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Biomedical subjects

A Uribe

Publications and source records attributed to A Uribe.

At least 37 records · Page 2Linked to original sources
PubMed1997

Indomethacin influences regulatory peptides and increases DNA synthesis in the gastrointestinal tract of the rat.

OBJECTIVE: To examine the effect of long-term administration of indomethacin on regulatory peptides and DNA synthesis. DESIGN: Sprague-Dawley rats were treated with 1 mg/kg indomethacin subcutaneously or indomethacin and 500 micrograms/kg oral prostaglandin E2 or solvents for 2 months before labelling with methyl-3H-thymidine. METHODS: The labelling index, growth fraction and the number of epithelial cells were determined on autoradiographs of the stomach small intestine and colon. Plasma and gastrointestinal tissue concentrations of regulatory peptides were analysed by radioimmunoassay. RESULTS: Indomethacin increased the concentration of somatostatin in the gastric fundus and ileum and reduced it in the colon. Prostaglandin E2 reduced the somatostatin concentration in the duodenum and colon. Indomethacin increased the concentration of neurotensin neurokinin A and glucagon in the distal small intestine and reduced the glucagon level in the colon. Prostaglandin E2 prevented such changes. Indomethacin increased DNA synthesis in the small intestine and produced hypoplasia of the villi. These changes were prevented by prostaglandin E2, except for the villous hypoplasia observed in the distal small intestine. Prostaglandin E2 reduced the labelling index in the antrum and colon. CONCLUSION: Endogenous prostaglandins selectively modulate the synthesis and/or release of regulatory peptides and regulate the outflow of cells from the epithelial surface. Indomethacin induces hypoplasia, which triggers a secondary trophic reaction in the epithelium that may, at least partially, be mediated by regulatory peptides.

Animals↗
PubMed1997

Three-dimensional estimation of the glandular volume, and of the number and volume of epithelial cells in two glands from the antral mucosa of five healthy volunteers.

Specimens of antral mucosa were taken from five healthy volunteers and processed for microscopic evaluation. Consecutive 50-micron-thick sections were cut to estimate the volume of two antral glands. Two glands in each section were followed throughout by projecting their profiles from two microscopes mounted in parallel. The glandular volume was estimated using Cavalieri's principle. The mean volume of epithelial cells was estimated by systematic random sampling of the sections with an optical disector of known sample volume. The total number of cells per gland was calculated after determination of the volume of the glands and the mean volume of the epithelial cells. The mean volume of the antral glands was 13.6 +/- 1.67.10(6) microns3, whilst the mean volume of the epithelial cells was 1256 +/- 240 microns3. The total number of epithelial cells per gland was 11216 +/- 1104. In conclusion, using stereological methods, the total number of cells as well as the cell volume and the volume of antral glands can be determined in routine biopsy specimens of human stomach provided that the total depth of the mucosa is present in the section.

Adult↗
PubMed1997

Sulphasalazine, olsalazine and sulphapyridine induce mitogenic actions in the rat intestinal epithelium.

Our aim was to study the influence of sulphasalazine (SASP), olsalazine (ADS) and sulphapyridine (SP) on the cell kinetics of the intestinal epithelium in conventional rats. Groups of rats were treated with SASP, ADS or SP for 9 days. After an intraperitoneal injection of a metaphase blocker, the rats were killed and the jejunum, ileum and colon were examined in histological sections by means of the cumulative mitotic index (MI), growth fraction and number of cells in crypts and villi. SP increased both the MI in the jejunum, ileum and colon and the number of crypt cells (p < 0.05 vs controls). In contrast, SASP and ADS increased the MI only in the colonic epithelium (p < 0.05 vs controls). The growth fraction was essentially unaffected. Our results suggest that SASP, SP and ADS have a selective compartment-dependent proliferative action on the epithelium of the intestinal tract.

Aminosalicylic Acids↗
PubMed1997

Prostaglandin E2 modulates serotonin- and gastrin/CCK-immunoreactive cells in the duodenal mucosa of the rat.

