bluuebunny/crossref_metadata_2025_split huggingface dataset:
Persistence of a defective tuberoinfundibular dopaminergic function in rats after long-term removal of oestrogen treatment. An in vivo study
Authors: Cocchi D. , Peñalva A. , Torpia R. , Rossi G. L. , Müller E. E. 
Published: December 2008

Abstract. The function of the tuberoinfundibular dopaminergic (TIDA) neurons of 49 rats bearing oestradiolvalerate (EV)-induced prolactin (Prl) secreting tumours (prolactinomas) was evaluated in vivo, 7 months after discontinuation of EV-treatment, with neuroactive drugs acting via stimulation or inhibition of DA neurotransmission. Based on the size and morphologic appearance of the pituitary and on determination of plasma Prl levels, rats previously treated with EV could be divided into those bearing macro- (31/49) and those bearing microprolactinomas (18/49). Administration of the indirect DA agonist drug nomifensine (10 mg/kg iv) lowered plasma Prl levels in control rats, but failed to do so in rats bearing either macro- or microprolactinomas. Administration of the DA receptor antagonist domperidone (50 μg/kg ip) or the synthetic enkephalin analogue FK 33-824 (1 mg/kg ip) failed to induce a rise in plasma Prl in rats with macro-, but induced a clear-cut rise in plasma Prl in those with microprolactinomas.
Prl unresponsiveness to all three neuroactive drugs indicates that long time after EV withdrawal TIDA neuronal function is still highly impaired in rats bearing EVinduced macroprolactinomas. The impairment of TIDA neuronal function would be of lesser extent in rats bearing microprolactinomas as revealed by a defective response to only one of the three applied neuroendocrine probes.
Sexual differences in the effect of serotonin on LH secretion in rats
Authors: Moguilevsky Jaime A. , Faigón María R. , Rubio Modesto C. , Scacchi Pablo , Szwarcfarb Berta 
Published: December 2008

Abstract. The effect of 5-hydroxytryptophan (5-HTP), a serotonin (5-HT) precursor, on luteinizing hormone (LH) secretion was studied in prepubertal male and female rats of different ages. In females 5-HTP stimulated LH release on days 16, 18 and 20 but not in older rats (26, 30, 35 days of age). No effects of 5-HTP on LH levels were observed in males. The positive feed-back mechanism of oestrogen-progesterone (E-P), that normally matures in the female between 20 and 26 days, was inhibited by 5-HTP in all the ages studied during prepuberty (26, 30 and 35 days old). On the other hand, in adult ovariectomized rats, 5-HTP administration not only decreased the high LH levels induced by ovariectomy, but the LH release response to E-P as well. These results indicate that there are sexual differences in the effect of 5-HT on LH in prepubertal rats younger than 26 days old.
Administration of p-chloroamphetamine (PCA) a serotonin neurotoxin selective for serotoninergic neurons that depletes 5-HT levels in the brain, induced a significant increase in the LH release response to LRH in females, but had no effect in males. These results, besides suggesting a probable pituitary participation in the 5-HT action on LH secretion in the female, appear to indicate the existence of sexual differences in the effect of 5-HT in adult rats.
'Cryptic' form of congenital adrenal hyperplasia due to 21-hydroxylase deficiency in the Yugoslav population
Authors: Dumić Miro , Brkljačić Ljerka , Mardešić Duško , Plavšić Vesna , Lukenda Milica , Kaštelan Andrija 
Published: December 2008

