Is dehydroepiandrosterone ( DHEA ) inhibition of monocyte binding by vascular endothelium associated with sialylation of neural cell adhesion molecule?
In these preliminary in vitro studies, DHEA increased PSA-NCAM expression and inhibited monocyte binding in an estrogen- and androgen receptor-dependent manner. Dehydroepiandrosteroneappears to act via its end metabolites, E2 and DHT. Dehydroepiandrosterone could furnish clinical prevention against atherogenesis and arteriosclerosis.
The use of dobutamine in addition to conventional therapy in patients with DCM provided improvements in some systolic parameters and quality of life particularly after the first treatment. In the late period of the treatment, however, it was determined that these beneficial effects tended to disappear and harmful effects became more evident.