[Pubic pain revealing postoperative pubic osteitis].
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Biomedical subjects
Publications and source records attributed to A Dubois.
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Short-chain fatty acids (SCFAs) alter ileal and colonic motility, but their effects on duodenojejunal motility are unknown. Simultaneous jejunal manometric recordings and hydrogen breath tests after lactulose were performed in eight healthy subjects during continuous duodenal infusion of either saline or SCFAs. These experiments were conducted in the fasting state and postprandially. The effects of various boluses of SCFAs on duodenojejunal motility were also determined in six subjects. During the fasting period, the number and characteristics of migrating motor complex, prolonged propagated contractions, discrete clustered contractions, motility index, and orocecal transit time were similar during saline and SCFAs. Similarly, the motility index and the duration of the postprandial period were not different between SCFAs and saline after the meal. The motility index was significantly increased after each of the 100-ml boluses (saline or SCFAs), but was not altered after the 12.5-ml boluses, suggesting a volume-related effect. Thus, SCFAs do not seem to affect proximal small bowel motility in healthy humans.
An important problem in the treatment of centrofacial ulcerations is to establish a precise diagnosis, since similar clinical and microscopic findings can result from many different causes (as in the centrofacial malignant granuloma syndrome [CFMG]). A comprehensive surgical biopsy protocol (known as SNFMI/GMCF), involving microbiology, parasitology, immunology and pathology laboratories, allowed us to evaluate and to treat 40 cases of CFMG, who form the basis of this report. In 13 of them, specific diagnoses were found and curative treatments could be given. In the remaining 27, the optical microscopy pattern met the criteria for CFMG without identifiable origin or the presence of so-called lethal midline granulomas; however, a more precise evaluation with the help of immunofluorescence studies led to the recognition of malignant lymphoma (ulcerative lymphoma of the midface [ULM]). Most of these lymphomas belonged to the T cell lineage; the others were of B lymphoid origin, or, more rarely, of histiocytic origin. Patients with ULM received radiotherapy and chemotherapy with a response rate of 70.3%; however, the toxicity was significant, with frequent occurrence of chemotherapy-induced neutropenia followed by severe infectious facial cellulitis. Six patients were enrolled in a preliminary open trial of treatment with recombinant alpha-2b interferon with little success. Three patients were treated with radiation therapy only, and survived. Thus, CFMG is a syndrome with specific causes and treatments, requiring multiple extensive biopsies to make the correct diagnosis. The recognition of ULM as the cause of the previously called "lethal midline granulomas" leads logically to the use of chemotherapy with growth factors in order to ameliorate its bad prognosis.
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The effect of the prostacyclin analog U-68,215 on gastric function and systemic blood pressure was evaluated in a primate model. Starting 30 min after histalog (1 mg/kg s.c.), gastric acid secretion and gastric emptying were determined over a 30-min period using a 99mTc-diethylene triamine pentaacetic acid dilution technique. Each animal then received an intragastric bolus of 0, 25, 50 or 100 micrograms/kg of U-68,215 and, after a 30-min equilibration period, gastric function was determined for an additional 60 min (histalog + U-68,215). Systemic blood pressure and heart rate were measured periodically using a pressure cuff and a Korotkoff microphone. U-68,215 produced a 94% maximum suppression of acid output from 60 to 90 min after 100 micrograms/kg U-68,215. Gastric emptying was significantly inhibited by all doses of U-68,215, and no diarrhea was observed in response to any dose of U-68,215. Systolic blood pressure was significantly inhibited (P less than .05) only after the 100 micrograms/kg, whereas diastolic blood pressure was reduced significantly (P less than .05) by both 50 and 100 micrograms/kg and was positively correlated with acid secretion (r = .53; P less than .05). These data demonstrate that U-68,215 produces a significant inhibition of acid secretion without the stimulatory effect on gastric emptying induced by PGE analogs. Thus, prostacyclin analogs may represent an attractive alternative to PGE analogs in the treatment of peptic ulcer disease.
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The anatomical localization of the increase in omega 3 (peripheral type benzodiazepine) binding site densities (an index of glial reaction) following intraperitoneal injection of convulsant doses of kainic acid has been studied by autoradiography in the rat brain. Consistent increases in omega 3 site densities were observed in the olfactory, piriform and entorhinal cortices, amygdaloid nucleus, hippocampal formation and thalamus. In the hippocampal formation, the most pronounced increases were seen in the stratum lucidum of the CA3 field and in the stratum oriens and pyramidale of the CA1 and CA2 fields. This pattern of changes in omega 3 site densities closely paralleled the pattern of neuropathological alterations (assessed by histological methods) observed in these brain regions. Thus, omega 3 site autoradiography may provide a sensitive and reliable index of the neuronal damage resulting from kainic acid administration.
