bluuebunny/crossref_metadata_2025_split huggingface dataset:
ABNORMAL PANCREATIC POLYPEPTIDE RESPONSE TO ORAL GLUCOSE LOADING IN DIABETES MELLITUS
Authors: TSUDA K. , SAKURAI H. , SEINO Y. , SEINO S. , TANIGAWA K. , KUZUYA H. , MORI K. , IMURA H. 
Published: March 2008

SUMMARYIn order to elucidate the abnormality of pancreatic polypeptide (PP) secretion in diabetes mellitus, basal plasma PP levels and their response to oral glucose loading were measured in normal subjects and diabetic patients. Fasting plasma PP levels were significantly elevated in patients with diabetes mellitus. Oral administration of 50g of glucose elicited an exaggerated rise in plasma PP in diabetic patients as compared with the response in normal subjects. This exaggerated PP response to oral glucose loading was partially but significantly improved after the treatment, with an augmented response of plasma insulin. These results indicate the existence of abnormal PP secretion in diabetes mellitus which is possibly caused by metabolic or endocrine derangements.
URINARY PROSTAGLANDINS FOLLOWING FRUSEMIDE TREATMENT AND SALT DEPLETION IN NORMAL SUBJECTS AND SUBJECTS WITH DIABETIC HYPORENINAEMIC HYPOALDOSTERONISM
Authors: FARESE R. V. , RODRIGUEZ‐COLOMÉ M. , O'MALLEY B. C. 
Published: March 2008

SUMMARYUrinary immunoreactive PGA and PGE, plasma and urinary aldosterone, and plasma renin activity (PRA) were determined in eleven control subjects and four patients with diabetic hyporeninaemic hypoaldosteronism (HH) before and during 4 days of sodium chloride restriction and frusemide administration. Aldosterone and PRA increased steadily in control subjects, but not in patients with HH. Increases in urinary PGA and PGE were observed during volume depletion. The basal levels and increases observed were comparable in both groups. The apparently normal stimulation of PGA and PGE in subjects with diabetic HH suggests that this syndrome is not associated with abnormal prostaglandin metabolism, despite the fact that drug‐induced abnormalities of the latter may precipitate or aggravate the clinical syndrome in susceptible individuals. The increase in PGA and PGE following frusemide treatment and salt depletion supports the possibility of a relationship between renal prostaglandin metabolism, frusemide‐induced natriuresis and/or renin secretion. While the nature of this relationship remains obscure, the increases in PGA and PGE in the absence of increases in renin‐angiotensin levels in subjects with HH suggests that these changes are not due to activation of the renin‐angiotensin system.
PITUITARY FUNCTION IN NORMOPROLACTINAEMIC INFERTILE MEN RECEIVING BROMOCRIPTINE
Authors: GLATTHAAR C. , DONALD R. A. , SMITH R. , McRAE C. U. 
Published: March 2008

SUMMARYA double blind trial of bromocriptine 7–5 mg daily versus placebo was carried out in ten infertile men. Pretreatment basal plasma prolactin, thyroid stimulating hormone (TSH) testosterone and luteinizing hormone (LH) concentrations were normal, but plasma follicle‐stimulating‐hormone (FSH) was raised in four individuals. After 4 months treatment with bromocriptine a significant fall in plasma prolactin was observed (P<0.01), both under basal conditions and following thyroid stimulating hormone releasing hormone (TRH). Basal plasma gonadotrophin, testosterone and thyroid stimulating hormone (TSH) concentrations did not alter. No change in sperm density, volume or motility was noted. However an apparent fall in the peak plasma LH (but not FSH) response to gonadotrophin releasing hormone (LHRH) was observed in patients receiving bromocriptine. This reduction in plasma LH responsiveness was significant when compared with the baseline response (P < 0.05) but failed to reach significance when compared with the placebo response. It is concluded that prolonged bromocriptine therapy in normoprolactinaemic men does not suppress FSH secretion, and any reduction in plasma LH responsiveness to LHRH is not accompanied by a significant fall in plasma testosterone.
OESTRONE SULPHATE IN PLASMA FROM POSTMENOPAUSAL WOMEN AND THE EFFECTS OF OESTROGEN AND ANDROGEN THERAPY
Authors: TOWOBOLA O. A. , CRILLY R. C. , OAKEY R. E. 
Published: March 2008

