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Audrey F Seasholtz Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA
Department of Biological Chemistry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Miina Öhman Department of Psychiatry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Amale Wardani Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Robert C Thompson Molecular and Behavioral Neuroscience Institute, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA
Department of Psychiatry, University of Michigan, 109 Zina Pitcher Place, BSRB Room 5035, Ann Arbor, Michigan 48109, USA

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Introduction Corticotropin-releasing hormone (CRH) is a key regulator of the endocrine, behavioral, and autonomic components of the mammalian stress response. Within the endocrine hypothalamic–pituitary–adrenal axis, this 41-amino acid peptide is

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Kristien Vandenborne Laboratory of Comparative Endocrinology, Zoological Institute, K U Leuven, Naamsestraat 61, B-3000 Leuven, Belgium

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Simon A Roelens Laboratory of Comparative Endocrinology, Zoological Institute, K U Leuven, Naamsestraat 61, B-3000 Leuven, Belgium

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Veerle M Darras Laboratory of Comparative Endocrinology, Zoological Institute, K U Leuven, Naamsestraat 61, B-3000 Leuven, Belgium

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Eduard R Kühn Laboratory of Comparative Endocrinology, Zoological Institute, K U Leuven, Naamsestraat 61, B-3000 Leuven, Belgium

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Serge Van der Geyten Laboratory of Comparative Endocrinology, Zoological Institute, K U Leuven, Naamsestraat 61, B-3000 Leuven, Belgium

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Introduction Thyrotropin-releasing hormone (TRH) is a neuroactive tripeptide ( l -pyroglutamyl- l -histidyl- l -prolinamide; pGlu-His-ProNH 2 ), that was originally isolated from porcine and ovine hypothalami as a first

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K. YAMASHITA
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M. MIENO
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ER. YAMASHITA
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The concentrations of 17-oxosteroids in the spermatic venous blood of anaesthetized dogs were used as an index of LH release to assess the effects of arginine-vasotocin on the response of the canine pituitary gland to exogenous luteinizing hormone releasing hormone (LH-RH). When injected into the carotid artery, arginine-vasotocin (1·0 μg/kg body wt) caused no significant alterations in the testicular output of 17-oxosteroids. The administration of LH-RH (5 μg/kg body wt, a standard dose) into the carotid artery produced typical stimulation of testicular 17-oxosteroid secretion. Administration of arginine-vasotocin (0·01, 0·1 or 1·0 μg/kg body wt) into the carotid artery 3 h before the administration of a standard dose of LH-RH inhibited the testicular secretion of 17-oxosteroids normally induced by LH-RH. However, pretreatment with arginine-vasotocin (1·0 μg/kg body wt) did not affect the testicular response to i.v. administration of human chorionic gonadotrophin (5 i.u./kg body wt). These results indicate that in the dog, arginine-vasotocin inhibits the LH-RH-induced release of LH by acting directly on the anterior pituitary gland.

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P. J. Trainer
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J. M. W. Kirk
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M. O. Savage
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A. B. Grossman
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G. M. Besser
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ABSTRACT

The GH response to insulin-induced hypoglycaemia and growth hormone-releasing hormone (GHRH) has been shown to be impaired in subjects with Cushing's syndrome and in healthy volunteers given oral glucocorticoids. Pyridostigmine is an anticholinesterase that stimulates GH secretion, probably by inhibition of hypothalamic somatostatin secretion. This work was designed to study the site of action of glucocorticoids in inhibiting the secretion of GH.

Eight healthy male volunteers were studied on three occasions in random order. They took 2 mg oral dexamethasone or placebo at precisely 6-hourly intervals for 48 h before receiving 120 mg oral pyridostigmine or placebo, followed 60 min later by GHRH (100 μg) i.v. Samples for measuring GH were obtained at 15 min intervals for 2 h.

The 'area under the curve' (AUC) for each of the treatments was significantly different: dexamethasone–pyridostigmine–GHRH (mean ± s.e.m., 1938 ± 631 mU/min per 1), dexamethasone–placebo–GHRH (634 ±211) and placebo–placebo–GHRH (4267 ± 1183) (P<0·02, Wilcoxon test).

In conclusion, dexamethasone given for 48 h significantly inhibited the AUC for GH following treatment with GHRH. However, pretreatment with pyridostigmine significantly reversed the inhibition although this was still partial. Our data suggested that this short-term suppressive effect of dexamethasone was independent of GHRH, and most probably relates to stimulation of the release of somatostatin.

