Search PubMed⌕ Search

Biomedical subjects

A Uribe

Publications and source records attributed to A Uribe.

At least 73 records · Page 4Linked to original sources
PubMed1989

Oral E2 prostaglandins affect endocrine cell populations in the gastric antrum of the rat.

The aim of the present study was to investigate antral endocrine cell populations and tissue and circulating hormone levels following a 4-week oral regimen with prostaglandin E2 (25, 250 and 5000 micrograms/kg-1 b.i.d.) or a stable methyl analogue (5 and 50 micrograms kg-1 b.i.d.). Epithelial hyperplasia of the gastric antrum was observed with the highest dose of prostaglandin E2 and both doses of the analogue, as evaluated by stereological methods and conventional cell count. The treatments significantly affected the endocrine cell population. Somatostatin-immunoreactive cells were increased in proportion to the increased epithelial cellularity and plasma levels of somatostatin were increased in parallel. The tissue content of somatostatin-like immunoreactivity differed according to the extraction procedure used, and was significantly higher than controls in specimens extracted in neutral water. In the neutral extracts an immunoreactive somatostatin of unidentified molecular structure dominated quantitatively over somatostatin 14 and 28, which were the major components in acetic acid extracts. The serotonin-immunoreactive cell population was also significantly increased by natural prostaglandin E2 and the analogue but the gastrin cell population was not significantly affected by treatments. Accordingly, no significant changes were observed in tissue or plasma gastrin levels. It is concluded that the epithelial hyperplasia of the antral epithelia produced by E2 prostaglandins is associated with selective changes of endocrine cell populations. The changes were proportional to the increases of epithelial cellularity and required quantitative determination of the total antral volume to be detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1988

Initial kinetic changes of prostaglandin E2-induced hyperplasia of the rat small intestinal epithelium occur in the villous compartments.

This study was performed to further identify the sequence of cell kinetics that occurs in the development of gastric and intestinal epithelial hyperplasia after orally administered prostaglandins of the E series. A high-dose, short-treatment schedule was used to examine the initial effects on kinetic parameters in the rat small intestinal epithelium. Groups of rats were killed after a single dose of oral prostaglandin E2 at 1 h after in vivo labeling with [methyl-3H]thymidine and during continued treatment at 6, 12, 24, 48, 72, and 96 h. As evidenced by autoradiography, the earliest change produced by prostaglandin E2 was an increased cellularity of the villous compartment (p less than 0.05 after 24 h). There was no change of labeling index of the villous compartment or of the leading edge of labeled cells within 24 h. At 48 h, the increased cellularity was accompanied by a significantly elevated labeling index of the villi. Throughout the study period no significant differences were observed between groups in the number of cells or labeling indices in the jejunal crypts, or in cellular input from the crypts to the villi. Epithelial turnover time in the placebo and treatment groups was 69 and 71 h, respectively. To exclude the possibility that prostaglandin E2 initially affects cell birth rate and mean cell cycle time, a metaphase blocker was given after 4 days of treatment in a second study. Animals were killed after 0, 0.5, 1.0, 1.5, and 2.5 h. The rate of entry into mitoses was 8.1% cells/h in controls compared with 8.2% cells/h in treated rats. The distribution of mitoses within crypts was identical in the two groups and the mean cell cycle time was 13.6 and 13.2 h, respectively. Also in this study there were trophic changes of the villi. It is concluded that the hyperplasia produced by oral prostaglandin E2 starts in the villi of the small intestine and is initiated by reduced cell exfoliation from the villous tips. Previously recorded retention of cellular elements in villi and crypts, increased cellularity of the proliferative compartments, and reduced mitotic index are secondary events.

Animals↗
PubMed1988

Effects of prostaglandin E2 on disease activity, gastric secretion and intestinal permeability, and morphology in patients with rheumatoid arthritis.