The possibility of using the rhesus monkey as a model for studying gastric function in the presence of infection with spiral bacteria was studied. Endoscopic evaluation of the gastric mucosa was performed under general anesthesia in 29 colony-bred rhesus monkeys, and gastric pinch biopsy specimens were obtained from each animal. On a separate day, gastric emptying and acid output were determined using a 99mTc dilution technique. Biopsy samples were fixed for light microscopy (H&E, Gram, and Warthin-Starry stains) and for transmission electron microscopy. The presence of spiral bacteria and gastritis was assessed and rated on coded slides. In 8 of 29 monkeys, Helicobacter pylori-like organisms were observed in close proximity to the mucosal epithelial cells or in the lumen of the gastric pits. In 14 other monkeys, "Gastrospirillum hominis"-like organisms were observed in the mucus covering the surface of epithelial cells, in the lumina of the gastric glands, and overlying parietal cells. Gastritis was present in 8 of 8 animals positive for H. pylori-like organisms, in 2 of 14 animals positive for "G. hominis"-like organisms, and in none of the uninfected monkeys, and the mean gastritis index was significantly greater in animals positive for H. pylori-like organisms. Moreover, acid output was significantly higher in monkeys positive for "G. hominis"-like organisms than in controls or animals positive for H. pylori-like organisms. Gastric emptying was not significantly different in the three groups. In conclusion, (a) H. pylori-like, but not "G. hominis"-like, organisms cause gastritis while not modifying acid output; (b) "G. hominis"-like, but not H. pylori-like organisms, invade and on occasion damage parietal cells while apparently causing hyperchlorhydria; and (c) the rhesus monkey appears to be a good model for the study of gastric infection with spiral bacteria.
The relation between the cutaneous electrogastrogram (EGG) and gastric emptying was investigated in six rhesus monkeys. Gastric emptying was measured using scintigraphy after administration of two 80-ml mixed solid liquid meals (1.5 and 5.0 kcal/kg) tagged with 99mTc-sulfur colloid and 111In-diethylenetriamine pentaacetic acid. Six epigastric bipolar recordings of the EGG were concurrently obtained, digitized, and band-pass filtered. Portions of the signal with motion artifacts were automatically detected and excluded using two microwave motion sensors. During the early postprandial period, gastric emptying was greater after the 1.5-kcal/kg meal than after the 5-kcal/kg meal, and EGG amplitude increased significantly compared with fasting only after the 1.5-kcal/kg meal. Both emptying and EGG amplitude subsequently decreased after the 1.5-kcal/kg meal, whereas these two parameters increased after the 5-kcal/kg meal. As a result, EGG amplitude was significantly correlated with gastric emptying of solids in all six animals. In contrast, EGG frequency was not significantly different between the two meals and was not correlated with emptying. These results indicate that both the EGG and gastric emptying are modified differently by meals with different caloric contents and that the EGG may represent a useful, although indirect, index of gastric emptying.
The fibrinolytic response to venous occlusion was studied in 17 patients with inflammatory bowel disease: 7 with Crohn's disease, 10 with ulcerative colitis and compared with those obtained in 20 controls. Patients with inflammatory bowel disease showed decreased tissue-type plasminogen activator antigen release (t-PA Ag), no significant Von Willebrand antigen release (vWF Ag), and a residual plasminogen activator inhibitor activity (PAI activity) after venous occlusion. These modifications were more important in the evolutive colitis group compared with the remission group. Hypofibrinolysis, as defined by a defective t-PA release, and a residual PAI activity after venous occlusion might contribute to digestive and/or extra digestive thrombotic manifestations observed during the course of inflammatory bowel diseases.
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Previous investigations have indicated that the detection and quantification of omega 3 (peripheral type benzodiazepine) binding site densities that are associated with reactive astroglia and macrophages could be of widespread applicability in the localization and indirect assessment of neural tissue damage in the central nervous system. In the present study, we analyze the usefulness of this approach in a number of experimental models that are characterized by (or putatively involve) neuronal degeneration. One week after the systemic administration of the excitotoxin, kainate, a marked increase in omega 3 site densities (as assessed by [3H]PK 11195 binding) was noted, an increase that was most prominent in known regions of selective vulnerability (hippocampus and septum). However, the kainate-induced omega 3 site proliferation was not a function of the dose administered, a marked interstudy variation was observed, and the binding increase was prevented by the administration of the anticonvulsant, clonazepam. The densities of omega 3 sites were studied, by autoradiography (using [3H]PK 11195 or [3H]PK 14105 as ligands), in 4 groups of Fischer 344 rats aged 3, 12, 22 and 30 months. No age-related changes were noted except in the 30-month-old group in which discrete and focal increases (reflecting tumoral processes) were observed in various brain regions. In spontaneously hypertensive, stroke-prone rats, omega 3 binding increases were observed concomitant with the development of stroke-related neurological signs. With autoradiography, the omega 3 site increase was localized to focal increases in the boundary zones between major cerebral arteries (and corresponding to regions of ischaemic or haemorrhagic infarction). Focal cerebral ischaemia was studied in rats and mice. Subsequent to middle cerebral artery occlusion in normotensive (Wistar/Kyoto) and spontaneously hypertensive rats, the density of omega 3 sites in the ipsilateral hemisphere was markedly elevated, the increase being greater in the spontaneously hypertensive rats. The increases in omega 3 labelling in these two strains matched the absolute volumes of infarctions, determined previously. Middle cerebral artery occlusion in the mouse also increased hemispheric levels of omega 3 sites; the maximum values were obtained between 4 and 8 days following the induction of focal ischaemia. These results demonstrate the feasibility of using omega 3 sites as a marker of excitotoxic, ischaemic and proliferative damage in the rodent brain. Binding measurement in tissue homogenates is an economic and time-efficient approach, whereas the autoradiographic detection of omega 3 sites allows the localization of brain lesions with a macroscopic or microscopic level of anatomical resolution.(ABSTRACT TRUNCATED AT 400 WORDS)
The venous occlusion test was applied to 17 patients with inflammatory bowel disease (IBD; 7 cases of Crohn's disease, 10 cases of ulcerative colitis). Results were compared to those obtained in 20 healthy matched control subjects. Patients with IBD had significantly decreased t-PA Ag release (p less than 0.001) and had no significant vWF Ag release. Residual PAI activity was evidenced after venous stasis in the IBD group but not in the control group. Hypofibrinolysis was more important in patients with an evolutive IBD than in patients with IBD in remission. Impaired systemic fibrinolytic capacity might contribute to an increased risk for thromboembolic complications and to the pathogenesis of inflammatory bowel disease.
The microscopic distribution of omega 3 (peripheral type benzodiazepine) binding sites in sections from normal and ischaemic rat brain has been determined by emulsion autoradiography with the photoaffinity ligand [3H]PK 14105. In the normal rat brain, high densities of omega 3 sites were present in the ependymal cells, the apical pole of the secretory cells in the choroid plexus and astrocyte-like cells in the outer cellular layer of the olfactory bulb. In ischaemic brain lesions caused by middle cerebral artery occlusion in spontaneously hypertensive rats or in spontaneous ischaemic and haemorrhagic lesions in spontaneously hypertensive stroke-prone rats, the proliferating omega 3 sites were associated with reactive glial cells and macrophages.
The relative roles of prostaglandins and mucosal injury in aspirin-induced changes in gastric function were evaluated. Conscious rhesus monkeys received a subcutaneous injection of sodium bicarbonate or aspirin (25, 50, 100, or 150 mg/kg) and sodium bicarbonate or 150 mg/kg aspirin subcutaneously plus oral sucralfate (25 mg/kg twice a day). Gastric emptying and fluid and H+ outputs were determined during a fasting period and after an 80-ml water load using a 99mTc-diethylenetriaminepentaacetic acid dilution technique. At the end of each study, the monkeys were gastroscoped to assess mucosal damage, which was ranked blindly on a scale of 0 to 5. Biopsy samples were taken from antrum and fundus for determination of prostaglandins and histological evaluation. All doses of aspirin significantly suppressed prostaglandins in both the antrum and fundus. In contrast, the aspirin-induced increase in gastric mucosal injury was dose dependent. Aspirin also produced a dose-dependent decrease in gastric emptying that was significantly correlated with erosions scores. When aspirin-induced lesions were prevented by sucralfate, the inhibition of gastric emptying was blocked during the fasting period and was attenuated following the water load. Acid secretion was also decreased significantly by aspirin. This action was not modified by sucralfate protection, suggesting that aspirin has a direct inhibitory effect on parietal cell secretion. These data show that mucosal damage contributes significantly to the aspirin-induced changes in gastric function. Moreover, prostaglandins may play a role in the control of gastric emptying, especially during early phase of the response to a water load.
The effects of chronic inflammatory lesions, induced by local injection of Freund's adjuvant into the rat hind limb, on omega 3 (peripheral type benzodiazepine) binding sites in the immune organs and leg infiltrate have been studied by autoradiography, using the specific photoaffinity ligand for omega 3 sites, 3H-PK 14105. In these arthritic rats, omega 3-site density in the thymus was about 2-fold greater than the values from control animals. Binding increases were similar in magnitude in the medulla and cortex. In contrast, omega 3 binding levels remained unchanged in the spleen. In the hyperplastic iliac lymph nodes, the morphological changes were accompanied by an increase in omega 3-site density in the proliferative centres and secondary follicles. In the inflammatory infiltrate of the leg an accumulation of omega 3-associated autoradiographic grains was observed over large multinucleated cells (possibly LE cells of Hargraves) and small thymocyte-like cells. Granulocyte-like cells located in the lumen of the vessels in the inflammatory lymph nodes and leg muscular infiltrate also had high amounts of autoradiographic grains. These findings demonstrate that in the inflammatory processes subsequent to the local injection of Freund's adjuvant, the activation of the immune system results in an increase in omega 3-site densities in immune organs and inflammatory lesions. This observation may be relevant to the proposed immunomodulatory role of these binding sites.