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Biomedical subjects

A Elewaut

Publications and source records attributed to A Elewaut.

At least 55 records · Page 3Linked to original sources
PubMed1984

Inhibition of adenylate cyclase activity of human thyroid membranes by gangliosides.

Gangliosides inhibit basal, thyrotropin-induced and fluoride-induced adenylate cyclase activity of human thyroid membranes in physiological conditions. In contrast neutral glycolipids, phospholipids and neuraminic acid containing oligosaccharides show no effect. The efficacy of inhibition is more dependent upon the position of the sialic acid residues than upon their absolute number. In general gangliosides with disialyl groups are more inhibitory than those with single sialyl moieties. The inhibitory effects of the individual gangliosides on the two modes of stimulation are parallel. This parallelism suggests that the inhibitory effect is located at the postreceptor level and that the gangliosides interact directly with the adenylate cyclase system. A possible role of thyroid membrane gangliosides as suppressive cofactors of adenylate cyclase is discussed in relation to recent findings of stimulating anti-ganglioside antibodies in Graves' disease.

Adenylyl Cyclase Inhibitors↗
PubMed1984

Fate of orally given isosorbide dinitrate in cirrhotic patients.

In 5 out of 7 patients with cirrhosis and extensive shunting, plasma concentrations of isosorbide dinitrate after oral administration of 10 mg of the substance were markedly higher than those found in subjects without hepatic disease. The explanation could be a higher bioavailability and/or a lower systemic clearance, due to shunting and hepatic cell dysfunction. The difference was confirmed by the calculation of the areas under the concentration-time curves.

Administration, Oral↗
PubMed1983

Immunoreactive thyrotrophin-releasing hormone like material (IR-TRH LM) in human cord blood: high circulating serum levels but possible non-identity with hypothalamic TRH.

Levels of immunoreactive thyrotrophin-releasing hormone like material (IR-TRH LM) were measured in paired maternal and umbilical cord serum samples (n = 45) and in serum of non-pregnant women (n = 63), using a sensitive and specific radioimmunoassay. In all pairs IR-TRH LM in venous cord serum (mean 91.3 pg/ml, range 20-270) was markedly elevated as compared to maternal serum (mean 13.5 pg/ml, range 0-37, P less than 0.001, the maternal levels being similar to those in non-pregnant women (mean 12.0 pg/ml, range 0-39, P greater than 0.1). In 23 cases IR-TRH LM was also measured in arterial cord serum: arterial and venous cord levels were highly significantly correlated (r = 0.904) with higher arterial levels in 22 out of 23 cases (mean 117.8 pg/ml, range 32-280 and 90.6 pg/ml, range 20-270, P less than 0.001), suggesting that cord IR-TRH LM is not of placental origin. There was no correlation between individual levels of IR-TRH LM and either TSH, T4, T3 or FT4 levels in either maternal or cord serum. Agar gel electrophoresis and equilibrium dialysis of adult and cord serum pre-incubated with [125I]TRH or [3H]TRH revealed no protein binding. Cord IR-TRH LM was immunologically, as well as in paper electrophoresis and in gelfiltration, indistinguishable from synthetic and hypothalamic TRH. In vitro degradation of synthetic TRH was much slower in cord serum as compared to maternal and control serum (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1981

Triiodothyronine binding to lymphocyte nuclei and plasma cyclic AMP response to intravenous glucagon in patients with peripheral resistance to thyroid hormones.

In vitro studies of nuclear binding of triiodothyronine (T3) in lymphocytes were performed in three members of a family with hereditary peripheral resistance to thyroid hormone action. Ficoll-Hypaque purified lymphocytes were used; the binding characteristics were analyzed by Scatchard's methods. In 5 euthyroid subjects the apparent mean equilibrium association constant (Ka) was 6.2 x 10(9) l/mol and the mean maximal binding capacity (Cap) 14.4 x 10(-15) mol/100 microgram DNA. In the 3 members of the family one single set os saturable T3 nuclear binding sites with affinity constants similar to those in the controls (mean Ka = 3.2 x 10(9) l/mol; mean Cap = 17.4 x 10(-15) mol/100 microgram DNA) were found. The glucagon stimulated increase in plasma cyclic AMP was studied in 6 healthy subjects and the four members of the family. The plasma cyclic AMP levels of the patients with hormone resistance were generally within the normal range. These observations demonstrate that in these patients with peripheral resistance to thyroid hormone binding of T3 to the receptor in the nucleus of lymphocytes is normal; in relation to the high circulating thyroid hormone levels, the thyroid hormone mediated cyclic AMP response is disturbed, suggesting that the defect is at the post-receptor effector level.

Adult↗
PubMed1981

Effect of domperidone on prolactin (PRL)and thyrotrophin (TSH) secretion.

Domperidone, a novel dopamine receptor blocking substance, unable to cross the blood brain barrier, was tested in twenty euthyroid volunteers of both sexes and in seven women with autonomous nodular goiter. Oral administration of 20 mg domperidone was followed by marked increase in serum PRL in all subjects; the response, being significantly greater in women as compared to men, was maintained in patients with autonomous goiter. The PRL response after oral domperidone was significantly greater than after 200 micrograms TRH intravenously. The PRL response obtained with oral domperidone followed by 200 microgram TRH i.v. was similar to the response obtained with domperidone alone before TRH administration. In euthyroid men the TSH response to 200 microgram TRH administered intravenously 120 min after oral domperidone was significantly greater than in a control TRH test. The data of the present study suggest that dopamine blockade at pituitary (or median eminence) level is able to stimulate maximally the lactotrophs and emphasize the important role of the dopaminergic system in the interrelated regulation of TSH and PRL secretion at the pituitary level.

Administration, Oral↗
PubMed1979

Testosterone metabolism in normal males and male cirrhotics.

The following physiopathological mechanisms for the abnormalities of testosterone metabolism observed in cirrhotic patients may be postulated: 1. The decreased testosterone secretion has a primary testicular origin; it seems probable that, as a result of direct toxicity the 17-beta-reductase is inhibited, resulting in decrease of testosterone and an increase of androstenedione. 2. The hypothalamic-pituitary function is nearly normal in cirrhotics. Basal level of LH and FSH are often slightly elevated, indicating a normal reactivity of the pituitary. 3. The conversion of androgens to oestrogens (androstenedione to oestrone) which occurs essentially extrahepatically, is increaed in cirrhosis.

Adipose Tissue↗