bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of methimazole treatment on growth hormone (GH) response to GH-releasing hormone in patients with hyperthyroidism
Authors: Giustina Andrea , Ferrari Carlo , Bodini Corrado , Buffoli Maria Grazia , Legati Fabio , Schettino Maurizio , Zuccato Fausto , Wehrenberg William B. 
Published: June 2009

Abstract.
In vitro studies have demonstrated that thyroid hormones can enhance basal and stimulated growth hormone secretion by cultured pituitary cells. However, both in man and in the rat the effects of high thyroid hormone levels on GH secretion are unclear. The aim of our study was to test the GH response to human GHRH in hyperthyroid patients and to evaluate the effects on GH secretion of short- and long-term pharmacological decrease of circulating thyroid hormones. We examined 10 hyperthyroid patients with recent diagnosis of Graves' disease. Twelve healthy volunteers served as controls. All subjects received a bolus iv injection of GHRH(1-29)NH2, 100 μg. Hyperthyroid patients underwent a GHRH test one and three months after starting antithyroid therapy with methimazole, 10 mg/day po. GH levels at 15, 30, 45, 60 min and GH peak after stimulus were significantly lower in hyperthyroid patients than in normal subjects. The GH peak was also delayed in hyperthyroid patients. After one month of methimazole therapy, most of the hyperthyroid patients had thyroid hormone levels in the normal range, but they did not show significant changes in GH levels after GHRH, and the GH peak was again delayed. After three months of therapy with methimazole, the hyperthyroid patients did not show a further significant decrease in serum thyroid hormone levels. However, mean GH levels from 15 to 60 min were significantly increased compared with the control study. The GH peak after GHRH was also earlier than in the pretreatment study. In conclusion, the GH response to GHRH is inhibited and delayed by hyperthyroidism and returns to the normal pattern after long-term euthyroidism has been achieved with methimazole.
Impaired prolactin response to hyperthermia in heroin addicts
Authors: Vescovi P. P. , Pedrazzoni M. , Maninetti L. , Pioli G. , Gerra G. , Passeri M. 
Published: June 2009

Abstract.
The response of PRL, FSH and LH to saunainduced hyperthermia was examined in 8 male former heroin addicts (studied after 14-24 days of abstinence) and 8 age- and sex-matched control subjects. The basal levels of PRL tended to be higher in former drug users than in control subjects (p=0.07). After sauna, there were no changes in the addict group, whereas a significant increase was observed in normal subjects (p<0.001). Baseline plasma LH and FSH levels were significantly lower in former drug users (p=0.02), but no change was found after sauna in either group. These findings are consistent with the existence of a deficient adaptation to thermal stress in chronic drug users, even after a relatively short drug-free period.
Effects of a V1-vasopressin antagonist on ACTH release following vasopressin infusion or insulin-induced hypoglycemia in normal men
Authors: Hader Oliver , Bähr Volker , Hensen Johannes , Hofbauer Karl G. , Oelkers Wolfgang K. H. 
Published: June 2009

