bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of the growth hormone receptor gene in chicken pituitary glands
Authors: Hull K. L. , Fraser R. A. , Harvey S. 
Published: December 2008

ABSTRACT
Although GH has no direct effect on GH release from chicken pituitary glands, GH receptor mRNA similar to that in the rabbit liver was identified by Northern blot analysis in extracts of adult chicken pituitaries. Complementary (c) DNA, reverse transcribed from chicken pituitary RNA, was amplified by the polymerase chain reaction (PCR) in the presence of 3′- and 5′-oligonucleotide primers coding for the extracellular domain of the chicken liver GH receptor and was found to contain an electrophoretically separable fragment of 500 bp, identical in size to that in chicken liver. Digestion of this pituitary cDNA with NcoI produced expected moities of 350 and 150 bp. Amplification of chicken pituitary cDNA in the presence of oligonucleotide primers for the intracellular sequence of the chicken liver GH receptor produced an electrophoretically separable fragment of approximately 800 bp, similar to that in chicken liver. This fragment was cut into expected moieties of 530 and 275 bp after digestion with EcoRI. These PCR fragments were identified in extracts of the pituitary caudal lobe, in which somatotrophs are confined and account for the majority of endocrine cell types, and in the cephalic lobe, in which somatotrophs are lacking. Translation of the GH receptor mRNA in the pituitary gland was indicated by the qualitative demonstration of radio-labelled GH-binding sites in plasma membrane preparations, in pituitary cytosol and in nuclear membranes. These results provide evidence for the expression and translation of the GH receptor gene in pituitary tissue, in which GH receptors appear to be widely distributed within cells and in different cell types. GH may therefore have paracrine, autocrine or intracrine effects on pituitary function.
Journal of Endocrinology (1992) 135, 459–468
Site-dependent effects of experimental hypo- and hyperthyroidism on resident macrophages in extraocular muscles of rats: a quantitative immunohistochemical study
Authors: Schmidt E. D. , van Hogerwou G. , van der Gaag R. , Wiersinga W. M. , Asmussen G. , Koornneef L. 
Published: December 2008

ABSTRACT
It has been suggested that the effects of dysthyroidism on resident immunocompetent cells of the extraocular muscles may play a role in the pathogenesis of Graves' ophthalmopathy. The distribution of such cells was therefore studied in extraocular muscles of rats that were made hyper- or hypothyroid by the oral administration of thyroxine or propylthiouracil respectively. Skeletal muscles were studied for comparison. The cell distributions were analysed in cryostat cross-sections subjected to a two-step immunoperoxidase method using well-characterized monoclonal antibodies against T cells, B cells, macrophages and MHC class II antigens.
The extraocular muscles of control (euthyroid) rats contained numerous macrophages, fewer MHC-II positive cells and T cells and no B cells. Differences in the distribution of immunocompetent cells were found in control rats, between skeletal and extraocular muscles as well as within the various recti eye muscles. This particular tissue distribution resembles that previously reported for human extraocular and skeletal muscles.
Quantitative analysis showed that experimental dysthyroidism only affected cell populations in the extraocular muscles. Significant effects on the number of macrophages were observed in the inferior rectus muscle of both hypo- and hyperthyroid rats, this was most pronounced in the orbital layer of the muscles. Both hyper- and hypothyroidism appear to affect local cell distributions in a tissue-specific manner. The presently observed site-dependent effects of dysthyroidism on local immunocompetent cell populations may have relevance for the differential involvement of muscular tissues in Graves' ophthalmopathy.
Journal of Endocrinology (1992) 135, 485–493
Age-related discrepancies between serum and pituitary gonadotrophin, and pituitary gonadotrophin subunit mRNA responses to castration and testosterone replacement in male rats
Authors: Pakarinen P. , Huhtaniemi I. 
Published: December 2008