The effects of oral natural prostaglandin E2 (PGE2) on symptoms, disease activity, and gastrointestinal functions in rheumatoid arthritis (RA) were studied in an open pilot trial. Twelve patients, six taking and six not taking non-steroidal anti-inflammatory drugs (NSAIDs), received 1 mg natural PGE2 three times a day for six weeks. The treatment was tolerated well and the only side effect noted was slightly looser stools in three patients. Half of the patients reported subjective improvement and none had aggravation of symptoms. The Ritchie articular index and several biochemical inflammation markers decreased and were significantly reduced at the end of the treatment period. The thickness of the small intestinal mucosa increased during the PGE2 treatment. The intestinal permeability pattern, measured by urinary excretion of polyethylene glycols (PEG 400), differed between the patients taking and not taking NSAIDs. The initially high urinary PEG 400 excretion values in the patients taking NSAIDs decreased and the initially low excretion values in patients not taking NSAIDs increased during the PGE2 treatment. The jejunal contents became sterile in 5/6 patients not taking NSAIDs and remained sterile in 1/6 patients taking NSAIDs at the end of the treatment. The treatment period was associated with a reduction of lactobacilli in patients not treated with NSAIDs. Thus the treatment appeared to decrease disease activity and to improve small intestinal functions in patients with RA, findings that need confirmation in a controlled trial.

Adult↗
PubMed1988

Alternating proliferative capacity in the rat gastrointestinal mucosa. Effects of E2 prostaglandins and indomethacin.

Having previously observed an apparent uneven distribution of proliferating cells in the gastric corporic mucosa of the rat, we examined the mitotic distribution along 8-mm sections of gastric and jejunal epithelia. Metaphases were arrested with vincristine to facilitate mitotic count, and the effects of treatment with a prostaglandin E2 analogue and a cyclooxygenase blocker were examined. Clusters of mitotic figures alternating with non-proliferating areas were observed in the gastric corporic epithelium of control rats. During 4 h mitotic activity was absent over 21% of the corporic mucosa. Extending the examined area to about 240 glands reduced substantially the error of mitotic counts. An uneven distribution of mitoses was found in the antral and jejunal epithelium, but areas without proliferating cells were uncommon. Treatment with the prostaglandin E2 analogue reduced the number of mitosis-free areas in the gastric corpus to 13%, and clusters were less easily identified. The total mitotic count was unaffected by treatment. In the jejunum prostaglandin increased the absolute number of mitoses. The mitotic span was also increased, reflecting the uneven distribution. Indomethacin produced the opposite effects to the prostaglandin analogue, including reduction of epithelial height. Of the gastric corporic mucosa 35% was non-proliferating during the observation period, but the clustering phenomenon was still apparent. Absence of dose relationship was attributed to ulcerogenic actions of high doses of indomethacin. It is concluded that mitoses are unevenly distributed in the upper gastrointestinal epithelium of the rat and that safe estimates of mitotic count require examination of large corporic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

A method for the quantitation of intestinal metaplasia of the stomach by morphometry.

A novel method to quantitate the extent of intestinal metaplasia in gastrectomy specimens is presented. Morphometric measurements of histochemically labeled mucin-producing goblet cells were done in three selected gastrectomies (one having a peptic ulcer, one with adenocarcinoma of the intestinal type, and one with adenocarcinoma of the diffuse type). The sectioning of the gastrectomy specimens was standardized. The results indicated that the intestinal metaplasia was significantly higher in the specimen with adenocarcinoma of the intestinal type (as compared to the other two specimens), both along the lesser and greater curvatures as well as in the fundic area. These quantitative results confirm nonquantitative reports based on subjective visual impressions. This quantitative histochemical method for measuring the actual length as well as the topographical distribution of intestinal metaplasia in resected stomachs will be used in future studies of intestinal metaplasia with the aim of disclosing possible differences among populations with disparate incidences of gastric carcinoma.