Abstract.
Experimental evidence indicates that arginine vasopressin contributes to the release of adrenocorticotropic hormone under certain conditions. We studied for the first time the AVP antagonist [d(CH2)5 Tyr(Me)AVP] in 6 normal men in order to evaluate the possible role of AVP as an ACTH-releasing hormone during insulin-induced hypoglycemia. To test the agent's capacity to inhibit an ACTH release by exogenous AVP, we compared the ACTH response to an infusion of 300 ng AVP/min a. 30 min after injection of 5 μg/kg of the antagonist, b. after injection of placebo (0.9% NaCl). Plasma ACTH levels during AVP infusion rose from 17.2±1.6 ng/l (3.8±0.35 pmol/l) to 31.7±4.2 ng/l (7.0±0.92 pmol/l) at 40 min after injection of the antagonist, the difference to the control-group (increment from 16.5±1.2 ng/l (3.6±0.26 pmol/l) to 41.8±3.5 ng/l) (9.2±0.77 pmol/l) being significant (p<0.05). Peak plasma cortisol levels were 323±42 and 529±52 nmol/l, respectively (p<0.05). We then tested the compound in the same subjects during an insulin-induced hypoglycemia; 30 min after administration of 10 μg/kg of the AVP antagonist or placebo, all subjects received 0.12 IU/kg of normal insulin, thus inducing a fall of blood glucose levels below 2 mmol/l. The AVP antagonist caused a moderate but insignificant reduction of the rise in plasma ACTH and a slightly greater, significant reduction of the increment in plasma cortisol (350±19 nmol/l with antagonist and 469±90 nmol/l with placebo, p<0.05) during insulininduced hypoglycemia. The results indicate that a. the AVP antagonist partly inhibits the stimulatory effect of infused AVP on ACTH release in normal men; b. a slightly higher dose of this competitive AVP antagonist inhibits ACTH and cortisol stimulation by hypoglycemia only very little. The importance of AVP as an ACTH-releasing factor in the latter condition may have been underestimated by our experiment, since AVP concentrations in hypophyseal portal blood during hypoglycemia probably were higher than during the AVP infusion experiment.
Lack of effects of hyperglycemia on the disposal of 3-hydroxybutyrate in insulin-dependent diabetic patients
Authors: Møller N. , Jørgensen J. O. L. , Møller J. , Ørskov L. , Pørksen N. , Alberti K. G. M. M. , Schmitz O. 
Published: June 2009

Abstract.
There is evidence that hyperketonemia in insulin-dependent diabetes may be aggravated by a decreased disposal rate for ketone bodies. To test the hypothesis that this decrease may be induced by concomitant hyperglycemia through substrate competition at the acetyl-CoA level, 5 young insulin-dependent diabetic subjects received at 2-h iv infusion of 0.9 mmol 3-hydroxybutyrate · kg−1 · h−1 at clamped 1. euglycemia (5 mmol/l) and 2. hyperglycemia (11 mmol/l) on separate occasions. To ensure similar metabolic conditions, a low-dose hyperinsulinemic euglycemic clamp was performed during the 5 h preceding the actual studies. Substrate fluxes in muscle were assessed through the forearm technique. The glucose infusion rate was 4.9 and 2.9 mg· kg−1·min−1, and the forearm arteriovenous difference for glucose was 0.72 during hyperglycemia and 0.39 mmol/l (p<0.05). during euglycemia. Hyperglycemia did not affect circulating levels of free insulin, glucagon, nonesterified fatty acids, 3-hydroxybutyrate (hyperglycemia: 665, euglycemia: 770 μmol/l, p>0.05) or acetoacetate, nor forearm uptake of 3-hydroxybutyrat (hyperglycemia, 152, euglycemia: 168 μmol/l, p>0.05). In conclusion, our results do not suggest any inhibitory role for hyperglycemia in the disposal of ketone bodies. In as much as extrapolation from the present well insulinized state is appropriate, the data indicate that alternative mechanisms may be involved in the observed impairment of ketone body clearance in hyperketonemic insulin-dependent diabetic patients.
Testicular responsiveness to hCG during infancy measured by salivary testosterone
Authors: Dunkel Leo , Huhtaniemi Ilpo 
Published: June 2009

