bluuebunny/crossref_metadata_2025_split huggingface dataset:
Insulin, insulin-like growth factor I (IGF-I) and IGF-II enhance basal and gonadotrophin-releasing hormone-stimulated luteinizing hormone release from rat anterior pituitary cells in vitro
Authors: Soldani Renza , Cagnacci Angelo , Yen Samuel SC 
Published: December 2008

Soldani R, Cagnacci A, Yen SSC. Insulin, insulin-like growth factor I (IGF-I) and IGF-II enhance basal and gonadotrophin-releasing hormone-stimulated luteinizing hormone release from rat anterior pituitary cells in vitro. Eur J Endocrinol 1994;131:641–5. ISSN 0804–4643
The role of insulin-like growth factor I (IGF-I) and IGF-II on luteinizing hormone (LH) release is still unclear. The present study was performed to investigate modifications of basal and gonadotrophinreleasing hormone (GnRH)-stimulated (109 mol/l) LH release, induced by a 4-h and a 24-h incubation with physiological doses of IGF-I (1, 5 and 10 nmol/l) and IGF-II (5, 10 and 15 nmol/l) in comparison with insulin (0.0017, 0.1722 and 1.722 nmol/l), from primary cultures of male rat anterior pituitary cells. Both during the 4-h and the 24-h incubation, basal and GnRH-stimulated LH release were increased by IGF-I, IGF-II and insulin in a dose-dependent fashion. Present data confirm insulin's capability of potentiating anterior pituitary LH release from dispersed rat anterior pituitary cells in vitro, and reveal similar effects for physiological doses of IGF-I and IGF-II.
Renza Soldani, Instituto di Ginecologia Ostetricia e Fisiopatologia della Riproduzione Umana, Ospedale S. Giovanni di Dio, via Ospedale 46, 09124 Cagliari, Italy
Effect of 6-hydroxydopamine injection into the arcuate hypothalamic nucleus on the osmotic release of vasopressin in conscious rats
Authors: Yamaguchi Ken'ichi , Hama Hitoshi , Watanabe Kazuo , Yamaya Kanemitsu 
Published: December 2008

Yamaguchi K, Hama H, Watanabe K, Yamaya K. Effect of 6-hydroxydopamine injection into the arcuate hypothalamic nucleus on the osmotic release of vasopressin in conscious rats. Eur J Endocrinol 1994;131:658–63. ISSN 0804–4643
The aim of the present study was to evaluate a role in vasopressin secretion of the catecholaminergic neurons, including the tuberohypophysial dopaminergic neurons situated in the arcuate hypothalamic nucleus. A neurotoxin, 6-hydroxydopamine (6 g/l), was injected locally into the arcuate nucleus and its effects on catecholamine levels of the hypothalamic tissue and the neurointermediate lobe, and on the plasma vasopressin concentrations before and during iv infusion (0.1 ml kg−1 min−1) of isotonic (0.15 mol/l) or hypertonic saline (2.5 mol/l), were examined in conscious rats. The infusion of hypertonic saline produced increases of plasma vasopressin 15 and 30 min later, accompanied by elevations of plasma osmolality, sodium, chloride and arterial pressure. The vasopressin response was potentiated markedly by the 6-hydroxydopamine injection performed 8 days before, which hardly affected the responses of the other variables. Histological examination indicated that the injection sites of 6-hydroxydopamine in those rats had been located in the area ranging from rostral to medial arcuate nucleus. The iv infusion of isotonic saline did not change plasma vasopressin, osmolality, sodium, chloride or arterial pressure, regardless of the presence or absence of pretreatment with 6-hydroxydopamine. It was confirmed that when 6-hydroxydopamine was injected into the arcuate nucleus region 8 days before, noradrenaline and adrenaline concentrations of the hypothalamic tissue containing the injection site were decreased remarkably, although we could not detect any signficant alteration in the dopamine concentration of the hypothalamic tissue or the neurointermediate lobe. On the basis of these results, we concluded that catecholaminergic neurons in the arcuate nucleus may act to inhibit osmotic vasopressin secretion.
Ken'ichi Yamaguchi, Department of Physiology, Niigata University School of Medicine, Asahimachi-Dori 1, Niigata City, Niigata 951, Japan
Thyroid-stimulating antibodies in sera from patients with Graves' disease are heterogeneous in epitope recognition
Authors: Ueda Yoshimichi , Sugawa Hideo , Akamizu Takashi , Okuda Jyoji , Ueda Michiko , Kosugi Shinji , Ohta Chizuko , Kihou Yukio , Mori Toru 
Published: December 2008

