal junction. Large mucosal protuberance, the torus pyloricus was observed in the side of the lesser curvature of the pyloric canal. In the lumen of pyloric canal region, numerous spines and small pebbles were observed. The muscle layers in the wall of this region were considerably thickened. The present results on the stomach of M. javanica are thought to be closely related to the toothless and eating habits of this animal species. [source]


Systemically administered trefoil factors are secreted into the gastric lumen and increase the viscosity of gastric contents

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2006
S Kjellev
Background and purpose: Trefoil factors (TFFs) secreted by mucus-producing cells are essential for the defence of the gastrointestinal mucosa. TFFs probably influence the viscoelastic properties of mucus, but this has not been demonstrated in vivo. We therefore studied the gastric secretion of systemically administered TFF2 and TFF3, and their influence on the viscosity of the secretions. Experimental approach: Mice and rats under general anaesthesia were injected intravenously with human (h) TFF2, hTFF3 (5 mg kg,1 to mice and 25 mg kg,1 to rats), murine (m) 125I-TFF3, or 125I-hTFF3 (300 000 cpm, mice only). The appearance of TFFs in the gastric mucosa and luminal secretions was analysed by autoradiography, gamma-counting, and ELISA, and the viscosity by rheometry. Key results: 125I-mTFF3 and 125I-hTFF3 were taken up by secretory cells of the gastrointestinal tract and detected at the gastric mucosal surface 15 min after injection. Stressing the stomach by carbachol (3.5 ,g kg,1) and pyloric ligation significantly increased the uptake. Injected hTFF2, hTFF3, and mTFF3 were retrieved from the gastric contents after 4 h. In rats, an approximately seven-fold increase in the viscosity was detected after injection of TFF2 compared to the controls, whereas TFF3 did not increase the viscosity. In mice, TFF2 increased the viscosity approximately 4-fold. Conclusions: These data indicate that systemically administered TFFs are transferred to the gastric lumen in a biologically active form. British Journal of Pharmacology (2006) 149, 92,99. doi:10.1038/sj.bjp.0706840 [source]