bluuebunny/crossref_metadata_2025_split huggingface dataset:
LONG‐TERM EFFECT OF IODIZED OIL ON SERUM THYROGLOBULIN LEVELS IN ENDEMIC GOITRE PATIENTS
Authors: LIMA N. , KNOBEL M. , MEDEIROS‐NETO G. 
Published: March 2008

SUMMARYSerum thyroglobulin (Tg) response to bovine TSH (bTSH) was evaluated in 44 goitrous patients (grades III and IV) living in conditions of chronic iodine (I) deficiency (iodine urinary excretion > 40 μg I/g) and in 26 normal subjects. After the initial clinical evaluation and laboratory tests (bTSH test, T4, T3, anti‐Tg and anti‐microsomal antibodies) all goitrous patients received 1 ml i.m. of iodized oil (I‐oil) and were followed up for 30 months. The bTSH test was repeated at 6, 12, 20 and 30 months after I‐oil in 21 subjects. A marked reduction in goitre size was observed in 85% of the patients with a concomitant significant increase in the mean serum T4 and T3 concentrations, a significant fall in the mean serum TSH level and a significant decrease in the T3/T4 ratio. Goitrous patients had elevated serum basal Tg levels (55 ± 8 SEM μg/l) and a significantly mean higher peak Tg value after bTSH (200 ± 65 μg/l) as compared with normal subjects (respectively, 11 ± 1·4 and 32 ± 3·4 μg/l). Larger goitres (grade IV) had a significantly higher mean peak Tg response as compared with grade III goitres. Treatment with I‐oil significantly reduced the mean peak Tg response to bTSH after 6 months (59 ± 10 μg/l) but at 12 and 20 months the peak Tg response after the injection rose, respectively, to 110 ± 19 μg/l and 92 ± 14 μg/l (P > 0·02 as compared with 6 months), returning to the normal range only at 30 months. (55 ± 10 μg/l). The absolute increment (ΔTg) was also reduced significantly at 6 and 30 months but not at 12 and 20 months after I‐oil. We conclude that two major factors may be involved in the increased secretion or release of Tg from the goitrous tissue: increased thyrotrophic stimulation and follicular derangement and necrosis. Both events seemed to be corrected with the long‐term action of I‐oil.
HYPOTHALAMIC HYPOPITUITARISM FOLLOWING CRANIAL IRRADIATION FOR NASOPHARYNGEAL CARCINOMA
Authors: LAM K. S. L. , WANG C. , YEUNG R. T. T. , MA J. T. C. , HO J. H. C. , TSE V. K. C. , LING N. 
Published: March 2008

SUMMARYEight patients, one male and seven females, with no pre‐existing hypothalamic‐pituitary disease, who developed symptoms of hypopituitarism following cranial irradiation for nasopharyngeal carcinoma were studied 5 years or more after radiotherapy. All were GH deficient. Four of the patients with no GH response during insulin tolerance tests (ITT) showed increased GH in response to synthetic human growth hormone releasing factor (GRF‐44). Four patients had impaired cortisol responses to ITT, and gradual but diminished cortisol responses to ovine corticotrophin releasing factor (CRF‐41). There was no significant difference between mean peak increments in response to ITT and those in response to CRF‐41. TSH responses to TRH were delayed in five and absent in two patients; four of these had low free T4 index. Prolactin was raised in all seven women and increased further in response to TRH. Two patients had impaired gonadotrophin responses to LHRH. None of the patients had clinical or biochemical evidence of diabetes insipidus. These data suggest that post‐irradiation hypopituitarism in these patients results from radiation damage to the hypothalamus leading to varying degrees of deficiency of the hypothalamic releasing or inhibitory factors.
THE EFFECT OF CHOLINERGIC BLOCKADE ON THE ACTH, β‐ENDORPHIN AND CORTISOL RESPONSES TO INSULIN‐INDUCED HYPOGLYCAEMIA
Authors: EVANS P. J. , DIEGUEZ C. , REES L. H. , HALL R. , SCANLON M. F. 
Published: March 2008

