bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hormone receptors in the epiphysial cartilage
Authors: Kan K. W. , Cruess R. L. , Posner B. I. , Guyda H. J. , Solomon S. 
Published: December 2008

ABSTRACT
In order to assess which hormones may exert direct effects on skeletal growth at the epiphysial growth plate, the specific binding of hormones to the epiphysial cartilage of growing dogs and rabbits was studied. Membrane fractions obtained by centrifugation of homogenates prepared from dog and rabbit growth plate cartilage at 600, 15 000 and 105 000 g showed significant specific binding of serum insulin-like activity and insulin. Binding of growth hormone and prolactin by the three membrane fractions was negligible. Saturable binding sites for triiodothyronine could be demonstrated in nuclei from the dog growth plate. Nuclear binding showed an apparent Kd of 11 ±3·6 nmol/l and a maximum binding capacity of 4·1 ± 1·6 pmol/mg DNA, a level comparable to dog liver. Using a viable chondrocyte suspension prepared from dog epiphysial cartilage, specific steroid binding in the cells could be demonstrated for [3H]dexamethasone but not 17α-methyltrienolone, oestradiol-17β or 1α,25-di-hydroxycholecalciferol. Scatchard analysis of dexamethasone binding showed high affinity binding sites having a Kd of 1·2 ± 0·35 nmol/l and a capacity of 1700 sites/cell, and a low affinity binding with a Kd of 109 ± 57 nmol/l and a capacity of 24 000 sites/cell. Steroid competition for the specific binding showed the following sequence of affinity: dexamethasone > corticosterone > 11-deoxycortisol > testosterone > oestradiol-17β. Although all of the hormones examined except prolactin have well-established physiological effects on skeletal growth, our present results suggest that some of the hormonal effects observed in intact animals are secondary and do not involve receptor–hormone interaction in cartilage as such.
J. Endocr. (1984) 103, 125–131
Stimulation of prolactin secretion by oestradiol in the rat is associated with increased hypothalamic release of thyrotrophin-releasing hormone
Authors: Franks S. , Mason H. D. , Shennan K. I. J. , Sheppard M. C. 
Published: December 2008

ABSTRACT
We have studied the effect of oestradiol (OE2) on secretion of prolactin and TSH by rat pituitary glands and correlated this with changes in hypothalamic content and release of thyrotrophin-releasing hormone (TRH). Ovariectomized Wistar rats received s.c. silicone elastomer implants of OE2 at a dose known to give pro-oestrous OE2 levels. After 1 week rats were decapitated, blood was collected for assay of prolactin and TSH, blocks of hypothalamus were dissected out and pituitary glands were removed and bisected. Medium bathing hemipituitary glands was collected for measurement of prolactin and TSH after a 30-min incubation. Immunoreactive TRH was measured in medium removed from hypothalami and in extracts of homogenized hypothalami. Serum prolactin was higher in OE2-treated than in control animals (59·3 ± 19·5 (s.e.m.) vs 9·4 ± 1·5 μg/l; P<0·05) and this was associated with a threefold increase in pituitary prolactin in the medium. By contrast, TSH concentrations in serum and pituitary incubation medium were not significantly different in the two groups. There was no difference between the groups in hypothalamic content of TRH but TRH release in the incubation medium was increased by OE2 (30·2 ± 6·5 vs 10·0 ± 1·3 pg/mg protein per 30 min; P<0·01). In summary, physiological levels of OE2 stimulated prolactin secretion without change in TSH and this was associated with a threefold increase in hypothalamic release of TRH. These findings suggest that the stimulating effect of OE2 on prolactin secretion may, in part, be mediated by hypothalamic TRH.
J. Endocr. (1984) 103, 257–261
Brain sites involved in the regulation of growth hormone secretion in the young male domestic fowl
Authors: Rabii J. , Knapp L. , De La Guardia A. , Zafian P. , Lauterio T. J. , Scanes C. G. 
Published: December 2008

