bluuebunny/crossref_metadata_2025_split huggingface dataset:
Jurkat cell proliferative activity is increased by luteinizing hormone-releasing hormone
Authors: Azad N , LaPaglia N , Kirsteins L , Uddin S , Steiner J , Williams D W , Lawrence A M , Emanuele N V 
Published: December 2004

Abstract
Jurkat cells were used to study the immunomodulatory role of luteinizing hormone-releasing hormone (LHRH) in immune cells. The Jurkat cell, a human mature leukemic cell line, phenotypically resembles resting human T lymphocytes and has been widely used to study T cell physiology. The data from this study demonstrate that the Jurkat cell concentration of immunoreactive LHRH was 210 ± 36 pg/106 cells and that of proLHRH was 188 ± 27 pg/106 cells (means ± s.e.m.). The authenticity of this LHRH immunoreactivity is documented in two ways. First, both Jurkat LHRH and proLHRH immunoreactivity demonstrate dilutional parallelism with hypothalamic LHRH and proLHRH. Second, Jurkat lysates show LHRH bioactivity by releasing luteinizing hormone from rat anterior pituitary cells in culture. The presence of substantial amounts of LHRH in medium in which Jurkat cells were cultured for 72 h indicated that LHRH can be released from the cells. Using specific primers to exons 2 and 4 of the LHRH gene, we have found that Jurkat cells (like human T cells) express LHRH mRNA.
The LHRH agonist, des-Gly10,d-Trp6-LHRH ethylamide, significantly increases the proliferative activity of Jurkat cells, as assessed by tritiated thymidine incorporation, from 15 980 ± 1491 c.p.m. in controls to 28 934 ± 3395, 30 457 ± 3861 (P=0·05 vs control) or 35 299 ± 5586 c.p.m. (P<0·01 vs control) with 10−11, 10−9 or 10−7 m agonist respectively. LHRH antagonist, [d-pGlu1,d-Phe2,d-Trp3,6]-LHRH, at a concentration of 10−8 m decreases Jurkat cell proliferative activity from 17 145 ± 526 c.p.m. in control medium to 10 653 ± 1323 c.p.m. (P=0·05). Co-incubation with the LHRH antagonist completely inhibits the proliferative stimulation induced by the LHRH agonist. Furthermore, applying monoclonal LHRH antibody to Jurkat cells inhibits the cell proliferative activity assessed by tritiated thymidine incorporation from 19 900 ± 2675 c.p.m. in controls to 15 680 ± 2254, 15 792 ± 1854 and 9700 ± 908 c.p.m. in media with 1:40, 1:20 and 1:10 dilution of purified antibody respectively (P<0·01, 1:10 dilution compared with control). In addition, the cAMP level in LHRH-stimulated Jurkat cells is decreased to 74, 27 and 57% of control levels after 15, 30 and 45 min respectively of exposure to 10−7 m LHRH agonist.
In summary, Jurkat cells produce, process and release immunoreactive and bioactive LHRH, as do normal human T cells. Endogenous and exogenous LHRH increase Jurkat cell proliferative activity, and cAMP may be involved in LHRH-induced Jurkat cell proliferation. The Jurkat cell may be a useful model with which to study the role of LHRH in human T cell function.
Journal of Endocrinology (1997) 153, 241–24
Testosterone-induced susceptibility to Plasmodium chabaudi malaria: persistence after withdrawal of testosterone
Authors: Benten W P M , Ulrich P , Kühn-Velten W N , Vohr H-W , Wunderlich F 
Published: December 2004