ABSTRACT
The responses of gonadotrophin gene expression, pituitary content and serum levels to castration alone and castration plus testosterone replacement (silicone elastomer implants) were compared in male rats at 10, 30, 60 and 90 days of age. Sham-operated animals served as controls. In addition, 30-day-old castrated rats were treated with dihydrotestosterone (DHT) and diethylstilboestrol (DES). When killed 7 days after castration, the increases in serum LH (six- to eightfold; P < 0·01) and FSH (two- to fourfold; P < 0·01) were similar at all ages studied. Likewise, testosterone reversed the effects of castration in a largely similar fashion at all ages. In contrast, great age-related differences were observed in the responses of gonadotrophin subunit mRNAs to the treatments. Castration increased the common α subunit mRNA two- to fourfold on days 10 and 30 (P < 0·01), sixfold on day 60 (P < 0·01), but not at all on day 90. Testosterone reversed the increases at all ages, but the levels were below those of controls only at 90 days (P < 0·01). The highest increases (sixfold; P < 0·01) of LH-β mRNA were seen on days 10 and 60, the others being two- to threefold higher (P < 0·05–0·01). Testosterone reversed this effect at 60 days and suppressed LH-β mRNA to below the control levels at other ages (P < 0·01). Castration had no effect on FSH-β subunit mRNA at 30 and 90 days but a four-to fivefold increase was seen on days 10 and 60 (P < 0·01). Testosterone suppressed these mRNAs at all ages, and they decreased to below the levels in controls at 30 and 60 days. Testosterone, DHT and DES had, at 30 days, practically the same effects on the LH parameters, whereas DHT was clearly less effective than testosterone and DES in suppressing those of FSH. In conclusion, although there was, in general, good agreement between gonadotrophin mRNA and serum levels in response to castration and testosterone replacement, there were specific ages when the post-castration increases in FSH and/or LH occurred with no detectable change in the respective mRNA levels. These findings indicate that altered transcription (or mRNA stability) is not solely responsible for the responses of the gonadotrophins to altered gonadal feedback, but that changes in translation efficiency and/or serum gonadotrophin stability are involved at specific ages of development.
Journal of Endocrinology (1992) 135, 507–515
Pituitary-dependent hyperadrenocorticism in a family of Dandie Dinmont terriers
Authors: Scholten-Sloof B. E. , Knol B. W. , Rijnberk A. , Mol J. A. , Middleton D. J. , Ubbink G. J. 
Published: December 2008

ABSTRACT
Adrenocortical function studies were performed in seven Dandie Dinmont terriers with pituitary-dependent hyperadrenocorticism. The ability of dexamethasone at a dose rate of 0·1 mg/kg body weight to suppress cortisol secretion was only moderate in four out of the six dogs tested. Concentrations of α-melanocyte-stimulating hormone in plasma were highly increased. Responses to stimulation with corticotrophin-releasing hormone and the dopamineantagonist haloperidol, examined in three animals, were moderate or absent. These results indicate that adrenocortical stimulation, i.e. hyperadrenocorticotrophism, was caused by pituitary lesions which were functioning autonomously.
In six of the seven animals there was a very close familial relationship and the coefficients of relationship and the coefficients of inbreeding were significantly higher than in a representative control population.
It was concluded that these seven related terriers with hyperadrenocorticotrophism had the biochemical characteristics of de-novo neoplasms of proopiomelanocortin-producing cells, and there was evidence for a genetic involvement in tumorigenesis.
Journal of Endocrinology (1992) 135, 535–542
Distribution and properties of endo-oligopeptidases A and B in the human neuroendocrine system
Authors: Medeiros M. S. , Iazigi N. , Camargo A. C. M. , Oliveira E. B. 
Published: December 2008

ABSTRACT
The thiol activated endo-oligopeptidases A and B were studied in the soluble fraction of human hypothalamus and various endocrine glands. For the identification, characterization and purification of the enzymes, Z-Gly-Pro-NH-Np and bradykinin were used as substrates. Endo-oligopeptidase B showed a molecular mass ranging from 55·5 to 65·5 kDa and isoelectric point from 4·7 to 4·95. Its activity in tissues was highest in the testis, with intermediate levels in the thyroid, neurohypophysis, adenohypophysis and hypothalamus and the lowest activity in the pineal gland. Endo-oligopeptidase A, 467-fold purified by immunoaffinity chromatography, exhibited a molecular mass of 65·5 kDa in the adenohypophysis but 58·5 kDa in other tissues. The isoelectric point ranged from 5·22 to 5·50. High endo-oligopeptidase A activity was observed in the adenohypophysis, testis and hypothalamus with lesser activity in the neurohypophysis and thyroid and the lowest in the pineal gland. Endo-oligopeptidase A cleaved the bonds Phe-Ser of bradykinin, Met-Arg of BAM-12P and Arg-Arg of neurotensin as described for rabbit brain and heart and bovine brain enzymes. This work shows that endo-oligopeptidase A also hydrolysed the bonds Tyr-Gly of LH-releasing hormone, Pro-Phe of angiotensin I and Tyr-Ile of angiotensin II.
Journal of Endocrinology (1992) 135, 579–588
Further studies on the mode of action of calcitonin on isolated rat osteoclasts: pharmacological evidence for a second site mediating intracellular Ca2+ mobilization and cell retraction
Authors: Alam A. S. M. T. , Bax C. M. R. , Shankar V. S. , Bax B. E. , Bevis P. J. R. , Huang C. L.-H. , Moonga B. S. , Pazianas M. , Zaidi M. 
Published: December 2008

