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Biomedical subjects

R D'Urso

Publications and source records attributed to R D'Urso.

At least 19 recordsLinked to original sources
PubMed2002

Sex-related variations in serum nerve growth factor concentration in humans.

A role of nerve growth factor (NGF) in the neuro-endocrine-immune interactions has been recently suggested by the presence of NGF and its receptors in cells of the immune and endocrine systems. The improvement in the comprehension of the role played by NGF in humans is linked to the availability of a sensitive and reliable method to quantify NGF concentrations in body fluids and tissues. As a consequence of different methods used, normal levels of human serum NGF reported in the literature show wide differences. The present results indicate that ELISA appears very sensitive (detection limit 1.4pg/ml) and allows the discrimination of subtle variations of serum NGF concentrations. ELISA performed in serum obtained from men indicated that NGF concentration was 40.8+/-10.8pg/ml, whereas women showed significantly lower levels that were influenced by the menstrual cycle. In particular, the mean value of this neurotrophin during the follicular phase was 8.2+/-1.4pg/ml; the luteal phase, in turn, showed levels up to 14.4+/-2.9pg/ml. The difference of serum NGF concentrations between the follicular and luteal phase in each woman was statistically significant. Differences in NGF concentrations between men and women (in both phases of the menstrual cycles) were also statistically significant. In conclusion, a possible role of sex steroids as modulators of NGF secretion in humans is strongly supported by the present paper. However, mechanisms underlying this phenomenon are still unknown. The evidence indicating physiological sex hormone-related variations in NGF levels would be of interest in view of the possible use of circulating NGF modifications as a laboratory biomarker in different diseases.

Adult↗
PubMed2001

High incidence of hyperandrogenism-related clinical signs in patients with multiple sclerosis.

A mild prevalence of multiple sclerosis (MS) is present in females (2:1). To elucidate the pathogenetic role of sex steroids on the disease, we studied 76 women affected by MS, compared to 50 healthy women (mean age +/- SD, 34.9 +/- 0.9 vs. 33.4 +/- 1.7 years). The menarche was at mean age of 12.3 +/- 0.2 vs. 12.4 +/- 0.2. Interval between menses was 28.0 +/- 0.3 vs 27.8 +/- 0.3 days, with duration of menstrual flow of 5.0 +/- 0.2 vs. 5.0 +/- 0.2 days. Oligo- or amenorrhea was present in 20% of patients and in 16% of controls. Oral contraceptives were assumed by 21% of patients and 34% of controls (n.s.). Premenstrual symptoms were found in 43% of patients and in 46% of controls (n.s.). The incidence of hyperandrogenism (greasy skin, acne and hirsutism), evaluated by a specific questionnaire, was higher and statistically significant in MS patients than in controls (28% vs. 10%, p<0.05). Further studies, including a complete clinical and laboratory evaluation of gonadal function, are necessary in order to clarify whether hyperandrogenism may influence MS disease activity.

Adult↗
PubMed1999

MRI in multiple sclerosis during the menstrual cycle: relationship with sex hormone patterns.

We investigated MRI activity in MS during the menstrual cycle in relation to physiologic sex hormone fluctuations. Eight women with relapsing-remitting MS were submitted to serial brain gadolinium-enhanced MRI examinations over a 3-month period in two alternate follicular and luteal phases of the menstrual cycle. The ratio of progesterone/17-beta-estradiol during the luteal phase was significantly associated with both number (r = 0.6, p = 0.03) and volume (r = 0.7, p = 0.009) of enhancing lesions, providing support for a role of these hormones as immunomodulatory factors in MS.

Adult↗
PubMed1997

Subacute thyroiditis during interferon-alpha therapy for chronic hepatitis C.