ABSTRACT
To study brain sites involved in the regulation of GH secretion in the domestic fowl, lesions were placed in and around the hypothalamus of 1-week-old cockerels. Circulating concentrations of GH were then measured at weekly intervals for 4 weeks after the placement of lesions. At the termination of the experiment, histological procedures were used to determine the exact site of the lesion in each bird. Although a fair degree of overlap existed between the lesion sites leading to stimulation and those causing an inhibition of GH secretion, a clear distinction could be made in the overall distribution of stimulatory and inhibitory sites of GH control. A high concentration of lesion sites resulting in GH decline (presumed GH-releasing factor-rich areas) appeared to reside in the general area of the ventromedial and the arcuate nucleus of the hypothalamus. Lesion sites causing a GH rise (presumed somatostatin-rich areas), on the other hand, seemed to have a more caudal distribution. In addition, some evidence of an anterior hypothalamic distribution of these presumed 'somatostatin' neurones was observed. These agree with the existing immunohistochemical data on the distribution of somatostatin and constitute experimental evidence for localization of presumed GH-releasing factor sites within the avian brain.
J. Endocr. (1984) 103, 327–332
Acute inhibition of rat myometrial responses to oxytocin by tamoxifen stereoisomers and oestradiol
Authors: Lipton A. , Vinijsanun A. , Martin L. 
Published: December 2008

ABSTRACT
The non-steroidal antioestrogen tamoxifen (trans-1-(4-β-dimethylaminoethoxyphenyl)-1,2-diphenylbut-1-ene), widely used in the treatment of breast cancer, and its oestrogenic cis-isomer rapidly inhibited contractile responses of isolated rat myometrium to supramaximal concentrations of oxytocin (1·28 × 10−6 mol/l). Both compounds were effective at concentrations comparable with the plasma concentrations of tamoxifen reached in therapy (i.e. 5 × 10−7to 5 × 10−6 mol/l). Inhibition was too rapid in onset ( < 3 min) to involve changes in RNA transcription and protein synthesis, and was not prevented or reversed by the addition of oestradiol to the bath. We conclude that the inhibition did not involve the classical oestrogen receptor pathway. Oestradiol-17β at concentrations above 10−6 mol/l also inhibited the myometrium and potentiated the effects of the antioestrogens. Our experiments suggest that the antioestrogens and oestradiol act via a similar route with tamoxifen having an equilibrium affinity approximately tenfold greater than that of oestradiol.
J. Endocr. (1984) 103, 383–388
TREATMENT OF PATIENTS WITH ADVANCED CANCER OF THE PROSTATE USING A SLOW-RELEASE (DEPOT) FORMULATION OF THE LHRH AGONIST ICI 118630 (ZOLADEX®)
Authors: Walker K.J. , Turkes A.O. , Turkes A. , Zwink R. , Beacock C. , Buck A.C. , Peeling W.B. , Griffiths K. 
Published: December 2008

ABSTRACT
Twenty two patients with advanced carcinoma of the prostate have been treated for up to 3 months with the slow-release (depot) formulation of the luteinizing hormone-releasing hormone (LHRH) agonist ICI 118630. Patients were randomized to receive one of three different doses of ICI 118630 of 0·9, 1.8 or 3.6 mg. The depot preparation was injected subcutaneously every 4 weeks. At the highest dose, the concentration of testosterone in serum was significantly reduced to castrate values after 2–3 weeks of therapy. The smaller doses of ICI 118630 (1.8 or 0.9 mg every 4 weeks) similarly reduced serum testosterone concentrations although, at the lowest dose, testosterone values were not suppressed in all patients during the first month. Hormonal changes were accompanied by subjective clinical improvement in symptomatic patients and there were no significant side effects. The data clearly demonstrate the considerable therapeutic potential of ICI 118630 in the depot formulation for the treatment of advanced carcinoma of the prostate.
Autoradiographic studies of androgen-binding sites in the rat urogenital sinus and postnatal prostate
Authors: Takeda H. , Mizuno T. , Lasnitzki I. 
Published: December 2008

ABSTRACT
Binding sites of [3H]testosterone and [3H]dihydrotestosterone in the rat fetal urogenital sinus and postnatal prostate and vagina grown in vitro were examined by steroid autoradiography. Distinct nuclear incorporation of both androgens appeared between 14·5 and 16·5 days of gestation in rat fetuses. Nuclear labelling in the sinus was restricted to the mesenchyme surrounding the epithelium which showed no nuclear labelling. A similar distribution of labelled cells was observed in male and female sinuses up to 18·5 days of gestation. By 20·5 days of gestation, the labelling in the ventral mesenchyme of female urogenital sinuses became less intense but persisted in the mesenchyme of the dorsal sinus wall from which the vagina is formed. In the postnatal prostate, the epithelium showed nuclear [3H]testosterone labelling at 10 days coinciding with the onset of its functional differentiation. Epithelial labelling became more intensive at 4 weeks post partum while that of the mesenchyme declined. The results suggest two phases of androgen action: formation of the prostatic buds mediated by the androgen-activated mesenchyme of the fetal urogenital sinus and the differentiation of the postnatal prostatic epithelium directly stimulated by androgens.
J. Endocr. (1985) 104, 87–92
Thyroxine treatment facilitates prolactin secretion and induces a state of photorefractoriness in thyroidectomized starlings
Authors: Goldsmith A. R. , Nicholls T. J. , Plowman G. 
Published: December 2008

