Gastric Pits (gastric + pit)

Distribution by Scientific Domains

Selected Abstracts

Dietary pectin up-regulates monocaboxylate transporter 1 in the rat gastrointestinal tract

Doaa Kirat
This work was undertaken to study the effect of pectin feeding on the expression level, cellular localization and functional activity of monocarboxylate transporter 1 (MCT1) in the gastrointestinal tract of rats. The results indicated that MCT1 protein level was significantly increased along the entire length of the gastrointestinal tract of pectin-fed rats in comparison with control animals. Immunohistochemical analysis revealed an increase in MCT1 in the stratified squamous epithelia of the forestomach as well as in the basolateral membranes of the cells lining the gastric pit of the glandular stomach of pectin-fed rats when compared with control animals. The parietal cells, which showed barely any or no detectable MCT1 in the control group, exhibited a strong intensity of MCT1 on the basolateral membranes in pectin-fed rats. In the small intestine of pectin-fed rats, strong immunopositivity for MCT1 was detected in the brush border and basolateral membranes of the absorptive enterocytes lining the entire villi, while in control rats, weak reactivity was detected on the brush border membrane in a few absorptive enterocytes in the villus tip. In the large intestine of control animals, MCT1 was detected on the basolateral membranes of the epithelia lining the caecum and colon. This staining intensity was markedly increased in pectin-fed rats, along with the appearance of strong reactivity for MCT1 on the apical membranes of the surface and crypt epithelia of caecum and colon. Our results also showed that MCT1 co-localizes with its chaperone, basigin (CD147), in the rat gastrointestinal tract, and that the pectin feeding increased the expression of CD147. In vivo functional studies revealed an enhanced acetate absorption in the colon of pectin-fed in comparison with control animals. We conclude that MCT1 is up-regulated along the gastrointestinal tract of pectin-fed rats, which might represent an adaptive response to the increased availability of its substrates. [source]

The Effect of Helicobacter pylori Infection on Levels of DNA Damage in Gastric Epithelial Cells

HELICOBACTER, Issue 5 2002
S. M. Everett
Abstract Background.Helicobacter pylori infection leads to an increased risk of developing gastric cancer. The mechanism through which this occurs is not known. We aimed to determine the effect of H. pylori and gastritis on levels of DNA damage in gastric epithelial cells. Methods. Epithelial cells were isolated from antral biopsies from 111 patients. DNA damage was determined using single cell gel electrophoresis and the proportion of cells with damage calculated before and 6 weeks after eradication of H. pylori. Cell suspensions generated by sequential digestions of the same biopsies were assayed to determine the effect of cell position within the gastric pit on DNA damage. Results. DNA damage was significantly higher in normal gastric mucosa than in H. pylori gastritis [median (interquartile range) 65% (58.5,75.8), n = 18 and 21% (11.9,29.8), n = 65, respectively, p < .001]. Intermediate levels were found in reactive gastritis [55.5% (41.3,71.7), n = 13] and H. pylori negative chronic gastritis [50.5% (36.3,60.0), n = 15]. DNA damage rose 6 weeks after successful eradication of H. pylori[to 39.5% (26.3,51.0), p = .007] but was still lower than in normal mucosa. Chronic inflammation was the most important histological factor that determined DNA damage. DNA damage fell with increasing digestion times (r = ,.92 and ,.88 for normal mucosa and H. pylori gastritis, respectively). Conclusions. Lower levels of DNA damage in cells isolated from H. pylori infected gastric biopsies may be a reflection of increased cell turnover in H. pylori gastritis. The investigation of mature gastric epithelial cells for DNA damage is unlikely to elucidate the mechanisms underlying gastric carcinogenesis. [source]


