bluuebunny/crossref_metadata_2025_split huggingface dataset:
Highly specific solid phase immunoextraction of TSH using anti-TSH antibodies purified by affinity chromatography
Authors: Ponsin Gabriel , Mornex René 
Published: December 2008

Abstract.
Highly specific anti-TSH antibodies were purified from a crude antiserum preparation by affinity chromatography using TSH-sepharose column as the adsorbant. This procedure completely eliminated the original LH binding activities. The purified anti-TSH antibodies were then coupled to CNBr activated sepharose 4 B and used in separating TSH from rat pituitaries by batch procedure. This method is demonstrated to be highly specific for purifying labelled TSH from pituitaries previously incubated in the presence of [14C]tyrosine. The effect of TRH on TSH biosynthesis is presented as a biological application of this procedure.
T4 degradation rate and plasma levels of TSH and thyroid hormones in ten young bulls during feeding conditions and 48 h of starvation
Authors: Tveit Borghild , Almlid Torbjørn 
Published: December 2008

Abstract.
The effect of starvation on thyroid hormones was studied during a starvation period of 48 h in 10 young bulls. Mean thyroxine degradation rate decreased from K/day 0.32 during feeding to 0.23 during fasting. Mean plasma concentration of T4 decreased to 75% of normal, and it was calculated that the mean thyroxine secretion rate during the starvation period was 24% of normal.
Plasma concentration of free thyroxine decreased to 54% of normal, indicating that the concentration of binding protein was not decreased.
T3 and reverse T3 decreased to about 60% of normal. This indicated a parallel decrease in the secretion of all 3 hormones. We did not find evidence of an inactivating pathway for T4 as has been shown in humans during starvation.
TSH decreased to 85% of normal.
T4, T3 and reverse T3 in the plasma of rats during the first 3 months of life
Authors: van der Heide D. , Ende-Visser M. P. 
Published: December 2008

Abstract.
A very sensitive radioimmunoassay for reverse T3 in rat plasma is described. The concentrations of T4, T3 and reverse T3 in the plasma of male and female rats were determined during the first 3 months of life. T4 concentrations reached a maximum value of 5.2±0.7 μg/100 ml (mean ± sd) when the rats were about 16 days old. As of day 28 the average serum T4 was approximately 4 μg/100 ml. Concentrations of T3 reached a maximum value of 168±34 ng/100 ml (mean ± sd) during the 16–20 day period. A plateau value of about 40 ng/100 ml was maintained after about 70 days. For reverse T3 a maximum value of 17.1±4.2 ng/100 ml (mean±sd) was found in rats between 13 and 16 days old, followed by a steep decrease to 8.2±0.9 ng/100 ml around the 28th day and a subsequent continuous slow increase. For the T3/reverse T3 ratio (as a parameter of the direction of the conversion pathway) the highest value of 16 was found during the fourth week of life. After 70 days the T3/reverse T3 ratio was only 3.5. The reciprocal fluctuations between T3 and reverse T3, as found in man and sheep, are less pronounced in the rat. The very high metabolic clearance rate of reverse T3 compared to that of T3 could be the explanation.
The long-term effect of lowering dialysate magnesium on circulating parathyroid hormone in patients on regular haemodialysis therapy
Authors: Parsons V. , Papapoulos S. E. , Weston M.J. , Tomlinson S. , O'Riordan J. L. H. 
Published: December 2008

Abstract.
Measurement of parathyroid hormone (PTH) in a group of patients on regular dialysis therapy (RDT) showed little acceleration of the development of raised concentrations until the dialysate concentration of magnesium was halved from 0.5 to 0.25 mmol/l. Patients with sustained concentrations of PTH changed less than those who were within the normal range at the outset.
Pancreatic hormonal release after glucose and arginine administration in anaesthetized pigs
Authors: Gustavsson S. , Johansson H. , Lundqvist G. 
Published: December 2008

Abstract.
Somatostatin, pancreatic polypeptide (PP), insulin and glucagon were measured in pancreatic venous effluent and in mixed venous blood of anaesthetized pigs. After stimulation of insulin release with glucose and arginine, respectively, a prompt decrease in PP levels was found in pancreatic venous blood. Somatostatin declined after glucose administration but was unaffected by arginine. The changes in PP and somatostatin levels were not evident in systemic blood. The present results emphasize the advantage of selective sampling of pancreatic venous blood in studies on the possible interactions between pancreatic hormones. The marked decrease in PP seen after stimulation of insulin release in the present study, indicates that PP should be included together with somatostatin in further studies on pancreatic hormonal interplay.
Role of androgens in hCG-induced ovulation in PMSG-primed immature rats
Authors: Peluso J. J. , Stude D. , Steger R. W. 
Published: December 2008

