bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of peptide nicking in the human chorionic gonadotropin β-subunit on stimulation of recombinant human thyroid-stimulating hormone receptors
Authors: Yoshimura Masayoshi , Pekary A Eugene , Pang Xuan-Ping , Berg Loretta , Cole Laurence A , Kardana Andrew , Hershman Jerome M 
Published: December 2008

Yoshimura M, Pekary AE, Pang X-P, Berg L, Cole LA, Kardana A, Hershman JM. Effect of peptide nicking in the human chorionic gonadotropin β-subunit on stimulation of recombinant human thyroid-stimulating hormone receptors. Eur J Endocrinol 1994;130:92–6. ISSN 0804–4643
It is now generally accepted that human chorionic gonadotropin (hCG) has thyroid-stimulating activity. Heterologous forms of the hCG molecule occur in the purified preparations extracted from urine of pregnant women and patients with trophoblastic diseases. This work was undertaken to determine the effect of peptide nicking in the hCG-β subunit on its thyrotropic potency. Using Chinese hamster ovary cells expressing functional human thyroid-stimulating hormone (TSH) receptors, we examined the effect of nicked hCG on cyclic AMP (cAMP) production and receptor binding. The effect of human leukocyte elastase (hLE), a nicking enzyme, on standard hCG also was examined in the cAMP assay and on receptor binding. We studied five hCG preparations extracted from the urine of normal pregnancy (CR-127 and P8) and trophoblastic diseases (C2, C5 and M4). Two preparations (C2, 96% nicked and M4, 100% nicked in the β44–49 region) showed about a 1.5-fold potency of standard hCG CR-127, which is also 20% nicked in the same region. Non-nicked hCG (P8) had the weakest potency among all of the samples tested. Treatment of standard hCG with hLE increased the cAMP response about two-fold. Dose-dependent displacement of bovine [125I]TSH by standard hCG and hLE-digested hCG was observed and was almost identical. We have confirmed the increased in vitro thyrotropic activity of hCG nicked in the β-intercysteine loop on recombinant human TSH receptors. These data suggest that peptide heterogeneity of the hCG molecule may modulate the in vivo thyrotropic activity of hCG in pregnant women and patients with trophoblastic diseases.
Jerome M Hershman, Endocrinology-W111D, West Los Angeles VA Medical Center, Los Angeles, California 90073, USA
Synthesis and characterization of anti-idiotypic anti-T4 antibodies
Authors: Juge-Aubry CE , Liang Hong , Lang Jochen , Barlow John W , Burger Albert G 
Published: December 2008

Juge-Aubry CE, Liang H, Lang J, Barlow JW, Burger AG. Synthesis and characterization of anti-idiotypic anti-thyroxine antibodies. Eur J Endocrinol 1994;130:107–12. ISSN 0804–4643
We injected rabbits with purified monoclonal murine immunoglobulin (IgG1) or polyclonal anti-thyroxine antibodies (anti-T4) and polyclonal anti-triiodothyroacetic acid (anti-Triac) antibodies to stimulate the production of anti-idiotypic antibodies. Purified immunoglobulins from all five rabbits immunized with monoclonal primary antibodies were able to inhibit the interaction between [125I]T4 and the primary antibody. The preimmune sera were inactive. This effect was not due to endogenous T4 contamination or contamination with the injected primary antibody. Half-maximal inhibition of binding of primary antibody with anti-idiotype was between 1.6 and 30 μg of total immunoglobulins. Addition of normal mouse IgG1 did not alter the inhibitory effect of the anti-idiotypic antibody. suggesting that this effect is specific. These anti-idiotypic antibodies reacted differently with different polyclonal antibodies, reflecting the heterogeneous nature of polyclonal antibody populations. Polyclonal antibodies were less effective in stimulating anti-idiotypic antibody production. One polyclonal anti-T4 and one anti-Triac antibody produced weak anti-idiotypic antibody that had to be used at a concentration of > 600 μg of total immunoglobulins to be inhibitory. Both inhibited the binding of T4 to the monoclonal anti-T4 antibody. However, they were ineffective in inhibiting the function of their own antigen, the polyclonal anti-T4 or anti-Triac antibody. We tested the most potent anti-idiotypic antibodies for their ability to compete with T4 for other T4-binding proteins. Specific inhibition of T4 binding to thyroid-binding globulin was observed with half-maximal effect at approximately 450 μg of total IgG. The antibody was negative when tested against Transthyretin, rat liver deiodinase type I, triiodothyronine cell uptake and liver cytoplasmic triiodothyronine binding. In conclusion, the technique described herein allows production of anti-idiotypic anti-T4, which can be useful in the characterization of the range of iodothyronine-binding sites involved in thyroid hormone action.
AG Burger, Unité de la Thyroïde, Hôpital Cantonal Universitaire, 1211 Genève 4, Switzerland
Identification and characterization of insulin-like growth factor I (IGF-I) and IGF-II/mannose-6-phosphate (IGF-II/M6P) receptors in bovine adrenal cells
Authors: Weber Matthias M , Kiess Wieland , Beikler Thomas , Simmler Pia , Reichel Martin , Adelmann Barbara , Kessler Ulrike , Engelhardt Dieter 
Published: December 2008

