bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions
Authors: Ohno Yasumasa , Kasugai Masahide , Kurauchi Osamu , Mizutani Shigehiko , Tomoda Yutaka 
Published: December 2008

Ohno Y, Kasugai M, Kurauchi O, Mizutani S, Tomoda Y. Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions. Eur J Endocrinol 1994;130:478–84. ISSN 0804–4643
Our objective was to clarify the mechanism of uterine contraction induced in pregnant women by intrauterine bacterial infection. The concentration of interleukin 2 (IL-2) was measured in amniotic fluids that had been obtained by amniocentesis, transvaginal amniotomy or by transuterine amniocentesis performed at cesarean section in 50 pregnant women. The concentration of IL-2 in those cases with intrauterine infection was significantly higher than that of those without intrauterine infection at preterm. The same tendency was found at term. Scatchard analysis demonstrated the presence of an IL-2 receptor in the fetal membranes. We collected the fetal membranes aseptically for the measurement of progesterone and prostaglandin E2 by radioimmunoassay following incubation with various concentrations of Interleukin I (IL-1) and IL-2 at 37°C for 16 h. The production of progesterone was inhibited significantly by 10 pmol/l IL-2 but not by 10 pmol/l IL-1. The production of prostaglandin E2 was accelerated significantly by either IL-1 or IL-2 at a dose of 10 pmol/l. The inhibitory effect of IL-2 on the production of progesterone was unaffected by indomethacin, which inhibits the production of arachidonate cycloxygenase metabolites such as prostaglandin E2. Our present data suggest that the presence of intrauterine bacterial infection may stimulate the intrauterine production of IL-2, and that the stimulation of IL-2 and the reduction of progesterone caused by IL-2 may in part explain the mechanism of uterine contraction associated with intrauterine infection during pregnancy.
Yasumasa Ohno, Department of Obstetrics and Gynecology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan
Does early administration of thyroxine reduce the development of Graves' ophthalmopathy after radioiodine treatment?
Authors: Tallstedt Leif , Lundell Göran , Blomgren Henric , Bring Johan 
Published: December 2008

Tallstedt L, Lundell G, Blomgren H, Bring J. Does early administration of thyroxine reduce the development of Graves' ophthalmopathy after radioiodine treatment? Eur J Endocrinol 1994:130: 494–7. ISSN 0804–4643
The roles of thyroid hormones and thryotropin (TSH) in the development of Graves' ophthalmopathy are not clear. Some studies suggest a protective effect of thyroid hormones on experimental exophthalmos and an adverse effect of increased TSH levels. In September 1988 we introduced early thyroxine (T4) administration after 131I therapy for hyperthyroidism caused by Graves' disease. We carried out a retrospective study of records from all patients with this disease treated with 131I for 4 years. During the first 2 years 248 patients were treated (group A). They received T4 when the serum concentration of TSH and/or T4 indicated hypothyroidism. During the next 2 years 244 patients were treated (group B). They were all given 0.05 mg of T4 daily, starting 2 weeks after therapy, and 0.1 mg after a further 2 weeks. With a follow-up of 18 months, 45 patients (18%) in group A and 27 patients (11%) in group B developed or deteriorated in an already present ophthalmopathy (p = 0.03, relative risk = 1.64, 95% confidence interval = 1.05–2.55). Twenty-six patients in group A required specific therapy for the ophthalmopathy (e.g. antithyroid drugs, steroids, etc.) compared to 11 patients in group B (p = 0.02, relative risk = 2.33; 95% confidence interval = 1.18–4.60). Our results suggest that early administration of T4 after 131I therapy reduces the occurrence of Graves' ophthalmopathy.
L Tallstedt, Department of Ophthalmology, Huddinge University Hospital, S-146 81 Huddinge, Sweden
Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas
Authors: Le Dafniet Michèle , Brandi Anne-Marie , Kujas Michèle , Chanson Philippe , Peillon Françoise 
Published: December 2008

