Biomedical subjects
B Lacour
Publications and source records attributed to B Lacour.
[Ability of isoelectric focusing to separate antitetanus antibodies in venous blood].
In a previous study, we have showed a great heterogeneity of antitetanus antibodies using polyacrylamide thin layer isoelectrofocusing. In this study, we have improved the resolution of the focused antitetanus antibodies by electrofocusing in sucrose density gradients, which is a suitable procedure for preparative work. After isoelectrofocusing the elution is performed according to any pH variation. For each fraction, we have determined pH, absorbance at 280 nm, protein level by method of Lowry, IgG concentration using immunonephelometric method and antitetanus antibodies concentration by radioimmunoassay. Furthermore, the purity of each fraction is verified by polyacrylamide slab gel isoelectrofocusing. It is concluded that the isoelectric point of antitetanus antibodies is alkaline range between 7.5 and 8.5. This precise knowledge could afford an opportunity for the industrial preparation of antitetanus antibodies.
Vitamin C and glucose measurement.
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[Urinary N-acetyl-beta-glucosaminidase as index of renal toxicity (author's transl)].
Urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG) has been studied in rats submitted to potentially nephrotoxic drugs (acetylsalicylic acid, gentamicin). Both drugs induced increase in NAG excretion which was reversible and dose-dependent. The date presented in this paper suggest that urinary NAG determination may have value as screening device for the study of nephrotoxic effects in experimental toxicology.
Carnitine improves lipid anomalies in haemodialysis patients.
51 chronic haemodialysis patients with hypertriglyceridaemia were given a daily oral dose of 2.4 g D,L-carnitine for 30 days to investigate a possible hypolipaemic effect. After 30 days' D,L-carnitine treatment the mean (+/- SEM) serum triglyceride concentration had decreased significantly from 3.50 +/- 0.39 to 2.87 +/- 0.27 mmol/l. Serum total cholesterol did not change. However, HDL cholesterol increased significantly from 0.89 +/- 0.05 to 1.35 +/- 0.07 mmol/l. This decrease in serum triglycerides and return of HDL cholesterol to normal levels in haemodialysis patients may be the result of correction of carnitine deficiency. Such treatment could reduce the risk factors for atherosclerosis and coronary-artery disease in uraemic patients.
[Unusual alpha-1-antitrypsin phenotype in a child with bronchial dilatation].
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Role of phosphate in the resistance to intestinal effects of parathyroid hormone in rats with chronic renal failure.
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Effect of acute ethanol loading on parathyroid gland secretion in the rat.
Acute ethanol loading in the rat induces hypocalcemia and hypermagnesemia. In addition, hypocalcemia is not corrected by exogenous PTH. In the rat the mechanism of these changes was investigated by measuring plasma immunoreactive parathyroid hormone (PTH). PTH was also measured in culture medium in which parathyroid glands were incubated. The addition of ethanol to test tubes did not interfere with PTH measurement. Absolute ethyl alcohol diluted to 50% with distilled water was administered via an intragastric tube. It failed to induce an increase in plasma immunoreactive PTH level. Similarly, it prevented an increase in plasma PTH after disodium EDTA injection. Thus in the presence of ethyl alcohol plasma PTH failed to increase in spite of a significant decrease of plasma calcium. In vitro studies showed that the decrease of calcium concentration of the medium from 1.50 to 0.75 mmol/l was associated with a 3 to 5 times increase in PTH secretion rate. This increase was suppressed when ethanol was added to the culture medium. In conclusion, ethanol loading via gastric tubing induced: 1) decrease in plasma calcium; 2) suppression of immunoreactive PTH secretion in the presence of hypocalcemia. It is postulated that the acute hypocalcemic effect of ethanol loading is mediated by a dual effect at the level of the bone and the parathyroid gland.
Effect of parathyroid hormone on jejunal electrolyte and water transport and cyclic nucleotide formation in the rat.
The effect of parathyroid hormone (PTH) on jejunal sodium, calcium, and water transport in situ was studied in thyroparathyroidectomized rats using the ligated loop instillation model. The acute administration of bovine PTH to the animals induced a significant increase in net sodium and water secretion when compared to animals receiving the vehicle only. This effect was due to an increase in unidirectional mucosa-to-lumen sodium flux. However, no change of calcium fluxes was observed. This acute in vivo effect on PTH could not be explained by an action via the adenyl or guanyl cyclase systems since bPTH failed to induce changes of cAMP or cGMP formation in isolated jejunal cells. Thus, other so far not elucidated mechanisms of action must be involved.
Plasma vitamin D metabolites in a patient with sporadic hypophosphataemic osteomalacia (adult-onset type).
Sporadic hypophosphataemic osteomalacia (adult-onset type) was demonstrated in a 40-year-old man on the basis of severe osteomalacia, hypophosphataemia, hyperphosphaturia and glycinuria. Plasma immunoreactive parathyroid hormone (iPTH) concentration was 9.3 ng prot./ml (normal range: 4-8 ng prot./ml). Plasma 25-hydroxy-vitamin D and 24,25-dihydroxy-vitamin D concentrations were 11 and 2.4 ng/ml respectively. Basal 1 alpha,25-dihydroxy-vitamin D concentrations were slightly elevated (116 and 96 pg/ml) and increased to 240 pg/ml after 3 days on a low-phosphorus diet. The patient was put on oral treatment with 25-hydroxycholecalciferol (100 microgram per day) and phosphorus (1500 mg per day). On the 4th month on treatment, a clinical improvement was apparent. Plasma 25(OH)D was 44 ng/ml, plasma 1,25(OH)2D was 256 pg/ml. However, plasma phosphorus remained low (0.77 mmol/l). On the 9th month of treatment a radiological improvement was evident despite a persistent hypophosphataemia (0.68 mmol/l). These facts suggest in our patient the existence of a vitamin D-independent renal phosphorus leak.
