bluuebunny/crossref_metadata_2025_split huggingface dataset:
MONOAMINE OXIDASE (MAO) ACTIVITY AND ITS FORMS IN NORMAL AND PATHOLOGICAL HUMAN THYROID TISSUES
Authors: CABANILLAS A. M. , MASINI‐REPISO A. M. , COLEONI A. H. 
Published: March 2008

SUMMARYMonoamine oxidase (MAO) activity and its forms were measured in normal human thyroid glands (39 samples from necropsy and four from perinodular tissues) and in pathological thyroid glands (13 multinodular goitres, three carcinomas, seven chronic thyroiditis, five Graves’ disease and seven follicular, seven foetal and five embryonal adenomas). MAO activity in carcinomas was lower than in normal perinodular thyroid control tissue; in Graves’ disease, foetal and embryonal adenomas it was significantly higher than in the normal control. The use of clorgyline (a selective MAO A inhibitor) and deprenyl (selective MAO B inhibitor) allowed estimation of the relative proportion of MAO forms. A high proportion of MAO A (more than 90%) was observed, both in normal and in pathological thyroid tissues. Changes in total thyroid MAO activity, but not in its forms, were found in different pathologies of the thyroid gland.
STEROID RESPONSES TO ACTH IN WOMEN WITH POLYCYSTIC OVARIES
Authors: HAGUE W. M. , HONOUR J. W. , ADAMS J. , VECSEI P. , JACOBS H. S. 
Published: March 2008

SUMMARYSixty‐three women with ultrasonically detected polycystic ovaries (PCO) were investigated for a disorder of adrenal steroid biosynthesis. Serum was obtained before, and at 30 and 60 min after, the administration of 250 μg tetracosactrin, and assayed for 17α‐OH‐progesterone, 21‐deoxycortisol, 17α‐OH‐pregnenolone and dehydroepiandrosterone by radioimmunoassay following paper chromatography. Results were compared with those in 11 women with normal ovaries, seven adult females with congenital adrenal hyperplasia (CAH) due to 21‐hydroxylase deficiency (21OHD), and 15 women heterozygous for this defect. Although the basal‐peak steroid concentration differences were significantly greater when ACTH tests were conducted between 1400 and 1700 h than between 0900 and 1000 h, absolute peak steroid concentrations were not different at either time of day. Four of 63 (6.4%) women with PCO had responses to ACTH characteristic of non‐classical (late onset) 21OHD CAH, and about half the remainder had responses characteristic of 21OHD heterozygotes. There was no clear cut evidence for a deficiency in 3β‐hydroxysteroid dehydrogenase activity in women with PCO.
REASONS FOR THE VARIABILITY IN GROWTH HORMONE (GH) RESPONSES TO GHRH CHALLENGE: THE ENDOGENOUS HYPOTHALAMIC‐SOMATOTROPH RHYTHM (HSR)
Authors: DEVESA J. , LIMA L. , LOIS N. , FRAGA C. , LECHUGA M. J. , ARCE V. , TRESGUERRES J. A. F. 
Published: March 2008

SUMMARYThe aims of this study were: (1) to test the possibility that pre‐GHRH plasma GH values could reflect the functional status of the hypothalamic‐somatotroph rhythm (HSR) at testing, and thus explain if it is responsible for the marked variability in GH responsiveness to GHRH challenge and (2) to see if exogenous somatostatin (SS) could disrupt this endogenous HSR and thus make the GH responses homogeneous.(1) Two to 14 GHRH acute tests (GRF‐29, 1 μg/kg, i.v. bolus) were performed in 12 normal men and 10 normal women at the same time (0830 h) at random intervals (2 to 60 days). Blood samples to measure plasma GH were drawn at 15 min intervals before and after GHRH challenge. Given that the increments in pre‐GHRH plasma GH values (I=value at 0 min minus value at ‐ 15 min) were highly correlated with either GHRH‐elicited peaks of GH (men, r= 0.81; women; r= 0.69; P<0.0001) or the rise in GH after the challenge (r=0.685; P<0.0001, in the total of tests performed), three theoretical HSR phases were proposed: (A) I > 0.4 μg/l Secretory Phase; (B) I < 0, (from GH at −15 min < 1.5 μg/l), Secretion Plateau; (C) I < 0, (from GH at − 15 min < 1.5 μg/l), Refractory Phase. Individually, 91% of the men and 86% of the women showed a constant HSR phase when tested at the same time of day independently of the intervals between tests. GH responses (peaks, mean‐± SEM, g/l) in Phase A (women, 51.5 ± 4.1; men, 31.4 ± 3.2) were significantly higher (P < 0.01) than those in Phase B (women, 22.6 ± 1.8; men, 19.7 ± 1.5), and these than those in Phase C (women, 9.2 ± 1.5; men, 6.2 ± 0.5). The great dispersion observed when GH peaks were analysed as a whole disappeared (except in Phase A in women) when they were evaluated according to the HSR Phase at testing.
CORTICOTROPHIN‐RELEASING FACTOR‐LIKE IMMUNOREACTIVITY IN HUMAN 24 H URINE
Authors: MASER‐GLUTH CHRISTIANE , VECSEI PAUL 
Published: March 2008

