[Adapting to the Italian population the methods of predicting the adult body height].
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Age Factors↗
Biomedical subjects
I Nicoletti
Publications and source records attributed to I Nicoletti.
Effect of the mobile phase composition on the retention behaviour of diphenylsilica pre-coated plates.
The retention of some rifamycins and steroids on diphenyl bonded pre-coated silica gel plates, in relation to the mobile phase used, was examined by thin-layer chromatography. Neat organic solvents, non-aqueous and aqueous binary mixtures were tested as eluents. By comparison of retention data for rifamycins and steroids, respectively, under non-aqueous and aqueous conditions, a dual retention mechanism on this diphenyl phase was found. Interactions with the residual silanol groups seemed to prevail when employing as mobile phase the more lipophilic solvents tested, such as chloroform or dichloromethane, whereas interactions with the aryl groups of the bonded phase prevailed when using high polarity alcohols or aqueous mixtures. As a consequence, by changing the mobile phase, a large variation in selectivity with a concomitant change in retention order of the test compounds was observed.
Chromatography, High Pressure Liquid↗
Effects of acute benzodiazepine administration on growth hormone, prolactin and cortisol release after moderate insulin-induced hypoglycemia in normal women.
Benzodiazepines are known to affect pituitary hormone release, and it has recently been hypothesized that the adenohypophysial hormone response to stress may be modified by previous benzodiazepine treatment. We investigated, therefore, whether a single dose of triazolam, a short-acting benzodiazepine, and flurazepam, a long-acting one, could influence the response of prolactin (PRL), growth hormone (GH) and cortisol to a mild hypoglycemic stress in young healthy volunteers. Neither triazolam nor flurazepam pretreatment resulted in a significant effect on the pituitary response to hypoglycemic stimulus. The GH, PRL and cortisol peaks after both benzodiazepines were similar to those observed after placebo. Our results seem to exclude, therefore, any relevant effect of acute benzodiazepine administration on the neuroendocrine response to mild stress.
Adult↗
Catecholamines and pituitary-function. V. Effect of low-dose dopamine infusion on basal and gonadotropin-releasing hormone stimulated gonadotropin release in normal cycling women and patients with hyperprolactinemic amenorrhea.
To verify the role of dopaminergic mechanisms in the control of gonadotropin secretion in normal and hyperprolactinemic women, we examined the gonadotropin response to GnRH (100 micrograms i.v.) administration in both basal conditions and during low-dose dopamine (DA, 0.1 microgram/kg/min) infusion. Hyperprolactinemic women, either with microadenoma or without radiological signs of pituitary tumor, showed significantly enhanced LH and FSH responses to GnRH in comparison with normal cycling women. 0.1 microgram/kg/min DA infusion did not result in any appreciable suppression of serum gonadotropin levels but significantly reduced the LH and FSH responses to GnRH in both normal and amenorrheic hyperprolactinemic women. Although both LH and FSH levels remained higher in hyperprolactinemic patients than in normal women after GnRH, the gonadotroph's sensitivity to DA inhibition was normal in the hyperprolactinemic group, as both control subjects and patients with hyperprolactinemic showed similar per cent suppression of GnRH-stimulated gonadotropin release during DA. These data confirm that hypothalamic DA modulates the gonadotroph's responsiveness to GnRH. The increased LH and FSH responses to GnRH in hyperprolactinemic patients and their reduction during low-dose DA infusion seem to indicate that endogenous DA inhibition of pituitary gonadotropin release is reduced rather than enhanced in women with pathological hyperprolactinemia.
Adenoma↗
Selective impairment of pancreatic A cell suppression by glucose during acute alloxan-induced insulinopenia: in vitro study on isolated perfused rat pancreas.
