bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of cytokines in the lipopolysaccharide-induced sick euthyroid syndrome in mice
Authors: Boelen A , Platvoet-ter Schiphorst M C , Bakker O , Wiersinga W M 
Published: December 2008

Abstract
To evaluate the role of cytokines in the sick euthyroid syndrome, we tried to establish an animal model of non-thyroidal illness in mice by the administration of a sub-lethal dose of bacterial endotoxin (lipopolysaccharide; LPS) which induces a variety of cytokines, including tumour necrosis factor (TNFα), interleukin-1 (IL-1α), interleukin-6 (IL-6) and interferon-γ (IFNγ). When compared with pair-fed controls, a single dose of LPS resulted in (a) systemic illness, (b) induction of TNFα and IL-6 and (c) a decrease of liver 5′-deiodinase mRNA from 4 h onwards followed by a decrease of serum tri-iodothyronine (T3) and thyroxine (T4) at 8 h and of serum free T3 (fT3) and free T4 (fT4) at 24 h; serum TSH remained unchanged.
We then studied whether a single dose or a combination of IL-1α, TNFα, IL-6 or IFNγ could induce the sick euthyroid syndrome in mice, again using pair-fed controls. None of the cytokines except IL-1α caused systemic illness, and IL-1α was the only cytokine that decreased liver 5′-deiodinase mRNA transiently. IL-1α, TNFα or IL-6 did not decrease serum T3, T4 and TSH, but administration of IFNγ decreased serum T4, T3 and fT3 in a dose-dependent manner without changes in serum TSH. Administration of all four cytokines together had no synergistic effects; observed changes were of a smaller magnitude than after LPS.
The following conclusions were reached. (1) Administration of LPS in mice is a suitable experimental model for the acute induction of the sick euthyroid syndrome. (2) Acute administration of IL-1α, TNFα or IL-6 in mice does not induce changes in thyroid hormones but IFNγ results in a dose-dependent decrease of serum T4, T3 and fT3 and IL-1α decreases liver 5′-deiodinase mRNA transiently. (3) Combined administration of IL-1α, TNFα, IL-6 and IFNγ had no synergistic effects; observed changes were of a smaller magnitude than after LPS. (4) The LPS-induced sick euthyroid syndrome is currently best explained by a direct thyroidal inhibition due to IFNγ and an extrathyroidal inhibition of liver 5′-deiodinase due to IL-1α, but other still unidentified factors seem to be involved as well.
Journal of Endocrinology (1995) 146, 475–483
Immuno-enhancement and -inhibition of GH-releasing factor by site-directed anti peptide antibodies in vivo and in vitro
Authors: Pell J M , James S 
Published: December 2008

Abstract
It is now well established that specific antibodies and binding proteins can potentiate rather than inhibit hormone activity. In order to investigate this phenomenon further, the current study was undertaken using a hormone with a characterised structure, in terms of receptor binding, and for which activity has already been manipulated in specific ways (prolongation of half-life, increased receptor affinity) using synthetic hormone analogues. GH-releasing factor (GRF) is a 40 or 44 residue peptide and is, together with somatostatin, responsible for the regulation of GH secretion. The effects of site-directed anti peptide antibodies were determined on the activity of GRF in vivo and in vitro as GH release. The peptide regions of GRF were: 1–14 (part of putative receptor-binding region) and 31–44 and 35–44 (sites thought to be distant from the receptor-binding region). Five sheep were administered GRF (1 μg/kg), anti peptide immunoglobulin (Ig; a calculated tenfold excess binding to GRF dose), or GRF together with anti peptide Ig (preincubated for 1 h). GRF induced a significant increase in plasma GH concentration over the next 240 min, this was abolished when GRF was administered with anti 1–14 Ig (P<0·05) and augmented (P<0·05) when GRF was administered with anti 35–44 Ig; anti 31–44 had no effect on GRF activity. Anti 35–44 Ig alone induced an increase in GH secretion which was equivalent to that for GRF alone, implying that the antibody had interacted and potentiated with endogenous GRF. The Ig effects on exogenous GRF activity were confirmed for GH release in vitro using primary cultures of sheep pituitary cells, except that anti 31–44 Ig also augmented GH release (P<0·05) when co-administered with GRF. These data are compatible with current findings on the regulation of GRF activity, namely that increases in hormone activity may be achieved by at least two mechanisms: protection from degradation (decreased clearance rate) and changed hormone–receptor interaction.
Journal of Endocrinology (1995) 146, 535–541
Levels of pro-opiomelanocortin and prolactin mRNA in the fetal sheep pituitary following hypoxaemia and glucocorticoid treatment in late gestation
Authors: Matthews S G , Challis J R G 
Published: December 2008

