bluuebunny/crossref_metadata_2025_split huggingface dataset:
CHANGES OF THYROID FUNCTION IN RESPONSE TO SEVERE NERVOUS STIMULATION
Authors: Árvay A. , Lampé L. , Kertész L. , Medveczky L. 
Published: December 2008

ABSTRACT
The effect of prolonged exposure to severe nervous traumatization on the activity of the thyroid gland has been studied. Good agreement between the results was obtained by using radioactive iodine 131I, measuring the activity over the thyroid gland and the radioautographs, as well as doing the histological examinations and determinations of the height of the epithelial cells lining the acini. According to these results intense nervous stimulations have a characteristic effect on the thyroid function. The initial phase of hyperfunction, lasting under our experimental conditions for 10 days, is followed by a state characterized by hypofunction. The effect is reversible. This effect of severe nervous traumatization on the thyroid function is markedly inhibited by chlorpromazine.
PLASMA PROTEIN-BOUND IODINE IN THE BEAVER AND OTHER ANIMALS
Authors: Kelsey Frances O. , Gullock A. , Clausen H. J. 
Published: December 2008

ABSTRACT
The plasma protein-bound iodine of beavers in South Dakota was found to be 8.2 ± 0.50 μg/100 ml. This value was appreciably higher than that found in the following other species: man, rabbit, coyote, and fox pups, guinea pig, rat, musk rat, opossum, pig, spider monkey, hedgehog and hawk. The 24-hour radioactive iodine thyroid uptake in one beaver was 8 %, the serum cholesterol 132 mg/100 ml and the serum inorganic iodine 3.0 μg/100 ml (PBI = 7.1 μg/100 ml). The radioiodine uptake and serum cholesterol in the spider monkey were quite similar to those of the beaver though the PBI was much lower (1.9 ± 0.28 μg/100 ml). The PBI was found to be significantly higher in dogs examined in October than those in March. Anaesthesia and/or various laboratory procedures caused a slight fall in PBI. The PBI was quite similar amongst pups of any given litter but varied considerably from litter to litter.
NEW VIEWS ON THE HORMONE-PRODUCING MESENCHYMOMAS OF THE OVARIES
Authors: Plate W. P. 
Published: December 2008

ABSTRACT
The hormone-producing mesenchymomas of the ovaries can be divided into androblastomas and gynaecoblastomas. The former are derived from »male« elements, and consist of Sertoli-cell tumours and Leydig-cell tumours. The latter arise from »female« elements and consist of granulosacell tumours and theca-cell tumours. Sertoli-cell tumours and granulosacell tumours produce oestrogens, while Leydig-cell tumours and theca-cell tumours produce oestrogens or androgens. Histologically, androblastomas and gynaecoblastomas are often difficult to distinguish. Since no »female« elements occur in a testicle, a granulosa-cell tumour in a testicle is improbable. Gynandroblastomas, therefore, can only be found in an ovary.
Diagnostic role of follicle-stimulating hormone (FSH) measurements during the menopausal transition—an analysis of FSH, oestradiol and inhibin
Authors: Burger Henry G 
Published: December 2008