Abstract.
To investigate the role of gonadotropins in postnatal testicular activation, testosterone responsiveness to human chorionic gonadotropin was studied in 11 male infants (aged 5-180 days). The boys were given a single im injection of 5000 IU/1.7m2 hCG, and serum and salivary testosterone responses were then measured for 7 days. The results were compared with the serum testosterone responses of 8 older prepubertal boys (aged 1.7-10.4 years) studied with the same protocol. The mean (±sem) basal serum testosterone levels were 2.67±1.27 nmol/l in the infants and 0.09±0.02 nmol/l in the prepubertal boys (p<0.05). Both groups gave a significant response to hCG stimulation (p<0.001, ANOVA, one-way). The stimulated concentrations of serum testosterone were higher in the infants than in the prepubertal boys (p<0.001). The mean basal level of salivary testosterone was 30.5 ±7.0 and the mean maximal level was 97± 10.3 pmol/l in the infants (p<0.001). No age-related changes were observed in either basal or hCG-stimulated levels. In infants the mean (±sem) maximal hCG-stimulated increase was 25 ± 10-fold in serum and 8±4-fold in saliva (p=0.13). A clear stimulatory effect of hCG on testicular testosterone production was found, suggesting that the postnatal increase in serum testosterone concentration in male infants is gonadotropin-mediated. Salivary testosterone concentrations can be increased by hCG, indicating that measurements of salivary testosterone may provide an optional, non-invasive method for assessing gonadal function in children.
Immunological quantitation of rat and mouse thyroxine-binding globulins. Ontogenesis and sex-dependence of the circulating levels of the thyroxine-binding globulins
Authors: Vranckx Roger , Savu Lia , Maya Michelle , Rouaze-Romet Marielle , Nunez Emmanuel A. 
Published: June 2009

Abstract.
We describe the preparation of monospecific antisera against a thyroxine-binding globulin partially purified from immature rat sera by affinity chromatography on thyroxine-Sepharose. The antisera are used for the rocket immunoelectrophoresis assay of rat thyroxinebinding globulin and also, owing to their partial crossreactivity with mouse thyroxine-binding globulin, for the quantitation of this serum binding protein in the mouse. The thyroxine-binding globulin is measured in developing rats and in sexually mature male and female rats and mice. The results of the ontogenetic study confirm the postnatal surge of serum thyroxine-binding globulin levels, formerly demonstrated with binding techniques. They allow further to define the correlations, dependent on age, of the immunoquantitated thyroxine-binding globulin and transthyretin levels with the abilities of the sera to bind thyroxine. In sexually mature rats and mice we demonstrate an opposite sexdependence of thyroxine-binding globulin levels, characterized by increased levels of the protein in the female rats versus increased levels of the protein in the male mice. This is the first report of immunological quantitation of rat and mouse thyroxine-binding globulins.
Antidiuretic effect of indapamide in central diabetes insipidus
Authors: Koçak Mustafa , Karademir Bülent Mustafa , Tetiker Tamer 
Published: June 2009

Abstract.
Indapamide produced a significant decrease in urinary output in three patients with central diabetes insipidus. The 24-h urinary volume was reduced from 5 to 2.3 1 in a 39-year-old woman; from 11 to 4.3 1 in a 30-year-old man, and from 16 to 9.2 1 in a 40-year-old man receiving 2.5 mg of indapamide per day. To our knowledge, the antidiuretic effect of indapamide in central diabetes insipidus has not been reported previously.
Basal and saline-stimulated plasma atrial natriuretic hormone in Cushing's syndrome
Authors: McKnight J. A. , McCance D. R. , Roberts G. , Sheridan B. , Atkinson A. B. 
Published: June 2009

Abstract.
The pathogenesis of hypertension associated with Cushing's syndrome is incompletely understood. We have studied basal and saline-stimulated levels of plasma atrial natriuretic hormone in 10 subjects with active Cushing's syndrome (8 F: 2 M), aged 43±4 years (mean±sem). Ten age- and sex-matched normal control subjects were also studied. Subjects fasted from 22.00 h, rose at 07.45 h, and remained ambulant until 09.45 h when blood was taken for plasma ANH, plasma renin activity and serum aldosterone. Subjects then rested supine until 10.00 h when blood was again taken, and blood pressure recorded. Then, while subjects remained supine, 2 1 of 0.9% NaCl were infused between 10.00 and 14.00 h. Blood was taken hourly. Basal plasma ANH was 8.0±0.9 pmol/l in Cushing's subjects and 6.9±2.5 pmol/l in controls. Levels increased in response to saline in both groups, and became significantly higher in the group of patients with Cushing's syndrome (14.00 h level 21.3±3.9 vs 10.4± 1.9 pmol/l; p<0.05). Serum aldosterone and plasma renin activity were not different between groups. Mean blood pressure was higher in patients (114±4 vs 91±7 mmHg; p<0.05). Urinary sodium excretion was not different between groups before saline, but during the four hours of saline was higher in Cushing's subjects (133±12 vs 67±11 mmols; N=6; p<0.05). Our results suggest that during salt loading the exaggerated natriuresis seen in the Cushing's group may have been caused by ANH.
Thyroid volume and goitre prevalence in the elderly as determined by ultrasound and their relationships to laboratory indices
Authors: Hintze Gerhard , Windeler Jürgen , Baumert Jörg , Stein Herbert , Köbberling Johannes 
Published: June 2009

