ライフサイエンスコーパス: adrenocorticotropin

1 a result of adrenal hypersensitivity toward adrenocorticotropin.

2 xpression in hypothalamic neurons regulating adrenocorticotropin.

3 es to release prolactin, growth hormone, and adrenocorticotropin.

4 of H4, but not an H3 peptide nor the peptide adrenocorticotropin.

5 -butyryl cyclic adenosine monophosphate, and adrenocorticotropin.

6 the pituitary and it was poorly processed to adrenocorticotropin.

7 in, and peptide fragments of substance P and adrenocorticotropin.

8 In the human adrenal cortex, adrenocorticotropin (ACTH) activates CYP17 transcription

9 and female rats, with females secreting more adrenocorticotropin (ACTH) and corticosterone than males

10 mulate the secretions of prolactin (PRL) and adrenocorticotropin (ACTH) and to inhibit the secretion

11 produced a dose-dependent increase in plasma adrenocorticotropin (ACTH) concentration.

12 homeostasis are accompanied by increases in adrenocorticotropin (ACTH) concentrations in fetal perip

13 he human adrenal cortex, the peptide hormone adrenocorticotropin (ACTH) directs cortisol and adrenal

14 ted after a variety of stimuli that increase adrenocorticotropin (ACTH) in the systemic circulation.

15 ma-melanocyte stimulating hormones (MSH) and adrenocorticotropin (ACTH) ligands.

16 elanocortin (POMC), the common precursor for adrenocorticotropin (ACTH) of pars distalis corticotrope

17 ry or adrenal, or stimulated by infusions of adrenocorticotropin (ACTH) or glucocorticoids.

18 The adrenocorticotropin (ACTH) receptor (melanocortin 2 rece

19 selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization st

20 hich peripheral IL-1 beta acutely stimulates adrenocorticotropin (ACTH) secretion are not clear.

21 Somatostatin inhibits adrenocorticotropin (ACTH) secretion from pituitary tumo

22 hypothalamus attenuate, but do not abolish, adrenocorticotropin (ACTH) secretion in response to acut

23 Adrenocorticotropin (ACTH) signaling increases glucocort

24 of S203 phosphorylation and is unaffected by adrenocorticotropin (ACTH) treatment, loss of SUMOylatio

25 Brachiocephalic occlusion (BCO) stimulated adrenocorticotropin (ACTH), cortisol and arginine vasopr

26 hesis in the adrenal cortex is controlled by adrenocorticotropin (ACTH), which increases intracellula

27 Cushing disease caused by adrenocorticotropin (ACTH)-secreting pituitary adenomas

28 90% of all budesonide patients had a normal adrenocorticotropin (ACTH)-stimulated cortisol response

29 ith a crude mouse anti-ACTH IgG solution and adrenocorticotropin (ACTH).

30 ondrial movement, by which activation of the adrenocorticotropin (ACTH)/cAMP signaling pathway stimul

31 2)-melanocyte stimulating hormones (MSH) and adrenocorticotropin (ACTH)], the antagonist agouti-relat

32 ncy (FGD), or hereditary unresponsiveness to adrenocorticotropin (ACTH; OMIM 202200), is an autosomal

33 Adrenocorticotropin acting through cyclic adenosine mono

34 n (POMC)-derived peptides (the melanocortins adrenocorticotropin, alpha-, beta- and gamma-melanocyte

35 They also suggest that adrenocorticotropin and cAMP function in these cells thr

36 muscarinic antagonist Scopolamine augmented adrenocorticotropin and corticosterone responses to rest

37 the early phase of LPS-induced increases in adrenocorticotropin and corticosterone secretion.

38 and 2DG exhibited increased levels of plasma adrenocorticotropin and corticosterone, indicating that

39 activity, thereby elevating plasma levels of adrenocorticotropin and corticosterone.