Abstract
It is well established that corticotrophin-releasing hormone and vasopressin can induce both synthesis and release of ACTH from the ovine pituitary gland, and that glucocorticoids can inhibit these responses. Changes in the abundance, localization and distribution of proopiomelanocortin (POMC) mRNA and prolactin (PRL) mRNA in the ovine fetal pituitary were examined by in situ hybridization following hypoxaemia applied in the presence or absence of concomitant cortisol in late gestation (day 135). Fetuses were distributed amongst four groups; saline-infused/normoxaemic, cortisol-infused/normoxaemic (0·3 mg/h), saline-infused/hypoxaemic and cortisol-infused/hypoxaemic. Hypoxaemia (6 h) was induced by reducing the maternal PaO2, resulting in a 6–8 mmHg decrease in fetal arterial PO2. Fetal infusions were commenced 5 h prior to and maintained throughout the treatment period. Hypoxaemia, which elevated fetal plasma ACTH and cortisol, caused a significant (P<0·05) increase in POMC mRNA in the pars distalis (PD), but was without effect on POMC mRNA in the pars intermedia (PI). Cortisol infusion attenuated the hypoxaemiainduced increase in POMC mRNA in the PD, but was without effect on non-stimulated steady-state POMC mRNA levels in either the PD or PI. PRL mRNA was only present in the PD and significantly (P<0·05) increased after cortisol infusion and hypoxaemia. In conclusion (i) POMC and PRL mRNA in the PD are increased following moderate hypoxaemia, (ii) cortisol attenuates changes in POMC mRNA but not PRL mRNA in the PD following hypoxaemia and (iii) cortisol increases PRL mRNA levels in the PD. Synthesis of POMC and PRL in the fetal PD is highly sensitive to homeostatic perturbations and glucocorticoids in late gestation.
Journal of Endocrinology (1995) 147, 139–146
Amniotic and allantoic fluid concentrations of thyroxine, 3,3′,5′-tri-iodothyronine, 3,3′-di-iodothyronine and 3′,5′-di-iodothyronine in the pig during the period of gestation
Authors: Brzezińska-Ślebodzińska E , Ślebodziński A B , Krysin E 
Published: December 2008

Abstract
Thyroxine (T4), 3,3′,5′-tri-iodothyronine (reverse T3; rT3) and di-iodothyronines (3,3′-T2 and 3′,5′-T2) were measured in pig amniotic fluid (AF) and allantoic fluid (Al) between 32 and 113 days of normal pregnancy. Low but measurable quantities of T4 in AF and Al (2·1 ± 0·3 and 3·2 ±0·5 nmol/l respectively) were found before the onset of fetal thyroid gland function, which indicates the maternal source of T4. The presence of rT3 (55·8 ±4·1 pmol/l in AF and 49·8 ± 5·3 pmol/l in Al), 3,3′-T2 (45·5 ± 0·6 pmol/l in AF and 49·2 ±9·2 pmol/l in Al) and 3′,5′-T2 (20·8 ±2·6 pmol/l in AF and 24·0 ± 2·2 pmol/l in Al) may be attributed to the monodeiodinase system already active in fetal pig tissues in early pregnancy, as demonstrated previously. T3 concentration was undetectable in both AF and Al. An approximately twofold increase in the levels of T4, rT3 and T2s in AF and Al at mid-gestation was observed. T4 and rT3 in AF showed a positive correlation with protein concentrations. AF rT3 concentration (but not T4) correlated with rT3 in the cord and maternal serum. The 3,3′-T2 and 3′,5′-T2 in AF and Al showed parallel changes to rT3, while the rT3/3,3′-T2 and rT3/3′,5′-T2 molar ratios remained constant. T4 concentrations in AF and Al were markedly lower than in corresponding maternal and fetal serum; the rT3 concentration in Al was equal to that in AF and two to four times lower than in fetal serum. In spite of differences between serum hormone patterns in the pig and human near term, iodothyronine concentrations in AF showed some similarities, mainly the following: undetectable T3, a strong correlation between rT3, T4 and AF total protein and the presence of 3,3′-T2 and 3′,5′-T2 in measurable levels. Comparative data for Al, except the ones in the present study in the pig, are not available.
Journal of Endocrinology (1995) 147, 245–251
Growth hormone (GH) receptor and GH-binding protein deficiency in the growth failure of potassium-depleted rats
Authors: Hochberg Z , Amit T , Flyvbjerg A , Dørup I 
Published: December 2008