Seishu Hayashi
Background:, We evaluated the endoscopic microvascular architecture of the gastric mucosa in portal hypertension patients using the prototype of narrow band imaging (NBI). Material and Methods:, The study included 103 Helicobacter pylori -negative patients with chronic liver disease (22 without portal hypertension (group 1), 81 with portal hypertension (group 2)). Results:, (i) Abnormality of collecting venules, reddening mucosa, red spots, a mosaic-like pattern, and gastric antral vascular ectasia (GAVE) were observed on the gastric mucosa, and an obscure change in collecting venules (73% vs 14%; P < 0.001), reddening mucosa (49% vs 5%; P < 0.001), red spots (36% vs 5%; P < 0.01) and a mosaic-like pattern (40% vs 5%; P < 0.01) were more frequently observed in group 2 than in group 1. (ii) On magnifying endoscopy with NBI, the mucosa with an obscure change in collecting venules was demonstrated as dilation of the capillaries surrounding the gastric pits in various degrees, and reddening mucosa was observed as extended and swollen gastric pits and various degrees of dilated and convoluted capillaries surrounding the gastric pits. Red spots were demonstrated as extended and swollen gastric pits, dilated and convoluted capillaries surrounding the gastric pits, and intramucosal hemorrhage around these capillaries. GAVE was recognized as partial and marked dilatation of the capillaries surrounding the gastric pits. Conclusion:, Abnormality of collecting venules, swelling of gastric pits, dilatation of capillaries surrounding the gastric pits, intramucosal hemorrhage around capillaries, and partial and marked dilatation of the capillaries were observed on the gastric mucosa in portal hypertension patients. [source]

Comparison of High Resolution Magnifying Endoscopy and Standard Videoendoscopy for the Diagnosis of Helicobacter pylori Gastritis in Routine Clinical Practice: A Prospective Study

HELICOBACTER, Issue 1 2009
Can Gonen
Abstract Background:, It has been shown that standard endoscopic features often labeled as gastritis has a poor correlation with histopathology. Recently, high resolution magnifying endoscopy has been reported to be an effective method to diagnose gastritis. The aim of the present study was to compare standard endoscopy with magnifying endoscopy for the diagnosis of Helicobacter pylori gastritis, and to determine whether gastritis can be diagnosed based on findings at magnification endoscopy. Materials and Methods:, A total of 129 patients were enrolled into the study. Erythema, erosions, prominent area gastrica, nodularity, and regular arrangement of collecting venules (RAC) were investigated by standard endoscopy. Standard endoscopy was followed by magnifying endoscopy in all patients, and repeated in 55 patients after indigo carmine spraying. Results:, None of the standard endoscopic features showed a sensitivity of more than 70% for H. pylori gastritis, except RAC pattern analysis. Absence of a corporal RAC pattern had 85.7% sensitivity and 82.8% specificity for predicting H. pylori infection. Under magnification, the sensitivity and specificity of regular corporal pattern (regular collecting and capillary vascular structures with gastric pits resembling pinholes) for predicting normal histology were 90.3% and 93.9%, respectively. Loss of collecting venules, or both collecting and capillary structures was correlated with chronic inflammation and activity. With the progression of mucosal atrophy, irregular collecting venules became visible. The values for irregularly arranged antral ridge pattern for the prediction of antral gastritis were 89.3% and 65.2%, respectively. Indigo carmine staining increased sensitivity and specificity up to 97.6% and 100% for corporal gastritis, and up to 88.4% and 75.0% for antral gastritis, respectively. Indigo carmine staining significantly increases the detection of intestinal metaplasia. Conclusions:, High resolution magnifying is superior to standard endoscopy for the diagnosis of H. pylori gastritis, and identification of specific histopathologic features such as atrophy and intestinal metaplasia seems possible. [source]

Enhanced Expression of Transcription Factor E2F in Helicobacter pylori -infected Gastric Mucosa