Weber MM, Kiess W, Beikler T, Simmler P, Reichel M, Adelmann B, Kessler U, Engelhardt D. Identification and characterization of insulin-like growth factor I (IGF-I) and IGF-II/mannose-6-phosphate (IGF-II/M6P) receptors in bovine adrenal cells. Eur J Endocrinol 1994;130:265–70. ISSN 0804–4643
We have identified and characterized insulin-like growth factor I (IGF-I) and IGF-II/mannose-6-phosphate (IGF-II/M6P) receptors in bovine adrenal cells. Iodine-125-labeled IGF-I ([125I]IGF-I) binding was characteristic of the IGF-I receptor, and binding kinetics as well as receptor densities were similar in cortical and medullary membranes. Scatchard analysis of [125I]IGF-I binding to cultured adrenocortical cells showed a single class of high-affinity binding sites with a Kd of 1.4 nmol/l and an average of 150 000 binding sites/cell. Affinity cross-linking experiments displayed a band at an apparent molecular weight of 135 kD, corresponding to the size of the α-subunit of the IGF-I receptor. In analogy, the binding of [125I]IGF-II to bovine adrenal membranes was characteristic of the IGF-II/ M6P receptor and no differences between cortical and medullary membrane fractions were found. Scatchard analysis revealed a single class of high-affinity binding sites in adrenocortical cells with a Kd of 1.1 nmol/l and an average of 280 000 binding sites/cell. The identity of the IGF-II/M6P receptor was confirmed by western blotting of adrenocortical membranes with an anti-IGF-II/M6P receptor antibody and by affinity cross-linking of adrenocortical cells with labeled IGF-II. In conclusion, we have identified and characterized IGF-I and IGF-II/M6P receptors in bovine adrenocortical as well as medullary cells. In both regions of the bovine adrenal gland the IGF-II/M6P receptor is much more abundant than the IGF-I receptor.
Matthias M Weber, Medizinische Klinik II, Klinikum Groβhadern, Marchioninistraβe 15, 81377 München, Germany
Effects of long-term treatment with the gonadotropin-releasing hormone analog nafarelin in patients with non-functioning pituitary adenomas
Authors: Colombo Paolo , Ambrosi Bruno , Saccomanno Katia , Bassetti Monique , Cortelazzi Donatella , Faglia Giovanni 
Published: December 2008

