bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship between growth and function of human thyroid cells in culture
Authors: Ollis C. A. , Davies R. , Munro D. S. , Tomlinson S. 
Published: December 2008

ABSTRACT
Subconfluent human thyroid cells in monolayer, isolated from thyrotoxic tissue or non-toxic goitres obtained at surgery, responded to the addition of epidermal growth factor (EGF) with an increase in cell growth as measured by increased incorporation of [3H]thymidine into trichloroacetic acid-precipitable material. The growth response to EGF was concentration-dependent and the characteristics of the responses were the same using EGF from murine or human sources. With concentrations which stimulated growth, EGF was found to inhibit human thyroid cell function as measured by the release of radioimmunoassayable tri-iodothyronine into the incubation medium. Thyrotrophin (TSH) was also found to stimulate human thyroid cell growth but at concentrations far lower than those used to stimulate thyroid cell function in this system. The effect of EGF on the differentiating action of TSH on human thyroid cells in culture was also investigated; the association of thyroid cells into two-dimensional follicular structures produced by the incubation of thyroid cells at a high cell density with TSH was found to be inhibited by the addition of EGF.
J. Endocr. (1986) 108, 393–398
Prolactin release, oestrogens and proliferation of prolactin-secreting cells in the anterior pituitary gland of adult male rats
Authors: Pérez R. L. , Machiavelli G. A. , Romano M. I. , Burdman J. A. 
Published: December 2008

ABSTRACT
Relationships among the release of prolactin, the effect of oestrogens and the proliferation of prolactin-secreting cells were studied under several experimental conditions.
Administration of sulpiride or oestradiol released prolactin and stimulated cell proliferation in the anterior pituitary gland of adult male rats. Clomiphene completely abolished the rise in cell proliferation, but did not interfere with the sulpiride-induced release of prolactin. Treatment with oestradiol plus sulpiride significantly increased serum prolactin concentrations and the mitotic index compared with the sum of the stimulation produced by both drugs separately. Bromocriptine abolished the stimulatory effect of oestradiol on the serum prolactin concentration and on cell proliferation. In oestradiol- and/or sulpiride-treated rats, 80% of the cells in mitoses were lactotrophs. The remaining 20% did not stain with antisera against any of the pituitary hormones. The number of prolactin-secreting cells in the anterior pituitary gland significantly increased after the administration of oestradiol or sulpiride.
The results demonstrate that treatment with sulpiride and/or oestradiol increases the proliferation and the number of lactotrophs in the anterior pituitary gland of the rat.
J. Endocr. (1986) 108, 399–403
Effects of LH and an LH-releasing hormone agonist on different second messenger systems in the regulation of steroidogenesis in isolated rat Leydig cells
Authors: Themmen A. P. N. , Hoogerbrugge J. W. , Rommerts F. F. G. , van der Molen H. J. 
Published: December 2008

ABSTRACT
The stimulation of steroid production in Leydig cells by LH is accompanied by increased cyclic AMP levels, activation of protein kinase A, increased phosphorylation of at least six phosphoproteins and requires protein synthesis. However, an LH-releasing hormone agonist (LHRH-A) can stimulate steroid production without stimulation of cyclic AMP levels. In the present study we have shown that LH action involves calcium fluxes through the plasma membrane, in addition to activation of protein kinase A. The action of LHRH-A, in contrast, does not require calcium fluxes and is not potentiated by 1-methyl-3-isobutylxanthine, indicating that cyclic AMP is not involved. Extracellular calcium is required for the action of both LH and LHRH-A. An increase in intracellular calcium concentration due to the effect of ionophore A23187 did not stimulate steroidogenesis and had deleterious effects on intracellular adenosinetriphosphate levels. LH and 4β-phorbol-12-myristate-13-acetate (PMA), an activator of protein kinase C, both stimulated phosphorylation of proteins of 17 000 and 33 000 mol. wt, whereas LHRH-A had no effect. However, compared with the effect of LH, PMA had a much smaller effect on steroid production, indicating that even if protein kinase C may be activated by LH its role in the regulation of steroid production may be less important than the role of protein kinase A. Action of LHRH-A does not appear to be mediated by calcium fluxes, protein kinase C activation or active protein phosphorylation.
J. Endocr. (1986) 108, 431–440
Colloidal carbon blocks oestrogen-induced migration of eosinophils to the uterus and the uterine water imbibition response
Authors: López M. , Castrillón M. A. , Tchernitchin A. N. 
Published: December 2008

