Disease relevance of Stomach

• Induction of intestinal metaplasia in the stomachs of rats by N-methyl-N'-nitro-N-nitrosoguanidine [1].
• Gastric ulcers were induced 5 days after submucosal injection of an acetic acid solution into the stomachs of rats [2].
• Quantitative distribution of gastrin cells was evaluated in three normal human stomachs and in four stomachs from patients with Zollinger-Ellison syndrome [3].
• To study the role of IL-10 in the host response to gastric Helicobacter infection, stomachs of IL-10(-/-) and wild-type mice were colonized with Helicobacter felis, as a model of human H. pylori infection [4].
• Helicobacter-specific cell-mediated immune responses display a predominant Th1 phenotype and promote a delayed-type hypersensitivity response in the stomachs of mice [5].

High impact information on Stomach

• 51Cr-labeled monolayers from rat stomachs were exposed to glucose oxidase-generated H2O2 or reagent H2O2, which both caused a dose-dependent increase in 51Cr release [6].
• Immunohistochemical demonstration of pyloric gland-type cells with low-pepsinogen isozyme 1 in preneoplastic and neoplastic tissues of rat stomachs treated with N-methyl-N'-nitro-N-nitrosoguanidine [7].
• Formation of a transplacental mutagen, 1,3-Di(4-sulfamoylphenyl)triazene, from sodium nitrite and sulfanilamide in human gastric juice and in the stomachs of hamsters [8].
• The formation of methylnitrosocyanamide (MNC), a carcionogenic N-nitroso compound, from methylguanidine (MG) and NaNO2 in simulated gastric juice (SGJ) and in the stomachs of rats was quantitatively investigated [9].
• Changes in the isozymes of pepsinogen (Pg) separated from the glandular stomachs of rats were studied by polyacrylamide gel electrophoresis during carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), from the beginning of MNNG administration to 3 months after the end of its 7-month regimen [10].

Chemical compound and disease context of Stomach

• To determine the relevance of gastric juice factors to gastric carcinogenesis, 56 patients with unoperated stomachs undergoing endoscopy for dyspepsia had gastric juice aspirated and analysed for pH, ascorbic acid, total bile acids, nitrite, nitrate and total nitroso compounds (NOCs) [11].
• Taken together, these results support the conclusion that glucocorticoid promotes a rapid increase in HDC synthesis in fetal liver histamine-forming cells, as well as in mouse mastocytoma P-815 cells and rat glandular stomachs [12].
• Cell proliferation and cell loss in intramucosal signet ring cell carcinoma of canine stomachs induced by N-ethyl-N'-nitro-N-nitrosoguanidine [13].
• During succinylcholine-induced muscle fasciculations, gastroesophageal barrier pressure in fasted adult dogs (n = 10) was compared by esophageal manometry with that in the same dogs with full stomachs [14].
• METHODS: Rats with experimentally induced chronic gastric ulcers were administered twice daily for 14 days either sucralfate at 100 mg/kg or vehicle, and at different stages of treatment their stomachs were used for macroscopic and biochemical assessments [15].

Biological context of Stomach

• In vivo, stomachs from gnotobiotic SCID mice that were colonized with a pure culture of C. albicans had low-grade infections and expressed inducible NOS (iNOS) mRNA [16].
• Ki67-labeled GSII-positive neck cells in Helicobacter felis-infected, but not G-/- stomachs, suggested that mucous neck cell proliferation accounted for expansion of this compartment in the H. felis model of gastritis, but not the G-/- model [17].
• In an ex vivo gastric chamber preparation, 40% ethanol incubation markedly lowered transmucosal potential difference and increased mucosal vascular permeability in rat stomachs [18].
• The extent of formation of N-nitrosodimethylamine (NDMA) in the stomachs of rats and mice after simultaneous oral administration of [14C]dimethylamine and potassium nitrite was determined by measuring the methylation of liver DNA [19].
• Histamine, infused intra-arterially, induced acid secretion of all ex vivo stomachs and this was significantly inhibited by intra-arterially or intra-gastrically administered dmPGE2: volume of secretion, output of HCl and concentration of H+ were decreased and gastric peripheral vascular resistance was significantly reduced [20].

