bluuebunny/crossref_metadata_2025_split huggingface dataset:
Localization of epidermal growth factor receptors in the human prostate by biochemical and immunocytochemical methods
Authors: Maddy S. Q. , Chisholm G. D. , Hawkins R. A. , Habib F. K. 
Published: December 2008

ABSTRACT
The receptor for epidermal growth factor (EGF) was characterized in the particulate fraction from human benign prostatic hyperplasia (BPH) and was present in 85% of tissues analysed. The uptake of 125I-labelled EGF by BPH was dependent on both time and temperature, with maximum specific uptake achieved after incubation for 90 min at 37 °C. Binding characteristics revealed two classes of binding sites of higher (mean dissociation constant (Kd)±s.d.= 0·8 ± 0·2 nmol/l) and lower (Kd = 7·6 ±2·8 nmol/l) affinities. Competition studies demonstrated the specificity of the receptor assay since the binding of labelled EGF was abolished with excess unlabelled EGF but not with excess unlabelled human GH, human insulin, venom nerve growth factor, human FSH, human LH and human prolactin. There was a complex biphasic relationship between specific binding and protein concentration in the range 0·1–8 mg/ml. Subcellular fractionation of BPH homogenates demonstrated that the bulk of the specific binding was confined to the 800 g (crude heavy pellet) and 15 000 g (mitochondrial pellet) fractions. The 105 000 g (microsomal pellet) and the 105 000 g (cytosol fraction) exhibited low and variable binding capacities for the growth factor. The presence of EGF receptor was also confirmed by immunocytochemical staining of frozen sections from BPH using monoclonal antibody specific for EGF receptors. A positive correlation between 125I-labelled EGF binding and the intensity of staining was found. The presence of a specific EGF-binding receptor protein in human BPH tissues suggests that EGF may play a role in the pathogenesis of human BPH.
J. Endocr. (1987) 113, 147–153
Preliminary investigations into the endocrine systems of subfertile cattle: location of a common lesion (rate-limiting step)
Authors: Dobson H. , Alam M. G. S. 
Published: December 2008

ABSTRACT
Dairy cows with a variety of clinical conditions were investigated in an attempt to identify the cause(s) of subfertility. Sequential or simultaneous injections of 20 μg gonadotrophin-releasing hormone (GnRH), 1 mg oestradiol benzoate and 0·06 mg ACTH(1–24) into five clinical cases of ovarian follicular cysts, two cases of poor body condition and one case of lameness and into control cows revealed a failure in the LH positive-feedback response to oestradiol in all eight clinical cases, but in only two out of twelve control cows. Two of the clinical cases and the two non-responding control cows had high or rising initial progesterone concentrations which would explain the absence of response. All cows studied responded similarly to GnRH and ACTH(1–24).
It is suggested that hypothalamus-pituitary control of LH release may involve a rate-limiting step (in the oestradiol positive-feedback system) and that lesions at this point result in subfertility in a variety of clinical situations.
J. Endocr. (1987) 113, 167–171
A novel technique for measuring hypothalamic and pituitary hormone secretion rates from collection of pituitary venous effluent in the normal horse
Authors: Irvine C. H. G. , Alexander S. L. 
Published: December 2008

ABSTRACT
We have described a novel technique for collecting pituitary venous effluent in the horse by placing a cannula in the intercavernous sinus close to the outlet of the pituitary veins using a venous pathway unique to equids. Cannula placement and blood collection are carried out painlessly in fully conscious, ambulatory, unstressed animals. There is no interference to hypothalamic, pituitary or target organ function. The blood collected contains readily measurable concentrations of gonadotrophin-releasing hormone, and LH concentrations which can be up to 40 times those in concurrent peripheral blood samples. Four millilitre blood samples, a quantity which permits simultaneous measurement of many hypothalamic and pituitary hormones, can be collected at 2-min intervals for several days. Intercavernous sinus blood flow can be calculated allowing secretion rates of hypothalamic and pituitary hormones to be determined for any time-period. This model is uniquely useful for investigating the normal functional characteristics of several neuroendocrine and endocrine systems.
J. Endocr. (1987) 113, 183–192
Calmodulin inhibitors and 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate do not prevent the inhibitory effect of prostaglandin F2α on cyclic AMP production in isolated rat corpora lutea
Authors: Lahav M. , Rennert H. , Sabag K. , Barzilai D. 
Published: December 2008