SUMMARYThis report is the first demonstration of the presence of corticotrophin‐releasing factor‐like immunoreactive material (CRF‐LI) in human urine. Our studies, using immunoaffinity chromatography for extraction, followed by reverse phase high performance liquid chromatography for further purification, and radioimmunoassay for final peptide measurement, suggest that CRF‐LI from human urine is similar, if not identical, to human CRF. Urinary CRF‐LI excretion in normal subjects was 1.48 ± 0.69 ng/24 h (mean ± SD; n= 20) with no significant differences between the sexes. During pregnancy, urinary CRF‐LI excretion increased, and a significant correlation between urinary CRF‐LI excretion and the gestational age was seen (r = 0.62; P <0.0001). We suggest that urinary 24‐h CRF‐LI excretion may reflect the secretion of CRF into the circulation. Measurements of CRF‐LI in the urine may have several advantages over determinations of hormone levels in plasma.
FREE RADICALS AND GRAVES' DISEASE: THE EFFECTS OF THERAPY
Authors: WILSON R. , CHOPRA M. , BRADLEY H. , MCKILLOP J. H. , SMITH W. E. , THOMSON J. A. 
Published: March 2008

SUMMARYPlasma thiol (PSH), caeruloplasmin (CP), intracellular lysate thiol (LSH) and superoxide dismutase (SOD) activity were measured in 30 patients with newly diagnosed Graves'disease (GD). Compared to control subjects (C) PSH and SOD were significantly reduced (C vs GD, 507 vs 449 pmol/l, P <0.01; 2. 1 vs 1.6 pmol/l, P<0.01 respectively) and LSH was significantly raised (C vs GD 181 vs 298 pmol/l). Treatment with carbimazole produced a significant rise in LSH and SOD. Propylthiouracil (PTU) treatment raised LSH levels but 131I treatment produced no significant change.All four parameters are involved in different ways in oxygen metabolism and together provide an indication of oxidative stress across the red‐cell membrane. In addition LSH is a general radical scavenger and SOD a specific O‐2 scavenger. In Graves'disease the increased oxidative stress and increased general radical scavenging may result from raised free‐radical activity. These changes, which have not previously been reported in Graves'patients, were modified by antithyroid drug therapy, but it is not clear whether this is a direct or indirect effect.
THE HALF‐LIFE OF EXOGENOUS GROWTH HORMONE AFTER SUPPRESSION OF ENDOGENOUS GROWTH HORMONE SECRETION WITH SOMATOSTATIN
Authors: HINDMARSH P. C. , MATTHEWS D. R. , BRAIN C. E. , PRINGLE P. J. , DI SILVIO L. , KURTZ A. B. , BROOK C. G. D. 
Published: March 2008

SUMMARYWe have estimated the half‐life of serum growth hormone (GH) in six subjects on 14 occasions following an intravenous bolus injection of either 50 or 500 mU of biosynthetic human growth hormone (B‐hGH) while endogenous GH secretion was suppressed by a continuous infusion of somatostatin. The disappearance curve of serum GH was mono‐exponential and the mean half‐life was 8.9 min (SD 1.5). This is less than previously reported and has important implications for the performance of GH profiles, which should be performed with 10–15 min sampling intervals, and the calculation of pituitary GH secretion rates.
SHORT‐TERM FASTING INHIBITS THE NOCTURNAL MELATONIN SECRETION IN HEALTHY MAN
Authors: RÖJDMARK S. , WETTERBERG L. 
Published: March 2008