Adenocarcinoma↗
PubMed1987

Reduction, the trace formula, and semiclassical asymptotics.

We state a theorem that relates the theory of dimensional reduction in Hamiltonian mechanics to the spectral properties of elliptic operators with symmetries on compact manifolds. As an application, we show that the spectrum of the Schrödinger operator, -[unk]hDelta + V, as [unk]h --> 0, contains geometric information about the closed trajectories of a classical particle with Hamiltonian p(2) + V(q). More generally, we show that this is true for particles with internal degrees of freedom and subject to an external Yang-Mills field, the classical limit being the Wong-Sternberg-Weinstein system for such particles.

Journal Article↗
PubMed1987

Cell proliferation of the rat gastrointestinal mucosa after treatment with E2 prostaglandins and indomethacin.

The frequency of arrested mitoses after vincristine injection was studied in the gastrointestinal mucosa of rats treated with either natural prostaglandin E2 (0.2-5.0 mg X kg-1, b.d.), 15-R-15 methyl prostaglandin E2 (2 mg X kg-1, b.d.) or indomethacin (1.0-3.0 mg X kg-1, b.d.). In addition to the mitotic index, morphometric measurements including the mucosal thickness and the thickness of the proliferative and functional zones of the gastric corpus, antrum and jejunum were performed. Natural prostaglandin E2, at the highest dose range, reduced significantly the mitotic index in the gastric antrum. Normal values were found in the gastric corpus and jejunum and in the antrum with the lower doses. The mitotic index was unaffected by treatment with 15-R-15 methyl prostaglandin E2. Natural prostaglandin E2 produced trophic changes (i.e. increased thickness and/or hyperplasia) in the antrum, functional epithelial zone of the gastric corpus and in the jejunum. More pronounced trophic changes were observed in the mucosa of rats treated with the analogue. Indomethacin reduced the mucosal thickness in all examined epithelia and lowered the mitotic index in the jejunum. It is concluded that the trophic effects of E2 prostaglandins on gastrointestinal epithelia are not caused by increased production of new cells. The reduced mitotic index observed in the antral mucosa of prostaglandin-treated rats could be secondary to a negative feedback from the hyperplastic epithelium. The antitrophic effects of the prostaglandin-synthesis blocker (indomethacin) indicates that endogenous prostaglandins may participate in the epithelial cell regulation of the gastrointestinal tract.

Animals↗
PubMed1987

Cell cycle distribution of proliferative and functional cells of the rat jejunum after treatment with oral E2 prostaglandins.

Proliferative and functional epithelial cells were isolated from jejunal specimens of the rat by means of vibrational treatment combined with differential air insufflation. This method gave a good separation between superficial cells of the villi and the crypt cells, as evaluated by flow cytometry, morphology, cytology, and incorporation of radioactive thymidine into DNA. Groups of Sprague-Dawley rats (260 g) were treated twice daily for 11 days with oral placebo, 15(R)15-methyl-prostaglandin E2 in the range of 0.125-2 mg X kg-1, or 5 mg X kg-1 natural PGE2. Isolated crypt cells and superficial cells of the jejunal villi were then analysed by flow cytometry. Morphometric measurements were performed on sections of some jejunal specimens not submitted to vibrational treatment. The cell cycle distribution of crypt cells was unaffected by treatment with the prostaglandin analogue despite the presence of trophic changes. The proportion of crypt cells in G2/M phase was slightly but significantly reduced in rats given natural PGE2 compared with controls. The cell cycle distribution of villus cells was not affected by prostaglandin treatment. Trophic changes in the absence of increased DNA synthesis (S phase) or increased mitotic activity suggests that the hyperplasia observed after prostaglandin treatment is due to a reduced cell loss and/or slower migration time of epithelial cells.

Administration, Oral↗
PubMed1987

[Gynecomastia].

Explore the source record for details and available documents.

