bluuebunny/crossref_metadata_2025_split huggingface dataset:
Review of Turkish patients with growth hormone insensitivity (Laron type)
Authors: Yordam Nurşen , Kandemir Nurgün , Erkul Ibrahim , Kurdoğlu Selim , Hatun Şükrü 
Published: December 2008

Yordam N, Kandemir N, Erkul I, Kurdoğlu S, Hatun S. Review of Turkish patients with growth hormone insensitivity (Laron type). Eur J Endocrinol 1995;133:539–42. ISSN 0804–4643
Clinical spectrum and endocrine details of thirteen Turkish children (age 0.3–14.2 years; eight females and five males; ten prepubertal, three pubertal) with growth hormone insensitivity are presented. All patients display phenotypical features of severe growth hormone deficiency, The diagnosis based on height standard deviation score (SDS), basal growth hormone (GH), basal insulin-like growth factor I (IGF-I, IGF-I response in an IGF generation test and growth hormone binding protein (GHBP) measurements. The median height SDS was −7.4 (range −3.2 to −10), weight for height index was 100 (range 81–152) and bone age/height age ratio was 2 (range 1.6–3.3). Endocrine investigations showed a median basal GH concentration of 61.4 mU/l (range 23.5–120 mU/l), Basal IGF-I level was below 10 ng/ml in all patients except one. None of the patients showed a significant IGF-I response to injections of GH (0.1 U/kg body weight for 4 days). The median IGFBP-3 level was 0.23 mg/l (range 0.1–0.56 mg/l). The GHBP level was undetectable in all of 10 patients. The high number of patients in our center may be due to the high rate of consanguinity among the Turkish population and the referral facility of our center in the area. These patients may benefit from the new therapy with recombinant human IGF-I.
Nurgün Kandemir, Hacettepe University, Department of Pediatrics, Division of Endocrinology, 06100 Ankara, Turkey
Identification and characterization of a corticotrophin-releasing hormone receptor in human placenta
Authors: Clifton Vicki L , Owens Phillip C , Robinson Phillip J , Smith Roger 
Published: December 2008

Clifton VL, Owens PC, Robinson PJ, Smith R. Identification and characterization of a corticotrophinreleasing hormone receptor in human placenta. Eur J Endocrinol 1995;133:591–7. ISSN 0804–4643
Corticotrophin-releasing hormone (CRH) causes vasodilatation in the human fetal–placental circulation and has paracrine actions in placental tissue, suggesting that CRH receptors may be present in the human placenta. We have now identified and characterized placental CRH binding sites and compared them to those described previously in human myometrium and rat pituitary. Radiolabelled ovine CRH binding to placental membranes was pH-, time-, temperature- and divalent cation-dependent and was reversible in the presence of 1 μmol/l unlabelled ovine CRH. Scatchard analysis of placentae delivered vaginally or by elective caesarean section revealed dissociation constants (Kd) of 214.5 ± 84 pmol/l (N = 8) and 45.4 ± 23.9 pmol/l (N = 9), respectively. The Kd for caesarean placental binding sites was similar to that of human myometrium (59.6 pmol/l, N = 3) and rat pituitary (82.5 pmol/l, N = 3) receptors. However, in vaginally delivered placentae the CRH binding sites had a much lower affinity (p < 0.05). The receptor densities (Bmax) of vaginally delivered and caesarean-delivered placentae were 28.6 ± 9.6 and 6.1 ± 2.8 fmol/mg, respectively (p < 0.05). Chemical cross-linking studies using disuccinimidyl suberate indicated that the molecular weight of the CRH receptor in the placenta and rat pituitary is 75 kD. We conclude that there is a high-affinity population of CRH binding sites in the human placenta that are physicochemically similar to pituitary and myometrial CRH receptors. The CRH receptor properties in the placenta change in response to labour, when CRH levels in maternal blood are highest, suggesting that placental CRH may regulate its receptor.
R Smith, Endocrinology Unit, John Hunter Hospital, Locked Bag 1, Hunter Regional Mail Centre, Newcastle, NSW 2310, Australia
Quantity of Na/K-ATPase and glucose transporters in the plasma membrane of rat adipocytes is reduced by in vivo triiodothyronine
Authors: Voldstedlund Marianne , Tranum-Jensen Jørgen , Handberg Aase , Vinten Jørgen 
Published: December 2008

