bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of dexamethasone on muscle protein homeostasis and on calpain and calpastatin activities and gene expression in rabbits
Authors: Yeh J-Y , Ou B-R , Forsberg N E 
Published: December 2008

Abstract
The objectives were to investigate the mechanisms by which glucocorticoids control proteolysis in muscle cells and the relationship between the calpain:calpastatin system and proteolysis in muscle. Female rabbits were treated with 1 mg dexamethasone (Dex)/kg body weight per day for 0, 1, 2 or 4 days after which animals were killed and muscle samples taken for analyses. Dex reduced urinary Nτ-methylhistidine (NMH) 48% (day 4 versus day 1 of Dex treatment) and muscle NMH concentrations by 49% (day 1) to 40% (day 2) respectively, suggesting that protein degradation was reduced. To investigate whether the changes in apparent proteolysis were related to calpains, we examined the effects of Dex on muscle calpain and calpastatin activities. These were unaffected by Dex. This implies that Dex-dependent changes in degradation are not mediated by changes in muscle calpain or calpastatin activities. We studied the effects of Dex on calpain and calpastatin gene expression as a means of clarifying the relationships between proteinase gene expression and proteinase activities. μ-Calpain mRNA concentration was unaffected by Dex but m-calpain mRNA and calpastatin mRNA concentrations were reduced by 42–55% and 40% respectively. Dex had a similar effect on β-actin mRNA. Although calpain and calpastatin genes behaved as housekeeping genes, changes in their expression mimicked apparent changes in proteolysis. The observation that calpain and calpastatin activities were unchanged indicates that additional regulation of the calpain:calpastatin system exists at other sites in muscle cells. To determine whether Dex-dependent changes in proteolysis were mediated indirectly, we assayed the effects of Dex on plasma thyroid hormone concentrations. Dex reduced both plasma triiodothyronine (T3) and thyroxine (T4) concentrations by as much as 68% and 67% respectively, and reduced the T3/T4 ratio by 74% following 4 days of Dex treatment. Thyroid hormones regulate muscle proteolysis and their lower concentrations in Dex-treated rabbits may account for the reductions in muscle NMH concentration and urinary NMH excretion caused by Dex.
Journal of Endocrinology (1994) 141, 209–217
Heterogeneity of the prolactin receptor in the rat mammary gland and liver during various physiological states
Authors: Guillaumot P , Cohen H 
Published: December 2008

Abstract
This work was undertaken to determine variations in the 125I-labelled ovine prolactin (oPRL) binding in rat liver and mammary gland membranes, and to study the molecular forms of prolactin receptor in different physiological situations. Prolactin binding was determined using 125I-labelled oPRL in the 100 000 g pellet. 125I-Labelled oPRL was cross-linked to receptors in membranes from rat liver and mammary gland and subjected to SDS-PAGE under reducing conditions, followed by autoradiography of dried gels.
In the mammary gland, the specific binding of oPRL to membranes, expressed as mean ± s.e.m. fmol/mg protein increased from 1·36 ±0·24 on the day of dioestrus to 3·26 ±0·60 on the day of oestrus. It remained very low during pregnancy but increased during lactation to reach 4·78 ±0·99. In the liver, the specific binding of oPRL to membranes was higher than in the mammary gland on the days of dioestrus 1, dioestrus 2 and oestrus, but not on the day of pro-oestrus. It increased until day 14 of pregnancy when the specific binding of 125I-labelled oPRL was 17·01 ±0·30.
Cross-linking revealed different molecular forms in the mammary glands and the liver. In the mammary gland we observed four prolactin-binding forms of 80, 50, 40 and 16 kDa, all of which were specific for prolactin. The 80, 50 and 40 kDa forms were also able to bind to a Concanavalin A–Sepharose column, indicating that these binding forms were glycosylated while the smaller one (16 kDa) appeared to be unglycosylated. The 40 kDa prolactin receptor was seen at all stages studied: the oestrous cycle (dioestrus, pro-oestrus and oestrus), pregnancy (days 8, 14 and 22) and lactation. The 50 kDa form was observed in the mammary gland during the day of pro-oestrus and gestation. It was also observed in ovariectomized rats treated with oestradiol (OE2), suggesting that OE2 could be one of the factors involved in the induction of this receptor form. The 16 kDa form of the receptor was found in the mammary gland only during lactation. This form, while unglycosylated, bound specifically to prolactin, suggesting that it might play a specific role during lactation.
In the liver, two forms were shown, a major one of 40 kDa and a minor one of 80 kDa. No variation in receptor molecular weight was found in the liver during the physiological stages studied.
Journal of Endocrinology (1994) 141, 271–278
Putative aromatase inhibitor induces male sex determination in a female unisexual lizard and in a turtle with temperature-dependent sex determination
Authors: Wibbels T , Crews D 
Published: December 2008

