There is now considerable evidence that nitric oxide is an important neuroregulatory agent, but there has been very little investigation of its possible role in neuroendocrine mechanisms in humans. We have investigated the effects of two nitric oxide precursors, L-arginine and molsidomine, under basal conditions on the pituitary hormones growth hormone (GH), prolactin, luteinizing hormone, follicle-stimulating hormone, thyrotrophin, adrenocorticotrophin (ACTH) and vasopressin, and also on serum cortisol; we have also studied the effect of L-arginine on circulating prolactin, ACTH and cortisol in normal human subjects under hypoglycaemic stress. L-Arginine stimulated both GH and prolactin release under basal conditions but had no effect on the other hormones studied, while the nitric oxide donor molsidomine showed no effect on any hormone studied. L-Arginine potentiated the hypoglycaemia-stimulated release of ACTH but did not influence the rise in GH. The current studies suggest that the effects of L-arginine on the stimulation of GH and prolactin release are unlikely to be mediated via the generation of nitric oxide.

In our in vitro model, MNPs are taken up by granulocytes through phagocytosis, whereas previously described methods were based on the use of a chelating agent that permit Cu to cross the cell membrane. Moreover, the (64)Cu-engulfed granulocytes showed a high stability of up to 80% of retained radioactivity after 24 h of incubation.

There are only scarce data on HIV progression in vertically infected children in developing countries. The aim of this study is to describe factors from neonatal period associated with long term non-progression (LTNP), in a Brazilian cohort. A cohort study, with data systematically collected from the "Peixe" Cohort (cohort study of children conducted at the main HIV Pediatric Center in Rio de Janeiro, from 1996 to 2005). The study included children who were vertically infected and started follow up at 5 years of age or younger. LTNP, defined as not reaching category C or severe immunosuppression before 5 years of age. Neonatal and demographic factors were studied. Variables with p-value<0.15 were included in a logistic regression model. 213 patients were included, of whom 42% (89/213) were classified as LTNP. Variables independently associated with LTNP were: baseline (at study entry) CD4+ cells (per %) (OR= 1.06, 95%CI=1.01-1.12); age of initiating follow-up, per month (OR= 1.03, 95%CI=1.01-1.06); ZDV use duriing newborn period (OR= 3.31, 95%CI=0.86-12.71); use of antiretroviral (ART) before classification C or severe immunosuppression (OR= 5.89, 95%CI=2.03-17.10). Adjusting for age at the beginning of follow-up, antiretroviral that was unsuccessfully used to prevent maternal-to-child transmission (ZDV use in neonatal period) was associated with better prognosis. ARTs initiation before category C or severe immunosuppression was also associated with LTNP. Key-Words: HIV, antiretroviral therapy, long term non-progressors, children, Brazil.It is estimated that 20-40% of HIV-1-infected children present with rapid disease progression and develop AIDS within the first years of life [1][2][3][4]. On the other hand, 60-80% of infected children manifest less severe symptoms and many survive through adolescence [3][4][5][6]. In developed countries, advanced maternal disease, high maternal viral load, and maternal and infant immune suppression were associated with rapid HIV progression in children [7]. In developing countries, where the majority of perinatal infections occur, there are only scarce data on HIV progression and risk factors. Meanwhile, in some developed countries, all HIV infected children are treated with highly active antiretroviral therapy (HAART) in early infancy. [8]. Brazilian guidelines [9] recommend that HIV infected infants should be treated only if they present any stage B or C symptoms and/or are in immune categories 2 or 3 (CDC) [10]. Although there is some evidence that infants benefit from treatment started in their first year of life, with early HIV replication control and preservation of the immune system [3,4,11], aspects associated with HAART adverse events, adherence and emergence to drug resistant virus must also be considered [5]. Another important issue is the possibility that almost 50% [1-4] of these infants would be long-term nonprogressors (LTNP), and would not benefit from HAART until five years of age or older. It is important to identify early life events that might be associated...

Naloxone is able to decrease the effect of a maximal dose of GHRH, thus suggesting the existence of an opioid stimulatory tone on GH secretion.

Summary:A 37 year old black female presented with congestive cardiac failure, 2 months postpartum. She developed spontaneous hypoglycaemia and symptoms of acute adrenal crisis (hypotension, nausea, abdominal pain and tachycardia with small thready pulse), which responded to i.v. dextrose, sodium chloride and hydrocortisone. Biochemical investigations revealed low serum cortisol and plasma adrenocorticotrophic hormone (ACTH) levels. The patient initially showed an impaired cortisol response to intramuscular aqueous tetracosactrin, but an exuberant response after priming with intramuscular tetracosactrin depot. These findings, together with the normal remainiing pituitary function, led us to conclude that this patient had isolated ACTH deficiency associated with congestive cardiac failure and acute adrenal crisis.

Exogenous growth hormone (hGH) administration in humans attenuates the endogenous growth hormone (GH) response to some pharmacological stimuli; in particular, pretreatment with hGH completely blocks the serum GH response to growth hormone-releasing hormone. In order to evaluate the mechanism(s) whereby opiods induce GH secretion in man, we gave the following treatments to six healthy male volunteers: (a) IV saline; (b) a met-enkephalin analog G-DAMME 250 micrograms IV as a bolus at time 0'; (c) hGH 2 IU as an IV bolus at time -180'; (d) G-DAMME as above, preceded by hGH as above. In our study, G-DAMME stimulated GH secretion both basally (peak 17.9 +/- 6.0 ng/ml) and, to a lesser extent, after hGH pretreatment (6.0 +/- 2.7 ng/ml). Since in our study G-DAMME was able to partially overcome the inhibitory effect of hGH administration, it is suggested that opioids act through an inhibition of somatostatin release and not through a GHRH-dependent pathway. However, an additional direct effect of hGH on pituitary somatotrophes cannot be excluded.

It has been previously shown that endogenous opioid peptides suppress human ACTH and gonadotropins secretion via hypothalamic mechanism. Since the angiotensin converting enzyme can participate in the metabolism of opioid peptides, this study examined the action of Captopril, an angiotensin converting enzyme inhibitor, on corticotropin and gonadotropin (LH and FSH) release induced by the opiate antagonist naloxone in man. Seven male hypertensive volunteers (aged 30-52) were treated with A) saline; B) naloxone 8 mg iv as a bolus followed by an iv infusion of 4 mg/h; C) naloxone as above after pretreatment with captopril 150 mg/day for 15 days; D) captopril alone. Naloxone significantly stimulated ACTH and LH secretion when compared with the saline infusion. This stimulating effect was taken as an indirect evidence for a tonic opioid inhibition on pituitary hormones release. The pre-medication with captopril significantly enhanced the ACTH and LH response to the opiate antagonist naloxone, but captopril alone did not modify ACTH and LH values when compared to saline. The results would suggest that captopril interferes with the opioid regulation of human ACTH and LH secretion probably by blocking the proteolytic degradation of opioid peptides.