Ueda Y, Sugawa H, Akamizu T, Okuda J, Ueda M, Kosugi S, Ohta C, Kihou Y, Mori T. Thyroidstimulating antibodies in sera from patients with Graves' disease are heterogeneous in epitope recognition. Eur J Endocrinol 1995;132:62–8. ISSN 0804–4643
Two synthetic peptides, P354-14 (amino acid nos. 354 to 367) and P338-16 (nos. 338 to 353), corresponding to the partial amino acid sequences of the hTSH receptor structure were studied for their ability to bind specifically serum IgGs from patients with Graves' disease and to inhibit thyroid stimulating TSH receptor antibody (TSH-R SAb) activity. IgG binding was measured by an ELISA using sera from 102 Graves', 20 Hashimoto patients, and 9 normal subjects. Both peptides showed significantly increased IgG binding of Graves' sera compared with those of Hashimoto and normal sera. There was a significant correlation (r = 0.529) between the amount of IgG bound by the two peptides, but neither of these values correlated well with their TSH-R SAb activity nor thyrotropin-binding inhibitor TSH receptor antibody (TSH-R IAb) activity. TSH-R SAb inhibiting effects of these peptides were then analysed by measuring TSH-R SAb activity after incubation with the peptides. Among eight Graves' IgGs tested the TSH-R SAb activity of three was inhibited by both peptides, two were inhibited only by P354-14 and three were not affected by either. These TSH-R SAb inhibiting effects were dose-dependent and reproducible. To confirm these findings, a peptide-sepharose gel affinity absorption study was performed. Eleven Graves' IgGs were applied to both peptide gels and the TSH-R SAb activity of the unabsorbed fraction was measured. The TSH-R SAb activity of five IgGs was strongly absorbed only by P354-14 and five others were absorbed by both peptides to an almost similar extent. One IgG was not affected by either of the peptides. None of the IgG activities tested was absorbed only or predominantly by P338-16. Most of Graves' IgGs could bind to region no. 338 to no. 367 of the hTSH receptor. There was apparent heterogeneity among Graves' TSH-R SAb IgGs as shown by their absorption by the peptides, and the existence of at least three heterogeneous species in epitopic recognition among Graves' TSH-R SAb was demonstrated.
Toru Mori, Department of Laboratory Medicine, Kyoto University School of Medicine, 54-Shogoin Kawaharacho, Sakyo-ku, Kyoto 606-01, Japan
Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus
Authors: Mattheij John AM , Swarts Hans JM 
Published: December 2008