Groups of Sprague-Dawley rats were given placebo or prostaglandin E2 (PGE2) at 25 or 5,000 micrograms/kg or 15,R,15-methyl-PGE2 (MePGE2) at 5 or 50 micrograms/kg, twice daily, orally, for 1 month. Histological sections from the proximal duodenum were processed for immunohistochemistry and the volume density of immunoreactive endocrine cells was determined using point-counting grids. The surface density of the villous lining was estimated by using a cycloid test system. Thereafter, the total volumes of endocrine cells and the total surface area of the villous lining were calculated after estimating the mucosal volume. The volume density of serotonin-immunoreactive cells was increased in the duodenum of rats given 25 or 5,000 micrograms/kg PGE2 (p < 0.05). The total volume of these cells increased in the animals given 25 micrograms/kg PGE2 (p < 0.05). The total volume of gastrin/CCK-immunoreactive cells was higher in rats given 25 micrograms/kg PGE2 or 50 micrograms/kg MePGE2 than in controls (p < 0.05). The volume density of somatostatin-immunoreactive cells increased in rats given 5 micrograms/kg MePGE2, but the total volumes were not different between the groups. The area of somatostatin-immunoreactive cell profiles was enlarged in the animals given 5,000 micrograms/kg PGE2 (p < 0.05). The mucosal volume was enlarged by prostaglandins. The epithelial thickness increased in rats given the highest doses of PGE2 (p < 0.05). The concentration of motilin-like immunoreactivity increased in the duodenum of rats given 5 micrograms/kg MePGE2 (p < 0.05). We conclude that oral administration of PGE2 for 1 month increased the total volumes of serotonin- and gastrin-CCK-immunoreactive cells and the tissue concentration of motilin-like immunoreactivity, which indicates that prostaglandins modulate endocrine cells in a stable steady-state condition.

Administration, Oral↗
PubMed1997

Endogenous prostaglandins and microflora modulate DNA synthesis and neuroendocrine peptides in the rat gastrointestinal tract.

BACKGROUND: Previous studies suggest that E2 prostaglandins and the microflora may participate in the regulation of endocrine cells and of gastrointestinal cell kinetics. Our aim is to examine the actions of endogenous prostaglandins and of the microflora on gastrointestinal cell proliferation and tissue levels of neuroendocrine peptides. METHODS: Germfree and ex-germfree rats were treated with subcutaneous placebo or 1.5 mg/kg indomethacin for 3 days. All rats were labeled with 3H-methyl-thymidine, and biopsy specimens from different parts of the gastrointestinal tract were processed for autoradiography. DNA synthesis was estimated by the labeling index, except in the oxyntic mucosa, where the total number of labeled cells present in 7.5 mm mucosa was used. The concentration of neuroendocrine peptides was determined by radioimmunoassay. RESULTS: In the germfree rat, indomethacin reduced DNA synthesis in the fundus, duodenum, and proximal jejunum (P < 0.05) and the number of villous cells throughout the small intestine (P < 0.05). Exposure to microflora increased DNA synthesis in the proximal and distal jejunum, ileum, and colon (P < 0.05 versus germfree controls) and the number of crypt cells in the distal small intestine and colon (P < 0.05) and reduced the number of villous cells in the small intestine (P < 0.05) but did not affect tissue concentrations of neuroendocrine peptides. Indomethacin increased the concentration of somatostatin in the stomach, duodenum, and colon of germfree rats (P < 0.001), the concentration of calcitonin gene-related peptide (CGRP) and enteroglucagon in the proximal and distal jejunum and ileum (P < 0.001), and the concentration of glucagon in the colon (P < 0.05). The concentrations of somatostatin, CGRP, and glucagon were lower in indomethacin-treated ex-germfree rats than in indomethacin-treated germfree rats (P < 0.01). CONCLUSIONS: Indomethacin selectively reduced DNA synthesis in the upper gastrointestinal tract of germfree rats, indicating a basal stimulatory role for endogenous prostaglandins on cell proliferation. Endogenous prostaglandins modulate synthesis or release of gastrointestinal neuroendocrine peptides. Somatostatin may mediate indomethacin-induced reduction of DNA synthesis. The microflora stimulates cell proliferation and influences tissue levels of neuroendocrine peptides in a manner opposite to that of indomethacin.

Animals↗
PubMed1997

Brachial plexus injury due to compression: an alternate mechanism of injury: case report and review of the literature.

We present a case of a brachial plexus injury due to compression of the nerves from a traumatic hematoma, with no associated bone or vascular injury. The paralysis in this case was not evident for 48 hours after the initial injury, implying that the brachial plexus was not damaged directly. Electromyograms documenting brachial plexopathy were obtained. The mechanism of injury in this case is different from the usual mechanisms of injury in brachial plexus trauma. The majority of brachial plexus injuries are associated with multisystem trauma. The mechanism of injury to the brachial plexus is either from extreme traction on the nerves or direct impact. Downward traction generally results in lesions in the upper cervical nerve roots, whereas upward traction results in lesions of the lower cervical nerve roots, C8 and T1. The usual symptoms of brachial plexus injuries include paralysis of the shoulder, arm, and/or hand with parasthesias and altered sensation. Temperature and color of the limb may be altered because of damage to the autonomic nervous system. The treatment of brachial plexus injuries varies depending on the mechanism and the time the injury is discovered in relation to the inciting trauma. Current treatment includes assessing function with physical examination, preoperative electromyogram, and then repair of viable nerve roots and associated vascular injuries.

