bluuebunny/crossref_metadata_2025_split huggingface dataset:
No correlation of growth hormone receptor gene mutation P561T with body height
Authors: Chujo Seiko , Kaji Hidesuke , Takahashi Yutaka , Okimura Yasuhiko , Abe Hiromi , Chihara Kazuo 
Published: December 2008

Chujo S. Kaji H, Takahashi Y. Okimura Y, Abe H, Chihara K. No correlation of growth hormone receptor gene mutation P561T with body height. Eur J Endocrinol 1996;134:560–2. ISSN 0804–4643
Analysis of the growth hormone receptor (GHR) gene in GH insensitivity syndrome revealed various mutations, mainly in the gene encoding the extracellular domain of GHR. On the other hand, the mutation of the gene encoding the cytoplasmic domain of GHR was not found. We have reported, in the cytoplasmic domain of a GHR gene, mutation P561T in a patient with Noonan syndrome who showed a blunted insulin-like growth factor I (IGF-I) response to an acute injection of GH. However, her mother possessing the same mutation had no growth failure. To clarify the significance of the GHR gene mutation P561T, 96 volunteers (41 males aged 21–80 years; 55 females, aged 20–80 years) were tested for the presence of this mutation. By the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, three of the 41 males and 11 of the 55 females examined revealed heterozygous missense mutation P561T, The body height (cm) was 168 ±5.3 (mean ± sd) in three males with the mutation and 164.1 ± 5.8 in 38 males without the mutation. The difference between them was not statistically significant. The body height in 11 females with the mutation was 152.6 ± 5.4, which did not differ significantly from 151.3 ± 6.2 in 44 females without the mutation. These findings suggest that the heterozygous missense mutation P561T in the cytoplasmic domain of GHR does not play a significant role in determining the final body height.
Hidesuke Kaji, Third Division, Department of Medicine, Kobe University School of Medicine. 7-5-1. Kusunokicho, Chuo-ku, Kobe 650, Japan
Adrenocorticotropin-independent bilateral macronodular adrenocortical hyperplasia: immunohistochemical studies of steroidogenic enzymes and post-operative course in two men
Authors: Wada Norio , Kubo Mitsumasa , Kijima Hiromichi , Ishizuka Tatsuya , Saeki Tomoko , Koike Takao , Sasano Hironobu 
Published: December 2008

Wada N, Kubo M, Kijima H, Ishizuka T, Saeki T, Koike T, Sasano H. Adrenocorticotropin-independent bilateral macronodular adrenocortical hyperplasia: immunohistochemical studies of steroidogenic enzymes and post-operative course in two men. Eur J Endocrinol 1996;134:583–7. ISSN 0804–4643
We treated two men with Cushing's syndrome due to adrenocorticotropin (ACTH)-independent bilateral macronodular adrenocortical hyperplasia (AIMAH). In both patients, plasma ACTH was low and plasma cortisol was not suppressed by a high dose of dexamethasone (8 mg) but was remarkably responsive to exogenous ACTH. The adrenal glands were extremely enlarged and contained multiple nodules composed of large clear cells and small compact cells. The immunore-activity of P-45017α was predominant in the small compact cells, while that of 3β-hydroxysteroid dehydrogenase (3 β-HSD) was observed exclusively in the large clear cells. Among various adrenocortical disorders, differential expression of 3β-HSD and P-45017α in clear and compact cells has heretofore been demonstrated only in AIMAH. Total adrenalectomy was done for one patient, and partial adrenalectomy for the other. In the former patient, the normal diurnal rhythm of plasma ACTH was restored 11 months postoperatively. In the latter patient, the normal dynamics in the hypothalamic-pituitary-adrenal axis became evident 15 months after surgery. Thus AIMAH is apparently a primary adrenocortical disorder and is not due to abnormalities of the hypothalamus or pituitary.
Mitsumasa Kubo, Department of Medicine II, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-Ku, Sapporo 060, Japan
Domestic cats show episodic variation in plasma concentrations of adrenocorticotropin, α-melanocyte-stimulating hormone (α-MSH), cortisol and thyroxine with circadian variation in plasma α-MSH concentrations
Authors: Kemppainen Robert J , Peterson Mark E 
Published: December 2008