ABSTRACT
Sexually immature male starlings were radiothyroidectomized while held under short daylengths. They were then subjected to long (18-h) photoperiods and the testes developed rapidly and apparently normally to full maturity. As expected, thyroidectomy prevented an onset of photorefractoriness and after 140 days the testes were still fully developed (testicular width 6·5 ± 0·8 mm). Half of the birds were then given thyroxine (0·011 mmol/l) in the drinking water for 14 days while the others were maintained as controls. At the end of this time the birds still had fully developed gonads (testicular width 7·8 ± 0·3 mm) but after a further 14 days testicular regression began in the thyroxine-treated birds. The testes of all individuals in this group were fully regressed (width 1·8 ± 0·1 mm) by 56 days after the end of thyroxine administration and moulting of the flight feathers had begun. No recrudescence of the gonads was subsequently noted in the next 2 months and the birds were apparently photorefractory. The short period of thyroxine treatment also caused a rapid and prolonged increase in plasma prolactin levels from 2·0 ± 0·3 to 16·8 ± 2·6 μg/l. No testicular regression or moulting was observed in the control birds and their plasma prolactin levels remained very low (below 4·0 μg/l) throughout the experiment.
In thyroidectomized and castrated starlings held on 18-h daylengths, 14 daily injections of thyroxine 100 μg/bird per day) caused a rapid and permanent decrease in circulating FSH to basal levels (reached about 36 days after thyroxine treatment began, at which time the birds moulted). The treatment also caused a marked increase in plasma prolactin lasting for about 50 days.
J. Endocr. (1985) 104, 99–103
Changes in concentrations and rate of decline of adrenaline in the medial preoptic area and mediobasal hypothalamus of acutely ovariectomized steroid-treated rats
Authors: MacKinnon P. , Clark C. , Clement E. M. , Sheaves R. 
Published: December 2008

ABSTRACT
The presence of adrenaline within the central nervous system appears to be essential for the occurrence of an oestrogen-stimulated surge of LH in both pro-oestrous and ovariectomized rats. Previous measurements of adrenergic activity based on the rate of decline of adrenaline (RDA) 2 h after injection of a synthesis inhibitor (SKF 64139) suggested that adrenergic activity increases in both the medial preoptic area (MPOA) and the mediobasal hypothalamus (MBH) at the start of the LH surge (15.00–17.00 h). The purpose of the present studies was to see whether oestrogen and progesterone affected this increase in adrenergic activity at the sites of the cell bodies (MPOA) and axon terminals (MBH) of the gonadotrophin-releasing hormone-synthesizing neurone. Rats ovariectomized at dioestrus showed a reduction in both plasma LH concentrations and RDA (P < 0·01) in the MBH between 15.00 and 17.00 h on the day of expected pro-oestrus. Oestrogen replacement at operation restored LH levels and the RDA to values found in intact rats. Injection of an antioestrogen (Cl-628), with or without oestrogen, also reduced plasma LH levels and the RDA (P < 0·01) in the MBH. Removal or replacement of oestrogen apparently had little effect on the RDA in the MPOA. In ovariectomized oestrogen-primed rats an injection of progesterone on the morning of expected pro-oestrus advanced and enhanced not only the LH surge but also the RDA in the MBH (P< 0·001). Moreover, concentrations of adrenaline in the MBH (but not the MPOA) decreased (P < 0·001) consistently over a 2-h period following injection of progesterone. These results support the suggestion that steroid-stimulated adrenergic activity in the MBH may be concerned with the preovulatory release of gonadotrophins.
J. Endocr. (1985) 104, 129–135
Passive immunization against progesterone inhibits endometrial sensitization in pseudopregnant mice and has antifertility effects in pregnant mice which are reversible by steroid treatment
Authors: Rider V. , McRae A. , Heap R. B. , Feinstein A. 
Published: December 2008