Mattheij JAM, Swarts HJM. Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus. Eur J Endocrinol 1995;132:91–6. ISSN 0804–4643
The cause of formation of luteinized unruptured follicles (LUF) is unknown. Formation of LUF was studied after injection of a varying small dose of luteinizing hormone (LH) with or without subsequent injection of gonadotrophin-releasing hormone (GnRH); in addition, the effect of suppression of prolactin on LUF formation was studied. Luteinization without ovulation occurred in virtually all graafian follicles, if 0.5–1.0 μg of LH was injected some hours before the presumed endogenous LH surge (suppressed by Nembutal); with increasing doses of LH progressively increasing numbers of ovulations were observed. If in early pro-oestrus 1 μg of GnRH was given 4 h after 1 μg of LH, formation of LUF was partly prevented; if the interval between LH and GnRH was 8 h or more, the great majority of graafian follicles developed into LUF. If early in pro-oestrus 1 μg of LH was given and 8 h later 0.1 μg of a potent GnRH analogue, about 50% of the follicles became LUF; in similarly treated rats, suppression of prolactin by ergocryptine reduced but did not prevent LUF formation. The data support the idea that deficient LH secretion in the period before ovulation may be involved in the formation of LUF.
John AM Mattheij, Department of Human and Animal Physiology, Haarweg 10, 6709 PJ Wageningen, The Netherlands
Erythropoietin and testicular steroidogenesis: the role of second messengers
Authors: Foresta Carlo , Mioni Roberto , Bordon Paola , Gottardello Francesco , Nogara Andrea , Rossato Marco 
Published: December 2008

Foresta C, Mioni R, Bordon P, Gottardello F, Nogara A, Rossato M. Erythropoietin and testicular steroidogenesis: the role of second messengers. Eur J Endocrinol 1995;132:103–8. ISSN 0804–4643
It has been demonstrated that erythropoietin (EPO) influences rat and human Leydig cell steroidogenesis, stimulating testosterone production through a direct and specific receptor-mediated mechanism. The aim of this study was to investigate the mechanism by which recombinant human erythropoietin (rHuEPO) exerts its stimulatory effect on rat Leydig cells. Recombinant human EPO did not induce, at any dose tested (10−10 to 10−13 mol/l), an increase in either cAMP or cGMP, suggesting that in Leydig cells the effect of rHuEPO does not involve the adenylate or guanylate–cyclase systems. The role of transmembrane calcium flux in rHuEPO-stimulated steroidogenesis was studied by evaluating the effect of calcium channel blocker, verapamil, and by the 45Ca2+ uptake method. Verapamil did not influence rHuEPO-induced testosterone secretion and rHuEPO did not modify calcium recycling, indicating that calcium transmembrane flux is not involved in the rHuEPO effect. The protein kinase C inhibitor staurosporine (10, 30, 100 and 300 nmol/l) inhibited rHuEPO-stimulated testicular steroidogenesis in a dose-dependent manner. This indirect evidence suggests that the stimulatory effect of rHuEPO on rat Leydig cells may involve protein kinase C activation.
Carlo Foresta, Institute of Internal Medicine, Via Ospedale Civile 105, 35128 Padova, Italy
Biosynthetic growth hormone increases the collagen deposition rate in rat aorta and heart
Authors: Brüel A , Oxlund H 
Published: December 2008

Brüel A, Oxlund H. Biosynthetic growth hormone increases the collagen deposition rate in rat aorta and heart. Eur J Endocrinol 1995;132:195–9. ISSN 0804–4643
Disorders of the cardiovascular system often are associated with alterations in the metabolism of the collagens of these tissues. A method for in vivo determination of collagen deposition rate in small tissue samples is delineated and used for assessment of the effect of biosynthetic growth hormone (GH) injections on the collagen deposition rate in rat aorta and cardiac musculature. Rats were injected with GH, and the controls with saline, twice daily for 7 days. The in vivo collagen deposition rate was measured by injecting iv a large dose of [3H]-proline with a flooding dose of "cold" proline, followed by determination of the production of [3H]-hydroxyproline during a 4-h labelling period. Extractable collagens that were not bound in the tissue and therefore do not contribute mechanical strength to it were removed from the samples. 3H-Labelled- and "cold" amino acids were assessed by reversed-phase HPLC combined with simultaneous flow scintillation detection on the same sample. In the control group the deposition per hour was 0.13 ± 0.02% (mean ± sem) in aortic intima media and 0.72 ± 0.09% in cardiac left ventricular musculature. Growth hormone induced a threefold increase (p < 0.001 and p < 0.01, respectively) in the collagen deposition rate: 0.45 ± 0.06% in aortic intima media and 2.43 ± 0.45% in cardiac left ventricular musculature. The method described enables a rapid and sensitive determination of collagen deposition per hour in small tissue samples from experimental animals. The collagen deposition rate of cardiac musculature is fivefold higher compared with that of aortic intima media. Biosynthetic GH induces a threefold increase in the collagen deposition rate of these tissues.
Hans Oxlund, Department of Connective Tissue Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C, Denmark
Epidermal growth factor stimulates the cell growth of the PA-1 teratocarcinoma cell line in an autocrine/paracrine fashion
Authors: Shigeta Hiroyuki , Taga Michiyoshi , Sakakibara Hideya , Minaguchi Hiroshi 
Published: December 2008

