bluuebunny/crossref_metadata_2025_split huggingface dataset:
RESPONSES OF NEUROHYPOPHYSIAL PEPTIDES TO HYPERTONIC SALINE AND INSULIN‐INDUCED HYPOGLYCAEMIA IN MAN
Authors: NUSSEY S. S. , ANG V. T. Y. , FINER N. , JENKINS J. S. 
Published: March 2008

SUMMARYIn order to investigate the possible role of oxytocin in osmoregulation and its response to stress, plasma immunoreactive oxytocin was measured during hypertonic saline infusion and insulin‐induced hypoglycaemia in a group of normal subjects, four patients with idiopathic diabetes insipidus and one patient with DIDMOAD syndrome (the syndrome of diabetes insipidus, diabetes mellitus, optic atrophy and deafness). The results were compared with those of plasma immunoreactive vasopressin to the same stimuli. As expected, there was a rise in plasma vasopressin in the normal subjects to both tests: this was absent in the patients with diabetes insipidus. Plasma oxytocin did not rise during hypertonic saline infusion in either group of subjects. The response of oxytocin to insulin‐induced hypoglycaemia (0.15 U/kg soluble insulin) in normal subjects was much more variable. One highly symptomatic volunteer showed a marked rise in oxytocin. Two subjects also showed a rise when retested with 0.19 U/kg soluble insulin. There was no response of oxytocin to a standard‐dose insulin test in the patients with diabetes insipidus. The data suggest that, in man, oxytocin is not involved in osmoregulation but that it may be secreted in response to marked hypoglycaemia.
THE EFFECT OF AMIODARONE ON THYROXINE KINETICS
Authors: PEARCE C. J. , HIMSWORTH R. L. 
Published: March 2008

SUMMARYAmiodarone was given by daily intraperitoneal injection (10 mg/kg body weight) to a group of 11 New Zealand white rabbits. Over 6 weeks there were significant increases (P<0–01) in plasma total T4 concentration (43±8 to 60±13 nmol/1; mean±l SD) and rT3 concentration (0.12±0.06 to 0.31 ± 0.16 nmol/1) and a significant fall in total plasma T3 (2.3±0.3 to 1.7 ± 0.2 nmol/1). The plasma clearance of T4 in rabbits treated with amiodarone for 6 weeks was significantly reduced relative to controls (64 ± 25 vs 109 ± 19 ml/kg per day, P<0.01) but the production rate was unchanged (3.8±1.8 vs 3.7±1.4 nmol/kg per day). In the amiodarone treated animals the increased plasma T4 concentration was entirely accounted for by the reduced clearance. It is inferred that the normal output of T4 by the thyroid is pituitary dependent and that TSH secretion is sustained in the presence of hyperthyroxinaemia because of amiodarone induced partial inhibition of T4 utilization by the thyrotroph.
HYPERPROLACTINAEMIA IN CONGENITAL HYPOTHYROIDISM
Authors: McCORMICK K. L. 
Published: March 2008

SUMMARYSerum prolactin concentrations were measured in nine untreated hypothyroid infants and 23 euthyroid controls. In the former group the serum prolactin concentrations were tenfold higher than the controls (352 vs 34 μg/1), declining gradually upon treatment. Although serum prolactin concentrations can be mildly elevated in adults with hypothyroidism, congenital hypothyroidism causes a profound and probably uniform hyperprolactinaemia; furthermore, the hormone concentration correlates directly with the simultaneous TSH concentration. The physiological importance, if any, of the hyperprolactinaemia in the fetus or neonate is uncertain.
INFLUENCE OF DOPAMINERGIC, ADRENERGIC AND CHOLINERGIC BLOCKADE AND TRH ADMINISTRATION ON GH RESPONSES TO GRF 1–29
Authors: JORDAN V. , DIEGUEZ C. , LAFAFFIAN I. , RODRIGUEZ‐ARNAO M. D. , GOMEZ‐PAN A. , HALL R. , SCANLON M. F. 
Published: March 2008

