Search PubMed⌕ Search

Biomedical subjects

R Mornex

Publications and source records attributed to R Mornex.

At least 91 records · Page 5Linked to original sources
PubMed1982

[Toxic adenoma].

Explore the source record for details and available documents.

Adenoma↗
PubMed1982

[Effects of propranolol and indomethacin upon urinary hydroxyproline in hyperthyroid patients (author's transl)].

Hydroxyproline excretion was increased by hyperthyroid patients. This increase was related to thyroid hormone levels. Propranolol administration induced a decrease in hydroxyproline excretion and in immunoreactive triiodothyronine. Indometacin administration induced a decrease in urinary excretion of prostaglandins but had no effect on hydroxyproline excretion. These data suggest that the increased bone resorption of hyperthyroidism may involve a catecholamine beta receptor-dependent mechanism and is probably independent of prostaglandins.

Adult↗
PubMed1982

Treatment of hypogonadotropic hypogonadal male patients with the luteinizing hormone-relasing hormone (LH-RH) anolog D-Ser(TBU)6 EA10 LH-RH: transient disappearance of gonadotropin stimulation.

We have studied the effect of prolonged treatment with a long-acting luteinizing hormone-releasing hormone (LH-RH) analog (D-Ser-(TBU)6 EA10 LH-RH in six patients with isolated gonadotropin deficiency. Before treatment, all subjects responded to LH-RH (100 microgram intravenously [IV]); one responded immediately, and five after 5 daily infusions of LH-RH (200 microgram). Treatment by LH-RH analog (348 microgram every 2 days with a nasal spray for 90 or 120 days) is only efficient for 1 month; a consistent increase in serum LH and a slight increase in testosterone (T) were observed in all patients, but no increase of serum follicle-stimulating hormone (FSH) was detectable. Then a paradoxical effect appeared: LH and T levels returned to the basal values. Moreover, this treatment induced refractoriness of the pituitary to LH-RH for several months after the end of treatment. The appearance of antibodies to LH-RH and LH-RH analog was eliminated. A pituitary response was obtained in three patients when a new LH-RH stimulation was repeated 7 and 11 months after the end of treatment. The mechanism of this pituitary desensitization is discussed.

Adolescent↗
PubMed1982

Metabolism of adiphenine. II. Identification of major excretion metabolites in rats.

1. Major metabolites isolated from rat urine after administration of a single dose of [14C]adiphenine or [3H]adiphenine were identified by chromatography and n.m.r. spectrometry, and by comparison with authentic reference compounds chemically synthesized. 2. Adiphenine was extensively metabolized by hydrolysis of the ester bond into diethylaminoethanol, diphenylacetic acid, diphenylacetic acid glucuronide and, in small quantities, the corresponding glycine and glutamine conjugates.

Animals↗
PubMed1981

Identification of an intracellular pathway of thyroxine synthesis by dispersed thyroid cells.

This study deals with the identification of the biochemical events involved in the metabolic sequence leading from the synthesis to the release of thyroxine in the dispersed thyroid cell system. (1) Using an experimental model allowing the differentiation between intracellular and extracellular sites of iodination, it is shown that thyroxine is synthesized inside the cells by an iodinating system sensitive to thyrotropin stimulation. (2) The secretion of thyroxine synthesized inside the cells is not mediated by an exocytotic-endocytotic phenomenon. Colchicine, vinblastine, fluoride, propanolol and chlorpromazine, at concentrations equal to or 10--100-times higher than those required to inhibit hormone release in follicular-organized thyroid tissue have no effect on thyrotropin-stimulated thyroxine secretion. (3) The secretion involves the intracellular proteolysis of hormone-containing iodoprotein(s) which, in addition to free thyroxine, generates free mono- and diiodotyrosines. Free thyroxine is released into the incubation medium and iodotyrosines are deiodinated under normal conditions and accumulate in the presence of an inhibitor of iodotyrosine deiodinase: 3,5-dinitrotyrosine. This proteolysis is inhibited by 5 mM chlorpromazine. These data indicate that the complete metabolic sequence leading from the uptake of iodide to the release of free thyroxine into the incubation medium can be described as an 'intracellular metabolic sequence for thyroxine synthesis'.

Animals↗
PubMed1981

Metabolism of adiphenine. I. Absorption, distribution and excretion in rats and mice.

