bluuebunny/crossref_metadata_2025_split huggingface dataset:
INTERACTION OF THYROTROPHIN RELEASING HORMONE AND THE ENKEPHALIN ANALOGUE DAMME ON PITUITARY HORMONE SECRETION
Authors: PICÓ A. , CACICEDO L. , VARELA C. , SáNCHEZ‐FRANCO F. 
Published: March 2008

SUMMARYBecause TRH counteracts the inhibitory effect of opiate peptides on LH secretion in cultured cells from normal pituitaries, six normal postmenopausal women were studied to determine whether TRH interacts in vivo with opioid peptides in the regulation of pituitary hormone secretion. At two different times a constant 3 h infusion of either saline or TRH (5 μg/min) was initiated. At 60 min a 250 μg bolus of the opiate agonist peptide D‐AIa2‐MePhe4‐metenkephalin‐0‐ol (DAMME) was injected in one of the two saline and TRH infusion tests. The four treatments, i.e. saline infusion alone, saline infusion with a DAMME bolus, TRH infusion alone; and TRH infusion with DAMME bolus were given at random with an interval of at least 7 d. Blood samples were taken every 15 min during the 3 h study. DAMME induced a significant fall (P < 0.05) in serum LH (from 35±8.5 to 18.3±5.1 mlU/ml) (mean±SEM) without significantly affecting FSH levels (from 29 ± 11.2 to 26.9 ± 12.4 mlU/ml). These changes were not antagonized by the continuous infusion of TRH. PRL had a monophasic response pattern to continuous isolated TRH infusion; the basal levels increased from 4.2 ± 1.2 to 24.5 ± 6.8 ng/ml at 30 min and then slowly decreased with a plateau from 90 min until the end of the study. DAMME administration at 60 min induced a significant second peak of PRL secretion (44±6.5 ng/ml) 30 min later (P < 005). Basal serum TSH levels increased progressively during the first 135 min of TRH infusion (from 2.4 ± 0.5 to 18.5 ± 5.2 μU/ml), and then remained stable until the end of treatment. DAMME induced an even more striking TSH response 30 min after its administration at 60 min (P < 0.05), which was later maintained. In the absence of TRH infusion, DAMME administration did not modify either PRL or TSH basal levels. GH values did not significantly change during saline or TRH infusion alone, nor after DAMME i.v. administration at 60 min in either test. These findings are against an antagonistic effect of TRH and opioid peptides on the regulation of pituitary hormones in postmenopausal women. DAMME potentiating activity on PRL and TSH stimulatory action of continuous TRH infusion is shown. Also confirmed is the inhibitory effect of DAMME on LH secretion in postmenopausal women. Some of these effects may at least partially be mediated by the opiate inhibition of dopamine secretion.
CHANGES IN THYROID‐STIMULATING AND TSH‐BINDING INHIBITORY ACTIVITIES IN A PATIENT WHO DEVELOPED HYPERTHYROIDISM DUE TO GRAVES' DISEASE FOLLOWING PRIMARY HYPOTHYROIDISM
Authors: KASAGI K. , KONISHI J. , IIDA Y. , MORI T. , TORIZUKA K. 
Published: March 2008

SUMMARYA 23‐year‐oid female who developed thyrotoxic Graves' disease following primary hypothyroidism was reported. She presented with symptoms of hypothyroidism and slight exophthalmos. After primary hypothyroidism was confirmed, she was treated with T4 in a dose of 50 μg/d. Two months after delivery, 1 year after the initial diagnosis of hypothyroidism, hyperthyroidism developed while she was taking T4. Graves' disease was confirmed by persistent thyrotoxicosis, high 99mTc thyroidal uptake, negative T3 suppressibility and detection of TSH‐receptor antibodies. During the hypothyroid phase, TSH‐binding inhibitory immunoglobulins (TBII) could not be detected, while thyroid stimulating antibodies (TSAb) were positive showing between 5.8 and 90 fold increases in the amount of cAMP produced in cultured porcine thyroid cells. Her IgG did not inhibit TSH‐induced cAMP increase in vitro. When she developed hyperthyroidism, TSAb activity became more potent (31.7 fold increase in cAMP) and TBII became positive (+61.3%).
PROLONGED LOW‐INTENSITY EXERCISE RAISES THE SERUM PARATHYROID HORMONE LEVELS
Authors: LJUNGHALL S. , JOBORN H. , ROXIN L.‐E. , RASTAD J. , WIDE L. , ÅKERSTRÖM G. 
Published: March 2008

