bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE RELATIONSHIP OF ERYTHROCYTE INSULIN RECEPTORS TO RED CELL AGE AND TO MONOCYTE INSULIN RECEPTORS
Authors: WARD G. M. , REES A. R. , NAYLOR B. A. , TURNER R. C. 
Published: March 2008

SUMMARYThis study examines the degree to which erythrocyte insulin receptors might be used instead of monocyte insulin receptors to assess overall insulin receptor status. Red blood cells from eight normal subjects were fractionated into older and younger populations by high speed centrifugation. Fractionated red cells (3·5 ± 109/ml) were incubated with 0·14 ng/ml of ‘monoiodo’125I‐insulin for 2·5 h at 15°C. The high reticulocyte fractions (mean 2·1% reticulocytes) had greater insulin binding than the low reticulocyte fractions (mean 0·6%), −9·0% compared with 6·0% specific binding, respectively. The difference (P > 0·05) appeared to be predominantly due to a greater number of high affinity sites per cell in the high reticulocyte fractions. Culture of high and low reticulocyte fractions, from both normal subjects and patients with high reticulocyte counts, in vitro for 2·5 days at 37°C, markedly reduced reticulocyte count and insulin binding of the high reticulocyte fractions, but produced little change in the low reticulocyte fractions. It appeared the reticulocytes had a ten‐ to twenty‐fold increase in binding sites compared with erythrocytes.There is little degradation of insulin by intact erythrocytes or reticulocytes at 37°C, with a dissociation between insulin binding and insulin degradation. The large degradative capacity of haemolysed red cells implies that insulin receptor assays would be invalid in the presence of haemolysis.Monocyte and erythrocyte receptors were compared in the same blood samples from overnight fasted subjects, with a correlation between insulin binding (r = 0·62). The inexact correlation may be partly due to the non‐homogeneous insulin binding of red cells, but correction for differences between reticulocyte content of the assayed red cells only increased the correlation to r = 0.67. Whilst the non‐homogeneity of red cells means that erythrocyte binding must be interpreted with caution, we cannot exclude similar non‐homogeneity of monocyte populations.
A COMPARATIVE STUDY OF THE BINDING OF GRAVES’ IMMUNOGLOBULINS BY THE PATIENT'S OWN AND OTHER THYROID MEMBRANES
Authors: GOSSAGE A. A. R. , BYFIELD P. G. H. , COPPING SUSAN , HIMSWORTH R. L. 
Published: March 2008

SUMMARYThyroid membrane preparations from six patients with active Graves’ disease were tested in an assay which detects the thyroid interactive immunoglobulins of Graves’ disease by their inhibition of binding of [125I]‐thyroid stimulating hormone (TSH). With all preparations inhibition of binding of 125I‐TSH by excess TSH could be demonstrated (specific binding). The patients’ own immunoglobulins were assayed against their own thyroid membranes and against each other's under exactly comparable conditions. Inhibition of binding by IgGs from the patients varied between membrane preparations: with one preparation 5/6 IgGs were inhibitory but with another none were effective. Of the six patients, their own IgG inhibited binding of 125I‐TSH to their own thyroid membrane preparation in only four instances, and when interaction did occur this did not reliably predict that the membrane preparation would interact with IgGs from other patients with Graves’ disease. The selection of a membrane preparation for this assay cannot be made solely on ability to specifically bind TSH but the measure of the specific interaction with a Graves’ IgG of proven potency must also be considered. Moreover, because of the variability between different membrane preparations, sequential clinical studies on individual patients, of the changes in concentration of Graves’ IgG, must be performed using the same selected thyroid membrane preparation.We infer from these observations that the membrane structure in the vicinity of the TSH binding site is an important determinant of the interaction of Graves’ IgGs with the TSH receptor, and that the configuration of this area is variable between individuals of the same species. The distinction between ‘human‐specific’ and ‘non‐species‐specific’ thyroid stimulating antibodies is therefore probably not valid. The observation that the patient's own IgG was not often the most potent IgG inhibitor of binding of TSH also suggests that the Graves’ IgG binding site is not identical or restricted to the TSH binding site; alternative explanations are discussed.
LACK OF EFFECT OF OESTROGENS ON ADRENAL ANDROGEN SECRETION IN CHILDREN AND ADOLESCENTS WITH A COMMENT ON OESTROGENS AND PUBIC HAIR GROWTH
Authors: SKLAR C. A. , KAPLAN S. L. , GRUMBACH M. M. 
Published: March 2008