ABSTRACT
Oestrogen induces a migration of eosinophil leukocytes to the uterus where, it is suggested, these cells mediate several responses to hormone stimulation. To investigate the mechanism of the recognition of the uterus by the eosinophils, the present study describes the effect of a blockade of the rat reticulo-endothelial system with colloidal carbon on oestrogen-induced uterine eosinophilia, and other responses to oestrogen stimulation that, it has been suggested, are mediated by eosinophils.
In the absence of oestrogen colloidal carbon induced an increase in the number of eosinophils in mesometrium but not in endometrium with myometrium, and a slight oedematous reaction in deep endometrium. Colloidal carbon abolished the oestrogen-induced increase in the number of eosinophils in endometrium with myometrium and drastically decreased the oestrogen-induced increase in uterine wet weight and the endometrial oedematous responses 6 h after the administration of oestrogen.
The present results agree with the hypothesis that most uterine water imbibition is mediated by eosinophils and suggest a possible mechanism for the interaction of colloidal carbon with eosinophil migration to the uterus.
J. Endocr. (1986) 109, 89–95
Transcortin and vitamin D-binding protein levels in mouse serum
Authors: Faict D. , De Moor P. , Bouillon R. , Heyns W. , Heiniger H.-J. , Corrow D. , Lesaffre E. 
Published: December 2008

ABSTRACT
The influence of age, sex and strain on the serum concentration of transcortin (corticosteroid-binding globulin) and vitamin D-binding protein (DBP) in mice was investigated. The effect of age was studied in two strains, C57BL/6JPfd and BALB/cmHeAPfd. The concentration of transcortin and DBP increased with age. In young animals the concentration of each protein showed a significant strain difference, which disappeared in older mice for DBP, but not for transcortin. In 7-day-old animals, no sex difference was observed for either protein, but in older animals a clear sex difference was found for transcortin. Adult males tended to have somewhat higher levels of DBP than adult females, but this difference was significant only on day 70.
The variation in transcortin and DBP levels was further investigated in a large number of mouse strains. The DBP concentration did not markedly vary among strains (5·98–9·65 μmol/l in males and 5·08–8·85 μmol/l in females). Transcortin, however, showed marked strain variations, ranging from 0·72 to 2·06 μmol/l in males and from 1·02 to 4·55 μmol/l in females and there was a significant correlation (r= 0·66, n= 26, P<0·001) between the mean transcortin levels in males and females of different strains. Interstrain variation was much higher than intrastrain variation or variation among related strains, suggesting that the transcortin concentration is largely controlled by genetically determined factors.
There was a significant correlation (r= 0·82, n = 9, P<0·01) between the mean corticosterone and transcortin concentrations (measured at 21.00 h). Consequently, differences in the free corticosterone levels in the serum of various mouse strains were smaller than the differences in the total corticosterone concentrations. The affinity of transcortin for corticosterone was similar in all but one strain; however, transcortin of the RIIIS/J strain showed a lower affinity for corticosterone.
J. Endocr. (1986) 109, 141–147
Steroid binding to feather follicles in the chicken
Authors: Kovács K. , Péczely P. , Szelényi Z. 
Published: December 2008

ABSTRACT
Steroid binding profiles in chicken feather follicles were studied in vitro. Progesterone and promegestone were bound specifically with high affinity (dissociation constant = 7·79 nmol/l in females and 2·0 nmol/l in males) and with low capacity to the high-speed supernatant fraction (cytosol) of homogenized feather follicles. The number of progestin-binding sites was significantly (P < 0·01) higher in females than in males (1·35 ± 0·07 (mean ± s.d.) vs 0·605 ± 0·15 pmol/mg protein). Significant cross-competition was observed between progestins and glucocorticoids for the binding sites. The heat-activated progestin–receptor complexes bound specifically to DNA-cellulose in vitro. The DNA-cellulose binding was 36·6% of the total specific binding. The presence of progestin-binding sites in the feather follicles implies a direct action of progesterone in this structure, which may be an important factor in the regulation of moulting. The lack of oestrogen binding to the cytosol prepared from the feather follicles suggests different regulation of progestin receptors in different target organs.
J. Endocr. (1986) 109, 187–191
Five new insulin-producing cell lines with differing secretory properties
Authors: Carrington C. A. , Rubery E. D. , Pearson E. C. , Hales C. N. 
Published: December 2008