ABSTRACT
In the rat corpus luteum, prostaglandin F2α (PGF2α) rapidly inhibits LH-induced cyclic AMP (cAMP) production when given in vivo or to isolated corpora lutea, but not to broken-cell preparations. The suggestion that increased cytosolic calcium concentration mediates PGF2α action was investigated in corpora lutea of pseudopregnancy induced in immature rats by administration of pregnant mare serum gonadotrophin (15 i.u.). Isolated 10-day-old corpora lutea were incubated for 90 min with LH (5 μg/ml), PGF2α (10 μmol/l) and other additions, and cAMP concentration in the tissue was estimated. The putative inhibitor of intracellular calcium release or action, 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8; 30 or 150 μmol/l), did not abolish the effect of PGF2α. Similarly ineffective was the combination of TMB-8 (150 μmol/l) and calcium-depleted medium (free ionized calcium concentration, 30 nmol/l). Calmodulin inhibitors of three different chemical structures were then tested. The phenothiazine trifluoperazine, at 300 as well as 30 μmol/l, did not interfere with the inhibitory effect of PGF2α on cAMP, while suppressing (at 300 μmol/l) progesterone secretion in LH-treated tissue. Furthermore, inhibition by PGF2α was not impaired by pimozide, a diphenylbutylpiperidine (25 and 50 μmol/l) nor by N-(6-aminohexyl)-5-chloro-1-naphthalene sulphonamide (W-7; 15 and 45 μmol/l). In the presence of LH alone, W-7 (45 μmol/l) inhibited and TMB-8 (30 μmol/l augmented cAMP accumulation, indicating that the luteal tissue was effectively exposed to these compounds. Thus, drugs known to inhibit calcium- and calmodulin-dependent processes in a variety of tissues did not abolish the inhibitory action of PGF2α on luteal cAMP production.
J. Endocr. (1987) 113, 205–212
Isolation of inhibin from ovine follicular fluid
Authors: Leversha L. J. , Robertson D. M. , de Vos F. L. , Morgan F. J. , Hearn M. T. W. , Wettenhall R. E. H. , Findlay J. K. , Burger H. G. , de Kretser D. M. 
Published: December 2008

ABSTRACT
Two forms of inhibin with molecular weights of 65 000 and 30 000 (65 and 30 kD) were isolated from ovine follicular fluid using a combination of gel permeation chromatography, reversed-phase high-performance liquid chromatography and preparative polyacrylamide gel electrophoresis. The 65 kD form was partially purified approximately 315-fold whilst the 30 kD form was isolated as two isoforms (29 and 30 kD) of similar biological activity and in >95% purity (1210-fold purification and 4·2% recoveries). On reduction the 30 kD form resolved into four components of 36, 31, 20–21 and 16 kD of which the 20–21 and 16 kD components were similar to the corresponding inhibin subunits isolated from porcine and bovine follicular fluid. The 36 kD component was established as a non-reducible inhibin-like material, based on its binding to antiserum raised against bovine 58 kD inhibin. The nature of the remaining non-reducible 31 kD component is unknown. Two NH2-terminal amino acid sequences (first 13 amino acids) identified in purified 30 kD inhibin were identical to the corresponding subunit amino acid sequences of bovine 31 kD inhibin.
J. Endocr. (1987) 113, 213–221
Effects of continuous intravenous infusion of an ovine placental extract enriched in placental lactogen on plasma hormones, metabolites and metabolite biokinetics in non-pregnant sheep
Authors: Thordarson G. , McDowell G. H. , Smith S. V. , Iley S. , Forsyth I. A. 
Published: December 2008

ABSTRACT
Continuous intravenous infusions of saline or of a placental extract containing ovine placental lactogen were given to three non-pregnant, non-lactating ewes over periods of 36 h, 1 week apart. During saline infusion no placental lactogen was detected in jugular vein plasma, but infusion of the placental extract raised the placental lactogen concentration from undetectable to 40-50 μg/l, similar to concentrations in ewes with one fetus on day 90 of pregnancy. By comparison with the saline control period, infusion of the placental extract consistently increased both plasma concentrations and irreversible loss of non-esterified fatty acids. Plasma concentrations of glucose and urea, but not irreversible loss of these metabolites, were consistently increased. Although the placental extract was not subjected to extensive purification, it was enriched in placental lactogen and contained no detectable contamination with insulin, prolactin or growth hormone. The results are suggestive of a role for placental lactogen in modifying metabolism and acting during pregnancy to provide nutrients for fetal metabolism.
J. Endocr. (1987) 113, 277–283
Leukotriene release by endometrium and myometrium throughout the menstrual cycle in dysmenorrhoea and menorrhagia
Authors: Rees M. C. P. , Di Marzo V. , Tippins J. R. , Morris H. R. , Turnbull A. C. 
Published: December 2008