SUMMARYTo assess the effect of cholinergic blockade on the ACTH, β‐endorphin and cortisol responses to insulin‐induced hypoglycaemia, six healthy male volunteers each underwent two insulin tolerance tests in random order, separated by at least 1 week with and without atropine. ACTH levels were significantly greater at + 45 min (mean ± SEM, 223 ± 21 pg/ml vs 148 ± 15 pg/ml, P > 0·01) and at + 120 min (54 ± 11 pg/ml vs 29 ± 10 pg/ml, P > 0·05). β‐endorphin levels were significantly greater at + 30 min (170 ± 45 pg/ml vs 96 ± 32 pg/ml, P > 0·05) and at + 105 min (81 ± 14 pg/ml vs 54 ± 7 pg/ml, P > 0·01). Cholinergic blockade had no effect on plasma glucose or cortisol concentrations. This study demonstrates that cholinergic blockade with atropine facilitates the ACTH and β‐endorphin responses to insulin‐induced hypoglycaemia without altering the cortisol responses.
LH PULSATILITY FOLLOWING ACUTE ETHANOL INGESTION IN MEN
Authors: BANNISTER P. , HANDLEY T. , CHAPMAN C. , LOSOWSKY M. S. 
Published: March 2008

SUMMARYAlcohol abuse leads to impotence, infertility and feminisation. Patients with chronic alcoholism have impaired hypothalamic‐pituitary function, but the effect of acute alcohol intake on hypothalamic function is unclear. The present study investigated the effect of ethanol ingestion on the pulsatile release of LH.Eight healthy male volunteers, aged 24–36 years, were investigated on a control day and a study day. Blood was sampled every 15 min for 8 h. On the study day ethanol was ingested, 1·5 ml/kg as an initial dose with supplements to maintain mean levels at 110–140 mg%. LH was measured on each sample by specific radioimmunoassay. Testosterone was measured at 0, 90 and 360 min. Data were analysed for pulsatile release by visual inspection, iterative computerized analysis and for longer period secretion by spectral analysis. Pulsatile release of LH was shown for all subjects on both days. Ethanol increased median LH levels (4·8 vs 5·55), but not by a significant amount. LH pulse amplitude was increased by ethanol ingestion, 3·7 vs 5·4 IU/I; P > 0.05. Spectral analysis demonstrated a release of LH with a wavelength of 240 min which was unchanged by ethanol administration. Testosterone levels were unchanged.
CHOLINERGIC MUSCARINIC RECEPTOR BLOCKADE WITH PIRENZEPINE ABOLISHES SLOW WAVE SLEEP‐RELATED GROWTH HORMONE RELEASE IN NORMAL ADULT MALES
Authors: PETERS J. R. , EVANS P. J. , PAGE M. D. , HALL R. , GIBBS J. T. , DIEGUEZ C. , SCANLON M. F. 
Published: March 2008

SUMMARYCholinergic pathways play an important role in the regulation of GH secretion from the anterior pituitary gland, and in this study we have investigated whether cholinergic muscarinic receptor blockade with pirenzepine displayed any inhibitory action on slow wave sleep‐related GH release in normal subjects. Six adult males (ages 24–37 years) were studied in a randomized order and fasted from 1800 h on each study day. All subjects showed episodes of slow wave sleep on each occasion and this was followed by peaks of GH release when placebo alone was administered (range of GH peaks 4–50 mU/l). In contrast, pirenzepine treatment (100 mg p.o. at 2200 and 2400 h) completely abolished nocturnal GH release in each individual without altering the occurrence of slow wave sleep itself. These data demonstrate clearly that cholinergic muscarinic receptor blockade completely abolishes slow wave sleep‐related GH release in normal adult subjects. Because of the striking effects it is reasonable to conclude that acetylcholine plays an important stimulatory role in mediating slow wave sleep‐related GH release. This finding may have investigational and therapeutic applications in young patients with Type 1 diabetes mellitus since GH is implicated in some acute metabolic and chronic microvascular complications of this disease.
THE EFFECT OF PERIPHERAL CATECHOLAMINE CONCENTRATIONS ON THE PITUITARY‐ADRENAL RESPONSE TO CORTICOTROPHIN RELEASING FACTOR IN MAN
Authors: MILSOM STELLA R. , DONALD R. A. , ESPINER E. A. , NICHOLLS M. G. , LIVESEY J. H. 
Published: March 2008