Shigeta H, Taga M, Sakakibara H, Minaguchi H. Epidermal growth factor stimulates the cell growth of the PA-1 teratocarcinoma cell line in an autocrine/paracrine fashion. Eur J Endocrinol 1995;132: 200–5. ISSN 0804–4643
In order to investigate the biological significance of epidermal growth factor (EGF) in the cell function of teratocarcinoma cells, we examined the production, binding and cell proliferative effect of EGF in PA-1 human ovarian teratocarcinoma cell line. The immunoreactivity of EGF in PA-1 cell-conditioned medium was detected by human EGF radioimmunoassay, and prepro-EGF mRNA was demonstrated in PA-1 cells by Northern blot analysis. An [125I] EGF binding study showed the presence of EGF receptor with very high binding affinity and relatively low numbers of binding sites in PA-1 cells. Furthermore, the growth of PA-1 cells was stimulated by EGF and inhibited by anti-EGF monoclonal antibody. These results suggest strongly that EGF plays an important role in controlling the growth of teratocarcinoma cells as an autocrine/paracrine growth factor.
Michiyoshi Taga, Department of Obstetrics and Gynecology, Yokohama City University School of Medicine, 3–9 Fukuura, Kanazawa-ku, Yokohama 236, Japan
Increase in human placental glucose transporter-1 during pregnancy
Authors: Sakata Masahiro , Kurachi Hirohisa , Imai Takashi , Tadokoro Chikae , Yamaguchi Masaaki , Yoshimoto Yasuhiro , Oka Yoshitomo , Miyake Akira 
Published: December 2008

Sakata M, Kurachi H, Imai T, Tadokoro C, Yamaguchi M, Yoshimoto Y, Oka Y, Miyaka A. Increase in human placental glucose transporter-1 during pregnancy. Eur J Endocrinol 1995;132:206–12. ISSN 0804–4643
Glucose transporter-1 (GLUT1) has been found in high abundance in human placentas. The purpose of this study was to analyze the changes in the level of GLUT1 during pregnancy. We have analzyed the gestational changes in human placental GLUT1 by [3H]cytochalasin B binding assay, immunoblot analysis and Northern blot analysis. Levels of [3H]cytochalasin B binding to placental membrane in pregnancy at 7–10, 18–20 and 38–40 weeks were 4.2 ± 0.47, 5.2 ± 0.46 and 7.2 ± 0.40 (mean±sem, N = 4) μmol/kg protein, respectively. Amounts of 49-kD and 60-kD proteins detected in immunoblot analysis increased during pregnancy in parallel with [3H]cytochalasin B binding to placental membrane. The GLUT1 mRNA levels also increased during pregnancy. Immunohistochemical examination showed that GLUT1 was localized in the plasma membranes of trophoblast cells. These findings showed that the GLUT1 level increased during pregnancy in human placentas and suggest that GLUT1 may play an important role in fetal development.
Masahiro Sakata, Department of Obstetrics and Gynecology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan
Effects of transforming growth factor α (TGF-α) on DNA synthesis and thyrotropin-induced iodine metabolism in cultured porcine thyroid cells
Authors: Arai Mariko , Tsushima Toshio , Isozaki Osamu , Demura Hiroshi , Shizume Kazuo , Emoto Naoya , Miyakawa Megumi , Nozoe Yasuko , Murakami Hitomi , Ohmura Eiji 
Published: December 2008