Abstract
Treatment of developing embryos of two diverse species of reptiles with fadrozole (a potent and specific nonsteroidal inhibitor of aromatase activity in mammals) resulted in the induction of male sex determination. In the first experiment, males were produced in an all-female parthenogenic species of lizard (Cnemidophorus uniparens). In the second experiment, male sex determination was induced in a turtle (Trachemys scripta) with temperature-dependent sex determination. The results support the hypothesis that the endogenous production of oestrogen may represent a pivotal step in the sex determination cascade of reptiles. Further, the production of male C uniparens indicates that the genes required for male sexual differentiation have not been lost in this parthenogenic lizard.
Journal of Endocrinology (1994) 141, 295–299
Net uptakes of oestradiol-17β and progesterone across the portal-drained viscera and the liver of ewes
Authors: Freetly H C , Ferrell C L 
Published: December 2008

Abstract
The objective of this study was to determine whether circulating concentrations or prior exposure to oestradiol-17β (OE2) and progesterone affected their uptake by splanchnic tissues. Catheters were surgically placed in the portal vein, a branch of the hepatic vein, a mesenteric vein and the abdominal aorta of three multiparous ovariectomized Dorset ewes. Blood and plasma flow across the portal-drained viscera (PDV) and the liver, and net uptake of OE2 and O2 consumption in these same tissues were determined in ovariectomized ewes (control), during OE2 infusion into the jugular vein, 7 days after an OE2 implant had been given, and during OE2 infusion into the jugular vein 7 days after an OE2 implant. The above treatments were repeated for progesterone. Plasma flows across visceral organs were determined by marker dilution (para-aminohippuric acid), and OE2 and progesterone concentrations were determined by radioimmunoassay. During the infusion with OE2, OE2 arterial concentration (mean ± s.d.) was 346 ± 199 pg/ml, PDV net uptake was 9·7±5·6 μg OE2/h and hepatic net uptake was 15·5 ± 9·5 μg OE2/h. Hepatic uptake was 82% of the jugular OE2 infusion rate. Blood flow and oxygen consumption by hepatic tissue increased when ewes were exposed to an OE2 implant for 7 days. During the infusion with progesterone, progesterone arterial concentration (mean ± s.d.) was 8·8 ±3·4 ng/ml, PDV net uptake was 220 ± 118 μg progesterone/h and hepatic net uptake was 238 ± 52 μg progesterone/h. Hepatic net uptake was 23% of the progesterone jugular infusion rate.
Journal of Endocrinology (1994) 141, 353–358
Blockade of the neonatal rise in testosterone by a gonadotrophin-releasing hormone antagonist: effects on timing of puberty and sexual behaviour in the male marmoset monkey
Authors: Lunn S F , Recio R , Morris K , Fraser H M 
Published: December 2008

Abstract
In primates, plasma testosterone concentrations are elevated for some 3 months from birth. The function of this rise is uncertain, but studies in rats suggest that its prevention by castration or administration of gonadotrophin hormone-releasing hormone (GnRH) analogues has effects on development and expression of social and sexual behaviours, and adverse long-term effects on fertility. The consequences of suppression of this rise in testosterone by treatment with the GnRH antagonist antide have been investigated in the marmoset monkey. Eight sets of male:male twins were used, one of each set receiving s.c. injections of antide (10 mg/kg), on days 0, 3 and 7, then weekly from birth to 98 days of age, with the twin receiving vehicle only. Plasma samples were taken at weekly intervals for the determination of testosterone concentrations from birth until 2 years of age. Treatment with antide completely abolished the neonatal rise in testosterone seen in control animals. The timing of the onset of the pubertal testosterone rise was not significantly affected by treatment; however, the subsequent pattern of circulating testosterone showed a tendency to decreased plasma concentrations in the neonatally treated group from weeks 25 to 42, relative to controls, and this difference was significant between 43 and 70 weeks. This was associated with a similar depression in bioactive LH concentrations around this time. Thereafter, the testosterone concentrations were similar between treated and control groups. There was no effect of treatment on growth, based on sequential body weight data. At 20 months the animals underwent behaviour tests with ovariectomized females. During these encounters, males showed the full panoply of normal sexual behaviours, with response to female proceptivity, tongue flicking, sustainable penile erections, mounts with pelvic thrusting, intromissions and intravaginal ejaculations. No significant differences were observed for any of these parameters between the control and treated animals. No changes in aggressive behaviours between groups were evident. These results show that blockade of the postnatal rise in testosterone in the male marmoset monkey may result in attenuation of the pubertal rise in testosterone but is without major effect on adult basal testosterone concentrations or reproductive behaviour.
Journal of Endocrinology (1994) 141, 439–447
A monoclonal antibody to C-type natriuretic peptide – preparation and application to radioimmunoassay and neutralization experiment
Authors: Hama N , Itoh H , Suga S , Komatsu Y , Yoshimasa T , Nakao K 
Published: December 2008

