Biomedical subjects
Publications and source records attributed to B Mallet.
We report 2 cases of aluminium sensitivity in adults. Each time, the means of sensitization was the inoculation of aluminium-precipitated pollen or dust extracts for hyposensitization. We conclude that aluminium allergy is not exceptional and that in these cases one can observe allergic reactions to the Finn Chamber tests.
In serum from 8 severely burned patients, haptoglobin (Hp), alpha 1-acid glycoprotein (AG) and alpha 1-antitrypsin (AT) were found to be increased by factors of 5, 6 and 2 respectively. Ceruloplasmin (Cp) was slightly decreased. In order to appreciate possible modifications to the structure of their attached N-glycans, whole sera were fractionated on concanavalin A (Con A)-Sepharose and respective glycoproteins measured by laser nephelometry using a monospecific antiserum. In the serum from normal as well as burned patients Hp was almost entirely bound to the immobilized lectin (but eluted with 300 mmol/l alpha 1-methylglucoside) and Cp was bound at about 92%. For AG, in contrast, the fraction without affinity for Con A, 25% in normal serum, decreased to 5% in patients, whereas the retained species increased in proportion. A very weakly reactive fraction (which was only retarded and eluted without alpha-methylglucoside) amounted to 72% in both types of serum. When reduced and alkylated, this intermediate fraction gave rise to both non-retained and retained species always in a proportion of about 1/3. On the whole one concludes that there is a significant shift for AG in burned patients towards species enriched in bi-antennary (Con A-reactive) glycans. For AT a minor part was not recognized by the lectin and about 27% was retarded. The latter, which increased in burned patients, gave rise mainly to retained species after reduction and alkylation. This again suggests a shift to bi-antennary glycans.
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Prealbumin was determined by radial immunodiffusion and laser immunonephelometry methods in serum or plasma from 86 adult subjects. Both methods were reliable in physiologic prealbumin range but immunonephelometry only was reliable for lower levels. Physiologic prealbumin level was 346 +/- 67 mg/l in adult males and 319 +/- 48 mg/l in adult females; no difference was noted for retinol binding protein (60 +/- 14 mg/l). When prealbumin and retinol binding protein levels were low, no close correlation was noted in their variations.
A method is reported for isolation and purification of human ceruloplasmin and apoceruloplasmin from serum. It involves a rapid and mild procedure by ion exchange chromatography on DEAE-Sephacel using a pH and ionic strength concave gradient. It was applied to serum of patients with oculocutaneous albinism, Wilson's disease, Menkes' disease and pregnant women. The ceruloplasmin obtained by this method is undegraded, and homogeneous by physico-chemical and immunochemical analysis.
Copper is an essential dietary component, being the coenzyme of many enzymes with oxidase activity, e.g. ceruloplasmin, superoxide dismutase, monoamine oxidase, etc. The metabolism of copper is complex and imperfectly known. Active transport of copper through the intestinal epithelial cells involves metallothionein, a protein rich in sulfhydryl groups which also binds the copper in excess and probably prevents absorption in toxic amounts. In hepatocytes a metallothionein facilitates absorption by a similar mechanism and regulates copper distribution in the liver: incorporation in an apoceruloplasmin, storage and synthesis of copper-dependent enzymes. Metallothioneins and ceruloplasmin are essential to adequate copper homeostasis. Apart from genetic disorders, diseases involving copper usually result from hypercupraemia of varied origin. Wilson's disease and Menkes' disease, although clinically and pathogenetically different, are both marked by low ceruloplasmin and copper serum levels. The excessive liver retention of copper in Wilson's disease might be due to increased avidity of hepatic metallothioneins for copper and decreased biliary excretion through lysosomal dysfunction. Menkes' disease might be due to low avidity of intestinal and hepatic metallothioneins for copper. The basic biochemical defect responsible for these two hereditary conditions has not yet been fully elucidated.