ABSTRACT
Endometrium and myometrium were collected at hysterectomy from 21 women with measured menstrual blood loss. Eight women complained of dysmenorrhoea and the remaining 13 had pain-free periods. Specimens were obtained throughout the menstrual cycle (menstrual, n = 5; follicular, n = 3; early luteal, n = 3; mid-luteal, n = 5; late luteal, n = 4). Leukotriene C4, leukotriene D4 and leukotriene E4 release were examined using a short-term incubation technique. Endometrial leukotriene release, which was always significantly greater than myometrial release, changed throughout the menstrual cycle and the highest concentrations were found during menstruation. Endometrial, but not myometrial, leukotriene concentrations were significantly higher in tissues obtained from women with a complaint of dysmenorrhoea compared with those in tissue from pain-free women. No correlation was found between leukotriene release in either endometrium or myometrium and menstrual blood loss (range 15–457 ml).
J. Endocr. (1987) 113, 291–295
Acetylcholine stimulates steroidogenesis in isolated frog adrenal gland through muscarinic receptors: evidence for a desensitization mechanism
Authors: Benyamina M. , Leboulenger F. , Lirhmann I. , Delarue C. , Feuilloley M. , Vaudry H. 
Published: December 2008

ABSTRACT
The effect of cholinergic agonists on glucocorticoid and mineralocorticoid production by frog interrenal (adrenal) tissue was studied in vitro by means of continuous perifusion. Acetylcholine, at doses ranging from 1 to 100 μmol/l, stimulated both corticosterone and aldosterone output in a dose-dependent manner, with a half-maximal effective dose of 2·5 μmol/l. Corticosteroid production was also stimulated by muscarine (10 μmol/l). In contrast, neither nicotine nor nicotine bitartrate (1–100 μmol/l) enhanced corticosteroid biosynthesis. The kinetics of the response of adrenal cells to acetylcholine and muscarine were similar to those observed during angiotensin II stimulation. In particular, a significant reduction (20–40%) in the spontaneous level of corticosteroid production was recorded after the initial infusion of muscarinic agents, but no further decrease in the basal level occurred after a second cholinergic administration. The effect of acetylcholine was blocked by the muscarinic receptor antagonist atropine (10 μmol/l). These results indicate that acetylcholine can stimulate frog adrenocortical cells through muscarinic receptors. Repeated 20-min pulses of acetylcholine (50 μmol/l) or muscarine (10 μmol/l), given at one pulse per 130 min, resulted in a marked reduction in the secretory response to the second pulse. No reduction in the stimulatory effect of acetylcholine or muscarine was observed when a 6·5-h interval separated two 20-min infusions of the secretagogue. In contrast with these findings, iterative pulses of the muscarinic agonist pilocarpine (in the range 1–100 μmol/l) did not cause any desensitization.
These data show that the neurotransmitter acetylcholine can modulate frog adrenocortical function and suggest that, in addition to more conventional regulators, i.e. ACTH and angiotensin II, the cholinergic endings of the splanchnic nerve might participate in the regulation of corticosteroid secretion, at least under some physiological conditions such as neurogenic stress.
J. Endocr. (1987) 113, 339–348
Effects of 4,4′-di-isothiocyano-2,2′-stilbene disulphonate on iodide uptake by primary cultures of turtle thyroid follicular cells
Authors: Chow S. Y. , Yen-Chow Y. C. , White H. S. , Woodbury D. M. 
Published: December 2008

