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Biomedical subjects

G M Besser

Publications and source records attributed to G M Besser.

At least 325 records · Page 18Linked to original sources
PubMed1984

Familial hypocalciuric hypercalcaemia: association with neonatal primary hyperparathyroidism, and possible linkage with HLA haplotype.

A kindred is described, six members of which fulfilled criteria for the syndrome of familial hypocalciuric hypercalcaemia (FHH). The majority of these individuals were asymptomatic: their hypercalcaemia was revealed by biochemical screening after parathyroid surgery had failed to diminish the elevated serum calcium concentration of the index case. In contrast to those members of the family diagnosed as adults, the daughter subsequently born to the index case included in her expression of FHH clinical features of severe neonatal primary hyperparathyroidism. Four hyperplastic parathyroid glands were excised, and following surgical intervention the baby improved clinically and accelerated the healing of her skeletal lesions. Her case suggests that an association does exist between FHH and neonatal primary hyperparathyroidism. Of the ten individuals at risk, inheritance of hypocalciuric hypercalcaemia was paralleled in eight cases by inheritance of the HLA haplotype All BW55 CW3 DR4. Such possible linkage has not previously been reported.

Adult↗
PubMed1984

Measurement of immunoreactive gamma-MSH in human plasma.

A radioimmunoassay for immunoreactive gamma-MSH (IR-gamma-MSH) in human plasma has been developed. The assay is capable of detecting normal basal circulating levels which range from less than 20-100 ng/1 at 0900 h. Plasma levels are raised concomitantly with ACTH during insulin induced hypoglycaemia and CRF stimulation and suppressed with dexamethasone. Chromatographic characterisation of IR-gamma-MSH in plasma demonstrates a major peak of IR-gamma-MSH, corresponding to purified glycosylated N-terminal pro-opiomelanocortin 1-76, when IR-gamma-MSH is secreted from the pituitary. In contrast IR-gamma-MSH produced ectopically appears to be heterogeneous.

ACTH Syndrome, Ectopic↗
PubMed1984

Responses to analogues of growth hormone-releasing hormone in normal subjects, and in growth-hormone deficient children and young adults.

Three analogues of growth hormone-releasing hormone (GHRH) have been compared in normal subjects. GHRH(1-29)NH2 is equipotent to GHRH(1-40); increasing doses from 10-200 micrograms per subject augments the duration of stimulated growth hormone (GH) release, but the peak serum GH shows only a poor correlation with dose. The derivative D-Ala2-GHRH(1-29)NH2 is no more potent than the unsubstituted GHRH(1-29)NH2. In 20 children and young adults with growth hormone deficiency by conventional criteria, eight showed normal or only slightly subnormal peak serum GH responses to GHRH(1-40) or GHRH(1-29)NH2. These included two patients with tumours of the hypothalamus, as well as six with idiopathic isolated growth hormone deficiency or panhypopituitarism. A poor response to GHRH was generally seen in patients on long-term GH therapy. Priming with GHRH, in either a single bolus or a continuous infusion, did not increase the GH response to GHRH. It is concluded that GHRH(1-29)NH2 is a useful analogue in the testing of GH reserve in patients with growth hormone deficiency, and has considerable potential for long-term therapy.

Adolescent↗
PubMed1984

Heterogeneous immunocytochemical reactivities of oCRF-41-like material in the human hypothalamus, pituitary and gastrointestinal tract.

Tissue specimens of human hypothalami, pituitaries and gastrointestinal tract were studied with an indirect immunoperoxidase technique using 6 different rabbit ovine corticotrophin-releasing factor (oCRF-41) antisera. All these antisera detected oCRF-41-like immunoreactivity in parvocellular neurones of the paraventricular nucleus of the hypothalamus and their nerve terminals adjacent to portal capillaries in the infundibular stem and posterior pituitary. 1 antiserum recognised oCRF-41-like immunoreactivity in the growth hormone cells of the anterior pituitary. 3 other antisera recognised oCRF-41-like immunoreactivity in mucosal cells of the gastric antrum. Pre-treatment of the antisera with sauvagine did not affect the immunostaining of the hypothalamic and gastric cells, but quenched the immunostaining of growth hormone cells in the anterior pituitary. It is concluded that (1) in human hypothalami a CRF is synthesized that is structurally very similar to oCRF-41; (2) in growth hormone cells of the anterior pituitary oCRF-41-like immunoreactive material can be detected which shares antigenic determinants with sauvagine; (3) in mucosal cells of the gastric antrum oCRF-41-like immunoreactivity is present that is comparable but probably not identical to hypothalamic CRF and is not sauvagine-like.

