bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recurrent miscarriage is associated with increased numbers of CD5/20 positive lymphocytes and an increased incidence of thyroid antibodies
Authors: Roberts Judith , Jenkins Carol , Wilson Rhoda , Pearson Charles , Franklin Ian A , MacLean Marjory A , McKillop James H , Walker James J 
Published: December 2008

Roberts J. Jenkins C, Wilson R, Pearson C, Franklin IA, MacLean MA, McKillop JH, Walker JJ. Recurrent miscarriage is associated with increased numbers of CD5/20 positive lymphocytes and an increased incidence of thyroid antibodies. Eur J Endocrinol 1996;134:84–6. ISSN 0804–4643
The aim of this study was to determine whether recurrent miscarriage (three or more miscarriages, no live children) was associated with an increased incidence of autoantibodies. Five groups were enrolled into the study; healthy non-pregnant women, healthy first-trimester pregnant women, women suffering spontaneous abortion, those undergoing termination of pregnancy and those with a previous history of miscarriage. The number of total B cells and the numbers of the antibody producing B cell subset CD5+/CD20+ were determined for each group. Samples were tested for anticardiolipin antibodies, antinuclear antibodies and thyroid microsomal and thyroglobulin antibodies. The results showed that compared to normal pregnancy or spontaneous abortion, recurrent miscarriage was associated with a significant increase in the number of CD5+/20+ positive cells (0.8 ± 0.3 vs 0.5 ± 0.1 vs 1.1 ± 0.3 × 108/l: p < 0.001). These women were also found to have a higher incidence of thyroid antibodies, with four out of the 11 patients being positive for thyroid microsomal antibodies. These results suggest that there may be an association between autoimmunity and recurrent miscarriage.
R Wilson, Department of Medicine, Glasgow Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK
5α-Androstane-3α, 17β-diol and 5α-androstane-3α, 17β-diolglucuronide in plasma of normal children, adults and patients with idiopathic hirsutism: a mass spectrometric study
Authors: Wudy Stefan A , Wachter Ulrich A , Homoki Janos , Teller Walter M 
Published: December 2008

Wudy SA. Wachter UA, Homoki J, Teller WM. 5α-androstane-3α, 17β-diol and 5α-androstane-3α, 17β-diol-glucuronide in plasma of normal children, adults and patients with idiopathic hirsutism: a mass spectrometric study. Eur J Endrocrinol 1996;134:87–92. ISSN 0804–4643
We investigated the developmental patterns of 5α-androstane-3α, 17β-diol (AD) and 5α-androstane-3α, 17β-diol-glucuronide (ADG) in plasma of normal children and adults of both sexes and in patients with idiopathic hirsutism using a physicochemical method: high-resolution gas chromatography/ mass spectrometry (HRGC/MS). In children below the age of 11 years, AD and ADG increased with age showing no differences between sexes (mean ±sd nmol/l): normal subjects 3–6 years: AD in females 0.08± 0.03. in males 0.07 ±0.03; ADG in females 0.15 ±0.05, in males 0.14± 0.04: normal subjects 7–10 years: AD in females 0.17 ± 0.03, in males 0.17 ± 0.07; ADG in females 0.59 ± 0.12, in males 0.47 ± 0.14. Thereafter, AD and ADG showed a greater increase in males (normal subjects 11–15 years: AD in females 0.24 ± 0.06, in males 0.41 ±0.14: ADG in females 1.47± 0.36. in males 3.36 ± 1.22). In adults, plasma levels did not overlap between females and males (AD in females 0.24 ±0.07. in males 0.99± 0.31; ADG in females 2.32 ± 0.68, in males 13.01 ± 3.05). 5α-Androstane-3β, 17β-diol-glucuronide discriminated better between sexes than AD. In idiopathic hirsutism, mean plasma concentrations of AD and ADG were higher than those of healthy females (ages 11–15 years: AD 0.31 ± 0.10. ADG 3.48 ± 2.00; ages > 16 years: AD 0.44 ± 0.27, ADG 6.46 ± 3.11). but 54% of patients had normal plasma concentrations of AD and 29% had normal ADG values. Thus, ADG reflected androgenicity better than AD. However, both metabolites were imperfect markers of androgenicity in idiopathic hirsutism. Therefore, our findings do not support the concept of increased 5α-reductase activity in all patients with idiopathic hirsutism.
Stefan A Wudy, Steroid Laboratory, First Department of Pediatrics, University of Ulm. D-89070 Ulm/Donau, Germany
Plasma free insulin-like growth factor I concentrations in growth hormone deficiency in children and adolescents
Authors: Hasegawa Yukihiro , Hasegawa Tomonobu , Takada Makoto , Tsuchiya Yutaka 
Published: December 2008

