bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of rifampicin on thyroid gland volume, thyroid hormones, and antipyrine metabolism
Authors: Christensen Hanne R. , Simonsen Kim , Hegedüs Laszlo , Hansen Bo M. , Døssing Martin , Kampmann Jens P. , Hansen Jens M. 
Published: December 2008

Abstract.
The influence of rifampicin (450 mg/day for 28 days) on the hepatic microsomal enzymes and thyroid function variables were investigated in 13 healthy male volunteers. After 14 and 28 days of treatment a significant increase in median thyroid volume (determined ultrasonically) was demonstrated (20 ml, range 13–28 before; 26 ml, range 18–48 at day 14, and 24 ml, range 17–40 at day 28) (p <0.01). A significant decrease in median serum free T4 index levels was seen (94.1 arbitrary units, range 80.1–123.4 before treatment; 86.8, range 71.7–102.0 at day 14, and 85.3, range 65.5–131.3 at day 28) (p <0.01). Serum T4, T3, T3 resin uptake, free T3 index and TSH levels were not significantly altered. Hepatic microsomal enzyme activity assessed by antipyrine clearance was significantly increased (approximately by 85%) at day 14 and 28, whereafter it normalized. The study supports the hypothesis that the increase in thyroid volume after treatment with rifampicin and other hepatic enzyme system inducers (e.g. phenytoin and carbamazepine) is a compensatory mechanism caused by an increased hepatic degradation of thyroid hormones.
Acute facilitory action of progesterone on gonadotropin secretion of perifused rat pituitary cells
Authors: Ortmann Olaf , Wiese Huberta , Knuppen Rudolf , Emons Günter 
Published: December 2008

Abstract.
The purpose of this study was to investigate the kinetics and estrogen dependence of the facilitory progesterone action on LH and FSH secretion from pituitary cells under dynamic culture conditions. Anterior pituitary cells obtained from ovariectomized or intact adult Wistar rats were cultivated on Cytodex 1 microcarrier beads. The perifusion experiments were performed with four separate perifusion chambers. The cells of chambers I+II had been pretreated with medium containing vehicle (0.1% ethanol), those of chambers III + IV with medium containing 1 nmol/l estradiol for 48 h. After perifusion was started, each of the chambers was challenged with an initial 2-min GnRH (1 nmol/l) pulse. Chamber I was further perifused with medium containing vehicle, chamber II with medium containing vehicle + 100 nmol/l progesterone, chamber III with medium containing 1 nmol/l estradiol, and chamber IV with medium containing 1 nmol/l estradiol + 100 nmol/l progesterone. Three further GnRH pulses were administered at 50-min intervals to each of the chambers. In estradiolprimed cells from intact rats, progesterone induced a positive effect on LH and FSH secretion after 50 min of exposure to progesterone. After 100 min of progesterone treatment, LH and FSH release were enhanced to 420 and 500 per cent, respectively. When such cells were not primed with estradiol, a slight though insignificant positive action of progesterone on LH release was present after 50 and 100 min of treatment, whereas FSH secretion was not influenced. The facilitory effect of progesterone occurred only after 100 min when estradiol-primed cells from ovariectomized rats were used. LH and FSH secretion were only enhanced by up to 210 and 233 per cent, respectively. When these cells were not primed with estradiol the positive progesterone effect was absent. In conclusion, progesterone induces an acute facilitory effect on GnRH-induced LH and FSH secretion which is estrogen-dependent.
In vivo responsiveness to glucocorticoid correlated with glucocorticoid receptor content in peripheral blood leukocytes in normal humans
Authors: Tanaka Hirotoshi , Ichikawa Yoichi , Akama Hideto , Homma Mitsuo 
Published: December 2008

Abstract.
Dexamethasone loading tests (0.1 mg dexamethasone/kg, iv) were performed in 18 normal males to evaluate the individual responsiveness to glucocorticoid. There were inter-individual differences in increase in peripheral blood polymorphonuclear leukocyte count, decrease in peripheral blood lymphocyte count, and increase in plasma free fatty acids levels after dexamethasone injection. In addition, there was a significant correlation between the maximum increase in polymorphonuclear leukocytes and the maximum decrease in lymphocytes (r = 0.7514, p < 0.0003). Simultaneous measurements of glucocorticoid receptor content by whole-cell assay revealed that glucocorticoid receptor content in polymorphonuclear leukocytes linearly correlated with that in the corresponding lymphocytes (r = 0.9482, p < 0.0001). There were also significant correlations between the maximum increase in polymorphonuclear leukocytes and glucocorticoid receptor content in polymorphonuclear leukocytes (r = 0.7239, p < 0.0007), and between the maximum decrease in lymphocytes and glucocorticoid receptor content in lymphocytes (r = 0.7703, p < 0.0002). These results suggest that individual differences are preserved both in glucocorticoid responsiveness and in glucocorticoid receptor content in peripheral blood leukocytes in normal humans.
The stimulated C-kinase activity in estradiol-treated rat pituitaries is reduced by chronic treatment with the dopamine agonist CV 205-502
Authors: Birman P. , Touraine Ph. , Bai-Grenier F. , Dubray C. , Kaabache T. , Peillon F. , Joubert (Bression) D. 
Published: December 2008

