Mapping of a gene for the Mr 48,000 tubular basement membrane antigen in the rat.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to P Mahieu.
Explore the source record for details and available documents.
In 10 adult patients acutely intoxicated with methanol, the base deficit and the total blood CO2 were highly correlated with blood formate level. No correlation was found between the same parameters and blood methanol level. Formate production is the main cause of acidosis in the early stages of methanol poisoning. The association of a latency period before treatment exceeding 10 hours and a blood formate level above 0.5 g/l (11.1 mmol/l) is predictive of severe methanol poisoning possibly leading to permanent sequelae.
Anti-alpha-galactosyl antibody (a-Gal Ab) is a human natural antibody belonging to the IgG class, found in high titres in all normal sera regardless of blood group, and specifically recognizing alpha (1-->3)-linked galactosyl residues. We have observed by radioimmunoassay, ELISA, passive haemagglutination and immunofluorescence blocking studies that affinity-purified a-Gal Ab reacted with mouse laminin, but not with the other mouse basement membrane proteins tested; it was able to fix complement in vitro. When injected intravenously into mice, the a-Gal Ab was found to mainly accumulate in kidneys, liver, spleen and lungs. No acute respiratory distress syndrome was observed shortly after the i.v. injection of 100 or 200 microg of antibodies. These doses of a-Gal Ab were also unable to induce acute glomerular injury. However, in primary cultures, the a-Gal Ab (100 or 200 microg per ml of medium) was shown to impair the attachment of mouse glomerular epithelial cells to mouse laminin and to elicit complement-dependent cell damage. The data indicate that the a-Gal Ab can interact in vitro and/or in vivo with alpha (1-->3)-linked galactosyl residues exposed on murine laminin or on murine cultured glomerular epithelial cells. Although this antibody fails to be pathogenic when administered at low doses in the intact animal, similar doses can alter some metabolic properties of these cells in vitro.
We report the case of a patient who presented with cardiac and neurological signs of lithium toxicity as the result of an association with amitriptyline. These manifestations disappeared spontaneously as medication was stopped. We review the possible physiopathological mechanisms that could account for these adverse effects.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The concentration of retinol-binding protein (RBP) in urine was determined in 20 healthy individuals and 119 patients with various renal diseases involving tubular or glomerular dysfunction. The sera from 4 healthy individuals and 33 patients were chromatographed on Sephadex G-75 to measure the concentration of free (i.e. not prealbumin-bound) RBP. In healthy individuals, the mean concentration of free RBP in serum was 5.8 mg/l and represented 14% of total RBP; the renal clearance and the fractional tubular uptake of free RBP averaged 0.032 ml/min and 99.97%, respectively. In patients, the concentration of free RBP and the percentage of free RBP in serum were on logarithmic scales inversely correlated with the endogenous creatinine clearance (r = -0.80 and -0.76) and increased in parallel with the serum creatinine (r = 0.67 and 0.66) and beta 2-microglobulin concentrations (beta 2-m, r = 0.76 and 0.89). The semi-logarithmic plot of urine versus serum concentration of free RBP suggests a renal threshold for the tubular reabsorption of this protein at a concentration of about 25 mg/l in serum. The existence of this threshold is confirmed by the relationship between urinary RBP and serum beta 2-m showing that urinary excretion of RBP is invariably high when the serum level of beta 2-m exceeds 5 mg/l. The latter value corresponds precisely to the renal threshold for the tubular reabsorption of beta 2-m. The corresponding value for free RBP derived from the relationship between both proteins is 24 mg/l.(ABSTRACT TRUNCATED AT 250 WORDS)
We reviewed the cardiac emergencies that occurred during or soon after pregnancy and required admission in an intensive care unit. The study sample consisted of 22248 pregnant women representing the whole obstetrical population collected from 3 hospitals over a ten-year period. Among the 88 patients admitted to our ICU during this decade, only 5 suffered from a specific cardiac disorder. Acute pulmonary edema was the common clinical presentation in the 4 cases reported. Despite the severity of cardiac involvement on admission none had previous evidence of heart disease that could have heralded acute left ventricular failure. From these observations it can be concluded that preexisting cardiovascular disease and circulatory changes related to pregnancy should no longer be regarded as the unique contributors to the development of severe heart failure during pregnancy.
