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Biomedical subjects

A Uribe

Publications and source records attributed to A Uribe.

At least 55 records · Page 3Linked to original sources
PubMed1993

Small intestinal bacterial overgrowth in patients with rheumatoid arthritis.

OBJECTIVES: To examine the microflora of the upper small intestine in patients with seropositive rheumatoid arthritis (RA) using a combination of microbial cultivation and tests for microbial metabolic activity. METHODS: Twenty five patients with seropositive RA, 12 achlorhydric control subjects, and 11 control subjects with normal gastric acid secretion were investigated. Disease activity was evaluated in the patients with RA by three different indices. Eight (32%) of the patients with RA had hypochlorhydria or achlorhydria. The acid secretory capacity was determined with pentagastrin stimulation. A modified Crosby capsule was used to obtain biopsy specimens and samples of intestinal fluid from the proximal jejunum; aerobic and anaerobic microbial cultivation of mucosal specimens/intestinal fluid was carried out, and gas production and microflora associated characteristics in jejunal fluid were determined. Additionally, a bile acid deconjugation breath test was performed. RESULTS: Subjects with at least one of the following findings were considered to have bacterial overgrowth: positive bile acid deconjugation test; growth of Enterobacteriaceae; positive gas production; or low tryptic activity. By these criteria half of the patients with RA with hypochlorhydria or achlorhydria and half of the achlorhydric controls had bacterial overgrowth. Thirty five per cent of the patients with RA with normal gastric acid secretion had bacterial overgrowth compared with none of the normal controls. Disease activity indices and rheumatoid factor titres were significantly higher in patients with RA with bacterial overgrowth than in those without. CONCLUSIONS: A high frequency of small intestinal bacterial overgrowth was found in patients with RA; it was associated with a high disease activity and observed in patients with hypochlorhydria or achlorhydria and in those with normal acid secretion.

Achlorhydria↗
PubMed1993

Contact diode laser microvascular anastomosis.

Contact diode laser microvascular anastomosis appears to be a valuable technique for anastomosing small arteries and veins. Significantly less foreign body reaction and markedly decreased operative time has been shown to be a major advantage of using contact diode laser technology. The authors have found that contact diode laser anastomosis can be performed in vessels as small as 1 mm in size using a 200-microns flat tip synthetic sapphire probe. Light microscopy has shown a significant decrease in foreign body reaction at the level of the anastomosis using laser techniques as compared to standard vessel anastomosis with 10-0 nylon sutures. The role of fibronectin and changes in collagen associated with laser anastomosis were also explored. Light microscopic electron-microscopic results as well as biotin-avidin immunoperoxidase fibronectin studies will be discussed.

Animals↗
PubMed1993

Functional alterations of the microflora in patients with ulcerative colitis.

The aim of the study was to examine microflora-associated characteristics in patients with inactive ulcerative colitis, receiving sulphasalazine, in relation to the spread of the disease. The conversion of cholesterol to coprostanol, the production of urobilinogen, and the degradation of tryptic activity (FTA) and beta-aspartylglycine were measured in faecal samples from patients with proctitis or left-sided or total ulcerative colitis and in age- and sex-matched controls. No significant differences in the results were observed in patients with various degrees of extension of inflammatory bowel disease. However, the coprostanol ratio and the urobilinogen level were lower and the FTA was higher in patients with colitis than in the controls (p < 0.05). Beta-aspartylglycine was not found in any faecal sample. The results indicate that patients with ulcerative colitis taking sulphasalazine have a microflora with abnormal metabolic characteristics.

Adult↗
PubMed1993

Ionophoretic-like properties of ketorolac for calcium.

Ketorolac is an analgesic drug known to induce its therapeutic effect by inhibiting prostaglandin synthesis. In this work we introduce the nonsteroidal antialgesic drug as a compound with ionophoretic properties for calcium ions, showing that ketorolac induces mitochondrial Ca++ release. This reaction did not depend on an uncoupler-like action, because the drug does not collapse the internal negative membrane potential nor does it affect oxidative phosphorylation. In addition, it is shown that ketorolac ferries calcium ions into energized liposomes and has a hydrophobic phase with an affinity constant of 4 x 10(-3). The therapeutic action of ketorolac is related to its ionophoretic properties in addition to its well known inhibitory effect on the cyclooxygenase enzyme.