Abstract.
The effect of pre-treatment with the anti-androgens, cyproterone acetate (C.A.) and Flutamide (Fl) on hCG-induced ovulation in immature PMSG-primed rats was studied. The results showed that pre-treatment with either anti-androgen reduced the ovulation rate by 50%. Not all pre-ovulatory follicles (≥ 600 μm in diameter) in control and anti-androgen-treated rats ovulated in response to hCG. In control rats, hCG induced cumulus cell dispersement and resumption of meiosis in the ova of these non-ovulatory follicles; while C.A. or Fl treatment prevented these pre-ovulatory responses (P < 0.05). In a subsequent study, PMSG-primed rats were pre-treated with Fl and autopsied 8 h after hCG. In control rats, hCG reduced ovarian oestradiol content, did not alter ovarian testosterone content, increased ovarian progesterone content (P < 0.05) and increased the percentage of follicles with 3B-HSD activity within their granulosa cell layers (P < 0.05). Fl did not alter ovarian steroid content but blocked the hCG-induced appearance of 3B-HSD activity in the granulosa cells of pre-ovulatory follicles. This lack of 3B-HSD activity could result in a local decrease in progesterone within the non-ovulatory follicle. It appears that androgens, presumably synthesized in the theca interna play an important role in either ovulation or in maintaining responsiveness of the pre-ovulatory follicle to LH.
Somatostatin and the 24 h levels of serum TSH, T3, T4, and reverse T3 in normals, diabetics and patients treated for myxoedema
Authors: Weeke Jørgen , Christensen Stig Engkjær , Hansen Aage Prange , Laurberg Peter , Lundbæk Knud 
Published: December 2008

Abstract.
The influence of somatostatin on serum TSH, 3,5,3′-triiodothyronine (T3), free T3, thyroxine (T4), free T4 and 3,3′,5′-triiodothyronine (reverse T3, rT3) was studied in 5 healthy young subjects, in 7 young patients with juvenile type diabetes on a fixed daily insulin dose, and in 5 patients with treated myxoedema. Blood samples were taken hourly during a 24 h control period and during a 24 h somatostatin infusion period.
Somatostatin infusion obliterated the night increase in serum TSH in all three groups. However, the lower daytime serum TSH was not altered by somatostatin. It has earlier been shown that somatostatin inhibits the TSH secretion induced by TRH. Taken together these findings suggest that the high TSH level at night is induced by a hypothalamic TRH surge, while the lower day level of TSH is quite independent of hypothalamic TRH.
Somatostatin infusion was accompanied by a minor fall in serum T4 in all groups. In normal subjects and diabetics serum free T3 fell 23 ± 6% and 25 ± 6%, respectively, during 24 h somatostatin infusion. In patients with treated myxoedema, serum free T3 was not significantly affected. These results are consistent with a decrease in thyroidal secretion during somatostatin infusion, as the cause for the fall in serum T3 in normal subjects and in patients with diabetes, while the monodeiodination of T4 to T3 in peripheral tissues is unaffected. However, an extrathyroidal effect of somatostatin on iodothyronine metabolism might also exist since serum rT3 increased 49 ± 19% in patients with treated myxoedema. In normal subjects and diabetic patients only a trend towards such a variation was observed.
Human thyroid stimulating activity and clinical state in antithyroid treatment of juvenile Graves' disease
Authors: Takata Ikuro , Suzuki Yukichi , Saida Kohki , Sato Tamotu 
Published: December 2008