SUMMARYTo evaluate the effect of changes in plasma catecholamines on the pituitary‐adrenal response to ovine corticotrophin releasing factor (CRF) in normal man, the response to CRF alone (10 subjects) was compared with responses after infusions of adrenaline (6 subjects), noradrenaline (6 subjects) and after oral administration of the α2 agonist clonidine (10 subjects). Compared to control levels, plasma adrenaline and noradrenaline concentrations were increased three‐ and four‐fold respectively by exogenous infusions, whereas plasma noradrenaline was significantly lowered by clonidine. Despite these changes in plasma catecholamine levels, the responses of plasma ACTH, cortisol and aldosterone to CRF did not differ significantly from control (CRF alone) in any of the three studies. Neither clonidine pretreatment nor catecholamine infusions altered basal levels of plasma ACTH, cortisol or aldosterone and no effect of CRF or catecholamine manipulations on plasma arginine vasopressin concentration was observed. These results show that modulation of peripheral plasma catecholamine levels within physiological limits does not affect CRF‐stimulated release of ACTH or the adrenal response in normal man.
HYPERSECRETION OF PROINSULIN DOES NOT EXPLAIN THE HYPERINSULINAEMIA OF PATIENTS WITH LIVER CIRRHOSIS
Authors: BALLMANN M. , HARTMANN H. , DEACON C. F. , SCHMIDT W. E. , CONLON J. M. , CREUTZFELDT W. 
Published: March 2008

SUMMARYA radioimmunoassay using a proinsulin‐specific antiserum that does not react preferentially with the split forms of proinsulin has been used to compare the response of circulating proinsulin to low (25 g) and high (75 g) oral glucose loads in healthy subjects and in patients with liver cirrhosis. The patients were divided into two groups: Group A (n= 7) with normal glucose tolerance and Group B with diabetic (n= 5) and impaired (n=1) glucose tolerance. There was no apparent correlation between glucose tolerance and the results of quantitative liver function tests. In the fasted state, the concentrations of serum proinsulin did not differ significantly in patients of Group A (0·022 ± 0·002 nmol/1) or Group B (0±026 · 0±004 nmol/1) from those in healthy subjects (0·021 ± 0·002 nmol/l). After 75 g glucose, the rise in serum proinsulin to a maximum concentration of 0·082 ± 0·012 nmol/1 in patients of Group A and to 0·070 ± 0·019 nmol/1 in Group B was not significantly different at any time point up to 180 min from the rise in healthy subjects (to 0·063 ± 0·005 nmol/1). After 25 g glucose, the response of serum proinsulin in Group B patients (maximum concentration 0·035 ± 0·003 nmol/1) was not significantly different from that in healthy subjects (maximum concentration 0·032 ± 0·003 nmol/1) but a slightly enhanced release was observed in the Group A patients (maximum concentration 0·049 ± 0·003 nmol/1) that was significantly greater (P>0·05) at 60 min post‐glucose. In contrast, the concentrations of serum immunoreactive insulin and immunoreactive C‐peptide in all patients with cirrhosis were significantly elevated compared with healthy subjects both in the fasted state and at several time points following high and low oral glucose. In the fasted state, the serum proinsulin/C‐peptide molar ratio, an index of the relative state of secretion of proinsulin and insulin, was significantly lower (P>0·05) in both groups of cirrhotic patients than in healthy subjects. After high and low glucose, this ratio fell in all patients and in the healthy subjects. We conclude that cirrhosis of the liver is associated with a hypersecretion of insulin but hyperproinsulinaemia does not contribute appreciably to the elevated concentration of immunoreactive insulin in the peripheral circulation.
PATTERN OF PLASMA LEVELS OF CORTISOL, DEHYDROEPIANDROSTERONE AND PREGNENOLONE SULPHATE IN NORMAL SUBJECTS AND IN PATIENTS WITH HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLAEMIA DURING ACTH INFUSION
Authors: BOIZEL R. , de PERETTI E. , CATHIARD A. M. , HALIMI S. , BOST M. , BERTHEZENE F. , SAEZ J. M. 
Published: March 2008