Axilla↗
PubMed1996

Immediate and long-term results of balloon mitral commissurotomy for rheumatic mitral stenosis: comparison between Inoue and double-balloon techniques.

We examined the immediate results and 2-year follow-up of percutaneous transvenous mitral commissurotomy (PTMC) using the Inoue balloon (IB) and double-balloon (DB) techniques. Short-term comparisons have been described, but long-term comparisons have not been available. PTMC was performed in 208 adult patients with symptomatic mitral stenosis (MS) and mitral valve area (MVA) of 0.94 +/- 0.2 cm2, by use of the IB in 157 (73.4%) and the DB technique in 56 (26.3%). Procedures were performed successfully and without complications in 198 (93%) cases. Adequate mitral dilatation (MVA = 1.6 cm2) without significant regurgitation was obtained in 179 (86%) of 192 patients. The final MVA was 2.0 +/- 0.43 cm2 after IB and 2.06 +/- 0.51 cm2 after DB (not significant). Technical difficulties and complications were more frequent with DB (16% vs 3.8%; p<0.001). Severe mitral regurgitation (grade III to IV) occurred in 4.6% of IB and 4.1% of DB (not significant), whereas grade 1 mitral regurgitation was greater with IB (21% vs 10.2%; p=0.01). A total of 172 patients were monitored an average of 23.8 +/- 10.6 months, with 83% in New York Heart Association functional class 1, echocardiographic MVA of 1.84 +/- 0.44 cm2, and restenosis rate of 22% at 36 months. PTMC is a safe, effective treatment for symptomatic MS. Results of both IB and DB techniques are similar, but the IB is simpler and safer, Long-term clinical improvement is maintained, although the restenosis rate seems to be progressive and related to inadequate immediate results.

Adolescent↗
PubMed1995

Indomethacin inhibits cell proliferation and increases cell losses in rat gastrointestinal epithelium.

Gastrointestinal cell proliferation was estimated in histological sections of rats treated with low and high doses of parenteral indomethacin for 3 to 60 days. Mitoses were arrested with vincristine and cells in S phase were labeled with tritiated thymidine. Short-term, low-dose treatments reduced the mitotic activity in the oxyntic and small intestinal epithelium, whereas moderate doses restored the mitotic index and high doses increased the proliferative activity and produced epithelial hyperplasia. Long-term, low-dose treatments increased cell proliferation in the small intestine and reduced the number of villous cells. Indomethacin did not affect the proliferative response elicited by refeeding in the oxyntic mucosa, but the simultaneous administration of prostaglandin E2 analog increased the number of arrested mitoses. The turnover of labeled cells was accelerated by indomethacin, particularly in the small intestine. These findings indicate that prostaglandins are regulators of the cell kinetics of the gastrointestinal epithelium but, at the same time, they disclose the presence of trophic mechanisms that are independent of the synthesis of endogenous prostaglandins.

Animals↗
PubMed1995

[Phyllodes tumor: diagnosis and treatment].

We reviewed 1.178 benign tumors treated between 1981/93 among which 39 appeared with a Phylodes Tumors diagnosis, disregarding 5 of them because they did not have a precise description and histologic classification, studying 34 proved cases which represented 2.89% of all benign tumors; if we add 89% cancers in these years, we have 2.074 and the relation becomes 1.64% of the total. We found 22 benign phylodes (64.7%) 7 border line (20.5%) and 5 malignant (14.8%) whose clinic, histologic and evolutive characteristics are presented in this paper.

Adolescent↗
PubMed1995

[Phase II trial with navelbine + cisplatin + etoposide in the treatment of inoperable non-small cell lung carcinoma].

40 patients with advanced non-small cell lung cancer not previously treated were included in a study at phase II with vinorelbine 20 mg/Sq.m days 1 and 8, etoposide 60 mg/sq.m days 1-3 and cisplatin 75 mg/sq.m day 1 each 28 days for 6 cycles. There were 31 men and 9 women, being the average age of 54 years, with "performance Status" grade 0-2. All of them could be evaluated for toxicity and 31 for responsiveness. 10 patients were in stage IIIb and 21 at stage IV. 42% of objective responses were obtained and an overall survival of 9 months, which justifies further studies.

Adult↗
PubMed1994

Characterization of Ca2+ transport in Euglena gracilis mitochondria.