Burger HG. Diagnostic role of follicle-stimulating hormone (FSH) measurements during the menopausal transition—an analysis of FSH, oestradiol and inhibin. Eur J Endocrinol 1994;130:38–42. ISSN 0804–4643
This review examines the role of follicle-stimulating hormone (FSH) measurement in assessing the significance of symptoms and possible continuing fertility during the menopausal transition. Follicle-stimulating hormone measurement is advocated frequently as a useful diagnostic tool in perimenopausal patients. Several investigators have shown that the serum FSH level increases in the early—midfollicular and early postovulatory phases in women over the age of 40 years who continue to experience regular menstrual cycles. The serum oestradiol level may fall (although this is controversial) and the immunoreactive inhibin level falls, being inversely correlated with the rising FSH level. When alterations in menstrual cyclicity or flow commence, signalling the onset of the menopausal transition, FSH levels may change abruptly, rising into the normal postmenopausal range and falling again into the range normally seen in young fertile women. Oestradiol and inhibin generally fluctuate in parallel with each other but inversely to FSH, although at times oestradiol in particular may be increased markedly. Postmenopausal FSH levels may be followed by endocrine evidence compatible with normal ovulation. After the menopause, FSH levels rise 10–1 5-fold, with low oestradiol and undetectable inhibin levels. It is concluded that FSH measurement is of little value, if any in the assessment of women during the menopausal transition because it cannot be interpreted reliably and because, apparently, ovulatory (and, presumably, potentially fertile) cycles may occur subsequent to the observation of postmenopausal FSH levels. Both oestradiol and inhibin are important negative feedback regulators of circulating FSH.
Henry G Burger, Prince Henry's Institute of Medical Research, PO Box 152, Clayton, Victoria 3168, Australia
Effect of bromocriptine and SMS 201-995 on growth of human somatotrophic and non-functioning pituitary adenoma cells in vitro
Authors: Renner Ulrich , Mojto Juri , Lange Manfred , Müller O Albrecht , von Werder Klaus , Stalla Günter K 
Published: December 2008

Renner U, Mojto J, Lange M, Albrecht Müller O. von Werder K, Stalla GK. Effect of bromocriptine and SMS 201-995 on growth of human somatotrophic and non-functioning pituitary adenoma cells in vitro. Eur J Endocrinol 1994;130:80–91. ISSN 0804–4643
The effect of the dopamine agonist bromocriptine and the somatostatin analog SMS 201-995 on growth of 12 human somatotrophic and 13 non-functioning adenoma cell cultures was investigated. When adenoma cells were maintained in medium supplemented with 5% fetal calf serum. cell counts of 10 of 12 somatotrophic cultures increased to 145±6 and 171 ±9% (mean±sd) and in 12 of 13 non-functioning cell cultures up to 125±12 and 217±15% after 3 days of incubation. In most cases bromocriptine and SMS 201-995 dose dependently (1 nmol/l to 10 μmol/l) inhibited adenoma cell growth but there was only (1.10 μmol/l) a significant inhibitory effect at high doses of both drugs. A 1 μmol/l concentration of bromocriptine decreased cell counts of 5 of 12 somatotrophic cell cultures (range 84±3 to 76±6% vs control = 100%) and in 5 of 13 non-functioning cell cultures (range 85±4 to 71 ± 7%). A 10 μmol/l concentration of bromocriptine decreased cell counts in all 12 somatotrophic (range 87±1 to 61 ±8%) and in 12 of 13 non-functioning adenoma cultures (range 87±6 to 57±3%). Bromocriptine specifically inhibited growth because its effect could be reversed by the dopamine D2-receptor antagonist haloperidol. Both 1 and 10 μmol/l SMS 201-995 significantly decreased cell counts in three of six somatotrophic (87± 3 to 38 ±3%) cell cultures. In two of five cases growth of non-functioning adenoma cultures was suppressed by 1 μmol/ISMS 201-995, and in four of five cases by 10 μmol/l(86± 3 to 74 ±4%). The growth inhibitory effect of both bromocriptine and SMS 201-995 was not just due to an effect on growth of fibroblasts contaminating the adenoma cell cultures, because it could be observed also when adenoma cells were maintained in a d-valine-supplemented medium that suppresses fibroblast growth. In summary, both bromocriptine and SMS 201-995 at high doses were able to inhibit cell growth of cultured somatotrophic and non-functioning adenomas in vitro. However, the mechanism of this inhibitory effect is not yet well understood.
Ulrich Renner, Max-Planck-Institute of Psychiatry, Clinical Institute, Kraepelinstr. 10, D-80804 Munich, Germany
Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness
Authors: Custro Nicola , Scafidi Vincenza , Gallo Salvatore , Notarbartolo Alberto 
Published: December 2008