This study was performed in order to investigate the role of insulin in the modulation of pancreatic A cell response to glucose. The isolated perfused rat pancreas model was used: intraislet insulinopenia was induced in vitro by 0.56 mM alloxan infusion over 15 min. Alloxan caused a transitory insulin release but did not affect glucagon secretion. Exposure to alloxan completely abolished insulin response to 20 mM arginine, 1.6 mM glucose, and 11.1 mM glucose. Glucagon response to 20 mM arginine and 1.6 mM glucose was unchanged by alloxan pretreatment compared to control pancreata not treated with alloxan. However, the suppression of glucagon release by 11.1 mM glucose was abolished in the alloxan experiments. Twenty milliunits per ml of insulin infused during 11.1 mM glucose infusion restored glycemic suppression of glucagon release, but it produced only a slight inhibitory effect on A cell function in the presence of 3.9 mM glucose. Our study indicates that glucose is the physiological suppressor of the pancreatic A cell and that, in this regard, insulin exerts only a permissive effect.
Alloxan↗
Catecholamines and pituitary function. IV. Effects of low-dose dopamine infusion and long-term bromocriptine treatment on the abnormal thyrotroph (TSH) dynamics in patients with pathological hyperprolactinaemia.
In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the effect of low-dose DA infusion on TRH stimulated TSH secretion in normally cycling women and in patients with pathological hyperprolactinaemia. The effect of long-term bromocriptine therapy on TSH dynamics was also evaluated in a selected group of hyperprolactinaemic women. Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values after TRH administration than 75 healthy controls. Furthermore, the TSH rises induced by the DA-synthesis inhibitor alpha-methyl-p-tyrosine (AMPT, 500 mg orally) were enhanced in both prolactinoma and 'idiopathic hyperprolactinaemia' patients as compared with controls. There was a positive correlation between the TRH- and AMPT-induced TSH rises in the hyperprolactinaemic group. Low-dose DA infusion (0.1 microgram/kg X min) reduced TSH response to TRH in both regularly cycling women and patients with hyperprolactinaemic amenorrhoea. Longterm bromocriptine therapy (2.5 mg tid over 60-150 days) not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had presented exaggerated TSH responses to the basal TRH test.(ABSTRACT TRUNCATED AT 250 WORDS)
Bromocriptine↗
Reduced number of natural killer cells in patients with pathological hyperprolactinemia.
Human natural killer (NK) cell activity, as measured against K-562 target cells, was evaluated in 23 untreated and in 11 bromocriptine-treated hyperprolactinemic female patients and in 63 age-matched healthy women using 51Cr-release assay. The NK cell activity was significantly reduced in untreated hyperprolactinemic patients with respect to that of normal subjects, but therapy with bromocriptine restored NK cell function of patients to the levels of normal controls. Moreover, a reduced number of Leu-7+ cells and of large granular lymphocytes in hyperprolactinemic patients, as compared to normal controls and bromocriptine-treated subjects, correlated well with the decreased NK activity. Finally, 'in vitro' incubation with purified human prolactin, did not affect NK cell activity of blood mononuclear cells. The present results demonstrate that pathological hyperprolactinemia, in which a tuberoinfundibular dopaminergic defect has been postulated, is also associated with a reduction in NK cell number and function and indicate a possible interaction between prolactin, neuroendocrine system and NK cell lineage in man.
Antigens, Differentiation, T-Lymphocyte↗
Estriol and its conjugates in late pregnancy determined by extraction with Carbopack B and liquid chromatography with fluorometric detection.
We report a method for measuring estriol and its intact conjugates in urine, serum, and amniotic fluid. A single assay can be done within about 50 min, eight samples assayed in less than 5 h. A 70-microL urine sample is diluted and the estriol conjugates are adsorbed from it onto graphitized carbon black (Carbopack B, Supelco). After two washings, the analytes are desorbed with chloroform/methanol (60/40, by vol) containing tetrapropylammonium bromide. After solvent evaporation, the residue is redissolved in 100 microL of water/acetonitrile and 20 microL is injected into the chromatograph. Or 1 mL of serum or 0.5 mL of amniotic fluid is deproteinized with cold methanol, then passed through the Carbopack column. After three washings, the estriol and its conjugates are desorbed and treated as for urine. Mean analytical recoveries of the analytes in any of these body fluids were within about 92-98%, except for estriol-3-sulfate-16 alpha-glucuronide in serum (mean recovery 88.3%). The limit of sensitivity is well below the concentrations of clinical interest, and the method is not susceptible to substantial interferences.