SUMMARYTo investigate whether short‐term fasting influences hormone release from human pinealocytes, nocturnal melatonin (MT) secretion was studied before and at the end of a 2‐day fast in seven normal subjects (group A). Serum MT was measured every second hour between 1800 and 0800 h, and the nocturnal MT secretion, as reflected by the MT incremental area (MT area appearing above the 1800 h level), was calculated and compared before and during the fast. MT excretion by the urine (between 2200 and 0700 h) was also determined before, during, and after the period of food deprivation. Body weight and blood glucose concentration fell by 2.5 ± 0.2 kg (mean ± SEM, P<0.001) and 1.7 ± 0.2 mmol/l (P<0.001) respectively during the fast. Nocturnal MT secretion declined by 19 ± 3% (P<0.002), in contrast to urinary MT excretion which remained unaffected. In order to prevent blood glucose from falling significantly during the period of food deprivation, six additional normal subjects (group B) were given eight small oral doses of glucose (each dose 0.5 g/kg) at regular intervals during the 2‐day fast. This did not prevent a weight loss (2.1 ± 0.5 kg, P<0.01) of similar magnitude as in group A, but it restored a normal nocturnal MT secretion. The fact that glucose supplementation during fasting returns a decreased MT secretion to normal suggests that human pinealocytes require a certain minimal glucose delivery to function normally.
ABNORMALITIES OF THYROTROPHIN (TSH) EVENING RISE AND PULSATILE RELEASE IN HAEMODIALYSIS PATIENTS: EVIDENCE FOR HYPOTHALAMIC‐PITUITARY CHANGES IN CHRONIC RENAL FAILURE
Authors: WHEATLEY TREVOR , CLARK PENELOPE M. S. , CLARK JOHN D. A. , HOLDER ROGER , RAGGATT PETER R. , EVANS DAVID B. 
Published: March 2008

SUMMARYUsing a sensitive enzyme amplified immunoassay for TSH, the evening rise and pulsatile release of TSH were studied in 10 men with chronic renal failure treated by haemodialysis. Compared to euthyroid male controls the evening rise of TSH was attenuated (median 0.066 vs 0.195 mU/l/h, P <0.01) and the rate of rise correlated with the TSH response to TRH (r= 0.93, P <0.001). All subjects showed TSH pulsatility in at least one method of data analysis but the less sensitive incremental method showed no significant difference in pulse frequency and amplitude between the two groups. However, with time series analysis, periodicity was shorter (median 45 vs 95 min, P= 0.013) and pulse amplitude smaller (median 0.06 vs 0.175 mU/l, P=0.017) in renal patients. Pulse amplitude, but not periodicity, correlated with the TSH response to TRH (r= 0.68, P <0.05). In addition, serum total thyroxine, free thyroxine and free triiodothyronine concentrations were reduced, while serum prolactin and 17 β‐oestradiol concentrations were raised. These changes in TSH evening surge and pulsatile release may contribute to the reduction in thyroidal hormone concentrations seen in renal failure and emphasize the value of sensitive methods of hormone and pulse data analysis.
ELEVATED SERUM LEVELS OF CALCITONIN GENE‐RELATED PEPTIDE (CGRP) BUT NO EVIDENCE FOR CGRP GENE EXPRESSION IN NON‐SMALL CELL LUNG CARCINOMAS
Authors: SCHIFTER SØREN , JOHANNSEN LIS , AAGAARD MICHAEL T. , GOLTERMANN NILS , PARKES HELEN C. , CRAIG ROGER K. 
Published: March 2008

