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Biomedical subjects

J C Legrand

Publications and source records attributed to J C Legrand.

At least 91 records · Page 5Linked to original sources
PubMed1983

[Catecholamines and their derivatives in the study of pheochromocytoma].

The biochemical diagnosis of pheochromocytoma is essentially based on the plasma and urinary levels of catecholamines and their derivatives, the metanephrines and vanyl-mandelic acid. The advantages and disadvantages of these investigations are reviewed, especially as regards the specificity and sensitivity of each test. The measurement of urinary metanephrine is the best test as its excretion is relatively higher, and it is rarely normal. The measurement of plasma catecholamines is more difficult but gives satisfactory results, but experience so far is limited.

Adrenal Gland Neoplasms↗
PubMed1982

CCK-8-Immunoreactivity distribution in human brain: selective decrease in the substantia nigra from parkinsonian patients.

The regional distribution of immunoassayable CCK-8 was determined in 12 regions of control and parkinsonian human brain, with specific attention to the possible regional coexistence of CCK-8 with dopamine. In Parkinson's disease, CCK-8-I levels were only decreased in the substantia nigra where dopamine cell bodies lie, and not in striatal and corticolimbic dopamine projecting areas. Our results suggest that the major proportion of dopaminergic neurones degenerated in Parkinson's disease may not contain the CCK-8 peptide.

Appetite Depressants↗
PubMed1982

Microtopography of methionine-enkephalin, dopamine and noradrenaline in the ventral mesencephalon of human control and Parkinsonian brains.

The topographical distributions of Met-enkephalin, dopamine and noradrenaline were determined in serial frontal sections of human substantia nigra (pars compacta and pars reticulata) and ventral tegmental area. Met-enkephalin was identified by Biogel and thin layer chromatography and assayed by a specific radioimmunoassay. In the substantia nigra (pars compacta and pars reticulata), the levels of Met-enkephalin increased progressively from the rostral to the caudal part of the structure. This pattern closely resembled that of dopamine levels, particularly in the pars compacta. Noradrenaline levels in the substantia nigra and those of Met-enkephalin, dopamine, and noradrenaline in the ventral tegmental area, exhibited only limited fluctuations from the anterior to the posterior part of each structure. Highly significant decreases in Met-enkephalin, dopamine and noradrenaline levels were observed in the substantia nigra and ventral tegmental area of Parkinsonian brains. This observation, together with the close topographical association of dopamine and Met-enkephalin in the substantia nigra, further supports the likely existence of important functional relationships between dopaminergic and enkephalinergic neurons in the human brain.

Aged↗
PubMed1982

Myelin basic protein in CSF and blood. Relationship between its presence and the occurrence of a destructive process in the brains of encephalitic patients.

Serum and CSF levels of myelin basic protein (MBP) were measured in 50 patients with encephalitis of various origins and severity. In nearly 50%, the CSF samples were found to display immunoreactivity of MBP. Positivity was found to be correlated with the severity of the clinical signs. More precisely, it corresponded to cases with suspected extensive brain destruction. No relationship could be observed with the cause of disease. Positive tests of sera were infrequent, even from patients whose CSF was rich in MBP. Longitudinal studies performed on 20 patients who were serially investigated during periods ranging from three weeks to 18 months demonstrated that after an attack, MBP liberation into the CSF persists for one to three weeks. The MBP assay should serve as an index for destruction of nervous tissue.

Encephalitis↗
PubMed1980

Relation between energy metabolism in mitochondria and conversion of 18 hydroxycorticosterone to aldosterone in adrenals.

The purpose of this study was to see whether there was any link between conversion of 18 hydroxycorticosterone to aldosterone and mitochondrial energy metabolism. In vitro incubations of duck adrenal mitochondria with 18 OH B were used in this study. Results show that 18 oxidation is inhibited by compounds blocking electron transport (antimycin A, cyanide, rotenone, amytal). Inhibition induced by cyanide and antimycin A is reversed with ATP. 2,4 dinitrophenol, oligomycin and DCCD inhibit 18 oxidation but guanidine stimulate this reaction. Thus aldosterone synthesis from 18 OH B depends on energy metabolism in mitochondria. This is a very new aspect related to the last step of aldosterone synthesis.

