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Biomedical subjects

J C Valcke

Publications and source records attributed to J C Valcke.

At least 19 recordsLinked to original sources
PubMed1990

[Inhibin].

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Activins↗
PubMed1988

Endocrine, paracrine and autocrine control of follicular development.

Development of a single follicle during the menstrual cycle is under control of hormones stimulating follicular maturation, ovulation and luteogenesis. Several factors intervene locally to prevent other follicles from developing at the same time as dominant follicle. These other follicles remain quiescent or evaluate to atresia. Atresia results from the action of several endocrine, paracrine and autocrine mechanisms which synergistically inhibit aromatase activity. The subsequent lack of estrogens reduces granulosa cell multiplication. The oocyte will not become fertilizable before the preovulatory peak of LH, after the resumption of meiosis and after reaching metaphase of the second meiotic division. Several factors are involved in the inhibition of spontaneous resumption of meiosis: cyclic nucleotides, sex steroids, somatostatin and oocyte maturation inhibitor(s) (OMI). Ovulation is related to breakdown of connective tissue synthesized by granulosa cells under the influence of FSH. Connective tissue lysis is dependent on proteolytic enzymes which are released and activated by FSH, LH and relaxin. A paracrine control could be involved in ovulation: LH induces the production of prostaglandin and relaxin by theca cells which, in turn, stimulate collagenase and proteoglycanase secretion by granulosa cells.

Endocrine Glands↗
PubMed1987

[Cardiothyreoses].

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Heart Diseases↗
PubMed1987

[Indications and results of pituitary radiotherapy after microsurgery in acromegaly. 15 cases].

The present treatment of acromegaly consists of selective adenomectomy followed, when unsuccessful, by pituitary gland irradiation. Fifteen acromegalic patients were evaluated after adenomectomy, then radiotherapy. Growth hormone assays were performed after carbohydrate load and administration of thyroid stimulating hormone. Somatomedins were measured by radiocompetition using the vector protein. Cure was obtained with adenomectomy alone in 3 of the 15 patients (mean follow-up 39 months). The remaining 12 patients were all cured by subsequent irradiation at the cost of pituitary insufficiency in one-third of them. Post-surgical cure of acromegaly can only be asserted from range of strict criteria. The best indicators of persisting activity are high levels of growth hormone and/or somatomedins. A solitary somatotropic dysregulation does not necessarily herald a relapse.

Acromegaly↗
PubMed1987

[Endocrine, paracrine and autocrine mechanisms involved in follicular development].

Development of a single follicle during the menstrual cycle is under control of hormones stimulating follicular maturation, ovulation and luteogenesis. Several factors intervene locally to avoid other follicles developing at the same time as the dominant follicle. These other follicles remain quiescent or go on to atresia. Atresia results from the action of several endocrine, paracrine and autocrine mechanisms which synergistically inhibit aromatase activity. The subsequent lack of oestrogens reduces granulosa cell multiplication. The oocyte will not become fertilizable before the preovulatory peak of LH, after the resumption of meiosis and after reaching the metaphase of the second meiotic division. Several factors are involved in this inhibition of spontaneous resumption of meiosis: cyclic nucleotides, sex steroids, somatostatin, oocyte maturation inhibitor(s) (OMI). Ovulation is related to breakdown of connective tissue synthesized by granulosa cells under the influence of FSH. Connective tissue lysis is dependent on proteolytic enzymes which are released and activated by FSH, LH and relaxin. A paracrine control could be involved in ovulation: LH induces the production of prostaglandin and relaxin by theca cells which, in turn, stimulate collagenase and proteoglycanase secretion by granulosa cells.

Female↗
PubMed1986

[Influence of gonadotropins on inhibin secretion].

Inhibin is produced by Sertoli cells in the male and by granulosa cells in the female. Follicular-stimulating hormone acts directly to stimulate production whereas luteinizing hormone exerts an indirect effect by stimulating production of androgens which themselves activate synthesis and release of inhibin. Prolactin has no effect on inhibin. These interpretations, derived from numerous in vivo and in vitro studies, explain why inhibin is not secreted in the hypophysectomized animal. Interruption of spermatogenesis by ligature of deferens canals, by experimental cryptorchidism in the rat, and in human primary azoospermias, provokes a reduction in production of inhibin and an increased secretion of FSH. The second must be the consequence of the first. Restoration of normal spermatogenesis results in normal production of inhibin. Biochemical mechanisms linking spermatogenesis and inhibin production are still unknown.

Animals↗
PubMed1977

Hormonal changes induced by bromocriptine (CB-154) at the early stage of treatment.

Fifteen female patients with amenorrhea and hyperprolactinemia were studied 1 to 3 times daily during the first 4 days of treatment with bromocriptine (2.5 mg b.i.d). Normal PRL levels were reached within one day in 12 while the mean value for the whole group showed no further significant decrease. Estradiol, LH and FSH levels did not vary significantly at this stage even in those 10 patients who subsequently resumed menstruation.

Adult↗
PubMed1977

Reversible gonadotropin deficiency in male Cushing's disease.

Twelve adult males with documented active Cushing's disease were studied. Mean plasma testosterone (T) was significantly decreased: 1.8 +/- 0.3 (SEM) ng/ml (N=6.8 +/- 0.5); gonadotropin measurements in 8 patients, in basal conditions and under LH-RH iv, showed a significant decrease in both FSH and LH. A further study of 11 patients in remission of Cushing's disease indicated a significant increase in plasma T and gonadotropins up to the normal range. One patient with an initial low T value had a normalized T while in remission, then a dramatic decrease when the disease relapsed. We conclude: a hypogonadotropic hypogonadism is found in male Cushing's disease; it disappears as early as hypercortisolism is suppressed. Some possible mechanisms are discussed.

Adolescent↗
PubMed1976

[Properties of anti-LH-RH serums induced by 2 different immunogens].

Several anti-LH RH antisera have been raised in Rabbits given as immunogen the synthetic decapeptide linked to bovine serum albumin by carbodiimide or bis-diazotized benzidine. Antibodies obtained with CDI as a coupling agent showed the highest titers and affinities enabling measurement of LH RH levels lower than 1 pg/tube. The specificity of the antisera, particularly toward 13 fragments of the molecule, were similar irrespective of the immunogen used.

Animals↗
PubMed1976

[Sexual side-effects of spironolactones. Possible mechanisms of their anti-androgen action].

Spirolactones (spironolactone, potassium canrenoate) may produce secundary sexual effects such as gynecomastia in man and menstrual disturbances in women. The mechanism of action of the antiandrogenic effects has been studied in man and rat. Acute i.v. injection of potassium canrenoate into man results in a decrease of plasma testosterone, without any change of gonadotropins. This decrease might be due to an impaired testicular steroidogenesis. On the other hand, spirolactones have an antiandrogenic effect at the target cells level. They do not modify the prostate 5alpha-reductase activity; however, they do inhibit the binding of androgens to their receptors. Thus the spirolactones interact with both biosynthesis and peripheral action of androgens.

Adult↗