Hasegawa Y, Hasegawa T, Takada M, Tsuchiya Y. Plasma free insulin-like growth factor I concentrations in growth hormone deficiency in children and adolescents. Eur J Endocrinol 1996;134:184–9. ISSN 0804–4643.
Serum levels of total insulin-like growth factor I (IGF-I) correlate with growth hormone (GH) secretory status and are a useful parameter in the diagnostic evaluation of GH deficiency. Serum total IGF-I levels represent the combined quantity of free or unbound IGF-I and IGF-I that is bound to specific IGF binding proteins. Free IGF-I (fIGF-I), which is postulated to be the bioactive fraction, accounts for only a small fraction of the total amount. We have recently developed a new immunoradiometric assay (IRMA) for plasma fIGF-I and have investigated fIGF-I in relation to GH status. The simple, non-extraction assay procedure involves the capture of unbound IGF-I by anti-IGF-I antibody coated to polystyrene beads and detection by a radiolabelled anti-IGF-I antibody directed to a separate epitope. Preliminary studies demonstrated that the f IGF-I IRMA does not measure IGF-I that is complexed to IGF-binding proteins and that the equilibrium between the free and bound fractions is not disturbed during the assay. Free IGF-I levels were compared to total IGF-I levels measured in the same IRMA after acid–ethanol extraction of the samples. Normal levels of fIGF-I from infancy through adulthood were found to have a close correlation with total IGF-I levels, with the lowest levels occurring in infancy and peak levels during puberty. Patients with complete GH deficiency had low levels of both fIGF-I and total IGF-I, with 94% and 100% of the levels below the 5th percentile for age, respectively. On the other hand, approximately 90% of patients with normal IGF binding protein-3 levels among partial GH deficiency and normal short children had free and total IGF-I levels above the 5th percentile for age. These data indicate that the clinical utility of plasma fIGF-I measurements is similar to measurements of total IGF-I in the evaluation of childhood GH deficiency.
Yukihiro Hasegawa, Division of Endocrinology and Metabolism, Tokyo Metropolitan Kiyose Children's Hospital, 1-3-1 Urnezono Kiyose, Tokyo 204, Japan
Proinsulin, C-peptide, and insulin in normal subjects during an 8-h hyperglycemic clamp
Authors: Hartling Svend G , Røder Michael E , Dinesen Bo , Binder Christian 
Published: December 2008

Hartling SG, Røder ME, Dinesen B, Binder C. Proinsulin C-peptide, and insulin in normal subjects during an 8-h hyperglycemic clamp. Eur J Endocrinol 1996;134:197–200. ISSN 0804–4643
Increased concentrations of proinsulin immunoreactive material (PIM) absolutely or relative to insulin is a characteristic finding in patients with non-insulin-dependent diabetes mellitus (NIDDM). The aim of this study was to test if 8 h or mild hyperglycemia (7–9 nmol/l in healthy subjects could induce a preferential secretion of PIM from B cells. Serum concentrations of insulin, C-peptide and PIM were measured every 10 min during the 8 h of continuous glucose infusion in nine normal-weight healthy subjects without diabetes among their first-degree relatives. After a gradual rise in B-cell peptides, a steady state was reached. From 4 to 8 h no further difference in insulin, C-peptide or PIM concentration was found. Fasting PIM/C-peptide and PIM/insulin ratios of 0.5% and 2.3% increased during the glucose clamp to levels of 1.4% and 7.6%, respectively. Neither testing the regression slope nor comparing individual time points showed any significant difference for the PIM/C-peptide ratio from 2 to 8 h and for the PIM/insulin ratio from 3 to 8 h. These results do not support the hypothesis that an increased glucose drive per se results in an altered B-cell function with increasing PIM/Cpeptide ratio. At least 8 h of mild hyperglycemia in healthy subjects does not progressively alter B-cell function.
Svend Hartling, Department of Internal Medicine, Sundby Hospital, Italiensvej 1, DK-2300 Sundby, Denmark
Androgen-dependent sex differences in the hypothalamic serotoninergic system
Authors: Borisova Nina A , Proshlyakova Evgeniya V , Sapronova Anna Ya , Ugrumov Michael V 
Published: December 2008

