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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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Department of Applied Biochemistry, Faculty of Agriculture, Utsunomiya University, Utsunomiya, Tochigi 321-8505, Japan
Freshwater Fisheries Research Division, National Research Institute of Fisheries Science, Nikko, Tochigi 321-1661, Japan
Laboratory of Brain Science, Faculty of Integrated Arts and Sciences, Hiroshima University, Higashi-Hiroshima 739-8521, Japan
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). GnIH-immunoreactive (ir) cell bodies and terminals were localized in the paraventricular nucleus and median eminence, respectively, indicating that GnIH acts directly on the pituitary ( Tsutsui et al. 2000 , Ubuka et al. 2003 , Ukena et al. 2003
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Introduction The hypothalamic–pituitary–adrenal (HPA) axis is a major regulator of immunity and inflammation via its secretion of glucocorticoids that suppress the immune activation of leukocytes and inhibit proinflammatory mediators. ACTH is the
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Introduction The anterior pituitary gland comprises five types of hormone-producing cells plus folliculo-stellate (FS) cells, which do not produce classical anterior pituitary hormones. FS cells have a star-like appearance ( Farquhar 1957 , Vila
Instituto de Biología y Medicina Experimental, Department of Medicine, Department of Cell Biology, Consejo Nacional de Investigaciones Científicas y Técnicas, Vuelta de Obligado 2490, 1428 Buenos Aires, Argentina
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Pituitary tumors Pituitary tumors are commonly benign, slow growing adenomas, and account for 10–15% of all intracranial neoplasms ( Farrell 2006 , Melmed 2015 ). The prevalence of these tumors is relatively high in the general population, with ∼77
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Introduction Pituitary adenomas are benign tumors which account for 15% of all intracranial neoplasms. Despite the extensive studies performed to elucidate the molecular defects present in pituitary adenomas, their pathogenesis is
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first exposure of the pituitary to GnRH ( de Koning et al. 1976 ). Progesterone receptor (PR) plays a key role in augmenting gonadotroph responsiveness to GnRH ( Waring & Turgeon 1992 , Turgeon & Waring 1994 ) and requires previous exposure of the
Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Gene Therapeutics Research Institute, Cedars-Sinai Medical Center and Department of Medicine and Molecular and Medical Pharmacology, David Geffen School of Medicine, UCLA, 8700 Beverly Blvd, Davis Building, Suite 5090, Los Angeles, California 90048, USA
Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA
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Introduction Although most pituitary tumors are benign, aggressive local growth can occur. Altered pituitary hormone release often leads to serious clinical disorders, such as acromegaly, Cushing’s disease and sexual dysfunction
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Introduction The anterior pituitary gland is composed of five types of hormone-producing cells and the folliculo-stellate cells (FS cells), which do not produce the classical anterior pituitary hormones. In vivo , these cells are surrounded by
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Introduction Pituitary adenomas account for 10–15% of all intracranial tumors. Ninety percent are represented by somatotroph adenomas (growth hormone (GH) secretors), clinically non-functioning adenomas (mainly gonadotroph) and
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Autoantibodies to cell surface antigens of human somatotropinoma (ASAS), human prolactinoma (ASAP) and rat adenohypophysis (ASARA) were assayed in the serum of patients with pituitary diseases associated with GH deficiency (GHD), such as pituitary dwarfism and primary empty sella syndrome (ESS), and in the serum of patients with hyperprolactinaemia of different etiologies: idiopathic hyperprolactinaemia, prolactinoma and ESS. The investigation was carried out with a cellular variant of an ELISA. Among children with GHD, the highest percentage of antibody-positive patients was found in the group with idiopathic isolated GHD (89% of ASAS(+) patients and 30% of ASARA(+) patients vs 33.3% and 0% respectively in the group with idiopathic combined pituitary hormone deficiency, and 33.3% and 9% in patients with pituitary hypoplasia associated with isolated GHD or combined pituitary hormone deficiency). Among hyperprolactinaemic patients, the highest ASAP and ASARA frequency was observed in patients with idiopathic hyperprolactinaemia (67.7% and 41.9% respectively) where it was twice as high as in the group of patients with prolactinoma. The proportion of ASAS(+) and ASARA(+) did not differ significantly between the groups of patients with ess with or without GHD. Similarly, there was no significant difference between the number of ESS ASAP(+) and ASARA(+) patients with or without hyperprolactinaemia. The data obtained suggested that autoimmune disorders may be primary, and responsible, at least in part, for pituitary dysfunction in the cases of idiopathic isolated GHD and idiopathic hyperprolactinaemia. At the same time, the autoimmune disorders in the patients with prolactinoma or ESS are probably secondary to the organic pituitary lesion and their significance in the development of the pituitary dysfunction is obscure.