The present study was designed to establish the characteristics of the Ca2+ fluxes in isolated mitochondria of the protist Euglena gracilis. Uptake of Ca2+ and Sr2+ was supported by succinate and lactate oxidation. Ca2+ influx was slightly inhibited by 5 microM Ruthenium red and completely blocked by La3+ with a half-maximal inhibition attained at 50 microM. The addition of inorganic phosphate induced a 3-fold stimulation of Ca2+ uptake. Ca2+ uptake was inhibited by Mg2+ only in the absence of phosphate. Ca2+ efflux was induced by Na+, Li+ and K+ through a diltiazem-insensitive reaction. Ca2+ release, collapse of membrane potential and swelling were induced by Hg2+ and Cd2+ but not by carboxyatractyloside; cyclosporin A did not prevent the Ca2+ release induced by the heavy metal ions. Ca2+ uptake was achieved in the presence of 3 microM antimycin or 0.1 mM cyanide; this finding indicates that the alternative respiratory chain present in Euglena mitochondria can support this energy-dependent reaction. The data obtained suggest similar pathways, but different regulatory mechanisms, for Ca2+ transport between protist and mammalian mitochondria.

Animals↗
PubMed1994

Microflora modulates endocrine cells in the gastrointestinal mucosa of the rat.

BACKGROUND/AIMS: Gastrointestinal peptides and biogenic monoamines participate in the regulation of gastrointestinal functions. The aim of this study was to examine the influence of the microflora on the distribution of endocrine cells and on the release of gastrointestinal peptides. METHODS: A quantitative morphological study using stereological methods was performed in gastrointestinal sections of conventional and germ-free rats. Tissue and plasma concentrations of peptides were measured. RESULTS: The total volumes of gastrin- and serotonin-immunoreactive cells were significantly increased in the gastric mucosa of germfree rats (P < 0.05), as well as the total volumes of serotonin- and motilin-immunoreactive cells in the ileum (P < 0.05) and serotonin-immunoreactive cells in the colonic mucosa (P < 0.05). The tissue concentration of somatostatin was significantly higher in the jejunum (P < 0.05) and lower in the ileum of germfree rats than in controls (P < 0.05). Plasma glucagon was significantly increased in germfree rats (P < 0.05). The total volume of the fundic mucosa was enlarged in germfree rats (P < 0.05), whereas the total volume, the mucosal thickness, and the number of crypt cells of the colonic mucosa were significantly reduced in these rats compared with controls (P < 0.05). CONCLUSIONS: Our findings suggest that the intraluminal microflora influences the release of biologically active peptides and that it participates in the regulation of gastrointestinal endocrine cells and the epithelial structure.

Animals↗
PubMed1994

Glutamine supplementation does not prevent small bowel mucosal atrophy after total parenteral nutrition in the rat.

Glutamine supplementation to non-lipid parenteral nutrition has been demonstrated to attenuate villus atrophy and increase mucosal DNA content in the rat. This study was performed in order to determine the effects of glutamine supplementation to a balanced TPN mixture (including lipids) on epithelial cell kinetics using autoradiography. Male Sprague-Dawley rats were used. Group 1 (control) received food and an intravenous saline infusion. Group 2 received an intravenous TPN mixture including lipids but without glutamine. The same TPN mixture, glutamine replacing an isonitrogenous amount of non-essential amino acids, was given to Group 3. Animals were fed for 7 days, whereafter blood and intestinal samples were taken 1 h after injection of tritiated thymidine. Microscopy of specimens from proximal jejunum revealed a significant reduction in the number of cells in crypts and villi in both TPN groups (2 and 3) compared to orally fed animals (p < 0.001). Epithelial cell numbers were not significantly different in Group 2 and 3. Similarly, the labelling index (number of labelled cells/number of crypt cells) was not affected by glutamine administration. In plasma, glucagon concentrations in Group 2 (TPN without glutamine) seemed to decrease compared to Group 1 and 3 (p = 0.06). In this study, glutamine supplementation did not affect apithelial atrophy or cell proliferation. It is concluded, that the effects of glutamine on mucosal atrophy and renewal in jejunum may depend on the composition of the TPN mixture supplied during parenteral feeding.

Journal Article↗
PubMed1994

Differential cell kinetics in the ileum and colon of germfree rats.

