AlGaN/GaN high electron mobility transistors are gaining commercial acceptance for use in high power and high frequency applications, but the degradation mechanisms that drive failure in the field are not completely understood. Since some of these mechanisms are current or field driven, reliability studies must go beyond the typical Arrhenius-accelerated life tests. In this paper, we summarize recent work on electric field or current driven degradation in devices with different gate metallization, device dimensions, electric field mitigation techniques (such as source field plates) and the effect of device fabrication processes for both dc and RF stress conditions.

A serious impediment to gene and protein replacement therapy in hemophilia A is the development of inhibitors. Mechanisms responsible for inhibitor development include T-cell-dependent adaptive immune responses and the CD28-B7 signaling pathway that eventually leads to the formation of antibodies directed against factor VIII (FVIII). Indoleamine 2,3-dioxygenase (IDO) is a potent immunosuppressive enzyme that can inhibit T-cell responses and induce T-cell apoptosis by regulation of tryptophan metabolism. Kynurenine, one of the metabolites of tryptophan, has been implicated as an immune modulator. Here we hypothesize that co-delivery of the genes for FVIII and IDO can attenuate inhibitor formation. Using transposon-based gene delivery, we observed long-term therapeutic FVIII expression and significantly reduced inhibitor titers when the genes were codelivered. Co-expression of FVIII and IDO in the liver was associated with increased plasma kynurenine levels, an inhibition of T-cell infiltration and increased apoptosis of T cells within the liver. These experiments suggest that modulation of tryptophan catabolism through IDO expression provides a novel strategy to reduce inhibitor development in hemophilia gene/protein therapy.