Abstract. Five individuals with the asymptomatic, 'nonclassical', 'cryptic' form of congenital adrenal hyperplasia (CAH) due to 21-hydroxylase (21-OH) deficiency from 5 unrelated families were discovered during hormonal studies and HLA-typing performed in a series of 24 families with CAH due to 21-OH deficiency.
Four of the 5 individuals with the 'cryptic' form of CAH belong to families where the index case was a patient with the classical form of CAH due to 21-OH deficiency. The fifth one originated from a family where the index case was a girl with the 'non-classical', 'late-onset' form of the disease. All the 5 individuals had no clinical symptoms in spite of clearcut biochemical signs of 21-OH deficiency: increased 17-OH-progesterone (17-OHP), dehydroepiandrosterone and androstenedione levels, particularly after ACTH-stimulation. The 17-OHP response upon ACTH stimulation of heterozygotes for this 'non-classical' form of 21-OH deficiency did not differ from the response of heterozygous individuals for the classical form of the disease. The results of this study confirm the hypothesis that individuals with the 'cryptic' form of CAH due to 21-OH deficiency are genetic compounds bearing one allele for the severe, classical form, and on the homologous locus, another one for the mild 'nonclassical' form of CAH due to 21-OH deficiency. Their genotype was 21-OHsevere/21-OHmild, The gene for 'cryptic' 21-OH deficiency, as well as the gene for the classical form of the disease is linked to the HLA system, but in our population apparently it is not in genetic disequilibrium with the antigens B 14 DR 1, as it was shown for other populations studied up to now.
Inhibition of phytohaemagglutinin-induced lymphocyte blastogenesis by serum from pregnant women: correlation between cortisol level and in vitro immunosuppression
Authors: Wajner Moacir , Papiha Surrinder , Arruda Neusa Bianchini 
Published: December 2008

Abstract. Peripheral human blood lymphocytes stimulated by optimal doses of phytohaemagglutinin (PHA) were cultured in the presence of serum obtained from non-pregnant (controls) and pregnant women at different stages of gestation. A significant inhibitory influence on cellular growth was identified in the serum from pregnant women from the second trimester onward but more pronounced at the end of gestation. This inhibition was strongly correlated with the levels of cortisol in the sera.
The action of commercial cortisol on lymphocyte reactivity in cultures stimulated by various concentrations of PHA and containing either a pool of pregnancy sera, or a pool of non-pregnancy sera, or a mixture of these pools was also investigated. The hormone provoked a significant inhibition more evident when low doses of PHA were used. The same finding occurred with the gravida's sera pool supplemented cultures.
Growth hormone releasing factor induces prolactin secretion in acromegalic patients but not in normal subjects
Authors: Losa Marco , Schopohl Jochen , Müller O. Albrecht , von Werder Klaus 
Published: December 2008

Abstract. The effect of an iv injection of growth hormone releasing factor (GRF) on Prl secretion in healthy volunteers and patients with active acromegaly was investigated. Thirteen normal subjects received 100 μg GRF 1-44, and 19 acromegalics received 100 μg GRF 1-44. Nine normals and 9 patients were given the diluent only and served as placebo control. In healthy volunteers GRF did not affect Prl secretion significantly when compared to placebo, whereas in acromegalics Prl levels after GRF were higher than after placebo.
We have divided acromegalics in Prl-responders to GRF (n = 11) and Prl-non-responders (n = 8) using the criterion of strict parallelism between GH and Prl secretion after GRF. In cases with no GH response to GRF a clear increase of Prl levels with the maximum 15–30 min after GRF was also regarded as a Prl response. Acromegalic Prl-responders and Prl-non-responders did not significantly differ in age, sex, previous therapy, and basal GH and Prl levels. However, Prl-non-responders had a significantly reduced response of both GH and Prl to TRH (GH: 147.3 ± 16.0 vs 590.1 ± 127.8%; mean ± se; Prl: 159.4 ± 32.6 vs 504.9 ± 109.3%). It is concluded that 50 or 100 μg GRF does not affect Prl secretion in normal subjects. In contrast, in acromegaly GRF leads to Prl secretion in more than half of all patients.
Thyrotrophin-releasing hormone (TRH) and hormone secretion from the follicular and C-cells of perfused dog thyroid lobes
Authors: Iversen E. , Laurberg P. 
Published: December 2008