Amniotic Fluid↗
Does the hypothalamic tyrosine-hydroxylase inhibition mediate the positive feedback of progesterone on gonadotropin release in women?
Neuropharmacological studies suggest a common inhibitory role for the hypothalamic dopaminergic pathway on gonadotropin and prolactin pituitary release, in humans. As a consequence, it has been hypothesized that the inhibition of hypothalamic tyrosine-hydroxylase and the subsequent fall in dopamine synthesis is involved in the positive feedback of progesterone on LH and PRL pituitary release in estrogen-primed hypogonadal women. The aim of our study was to verify whether an inhibition of tyrosine-hydroxylase may really account for the progesterone action on gonadotropin and prolactin secretion. For this purpose, we compared the effect of a specific tyrosine-hydroxylase inhibitor (alpha-methyl-p-tyrosine, AMPT) with the effect of progesterone on gonadotropin and prolactin release in estrogen-primed postmenopausal women. Progesterone induced a marked release of LH (delta: 129.7 +/- 16.5 mlU/ml, mean +/- SE) and a slight increase in FSH (delta: 39.4 +/- 11.6 mlU/ml) and PRL (delta: 15.3 +/- 2.8 ng/ml) serum levels. Acute or two-day administration of AMPT was followed by a marked rise in PRL serum levels (delta: 82.9 +/- 13.8 and 88.3 +/- 8.2 ng/ml, respectively) while there were no significant increases in serum LH (delta: 5.4 +/- 2.6 and 3.3 +/- 4.6 mlU/ml) and FSH (delta: 3.4 +/- 0.9 and -0.4 +/- 2.9) concentrations. The ineffectiveness of a specific tyrosine-hydroxylase inhibitor in simulating the progesterone effect on gonadotropin secretion seems to negate the hypothesis that a reduction in hypothalamic dopaminergic activity mediates the positive feedback of progesterone on gonadotropin release.
Aged↗
Catecholamines and pituitary function. 2. Prolactin response to different dopamine doses in normal cycling women and patients with prolactin-secreting pituitary tumors, both before and after endogenous catecholamine synthesis inhibition.
The inhibitory effect of various doses of dopamine on serum PRL levels was assessed in both normal cycling women and patients with tumoral hyperprolactinemia before and after endogenous catecholamine synthesis inhibition by alpha-methyl-p-tyrosine, a strong and specific tyrosine-hydroxylase inhibitor. Dopamine infusion induced a significant decrease in the serum PRL levels in both normal cycling and hyperprolactinemic subjects. The mean percent inhibition of baseline PRL induced by the various dopamine infusion rates (0.1, 0.5, 1.0 and 2.0 micrograms/kg/min) was similar in regularly cycling women and in patients with tumoral hyperprolactinemia both before and after endogenous catecholamine synthesis inhibition by alpha-methyl-p-tyrosine. Alpha-methyl-p-tyrosine pretreatment significantly increased serum PRL concentrations in normal women and enhanced their responsiveness to the exogenously administered dopamine. Hyperprolactinemic patients, on the contrary, did not show any significant variation in either basal PRL release or the PRL sensitivity to dopamine infusion after endogenous catecholamine synthesis inhibition. These data indicate that reduced dopamine delivery to the adenomatous lactotroph, either due to a primary hypothalamic abnormality or to a deranged vascular pituitary arrangement, rather than a reduced PRL sensitivity to dopamine inhibition, is the main event accounting for PRL hypersecretion in women with PRL-secreting pituitary tumors.
Catecholamines↗
Catecholamines and pituitary function. I. Effects of catecholamine synthesis inhibition and subsequent catecholamine infusion on gonadotropin and prolactin serum levels in normal cycling women and in women with hyperprolactinemic amenorrhea.