SUMMARYTwelve healthy males performed 5 h exercise on a bicycle ergometer at a constant work load of approximately 50% of their maximum capacity. The serum concentrations of parathyroid hormone (PTH) increased after the first hour and were continuously elevated throughout the exercise period. The rise in PTH was 5–7% above pre‐exercise levels, corresponding to 20–30% of the maximal increase obtained by the same assay during prolonged hypocalcaemia. The probable cause for the rise in PTH was that the plasma ionized calcium tended to be lowered during exercise. Since the total serum calcium concentrations were raised (by 3–5%) during exercise the reduction of the free, ionized, fraction was presumably largely due to increased complex‐binding although an outward transport from plasma was not excluded. The serum concentrations of magnesium were gradually reduced during exercise while those of phosphate and potassium were raised throughout, probably as a result of leakage from the working muscle.
ASYMPTOMATIC HYPERPROLACTINAEMIA AND PROLACTINOMA IN THE GENERAL POPULATION—MASS SCREENING BY PAIRED ASSAYS OF SERUM PROLACTIN
Authors: MIYAI K. , ICHIHARA K. , KONDO K. , MORI S. 
Published: March 2008

SUMMARYA total of 10 550 ‘normal’ adults (8450 men and 2100 women) in the general population were screened by a paired assay method for serum PRL and 40 subjects with hyperprolactinaemia (>75 μg/1) were detected. Of these, five patients (three men and two women) with pituitary prolactinoma, one man with empty sella syndrome, 10 cases of ‘big’ prolactinaemia, seven pregnant women and 13 subjects with drug‐induced hyperprolactinaemia were found. The patients with prolactinoma had few if any complaints (asymptomatic prolactinoma).
NON‐FUNCTIONING PITUITARY ADENOMAS DO NOT REGRESS DURING BROMOCRIPTINE THERAPY BUT POSSESS MEMBRANE‐BOUND DOPAMINE RECEPTORS WHICH BIND BROMOCRIPTINE
Authors: BEVAN J. S. , BURKE C. W. 
Published: March 2008

SUMMARYDopaminergic binding to membranes from 20 well‐characterized non‐functioning pituitary tumours was investigated using the radioligand [3H]spiperone; nine had failed to regress during pre‐operative bromocriptine therapy. Five macro‐prolactinomas and six normal pituitaries were similarly investigated. High affinity dopaminergic binding sites were defined in all tissues studied. Mean dissociation constants were similar for the three groups (0.92, 0.55 and 0.51 nmol/l, respectively) but mean site numbers were greater in the prolactinomas (698) than in non‐functioning tumours (131) or normal pituitaries (136 fmol/mg protein). In a pool of non‐functioning tumour membranes ligand competition experiments confirmed that binding was dopaminergic. Stereospecificity was demonstrated using the (+) and (−) isomers of butaclamol. Bromocriptine was present in three non‐functioning tumours that had been exposed to the drug within 24 h of surgery and it largely prevented [3H]spiperone binding; membrane washing restored [3H]spiperone binding to control values. We conclude that non‐functioning tumours possess high affinity membrane‐bound dopaminergic binding sites similar to those in normal pituitary and macroprolactinomas, but apparently fewer in number than in the latter. Though bromocriptine binds to dopamine receptors on non‐functioning tumours in vivo, this does not result in tumour regression.
EFFECT OF INJECTION SITE ON THE PHARMACOKINETICS AND PHARMACODYNAMICS OF SUBCUTANEOUSLY ADMINISTERED LUTEINIZING HORMONE RELEASING HORMONE
Authors: BLUNT S. M. , CLAYTON R. N. , BUTT W. R. 
Published: March 2008