Abstract.
To investigate whether the modulation of lactotrope cell multiplication and prolactin secretion in rat pituitary glands implicated the phosphoinositide C-kinase system, female Wistar rats were treated or not with the dopamine agonist CV 205-502 or 8 days or with estradiol cervical implants for 8 for 15 days, alone or in combination with CV 205-502 for the last 8 days. CV 205-502 treatment induced a significant reduction in plasma PRL levels and in pituitary weights, whereas estradiol treatment induced a significant increase in both parameters. CV 205-502, in association with estradiol, counteracted estradiol stimulation of PRL levels and of pituitary weights. Total C-kinase activity in controls was 29.8 ± 9.9 pmol 32phosphorus/min (N = 7, mean±sem), mainly found in the soluble fraction (84%). When administered alone, CV 205-502 induced a significant reduction (–58%, p < 0.02) in C-kinase activity in the particulate fraction with no modification in the soluble fraction. Both 8 and 15 days estradiol treatment induced a significant stimulation of total C-kinase activity, 74% and 155% respectively. When combined with estradiol, CV 205-502 significantly (p < 0.02) counteracted the estradiol increase in total C-kinase activity, which was only 45% over control values. We conclude that treatment with a dopamine agonist and estradiol, which have antagonistic effects on the pituitary, exerts an opposite regulation of C-kinase activity. Whether this may be one of the mechanisms involved in their interaction on pituitary lactotropes remains to be determined.
Effect of congenital renal disease and neonatal thyroid status on urinary human epidermal growth factor concentrations
Authors: Scott Susan M. , Guardian Carmela , Rogers Cathy , Angelus Pam , Werner Sher 
Published: December 2008

Abstract.
We have previously demonstrated that changes in urinary epidermal growth factor/creatinine ratios relate to gestational age and gender. It is unclear what controls this developmental pattern although chronic renal disease and thyroid aberrations have significant effects on epidermal growth factor and creatinine excretion in childhood and in adults. Therefore, we chose to explore the effects of these disease states on epidermal growth factor excretion during the perinatal time period. We collected urine samples from 8 infants with congenital renal disease and 45 infants with low T4 and normal TSH values who 'failed' the newborn screen. In addition, 2 infants with hypothyroidism and 2 infants with neonatal Grave's disease had urine samples examined. Values were compared with the epidermal growth factor and creatinine excretion from 190 infants. We demonstrated that epidermal growth factor excretion increased earlier in gestation than does creatinine excretion. In infants with renal disease or hypothyroidism, epidermal growth factor excretion was decreased while hyperthyroidism enhanced excretion. Epidermal growth factor excretion increased with relief of an obstruction but still remained low and creatinine excretion was unchanged. We confirm that in preterm infants as in childhood there are similar effects of thyroid and renal diseases on epidermal growth factor excretion.
On the nature of the galanin action on the endocrine pancreas: studies with six galanin fragments in the perfused dog pancreas
Authors: Hermansen Kjeld , Yanaihara Noboru , Ahrén Bo 
Published: December 2008