Animals↗
PubMed1992

Indomethacin accelerates clearance of labeled cells and increases DNA synthesis in gastrointestinal mucosa of the rat.

Sprague-Dawley rats treated with placebo, parenteral indomethacin, or oral prostaglandin E2 for six days were given an intraperitoneal injection of [3H] methyl-thymidine and killed at 45 min and 96 hr after labeling. Treatments were continued until death. The dpm/DNA index was determined in mucosal scrapings of the stomach, duodenum, and jejunum and used to estimate DNA synthesis (45 min) and the clearance of labeled cells (96 hr). Indomethacin increased the DNA synthesis in both the duodenal and jejunal mucosa (P less than 0.05). In comparison to the controls, the clearance of labeled cells from the antral, duodenal, and jejunal mucosa was accelerated by indomethacin treatment, whereas the elimination of labeled cells from the antral and jejunal mucosa was slowed by PGE2 treatment (P less than 0.05). DNA synthesis of the antral mucosa was significantly reduced by PGE2 (P less than 0.05). The cyclooxygenase blocker did not affect the cell kinetic parameters of the oxyntic mucosa. The plasma levels of somatostatin were significantly higher both in PGE2- and indomethacin-treated rats than in controls (P less than 0.05). It is concluded that indomethacin treatment increases the cell losses from the epithelial surface, which in turn trigger a compensatory trophic reaction. It is suggested that an important physiological action of endogenous prostaglandins is to regulate the outflow of cells from the superficial zones of the epithelium. Finally, this study disclosed the presence of hitherto unknown regulatory mechanisms that promote cell proliferation in the gastrointestinal mucosa despite inhibition of the synthesis of endogenous prostaglandins.

Animals↗
PubMed1992

Fluorescamine-induced membrane permeability in mitochondria.

1. Addition of fluorescamine (75 microM) to mitochondria induced an increase in membrane permeability. 2. The leakiness of the inner mitochondrial membrane is characterized by extensive release of accumulated Ca2+, collapse of the transmembrane potential, mitochondrial swelling and efflux of matrix proteins, among them, malate dehydrogenase. 3. These effects were diminished by supplementing the media with 1 mM phosphate, and partially prevented by Mg2+. 4. These results indicate that the primary amino groups of membrane components contribute, partially, to the maintenance of the permeability barrier in mitochondria.

Animals↗
PubMed1992

The characteristics of mitotic figures in jejunal mucosa of patients with celiac disease.

The morphologic characteristics of the mitotic figures present in the jejunal mucosa of 23 pediatric patients having gluten enteropathy were recorded. Of the 851 mitoses found, 4.9% were in prophase, 39.9% in prometaphase, 29.5% in metaphase, 22.3% in anaphase, and 3.3% in telophase. Of the 851 mitoses found, 98.8% were considered to be morphologically normal and the remaining 1.2% were considered atypical. The occurrence of atypical mitoses in the jejunal mucosa of pediatric patients was unexpected. However, because jejunal adenocarcinomas in celiac patients are known to be rare, the plausible explanation for the present findings is that the occurrence of atypical mitoses may mirror morphologic variations from the normal mitotic pattern occurring in a rapidly proliferating mucosa, such as that of patients with gluten enteropathy.

Celiac Disease↗
PubMed1992

Oral prostaglandin E2 influences the enterochromaffin-like and somatostatin cell populations in the oxyntic mucosa of the rat.