Adolescent↗
PubMed1986

Effect of oral prostaglandin E2 on DNA turnover in gastric and intestinal epithelia of the rat.

The mucosal incorporation and clearance of a DNA precursor was examined in the rat stomach and intestine following oral treatment with natural prostaglandin E2 (PGE2) or 15(R) 15 methyl prostaglandin E2 (Me PGE2). Control groups received vehicle or pentagastrin. After five days of treatment animals were labelled with methyl-3H-thymidine. Groups of rats were killed at 0.75, 24, 72, 96 and 120 h after labelling. Treatments continued until killed. Mucosal scrapings were analysed for radioactivity and DNA. Morphometric measurements were performed and plasma levels of gastrin and somatostatin determined. PGE2 and its stable analogue produced hyperplasia within one week of treatment, in particular of the gastric antrum and changed the incorporation and clearance of radioactive thymidine from gastric and intestinal epithelia. The most consistent finding was a delayed elimination of thymidine from the mucosa, indicating a slowing of the DNA turnover. The DNA synthesis was differently affected along the gastrointestinal tract, being unchanged or reduced in the stomach and moderately increased in the intestine. Prostaglandin treatment was associated with a three- to ten-fold increase of the gastric acid contents and with elevated plasma levels of gastrin and somatostatin. It is concluded that E2 prostaglandins produce hyperplasia of gastric and intestinal epithelia in the rat by prolonging the cell survival time rather than by increasing new cell production. Hypergastrinemia is not a likely mediator of trophic actions of E2 prostaglandins, which develop despite elevated plasma levels of somatostatin.

Administration, Oral↗
PubMed1986

Cell kinetics of rat gastrointestinal mucosa. Autoradiographic study after treatment with 15(R)15-methyl-prostaglandin E2.

Forty Sprague Dawley rats (120 g) were divided in groups of five rats each, and 2 mg , kg-1 15(R)15-methyl-prostaglandin E2 or vehicle was administered orally, twice daily for 5 days. On the 6th day, 1 mCi . kg-1 methyl-3H-thymidine was given intraperitoneally to all rats. Groups of rats were killed at 45 min and 24 h, 72, and 120 h after the labelling. Treatments were continued until death. Samples were taken from the corpus, antrum, and jejunum and processed for autoradiography. Microscopic evaluation of the proliferative and functional compartments included cell counts and determination of the labelling index (LI) and mitotic index (MI). Prostaglandin treatment increased the number of cells in the jejunal and gastric epithelia. The DNA synthesis, evaluated from the LI and 45 min after thymidine injection, was unaffected by treatment. The clearance of label from jejunal crypts and villi was significantly slower in the prostaglandin groups. Similar observations were made in the proliferative zone of the corporal and antral epithelia. The MI was unchanged or reduced by prostaglandin treatment, the reduction being significant after 8 to 10 days' treatment. It is suggested that the trophic action of prostaglandin E2 is produced by reduction of epithelial cell losses, thereby prolonging the cell survival time. The reduced MI may be secondary to negative feedback from the hyperplastic epithelium. Trophic actions are produced by short-term treatments.

Animals↗
PubMed1985

Trophic actions of E2 prostaglandins in the rat gastrointestinal mucosa. A quantitative morphologic study.