SUMMARYSerum concentrations of LHRH and the subsequent LH responses were compared following s.c. injections of 20 μg LHRH into the upper arm and the lower abdominal wall, in 9 hypogonadal women responsive to pulsatile LHRH therapy. Tests were carried out at the two sites in random order. Peak LHRH concentrations were reached by 5 min after upper arm and by 20 min after lower abdominal wall injections, the maximum concentrations being significantly greater following injections into the former. There was no increase in LH until 10 min and then maximum concentrations were reached at 30 min following injection into both sites. There was no significant correlation between the LHRH increments and the LH response but there was a negative correlation between the Ponderal Index of the patients and the LHRH increments following injections into the lower abdominal wall only. There was no significant overall difference between the LH increments related to the site of injection, but the order of injections affected the responses. When upper arm injections were given first the LH responses were significantly greater, but when lower abdominal wall was injected first the subsequent responses to upper arm injections were impaired. A possible reason for this is that the absorption from the lower abdominal wall was delayed so prolonging the exposure of the pituitary gonadotrophs to LHRH, resulting in pituitary desensitization at the time of the second test.
DOSAGE‐RELATED EFFECTS OF DANAZOL ON SEX HORMONE BINDING GLOBULIN AND FREE AND TOTAL ANDROGEN LEVELS
Authors: FORBES K. L. , DOWSETT M. , ROSE GILLIAN L. , MUDGE JOANNE E. , JEFFCOATE S. L. 
Published: March 2008

SUMMARYDanazol is known to cause marked suppression of sex hormone binding globulin (SHBG) levels in plasma and to increase the proportion of plasma testosterone unbound to protein but the effect on the concentration of total and free testosterone is unclear. Twenty‐five patients with endometriosis were treated daily for 6 months with doses of danazol ranging from 50 to 600 mg. The fall in SHBG and rise in percent free testosterone was dose‐related during the early part of treatment. Suppression of total testosterone and 5α‐dihydrotestos‐terone levels occurred and was probably due to increases in metabolic clearance rates. The observed fall in androstenedione levels was related to the incidence of menstrual abnormality, suggesting that this might be due to reduced ovarian activity. The concentration of free testosterone increased by a factor of two in the first week but subsequently returned to levels of between 25 and 50% above pretreatment levels. This pattern of changes may be due to the rise in metabolic clearance rates being dependent on induction of enzymes of androgen metabolism.
INCREASED CIRCULATING RADIORECEPTOR‐ACTIVE GROWTH HORMONE IN INSULIN‐DEPENDENT DIABETICS
Authors: MACFARLANE I. A. , STAFFORD S. M. , WRIGHT A. D. 
Published: March 2008

SUMMARYA radioreceptor assay (RRA) for GH, using pregnant rabbit liver membranes, was used to evaluate the receptor‐hormone interaction of circulating (serum) GH in diabetics. Multiple morning blood samples were taken from 18 fasted insulin‐dependent diabetics on three occasions and assayed for GH by the RRA and radioimmunoassay (RIA). Samples from 12 normal subjects (GH secretion stimulated by exercise and hypoglycaemia) and 11 acromegalics were also studied. The RRA/RIA ratio was higher in samples from the acromegalics than in normal subjects (0.85 vs 0.65, P < 0.01) and only a few samples had RRA values greater than RIA. All the samples from 14 of the diabetics had lower RRA values than RIA, but 40% (39 of 96) of samples from the remaining four diabetics had RRA concentrations markedly in excess of the levels measured by RIA. Sephadex chromatography (G100) of serum samples revealed similar proportions of immunoreactive GH forms in the diabetics with high RRA values compared with the diabetics with low RRA values. These findings may indicate intermittent secretion of highly bioactive GH in some insulin‐dependent diabetics. Further studies on the biological properties of circulating GH are needed to clarify the role of GH secretion in the development of diabetic microvascular complications.
VITAMIN D NUTRITION AND VITAMIN D METABOLISM IN THE PREMATURE HUMAN NEONATE
Authors: MAWER E. BARBARA , STANBURY S. W. , ROBINSON M. J. , JAMES J. , CLOSE C. 
Published: March 2008