Voldstedlund M. Tranum-Jensen J, Handberg A, Vinten J. Quantity of Na/K-ATPase and glucose transporters in the plasma membrane of rat adipocytes is reduced by in vivo triiodothyronine. Eur J Endocrinol 1995:133:626–34. ISSN 0804–4643
The expression of sodium-potassium pumps and glucose transporters in pure adipocyte plasma membranes from a hyperthyroid animal model was studied. Hyperthyroidism was induced by enteral administration of five doses of 90 μg of triiodothyronine every second day to 8-week-old rats. Following isolation of epididymal adipocytes, 3-O-methylglucose transport was measured and the number of Na/K-ATPase-(α1- and α2-isoforms) and glucose transporter (GLUT1 and GLUT4) molecules in sheets of adipocyte plasma membrane were determined by quantitative immunoelectron microscopy, using gold labelling. Maximal in vitro insulin stimulation of adipocytes increased the glucose transport rate and the amount of GLUT4 in the plasma membrane 15-fold, whereas the amount of α2 was unaffected, In adipocytes from hyperthyroid rats, mean adipocyte volume was decreased by 18% and the quantities of GLUT4 per unit area of plasma membrane (maximal insulin stimulation) and of α2 were decreased by 19% and 15% respectively. Thus, hypotrophia of fat tissue in the hyperthyroid state is associated with a decreased expression in the plasma membrane of the glucose transporter GLUT4 and the α2 -isoform of Na/K-ATPase.
Marianne Voldstedlund, Department of Medical Physiology, The Panum Institute, University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark
Regulation of luteal function by luteinizing hormone and prolactin at different times of the luteal phase
Authors: Hinney Bernd , Henze Christina , Wuttke Wolfgang 
Published: December 2008

Hinney B, Henze C, Wuttke W. Regulation of luteal function by luteinizing hormone and prolactin at different times of the luteal phase. Eur J Endocrinol 1995;133:701–17. ISSN 0804–4643
In 54 healthy women luteal function was assessed by sequential withdrawals of blood samples at 10-min intervals for 8–10 h. Subgroups of the women were studied during the early and late ovulatory period and during the early, mid- and late luteal phase. Bio- and immunoreactive luteinizing hormone (LH), prolactin, testosterone, estradiol and progesterone levels were determined in each sample. While the bio- and immunoreactivity of LH pulses correlated fairly well, a number of bio- or immunoreactive LH pulses were observed that were not detected by the respective other method. Responsivity of the corpus luteum to LH episodes developed during the second half of the luteal phase and was most marked in cases where LH episodes were accompanied by prolactin episodes. In the absence of prolactin episodes, LH episodes did not stimulate progesterone or estradiol secretion. The highest incidence of coincident LH and prolactin pulses was observed during the mid- and late luteal phase. Serum testosterone levels showed also some fluctuations but these were independent of immuno- or bioactive LH episodes and therefore most likely not of luteal origin. Prior to menstruation LH episodes were not any more stimulatory to progesterone secretion, indicating that it is not the withdrawal of LH but, rather, another possibly intraovarian mechanism that results in luteolysis. In a number of women, increased estradiol and progesterone secretion was strictly related to the prior occurrence of LH and prolactin pulses. In other subjects, both gonadal steroids fluctuated largely with no discernible correlation to LH fluctuations. This may indicate that in these subjects the corpora lutea have some degree of autonomous regulation.
W Wuttke, Abteilung für Klinische und Experimentelle Endokrinologie, Universitäts-Frauenklinik, Robert-Koch-Strasse 40, D-37075 Gottingen, Germany
A clinically useful diabetes electronic medical record: Lessons from the past; pointers toward the future
Authors: Gorman Colum , Looker James , Fisk Tom , Oelke William , Erickson David , Smith Steven , Zimmerman Bruce 
Published: December 2008

