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Biomedical subjects

M Begeot

Publications and source records attributed to M Begeot.

42 records · Page 3Linked to original sources
PubMed1977

Growth hormone and ACTH in the pituitary of normal and anencephalic human fetuses: immunocytochemical evidence for hypothalamic influences during development.

The influence of the hypothalamus on the development of the anterior pituitary cells was studied in normal and anencaphalic human fetuses. An immunocytological method was applied to study the quantitative evolution of the size of the cells during gestation. The somatotropic and corticotropic cells appeared at the end of the 2nd month of gestation. After the 3rd month of gestation their normal development required the presence of brain. The results suggest that hypothalamic factors are needed for the normal development of cells containing these pituitary hormones.

Adrenocorticotropic Hormone↗
PubMed1977

[Human fetal antehypophysis in vitro. II. Immunocytological study and radioimmunoassay of LH and FSH (author's transl)].

Human fetal antehypophysis (16 males, 16 females and 4 unknown sex) were cultivated during several weeks. By immunocytochemistry LH gonadotroph cells were determined with anti-hTSH and anti-pLH serum. The release in vitro of LH and FSH was studied by radioimmunoassay. At the first medium change, the quantity of LH and FSH release was related to the gestational age and sex. A rapid decline of both LH and FSH occured over the 10 first days. There after, a basal release of LH was maintained during several months; the release of FSH was generally maintained at the lower limit of the assay. After 1 month in vitro, the level of LH could not be related to the sex. Release of LH was stimulated by synthetic LRF. A significant increase was observed independently of the sex and age of the fetuses studied.

Culture Techniques↗
PubMedDate not supplied

Syndrome of congenital adrenocortical unresponsiveness to ACTH. Report of six patients.

Familial glucocorticoid deficiency (FGD) or unresponsiveness to ACTH at the receptor level is a rare autosomal recessive hereditary syndrome characterized by a low cortisol level despite high serum ACTH concentration. Aldosterone levels are normal. The clinical entity generally presents in the first year of life with skin hyperpigmentation and hypoglycemic convulsions. Cortisol response to exogenous ACTH is also absent. Unresponsiveness to ACTH may be due to a mutation in the ACTH receptor; sometimes no mutation is found. We discuss the clinical and laboratory findings and genetic studies in six patients with a diagnosis of FGD. A homozygous V142L mutation was detected in three of the patients and a homozygous D103N mutation was detected in two patients.

Adrenal Cortex↗