bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phosphorylated forms of adrenocorticotropin and corticotropin-like intermediary lobe peptide in human tumors
Authors: Massias Jean Francis , Hardouin Sandrine , Vieau Didier , Lenne Frédéric , Bertagna Xavier 
Published: December 2008

Massias JF, Hardouin S, Vieau D, Lenne F, Bertagna X. Phosphorylated forms of adrenocorticotropin and corticotropin-like intermediary lobe peptide in human tumors. Eur J Endocrinol 1994;131:341–6. ISSN 0804–4643
Many peptides contribute to the heterogeneity of immunoreactive adrenocorticotropin (ACTH) in man. The use of a radioimmunoassay (RIA) specifically directed against the C-terminal end of ACTH allowed us to study precisely the following four peptides: ACTH itself, corticotropin-like intermediary lobe peptide (CLIP) or ACTH(18–39) and their phosphorylated forms on Ser31. We have set up a highperformance liquid chromatography system that separates these four molecules in a single run, to establish their relative distributions in tumors responsible for Cushing's disease or for the ectopic ACTH syndrome, and to evaluate the possible interference of phospho-Ser on various RIA or immunoradiometric assay (IRMA) recognition systems for ACTH. In this system, alkaline phosphatase treatment shifted the retention time of the phosphorylated peptides to that of their non-phosphorylated counterparts. In three tumors responsible for the ectopic ACTH syndrome, CLIP peptides were predominant in two and phosphorylated molecules represented between 22% and 50% of immunoreactive materials. In five pituitary tumors responsible for Cushing's disease, ACTH peptides were predominant and the phosphorylated molecules varied between 35% and 75% in four of them. In the same tumor the ratios of phosphorylated to non-phosphorylated CLIP or ACTH were identical. The presence of phospho-Ser31 did not affect the recognition ability of two mid-ACTH and two C-terminal ACTH RIAs, nor of the ACTH IRMA (Allegro, Nichols).
Xavier Bertagna, CJF 92-08 Endocrinologie, Faculté Cochin-Port Royal, 24 rue du Faubourg Saint Jacques, 75014 Paris, France
Retinoic acid differentially modulates triiodothyronine and retinoic acid receptors in rat liver according to thyroid status
Authors: Pallet Véronique , Audouin-Chevallier Isabelle , Verret Catherine , Garcin Henri , Higueret Paul 
Published: December 2008

Pallet V, Audouin-Chevallier I, Verret C, Garcin H, Higueret P. Retinoic acid differentially modulates triiodothyronine and retinoic acid receptors in rat liver according to thyroid status. Eur J Endocrinol 1994;131:377–84. ISSN 0804–4643
Triiodothyronine (T3) receptors (TRs) and retinoic acid (RA) receptors (RARs) exert their effects on growth, differentiation and cellular homeostasis by acting as transcription factors. The binding characteristics of these receptors have been studied in liver of hypothyroid and hyperthyroid rats, with or without treatment with T3, RA or T3 + RA together. The changes in binding induced by RA treatment depended on the hormonal status of the rat. In hypothyroid rats the T3 binding capacity was unaltered by administration of T3 or RA alone but increased by 48% after treatment with T3 and RA together. In these rats administration of RA, T3 or T3 + RA increased the RAR binding capacity by 45, 79 and 112%, respectively. In hyperthyroid rats the administration of RA reduced the TR and RAR binding capacities by 22 and 37%, respectively. We found also that the affinity constants of TRs and RARs were reduced in hypothyroid rats after treatment with T3 or T3+RA. It is suggested that this change of the properties of receptors is related to a ligand-dependent conformational change in these receptors.
Paul Higueret, Laboratoire de Nutrition, Avenue des Facultés, 33405 Talence Cedex, France
Diagnosis and treatment of thyrotoxicosis in childhood A European questionnaire study
Authors: Perrild Hans , Grüters-Kieslich Anette , Feldt-Rasmussen Ulla , Grant David , Martino Enio , Kayser Lars , Delange Francois 
Published: December 2008