Le Dafniet M, Brandi A-M, Kujas M, Chanson P, Peillon F. Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas. Eur J Endocrinol 1994:130:559–64. ISSN 0804–4643
In order to see whether, in thyrotropic adenomas with thyrotoxicosis, plasma thyroid hormones regulate the thyrotropin-releasing hormone (TRH) binding sites and the thyrotropin (TSH) response to TRH, we investigated: the presence of TRH binding sites in two cases of thyrotropic adenomas associated with hyperthyroidism and in one case of thyrotropic adenoma secondary to thyroid failure; and the in vitro effect, in a perifusion system, of triiodothyronine (T3) on the response of TSH to TRH in three cases of TSH-secreting adenomas associated with hyperthyroidism. The TRH binding sites were absent in the adenomas associated with high levels of circulating thyroid hormones, whereas they were present in the adenoma secondary to primary thyroid failure (K4 =47 nmol/l, Bmax = 40 nmol/ kg membrane proteins). In vitro, the three adenomas spontaneously released TSH in the perifusion medium (1.49 ±0.06 (mean ± sem), 7.25±0.12 and 16.73±0.36 mIU·−1·106 cells−1·2 min−1) and exhibited an ample TSH response to 10−7 mol/l TRH pulses. In two cases, tumoral secretion of fragments was compared with those of fragments maintained since the time of surgical removal in the presence of 10−8 mol/l T3. The TSH responses to TRH were abolished in the presence of T3 in these two cases. We conclude that thyrotropic adenomas associated with hyperthyroidism are still controlled in vivo by T3. In particular, T3 regulates the TSH response to TRH, probably via a down-regulation of the TRH binding sites.
Michèle Le Dafniet, Unité INSERM 223, Faculté de Médecine, Pitié-Salpêtrière, 105 Boulevard de l'Hôpital, 75013 Paris, France
Single amino acid substitution (840Arg → His) in the hormone-binding domain of the androgen receptor leads to incomplete androgen insensitivity syndrome associated with a thermolabile androgen receptor
Authors: Imasaki Kyosuke , Hasegawa Tomonobu , Okabe Taijiro , Sakai Yoshiyuki , Haji Masafumi , Takayanagi Ryoichi , Nawata Hajime 
Published: December 2008

Imasaki K, Hasegawa T. Okabe T. Sakai Y. Haji M. Takayanagi R, Nawata H. Single amino acid substitution (840Arg → His) in the hormone-binding domain of the androgen receptor leads to incomplete androgen insensitivity syndrome associated with a thermolabile androgen receptor. Eur I Endocrinol 1994;130:569–74. ISSN 0804–4643
We have characterized the androgen receptor in a Japanese girl and her maternal cousin in a family with incomplete androgen insensitivity syndrome, and have investigated the molecular basis. Wholecell androgen binding assay in cultured genital skin fibroblasts from both patients showed a normal maximum binding capacity and a normal apparent dissociation constant. However, androgen binding in fibroblasts from both patients decreased to 30% when the assay temperature was raised from 30°C to 41°C, indicating the presence of the thermolability of ligand binding to the androgen receptor. Sequence analysis of the coding exons of the androgen receptor gene from the patients revealed a single nucleotide substitution at position 2881 in exon G, resulting in the conversion of arginine (CGT) to histidine (CAT) at amino acid position 840 in the hormone-binding domain of the androgen receptor. The family study showed that the mothers and the maternal grandmother of the patients are heterozygous carriers for this mutation, whereas the father does not carry it, supporting the view that androgen insensitivity syndrome is an X chromosome-linked disorder. The single amino acid substitution may explain the qualitative abnormality of the androgen receptor displaying thermolability, which is thought to be the pathogenesis of incomplete androgen insensitivity syndrome in the patients.
Kyosuke Imasaki, Third Department of Internal Medicine, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812, Japan
Detection of autoantibodies to the 65-kD isoform of glutamate decarboxylase by radioimmunoassay
Authors: Lühder Fred , Woltanski Klaus-Peter , Mauch Ludwig , Haubruck Heinz , Kohnert Klaus-Dieter , Rjasanowski Ilona , Michaelis Dietrich , Ziegler Manfred 
Published: December 2008