To investigate the role of catecholamines in the control of gonadotropin and prolactin release, we examined the effects of a catecholamine synthesis inhibitor (alpha-methyl-p-tyrosine, AMPT) administration and those of dopamine (DA) or epinephrine (EPI) infusion after endogenous catecholamine synthesis inhibition, on FSH, LH and PRL serum levels, in regularly cycling women and in patients with hyperprolactinemic amenorrhea. AMPT administration was followed by a prompt increase in serum PRL in regularly cycling women, but not in women with hyperprolactinemia either due to a PRL-secreting pituitary microadenoma or 'idiopathic'. Gonadotropin serum levels did not show any significant variation after AMPT in both normal and hyperprolactinemic women. DA infusion after endogenous catecholamine synthesis inhibition by AMPT, induced an appreciable decline in PRL levels in both normal and hyperprolactinemic subjects. Although the net decrements were higher in the hyperprolactinemic group, the PRL fall was similar in the two groups when expressed as a percentage of preinfusion PRL concentrations. LH serum levels similarly fell during DA infusion in normal women and in hyperprolactinemic patients, while FSH concentrations did not show any significant change. EPI infusion after analogous AMPT pretreatment was followed by an evident decrease in serum PRL in both normal and hyperprolactinemic subjects. No significant changes in FSH and LH serum concentrations were observed during EPI administration. These data, while confirming the existence of a functional derangement in the neural inhibitory control of PRL secretion in hyperprolactinemia either due to a PRL-secreting pituitary microadenoma or so-called 'idiopathic', do not agree with the hypothesis that tubero-infundibular DA hyperactivity inhibits gonadotropin secretion in hyperprolactinemic patients. The inhibitory action of exogenously administered DA might represent rather a pharmacological effect than express a physiological inhibitory role of hypothalamic DA pathway on gonadotropin secretion in humans.
Adult↗
Catecholamines and pituitary function. III. Restoration of the prolactin response to thyrotropin-releasing hormone by low-dose dopamine infusion in women with pathological hyperprolactinemia.
Previous studies in Rhesus monkeys have demonstrated that a dopamine (DA) infusion rate of 0.1 microgram/kg X min induces peripheral DA levels similar to those measured in hypophysial stalk blood and normalizes serum prolactin (PRL) levels in stalk-transected animals. We therefore examined the effect of such DA infusion rate on basal and thyrotropin-releasing hormone (TRH)-stimulated PRL secretion in both normal cycling women and women with pathological hyperprolactinemia. 0.1 microgram/kg X min DA infusion fully normalized PRL serum levels in 8 normal cycling women whose endogenous catecholamine synthesis had been inhibited by alpha-methyl-p-tyrosine (AMPT) pretreatment. Furthermore, DA significantly reduced, but did not abolish, the rise in serum PRL concentrations induced by both acute 500 mg AMPT administration and 200 micrograms intravenous TRH injection in normal women. A significant reduction in serum PRL levels in response to 0.1 microgram/kg X min DA, similar to that observed in normal cycling women when expressed as a percentage of baseline PRL, was documented in 13 amenorrheic patients with TRH-unresponsive pathological hyperprolactinemia. However, a marked rise was observed in the serum PRL of the same patients when TRH was administered during the course of a 0.1-microgram/kg X min DA infusion. The PRL response to TRH was significantly higher during DA than in basal conditions in hyperprolactinemic patients, irrespective of whether this was expressed as an absolute increase (delta PRL 94.4 +/- 14.2 vs. 17.8 +/- 14.1 ng/ml, p less than 0.002) or a percent increase (delta% PRL 155.4 +/- 18.9 vs. 17.9 +/- 7.1, p less than 0.0005), and there was a significant linear correlation between the PRL decrements induced by DA and the subsequent PRL responses to TRH. These data would seem to show that the 0.1-microgram/kg X min DA infusion rate reduces basal PRL secretion and blunts, but does not abolish, the PRL response to both TRH and acute AMPT administration. The strong reduction in PRL secretion and the restoration of the PRL response to TRH by 0.1 microgram/kg X min DA infusion in high majority of hyperprolactinemic patients, seem to indicate that both PRL hypersecretion and abnormal PRL response to TRH in women with pathological hyperprolactinemia are due to a relative DA deficiency at the DA receptor site of the pituitary lactotrophs.
Adult↗
Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation.
