[Severe cytolytic hepatitis caused by imolamine].
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Biomedical subjects
Publications and source records attributed to P Rampal.
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A new model to study cholesterol uptake in the human intestine in vitro is described. Human small intestine organ cultures were incubated with mixed micelles containing bile acid, phospholipid, and cholesterol or its nonabsorbable analogue, sitosterol; trace amounts of labeled cholesterol or sitosterol were added to the micelles. After incubation, the lipids were extracted from the cells and cholesterol and sitosterol uptake was evaluated. Specific cholesterol uptake was determined as a difference between cholesterol and sitosterol uptake. Cholesterol, but not sitosterol, uptake was time- and dose-dependent. Rapid and slow phases of cholesterol uptake were observed. Cholesterol uptake was also temperature-dependent. Removal of epithelial cells from human intestine explants reduced cholesterol, but not sitosterol, uptake. Inhibition of acyl CoA:cholesterol acyltransferase by Sandoz compound 58-035 and treatment with monensin reduced cholesterol uptake, but not sitosterol uptake, in a dose-dependent manner. In contrast, treatment of cultures with an inhibitor of 3-hydroxy-3-methyl-glutaryl coenzyme A reductase, lovastatin, stimulated cholesterol, but not sitosterol, uptake in a dose-dependent manner; mevalonic acid reversed the effect of lovastatin. The presented model allows large-scale in vitro studies of different stages of cholesterol absorption in the human intestine.
Chronic gastritis (CG) which can be associated with severe complications, is a frequent phenomenon in gastroenterological practice. No data concerning the prevalence of GC are available in France. The aim of this study was to evaluate the prevalence of CG on biopsy specimens in the French population. All outpatients coming from different towns of seven French areas and undergoing an upper endoscopy on one or two randomly selected consecutive days were included in the study. A case report form was filled out and 5 biopsy specimens were taken from the fundus and antrum. Pathologists graded the specimens on the basis of Whitehead's classification. Seven hundred and forty-two patients were enrolled by 102 private gastroenterologists. Mean age was 53 years; 52% were males. Endoscopically, the gastric mucosa was abnormal in 53%. Superficial and atrophic CG was diagnosed in 53% of cases. Superficial gastritis was observed in 101 patients (14%), antral chronic atrophic gastritis (CAG) in 189 (26%) and fundic CAG in 17 (2%). Patients with CAG were significantly older than the other patients. There were more smokers and heavy alcohol drinkers in the group of CAG patients. Endoscopy and histology were in accordance in only 55.2% of the patients: most cases of CAG were not detected by endoscopy. These results are similar to other studies in European populations. The principal pattern among the various types of gastritis was CAG. The other forms were rare. Autoimmune gastritis was uncommon in this French population (4% of the CAG patients).
Several studies have demonstrated that certain essential fatty acids present a specific cytotoxicity for tumor cells. However, no investigation of this type has been performed on human colon cancer cells to date. This study investigated the effect of gamma-linolenic acid (GLA), eicosapentaenoic acid (EPA) and prostaglandin (PG) E1 on the proliferation and metabolism of three human colon cancer cell lines: HT 29, HRT 18, and CACO 2. GLA, EPA and PGE1 all inhibited the proliferation of the three cell lines, but with a decreasing gradient of sensitivity: HRT 18 > HT 29 > CACO 2, and with different IC50 values. PGE1 was markedly less effective than the other two. GLA and EPA increased lipid peroxidation and membrane fluidity in a dose-dependent manner. The presence of indomethacin did not modify the effects of GLA and EPA. In addition, PGE1 had little effect on membrane fluidity and lipid peroxidation. The antitumoral effect thus does not appear to be mediated by PGE1. Addition of vitamin E decreased the effects of GLA and EPA, which supports the hypothesis of direct action by these fatty acids. In conclusion, while EPA and GLA have an antitumoral effect in vitro, their effect on primary cultures of normal human colon cells must be investigated to determine whether this effect is specific to tumoral cells, as has been observed for other cell types.
We report two cases of Hashimoto's thyroiditis associated with chronic active hepatitis C virus (HCV). Our data suggest that HCV infection might be involved in this autoimmune disease.
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This study was designed to evaluate the efficacy and tolerance of cyclic (nocturnal) enteral nutrition in ambulatory malnourished patients. A ternary polymeric diet was administered to a total of 28 women and 23 men (mean age: 58 years) for a nocturnal period of 12-14 hours during 24.5 +/- 1.1 days. This diet provided an average of 28.3 +/- 0.6 kcal/kg ideal body weight/day. The nutritional program was administered as planned and well tolerated in 50 of the 51 patients. Voluntary oral caloric intake improved significantly during the treatment period (18.2 +/- 1.4 kcal/kg ideal body weight/day during the first week of enteral nutrition and 22.7 +/- 1.6 kcal/kg ideal body weight/day during the last week). The global nutritional deficit based on 10 anthropometric and biological parameters improved by an average of 36.8 +/- 2.2 percent. Overall, 71 percent of the patients exhibited a favorable nutritional course. Results were identical regardless of the pathology responsible for malnutrition. The main advantages of cyclic enteral nutrition include the possibility for patients to engage in physical activities and to eat normally during the day.
