Is the microvascular response to transdermal iontophoresis of insulin mediated by nitric oxide?
The main finding is that iontophoresis of insulin induces a dose-dependent vasodilation in the skin, which could be suppressed after pretreatment with a NO synthase inhibitor. This suggests that vasodilation in the skin after iontophoresis of insulin is mediated by the NO pathway.
These results demonstrate that RB reconstitution into RB-deficient NSCLC lines establishes regulation of certain RB/E2F target genes and restores G1 arrest mechanisms. Furthermore, introduction of RB enhances the G1 checkpoint response to chemotherapeutics and decreases chemosensitivity. Knowledge of RB-dependent chemosensitivity may ultimately contribute to individualized therapy based on molecular characterization of tumors.