SUMMARYThe concentration of oestrone sulphate in peripheral plasma from postmeno‐pausal women was investigated using a method which involved extraction of the conjugate, which was then hydrolysed with acid, and determination (by radioimmunoassay) of the purified oestrone fraction obtained. The concentration of unconjugated oestrone in the same plasma samples was also measured. Postmenopausal women had concentrations of oestrone sulphate in plasma (1.1 ± 0.36 nmol/1, mean ± SD, n = 39) similar to those found in women in the follicular phase of the menstrual cycle and less than those found in males (3.2 ± 0.61 nmol/1, n= 21). The mean ratio of the concentration of oestrone sulphate to that of oestrone in plasma from postmenopausal women (7.9 ± 3.3) was significantly lower (P < 0.001, t test) than the mean ratio in men (19.8 ± 3.8). Treatment with conjugated oestrogens, oestradiol in a cream, oestradiol valerate or ethinyl oestradiol, increased the concentration of oestrone sulphate in the peripheral circulation. In contrast, chronic corticosteroid therapy reduced the level of oestrone sulphate (0.5 ± 0.11 nmol/1, n = 10) but this was partly restored (to 0.7 ± 0.13 nmol/1) by concomitant oral dehydroepiandrosterone. Ingestion of piperazine oestrone sulphate (Harmogen, 1.5 mg) by three fasting postmenopausal women was followed 4 h later by oestrone sulphate concentrations five to ten times those found at midcycle.
THERAPY OF PRIMARY HYPOTHYROIDISM WITH L‐TRIIODOTHYRONINE: DISCORDANT CARDIAC AND PITUITARY RESPONSES
Authors: RIDGWAY E. C. , COOPER D. S. , WALKER HARRIET , DANIELS G. H. , CHIN W. W. , MYERS G. , MALOOF FARAHE 
Published: March 2008

SUMMARYCardiac systolic time intervals were studied in ten patients with primary hypo‐thyroidism before and during therapy with increasing doses of oral L‐triiodo‐thyronine (L‐T3). Therapy was increased sequentially from 10, 20, 25 to 50 μg of L‐T3 daily on a monthly basis. On L‐T3, 20 to 25 μg/day, cardiac systolic time intervals and other peripheral responses to thyroid hormone including serum cholesterol concentration, serum creatine phosphokinase (CPK) activity, and basal metabolic rate had normalized. However, serum thyrotrophin (TSH) levels and peak TSH responses to thyrotrophin‐releasing hormone (TRH) remained elevated on these doses of L‐T3. As the dose of L‐T3 was increased from 20 to 50 μg/day, mean basal serum TSH levels decreased from 55 to 16 μu/ml, and the peak TSH response to TRH decreased from 243 to 58 μu/ml (P < 0.001) while systolic time intervals did not decrease further. Changing to L‐thyroxine (L‐T4) therapy at this point resulted in further suppression of TSH secretion, without significantly altering systolic time intervals or the other peripheral responses to thyroid hormone. These data suggest (a) that some biological responses to thyroid hormone were normalized on lower doses of L‐T3 than were required to normalize TSH secretion, and (b) that higher doses of L‐T3 or substituting L‐T4 therapy could suppress TSH secretion further without altering the other peripheral responses to thyroid hormone.
METABOLIC ASPECTS OF THE CALORIGENIC EFFECT OF THYROID HORMONE IN MAMMALS
Authors: SESTOFT L. 
Published: March 2008