ABSTRACT
Calcitonin is a circulating polypeptide that inhibits bone resorption by inducing both quiescence (Q effect) and retraction (R effect) in osteoclasts. Two structurally related members of the calcitonin gene peptide family, calcitonin gene-related peptide (CGRP) and amylin, inhibit osteoclastic bone resorption selectively via the Q effect. In the present study, we have made measurements of cell spread area in response to the application of amylin, CGRP and a peptide fragment of CGRP, CGRP-(Val8Phe37). We found that, over a wide concentration range (50 pmol/l to 2·5 μmol/l), the selective Q effect agonists did not produce an R effect. Furthermore, the peptides, when used at a 50-fold higher molar concentration than calcitonin, did not antagonize calcitonin-induced cell retraction. Additionally, experiments designed to measure changes in the intracellular free calcium concentration ([Ca2 + ]i) in single osteoclasts revealed that, unlike calcitonin, the non-calcitonin Q effect agonists did not produce a rise in [Ca2+]i. The peptides were also unable to attenuate the peak rise in [Ca2+]i induced by calcitonin. The results support our hypothesis that the inhibitory activity of calcitonin on osteoclastic bone resorption is mediated by two sites which may or may not be part of the same receptor complex. One of these is the classical Q effect site coupled to adenylate cyclase via a cholera toxin-sensitive Gs. This site can be activated by nanomolar concentrations of calcitonin, amylin, CGRP or CGRP-(Val8Phe37). A novel R effect site, possibly coupled via a pertussis toxin-sensitive G protein to a [Ca2+]i elevating mechanism is predicted from this study. The site is highly specific for calcitonin and is not activated, even at micromolar concentrations, by amylin, CGRP or CGRP-(Val8Phe37). Whether or not the two sites are part of the same receptor complex or are two receptor subtypes remains to be determined.
Journal of Endocrinology (1993) 136, 7–15
Evidence that inhibin is an important factor in the regulation of FSH secretion during the mid-luteal phase in cows
Authors: Kaneko H. , Nakanishi Y. , Taya K. , Kishi H. , Watanabe G. , Sasamoto S. , Hasegawa Y. 
Published: December 2008

ABSTRACT
To investigate the physiological importance of inhibin in the regulation of FSH secretion in cows, seven cyclic cows were treated with an inhibin antiserum raised against bovine 32 kDa inhibin in a castrated goat. The same animals treated with a castrated goat serum (control serum) served as controls. On day 12 of the oestrous cycle (day 0 = day of oestrus), four of seven cows were injected with 100 ml inhibin antiserum first, and the remaining three cows with 100 ml control serum first. Twelve days after the second oestrus following the first serum injection (42–46 days after the first serum injection), the former four cows were injected with control serum and the latter three with inhibin antiserum. Follicular development after the injections of control serum or inhibin antiserum was assessed by daily ultrasonographic examination.
Treatment with inhibin antiserum resulted in a marked increase (P < 0·01) in plasma concentrations of FSH and oestradiol-17β but not LH or progesterone, compared with those after treatment with control serum. Plasma concentrations of FSH increased significantly (P < 0·01) at 8 h after injection of antiinhibin serum when compared with the control value. Concentrations of FSH in the plasma remained high for 72 h, then declined to the control level by 84 h, concomitant with an abrupt decrease in the titre of free inhibin antibody in the plasma. High concentrations of oestradiol-17β were observed between 36 and 96 h after treatment. Treatment with inhibin antiserum markedly increased the number of small (≥ 4 < 7 mm in diameter), medium (≥ 7 < 10 mm) and large (≥ 10 mm) follicles by 48, 72 and 96 h after treatment when compared with the value before treatment. The number of large follicles returned to the pretreatment value at 168 h, whereas the number of small and medium follicles remained increased.
The present results provide strong evidence that inhibin is an important factor in the inhibitory regulation of FSH secretion during the mid-luteal phase of cows, and demonstrate that an increase in endogenous FSH secretion after immunoneutralization of circulating inhibin stimulates the rapid growth of a large number of follicles.
Journal of Endocrinology (1993) 136, 35–41
Effect of 3,3′-di-iodothyronine and 3,5-di-iodothyronine on rat liver mitochondria
Authors: Lanni A. , Moreno M. , Cioffi M. , Goglia F. 
Published: December 2008