SUMMARYTo study the effect of oestrogen on adrenarche and adrenal androgen secretion we measured plasma concentrations of dehydroepiandrosterone‐sulphate (DHEA‐S), androstenedione (Δ4A) and oestradiol (E2) in the following groups: children with premature adrenarche; agonadal patients before and after initiation of oestrogen replacement therapy; and, children exposed to increased concentrations of endogenous oestrogen at a precocious age.Fourteen of fifteen patients with premature adrenarche had plasma E2 levels in the normal prepubertal range (> 10 pg/ml), despite a mean DHEA‐S concentration that was significantly elevated for age (6–8 years: 72·5 ± 12·6 μg/dl v. 11·4 ± 2·9 μg/dl, P 0·002). DHEA‐S and Δ4 A concentrations in fifteen patients with gonadal dysgenesis before and 2–14 months after initiation of oestrogen replacement therapy were not significantly different despite the appearance of oestrogen‐induced secondary sex characteristics. Six of fifteen patients developed increased pubic hair during oestrogen therapy but had no increase in the concentrations of plasma DHEA‐S. Two patients (aged 1 year 4 months and 4 years 10 months) with oestradrol secreting ovarian follicular cysts (plasma E2 11–796 pg/ml) and one patient (aged 6 years 10 months) who had had a granulosa cell tumour of the ovary maintained preadrenarchal DHEA‐S levels (> 6·2 μg/dl) despite exposure to concentrations of circulating oestrogen that were high for their chronological age.We interpret the results as follows: (1) Initiation of premature adrenarche occurs without an increase into the early pubertal range of E2 levels. (2) Administration of replacement doses of oestrogen does not increase adrenal androgen concentrations in adolescent patients with gonadal dysgenesis. (3) Elevated plasma concentrations of endogenous ovarian oestrogens at a precocious age did not increase adrenal androgen secretion in childhood. Thus, it appears that circulating oestrogens are either required for the activation or maintenance of adrenarche nor do they significantly affect the plasma concentrations of adrenal androgens in children and adolescents. (4) The pubic hair growth associated with the institution of oestrogen replacement in adolescent patients with gonadal dysgenesis is not mediated by an increase in adrenal androgen secretion and may result from a specific effect of oestrogen on androgen action at the target tissue (pubic skin).
CLINICAL RESPONSE TO METYRAPONE AS INDICATED BY MEASUREMENT OF MINERALOCORTICOIDS AND GLUCOCORTICOIDS IN NORMAL CHILDREN
Authors: SONINO NICOLETTA , CHOW DIANE , LEVINE LENORE S. , NEW MARIA I. 
Published: March 2008

SUMMARYThe effect of 24‐h metyrapone administration on adrenal mineralocorticoid and glucocorticoid pathways has been studied in normal children. Urine and serum steroid concentrations were evaluated. Simultaneous determinations of deoxycorticosterone (DOC), corticosterone (B), cortisol (F), and aldosterone (aldo), in both urine and serum, were carried out by celite column chromatography and radioimmunoassay. 11‐deoxycortisol (Compound S) in serum and urine, urinary free 18‐hydroxydeoxycorticosterone (18‐OH‐DOC), urinary free 18‐hydroxycorticosterone (18‐OH‐B), and urinary aldosterone‐18‐glucuronide (pH 1 aldo) were measured separately by specific methods. Conclusions drawn were that (1) Useful indices of metyrapone effect were the marked rise of 11‐deoxysteroids (DOC and S), and the fall of aldo and 18‐OH‐B; no changes occurred in 18‐OH‐DOC and the 11‐hydroxylated steroids (B, F); (2) Serum and urine values were significantly correlated, indicating that both were equally reliable in the evaluation of the metyrapone test; (3) Hormonal ratios indicate that metyrapone inhibition affected the 11‐hydroxylation of DOC and Compound S, and the 18‐hydroxylation of DOC and B; and (4) The correlation between DOC/B and S/F ratios was highly significant (r = 0·86; P < 0·0001), showing the same degree of inhibition of 11‐hydroxylase functions for both 17‐hydroxy (17‐OHS) and 17‐deoxysteroids.
THE OPIOID CONTROL OF LH AND FSH RELEASE: EFFECTS OF A MET‐ENKEPHALIN ANALOGUE AND NALOXONE
Authors: GROSSMAN A. , MOULT P. J. A. , GAILLARD R. C. , DELITALA G. , TOFF W. D. , REES LESLEY H. , BESSER G. M. 
Published: March 2008