Kemppainen RJ. Peterson ME. Domestic cats show episodic variation in plasma concentrations of adrenocorticotropin, α-melanocyte-stimulating hormone (α-MSH), cortisol and thyroxine with circadian variation in plasma α-MSH concentrations. Eur J Endocrinol 1996:134:602–9. ISSN 0804–4643
Blood samples were collected from 31 healthy domestic cats to characterize possible episodic and/or circadian variation in plasma concentrations of adrenocorticotropin (ACTH), cortisol, thyroxine and α-melanocyte-stimulating hormone (α-MSH). Samples were collected with minimal disturbance through indwelling jugular cannulae at two frequencies: at 20-min intervals for 3 h for evaluation of episodic variation, and at 2-h intervals for 48 or 72 h to identify possible circadian changes. Episodic peaks in profiles of all hormones were found in the majority of cats. When data were compared across four bleed periods (each of 3 h duration), no differences were detected in average hormone concentrations or characteristics of episodic pulses. Correlation analyses showed a significant (p < 0.001) relationship between concentrations of ACTH and cortisol (r = 0.44) when these hormones were measured in the same plasma sample. A weaker but significant correlation (r = 0.13,p < 0.05) was also detected between concentrations of ACTH and α-MSH, suggesting that proopiomelanocortin peptide secretion from the pars distalis and pars intermedia occurs at least on occasion in synchrony. No differences in hormonal profiles were noted when comparing data across sexes. Data from the studies designed to evaluate circadian change (48 and 72-h bleed periods) indicated that, of the four hormones, only concentrations of α-MSH changed with a significant circadian periodicity. A significant circadian component of period length 24–25 h was detected in 37% (seven of 19) of cats examined. Concentrations of α-MSH were greatest coincident with or shortly after the onset of darkness. These findings indicate that pituitary–adrenocortical hormones are secreted episodically in domestic cats and that, in contrast to the patterns shown by ACTH and cortisol, secretion of the pars intermedia product α-MSH occurs with a circadian rhythm in about one-third of cats.
Robert J Kemppainen, Department of Physiology & Pharmacology, Auburn University College of Veterinary Medicine, Auburn, Alabama 36849, USA
Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro
Authors: Ritchie Paul K , Ashby Marilyn , Knight Heather H , Judd Allan M 
Published: December 2008

Ritchie PK, Ashby M, Knight HH, Judd AM. Dopamine increases interleukin 6 release and inhibits tumor necrosis factor release from rat adrenal zona glomerulosa cells in vitro. Eur J Endocrinol 1996:134:610–6. ISSN 0804–4643
Interleukin 6 (IL-6) and tumor necrosis factor (TNF) are released from the zona glomerulosa of rat adrenal glands. The release of these cytokines from adrenal cells is regulated by interleukin 1β (IL-1β) and lipopolysaccharide (LPS), which are involved in the immune and inflammatory responses. Adrenocorticotropic hormone (ACTH) and angiotensin II, hormones that regulate the adrenal cortex, likewise regulate release of cytokines from adrenal glands. Dopamine inhibits aldosterone release from the adrenal cortex. Therefore, effects of dopamine on IL-6 and TNF release from rat adrenal zona glomerulosa were investigated. Primary cultures of rat adrenal zona glomerulosa cells were exposed to test agents and IL-6 and TNF release determined by the 7TD1 and WEHI bioassays, respectively. Dopamine increased basal IL-6 release and potentiated IL-6 release stimulated by ACTH, LPS or IL-1β. Dopamine inhibited basal and secretagogue-stimulated (LPS and IL-1β) TNF release. These effects of dopamine were mediated by D2 receptors because N-04 37, a D2 agonist, had effects on TNF and IL-6 release identical to those of dopamine. Therefore, dopamine, through D2 receptors, regulates the release of IL-6 and TNF from adrenal cells. Because TNF and IL-6 regulate adrenal steroid release, these cytokines may serve as autocrine or paracrine mediators of adrenal gland function.
Allan M Judd, Department of Zoology, Brigham Young University, Provo, UT 84602, USA
Stimulation of thyroid cell proliferation by epidermal growth factor is different from cell growth induced by thyrotropin or insulin-like growth factor I
Authors: Bechtner Günther , Schopohl Dorothee , Rafferzeder Michael , Gärtner Roland , Welsch Ulrich 
Published: December 2008