Abstract
Testosterone induces susceptibility to Plasmodium chabaudi malaria by imposing restrictions on those mechanisms which mediate resistance controlled by genes of the H-2 complex and the non-H-2 background in mice. This study investigated whether these restrictions are abolished after withdrawal of testosterone. Female mice of the inbred strain C57BL/10 were treated with 0·9 mg testosterone twice a week for 3 weeks and testosterone was then withdrawn for 12 weeks. The treatment raised plasma testosterone levels from 0·18 ng/ml to 3·79 ng/ml. After the testosterone treatment, these levels progressively dropped and reached 0·21 ng/ml by week 12 after testosterone withdrawal. Surprisingly, however, the testosterone-induced susceptibility still persisted. When mice were challenged on week 12 after testosterone withdrawal, P. chabaudi infections were still fatal in testosterone-treated mice, in contrast to self-healing infections in resistant, i.e. untreated, control mice. In addition, testosterone caused a persistent decrease in the levels of total IgG antibodies, especially IgG1 and IgG2b isotypes. In contrast, testosterone-induced changes in spleen cells, such as the reduction in number by 50%, the relative increase in CD8+ cells and the decrease in Ig+ cells, as well as the acquisition of the susceptible phenotype, were completely reversed on week 10 after testosterone withdrawal at the latest. Testosterone did not affect the production of the TH1-signalling cytokine interferon-γ and the TH2-signalling cytokines interleukin (IL)-4 and IL-10 in response to P. chabaudi malaria. Together, our data indicated that the gene-controlled host resistance to P. chabaudi malaria is subject to superior hormonal imprinting: when once induced by testosterone, mechanisms which suppress resistance thus causing susceptibility persist independently of testosterone.
Journal of Endocrinology (1997) 153, 275–281
Stem cell factor and c-kit in the mammalian testis: lessons originating from Mother Nature's gene knockouts
Authors: Loveland K L , Schlatt S 
Published: December 2004

Abstract
Analysis of mice with naturally occurring mutations in the genes encoding the tyrosine kinase receptor protein, c-kit, and its ligand, stem cell factor (SCF), has implicated these proteins in testicular development and function because of the phenotype of these mice of reduced or absent fertility. Descriptive and functional studies have highlighted the involvement of these proteins in primordial germ cell migration and survival, and in spermatogonial proliferation, survival and adhesion. This review summarises the current knowledge regarding functions of c-kit and SCF in the testis and discusses the implications of information gleaned from other biological systems.
Journal of Endocrinology (1997) 153, 337–344
Platelet-derived growth factor, insulin-like growth factors, fibroblast growth factors and transforming growth factor β do not account for the cell growth activity present in bovine milk
Authors: Belford D A , Rogers M-L , Francis G L , Payne C , Ballard F J , Goddard C 
Published: December 2004

Abstract
Cation-exchange chromatography effectively concentrates the cell growth activity present in whey and we have used this process as a basis to characterise further the growth factors present in bovine milk. Under neutral conditions, total bioactivity in the growth factor-enriched cation-exchange fraction chromatographed with an apparent molecular mass of 80–100 kDa. In contrast, acid gelfiltration chromatography resolved two peaks of cell growth activity. A peak at 15–25 kDa contained the bulk of growth activity for Balb/c 3T3 fibroblasts while bioactivity for L6 myoblasts and skin fibroblasts eluted with a molecular mass of 6 kDa. A peak of inhibitory activity for Mv1Lu and MDCK cells also eluted at 15–25 kDa. Both IGF-I and IGF-II were purified from fractions that eluted at 6 kDa, although the IGF peptides alone did not account for the total bioactivity recovered. Platelet-derived growth factor (PDGF), identified by radioreceptor assay, eluted at a slightly higher molecular mass than the peak of growth activity for Balb/c 3T3 cells, and an anti-PDGF antibody was without effect on the growth of Balb/c 3T3 cells in response to the whey-derived factors. Further purification of the inhibitory activity for epithelial cells yielded a sequence for transforming growth factor β (TGF-β), and all inhibitory activity for Mv1Lu cells was immuno-neutralised by an antibody against TGF-β. In contrast, this antibody decreased the growth of Balb/c 3T3 fibroblasts in the whey-derived extract by only 10%. Finally, a cocktail of recombinant growth factors containing IGF-I, IGF-II, PDGF, TGF-β and fibroblast growth factor 2 stimulated growth of Balb/c 3T3 cells to a level equivalent to only 51% of that observed in the milk-derived growth factor preparation. We conclude that: (i) cell growth activity recovered from bovine whey is present in acid-labile high molecular weight complexes; (ii) all cell growth inhibitory activity for epithelial cells can be accounted for by TGF-β; (iii) IGF-I and IGF-II co-elute with the major peak of activity for L6 myoblasts and skin fibroblasts, although the IGF peptides alone do not explain the growth of these cells in the whey-derived extract; and (iv) neither PDGF nor TGF-β account for the 15–25 kDa peak of Balb/c 3T3 growth activity. These data suggest the presence of additional mitogenic factors in bovine milk.
Journal of Endocrinology (1997) 154, 45–55
Age and sex related differences in serum levels of unconjugated dehydroepiandrosterone and its sulphate in normal subjects
Authors: Šulcová J , Hill M , Hampl R , Stárka L 
Published: December 2004