SUMMARYThe effect of supplementation with daily doses of vitamin D2 (1000 IU or 3000 IU, 25–75 μg, 63–189 nmol) has been studied in 39 premature neonates, initial gestational age 25–32 weeks. The initial mean plasma 25‐hydroxyvitamin D was 25.8 nmol/l (10.3 ng/ml) but in 12 infants, most of whom were born in the winter months, the level was < 15 nmol/l (6 ng/ml), and in seven babies plasma 1,25‐dihydroxyvitamin D was <48 pmol/l (20 pg/ml). These findings suggest a considerable degree of maternal vitamin D‐deficiency. Maximum attained concentrations of 25‐hydroxyvitamin D on treatment were 77.3 nmol/l (30.9 ng/ ml), high dose and 86.8 nmol/l (34.7 ng/ml), low dose; the mean rate of increase was greatest during the first two weeks (2.2 nmol/l/d; 0.88 ng/ml/d) and declined over the next 4 weeks. Mean maximum concentrations of 1,25‐dihydroxyvitamin D2 were 283 pmol/l, (121 pg/ml), high dose and 309 pmol/l (129 pg/ml), low dose. Apart from a minor contribution to the initial plasma 1,25‐dihydroxyvitamin D concentration, no effect of gestational age could be discerned in any of the measured variables. The endogenous pool of 1,25‐dihydroxyvitamin D3 decayed with a T of 22.5 d, indicating that vitamin D supplementation of these infants was necessary to avoid vitamin D‐deficiency.
CALCITONIN GENE‐RELATED PEPTIDE AND CALCITONIN IN MEDULLARY THYROID CARCINOMA
Authors: SCHIFTER S. , WILLIAMS E. D. , CRAIG R. K. , HANSEN H. H. 
Published: March 2008

SUMMARYWe have investigated the levels of serum calcitonin and calcitonin‐gene related peptide (CGRP) in 35 patients with well‐documented medullary thyroid carcinoma (MTC). Immunohistochemical investigations for calcitonin and CGRP have been performed on tumour tissue from 9 patients to clarify the cellular pattern of production. In four patients with aggressive disease, serum calcitonin and CGRP values have been monitored in relation to progression of disease after surgery. All 35 patients with MTC have elevated calcitonin and 26 elevated CGRP levels. Generally calcitonin values were found to be higher than those of CGRP, although the ratio of the two peptides varied from patient to patient. The immunohistochemical investigations corresponded with these findings, generally showing diffuse staining for calcitonin in MTC tumour‐cells and only a small number of CGRP positive cells. Calcitonin and CGRP are produced by alternative processing of the common precursor gene transcript. Our results suggest that absolute values of either calcitonin or CGRP in serum have no direct relationship to aggressiveness of disease. Thus whilst serum CGRP measurements appear to be a useful additional marker for the disease, they can be considered to be only a useful adjunct to serum calcitonin as a marker for tumour progression.
THE DIAGNOSTIC VALIDITY OF LOCAL AND TOTAL BONE MINERAL MEASUREMENTS IN POSTMENOPAUSAL OSTEOPOROSIS AND OSTEOARTHRITIS
Authors: NILAS LISBETH , GOTFREDSEN A. , RIIS B. J. , CHRISTIANSEN C. 
Published: March 2008