SUMMARYThe effect of a long‐acting analogue of met‐enkephalin (DAMME) and naloxone on gonadotrophin secretion has been investigated in man. In menopausal women DAMME induced a progressive fall in LH to approximately 60% of basal levels at 3 h, which was blocked by naloxone; there was a smaller fall in FSH that did not attain statistical significance. However, the LHRH‐induced rise in LH and FSH in young male volunteers was unaffected by pretreatment with a high‐dose DAMME infusion. Naloxone infusion in young male and female normal subjects produced a significant rise in both LH and FSH. Long‐term infusion of naloxone appeared to increase the rate, and possibly the amplitude, of LH pulsatility. These results suggest that met‐enkephalin‐like opioid peptides exert a tonic inhibitory control of LH release in both menopausal and young subjects of both sexes. This control is most likely to be at the level of the hypothalamus, and involves modulation of pulsatile LHRH release.
ORBITAL PSEUDOTUMOUR AND LACRIMAL INVOLVEMENT DEVELOPING IN A PATIENT WITH RIEDEL'S STRUMA RECEIVING STEROIDS
Authors: WILMSHURST P. , MELSOM R. , GOSTELOW B. 
Published: March 2008

SUMMARYWe present a patient with hypothyroidism secondary to Riedel's struma, treated with thyroxine and prednisolone, who developed clinical and radiological features of a unilateral orbital pseudotumour with lacrimal gland involvement; the histology of which was indistinguishable from that of the thyroid gland.
PREVALENCE OF VARIOUS DEGREES OF HYPOTHYROIDISM AMONG PATIENTS OF A GENERAL MEDICAL DEPARTMENT
Authors: RINIKER M. , TIÈCHE M. , LUPI G. A. , GROB P. , STUDER H. , BÜRGI H. 
Published: March 2008

SUMMARYWe have measured basal thyrotropin (TSH) in 945 consecutive patients of a general medical department. Additional thyroid tests were carried out in patients with elevated TSH. Thirty patients (3·1%) had subclinical hypothyroidism, i.e. an elevated TSH with no clinical signs and with a normal free thyroxine index. A cause was found in only fifteen of these thirty patients. Thirteen additional patients (1·37%) had mild or overt primary hypothyroidism, three of which were already diagnosed. This prevalence is three times higher than that found in a retrospective survey at the same hospital. Of the ten newly‐detected cases five were discharged on thyroid hormone replacement. In two patients the antithyroid drugs which were the cause of hypothyroidism were discontinued. The remaining three patients had severe non‐thyroidal illnesses and thyroid hormone was not prescribed. A cause for the hypothyroidism (autoimmune thyroid disease, post‐radioiodine, post‐thyroidectomy or antithyroid drugs) was established in all but two cases. The data suggest that thyroid function tests (preferably a TSH) should be performed on any patient with prior treatment to the thyroid and, in addition with very broad indications, perhaps even routinely, in all women over 50 years of age.
HUMAN POST‐MORTEM PINEAL ENZYME ACTIVITY
Authors: SMITH J. A. , MEE T. J. X. , PADWICK D. J. , SPOKES E. G. 
Published: March 2008