Abstract
Dehydroepiandrosterone sulphate (DHEAS) and unconjugated dehydroepiandrosterone (DHEA) have been determined in the blood serum of normal subjects of both sexes from 1 month to 100 years of age. In total, 92 girls, 49 boys, 211 women and 110 men were investigated. The effects of age and sex on the levels of the hormones were measured.
DHEAS levels declined rapidly during the first year of life and were maintained at a minimum level for 5 years. They increased significantly from 6 to 7 years of age and reached maximum levels in women at about 24 years and in men at about 30 years of age. They then declined rapidly in both sexes but the fall which occurred after 50 and 60 years of age respectively was only moderate. Age-related unconjugated DHEA levels were different. After the first month of life DHEA levels were relatively high and declined more slowly. The minimum level was observed in girls between 5 and 7 years and in boys between 5 and 9 years of age. A significant rise then began and levels reached a maximum in women as well as in men at about 20 years of age. In men levels then declined up to the age of 80. In women the DHEA levels declined during the next 15 years and from approximately 36 years of age they again rose significantly up to a second peak. A mild but significant decline then resumed.
There was a difference in the levels of DHEA and DHEAS depending on sex. Unlike DHEAS, unconjugated DHEA was higher in women than in men. However, this difference was significant only in some age groups: during puberty (between 11 and 15 years of age), in the premenopausal period (between 36 and 45 years of age) and in the older group (after 60 years of age).
Age- and sex-related dependencies were different between DHEAS and DHEA. They indicate the possible variable secretion and dynamics of their (inter)conversion. We have concluded that DHEA measurements cannot be a substitute for DHEAS and vice versa.
Journal of Endocrinology (1997) 154, 57–62
Evidence suggesting that cadmium induces a non-thyroidal illness syndrome in the rat
Authors: Pavia M A , Paier B , Noli M I , Hagmüller K , Zaninovich A A 
Published: December 2004

Abstract
The effect of in vivo administration of cadmium chloride on the pituitary-thyroidal axis was assessed in 200 g body weight Wistar rats. A dose of 2·5 mg/kg body weight was injected i.v. 24 h before the experiments were initiated. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations in cadmium-treated rats were significantly (P<0·01) decreased, whereas plasma TSH failed to increase in response to low T4 and T3. However, the TSH response to TRH and the pituitary content of TSH in these rats were both normal. Cadmium induced a significant (P<0·01) decrease in 4-h thyroidal 131I uptake and in thyroid/plasma radioactivity ratio. The in vitro conversion of T4 to T3 in the pituitary was significantly (P<0·01) blocked by cadmium whereas there was no in vivo effect. Parameters of peripheral T4 kinetics in cadmium-treated rats, such as metabolic clearance rate (P<0·01), fractional turnover rate (P<0·01), absolute disposal rate (P<0·05), urinary clearance (P<0·05) and faecal clearance (P<0·05), were all decreased by cadmium. The lack of response of TSH to low plasma T4 and T3 and the normal response to exogenous TRH in this and in other non-thyroidal illness syndromes produced by other pathologies suggest a decreased stimulation of pituitary thyrotrophs by endogenous TRH.
Journal of Endocrinology (1997) 154, 113–117
Characterization of the binding of 3,3′-di-iodo-l-thyronine to rat liver mitochondria
Authors: Lombardi A , Moreno M , Horst C , Goglia F , Lanni A 
Published: December 2004