Bechtner G, Schopohl D, Rafferzeder M, Gärtner R, Welsch U, Stimulation of thyroid cell proliferation by epidermal growth factor is different from cell growth induced by thyrotropin or insulin-like growth factor I. Eur J Endocrinol 1996;134:639–48. ISSN 0804–4643
Isolated intact porcine thyroid follicles free of contaminating single cells were embedded in "Matrigel". which is a gel-forming basement membrane preparation containing mainly collagen type IV, laminin, heparan sulfate proteoglycans and entactin. Follicles were treated with different growth factors: thyrotropin (TSH), insulin-like growth factor I (IGF-I), epidermal growth factor (EGF) or transforming growth factor beta. Cell proliferation was quantified by counting cell numbers. Morphological studies were done by photodocumentation and analysis of histology by light and electron microscopy. The thyrocytes had the physiological polarity with follicular cell arrangement, microvilli at the apical membrane, desmosomes and tight junctions. The lumen contained colloid. Iodide organification (10.2 ± 2.1 vs 26.1 ± 5.8 pmol/106 cells; TSH 0.1 mU/ml) and release of thyroid hormones thyroxine, 1754 ± 207 vs 2890 ± 460 pg/106 cells; triiodothyronine. 164 ± 22 vs 412 ± 106 pg/106 cells; TSH, 1 mU/ml) were significantly stimulated by TSH. There was no basal growth rate in serum-free medium but proliferation was slightly stimulated with TSH (1 mU/ml;149 ± 19%) and in the same order of magnitude with IGF-I (10 ng/ml; 159 ± 23%) but without follicle neoformation. In contrast, EGF (1.0–5.0 ng/ml) induced thyrocyte proliferation dose dependently three- to sixfold. With EGF up to 2 ng/ml, buds of new follicles formed surrounding pre-existing follicles. With EGF higher than 3 ng/ml, typical papillary structures developed. Transforming growth factor beta inhibited this dedifferentiated growth. A migration of single cells into the gel was never observed. Thus, three-dimensional culture of isolated thyroid follicles in "Matrigel" provides a tool for investigating the regulation of follicular growth and neoformation close to the in vivo situation.
G Bechtner, Medizinische Klinik, Klinikum Innenstadt, Ludwig-Maximilians-Universität München, Ziemssenstraße 1, 80336 München, Germany
Analysis of vasopressin receptor type II (V2R) gene in three Japanese pedigrees with congenital nephrogenic diabetes insipidus: identification of a family with complete deletion of the V2R gene
Authors: Jinnouchi Hideaki , Araki Eiichi , Miyamura Nobuhiro , Kishikawa Hideki , Yoshimura Ryohei , Isami Satoshi , Yamaguchi Kohei , Iwamatsu Hiroko , Shichiri Motoaki 
Published: December 2008