Colombo P, Ambrosi B, Saccomanno K, Bassetti M, Cortelazzi D, Faglia G. Effects of long-term treatment with the gonadotropin-releasing hormone analog nafarelin in patients with non-functioning pituitary adenomas. Eur J Endocrinol 1994;130:339–45. ISSN 0804–4643
The supposed origin of non-functioning pituitary adenomas (NFPA) from gonadotrophs prompted us to investigate the effects of the gonadotropin-releasing hormone (GnRH) analog nafarelin on hormonal and tumoral parameters in eight patients with NFPA, previously unsuccessfully operated and all hypogonadal. Nafarelin was administered intranasally for 1 year to all patients. Four patients received a dose of 1200 μg/day; the remaining four received 800 μg/day for 3 months, which was subsequently increased to 1200 μg/day. Basal gonadotropin and α-subunit (αSU) levels were low–normal. In four patients (nos. 1,2,3,5) nafarelin significantly lowered luteinizing hormone (LH) levels, and also folliclestimulating hormone (FSH) in three of them (nos. 1,2,3). Persistent FSH stimulation occurred in three patients (nos. 6,7,8), with a transient slight LH increase only in patient no. 8. In one patient (no. 7), αSU levels were persistently stimulated. Hormonal responses to an acute GnRH test during nafarelin administration were generally blunted when compared to the pretreatment responses. Immunofluorescence results, obtained before treatment in five adenomas (nos. 2,3,4,6,7), had been as follows: positive for FSH-β in all; negative for LH-β in all, except a few positive cells in case no. 4; positive for αSU in three (nos. 2,3,7). No changes of visual field and tumor size occurred in any patient during treatment. However, one patient who showed a persistent increase in FSH levels exhibited left palpebral ptosis after 12 months of therapy and underwent a second transsphenoidal surgery. In conclusion: NFPA behave heterogeneously in terms of hormonal responses to GnRH analog therapy; long-term nafarelin treatment was unsuccessful in reducing the size of NFPA; and stimulation rather than inhibition of gonadotropin levels may suggest discontinuance of GnRH analog therapy in NFPA.
Paolo Colombo, Istituto di Scienze Endocrine, Ospedale Maggiore IRCCS-Pad, Granelli, via F. Sforza 35, 20122 Milano, Italy
Effect of pericardiocentesis on circulating concentrations of atrial natriuretic hormone and arginine vasopressin in dogs with spontaneous pericardial effusion
Authors: Stokhof Arnold A , Overduin Lisette M , Mol Jan A , Rijnberk Ad 
Published: December 2008

Stokhof AA, Overduin LM, Mol JA, Rijnberk A. Effect of pericardiocentesis on circulating concentrations of atrial natriuretic hormone and arginine vasopressin in dogs with spontaneous pericardial effusion. Eur J Endocrinol 1994;130:357–60. ISSN 0804–4643
Factors regulating the secretion of atrial natriuretic hormone (ANH) and arginine vasopressin (AVP) have not been elucidated fully. In several studies the release of these peptides has been studied by inducing both increased atrial pressure and atrial distension. A few studies employ cardiac tamponade, allowing the effect of atrial pressure and atrial stretch to be studied separately. In eleven dogs with spontaneous cardiac tamponade the effect of pericardiocentesis on circulating concentrations of ANP and AVP was studied. Pericardiocentesis was followed by a prompt rise in (non-elevated) plasma ANH concentrations from 21.6 ± 7.3 to 65.4 ± 17.1 pmol/l (mean ± sem). The initially slightly elevated AVP concentration of 5.5 ± 1.5 pmol/l declined following pericardiocentesis to 2.1 ± 0.5 pmol/l. In three dogs the systolic arterial pressure was measured indirectly and the central venous pressure was measured with a fluid-filled catheter. Before and after pericardiocentesis arterial pressure readings did not change significantly. Central venous pressure values showed an immediate very steep significant decrease after centesis. It is concluded that ANH release is primarily regulated by stretch and not by atrial pressure, that plasma AVP concentrations are moderately elevated in cardiac tamponade and that in cardiac tamponade pericardiocentesis causes a rapid decline in plasma AVP concentration.
Arnold A Stokhof, Department of Clinical Sciences of Companion Animals, Yalelaan 8, 3584 CN Utrecht, The Netherlands
Role of thyroid hormone in controlling the concentration of luteinizing hormone/human chorionic gonadotropin receptors in rat ovaries
Authors: Fitko Remigiusz , Szlezyngier Beata 
Published: December 2008

Fitko R, Szlezyngier B. Role of thyroid hormone in controlling the concentration of luteinizing hormone/human chorionic gonadotropin receptors in rat ovaries. Eur J Endocrinol 1994;130:378-80. ISSN 0804–4643
Little is known about the mechanism by which thyroid hormones influence ovarian function, especially in gonadotropin receptor formation. In this study the concentration of Iuteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptors in the ovaries of hypo- and hyperthyroid rats was estimated. Rats were made experimentally hypothyroid by thyroidectomy (N = 10) and hyperthyroid by injections of 40 μg of l-thyroxine daily for 21 days (N = 14). After 3 weeks the ovaries were excised, weighed, immersed in liquid nitrogen and then, after 24 h of incubation with 125I-labeled hCG (CR-121), the concentration of receptors (cpm) for one ovary and 1 mg of tissue was counted in their respective homogenates. The ovaries of the hyperthyroid group were diminished in size and consequently the level of receptors per ovary also was reduced when compared with control animals. The number of receptors per ovary and per milligram of tissue of hypothyroid rats was three times higher than in the control. In hyperthyroid animals a significant decrease in these values was noted when compared with hypothyroid rats, especially in the calculation of receptor concentration per ovary. It may be concluded that thyroid function may affect the size of the gland and also the number of LH/hCG-binding sites in rat ovaries. These data may be useful for interpretation of the pathophysiology of polycystic ovary syndrome in women and animals.
R Fitko, Department of Experimental Pathology, Centre for Agrotechnology and Veterinary Sciences, 10-718 Olsztyn, ul. Prawocheñskiego 5, Poland
Drug competition for intracellular triiodothyronine-binding sites
Authors: Barlow John W , Curtis Andrea J , Raggatt Lorna E , Loidl Nicole M , Topliss Duncan J , Stockigt Jan R 
Published: December 2008