HELICOBACTER, Issue 3 2002
Hajime Isomoto
Abstract Objective.Helicobacter pylori is implicated in gastric carcinogenesis through increased gastric epithelial cell turnover. In fact, high proportions of proliferating and apoptotic epithelial cells are found in H. pylori -infected gastric mucosa. E2F, a transcription factor, induces coordinated transactivation of a set of genes involved in cell cycle progression. The aim of this study was to investigate the expression of E2F in H. pylori -infected gastric mucosa and examine the correlation between such expression and gastric epithelial cell proliferation and apoptosis. Methods. Twenty-five patients with H. pylori -associated gastritis (HAG) and 13 control subjects negative for H. pylori were examined. E2F expression was studied in situ by Southwestern histochemistry, a method used to localize transcription factors. Labeled double-stranded oligo-DNA with specific consensus sequence for E2F binding sites was reacted with frozen sections from antral biopsy specimens obtained at endoscopy. Gastric epithelial cell proliferation was assessed by immunostaining of proliferating cell nuclear antigen (PCNA), while apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). The percentages of epithelial cells with nuclear staining for PCNA and E2F were expressed as a positivity index (PI). The percentage of TUNEL-positive epithelial cells was defined as apoptotic index. Results. E2F was expressed in the nuclei of gastric epithelial cells within gastric pits. E2F PI in H. pylori -infected gastric mucosa was significantly higher than that in noninfected. Expression of E2F correlated well with PCNA-positive epithelial cells. We also demonstrated colocalization of PCNA with E2F expression in the same epithelial cells. Apoptotic index was also high in H. pylori -infected mucosa, and correlated with E2F PI. Conclusion. Our results demonstrated a significant increase in the expression of E2F in H. pylori -infected mucosa, which correlated with both the percentages of PCNA- and TUNEL-positive cells. Our results suggest that enhanced E2F expression in gastric mucosa may be involved in H. pylori -related gastric carcinogenesis through accelerated cell turnover. [source]

Morphometric and immunohistochemical study of the abomasum of red deer during prenatal development

A. J. Masot
Abstract The red deer is well suited to scientific study, given its economic importance as an animal to be hunted, and because it has a rich genetic heritage. However, there has been little research into the prenatal development of the stomach of ruminants in general, and none for the red deer. For this reason, we undertook histological evaluation of the ontogenesis of the abomasum in red deer. Histomorphometric and immunohistochemical analyses were carried out on 50 embryos and fetuses from the initial stages of prenatal life until birth. The animals were divided for test purposes into five experimental groups: group I [1.4,3.6 cm crown,rump length (CRL); 30,60 days, 1,25% of gestation]; group II (4.5,7.2 cm CRL; 67,90 days, 25,35% of gestation); group III (8,19 cm CRL; 97,135 days, 35,50% of gestation); group IV (21,33 cm CRL; 142,191 days, 50,70% of gestation) group V (36,40 cm CRL; 205,235 days, 75,100% of gestation). In the organogenesis of the primitive gastric tube of red deer, differentiation of the abomasum took place at 67 days, forming a three-layered structure: the epithelial layer (pseudostratified), pluripotential blastemic tissue and serosa. The abomasal wall displayed the primitive folds of the abomasum and by 97 days abomasal peak areas were observed on the fold surface. At 135 days the abomasal surface showed a single mucous cylindrical epithelium, and gastric pits were observed in the spaces between abomasal areas. At the bottom of these pits the first outlines of glands could be observed. The histodifferentiation of the lamina propria-submucosa, tunica muscularis and serosa showed patterns similar to those described for the forestomach of red deer. The abomasum of red deer during prenatal life, especially from 67 days of gestation, was shown to be an active structure with full secretory capacity. Its histological development, its secretory capacity (as revealed by the presence of neutral mucopolysaccharides) and its neuroendocrine nature (as revealed by the presence of positive non-neuronal enolase cells and the neuropeptides vasoactive intestinal peptide and neuropeptide Y) were in line with the development of the rumen, reticulum and omasum. Gastrin-immunoreactive cells first appeared in the abomasum at 142 days, and the number of positive cells increased during development. As for the number of gastrin cells, plasma gastrin concentrations increased throughout prenatal life. However, its prenatal development was later than that of the abomasum in sheep, goat and cow. [source]