ABSTRACT
Pregnant mice were injected 32 h post coitum (p.c.) with a monoclonal antibody against progesterone (5·7 or 9·5 nmol immunoglobulin G (IgG)) or 0·9% (w/v) NaCl (controls). Progesterone was injected starting on day 2, 3, 4 or 5 p.c. Progesterone reversed the antifertility effect of the lower dose of antibody when replacement began on day 2, 3 or 4, though the number of implantation sites was reduced when treatment started on day 3 or 4. By day 5 only one of six treated animals remained pregnant, showing that antibody action was reversible only up to day 4. At the higher dose of antibody, exogenous nidatory oestrogen was also required.
Pseudopregnant mice were injected 32 h p.c. with this antibody (5·7 nmol IgG) or 0·9% NaCl (controls). At 16.00 h on day 4 p.c., oil was injected into the lumen of one uterine horn and the magnitude of the decidual cell reaction was assessed 72 h later. Injected horns of antibody-treated females did not respond to intraluminal oil, whereas those of control mice increased fivefold in weight. Steroid treatment after the induction stimulus did not promote decidual growth, indicating that passive immunization reduced endometrial sensitivity. The results show that in the event that antibody fails to arrest the development of all embryos, the absence of endometrial sensitization will preclude the initiation of implantation, unless progesterone is given within 48 h of antibody treatment.
J. Endocr. (1985) 104, 153–158
Monosodium l-glutamate administration: effects on gonadotrophin secretion, gonadotrophs and mammotrophs in prepubertal female rats
Authors: Dada M. O. , Blake C. A. 
Published: December 2008

ABSTRACT
We have studied gonadotrophin secretion and immunocytochemically stained gonadotrophs and mammotrophs in 35-day-old female rats which had been treated with monosodium glutamate (MSG) as neonates. We also compared our morphometric data in the saline-treated controls with those we have previously obtained in normal adult female rats. The size of the anterior pituitary glands was reduced but the serum levels, the pituitary gland concentrations and contents, and the in-vitro basal release rates of LH and FSH were not significantly altered by MSG treatment. The size of the LH and FSH cells was reduced by MSG administration, but the volume and numerical densities of LH and FSH cells, and the percentage of LH and FSH cells in the pars distalis were not affected. The results suggest that in spite of the smaller size of LH and FSH cells and of the anterior pituitary glands in the MSG-treated rats, the cells contain normal amounts of hormone and the basal LH and FSH secretion rates of the glands are not significantly depressed, contributing to the maintenance of normal serum gonadotrophin concentrations. The volume density of prolactin cells was not increased by MSG treatment. The volume density of gonadotrophs and the percentage of cells which are gonadotrophs in anterior pituitary glands of prepubertal female rats were greater than those in adult female rats, but the reverse was true for the volume density of prolactin cells, suggesting a reciprocal relationship between the relative numbers of gonadotrophs and mammotrophs in prepubertal and adult female rats.
J. Endocr. (1985) 104, 185–192
Oxytocin and vasopressin in rat hypophysial portal blood: experimental studies in normal and Brattleboro rats
Authors: Horn A. M. , Robinson I. C. A. F. , Fink G. 
Published: December 2008