Abstract.
In 569 unselected elderly subjects over 60 years from the general population of an iodine-deficient area, a palpation and an ultrasound investigation of the thyroid were performed. Additionally, thyroid hormone values were determined in 466 of the 569 subjects (81.9%) and urinary iodine excretion in 491 subjects (86.3%). By palpation, no thyroid enlargement was noticed in 302 subjects (54.2%), goitre Ia in 98 (17.6%), goitre lb in 94 (16.9%), goitre II in 53(9.5%), and goitre III in 10(1.8%). The thyroid volumes (medians) by ultrasound were 18.6 ml in the entire group, in women (N=489) 19.2 ml, and in men (N=80) 16.6 ml. One hundred and one subjects had a thyroid nodule (17.6%), 43 persons cystic lesions (7.6%). If, according to the literature, a goitre is defined as a thyroid enlargement of more than 18 ml in women and more than 25 ml in males, a goitre prevalence of 54.2% in females and of 22.5% in males was obtained. The goitre prevalence in the entire group was calculated as 49.7%. Thyroid hormone measurements showed in subjects with goitre a significant lower TSH value (p<0.001) and a higher thyroglobulin value (p<0.001). In summary, the study shows a high prevalence of goitre in elderly subjects, a high prevalence of nodules in these thyroids, a negative correlation of goitre volume with TSH, and a positive correlation of goitre volume with the thyroglobulin concentration.
Effects of ketoconazole in hirsute women
Authors: Akalin Sema 
Published: June 2009

Abstract.
To determine the efficacy of ketoconazole in the treatment of hirsutism, clinical and hormonal effects of this agent were evaluated with a randomized, placebocontrolled, double-blind cross-over study design. Nine hirsute women were given ketoconazole (600 mg/day) or placebo for 6 months and then crossed over. The severity of hirsutism was assessed according to the scale of Ferriman & Gallwey. Baseline serum testosterone, dehydroepiandrosterone sulphate, progesterone, estradiol, basal and stimulated cortisol and 17-alpha hydroxyprogesterone were measured. Blood was also drawn for FSH and LH levels at 0, 30, 60, and 90 min of a GnRH stimulation test. The same parameters were determined following administration of placebo or ketoconazole for 6 months. The pretreatment (28.3±0.9) and post-placebo (27.7±1.4) Ferriman-Gallwey scores were significantly higher than the post-ketoconazole score (16.6±1.3, p≤0.01). Basal and stimulated cortisol levels were not blunted after ketoconazole, but basal and stimulated 17-hydroxyprogesterone levels were significantly higher, indicating sufficient enzymatic inhibition. Serum dehydroepiandrosterone sulphate and testosterone levels were significantly lowered following ketoconazole (p≤0.05). Although E2 levels did not change significantly at any time, E2:testosterone ratios were significantly higher after ketoconazole (p≤0.01), and the LH:FSH area ratio was also significantly greater than 3 after ketoconazole. It is concluded that ketoconazole significantly alleviates hirsutism by inhibiting steroid synthesis.
Pituitary function in thalassemic patients and the effect of chelation therapy
Authors: Vannasaeng Sathit , Fucharoen Suthat , Pootrakul Pensri , Ploybutr Sirirat , Yansukon Pornpun 
Published: June 2009