Perrild H, Grüters-Kieslich A, Feldt-Rasmussen U, Grant D, Martino E, Kayser L, Delange F. Diagnosis and treatment of thyrotoxicosis in childhood. A European questionnaire study. Eur J Endocrinol 1994;131:467–73. ISSN 0804–4643
A covering letter and a questionnaire covering the diagnosis and treatment of thyrotoxicosis in childhood was circulated between October 1992 and February 1993 amongst 672 European members of the European Thyroid Association (ETA) and members of the European Society for Pediatric Endocrinology (ESPE). Almost 50% replied to the letter and 99 individuals or groups from 22 countries completed the questionnaire. A consensus was reached on the use of total thyroxine (T4) and/or free T4 and thyrotropin as routine diagnostic tools. Two-thirds included total triiodothyronine (T3) and/or free T3 and 32% used a thyrotropin-releasing hormone test. Surprisingly, thyroglobulin autoantibodies were used as a routine test by 78%; 63% included thyrotropin receptor antibodies and 60% microsomal antibodies, whereas only 50% measured thyroperoxidase antibodies. For thyroid imaging, 40% performed a thyroid scintigram and 56% measured the size of the thyroid gland by ultrasound. Antithyroid drugs (ATD) were the basic initial treatment of choice given by 99% of the respondents for children with uncomplicated Graves' disease. Carbimazole, methimazole and thiamazole were the most frequently used drugs, with a median initial dose of 0.8 mg · kg1 · day1. Two-thirds added betablockers and a few used sedatives. The ATD dose was adjusted for each patient by 39%, whereas 56% combined ATD with T4 for long-term treatment; 84% gave treatment for a fixed period (44% for 1–2 years). Surgery was considered the treatment of choice in children with an adenoma (83%), with a nodular (53%) or large goiter (16%) and recurrence after ATD (14%). Radioiodine was the treatment of choice by 18% of the respondents for patients with recurrence after surgery and recurrence after ATD (7%).
Hans Perrild, Department of Medicine B, Bispebjerg University Hospital, 2400 Copenhagen, Denmark
Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men
Authors: Veldhuis Johannes D , Iranmanesh Ali , Wilkowski Michael J , Samojlik Eugeniusz 
Published: December 2008

Veldhuis JD, Iranmanesh A, Wilkowski MJ, Samojlik E. Neuroendocrine alterations in the somatotropic and lactotropic axes in uremic men. Eur J Endocrinol 1994;131:489–98. ISSN 0804–4643
To investigate the pathophysiology of altered growth hormone (GH) and prolactin secretion in endstage renal disease, we sampled blood at 10-min intervals for 24 h and applied deconvolution analysis to calculate hormone half-lives and pulsatile secretion rates. Two-site immunoradiometric assays were employed to quantitate presumptively intact GH and prolactin in nine middle-aged men with chronic renal failure and 14 gender-, age-, body weight- and community-matched controls. We observed that the half-lives of endogenous GH and prolactin were prolonged significantly in uremia: for GH, control 17 ±1.4 versus uremia 21 ±1.3 min (p < 0.05); for prolactin, control 66 ±9.3 versus uremia 112 ± 10 min (p < 0.01). Daily GH secretion rates exceeded sex-, age- and weight-predicted values in eight of nine uremic individuals, while values for prolactin were variable but on average twofold higher in uremia. In both the somatotropic and lactotropic axes, the frequency of secretory bursts was increased significantly (for GH, control 11 ± 1.1 versus uremia 15 ± 0.84 secretory events/24 h; for prolactin, control 20 ± 0.90 versus uremia 27 ± 1.3 pulses/24 h. p < 0.05). Although there were no significant alterations in the mean amplitude, duration or mass of GH secretory bursts, prolactin secretory burst amplitudes were elevated threefold in uremia (p < 0.01). These distinctive mechanisms brought about higher 24-h mean serum concentrations of GH (0.70 ±0.17 control versus 1.22 ± 0.32 μg/l uremia) and prolactin (7.3 ± 2.4 control versus 26 ± 6.1 μg/l uremia, p < 0.05). Lastly, serum concentrations of estradiol were increased but those of unconjugated estriol decreased in uremia. We conclude that hypersomatotropinemia and hyperprolactinemia in uremic men result from prolonged hormone half-lives combined with increased frequencies of secretory events driven by unknown stimuli within the respective axes, and/or by defects in their negative-feedback regulation. We postulate that the latter may arise from partial tissue resistance to hormone action in hemodialyzed men.
JD Veldhuis, Division of Endocrinology, Department of Internal Medicine, National Science Foundation Center for Biological Timing, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
Effect of glucocorticoid on prostaglandin F2α-induced prostaglandin E2 synthesis in osteoblast-like cells: inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2
Authors: Kozawa Osamu , Tokuda Haruhiko , Suzuki Atsushi , Kotoyori Jun , Ito Yoshiaki , Oiso Yutaka 
Published: December 2008