SUMMARYIn order to establish the influence of dopaminergic, á‐adrenergic and cholinergic pathways on GRF‐mediated GH release we have studied the GH responses to GRF 1–29 (100 or 50 μg as i.v. bolus) alone and in combination with metoclopramide (MCP, 10 mg, i.v.), thymoxamine (THYM, 210 μg/min, 150 min infusion), and atropine (1.2 mg, i.v.). We have also investigated any possible interaction between TRH and GRF in view of the reported inhibitory effects of TRH infusion on stimulated GH release. Dopaminergic and á‐adrenergic blockade with MCP and THYM respectively, did not have any effect on the GH responses to GRF. This lack of effect strongly suggests that any action which these neurotransmitters may exert on GH secretion is not at a pituitary level. TRH did not modify the GH response to GRF suggesting that the inhibitory effect on stimulted GH secretion is exerted at a hypothalamic level. In contrast, GH responses to GRF were significantly reduced by prior administration of atropine. These data support the view that cholinergic pathways play an important role in the regulation of GH secretion and such control may be exerted at both hypothalamic and pituitary levels.
FAMILIAL CUSHING'S SYNDROME DUE TO NODULAR ADRENOCORTICAL DYSPLASIA. A PUTATIVE RECEPTOR‐ANTIBODY DISEASE?
Authors: VAN BERKHOUT F. TEDING , CROUGHS R. J. M. , KATER L. , SCHUURMAN H. J. , MEYLING F. J. H. GMELIG , KOOYMAN C. D. , VAN DER GAAG R. D. , JOLINK D. , DREXHAGE H. A. 
Published: March 2008

SUMMARYTwo sisters aged 13 and 19 years suffering from familial Cushing's syndrome due to nodular adrenocortical dysplasia are described. Pituitary adrenocortical function tests indicated the presence of adrenal autonomy. Adrenal scintigraphy showed bilateral symmetrical uptake indicating the bilateral character of the autonomous process. Complete adrenalectomy was performed in both girls. The adrenals were of about normal weight showing numerous dark brown pigmented nodules and small perivascular lymphocytic infiltrates. Serum immunoglobulin preparations obtained from both girls stimulated adrenocortical cell growth in a cytochemical bioassay system. It is proposed that circulating growth factors may be involved in the pathogenesis of the disease.
PSEUDOHYPOALDOSTERONISM: DECREASED ALDOSTERONE LEVELS WITH AGE WITHOUT SIGNIFICANT CHANGE IN URINARY SODIUM EXCRETION
Authors: YASUDA T. , NODA‐CHO H. , NISHIOKA T. , SASAKI N. , NIIMI H. , NAKAJIMA H. 
Published: March 2008

SUMMARYTo clarify age‐related changes in the plasma renin activity (PRA)‐aldosterone (ALDO) system in relation to urinary sodium (Na) excretion in pseudohypoal‐dosteronism type I (PHA), we followed a patient with PHA serially by measuring the hormonal balance and urinary electrolyte excretion for 5 years. The patient was diagnosed as PHA mainly on the basis of extremely high PRA (170 ng/ml/h) and ALDO (1670 ng/dl) despite massive urinary Na excretion, a normal ALDO/PRA ratio (mean value = 11), and the ineffectiveness of 9a‐fluorocortisol (Florinef) to reduce urinary Na excretion and PRA‐ALDO. The pattern of reduction in PRA‐ALDO with age in this patient was almost identical with that of normal infants and children and was most remarkable during the first 18 months of life. During this period, there were statistically significant correlations between age and each of the following values: PRA (r=−0.753, n= 9, P<0.05), ALDO (r=−0.736, n= 11, P<0.01) and urinary ALDO excretion (r=−0.840, n= 9, P<0.01). But the reduction of PRA‐ALDO in this patient was not the result of increased urinary Na excretion with age. Although PRA and ALDO values in this patient did decrease with age, they were still high compared with age‐matched controls, suggesting a marginal state of Na balance. Thus, we conclude that PRA‐ALDO levels in PHA decrease with age in the same pattern as in normal infants and children without a significant change in urinary Na excretion, possibly through increased renal conservation of Na, the mechanism of which should be clarified in a future study.
NALOXONE PROVOKES CATECHOLAMINE RELEASE IN PHAEOCHROMOCYTOMAS AND PARAGANGLIOMAS
Authors: BOULOUX P.‐M. G. , GROSSMAN A. , BESSER G. M. 
Published: March 2008