ABSTRACT
Iodide uptake by primary cultures of turtle thyroid follicular cells is directly proportional to the Na + concentration and is inversely proportional to the HCO3− concentration in culture medium, but is not affected by the Cl− concentration. Addition of 4,4′-di-isothiocyano-2,2′-stilbene disulphonate (DIDS; 10 μmol/l and higher doses) to medium containing different concentrations of Na+ (5–140 mmol/l), HCO3− (0–40 mmol/l) and Cl − (120 mmol/l) generally enhanced iodide uptake by the cultured cells; however, there was no significant effect in Na+-free and in low Cl− (90 mmol/l and less) medium. The inhibitory effects on iodide uptake of ouabain, frusemide and perchlorate were attenuated by DIDS which also antagonized the stimulatory effects on iodide uptake of TSH, although both DIDS and TSH increased the 125I− cell/medium ratio when they were given alone. At doses of 100 μmol/l and higher, DIDS lowered the intracellular pH of cultured cells when the pH of the medium was maintained at a constant level. It also increased the intracellular Cl − concentration, but had no effect on intracellular Na+ or K +. The input and specific resistances of cell membranes in cultured thyroid cells and in isolated thyroid slices increased (decreased conductance) after adding DIDS to the perfusion fluids. Both Na+/K+- and HCO3−-ATPase activities in homogenates of turtle thyroid tissue were inhibited by DIDS. Results from this investigation demonstrate (1) that in addition to preventing the leak of iodide from thyroid cells, DIDS may act to increase the sensitivity of the Na + -anion carrier to I− and thereby increases iodide uptake, and (2) that a HCO3−–Cl− exchange system is present in the thyroid cell membrane and appears to be linked to the transport of iodide into thyroid cells.
J. Endocr. (1987) 113, 403–412
The significance of small pulses of gonadotrophin-releasing hormone
Authors: Clarke I. J. , Cummins J. T. 
Published: December 2008

ABSTRACT
A series of experiments was conducted to ascertain the significance of 'small' pulses of gonadotrophin-releasing hormone (GnRH). In the first experiment, ovariectomized hypothalamo-pituitary disconnected (HPD) ewes were given 250 ng pulses of GnRH every 2 h for 1 week, 25 ng pulses every 2 h for 24 h, 25 ng pulses hourly for 24 h and then alternating hourly pulses of 25 and 250 ng. During the 25 ng pulses, LH was not detectable in plasma and FSH concentrations declined after 2 days. Following the 25 ng pulses, the resumption of 250 ng pulses led to exaggerated LH responses (mean ± s.e.m. pulse amplitude 18·7 ± 1·7 vs 10·2 ± 1·2 μg/l in the first week). In a second experiment, ovariectomized–HPD ewes were maintained on 250 ng GnRH pulses every 2 h for 1 week and were then given three 25 ng pulses mid-way between the 250 ng pulses. Samples of blood were taken over three 250 ng pulses without 25 ng insertions and over three pulses with insertions. The insertion of 25 ng GnRH pulses did not cause LH pulses in their own right and did not alter the LH responses to the 250 ng pulses. In a third experiment, 50 ng GnRH pulses were inserted between the 250 ng GnRH pulses, as in experiment 2; these 50 ng pulses caused small LH pulses and led to a reduction in the response of the LH pulse amplitude to the 250 ng pulses. The 'small' LH pulses which occurred in response to 50 ng GnRH compensated for the reduced responses to the 250 ng pulses. Hence, the integrated area under the LH curve and between successive 250 ng pulses remained the same, irrespective of the 50 ng insertions.
From these data we conclude that 'small' GnRH pulses alone can sustain ongoing LH synthesis without release, leading to an accumulation of releasable LH, and that the insertion of 'small' GnRH pulses may modify the pattern of pituitary responsiveness to 'large' GnRH pulses.
J. Endocr. (1987) 113, 413–418
Naloxone reverses post-ejaculatory inhibition of sexual behaviour in female rats
Authors: Forsberg G. , Bednar I. , Eneroth P. , Södersten P. 
Published: December 2008

ABSTRACT
Sexual receptivity was inhibited in ovariectomized rats treated with oestradiol benzoate (OB: two injections of 2 μg) and progesterone (0·5 mg) immediately after ejaculation by the male and restored after the end of the post-ejaculatory refractory period in the male. The post-ejaculatory inhibition of sexual receptivity was reversed by i.p. (5 mg), intracerebroventricular (50 μg) or intrathecal (50 μg) injection of the opioid peptide receptor antagonist naloxone. The concentration of serum β-endorphin-like immunoreactivity in ovariectomized rats treated with OB plus progesterone was unaltered by sexual interactions with males (18·3 ± 6·0 (s.e.m.), 26·4 ± 2·1 and 21·8 ± 6·1 pmol/l before sexual activity, after ejaculation and after the end of the post-ejaculatory interval) but reduced to non-detectable by hypophysectomy. Subcutaneous injection of 10 μg β-endorphin raised serum concentrations of β-endorphin-like immunoreactivity but did not affect the display of sexual behaviour. The behaviour was also unaffected by intracerebroventricular injection of 0·1, 0·2 or 1·0 μg β-endorphin or by injections of 0·25 μg β-endorphin in the periaqueductal central grey of the mesencephalon. The results show that ejaculation by male rats causes a transient inhibition of sexual receptivity in the female which may be dependent upon opioid peptide receptor mechanisms in the brain and spinal cord. It is unlikely that the peptide is β-endorphin.
J. Endocr. (1987) 113, 429–434
Hormone profiles for progesterone, oestradiol, prolactin, plasma renin activity, aldosterone and corticosterone during pregnancy and pseudopregnancy in two strains of rat: correlation with renal studies
Authors: Garland H. O. , Atherton J. C. , Baylis C. , Morgan M. R. A. , Milne C. M. 
Published: December 2008