We evaluated the effect of a cimetidine continuous infusion (2 g in 24 h) on the intragastric pH of 16 critically ill patients (11 men, 5 women, mean age 45 years). During the 24 h pre-trial period and the subsequent 24 h cimetidine infusion, an intragastric combined electrode was placed in the fundus and the pH recorded with a portable pH module and data collection unit. In each patient, the cimetidine infusion induced a prolonged rise of intragastric pH. For all patients the mean percentage of readings above pH 4.0 was 11% pre-trial and 75% during the cimetidine 24 h infusion (p less than 0.001). The percentages of readings above 5.0, 6.0, 7.0 were also significantly higher during infusion than pre-trial in the 16 patients. After starting the cimetidine infusion, there was a concomitant rise of median plasma cimetidine and median intragastric pH in the 7 patients studied. After 6 h, median plasma cimetidine remained above 1 mcg/ml. These results and recent data from the literature suggest that in critically ill patients a continuous infusion of cimetidine might prevent stress ulcerations better than bolus injections by maintaining intragastric pH above 4.0 during longer time intervals.
Using an original technique permitting repeated plasma exchange in the rat, we have tested this therapeutic approach in animals actively immunised with horseradish peroxidase, and in rats with HgCl2-induced autoimmune glomerulonephritis. Plasma exchange effectively removes circulating IgG anti-horseradish peroxidase antibodies from the sera of immunised rats. When applied to the model of HgCl2-induced antiglomerular basement membrane glomerulonephritis in Brown-Norway rats, this technique is also remarkably effective. In these rats, proteinuria is abolished during the plasma exchange treatment period and no circulating antiglomerular basement membrane antibodies can be detected. These antibodies are, however, found in the ultrafiltrates of exchanged rats. Serum IgE, characteristically elevated in HgCl2-treated rats, is also markedly diminished in exchanged rats. Control rats treated with infusions of fresh frozen plasma or with heparin alone did not show any improvement in disease severity. These results suggest that plasma exchange alone can attenuate antiglomerular basement membrane nephritis in HgCl2-treated rats. This observation may be of relevance for the treatment of human antiglomerular-basement membrane-mediated glomerulonephritis.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Nine patients with severe Graves' ophthalmopathy were treated by intensive plasma exchange, followed by immunosuppression. Severity of ocular involvement and response to therapy were evaluated by numerical scoring (ophthalmopathy index) and clinically. Serum thyroid stimulating immunoglobulins (TSI) and urinary excretion of glycosaminoglycans (GAG) were measured immediately before and immediately after plasmapheresis. Plasma exchange was rapidly accompanied by marked clinical improvement in 8/9 patients. The most marked effects were on soft tissue involvement, proptosis, intraocular pressure, and visual acuity. The ophthalmopathy index decreased from 9.7 +/- 4.1 to 5.7 +/- 2.2 (p less than 0.001) after plasmapheresis. Serum TSI levels were initially elevated in 6 patients and remained positive in 3 patients after treatment. Urinary GAG excretion was initially 2- to 12-fold normal levels and was decreased by 60%. After plasmapheresis, patients received immunosuppressive drugs for 3-6 months. The follow-up period, after withdrawal of drugs, ranged from 5 to 38 months with a median of 17 months. The ocular condition remained stable in 6 patients. Three patients had a relapse 1 year after plasmapheresis: they were treated a second time by plasma exchange with subsequent improvement. In conclusion, intensive plasma exchange provided prompt and effective improvement in patients with severe progressive Graves' ophthalmopathy. This therapeutic procedure, followed by immunosuppression, gave long lasting results. Relapses were responsive to plasmapheresis therapy. The data suggest that plasma exchange may represent the best primary treatment for severe progressive Graves' ophthalmopathy.
Interactions of malignant or non-malignant human and rodent cells with the vascular wall were studied using perfused human umbilical cord veins. The integrity of perfused endothelium was confirmed by morphological and functional criteria. Highly malignant cells in vivo adhered to the endothelial cells, as shown by scanning electron microscopy. The specific attachment of radiolabelled malignant cells to the whole vein was already maximal within 30-60 min and remained stable for perfusion flow rates ranging between 10 and 60 ml/min. It increased proportionally to the number of cells infused and could be modulated by human platelets, human fibronectin and rabbit anti-laminin antibodies. In contrast, the binding of human or rodent non-malignant cells in vivo, of human red blood cells and of human platelets to the endothelial cells was negligible under similar experimental conditions. This perfusion system therefore represents a new model for elucidating some mechanisms involved in tumour cell arrest in vivo.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.