Abstract. Recently we found small amounts of TRH immunoreactivity in the thyroid gland of dogs and pigs. In the present study we investigated if exogenous TRH influences the release of T4, T3 and cAMP from the follicular cells, and calcitonin and somatostatin from the C-cells of perfused dog thyroid lobes.
10−5 mol/l TRH inhibited the TSH induced iodothyronine and cAMP release from the thyroid while 10−8 mol/l TRH had no effect. The relative proportions of T4 and T3 in thyroid secretion were not altered by TRH infusion. TRH did not influence the basal or the Ca++ induced release of somatostatin and calcitonin.
Hence TRH has a direct inhibitory effect on the hormone secretion from thyroidal follicular cells. This opens the possibility that TRH in the thyroid participate in the regulation of thyroid hormone secretion.
Even though the concentration of TRH found to be effective is high our results may indicate that TRH in the thyroid participates in the regulation of thyroid hormone secretion as an antagonist to TSH.
Immunocytochemical demonstration of oxytocin in bovine ovarian tissues
Authors: Kruip Th. A. M. , Vullings H. G. B. , Schams D. , Jonis J. , Klarenbeek A. 
Published: December 2008

Abstract. The presence of oxytocin in ovarian tissue was examined immunocytochemically. Bovine antral follicles and corpora lutea were fixed with glutaraldehyde, picric acid and acetic acid fixative and immuno-stained by the indirect peroxidase-antiperoxydase (PAP) technique. Immunoreactive oxytocin was demonstrated in the granulosa cells of small and large follicles, in the granulosalutein cells of the young corpus luteum and in the large luteal cells of the mature corpus luteum.
The regressing corpus luteum was not stainable. It is discussed that these findings additionally support the view that oxytocin is actually synthesized in ovarian tissues.
Endocrinological and histological changes induced by continuous low dose γ-irradiation of the rat testis
Authors: Pinon-Lataillade G. , Viguier-Martinez M. C. , maas J. 
Published: December 2008

Abstract. Young adult Sprague-Dawley rats were continuously whole-body irradiated with γ rays at a dose-rate of 7 cGy/day for 92 days. Plasma LH, FSH and testosterone concentrations and testicular histology were quantified at different times during exposure. Irradiation selectively decreased spermatogonial numbers until 17 days of irradiation, following which a maturation depletion was observed. By the end of the exposure all germ cell types were reduced in number to about 10% of the control values.
No significant changes were found in testosterone concentration nor in the weights of testosterone dependent accessory sex organs, LH plasma concentration increased slightly but not significantly at the end of irradiation. A significant increase in plasma FSH concentration occurred after the numbers of a spermatogonia and preleptotene spermatocytes had been reduced, when number of stage VII pachytene spermatocytes decreased to 36% of control values, whereas numbers of round spermatids and Sertoli cells were respectively 86% and 100% of the control values. These results suggest a possible role of pachytene spermatocytes in the regulation of inhibin production by the testis.
Antibodies against animal growth hormones appearing in patients treated with human growth hormone: their specificities and influence on growth velocity
Authors: Pérez A. R. , Peña C. , Poskus E. , Paladini A. C. , Domené H. M. , Martínez A. S. , Heinrich J. J. 
Published: December 2008

Abstract. The appearance of anti-human growth hormone (hGH) and anti-non-hGHs antibodies in 27 patients with idiopathic hypopituitarism, treated for periods of 6—18 months with three different preparations of hGH, was investigated.
The preparations induced antibodies to GH in 21 out of the 27 patients: 10 patients produced exclusively an anti-non-hGH response, whereas 11 generated both anti-non-hGH and anti-hGH antibodies. The levels of antibodies against hGH had low correlation with decreased growth velocity, whereas those for the antibodies against non-hGHs did not correlate with decreased growth velocity.
Glucagon release and glucose counter-regulation during hypoglycaemia
Authors: Lager Ibe , von Schenck Henning , Smith Ulf 
Published: December 2008