ABSTRACT
In the present study we report that 3,3′,5-tri-iodothyronine (T3) as well as two iodothyronines (3,5-diiodothyronine (3,5-T2) and 3,3′-di-iodothyronine (3,3′-T2)) significantly influence rat liver mitochondrial activity.
Liver oxidative capacity (measured as cytochrome oxidase activity/g wet tissue) in hypothyroid compared with normal rats was significantly reduced (21%, P > 0·01) and the administration of T3 and both iodothyronines restored normal values. At the mitochondrial level, treatment with T3 stimulated respiratory activity (state 4 and state 3) and did not influence cytochrome oxidase activity. On the other hand, both the mitochondrial respiratory rate and specific cytochrome oxidase activity significantly increased in hypothyroid animals after treatment with 3,3′-T2 or 3,5-T2 (about 50 and 40% respectively). The actions of both iodothyronines were rapid and evident by 1 h after the injection. The hepatic mitochondrial protein content which decreased in hypothyroid rats (9·6 mg/g liver compared with 14·1 in normal controls, P < 0·05) was restored by T3 injection, while neither T2 was able to restore it.
Our results suggest that T3 and both iodothyronines have different mechanisms of action. T3 acts on both mitochondrial mass and activity; the action on mitochondrial activity was not exerted at the cytochrome oxidase complex level. The action of the iodothyronines, on the other hand, is exerted directly on the cytochrome oxidase complex without any noticeable action on the mitochondrial mass.
Journal of Endocrinology (1993) 136, 59–64
Oestradiol negative feedback inhibition on LH secretion during lactation is prolonged in adolescent primiparous rhesus monkeys
Authors: Wilson M. E. 
Published: December 2008

ABSTRACT
Lactational infertility in rhesus monkeys is significantly prolonged in adolescent primiparous compared with adult multiparous mothers. In order to determine if this longer period of infertility for young mothers is the result of a greater sensitivity to nursing-induced inhibition of LH release either by enhanced oestradiol negative feedback or a direct non-gonadally mediated suppression, the effects of periodic administration of oestradiol on serum LH concentrations in nursing ovariectomized adolescent primiparous (Prp; n = 5) and adult multiparous (Mlt; n = 7) mothers was assessed. Females were treated every 5–6 weeks with a 21-day time-release capsule of oestradiol which produced serum concentrations of approximately 250, 90 and 45 pmol/l by +6, +13 and +20 days after treatment. Thus, the design permitted assessment of LH and prolactin concentrations under a regime of 21 days of decreasing oestradiol levels followed by 2–3 weeks of no oestradiol treatment. Females were studied from week 3 to week 42 post partum and oestradiol treatment occurred during weeks 5, 11, 21, 26, 31, 36 and 41.
Behavioural observations indicated that the amount of time mothers nursed their offspring decreased in a similar fashion throughout the lactational period for both Prp and Mlt females. LH concentrations under the 'no oestradiol' conditions progressively increased throughout lactation reaching maximum levels by week 36 post partum in a similar manner for both Prp and Mlt mothers. These data suggest that differences in fertility between adolescent and adult nursing mothers observed previously cannot be attributed to a difference in a direct non-gonadally-mediated affect on LH.
With respect to oestradiol negative feedback inhibition of LH, oestradiol treatment effectively suppressed serum LH concentrations at all points during lactation up to week 31, at which time LH concentrations were maximally suppressed in both Prp and Mlt mothers at + 6 days after treatment but by day + 13 LH values were significantly higher in Mlt females. After oestradiol treatment during week 36, LH values were again maximally suppressed on day +6 in Prp females but not in Mlt females. However, the response of serum LH after oestradiol treatment during week 41 was similar between Prp and Mlt females at all sampling points. Thus, the effectiveness with which oestradiol suppressed LH concentrations diminished at an earlier point in lactation in Mlt compared with Prp mothers. Furthermore, this parity/age difference in oestradiol negative feedback inhibition of LH was not associated with differences in nursing behaviour. These data suggest that the prolonged period of lactational infertility in adolescent primiparous monkey mothers is the result of a hypersensitivity to oestradiol negative feedback inhibition of LH which is still functional at a time when the nursing stimulus has diminished.
Journal of Endocrinology (1993) 136, 127–136
Cell interactions in initiation of mammary epithelial proliferation by oestradiol and progesterone in prepubertal heifers
Authors: Woodward T. L. , Beal W. E. , Akers R. M. 
Published: December 2008