ABSTRACT
Five cell lines have been derived from a rat transplantable islet cell tumour using two different methods. The lines differ in morphology and contain and release different amounts of insulin and glucagon (insulin content, 1–90 pmol/106 cells; insulin release, 6–250 pmol/106 cells per 24 h; glucagon content, < 0·005–35 pmol/106 cells; glucagon release, < 0·05– 10 pmol/106 cells per 24 h). All the lines responded to the presence of the secretagogues leucine (20 mmol/l) plus theophylline (5 mmol/l) by increasing the rate of release of insulin approximately twofold. A high extracellular concentration of potassium (40 mmol/l) caused a three- to tenfold calcium-dependent increase in release of insulin and a parallel release of glucagon. Increasing the concentration of glucose from 2·8 to 16·7 mmol/l did not alter the rate of insulin release by any of the cell lines.
J. Endocr. (1986) 109, 193–200
Dexamethasone and 8-bromo-cyclic AMP depress the incorporation of [3H]thymidine into mouse condylar cartilage by different pathways
Authors: Kraiem Z. , Maor G. , Silbermann M. 
Published: December 2008

ABSTRACT
We examined whether cyclic AMP (cAMP) affects the incorporation of [3H]thymidine into cartilage cells and, if so, whether this action could be related to the inhibitory effect of glucocorticoid hormones on the growth of ossifying cartilage. Incorporation of [3H]thymidine into trichloroacetic acid-precipitable material by mouse cartilage was measured concomitantly with the concentration of cAMP. Dexamethasone (1 μmol/l) significantly (P < 0·05) depressed the incorporation of [3H]thymidine. The cAMP analogue 8-bromo-cAMP (0·01–1 mmol/l) also depressed the incorporation of the radionucleotide in a dose-dependent fashion. When various concentrations of 8-bromo-cAMP were added with dexamethasone (1 μmol/l), no apparent changes took place compared with the effect of dexamethasone alone. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0·2-1 mmol/l) elicited an inhibitory effect on [3H]thymidine incorporation and a stimulatory influence on cartilage cAMP concentrations. Dexamethasone, at doses (0·01–1 μmol/l) causing significant inhibition of [3H]thymidine incorporation, failed to increase cartilage levels of cAMP. It seems, therefore, that the depressive effect of dexamethasone on [3H]thymidine incorporation in condylar cartilage is not mediated through an increase of cAMP in the tissue.
J. Endocr. (1986) 109, 209–213
Regulation of the level of epidermal growth factor by oestrogen in the submandibular gland of female mice
Authors: Kurachi H. , Oka T. 
Published: December 2008

ABSTRACT
The concentration of epidermal growth factor (EGF) in the submandibular gland of immature female mice (less than 6 weeks old) was low, ranging from 0·07 to 0·17 pmol (0·4 to 1·0 ng)/mg wet wt, but increasing to 7·61 pmol/mg wet wt by 8 weeks of age. It remained relatively constant up to 24 weeks of age, but thereafter the glandular EGF concentration increased again during the post-reproductive period to reach 62·9 pmol/mg wet wt. In contrast, the glandular EGF content in male mice increased greatly during the first 17 weeks of age to about 310 pmol/mg wet wt, and thereafter remained relatively constant up to 48 weeks of age. Ovariectomy of mature virgin mice markedly increased the glandular concentration of EGF to about 74·4 pmol/mg wet wt 4 weeks after the operation. This increase was suppressed by oestradiol-17β administered to ovariectomized mice at a dose of 1 μg/mouse per day but not by 1 mg progesterone. Histological studies indicated that granular convoluted tubular cells that produced EGF in the submandibular gland were much less abundant in 12-week-old female and in oestrogen-treated ovariectomized mature mice than in 40-week-old female and ovariectomized mature mice. We conclude that oestrogen suppresses the concentration of EGF in the submandibular gland of female mice.
J. Endocr. (1986) 109, 221–225
The actions of N-terminal fragments of corticotrophin on steroidogenesis in dispersed rat adrenal cells in vitro
Authors: Vinson G. P. , Whitehouse B. J. , Bateman A. , Dell A. , Laird S. M. 
Published: December 2008