Borisova NA, Proshlyakova EV, Sapronova AY, Ugrumov MV. Androgen-dependent sex differences in the hypothalamic serotoninergic system. Eur J Endocrinol 1996;134:232–5. ISSN 0804–4643
This study has attempted to fulfil our knowledge on the sex differences in the hypothalamic serotoninergic (5-HT) system in adult rats, and also to evaluate the role of neonatal androgens in the appearance of this sexual dimorphism. Such integrative characteristics of the 5-HT system as 5-HT content and specific uptake were estimated and compared in the anterior and middle hypothalami in intact adult females and males, as well as in neonatally castrated adult males. According to our data, the 5-HT content and [3H]5-HT specific uptake both in the anterior and middle hypothalami of intact females exceeded significantly those in intact males. Neonatal castration of males resulted in an increase of the 5-HT content and [3H]5-HT uptake in both hypothalamic regions up to their levels in intact females. Thus, the present study provides new information on the sex differences in the hypothalamic 5-HT system, which are apparently related to the neonatal masculinization of the hypothalamus.
Michael V Ugrumov, Institute of Developmental Biology, Russian Academy of Sciences, Vavilov str., Moscow 117808, Russia
New insights into pancreatic β-cell metabolic signaling in insulin secretion
Authors: Prentki Marc 
Published: December 2008

Prentki M. New insights into pancreatic β-cell metabolic signaling in insulin secretion. Eur J Endocrinol 1996;134:272–86. ISSN 0804–4643
In recent years, it has become apparent that second messengers and factors other than ATP, metabolically sensitive KATP+ channels and Ca2+ play essential roles in nutrient-induced insulin release. This paper reviews the evidence in support of several new concepts and hypotheses in the field of β-cell signaling. These include in particular that: a rise in cytosolic Ca2+ is not sufficient to explain the kinetics and extent of secretion induced by glucose: variations in ADP, rather than ATP, regulate β-cell metabolism and the KATP+ channel; anaplerosis (the replenishment of the citric acid cycle with intermediates) is essential for β-cell activation; a shift from fatty acid oxidation to esterification is an important event in β-cell signaling; malonyl-CoA and long chain acyl-CoA esters may act as metabolic coupling factors; glycolytic oscillations underlie, in part, oscillations in electrical activity, cytosolic Ca2+ and insulin release. A metabolic model of fuel sensing that integrates the mode of action of all classes of nutrient secretagogues is proposed.
Marc Prentki, Department of Nutrition, University of Montreal, CP6128, Succ, Centre-Ville, Montreal, PQ H3C3J7, Canada
High frequency of endocrine autoimmunity in patients with sarcoidosis
Authors: Papadopoulos Konstantin I , Hörnblad Yngve , Liljebladh Harriet , Hallengren Bengt 
Published: December 2008

Papadopoulos KI, Hörnblad Y, Liljebladh H, Hallengren B. High frequency of endocrine autoimmunity in patients with sarcoidosis. Eur J Endocrinol 1996;134:331–6. ISSN 0804–4643
Autoimmune diseases and sarcoidosis may be related and, especially, the association between sarcoidosis and autoimmune thyroid disease has long been recognized. The frequency and type of endocrine autoimmunity was examined in a series of Swedish patients with sarcoidosis. Of all patients (N = 89) with documented sarcoidosis attending the Department of Pulmonary Medicine between January 1980 and December 1991, 78 patients (44 males and 34 females; median age at the time of the study 48 years, range 22–81 years) were examined at the Department of Endocrinology, Malmö University Hospital, in the present study. Fifteen patients (19.2%) had clinical or serological evidence of endocrine autoimmunity. Two patients had Addison's disease, both with polyglandular autoimmune (PGA) syndrome type II; evidence of thyroid autoimmunity was found in 13 patients, eight with clinical autoimmune thyroid disease (ATD) (two with Graves' disease and six with autoimmune thyroiditis), of whom two had PGA syndrome type III, and five with isolated positive thyroid serology: two patients had insulin-dependent diabetes mellitus and one had premature ovarian failure. The frequencies of Addison's disease, clinical ATD and PGA syndrome type II were significantly higher compared with the frequencies found in the general population. In conclusion, a high frequency of endocrine autoimmunity in patients with sarcoidosis, occurring in about 20% of the cases, was demonstrated. Thyroid autoimmunity and polyglandular autoimmune syndromes occurred most frequently. Complex immunological and genetic mechanisms might explain the association of sarcoidosis and endocrine autoimmune diseases.
Bengt Hallengren, Department of Endocrinology, Malmö University Hospital, S-205 02, Malmö, Sweden
Prophylactic application of thyrostatic drugs during excessive iodine exposure in euthyroid patients with thyroid autonomy: a randomized study
Authors: Nolte Wilhelm , Müller Ralf , Siggelkow Heide , Emrich Dieter , Hüfner Michael 
Published: December 2008

