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1 nticatabolic agents to reduce the effects of hypercortisolemia.
2 specially in the hippocampus, are related to hypercortisolemia.
5 ACTH-secreting pituitary adenomas lead to hypercortisolemia and cause significant morbidity and mo
6 ortisol-metabolizing enzymes, contributed to hypercortisolemia and hence corticotropin suppression.
7 PA axis activity, characterized by overnight hypercortisolemia and increased activity in ultradian se
8 te that chronic stress, associated with mild hypercortisolemia and prolonged SNS activation, favors a
9 stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation i
10 To address this, the authors have modeled hypercortisolemia by administering corticosterone in the
11 excess, due to primary aldosteronism (PA) or hypercortisolemia, causes hypertension and cardiovascula
12 a novel approach for treating patients with hypercortisolemia due to pituitary corticotroph adenomas
13 ught to better define the role of antecedent hypercortisolemia in generating HAAF, using two complime
14 ed in the overreaction to the stress and the hypercortisolemia in the development of depression--prob
16 icosterone levels; it also reversed signs of hypercortisolemia, including elevated glucose levels and
17 he disorders, a causal relationship in which hypercortisolemia induces diabetes or diabetic vascular
20 de strong evidence that hypoglycemia-induced hypercortisolemia is not primarily responsible for the g
22 ies have suggested that hypoglycemia-induced hypercortisolemia may be responsible for blunting subseq
24 motional neglect during childhood as well as hypercortisolemia may lead to heightened threat-related
25 Our results showed no effect of antecedent hypercortisolemia on epinephrine responses to subsequent
26 (ACTH)-secreting pituitary adenomas leads to hypercortisolemia predisposing to diabetes, hypertension
27 rs may counteract the deleterious effects of hypercortisolemia seen in bipolar disorder by upregulati
29 Critical illness is often accompanied by hypercortisolemia, which has been attributed to stress-i
30 ion was regulated through DNA methylation in hypercortisolemia with cortisol-producing adenoma (CPA),
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