bluuebunny/crossref_metadata_2025_split huggingface dataset:
Retrospective evaluation of subtotal and total thyroidectomy in Graves' disease with and without endocrine ophthalmopathy
Authors: Winsa Brita , Rastad Jonas , Åkerström Göran , Johansson Henry , Westermark Kerstin , Karlsson F Anders 
Published: December 2008

Winsa B, Rastad J, Åkerström G, Johansson H, Westermark K, Karlsson FA. Retrospective evaluation of subtotal and total thyroidectomy in Graves' disease with and without endocrine ophthalmopathy. Eur J Endocrinol 1995;132:406–12. ISSN 0804–4643
A retrospective analysis was performed in 173 consecutive patients with Graves' disease (GD) with the principal aim of evaluating the influences of subtotal (N = 157) and total (N = 19) thyroidectomy on postoperative recurrence rates, endocrine ophthalmopathy (EO) and thyrotropin receptor antibody (TSH-R-ab) titres. Postoperatively recurrent disease, identified by increased thyroid hormone levels, occurred in 32 patients (20%) who underwent subtotal resection. These recurrences were associated with over-representation of preoperative EO (p < 0.001) as well as high TSH-R-ab levels post-operatively (p < 0.05–0.01). Subtotal and total resections were followed by an aggravation of preoperative EO in nine (16%) and one (6%), and by a development of EO in two and none of the patients, respectively. Persistently elevated TSH-R-ab titers during thyrostatic therapy became close to normalized in seven (32%) and 15 (88%) of the patients undergoing subtotal or total thyroidectomies, respectively, which illustrates a thyroid tissue dependency of the autoantibody production. Among the total material of 173 patients, altogether 75 cases exhibited persistent or progressive EO and/or TSH-R-ab elevation after more than 1 year of preoperative thyrostatic treatment. In this group, recurrent GD or aggravated EO occurred in 23 (39%) of those operated with subtotal resection and in one (6%) of those undergoing total thyroidectomy (p < 0.05). The results thus indicate that EO, particularly at the time of surgery, and prevailing TSH-R-ab titers are associated with an increased risk of recurrent GD and suggest that patients exhibiting these characteristics should benefit from total rather than subtotal thyroidectomy.
Brita Winsa, Department of Internal Medicine, University Hospital, S-751 85 Uppsala, Sweden
Kinetic analysis of thyroid hormone action on glucose metabolism in man
Authors: Müller MJ , Reynard CA , Burger AG , Toffolo G , Cobelli C , Ferrannini E 
Published: December 2008

Müller MJ, Reynard CA, Burger AG, Toffolo G, Cobelli C, Ferrannini E. Kinetic analysis of thyroid hormone action on glucose metabolism in man. Eur J Endocrinol 1995;132:413–18. ISSN 0804–4643
Thyroid hormone action on insulin's effect on glucose kinetics was investigated with the use of a physiological three compartment model. In six healthy volunteers before and after 14 days of thyroxine treatment (300 μg/day), a bolus of [3-H3]glucose was injected and the time course of plasma radioactivity was followed closely for 150 min. Then a hyperinsulinemic (1 mU · min−1 · kg−1) and euglycemic clamp was started, and euglycemia was maintained for another 250 min. A second bolus of the tracer was then given at 240 min, and the plasma radioactivity was followed for 160 min. Insulin stimulated basal plasma glucose clearance fourfold (p < 0.001) and completely suppressed basal hepatic glucose production (p < 0.001). Concomitantly, the total distribution volume of glucose was increased by 19% (p < 0.05); this change was accompanied by about 50% expansion of the slowly exchanging glucose pool (putatively representing the insulin-dependent compartment). Thyroxine treatment increased plasma triiodothyronine by about 20% (0.1 > p > 0.05) but did not affect basal glucose turnover, insulin-stimulated plasma glucose clearance or the insulin-induced suppression of endogenous glucose output. However, thyroxine treatment blunted the insulin-induced increases in total distribution volume and the slowly exchanging pool of glucose (p = NS vs the basal state). We conclude that minor changes in plasma triiodothyronine (such as occur during overfeeding) do not interfere with the ability of insulin to stimulate the rate of disappearance of glucose or suppress endogenous glucose release; however, our data suggest that they induce finer changes in glucose kinetics, possibly reflecting acceleration or intracellular glucose degradation.
Manfred J Müller, Institut für Humanernährung und Lebensmittelkunde, Christian-Albrechts-Universität zu Kiel, Düsternbrooker Weg 17, D-24105 Kiel, Germany
Identification and quantification of human kidney atrial natriuretic peptide receptors
Authors: Kahana Luna , Yechiely Haya , Mecz Yoel , Lurie Aharon 
Published: December 2008