Our aim was to study the effects of long-term oral administration of different doses of prostaglandin E2 (PGE2) and of a synthetic analogue on the endocrine cells and on selected epithelial cells of the rat oxyntic mucosa. The endocrine cells were visualized by immunohistochemical staining and by the Sevier-Munger method. Quantification of the mucosal cells was performed at a light-microscopic level using stereological methods. The highest dose of 15-R-15-methylprostaglandin E2 (MePGE2) increased the total volume of enterochromaffin-like (ECL) cell profiles whereas no changes were observed after treatment with PGE2. On the other hand, the total mucosal volume of chromogranin A-immunoreactive cells was significantly reduced by both doses of natural PGE2. The highest dose of PGE2 increased the total volume of somatostatin-immunoreactive cells. The serotonin-immunoreactive cells were very few and unaffected by treatments. E2 prostaglandins induced hyperplasia and hypertrophy of epithelial cells. A selective trophic action on the mucous but not on the parietal cells was observed. The area of the parietal cells was increased in rats treated with the analogue. The gastric acid content was increased in rats treated with the highest doses of E2 prostaglandins. The plasma level of somatostatin was significantly increased in rats given MePGE2 and the highest dose of PGE2. The cell population of chromogranin A-immunoreactive cells did not reach the levels of the NECL cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

E2 prostaglandins modulate cell proliferation in the small intestinal epithelium of the rat.

Groups of Sprague-Dawley rats were administered 1 mg/kg indomethacin subcutaneously, indomethacin subcutaneously plus 200 micrograms/kg oral 15-R-15 methyl-prostaglandin E2 (MePGE2) or oral MePGE2 twice daily for 10 days. The animals were treated with antibiotics to prevent mortality. Two control groups were used: control 1 was given placebo and control 2 was treated with antibiotics. All rats were killed 4 h after injection of a metaphase blocker, and the proliferative activity of the distal small intestine was examined in histological sections by means of the cumulative mitotic index (MI). A reduction in the number of villous cells was observed in the rats given antibiotics (p < 0.05 vs. control 1). The small intestinal villi of the rats treated with indomethacin had fewer cells than those of both control groups (p < 0.05) whereas the crypts contained more cells (p < 0.05) and had a higher MI than those of the controls (p < 0.05 vs. controls 1 and 2). These changes were reverted by the prostaglandin analogue. The number of cells of the small intestinal crypts and the cumulative MI in the rats who received indomethacin and the prostaglandin analogue were similar to controls, and they were significantly lower than the values observed in the animals treated with indomethacin (p < 0.05). The animals treated with the prostaglandin analogue and placebo developed a marked hyperplasia of the small intestinal villi (p < 0.05 vs. both control groups), but the atrophy of the villi induced by indomethacin was not prevented by simultaneous administration of the analogue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Somatostatin cells in the oxyntic mucosa of hypo- or hypergastrinemic rats.

The present report describes the long-term effects of antrectomy, antrum exclusion, portacaval shunt, omeprazole treatment, or the combination of omeprazole treatment and portacaval shunt on the number and density of somatostatin cells in the oxyntic mucosa of the rat. Antrectomy, which is associated with hypogastrinemia, raised the number and density of the somatostatin cells, whereas antrum exclusion and omeprazole treatment, which are associated with hypergastrinemia, reduced the number and density of the somatostatin cells. Portacaval shunt, which is associated with hypogastrinemia, increased both the number and the density. Omeprazole treatment of portacaval--shunted rats suppressed or even reversed the somatostatin cell hyperplasia after portacaval shunt alone. From these findings it is unlikely that gastrin stimulates the proliferation of somatostatin cells in the oxyntic mucosa. In fact, there seems to be an inverse relationship between the serum gastrin concentration and the somatostatin cell number.

Animals↗
PubMed1992

Trophic doses of E2 prostaglandins do not influence the exocrine and endocrine pancreas in the presence of high levels of plasma somatostatin.