18-Hydroxycorticosterone↗
PubMed1980

Radioimmunoassay of the myelin basic protein in biological fluids, conditions improving sensitivity and specificity.

The radioimmunoassay (RIA) for myelin basic protein (MBP) in biological fluids was reassessed in order to improve its sensitivity and eliminate some interferences. By using the preincubation technique and the charcoal-dextran-horse serum mixture for the separation step, the detection limit could be lowered to 200 pg/ml for cerebrospinal fluids (CSF), amniotic fluids (AF) and nervous tissue extracts and 600 pg/ml for sera. The RIA could be used directly on CSF, AF and nervous tissue extracts. Sera, however, had to be heated in citrate buffer at 100 degrees C in order to discard interfering material. The present method is 10 to 20 times more sensitive than others previously published. Moreover, it can be applied to amniotic fluid. The biological fluids had to be promptly frozen to avoid degradation of MBP.

Amniotic Fluid↗
PubMed1979

[Cytochrome P-450 and transformation from 18-hydroxycorticosterone to aldosterone].

The authors have studied the in vitro conversion of 18 hydroxycorticostérone to aldosterone (18 oxidation) by duck adrenal subcellular fractions. Considering the new hypothesis about the mechanism of this step (hydroxylation mechanism) the authors have investigated a possible relationship between this reaction and cytochrome P450. With experimental conditions described, data show that metyrapone, a cytochrome P450 competitive inhibitor does not inhibit 18 oxidation. In contrast, 18 oxidation is inhibited by spirolactones (spironolactones, canrenone, potassium canrenoate). These compounds act at the cytochrome P450 level but have also an uncoupling effect which has been recently discovered. The effects of metyrapone and spirolactones on 18 oxidation as well as the different behaviour between biologicaly and organically synthetised 18 hydroxycorticosterone allow us to propose hypotheses for the mechanism of this step.

18-Hydroxycorticosterone↗
PubMed1978

Circadian and circannual rhythms in plasma hormones and other variables of five healthy young human males.

Every other month (plasma) and every month (urine) circadian rhythms were documented during the course of 14 months. Annual changes were validated in the 24 h mean of: plasma FSH (annual crest time: February), LH (March), thyroxine (September), cortisol (February), renin activity (April), testosterone (October), urinary 17-hydroxycorticosteroids (March), aldosterone (March), potassium (May) as well as sexual activity (September) [self-recorded daily]. Plasma prolactin did not show an annual variation. In addition, annual changes in the circadian acrophase (crest time location in the 24 h scale) occurred for some of the documented variables: plasma thyroxine, cortisol, renin activity, testosterone, urinary aldosterone and potassium.

17-Hydroxycorticosteroids↗
PubMed1978

[Antialdosterones and enzymes of the adrenal gland].

With subcellular fractions of animal adrenals, the authors have looked for the effect of antialdosterones on different aspects of adrenal metabolism (steroidogenesis, some enzymes of intermediary metabolism, mitochondrial respiration). Antialdosterones act on mitochondrial respiration by inducing an uncoupling effect. Nature of this uncoupling cannot yet by precised. Antialdosterones inhibit steroidogenesis with concentrations corresponding to blood concentrations observed during treatment with these compounds. This inhibition could explain the annulation of hyperaldosteronism secondary to sodium loss and kaliemic replenishment. This enhance the interest of antialdosterones over other diuretics.

Adrenal Cortex Hormones↗
PubMed1978

[Effect of spironolactones on aldosterone synthesis and adrenal metabolism].