ABSTRACT
Oxytocin (OT) and vasopressin (VP) were measured by radioimmunoassay in hypophysial portal and peripheral blood from male Wistar rats and heterozygous and homozygous Brattleboro rats anaesthetized with urethane. In Wistar rats the concentrations of OT and VP were about 50 times greater than the concentrations in peripheral blood, whether or not the pituitary gland was left in situ during collection, and also considerably greater than the reported concentrations of the peptides in the cerebrospinal fluid. The release of both peptides was increased significantly by a lesion of the supraoptico-hypophysial tract that led to diabetes insipidus, but which left intact the external layer of the median eminence (ME). Concentrations of VP were undetectable in plasma from homozygous Brattleboro rats, but the portal plasma concentrations of VP in heterozygous Brattleboro rats were not significantly lower than in Wistar rats. The concentrations of OT in portal plasma from both types of Brattleboro rat were significantly higher than in Wistar rats.
The output of VP and OT into hypophysial portal blood of Wistar rats was not significantly affected by electrical stimulation of the suprachiasmatic, supraoptic or paraventricular nuclei or the ME using two types of stimuli, one of which produced an increase in peripheral plasma concentrations of VP and OT in intact rats and a significant increase in the release of LH-releasing hormone into hypophysial portal blood. The output of VP and OT into portal blood was also not significantly affected by either adrenalectomy with or without injection of dexamethasone or the injection of either the 5-hydroxytryptamine (5-HT) synthesis blocker, parachlorophenylalanine, or the 5-HT uptake blockers, alaproclate or zimelidine.
These results show that large amounts of OT as well as VP are released into hypophysial portal blood from fibres of the hypothalamo-neurohypophysial system that terminate in the external layer of the ME. Although distinct from the fibres that terminate in the pars nervosa (PN), the findings in Brattleboro rats show that the VP fibres of the ME system originate in neurones with a genomic mechanism for VP synthesis similar to that of the VP neurones that project to the PN. The lack of effect of adrenalectomy and the administration of 5-HT synthesis and uptake blockers must be interpreted with caution since the results obtained with electrical stimulation suggest that when the pituitary stalk is cut the release of OT and VP into portal blood approaches a maximum and may therefore be difficult to alter by experimental manipulation. The concentrations of OT and VP in portal blood are sufficiently high for these peptides to play a significant role in neural control of the anterior pituitary gland.
J. Endocr. (1985) 104, 211–224
Plasma concentrations of somatomedin-C in hypophysectomized, dwarf and intact growing domestic fowl as determined by heterologous radioimmunoassay
Authors: Huybrechts L. M. , King D. B. , Lauterio T. J. , Marsh J. , Scanes C. G. 
Published: December 2008

ABSTRACT
The application of a human somatomedin-C radioimmunoassay for the determination of somatomedin-C in chicken plasma has been examined. Parallel inhibition of binding of 125I-labelled somatomedin-C to antisera raised against somatomedin-C was observed with acid-treated human and chicken plasma. The concentration of immunoreactive (IR)-somatomedin-C in the plasma of the domestic fowl appears to be GH dependent. Plasma concentrations of IR-somatomedin-C were reduced after hypophysectomy and partially restored by replacement therapy with chicken GH. The age/development pattern of circulating concentrations of IR-somatomedin-C has been determined in normal and dwarf strains of domestic fowl. Increases in the plasma concentration of IR-somatomedin-C were observed between 1 and 6 weeks of age in control male domestic fowl of either heavy (broiler type) or light (White Leghorn) strains. Thereafter, the plasma concentrations of IR-somatomedin-C remained constant in the heavy strain birds but declined in White Leghorn chicks. Plasma concentrations of IR-somatomedin-C were reduced in sex-linked dwarf chickens, in both light and heavy strains of fowl, but were unaffected in autosomal dwarf chickens.
J. Endocr. (1985) 104, 233–239
On the origin of dehydroepiandrosterone sulphate in the blood of fetal sheep
Authors: Liggins G. C. , Schellenberg J.-C. , Amato F. , Godfrey B. , Seamark R. F. 
Published: December 2008

ABSTRACT
Total sulphoconjugated and unconjugated dehydroepiandrosterone (DHA) and total oestrone were measured in plasma of intact sheep fetuses, fetuses hypophysectomized at 104–112 days and fetuses bilaterally adrenalectomized at 98–101 days. At 120–127 days, the mean concentrations of total DHA and oestrone in intact fetuses (n = 13) were 29·7 ± 4·2 (s.e.m.) nmol/l and 14·3 ± 2·8 nmol/l respectively. At term, the values for total DHA and oestrone in hypophysectomized fetuses (n = 13) of 18·0 ± 1·9 nmol/l and 9·1 ±2·0 nmol/l were significantly (P <0·05) lower than the intact group whereas in the adrenalectomized fetuses (n = 8) total DHA (80·8±13·0 nmol/l) was higher (P < 0·05) and total oestrone values were similar to the intact animals. Intrafetal infusion of cortisol at term (1 mg/h for 84 h) raised levels of total oestrone in intact (n = 6; 12·3 ± 2·9 vs 31·6± 8·5 nmol/l) and adrenalectomized (n = 4; 14·2 ± 2·6 vs 190·6 ± 53·0 nmol/l) fetuses and of total DHA in hypophysectomized fetuses (n = 7; 16·0±1·9 vs 31·6 ± 8·5 nmol/l) while infusion of ACTH(1–24) (5 μg/h) was without significant effect in any group. It is concluded that the ovine fetal adrenal in late pregnancy makes no significant contribution either to the high circulating concentrations of DHA sulphate or to the substrates for placental oestrogen synthesis.
J. Endocr. (1985) 104, 279–283