ABSTRACT
The finding that the rat adrenal zona glomerulosa cell shows specific sensitivity to stimulation by α-MSH and related peptides has been confirmed both in vivo and in vitro, raising the possibility that α-MSH may have a physiological role in the control of glomerulosa function and aldosterone secretion. To define more closely the structural features which confer the specificity of the glomerulosa response, other ACTH derived peptides have been tested for their specificity of actions on rat adrenal cells in vitro. The peptides tested were ACTH(5–24), ACTH(1–12), ACTH(1–14), ACTH(1–15), ACTH1–16) and ACTH(1–17). Their actions were compared with those of α-MSH and ACTH(1–24). All of the ACTH-derived peptides stimulated glomerulosa corticosterone production with sensitivities similar to that of α-MSH; minimum effective concentration was 10 nmol/l. Also, like α-MSH, the shorter ACTH peptides stimulated aldosterone production only relatively weakly in these cells from animals on normal sodium intake. Only ACTH(5–24), ACTH(1–16) and ACTH(1–17) stimulated fasciculata/reticularis cells at concentrations up to 1 μmol/l. The actions of all of the shorter peptides were thus unlike those of ACTH(1–24) which stimulates both cell types with approximately equal sensitivity, and which furthermore strongly stimulates aldosterone production.
The data suggest that the 18–24 region of the ACTH molecule contains the signal for a fasciculata/ reticularis response, and the region 1–13 that for glomerulosa specificity. They confirm the view that, in the rat, α-MSH itself may be the specific pituitary glomerulosa-stimulating agent which much experimental work has predicted. They also indicate that synthetic ACTH(1–17) analogues should be used with caution.
J. Endocr. (1986) 109, 275–278
Pulsatile growth hormone secretion in the ovine fetus and neonatal lamb
Authors: Bassett N. S. , Gluckman P. D. 
Published: December 2008

ABSTRACT
The ontogenesis of the pulsatility of GH in the ovine fetus was determined by obtaining blood samples at 20-min intervals for 3-h periods from fetuses (n = 33) at various stages of development (76–147 days gestation), and in neonatal life (n = 19). A significant increase (P <0·01) in the GH mean, nadir and maximum, and pulse height was observed between the ages of 100 and 130–139 days of gestation. An analysis of the difference in the mean, maximum and nadir concentrations between 100 and 139 days of gestation revealed that males had higher GH levels than females (P <0·05).
There was a significant fall in plasma GH concentrations from 140 days of gestation to term, but before the onset of active labour. There was a more rapid fall in the circulating levels of fetal GH directly following birth. Immediately before birth fetal GH levels were still relatively high, but within 60 min of birth they had fallen by more than 80%.
It is suggested that these changes in the pulsatile pattern of GH release are a consequence of both maturational changes in the hypothalamic-pituitary unit and the effects of pregnancy-related factors on GH release. The sexually dimorphic nature of GH release in the adult is also observed in the sheep fetus during late gestation.
J. Endocr. (1986) 109, 307–312
Kinetics of transfer of 125I-labelled epidermal growth factor from blood into mammary secretions of goats
Authors: Brown K. D. , Blakeley D. M. , Fleet I. R. , Hamon M. , Heap R. B. 
Published: December 2008