Abstract.
Human thyroid stimulating activity in 37 patients with juvenile hyperthyroidism was studied during the course of antithyroid drug treatment. Observation periods varied from 6 months to 6 years (average 3 years). The existence of human thyroid stimulator (HTS) in their sera was determined by triiodothyronine (T3) release from resected thyroid adenomas. A measurement of T3 above the control value of 140% was judged to be positive. Before treatment, 25 of the 28 patients with Graves' disease had HTS in their sera, one of the 7 patients with Hashimoto's thyroiditis had HTS, and none of the 19 normal children had HTS in their sera. During the therapy, 7 of 18 Graves' patients had HTS. After cessation of the therapy, 9 of 22 patients remained HTS-positive, and 8 of the 9 patients with positive HTS relapsed within 6 months, whereas in 13 HTS-negative patients, 3 escaped and 10 remained in remission. There was no significant correlation between human thyroid stimulating activity (HTSA) and the following: serum T3 concentration, 131I-thyroidal uptake, TSH responsiveness to TRH and antithyroid antibody titre. These results indicate that (1) almost all patients with Graves' disease have HTS when they are in a state of hyperthyroidism, (2) HTS tends to disappear with the clinicial remission, but its persistence seems to predict relapse in the future, and (3) routine laboratory tests cannot serve as alternative to HTS.
Binding of thyrotrophin to low molecular weight fragments of human thyroid membranes
Authors: Adlkofer Franz , Kotulla Peter , Schleusener Horst 
Published: December 2008

Abstract.
The LATS absorbing activity from thyroid homogenates which is associated with the soluble thyroid fraction (4S-LAA) binds TSH in addition to LATS. This may indicate that 4S-LAA originates from the receptor sites for TSH at the thyroid cell surface. The affinity of 4S-LAA for TSH is much lower than that of thyroid membranes suggesting that 4S-LAA represents incomplete receptor sites or receptor sites which are altered in their structure.
Acceleration of puberty in boys with delayed puberty by clomiphene citrate. A clinical and laboratory study
Authors: Dickerman Zvi , Prager-Lewin Ruth , Lahmy Osnat , Laron Zvi 
Published: December 2008

Abstract.
Clomiphene citrate was administered at a dose of 50 mg/day for 3 months to 29 boys with delayed puberty, 15 in a stage of early puberty (group 1) and 14 in stages of mid puberty (group 2). In both groups a significant acceleration in the advancement of pubertal signs was noted in the 6-month period following initiation of therapy as compared to a non-treated control group. A significant rise in the mean (± sd) basal plasma LH levels, from 1.0 ± 0.4 to 2.7 ± 2.2 mU/ml in group 1 (P < 0.05) and from 1.0 ± 0.6 to 2.2 ± 1.7 mU/ml in group 2 (P < 0.05) was observed following the treatment period with clomiphene. Concomitantly there was a rise of the mean basal plasma FSH level from 1.1 ± 0.4 to 2.0 ± 1.5 mU/ml in group 1 (P ± 0.05) and from 1.9 ± 1.6 to 3.4 ± 3.0 mU/ml in group 2 (P < 0.02). The mean LH peak response to an iv bolus of LRH (50 μg/m2 iv) rose from 8.3 ± 4.2 to 13.0 ± 5.3 mU/ml in group 1 (P < 0.05) and from 9.2 ± 5.8 to 12.6 ± 6.8 mU/ml in group 2 (NS). The mean peak plasma FSH response to LRH rose from 2.0 ± 0.6 to 5.9 ± 4.2 mU/ml in group 1 (P < 0.05) and from 4.3 ± 4.0 to 7.0 ± 6.8 mU/ml in group 2 (NS).
Clomiphene therapy caused a rise of the basal plasma testosterone level from 68 ± 53 to 313 ± 270 ng/100 ml in group 1 (P < 0.01) and from 103 ± 67 to 392 ± 248 ng/100 ml in group 2 (P < 0.01). The plasma testosterone response to one hCG stimulation (5000 U im), tested in 4 boys immediately before and after the 3-month period of clomiphene administration revealed an increase in both the basal and the peak testosterone levels (P < 0.05 and P < 0.001, respectively).
A standard clomiphene test consisting of the administration of 100–200 mg/day clomiphene citrate for 8 days was performed in 8 boys before initiation of clomiphene treatment for the 3-month period. In 4, including 2 boys in an early stage of puberty, there was a suppression of the basal level of gonadotrophins and their response to synthetic LRH. The other 4 boys, all of them in stages of mid-puberty, showed an increase in the basal and peak plasma gonadotrophin levels following LRH stimulation. In all 8 boys there was a significant rise of the basal plasma testosterone level. Despite the varying response to the short clomiphene test in these 8 boys, all gave a good response to the prolonged administration of clomiphene citrate. It was concluded that treatment with small doses of clomiphene citrate for a period of 3 months induces an acceleration of puberty in boys with delayed or slowlyprogressing puberty, once the stage of initiation of puberty has been passed.
Lithium and iodine combination therapy for thyrotoxicosis
Authors: Boehm Timothy M. , Burman Kenneth D. , Barnes Susan , Wartofsky Leonard 
Published: December 2008