Abstract
C-type natriuretic peptide (CNP), the third member of natriuretic peptides, has recently been discovered from the porcine brain. Using a polyclonal antiserum to CNP, we demonstrated that CNP-like immunoreactivity (CNP-LI) is present mainly in the central nervous system. Recently, however, we have discovered the production and secretion of CNP in vascular endothelial cells. These observations suggested that CNP may act not only as a neuropeptide but also as a local regulator of vascular tone or growth. In order to further clarify the pathophysiological significance of CNP, we aimed at the preparation of a monoclonal antibody to CNP.
A monoclonal antibody to CNP, KY-CNP-I, has been produced. This monoclonal antibody belongs to the immunogloblin G1 subclass and has high affinity for CNP. Using this monoclonal antibody, we established a specific radioimmunoassay (RIA) for CNP. The RIA detected CNP-LI in rat brain extracts and culture media conditioned with bovine endothelial cells. In addition, the pretreatment of cultured aortic smooth muscle cells with KY-CNP-I attenuated cyclic GMP production induced by CNP in vitro. The preadministration of KY-CNP-I to rats also attenuated plasma cyclic GMP increase after intravenous injection of CNP in vivo.
These results indicate that this monoclonal antibody is a useful tool to clarify the pathophysiological role of CNP as a neuropeptide and as a local vascular regulator.
Journal of Endocrinology (1994) 141, 473–479
Cellular mechanisms mediating the stimulation of ovine endometrial secretion of prostaglandin F2α in response to oxytocin: role of phospholipase A2
Authors: Lee J-S , Silvia W J 
Published: December 2008

Abstract
Four experiments were conducted to determine whether phospholipase (PL) A2 mediates the stimulatory effect of oxytocin on the release of prostaglandin (PG) F2α from ovine endometrial tissue. Caruncular endometrial tissue was collected from ovariectomized ewes on the day after a steroid replacement protocol had been completed. The replacement protocol consisted of progesterone for 10 days (12 mg/day) followed by oestradiol on days 10 and 11 (100 μg/day) and had been shown previously to provide endometrial tissue that would release PGF2α in response to oxytocin in vitro. In experiment 1, oxytocin (10−7 m) and melittin (1·76 × 10−6 m; a stimulator of PLA2) stimulated release of PGF2α from tissue explants (P<0·05). Aristolochic acid (10−4 m; an inhibitor of PLA2) decreased oxytocin-and melittin-induced release of PGF2α by 77% and 71% respectively (P<0·05). Experiment 2 was conducted to establish the minimum inhibitory dose of aristolochic acid. Basal release of PGF2α was inhibited at 10−5 m aristolochic acid, but 10−4 m was required to block the stimulatory effect of oxytocin. Experiment 3 was carried out to identify the precise intracellular locus at which aristolochic acid was exerting its effect. Oxytocin (10−7 m), AlF4− (5 × 10−2m NaF, 10−5m AlCl3), melittin (1·76 × 10−6 m) and arachidonic acid (AA; 20 μg/ml) stimulated release of PGF2α (P<0·05). Aristolochic acid (10−4 m) blocked the release of PGF2α stimulated by oxytocin, AlF4− or melittin by >80% (P<0·05). However, aristolochic acid reduced AA-induced release by only 22% (P=0·09). Thus, aristolochic acid blocked responsiveness to stimulatory agents that act on, or proximal to, PLA2 but not responsiveness to AA whose stimulatory effect is exerted distal to PLA2. Experiment 4 was intended to establish the specificity of the inhibitory effect of aristolochic acid. This was accomplished by examining the effect of aristolochic acid on the ability of oxytocin to stimulate activity of PLC. Aristolochic acid (10−4 m) increased basal PLC activity by 29% (P<0·05) but had no effect on the activity induced by oxytocin (P>0·1). Thus, aristolochic acid blocked the ability of oxytocin to stimulate PGF2α release (experiments 1–3) but not its ability to stimulate the activity of PLC (experiment 4). The effects of melittin and aristolochic acid are consistent with the hypothesis that the stimulatory effect of oxytocin on PGF2α release from ovine endometrial tissue is mediated through PLA2.
Journal of Endocrinology (1994) 141, 491–496
IMMUNOFLUORESCENT EVIDENCE FOR THE ABUNDANCE OF FOCAL ADHESION KINASE IN THE HUMAN AND AVIAN OSTEOCLASTS AND ITS DOWN REGULATION BY CALCITONIN
Authors: Berry V , Rathod H. , Pulman L. B. , Datta H. K. 
Published: December 2008