A 34-year-old woman with chronic hepatitis C received interferon-alpha (IFN-alpha) therapy. Her thyroid function was normal and thyroid autoantibodies were negative before treatment. Four months after the beginning of the therapy she presented a clinical course of thyroiditis with a transient thyrotoxicosis. The diagnosis of subacute thyroiditis was confirmed by laboratory, ultrasonography, radioiodine scanning and fine needle aspiration findings. Thyroid autoantibodies were persisting negative. She suspended IFN-alpha therapy and she started non steroidal anti-inflammatory agents and beta-blockers. Latent hypothyroidism subsequently developed, but L-thyroxine therapy resulted in a rapid normalization of thyroid function tests.

Adult↗
PubMed1997

Effect of r-interferon alpha administration on hypothalamus-pituitary-thyroid axis in chronic hepatitis.

Recent studies pointed out the development of autoimmune thyroid diseases during interferon (IFN) therapy, mainly in patients with positive thyroid autoantibodies (MsAb and TgAb) before treatment. The effects of recombinant human IFN alpha (rhIFNalpha) on thyroid function and thyroid autoantibodies were studied in 12 patients with chronic active hepatitis associated with virus B or C, selected on the basis of negative results for MsAb and TgAb. No significant variation in T3, T4 and TSH levels was observed either after the first administration of rhIFN alpha (3 million IU i.m.) or after three months of therapy (3 million IU i.m. 3 times a week). TSH response to TRH was in the normal range either before or after the therapy. The absence of MsAb and TgAb was confirmed in all the patients at the end of the treatment. These results indicate that no patient developed thyroid disorder during IFN therapy. Nevertheless, since positive MsAb and TgAb have been considered as a risk factor for thyroid diseases, in patients selected for IFN therapy they should be carefully assessed for autoantibodies before undergoing IFN treatment.

Adult↗
PubMed1991

Nimodipine in migraine: clinical efficacy and endocrinological effects.

Serum prolactin is increased during chronic flunarizine treatment of patients suffering from migraine. In order to clarify the role of calcium in control of the secretion of anterior pituitary hormones, a study has now been made of the effects of chronic nimodipine and propranolol treatment of migraine patients on prolactin (PRL), luteinizing hormone (LH) and growth hormone (GH) levels. 11 patients were treated with nimodipine and 8 with propranolol for four months. A statistically significant reduction in the frequency of the attacks was demonstrated in both groups. No significant change was found in the hormones levels during nimodipine treatment.

Adult↗
PubMed1991

Effect of ritanserin, specific 5HT-2 antagonist, on PRL secretion in normal subjects and in different hyperprolactinaemic conditions.

The availability of a new specific anti 5HT-2 compound, ritanserin (RTS), led us to further investigate the role of serotonin in controlling PRL secretion. The drug was administered to normoprolactinaemic subjects and to patients with differing hyperprolactinaemic conditions. While RTS failed to modify PRL levels in normoprolactinaemic subjects and in patients with PRL-secreting pituitary adenomas, a marked decrease in the hormone was obtained in patients with functional and puerperal hyperprolactinaemia. The lack of effect of RTS in PRL-secreting pituitary adenomas suggests that the reported suppression of PRL by other antiserotoninergic drugs, such as metergoline, is probably due to their concomitant dopaminergic activity.

Adenoma↗
PubMed1991

Calcium and calmodulin mediation of growth hormone-releasing hormone release from the rat hypothalamus in vitro.