Jinnouchi H, Araki E, Miyamura N, Kishikawa H, Yoshimura R, Isami S, Yamaguchi K, Iwamatsu H, Shichiri M. Analysis of vasopressin receptor type II (V2R) gene in three Japanese pedigrees with congenital nephrogenic diabetes insipidus: identification of a family with complete deletion of the V2R gene. Eur J Endocrinol 1996;134:689–98. ISSN 0804–4843
To investigate the association of mutations in the arginine vasopressin receptor type II (V2R) gene with congenital nephrogenic diabetes insipidus (CNDI) in the Japanese, we analyzed the V2R gene, located on the X chromosome, in three Japanese pedigrees with CNDI. In one pedigree, a large deletion spanning the entire coding region of the V2R gene was identified. In another pedigree, a G to A transition responsible for a substitution of Met88 (ATG) for Val88 (GTG) was detected. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis revealed that this was a de novo mutation that had occurred in the proband's mother. Because CNDI was observed only in those with this mutation, the pathogenicity of this mutation seemed clear. In the last pedigree, only a silent mutation at Leu309 (CTA→CTG) was found. All the individuals studied in this pedigree by allele-specific oligonucloetide-polymerase chain reaction (ASO-PCR) analysis showed a complete association of this mutation to the clinical symptoms. Because the silent mutation detected was unlikely to be a direct cause of CNDI. mutations in other regions of the V2R gene, such as a promoter region or other regulatory regions, may be responsible for the cause of CNDI in this pedigree. Thus, association of the V2R gene abnormality to clinical symptoms of CNDI was confirmed in three Japanese pedigrees, and a strong contribution of the V2R gene mutation to the development of CNDI was suggested.
E Araki, Department of Metabolic Medicine, Kumamoto University School of Medicine, 1-1-1 Honjo, Kumamoto 860, Japan
Desensitization from long-term intranasal treatment with hexarelin does not interfere with the biological effects of this growth hormone-releasing peptide in short children
Authors: Klinger Beatrice , Silbergeld Aviva , Deghenghi Romano , Frenkel Jenny , Laron Zvi 
Published: December 2008

Klinger B, Silbergeld A, Deghenghi R, Frenkel J, Laron Z. Desensitization from long-term intranasal treatment with hexarelin does not interfere with the biological effects of this growth hormonereleasing peptide in short children. Eur J Endocrinol 1996;134:716–9. ISSN 0804–4643
A clinical, prospective experiment was carried out to determine whether long-term intranasal administration of the growth hormone-releasing peptide hexarelin (His-d-2-methyl-Trp-Ala-Trp-d-Phe-Lys-NH2) affects pituitary growth hormone secretion. Hexarelin (60 μg/kg t.i.d.) was administered to seven prepubertal constitutionally short children (mean age ±sd = 7.6 ± 2.4 years). Serum human growth hormone (hGH) response to an intranasal (20 μg/kg) and intravenous (1 μg/kg) bolus of hexarelin before, during and after 6–10 months of treatment was measured. The mean (±sd) peak rise of hGH to the intranasal bolus before treatment was 70.6 ± mU/I. After 7 days of hexarelin treatment, mean peak values dropped to 34.1 ±15.7 mU/l (p < 0.002) and thereafter remained constant for 6 months of treatment at 37.5 10.3 ±mU/l (p < 0.03). The pretreatment peak to the iv hexarelin bolus was 84.8 52.5 ±mU/l, and at the end of the treatment period it was 19.8 10.9 ±mU/l (p < 0.05). Three months after stopping treatment the mean (±sd) hGH response rose to 42.1 ±4.7 mU/l (p < 0.005). Growth velocity increased from 5.3±0.9 cm/year (before treatment) to 7.4 1.6 cm/year at ±6–10 months of treatment (p < 0.005). In conclusion, the partial suppression of pituitary hGH responsiveness to long-term intranasal hexarelin treatment, probably due to desensitization, does not affect the observed increase in growth velocity.
Z Laron, Pediatric Endocrinology, 11 El Al Street, Ramat Efal, 52960, Israel
Hormonal regulation of human protein metabolism
Authors: De Feo Pierpaolo 
Published: December 2008