SUMMARYThe increased BMR in hyperthyroidism may be accounted for by the use of chemical energy for metabolic processes and work. Major contributors are the heart work and futile cycling of FFA into triglyceride in adipose tissue, whereas gluconeogenesis in liver and the maintenance of sodium and potassium concentration gradients across the plasma membranes are unlikely to play any significant role. Information on the use of energy for protein turnover and urea production is lacking. The rate of oxygen uptake is not increased in the brain, spleen and testis. The main metabolic fuel seems to be free fatty acid.The mechanism which enables the hyperthyroid tissue to maintain normal concentrations of ATP, ADP and inorganic phosphate, (Pi) despite an increased turnover of energy‐rich phosphates, is not fully elucidated. However, ultimately the increased rate of oxygen uptake in hyperthyroidism seems to rely upon an increased capacity for the transport of cytosolic ADP and Piinto mitochondria. The transport capacity is increased by an increased area of the mitochondrial membrane per g tissue and by a change in the kinetics of translocation of substrates for oxidative phosphorylation. Other transport processes across the mitochondrial membrane are also changed by hyperthyroidism, e.g. long chain fatty acid transport via carnitine acyl transferase, and oxaloacetate transport via substrate shuttles.
EFFECT OF DOPAMINE INFUSION ON SERUM PROLACTIN CONCENTRATION IN NORMAL AND HYPERPROLACTINAEMIC SUBJECTS
Authors: RESCHINI E. , FERRARI C. , PERACCHI M. , FADINI R. , MESCHIA M. , CROSIGNANI P. G. 
Published: March 2008

SUMMARYThe serum prolactin response to intravenous dopamine infusion (5μg.kg−1 min−1) was measured in twenty‐one healthy subjects, in seven hyperprolactinaemic patients without evidence of a pituitary tumour, and in twenty‐one patients with prolactinomas. Mean serum prolactin values were significantly suppressed in all three groups, without any significant difference between the degree of suppression. A decrease of serum prolactin to below 50% of basal values occurred in fifteen healthy subjects, in four patients without evidence of pituitary tumour, and in fourteen patients with prolactinomas. These findings demonstrate that most human prolactin‐secreting pituitary adenomas are normally suppressible by exogenously administered dopamine and that dopamine infusion is not able to distinguish between tumorous and non‐tumorous hyper‐prolactinaemia. Since intravenously infused dopamine is believed to inhibit prolactin secretion by acting at pituitary level, it is suggested that a normal functioning of pituitary dopamine receptors is maintained in most human prolactinomas.
EVALUATION OF TWO INHIBITORY TESTS (NOMIFENSINE AND L‐DOPA + CARBIDOPA) FOR THE DIAGNOSIS OF HYPERPROLACTINAEMIC STATES
Authors: MORIONDO PAOLA , TRAVAGLINI P. , NISSIM MARINA , FAGLIA G. 
Published: March 2008

SUMMARYIt has been reported that administration of nomifensine (Nom) or of L‐dopa + carbidopa (L‐dopa + Carb) potentiates central dopaminergic tonus, resulting in decreased prolactin (PRL) secretion. It has been proposed that these drugs would help to discriminate patients with PRL‐secreting pituitary tumours from those with so‐called ‘functional’ hyperprolactinaemia.In this study, oral Nom (200 mg) was given to forty‐three hyperprolactinaemic patients and L‐dopa + Carb (50 mg Carb every 6 h for four doses followed by L‐dopa 100 mg and Carb 35 mg) to thirty of them and both treatments to ten normal subjects. The hyperprolactinaemic patients were divided into four clinical groups. Group A, twenty patients with proven PRL‐secreting pituitary tumours; Group B, thirteen women with elevated PRL levels (<100 ng/ml) without any radiological evidence of a pituitary tumour (hyperprolactinaemia of unknown aetiology or ‘functional’ hyperprolactinaemia); Group C, four women with polycystic ovarian disease and mildly elevated serum PRL; Group D, six patients with various other disorders associated with hyperprolactinaemia.PRL levels decreased in the normal controls below the basal values by 61.3%±6.2 (SEM) after Nom and 77.6%± 4.2 after L‐dopa + Carb. Decreases in serum PRL of at least 50% (in three consecutive determinations) were found in group A in 20% of patients after Nom and in 25% after L‐dopa + Carb; in group B in 15% and 40% of cases; in most of the hyperprolactinaemic women in group C; and some in group D.In conclusion, these two treatments did not discriminate between tumorous and non‐tumorous causes of PRL hypersecretion.
GRAVES' DISEASE AND HLA: CLINICAL AND EPIDEMIOLOGIC ASSOCIATIONS
Authors: FARID N. R. , STONE E. , JOHNSON G. 
Published: March 2008