Abstract
Potassium (K+) deficiency is associated with growth retardation in both man and experimental animals. Growth hormone (GH) administration to such animals prevents, to some extent, weight loss and selective muscle atrophy, but does not affect tail and tibia length even with supraphysiological doses. The present study was undertaken to investigate the possible effect of K+ deficiency on the hepatic GH receptor and GH-binding protein (BP). Young female Wistar rats were maintained on K+-deficient fodder and distilled water, and compared with pair-fed and ad-libitumfed control groups. After 15 days GH-BP and electrolytes were measured in sera, GH receptors were studied in liver membranes by 125I-labeled human GH binding and muscles were weighed and saved for electrolyte measurements. K+-deficient rats showed complete growth arrest compared with an intermediate weight gain of the pair-fed group. Serum K+ was very low, at 1·5 ±0·1 mmol/l, compared with the mean value of 5·3 mmol/l of control animals. Somatogenic and lactogenic receptors in liver membranes and serum GH-BP levels were significantly (P<0·05) lower in K+ deficiency, as compared with their pair-fed controls. Liver GH receptors correlated significantly (P<0·05) with serum GH-BP levels. The growth variables correlated positively with both hepatic somatogenic and lactogenic receptors and serum GH-BP levels, with correlation coefficients that were highest against serum GH-BP and lowest against liver lactogenic receptors. Serum and muscle K+ correlated significantly (P<0·05) with both liver GH receptors and serum GH-BP, with correlation coefficients that were higher against serum GH-BP. Lactogenic receptors had a lower or no correlation. It is concluded that GH receptor deficiency may be involved in the growth retardation of K+ deficiency.
Journal of Endocrinology (1995) 147, 253–258
Inhibition of 5α-reductase in genital skin fibroblasts and prostate tissue by dietary lignans and isoflavonoids
Authors: Evans B A J , Griffiths K , Morton M S 
Published: December 2008

Abstract
Isoflavonoids and lignans, constituents of many plant foods, have been proposed as protective agents in those populations with a low incidence of hormone-dependent cancers. They may act by their inhibition of the metabolism of growth-promoting steroid hormones. This report describes the inhibition of 5α-reductase and 17β-hydroxysteroid dehydrogenase by six isoflavonoids and two lignans in human genital skin fibroblast monolayers and homogenates, and in benign prostatic hyperplasia tissue homogenates. In genital skin fibroblasts, genistein, biochanin A and equol were the most potent inhibitors of 5α-reductase activity, each resulting in greater than 80% inhibition at a concentration of 100 μm. The IC50 values for genistein and a seven-compound mixture were approximately 35 μm and 20 μm (2·9 μm of each compound) respectively. Of the lignans, enterolactone was the most potent inhibitor. Inhibition by biochanin A was shown to be reversible. When genital skin fibroblast homogenates were used, biochanin A was found to inhibit 5α-reductase isozymes 1 and 2 to differing extents (30% and 75% respectively). Genistein was shown to inhibit 5α-reductase 2 in a non-competitive nature (Vmax and Km values without and with inhibitor were 30 and 20 pmol/mg protein per h and 177 and 170 nm respectively). All of the compounds tested inhibited 17β-hydroxysteroid dehydrogenase activity in genital skin fibroblast monolayers. When prostate tissue homogenates were used, the compounds tested were better inhibitors of 5α-reductase 1 than 2. It is possible that a life-long dietary exposure to these lignans and isoflavonoids may have a significant influence on the development of hormone-dependent tumours.
Journal of Endocrinology (1995) 147, 295–302
Two-step development of Hashimoto-like thyroiditis in genetically autoimmune prone non-obese diabetic mice: effects of iodine-induced cell necrosis
Authors: Many M-C , Maniratunga S , Varis I , Dardenne M , Drexhage H A , Denef J-F 
Published: December 2008