Amphibian Proteins↗
PubMed1984

CRF-41 stimulates the release of beta-lipotrophin and beta-endorphin in normal human subjects.

A prompt rise in circulating immunoreactive N- and C-terminal lipotrophin (LPH) accompanied the increase in ACTH when 100 micrograms CRF-41 was given to 6 normal male subjects. Chromatography of the basal and peak 15-min values showed that there was an equimolar increase in beta-LPH and beta-endorphin, to cause parallel release of ACTH, beta-endorphin and beta-LPH from the pro-opiocortin precursor.

Adult↗
PubMed1984

High dose androgen therapy in male pseudohermaphroditism due to 5 alpha-reductase deficiency and disorders of the androgen receptor.

We describe the clinical and biochemical features of six men with male pseudohermaphroditism due to androgen resistance. Each of the subjects had male-gender behavior but incomplete virilization. The underlying defects in androgen metabolism were defined by studies of the 5 alpha-reductase enzyme and the androgen receptor in fibroblasts cultured from biopsies of genital skin. Four of the six have 5 alpha-reductase deficiency, and two have defects of the androgen receptor (the Reifenstein syndrome). The responses of these men to androgen treatment were assessed by monitoring nitrogen balance, plasma luteinizing hormone (LH) values, and clinical parameters of virilization including penile growth, potency and ejaculatory volume, muscle bulk, and growth of body and facial hair. In all of the subjects with 5 alpha-reductase deficiency and one man with the Reifenstein syndrome significant response occurred, as evidence by nitrogen retention, lowered plasma LH levels, and improved virilization, with doses of parenteral testosterone esters that raised plasma testosterone levels above the normal male range and brought plasma dihydrotestosterone levels into the normal male range. The subject who did not respond with clinical virilization nevertheless showed nitrogen retention in response to acute testosterone administration. This patient had a profound deficiency of the androgen receptor, whereas the man with a receptor defect who did respond clinically to therapy had normal amounts of a qualitatively abnormal receptor. We conclude that high dose androgen therapy may be of benefit in improving virilization, self-image, and sexual performance in subjects with 5 alpha-reductase deficiency who have male-gender behavior and in some subjects with defects of the androgen receptor.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1984

Corticotrophin-releasing factor--mediated adrenocorticotrophin release from rat anterior pituitary cells is potentiated by C-terminal gastrin-releasing peptide.

The remission of Cushing's syndrome following surgical removal of a tumour containing bombesin-like immunoreactivity (BLI), but insignificant levels of ACTH, is described. However, an acid extract of the tumour tissue caused the release of ACTH from isolated rat anterior pituitary cells in vitro. These observations led to an investigation of the effects of synthetic C-terminal gastrin-releasing peptide (GRP(14-27] on ACTH release from isolated rat anterior pituitary cells. GRP(14-27) (10-1000 ng/ml) directly stimulated the release of ACTH in vitro, whereas lower doses (10-1000 pg/ml), ineffective themselves in eliciting ACTH release, potentiated the CRF-mediated in-vitro release of ACTH.

ACTH Syndrome, Ectopic↗
PubMed1983

Endorphin-related peptides in rat cerebrospinal fluid.

Cerebrospinal fluid (CSF) samples were taken from rats implanted with chronic cisternal cannulae and assayed for methionine-enkephalin, beta-endorphin and corticotropin (ACTH). Immobilization stress had little apparent effect on immunoreactive levels of the peptides in the CSF. Gel chromatographic analysis of the beta-endorphin- and ACTH-immunoreactive profiles in rat CSF revealed several peaks. beta-Endorphin-immunoreactive peaks were present at the expected positions of pro-opiocortin, beta-lipotropin and beta-endorphin. ACTH-immunoreactive peaks eluted at positions corresponding to pro-opiocortin, the 20-23K ACTH biosynthetic intermediate, 14K ACTH, and 4.5K ACTH. These results suggest that rat CSF contains peptides of the pro-opiocortin family similar to those previously described in rat pituitary.

Adrenocorticotropic Hormone↗
PubMed1983

Treatment with gonadotrophin releasing hormone analogue in advanced prostatic cancer.