SUMMARYCorrelation between clinical and epidemiological features of Graves' disease and HLA were sought in 175 patients, eighty‐three of whom were typed for HLA DR antigens. The relative risks (x) conferred by HLA‐B8 and DR3 were 3.1 and 5–7 respectively (P<0.0005 uncorrected). The disease occurred at an earlier age in HLA‐DR3 positive patients compared to negative patients (P<0.005 in females> and <30‐years‐old). Eighty‐four out of ninety‐two patients could specify the season of onset of hyperthyroidism; an excess of HLA‐B8 positive patients in the summer and a lack of these in the spring and autumn was found. No associations between B8 and exophthalmos and/or soft tissue eye changes were observed. However, significant associations between exophthalmos and either exophthalmos and/or soft tissue changes were found with DR3 (x=3.6 and 3.8 respectively). HLA‐DR3 positive patients were found to be more resistant to radioiodine therapy than patients negative for these antigens. No heterogeneity in the distribution of HLA antigens was found when the following indices were examined: sex, goitre size, severity of disease, pretibial myxoedema, antecedent psychological disorder, consumption of oral contraceptives, family history of Graves' disease or thyroid antibody titre. HLA does not appear to distinguish subvariants of Graves' disease, rather it influences the susceptibility to disease and its persistence once it becomes clinically manifest.
THE EFFECT OF FENCLOFENAC ON THYROID FUNCTION TESTS IN VIVO AND IN VITRO
Authors: RATCLIFFE WENDY A. , HAZELTON R. A. , THOMSON J. A. , RATCLIFFE J. G. 
Published: March 2008

SUMMARYClinically euthyroid patients on long term maintenance therapy with the non‐steroidal anti‐inflammatory drug fenclofenac (Flenac) show an unusual and abnormal pattern of serum thyroid function tests. In all twelve patients studied, total T4 concentrations were grossly subnormal (mean 28.4±9.9 (SD) nmol/1 and total T3 levels low‐normal (mean 1.4 ± 0.3 (SD) nmol/1), whereas rT3 (mean 0.36 ± 0.06 (SD) nmol/1) and basal TSH levels (mean 1.9 ± 0.5 (SD) mu/1) were within their respective normal ranges. Free T4 levels were low normal (mean 11.0 ± 1.0 (SD) pmol/1) while TSH, T4 and T3 responses to intravenous TRH were similar to those found in euthyroid subjects. These effects appear to be due predominantly to in vivo inhibition of binding of thyroid hormones to carrier proteins in serum, rather than in vitro drug interference in the radioimmunoassays employed. Fenclofenac does, however, interfere in those laboratory methods employing serum proteins as binding agents. Thus the Thyopac 4 method for serum total T4 grossly over‐estimates T4 levels, while thyroid hormone binding capacity (Thyopac 3) is low. Since fenclofenac is one of the most potent drugs interfering with routine indices of thyroid status, it is suggested that suspected thyroid dysfunction is excluded before commencing therapy with the drug.
THE FUNCTION OF THE PITUITARY‐THYROIDAL AXIS IN ACROMEGALIC PATIENTS V. PATIENTS WITH HYPERPROLACTINAEMIA AND A PITUITARY TUMOUR
Authors: KLIJN J. G. M. , LAMBERTS S. W. J. , DOCTER R. , JONG F. H. DE , VAN DONGEN K. J. , BIRKENHAGER J. C. 
Published: March 2008