ABSTRACT
Plasma samples were obtained throughout pregnancy and pseudopregnancy from Sprague–Dawley (SD) rats and during pregnancy from rats of the Munich Wistar (MW) strain. The concentrations of progesterone, oestradiol, prolactin, plasma renin activity (PRA), aldosterone and corticosterone were measured by radioimmunoassay to establish hormonal profiles in the two strains of rat.
Circulating progesterone concentrations in both strains of rat were significantly higher during pregnancy than in virgin controls, except at term in the SD group. The hormonal pattern for pseudopregnancy was similar to that of the first half of pregnancy. Oestradiol concentrations were similar to, or lower than, those in virgin controls throughout pseudopregnancy and for the first 2 weeks of pregnancy in both strains of rat. Increased concentrations of steroid were seen only in the pregnant groups towards term. In SD rats, highest prolactin concentrations were apparent during the first half of pregnancy and pseudopregnancy, and at term in the pregnant group. Pregnant MW rats showed a different profile for this hormone, with low levels throughout pregnancy except at term. In all groups PRA rose to a peak at day 9 and decreased to day 16. Pregnant SD rats also showed a significant increase at term. Aldosterone concentrations were significantly increased at several stages of pregnancy in both strains of rat, particularly during the second half of gestation. Pseudopregnant animals showed a different hormone profile, with no significant changes until day 16 when lower concentrations were recorded. There was little variation in the circulating corticosterone concentration except in pregnant rats at term when levels fell.
These findings are discussed in relation to the known renal changes of pregnancy and pseudopregnancy.
J. Endocr. (1987) 113, 435–444
Prostaglandin production by the guinea-pig endometrium: is calcium necessary?
Authors: Riley S. C. , Poyser N. L. 
Published: December 2008

ABSTRACT
The output of prostaglandin (PG) F2α from guinea-pig endometrium obtained on day 15 of the oestrous cycle and maintained in tissue culture was significantly (P<0·05) reduced by the use of Ca2+-depleted medium, EGTA (a Ca2+ chelator), 8-(N,N-diethyl-amino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8; an intracellular Ca2+ antagonist), trifluoperazine (TFP) and N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7; both calmodulin antagonists). Nifedipine inhibited PGF2α output at a concentration (100 μmol/l) much greater than that usually required to block Ca2+ channels. Verapamil had a small but significant (P < 0·05) inhibitory effect on PGF2α output at 10–100 μmol/l. The outputs of PGE2 and, to a lesser extent, 6-keto-PGF1α (the hydrated product of PGI2) were also reduced by using Ca2+-depleted medium. EGTA reduced the outputs of PGE2 and 6-keto-PGF1α on day 1 of culture, but stimulated 6-keto-PGF1α output on day 3 of culture. The outputs of PGE2 and 6-keto-PGF1α were increased by TMB-8 (100 μmol/l) on day 3 of culture and by TFP and, to a smaller extent, by W-7 on all 3 days of culture. Nifedipine (100 μmol/l by not 1 or 10 μmol/l) reduced the outputs of PGE2 and 6-keto-PGF1α on all 3 days of culture, whereas verapamil (100 μmol/l but not 1 or 10 μmol/l) increased the outputs of these two prostaglandins on days 2 and 3 of culture. Phorbol 12-myristate 13-acetate (an activator of protein kinase C) had no effect on the outputs of PGF2α, PGE2 and 6-keto-PGF1α from cultured guineapig endometrium obtained on days 7 and 15 of the oestrous cycle. It is concluded that extracellular Ca2+ is necessary for the high output of PGF2α from the guinea-pig uterus after day 11 of the oestrous cycle, and that the action of Ca2+ is not potentiated by the activation of protein kinase C.
J. Endocr. (1987) 113, 463–471