Adult, male Sprague-Dawley rats in groups of 10 received one of the following treatments orally twice daily for 3 wk: prostaglandin E2 (PGE2) 7.5 mg X kg-1, 15(R)-15-methyl prostaglandin E2 (MePGE2) at 0.2 or 2.0 mg X kg-1, or vehicle. After 18 h of fasting and 10-12 h after the last dose, the rats were anesthetized, and the gastrointestinal tract was fixed and processed for macroscopic and microscopic investigations. Trophic changes were more pronounced in the gastric antrum than in the gastric corpus or small intestine. The thickness of the antral mucosa was significantly increased by PGE2 and in a dose-related way by MePGE2. The mucosa of the gastric corpus became significantly thicker only with the higher dose of MePGE2. In all the prostaglandin-treated groups, the proportion of endocrine cells was reduced. Small--but sometimes significant--changes were registered in the proportions of the various exocrine cells. The parietal cells became significantly larger (+88%) in the rats treated with high doses of MePGE2. The secretory surface of the parietal cells was markedly increased by PGE2 and MePGE2. The enlargement of the secretory surface in animals treated with prostaglandins corresponded to a marked elevation of the basal gastric acid secretion and an increase in plasma gastrin levels. Hypergastrinemia can explain some, but not all, of the trophic changes observed in this study. Light microscopic examination of the duodenal and jejunal mucosa showed dose-related increases in villus heights and crypt lengths after treatment with MePGE2. Only the duodenal villus heights were increased by PGE2.

Animals↗
PubMed1985

Protection of the gastroduodenal mucosa by prostaglandins.

Like other nucleated cell populations in the body, the cells of the gastroduodenal mucosa are capable to metabolise arachidonic acid into prostaglandins, with prostaglandin E2 as the probable major metabolite. The production increases on demand and can be followed in the gastric lumen, where the output of prostaglandin E2 increases two to fourfold after exposure of the mucosa to hydrochloric acid. Exogenous prostaglandins, in particular of the E series, stimulate several identified mucosal defense factors in the upper gastrointestinal tract. Prostaglandins of the E series stimulate the transport of bicarbonate and the production and release of mucus glycoproteins from the gastroduodenal mucosa. They have trophic effects on gastrointestinal epithelia by increasing the survival time of mucosal cells and have cytoprotective properties. In addition, E2 prostaglandins suppress the gastric acid secretion and accelerate peptic ulcer healing. Non steroidal antiinflammatory drugs, which block the biosynthesis of prostaglandins, suppress the bicarbonate secretion, the production of mucus glycoproteins and cytoprotective properties. They interfere with the inhibitory feedback regulation of the gastric acid secretion and are ulcerogenic in experimental and clinical situations. These actions of PG biosynthesis blockers provide indirect information on the importance of local prostaglandin formation for maintenance of gastrointestinal mucosal integrity. It is hypothesised that biosynthesis of prostaglandins in the gastroduodenal mucosa is of importance and may be a key event in triggering the different components of the mucosal defense.

Animals↗
PubMed1984

Effects of 16,16 dimethyl prostaglandin E2 on irradiation damage of the small intestine.

The effects of oral 16,16 dimethyl prostaglandin E2 on irradiation induced damage of the small intestine was examined in the rat. Groups of Sprague-Dawley rats received graded doses of the analogue or placebo at 24, 8 and 0.5 hours before and at 16 and 24 hours following whole abdominal exposure to 10 Gy. Rats were killed 72 hours after irradiation. Pretreatment within the lower dose range had a moderate protective effect with better preserved crypts and crypts to villus ratio. Larger doses seemed to increase the intestinal damage. The prostaglandin treated sham irradiated rats had higher villous height and larger epithelial surface compared with controls.

16,16-Dimethylprostaglandin E2↗
PubMed1984

A quantitative method of estimating inflammation in the rectal mucosa. IV. Ulcerative colitis in remission.

Histological preparations of the rectal mucosa were analyzed quantitatively in 61 patients with ulcerative colitis in remission (UCR). Four histological variables were recorded: the diameter (minor axis) of the lumen of 10 consecutive (transversally cut) glands, the interglandular linear distance between 10 consecutive glands, the number of glands at high-power field examination, and the number of nuclei in 10 consecutive areas of lamina propria. The most important feature to differentiate UCR patients from non-colitic patients was the distance between glands and the number of glands per area. The sum of the values of the four variables demonstrated that 84% of the patients with UCR had scores of 22 or more, whereas only 1 of 124 non-colitic patients (that is, 0.8%) had similar scores.

Cell Count↗