SUMMARYThe function of the pituitary‐thyroidal axis was examined in fifty‐three of sixty‐two patients with hyperprolactinaemia and a pituitary tumour and in forty of forty‐four acromegalic patients, in whom one or more indices of the pituitary‐thyroid function were determined before treatment. In the patients with hyperprolactinaemia and a pituitary tumour, sellar + extrasellar tissue (EST) size showed a significant negative correlation with the response of TSH to TRH (ΔTSH) as well as with the circulating T4 and T3 levels. These correlations were not present in the acromegalic patients. In the prolactinoma group a sharp decrease in mean serum T4 and T3 levels was found at sellar + EST sizes exceeding 3 cm2. In twenty‐three patients with a sellar + EST size of 3 cm2 or more, thirteen (57%) showed a T4 level of less than 6 μg/dl against none of twenty‐eight patients with a sellar + EST size of less than 3 cm2. For T3, using a limit of 120 ng/dl, the corresponding numbers were eight out of thirteen (62%) and none of ten patients respectively. A positive correlation was observed between ΔTSH and the T3 levels but not between ΔTSH and T4, while in the acromegalic patients there was no correlation between TSH reserve and T3 or T4. In the patients with hyperprolactinaemia and a pituitary tumour positive correlations between basal TSH and ΔTSH as well as between T4 and T3 levels were observed. These correlations were not found in the acromegalic patients.In conclusion: (1) Thyroid function appears to be independent of pituitary tumour size in patients with acromegaly but not in patients with hyperprolactinaemia and a pituitary tumour. (2) In acromegalic patients the high incidence of an impaired TSH response (without hypothyroidism and independent of tumour size) may be caused by suppression of TSH secretion rather than by destruction of thyrotrophic cells.
THE EFFECT OF INCREASING DOSES OF INGESTED GLUCOSE ON INSULIN AND GASTRIC INHIBITORY POLYPEPTIDE (GIP) CONCENTRATIONS IN MAN
Authors: FALKO J. M. , CROCKETT S. E. , CATALAND S. , O'DORISIO T. M. , KRAMER W. , MAZZAFERRI E. L. 
Published: March 2008

SUMMARYGastric inhibitory polypeptide (GIP) is insulinotropic in vivo and in vitro. It is released following glucose ingestion and is a leading candidate as a mediator of the enteroinsular axis. To investigate the GIP response to increasing amounts of oral glucose, and its relationship to glucose levels and insulin secretion, fourteen normal volunteers ingested 25, 50 and 75 g of glucose at random with 5–7 days between each test. Serum insulin, glucose and GIP concentrations were measured and total integrated incremental responses were determined. Peak mean responses to glucose, insulin and GIP occurred at 30 min following each glucose ingestion. There were no significant differences in glucose concentrations at any interval with the varying glucose doses. Mean peripheral insulin concentrations were significantly increased ater 50 or 75 g of glucose as compared with the 25 g dose (P<0.02). Mean GIP concentrations were significantly greater (P<0.03) between 15 and 180 min with both the 50 and 75 g glucose stimulus. Total integrated areas under the response curves for glucose, insulin and GIP showed a graded increase in circulating insulin and GIP (P<0.01) as the amount of ingested glucose was increased from 25 to 75 g. These findings show that increasing doses of glucose stimulated greater levels of GIP and insulin and further support the insulinotropic properties of endogenous GIP in man.
ADRENAL FUNCTION IN SUBGROUPS OF THE PCO SYNDROME ASSESSED BY A LONG ACTH TEST
Authors: KANDEEL F. R. , LONDON D. R. , BUTT W. R. , DAVILA N. , RUDD B. T. , SADEGHIAN S. , LYNCH S. S. , EDWARDS R. LOGAN , HORDER M. 
Published: March 2008