Abstract.
In order to compare the relative therapeutic efficacy of iodine (I) and lithium (Li) in thyrotoxicosis, investigate possible additive effects of these agents, and examine their effect upon thyroidal release, 17 thyrotoxic patients were assigned to groups given either I (n = 9) or Li (n = 8) alone during an initial treatment period, with the alternate drug added as combination treatment during a second treatment period. Half of the patients received methimazole (MMI). Three additional thyrotoxic patients received I during both treatment periods to evaluate the possibility of cumulative I effect upon thyroidal release during the second treatment period. A double isotope technique was utilized as an index of thyroidal release, employing 125I as an intra-thyroidal label and [131I] T4 as a marker of T4 disposal. During the first treatment period either I or Li induced comparable, significant (P < 0.05) decreases in thyroidal release, as measured by slopes of ratios of serum PB125I: PB131I and by percentage inhibition of fractional T4 release rate. In response to Li, there was a 55% decrease in the slope of PB125I: PB131I with MMI and a 52% decrease without MMI. In response to I, there was a 70% dercrease in the slope of PB125I: PB131I with MMI and a 57% decrease without MMI. Further significant (P < 0.05) decreases in the slopes of these ratios during the second, combined treatment period (I + Li) occurred only in those patients who had initially received I. No further decreases in the second treatment period were seen in patients receiving I during both treatment periods. Thus, I and Li together display additive inhibition of thyroidal release only if I is administered initially, but the combination, if Li is used first, does not appear to be more effective than Li alone.
Influence of corticotrophin on plasma testosterone in normal women
Authors: Vérine A. , Trouvé-Blanqui E. , Oliver C. , Boyer J. 
Published: December 2008

Abstract.
The concentrations of ACTH and testosterone (T) in the plasma from 12 normal women (aged 18–35 years) were simultaneously determined at various times after im injection of 1 mg corticotrophin. The increase in the plasma level of total immunoreactive ACTH was maximal 0.5 h after the injection (mean value 1123 as compared to 36 pg/ml in the basal state); at 48 h, the ACTH level was still 2.4-fold that measured in the basal state. The administration of corticotrophin induced a broad increase in the mean level of plasma T which was highly significant (P < 0.001) at 4, 6, 8, 16 and 24 h after the injection. The maximum T response was detected at 16 h (mean value 477 as compared to 338 pg/ml in the basal state). The results indicate that plasma T is susceptible to stimulation by a pharmacological dose of ACTH in normal women. This effect should be taken into account in evaluating the indication of ACTH as a therapeutic agent.
Investigation of the secretion and metabolism of cortisol during a 100 km race using [4-14C] and [1 1α-3H] cortisol
Authors: Few J. D. , Thompson M. W. 
Published: December 2008

Abstract.
A mixture of [11α-3H] and [4-14C]cortisol was administered orally to healthy men, following which urine was collected for 24 h. Four subjects acted as basal controls, going about their normal (sedentary) work; a further 3 resting subjects also received 100 mg cortisol orally (high cortisol controls) and 6 subjects competed in a 100 km race. Decreases in the carbon-14 specific activity of the cortisol metabolite excreted by the runners suggested that they seceted cortisol at 2–4 times the rate of the basal controls. This change was mirrored by the excretion of urine free cortisol but not by that of 17-hydroxycorticosteroids.
The isotope ratio (3H:14C) of 11-hydroxy metabolites of cortisol from the runners was intermediate between those of the basal and high cortisol controls, from which we conclude that though the fractional oxidation of cortisol to cortisone is reduced by increasing the cortisol pool, it is not affected by exercise per se. This and other results show that although continuous running for 6–8 h, involving energy expenditure in excess of 25 megajoules, leads to a moderate increase in the rate of cortisol secretion, running per se does not appear to markedly affect the metabolism of cortisol.
Effects of angiotensin I converting enzyme inhibitor (SQ 14225) on control of aldosterone
Authors: Eguchi Toyohisa , Saito Ikuo , Nakamura Ryuichi , Yasui Toshiyuki , Saruta Takao 
Published: December 2008

