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(December 7, 2010)

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Further investigations revealed that the disorder is associated with mutations in the gene for the GH receptor that result in defective hormone binding or a reduced efficiency of dimerization of the receptor after hormone occupancy, as well as exceptionally low levels of insulin-like growth factor 1 (IGF-1) [2]

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Mechanistically, the consistent threads are collagen up-regulation, angiogenesis support, and modulation of nitric-oxide pathways all of which are biologically plausible drivers of the observed soft-tissue effects