Barlow JW, Curtis AJ, Raggatt LE, Loidl NM, Topliss DJ. Stockigt JR. Drug competition for intracellular triiodothyronine-binding sites. Eur J Endocrinol 1944;130:417–21. ISSN 0804–4643
A variety of substances, including frusemide, non-esterified fatty acids (NEFAs) and non-steroidal antiinflammatory drugs (NSAIDs), can compete for triiodothyronine (T3)-binding sites in serum and at the cell surface. We examined the competitive potency of these agents at intracellular T3-binding sites in order to assess their potential to act as T3 antagonists. Competition for [125I]T3 binding was determined using hydroxyapatite separation in cytosols and nuclear extracts prepared from livers of Macaca fascicularis. The T3 affinities were 15.8 ± 1.2 nmol/l in cytosol and 0.23 ± 0.02 nmol/l in nuclear extract. Does–response curves were analysed by a four-parameter sigmoid curve-fitting program to determine competitor potency. The nineteen agents tested included various NSAIDs, NEFAs, non-bile acid cholephils (NBACs), frusemide, amiodarone and the flavonoid EMD 21388. In nuclear extract the most active competitors were linoleic acid (8.5 μmol/l) and linolenic acid (7.8 μmol/l), Potencies of NSAIDs varied between 66 μmol/l (meclofenamic acid) and 525 μmol/l (diclofenac). In cytosol, NEFAs were less potent but NSAIDs were stronger competitors than in nuclear extract. Half-inhibitory potencies in cytosol were between 13.2 μmol/l (meclofenamic acid) and 63.1 μmol/l (flufenamic acid). The NBAC bromosulphthalein was one of the most potent inhibitors in both cytosol and nuclear extract. When expressed relative to T3, diclofenac was a more effective competitor in cytosol than it was in nuclear extract. Amiodarone and EMD 21388 were without effect both in cytosol and nuclear extract. Frusemide (759 μmol/l) was weakly active in cytosol only. The action of T3 was assessed by measuring secretion of sex hormone-binding globulin (SHBG) in Hep-G2 cells. After 3 days with total T3 (0.1 μmol/l), SHBG was 155 ± 15% of the control. Amiodarone (100 μmol/l) and meclofenamic acid (100 μmol/l) were cytotoxic. Bromosulphthalein (10 μmol/l), one of the most potent competitors at both the cytoplasmic and the nuclear level, did not influence the T3-induced rise in SHBG secretion. None of the drugs tested affected the magnitude of maximal induction of SHBG by T3. Substances that compete for serum and cell surface T3-binding sites are also weak competitors for intracellular T3-binding proteins, although the heirarchy of potency differs. Frusemide and diclofenac, with a greater relative potency for cytosolic binding than nuclear binding, may have potential use in investigating the function of cytosolic T3-binding. Amiodarone shows no binding activity and is not a hormone antagonist in primate hepatic tissue.
John W Barlow, Ewen Downie Metabolic Unit, Alfred Hospital, Commercial Road, Melbourne, Victoria 3181, Australia
Lanreotide, a somatostatin analogue, reduces insulin-like growth factor I accumulation in proliferating aortic tissue in rabbits in vivo. A preliminary study
Authors: Howell Marcus , Ørskov Hans , Frystyk Jan , Flyvbjerg Allan , Grønbæk Henning , Foegh Marie 
Published: December 2008