Arai M, Tsushima T, Isozaki 0, Demura H, Shizume K, Emoto N, Miyakawa M, Nozoe Y, Murakami H, Ohmura E. Effects of transforming growth factor α (TGF-α) on DNA synthesis and thyrotropin-induced iodine metabolism in cultured porcine thyroid cells. Eur J Endocrinol 1995;132:242–8. ISSN 0804–4643
Transforming growth factor α (TGF-α) is a potent mitogen that is similar structurally to epidermal growth factor (EGF). As EGF is a potent growth stimulator and an inhibitor of iodine metabolism in cultured thyroid cells of several species, we studied whether TGF-α has similar effects using porcine thyroid cells in culture. Recombinant human TGF-α dose-dependently stimulated DNA synthesis of thyroid cells, with maximal stimulation (eight- to ninefold above basal) occurring at 2 nmol/l. The potency was approximately 50% that of mouse EGF and correlated with the ability to compete with EGF for receptor binding, suggesting that the action of TGF-α is mediated by interaction with EGF receptors. When thyroid cells were cultured for 3 days with thyrotropin (TSH) in the presence of TGF-α, TSH-induced iodide uptake was inhibited in a dose-dependent manner. The potency of TGF-α again was approximately 50% that of EGF. Transforming growth factor α did not inhibit TSH-stimulated cAMP production. Moreover, iodide uptake stimulated by either forskolin or 8-bromo-cAMP also was inhibited by TGF-α. Thus, we conclude that TGF-α inhibits TSH-induced iodine metabolism largely by acting at the steps distal to cAMP production. Northern blot analysis revealed expression of TGF-α mRNA in porcine thyroid cells. These observations suggest that TGF-α acts as an autocrine modulator of growth and differentiated functions in porcine thyroid cells.
T Tsushima, Department of Medicine 2, Tokyo Women's Medical College, Kawadacho 8–1, Shinjukuku, Tokyo 162, Japan
Missense mutation in CYP11B1 (CGA[Arg-384] → GGA[Gly]) causes steroid 11β-hydroxylase deficiency
Authors: Nakagawa Yuichi , Yamada Masao , Ogawa Haruo , Igarashi Yoshio 
Published: December 2008

Nakagawa Y, Yamada M, Ogawa H, Igarashi Y. Missense mutation in CYP11B1 (CGA[Arg-384] → GGA[Gly]) causes steroid 11β-hydroxylase deficiency. Eur J Endocrinol 1995;132:286–9. ISSN 0804–4643
Steroid 11β-hydroxylase deficiency (11β-OHD) is an autosomal recessive hereditary defect and one of the causes of congenital adrenal hyperplasia. The 11β-hydroxylase enzyme is encoded by the CYP11B1 gene on chromosome 8q22. Twelve types of mutations of this gene have been reported previously in patients with 11β-OHD, including one Japanese patient. We detected an additional previously uncharacterized mutation: R384G mutation, a single C→G base substitution in the codon 384 of the exon 7 changing an arginine (CGA) to a glycine (GGA) by sequencing the CYP1 1B1 gene of Japanese siblings with 11β-OHD. We analyzed also the CYP11B1 gene of their unaffected family members. Their grandfather was homozygous for the normal gene, whereas their grandmother, parents and younger brother were heterozygous for the mutation. These results indicate that the cause of 11β-OHD is heterogeneous even in the Japanese population, which is ethnically homogeneous.
Yuichi Nakagawa, Department of Pediatrics, Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu 431-31, Japan
Percutaneous computed tomography-guided ethanol injection in aldosterone-producing adrenocortical adenoma
Authors: Rossi Riccardo , Savastano Silvia , Tommaselli Antonio P , Valentino Rossella , Iaccarino Vittorio , Tauchmanova Libuse , Luciano Antonio , Gigante Marianna , Lombardi Gaetano 
Published: December 2008