Nolte W, Müller R, Siggelkow H, Emrich D, Hüfner M. Prophylactic application of thyrostatic drugs during excessive iodine exposure in euthyroid patients with thyroid autonomy: a randomized study. Eur J Endocrinol 1996;134:337–41. ISSN 0804–4643
In a prospective, randomized study we examined the influence of prophylactic short-term thyrostatic therapy on thyroid iodine metabolism in patients with euthyroid autonomy undergoing elective coronary angiography. From a total of 1177 patients, 51 fulfilled the criteria of euthyroid autonomy before coronary angiography (negative thyrotropin-releasing hormone test, 10-min uptake of at least 1.2% 99mTc and no elevation of free thyroxine and free triiodothyronine indices) and were randomized into three groups: group I (N = 17) received 20 mg/day of thiamazole and group 2 (N = 17) received 900 mg/day of sodium perchlorate; thyrostatic therapy was begun on the day before angiography and continued for 14 days; group 3 (N = 17) served as controls without treatment. Parameters of thyroid function-free thyroxine (FT4) index and free triiodothyronine (FT3) index, thyrotropin (TSH) and delta-TSH–urine iodine excretion and 99mTc uptake were determined before and 30 days after coronary angiography. At the end of the study the mean FT4 index and FT3 index were elevated significantly in the control group compared with baseline values, but were still within the normal range. In contrast, the mean FT4 index and FT3 index remained unchanged in the treated groups. Four mild cases of hyperthyroidism were observed at the end of the study: two cases in the control group and one case in each of the treated groups. Thyrotropin suppression, urine iodine excretion and 99mTc uptake differed significantly between the treated groups and the control group. In the treated groups TSH suppression, urine iodine excretion and 99mTc uptake remained unchanged 30 days after coronary angiography compared with baseline values. In the control group the degree of TSH suppression and the level of urine iodine excretion increased (about twofold) significantly after coronary angiography, whereas 99mTc uptake decreased significantly (ca. 50%). In conclusion, short-term prophylactic thyrostatic therapy seems to have a protective effect against iodine excess in patients with euthyroid autonomy. However, mild hyperthyroidism could not be prevented in some cases. Probably a combination therapy of thiamazole and perchlorate would be more effective.
Wilhelm Nolte, Department of Gastroenterology and Endocrinology, Medizinische Klinik, Robert-Koch-Straße 40, 37075 Göttingen, Germany
Aggressive thyroid cancer associated with toxic nodular goitre
Authors: Hayes Frances J , Sheahan Kieran , Heffernan Andrew , McKenna T Joseph 
Published: December 2008

Hayes FJ, Sheahan K, Heffernan A, McKenna TJ. Aggressive thyroid cancer associated with toxic nodular goitre. Eur J Endocrinol 1996:134:366–70. ISSN 0804–4643
Reports of concurrent thyrotoxicosis and thyroid cancer have appeared in the last three decades. While most of the tumours have been clinically inconsequential, it has been suggested that thyroid carcinomas arising in patients with Graves' disease tend to behave aggressively, while those associated with toxic nodular goitre follow a more benign course. We report a contrary clinical experience with four cases of thyrotoxicosis associated with metastatic thyroid cancer, two of which were fatal. All four patients had toxic nodular goitre. Thyroid eye signs were uniformly absent. Two patients had received 131I therapy; none had other history of irradiation to the head or neck. Antimicrosomal and antithyroglobulin antibodies were absent in all four patients. Thyroid-stimulating immunoglobulin, which was measured in one patient, was also absent. Histopathological examination of the resected thyroid glands revealed two papillary cancers, one mixed anaplastic/papillary and one anaplastic cancer. All four patients had cervical node involvement and one had pulmonary metastases, Both patients with anaplastic carcinoma succumbed to their disease within 6 months; neither of the patients with papillary cancer had disease recurrence after 2 and 4 years, respectively. The experience reported here of aggressive thyroid cancer associated with toxic nodular goitre may represent coincidence or, alternatively, it may represent the early recognition of a change in the natural history of toxic nodular goitre.
TJ McKenna, Department of Endocrinology & Diabetes Mellitus, St Vincent's Hospital, Elm Park, Dublin 4, Ireland
Influence of oestrous cycle on the pressor recovery following haemorrhage in anaesthetized Brattleboro rats
Authors: Morrissey Sinead E , Baden-Fuller Joanna , Murugananthan Nirodhini , whitehead Saffron A , Laycock John F 
Published: December 2008