SUMMARYAssessment of different forms of prevention and treatment of bone mineral loss depends upon valid and precise methods to assess bone mass. We have here studied four groups of women: 45 healthy premenopausal women, 37 healthy postmenopausal women, 21 women with osteoarthritis and 20 with hip fractures. Bone mass was measured in the spine and total body by dual photon absorptiometry and in two forearm sites (proximal and distal bone mineral content (BMC) by single photon absorptiometry. The long‐term (1 year) reproducibility was 1.2% for proximal BMC, 1.6% for distal BMC, 5.5% for spinal BMC, and 21% for total body bone mass (TBBM). In the early postmenopausal years bone mass was mainly reduced in areas with a high content of trabecular bone. In elderly postmenopausal women and women with hip fractures bone mass was almost identical in all four sites studied. The osteoarthritic patients had an 18% reduction of bone mass in the forearms and in TBBM, whereas the spinal bone mass was only reduced by 6%. In all subgroups TBBM could be predicted from the forearm measurements with standard errors of estimates of 9–13%. When the osteoarthritic women were excluded spinal bone mass could be predicted from both forearm measurements with a standard error of 15% (r= 0.74). The distal forearm BMC seems to be a more accurate estimate of spinal bone mass than does the proximal measurement. Of the 20 patients with hip fracture 16 had a distal forearm value below the premenopausal normal range, whereas spinal bone mass was subnormal in only eight (P < 005). We conclude that bone loss is universal in patients with hip fracture and measurements of forearm bone mass will meet most clinical and research demands.
DOES SHORT‐TERM FASTING DESENSITIZE HUMAN SOMATOTROPHS TO ORAL L‐DOPA STIMULATION?
Authors: RÖJDMARK S. 
Published: March 2008

SUMMARYTo investigate whether short‐term fasting influences hormone release from human somatotrophs and lactotrophs, two oral L‐dopa tests, using 0.5 g L‐dopa, were carried out in seven normal subjects. The first test was performed after an overnight fast (8 h), the second after an additional 48 h of total food withdrawal. Basal blood glucose declined by 21 ±2% (mean ± SEM) between the two tests (P < 0001). Free T3 in serum (FT3) fell by 32 ±4% (P < 0001). GH responsiveness to L‐dopa—as reflected by the GH incremental area (ng/ml ± min)—decreased from 588 ± 162 to 24 ± 240 (P < 0.02). The latter response area did not even differ significantly from zero. Food deprivation failed to affect the lactotrophs, inasmuch as similar PRL decremental areas (ng/ml ± min) were obtained in response to L‐dopa before (704 ± 165) and after (686 ±128) the prolonged fast. In order to prevent blood glucose from falling significantly during the period of food deprivation eight additional normal subjects were given 9 small oral doses of glucose (each dose 0.5 g/kg) at regular intervals between the two L‐dopa tests. This resulted in similar FT3 concentrations before and after the prolonged fast. Furthermore, glucose supplementation restored normal GH responsiveness to L‐dopa, as evidenced by similar GH incremental areas before and after the glucose fast. These results imply that short‐term fasting desensitizes human somatotrophs to exogenous L‐dopa. The finding that the decreased GH responsiveness returns to normal if a decline in FT3 is prevented by oral glucose supplementation, suggests that changes in FT3 might contribute to the abolished GH responsiveness to L‐dopa in fasting.
RELATIONSHIP BETWEEN HUMAN PROSTATIC EPITHELIAL CELL PROTEIN SYNTHESIS AND TISSUE DIHYDROTESTOSTERONE LEVEL
Authors: GELLER J. , LIU J. , ALBERT J. , FAY W. , BERRY C. C. , WEIS P. 
Published: March 2008

SUMMARYTo evaluate the role of small amounts of prostatic tissue dihydrotesterone (DHT) as a stimulus to epithelial cell protein synthesis, we studied tissue from 27 patients given various androgen‐blocking drugs for 1 week before transurethral resection of the prostate (TURP) and measured epithelial protein synthesis and DHT levels in the tissue specimens. Test drugs before TURP included megestrol acetate 160 mg per day, with and without Tamoxifen 40 mg per day, or ketoconazole 1200 mg per day. The tissue was processed immediately and epithelial cells separated by digestion of tissue with 0.5% collagenase. After separation, epithelial cells were labelled with either 3H‐leucine or l‐35S‐methionine. The DHT level was measured in whole prostatic tissue. Megesterol acetate alone and with tamoxifen significantly decreased both the incorporation of 3H‐leucine into protein and the tissue concentration of DHT; megestrol acetate plus ketoconazole significantly decreased l‐35S‐methionine incorporation into protein and the DHT level. When the data correlating DHT with protein synthesis using both labelling techniques were combined, the curves were parallel and a strong correlation was noted between DHT and protein synthesis over a wide range of values (P < 0–001). These results suggest that in hormone‐dependent prostatic cancer even small amounts of prostatic DHT such as may occur from adrenal androgens following castration may significantly stimulate protein synthesis of the tumour epithelial cells.
HYPERMINERALOCORTICOIDISM DUE TO ADRENAL CARCINOMA: PLASMA CORTICOSTEROIDS and THEIR RESPONSE TO ACTH and ANGIOTENSIN II
Authors: ISLES C. G. , MACDOUGALL I. C. , LEVER A. F. , FRASER R. 
Published: March 2008