Abstract
The binding of labelled 3,3′-di-iodo-l-thyronine (3,3′-T2) to isolated rat liver mitochondria has been characterized. Specific binding could be detected only in the inner mitochondrial membrane, not in other mitochondrial subfractions. The composition of the incubation medium influenced the binding capacity, the best combination of high specific binding and low non-specific binding being observed in phosphate buffer, pH 6·4.
The specific binding of 3,3′-T2 to mitochondria requires low ionic strength: concentrations of K+ and Na+ higher than 10 mmol/l and 0·1 mmol/l respectively resulted in a decreased binding capacity. The optimal calcium ion concentration was in the range 0·01–1·0 mmol/l. Varying magnesium ion, over the range of concentrations used (0·1–100 mmol/l), had no effect. Both ADP and ATP, at over 1 mmol/l, resulted in an inhibition of the specific binding. Incubation with protease resulted in a decrease in specific binding and an increase in non-specific binding, thus indicating the proteic nature of the binding sites. In addition to the above factors in the local environment the thyroid state of the animal might influence the 3,3′-T2-binding capacity. In fact, the thyroid state of the animal seemed not to have an influence on the affinity constant, but it did affect binding capacity.
Journal of Endocrinology (1997) 154, 119–124
Mitogenic effects of thyroxine and TRH on thyrotrophs and somatotrophs of the anterior pituitary gland in thyroidectomized rats
Authors: Quintanar-Stephano A , Valverde-R C 
Published: December 2004

Abstract
The question of whether thyroxine (T4) and TRH have a mitogenic effect on pituitary thyrotrophs and somatotrophs in thyroidectomized rats was investigated. Mitoses were counted in hematoxylin–eosin-stained or periodic acid–Schiff–hematoxylin-stained pituitary slides or immunostained for TSH or GH using male rats thyroidectomized for 5 months. Ten days before they were killed groups of rats were injected with different doses of T4 (0·5, 3 or 10 μg i.m. every second day for 10 days), TRH alone (100 ng s.c. three times a day for 10 days), or T4 plus TRH (same doses as above). Mitoses (stopped with colchicine) were counted in 1 mm2 areas at a magnification of × 1000. In thyroidectomized rats, mitoses were not significantly increased and treatment with TRH or 0·5 μg T4 alone in thyroidectomized rats did not affect mitotic counts. In thyroidectomized rats treated with higher doses of T4, mitoses were increased in a dose-dependent fashion. Simultaneous administration of TRH and T4 had a significant synergistic effect on pituitary mitoses in a T4 dose-dependent manner. The treatments also had differential effects on the relative percentages of cellular types in mitosis. Thus, 60% somatotrophs and 12·5% thyrotrophs were found in the euthyroid group. In thyroidectomized and thyroidectomized plus TRH groups, no somatotrophs in mitosis were seen, while thyrotrophs were 28·5% and 33·3% respectively. In thyroidectomized rats treated with low doses of T4, somatotrophs and thyrotrophs in mitosis increased to 38·4% and 80% respectively and, with simultaneous administration of a low dose of T4 plus TRH, although less effective than T4 alone, mitosis increased in somatotrophs and thyrotrophs to 11·1% and 54·5% respectively. A high dose of T4 alone did not increase the mitotic figures in somatotrophs (38·8%), while it diminished the percentage of thyrotrophs to 25%. The administration of high doses of T4 plus TRH had an opposite effect on the mitotic figures of somatotrophs and thyrotrophs and thus the percentage of somatotrophs increased to 50% while thyrotrophs decreased to 5·5%. Ten days of treatment with T4 were insufficient to reverse the histology to euthyroidism. It can be concluded that in long-standing hypothyroidism: (1) thyroid hormone replacement elicits a dose-dependent and differential proliferative response on pituitary thyrotrophs and somatotrophs, (2) TRH is devoid of mitogenic effects when administered alone and (3) the proliferative response of somatotrophs to T4 is enhanced by its co-administration with TRH, suggesting a permissive and/or synergistic effect of the thyroid hormone and TRH.
Journal of Endocrinology (1997) 154, 149–153
Glucose homeostasis with infinite gain: further lessons from the Daisyworld parable?
Authors: Koeslag J H , Saunders P T , Wessels J A 
Published: December 2004