SUMMARYThe aim of this study was to determine whether patients with homozygous familial hypercholesterolaemia (FH) have impaired adrenal cortical function. Plasma levels of cortisol, dehydroepiandrosterone (DHA), pregnenolone sulphate (PS) and DHA sulphate (DHAS) were measured during an 8 h ACTH infusion in six controls and two patients with homozygous FH. The basal PS levels of both patients and the basal DHA level of one were abnormally low for age and pubertal stage. During ACTH infusion we observed in both patients: (1) a mild impairment of control response after sustained stimulation (P> 0·002); (2) a clear impairment of PS response (values less than 2 SD of those in controls); (3) a clear impairment of DHA response (values less than 2 SD) until 4 h in the boy who was at pubertal stage 4 and whose response could be compared to controls; no increase at all in the affected girl (pubertal stage 2) at a stage where normal subjects respond with significant increase. These results suggest that patients with FH lack cholesterol for corticosteroid biosynthesis under maximal ACTH stimulation and that mild chronic ACTH stimulation due to a deficit in the cholesterol supply to adrenal cells might increase the conversion of Δ5 to Δ4‐steroids. They provide further evidence to support the primordial role of low density lipoprotein (LDL)‐cholesterol in adrenal steroidogenesis in vivo.
ANALYSIS OF THE RELATION BETWEEN ALOPECIA AND RESISTANCE TO 1,25‐DIHYDROXYVITAMIN D
Authors: MARX S. J. , BLIZIOTES M. M. , NANES M. 
Published: March 2008

SUMMARYAlopecia is a frequent feature in hereditary resistance to (1,25(OH)2D). We sought insight into this feature by analysing data from affected members of 30 kindreds. We assessed indices of mineral metabolism in one group with normal hair compared with a group with alopecia. Hereditary resistance to 1,25(OH)2D was diagnosed at an earlier age in alopecic patients (0·9 vs 3·3 years, P> 0·05); this reflected late presentation of metabolic bone disease in some cases with normal hair and could not be attributed to early diagnosis resulting from the striking feature of alopecia. For untreated subjects, serum concentrations of calcium and 1,25(OH)2D were similar in both groups of patients. During calciferol therapy, however, the cases with alopecia showed lower serum calcium (1·9 vs 2·4 mmol/1, P > 0·005), but higher serum 1,25(OH)2D (2900 v 340 pg/ml, P> 0·005). Hair status did not predict the type of defect identified with cultured skin fibroblasts but did correlate with responsiveness of 25(OH)D 24‐hydroxylase to 1,25(OH)2D3 in those cells. Cells from seven of eight kindreds with alopecia showed no 24‐hydroxylase response to high doses of 1,25(OH)2D3 while cells from five of six kindreds with normal hair showed a 24‐hydroxylase response to high doses of 1,25(OH)2D3. We conclude that in cases with hereditary resistance to 1,25(OH)2D alopecia reflects the more severe grades of this resistance based upon earlier age at time of diagnosis, lower potential for calcaemic response to calciferols, and lower potential for 24‐hydroxylase response to 1,25(OH)2D3 by cultured skin fibroblasts.
DEFINITION OF BIOACTIVE PROLACTIN PULSATIONS DURING THE MENSTRUAL CYCLE
Authors: BLANK M. S. , DUFAU MARIA L. 
Published: March 2008