Abstract. The importance of a short-term elevation of the ambient glucose level for the release of counter-regulatory hormones and the glucose recovery rate during a subsequent hypoglycaemia was studied in healthy subjects. Hypoglycaemia was induced with insulin infusion after a previous 80 min of euglycaemic (E: 5 mmol/l) or hyperglycaemic (H: 15 mmol/l) glucose clamp. By infusing insulin during the euglycaemic clamp similar levels were reached during both glucose clamps. The same level of hypoglycaemia was reached in both studies (E: 1.5 ± 0.1, H: 1.5 ± 0.2 mmol/l) and the insulin levels were also similar both at glucose nadir and during the recovery period. In spite of this, both the mean glucagon levels at nadir at the mean individual maximal increase were significantly lower after the hyperglycaemic clamp (E: 101 ± 25, H: 54 ± 7 pg/ml, P < 0.05). The glucose recovery rate was also significantly impaired following the hyperglycaemic clamp.
The results show that a short-term elevation of the ambient glucose level impairs the glucagon release during a subsequent hypoglycaemia. This finding may be of importance for the development of the blunted glucagon release in response to low glucose levels in diabetics.
The effect of naloxone on ATCH and β-endorphin in patients with Cushing's disease
Authors: Baranowska B. , Dorobek W. , Misiorowski W. , Jeske W. , Abdel-Fattah M. H. 
Published: December 2008

Abstract. Endogenous opiates may be important in the control of ACTH secretion in men. The effect of opiate receptor blockade by naloxone on ACTH, β-endorphin-like substance and cortisol release was studied in healthy women and in 9 patients with Cushing's disease.
In the healthy subjects, ACTH, β-endorphin and cortisol levels were increased in response to naloxone. However, in 3 our of the 9 patients with Cushing's disease, a paradoxical decrease in serum ACTH, cortisol and β-endorphin concentrations was observed after naloxone administration. In the patients with a paradoxical response to naloxone, transsphenoidal microadenomectomy was ineffective.
Effects of bromocriptine on hormone production and cell growth in cultured rat pituitary cells
Authors: Johansen P. W. , Haug E. , Gautvik K. M. 
Published: December 2008

Abstract. Rat pituitary adenoma cells (GH3) that spontaneously synthesize and secrete both prolactin (Prl) and growth hormone (GH) were used in this study. Bromocriptine (5 × 10−5 mol/l), a dopamine (DA) agonist, induced a rapid reduction in Prl and GH secretion with maximum effect (approximately 60%) after 15 min of treatment. Bromocriptine also inhibited Prl and GH production in a time- and dose-dependent manner with ED50 at 4 × 10−6 mol/l and 7 × 10−6 mol/l, respectively. Maximum effect was obtained at 5 × 10−5 mol/l of bromocriptine which after 24 h of treatment reduced the production of Prl and GH by ∼ 70 and ∼ 50%, respectively. After 9 days of treatment both Prl and GH production was reduced by more than 95%. Bromocriptine also reduced cellular growth rate. The ED50 was ∼ 1 × 10−5 mol/l and the maximum effect (> 50%) was observed at 5 × 10−5 mol/l. All effects of bromocriptine were reversible upon cessation of treatment. The anti-proliferative effect of bromocriptine was also observed using a rat hepatoma cell line (MH1C1) and a human epithelial cell line (HE), suggesting a non-receptor mediated growth inhibition at high concentrations of the drug.
In conclusion, the inhibitory effect of bromocriptine on secretion and production of both Prl and GH in GH3 cells occurs at a lower concentration than its effect on cell proliferation. The pharmacological effects of bromocriptine in vivo on Prl and GH producing adenomas may be explained by an action directly at the pituitary level.
Renal sodium retention and vasopressin induced kaliuresis in ethanol anaesthetised rats
Authors: Musabayane C. T. , Brimble M.J. , Balment R.J. 
Published: December 2008