Lühder F, Woltanski K-P, Mauch L, Haubruck H, Kohnert K-D, Rjasanowski I, Michaelis D, Ziegler M. Detection of autoantibodies to the 65-kD isoform of glutamate decarboxylase by radioimmunoassay. Eur J Endocrinol 1994:130:575–80. ISSN 0804–4643
Autoantibodies (AAb) to glutamate decarboxylase (GAD) occur with a high prevalence in sera of newly diagnosed type I (insulin-dependent) diabetic patients. The aim of this study was to establish a GAD-AAb radioimmunoassay using 125I-labelled GAD65 and to evaluate this assay in a cross-sectional study with newly diagnosed type I diabetic patients (diabetes duration < 6 weeks). Furthermore, subjects at high risk of developing type I diabetes and individuals suffering from other autoimmune diseases were examined in this assay. For GAD-AAb detection, 125I-labelled GAD65 was incubated with 10 μl of human serum overnight on ice. Thirty of 51 (59%) type I diabetic patients but none of the 54 healthy blood donors tested were found to be positive. A displacement step using 100 000 g supernatant from rat brain containing or not containing GAD showed the specificity of the binding of 125I-GAD65. Concerning the individuals at high risk of developing diabetes, 9/12 (75%) islet cell antibody (ICA)-positive non-diabetic and 4/34 (12%) ICA-negative subjects with metabolic abnormalities were GAD-AAb positive. These results show the association between type I (insulin-dependent) diabetes mellitus and the occurrence of GAD65-AAb, which possibly predicts a risk of developing the disease.
F Lühder, Department of Immunochemistry, Institute of Diabetes "Gerhardt Katsch", Greifswalder Str. I la, D-17495 Karlsburg, Germany
Effect of octreotide on glucose tolerance in acromegaly
Authors: Koop Brenda L , Harris Alan G , Ezzat Shereen 
Published: December 2008

Koop BL, Harris AG. Ezzat S. Effect of octreotide on glucose tolerance in acromegaly. Eur J Endocrinol 1994;130:581–6. ISSN 0804–4643
To determine the effect of the somatostatin analog octreotide on glucose tolerance in acromegaly, we examined glucose profiles, oral glucose tolerance and the insulinogenic index in patients treated with this analog. Ninety patients participated in a long-term, prospective, open-label study. There was no significant change between mean daily blood glucose profiles at baseline or during octreotide treatment. Using glucose tolerance test criteria, 61% of 90 patients had normal baseline glucose tolerance. While on octreotide, 20% and 29% of these patients, respectively, developed impaired glucose tolerance or became frankly diabetic. Conversely, three of the patients who were diabetic at baseline (N = 11) became normal (18%) or developed impaired glucose tolerance (9%) during octreotide therapy. There was no relationship between the dose of octreotide and change in glycemic state. The insulinogenic index (insulin/glucose) response to a glucose challenge decreased uniformly in octreotide-treated patients. Female patients and those with elevated baseline insulin levels were more likely to develop diabetes mellitus during octreotide therapy. In conclusion, octreotide significantly alters glucose tolerance in patients with acromegaly, mandating glucose monitoring during this form of therapy.
Alan G Harris, Division of Clinical Pharmacology, Department of Medicine, Cedars-Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, CA 90048, USA
The degree of inhibition of thyroid follicular cell proliferation by iodide is a highly individual characteristic of each cell and differs profoundly in vitro and in vivo
Authors: Aeschimann Simon , Gerber Hans , von Grünigen Christine , Oestreicher Madeleine , Studer Hugo 
Published: December 2008