Kahana L, Yechiely H, Mecz Y, Lurie A. Identification and quantification of human atrial natriuretic peptide receptors. Eur J Endocrinol 1995;132:465–71. ISSB 0804–4643
The present study determined 125I-label atrial natriuretic peptide (ANP) binding sites in human kidney glomerular and papillary membranes. The membranes were prepared from non-malignant renal tissue obtained at nephrectomy of patients with renal carcinoma. To evaluate the proportion of ANP receptor classes ANP-R1 (ANPR-A, -B) versus ANP-R2 (ANPR-C), competitive binding studies were performed using [125I]-ANP in the presence of increasing concentrations of ANP or an internally ring-deleted analog, des(Gln116, Ser117, Gly118, Leu119, Gly120)ANP(102–121), called C-ANP, which binds selectively to ANPR-C receptors. Analysis of the competitive binding curve with ANP in glomerular membranes suggested the presence of one group of high-affinity receptors with dissociation constant Kd = 26 ± 12 pmol/l and density Bmax = 101 ± 47 nmol/kg protein. A decrease of 10–30% in Bmax with no change in Kd was obtained in the presence of excess (10−6 mol/l) C-ANP, suggesting the existence of a small amount of a second class of receptors, the ANPR-C class. The densities of ANPR-A, -B versus ANPR-C receptors in human glomeruli, calculated from competitive inhibition experiments, were 75 ± 42 and 22 ± 16 nmol/kg protein (N = 8). Autoradiography of the sodium dodecyl sulfate polyacrylamide gel electrophoresis under reducing conditions showed two bands: a highly labeled 130kD band and a weakly labeled 66kD band, both displaced by ANP. Only the 66-kD band was displaced by the C-ANP analog. Human papilla membrane, as shown by competition binding studies and SDS gel electrophoresis, presented only one class of receptors with Kd = 40 ± 23 pmol/l (mean ± SD, N = 3) and Bmax = 17 ± 6.3 nmol/kg protein. No displacement of [125I]ANP with C-ANP analog could be detected. The Kd of the binding sites in human kidney papilla was not statistically different (p > 0.05) from the Kd values of the two receptor subtypes for ANP in glomeruli. Thus, human kidney, much like that of the rat, presents: two classes, the high- (ANPR-A, -B) and low (ANPR-C)-molecular-weight receptors, in glomerular membranes; only one class, the high-molecularweight receptors, in papillary membranes. In contrast to rat kidney, the high-molecular-weight ANPR-A, -B is the dominant class in human glomerular membranes.
Luna Kahana, Endocrine Laboratory, Carmel Medical Center, 7 Michal Street, Haifa 34362, Israel
Biphasic effect of interleukin-1β on arginine vasopressin-induced cellular cyclic adenosine monophosphate production in cultured rat renal papillary collecting tubule cells
Authors: Ishikawa San-e , Saito Toshikazu 
Published: December 2008