SUMMARYThe effects of low‐ (2 mg) and high–dose (10 mg) intravenous naloxone administration on circulating plasma catecholamines in four patients with proven and two patients with suspected phaeochromocytomas have been evaluated. In three out of four patients with confirmed phaeochromocytomas or paragangliomas, 10 mg naloxone resulted in a marked rise (290–575%) in circulating noradrenaline; despite combined alpha and beta‐adrenoceptor blockade, in two out of four cases systolic and diastolic pressures rose whilst pulse rate fell. No response was seen to 2 mg naloxone in any patient. No humoral or pressor response was obtained in the fourth patient, who may have been secreting maximal levels of plasma noradrenaline at the time of study. In the two patients with suspected phaeochromocytoma, there was no response to naloxone: further investigations failed to reveal a source of abnormal catecholamine secretion in these patients. It is concluded that naloxone represents a new pharmacological agent which can provoke catecholamine release in patients with phaeochromocytomas; in such patients, endogenous opioids may regulate catecholamine release either from the tumour itself or from the enhanced peripheral catecholamine stores.
THE ROLE OF IMMUNOPEROXIDASE TECHNIQUES ON PARAFFIN EMBEDDED TISSUE IN DETERMINING THE HISTOGENESIS OF UNDIFFERENTIATED THYROID NEOPLASMS
Authors: MYSKOW M. W. , KRAJEWSKI A. S. , DEWAR A. EDNA , MILLAR E. P. , MCLAREN KATHYRYN , FABRE J. W. 
Published: March 2008

SUMMARYTwenty cases of undifferentiated thyroid tumours were reviewed histologically. In seven cases the histogenesis was difficult to determine using morphological criteria. Immunohistochemical staining with a panel of antibodies to lymphoid and epithelial cells, including monoclonal antibodies directed against the leucocyte common antigen, cytokeratin, and epithelial membrane antigen confirmed that four of these cases were lymphomas and that one was a medullary carcinoma. In the remaining two cases immunohistochemistry was unhelpful. In the thirteen histologically typical tumours, the immunohistochemical profile was in keeping with their histogenesis as determined by morphological criteria. Immunohistochemical staining with a panel of selected antibodies allows the reliable diagnosis of undifferentiated thyroid neoplasms, when this cannot be reached using routine histological techniques.
3,5‐DIIODOTYROSINE AND THYRONINE IN THE URINE OF PATIENTS WITH CHRONIC RENAL DISEASE
Authors: RAMSDEN D. B. , FARMER M. , MOHAMMED M. N. , Gonigle R. S. S. Mc , SHEPPARD M. C. 
Published: March 2008

SUMMARYUrinary 3,5‐diiodotyrosine (DIT) and thyronine (T0) excretion was investigated in 18 patients with chronic renal disease. In accord with previous findings serum T4 and thyroid hormone binding proteins measured in 17 patients were in the low or normal range. Urinary albumin excretion was elevated in all 18 and T4 binding prealbumin (TBPA) in 15 of the 18. Urinary T0 excretion measured in 12 patients was also significantly lower than normal (mean±SD 4.4±2.6 vs 15.8±5.8 nmol/24 h renal vs normal 2 P<0.001). In contrast urinary DIT excretion was significantly elevated in renal patients compared with normal subjects (2.0±1.5 vs 0.75±0.41 nmol/24 h, respectively). Possible sources of the increased DIT are discussed.
PARENTERAL BROMOCRIPTINE IN THE TREATMENT OF HORMONALLY ACTIVE PITUITARY TUMOURS
Authors: BENKER G. , GIESHOFF B. , FREUNDLIEB O. , WINDECK R. , SCHULTE H. M. , LANCRANJAN IONA , REINWEIN D. 
Published: March 2008