SUMMARYA 47‐year‐old female presented with hypertension, hypokalaemia, low plasma renin, high plasma aldosterone and was found to have a left adrenal tumour 4 cm in diameter by computerized tomography. Detailed biochemical studies showed high plasma levels of 11‐deoxycorticosterone and corticosterone in addition to aldosterone and 18‐hydroxycorticosterone, Basal 11‐deoxycorticosterone levels were particularly high. Corticosterone, 18‐hydroxycorticosterone and aldosterone concentrations were abnormally sensitive to infusions of ACTH and angiotensin II. Plasma Cortisol and assays for sex hormones were normal although there was evidence that Cortisol derived from the neoplasm. At operation a well‐differentiated adrenocortical carcinoma weighing 50 g (56 × 30 × 36 mm) was removed. There was no evidence of metastases following surgery. Adrenal function returned to normal. Review of the literature suggests that adrenocortical carcinoma should be suspected in patients who otherwise have typical features of Conn's syndrome, but whose tumours are more than 3 cm in diameter. Measurement of steroids such as 11‐deoxycorticosterone in addition to aldosterone is recommended since abnormally high values may also help to distinguish between hyperaldosteronism due to adenoma and carcinoma. Previously reported cases of isolated aldosterone production by a carcinoma cannot be substantiated.
DETERMINATION OF ENOLASE ISOZYMES IN VARIOUS ADRENAL GLAND TUMOURS
Authors: YONEDA M. , TAKATSUKI K. , YAMAUCHI K. , OISO Y. , TOMITA A. , MIZUNO S. , KATO K. 
Published: March 2008

SUMMARYEnolase isozymes (α enolase and γ enolase) in the extracts of adrenal tumours (phaeochromocytoma, adenoma of primary aldosteronism and Cushing's syndrome, and neurinoma) were determined by means of enzyme immunoassay systems. The mean ± SEM, respectively, of α and γ enolase levels were 2.5 ± 0.37 μg/mg protein and 3‐2 ± 0–69 μg/mg protein for 9 phaeochromocytomas, 15.2 + 3.1 μg/mg protein and 0.65 ± 0.18 μg/mg protein for three adenomas with primary aldosteronism, 10.8 ± 3.0 μg/mg protein and 0.23 ± 0.02 μg/mg protein for five adenomas causing Cushing's syndrome, and 3.8 ± 0.88 μg/mg protein and 0.30 ± 0.15 μg/mg protein for three neurinomas. Thus, the γ enolase concentration in the extract of phaeochromocytoma was higher than that of other adrenal tumours. The serum level of γ enolase was determined in 36 patients with adrenal tumours and 26 normal controls by radioimmunoassay. The mean + SEM of γ enolase level was 5.4 ± 0.3 ng/ml in normal controls, 91 ± 0.9 ng/ml for 10 patients with phaeochromocytoma, 6.3 ± 0.3 ng/ml for 11 with primary aldosteronism, 5.5 ± 0.4 ng/ml for 11 with Cushing's syndrome, and 5.1 ± 0.7 ng/ml for four with neurinoma. Thus, patients with phaeochromocytoma had a significantly higher serum γ enolase levels than did those with tumours derived from adrenal cortex and normal controls. In patients with phaeochromocytoma, serum γ enolase levels showed a significant positive correlation with urinary adrenaline levels (P<0.05), and after resection the elevated level of γ enolase fell significantly (P<0.05) and returned to normal. These results indicate that γ enolase in serum may be a useful marker for the differential diagnosis of adrenal tumours and therapeutic monitoring of phaeochromocytoma.