Ishikawa S, Saito T. Biphasic effect of interleukin-1β on arginine vasopressin-induced cellular cyclic adenosine monophosphate production in cultured rat renal papillary collecting tubule cells. Eur J Endocrinol 1995;132:472–8. ISSN 0804–4643
The present study was undertaken to determine whether interleukin (IL)-1β affects the response of cellular cyclic adenosine monophosphate production to arginine vasopressin (AVP) in cultured rat renal papillary collecting tubule cells. Arginine vasopressin increased cellular cAMP production in a dose-dependent manner. A 10-min exposure of cells to IL-1β at a concentration of 1 × 10−12 mol/l or higher significantly reduced the AVP-induced increases in cellular cAMP production but did not affect the 2 × 10−8 mol/l forskolin-induced increases in cellular cAMP production. The IL-1β inhibition disappeared totally when cells were pretreated with 100 μg/1 pertussis toxin for 2 h. In contrast, more than a 30-min exposure of cells to IL-1β increased basal cAMP levels and enhanced both the AVP- and forskolin-induced increases in cellular cAMP production. These results indicate that IL-1β produces biphasic regulation of AVP-induced cellular cAMP production in renal papillary collecting tubule cells. The inhibition by IL-1β is dependent on the activation of pertussis toxin-sensitive G protein. However, the mechanism whereby the longer exposure to IL-1β enhances cAMP production remains to be determined.
San-e Ishikawa, Division of Endocrinology and Metabolism, Department of Medicine, Jichi Medical School, 3311-1 Yakushiji Minamikawachi-machi, Tochigi 329-04. Japan
Insulin-like growth factor I messenger ribonucleic acid expression in porcine thyroid follicles is regulated by thyrotropin and iodine
Authors: Hofbauer Lorenz C , Rafferzeder Michael , Janssen Onno E , Gärtner Roland 
Published: December 2008

Hofbauer LC, Rafferzeder M, Janssen OE, Gartner R. Insulin-like growth factor I messenger ribonucleic acid expression in porcine thyroid follicles is regulated by thyrotropin and iodine. Eur J Endocrinol 1995;132:605–10. ISSN 0809–4643
Insulin-like growth factor I (IGF-I) has been shown to be released from thyrocytes in vitro. We investigated IGF-I mRNA expression during treatment with thyrotropin (TSH), forskolin and potassium iodide (KI) in intact porcine thyroid follicles ex vivo. Porcine thyroid follicles were prepared by collagenase digestion and cultured in the presence of TSH, forskolin or KI. After different incubation times, mRNA was isolated and examined by Northern hybridization with a porcine IGF-I cDNA probe of 405 bp in length. In untreated follicles no IGF-I mRNA was found, whereas in follicles stimulated with TSH an IGF-I mRNA of 7.0 kb was detected after 24 h, which persisted for another 24 h. Forskolin treatment mimicked the TSH effect, indicating that IGF-I mRNA expression may be stimulated by the adenylate cyclase pathway. Preincubation of the porcine follicles with KI decreased dose dependently the TSH-induced IGF-I mRNA expression, with complete inhibition at 10 μmol/l KI. These results suggest that TSH acts via the cAMP pathway to enhance IGF-I mRNA expression, which then may lead to an autocrine IGF-I stimulation. The IGF-I mRNA expression is under negative control of iodide.
Roland Gärtner, Medizinische Klinik, Ludwig Maximilians University, Ziemssenstrasse 1, 80336 München, Germany
Decreased serum testosterone and free triiodothyronine levels in healthy middle-aged men indicate an age effect at the pituitary level
Authors: Erfurth Eva Marie T , Hagmar Lars E 
Published: December 2008