SUMMARYFifteen patients with the polycystic ovarian (PCO) syndrome were classified into Group A (n= 6) and Group B (n= 9) based on their LH responses to LHRH before and at 44 and 92h after administration of oestradiol benzoate. Adrenal function in both groups was assessed by comparing the hormone responses to ACTH (0.5mg twice daily for 4 days) with those obtained in nine normally ovulating women during the early follicular phase of their cycles. In Group A patients there was no significant difference from normals in the serum concentration of dehydroepiandrosterone sulphate (DHAS), 17α‐hydroxy‐progesterone (17‐OHP) or androgens (testosterone and dihydrotestosterone). In contrast, the serum concentrations in Group B were significantly higher (P<0.01) for each of these steroids before ACTH, and remained higher at 2 and 4 days for DHAS, but not for the other two steroids. The concentration of oestrone was significantly higher (P<0.05) in Group B patients before, and 2 days after, ACTH, while in Group A patients higher concentrations (P<0.02) were found only after 2 days. The concentrations of oestradiol, on the other hand, were not different from normal in either group before ACTH and became lower than normal in both groups at 2 days and remained lower at 4 days in Group B. The concentration of cortisol was within the normal range throughout in Group A, but was lower than normal after 4 days in Group B patients (P<0.05). The ratios between the sums of concentrations of DHAS to cortisol on days 2 and 4 (P<0.001) or 17‐OHP to cortisol (P<0.05) were elevated in Group B compared with normal subjects. LH, FSH and prolactin values were normal throughout in Group A, but in Group B patients the mean value for LH was significantly elevated before ACTH and at 4 days after ACTH (P<0.02).
SOMATOSTATIN SECRETION BY LUNG AND THYMIC TUMOURS
Authors: PENMAN ERICA , WASS J. A. H. , BESSER G. M. , REES LESLEY H. 
Published: March 2008

SUMMARYEctopic secretion of somatostatin in one patient with a thymic tumour and in two patients with lung tumours is described. All three patients also had ectopic ACTH secretion. Gel filtration chromatography under dissociating conditions showed the two lung tumour extracts to contain predominantly 1600 MW somatostatin monomer while the thymic tumour contained predominantly a 3000–3500 MW form of somatostatin, 77% of which was not converted to 1600 MW somatostatin by dithiothreitol (an agent which reduces disulphide bridges). This form may therefore represent a covalently‐bound precursor of somatostatin rather than a dimer of two somatostatin monomers. Plasma from all three tumour patients and from normal subjects contained both 1600 and 3000–3500 MW somatostatin. It is suggested that somatostatin secretion may frequently be associated with multiple hormone producing tumours.
STUDIES OF DIURNAL CHANGES IN PLASMA RENIN ACTIVITY, AND PLASMA NORADRENALINE, ALDOSTERONE AND CORTISOL CONCENTRATIONS IN MAN
Authors: LIGHTMAN S. L. , JAMES V. H. T. , LINSELL C. , MULLEN P. E. , PEART W. S. , SEVER P.S. 
Published: March 2008

SUMMARYDiurnal studies were performed on ten normal volunteers taking a normal sodium diet. Half‐hourly blood samples were taken throughout 25 h and assayed for plasma renin activity (PRA) and the plasma concentrations of noradrenaline, aldosterone and cortisol. Sleep was recorded polygraphically and scored by standard criteria. Circadian rhythms were demonstrated for plasma cortisol, aldosterone and noradrenaline concentrations, but not for plasma renin activity. The nadir of the rhythm for the noradrenaline concentration appeared to be related to sleep itself rather than to any chronological index. Only PRA was effected by the stage of sleep, falling sharply during periods of REM sleep. Plasma cortisol and aldosterone concentrations showed a positive correlation over the 24 h. There was, however, no correlation between PRA and plasma aldosterone concentrations, except when the subjects arose after their night's recumbency. Plasma noradrenaline concentration did not correlate with the concentration of any of the other hormones measured.