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adrenocortical adenoma/arginīns

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ractText>Adrenocorticotropic hormone (ACTH)-independent Cushing's syndrome (CS) is mostly due to unilateral tumors, with bilateral tumors rarely reported. Its common causes include primary pigmented nodular adrenocortical disease, ACTH-independent macronodular adrenal hyperplasia, and bilateral
An absent or severely blunted hGH response to an i.v. bolus injection (100 micrograms) of human pancreatic growth hormone releasing hormone (hpGRF 1-44) was found in seven female patients with Cushing's syndrome (five with pituitary dependent Cushing's disease and two due to an adrenal adenoma) and
We have studied the diurnal rhythm of pars distalis and pars intermedia-type immunoreactive (IR)-POMC peptides and cortisol in 3 normal dogs and 1 dog with Cushing's syndrome and have documented the responses to a variety of agents in 42 dogs with Cushing's disease, 2 of which were known or presumed

A MEN1 syndrome with a paraganglioma.

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Germline mutations of the MEN1 gene cause multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant disorder characterized by tumors of the parathyroids, the pancreas, and the anterior pituitary. Paraganglioma (PGL) is a rare endocrine tumor, which can be sporadic or genetically determined.
Secretin, glucagon, gastric inhibitory polypeptide (GIP), and parathyroid hormone (PTH) belong, together with vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase (AC)-activating polypeptide, to a family of peptides (the VIP-secretin-glucagon family), which also includes growth

Effects of serotonin and vasopressin on cortisol production from an adrenocortical tumor causing subclinical Cushing's syndrome.

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In dexamethasone-suppressed healthy volunteers, the serotonin4 (5-HT4) receptor agonist cisapride and lysine vasopressin [LVP, an analog of arginine vasopressin (AVP)] have no influence on plasma cortisol levels (PCL). In contrast, cisapride and AVP have been shown to stimulate cortisol secretion in
OBJECTIVE Abnormal responsiveness to arginine vasopressin (AVP) was previously observed in cortisol-producing adrenocortical tumours but the mechanism remains unclear. The aim of this study was to characterize the effect of AVP on cortisol secretion from adrenocortical tumours compared to normal

Mutations of the p53 gene in human functional adrenal neoplasms.

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To clarify gene alterations in functional human adrenal tumors, we performed molecular analysis for p53 abnormalities in 23 cases with adrenal neoplasms. The immunohistochemical study with anti-p53 monoclonal antibody pAb1801 demonstrated that 10 of 23 (43.5%) cases overexpressed p53 protein in the
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