Erfurth EMT, Hagmar LE. Decreased serum testosterone and free triidothyronine levels in healthy middle-aged men indicate an age effect at the pituitary level. Eur J Endocrinol 1995;132:663–7. ISSN 0804–4643
In an attempt to study further the age-specific influence on the hypothalamo-pituitary–gonadal axis as well as the hypothalamo–pituitary–thyroid axis, we have now investigated young and middle-aged men, considering possible confounding factors. Both serum total testosterone, free testosterone and the total ratio of testosterone to sex-hormone binding globulin were significantly lower among middle-aged men as compared with young men (p = 0.02, p = 0.002 and p = 0.0003, respectively). In accordance with these findings there was also a decrease in the luteinizing hormone response to gonadotrophin-releasing hormone in the middle-aged men (p= 0.02). Free testosterone was correlated significantly with the luteinizing hormone response (r = 0.32, p = 0.02). Serum free triiodothyronine was significantly higher among young men as compared with middle-aged men (p = 0.002) and the thyrotrophin-releasing hormone-stimulated thyrotrophin response was also higher in the young group compared with the middle-aged group. The present results may indicate that the age effect on serum levels of testosterone and free triidothyronine is mediated at the pituitary level.
Eva Marie Erfurth, Dept. of Internal Medicine, University of Lund, S-221 85 Lund, Sweden
Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment
Authors: Çelik Ismail , Akalin Sema , Erbaş Tomris 
Published: December 2008

Çelik I, Akalin S, Erbaş T. Serum levels of interleukin 6 and tumor necrosis factor-α in hyperthyroid patients before and after propylthiouracil treatment. Eur J Endocrinol 1995;132:668–72. ISSN 0804–4643
Contrary to the usual inhibitory role of tumor necrosis factor-α (TNF-α) thyroid metabolism, it also has specific stimulatory effects in autoimmune thyroid disorders, including induction of HLA class II antigen-presenting cell—T cell interaction. Despite high intrathyroidal concentrations, various studies were not able to demonstrate high serum levels of TNF-α in patients with Graves' disease. To investigate this discrepancy we determined TNF-α and interleukin 6 (IL-6) levels in 25 hyperthyroid patients who responded to propylthiouracil treatment (16 with Graves' disease and nine with toxic multinodular goiter) and compared them with the levels found in euthyroid patients with simple diffuse goiter (n = 15) and normal healthy controls (n = 15). Median IL-6 levels were high in both Graves' disease and toxic multinodular goiter patients before propylthiouracil treatment (23 and 26.5 pg/ml, respectively). After restoring euthyroidism there was a statistically significant decline to near-normal levels (3 and 10 pg/ml, respectively). On the other hand, median serum TNF-α levels were high only in Graves' disease patients (20 pg/ml) and could not be normalized with antithyroid medication (20 pg/ml) compared to that of controls (5 pg/ml). Tumor necrosis factor-α, but not IL-6, was found to be high in the sera of Graves' disease patients when euthyroid, which may be due to an ongoing antigen–antibody interaction, a feature of autoimmune attack. It remains to be determined whether the degree of TNF-α and/or IL-6 elevation will be a predictor of disease recurrence.
Ismail Çelik, Section of Oncology, Dept. of Medicine, Hacettepe University Institute of Oncology, Ankara 06100, Turkey
Treatment of central precocious puberty with depot leuprorelin
Authors: Carel Jean-Claude , Lahlou Najiba , Guazzarotti Laura , Joubert-Collin Maryse , Roger Marc , Colle Michel , _ _ , Chaussain Jean Louis 
Published: December 2008