40 HPA axis assessment included monitoring of adrenocorticotropin and cortisol over a full circadian c

41 l activity was monitored by measuring plasma adrenocorticotropin and cortisol, 24 hr urinary cortisol

42 iencies include growth hormone, thyrotropin, adrenocorticotropin and gonadotropin deficiencies, prima

43 outing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pit

44 , the anterior lobe corticotropes, producing adrenocorticotropin, and the intermediate lobe melanotro

45 nt increase in circulating concentrations of adrenocorticotropin, cortisol, and norepinephrine after

46 of the corticotropin-releasing hormone (CRH)-adrenocorticotropin-glucocorticoid axis, mediated by the

47 paraventricular nucleus (PVN), the pituitary adrenocorticotropin hormone (ACTH) and adrenal corticost

48 Adrenocorticotropin hormone (ACTH) and adrenal steroids

49 In addition, IL-1beta, adrenocorticotropin hormone (ACTH) and corticosterone co

50 adrenocortical (HPA) axis and the release of adrenocorticotropin hormone (ACTH) and corticosterone in

51 holino-sydnonimine (SIN-1) on the release of adrenocorticotropin hormone (ACTH) and the neuronal resp

52 plasma concentrations of corticosterone and adrenocorticotropin hormone (ACTH) are unchanged, and a

53 ng inflammation CRH is required for a normal adrenocorticotropin hormone (ACTH) increase but not for

54 s as determined by plasma corticosterone and adrenocorticotropin hormone (ACTH) levels.

55 oopiomelanocortin (POMC) mRNA expression and adrenocorticotropin hormone (ACTH) secretion.

56 proopiomelanocortin (POMC) transcription and adrenocorticotropin hormone (ACTH) secretion.

57 sequent cortisol biosynthesis in response to adrenocorticotropin hormone (ACTH) stimulation.

58 By stimulating the release of adrenocorticotropin hormone (ACTH), CRF acts as a key me

59 For acromegaly and adrenocorticotropin hormone (ACTH)-secreting, thyroid-st

60 a2-melanocyte stimulating hormones (MSH) and adrenocorticotropin hormone (ACTH).

61 emical immunosensor for the determination of adrenocorticotropin hormone (ACTH).

62 ing for growth hormone deficiency (GHD), and adrenocorticotropin hormone deficiency.

63 Plasma corticosterone and adrenocorticotropin hormone levels were higher after 30

64 treated with conventional therapies such as adrenocorticotropin hormone, corticosteroids, and/or int

65 gene expression and subsequent production of adrenocorticotropin hormone.

66 Finally, given the clinical efficacy of adrenocorticotropin in joint diseases, AP1189 was tested

67 ogression of ventral cell types and inducing adrenocorticotropin in rostral tip cells.

68 of alpha-melanocyte stimulating hormone and adrenocorticotropin in the epidermis and melanocytes has

69 a cascade of events which culminates in the adrenocorticotropin-induced release of corticosteroids f

70 only a modest elevation of their concurrent adrenocorticotropin levels (57 +/- 13 vs. 29 +/- 9 pmol/

71 t stress, whereas their plasma and pituitary adrenocorticotropin levels were either unchanged or lowe

72 one to cortisol does not occur, resulting in adrenocorticotropin-mediated androgen excess and a pheno

73 ycytes rarely contained detectable levels of adrenocorticotropin or alpha-melanocyte-stimulating horm

74 gainst alpha-melanocyte stimulating hormone, adrenocorticotropin, prohormone convertases 1 and 2 (PC1

75 pituitary gland where both peptides inhibit adrenocorticotropin release.

76 ccompanied by elimination of the exaggerated adrenocorticotropin responses to a saline injection (min

77 cts of adrenal corticosteroids on subsequent adrenocorticotropin secretion are complex.

78 PDE8s have their greatest control under low adrenocorticotropin-stimulated conditions, whereas other

79 elective inhibitor (PF-04957325) potentiates adrenocorticotropin stimulation of steroidogenesis by in

80 Diagnostic testing by adrenocorticotropin stimulation tests should be done in

81 eveloped a protocolized approach to low-dose adrenocorticotropin testing and empirical low-dose gluco

82 sor-dependent shock receiving protocol-based adrenocorticotropin testing and low-dose steroid supplem

83 Use of low-dose adrenocorticotropin testing may help further delineate p

84 By adrenocorticotropin testing, 44 (56%) had absolute adren

85 Effects of adrenocorticotropin therapy on the development of age-sp

86 importantly, renders the spasms sensitive to adrenocorticotropin therapy.

87 enzyme 2, which catalyzes the conversion of adrenocorticotropin to alpha-MSH, thereby decreasing alp

88 , and CSF cortisol were elevated, and plasma adrenocorticotropin was reduced in the active treatment

89 O-Nitrophenyl,sulfenyl-adrenocorticotropin, which produces a minimal increase i