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Glucocorticoid deficiency can be caused by inherited genetic disorders that affect the production of cortisol in the adrenal glands, such as familial glucocorticoid deficiency (FGD). [3] FGD is a group of monogenic recessive disorders caused by disease-causing variants in genes involved in cortisol biosynthesis. [ 4 ]
Glucocorticoid deficiency 1 is an adrenocortical failure characterized by low levels of plasma cortisol produced by the adrenal gland despite high levels of plasma ACTH. This is an inherited disorder with several different causes which define the type.
The glucocorticoids provide a reliable substitute for cortisol, thereby reducing ACTH levels. Reducing ACTH also reduces the stimulus for continued hyperplasia and overproduction of androgens. In other words, glucocorticoid replacement is the primary method of reducing the excessive adrenal androgen production in both sexes.
The mutations in the MRAP gene caused the congenital disorder familial glucocorticoid deficiency type 2 (FGD-2). FGD-2 is an autosomal recessive disease with early childhood onset of recurrent infections, hypoglycaemia, skin hyperpigmentation, and failure to thrive due to low glucocorticoids levels. If left untreated, it could be fatal.
The dose ratio r is the ratio of the dose of agonist required for half maximal response with the antagonist present divided by the agonist required for half maximal response without antagonist ("control"). In other words, the ratio of the EC50s of the inhibited and un-inhibited curves. Thus, r represents both the strength of an antagonist and ...
Such a curve is referred to as a quantal dose–response curve, distinguishing it from a graded dose–response curve, where response is continuous (either measured, or by judgment). The Hill equation can be used to describe dose–response relationships, for example ion channel-open-probability vs. ligand concentration. [9]
Pharmacogenomics, often abbreviated "PGx," is the study of the role of the genome in drug response. Its name (pharmaco-+ genomics) reflects its combining of pharmacology and genomics. Pharmacogenomics analyzes how the genetic makeup of a patient affects their response to drugs. [1]
The glucocorticoid receptor (GR or GCR) also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1) is the receptor to which cortisol and other glucocorticoids bind. The GR is expressed in almost every cell in the body and regulates genes controlling the development , metabolism , and immune response .