Carel J-C, Lahlou N, Guazzarotti L, Joubert-Collin M, Roger M. Colle M, The French Leuprorelin Trial Group, Chaussain JL. Treatment of central precocious puberty with depot leuprorelin. Eur J Endocrinol 1995;132:699–704. ISSN 0804–4643
We evaluated the pituitary and gonadal suppression in 40 girls and nine boys treated with depot leuprorelin (3.75 mg sc if body weight ≥20kg, 1.87 mg if body weight <20 kg) every 28 days for central precocious puberty. Gonadal suppression was obtained in most of the children with this dose: 3 months after initiation of the treatment, 85% of children had a peak plasma luteinizing hormone response to gonadotropin-releasing hormone <3 IU/l and the gonadal axis remained suppressed throughout the duration of the study (up to 24 months). Four patients required higher doses of leuprorelin to achieve suppression. In two girls, a cutaneous reaction to the drug was associated with incomplete suppression and the treatment had to be interrupted. Plasma leuprorelin levels tended to increase from day 3 to day 28 after injection. Residual leuprorelin levels measured 28 days after injection were stable during the first year of the study. We conclude that an initial dose of depot leuprorelin of 3.75 mg sc every 28 days is efficient in most children with central precocious puberty.
Jean-Claude Carel, INSERM U342, Hôpital Saint Vincent de Paul, 82 av Denfert Rochereau, 75014 Paris, France
Growth hormone treatment during pregnancy in a growth hormone-deficient woman
Authors: Müller Jørn , Starup Jørgen , Christiansen J Sandahl , Jøgensen Jens OL , Juul Anders , Skakkebaek Niels E 
Published: December 2008

Müller J, Starup J, Christiansen JS, Jørgensen JOL, Juul A, Skakkebaek NE, Growth hormone treatment during pregnancy in a growth hormone-deficient woman. Eur J Endocrinol 1995;132:727–9. ISSN 0804–4643
Information on the course and outcome of pregnancies in growth hormone (GH)-deficient patients is sparse, and GH treatment during pregnancy in such women has not been described previously. We have studied fetal growth and serum levels of GH, insulin-like growth factor I (IGF-I) and IGF binding protein 3 (IGFBP-3) during pregnancy, as well as birth weight and hormone levels after delivery in a 2 5-year-old woman with idiopathic, isolated GH deficiency diagnosed at the age of 7 years. As part of a clinical trial, the patient was treated with 2 IU/M2 GH for a period of 5 years. At this time she became pregnant after donor insemination. The GH treatment was continued until variant GH production from the placenta was evident. Serum levels of GH, IGF-I and IGFBP-3 were measured monthly during pregnancy after 3 days off GH therapy. Abdominal ultrasound was performed five times. Hormonal levels were measured immediately after delivery and during the following days. Serum GH and IGF-I levels increased during the second half of pregnancy: serum IGFBP-3 remained constant throughout pregnancy at a normal level. Serum levels of GH fell within 1 h after delivery, and levels of IGF-I and IGFBP-3 decreased into the range of GH-deficient women 4 days after. The fetal biparietal diameter increased normally, and birthweight was 3.564kg, length 52 cm. No adverse events were recorded. We conclude that the role of GH replacement during pregnancy of GH-deficient women should be investigated further.
Jørn Müller, Department of Growth and Reproduction, GR 5064, Rigshospitalet, 9 Blegdamsvej, DK-2100 Copenhagen ø, Denmark
Long-lasting effects of Triac and thyroxine on the control of thyrotropin and hepatic deiodinase type I
Authors: Juge-Aubry Cristiana E , Morin Odette , Pernin Agnés T , Liang Hong , Philippe Jacques , Burger Albert G 
Published: December 2008