1. The disposition of adiphenine labelled with 14C in two positions has been investigated in rats and mice after i.v. administration, and has been compared with that of the [14C]diethylethanolamine HCl and of the [14C]diphenylacetic acid. 2. Radioactivity in the blood declined in a biphasic manner. Biliary elimination depended upon the 14C-labelled compound administered: less than 5% dose for the diethylethanolamine moiety, 100% dose for the carboxylic moiety. Of the radioactivity appearing in rat bile, less than 1% is associated with unchanged adiphenine. 3. In preliminary metabolic studies, three major metabolites have been identified: diphenylacetic acid, diethylethanolamine and a diphenylacetic acid glucuronide. 4. Uptake by the brain of [14C]adiphenine shortly after dosing is 15 times greater than that of blood. Radioactivity is also found in the hypophysis, the adrenals and melanoid pigments, with a concn. up to 30 times greater than that found in the blood.

Absorption↗
PubMed1980

Intracellular and extracellular sites of iodination in dispersed hog thyroid cells.

Iodination and hormone synthesis has been studied in isolated hog thyroid cells in suspension. We characterized three iodination processes by use of pharmacological agents. (1) Intracellular iodination dependent on active iodide transport, which was inhibited by NaClO4 or ouabain, but not by catalase. This iodination was linear for 6h with no apparent Km for iodide of 1.5 muM, was stimulated by thyrotropin or N6O2'-dibutyryladenosine 3':5'-cyclic monophosphate, yielded mostly iodinated thyroglobulin and was efficient for tetraiodothyronine synthesis. (2) Extracellular iodination, which was sensitive to catalase, but not to NaClO4 or ouabain. This iodination plateaued after 2h and the apparent Km was 16.5 muM. This process was insensitive to thyrotropin and dibutyryl cyclic AMP. The major products were iodoprotein other then thyroglobulin and iodolipid and the yield of tetraiodothyronine was low. (3) Intracellular iodination from passively diffused iodide, which was not sensitive to inhibitors. Other characteristics of passive intracellular iodination were intermediate between active intracellular iodination and extracellular iodination. The fact that the three processes are inhibited by similar concentrations of methimazole, and their apparent Km values, when corrected for the concentrating effect of iodide trapping, are all of the same order as the Km of purified thyroid peroxidases, suggest that although their locations are different, the enzymic systems involved are identical. These results show that, besides an extracellular site of iodination, dispersed thyroid cells process an intracellular site of iodination with biochemical characteristics of physiological relevance.

Animals↗
PubMed1980

Sex differences in the adrenergic response to hypoglycemic stress in human.

We have found different patterns of adrenergic response to insulin-induced hypoglycemia in men and women. The differences involve the readiness of adrenergic reactivity, the magnitude of the responses, and the nature of secreted amines. In men, a strong and transient discharge of epinephrine (E) is observed in plasma, corresponding to a great increase in the urinary level of this amine in the 2 h period following insulin. In women, the adrenergic response is delayed and consists of moderately increased amounts of E and norepinephrine (NE) which persist in plasma for a longer period. From the correlations observed between urinary amount and the increase of plasmatic catecholamines after 30, 45, and 60 min, it may be assumed that urinary data may reflect the cumulative plasma levels of catecholamines in the corresponding period, but not the precise pattern of plasmatic changes. Our findings show that the differences in adrenergic behavior previously observed in men and women under the effect of psychological stress, may also be induced by a metabolic stimulus such a insulin hypoglycemia; however, women, but not men, exhibit a mild release of NE under this metabolic stress.

Adult↗
PubMed1980

Highly specific solid phase immunoextraction of TSH using anti-TSH antibodies purified by affinity chromatography.

Highly specific anti-TSH antibodies were purified from a crude antiserum preparation by affinity chromatography using TSH-sepharose column as the adsorbant. This procedure completely eliminated the original LH binding activities. The purified anti-TSH antibodies were then coupled to CNBr activated sepharose 4 B and used in separating TSH from rat pituitaries by batch procedure. This method is demonstrated to be highly specific for purifying labelled TSH from pituitaries previously incubated in the presence of [14C]tyrosine. The effect of TRH on TSH biosynthesis is presented as a biological application of this procedure.

Animals↗
PubMed1980

Serotonin and endocrine rhythms.

The biological rhythms belong partly to the genetic patrimony and partly to the environmental patterns. The main results have been obtained on the hormonal fluctuations which are mostly controlled by the hypothalamopituitary system. Thus they include modulations of neurotransmitters activity especially serotonin. Experimental facts have been gathered in different species for ACTH, growth hormone, prolactin TSH and gonadotropins rhythms. These phenomenona are integrated in a general organization which includes sleep-waking cycle.

Adrenocorticotropic Hormone↗