1,721,017 research outputs found
Chronic lisuride treatment decrease ACTH but not 3-EP and β-LPH plasma levels in children Auteur(s) / Author(s)
No full textChronic lisuride treatment decrease ACTH but not 3-EP and β-LPH plasma levels in childre
Impaired pregnenolone secretion after combined cyproterone acetate and ethynyl estradiol therapy in hirsute patients.
No full text6 women affected by hirsutism, either of idiopathic origin or due to polycystic ovary syndrome, have been treated with cyproterone acetate and ethynyl estradiol in combined therapy using, respectively, 100 mg and 50 micrograms/day, from the 5th to the 25th day of the cycle. The adrenal function was assessed before treatment and at the end of the 4th month of therapy, evaluating the peripheral plasma concentrations of pregnenolone (delta 5P), progesterone, 17-OH-progesterone, dehydro-epiandrosterone sulfate, androstenedione, testosterone, and cortisol in basal conditions and after dexamethasone suppression and an adrenocorticotropic hormone (ACTH) stimulation test. A group of healthy, untreated females were examined in the early follicular phase, as controls, Before therapy, the hirsute patient showed testosterone and androstenedione plasma levels, which were significantly higher than in the controls, and a significant reduction in pregnenolone response to ACTH. After 4 months of therapy with cyproterone acetate plus ethynyl estradiol, a significant decrease was found in testosterone and androstenedione plasma levels, and pregnenolone basal plasma levels, dexamethasone suppressibility, and response to ACTH were also markedly reduced, showing a significant difference versus the same patients before therapy and versus the control group. The existence of an impairment in adrenal function after cyproterone acetate plus ethynyl estradiol therapy at the given dose seems to be evident only in the case of directly ACTH-dependent adrenal enzymatic activities responsible for cholesterol cleavage to pregnenolone
Chronic lisuride treatment decrease ACTH but not 3-EP and β-LPH plasma levels in children
No full textSomatostatin and oxytocin infusion inhibits the rise of plasma beta-endorphin, beta-lipotrophin and cortisol induced by insulin hypoglycaemia.
No full textThe present study investigated the possible effect of somatostatin and oxytocin on the basal and stress-induced rise of beta-endorphin (beta-END), beta-lipotrophin (beta-LPH) and cortisol in the human. For this purpose somatostatin (4.1 micrograms/min for 120 min or oxytocin (0.4 micrograms/min for 120 min) was infused into two different groups of seven healthy subjects; 30 min after the start of the infusion, placebo or insulin (0.1 IU/kg body weight, B.W.) was injected on two different days. In a third experimental step, an insulin tolerance test was performed during saline infusion to evaluate stress-related effects on the different hormonal secretions under basal conditions. Plasma levels of beta-END, beta-LPH and cortisol were measured by radioimmunoassay. Extraction and chromatographic procedures preceded the assay for beta-END and beta-LPH. Neither somatostatin nor oxytocin significantly modified basal plasma levels of beta-END, beta-LPH and cortisol. However these treatments blunted the rise of the three hormones seen at 45 and 60 min during insulin-induced hypoglycaemia (P less than 0.01). These results indicate that somatostatin and oxytocin may influence the beta-END, beta-LPH and cortisol increase induced by stress in humans, without affecting their basal secretion
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Hypothalamic amenorrhea: evidence for a central derangement of hypothalamic-pituitary-adrenal cortex axis activity
No full textOBJECTIVE:
To evaluate the activity of the hypothalamic-pituitary-adrenal axis (HPA) in patients with hypothalamic amenorrhea.
PATIENTS, PARTICIPANTS:
Amenorrheic women with a history of emotional stressful events and eumenorrheic women as control group were studied.
DESIGN:
Pulsatile cortisol (F) secretion over a 4-hour period of time and plasma F responses to various neuroendocrine tests (naloxone, fenfluramine, corticotropin-releasing hormone [CRH], adrenocorticotropic hormone) were investigated.
RESULTS:
Women with hypothalamic amenorrhea showed a F secretory pattern higher than normal women. In addition, the lack of naloxone or fenfluramine-induced release of F and a blunted F response to CRH test were observed.
CONCLUSION:
The increased activity of HPA in patients with hypothalamic amenorrhea is associated with an impaired activity of some central pathways (opioids and serotonin), suggesting multiple alterations in the hypothalamic control of pituitary-adrenal axis in amenorrheic women
Growth hormone (GH)-releasing hormone-induced GH response in hypothalamic amenorrhea: evidence of altered central neuromodulation
No full textOBJECTIVE:
To evaluate the GH-releasing hormone (GH-RH)-induced response of GH in patients affected by hypothalamic amenorrhea.
DESIGN:
Patients affected by weight-loss-related hypothalamic amenorrhea (n = 28) were studied and compared with 20 healthy controls. Among patients with weight-loss amenorrhea, both hypogonadotropic and normogonadotropic conditions were present. All subjects underwent a GH-RH test (GEREF, Sereno, Rome, Italy) (1 microgram/kg body weight IV). Plasma GH concentrations were determined using commercially available RIAs. Also, in selected samples insulin-like growth factor-I (IGF-I) levels were measured.
RESULTS:
Basal plasma IGF-I levels as well as body mass index (BMI) were lower in amenorrheic patients than in healthy controls. No significant correlation was found between BMI and IGF-I or E2 plasma levels or between LH and IGF-I plasma levels. The basal GH plasma levels were comparable in all groups of subjects. The GH-RH--induced GH response evaluated as maximal release and as area under the curve (AUC) was higher in amenorrheic patients than in control subjects.
CONCLUSIONS:
The amenorrheic condition associated with reduced BMI changes the GH-RH--induced GH response in hypothalamic amenorrhea, supporting a GH and a IGF-I disregulation in weight-loss--related amenorrhe
- …