Kozawa O, Tokuda H, Suzuki A, Kotoyori J, Ito Y, Oiso Y. Effect of glucocorticoid on prostaglandin F2α-induced prostaglandin E2 synthesis in osteoblast-like cells: inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2. Eur J Endocrinol 1994;131:510–15. ISSN 0804–4643
It is well known that osteoporosis is a common complication of patients with glucocorticoid excess. We showed previously that prostaglandin (PG) F2α stimulates the synthesis of PGE2, a potent bone resorbing agent, and that the activation of protein kinase C amplifies the PGF2α-induced PGE2 synthesis through the potentiation of phospholipase A2 activity in osteoblast-like MC3T3-E1 cells. In the present study, we examined the effect of dexamethasone on PGE2 synthesis induced by PGF2α in MC3T3-E1 cells. The pretreatment with dexamethasone significantly inhibited the PGE2 synthesis in a dose-dependent manner in the range between 0.1 and 10 nmol/l in these cells. This effect of dexamethasone was dependent on the time of pretreatment up to 8 h. Dexamethasone also inhibited PGE2 synthesis induced by melittin, known as a phospholipase A2 activator. Furthermore, dexamethasone significantly inhibited the enhancement of PGF2α- or melittin-induced PGE2 synthesis by 12-O-tetradecanoylphorbol-13-acetate, known as a protein kinase C activator. In addition, dexamethasone significantly inhibited PGF2α-induced formation of inositol phosphates in a dose-dependent manner between 0.1 and 10 nmol/l in MC3T3-E1 cells. These results strongly suggest that glucocorticoid inhibits PGF2α-induced PGE2 synthesis through the inhibition of phosphoinositide hydrolysis by phospholipase C as well as phospholipase A2 in osteoblast-like cells.
Osamu Kozawa, Department of Biochemistry, Institute for Developmental Research, Aichi Prefectural Colony, Kasugai, Aichi 480-03, Japan
G-Proteins: implications for pathophysiology and disease
Authors: Gordeladze Jan O , Johansen Per W , Paulssen Ruth H , Paulssen Eyvind J , Gautvik Kaare M 
Published: December 2008

Gordeladze JO, Johansen PW, Paulssen RH, Paulssen EJ, Gautvik KM. G-Proteins: implications for pathophysiology and disease. Eur J Endocrinol 1994;131:557–74. ISSN 0804–4643
This article focuses on the involvement of G-proteins in neuroendocrine secretion, cell growth and phenotype alterations. The current concept of hormonal activation of the GTPase cycle, as well as the molecular diversity of G-protein families and receptor * G-protein * effector coupling, are described. Also described are certain G-proteins as possible proto-oncogenes and how point mutations and frame shift mutations alter G-protein function and determine the characteristics of various endocrine diseases. The article outlines in detail how receptors and G-proteins interact in prolactin and growth-hormone-secreting pituicytes, how G-proteins are involved in the growth and differentiation of preadipocytes and osteoblasts. All in all, it seems that hormonal activation through G-proteins is modulated through direct intra- and inter-signalling system cross-talk at the plasma membrane level (short-term) and through interactions on the level of transcription (HREs) from tyrosine kinases, steroid-like hormones and metabolic pathways. Pharmacological intervention to treat diseases where G-proteins are involved should take both long and short-term regulatory phenomena into consideration.
JO Gordeladze, Institute of Medical Biochemistry, University of Oslo, PO Box 1112, Blindern, 0317 Oslo, Norway
Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion
Authors: Pineda Jaime , Martul Pedro , Casanueva Felipe F , Dieguez Carlos , Rica Itxaso , Loridan Liliane 
Published: December 2008

Pineda J, Martul P, Casanueva FF, Dieguez C, Rica I, Loridan L. Oral dexamethasone administration: new pharmacological test for the assessment of growth hormone secretion. Eur J Endocrinol 1994;131:598–601. ISSN 0804–4643
Acute intravenous (iv) dexamethasone administration has been described recently as a new test for the diagnosis of growth hormone (GH) deficiency. In the present study, a new protocol of dexamethasone administration was evaluated. Twelve normal adults and 18 normal prepubertal children were studied. The dexamethasone iv test was performed in six adults at a dose of 4 mg and 12 children at a dose of 2 mg/m2. Blood samples were collected 15 min before, at time zero and every 15 or 30 min during 5 h, resulting in a total of 16 samples. In the remaining six adults and six children, 8 and 4 mg, respectively, of dexamethasone were administered orally at the subject's home, and blood sampling started 90 min later when they arrived at the hospital. Plasma GH was measured by radioimmunassay. The dexamethasone-induced GH response (mean ± sem, μg/1) to the iv or oral protocol did not differ in either the adults (iv 8.2 ± 2.1; oral 8.0 ± 1.6) or the children (iv 14.9 ± 1.3; oral 13.6 ± 1.8). It is concluded that the simpler protocol of acute oral dexamethasone administration hereby presented can be a safe and suitable test of GH secretion.
J Pineda, Sección de Endocrinologia Pediátrica, Hospital de Cruces, 48903 Baracaldo (Vizcaya), Spain
Expression of chorionic gonadotrophin in human pituitary adenomas
Authors: Levy A , Biswas S , Burton PA , Lightman SL 
Published: December 2008