A major role for Ca2+ and calmodulin in stimulus-secretion coupling has been suggested for several neuropeptides; however, the cellular mechanisms of GH-releasing hormone (GHRH) release have been little investigated so far. We have used a previously validated acute rat hypothalamic explant system in order to elucidate whether Ca2+ acts as a second messenger in the regulation of GHRH release, and whether calmodulin-dependent pathways are involved. Calcium dependence of somatostatin (SRIH) release was assessed in the same experiments. Calmodulin dependence of SRIH was not investigated in detail, as it has been established previously. The calcium-entry antagonist, verapamil, antagonized K(+)-stimulated GHRH and SRIH release in a dose-dependent manner, with maximal inhibition shown at 10(-4) M. The calmodulin antagonist W7 also blocked K(+)-evoked GHRH release in a dose-dependent manner, with significant inhibition in the dose range 5 X 10(-5) M to 2 X 10(-4) M; similarly, a more specific calmodulin inhibitor, the W7 derivative 5-iodo-C8 (W8), reversed K(+)-stimulated GHRH release, showing slightly higher potency than W7. W7 also reversed GHRH release in response to the calcium-ionophore A23187, although verapamil had no effect on A23187-evoked GHRH or SRIH release. Thapsigargin, which increases the efflux of Ca2+ from calciosomes, did not affect either GHRH or SRIH release at 10(-5) M or 10(-4) M. The basal release of GHRH was clearly suppressed by W7 and W8 (10(-4) M), whereas verapamil had no effect. We conclude that calcium influx is crucial for depolarization-induced GHRH and SRIH release. Calcium entrance in response to A23187 appears to be independent of verapamil-sensitive calcium channels. The lack of effect of thapsigargin suggests that increased intracellular Ca2+ from intracellular stores is not equivalent to an increase in Ca2+ influx. Both basal and depolarization-induced release of GHRH in this system are calmodulin dependent.

Animals↗
PubMed1991

Interleukin-1 beta modulates the acute release of growth hormone-releasing hormone and somatostatin from rat hypothalamus in vitro, whereas tumor necrosis factor and interleukin-6 have no effect.

There is clear evidence for communication between the immune and neuroendocrine systems. However, the effect of cytokines as major immune mediators on the hypothalamic growth peptides, GHRH and somatostatin (SRIH), is not well established. To investigate a possible hypothalamic action of the cytokines interleukin-1 beta (IL-1), interleukin-6, and tumor necrosis factor-alpha, on the release of GHRH and SRIH, we used a previously validated acute rat hypothalamic explant system. IL-1 caused a pronounced dose-dependent stimulation of SRIH in the dose-range 1-100 U/ml (P less than 0.01). GHRH showed a slight, but significant, increase in response to IL-1 tested in the dose-range 10-100 U/ml. Similar studies with mediobasal hypothalamic (GHRH and SRIH) or median eminence (SRIH) fragments produced no change in either GHRH or SRIH release. The effects of IL-1 were antagonized by the cyclo-oxygenase inhibitor, indomethacin (10 micrograms/ml). Stimulation of GHRH and SRIH could not be blocked by the CRH-antagonist alpha-helical CRH (9-41) at 10(-6) M. Interleukin-6, in the dose range 10-100 U/ml, and tumor necrosis factor-alpha, in the dose range 10-10,000 U/ml, had no effect on the acute hypothalamic release of either GHRH or SRIH. It is concluded that IL-1 stimulates the acute hypothalamic release of GHRH and SRIH, and that this effect is mediated by cyclo-oxygenase products. The marked IL-1 stimulation of hypothalamic SRIH release may override the minor increase of GHRH increase, and may thus contribute to disturbances in growth seen in the presence of chronic inflammation.

Animals↗
PubMed1986

Role of arachidonate metabolism on the in vitro release of luteinizing hormone and prolactin from the anterior pituitary gland: possible involvement of lipoxygenase pathway.

The aim of the present study was to evaluate whether arachidonic acid metabolism may play a role on luteinizing hormone (LH) and prolactin (PRL) release directly at the pituitary level. To this purpose, exogenous arachidonic acid, alone or in presence of inhibitors of cyclooxygenase (indomethacin:IND) and lipoxygenase pathways (nordihydroguaiaretic acid:NDGA), was added to perfused rat anterior pituitary cells. PGE, PGF alpha, LH and PRL levels present in the eluate were assayed with specific RIA methods. Both PGE and PGF alpha show a dose-related response after the addition of increasing doses of arachidonic acid. The addition of 0.05 mM arachidonic acid induces an increase of LH and PRL. The addition of IND to the perfusion medium highly potentiates the stimulatory effects induced by arachidonic acid on LH and PRL release. On the contrary, the addition to the medium of either NDGA or IND plus NDGA completely reverses the stimulatory action induced by arachidonic acid alone. The present results suggest that: adenohypophyseal cells are able to metabolize exogenous arachidonic acid; arachidonic acid induces an elevation in LH and PRL levels; lipoxygenase pathway metabolite(s) are likely involved in these activities, and the site of action of arachidonic acid is at the pituitary level.