Repeated administration of long acting analogues of gonadotrophin releasing hormone diminishes gonadal function and in men decreases testosterone concentrations; for this reason the effect of the analogue buserelin was studied in prostatic carcinoma. Twelve consecutive patients with newly diagnosed locally advanced or metastatic carcinoma of the prostate were treated. Each patient received intranasal buserelin in divided dosages of either 600 or 1000 micrograms daily. Suppression of the gonadotrophins and testosterone occurred in all patients. Objective and subjective signs of regression of disease were seen in nine patients. Buserelin offers an effective treatment of metastatic prostatic cancer without the side effects and cardiovascular risks associated with oestrogen treatment.

Administration, Intranasal↗
PubMed1983

The relationship between prolactin levels and clinical ratings in manic patients treated with oral and intravenous test doses of haloperidol.

Twelve manic patients were treated for 2 weeks with oral haloperidol; in 6 patients treatment commenced with intravenous haloperidol, and intravenous 'test' doses were given after 1, 3-5 and 14 days of oral medication. From 24 hours to 14 days baseline serum prolactin levels rose towards a plateau, as did the improvement in clinical ratings. After the first intravenous test doses of haloperidol, prolactin levels peaked at 1 hour; however, they fell to a low point at 24 hours, and no response to further test doses was seen for 3-5 days. The response tended to return at 14 days. The mechanisms underlying the changes in prolactin levels, and in clinical state, are discussed.

Adolescent↗
PubMed1983

Low dose prednisolone or oestrogen in the treatment of women with late onset or persistent acne vulgaris.

Women with persistent or late onset acne vulgaris were divided into two treatment groups. The first received continuous low dose prednisolone to suppress ACTH-dependent androgen secretion and the second was treated with cyclical oestrogens with medroxyprogesterone to elevate sex hormone binding globulin (SHBG). In both groups there was a significant improvement in the severity of the acne after 4 months' treatment. Although pre-existing hormonal abnormalities were corrected, the improvement in the acne did not correlate with the baseline hormone levels. However, suitable oestrogen-progesterone combinations or low dose prednisolone may be given, alone or in combination, to suppress free circulating androgens in these patients with a high probability of improving their acne.

Acne Vulgaris↗
PubMed1983

The participation of hypothalamic dopamine in morphine-induced prolactin release in man.

In order to assess the role of dopamine in opiate-induced prolactin secretion, morphine alone or in combination with the dopamine blocker metoclopramide, or the L-aromatic aminoacid decarboxylase inhibitor benserazide, was administered to a group of normal adult men. Morphine (10 mg) stimulated prolactin release in all subjects; however, the effect was totally abolished when 10 mag metoclopramide or 200 mg benserazide were given before the opiate agonist. The prolactin releasing effect of a sub-maximal metoclopramide dose (1 mg) was potentiated by morphine. In vitro, benserazide was totally inactive in stimulating prolactin release by isolated anterior pituitary cells. Moreover, benserazide failed to alter the inhibiting action of dopamine on prolactin release. The data suggest that opiates stimulate prolactin release in man by acting through dopaminergic mechanisms.

Adult↗
PubMed1983

Opiate peptides control growth hormone through a cholinergic mechanism in man.

Opiate peptides are known to elevate circulating GH in man, and data in other animals suggest that acetylcholine may be involved. We have administered the long-acting met-enkephalin analogue DAMME to 6 normal males, and have shown that the resulting elevation in GH is blocked by the specific cholinergic antagonist, pirenzepine. It seems likely that a cholinergic mechanism may interact with opiate-induced changes in GH in man.

Adult↗
PubMed1983

Naloxone inhibits exercise-induced release of PRL and GH in athletes.

Opiate peptides stimulate the release of GH and PRL, and such changes have also been reported following physical exercise. To investigate opiate involvement in the exercise-induced release of these hormones, eight professional athletes were exercised to 80% of their maximal heart rate on a bicycle ergometer. This exercise alone induced an increase in circulating mean GH (basal to maximal level, 3.1 +/- 0.9 ng/ml-27.3 +/- 5.9 ng/ml) and mean PRL level (6.1 +/- 1.1 ng/ml-19.5 +/- 1.9 ng/ml). Infusion of naloxone (0.3 mg/min) antagonized these responses in mean serum GH (5.6 +/- 1.0 ng/ml to 8.6 +/- 1.1 ng/ml) and PRL levels (6.4 +/- 1.1 ng/ml-8.1 +/- 1.2 ng/ml), which were both significantly less than during the control infusions (P less than 0.01). It is suggested that certain forms of stress stimulate the release of PRL and GH via endogenous opiate peptides.

Adult↗