ABSTRACT
We show here that osteoclasts possess an abundant level of focal adhesion kinase, a novel cytosolic tyrosine kinase with unique structural features that may play an important role in the action of pp60c-src, cell surface integrins, and hormonal peptides. The presence of focal adhesion kinase in the bone cell osteoclast was determined using monoclonal antibodies to the kinase by employing immunofluorescent staining. The expression of focal adhesion kinase in the osteoclast was markedly suppressed following exposure to calcitonin. However, calcitonin-induced down regulation of the kinase was apparent only following a prolonged exposure. Our hypothesis that focal adhesion kinase is maximally expressed in the osteoclasts was confirmed when the transfection of avian osteoclasts and fibroblasts, with v-src containing plasmid pATV-8, induced increased expression of the kinase in the fibroblasts but did not alter the expression level of FAK in the osteoclasts.
Effects of close-arterial (external pudic) infusion of insulin-like growth factor-II on milk yield and mammary blood flow in lactating goats
Authors: Prosser C G , Davis S R , Farr V C , Moore L G , Gluckman P D 
Published: December 2008

Abstract
Five lactating goats were infused, via an external pudic arterial catheter, directly into the mammary gland with 0·9% (w/v) NaCl (20 ml/h), recombinant human insulin-like growth factor-I (IGF-I; 80 nmol/h), recombinant human IGF-II (133 nmol/h) or IGF-I and IGF-II combined. The infusion was for 6 h and milk yield was determined every 2 h. The ratio of milk yield in the infused relative to the non-infused gland was changed only slightly by saline (2%), but increased to 9% (P<0·05) in response to IGF-I and 8% (P<0·05) in response to IGF-II. When combined, both peptides increased this ratio by 6%. These effects were elicited within 2–4 h of the beginning of infusion. Mammary blood flow increased 50–80% (P<0·05) during all IGF infusions, but only 28% during saline treatment. Plasma insulin decreased 50% (P<0·01) during the infusion of IGF-I alone or in combination with IGF-II and 25% in response to IGF-II alone. Whereas plasma glucose increased by approximately 10% during infusion of IGF-I alone or with IGF-II, it was not altered by infusion of IGF-II only.
The rapidity and unilateral nature of the milk-yield response to IGF-I and IGF-II is consistent with their acting directly on mammary tissue itself. Thus, the present results demonstrate similar local and systemic actions induced by intramammary infusion of IGF-II and IGF-I, although the magnitude of the response to IGF-II tends to be less than that to IGF-I.
Journal of Endocrinology (1994) 142, 93–99
Effects of the opioid antagonist naloxone on release of luteinizing hormone in mares during the anovulatory season
Authors: Aurich C , Schlote S , Hoppen H-O , Klug E , Hoppe H , Aurich J E 
Published: December 2008

Abstract
To investigate an involvement of endogenous opioids in the regulation of circannual changes in reproductive activity, effects of the opioid antagonist naloxone on the concentration of immunoreactive and bioactive luteinizing hormone (LH) in plasma were measured in mares during the anovulatory season. Naloxone (0·5 mg/kg i.v.) caused a significant increase (P<0·05) in immunoreactive as well as bioactive LH concentration in plasma. The amplitude of the increase in LH concentrations measured with an in vitro bioassay was more pronounced than the amplitude of the increase in LH secretion determined by radioimmunoassay. This indicates that although in seasonal anovulatory mares the bioactivity of LH in plasma is low, highly bioactive LH is present in the anterior pituitary and can be released by naloxone. The LH response to naloxone did not depend on the degree of ovarian follicular activity. It can be concluded that a tonic opioid inhibition of LH release is present in mares during at least part of the anovulatory season and that endogenous opioids seem to be involved in the regulation of seasonal reproductive activity in the horse. In contrast to the situation during the breeding season, the opioid systems regulating LH release are activated independently of luteal progesterone.
Journal of Endocrinology (1994) 142, 139–144
Developmental changes in chicken and turkey insulin-like growth factor-I (IGF-I) studied with a homologous radioimmunoassay for chicken IGF-I
Authors: McMurtry J P , Francis G L , Upton F Z , Rosselot G , Brocht D M 
Published: December 2008