SUMMARYCalcitonin gene‐related peptide (CGRP) is a hormone formed by alternative post‐transcriptional processing of the calcitonin gene. It is a neuropeptide localized to discrete regions of the central nervous system (CNS) and in nerve fibres associated with blood vessels. It is also expressed in medullary carcinomas of the thyroid and lung carcinoma cell lines. The latter finding suggests a possible value for CGRP as tumour marker in lung carcinomas. In this investigation of 22 patients undergoing operation for lung tumours, pre and post‐operative levels of serum CGRP were measured. Preoperative as well as postoperative serum CGRP levels were significantly elevated when compared to age‐matched normals. However, no evidence could be found for CGRP gene expression in tumour tissue from the same patients as judged by immunocyto‐chemistry or in‐situ hybridization using CGRP cRNA probes. CGRP has been localized to nerve fibres in relation to pulmonary blood vessels and has been shown to be a potent vasodilator. These findings, and the absence of evidence for synthesis in tumours, as opposed to cell lines derived from lung carcinomas, suggests that the lack of post‐operative normalization of serum CGRP concentrations may be related to physiological changes in cardiovascular haemodynamics following surgery. Elevated pre‐operative serum CGRP levels may also reflect a consequence of the lung carcinoma leading to increased release of CGRP from sites in the vasculature yet to be determined, but does not indicate synthesis de novo and secretion of CGRP by the tumours.
EVIDENCE FOR A SLOW TISSUE ADAPTATION TO CIRCULATING THYROXINE IN PATIENTS WITH CHRONIC L‐THYROXINE TREATMENT
Authors: NYSTRÖM E. , LUNDBERG P. ‐A. , PETERSEN K. , BENGTSSON C. , LINDSTEDT G. 
Published: March 2008

SUMMARYWe measured serum procollagen‐III‐peptide in 67 women with long‐term L‐thyroxine treatment and compared the results with age‐matched controls. The strong correlation between serum free thyroxine and procollagen‐III‐peptide concentrations previously found after 6 months of L‐thyroxine treatment was not found after long‐term treatment. There were slightly higher procollagen‐III‐peptide concentration values in those chronically treated patients who had high free thyroxine levels but this increase was less marked than in patients previously studied after short‐term treatment.An increase in procollagen‐III‐peptide concentration reflects an increased biosynthesis of collagen III, which is present in connective tissues throughout the body, and our findings may be explained by slow tissue adaptation to increased levels of thyroxine. We conclude that the increased thyroxine levels found in L‐thyroxine‐treated patients are of less clinical importance than thought previously. We also conclude that peripheral markers of thyroid hormone peripheral effects such as procollagen‐III‐peptide may be of less use than thought previously due to this slow tissue adaptation to changes in thyroxine concentration.
GnRH AGONIST ADMINISTRATION IN POLYCYSTIC OVARY SYNDROME
Authors: BUCKLER H. M. , PHILLIPS S. E. , KOVACS G. T. , BURGER H. G. , HEALY D. L. 
Published: March 2008

SUMMARYThe study was designed to examine (1) the effects of the luteinizing hormone releasing hormone (GnRH) agonist, buserelin, on pituitary and ovarian hormone secretion, and (2) the effect that pituitary—ovarian suppression with a GnRH agonist has on subsequent ovulation induction with exogenous gonadotrophins (hMG), in polycystic ovary syndrome (PCOS). Two protocols were studied where buserelin was administered intranasally to all patients in a dose of 200 μg, six times daily. Ten patients received buserelin until an oestrogen withdrawal bleed occurred while a further 12 patients received buserelin for 4 weeks, before hMG was co‐administered. Nine of the above subjects also underwent conventional ovulation induction with hMG. Blood samples were taken daily for radioimmunoassay of LH (LH‐RIA), FSH, sex steroids and inhibin and for immunoradiometric assay of LH (LH‐IRMA). Following buserelin administration there was an initial rise in LH‐RIA, FSH, oestradiol (E2) and inhibin (P < 0.01). Fourteen days were needed for LH‐RIA to return to the normal range, with both protocols resulting in a fall in LH‐RIA and FSH (P < 0.01) before hMG was co‐administered. Twenty‐eight days of buserelin administration were needed to suppress E2 into the castrate range. Inhibin and both E2 and FSH were closely correlated throughout buserelin administration (P < 0.01). There was failure to respond to an intravenous bolus of 100 μg of GnRH from 7 days of buserelin administration onwards, despite the serum LH‐RIA still being raised at 7 days. Serum samples assayed for LH by RIA using WHO Matched Reagents and by IRMA were closely correlated (r = 0.96, P < 0.01). There was no difference in the proportion of ovulations (52%vs 66%) or pregnancies (1 vs 1) in the GnRH agonist or control group. Similar amounts of hMG were needed in both groups and there was multiple follicular development (> 3 follicles > 15 mm diameter; 41%vs 38%) following hMG administration. There was a close correlation between E2 and inhibin levels (P < 0.01). This study demonstrates that (a) 28 days of buserelin administration in a dose of 200 μg, six times daily intranasally is needed to achieve suppression of ovarian function; (b) the GnRH stimulation test is unsatisfactory as an indicator of whether inhibition of pituitary secretion has occurred; (c) following a rise in endogenous and exogenous gonadotrophin levels, E2 and inhibin are stimulated and are closely correlated; (d) there was no benefit of pituitary—ovarian suppression with a GnRH agonist on subsequent ovulation induction, and multiple follicle development was not prevented.
FAMILIAL CUSHING'S SYNDROME DUE TO NODULAR ADRENOCORTICAL DYSPLASIA IS AN INHERITED DISEASE OF IMMUNOLOGICAL ORIGIN
Authors: VAN BERKHOUT F. TEDING , CROUGHS R. J. M. , WULFFRAAT N. M. , DREXHAGE H. A. 
Published: March 2008