Gorman C, Looker J, Fisk T, Oelke W, Erickson D, Smith S, Zimmerman B. A clinically useful diabetes electronic medical record. Lessons from the past; pointers toward the future. Eur J Endocrinol 1996;134:31–42. ISSN 0804–4643
We have analysed the deficiencies of paper medical records in facilitating the care of patients with diabetes and have developed an electronic medical record that corrects some of them. The diabetes electronic medical record (DEMR) is designed to facilitate the work of a busy diabetes clinic. Design principles include heavy reliance on graphic displays of laboratory and clinical data, consistent color coding and aggregation of data needed to facilitate the different types of clinical encounter (initial consultation, continuing care visit, insulin adjustment visit, dietitian encounter, nurse educator encounter, obstetric patient, transplant patient, visits for problems unrelated to diabetes). Data input is by autoflow from the institutional laboratories, by desk attendants or on-line by all users. Careful attention has been paid to making data entry a point and click process wherever possible. Opportunity for free text comment is provided on every screen. On completion of the encounter a narrative text summary of the visit is generated by the computer and is annotated by the care giver. Currently there are about 7800 patients in the system. Remaining challenges include the adaptation of the system to accommodate the occasional user, development of portable laptop derivatives that remain compatible with the parent system and improvements in the screen structure and graphic display formats.
Colum Gorman, Division of Endocrinology and Metabolism, Mayo Clinic, Rochester. MN. USA
Study of serum 3,5,3′-triiodothyronine sulfate concentration in patients with systemic non-thyroidal illness
Authors: Santini Ferruccio , Chiovato Luca , Bartalena Luigi , Lapi Paola , Palla Roberto , Panichi Vincenzo , Velluzzi Fernanda , Grasso Lucia , Chopra Inder J , Martino Enio , Pinchera Aldo 
Published: December 2008

Santini F, Chiovato L, Bartalena L, Lapi P, Palla R. Panichi V, Velluzzi F, Grasso L, Chopra IJ, Martino E. Pinchera A. Study of serum 3,5,3′-triiodothyronine sulfate concentration in patients with systemic non-thyroidal illness. Eur J Endocrinol 1996;134:45–9. ISSN 0804–4643
Sulfation is an important pathway of triiodothyronine (T3) metabolism. Increased serum T3 sulfate (T3S) values have been observed during fetal life and in pathological conditions such as hyperthyroidism and selenium deficiency. Similar variations have also been reported in a small number of patients with systemic non-thyroidal illness, but the underlying mechanisms have not been elucidated. In this study, serum T3S concentrations have been measured by a specific radioimmunoassay in 28 patients with end-stage neoplastic disease (ESND) and in 44 patients with chronic renal failure (CRF); 41 normal subjects served as controls. Both ESND and CRF patients had lower serum total T4 (TT4) and total T3 (TT3) than normal controls, while serum reverse T3 (rT3) was increased significantly in ESND (0.7 ±0.5 nmol/l; p < 0.001 vs. controls) but not in CRF (0.3 ± 0.1 nmol/l). The TT3/rT3 ratio, an index of type I iodothyronine monodeiodinase (type I MD) activity, was reduced significantly in both groups of patients. Serum T4-binding globulin (TBG) was decreased in CRF but not in ESND patients. Serum T3S was significantly higher both in ESND (71 ± 32 pmol/l) and CRF 100 ± 24 pmol/l) than in controls (50 ± 16 pmol/l, p < 0.001). Serum T3S values showed a positive correlation with rT3 values and a negative correlation with both TT3 and FT3 values in ESND, but not in CRF. In the latter group a positive correlation was observed between T3S and TBG values. The T3S/FT3 ratio was higher both in CRF (18 ± 5) and in ESND (23 ± 18) as compared to controls (10 ± 4). Serum inorganic sulfate was increased and correlated positively with T3S values in CRF patients. In conclusion, the results of this study in a large series of patients confirm that patients with systemic non-thyroidal illness have increased serum T3S levels. The mechanisms responsible for these changes appear to be different in ESND and CRF patients. In ESND the increase in serum T3S levels is mainly related to reduced degradation of the hormone by type I MD, whereas in CRF it might be driven by the enhanced sulfate ion concentration, and could be partially dependent on the impaired renal excretion of T3S Because T3S can be reconverted to T3. it is possible that increased T3S concentrations contribute to maintenance of the euthyroid state in systemic non-thyroidal disease.
Ferruccio Santini, Institute of Endocrinology, University of Pisa. Viale del Tirreno 64. 56018 Tirrenia, Pisa, Italy
Plasma GH responses to human GHRH-antagonist in normal subjects
Authors: Hanew Kunihiko , Tanaka Aki , Utsumi Atsushi , Sugawara Akira , Abe Keishi 
Published: December 2008