SUMMARYPatterns of circulating prolactin bioactivity during three stages of the menstrual cycle were studied in detail in four normally cycling women. Serial blood samples were withdrawn at 10 or 15 min intervals for up to 8 h. Plasma prolaction concentrations were quantitated by a bioassay which is based on the replication of a rat lymphoma cell line (Nb2 node) and by conventional radioimmunoassay. A total of 50–103 samples from each patient was analysed. Using a threshold‐based algorithm, definite pulsations of prolactin biological (B) and immunological (I) activity were detected at most stages of the menstrual cycle. The periodicity of these peaks ranges from 1 to 11/2 h. However, pulsations were less evident in one subject who had asymptomatic hyperprolactinaemia although circulating prolactin was fully bioactive (mean B:I ratios being 1 02–1.25). B:I ratios in the three normoprolactinaemic women were generally lower, ranging from 0.39±0.02 to 0–93±0.03. Elevations in the B:I ratio of normoprolactinaemic women were associated with bioactive peaks; this was not always the case in the hyperprolactinaemic subject. Thus, the lack of symptoms in this hyperprolactinaemic subject could not be due to bioinactive prolactin, but might perhaps be due to the absence of episodic prolactin secretion which would desensitise target organs.
LOSS OF LUTEINIZING HORMONE BIOACTIVITY IN PATIENTS WITH PROSTATIC CANCER TREATED WITH AN LHRH AGONIST AND A PURE ANTIANDROGEN
Authors: ST‐ARNAUD R. , LACHANCE R. , KELLY SUSAN J. , DUPONT BELANGER. A. , LABRIE F. 
Published: March 2008

SUMMARYChronic treatment of adult men with LHRH agonists causes a decrease in serum testosterone and 5α‐dihydrotestosterone to castrate levels. In the presence of such low levels of circulating testicular androgens, the concentration of serum LH measured by radioimmunoassay (RIA) sometimes remains normal or is only partially inhibited. In order to assess the biological activity of circulating LH, we have used the mouse interstitial cell assay. Blood samples were obtained from patients with prostatic carcinoma treated with the LHRH agonist [D‐Trp6] LHRH ethylamide in combination with the pure antiandrogen Flutamide (Euflex). While serum LH levels measured by RIA were only partially reduced from 2.2±0.3 (SEM) to 1.1±0.1 ng/ml after 3 months of therapy, bioactive LH was markedly inhibited from 0.43±0.04 to 0.030±0.007 ng/ml, thus causing the ratio of biologically active to radioimmunoassayable LH to drop from 0.26±0.03 to 0.03±0.01. In the same patients, serum testosterone levels were decreased from 3.91±0.51 to 0.14±0.05 ng/ml after 3 months of treatment. In patients treated for 6 months, the bio/immuno ratio was still reduced at 0.032±0.005. These data show a marked loss of LH biological activity during treatment of adult men with an LHRH agonist and an antiandrogen. The close parallelism observed between serum testosterone and bioactive LH levels suggests that the loss of biological activity of the gonadotrophin is mainly, if not exclusively, responsible for the inhibition of testicular androgen secretion observed during chronic treatment with LHRH agonists.
COMPARISON OF BLOOD SPOT, SALIVARY AND SERUM PROGESTERONE ASSAYS IN THE NORMAL MENSTRUAL CYCLE
Authors: PETSOS P. , RATCLIFFE WENDY A. , HEATH D. F. , ANDERSON D. C. 
Published: March 2008

SUMMARYSensitive direct (non‐extraction) radioimmunoassays for assay of progesterone (Po) in saliva and capillary blood dried on filter paper have been developed to facilitate collection of specimens for the assessment of luteal function in the investigation of infertility. The antiserum had been raised to a Po I lα‐hemisuccinyl conjugate and the assays employ Po 11α‐glucurony 1‐[25I] tyramine as tracer with separation by solid phase double antibody. Po levels in saliva and capillary blood were compared with those in serum in matched specimens collected daily throughout the menstrual cycle from six female volunteers. The correlation between blood (y) and serum (x) Po levels (y= 0.439x‐2.98, r=0.98) was superior to that between salivary (y) and serum levels (x) (y=0.0637x+0.020. r= 0.89). Blood spot and serum Po levels were uniformly undetectable throughout the follicular phase, whereas in 2 out of 72 saliva specimens Po was inappropriately raised (60 and 120 pmol/l) possibly reflecting contamination of the specimens. Salivary and blood progesterone assays both lack adequate sensitivity to measure Po reliably in early or late luteal phases when serum levels are <12 nmol/l but are well suited to assess luteal function during the mid‐luteal phase of the cycle (4–10 d before menses) when serum levels in the six subjects ranged from 22–84 nmol/l, with corresponding blood levels of 6.2–35 nmol/l and saliva levels of 130–620 pmol/l. We conclude that blood spot and saliva Po levels both correlate well with Po levels in serum, but that blood spot Po levels are more reliable.
THE EFFECT OF PHYSIOLOGICAL CHANGES IN OVARIAN STEROIDS ON THE PROLACTIN RESPONSE TO GONADOTROPHIN RELEASING FACTOR
Authors: TAN Y. M. , STEELE P. A. , JUDD S. J. 
Published: March 2008