Abstract
The administration of a high iodide dose (HID; 10 μg/day) to goitrous mice is known to induce thyroid cell necrosis and inflammation, which, in most strains, is transient. In this study, we analyzed the effects of iodide in autoimmune prone non-obese diabetic (NOD) mice.
Control NOD mice fed a standard diet (MID; 1 μg I/day) or HID did not spontaneously develop thyroiditis. In NOD mice previously made goitrous, HID provoked thyroid cell necrosis and diffuse inflammation within 4 days. Inflammatory cells consisted of MHC-class II+ antigen-presenting cells, CD4+ T helper cells and CD8+ T suppressor/cytotoxic cells. After 96 days of treatment with HID, thyroiditis similar to Hashimoto's disease was obtained in 100% of the animals, with destruction of thyroid follicles, large clusters of T and B cells, and antithyroid antibodies in the plasma. When treating goitrous mice with MID, no cell necrosis was observed and no autoimmune thyroiditis was obtained. The early iodide-induced cell necrosis and inflammation may thus be considered as an important factor in the induction and persistence of autoimmune thyroiditis in individuals carrying a genetic susceptibility to autoimmune disease.
Journal of Endocrinology (1995) 147, 311–320
Prolactin receptor expression in lymphocytes from patients with hyperprolactinemia or acromegaly
Authors: Leite-de-Moraes M C , Touraine P , Kelly P A , Kuttenn F , Dardenne M 
Published: December 2008

Abstract
Previous reports demonstrated that prolactin receptors (PRL-R) are widely expressed on cells of the immune system. We analyzed a possible regulation of PRL-R expression on human mononucleated blood cells by prolactin (PRL) itself. PRL-R expression was analyzed by immunofluorescence on T and B lymphocytes and monocytes from peripheral blood mononucleated cells (PBMC) of patients with hyperprolactinemia or acromegaly compared with sex- and age-matched control subjects. The frequency of PRL-R positive cells and the intensity of PRL-R expression was only modified among the CD8+ T cell population of hyperprolactinemic patients with macroadenoma. No correlation was reported between PRL-R expression and circulating PRL levels. The percentage of PRL-R+ cells on B or T lymphocytes and monocytes as well as the capacity of PBMC to proliferate in response to T cell mitogens were not significantly different in bromocriptine-treated compared with untreated patients. These findings suggest that factors other than pituitary PRL play the major role in regulating PRL-R expression on cells of the immune system.
Journal of Endocrinology (1995) 147, 353–359
Changes in lipid peroxidation and free radical scavengers in the brain of hyper- and hypothyroid aged rats
Authors: Mano T , Sinohara R , Sawai Y , Oda N , Nishida Y , Mokuno T , Asano K , Ito Y , Kotake M , Hamada M , Nakai A , Nagasaka A 
Published: December 2008

Abstract
To determine how lipid peroxides and free radical scavengers are changed in the brain of hyper- or hypothyroid rats, we examined the behavior of lipid peroxide and free radical scavengers in the cerebral cortex of aged (1·5 years old) rats that had been made hyper- or hypothyroid by the administration of thyroxine or methimazol for 4 weeks. Concentrations of catalase, Mn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were increased in hyperthyroid rats compared with euthyroid rats. Concentrations of total SOD, Cu,Zn-SOD and GSH-PX were increased but that of Mn-SOD was decreased in hypothyroid animals. There were no differences among hyperthyroid, hypothyroid and euthyroid rats in the levels of coenzymes 9 or 10. The concentration of lipid peroxides, determined indirectly by the measurement of thiobarbituric acid reactants, was decreased in hyperthyroid rats but not in hypothyroid rats when compared with euthyroid animals.
These findings suggest that free radicals and lipid peroxides are scavenged to compensate for the changes induced by hyper- or hypothyroidism.
Journal of Endocrinology (1995) 147, 361–365
Inhibition of mouse placental lactogen-II release from placental cells by interleukin-1 after mid-pregnancy
Authors: Yamaguchi M , Sakata M , Ogura K , Adachi K , Mammoto A , Miyake A 
Published: December 2008