SUMMARYEleven patients with PRL and three with GH‐secreting pituitary adenomas were treated with a single intramuscular injection of 50 mg of bromocriptine retard (Parlodel, LA (long‐acting)). There was a marked PRL suppression in 9 prolactinoma patients, in four for a period of at least 6 weeks. In one patient with acromegaly GH plasma levels decreased into the normal range. The size of the pituitary adenoma diminished considerably, as shown by CT scan, in three out of the 9 responding patients with prolactinoma and in the above acromegalic patient. Visual fields normalized within 14 d in one patient with a PRL‐secreting macroadenoma and bitemporal hemianopsia who also had CT scan‐documented shrinkage of the tumour. There were no side‐effects except slight hypotension in two and local tenderness at the injection site in one patient; these symptoms disappeared without treatment. It is concluded that bromocriptine retard is a safe and effective therapeutic tool for shrinking hormonally active pituitary tumours in selected patients. Due to its good tolerance and the rapid hormonal and clinical improvement it may be also considered as the best therapeutic approach to initiate the treatment of PRL‐ and/or GH‐secreting pituitary tumours.
SUPPRESSION OF PARATHYROID HORMONE INHIBITORY ACTIVITY OF PLASMA IN PSEUDOHYPOPARATHYROIDISM TYPE I BY IV CALCIUM
Authors: LOVERIDGE N. , FISCHER J. A. , DEVOGELAER J.‐P. , DE DEUXCHAISNES C. NAGANT 
Published: March 2008

SUMMARYThe biological response, as measured in the cytochemical bioassay, to the high circulating levels of immunoreactive parathyroid hormone (iPTH) in patients with pseudohypoparathyroidism type I (PSPI) is affected by the presence of an endogenous inhibitor. This is evidenced by the reduced recovery of the biological activity of PTH added to the plasma. Here we have used i.v. calcium infusion to inhibit the release of PTH and studied endogenous PTH bioactivity and immunoreactivity as well as the recovery of the bioactivity of added PTH in a normal subject and two patients with PSPI. In the control subject both bioactive PTH (bioPTH) and iPTH fell in response to the increased levels of plasma calcium and the recovery of the biological activity of PTH added to the plasma remained unchanged. In the PSPI patients, although the level of iPTH fell, the level of bioPTH remained unchanged. However, the level of inhibitory activity of the plasma, as determined by the recovery of added PTH, was transiently normalized in response to the rise in plasma calcium. Thus i.v. calcium infusions not only suppress the release of endogenous iPTH but also the inhibitory activity present in the plasma of PSPI patients.
IMMUNOLOGICAL DISTURBANCES IN PATIENTS WITH PREMATURE OVARIAN FAILURE
Authors: PEKONEN F. , SIEGBERG R. , MÄKINEN T. , MIETTINEN A. , YLI‐KORKALA O. 
Published: March 2008

SUMMARYEighteen patients with postmenopausal gonadotrophin levels and secondary amenorrhoea before the age of 35 years (premature ovarian failure, POF) were examined for the presence of cellular and humoral immune defects. Six patients had an abnormally low natural killer (NK) cell activity. The levels of circulating immune complexes were increased in six patients. Tissue antibodies were detected in six patients and two of these possessed ovarian antibodies. Leukocyte migration inhibition in the presence of ovarian antigen was slightly enhanced in three patients. Altogether 12 patients (66%) with POF had some immunological defect or defects suggesting that immune mechanisms are often involved in the aetiology of POF.
THYROID AUTOANTIBODIES IN HLA‐GENOTYPED TYPE 1 DIABETIC FAMILIES: SEX‐LIMITED DR5 ASSOCIATION WITH THYROID MICROSOMAL ANTIBODY
Authors: ROMAN SHEILA H. , DAVIES T. F. , WITT MARY E. , GINSBERG‐FELLNER FREDDA , RUBINSTEIN P. 
Published: March 2008