Custro N, Scafidi V, Gallo S, Notarbartolo A. Deficient pulsatile thyrotropin secretion in the low-thyroid-hormone state of severe non-thyroidal illness. Eur J Endocrinol 1994;130:132–6. ISSN 0804–4643.
Twenty-four-hour thyrotropin (TSH) profiles in eight severely ill patients were compared with those of six healthy subjects. The profiles were assessed using the cosinor method to evaluate circadian variations and using the Pulsar algorithm to analyze episodic secretion. In the normal subjects, the typical periodicity of TSH secretion showed a mean level in the rhythm (mesor) of 2.03 mU/l, The amplitude (half the extent of rhythmic change in the cycle) was 0.58 mU/l; the acrophase (the delay from midnight (0 degrees) of the highest level in the rhythm) was −9.9 degrees. In contrast, severely ill patients showed only slight and anticipated elevations of serum TSH levels (mesor 0.93 mU/l, amplitude 0.22 mU/l, acrophase +82.4 degrees). Moreover, whereas the episodic TSH secretion in healthy individuals consisted of 5–8 pulses/24 h, mainly clustered around midnight, only one pulse of reduced amplitude was detected in two of the eight severely ill patients and no pulses in the other six. Since earlier studies have indicated that the loss of TSH pulsatility is associated with the relative insensitivity of the thyrotrophs to low thyroid hormone levels and our analytical procedures have demonstrated that 24 h pulsatile pattern of TSH closely overlapped with baseline TSH secretion, it seems reasonable to assume that low-thyroid-hormone state, deficient pulsatile TSH secretion and altered nyctohemeral TSH periodicity do not coincide by chance, but that there is a causal relationship between such abnormalities in severely ill patients.
Nicola Custro, Cattedra di Patologia Medica, Via del Vespro, n.141, 90127 Palermo, Italy
Calcium mobilization is a prerequisite for the expression of phorbol ester-stimulated luteinizing hormone secretion from pituitaries of male and acutely ovariectomized rats
Authors: Das Saswati , Fahmy Nabil W , Bourne Gregory A 
Published: December 2008

Das S, Fahmy NW, Bourne GA. Calcium mobilization is a prerequisite for the expression of phorbol esterstimulated luteinizing hormone secretion from pituitaries of male and acutely ovariectomized rats. Eur J Endocrinol 1994;130:151–8. ISSN 0804–4643
Ionomycin, which mobilizes Ca2+, and phorbol 12-myristate 13-acetate (PMA) which activates protein kinase C (PKC), were used to compare the effects/interactions of Ca2+ and PKC on luteinizing hormone (LH) secretion from pituitaries of intact male and acutely ovariectomized (72 h) rats. Quartered pituitaries from donor animals were perifused at 0.25 ml/min and sequential effluent fractions were collected every 10 min. Continuous administration (4 h) of 1 nmol of gonadotropin-releasing hormone (GnRH) resulted in an increase in LH secretion. Cycloheximide (5 μmol) dissociated the GnRH-stimulated LH responses into protein synthesis-independent and -dependent components. While ionomycin (10 μmol) stimulated LH secretion from pituitaries of both sexes by protein synthesis-independent mechanisms, PMA (1 μmol) and the inactive phorbol ester, 4α-phorbol 12,13-didecanoate (PDD), were ineffective secretagogues. However, PMA (but not PDD) interacted synergistically with ionomycin and GnRH to augment LH secretion by protein synthesis-dependent mechanisms. These results suggest a similarity in the effects/interactions of Ca2 + and PKC in gonadotropes from male and ovariectomized rats. If the effects of PMA can be attributed to PKC activation, then it also appears that Ca2+ mobilization is necessary for the manifestation of PKC as a mediator of LH secretion from these gonadotropes. While PKC activity can be divorced from the protein synthesis-independent component of LH release (this component appears to be mediated by Ca2+ mobilization), the enzyme might be involved in amplifying the response to Ca2+ mobilization through synergistic, protein synthesis-dependent mechanisms.
Gregory Bourne, Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada S7N OWO
Stimulation of sex hormone-binding globulin mRNA and attenuation of corticosteroid-binding globulin mRNA by triiodothyronine in human hepatoma cells
Authors: Barlow John W , Crowe Timothy C , Cowen Neil L , Raggatt Lorna E , Topliss Duncan J , Stockigt Jan R 
Published: December 2008