ABSTRACT
The acute temporal effects of exogenous oestradiol (0·1 mg/kg per day), progesterone (0·25 mg/kg per day) or both together on the proliferative response of epithelial cells, fibroblasts, adipocytes and endothelial cells in the mammary tissue of prepubertal cross-bred heifers were determined. Mammary biopsies were taken immediately before, then 24, 48 and 96 h after the initiation of daily administration of hormones to three heifers per treatment group. Incorporation of [3H]thymidine into explants prepared from biopsies was evaluated after a 1-h incubation by measuring trichloroacetic acid (TCA)-insoluble radioactivity in explant homogenates as well as by quantitative histoautoradiography. Incorporation expressed as d.p.m./mg tissue or d.p.m./μg DNA was increased (P ≤ 0·05) approximately 11-fold by 96 h in oestradiol-treated heifers. Progesterone-treated animals were unresponsive and heifers treated with both hormones were intermediate in response compared with oestradiol-treated heifers. Autoradiographic data for ductal or terminal duct epithelial cells showed similar dramatic increases in labelling by 24 h with further increased (P < 0·01) labelling by 96 h (5·1% vs 0·1%) in heifers given oestradiol. As with incorporation, tissue from progesterone-treated heifers showed no time or treatment response compared with pretreatment biopsies and tissue from heifers given both showed intermediate responses, i.e. significantly increased labelling by 96 h compared with pretreatment (P ≤ 0·05) but less labelling (P < 0·05) than oestradiol-treated heifers. A proliferative response of epithelial cells in oestradiol-treated heifers occurred prior to the response of fibroblasts adjacent to epithelial cells (≤ 50 μm). Interestingly, labelling of endothelial cells was also markedly increased by 48 h in oestradiol-treated heifers. Non-adjacent fibroblasts (≥ 100 μm from ductal epithelial cells) and adipocytes showed no time or treatment response. These data demonstrate that exogenous oestradiol markedly and acutely stimulates proliferation of mammary ducts, while progesterone has no effect and may decrease the effectiveness of oestradiol. In contrast to mice, mammary epithelial response to oestradiol in prepubertal heifers is not first exhibited after a proliferative response of stromal cells. This suggests that the cell-type interactions involved in the control of mammogenesis are dissimilar in ruminants and rodents.
Journal of Endocrinology (1993) 136, 149–157
Reproducibility of the cortisol response to stimulation with a low dose of ACTH(1–24): the effect of basal cortisol levels and comparison of low-dose with high-dose secretory dynamics
Authors: Crowley S. , Hindmarsh P. C. , Honour J. W. , Brook C. G. D. 
Published: December 2008

ABSTRACT
We compared the reproducibility and repeatability of the acute adrenal response to low doses (90 and 500 ng/1·73 m2) of Synacthen (ACTH(1–24)) with that of the standard dose (250 μg/1·73 m2). We also examined the effect of basal cortisol levels on peak values achieved after stimulation with a low dose.
ACTH(1–24) was given to six male volunteers: 90 ng/1·73 m2 twice at 90-min intervals on day 1, and 90 and 500 ng/1·73 m2 once on day 2 and 250 μg/1·73 m2 once on day 3. The rise in serum cortisol concentration with repeated low doses of ACTH was not attenuated (161 ± 49 (s.d.) nmol/l on initial vs 150 ± 41 nmol/l on repeat stimulation; P = 0·5) and this was reproducible (161 ± 49 nmol/l on day 1 vs 148 ± 15 nmol/l on day 2; P = 0·6). A dose of 500 ng ACTH(1–24)/1·73 m2 produced a maximal adrenal response in that the rise in serum cortisol concentration at 20 min was identical with that produced at the same time by the standard dose of 250 μg/1·73 m2. There was a strong positive correlation between the basal cortisol level and peak cortisol concentration after low-dose ACTH stimulation (r = 0·93, P < 0·001) but not between the basal cortisol level and the incremental rise (r= −0·1, P = 0·69).
These results suggest that the cortisol response to low-dose ACTH stimulation is reproducible and not attenuated by repeat stimulation at 90-min intervals. The incremental rise in serum cortisol concentration after ACTH stimulation appears constant in these situations and is not influenced by the basal cortisol level. When there is concern that the standard dose may be excessive and mask subtle but important changes in adrenal function, the low dose (500 ng) of ACTH should be used.
Journal of Endocrinology (1993) 136, 167–172