Abstract
The development of a homologous radioimmunoassay (RIA) for chicken insulin-like growth factor-I (cIGF-I) and its use to investigate the developmental changes in IGF-I in the chicken and turkey is described. A doubleantibody RIA has been developed using recombinantly derived cIGF-I as antigen, radiolabelled tracer and standard. The resulting immunoassay has a minimum detection limit of 0·035 ng and effective dose of 2·5 ng. Dose–response curves of chicken and turkey plasma and tissue extracts were parallel with cIGF-I standard. The antiserum is specific for IGF-I as no cross-reactivity with chicken IGF-II, insulin, glucagon, gastrin or avian pancreatic polypeptide was observed. We have also established that acid/ethanol extraction of chicken and turkey plasma reduced possible interference of IGF-binding proteins (IGFBPs) in the RIA. Comparison of IGF-I immunoactivity in unextracted and acid/ethanol-extracted samples following gel filtration under acidic and neutral conditions indicates that the cIGFBPs may be acid-labile. Analyses of samples from growing chickens and turkeys using the homologous avian reagents revealed higher IGF-I concentrations than if the IGF were quantified using heterologous mammalian-derived reagents. A similar pattern was observed when tissue extracts were assayed for IGF-I content. The application of the homologous RIA to monitor blood and tissue IGF-I levels during embryonic development and posthatch growth in avian species will provide more accurate comparisons of results from studies on the role of IGF-I in growth and metabolism of domestic birds.
Journal of Endocrinology (1994) 142, 225–234
The regulation of plasma relaxin levels during human pregnancy
Authors: Johnson M R , Abbas A A , Allman A C J , Nicolaides K H , Lightman S L 
Published: December 2008

Abstract
The factors that determine the circulating levels of relaxin during pregnancy have been investigated by comparing the plasma levels of relaxin throughout pregnancy in women who became pregnant spontaneously (singleton, n=240) or following superovulation (singleton and multifetal pregnancies (two to ten conceptuses), n=83). Some of the women with multifetal pregnancies underwent selective fetal reduction to twin pregnancies. Relaxin levels were higher at 7–34 weeks of gestation in singleton pregnancies achieved following superovulation when compared with levels in spontaneously conceived singleton pregnancies (P<0·05–0·001). In samples obtained between 10 and 12 weeks of gestation (before fetal reduction for the multifetal pregnancies), plasma relaxin levels correlated with fetal number (r=0·526, P=0·0001). Reduction in fetal number to a twin pregnancy did not alter relaxin levels. These data suggest that the circulating levels of relaxin throughout pregnancy are determined during the cycle of conception by gonadotrophin stimulation, and within the first 10 weeks of pregnancy by the luteotrophic stimulus from the conceptus. Furthermore, once corpus luteum synthesis of relaxin is established, then reduction in the luteotrophic stimulus does not appear to affect it.
Journal of Endocrinology (1994) 142, 261–265
Biological effects of prostate specific antigen as an insulin-like growth factor binding protein-3 protease
Authors: Cohen P , Peehl D M , Graves H C B , Rosenfeld R G 
Published: December 2008

Abstract
Prostate specific antigen (PSA) is an insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) protease found in seminal plasma and produced by prostatic epithelial cells (PC-E) in vivo. We examined the effects of PSA-proteolysis of IGFBP-3 on the affinity of IGFBP-3 fragments for IGFs and on the mitogenic action of IGFs on PC-E. Recombinant human IGFBP-3 was cleaved by PSA, then incubated with 125I-IGF-I or -II in the presence of varying concentrations of unlabelled peptides, and then cross-linking electrophoresis and densitometric analysis were performed. While the affinity of IGF-II for the PSA-generated IGFBP-3 fragments fell slightly compared to intact IGFBP-3, the affinity of the PSA-generated IGFBP-3 fragments for IGF-I fell by ten fold. The addition of IGF-I or -II to PC-E in serum-free culture conditions resulted in a two-fold stimulation of cell number compared to control. The presence of IGFBP-3 in the media blocked the IGF-induced stimulation, but had no independent effect in the absence of IGFs. When PSA was added to PC-E cultures to which both IGF-I or -II and IGFBP-3 were added, the inhibitory effects of IGFBP-3 on IGF mitogenesis were reversed. We conclude that PSA decreases the affinity of IGFBP-3 for IGF and can potentiate IGF action in the presence of inhibitory IGFBP-3. This phenomenon may contribute to normal and malignant prostate growth.
Journal of Endocrinology (1994) 142, 407–415