Barlow JW, Crowe TC, Cowen NL, Raggatt LE, Topliss DJ, Stockigt JR. Stimulation of sex hormone-binding globulin mRNA and attenuation of corticosteroid-binding globulin mRNA by triiodothyronine in human hepatoma cells. Eur J Endocrinol 1994;130:166–70. ISSN 0804–4643
We examined the time course and dose response of the triiodothyronine (T3) effect on mRNAs for sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) in cells of the human hepatoma line HepG2. After 7 h of exposure to a saturating dose of T3, SHBG mRNA was unchanged but increased to 1.5±0.1 times the unstimulated control at 22 h. Maximal stimulation (2.3±0.6) was observed at 2–3 days. Corticosteroid-binding globulin mRNA was unchanged for 22 h after exposure to T3 but diminished thereafter to 64% by day 3. At 3–4 days of exposure, the changes in both SHBG mRNA and CBG mRNA were dose-responsive to the T3 concentration. For both mRNAs, half-maximal response occurred between 10 and 20 pmol/l bioavailable T3. Cortisol-binding proteins secreted by HepG2 cells after 3 days in culture also were T3 dose-responsive. No re-uptake of secreted CBG by the cells was observed, suggesting that the T3 effect on CBG secretion occurs during production of the mature protein. These data suggest that T3 stimulates the expression of the SHBG gene and attenuates the expression of the CBG gene. The effects of T3 on these genes are consistent with the increase in circulating SHBG and decrease in circulating CBG observed in hyperthyroidism. The HepG2 cells may be a useful human cell line in which to study the diversity of the molecular mechanisms of T3 action.
JW Barlow, Ewen Downie Metabolic Unit, Alfred Hospital, Commercial Rd. Melbourne, Victoria 3181, Australia
Effect of the antiglucocorticoid RU486 on adrenal steroidogenic enzyme activity and steroidogenesis
Authors: Albertson Barry D , Hill R Blake , Sprague Kellie A , Wood Karen E , Nieman Lynnette K , Loriaux D Lynn 
Published: December 2008

Albertson BD, Hill RB, Sprague KA, Wood KE, Nieman LK, Loriaux DL. Effect of the antiglucocorticoid RU486 on adrenal steroidogenic enzyme activity and steroidogenesis. Eur J Endocrinol 1994;130: 195–200. ISSN 0804–4643
RU486, a synthetic steroid receptor antagonist, has strong antiprogesterone and antiglucocorticoid properties. Chronic RU486 administration in two patients with ectopic secretion of adrenocorticotropin (ACTH) has been associated with decreasing plasma cortisol concentrations. One explanation of this finding is that RU486 may directly inhibit adrenal steroidogenesis. To test this hypothesis, we measured the effect of RU486 on specific steroidogenic enzymatic steps using an in vivo rat and an in vitro monkey model. Hypophysectomized–castrated–ACTH-replaced Sprague-Dawley rats were given RU486 i.p. at daily doses of 0, 0.0005, 0.005, 0.05, 0.5 and 5 mg/kg body weight per day for 7 days. The animals were sacrificed, and blood and adrenal glands collected. Adrenal cortical mitochondria and microsomes were purified from the rats and from two untreated Cynomolgus macaque monkeys. Specific steroidogenic enzyme activities were measured in the rat by the incorporation of 14C-labeled steroid substrates into products. A similar protocol was used to assay the steroidogenesis in the monkey adrenal fractions in the presence and absence of added RU486. Although rat adrenal weights decreased significantly at the highest RU486 dose, plasma levels of corticosterone were similar in control and treated rats. Rat adrenal 3β-hydroxysteroid dehydrogenase/isomerase (3-HSD), 21-hydroxylase (21-OH) and 11-hydroxylase (11-OH) activities decreased with increasing RU486 doses, with 21-OH and 11-OH being most severely affected. Monkey adrenal 3-HSD, 21-OH, 11-OH, 1 7-hydroxylase and 17,20-desmolase similarly decreased in the presence of increasing in vitro concentrations of RU486. Taken together, these results suggest that RU486 directly inhibits adrenal steroidogenesis, with a locus of action at several key enzymatic steps in the glucocorticoid pathway. This steroidogenic blockade may account for the observed decreases in glucocorticoids during RU486 treatment.
Lynette K Nieman, Developmental Endocrinology Branch, NICHD, Building 10, Room 10N262, NIH, Bethesda, MD 20892, USA
Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression
Authors: Mehta Vivek K , Hao Wei , Brooks-Worrell Barbara M , Palmer Jerry P 
Published: December 2008