Our aim was to study the cell kinetics and epithelial structure in the ileum and colon of conventional and germfree AGUS rats by means of a classic stathmokinetic technique. A slight hyperplasia was observed in the villi of germfree animals (p < 0.05), associated with a comparatively short cell cycle time. The crypt cell production rate was reduced in the colon of germfree rats (p < 0.05), and their crypts contained fewer cells than those of conventional animals (p < 0.05). It is concluded that intraluminal bacteria influence cell proliferation in the colon. The absence of microflora prolongs the cell cycle time and reduces the proliferative activity in the colonic crypts, which contributes to a steady state that is different from that of conventional animals.

Animals↗
PubMed1994

Abnormal colonic microbial function in patients with rheumatoid arthritis.

The aim of this study was to examine the microflora-associated characteristics (MACs) of faecal samples of patients with rheumatoid arthritis (RA) and to evaluate the actions of sulphasalazine (SASP) on these MACs. The conversion of cholesterol to coprostanol, the production of urobilinogen, the degradation of faecal tryptic activity (FTA) and of beta-aspartylglycine were measured in faecal samples from 19 patients treated with SASP and 21 patients not treated with this medication. A control group of 21 healthy subjects was sex- and age-matched with the untreated patients. The conversion of cholesterol to coprostanol showed a bimodal distribution. The frequency of high converters in patients without SASP treatment was higher than in healthy subjects (p < 0.05). Treatment with SASP markedly increased the FTA and reduced the urobilinogen values, as compared to the untreated patients (p < 0.05). Beta-aspartylglycine was not found in any faecal samples. The results indicate that patients with RA have an abnormal formation of coprostanol, which is ascribed to alterations in the function of the Eubacteria species. In patients with RA, SASP treatment induces disturbances in the metabolism of the microflora.

Aged↗
PubMed1993

Helicobacter pylori infection, ABO blood group, and effect of misoprostol on gastroduodenal mucosa in NSAID-treated patients with rheumatoid arthritis.

Our aim was to investigate the effect of misoprostol on NSAID-induced gastroduodenal mucosal damage in patients with rheumatoid arthritis. The study included 40 patients, and it was designed as a double-blind, placebo-controlled trial. Misoprostol significantly reduced the gastroduodenal mucosal lesions found at endoscopy (P < 0.05) and prevented the development of ulcers. The cumulative incidence of ulcers at four weeks was 5% in the placebo group and 0% in the misoprostol group. The basal and pentagastrin-stimulated acid output as evaluated after 23 days of treatment with misoprostol was not significantly affected. Forty-one percent of the patients had signs of current Helicobacter pylori infection, 33% had positive serology only, and 26% had no evidence of infection. Most of the patients with current infection belonged to blood group O (P < 0.05). Misoprostol treatment did not affect the occurrence of Helicobacter pylori or the rheumatic disease activity. It is concluded that the protective actions of misoprostol on the gastroduodenal mucosa of NSAID-treated patients are largely mediated by mechanisms other than inhibition of acid secretion. The relationship among active Helicobacter pylori infection, blood group O, and peptic ulcer may be helpful to identify a subpopulation of patients taking NSAIDs at risk of developing peptic ulcers.

ABO Blood-Group System↗
PubMed1993

Indomethacin inhibits cell proliferation in the oxyntic epithelium of the rat.

The aim of this investigation was to examine the action of parenteral indomethacin and oral prostaglandin E2 on cell proliferation in the rat oxyntic mucosa. Groups of Sprague Dawley rats were treated with either 1.5 mg/kg indomethacin subcutaneously, 5 mg/kg oral prostaglandin E2 or placebo, twice daily during 5 days. All rats were killed exactly 4 hours after mitotic arrest with vincristine, and a biopsy specimen from the oxyntic mucosa was processed for routine microscopic evaluation. Mitotic figures were distributed cluster-like along the oxyntic mucosa alternating with mitosis-free areas. The total number of mitotic figures in 8 mm of mucosa was significantly reduced by administration of indomethacin (p < 0.05). In rats given indomethacin, 32.5% of the examined mucosa did not have mitotic figures, which is significantly higher than 14.3% as observed in placebo-treated rats (p < 0.05). Both rats treated with indomethacin and with prostaglandin E2 had fewer microscopic fields containing 5-6 mitotic figures than placebo-treated animals (p < 0.05). The maximal length of mitosis-free areas was 0.6 (0.6-0.9) mm in rats given indomethacin which is significantly larger than 0.4 (0.2-0.4) mm observed in controls (p < 0.05). Indomethacin produced epithelial atrophy as shown by a significant reduction of the epithelial height observed in those rats compared to controls (p < 0.05). The inhibition of cell proliferation observed in the oxyntic mucosa of rats treated with the cyclooxygenase blocker indicates that an important physiological role of endogenous prostaglandin is to maintain the proliferative activity of the epithelium at a high level.

Animals↗