Morrissey SE, Baden-Fuller J. Murugananthan N, Whitehead SA, Laycock JF. Influence of oestrous cycle on the pressor recovery following haemorrhage in anaesthetized Brattleboro rats. Eur J Endocrinol 1996;134:379–85. ISSN 0804–4643
A sexual dimorphism in the pressor responsiveness to the neurohypophysial hormone vasopressin may be associated with a peripheral interaction between ovarian steroids and the neurohypophysial hormone. Indeed, the ovarian steroids may inhibit the vasopressin-dependent component of the pressor response to haemorrhage. The present study examined the recovery of the arterial blood pressure following a single large 2%v/w) haemorrhage in anaesthetized male Long Evans (LE) rats and females of the same strain during either pro-oestrous or di-oestrous phases of the reproductive cycle. In addition the same recovery process was examined in Brattleboro rats with diabetes insipidus (BDI) lacking circulating vasopressin. All BDI rats had an impaired blood pressure recovery following haemorrhage compared with male rats of the parent LE strain, and this was irrespective of sex or stage of the oestrous cycle. While the blood pressure recovery was more impaired in both groups of BDI female rats than in the males of the same strain during the first 20 min after haemorrhage (both comparisons p < 0.001: ANOVA), there was no difference between the recoveries of the female rats in pro-oestrus or di-oestrus. In contrast a significantly impaired blood pressure recovery was observed in female LE rats at pro-oestrus, when circulating ovarian steroid concentrations are raised, compared with male (p < 0.001; ANOVA) and di-oestrous (p < 0.02; ANOVA) rats of the same strain. Heart rate responses to haemorrhage showed strain differences, with LE rats having initial decreased heart rates followed by a recovery process, while the heart rate responses of BDI rats increased immediately. The novel use of the female Brattleboro rat in this study provides evidence for the existence of an important inhibitory interaction between ovarian steroids and vasopressin during the blood pressure recovery phase following haemorrhage, and indicates a possible direct influence of gonadal steroids on the recovery process.
JF Laycock, Department of Physiology, Charing Cross & Westminster Medical School, Fulham Palace Rd, London W6 8RF, UK
Angiotensin II receptors: protein and gene structures, expression and potential pathological involvements
Authors: Clauser E , Curnow KM , Davies E , Conchon S , Teutsch B , Vianello B , Monnot C , Corvol P 
Published: December 2008

Clauser E, Curnow KM, Davies E, Conchon S, Teutsch B, Vianello B, Monnot C, Corvol P. Angiotensin II receptors: protein and gene structures, expression and potential pathological involvements. Eur J Endocrinol 1996;134:403–11. ISSN 0804–4643
Two distinct types of cell-surface angiotensin II receptors (AT1 and AT2) have been defined pharmacologically and cDNAs encoding each type have been identified by expression cloning. These pharmacological studies showed the AT1 receptors to mediate all the known functions of angiotensin II in regulating salt and fluid homeostasis. Further complexity in the angiotensin II receptor system was revealed when homology cloning showed the existence of two AT1 subtypes in rodents and in situ hybridization and reverse transcription-polymerase chain reaction analyses showed their level of expression to be regulated differently in different tissues: AT1A is the principal receptor in the vessels, brain, kidney, lung, liver, adrenal gland and fetal pituitary, while AT1B predominates in the adult pituitary and is only expressed in specific regions of the adrenal gland (zona glomerulosa) and kidney (glomeruli). Expression of AT1A appears to be induced by angiotensin II in vascular smooth-muscle cells but is inhibited in the adrenal gland. Preliminary analysis of the AT1 promoters is also suggestive of a high degree of complexity in their regulation. Investigation of a potential role for altered AT1 receptor function has commenced at a genetic level in several diseases of the cardiovascular system. No mutations affecting the coding sequence have been identified in Conn adenoma and no linkage has been demonstrated with human hypertension by sib-pair analysis. None the less, certain polymorphisms that do not alter the protein structure have been found to be associated with hypertension and to occur at an increased frequency in conjunction with specific polymorphisms in the ACE gene in individuals at increased risk for myocardial infarction. Further characterization of the regions of the AT1 gene that regulate its expression are therefore needed. The physiological importance of the AT2 gene product still remains a matter of debate.
E Clauser, INSERM U36, Collège de France, 3 rue d'Ulm, 75005 Paris, France