Mehta VK, Hao W, Brooks-Worrell BM, Palmer JP. Low-dose interleukin 1 and tumor necrosis factor individually stimulate insulin release but in combination cause suppression. Eur J Endocrinol 1994;130:208–14. ISSN 0804–4643
The macrophage-derived cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have direct effects on pancreatic beta cells and have been hypothesized to play important roles in the autoimmune beta cell lesion of type I diabetes because of two major effects on beta cells: altered insulin secretion and beta cell cytotoxicity. High doses of IL-1 are cytotoxic to beta cells and strongly inhibit insulin release; high-dose IL-1 plus TNF acts synergistically to suppress further the insulin release. In contrast, we observed that the predominant effect of low-dose IL-1 and TNF when administered separately was the stimulation of insulin release. We therefore asked whether the combination of low-dose IL-1 plus TNF would act synergistically to stimulate or suppress insulin release. Studies were performed on cultured rat islets and both insulin release and cytotoxicity (51Cr release) were measured. After 2 days of culture, increasing doses of IL-1—25, 50, 75 and 100 ng/l—caused progressively increased cytotoxicity and impaired insulin release. In contrast, the lowest dose of IL-1 tested, 10 ng/l, increased insulin release but was still slightly cytotoxic. Tumor necrosis factor at doses of 10, 25, 62.5, 75 and 100 μg/l also was slightly cytotoxic but increased insulin release. The augmented insulin release declined progressively with increasing TNF dose. However the combination of insulin stimulatory doses of IL-1 (10 ng/l) and TNF (62.5 μg/l) suppressed insulin release. The effects of these two cytokines on insulin release demonstrated a similar pattern after 4 and 6 days of culture. Although both IL-1 and TNF are cytotoxic to cultured islets cells, the effects of these two cytokines on insulin release are markedly different: with IL-1 primarily suppressing and TNF increasing insulin release. In combination, IL-1 and TNF always inhibits insulin release. The lack of concordance between insulin release and cytotoxicity suggests that these cytokines may alter insulin release by at least two mechanisms, one dependent on and the other independent of cytotoxicity.
Jerry P Palmer, Veterans Affairs Medical Center, Endocrinology (111) ZB-21. 1660 S Columbian Way, Seattle, WA 98108, USA
Androgen manipulation and vasopressin binding in the rat brain and peripheral organs
Authors: Gao Xin , Phillips Paddy , Oldfield Brian , Trinder Deborah , Risvanis John , Stephenson Jayne , Johnston Colin 
Published: December 2008