SUMMARYThis study was designed to assess the effect of an altered level of serum oestrogen and progesterone on the prolactin (PRL) response to gonadotrophin releasing hormone (GnRH). Six normal women were studied in the early follicular phase and the mid‐luteal phase of one cycle and five menopausal women were studied before and after treatment with progesterone. Blood samples were collected at 15 min intervals for 6 h after a basal collection period of 30 min. Intravenous boluses of GnRH (1 μg, 10 μg and 50 μg) were given at 0, 2 and 4 h. Basal samples were assayed for 17β‐oestradiol (E2), oestrone (E1) and progesterone (P); LH, FSH and PRL were measured in all samples. Serum PRL was significantly elevated in all groups after 10 μg of GnRH with maximum increments (±SEM) ranging from 3.9±1.3 μg/l in early follicular phase women to 14.7 ± 4.7 μg/l in progesterone‐treated menopausal women. The PRL response to GnRH was significantly greater in the luteal phase and in menopausal women compared to early follicular phase women. There was a significant correlation between the maximum PRL response and the maximum LH response to GnRH in all the women studied (r= 0.7; P < 0.01). A significant correlation was also found between the maximum PRL response and the basal serum oestrogen concentration in the normal cycling women (r= 0.8; P < 0.01), but not when the menopausal women were included in the analysis. Administration of progesterone to menopausal women did not significantly affect the PRL response to GnRH and no significant correlation was found between the basal serum progesterone and the PRL response to GnRH. We conclude that GnRH stimulates the secretion of PRL in normal, cycling and in menopausal women to a degree which is more closely correlated with the LH response than with the circulating oestrogen or progesterone concentration. This is consistent with the hypothesis that GnRH exerts an indirect effect on the lactotrophe by stimulating the prodution of a paracrine factor from the gonadotrophe. We suggest that the action of GnRH on the lactotrophe may be physiological in view of its reported action in synchronizing the secretion of LH and PRL and in maintaining the acute releasable pool of PRL in the lactotrophe.
HORMONAL AND CARDIOVASCULAR RESPONSES TO DDAVP IN MAN
Authors: WILLIAMS T. D. M. , LIGHTMAN S. L. , LEADBEATER M. J. 
Published: March 2008

SUMMARYHormonal and cardiovascular responses to 1‐desamino‐8‐d‐arginine vasopressin (DDAVP) were investigated in six normal adult volunteers. After overnight fluid deprivation, an intravenous injection of either DDAVP (0.4 μg/kg) or the same volume of normal saline was administered. One hour later an intravenous infusion of hypertonic saline was commenced and continued over two hours. Five minutes following the DDAVP injection, facial flushing, a fall in diastolic blood pressure by an average of 13% and a rise in pulse rate by an average of 18% were observed. There was a significant increase in plasma renin activity and plasma cortisol concentration, but no significant changes were observed in plasma concentrations of LH, FSH, TSH, prolactin or GH. Following osmotic stimulation by hypertonic saline plasma AVP rose to the same extent in both the DDAVP and control studies. DDAVP (0.4 μg/kg) was also administered to five subjects with cranial diabetes insipidus. Again facial flushing, increased facial temperature, a fall in diastolic pressure and a rise in heart rate were all observed, suggesting that DDAVP exerts its cardiovascular actions by a mechanism other than antagonism of circulating endogenous AVP.