SUMMARYThe synthetic enzymes for melatonin production, serotonin‐N‐acetyltransferase (SNAT) and hydroxy‐indole‐O‐methyltransferase (HIOMT) were measured in post‐mortem pineal organs from eighty‐eight men and women. The activity of each enzyme was correlated with age and sex. No difference was seen in either parameter when the maximum or minimum activities were measured in the death time periods of the diurnal rhythm established earlier. However, an annual bimodal rhythm was seen in HIOMT activity with maximal values occurring in January and July and minimum activities in March and October. The SNAT and HIOMT enzymes have previously been shown to be stable when measured in pineal organs held under the usual post‐mortem conditions. Pineal HIOMT has also been measured in twenty‐one psychotic individuals. Whilst the schizophrenic group showed significantly increased values, the schizophrenic‐like group had normal values. The results were not affected by ante‐mortem or post‐mortem states or by drug treatment. Any clinical interpretation of pineal dysfunction in disease states need not, therefore, take into consideration age, or possibly sex, but should be aware of the normal diurnal rhythm as well as the bimodal annual rhythm.
A SENSITIVE TECHNIQUE FOR DETERMINATION OF THYROID‐STIMULATING IMMUNOGLOBULIN (TSI) IN UNFRACTIONATED SERUM*
Authors: ETIENNE‐DECERF J. , WINAND R. J. 
Published: March 2008

SUMMARYA new sensitive and reproducible technique for the determination of thyroid stimulating immunoglobulins is described. This procedure employs cells obtained from primary culture of human thyroid gland. We measured the increase of cyclic AMP after addition of patient sera. The major advantages of this procedure are the improved sampling throughout with the ability to measure eighty samples simultaneously without fractionation of serum. This large sample allows us to test forty sera together and to assay in duplicate, thus increasing the validity of the results. The TSI activity is associated with the immunoglobulins G (IgG) fraction and we obtained a linear dose response curve with IgG as well as with whole serum. The results obtained in various thyroid diseases are discussed.
ALTERATIONS IN CIRCULATING THYROID HORMONES AND THYROXINE BINDING GLOBULIN IN CHRONIC ALCOHOLISM
Authors: GEURTS J. , DEMEESTER‐MIRKINE N. , GLINOER D. , PRIGOGINE T. , FERNANDEZ‐DEVILLE M. , CORVILAIN J. 
Published: March 2008

SUMMARYThe present study concerns eighteen chronic alcoholics with minimal liver damage. A significant reduction in total serum T4 with an accompanying drop in circulating TBG was observed in these otherwise euthyroid patients. During alcohol withdrawal, we observed a rapid increase in T4 and TBG into the normal range. We suggest that the fall in the level of circulating thyroxine‐binding globulin is related to a defect in its synthesis or secretion by the liver due to ethanol consumption. Caution is recommended in the interpretation of thyroid function tests in chronic alcoholics.
FAMILIAL HYPERCHOLESTEROLAEMIA AND PRIMARY HYPOTHYROIDISM: COEXISTENCE OF BOTH DISORDERS IN A YOUNG WOMAN WITH SEVERE HYPERCHOLESTEROLAEMIA
Authors: ILLINGWORTH D. R. , McCLUNG M. R. , CONNOR W. E. , ALAUPOVIC P. 
Published: March 2008

SUMMARYSevere hypercholesterolaemia in a 17‐year‐old girl was found to be due to the coexistence of heterozygous familial hypercholesterolaemia and chronic lymphocytic thyroiditis with primary hypothyroidism. Her cultured skin fibroblasts showed a 70–75% reduction in the binding, internalization and degradation of 125I‐labelled low density lipoprotein and several other family members were hypercholesterolaemic. Replacement therapy with L‐thyroxine reduced the concentrations of total and low density lipoprotein cholesterol and apoprotein B in the patient's plasma to values similar to those in other sibs with only heterozygous familial hypercholesterolaemia. Severe hypercholesterolaemia attributable to coexistent heterozygous familial hypercholesterolaemia and hypothyroidism in teenage girls may be estimated to occur with a frequency of between 1 in 500 000 and 1 in 106. This value is similar to the gene frequency for homozygous familial hypercholesterolaemia.
FAILURE OF HAEMAGGLUTINATION AND IMMUNOFLUORESCENCE METHODS TO DETECT SERUM ORBITAL ANTIBODIES IN PATIENTS WITH GRAVES' OPHTHALMOPATHY
Authors: HENDERSON JANICE , WALL J. R. 
Published: March 2008