Abstract
The effects of interleukin (IL)-1 and granulocytemacrophage colony stimulating factor (GM-CSF), which are present in the mouse placenta, on the secretion of mouse placental lactogen (mPL)-1 and mPL-II by placental cells were tested in vitro. IL-lα and IL-1β, 2·5 nmol/l each, significantly inhibited mPL-II secretion by cells from days 9 and 12 of pregnancy, but did not affect mPL-II secretion by cells from day 7 of pregnancy or mPL-I secretion by cells from days 7, 9 or 12 of pregnancy. GM-CSF had no effect on mPL-I and mPL-II secretion by cells from days 7, 9 or 12 of pregnancy. The inhibitory effects of IL-1α and IL-1β on mPL-II secretion were completely eliminated by the addition of antibodies to IL-1α and IL-1β respectively. Western blot analysis for mPL-II indicated that IL-1α significantly reduced the intensity of the mPL-II band. Steady-state levels of mPL-II mRNA, assessed by Northern blot analysis, were reduced by incubation of placental cells from day 12 of pregnancy with 2·5 nmol/l IL-1α for 5 days. Co-incubation of 0·25 pmol/l IL-1α, 25 pmol/l IL-6, and 25 pmol/l tumor necrosis factor-α, each of which did not significantly inhibit mPL-II secretion by itself, together inhibited mPL-II secretion. These results suggest that IL-1, but not GM-CSF, is a potent inhibitor of mPL-II secretion after mid-pregnancy, and that the combined action of cytokines can inhibit mPL-II secretion.
Journal of Endocrinology (1995) 147, 423–429
Differences in cellular transport of tri-iodothyronine and thyroxine: cell cycle-dependent alteration of tri-iodothyronine uptake
Authors: Nagasawa T , Ichikawa K , Minemura K , Hara M , Yajima H , Sakurai A , Kobayashi H , Hiramatsu K , Shigematsu S , Hashizume K 
Published: December 2008

Abstract
Cellular and nuclear uptake of tri-iodothyronine (T3) and thyroxine (T4) was examined using the cultured cell line derived from rat liver, clone 9, and rat hepatoma, dRLH-84. The saturable cellular uptake of T3 and T4 was demonstrated in these cells. First we examined the cell cycle-dependent alteration of thyroid hormone uptake. Cellular T3 uptake was minimal in the early G1 phase and increased in the late G1 phase, reaching a maximal level in the S phase. Alterations in nuclear T3 uptake were in accordance with the changes in cellular T3 uptake. On the other hand, cellular and nuclear T4 uptake was unchanged throughout the cell cycle, suggesting the T3 specificity of the cell cycle-dependent alteration of cellular hormone transport. Next we examined the effect of sodium butyrate on the cellular transport of thyroid hormones. After treatment with 5 mm sodium butyrate, cellular and nuclear uptake of T3 was increased, reaching a maximal level (four- to sevenfold increase) after 48 h. When cells were incubated for 48 h with various concentrations of sodium butyrate, T3 uptake was enhanced by 1 mm sodium butyrate, reaching a maximal level with 5 mm. Although cellular T4 uptake was also increased after treatment with sodium butyrate, the degree and time-course of the increase were different from those of T3. The maximal increase in cellular T4 uptake (two- to threefold increase) was attained 20 h after treatment. Despite the increase in cellular T4 uptake, nuclear T4 uptake was decreased after treatment with sodium butyrate. For both T3 and T4, the enhanced cellular uptake was due to the increased Vmax without changes in the Michaelis–Menten constant. These data indicate that cellular transport of T4 is different from that of T3 in rat hepatic cells.
Journal of Endocrinology (1995) 147, 479–485
Successful Drilling of Oil and Gas Wells by Optimal Drilling-Fluid/Solids Control— A Practical and Theoretical Evaluation
Authors: Dahl B. , Saasen A. , Omland T. H. 
Published: December 2008

Summary
Since the development of the drilling industry, the process for removing drill solids from the drilling fluid has culminated in the use of shaker screens as the primary or sole solution. It is, therefore, necessary to optimize both filtration efficiency and the screen life to hinder drilled solids from entering the drilling fluid. Optimum solids control can be obtained by using knowledge of how damage to the filtration cloth arises, of how to reduce it, and of how the particles in the circulation system influence the general picture of the drilling process. When this knowledge is accepted, established, and implemented in the drilling industry, it is possible to maintain efficient drilling.
This paper describes, in detail, the theory and field examples on how wear arises on the shaker-screen cloth. As will be shown, this knowledge has been used to increase the solids-control efficiency and to reduce the screen wear by more than 90% in several field cases where 17½-in. sections have been drilled with oil-based mud. This has been achieved by use of a different screen configuration, running with top screens with finer cut points than normal. This leads to removal of 90 to 95% of the solids from the fluid using the top deck, thereby minimizing the wear on the finer bottom-deck screens. The documentation is based on practical off-shore results from these drilling operations, including data from the drilling log, laboratory analyses of the drilling fluid, and of the particle-size distribution (PSD) of the drilling fluid. The particular focus of this article is the application of double-deck shakers.