Abstract.
This study examined anterior pituitary function and the effect of chelation therapy in 31 patients with β-thalassemia/HbE disease. Patients were divided into those receiving chelation therapy by deferoxamine and those receiving no such therapy (control group). Pituitary function studies were repeated in both groups 18 months later. The results showed decreased pituitary responses following stimulation in 22 patients. Among these, gonadotropin and PRL responses were most affected. After 18 months, serum ferritin levels had significantly decreased in the deferoxamine group. PRL and GH responses were improved in 3 patients receiving chelation therapy without changes in other hormone responses. In contrast, no changes in pituitary responses were shown in the control group at the end of follow-up. There were 6 drop-outs (4 in the control and 2 in the deferoxamine group) and 3 deaths (2 in the control and 1 in the deferoxamine group) during 18 months. In conclusion, gonadotropin and PRL deficiencies occur most frequently in thalassemic patients. Chelation therapy for 18 months markedly reduced serum ferritin level and might preserve or improve PRL and GH secretions, but seems to have no beneficial effects on other pituitary hormone reserves.
Impaired secretion of growth hormone-releasing hormone, growth hormone and IGF-I in elderly men
Authors: Bando Hiroshi , Zhang Chenyu , Takada Yukinobu , Yamasaki Ryuichi , Saito Shiro 
Published: June 2009

Abstract.
The GHRH test and L-dopa test were performed in 12 normal young men (24.1 ± 1.1 years) and 12 normal elderly men (77.8±1.4 years) to investigate age-related changes in secretion of GHRH, GH and IGF-I. The basal plasma levels of GHRH and GH were not significantly different in young and elderly men, but the basal plasma level of IGF-I was higher in the young men (159.0± 11.7 vs 86.7± 11.6 μg/1). The area under the curve for plasma GH in the GHRH test was less in the elderly group (35.1 ±5.9 vs 11.2 ± 2.1 μg · h−1 · 1−1, p<0.001). The AUCs for the plasma GHRH and GH responses in the L-dopa test in young and elderly men were 32.0±2.7 vs 20.3±1.8 ng · h−1 · 1−1 (p<0.001), and 21.8±4.6 vs 5.4±1.1 μg · h−1 · 1 (p<0.01), respectively, indicating decreased releases of GHRH and GH in the elderly. Correlations between the AUCs for plasma GHRH and GH responses in L-dopa were found in both groups, but the ratio of the AUCs for GH/GHRH was lower in the elderly group. The elderly group showed a significant correlation between the basal plasma IGF-I level and the AUCs for plasma GH in the GHRH and L-dopa tests. These results suggest that elderly men have a decreased reserve of hypothalamic GHRH, resulting in secondarily impaired GH release, which may lead to a lower level of IGF-I than in young men.
Amyloid protein in somatostatinoma differs from human islet amyloid polypeptide
Authors: Ohsawa Haruhiko , Kanatsuka Azuma , Tokuyama Yoshiharu , Yamaguchi Takahide , Makino Hideichi , Yoshida Sho , Horie Hiroshi , Mikata Atsuo , Kohen Yoshibumi 
Published: June 2009

Abstract.
Amyloid deposits in somatostatinomas are rare observations. To examine the characteristics of this amyloid, we compared amyloid deposits in a somatostatinoma to those found in pancreatic tissue in patients with Type II diabetes mellitus and in insulinomas, using immunohistochemical techniques and specific antibodies to islet amyloid polypeptide or other pancreatic hormones, as well as electron-microscopy. Antibodies to islet amyloid polypeptide regions 8-17 or 25-37 were confirmed to be specific. Amyloid deposits in patients with Type II diabetes mellitus and in insulinomas, but not those in the somatostatinoma strongly reacted with these antibodies, or to an antibody to amyloid P component. Amyloid deposits in the somatostatinoma were not reactive with antibodies to somatostatin or to other pancreatic hormones. Electron-microscopic examinations revealed that amyloid fibrils in the somatostatinoma were thinner and more randomly distributed than were those in islets from patients with Type II diabetes mellitus. As amyloid in somatostatinomas is unlike that consisting of islet amyloid polypeptide or other mature pancreatic hormones, it may be a novel type of local amyloid in pancreatic islets.
Vasoactive intestinal polypeptide stimulates parathyroid hormone release by interaction with cyclic adenosine monophosphate production of bovine parathyroid cells
Authors: Joborn Henrik , Larsson Rolf , Rastad Jonas , Nygren Peter , Åkerström Göran , Ljunghall Sverker 
Published: June 2009