[Evidence for a glucose-dependent renal phosphorus leak in normo- and hypercalciuric stone-formers (author's transl)].
Changes in phosphatemia and in maximum renal threshold phosphate concentration (TmP/GFR) have been measured before and 45 and 75 min after oral ingestion of 75 g of glucose in 10 hypercalciuric lithiasic patients (HCI), 8 normocalciuric lithiasic patients (NCI) and 7 control subjects. After glucose ingestion, whereas plasma phosphorus decreased in all 3 groups, TmP/GFR decreased significantly in HCI and NCI but not in controls. A slight increase in calcium excretion was noted in the subjects with HCI and NCI after glucose load. Plasma concentration of 1,25(OH)2D was measured in 8 HCI and 7 controls before and after glucose: there was a significant increase in HCI 45 min after glucose and no modification in control subjects. These results show that a glucose load causes a decrease in TmP/GFR in lithiasic subjects. The results demonstrate the existence in lithiasic patients of perturbations of renal handling of phosphates which could, at least in part, be related to glucose metabolism. This trouble could contribute to the elevation of the serum 1,25(OH)2D observed in these patients.
[Efficacy of a French hepatitis B vaccine. Results of a multicenter clinical trial, using a placebo, with double-blind randomized administration].
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Plasma 1,25(OH)2D3 and iPTH in transplanted adults with persisting hypophosphataemia.
Hypophosphataemia is a common finding among kidney transplanted patients [1,2]. In a previous study in kidney transplanted children with plasma creatinine below 1.1mg/dl, we demonstrated [3] a negative correlation between plasma phosphorus and 1 alpha, 25-dihydroxyvitamin D3 (1,25(OH)2D3), the renal hormonal form of vitamin D. No such correlation was apparent in children with minimal increase in plasma creatinine. The aim of the present investigation carried out in hypophosphataemic transplanted adults was two-fold: 1) to determine whether hypophosphataemia results from persisting hyperparathyroidism or from a renal phosphorus leak, or both, and 2) to study the relation between plasma phosphorus, iPTH and 1,25(OH)2D3 in these patients.
Improvement of post-heparin lipolytic activity (PHLA) after haemofiltration, in uraemic patients.
UNLABELLED: The decrease of serum PHLA in uraemic patients has been attributed to toxic effects of 'middle molecules' on lipoprotein lipase. Haemofiltration could improve PHLA by increasing 'middle molecule' clearance. Serum triglyceride concentration decreased and PHLA improved in three uraemic patients who received haemofiltration during three weeks as the initial treatment schedule. Activated PHLA of a healthy subject failed to be inhibited by uraemic sera and uraemic plasma ultrafiltrates obtained in vitro using polyacrylonitrile and cuprophane membranes. CONCLUSION: haemofiltration is able to improve PHLA and to restore normal serum triglyceride concentrations. The reported toxicity of uraemic serum may affect metabolic steps preceding the activation of the circulating lipolytic enzymes.
[Hyperparathyroidism and anemia: experimental study in the rat (author's transl)].
Red blood cell (RBC) production has been explored in hyperparathyroid as compared to normal rats. The hyperparathyroid state was obtained by feeding the rats a calcium-deficient diet during 30 days. A significant decrease (p less than 0.001) in reticulocyte count and in erythrocyte 59Fe incorporation was observed in hyperparathyroid rats when compared to control animals. A comparable inhibition of erythrocyte 59Fe incorporation in hyperparathyroid rats was found when the study was performed after stimulating bone marrow activity by acute arterial hemorrhage. These results of decreased RBC production using a model of endogenous hyperparathyroidism could be confirmed in additional experiments using a model of exogenous hyperparathyroidism. In this model, the rats received either parathyroid extract (3 x 10 USP/day during 8 days) or vehicle only. Again, a decrease in erythrocyte 59Fe incorporation was observed in hyperparathyroid animals when compared to control animals. It is concluded that the hyperparathyroid state is accompanied by a decrease of RBC production in the rat. It is probable that a similar pathogenesis underlies the anemia of patients with primary or secondary hyperparathyroidism.
Successful parathyroid gland autotransplantation in the rat using a simplified cryopreservation technique.
In the present work a simplified technique for cryopreservation of parathyroid glands was compared to the generally used technique needing a programmed freezer. Four groups of rats had total parathyroidectomy. In two of them the glands were cryopreserved and reimplanted 10 days after ablation. The other two groups had, respectively, immediate parathyroid autotransplantation and no autotransplantation. During a follow-up of 60 days, plasma calcium remained low and plasma phosphorus elevated in all aparathyroid rats of the last group. In the group of rats with immediate parathyroid reimplantation, both mean plasma calcium and phosphorus values rapidly returned to the normal values observed before operation. In the rats that had the simplified parathyroid cryopreservation technique, mean plasma phosphorus also returned to the normal range and mean plasma calcium to nearly normal. However, in the group of rats with the classical cryopreservation method, the mean plasma calcium and phosphorus levels remained far from normal in the majority of animals. It was concluded that parathyroid glands of the rat could be successfully autografted after previous freezing using a simplified cryopreservation technique. The results obtained were comparable with, even though not as perfect as, that observed after immediate autotransplantation. If suitable for human parathyroid gland fragments, this technique would allow a more general application of parathyroid tissue cryopreservation.
[Idiopathic hypercalciuria: effects of acute phosphorus deficiency (author's transl)].
Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.
Early stimulation of alkaline phosphatase activity in response to 1 alpha, 25-dihydroxycholecalciferol.
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