Abstract
A major unresolved physiological problem is how the rate of hepatic glucose production is increased to match the increased rate of glucose utilization during exercise without a change in arterial blood glucose level. A homeostat with such capabilities is said to have infinite gain.
Daisyworld is an imaginary planet orbiting a variable star. The only life is black and white daisies. Black daisies retain heat, slightly warming the planet; white daisies cool it. When the two types of daisies grow best at slightly different temperatures, variations in solar luminosity (over a wide range) cause the ratio of white:black daisies to vary in a manner that keeps the planetary temperature constant. This model therefore achieves infinite gain by having two opposing but interdependent controllers.
Here we suggest that the pancreatic islet α- and β-cells might act as black and white daisies. For the analogy to apply, glucagon and insulin must not only have opposing effects on the blood sugar concentration, but the secretion of the one has, at some quantum level, to be at the expense of the other. Electrical coupling between heterocellular groups of α- and β-cells within the pancreatic islets suggests that this might indeed be the case. α-Cell activity must, furthermore, promote secretory activity in other α-cells; similarly with β-cells. This is probably mediated via pancreastatin and γ-amino butyric acid (GABA) which are paracrinically co-secreted with glucagon and insulin, respectively. α-Cell activity spreads (at the expense of β-cell activity) when the blood glucose level is below set point, while β-cell activity progressively replaces α-cell activity above set point. At set point changes in the ratio of α:β-cell activity are inhibited.
Journal of Endocrinology (1997) 154, 187–192
Evidence for steroidogenic luteal cell hypertrophy and hyperplasia during pregnancy in the rat
Authors: Gaytán F , Bellido C , Morales C , Aguilar E , Sánchez-Criado J E 
Published: December 2004

Abstract
The proliferative activity of the rat corpus luteum was studied on days 2, 3, 6, 9, 12, 15, 17, 19 and 21 of pregnancy. Proliferating cells were detected by the immunohistochemical demonstration of DNA-incorporated 5-bromodeoxyuridine (BrdU) and by the presence of mitoses. Steroidogenic luteal cells showed two proliferative waves on days 12–15 and on day 21, when relatively abundant BrdU-labeled and mitotic cells were observed. These cells were clearly distinguishable from non-steroidogenic cells by their round nuclei and large polygonal cytoplasm. The proliferative activity on days 12–15 was coincident with an increase in the size of the cells and in progesterone concentrations. On the other hand, the proliferative activity of non-steroidogenic luteal cells (especially endothelial cells of the blood and lymphatic vessels) followed a different pattern. These cells intensely proliferated on days 2–3 of pregnancy and this proliferative activity was significantly higher than that observed in non-pregnant rats on metestrus and diestrus. A new proliferative wave was observed on days 12–15, in association with the increase in the proliferative activity of steroidogenic cells. The presence of both BrdU-labeled and mitotic steroidogenic luteal cells provides evidence that these cells do proliferate and that both hypertrophy and hyperplasia are involved in the increase in the parenchyma of the corpus luteum during pregnancy. Also, the results suggest that different mechanisms are involved in the regulation of the proliferative activity in the corpus luteum at different times during pregnancy.
Journal of Endocrinology (1997) 154, 211–217
Changes in tyrosine phosphorylation of insulin receptor and insulin receptor substrate-1 (IRS-1) and association of p85 subunit of phosphatidylinositol 3-kinase with IRS-1 after feeding in rat liver in vivo
Authors: Ito Y , Ariga M , Takahashi S-I , Takenaka A , Hidaka T , Noguchi T 
Published: December 2004