Aeschimann S, Gerber H, von Grünigen C, Oestreicher M, Studer H. The degree of inhibition of thyroid follicular cell proliferation by iodide is a highly individual characteristic of each cell and differs profoundly in vitro and in vivo. Eur J Endocrinol 1944;130:595–600. ISSN 0804–4643
Pharmacological concentrations of iodide (>1 × 10−6 mol/l) are known to inhibit thyroid follicular cell growth in vitro. However, the inhibitory effect varies widely, depending on experimental conditions, and usually does not exceed 50%. We demonstrate that iodide (10−4 mol/l) inhibits the growth of FRTL-5 cells in different passages by 11–67%. When five subclones of FRTL-5 cells were compared to the wild type, iodide-induced growth inhibition varied between 25% and 46%. The individual degree of inhibition of each clone was reproducible in two subsequent passages, suggesting that it is a stable constitutive trait. When FRTL-5 cells were grown first in three-dimensional clusters and then transplanted onto nude mice with high endogenous thyrotropin secretion, iodide at a serum concentration of less than 5.7 × 10−7 mol/l nearly completely blocked cell replication in the transplants but not in the mice's own thyroid. Five cell lines, prepared from autonomously growing hyperthyroid feline multinodular goiters, were nearly completely resistant to the growth-inhibitory effect of iodide. These observations suggest that the sensitivity towards the growth-inhibiting effect of iodide is a highly variable, stable trait of each thyrocyte, even in cloned cell populations. Some FRTL-5 cells and, even more so, cells prepared from autonomously growing nodular feline goiters are resistant constitutively to the growth-inhibiting effect of iodide. Three-dimensional clusters of FRTL-5 cells growing as transplants in recipient mice are growth-arrested totally by iodide concentrations more than 175 times lower than those partially inhibiting monolayer cultures, while growth of the intact thyroid of the recipient mouse remains unaffected or is even enhanced. Thus, the sensitivity of thyrocytes toward iodide is different fundamentally in vitro and in vivo.
Hugo Studer, Medizinische Universitaetsklinik, Inselspital, CH-3010 Bern, Switzerland
Growth hormone (GH) treatment increases serum insulin-like growth factor binding protein-3, bone isoenzyme alkaline phosphatase and forearm bone mineral content in young adults with GH deficiency of childhood onset
Authors: Juul Anders , Pedersen Søren A , Sørensen Steen , Winkler Kjeld , Jørgensen Jens OL , Christiansen Jens S , Skakkebæk Niels E 
Published: December 2008