Hanew K, Tanaka A, Utsumi A, Sugawara A, Abe K, Plasma GH responses to human GHRH-antagonist in normal subjects. Eur J Endocrinol 1996;134:67–72. ISSN 0804–4643
The effect of GHRH-antagonist {N-Ac-Tyr1, d-Arg2) GRF-(1–29)-NH2} on plasma GH morning and evening secretion was evaluated in 14 normal subjects (10 males, 4 females, aged 19–25 years). Plasma GH was determined using a high sensitivity IRMA kit (detection limit, 0.006 μg/l). After intravenous infusion of GHRH-antagonist (100 μg/100 ml saline over 75 min) in the morning, plasma GH remained constant during the 150 min post-infusion (N = 6). In contrast, when GHRH-antagonist was administered in the evening, plasma GH showed a clear and gradual decrease through the initial 90 min and returned to baseline levels at 150 min. Plasma GH values were also significantly lower from 75 min to 135 min when compared to physiological fluctuations in plasma GH (P < 0.05). Other anterior pituitary hormones remained unaffected by GHRH-antagonist. In conclusion, our data suggest that evening basal GH secretion, but not morning GH secretion, is maintained by endogenous GHRH.
K Hanew, The Second Department of Internal Medicine, Tohoku University School of Medicine. 1-1 Seiryocho, Sendai 980, Japan
Overnight dexamethasone suppression test: comparison of plasma and salivary cortisol measurement for the screening of Cushing's syndrome
Authors: Barrou Zina , Guiban Dominique , Maroufi Amel , Fournier Claudine , Dugué Marie-Annick , Luton Jean-Pierre , Thomopoulos Pierre 
Published: December 2008

Barrou Z, Guiban D, Maroufi A, Fournier C, Dugué M-A, Luton J-P. Thomopoulos P. Overnight dexamethasone suppression test: comparison of plasma and salivary cortisol measurement for the screening of Cushing's syndrome. Eur J Endocrinol 1996:134:93–6. ISSN 0804–4643
The overnight 1-mg dexamethasone suppression test is a very good screening test for subjects suspected of having Cushing's syndrome. To simplify the procedure, we evaluated the 1-mg dexamethasone suppression test with measurement of salivary cortisol. We performed this test with plasma and salivary cortisol measurements in 27 patients with Cushing's syndrome and 64 normal controls. The sensitivity and specificity of plasma cortisol measurements were 100% and 87%, respectively, for a cut-off point of 100 nmol/l, in accordance with previous studies. The results of salivary cortisol showed the absence of overlap between the two groups, with a sensitivity and specificity of 100% for a cut-off point of 2.8 nmol/l, On a larger series, however, one might occasionally miss the diagnosis of a patient with Cushing's syndrome. Therefore, we favor a cut-off point of 1.9 nmol/l, the sensitivity remaining at 100% and the specificity being 94%. In conclusion we recommend the overnight dexamethasone suppression test with measurement of salivary cortisol as a screening test for Cushing's syndrome.
Pierre Thomopoulos. Clinique des maladies endocriniennes et métaboliques. Hôpital Cochin, 27 rue du Faubourg Saint-Jacques, 75014 Paris, France
Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats
Authors: Gøtzsche Liv Bjørn-Hansen , Rosenqvist Ninna , Grønbæk Henning , Flyvbjerg Allan , Gøtzsche Ole 
Published: December 2008

Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643.
In order to elucidate further the abnormal myocardial Ca+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and β-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca+ channels was reduced by 25% at day 4 p<0.05) and the β-receptor MBC was reduced by 48% p<0.05). A normalizing tendency was observed at day 7 for both receptor types; insulin-treated rats did not differ from controls at that time. After 90 and 200 days of untreated diabetes the Ca+ channel MBC had increased by 36% and 27%, respectively (p < 0.05). Twenty days of strictly regulated blood glucose following 180 days of untreated diabetes totally normalized the Ca+ channel MBC. This is in contrast to a previous report where insulin treatment did not normalize the Ca+ channel MBC. Total β-receptor MBCs did not differ from control values 90 and 200 days after STZ. In conclusion, an increase in rat myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could serve to compensate for a defect coupling of the β-receptor to adenylate cyclase. An elevated Ca+ channel number may, at least theoretically, lead to increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration.
Liv Bjørn-Hansen Gøtzsche, Dept. of Internal Medicine M, (Diabetes and Endocrinology), Aarhus Kommunehospital, University Hospital of Aarhus, DK-8000 Aarhus C, Denmark.
Effect of growth hormone on follicular fluid androgen levels in patients treated with gonadotropins before in vitro fertilization
Authors: Bergh Christina , Carlström Kjell , Selleskog Ulrika , Hillensjö Torbjörn 
Published: December 2008