SUMMARYThyroid autoantibodies are common in Type I diabetics and their first degree relatives and may be part of the autoimmune diathesis present within such families. We have measured the prevalence of microsomal (M‐Ab) and thyroglobulin (Tg‐Ab) autoantibodies in 84 HLA‐typed families having a Type 1 diabetic child, using enzyme‐linked immunosorbent assay techniques. Thyroid autoantibodies were detectable in 201/407 (49%) individuals in these families. Both autoantibodies were significantly more frequent in the subsets of parents, diabetic children and their non‐diabetic siblings than in groups of control adults and children. The prevalence of these autoantibodies in the diabetic families was increased in both sexes with a female:male ratio of 1.4:1. Antigen DR5 was significantly associated with M‐Ab production but only for male subjects (P= 0.005 after correction for the number of DR antigens tested). No significant associations were encountered for Tg‐Ab. Within‐family analyses indicated that thyroid autoantibodies occurred with increased prevalence in HLA‐identical or haplo‐identical siblings of autoantibody‐positive index cases in comparison to control children. We conclude (1) the DR association with thyroid autoantibody production in this diabetes‐selected population was thyroiditis‐related and not diabetes‐related, and (2) the DR5 association was restricted to males and the production of M‐Ab. These data are consistent with the hypothesis that multiple genetic and non‐genetic factors played a role in the high prevalence of thyroid autoantibodies in this population.
TSH RECEPTOR ANTIBODY INDUCTION OF THYROGLOBULIN RELEASE FROM HUMAN THYROID CELL MONOLAYERS
Authors: FELDMAN A. , SCHWARTZ A. E. , FRIEDMAN E. W. , DAVIES T. F. 
Published: March 2008

SUMMARYWe investigated the influence of TSH receptor antibody (TRA), as detected by inhibition of 125I‐bTSH binding to detergent solubilized porcine TSH receptors, on in‐vitro thyroglobulin (hTg) production using normal thyroid cells in monolayer. Secretion of hTg into the culture medium was analysed by a noncompetitive enzyme immunosorbent (ELISA) technique utilizing two murine monoclonal antibodies. Basal hTg release (mean ± SD 124 ± 27 ng/105 cells/6 d, n= 5) was stimulated by bTSH (10, 102, 103μU/ml) in a dose related manner (mean ± SD 191 ±24, 587 ±80, 695 ±66 ng/105 cells/6 d, respectively). IgG (2 mg/ml) from seven patients with hyperthyroid Graves' disease, and known titres of TRA, similarly enhanced production of hTg, in a dose and time‐dependent manner, when compared to control IgG. The degree of induction varied from a 140–230% increase in total hTg release over a 6‐day incubation period. There was a direct correlation between the degree of 125I‐bTSH binding inhibitory activity and the hTg response (r= 0.9, P < 001). These data demonstrate that TSH receptor antibodies enhance hTg release from human thyroid cell monolayers and allow an assessment to be made of antibody‐activated post receptor mechanisms.
INSULIN‐LIKE GROWTH FACTOR I (IGF‐I) IN HEALTHY CHILDREN, ADOLESCENTS AND ADULTS AS DETERMINED BY A RADIOIMMUNOASSAY SPECIFIC FOR THE SYNTHETIC 53–70 PEPTIDE REGION
Authors: SILBERGELD A. , LITWIN A. , BRUCHIS S. , VARSANO I. , LARON Z. 
Published: March 2008