De Feo P. Hormonal regulation of human protein metabolism. Eur J Endocrinol 1996:135:7–18. ISSN 0804–4643
This review focuses on the effects of hormones on protein kinetics in humans. Most of the recent knowledge on the regulation of protein metabolism in humans has been obtained by tracing protein kinetics in vivo, using labelled isotopes of essential or non-essential amino acids. This technique allows the rates of the whole-body protein synthesis and breakdown to be estimated together with amino acid oxidation and the fractional synthetic rates of mixed muscle proteins or of single plasma proteins. Changes induced within these parameters by hormonal administration or endocrine diseases are also discussed. Hormones, on the basis of their net effect on protein balance (protein synthesis minus protein breakdown), are divided into two categories: those provided with an anabolic action and those with a prevalent catabolic action. The effects on protein metabolism of the following hormones are reviewed: insulin, growth hormone, IGF-I, adrenaline, androgens, estrogens, progesterone, glucagon, glucocorticosteroids, thyroid hormones. The review concludes with a report on the effects of multiple hormonal infusions on whole-body protein kinetics and a discussion on the potential role played by the concomitant increase of several hormones in the pathogenesis of protein wasting that complicates stress diseases.
Pierpaolo De Feo, DIMISEM, Via E. Dal Pozzo, 06126 Perugia, Italy
Activated and interferon-γ producing thyroid-derived T cells are detected in Graves' disease, thyroid autonomy as well as in non-toxic multinodular goiter
Authors: Aust Gabriela , Lehmann Irina , Laue Sandy , Scherbaum Werner A 
Published: December 2008

Aust G, Lehmann I, Laue S, Scherbaum WA. Activated and interferon-γ producing thyroid-derived T cells are detected in Graves' disease, thyroid autonomy as well as in non-toxic multinodular goiter. Eur J Endocrinol 1996;135:60–8. ISSN 0804–4643
The relative numbers of activated and interferon gamma (IFN-γ)-producing peripheral blood lymphocytes (PBL) and thyroid-derived lymphocytes (TL) were determined using double surface and intracellular labeling techniques in flow cytometry. Cells were analyzed from 10 patients with Graves' disease (GD), eight patients with thyroid autonomy (TA) and five patients with non-toxic multinodular goiter (NTG). A maximum of 1% IFN-γ+ cells were detected both in unstimulated PBL and TL. Stimulation caused a two- to threefold higher number of IFN-γ+ cells in TL (GD, 48 ± 12%; TA, 48 ± 11%; NTG, 50± 15%) as compared to PBL (GD, 15 ± 7%: TA, 16 ± 8%; NTG, 18 ± 10%) of the same patients. Nearly all IFN-γ+ TL in GD were CD3+ T cells, whereas 10–20% of IFN-γ+ TL in TA and NTG were NK cells. In PBL 80% and in TL almost 100% of IFN-γ+ cells were antigenprimed CD45RO+ cells. Only 25–35% of IFN-γ+ thyroid-derived T cells expressed the CD4 antigen. About 42 ± 10% thyroid-derived T cells in GD, 33 ± 11% in TA and 34 ± 13% in NTG expressed the HLA-DR molecule but not the interleukin 2 (CD25) or the transferrin receptor (CD71). Forty per cent of these HLA-DR+ T cells showed an intracellular staining for IFN-γ and half of them co-expressed the activation antigen CD69. Immunofluorescence double labeling on thyroid cryostat sections demonstrated that HLA-DR+ T cells were also present in situ. The presence of activation antigens on thyroid-derived T cells not only in patients with GD but also in TA and NTG suggests failsafe mechanisms such as anergy, suppression or cytokine regulation in so-called non-immunogenic goiter.
Gabriela Aust, Department of Internal Medicine III, Endocrinology, University of Leipzig, Ph.-Rosenthal-Str. 27, Leipzig, D-04103, Germany
Relationships between plasma thyrotropin receptor antibodies and lipid or lipoprotein parameters in Graves' disease
Authors: Rieu Max , Revue Eric , Bonete Rémi , Nunez Sébastien 
Published: December 2008