Bergh C, Carlström K, Selleskog U, Hillensjö T. Effect of growth hormone on follicular fluid androgen levels in patients treated with gonadotropins before in vitro fertilization. Eur J Endocrinol 1996;134:190–6. ISSN 0804–4643
Forty normally ovulating women aged 25–38 years from one private and two university in vitro fertilization (IVF) centres were used in this randomized, double-blind, parallel, placebo-controlled study to explore the effect of recombinant human growth hormone (GH) on follicular fluid (FF) levels of steroid hormones, particularly androgens. All the women had tubal factor infertility and were classified as poor responders with at least two previously performed and failed IVF treatments in which less than five oocytes had been retrieved following ovarian hyperstimulation. Growth hormone (GH 0.1 IU/kg body wt per day) or placebo was given as pretreatment during down-regulation with gonadotropin-releasing hormone agonist and during stimulation with human menopausal gonadotropin (hMG) according to the randomized protocol. Follicular fluid concentrations of steroids were measured and changes related to the levels of insulin-like growth factor I (IGF-I) and IGF binding proteins 1 and 3 and to the mode of GH administration. Pretreatment with GH, i.e. administration of GH before hMG stimulation only, caused significantly elevated follicular fluid concentrations of estrone, testosterone and dehydroepiandrosterone (DHEA) and higher values for markers of aromatase activity (ratios between estrone and androstenedione and between estradiol-17β and androstenedione) than in the placebo group, as well as in the two groups receiving GH during hMG stimulation. The highest values for markers of steroid sulfatase activity (ratios between DHA and DHEA sulfate and between unconjugated and conjugated estrone) were found in the patients pretreated with GH. Positive correlations were found between follicular fluid IGF-I and IGF binding protein 3 on the one hand and androgens on the other. This study showed that the administration of adjuvant GH to women who were poor responders to gonadotropins alters the endocrine/paracrine ovarian response to gonadotropins.
Torbjörn Hillensjö, Department of Obstetrics and Gynecology, Huddinge University Hospital, S-141 86 Huddinge, Sweden
Relationship between serum dehydroepiandrosterone sulfate, androstenedione, and sex hormones in men and women
Authors: Phillips Gerald B 
Published: December 2008

Phillips GB. Relationship between serum dehydroepiandrosterone sulfate, androstenedione, and sex hormones in men and women. Eur J Endocrinol 1996;134:201–6. ISSN 0804–4643
Previous reports of a correlation between serum dehydroepiandrosterone sulfate (DHEAS) and testosterone in both men and women have led to the suggestion that adrenal and gonadal secretion are related. In the present study, the correlation of DHEAS with testosterone and free testosterone (FT) in both normal men and women was tested. Androstenedione, estradiol, sex hormone binding globulin (SHBG), and insulin were also measured and their correlations determined. All correlations were controlled for age and body mass index. In the men in the study, DHEAS did not correlate with testosterone or FT but correlated strongly with androstenedione. In the women, DHEAS correlated strongly with testosterone, FT. and androstenedione; androstenedione in turn correlated strongly with testosterone and FT. DHEAS showed no correlations with estradiol, SHBG, or insulin in the men or women. The lack of a correlation between DHEAS and testosterone in normal men is consistent with the independent secretion of these hormones by the adrenal and testis, respectively. The finding of a strong DHEAS-testosterone correlation in normal women may be explained by parallel adrenal secretion in response to trophic stimuli, i.e., without invoking an adrenal-gonadal interaction.
GB Phillips, Roosevelt Hospital, 428 West 59th Street, New York, NY 10019, USA