SUMMARYSerum antibodies against human, bovine, and guinea‐pig, orbital antigens were tested for in patients with Graves' ophthalmopathy using haemagglutination and immunofluorescence techniques. Although low titres of antibodies were demonstrated in a small proportion of patients with Graves' ophthalmopathy, the prevalence was similar to that for normal subjects using both tests. The significance of these findings and the evidence for a role of autoantibodies in the pathogenesis of Graves' ophthalmopathy are discussed.
A RADIOIMMUNOASSAY FOR NEUROTENSIN
Authors: KRONHEIM S. , SHEPPARD M. C. , MILLER J. 
Published: March 2008

SUMMARYA specific radioimmunoassay for neurotensin has been developed with a sensitivity of 40 pg/ml. Neurotensin‐like immunoreactivity in human plasma shows characteristics similar to synthetic neurotensin on Sephadex G‐25 (f) gel chromatography.
EFFECT OF EXOGENOUS INSULIN ON FASTING SERUM LEVELS OF GASTRIC INHIBITORY POLYPEPTIDE (GIP) IN JUVENILE DIABETES
Authors: TALAULICAR M. , EBERT R. , WILLMS B. , CREUTZFELDT W. 
Published: March 2008

SUMMARYThe effect of insulin on fasting levels of immunoreactive gastric inhibitory polypeptide (IR‐GIP) has been examined in insulin‐dependent, juvenile‐type diabetics who were well‐controlled with two doses of an intermediate insulin. After withdrawal of the evening insulin injection the fasting blood glucose and serum IR‐GIP levels were elevated and decreased significantly following intravenous insulin towards normal values. There was a significant positive correlation between levels of blood glucose and serum IR‐GIP before and during insulin application. It is suggested that fasting serum GIP levels increase in case of insulin deficiency because basal GIP secretion is suppressed by normal insulin levels.
GROWTH HORMONE (GH) SECRETION IN HEPATIC ENCEPHALOPATHY
Authors: LANGER MARIA , MASALA A. , ALAGNA S. , RASSU S. , MADEDDU G. , SOLINAS A. , CHIANDUSSI L. 
Published: March 2008

SUMMARYElevated plasma concentrations and abnormal secretory patterns of GH have been found in patients with cirrhosis of the liver. Displacement of brain dopaminergic monoamines by false ‘neurotransmitters’ produced in the gut has been postulated as a cause of encephalopathy. In this study basal GH plasma levels and their response to TRH and l‐DOPA were determined in thirty‐nine cirrhotic patients and fifteen controls. Eleven patients had evidence of encephalopathy (Group 1), twenty‐eight did not (Group 2). Both basal levels and the mean peak response to TRH were significantly higher in the cirrhotic patients than in the controls (Group 3). Peak values were moderately, but not significantly, higher in Group 1 than in Group 2. The response to l‐DOPA was considerably lower in the encephalopathic patients in comparison with the subjects of both Group 2 and Group 3. This finding is consistent with depletion of active ‘neurotransmitters’ in CNS. Our data fail to demonstrate clearly whether the paradoxical response to TRH can also be related to these abnormalities of monoamine metabolism in cirrhotics.
FACTORS RELATING TO ALDOSTERONE SECRETION RATE, THE EXCRETION OF ALDOSTERONE 18‐GLUCURONIDE, AND THE PLASMA ALDOSTERONE CONCENTRATION IN CIRRHOSIS
Authors: WILKINSON S. P. , WHEELER P. G. , JOWETT T. P. , SMITH I. K. , KEENAN J. , SLATER J. D. H. , WILLIAMS R. 
Published: March 2008