Abstract.
Influence of vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and substance P was investigated on dispersed parathyroid cells of adult cattle. At a physiological concentration of extracellular calcium, vasoactive intestinal polypeptide stimulated the parathyroid hormone release in a dose-dependent manner, whereas no effects were noted for the other peptides. The dependency of PTH secretion upon extracellular calcium was shifted to the right by vasoactive intestinal polypeptide at 10−6 mol/l, with a tendency for greater effects at low (0.5 mmol/l) than high concentrations (2.0-3.0 mmol/l) of the cation. Vasoactive intestinal polypeptide significantly enhanced cAMP release of the parathyroid cells, whereas no influence was noted on cytoplasmic calcium or pH within the cells. The results suggest that vasoactive intestinal polypeptide stimulates the PTH release by interaction with cAMP production of the parathyroid cells. This effect may contribute to the development of hypercalcemia in patients with neuroendocrine tumours secreting vasoactive intestinal polypeptide.
Effects of interleukin 1 on growth and adenosine 3',5'-monophosphate generation of the rat thyroid cell line, FRTL-5 cells
Authors: Zeki Kazuya , Azuma Hiroyuki , Suzuki Hidero , Morimoto Isao , Eto Sumiya 
Published: June 2009

Abstract.
We investigated the effects of IL-1, IL-2, IL-6, interferon-γ and tumour necrosis factor-α on growth and cAMP generation of FRTL-5 cells. IL-1 produced a significant stimulation of [3H]thymidine incorporation into FRTL-5 cells without TSH, whereas IL-1 caused significant reductions in [3H]thymidine incorporation induced by TSH or forskolin, which is known as an adenylate cyclase activator. Intracellular cAMP generation of FRTL-5 cells was stimulated by IL-1, whereas TSH-stimulated cAMP generation was inhibited by IL-1. These effects of IL-1 was neutralized by addition of anti-IL-1 antibody. The studies suggested that IL-1 blocks the effects of TSH on proliferation and cAMP generation of FRTL-5 cells on a post-receptor site of TSH.
Intracellular calcium and phospholipid turnover are not involved in the inhibition of iodothyronine 5'-deiodinase type II activity by T4
Authors: Juge-Aubry Cristiana , Dôme Pierre , Siegrist-Kaiser Catherine A. , Capponi Alessandro M. , Burger Albert G. 
Published: June 2009

Abstract.
In glial cell cultures, iodothyronine 5'-deiodinase type II is stimulated by dibutyryl cAMP. Serum-free medium increases enzyme activity and prolongs the half-life of the enzyme. T4 and rT3 specifically inhibit this activity. We tested whether enzyme inactivation by T4 was mediated by changes in cytosolic free calcium concentration and/or phospholipid turnover. Intracellular calcium concentration was decreased either by chelation of extracellular calcium or by chelation of extracellular and intracellular calcium. Neither basal hypothyroid 5'-deiodinase activity nor its inactivation by T4 were modified in such experimental conditions, compared with control cells incubated in normal calcium-containing medium. T4 by itself had no effect on the cytosolic free calcium concentration for up to 20 min. Studies on phospholipid turnover included norepinephrine in parallel to T4 as positive stimulation control. While norepinephrine clearly accelerated phosphoinositide turnover, there was no effect of T4 on any phospholipid turnover. These results suggest that neither cytosolic free calcium nor phospholipid turnover is involved in T4-dependent modulation of 5'-deiodinase type II activity in astrocytes in culture.