Abstract.
To study effects of angiotensin I converting enzyme inhibitor (CEI), SQ 14225, on plasma aldosterone (PA), angiotensin I (AI), angiotensin II (AII), potassium and ACTH were administered with or without the simultaneous injection of SQ 14225 in rabbits. The direct effect of bradykinin on PA was also examined, since it is suspected to augment the action of kinin under the administration of CEI.
In rabbits the dose of 1 mg/kg of SQ 14225 by a bolus injection resulted in a marked elevation of plasma renin activity (PRA) and moderate but significant decreases in circulating AII and PA with only a little change of blood pressure. Decrements in circulating AII and those in PA observed after the injection of SQ 14225 were well correlated (r = 0.585, P < 0.05). Stimulatory effects of AII, potassium and ACTH on PA were not affected by SQ 14225, however, those of AI on PA and blood pressure were completely inhibited by pre-treatment of SQ 14225. The infusion of bradykinin showed a remarkable reduction in blood pressure and a small increment in PRA, circulating AII and PA.
These results may suggest that the inhibitory effect of acutely administered SQ 14225 on PA is mainly due to the inhibition of conversion from AI to AII, but not direct effects on adrenal glands. Furthermore, it was suggested that the augmented kinin is not related to the inhibitory effect of SQ 14225 on PA. In addition, the administration of SQ 14225 does not change the effects of potassium and ACTH on PA.
Radioimmunoassay of three oestrogens and three androgens in the same plasma sample after extraction and chromatographic separation
Authors: Paradisi Roberto , Lodi Sergio , Bolelli Gianfranco , Venturoli Stefano 
Published: December 2008

Abstract.
The plasma levels of oestrone (Oe1), 17β-oestradiol (Oe2), oestriol (Oe3), testosterone (T), 5α-dihydrotestosterone (DHT) and androstenedione (A) were assayed by RIA in plasma obtained from peripheral venous blood. The hormones are isolated from the plasma extract, first by Sephadex LH-20 column chromatography (Oe2/Oe3/Oe1, T, DHT, A) and after Oe1, T, DHT, A by TLC on silica gel 60 F254. The accuracy, reproducibility and sensitivity of the method make it satisfactory for clinical studies.
Prevention of cystic ovary induction in rabbits by aminoglutethimide
Authors: Albrecht Eugene D. 
Published: December 2008

Abstract.
Polycystic ovaries were induced in thyroidectomized rabbits by the administration of either 25 IU human chorionic gonadotrophin or 10 IU pregnant mare serum daily for a period of 20 days. Cystic ovaries in rabbits exhibited subnormal (P < 0.01) ovarian Δ5-3β-hydroxysteroid dehydrogenase (3β-HSD) concentration and specific activity. Since weight of cystic ovaries was markedly elevated, however, total capacity for Δ4-3-ketosteroid production was enhanced.
Concomitant administration of chorionic gonadotrophin and aminoglutethimide phosphate to thyroidectomized rabbits prevented the formation of cystic ovaries indicating that a steroid, or steroids formed beyond cholesterol in the biosynthesic pathway is necessary for the experimental induction of cystic ovaries in this laboratory animal.
Iodine induced thyrotoxicosis in apparently normal thyroid glands
Authors: Skare ståle , Frey Harald M. M. 
Published: December 2008

Abstract.
Two male patients aged 36 and 52 years with thyrotoxicosis revealed a serum T3 of 2.8 and 6.5 nmol/l and a serum T4 of 166 and 238 nmol/l, respectively. Both had been exposed to iodine (2–10 mg daily) for 2–12 months before thyrotoxicosis was diagnosed. Urinary iodine excretion was high, 5000 and 10000 nmol/24 h (624–1250 μg). The uptake of 131I in the thyroid glands were low, none had goitre.
Their iodine intake was interrupted, urinary iodine excretion gradually decreased, and T3 and T4 in serum concomitantly normalized. They were clinically and biochemically euthyroid 9 and 11 weeks after withdrawal. After 14 and 22 weeks they had normal thyroid uptake of 131I, and thyroid scans showed glands of normal size and configuration, TRH-stimulation and a T3-suppression tests became normal. ESR was not elevated in any of the cases, thyroid antibodies against thyroglobulin and follicular cell microsomes were absent and TSAb was undetectable during the thyrotoxic stage.
Thus no evidence of any pre-existing and/or pre-disposing pathological condition in the thyroid glands were found. The mechanism for the iodine-induced thyrotoxicosis in such cases remains obscure.