ABSTRACT
125I-Labelled mouse epidermal growth factor (125I-EGF) was transferred intact and undegraded from circulating blood into milk in conscious lactating goats. Greater than 90% of the total radioactivity present in milk from the infused gland was in the aqueous phase and more than 72% was acidprecipitable. This radiolabelled material co-eluted with authentic EGF through gel filtration and was immunoprecipitable by a specific rabbit anti-mouse EGF immunoglobulin. Mammary uptake of125I-EGF infused into mammary arterial blood (close-arterial infusion) for 1 h varied from 20 to 83% at different stages of the reproductive cycle. Only 0·5–2·9% of the infused 125I-EGF was transferred into milk during the first 3 h after the start of the infusion, which represents 0·7–6·3% of mammary uptake of EGF.
The kinetics of transfer of 125I-EGF were followed in two lactating goats. Radioactivity reached peak levels in milk about 120 min after the start of a 1 h close-arterial infusion into the mammary gland, with an initial lag of about 30 min when little transfer occurred. Transfer was slower in two non-lactating goats with maximal levels of activity in milk being reached after about 180 min. The results are consistent with a transcellular transfer, whereby the factor is bound to receptors on the baso-lateral membrane, internalized by epithelial cells and subsequently secreted across the apical membrane into the alveolar lumen. The low level of degraded labelled EGF in milk (and mammary vein blood) suggests a modification of the normal pathway of EGF degradation such that the delivery of internalized factor to lysosomes is avoided.
J. Endocr. (1986) 109, 325–332
Dopamine effects on adrenocorticotrophin-stimulated aldosterone, cortisol, corticosterone and 11-deoxycorticosteroid concentrations in sodium-replete and sodium-deplete man
Authors: Connell J. M. C. , Kenyon C. J. , Ball S. G. , Davies D. L. , Fraser R. 
Published: December 2008

ABSTRACT
The effect of dopamine (1 μg/kg per min) on corticosteroid response to ACTH (0·1, 1 and 10 ng/kg per min) was compared with that of a placebo in sodium-replete (150 mmol/day) and -deplete (10 mmol/day) normal man. Dopamine had no effect on aldosterone, cortisol or corticosterone responses in either dietary phase, but increased deoxycorticosterone (897·0 ± 126·4 (s.e.m.) vs 590·0 ±84·3 pmol/l, normal Na+; 1264·2 ±84·3 vs 764·5 ±84·3 pmol/l, low Na+) and deoxycortisol (6·033 ± 0·583 vs 5·048±0·680 nmol/l, normal Na+; 5·112 ± 0·600 vs 4·130± 0·367 nmol/l, low Na+) levels during ACTH administration (all P <0·01). Deoxycorticosterone and corticosterone responses to ACTH were greater during sodium depletion than repletion (both P <0·01).
Dopamine therefore increased 11-deoxycorticosteroid concentrations during ACTH-stimulated steroidogenesis. This may reflect action of dopamine to increase extra-adrenal formation of 11-deoxycorticosteroids.
J. Endocr. (1986) 109, 339–344
Hypothyroidism of hypothalamic origin in pyridoxine-deficient rats
Authors: Dakshinamurti K. , Paulose C. S. , Vriend J. 
Published: December 2008

ABSTRACT
Pyridoxine-deficient young rats (3 weeks old) had significantly reduced levels of pituitary TSH, serum thyroxine (T4) and tri-iodothyronine (T3) compared with pyridoxine-supplemented rats. The status of the pituitary-thyroid axis of normal, pyridoxine-supplemented and pyridoxine-deficient rats was evaluated by studying the binding parameters of [3H](3-methyl-histidine2)TRH in the pituitary of these rats. The effects of TRH and T4 injections on pituitary TSH and serum TSH, T4 and T3 of these two groups were also compared. The maximal binding of TRH receptors in the pituitary of pyridoxine-deficient rats was significantly higher than that of pyridoxine-supplemented control and normal rats, but there was no change in the binding affinity. Treatment with TRH stimulated TSH synthesis and release. It also increased serum T4 and T3 in both pyridoxine-supplemented and pyridoxine-deficient rats. Treatment with T4 decreased serum and pituitary TSH in both pyridoxine-supplemented and pyridoxine-deficient rats, compared with saline-treated rats. The increased pituitary TRH receptor content, response to TRH administration and the fact that regulation at the level of the pituitary is not affected in the pyridoxine-deficient rat indicates a hypothalamic origin for the hypothyroidism of the pyridoxine-deficient rat.
J. Endocr. (1986) 109, 345–349
Effects of porcine relaxin on oxytocin release from the neurohypophysis in the anaesthetized lactating rat
Authors: O'Byrne K. T. , Eltringham L. , Clarke G. , Summerlee A. J. S. 
Published: December 2008

ABSTRACT
The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat.
The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2·5–10 μg/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6–10 min and lasted for 10–60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500–2000 ng/ml) failed to inhibit oxytocin release in vitro.
The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release.
J. Endocr. (1986) 109, 393–397