The aim of the present investigation was to study the effect of a long-term and a short-term treatment regimen with 15-R-15-methyl prostaglandin E2 and natural prostaglandin E2 (PGE2) on the endocrine cell populations of the rat pancreas. Graded oral doses of the analogue (5 and 50 micrograms/kg) and PGE2 (5000 micrograms/kg) were given twice daily for 4 weeks. The pancreas was carefully excised and weighed. Sections from randomly taken pancreatic biopsy specimens were processed for immunohistochemistry or hematoxylin and eosin staining before quantitative estimations were made, using stereologic methods. The total pancreatic volumes of insulin-, glucagon-, polypeptide P-, somatostatin-, and chromogranin A-immunoreactive cells were not affected by E2 prostaglandins. Neither the total volume of the islets of Langerhans nor that of the pancreatic cell nuclei was affected. The size of pancreatic cell nuclei was the same in the groups. The plasma levels of the antitrophic peptide somatostatin were significantly increased in rats treated with doses of both the analogue and PGE2 (p less than 0.05). In an additional short-term study rats were given oral placebo or 5000 micrograms/kg PGE2 twice daily for 5 days. The total endocrine pancreatic volume was not affected by PGE2. As in the long-term study, natural PGE2 did not affect the total pancreas volume or the total volume of pancreatic cell nuclei. These findings indicate that E2 prostaglandins produce no changes in the exocrine or endocrine pancreas in a dose range known to induce hyperplasia in the gastrointestinal epithelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1991

Distribution of control of oxidative phosphorylation in mitochondria oxidizing NAD-linked substrates.

The flux control distribution of the net rate of state 3 respiration was determined in heart and kidney mitochondria incubated with low concentrations of pyruvate (0.5 mM) or 2-oxoglutarate (1 mM), and in conditions that led to activation of NAD-linked dehydrogenases, i.e., high substrate or Ca2+ concentrations. Control of flux was exerted by the ATP/ADP carrier (flux control coefficient, ci = 0.37) and Site 1 of the respiratory chain (ci = 0.28) when dehydrogenase activity was low. Control of the process shifted to the ATP synthase (ci = 0.32) and the Pi carrier (Ci = 0.27) when dehydrogenases were activated by high pyruvate and high Ca2+. The changes in the control exerted by the ATP/ADP carrier and the ATP synthase were not due to changes in the transmembrane potential, nor to a modification of intramitochondrial ATP/ADP ratios. Applying the summation theorem of the control analysis, it was found that at low Ca2+ and pyruvate concentrations the dehydrogenases shared the control of state 3 respiration with other steps. The NAD-linked dehydrogenases did not exert any significant control at high Ca2+ or high pyruvate concentrations.

Animals↗
PubMed1991

Diagnostic laparoscopy.

Laparoscopy is a unique procedure which can be used in diagnostic or therapeutic situations involving intra-abdominal pathology. Until recently, open laparotomy has been the preferred method for such evaluations. The following cases indicate the increased sensitivity, specificity, safety, and cost effectiveness of laparoscopy in diagnostic situations.

Abdominal Neoplasms↗
PubMed1990

Prostaglandin E2-induced hyperplasia of the rat antral epithelium is followed by a secondary inhibition of the mitotic activity.

The aim of the study was to examine the mitotic activity in the antral and duodenal epithelium of Sprague-Dawley rats given trophic doses of E2 prostaglandins during a prolonged period of time. Natural prostaglandin E2 (dose range: 0.2-5.0 mg.k-1) and 15 (R) 15 methyl prostaglandin E2 (dose range: 0.03-2.0 mg.kg-1) were administered for 11 days, and mitoses were arrested with vincristine for 4 h before estimation of the cumulative mitotic index. A dose-related hyperplasia of the antral glands was observed after treatment with prostaglandin E2 and the synthetic analogue (p less than 0.05). The proliferative zone was enlarged in rats treated with high doses of the analogue but natural prostaglandin E2 did not affect the limits of the proliferative zone. A dose-related reduction of the mitotic index was observed in animals treated with prostaglandin E2 despite the presence of hyperplastic changes. All doses of the analogue induced antral hyperplasia without affecting the mitotic index except in rats given the highest dose who had a significantly lower mitotic index than controls (p less than 0.05). Hyperplasia of both crypts and villi was observed in the duodenum of rats given high doses of E2 prostaglandins (p less than 0.05) whereas the mitotic index and the growth fraction were not affected by treatments. It is concluded that hyperplasia by prostaglandins is developed in absence of changes of the mitotic activity. The observed reduction of the mitotic index is interpreted as a secondary phenomenon, possibly mediated by a regulatory mechanism of cell proliferation which is triggered to reduce further epithelial growth. It is suggested that prostaglandin E2 might influence such regulatory mechanisms.

Administration, Oral↗