Abstract.
Galanin, a 29 amino acid peptide, inhibits insulin and somatostatin secretion from the isolated, perfused dog pancreas. To assess the nature of the influences of galanin on the endocrine pancreas, we examined the effects of porcine galanin and six different galanin analogues at the equimolar concentration of 1 nmol/l on the hormone release from the isolated, perfused dog pancreas. It was found that galanin2–29 (by 75 ± 4%), like the native galanin1–29 (by 90 ± 3%) potently inhibited insulin secretion (p < 0.001). In contrast, galanin3–29 did not significantly affect insulin secretion. This indicates that removal of the two N-terminal amino acids markedly reduces the potency of galanin. Also, the replacement of the amino acid number 2 (Trp) by Tyr or Phe was followed by a loss of the insulin lowering effect of galanin at this dose level. Likewise, galanin 10–29 had no significant effect on insulin secretion. In contrast, the C-terminally deleted galanin1–15 significantly inhibited insulin secretion (by 24 ± 5%; p < 0.01), though with a lower potency than did native galanin (p < 0.05). Consequently, the C-terminal end of galanin is also of importance for the effect. Somatostatin secretion was inhibited by galanin (p < 0.001), but not by any of the other investigated peptides. Glucagon secretion was not affected by galanin. It is concluded that the two N-terminal amino acids of galanin are essential for the inhibitory action on the insulin secretion. The removal of the N-terminal Gly residue decreases the action of galanin on insulin secretion to a much smaller extent than does the removal of, in addition, the Trp residue. However, the remainder of the molecule seems necessary for full potency. It is also concluded that the inhibition by galanin of somatostatin secretion seems to require the entire molecule.
Sn-1,2-diacylglycerols and phorbol ester stimulate the production of progesterone from the human placenta
Authors: Kato Hiromi , Kato Masayuki , Kasugai Masahide , Mizutani Sigehiko , Ninagawa Terumi , Tomoda Yutaka 
Published: December 2008

Abstract.
Human term placental explants were used to investigate the possible role of phospholipid-sensitive and Ca2+ dependent protein kinase in the regulation of human placental progesterone production. Placental tissue was incubated with low density lipoprotein as a precursor of progesterone in the presence or the absence of phorbol 12-myristate-13-acetate, 1-oleoyl-2-acetyl-glycerol, and the calcium ionophore A23187. The rate of progesterone production by placental tissue was 21.7 ± 4.6 ng · (mg wet wt)−1 · (2 h)−1 (mean ± sem) with 500 mg low density lipoprotein/1 (control). The rate of progesterone production was accelerated 2-fold by l nmol/1 phorbol 12-myristate-13-acetate, 1.6-fold by 250 μmol/1 1-oleoyl-2-acetyl-glycerol and this increase was dose-related (25–250 μmol/1 1-oleoyl-2-acetyl-glycerol). A non-promoting derivative, 4α-phorbol-12,13-didecanoate had no effect. The phorbol 12-myristate-13-acetate or 1-oleoyl-2-acetyl-glycerol induced stimulation of progesterone production was not associated with a change in the intracellular cAMP level. Addition of 10 μmol/1 A23187 further increased progesterone production with 125 μmol/1 1-oleoyl-2-acetyl-glycerol. The rate of progesterone production was accelerated 1.6-fold by 125 μmol/1 1-oleoyl-2-acetyl-glycerol and 10 μmol/1 A23187 as compared with control. The effects of the phorbol ester and the diacyl glycerol were completely blocked by the addition of the protein synthesis inhibitor cycloheximide. We conclude that these phorbol regents are able to stimulate human placental progesterone production. The possible roles of intracellular Ca2+ and protein kinase C in placental steroidogenesis are discussed.
Infusion of atrial natriuretic hormone in DOCA/salt and spontaneously hypertensive rats
Authors: Fujimura Akio , Kyker Kimberly D. , Kem David C. 
Published: December 2008

Abstract.
The effects of a 6-day infusion of atrial natriuretic hormone (ANH) on blood pressure and urinary sodium excretion were determined in conscious DOCA/salt and spontaneously hypertensive rats. The DOCA/salt rats were randomly divided into two groups after 4 weeks and either infused by osmotic minipump with 32.5 pmol/h of ANH in 0.1 % gelatin vehicle or sham operated with emplacement of a blind cannula. Thirteen-week-old spontaneously hypertensive rats were studied in a similar fashion. The baseline systolic blood pressure prior to the infusion was 176 ± 7 mmHg (x ± sem) in the ANH group and 169±5 mmHg in the sham group of DOCA/salt animals. The ANH infusion in the DOCA/salt animals dropped their blood pressure to 160 ± 10 mmHg (p < 0.01) compared to that in the sham controls which continued to rise to 200 ± 7 mmHg. The blood pressure response to ANH infusion in the spontaneously hypertensive rats was slightly greater, with a blood pressure of 192 ± 5 mmHg in the sham group and 132 ± 3 mmHg in the ANH-infused animals. ANH infusion produces a qualitatively similar blood pressure response in the DOCA/salt rat as well as the other hypertensive models. This response is relatively less on a quantitative basis than that observed in the spontaneously hypertensive rats and is not related to changes in sodium balance or volume contraction.
Physiological levels of immunoreactive ANH-like peptides in human follicular fluid
Authors: Sundsfjord J. A. , Forsdahl F. , Thibault G. 
Published: December 2008