The authors study antialdosterones action on several enzymatic systems in subcellular fractions of animal adrenals. They report an inhibition of aldosterone synthesis located at the corticosterone 18 hydroxylation step but also at the following step of oxydation of 18 hydroxycorticosterone into aldosterone (in the duck as well as in the sheep). In contrast, these drugs do not modify the activity of several enzymes not involved in aldosterone biosynthesis. In addition, anti-aldosterones have decoupling action on mitochondrial respiration. This effect, observed by many authors on adrenal mitochondria can be considered as an illustration of competition between two electron transport chains (phosphorylative oxydation and hydroxylation) and not as a toxic effect. These in vitro results are of clinical interest as they are obtained with antialdosterones concentrations similar to that found in plasma of subjects treated with these diuretics and could explain the absence of secondary hyperaldosteronism in these subjects.

Adrenal Glands↗
PubMed1977

Comparative study of urinary excretion rates of para-hydroxy-mandelic acid, homovanillic acid, vanylmandelic acid in cirrhotic patients with and without encephalopathy.

A comparative study of urinary excretion of octopamine, dopamine, and noradrenaline catabolic products, respectively parahydroxymandelic acid (PHMA) homovanillic acid (HVA) and vanylmandelic acid (VMA) was carried out in 27 cirrhotic patients with (11) and without (16) porto-systemic encephalopathy (P.S.E). PHMA, HVA and VMA were significantly higher in patients with PSE, and there was a positive correlation between PHMA and HVA, and between PHMA and VMA. Higher excretion of PHMA in patients with PSE strongly suggests an increased metabolism of octopamine. HVA and VMA increased excretion, and the positive correlations could be explained by the depletion of stored dopamine and noradrenaline. These observations support the hypothesis that octopamine acts as a false neurotransmitter, and the resulting depletion of dopamine and noradrenaline could explain the neuropsychic phenomena of PSE, and the awakening effect of L. Dopa treatment.

Aged↗
PubMed1977

Radioimmunological determination of urinary tetrahydroaldosterone.

A method is presented for radioimmunological determination of 3alpha, 5beta-tetrahydroaldosterone. It is based upon the reactivity of this steroid with an antiserum induced by the 3-carboxymethyloxime of 18, 21-aldosterone diacetate conjugated with bovine serum albumin. One hundred microliters of urine enzymatically hydrolyzed with an helix pomatia preparation, containing tritiated tetrahydroaldosterone for the yield calculation, were extracted with dichloromethane and chromatographed on a small celite column. The yield after extraction and chromatography was 64 +/- 17%. The radioimmunological determination was carried out in a conventional manner. The method is specific, sensitive (10 pg/tube), exact, reproducible, very simple and extremely rapid. The results showed good agreement with values given by a colorimetric method (p less than 0.001). The median value measured in 45 healthy adult subjects under standard sodium diet was 53.3 microgram/24h (95 % of the population within a 16.6 to 131.1 microgram/24h range). In 78 cases of adrenocortical insufficiency, 60 cases of obesity and 28 cases of hypokalemia, the median values (and the ranges : microgram/24h) were respectively 7.7 (1.0 - 51.0), 80.9 (17.0 - 503.0) and 64.3 (8.0 - 181.0). In 330 hypertensive patients the excretion of tetrahydroaldosterone exceeded the normal range in 115 cases (35%) with a median of 199.7 microgram/24h (131 to 620 microgram/24h).

Aldosterone↗
PubMed1977

[Enzymatic character and subcellular localization of the transformation reaction of 18 hydroxycorticosterone to aldosterone].

The authors study in vitro the conversion of 18 hydroxycorticosterone into aldosterone in duck adrenal subcellular fractions. The enzymatic nature of this conversion is studied by classical enzymologic tests. All results are in favor of an enzymatic conversion and this enzyme is strictly located in the mitochondrial fraction. Results concerning this localisation are expressed as specific activity and relative specific activity. Preliminary results on further experimental data point out that this conversion depends on the energetic state of mitochondria. Complete electron transfer blokage inhibits this transformation whereas respiratory chain blokage with a NADPH generating system and ATP supplementation does not seem to produce any inhibition. Oligomycine and guanidine stimulation suggest that ATP or its precursors may be involved in this reaction.

18-Hydroxycorticosterone↗