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Biomedical subjects

I Nicoletti

Publications and source records attributed to I Nicoletti.

At least 109 records · Page 6Linked to original sources
PubMed1982

DHT-receptor in cultured human fibroblasts: binding study in a family with androgen insensitivity (complete testicular feminisation).

3H-DHT binding was examined in cultured skin fibroblasts from a patient with complete testicular feminisation (CTF), from his heterozygote mother, and his clinically normal sister, who menstruated normally. Binding parameters were: Bmax less than 1 fmol/mg protein and KD unmeasurable in CTF; Bmax = 24 fmol/mg protein and KD = 3.63 X 10(-9) mol/l in the mother; and Bmax = 46 fmol/mg protein and KD = 3.7 X 10(-9) mol/l in the sister. Five cultures obtained from genital and non-genital skin of normal male and female subjects were used as controls, in which Bmax ranged from 37 to 62 fmol/mg and KD from 2.0 to 3.6 X 10(-9) mol/l. The considerable reduction of Bmax in the obligate heterozygote and the normal binding capacity in the sister, a probable heterozygote, suggests that it may be possible to use the DHT-receptor assay to identify carriers in families with androgen resistance.

Adolescent↗
PubMed1982

Characterization of adrenergic control of glucagon secretion from isolated perfused rat pancreas.

In order to characterize the adrenergic control of the pancreatic A cell the effect on glucagon secretion of three sympathomimetic substances - epinephrine, isoproterenol and phenylephrine - and two adrenergic blocking agents - propranolol and phentolamine - were tested separately in the basal state and during glucagon hypersecretion induced by arginine infusion or glucopenia, using the isolated perfused rat pancreas. Epinephrine and isoproterenol infusion caused a prompt and sustained glucagon release in the basal state and potentiated glucagon response to metabolic stimuli. Insulin secretion was suppressed by epinephrine and slightly stimulated by isoproterenol. The stimulatory effect on glucagon secretion observed during phenylephrine infusion was abolished by concomitant propranolol infusion and potentiated by phentolamine. Insulin secretion was markedly depressed by phenylephrine: this effect was reserved by concomitant phentolamine infusion, while no effect was observed by concomitant propranolol infusion. Propranolol caused a suppression of both glucagon and insulin secretion, while phentolamine slightly enhanced glucagon and insulin production. In conclusion, beta-adrenergic receptor stimulation markedly increased pancreatic glucagon secretion and slightly enhanced pancreatic beta-cell activity; conversely, alpha-adrenergic agents markedly depressed insulin secretion while scarcely influencing glucagon production.

Animals↗
PubMed1981

[Adrenergic control of pancreatic glucagon secretion].

In order to characterize the adrenergic control of pancreatic A cell, the effect on the glucagon secretion of three sympathomimetic substances (epinephrine, isoproterenol, phenylephrine) and two adrenergic blockers (propranolol and phentolamine) have been separately examined by the isolated perfused rat pancreas. The study was performed in basal state and during glucagon hypersecretion induced by arginine or glucopenia. Epinephrine and isoproterenol infusion determined a prompt an sustained glucagon release both in the basal state and during glucagon hypersecretion. The effect of phenylephrine infusion was slight. In the presence of propranolol, glucagon secretion induced by metabolic stimulus was significantly depressed. The glucagon secretion in the same experimental conditions was insignificantly enhanced by phentolamine. Finally propranolol infusion reverse the glucagon secretion induced by phenylephrine. In conclusion the pancreatic glucagon secretion in our model of study is clearly induced by B adrenergic receptor stimulation.

Animals↗
PubMed1981

[Typing of the alpha adrenergic receptors of pancreatic B cells. In vitro studies with the isolated and perfused rat pancreas].

Two groups of receptors, one which develops a stimulating effect (alpha 1), the other an inhibitory effect hae recently been isolated in the alpha adrenergic group. In order to type the B cell adrenergic receptor of the endocrine pancreas, which mediates the inhibitory action exerted by the catecholamines on insulin secretion, the release of this hormone was evaluated in the presence of five alpha simpathomimetic substances that have a decreasing degree of efficiency on the adrenergic alpha 2 receptor of the presynaptic sympathic nerve terminal. The order of potency with which the alpha agonists tested depressed IRI secretion is superimposable on that of their potency on the sympathetic nerve and alpha 2 receptor. We concluded that adrenergic inhibition of insulin secretion is mediated by an alpha 2 receptor.

Adrenergic alpha-Agonists↗
PubMed1981

[A new model for the in vitro study of the entero-island of Langerhans axis].

A new in vitro pancreas-intestine model which makes it possible to study the physiopathology of the intero-insular axis in greater depth, as it eliminates interference from other system, is proposed. The model, which is composed of the rat pancreas, duodenum and the first 25 cm of the small intestine, conserves both the circulation and the in vivo anatomical reltionship intact. Experiments were designed to evaluate the effect of a drug-induced disaccharidase-activity block on insulin secretion. The results obtained confirm the validity of the proposed model in investigating the entero-insular axis.

Acarbose↗
PubMed1981

[Anemia in primary hyperparathyroidism. Description of 2 case].

Two cases of hyporigenerative anaemia in primary hyperparathyroidism are reported. The absence of other causes of anaemia and the correction of hematological disorder after parathyroidectomy, indicates that PTH hypersecretion is responsible for anaemia. The relationships between calcium levels controlling mechanisms and erithropoiesis are discussed.

Adenoma↗
PubMed1981

Progesterone positive feedback on gonadotropin release in estrogen-primed postmenopausal women: central nervous system and pituitary as possible sites of action.