SUMMARYCirculating immunoglobulins may be involved in the pathogenesis of familial Cushing's syndrome due to nodular adrenocortical dysplasia. The disease may also be part of a complex including cutaneous and cardiac myxomas, spotty pigmentation of the skin, and other signs of endocrine overactivity. In the present study of two sisters treated by complete adrenalectomy for Cushing's syndrome due to nodular adrenocortical dysplasia, and of their first‐degree relatives, no evidence of associated disorders was present. However, the serum of both girls and of their mother contained immunoglobulins capable of stimulating adrenal DNA synthesis and cortisol production in vitro. The study supports the theory that familial Cushing's syndrome due to adrenocortical dysplasia is an inherited disease of immunological origin.
EFFECTS OF HYPERTHYROIDISM ON BINDING PROTEINS FOR STEROID HORMONES
Authors: CARON PH. , BENNET A. , BAROUSSE C. , NISULA B. C. , LOUVET J. P. 
Published: March 2008

SUMMARYSex hormone binding globulin (SHBG) and corticosteroid binding globulin (CBG) binding capacities were examined weekly in eight normally cycling women and three women taking birth control pills during a 5‐week baseline period and after daily ingestion of 75 μg of L‐triiodothyronine (T3) for 30 days. The SHBG binding capacity increased whereas the CBG binding capacity decreased after T3 therapy. The binding capacities of proteins for steroid hormones were measured in 18 hyperthyroid subjects (Graves' disease) prior to and after 3 months of antithyroid drug therapy. SHBG binding capacity in hyperthyroid men or women was higher, and CBG binding capacity lower than those in euthyroid subjects. Thus, during hyperthyroidism, binding capacities of sex hormone binding globulin and corticosteroid binding globulin vary in opposite directions. A statistically significant correlation between the ratio of the sex hormone binding globulin to the corticosteroid binding globulin and triiodothyronine levels was found (P < 0.01). Therefore the ratio of the sex hormone binding globulin to the corticosteroid binding globulin might be potentially useful as a biochemical index of thyroid hormone action in peripheral tissues.
STIMULATION OF CYCLIC AMP PRODUCTION IN FRTL‐5 THYROID CELLS BY CRUDE IMMUNOGLOBULIN FRACTIONS OF SERUM FROM PREGNANT WOMEN
Authors: KASAGI K. , HIDAKA A. , HATABU H. , TOKUDA Y. , MISAKI T. , IIDA Y. , YOSHIDA M. , FUJII S. , TAII S. , TAMAI H. , KONISHI J. 
Published: March 2008

