Local-field enhancement effect on the nonlinear optical response of gold-silver nanoplanets.

We report on the nonlinear optical properties of Au-Ag nanoplanets produced by ion implantation and irradiation in silica, experimentally investigated by means of the single beam z-scan technique. The measurements provided experimental evidence of the intense local-field enhancement effect theoretically demonstrated for these plasmonic nanosystems. In particular, this has a dramatic impact on their nonlinear absorption behavior and results in a tunable changeover from reverse saturable absorption to saturable absorption by slightly varying the pump intensity and in the possibility to activate and observe nonlinear phenomena of the electron dynamics otherwise unaccessible in the intensity range that can be employed to study these materials. Finally, for the nanoplanet configuration we found a dramatic decrease of the intensity-dependent absorption coefficient, which could be very promising for obtaining optical gain materials.

Hypothalamic-pituitary-adrenal axis function and cytokine production in multiple sclerosis with or without interferon-beta treatment.

OBJECTIVES: Pro-inflammatory cytokines mediate brain damage in multiple sclerosis (MS); they can also influence the hypothalamic-pituitary-adrenal (HPA) axis function. We evaluated the possible abnormalities of HPA axis function in relapsing-remitting MS (RR-MS). MATERIAL AND METHODS: IFN-gamma, TNF-alpha and IL-6 production by ex-vivo lymphocytes from 10 normal volunteers and 10 RR-MS patients before and during IFN-beta therapy was assessed; pituitary-adrenal function was evaluated by means of CRH and ACTH stimulation tests. RESULTS: In untreated patients the production of IFN-gamma, TNF-alpha, IL-6 was increased, and was significantly decreased by IFN-beta. Neither basal, nor stimulated ACTH, cortisol, DHEA, DHEAs, 17-alpha-OH-progesterone levels differed between controls and RR-MS patients, both before and during treatment. Moreover, no correlation was found between endocrine and immune parameters. CONCLUSION: In MS the HPA axis function seems normal and not influenced by IFN-beta treatment. This result is discussed in relation to the increased production of pro-inflammatory cytokines found in this disease.

Neuroendocrine effects of subcutaneous sumatriptan in patients with migraine.

We evaluated the sensitivity of 5-HT1D receptors in patients with migraine using sumatriptan as a pharmacological probe. The drug inhibits the release of ACTH, cortisol and prolactin and this effect may be used to explore the function of serotoninergic systems in vivo. We administered sumatriptan (6 mg sc) and placebo to 15 migraineurs, during the headache-free period, and to 10 healthy controls. Blood samples were collected -15, 0, 15, 30, 45, 60 and 90 min after injections. Sumatriptan induced a significant (p<0.01) decrease of ACTH, cortisol and prolactin concentrations both in patients with migraine and in controls. The neuroendocrine response was not significantly different in the two groups. Our results suggest that 5-HT1D receptor sensitivity is not altered in migraine.

Effects of subcutaneous sumatriptan on plasma growth hormone concentrations in migraine patients.

The purpose of this study was to assess the sensitivity of 5-HT1D receptors in migraine using sumatriptan as a pharmacological probe. The drug stimulates the release of growth hormone (GH) and this effect may be used to explore the function of cerebral serotonergic systems in vivo. We administered sumatriptan and placebo to 15 migraineurs and to 10 controls. Blood samples were collected -15, 0, 15, 30, 45, 60 and 90 min after injection. Placebo had no effect on hormone concentrations. Sumatriptan induced a significant (P<0.01) increase in GH concentrations both in migraine patients and healthy controls. The GH increase was not significantly different in the two groups. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are not altered in migraine. Sumatriptan overuse could lead to adverse effects mediated by its neuroendocrine activity.

Evidence for a positive correlation between serum cortisol levels and IL-1beta production by peripheral mononuclear cells in anorexia nervosa.

A hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis has been reported in anorexia nervosa (AN), together with some immunological abnormalities, involving citokine - and particularly Tumor Necrosis-Factor-alpha (TNF-alpha) - production by polymorphonuclear cells. The ability of pro-inflammatory cytokines to activate the HPA axis is well known; however, there are no data demonstrating an interdependence between immunological and endocrine response in AN. To investigate the presence of a correlation between immune response and pituitary-adrenal function, plasma ACTH and serum cortisol concentrations were measured in 13 AN patients and in the same number of controls. TNF-alpha and interleukin (IL)-1beta production by ex-vivo unstimulated and LPS-stimulated peripheral mononuclear cells was also assessed. Circulating cortisol concentrations were higher (p<0.01) in AN (156.7 +/- 45.1 microg/l, mean +/- SD) than in controls (105.9 +/- 25.7 microg/l). Unstimulated IL-1beta release in supernatants of mononuclear cell cultures was slightly but not significantly higher in AN than in controls, while TNF-alpha release was similar in the two groups. A positive correlation was found between IL-1beta concentrations in unstimulated culture supranatants and serum cortisol levels in AN (r=0.782, p=0.002), while in normal subjects there was a trend toward a negative correlation; a slight positive correlation, while not significant, between IL-1beta and plasma ACTH, as well as between TNF-alpha and serum cortisol was also found in AN. These data suggest that the normal relationship between pro-inflammatory cytokines release, particularly IL-1beta, and cortisol secretion is deranged in AN.

[Primary hyperaldosteronism. Update on a topic of physiopathology and clinical features]. / L'iperaldosteronismo primitivo. Attualità in tema di fisiopatologia e clinica.

The authors examine the various forms of primary hyperaldosteronism, outlining the most recent acquisitions in terms of etiopathogenesis and physiopathology. While Conn's original description of primary hyperaldosteronism is a syndrome based on corticoadrenal aldosteronesecreting adenoma, it was later seen that this condition could recognise other anatomic substrates, such as carcinoma and in particular bilateral corticoadrenal hyperplasia. A peculiar form of the latter can be suppressed with glucocorticoids sustained by an anomalous recombination of aldosterone-synthase and 11-beta-hydroxylase. The main focus in this paper is on clinical management, in particular the current diagnostic criteria which show that primary hyperaldosteronism affects a higher percentage of the hypertense population that was estimated in the past. Above all, the significance of the aldosterone/PRA (ARR) ratio in screening for this condition is discussed, above all in normokalemic forms, together with the role of molecular biology in identifying glucocorticoid-suppressible forms. Lastly, the principles of medical and surgical management are outlined, emphasising the role of laparoscopic surgery.

Evidence for an interaction between alpha-MSH and opioids in the regulation of gonadotropin secretion in man.

Gonadotropin secretion is inhibited by the endogenous opioids and stimulated by their antagonist naloxone. LH secretion is stimulated by alpha-MSH, a tridecapeptide derived from the post-translational processing of POMC. The possibility that alpha-MSH interacts with the opioids, as suggested by the experimental evidence, was investigated in 7 normal males aged 24-29 through the performance of seven tests: naloxone (0.8 mg i.v. bolus, followed by infusion of 1.6 mg/h for 120'); alpha-MSH (2.5 mg i.v. bolus); naloxone + alpha-MSH (2.5 mg i.v. 15' after commencement of the naloxone infusion); naloxone + GnRH (100 micrograms i.v. 15' after commencement of the naloxone infusion); alpha-MSH + GnRH (respectively 2.5 mg and 100 micrograms at time 0), GnRH alone (100 micrograms at time 0), placebo (150 nmol/l NaCl solution). The LH AUCs during both naloxone (30.3 +/- 2.7 mIU/ml.min-1) and alpha-MSH test (32.9 +/- 4.6 mIU/ml.min-1) were significantly greater (p < 0.005) than that observed during placebo (16.9 +/- 3.6 mIU/ml.min-1). The LH AUC during alpha-MSH + naloxone (37.6 +/- 2.6 mIU/ml.min-1) was not significantly different from that recorded during their separate administration. GnRH injected alone, during the naloxone infusion and with alpha-MSH produced similar increases in LH, that were significantly higher than that observed during the other tests (AUCs: GnRH 89.4 +/- 10.6, GnRH + naloxone 100.5 +/- 9.1, GnRH + alpha-MSH 94.6 +/- 7.9 mIU/ml.min-1, p < 0.001). Significant increase in FSH (p < 0.001) was only observed during GnRH, GnRH + naloxone and GnRH + aMSH tests (AUCs: placebo 13.3 +/- 1.7; naloxone 14.7 +/- 2.5; alpha-MSH 15.5 +/- 2.3; alpha-MSH + naloxone 16.9 +/- 1.9; GnRH 19.1 +/- 1.1; GnRH + alpha-MSH 20.7 +/- 1.3; GnRH + naloxone 21.2 +/- 1.8 mIU/ml.min-1). These results are in line with the possibility of an interaction between alpha-MSH and the opioids in the regulation of gonadotropin secretion, perhaps with opposing effects on a final common pathway.