The present study was carried out on 76 industrial workers divided in four working sections and exposed to cadmium and copper fumes and/or dust for periods ranging from 2 to 32 years. There were no signs of chronic copper poisoning associated with long term industrial exposure. In all cases indeed, normal blood copper level (near 15,5 mumol/l) and normal urine copper level (53 mumol/mol creat) were found. Moreover, in the plasma, the copper/ceruloplasmin ratio was approximately 8, with both normal values in micromoles. The great elimination of copper in feces assured probably the copper homeostasis. On the contrary, particularly near the furnace, the atmospheric cadmium level was to be considered; 9 out of 11 furnacemen who worked during more than 5 years showed neither respiratory or hepatic failure nor bone mineral metabolism disturbances, in spite of urine cadmium level greater than 10 mumol/mol creat, "early warning" for renal damage. There was no significant correlation between urine and blood cadmium levels when the latter was greater than 4,5 micrograms/l (40,2 nmol/l). The high beta 2 microglobulin level for 66 p. cent of furnacemen, was the indicator of tubular damage. Therefore the urine cadmium in combination with beta 2m should be determined to detect early effects of cadmium in exposed workers.
The control of the air pollution by cadmium in Marseille was realized between July 1st 1977 and June 30 1979 by determining the metal in the air dust by atomic absorption spectrophotometry without flame. The samples were taken on eight different stations located in the urban-center and in the suburbs. The atmospheric levels of cadmium in Marseille are low but a note-worthy increase was noticed from september 1978. A principal components analysis of the data compared with these obtained with other atmospheric pollutants, revealed the particular characteristic of cadmium in Marseille, which seems to be bound neither with the pollutants issued from motor vehicles, nor with zinc of which it is yet an impurity. However vigilance is indispensable against the environmental contamination by cadmium in consideration of its potential risks for the health.
Three major forms CI, CII and CX and the minor component CI1v of ovine erythrocyte carbonic anhydrase have been identified in the ethanol chloroform extract of the hemolysate by electrophoresis on cellulose acetate and isoelectrofocusing. Isolation of the four forms was achieved by chromatography on DEAE-Sephadex A-50. Comparative studies suggest that: (1) form CI1v is a modified form of CI, (2) form CX is CI plus glutathione and (3) forms CI and CII are isoenzymes which differ in their primary structure by one Lys leads to Thr substitution 35 residues from the N-acetylated terminus.
Limiting viscosity numbers of bovine and ovine erythrocytes carbonic anhydrase variants were calculated by the objective method of comparing viscosimetric data obtained from low-activity-human erythrocyte carbonic anhydrase and its natural variant. Shifts of mobilities and isoelectric points are shown for all species variants, but variations of limiting viscosity numbers were only detected for human and bovine variants. Results of the study are consistent with the observation that variants arise by deamidation of erythrocyte carbonic anhydrases, and that deamidation is responsible for changes in structure and hydration (i. e. "conformational" modifications). Thus, all the variants so far investigated are stable conformational variants or erythrocyte carbonic anhydrases.
Erythrocyte superoxide dismutase is a cuproprotein displaying increased activity in cases of trisomy 21. In this study, the three erythrocyte copper fractions were compared at constant serum copper levels in children with and without trisomy 21. The labile erythrocyte copper level was found to be identical in both groups of children. Total erythrocyte copper, especially the stable fraction, was increased in cases of trisomy 21. The approximately fifty per cent ob served increase correlates with the augmented superoxide dismutase activity related to the presence of an extra chromosome 21. Measurement of the stable erythrocyte copper fraction could constitute an indirect method for evaluating superoxide dismutase activity.
The two major forms of bovine erythrocyte carbonic anhydrase have been designated as CI and CII because their high activity of the C type. Separation of both forms and isolation of CI from the ethanol chloroform extract of the hemolysate were obtained by either column chromatography on DEAE-cellulose DE 23 or on DEAE-sephadex A-50. But pure preparations of the CII form were only obtained from DEAE-sephadex A-50 which separated CII from a minor component CIv1. Comparative studies of the CI and CII forms and of the minor component CIv1 strongly suggest that CIv1 is a conformational variant of CI and CII are genetic variants differing at least in their primary structure by one Arg yields Gln substitution 56 residues from the N-acetylated terminus. Based on the large variability of the proportion of the two isozymes in heterozygous individuals, the modality of the inheritance of these enzymes is discussed.