Juge-Aubry CE, Morin 0, Pernin AT, Liang H, Phillipe J, Burger AG. Long-lasting effects of Triac and thyroxine on the control of thyrotropin and hepatic deiodinase type I. Eur J Endocrinol 1995;132:751–8.
The purpose of this study was to investigate the relation between the serum levels of thyroid hormones and their biological effects. For this purpose, hypothyroid rats were studied after stopping treatment with a long-acting thyroid hormone, thyroxine (T4) and a short-acting one, triiodothyroacetic acid (Triac). Based on preliminary experiments with different doses of T4 and Triac, hypothyroid rats (N= 84) received over 6 days' injections of lOnmol Triac or 2 nmol T4/100 g body wt per day. Biological effects of Triac and T4 were measured in the pituitary, liver and kidney up to 8 days after stopping treatment. With Triac, serum thyrotropin (TSH) levels were inhibited completely 6 h after injection, yet after 24 h they were 4.9 ± 1.8 μ/l (hypothyroid 14.5 ± 0.8 μg/l). The rapid changes in serum TSH levels were followed by a more gradual increase in serum TSH levels were followed by a more gradual increase in serum TSH, which was similar to that after T4 injection. Even 8 days after Triac treatment, serum TSH levels did not reach the hypothyroid control levels. Changes in β-TSH mRNA levels also showed a prolonged inhibition after both treatments and a slow return to hypothyroid values, which was not complete 8 days after stopping treatment. A second parameter was hepatic 5′-deiodinase type I (5′D-I), The 6-day treatment with Triac had a markedly stronger effect on 5′D-I enzyme activity and mRNA levels than treatment with T4. Again, the effect disappeared slowly because hepatic activity was still above control levels 8 days after treatment. The mRNA levels of spot 14 also were higher with Triac. However, 4 days after stopping treatment with both hormones, mRNA levels had returned to hypothyroid values. These data suggest that at the pituitary level one can distinguish between rapid and slower effects. For 5′D-I activity, however, the effects are longlasting and there is no apparent difference in the duration of the effects between Triac or T4. They last much longer than the injected hormone. Our results show that even for parameters closely controlled by thyroid hormones, the expression and duration of thyroid hormone effects vary markedly, not only from organ to organ TSH/5′D-I but also within the same organ, depending on the parameters (5′D-I/ spot 14).
Cristiana E Juge-Aubry, Thyroid Unit, Hôpital Cantonal Universitaire, 1211 Geneva 14, Switzerland
Follicle-stimulating hormone–testosterone interaction in modulating steroidogenesis in bovine granulosa cells. I. Effect on progesterone production
Authors: Grasselli Francesca , Basini Giuseppina , Bussolati Simona , Tamanini Carlo 
Published: December 2008

Grasselli F, Basini G, Bussolati S, Tamanini C. Follicle-stimulating hormone–testosterone interaction in modulating steroidogenesis in bovine granulosa cells. I. Effect on progesterone production. Eur J Endocrinol 1995;132:759–64. ISSN 0804–4643
The aim of this study was to investigate the effects of testosterone on basal and follicle-stimulating hormone (FSH)-induced progesterone production by cultured bovine granulosa cells. Granulosa cells were isolated from small (< 5 mm) and large (>8 mm) follicles and cultured for 48 h in 1 ml of Medium-199 with different concentrations of FSH (0.1, 1, 10 and 35 mg/l). In addition, the combined effects of different amounts of testosterone (1 nmol–10 μmol) and 1 mg/l FSH for 48 h on progesterone production by granulosa cells of both groups of follicles were studied; progesterone production during the subsequent 24-h incubation period was evaluated in the absence of hormones. In a third experiment, granulosa cells were treated with 500 μg of dibutyryl-cAMP and 10 μmol of testosterone for 48 h. At the end of each incubation period, the progesterone content in the culture media was determined by a validated radioimmunoassay. Basal progesterone release during the 48-h incubation period was higher in granulosa cells from small as compared to cells from large follicles; in both groups of cells, progesterone production was stimulated maximally by 1 mg/l FSH. The treatment with 10 μmol of testosterone induced a decrease of progesterone production in both groups of cells, while lower amounts exerted an inhibitory effect only in cells from large follicles. Furthermore, 10 μmol of testosterone inhibited FSH-induced progesterone release, while lower dosages were ineffective. Dibutyryl-cAMP stimulated significantly the progesterone output by granulosa cells of both groups and testosterone was effective in suppressing this increase. Our data demonstrate that testosterone plays an important role in regulating progesterone production by granulosa cells in that it inhibits (at high dosages) both basal and FSH-induced progesterone output. These data also suggest that the site of inhibition is distal to cAMP formation.
Carlo Tamanini, Istituto di Fisiologia Veterinaria. Via del Taglio 8, 43100 Parma, Italy