Hypertension and oedema caused by cortexone hyperproduction and cured by monolateral adrenalectomy. Case report.

Excess 11-deoxycorticosterone (DOC) production, mostly due to an enzyme defect 11-beta-hydroxylase, is a rare cause of secondary hypertension. Even rarer are those forms due to an adrenal adenoma or to a bilateral hyperplasia. In this paper we report the case of 23-year-old woman with excess DOC production, presenting with arterial hypertension and oedema, whom we first observed in 1961. Complete clinical remission, persisting more than 30 years later, was obtained by monolateral adrenalectomy. The literature reports of DOC-induced hypertension due to adrenal adenoma or hyperplasia are reviewed and the possible pathogenetic mechanisms are discussed.

Alpha-melanocyte-stimulating hormone antagonizes the inhibitory effect of corticotropin-releasing hormone on luteinizing hormone secretion during the luteal phase in normal women.

CRH inhibits the secretion of gonadotropins by activating endogenous opioids, whereas alpha MSH, which displays various behavioral and neuroendocrine effects contrary to those of the opioids, stimulates their release. To evaluate the possible interaction of CRH and alpha MSH, eight women in the luteal phase underwent the following tests: 1) ovine CRH infused at 100 micrograms/h for 3 h, 2) alpha MSH (2.5 mg as an iv bolus 60 min after the start of saline infusion), 3) CRH plus alpha MSH (injected 60 min after the start of CRH infusion), and 4) placebo. LH, FSH, PRL, ACTH, and cortisol were determined every 15 min for 180 min. CRH significantly (P < 0.001) reduced serum LH. alpha MSH alone significantly (P < 0.001) increased LH to a peak within 15-30 min (baseline, 3.3 +/- 0.7 mIU/mL; maximum increase, 3.5 +/- 0.9 mIU/mL) and induced an even greater rise when injected during the CRH infusion (baseline, 2.8 +/- 03 mIU/mL; maximum increase 7.5 +/- 1.6 mIU/mL; P < 0.05 vs. alpha MSH alone). FSH was always unaffected. ACTH and cortisol increased (P < 0.001) during the CRH infusion and fell significantly (P < 0.001) during the placebo infusion. alpha MSH had no effect on these changes. PRL fell during the placebo infusion (P < 0.001). No changes were induced by CRH or alpha MSH. In conclusion, alpha MSH antagonizes CRH inhibition of LH secretion. This finding lends support to the view that differential posttranslational processing of POMC contributes to the regulation of LH secretion. Further investigation is needed to clarify the mechanism of the antagonism between alpha MSH and CRH.

[Correlation between blood concentrations of E2, P, T, A and HCS in induction of abortion in trimester II and ultrasonic monitoring]. / Correlazione tra le concentrazioni plasmatiche di E2, P, T, H, HCS nell'induzione dell'aborto al ii trimestre e monitoraggio ultrasonico.

PIP: The authors studied plasma HCS, estradiol (E2), progesterone (P), testosterone (T), and androgen (A) changes in 8 cases of therapeutic abortion by intraamniotic injection of prostaglandin F2 alpha (PGF2alpha). During abortion, the mean plasma concentrations of A and T did not change considerably, while mean plasma concentrations of HCS, E2, and P showed a progressive fall correlated to PGF2alpha dosages used to induce abortion. During the induction of abortion, monitoring by ultrasound showed no correlation between fetal movements, fetal distress, and fetal death. (author's modified)^ieng