Anatomical context of Stomach

• Rat stomachs were perfused in situ with Krebs-Ringer bicarbonate buffer containing 10% ovine erythrocytes and gassed with 95% O2-5% CO2 [21].
• To determine whether local hormones may mediate CRF-induced acid inhibition, we examined the peptide's effect on the release of somatostatin and gastrin from cultured canine gastric D and G cells and from isolated perfused rat stomachs [22].
• PCFS was seen around the glands of intestinal metaplastic mucosa in both Cdx2 transgenic mouse and human stomachs [23].
• METHODS: The stomachs of IP(-/-) or their wild-type counterparts (IP(+/+)), anaesthetised with urethane (1.225 g/kg), were doubly cannulated from the oesophageal and duodenal sides, and the gastric mucosa was perfused (1 ml/min) with physiological saline [24].
• These morphological data correlated with total immunoreactive TRH content extracted from the whole stomachs of six fetuses and two preterm infants [25].

Associations of Stomach with chemical compounds

• The morphology of ligated rat stomachs filled with absolute ethanol for 1, 7, 15, 30, and 60 min was studied [26].
• Bioassays of plasma extracts were performed in anesthetized rats with perfused stomachs and acid out-puts were compared with those produced by normal saline and by 50 ng pentagastrin given in random order [27].
• We have quantitatively evaluated in semithin sections the amount and depth of gastric mucosal damage to rat stomachs exposed to absolute ethanol with and without prostaglandin (16,16-dimethyl PGE2) pretreatment [28].
• Chambered stomachs were damaged by hypertonic saline followed by either acidic or neutral isotonic saline [29].
• METHODS: The passage of intragastrically administered Evans blue in the small bowel of unanesthetized rats was followed, and the stomachs were weighted after killing the rats [30].

Gene context of Stomach

• Immunocytochemical, histological, and ultrastructural analyses of Atp4a(-/-) stomachs revealed the presence of chief cells, demonstrating that the lack of acid secretion does not interfere with their differentiation [31].
• Other prostaglandins (thromboxane B2, PGD2, PGF(2alpha), and 6-keto-PGF(1alpha)) were significantly elevated in stomachs of mPGES-1-null mice but not in other tissues [32].
• Activin has a positive growth effect on gonadal tumor cells in culture and directly causes the cancer cachexia-like syndrome in inhibin-deficient mice via interaction with activin receptor type IIA in livers and stomachs [33].
• These results demonstrate that two HMFG glycoproteins implicated in prevention of infection, MUC-1 mucin and lactadherin, survive and maintain their integrity in the stomachs of human milk-fed preterm infants [34].
• The present study examines the role of endogenous ANP in regulating endocrine secretion in rat and human stomachs [35].

Analytical, diagnostic and therapeutic context of Stomach

• Parietal cells were released by pronase digestion of everted stomachs from adult male and female rats and were purified by density gradient centrifugation on Nycodenz [36].
• Perfusion of TC-treated stomachs with 50 mM HCl caused only minimal damage, yet this treatment produced gross lesions in the presence of indomethacin or SC-560 [37].
• Moreover, oral administration of 100% ethanol produced severe haemorrhagic lesions in rat stomachs, all of which rapidly healed within 7 days after lesion induction [38].
• These ulcerogenic factors were effectively inhibited in acid-perfused stomachs of food-deprived rats by daily intraperitoneal injection of the amino acid mixture (150 mg/kg) or by an average daily consumption via drinking water of glucose (10 g) or ascorbate (1.2 g) [39].
• Electrical stimulation of the vagal trunks resulted in a significantly greater elevation in gastrin secretion from control stomachs compared to TPN animals (4-fold vs. 2.4-fold increase, P less than 0.05) [40].

References