Rieu M, Revue E, Bonete R, Nunez S. Relationships between plasma thyrotropin receptor antibodies and lipid or lipoprotein parameters in Graves' disease. Eur J Endocrinol 1996:135:77–81. ISSN 0804–4643
Functional thyrotropin receptors (TSH-R) have recently been detected in fat cells but not in liver cells from rat, and it seems that in infant adipocytes stimulatory TSH-R antibodies (TSH-R-ab) act through this receptor pathway, resulting in increased triglyceride catabolism. We investigated the relationships between plasma TSH-R-ab and free thyroxine (FT4) levels and plasma lipid or lipoprotein values in 49 untreated adult women with Graves' disease, all positive for these antibodies. A simple positive correlation (p < 0.01) was found between TSH-R-ab levels and FT4 values (r = 0.40). Simple positive correlations (p < 0.001) were found between triglyceride levels and FT4 (r = 0.51) or TSH-R-ab (r = 0.52) values. Multiple regression analysis confirmed that both FT4 and TSH-R-ab are strong (p < 0.005) predictors of triglyceride (FT4: partial r = 0.40; TSH: partial r = 0.39). Simple negative correlations (p < 0.05, at least) were found between FT4 levels and total cholesterol (TC) (r = −0.45), low-density lipoprotein (LDL)-C (r = -0.46), apoprotein (apo)-B (r = −0.31) or high-density lipoprotein (HDL)-C (r = −0.55) values. Among these lipid parameters, only HDL-C levels (r = −0.31, p < 0.05) correlated to TSH-R-ab values. However, multiple regression analysis revealed that while FT4 is a strong predictor (p < 0.005) of TC (partial r = −0.42), LDL-C (partial r = −0.43) or HDL-C (partial r = 0.47), TSH-R-ab are not. Thus, the apparent positive relationship between TSH-R-ab and HDL-C results from the positive correlation between TSH-R-ab and FT4. In conclusion, this study suggests that stimulating TSH-R-ab are involved in triglyceride metabolism. In contrast to thyroid hormones, these antibodies seem not to be related to cholesterol metabolism.
Max Rieu, Hôpital Saint Michel, 33 rue Olivier de Serres, 75015 Paris, France
Evaluation of growth hormone (GH) responses to pulsed GH-releasing hormone administration using the MTT–ESTA bioassay
Authors: Dattani Mehul T , Winrow Andrew P , Tuil'Pakov Anatoly , Pringle P Jane , Hindmarsh Peter C , Brook Charles GD , Marshall Nicholas J 
Published: December 2008

Dattani MT, Winrow AP, Tuil'Pakov A, Pringle PJ, Hindmarsh PC, Brook CGD, Marshall NJ. Evaluation of growth hormone (GH) responses to pulsed GH-releasing hormone administration using the MTT–ESTA bioassay. Eur J Endocrinol 1996;135:87–95. ISSN 0804–4643
We compared the immunoactivity of human growth hormone (hGH) with its bioactivity after stimulation of hGH release into the circulation by the administration of growth hormone-releasing hormone [GHRH(1–29)-NH2] according to a pre-determined protocol to four normal adult volunteers. We used the Hybritech immunoradiometric assay to measure the immunoactive GH concentrations. Bioactive GH concentrations were measured using the highly quantitative and precise eluted stain bioassay system (ESTA). The high sample capacity of the ESTA bioassay permitted us to monitor the bioactivities in closely timed sequential samples, and in far greater detail than has previously been possible. Two pulses of GHRH(1–29)-NH2 were administered intravenously to the four adult male volunteers (aged 24–37 years) on a weekly basis over a 4-week period. Two different doses of GHRH(1–29)-NH2 (0.1 and 1.0 μg/kg) were tested. These were separated by specified time intervals (60 or 120 min). Responses in the four individuals were variable. However, although the immunoand bioactivities generally agreed well, there was a systematic and progressive increase in the bioactivity/immunoactivity (B/I) ratios as half of the response peaks were approached. After these peak concentrations, the B/I ratios subsequently returned to values that were close to unity. The enhanced bioactivity of the peak samples from the two volunteers in whom the largest magnitudes of response were observed was found to be labile after long-term storage at −20°C. We suggest that the preferential rise in GH bioactivity, as opposed to immunoactivity, in response to GHRH(1–29)-NH2 was due to progressive changes in the concentrations of isoforms of GH that are not detectable in the Hybritech immunoassay.
NJ Marshall, Division of Molecular Pathology, University College London, The Windeyer Building, 46 Cleveland Street, London W1P 6DB, UK