An anomalous kink effect has been observed in the
room-temperature drain current ID versus drain voltage VDS
characteristics of GaN high electron mobility transistors. The kink
is originated by a buildup (at low VDS) and subsequent release
(at high VDS) of negative charge, resulting in a shift of pinch-off
voltage VP toward more negative voltages and in a sudden increase
in ID. The kink is characterized by extremely long negative
charge buildup times and by a nonmonotonic behavior as
a function of photon energy under illumination. The presence
of traps in the GaN buffer may explain both spectrally resolved
photostimulation data and the slow negative charge buildup
We investigate the role of the 0.5 eV traps in determining GaN HEMT degradation by means of DC and rf testing, and 2D numerical simulation. We demonstrate that generation of deep levels, having an activation energy of 0.5 eV, is responsible for the degradation observed during rf aging; we show that the occurrence of trap-induced degradation depends on rf driving conditions. We also show that degradation can be explained by the generation of a damaged region within the AlGaN layer at the gate-drain edge, and that the DC and pulsed device degradation effects have a different dependence on the width and depth of the damaged region
This longitudinal study assessed the influence of post-transplant clinical and therapeutic variables in 50 kidney transplant recipients aged 2-19 yr receiving a triple immunosuppressive regimen consisting of cyclosporine microemulsion (CsA), steroids and MMF (300-400 mg/m(2) body surface area twice daily), the full pharmacokinetic profile (10 points) of which was investigated on post-transplant days 6, 30, 180 and 360. Total plasma MPA was measured by Enzyme Multiplied Immunoassay Technique. CsA therapeutic drug monitoring (TDM) was performed via C2 blood monitoring, while MPA TDM via C0. MPA Cmax, tmax, AUC0-12 and AUC0-4 pharmacokinetic profile changed significantly during the first post-transplant year. C0 was a poor predictor of the total MPA exposure [as measured by the area under the concentration-time curve AUC)], while a truncated AUC was a good surrogate of the 12-h profile (r = 0.91; p < 0.001) Graft function and cyclosporine therapy influenced MPA pharmacokinetics, as shown by the univariate and multivariate analyses. We conclude that because after transplantation MPA exposure varied over time, a strict TDM is advisable in the pediatric population.
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