Abstract.
The concentrations of immunoreactive C-terminal (ANH-(99-126)) and N-terminal (ANH-(1-98)) portions of pro-ANH were measured in follicular fluid and plasma samples from 9 young women undergoing in vitro fertilization. ANH-(99-126) and ANH-(1-98)-like immunoreactivity levels in plasma were 6.0–25.4 (mean 12.2) pmol/1 and 184–427 (mean 300) pmol/1, respectively, whereas the corresponding levels in follicular fluid were 3.8–8.0 (mean 4.9) pmol/1 and 169–385 (mean 262) pmol/1. The concentrations of both ANH-like peptides were consistently lower (p < 0.01) in the follicular fluid than in the matched plasma samples, but within the variation found in plasma controls. It is concluded that ANH-like peptides in the follicular fluid, whether secreted locally or derived from circulating ANH, might play a physiological role in the biosynthesis of ovarian steroid hormones or follicular maturation and fluid dynamics.
Serum GH binding protein activities identifies the heterozygous carriers for Laron type dwarfism
Authors: Laron Z. , Klinger B. , Erster B. , Silbergeld A. 
Published: December 2008

Abstract.
Measurement of GH-binding protein activity and IGF-I was carried out in the sera of 13 patients with Laron type dwarfism, a syndrome caused by a lack of GH receptors which leads to impairment of IGF-I generation, and those of 16 of their close relatives. GH binding protein activity was measured by incubating 125I-hGH with 100 μl serum in the presence and in the absence of excess unlabelled hGH, followed by separation of specifically bound 125I-hGH binding protein complexes from free 125I-hGH by gel filtration. The results are expressed as percent specific binding relative to an adult reference serum. IGF-I was determined by RIA after acid extraction on octadecylsilane silica columns. All Laron type dwarfism patients had no, or only negligible GH binding protein activity, which supports the evidence that serum GH binding protein corresponds to the extracellular domain of the membranal GH receptor. Eight of the 16 relatives had serum GH binding protein activity more than 2 sd below the mean for age, a finding considered to denote heterozygocity for their molecular defect disease. The significant correlation (p < 0.001) between serum GH binding protein activity and IGF-I levels supports this conclusion. The ability to define heterozygotes of Laron type dwarfism will be helpful in genetic counselling.
Discordant immune and growth response to pituitary and biosynthetic growth hormone in siblings with isolated growth hormone deficiency type IA
Authors: Hauffa Berthold P. , Illig Ruth , Torresani Toni , Stolecke Herbert , Phillips John A. 
Published: December 2008

Abstract.
Two brothers with familial isolated growth hormone deficiency type IA homozygous for the same 6.7 kb deletion on chromosome 17 including the growth hormone gene were intermittently treated with various forms of hGH for more than 7 years. While the elder brother (Patient 1) showed a good growth response to pituitary hGH, the younger one (Patient 2) developed high titre growth blocking hGH antibodies early in the course of treatment and grew only 2.2–3.9 cm/year on a hGH dose of 12–26 IU/m2 per week. When the younger brother was changed to a higher dose (33 IU/m2 per week) of biosynthetic methionyl hGH he had striking catch-up growth and he has subsequently maintained a height velocity of 10.0 cm/year for the last 2 years. During this time his antibody titres have decreased over 1000-fold. These findings demonstrate that therapy with biosynthetic methionyl hGH may provide an effective form of treatment for subjects with isolated growth hormone deficiency type IA who do not grow in response to native hGH, and imply that biosynthetic methionyl hGH may be less antigenic than pituitary derived hGH.
Effects of lithium on stimulated metabolic parameters in dog thyroid slices
Authors: Tseng Fen-Yu , Pasquali Daniela , Field James B. 
Published: December 2008