To investigate the site and mode of action of progesterone in inducing gonadotropin release, the effects of catecholamine-depleting (methyldopa) or dopamine agonist (bromocriptine) drugs on progesterone positive feedback and the gonadotropin response to a centrally acting noradrenergic drug (clonidine) were evaluated in estrogen-primed postmenopausal women. Progesterone administration induced a significant rise in LH, FSH, and PRL serum levels in the control group. Bromocriptine administration was followed by a marked suppression of PRL release but did not modify the gonadotropin response to progesterone. Methyldopa pretreatment significantly reduced the progesterone-induced LH surge, while PRL release was unaffected. After estrogen priming, clonidine administration did not result in an increase in serum LH or FSH concentrations. The dissociated responses of LH and PRL in bromocriptine-pretreated subjects and the significant reduction of the LH rise after progesterone in methyldopa-pretreated women seem to invalidate the hypothesis that a fall in endogenous dopamine is responsible for progesterone positive feedback and suggest that neural noradrenergic mechanisms are involved in progesterone-induced gonadotropin release. The ineffectiveness of a centrally acting noradrenergic agonist in inducing gonadotropin rise provides indirect evidence that an increased pituitary responsiveness may also be involved in progesterone positive feedback.

Aged↗
PubMed1981

Effect of estrogens and progesterone on gonadotropin and prolactin release in a patient with androgen insensitivity.

Response of serum levels of gonadotropins and prolactin to doses of estrogen and progesterone was measured in a patient with the complete form of androgen insensitivity, ie, testicular feminization. Before gonadectomy a single 2.5-mg dose of estradiol benzoate (E2B) produced a decrease in gonadotropin levels. Gonadectomy resulted in a rise of serum levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) but had no effect on levels of prolactin. The following results were obtained after gonadectomy: During low-dosage therapy with ethinyl estradiol (EE) a single 2.5-mg dose of E2B produced a decrease in FSH and LH levels, no LH surge, and a small rise in prolactin levels. With a tenfold higher EE priming, the same dose of E2B provoked an LH surge; progesterone administration produced FSH, LH, and prolactin release. However, progesterone priming blocked the positive feedback of estradiol and enhanced its negative feedback. Pituitary sensitivity ot nonandrogenic steroids appears to be normal in cases of testicular feminization. Under this condition, after gonadectomy, the dynamics of gonadotropins and prolactin in response to estrogens or progesterone administration are similar to those in normal women and suggest that aromatization products of testosterone do not produce any irreversible effects on neuroendocrine differentiation of androgen-insensitive patients

Adult↗
PubMed1980

[The amenorrhea-galactorrhea syndrome. Clinical and therapeutic aspects of 5 treated cases].

The behaviour of plasma prolactin in response to various pharmacological tests has been examined together with that of other hypophyseal function parameters in five patients suffering from amenorrhoea-galactorrhoea syndrome. Evaluation of plasma prolactin and hypophyseal tropinic reserve levels did not prove sufficient to discriminate between functional and organic forms of hyperprolactinaemia. A woman patient was submitted to neurosurgical operation for removal of a hypophyseal microadenoma. The other patients were treated medically with 2-alpha-bromoergocryptin which produced quick normalization of prolactinaemia with restoration of normal memstrual cycles and cessation of galactorrhoea.

Adenoma↗
PubMed1979

[Adrenergic activity and glycometabolic compensation in patients with diabetes mellitus].

In an assessment of the degree of adrenergic activity in the course of diabetes mellitus, plasma levels and urinary excretion of norepinephrine and epinephrine were determined in 20 normal subjects and 47 diabetics: 11 in good control (group I), 23 in poor control (group II), 13 with frank ketoacidosis (group III). The study was repeated in groups II and III once good glycometabolic control had been achieved. Slightly above normal catecholamine levels were noted in group I, while there was a marked increase in group II. Group III shaved an enormous increase by comparison with the other two groups. After medical treatment values in group III fell to within the group I range. The conclusion is drawn that a close relationship exists between adrenergic acitivity and the degree of control of diabetes. The sympathetic nervous system, therefore, interferes in the course of diabetes with blood sugar control via numerous, complex mechanisms.

Adolescent↗
PubMed1976

Amikacin in obstetric, gynecologic, and neonatal infections: laboratory and clinical studies.

Based on the proportion of resistant, moderately sensitive, and sensitive strains, the descending order of activity of amikacin against clinical isolates of urinary pathogens was Salmonella, Klebsiella, Enterobacter, Escherichia coli, Staphylococcus aureus, Citrobacter, Proteus species, and Pseudomonas aeruginosa. However, amikacin was the most active of the antibiotics tested (including gentamicin and tobramycin) against 100 strains of P. aeruginosa. The calculated half-life of amikacin was substantially longer in patients with compromised renal function than in normal subjects. Immaturity of renal function, characteristic of the newborn, similarly slowed the rate of excretion of amikacin. The cure rate (complete clinical remission and eradication of the pathogen) was 91% in 22 patients with urinary tract infection (including 16 with chronic pyelonephritis) treated with 500 mg of amikacin every 8 or 12 hr for eight to 17 days. After single injections of 7.5 mg/kg 2-3 hr before delivery, appreciable amounts of the drug were recovered from the cord blood. No local or systemic intolerance or laboratory abnormalities were observed in a total of 42 patients (including eight infants) treated for a maximum of two weeks. No ototoxicity was demonstrable in any of the 12 patients subjected to audiometry; nystagmography revealed slight vestibular dysfunction in two elderly patients.

Amikacin↗