Abstract. Renal electrolyte excretion has been examined in water loaded ethanol anaesthetised rats receiving continuous iv saline (0.077 m NaCl) infusion. These animals exhibited very low rates of Na+, K+ and Cl− excretion by comparison with Inactin anaesthetised rats. Water loaded Inactin anaesthetised rats also showed a degree of Na retention but both Na+ and K+ excretory rates were higher than in ethanol anaesthetised animals. Plasma aldosterone levels did not differ between ethanol and Inactin anaesthetised groups.
Vasopressin administration did not effect Na+ but potentiated K+ excretion in ethanol anaesthetised animals. This contrasted with the potent natriuretic and weak kaliuretic action of vasopressin in water loaded Inactin anaesthetised rats. The significance of abnormal renal electrolyte handling and the marked kaliuretic effect of vasopressin to the use of ethanol anaesthetised animals for vasopressin bioassay is discussed.
Activation of adrenal adenyl cyclase by anti-thyroid plasma membrane antibodies
Authors: Ong M. , Malkin D. G. , Malkin A. 
Published: December 2008

Abstract. We have previously shown that IgG isolated from rabbit anti-bovine thyroid plasma membrane (anti-BTPM) antiserum exhibits properties similar to thyroid stimulating antibodies (TSAb) in that it activates thyroid adenyl cyclase. In this study, the organ non-specificity of this reaction was investigated. It was observed that anti-BTPM IgG stimulated not only adenyl cyclase of bovine thyroid but also that of the adrenal. The stimulatory activities on the thyroid and adrenal adenyl cyclase were abolished by absorption of the IgG with bovine adrenal plasma membrane (BAPM). These results indicate that anti-BTPM antibodies, similar to TSAb, exert both thyroidal and extra-thyroidal effects. Thus anti-BTPM antibodies may be directed against antigenic determinants that are common to both thyroid and adrenal plasma membranes.
Like the anti-BTPM IgG, anti-BAPM IgG also activated both thyroid and adrenal adenyl cyclase. However, when IgG of the anti-BAPM antiserum was absorbed with thyroid plasma membranes, only the thyroid, but not the adrenal stimulating activity was abolished. It was concluded that the anti-BAPM antiserum contained antibodies directed against membrane antigens specific for the adrenal as well as common antigens shared by the thyroid.
Effects of bromocriptine on cell cycle distribution and cell morphology in cultured rat pituitary adenoma cells
Authors: Johansen P. W. , Clausen O. P. F. , Haug E. , Fossum S. , Gautvik K. M. 
Published: December 2008

Abstract. The effects of bromocriptine, a dopamine (DA) agonist, on cell cycle distribution and cell morphology have been studied in a clonal strain of rat pituitary adenoma cells (GH3) which produce and secrete spontaneously both prolactin (Prl) and growth hormone (GH). DNA flow cytometry showed that bromocriptine caused a dose-dependent delay in cell cycle traverse concomitantly with a reduction in cellular growth rate. The lowest concentration of bromocriptine (5 × 10−6 mol/l) significantly (P < 0.05) increased the relative number of cells in the S phase and reduced the proportion of cells in the G1 phase. At higher concentrations (1 × 10−5–5 × 10−5 mol/l) bromocriptine delayed cell cycle traverse through effects on cells in the S, G1 and G2 phases. These effects occurred already after 24 h of treatment. These results were supported by autoradiography of nuclear uptake of [3H]thymidine and by measurements of the number of cells arrested in metaphase after colcemide treatment (mitotic rate).
Bromocriptine at 5 × 10−5 mol/l altered profoundly GH3 cell structure inducing cell clustering and typical changes in mitochondrial and nuclear ultrastructures.
Since Prl and GH production is a characteristic of cells in G1 phase, the inhibitory effect of the lowest antiproliferative concentration of bromocriptine (5 × 10−6 mol/l) can only partly be explained by alterations in phase distribution. At the highest concentration of bromocriptine (5 × 10−5 mol/l) hormone production and cell division are also inhibited due to general toxic effects as reflected by the ultrastructural changes.
Regulation of vasopressin secretion in a patient with chronic hypernatraemia
Authors: Smitz Simon , Legros Jean-Jacques 
Published: December 2008