Abstract.
Thyroid abnormalities may develop during chronic lithium therapy for affective disorders. Lithium, like iodide, inhibits TSH stimulation of adenylate cyclase and thyroid hormone release. The present study examined the effect of lithium on stimulation of intrathyroidal intermediary metabolism by several agonists. LiCl (5 mmol/l) did not inhibit basal cAMP, glucose oxidation or 32P incorporation into phospholipids in dog thyroid slices. Although LiCl inhibited TSH stimulation of cAMP, it did not abolish the hormone's effect on cAMP-dependent protein kinase. The stimulation of iodide organification, glucose oxidation or 32P incorporation into phospholipids by TSH, carbachol and phorbol esters was not inhibited by lithium. This is in contrast to the effects of iodide, which inhibited stimulation of glucose oxidation and 32P incorporation into phospholipids by various agonists. Thus, although both lithium and iodide inhibited TSH-stimulated cAMP formation, they act differently on intrathyroidal intermediary metabolism.
High and low doses of luteinizing hormone induce different changes in testicular microcirculation
Authors: Widmark Anders , Damber Jan-Erik , Bergh Anders 
Published: December 2008

Abstract.
To study the effects of LH on total testicular blood flow and microcirculation, rats were treated with 2.5 or 25 μg LH sc and measurements were made on control rats and on LH-treated rats 1, 2, 3, 4, 6 and 12 h, after treatment. After treatment with 25 μg LH, total testicular blood flow, as measured with the radioactive microsphere method, was decreased at 6 h and increased at 12 h. Testicular microcirculatory blood flow was recorded with laser Doppler flowmetry and regular oscillations in blood flow, vasomotion, was observed in control rats. Vasomotion was not present 4 and 6 h after treatment with 25 μg LH, but returned at 12 h. Prior to and concomitantly with these changes in vasomotion, polymorphonuclear leukocytes accumulated in testicular microvessels and migrated into the interstitial tissue. These changes were followed, 6 h after treatment, by an increased vascular permeability, measured as increased testicular interstitial fluid volume. The lower dose of LH (2.5 μg), doubled plasma testosterone concentration and initially decreased interstitial fluid volume, and later induced a slight increase in blood vessel leukocytes. At the times studied, no changes could be observed in the other vascular parameters. In conclusion, it is suggested that LH, probably via some Leydig cell product, promotes regulatory effects on testicular microcirculation, but different magnitudes of LH stimulation induce different responses.
Pharmacokinetics of 3,5,3'-triiodothyroacetic acid and its effects on serum TSH levels
Authors: Menegay C. , Juge C. , Burger A. G. 
Published: December 2008

Abstract.
3,5,3'-triiodothyroacetic acid is an effective inhibitor of TSH secretion in central hyperthyroidism. Serum 3,5,3'-triiodothyroacetic acid was measured with an RIA preceded by immunoprecipitation. An anti-3,5,3'-triiodothyroacetic acid antibody was obtained in rabbits, using 3,5,3'-triiodothyroacetic acid coupled to hemocyanin and diazotized benzidine as antigen (crossreactivity with T4, T3, tetraiodothyroacetic acid was 0.2, 1.1, and 5%, respectively). Endogenous 3,5,3'-triiodothyroacetic acid levels could not be detected in 14 euthyroid, 10 hypothyroid and 10 hyperthyroid sera (detection limit 0.055 nmol/l). Kinetic studies were performed in 6 healthy male subjects who received an oral and an iv dose of 1050 μg of 3,5,3'-triiodothyroacetic acid. The serum measurements were analysed according to a non-compartmental method. The half-life of 3,5,3'-triiodothyroacetic acid was 6 h 22 min ± 29 min, the volume of distribution was 114 ± 9 1/70 kg, and the plasma clearance rate was 298 ± 14 1 · (70 kg)−1 · day−1. Highest 3,5,3'-triiodothyroacetic acid levels were measured after 40 min (for T3 2–3 h) and its absorption was 67±6%. The nadir of the mean TSH levels was 0.72 ± 0.09 mU/l 6 h after 3,5,3'-triiodothyroacetic acid administration. However, the time course of serum TSH response did not differ from that obtained after administration of 37.5 μg T3. The dose-response effect for TSH was studied using oral doses of 350, 700, 1400 and 2800 μg 3,5,3'-triiodothyroacetic acid. TSH was measured 9 h after 3,5,3'-triiodothyroacetic acid administration at 17.00 h, and compared with control serum TSH levels obtained at 08.00 h (1.53 ± 0.11) and at 17.00 h the day before the test (1.87 ± 0.11). They were 1.05 ± 0.15 (N = 9, mean ± sem), 0.83 ± 0.08 (N = 24), 0.66 ± 0.06 (N = 24), and 0.43 ± 0.02 mU/l (N = 6), respectively. In conclusion, TSH inhibition by 3,5,3'-triiodothyroacetic acid is similar to T3, with a potency ratio of 1 to 18.