Animals↗
PubMed1984

Dermorphin stimulates prolactin secretion in the rat.

The effect of dermorphin, a new opioid peptide originally isolated from amphibian skin, on the release of prolactin (Prl) was studied in vivo and in vitro. In vivo experiments: subcutaneous administrations of different doses of dermorphin ranging from 0.1 to 5 mg/kg body weight to normal male rats induce a statistically significant, dose-related increase in serum Prl levels. Pretreatment with the specific opioid antagonist, naloxone (2 mg/kg i.p.) completely prevents the rise in serum Prl, induced by 2 mg/kg of dermorphin. In normal male rats, the intraventricular injection of 0.25 micrograms/kg of dermorphin is not able to induce any significant changes in serum Prl levels 10 min after injection. Serum Prl levels show a significant enhancement 30 min after the administration of this dose of dermorphin, and return to control values at 60 min. On the contrary, 1 microgram/kg of dermorphin significantly elevates Prl concentrations 10 min after injection, leaving serum Prl levels unchanged 30 and 60 min after the administration. Naloxone (25 and 100 micrograms/kg) alone does not substantially modify serum Prl concentrations at any time interval considered. Treatment with either dose of naloxone performed together with either 0.25 or 1 microgram/kg of dermorphin completely counteracts the stimulatory effect of the peptide at all time intervals in which dermorphin was active when given alone. In orchidectomized (3 weeks) rats, the intraventricular administration of dermorphin at the dose of 0.25 micrograms/kg appears effective in enhancing Prl levels only 30 min after treatment. No statistically significant modifications are observed at 10 and 60 min with this dose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Sauvagine induces release of adrenocorticotropin, beta-endorphin and corticosterone in rats.

The effect of sauvagine, a frog skin peptide, on ACTH, beta-endorphin and corticosterone secretion, was studied in rats. A subcutaneous injection of 5 micrograms kg-1 of sauvagine in rats produced a prompt increase in immunoreactive plasma concentration of ACTH and beta-endorphin, which reached a peak value 15-30 min after the peptide injection. The stimulatory action of sauvagine on ACTH and beta-endorphin secretion was dose related. Intensity and duration of corticosterone secretion, produced by sauvagine mediated ACTH release, was dose-dependent, the threshold dose being 0,5 microgram kg-1 s.c. Pretreatment of rats with dexamethasone-21-phosphate, prevented the corticosterone releasing effect of sauvagine. Sauvagine perfusion (2,1 nM/h) of biogel columns containing isolated and dispersed anterior pituitary cells induced a sharp increase of ACTH levels in the eluate. Considering the high corticotropin releasing potency of sauvagine and its chemical similarity to ovine CRF, it is interesting to hypothesize whether this peptide may represent, in lower vertebrates, an ancestral form of the mammalian hypothalamic releasing factor.

Adrenocorticotropic Hormone↗
PubMed1983

Effect of long term administration of ovine prolactin on hypothalamic-pituitary testicular axis in rat.

The effect of hyperprolactinaemia on testicular morphology and on hypothalamic-pituitary-testicular axis was studied in adult male Wistar rats. Animals received ovine prolactin (oPRL) 200 micrograms twice daily s.c.) for 24 and 36 days and were killed by exanguination. Blood was collected for hormonal determinations and sex accessory glands were removed for histological studies. Circulating testosterone (T) and luteinizing hormone (LH) levels showed a significant reduction after 36 days of treatment whereas plasma follicle-stimulating hormone (FSH) levels were unchanged in all animals. No macroscopic or light microscopic histological modifications were observed in the testes. The present results, while excluding a direct effect of hyperprolactinaemia on seminiferous tubules, suggest that LH suppression is the consequence of a central effect of the ovine PRL long-term administration. The increased DA turnover in the hypothalamus suggested as inhibitory on GnRH neurons could account for this effect. The reduction of T levels seems to be mediated by the LH suppression, even though a direct effect of oPRL on Leydig cell receptors could be hypothesized.