Howell M, Ørskov H, Frystyk J. Flyvbjerg A, Grønbæk H, Foegh M. Lanreotide, a somatostatin analogue, reduces insulin-like growth factor I accumulation in proliferating aortic tissue in rabbits in vivo. A preliminary study. Eur J Endocrinol 1994;130:422–5. ISSN 0804–4643
Coronary artery restenosis following percutaneous transluminal angioplasty occurs with a very high incidence. Major efforts have been aimed at revealing the mechanisms and at developing therapies that might prevent or delay the myointimal proliferation. Most clinical trials have been unsuccessful. Endothelial denudation was induced in 30 rabbits using balloon catheterization of iliac arteries and aorta. Immunoreactive insulin-like growth factor I (IGF-I) was measured in arterial tissue samples obtained 1, 2 and 4 days postoperatively using a double extraction procedure to remove IGF-I binding proteins. Half of the animals were treated with subcutaneous injections of lanreotide, 10 μg/kg twice daily, and the other half served as controls. In the latter group, arterial IGF-I was unaltered from baseline at day 1 and increased by 300 and 400% at days 2 and 4. No increase was observed in the rabbits treated with lanreotide. The results indicate that initial local accumulation of IGF-I may be one of the mechanisms involved in myointimal proliferation after experimental arterial injury. The reduction of local IGF-I accumulation by lanreotide may be involved in the previously observed reduction in myointimal proliferation.
Hans Ørskov, Institute of Experimental Clinical Research, University Hospital, DK-8000 Aarhus C, Denmark
Relationship between calcitrophic hormones and blood pressure in elderly subjects
Authors: John Andrew St , Dick Ian , Hoad Kirsten , Retallack Robert , Welborn Timothy , Prince Richard 
Published: December 2008

St John A, Dick I, Hoad K, Retallack R, Welborn T, Prince R. Relationship between calcitrophic hormones and blood pressure in elderly subjects. Eur J Endocrinol 1994;130:446–50. ISSN 0804–4643
The relationship between calcitrophic hormones and blood pressure has been investigated in 583 elderly subjects who were untreated for hypertension. Univariate analysis demonstrated that serum parathyroid hormone, calcitriol, albumin and calcium were correlated significantly with mean blood pressure (r = +0.15, +0.10, +0.14 and +0.11, respectively), as were body mass index and age (r = +0.19 and +0.10, respectively). Parathyroid hormone also was correlated positively with both age and calcitriol (r = +0.34 and +0.15, respectively) and negatively with plasma calcium and albumin (r = −0.09 and −0.09, respectively). Multivariate analysis demonstrated that when allowing for age and body mass index, parathyroid hormone and calcitriol were both significant independent determinants of the mean blood pressure. When other independent variables were included in the analysis, parathyroid hormone but not calcitriol remained a significant predictor of mean blood pressure. This study has demonstrated a weak but significant relationship between blood pressure and calcitrophic hormones in a group of elderly people. The data are consistent with the hypothesis that hypertension may be due in part to calcium deficiency.
Andrew St John, Department of Biochemistry, Royal Perth Hospital, GPO Box X2213, Perth, Western Australia
Efficacy of intermittent therapy in growth hormone-deficient children
Authors: Bougnères Pierre 
Published: December 2008

Bougnères P. Efficacy of intermittent therapy in growth hormone-deficient children. Eur J Endocrinol 1994;130:459–62. ISSN 0804–4643
Eighty-six growth hormone-deficient children treated with extractive growth hormone were transferred to recombinant growth hormone (rGH): 57 children were transferred directly to rGH, but 29 experienced a 9.7 ± 1-month pause in growth hormone administration. The retrospective analysis of growth from 1 year before to 1 year after initiation of rGH showed that the interruption of growth hormone administration did not modify the final height gain. During the 2 years, children with continuous therapy gained 12.2 ± 0.5 cm with a cumulative growth hormone dose of 43 ± 3 U/kg, while those who paused gained 12.1 ±0.3 cm with a cumulative growth hormone dose of only 24 ± 2 U/kg (p < 0.0005). As expected, during the year preceding the onset of rGH, the children who paused gained less height than those treated continuously, but grew more rapidly during the first year of rGH administration. This was due to an important re-acceleration of growth rate at re-initiation of therapy after the pause. Our observation suggests that regimens of discontinuous rGH administration could be as efficient as continuous treatment. If confirmed in prospective randomized trials, this could have important consequences for improving the clinical efficiency of a given dose of rGH, as well as for the patient's comfort, secondary effects and cost of therapy.
Pierre Bougnères, Service d'Endocrinologie Pédiatrique, Hôpital Saint Vincent de Paul, 82 avenue DenfertRochereau, 75014 Paris, France