A case of a patient with hypopituitarism due to a disturbance of hypothalamo-pituitary regulation is presented, who developed high-grade hyperprolactinaemia after the initiation of substitutive therapy with testosterone esthers. The increase in serum Prl was strictly related to testosterone aromatization to oestradiol, since anti-oestrogen compounds were effective in reducing (clomiphene) or abolishing (tamoxifen) the enhanced Prl secretion. The oestrogen effect in raising Prl release was not attributable to a reduction in the dopamine inhibition of Prl-secreting cells, as the dopamine-antagonist domperidone failed to increase Prl serum levels in the same patient. This suggests that, in man, the oestrogen effect in enhancing Prl release is mainly enacted directly on the pituitary lactotrophs rather than exerted through a reduction in the hypothalamic dopamine activity.
Adult↗
[Current methods for the evaluation of skeletal maturation. A rapid method for screening changes in skeletal maturation].
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Adolescent↗
[Current methods for the evaluation of the skeletal maturation. 1. Adaptation of the T.W.2 method to the Italian population].
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Age Determination by Skeleton↗
Suppressive effect of long term sulfonylurea treatment on A, B, and D cells of normal rat pancreas.
The effect of chronic administration of tolbutamide (150 mg/kg X day, orally, over 60 days) and glibenclamide (1 mg/kg X day, orally, over 60 days) on pancreatic A, B, and D cell function was investigated in male nondiabetic rats. In a first set of experiments pancreatic hormonal response to metabolic stimuli was evaluated during glucose (11.1 mM) or arginine (10 and 20 mM) infusion in the isolated perfused rat pancreas. The basal levels of insulin (IRI) and glucagon (IRG) were similar in control and in sulfonylurea-treated rats. Tolbutamide treatment markedly depressed the IRI response to glucose (P less than 0.005) or arginine (P less than 0.0005) infusion and the IRG response to arginine (P less than 0.01). After glibenclamide treatment, IRI decreased significantly (P less than 0.0005 and P less than 0.005, respectively) only in response to arginine infusion. This effect was still evident 10 days after the end of treatment. Furthermore, long term glibenclamide administration suppressed somatostatin (SRIF) response to glucose (P less than 0.0005) or arginine (P less than 0.0005). In a different group of rats treated with glibenclamide (1 mg/kg X day, orally, over 60 days) IRI, IRG, and SRIF plasma concentration and blood glucose levels were examined at the end of treatment. The results did not differ significantly from those of a control group. In the same animals, pancreatic IRI, IRG, and SRIF content, measured on acid-ethanol extracts, was reduced (P less than 0.1 vs. controls). These data clearly indicate that long term treatment with sulfonylurea drugs has a suppressive effect on pancreatic endocrine function in rats. The concomitant involvement of A, B, and D cell suggests that this effect is not specific.
Animals↗
[Evaluation of bone maturity: the simplified percentile method of the skeletal profile].
A new method is presented for the evaluation of skeletal growth; it is a simplification of an already known too time-consuming method. A single left wrist-and-hand X-ray is required; examining the morphology of five hand and wrist bones (different according to age) the examined subject can be judged either normal, or requiring a more thorough examination. The results shown were achieved comparing, on 286 roentgenograms, the new simplified method with the already standardized ones. The use of the new method is not only advised because of its simplicity but because of its lack of false negatives as well in the authors' experience.
Adolescent↗
[Hypokalemic myopathy in arterial hypertension].
Three cases of arterial hypertension and severe hypokaliemia are reported; in two cases an acute rhabdomyolisis was also observed. The syndrome was iatrogenic in two cases depending on the licorice eating and the combined use of diuretics and a 9-alpha-fluoroprednisolone-containing nasal spray in one patient, and on a long-term use of the same nasal decongestant in the other. In the patient 2 the persistence of low PRA and aldosterone levels seems to indicate an excess of mineralcorticoid activity other than aldosterone. The syndrome of factitious mineralcorticoid excess should, therefore, be considered in the differential diagnosis of arterial hypertension with hypokaliemia; the risks of a long-term administration of steroid-containing nasal sprays, responsible of serious side effects, should also be stressed.
Adult↗