SUMMARYIn an assay for thyroid‐stimulating antibodies, in which FRTL‐5 thyroid cells were incubated with crude immunoglobulin (Ig) fractions precipitated from serum with 15|X% polyethylene glycol, significant increase in cAMP production was elicited by the samples from 25 (35·7%) out of 70 pregnant women. The highest value was 529·5%. There was a close correlation between thyroid stimulating activities and serum hCG concentrations (r= 0‐708, P < 0·001). When 125I‐hCG was added to serum from pregnant women, about 20% of the radioactivity was incorporated into the Ig fractions. hCG preparations within a range of concentrations of 30‐300 IU/m elicited 2·3–16·5 times increase in cAMP in a dose‐dependent manner.Nine pregnant women with serum TSH concentrations less than the lower limit of the normal range (< 0·25 mU/1) displayed significantly higher values for both thyroid stimulating activities and serum hCG concentrations (P < 0·001, respectively) compared with those who had normal TSH levels in serum. These data suggest that hCG or its variant may stimulate the thyroid sufficiently to suppress secretion of TSH from the pituitary in some pregnant women.
ENHANCEMENT OF THE ACTIVITY OF THYROID‐STIMULATING ANTIBODIES BY ANTI‐HUMAN IgG ANTIBODIES IN VITRO
Authors: SAITO T. , SHIMURA H. , ENDO T. , ONAYA T. 
Published: March 2008

SUMMARYIn an attempt to determine whether or not anti‐human IgG antibodies could influence the activity of thyroid‐stimulating antibodies (TSAb), we investigated the effects of anti‐human Fc antibody (anti‐Fc antibody) and IgG from rheumatoid arthritis patients (RA‐IgG) on TSAb activity using FRTL‐5 cells. It was found that these anti‐human IgG antibodies enhanced the TSAb activity in vitro. FRTL‐5 cells were first incubated with Graves' disease IgG for 30 min at 37|MoC, then washed and incubated in Hanks’balanced salt solution with anti‐human IgG antibodies for 60 min at 4|MoC, and then for a further 120 min at 37|MoC. The level of cAMP accumulated in the medium was determined by RIA. Anti‐Fc antibody significantly augmented the cAMP formation stimulated by 16 out of 24 Graves' IgGs, whereas anti‐F(ab')2 antibody did not potentiate cAMP accumulation. Three of five RA‐IgGs, which are usually defined as specific antibodies for the Fc fragment of human IgG, mimicked these stimulatory effects. Protein A also potentiated the cAMP formation stimulated by Graves' IgGs. Furthermore, there was a significant correlation between the TSAb titres of these Graves' IgGs and the potentiating effects of anti‐Fe antibody (r= 0.495, P < 0.05, n= 21). These results suggest that the interaction of TSH receptor antibody with anti‐human IgG antibodies might modulate thyroid function in Graves' disease.
RADIATION‐INDUCED HYPOPITUITARISM IS DOSE‐DEPENDENT
Authors: LITTLEY M. D. , SHALET S. M. , BEARDWELL C. G. , ROBINSON E. L. , SUTTON M. L. 
Published: March 2008

SUMMARYRadiation‐induced hypopituitarism has been studied prospectively for up to 12 years in 251 adult patients treated for pituitary disease with external radiotherapy, ranging in dose from 20 Gy in eight fractions over 11 days to 45 Gy in 15 fractions over 21 days. Ten further patients were studied 2–4 years after whole‐body irradiation for haematological malignancies using 12 Gy in six fractions over 3 days and seven patients were studied 3–11 years after whole‐brain radiotherapy for a primary brain tumour (30 Gy, eight fractions, 11 days). Five years after treatment, patients who received 20 Gy had an incidence of TSH deficiency of 9|X% and in patients treated with 35–37 Gy, 40 Gy and 42–45 Gy, the incidence of TSH deficiency (22, 35 and 52% respectively) increased significantly (P < 0.001) with increasing dose. A similar relationship was observed for both ACTH and gonadotrophin deficiencies when the 20 Gy group was compared to patients treated with 35–45 Gy (P < 0.01 and P < 0.05 respectively). Growth hormone deficiency was universal by 5 years over the dose range 35–45 Gy. In seven patients who were treated with 30 Gy in eight fractions over 11 days, deficiencies were observed at a similar frequency to the 40 Gy group (15 fractions, 21 days). No evidence of pituitary dysfunction was detected in the ten patients who received 12 Gy (six fractions, 3 days). Both total radiation dose and fractionation schedule may determine the incidence of pituitary hormone deficiencies. The dose below which deficiencies do not occur is probably irrelevant to therapeutic irradiation of pituitary and other intracranial neoplasms.