Juul A, Pedersen SA, Sørensen S, Winkler K, Jørgensen JOL, Christiansen JS, Skakkebæk NE. Growth hormone (GH) treatment increases serum insulin-like growth factor binding protein- bone isoenzyme alkaline phosphatase and forearm bone mineral content in young adults with GH deficiency of childhood onset. Eur J Endocrinol 1994;131:41–9. ISSN 0804–4643
Recent studies have demonstrated that growth hormone (GH)-deficient adults have a markedly decreased bone mineral content compared to healthy adults. However, there are conflicting results regarding the effects of GH treatment on bone mineral content in GH-deficient adults. Therefore, we evaluated the effect of GH treatment on a marker of bone formation (bone alkaline phosphatase), hepatic excretory function and distal forearm bone mineral content in GH-deficient adults. Growth hormone was administered subcutaneously in 21 adults (13 males and 8 females) with GH deficiency of childhood onset for 4 months in a double-blind, placebo-controlled GH trial, while 13 of the patients then received further GH for an additional 14 months. Serum insulin-like growth factor I (IGF-I) increased significantly from 100 to 279 μg/l and IGF binding protein-3 (IGFBP-3) from 1930 to 3355 μg/l after 4 months of GH treatment (p < 0.0001). In addition, the molar ratio between IGF-I and IGFBP-3 increased significantly from 0.22 to 0.33 after GH treatment (p < 0.0001), Bone alkaline phosphatase increased significantly from 38.6 to 92.9 U/l during GH therapy in male patients (p < 0.0001), whereas liver-derived alkaline phosphatase was unaltered by GH. In the females, the increase in bone alkaline phosphatase did not reach statistical significance (19.1 vs 40.0 U/l, p = 0.06). The GH-induced increase in bone alkaline phosphatase correlated significantly with the increase in serum IGFBP-3 (r = 0.46, p = 0.04) but not with the increase in serum IGF-I (p = 0.16). Liver function as assessed by the galactose elimination capacity was within the normal range for healthy adults and did not change after GH treatment. Bone mineral content increased significantly between 7 and 14 months of GH treatment (mean increase in bone mineral content Z score = 0.24 sd/ 7 months), but remained low even after 14 months of GH treatment (Z score = –2.2 ± 0.24 (mean ± sem)). We conclude that GH administration increases serum levels of bone-derived alkaline phosphatase in male patients and has a potentially beneficial impact on bone mineral content in young adults with GH deficiency of childhood onset.
Anders Juul, Department of Growth and Reproduction, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark
ACTH-independent massive bilateral adrenal disease (AIMBAD): A subtype of Cushing's syndrome with major diagnostic and therapeutic implications
Authors: Lieberman Steven A , Eccleshall T Ross , Feldman David 
Published: December 2008

Lieberman SA, Eccleshall TR, Feldman D. ACTH-independent massive bilateral adrenal disease (AIMBAD): a subtype of Cushing's syndrome with major diagnostic and therapeutic implications. Eur J Endocrinol 1994:131:67–73. ISSN 0804–4643
A 49-year-old man with classic manifestations of Cushing's syndrome had undetectable levels of ACTH, lack of suppression of hypercortisolism with dexamethasone in doses of 2, 8, or 16 mg per day, bilaterally enlarged adrenal glands on MRI, and bilateral adrenal uptake of iodocholesterol. Preoperative treatment with ketoconazole lowered blood pressure and serum cortisol and produced symptoms of steroid withdrawal. Bilateral adrenalectomy revealed massively enlarged adrenal glands (left: 199 g, right: 93 g). Sequencing of the gene encoding the stimulatory G protein, Gsα, did not show either of two activating mutations previously reported in patients with McCune–Albright syndrome or acromegaly. Twenty-three previous cases of Cushing's syndrome due to ACTH-independent massive bilateral adrenal disease (AIMBAD) have been reported. AIMBAD may cause confusion in the differential diagnosis of Cushing's syndrome as endocrine testing suggests a unilateral, ACTHindependent process while adrenal imaging demonstrates bilateral abnormalities. Bilateral adrenalectomy is curative and appears to carry little risk of Nelson's syndrome. The pathogenesis of AIMBAD appears to be heterogeneous, as recent reports have demonstrated GIP-mediated hypercortisolism and familial AIMBAD. Transition from Cushing's disease to ACTH-independence is not supported by the available data. Future cases of AIMBAD should be investigated carefully to further elucidate the pathogenesis of this disorder.
David Feldman, Division of Endocrinology, Dept. of Medicine, Room S-005, Stanford University Medical Center, Stanford, CA 94305, USA
Primary hypothyroidism manifested in childhood with special reference to various types of reversible hypothyroidism
Authors: Okamura Ken , Sato Kaori , Ikenoue Hiroshi , Nakagawa Mizuho , Kuroda Takeo , Yoshinari Mototaka , Fujishima Masatoshi 
Published: December 2008