SUMMARYA radioimmunoassay (RIA) specific for the synthetic 53–70 peptide region of human insulin‐like growth factor I (IGF‐I) was used to determine IGF‐I in the serum of 191 healthy newborns, children and adolescents and in 26 adults. The results compare favourably with reported values obtained using RIA systems for the native IGF‐I molecule. Intra‐ and inter‐assay CV were 3.3 and 7.2% respectively. In childhood, mean ± SD IGF‐I levels rise from 60 ± 3.5 nmol/l in newborns to 16.5±4.0 nmol/l at 8–11 years in both sexes. At the onset of puberty, IGF‐I levels in females (24.9 ± 6.6 nmol/l) are significantly (P > 0.005) higher than in males (17.2 ± 4.2 nmol/l). With further pubertal development IGF‐I levels continue to rise, reaching peak values at pubertal stage P4 (40.6 ± 4.5 nmol/l in males, 42.8 ± 5.1 nmol/l in females) and decline thereafter to lower values during adulthood: 16.5 ± 5.8 nmol/l (males) and 24.2 ± 7.0 nmol/l (females) (P > 0.001). In pubertal males, IGF‐I correlates significantly with height (r= 0.66, P < 0.001), bone age (r= 0.69, P > 0.001) and growth velocity (r= 0.64, P= 0.025) as well as with testosterone levels (r= 0.69, P < 0.001). In pubertal females a significant correlation is found between IGF‐I and height (r= 0.55, P < 0.020). The ready availability of a simple, precise and reproducible IGF‐I RIA, should contribute much to evaluating the importance of IGF‐I measurements in normal growth and in the diagnosis and therapy of various growth disorders.
THE EFFECT OF OVINE CORTICOTROPHIN RELEASING FACTOR (oCRF), BROMOCRIPTINE AND TRH ON THE SECRETION OF ACTH AND α‐MSH IN NELSON'S SYNDROME AND CUSHING'S DISEASE
Authors: ABRAHAM R. R. , CAMPBELL E. A. , GILLHAM B. , THODY A. J. , ALTAHER A. R. H. , PRYSOR‐JONES A. , WYNN V. , JONES M. T. , JENKINS J. 
Published: March 2008

SUMMARYThe circulating levels of ACTH and α‐melanocyte stimulating hormone (α‐MSH) were measured in 9 patients with Nelson's syndrome after the administration of saline, ovine corticotrophin releasing factor (oCRF), bromocriptine or TRH. The concentrations of ACTH were grossly elevated and α‐MSH levels ranged from undetectable to higher than the normal range. In seven of eight subjects there was a rapid corticotrophic response, but no change in the α‐MSH level, following oCRF. This response was delayed in one subject. Following oCRF injection, the plasma oCRF profile was variable but circulating oCRF was detectable even at the end of the experiment in all cases. There was no significant change in circulating ACTH or α‐MSH following either bromocriptine or TRH. Cultured tumour cells from one case of Cushing's disease showed a corticotrophic response but no change in α‐MSH to oCRF and the response was enhanced by vasopressin. Bromocriptine added to the same tumour depressed ACTH secretion without affecting the output of α‐MSH. The present data suggest that the tumours in these subjects are responsive to oCRF and arise from corticotrophs rather than melanotrophs.
ADRENERGIC ACTIVITY AND ALDOSTERONE REGULATION: NO EVIDENCE FOR AN ALPHA‐1 ADRENOCEPTOR‐MEDIATED INFLUENCE IN NORMAL SUBJECTS
Authors: BIANCHETTI L. , FERRIER C. , BERETTA‐PICCOLI C. , FRASER R. , MORTON J. J. , ZIEGLER W. H. 
Published: March 2008

SUMMARYIn normal man the sympathetic nervous system could exert an inhibitory influence on aldosterone responsiveness to angiotensin II. The possible role of alpha‐1 adrenoceptors in the modulation of aldosterone response was assessed by studying the changes of plasma aldosterone during infusion of angiotensin II at the doses of 1, 2, 5 and 10 ng/kg.min or after 1–24corticotrophin injection, 0.25 mg, in 9 normal subjects before and after treatment with the selective alpha‐1 adrenoceptor antagonist, prazosin. Prazosin, given during 3 weeks, did not modify supine arterial pressure, heart rate and the plasma levels of angiotensin II, renin, aldosterone or adrenaline but caused a significant (P < 005) increase of plasma noradrenaline. The correlation relating plasma aldosterone to plasma angiotensin II levels before and during angiotensin II infusion and the response of plasma aldosterone to corticotrophin was not modified by prazosin. These findings suggest that in normal man there is no inhibitory influence of the noradrenergic system on aldosterone responsiveness to angiotensin II mediated by an alpha‐1 dependent mechanism.