We report what is probably the first case of para-oesophageal bronchogenic cyst treated by video-thoracoscopy. The patient was a 26-years old woman who presented with dysphagia to solid foods. Preoperative investigations showed that the lesion was a cyst and that it was located in the superior and posterior mediastinum; they also enabled us to determine its relations with nearby structures, notably the oesophagus, and to make the diagnosis of para-oesophageal bronchogenic cyst. Treatment consisted of excision of the cyst by video-thoracoscopy. The postoperative period was uneventful, and the patient was discharged on the fourth day.
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Between 1987 and 1989 we treated 18 patients with advanced pancreatic adenocarcinoma with a long acting LH-RH analogue: triptorelin. Seventeen patients were evaluated. We obtained no objective responses. The median survival time was 4.5 months. The treatment was well tolerated without any major secondary effects. The absence of dosage of hormonal receptors did not allow the selection of hormone sensitive patients. The future study of hormone therapy will analyse the pancreatic hormonal receptors.
In vivo, Clostridium difficile acts by releasing 2 toxins: toxin A, an enterotoxin, and toxin B, a cytotoxin. This study was performed to determine: a) whether the rat epithelial intestinal cell line IRD 98 responds to Clostridium difficile toxin A and B; b) whether the yeast Saccharomyces boulardii has an effect on this model. Evaluation of 3H-thymidine incorporation into IRD 98 cells exposed to toxin B revealed that DNA synthesis was inhibited for low concentrations (10 ng/ml). For higher concentrations, DNA synthesis was not modified. Evaluation of 14C-leucine incorporation into IRD 98 cells exposed to toxin B revealed that this toxin affected protein synthesis. Whereas cholera toxin stimulates adenylate cyclase in IRD 98 cells, cAMP levels in cells exposed to various quantities of toxin A was similar to that in control cells. As opposed to cholera toxin, which does not affect the cytoskeletal structure of IRD 98 cells, 7 micrograms/ml of toxin A and even smaller amounts of toxin B (1 ng/ml) were found to cause structural alterations by immunofluorescence studies. Prior exposition of cells to Saccharomyces boulardii reduced or prevented the rounding of cells in the presence of these toxins. IRD 98 cells can thus be considered a good model for in vitro investigation of the effects of Clostridium difficile toxins A and B, and findings suggest that Saccharomyces boulardii has a protective effect against the action of these toxins.
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Endogenous mitotic inhibitors act as control-mechanisms in intestinal epithelium proliferation. The presence of an inhibitor of cultured intestinal epithelial cell from a villous extract of rat jejunum has been reported in one of our papers. The object of the study now reported was to find the presence of a growth inhibitor in the villous extract from man's small intestine and to purify and characterize this factor when found. Our results reveal that: (1) Such an inhibitor was found in a supernatant preparation obtained from human intestinal epithelial cells. The inhibition of the proliferation of epithelial cells (IRD-98) it induced was seem to be dose-dependent and non-cytotoxic. (2) After chromatography on hydroxylapatite, on DEAE and then on ACA 54 (gel permeation), a low-molecular-weight protein (15 kDa) called purified intestinal inhibitor (PII) was isolated (purification factor of approx. 50,000 with respect to the supernatant fraction). This fraction proved to inhibit the IRD-98 cells in a reversible manner. When cells are incubated with this protein, cells prove to be arrested in phase G1 of the cell cycle as is revealed by the flow cytometry studies. The results obtained support the hypothesis that regulation of cell proliferation is mediated by endogenous inhibitors at the epithelial level.
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The effect of exposure of an intestinal epithelial cell line to various concentrations of ethanol [217 mM (1%) to 652 mM (3%)] during 24, 48, and 72 hr was investigated in vitro using a rat intestinal epithelial cell line (IRD 98). Incubation of these cells in the presence of ethanol significantly decreased cell growth. This inhibition was accompanied by a strong increase in cellular protein. Stimulation of specific disaccharidases, gamma-glutamyl transferase, and aminopeptidase activities by ethanol was dose- and time-dependent. Ethanol induces a change in the relative proportions of the different lipid classes synthesized; triglycerides, fatty acids, and cholesterol esters were preferentially synthethysed. Our findings show that cell lines are good models for investigation of the effects of ethanol, and that alcohol considerably modifies the functions of intestinal epithelial cells.
Endogenous mitotic inhibitors have been implicated as controlling mechanisms of intestinal epithelium proliferation. We previously reported the purification of an inhibitor of intestinal epithelial cells in culture isolated from a villous extract of human jejunum. This article describes the biologic effects of this inhibitor on organ cultures of rabbit intestinal mucosa. Our results reveal that (1) this factor is not cytotoxic; (2) it inhibits intestinal epithelial cell proliferation in a dose-dependent and reversible manner; (3) it does not appear to be species-specific; (4) it is specific to the digestive tract, and more particularly to the small intestine.