SUMMARYIn a group of eight patients with cirrhosis the rate of renal excretion of the 18‐glucuronide metabolite of aldosterone (UAldoV) was found to be closely related to the aldosterone secretion rate (ASR). UAldoV was therefore used as an index of ASR in a further group of fifty patients in order to evaluate the possible importance of factors known to regulate aldosterone secretion. UAldoV showed statistically significant relationships to both plasma renin activity (PRA) and the plasma sodium concentration (PNa), but not to the plasma potassium concentration (PK) or the renal excretion of cortisol (UCortV), the latter used as an index of adrencorticotrophic hormone activity. The plasma aldosterone concentration (PAido) was determined in fifty‐eight patients and also found to show statistically significant relationships to PRA and PNa. PAldo showed a weak, though statistically significant, relationship to PK, but not to UCortV. These findings are in keeping with a role for the renin‐angiotensin system in the control of aldosterone secretion in cirrhosis although evidence from other studies suggest other factors to be involved also. Whether PNa was another determinant of ASR, or whether aldosterone was a determinant of PNa through regulating sodium reabsorption by the proximal tubule of the nephron, is uncertain.
PROLACTIN RESPONSE TO METOCLOPRAMIDE AND CHLORPROMAZINE IN PRIMARY TESTICULAR FAILURE AND ISOLATED GONADOTROPHIN DEFICIENCY
Authors: SPITZ I. M. , HALPERIN Y. , ZYLBER‐HARAN E. , SHILO S. , LEROITH D. , LIEL Y. , LIVSHIN J. , LAUFER N. , SCHENKER J. 
Published: March 2008

SUMMARYThe aim of the present study was to measure the PRL response to metoclopramide (MET) and chlorpromazine (CPZ) in seventeen patients with primary testicular failure and eight patients with isolated gonadotrophin deficiency (IGD). The responses were compared with those to TRH. Basal gonadotrophins and peak responses to LHRH were increased in testicular failure and reduced in IGD. Basal PRL levels were normal in both groups of patients. However, when compared with controls, the PRL response to both MET and CPZ as well as to TRH was exaggerated in primary testicular failure, whereas the responses were decreased in IGD. In both patient groups, as well as in the controls, the PRL response to MET exceeded that to TRH and CPZ. It is suggested that alterations in the steroid milieu are responsible for the exaggerated PRL response to MET, CPZ and TRH in primary testicular failure and the reduced response observed in IGD.
PROLACTIN PULSATILITY IN PATIENTS WITH GONADAL DYSFUNCTION
Authors: MOULT P.J.A. , DACIE JANET E. , REES LESLEY H. , BESSER G.M. 
Published: March 2008

SUMMARYSerum prolactin concentrations have been measured at 15 min intervals for 2 h on 240 occasions in 227 patients with symptoms which could have been due to hyperprolactinaemic gonadal dysfunction. Of the 227, 138 had at least one elevated random prolactin level. Overall, 22% showed no significant fluctuation in prolactin. In 38% the levels fell progressively from the start of the sampling period, this pattern being found most commonly in patients complaining of infertility. The sampling method yielded a basal or unstressed prolactin concentration which was, on average, 27% lower than random prolactin concentrations. However, a comparison with clinical data, the radiological appearances of the pituitary fossa, and the response to bromocriptine therapy, has shown that there is no predictive information in the multiple sampling results that could not have been obtained from two or three random prolactin levels.
LACK OF RESPONSE OF 1,25‐DIHYDROXYCHOLECALCIFEROL TO EXOGENOUS PARATHYROID HORMONE IN A PATIENT WITH TREATED PSEUDOHYPOPARATHYROIDISM
Authors: BRAUN J. J. , BIRKENHÄGER J. C. , VISSER T. J. , JUTTMANN J. R. 
Published: March 2008

SUMMARYThe response of serum 1,25‐dihydroxycholecalciferol (1,25‐OH2CC) concentration to the administration of parathyroid extract (PTE) was studied in a patient with pseudohypoparathyroidism (PHP) type I, 3 days after withdrawal of dihydrotachysterol (DHT) treatment. The patient had had a normal serum calcium (Ca), phosphorus (P) and immunoreactive parathyroid hormone (iPTH) level on DHT for 6 years. After PTE administration no rise of the 1,25‐OH2CC concentration and no response of urinary cAMP and P were seen.