Abstract
The binding of insulin to its receptor rapidly induces intrinsic insulin receptor tyrosine kinase activity, resulting in tyrosine phosphorylation of various cytosolic substrates, such as insulin receptor substrate-1 (IRS-1) which, in turn, associates with a p85 subunit of phosphatidylinositol 3-kinase (PI 3-kinase) followed by activation of this enzyme.
In the present study, we have examined these early steps of insulin signalling in rat liver in vivo after food ingestion. After fasting for 22 h, a 12% casein diet was available ad libitum throughout the 8-h experimental period. Plasma insulin concentrations increased within 45 min after feeding, reached a maximum at 1·5 h and gradually decreased until 8 h. Autophosphorylation of the insulin receptor β-subunit in liver was detected even during fasting and increased about 1·5-fold at 1·5 h after feeding. Basal tyrosine phosphorylation of IRS-1 was detectable during starvation, increased about twofold at 3 h after feeding and levels were maintained until 8 h. The content of the p85 subunit of PI 3-kinase associated with IRS-1 also increased after feeding in parallel with the changes in tyrosine phosphorylation of IRS-1.
Because tyrosine phosphorylation of the insulin receptor β-subunit and IRS-1 and the association of the p85 subunit of PI 3-kinase with IRS-1 in liver were closely correlated with the changes in the plasma concentration of insulin, we concluded that endogenous insulin secreted in response to eating caused these insulin-dependent intracellular changes in the liver.
Journal of Endocrinology (1997) 154, 267–273
Central cholinergic regulation of pancreatic polypeptide secretion in conscious dogs
Authors: Okita M , Inui A , Baba S , Kasuga M 
Published: December 2004

Abstract
The secretion of pancreatic polypeptide (PP) is regulated by fluctuations in blood glucose concentrations and food intake, in which vagal-cholinergic mechanisms play an important role, especially for the cephalic phase of PP secretion. In this study, we examined whether central cholinergic mechanisms are also important for PP secretion by relaying information in the brain to the vagus nerve and the muscarinic cholinergic receptors in the pancreas.
Atropine sulfate (20–200 μg) was administered into the lateral cerebral ventricle and its effects on the basal secretion of PP as well as the secretions stimulated by insulin-induced hypoglycemia (Actrapid MC, 0·25 U/kg) and a mixed meal (243 kcal) were studied in seven dogs. Intralateral cerebroventricular (ILV) atropine (100 and 200 μg) abolished the fluctuations in basal PP secretion without appearing in the plasma. Pretreatment with 20, 100, and 200 μg ILV atropine significantly decreased the PP response to insulin-induced hypoglycemia, with the integrated PP response to 58, 32, and 26% of that of controls respectively. Atropine (100 μg ILV) significantly reduced the postprandial PP secretion in both the cephalic and the gastrointestinal phases, whereas increased insulin and glucose levels were unaffected.
Centrally administered atropine was able to suppress the basal secretion of PP as well as the secretions stimulated by hypoglycemia and food intake. These findings suggest that (1) the spontaneous release of PP is governed by an oscillating, central cholinergic tone, and (2) the stimulating PP secretion is, at least in part, regulated by the central cholinergic system.
Journal of Endocrinology (1997) 154, 311–317