Levy A, Biswas S, Burton PA, Lightman SL. Expression of chorionic gonadotrophin in human pituitary adenomas. Eur J Endocrinol 1994;131:615–22. ISSN 0804–4643
In addition to the classical anterior pituitary hormones, many human pituitary adenomas express hormone genes ectopically. Expression of glycoprotein hormone α-subunit and, less commonly, free luteinizing hormone β (LH-β) or follicle-stimulating hormone β is characteristic of endocrinologically inactive adenomas, a subgroup thought to be derived predominantly from the gonadotroph line. Thyrotrophin β expression in these tumours is unusual, and specific chorionic gonadotrophin β (CG-β) expression, identified using oligonucleotide probes that reliably distinguish LH-β and CG-β in situ, is not well described. Using in situ hybridization histochemistry with a CG-β transcript-specific oligonucleotide probe and a non-specific LH/CG-β oligonucleotide and riboprobe, we have demonstrated specific CG-β expression in two of 35 random pituitary adenomas; LH-β expression occurred in a further eight adenomas. Unlike prolactin, growth hormone and proopiomelanocortin, which are transcribed in the vast majority of cells in their respective hormone-positive tumour subtypes, the pattern of LH/CG-β was typically a scattering of single or small clusters of hormone-positive cells in a predominantly LH/CG-β-negative tumour. Finally, although bona fide CG-β expression in human pituitary adenomas does occur, it is only at an incidence similar to that described for carcinomas of other tissues.
A Levy, Department of Medicine, University of Bristol, Bristol Royal Infirmary, Marlborough Street, Bristol BS2 8HW, UK
Sex hormone-binding globulin mRNA levels in human uterine endometrium
Authors: Misao Ryou , Itoh Naoki , Mori Hidehiro , Fujimoto Jiro , Tamaya Teruhiko 
Published: December 2008

Misao R, Itoh N, Mori H, Fujimoto J, Tamaya T. Sex hormone-binding globulin mRNA levels in human uterine endometrium. Eur J Endocrinol 1994;131:623–9. ISSN 0804–4643
Sex hormone-binding globulin (SHBG) is a specific steroid hormone-binding protein that plays a role in transporting dihydrotestosterone, testosterone and estradiol-17β (E2), altering their concentration in blood and influencing their biological action. Recently it has been reported that immunoreactive SHBG is localized in target tissues and that SHBG mRNA was identified in human endometrial and prostatic cell lines. In the present work, SHBG mRNA was detected in human normal endometrial tissues using Northern blot analysis and polymerase chain reaction. Its level was higher (p < 0.02) in the secretory phase than in the proliferative phase. In the secretory phase, the endometrial SHBG mRNA level was correlated positively with serum E2 and progesterone level (p < 0.05). However, there was a negative correlation between endometrial SHBG mRNA level and serum E2 /progesterone ratio (p < 0.01). These findings suggest that SHBG is synthesized in the uterine endometrium and a part of its synthesis is regulated complexly by sex steroid hormones such as E2 and progesterone.
Ryou Misao, Department of Obstetrics and Gynecology, Gifu University School of Medicine, Tsukasamachi-40. Gifu 500, Japan
Effects of deflazacort and cortisone on body growth, thymus weight and gene expression of growth-related proteins in the rat
Authors: Latta Kay , Krieg Richard J , Chan Winnie , Hisano Satoshi , Chan James CM 
Published: December 2008

