It was found that after RU486 was given at 20:00, the 8Am levels of plasma ACTH and plasma cortisol were increased significantly (P<0.01,P<0.001) on the next two consecutive days and 24h urine cortisol was increased remarkably(P<0.01)on the next day.
Contents of serum cortisol (F), adrenocorticotropin (ACTH), plasma testosterone (T), estradiol (E_2), Luteinizing hormone (LH),foelicle-stimulating hormone (FSH) and prolaction (PRL) in 60 cases of chronic pulmonale heart disease (CPHD) and in 23 healthy men were determined using the method of radioimmunoassay.
Hemorheological indexes, brain noradrenaline (NE), adrenocorticotropine(ACTH), β endorphin, cortisol, estradiol, testoderone, interleukin-Ⅱ (IL-2), tumour necrosis factor (TNF) in the blood, and rat spleen's lymphocyte transformation and induction of IL-2 and the activity of natural killer cells (NKC).
During late gestation in sheep, fetal plasma adrenocorticotrophin (ACTH) and cortisol levels increase, and these are associated with increased pro-opiomelanocortin (POMC) mRNA levels in the anterior pituitary.
Surgery was performed to remove the suprasellar part of the tumour, and histology revealed an adrenocorticotrophin (ACTH) secreting pituitary adenoma.
Plasma adrenocorticotrophin (ACTH) and cortisol (F) concentrations were studied in six male subjects under normoxic (N) and acute hypoxic (H) conditions (altitude 3000 m) in a hypobaric chamber.
We investigated the mechanisms of stress-induced alterations in adrenocorticotrophin (ACTH) release.
There were no consistent significant differences between the concentrations of luteinizing hormone (LH) and adrenocorticotrophin (ACTH) in the rostral compared with the caudal zone of the echidna pars distalis.
Auditory brain-stem responses (ABRs) were compared in two groups of multiple sclerosis (MS) patients receiving standard treatment with adrenocorticotropin (ACTH) and with dexamethasone (DEX).
Adrenocorticotropin (ACTH) has indirect effects via the action of glucocorticoid on bones, muscles, and the immune system.
Corticotropin releasing factor (CRH) is released from the hypothalamus and travels to the anterior pituitary where it stimulates the release of adrenocorticotropin (ACTH).
In pituitary cells in culture, both basal and releasing factor-stimulated adrenocorticotropin (ACTH) secretion is inhibited by AM.
Instead, the proopiomelanocortin (POMC) producing, adrenocorticotropin (ACTH)- and β-endorphin-immunoreactive PI cells are incorporated within the pars anterior, thereby participating in the formation of the pars distalis.
The cells were then exposed to serum-free RPMl-1640 medium containing vehicle (RPMl medium alone), serotonin, and/or endotoxin, interleukin-1β, or adrenocorticotrophic hormone (ACTH).
We have previously shown that lipopolysaccharide (LPS) administration induces hypothalamic and pituitary LIF expression in vivo, which is associated with the acute rise in circulating adrenocorticotrophic hormone (ACTH) levels.
ICH on serial sections with EGF or EGFr and adrenocorticotrophic hormone (ACTH) or S-100 protein revealed that EGF and EGFr are localized specifically in corticotrophs and EGFr in stellate cells of nontumorous adenohypophysis.
A 64-year-old woman with long-standing Addison's disease owing to destructive immune adrenalitis presented with hyperpigmentation and progressively increasing blood adrenocorticotrophic hormone (ACTH) levels.
Interventions: A short adrenocorticotrophic hormone (ACTH) stimulation test was performed.
Tritium-labeled synthetic fragments of human adrenocorticotropic hormone (ACTH) [3H]ACTH (11-24) and [3H]ACTH (15-18) with a specific activity of 22 and 26 Ci/mmol, respectively, were obtained.
Plasma profiles of prolactin, growth hormone, adrenocorticotropic hormone (ACTH) and cortisol were evaluated in a group of untreated patients with idiopathic Parkinson's disease and a group of healthy age-matched controls.
Any type of corticosteroids or adrenocorticotropic hormone (ACTH) treatment was considered, as was any dosage, route of administration, and length of treatment.
Cervical sympathetic nerves may affect blood adrenocorticotropic hormone (ACTH), cortisol (CS), melatonin or serotonin levels.
Mineralocorticoid synthesis in these pathologic states can be constitutive or driven by pituitary adrenocorticotropic hormone (ACTH), due to genetic defects that cause disordered steroid synthesis or catabolism.