Abstract. A patient with the chronic hypernatraemia syndrome is described. Using a sensitive and specific radioimmunoassay, the plasma arginine-vasopressin (AVP) level was measured under various conditions.
With an unrestricted diet, the plasma AVP level was inappropriately low for the degree of plasma hyperosmolality (0.9 pmol/l and 302 mOsm/kg, respectively).
After chronic water loading, plasma osmolality was 271 mOsm/kg, plasma AVP level 1.5 pmol/l, and the urine remained hypertonic with respect to the plasma.
During hypertonic saline infusion, plasma osmolality increased from 271 to 294 mOsm/kg without a concomitant increase in the plasma AVP concentration. After sc injection of apomorphine and after haemodynamic stimulation, the plasma AVP concentration increased from 0.8 to 36 pmol/l and from 1.2 to 6.3 pmol/I, respectively. These data demonstrate a selective deficiency in the osmoregulation of the AVP secretion. The observed neuroendocrine abnormalities may be linked to a congenital malformation of the brain.
Hyperthyroidism caused by a pituitary thyrotrophin-secreting tumour with excessive secretion of thyrotrophin-releasing hormone and subsequently followed by Graves' disease in a middle-aged woman
Authors: Kamoi Kyuzi , Mitsuma Terunori , Sato Hiroshi , Yokoyama Motoharu , Washiyama Kazuo , Tanaka Rhuichi , Arai Okuhiro , Takasu Nobuyuki , Yamada Takashi 
Published: December 2008

Abstract. A 46-year-old woman had signs of thyrotoxicosis and galactorrhoea. Serum immunoreactive TSH and its α-subunit increased in the presence of high serum triiodothyronine (T3), thyroxine (T4), and free T4 concentrations, whereas β-subunit TSH was undetectable. Exogenous TRH failed to increase serum TSH. Serum TSH was markedly suppressed by glucocorticoid, but was increased by antithyroid drug. l-Dopa or bromocriptine partially suppressed, but nomifensine had no influence on serum TSH.
Serum prolactin (Prl) was above normal and markedly increased by TRH, but depressed by bromocriptine and not suppressed by nomifensine. Plasma TRH was normal in the hyperthyroid state, but was increased by glucocorticoid and antithyroid drug. Excess thyroid hormone depressed plasma TRH concentrations. Basal serum GH levels were constantly low. Transsphenoidal removal of the tumour normalized serum hormones (T3, T4 free T4, TSH, α-subunit and Prl), and eradicated the clinical signs of hyperthyroidism and galactorrhoea. Histological study of the tumour tissue demonstrated both thyrotrophes and somatotrophes. A reciprocal relationship between serum TSH and T4 concentrations shifted to a higher level before but was normalized after removal of the tumour. Ten months later, the clinical signs of thyrotoxicosis and the increase in serum thyroid hormone recurred without a concomitant increase in serum TSH and its α-subunit. Thyroidal auto-antibodies were slightly positive, but thyrotrophin-binding inhibitor immunoglobulin (TBII) was negative. Administration of antithyroid drug produced a euthyroid state, but 3 years later, discontinuation of the treatment resulted in recurrent hyperthyroidism without suppressed plasma TRH and with no evidence of regrowth of the pituitary tumour.
It is suggested that the patient initially had hyperthyroidism owing to excessive TSH secretion from the tumour caused by abnormal TRH secretion, and subsequently had hyperthyroidism owing to Graves' disease.