Animals↗
PubMed1983

Reproductive parameters in prolactinaemic men.

The sexual behavior, hypothalamic-pituitary-testicular axis and seminal fluid parameters in three different models of hyperprolactinaemia were studied: patients with prolactin secreting pituitary adenomas, normal volunteers before and during metoclopramide, and psychotic patients on chronic neuroleptic therapy. Hyperprolactinaemia is always accompanied by a reduced seminal volume but there is no clearcut evidence that it can induce spermatogenesis modifications. Impotence is constantly present in the hyperprolactinaemic syndromes. The mildly impaired androgen production by the Leydig cells during hyperprolactinaemia does not seem to explain the impotence. Hypotheses on the pathogenesis of this symptom are suggested.

Adenoma↗
PubMed1982

Phospholipid liposomes and prolactin secretion: effects on spontaneous and drug-induced hyperprolactinaemia.

Bovine brain phospholipid liposomes (BC-PL) reduce plasma prolactin (PRL) levels in humans after acute administration and counteract the metoclopramide- and sulpiride-induced hyperprolactinaemia. However, BC-PL, like nomifensine, a dopamine (DA) reuptake inhibitor and therefore an indirect dopaminergic compound, does not influence TRH-induced hyperprolactinaemia. Moreover, BC-PL and nomifensine reduce plasma PRL levels in hyperprolactinaemic PCO syndromes but not in PRL secreting pituitary adenomas. The results obtained indicate that BC-PL antagonizes the DA blockade-induced hyperprolactinaemia and that the main site of action of BC-PL seems to be at the hypothalamic level; however a concomitant pituitary effect cannot be ruled out.

Adult↗
PubMed1982

Prolactin response to acute administration of different L-dopa plus decarboxylase inhibitors in Parkinson's disease.

Plasma prolactin (PRL) levels modifications after acute administration of L-dopa, L-dopa plus carbidopa and L-dopa plus benserazide were studied in parkinsonian patients. PRL increase after benserazide was compared with PRL response after carbidopa at the same dosage in untreated parkinsonian patients. A further study of the hyperprolactinemic effect of benserazide was performed in vitro on isolated and dispersed rat pituitary cells. The data gathered indicate that benserazide-induced hyperprolactinemia in parkinsonian patients could be due to a direct effect of the drug at the hypothalamic level and consequently to an inhibition of dopamine decarboxylation in the tuberoinfundibular dopaminergic system. It is not possible to exclude, however, that benserazide could exert its biological activity through the production of active metabolites in vivo.

Aged↗
PubMed1982

Potent in vivo and in vitro prolactin inhibiting activity of sauvagine, a frog skin peptide.

The effect of sauvagine (SAU), a frog skin peptide, on prolactin (PRL) levels was studied in vivo and in vitro. Subcutaneous administration of SAU (20 micrograms/kg) reduced plasma PRL levels in normal adult male rats and suppressed the suckling-induced rise of PRL in lactating rats even at doses of 1 and 5 micrograms/kg. Perfusion of isolated and dispersed rat pituitary cells in vitro with increasing doses of SAU (from 5 x 10(-10) to 1.7 x 10(-8)M) induced a significant dose-related decrease of PRL secretion in the eluate. These results indicate that SAU is a potent PRL inhibiting factor and that its action is exerted at the pituitary level. If SAU or a SAU-related peptide is present in the mammalian brain, it can be tentatively hypothesized that this peptide plays an important role in the control of PRL secretion.

Amphibian Proteins↗