The anti-inflammatory effect of natural glucocorticoids is often overlooked, as shown by these two cases of inflammatory rheumatism flare-up which occurred after surgical treatment of Cushing's syndrome. The disorder in the first case was exacerbation of a probable rheumatoid arthritis; in the second case an unlabelled inflammatory rheumatism appeared in a context of postoperative corticotropic deficiency. In both cases a purely substitutive hydrocortisone therapy resulted in dramatic regression of the articular symptoms. It is well known that rheumatismal manifestations may occur in patients with slow adrenal failure. The determinant factor seems to be a glucocorticoid deficiency, either isolated or associated with others, since cortisol exerts and anti-inflammatory activity. In patients with corticotropic deficiency following surgical treatment of Cushing's disease, the endogenous corticosteroid therapy of hypercortisolism is interrupted, allowing the aggravation or emergence of inflammatory rheumatism.
Growth hormone and growth factors have been implicated in the pathogenesis of diabetic retinopathy. Hypophysectomy has been proposed as a treatment for proliferative diabetic retinopathy unresolved by panretinal photocoagulation (PPC). SMS 201-995, a long acting somatostatin analogue which slows down growth hormone secretion, may provide a non-invasive therapy for these rare cases. To assess this possibility, we studied the feasibility and efficiency of long-term SMS 201-995 treatment in diabetics. SMS 201-995 was injected subcutaneously with a continuous pump system at a dose of 400 micrograms/d into 4 insulin dependent diabetic patients suffering from proliferative diabetic retinopathy progressing despite a pan-photocoagulation. The mean age of these patients was 29 +/- 3 years and mean disease duration 18 +/- 3 years. Treatment periods lasted from 6 to 20 months (mean 15 months). Mean 24-hour growth hormone levels decreased by 57% after only one month of treatment (7.4 +/- 1.9 mU/l to 3.2 +/- 0.9 mU/l). The decline continued up to the third month. After the sixth month, signs of resistance to the drug were noted. The frequency of 24-hour GH peaks over 10 mU/l followed a parallel pattern. No rebound was observed when the treatment was progressively discontinued. In 2 patients neovascularization stopped. In the other 2 the process regressed. In all treatment had beneficial effects on the retina. Overall visual acuity improved (7.8 +/- 0.8/10e vs 5.5 +/- 0.8/10e). These effects were obtained within 3 to 6 months. Glycosylated haemoglobin levels did not change (8.8 +/- 1.3% to 9.0 +/- 0.8%). Insulin doses decreased 41% (46.5 +/- 1.7 U/d to 27.3 +/- 3.0 U/d). No severe hypoglycaemia occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
Urinary iodine is largely measured in microtiter plates by a colorimetic ceric-arsenic assay based on the Sandell-Kolthoff reaction. However, a preliminary digestion step is necessary and requires a particular care not only to transform all the iodo-compounds into iodide but also to prevent the formation of substances liable to the disturb of the subsequent redox reaction. In the present study we tested three types of digestion processes, among them two conventional methods (ammonium persulfate and chloric acid) and a new one using combined nitric acid/hydrochloric acid. Results showed that important errors may be obtained with the chloric acid and the ammonium persulfate digestions. These discordances were the consequence of either an incomplete transformation of iodo-compounds or an oxidation of iodide into molecular iodine or a colorimetric assay disturbance due to a residual yellow coloring. No problems were evidenced with the combined nitric acid/hydrochloric acid process, which remains the better alternative to evaluate the urinary iodine. It could also provide a particularly useful means of assessing the iodine status in epidemiological studies.