Journal of Endocrinology (1992) 134, 513–517

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Sean C Lema
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Jon T Dickey Physiology Program, School of Aquatic and Fishery Sciences, Pacific Northwest Division, Northwest Fisheries Science Center, NOAA Fisheries, Seattle, Washington 98112, USA

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Irvin R Schultz Physiology Program, School of Aquatic and Fishery Sciences, Pacific Northwest Division, Northwest Fisheries Science Center, NOAA Fisheries, Seattle, Washington 98112, USA

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Penny Swanson
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Introduction The hypothalamic–pituitary–thyroid (HPT) axis regulates metabolism and growth, reproduction, and brain development in vertebrates. Similarly, in fish, thyroid hormones (THs) have been demonstrated to regulate growth ( Huang et al

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S. M. Farrow
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For many years hormone secretion was the sole indicator of hormone synthesis available but the emergence of molecular biology and the provision of cDNA probes enabled synthesis to be studied in more detail, particularly with regard to changes in the rate of gene transcription and steady-state mRNA levels. However, the limitations of these approaches have become apparent, with paradoxical results whereby changes in the rate of transcription do not parallel changes in hormone production. These observations provided evidence for the presence of posttranscriptional sites of regulation in addition to those at transcription and secretion.

Over the last few years, post-transcriptional regulation has been studied in detail for many proteins, including a range of intracellular 'housekeeping' proteins and exported products including hormones. Figure 1 depicts the protein synthetic pathway from gene transcription to polypeptide production on ribosomes and serves to illustrate some of the sites at which regulation may occur. The

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M. G. Parker
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Hormone receptors which function in the cell nucleus to regulate the expression of specific genes appear to be members of a discrete family of proteins. The best characterized of these are the steroid receptors which, not too surprisingly, share similar structural and functional properties with one another (King, 1987) but it is now emerging from molecular cloning studies that the receptors for thyroid hormone and retinoic acid and a number of novel receptors are also members of this same family of proteins (Table 1). The justification for assigning all these nuclear-acting receptors to a single family of proteins is the subject of this commentary.

table 1. Members of the nuclear receptor family. Receptors which have been cloned are listed together with the chromosomal location of the human genes if known

Androgens (X) Thyroid hormone α (17)

Glucocorticoids (5) Thyroid hormone β (3)

Mineralocorticoids (4)

Oestrogens (6) Retinoic acid α (17)

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Ana Sofia Rocha IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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Ricardo Marques IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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Inês Bento IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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Ricardo Soares IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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João Magalhães IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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Inês Vieira de Castro IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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Paula Soares IPATIMUP, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Roberto Frias s/n, 4200-065 Porto, Portugal
Department of Pathology, Hospital São João, Porto, Portugal
Department of Pathology, Medical Faculty, University of São Paulo, São Paulo, Brazil
Department of Pathology, Medical Faculty, University of Porto, Porto, Portugal

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( Castro et al. 2006 ). At variance with PTC, a mouse model for FTC was lacking until Kaneshige et al. (2000) described a mutant mouse with a mutation ( PV ) targeted to the thyroid hormone receptor β (THRB) locus. In a heterozygous condition

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Christopher J Charles Christchurch Cardioendocrine Research Group, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand

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Miriam T Rademaker Christchurch Cardioendocrine Research Group, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand

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A Mark Richards Christchurch Cardioendocrine Research Group, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand

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increased AVP release from hypothalamic explants ( Taheri et al. 2002 ) but reduced AVP secretion reported in vivo in response to i.c.v. apelin ( Reaux et al. 2001 , De Mota et al. 2004 ). Apelin also increases corticotrophin releasing hormone

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Tabata M Bohlen Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Thais T Zampieri Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Isadora C Furigo Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Pryscila D S Teixeira Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Edward O List Edison Biotechnology Institute and Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA

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John J Kopchick Edison Biotechnology Institute and Heritage College of Osteopathic Medicine, Ohio University, Athens, Ohio, USA

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Jose Donato Jr Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Renata Frazao Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo, São Paulo, Brazil

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Introduction Puberty is a complex phenomenon modulated by genetic, epigenetic, environmental, nutritional and hormonal factors. Both the onset and proper development of sexual maturation depend on augmented sex steroid levels, and the ability

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