Rossi R, Savastano S, Tommaselli AP, Valentino R, Iaccarino V, Tauchmanova L, Luciano A, Gigante M, Lombardi G. Percutaneous computed tomography-guided ethanol injection in aldosteroneproducing adrenocortical adenoma. Eur J Endocrinol 1995;132:302–5. ISSN 0804–4643
The feasibility, safety and effectiveness of percutaneous computed tomography-guided ethanol injection (PEI-CT) was investigated in a patient affected by aldosterone-producing adenoma (APA). A 42-year-old male patient with typical features of hyperaldosteronism presented a solitary left adrenal adenoma measuring 2 cm, with a normal contralateral gland, evidenced by both CT scan and adrenal [75Se-19]-nor-cholesterol scintigraphy. After normalization of potassium plasma levels, 4 ml of sterile 95% ethanol with 0.5 ml of 80% iothalamate sodium was injected. The procedure was completed in about 30 min. No severe pain or local complication was noted. Five hours after PEI, a fourfold and a twofold increase in aldosterone and cortisol plasma levels were observed, respectively. After 11 days on a normal sodium and potassium diet, normal potassium plasma levels and reduced aldosterone plasms levels were present, with reappearance of an aldosterone postural response. Plasma renin activity and aldosterone plasma levels normalized I month later, with reappearance also of a plasma renin activity postural response and maintenance of normal potassium plasma levels even on a high sodium and normal potassium diet. The patient has remained hypertensive, although lower antihypertensive drug dosages have been employed. After 17 months, normal biochemical, hormonal and morphological findings were still present. Thus, we suggest PEI-CT as a further alternative approach to surgery in the management of carefully selected patients with APA.
Riccardo Rossi, Chair of Endocrinology, "Federico II" University of Naples, via Sergio Pansini 5, 80131 Naples, Italy
Insulin-like growth factors I and II in healthy women with and without established osteoporosis
Authors: Ravn P , Overgaard K , Spencer EM , Christiansen C 
Published: December 2008

Ravn P, Overgaard K, Spencer EM, Christiansen C. Insulin-like growth factors I and II in healthy women with and without established osteoporosis. Eur J Endocrinol 1995;132:313–9. ISSN 0804–4643
We measured serum concentrations of insulin-like growth factors I and II (IGF-I and IGF-II) by radioimmunoassay in 107 healthy women aged 28–78 years and in 116 women with established osteoporosis. The women with established osteoporosis were randomized to a 1-year double-blind, placebo-controlled treatment with continuous estrogen/progestogen, anabolic steroids, salmon calcitonin or placebo and the IGFs were measured every 6 months. Women less than 35 years of age had 29% higher levels of IGF-I (p < 0.001) as compared to women above that age. For women more than 35 years of age, we found no correlation between IGF-I and age (r = 0.02). Correspondingly, we found no significant changes in serum IGF-I in 10 women, who were followed with serial measurements of IGFs every 3 months from 2 years before to 1 year after menopause; IGF-II revealed no correlation with age (r = 0.04). In the group of 116 women with established osteoporosis, IGF-I was 30% lower (p < 0.01) as compared to a group of 19 height-, weight- and age-matched nonfractured women (mean age 64 years). The IGF-II levels were equal in the two groups. Over the 1-year therapeutic intervention period, an increase in IGF-I of 13–15% (p < 0.05) was seen in the nandrolone decanoate-treated group. The same tendency was seen for hormone replacement therapy, although it was not significant. In conclusion, the serum level of IGF-I is high in young women, when peak bone mass is attained, and low in postmenopausal women with established osteoporosis.
Pernille Ravn, Center for Clinical & Basic Research, Ballerup Byvej 222, DK-2750 Ballerup, Denmark