Gao X, Phillips P, Oldfield B, Trinder D, Risvanis J, Stephenson J, Johnston C. Androgen manipulation and vasopressin binding in the rat brain and peripheral organs. Eur J Endocrinol 1994;130:291–6. ISSN 0804–4643
It is now widely recognized that there is a sexual dimorphism in the development of arginine vasopressin (AVP) immunoreactivity in certain parts of the brain, and that changes in brain AVP immunoreactivity change with manipulation of androgen status. The aim of this experiment was to determine specifically any AVP receptor changes in response to manipulation of androgen levels using a selective V1 antagonist radioligand. Following castration, plasma testosterone levels fell and AVP immunoreactivity was reduced in the lateral septum and bed nucleus of the stria terminalis. With testosterone supplementation in castrated animals, the immunoreactivity in these regions was restored to a higher degree than in sham-operated animals. Central and peripheral V1 AVP receptor binding (as determined using the selective AVP V1 antagonist radioligand [125I](d(CH2)5,sarcosine7)AVP was not changed in any of the brain regions studied or in liver or kidney membranes from the three groups. This study demonstrates that there is no change in brain AVP receptor binding despite changes in regional AVP immunoreactivity in the brain, and excludes any confounding interaction with changes in oxytocin receptors.
P A Phillips, Department of Medicine, The University of Melbourne, Austin Hospital, Heidelberg, Victoria 3084, Australia
Effect of thyroid status on the oxidative capacity of Sertoli cells isolated from immature rat testis
Authors: Palmero S , Trucchi P , Prati M , Fugassa E , Lanni A , Goglia F 
Published: December 2008

Palmero S, Trucchi P, Prati M, Fugassa E, Lanni A, Goglia F. Effect of thyroid status on the oxidative capacity of Sertoli cells isolated from immature rat testis. Eur J Endocrinol 1994;130:308–12. ISSN 0804–4643
Our previous studies indicate the Sertoli cell as a target for thyroid hormone action at testis level. In the present study we evaluated the effect of thyroid hormone on Sertoli cell oxidative capacity measured by specific cytochrome oxidase (COX) activity and intracellular adenosine triphosphate (ATP) content. Sertoli cells were isolated from 21-day-old rats. Hypothyroidism, induced from the day of birth by administration of 0.025% methimazole, was characterized by a severe delay of body and testis growth and resulted in a lower COX activity (−40%, p ≥ 0.01) and a lower ATP content (−35%, p ≥ 0.01) by isolated Sertoli cells. Administration of triiodothyronine (10 μg/100 g body wt on alternate days) to hypothryoid rats improved body and testis growth and restored both COX activity and ATP content. The presence of high-affinity, low-capacity binding sites for triiodothyronine in Sertoli cell mitochondria also was demonstrated. This study, unlike that carried out on the whole testis from adult rats, demonstrates that thyroid hormone affects the energy metabolism of Sertoli cells from midpubertal rat testes.
Silvio Palmero, Istituto di Fisiologia Generale, Università di Genova, Corso Europa 26,1-16132 Genova, Italy
Cortisol decreases 2[125I]iodomelatonin binding sites in the duck thymu
Authors: Poon AMS , Liu ZM , Tang F , Pang SF 
Published: December 2008

Poon AMS, Liu ZM, Tang F, Pang SF. Cortisol decreases 2[125I]iodomelatonin binding sites in the duck thymus. Eur J Endocrinol 1994;130:320–4. ISSN 0804–4643
The immunosuppressive effect of chronic glucocorticoid treatment on 2[125I]iodomelatonin binding in the duck thymus was studied. Two-week-old ducks were injected intraperitoneally with either 1 mg of cortisol per day (experimental group) or an equivalent volume of vehicle (control group) in the middle of the light period for 7 days. 2[125I]Iodomelatonin binding assays were performed on thymic membranes. Cortisol injection reduced the body weight gain, size of the bursa of Fabricius and absolute weights of the primary lymphoid organs but had no effect on the spleen weights. The relative weights of the spleen were increased while those of the primary lymphoid organs were unchanged. The density of the thymus 2[125I]iodomelatonin binding sites was decreased while the affinity was not affected. The modulation of the thymic 2[125I]iodomelatonin binding sites by changes in the immune status of the duck suggests that these binding sites represent physiologically relevant melatonin receptors and that melatonin exerts its action on the lymphoid tissues directly. Our findings support the hypothesis that the thymus is the target site for the immunomodulatory interactions between the pineal melatonin and the adrenal steroids. A possible inhibitory influence of adrenal steroids on the immuno-enhancing effect of melatonin is also suggested.
AMS Poon, University of Hong Kong, 5 Sassoon Rd, Hong Kong