Okamura K, Sato K, Ikenoue H, Nakagawa M, Kuroda T, Yoshinari M, Fujishima M. Primary hypothyroidism manifested in childhood with special reference to various types of reversible hypothyroidism. Eur J Endocrinol 1994;131:131–7. ISSN 0804–4643
The clinical courses of 15 patients with overt primary hypothyroidism manifested in childhood were studied. Nine female patients with goitrous hypothyroidism due to chronic thyroiditis showed almost normal height and became euthyroid spontaneously during iodine restriction. The other 6 non-goitrous patients (3M and 3F) (atrophic thyroiditis in 2, lingual goiter in 2 and probable hypoplastic thyroid in 2) showed physical growth retardation and remained irreversibly hypothyroid requiring replacement therapy. In the reversible group, the characteristic findings were high thyroidal radio-active iodine uptake (58 ± 19%/24 h, N = 8) and positive perchlorate discharge test. Serum non-hormonal iodine levels were high in 4 of 6 patients measured. During the long-term follow-up period of 6 years in 6 patients, 2 patients remained euthyroid with normal growth and regular menstrual cycle and 4 patients became hypothyroid again (after eating seaweed in 1, despite iodine restriction in 2 and after the episode of painless thyroiditis in 1). Transient retardation of growth was observed during the second episode of hypothyroidism. In the irreversible group, one patient with blocking type TSH binding inhibitor immunoglobulin (TBII) became thyrotoxic 4 years later with the decrease in activity of blocking type TBII. These results suggested that reversible recovery of the thyroid function could be expected in patients with juvenile hypothyroidism due to chronic thyroiditis after (1) iodine restriction, (2) improvement of immunological perturbation, or (3) disappearance of blocking type TBII. However, careful follow-up is necessary, because hypothyroidism would recur again with transient retardation of growth in children.
Ken Okamura, Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Higashiku, Fukuoka 812, Japan
No evidence for reduced spontaneous or growth-hormone-stimulated serum levels of insulin-like growth factor (IGF)-I, IGF-II or IGF binding protein 3 in women with spinal osteoporosis
Authors: Kassem M , Brixen K , Blum W , Mosekilde L , Eriksen EF 
Published: December 2008

Kassem M, Brixen K, Blum W, Mosekilde L, Eriksen EF. No evidence for reduced spontaneous or growth-hormone-stimulated serum levels of insulin-like growth factor (IGF)-I, IGF-II or IGF binding protein 3 in women with spinal osteoporosis. Eur J Endocrinol 1994;131:150–5. ISSN 0804–4643
To test the hypothesis that a dysfunctional growth hormone (GH)–insulin-like growth factor (IGF) axis may play a role in the pathogenesis of osteoporosis, we compared the levels of IGF-I, IGF-II and IGF binding protein 3 (IGFBP-3) in 15 women with spinal osteoporosis (i.e. at least one non-traumatic vertebral fracture) and 15 normal age-matched women. Furthermore, the response to 3 days' treatment with recombinant human GH (r-hGH) (0.2 IU kg−1·day−1) was determined. The basal levels of IGF-I, IGF-II and IGFBP-3 were similar in patients and controls (mean ± sem): IGF-I, 16.5 ± 1.3 versus 16.0 ± 1.3 nmol/l (NS); IGF-II, 79.9 ± 3.6 versus 72.5 ± 4.1 nmol/l (NS); and IGFBP-3, 125.7 ± 6.5 versus 130.3 ± 7.8 nmol/l (NS). Stimulation with r-hGH elicited increased levels of IGF-I, IGF-II and IGFBP-3 within both groups (p < 0.001). The maximal values expressed as a percentage of baseline were: IGF-I, 341 ± 26% versus 369 ± 22%, IGF-II, 125 ± 4% versus 119 ± 5%, IGFBP-3, 141 ± 5% versus 147 ± 7% in osteoporotic patients and controls, respectively. No significant differences were observed between patients and controls in either their maximal response or in the area under the response curves. Our results do not support the hypothesis of a dysfunctional GH–IGF axis in women with spinal osteoporosis.
Kim Brixen, University Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Tage-Hansens gade 2, DK-8000 Aarhus C, Denmark