Latta K, Krieg RJ, Chan W, Hisano S, Chan JCM. Effects of deflazacort and cortisone on body growth, thymus weight and gene expression of growth-related proteins in the rat. Eur J Endocrinol 1994;131:652–7. ISSN 0804–4643
Deflazacort is an oxazoline derivative of cortisone with presumably less serious side effects, but its effects on growth factors are unknown. The present experiments in Long Evans rats were carried out to investigate how deflazacort administration affected the growing rat, especially in relation to hepatic insulin-like growth factor I (IGF-I) and growth hormone receptor (GHR) messenger ribonucleic acid (mRNA). Four groups of animals were used: those treated with cortisone, with two different doses of deflazacort and with vehicle. Subcutaneous injections were given daily for 8 days. Thymus weight was reduced in all treated groups, with a comparable magnitude of reduction in the groups treated with cortisone and the higher dose of deflazacort (DF1). Daily weight gain was reduced significantly after cortisone treatment, but less so in the DF1 rats. Liver IGF-I and GHR mRNA were lower in the cortisone and deflazacort than in controls. However, GHR mRNA was reduced significantly only by cortisone and not by DF1. We conclude that growth failure is less severe in the DF1 rats compared to cortisone rats, which corresponds to the reduction in hepatic GHR mRNA.
Kay Latta, Kinderklinik der Medizinischen Hochschule Hannover, Konstanty-Gutschow-Str. 8, 30625 Hannover, Germany
Reduction in goiter size by 131I therapy in patients with non-toxic multinodular goiter
Authors: Wesche Maria F , Tiel-v-Buul Monique M , Smits Nico J , Wiersinga Wilmar M 
Published: December 2008

Wesche MF, Tiel-v-Buul MM, Smits NJ, Wiersinga WM. Reduction in goiter size by 131I therapy in patients with non-toxic multinodular goiter. Eur J Endocrinol 1995;132:86–7. ISSN 0804–4643
A retrospective follow-up study of 131I treatment was performed in 10 females (median age 48 years, range 40–74 years) with non-toxic multinodular goiter. The median dose of 131I given was 20 mCi (range 14–65 mCi). Thyroid volume was measured by ultrasonography. The median follow-up period was 26 months (range 12–68 months). Nine patients had a reduction of goiter size: thyroid volume decreased from 88 ± 14.9 ml (mean±sem) to 49 ± 10.9 ml 1 year after 131I treatment. The relative decrease of goiter size was 48% after 1 year (N = 9) and 59% after 2 years (N = 5). One patient did not respond and was referred for operation. Side effects were mild spontaneously resolving radiation thyroiditis in one patient and subclinical hypothyroidism in four patients. In conclusion, 131I treatment of non-toxic goiter is an effective treatment at the expense of post-radiation (subclinical) hypothyroidism.
Maria F Wesche, Academic Medical Center, University of Amsterdam, Department of Internal Medicine, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
Production of insulin-like growth factor binding protein (IGFBP), IGFBP-3 protease, and expression of IGF-I receptors by cells of the sheep immune system
Authors: Tonner Elizabeth , Beattie James , Flint David J 
Published: December 2008

Tonner E, Beattie J, Flint DJ. Production of insulin-like growth factor binding protein (IGFBP), IGFBP-3 protease, and expression of IGF-I receptors by cells of the sheep immune system. Eur J Endocrinol 1995;132:118–22. ISSN 0804–4643
Single-cell suspensions of sheep thymus cells were cultured in serum-free medium with or without polyclonal activators (phytohaemagglutinin or concanavalin A) and the resultant conditioned medium was assayed for insulin-like growth factor binding protein (IGFBP) activity by binding of [125I]IGF-I, using charcoal to separate free from bound. All cultures produced IGFBP but mitogen stimulation significantly increased IGFBP concentrations, indicating production by lymphoid cells. Conditioned medium also degraded recombinant human [125I]IGFBP-3, suggesting IGFBP-3 protease production within the thymus. This degradation was inhibited by several protease inhibitors (phenylmethylsulphonyl fluoride, aprotinin, N-α-p-tosyl-l-lysine chloromethyl ketone), suggesting the presence of a serine protease. Cell surface [125I]IGF-I binding was demonstrated on cells from thymus, mesenteric lymph node, peripheral blood mononuclear cells and platelets. The [125I]IGF-I binding to platelets could be inhibited by unlabelled peptides, with relative potencies IGF-I > IGF-II ≫ insulin. Scatchard analysis of IGF-I competitive binding revealed a Kd of 266 pmol/l and approximately 40 receptor sites per cell. The high-affinity binding of IGF-I and competition by insulin suggested that the [125I]IGF-I binding was to an IGF-I receptor rather than to a membrane-associated IGFBP, to which insulin does not bind. These data provide further support for the role of the IGF-IGFBP axis in the immune system, particularly in relation to the thymus.
Elizabeth Tonner, Hannah Research Institute, Ayr, UK