Impact of sidewall etching on the dynamic performance of GaN-on-Si E-mode transistors

Abstract The aim of this paper is to investigate the role of the etching of the sidewalls of p-GaN on the dynamic performance of normally-off GaN HEMTs with p-type gate. We analyze two wafers having identical epitaxy but with different recipes for the sidewall etching, referred to as "Etch A" (non-optimized) and "Etch B" (optimized). We demonstrate the following relevant results: (i) the devices with non-optimized etching (Etch A), when submitted to positive gate bias, show a negative threshold voltage shift and a decrease in Ron, which are ascribed to hole injection under the gate and/or in the access regions; (ii) transient characterization indicates the existence of two trap states, with activation energies of 0.84 eV (CN defects) and 0.30 eV. The latter (with time-constants in the ms range) is indicative of the hole de-trapping process, possibly related to trap states in the AlGaN barrier or at the passivation/AlGaN interface; (iii) by optimizing the p-GaN sidewall etching (for the same epitaxy) it is possible to completely eliminate the threshold voltage shift. This indicates that hole injection mostly takes place along the sidewalls

Buffer breakdown in GaN-on-Si HEMTs: A comprehensive study based on a sequential growth experiment

Abstract The aim of this work is to investigate the breakdown mechanisms of the layers constituting the vertical buffer of GaN-on-Si HEMTs; in addition, for the first time we demonstrate that the breakdown field of the AlN nucleation layer grown on a silicon substrate is equal to 3.2 MV/cm and evaluate its temperature dependence. To this aim, three samples, obtained by stopping the epitaxial growth of a GaN on Silicon stack at different steps, are studied and compared: Si/AlN, Si/AlN/AlGaN, full vertical stack up to the Carbon doped buffer layer. The current-voltage (IV) characterizations performed at both room temperature and high temperature show that: (i) the defectiveness of the AlN nucleation layer is the root cause of the leakage through an AlN/Silicon junction, and causes the vertical I-V characteristics to have a high device-to-device variability; (ii) the first AlGaN layer grown over the AlN, beside improving the breakdown voltage of the whole structure, causes the leakage current to be more stable and uniform across the sample area; (iii) a thick strain-relief stack and a carbon-doped GaN buffer enhance the breakdown voltage up to more than 750 V at 170 °C, and guarantee a remarkably low device-to-device variability. Furthermore, a set of constant voltage stress on the Si/AlN sample demonstrate that the aluminum nitride layer shows a time dependent breakdown, with Weibull-distributed failures and a shape factor greater than 1, in line with the percolation model

Mice Null for Calsequestrin 1 Exhibit Deficits in Functional Performance and Sarcoplasmic Reticulum Calcium Handling

In skeletal muscle, the release of calcium (Ca2+) by ryanodine sensitive sarcoplasmic reticulum (SR) Ca2+ release channels (i.e., ryanodine receptors; RyR1s) is the primary determinant of contractile filament activation. Much attention has been focused on calsequestrin (CASQ1) and its role in SR Ca2+ buffering as well as its potential for modulating RyR1, the L-type Ca2+ channel (dihydropyridine receptor, DHPR) and other sarcolemmal channels through sensing luminal [Ca2+]. The genetic ablation of CASQ1 expression results in significant alterations in SR Ca2+ content and SR Ca2+ release especially during prolonged activation. While these findings predict a significant loss-of-function phenotype in vivo, little information on functional status of CASQ1 null mice is available. We examined fast muscle in vivo and in vitro and identified significant deficits in functional performance that indicate an inability to sustain contractile activation. In single CASQ1 null skeletal myofibers we demonstrate a decrease in voltage dependent RyR Ca2+ release with single action potentials and a collapse of the Ca2+ release with repetitive trains. Under voltage clamp, SR Ca2+ release flux and total SR Ca2+ release are significantly reduced in CASQ1 null myofibers. The decrease in peak Ca2+ release flux appears to be solely due to elimination of the slowly decaying component of SR Ca2+ release, whereas the rapidly decaying component of SR Ca2+ release is not altered in either amplitude or time course in CASQ1 null fibers. Finally, intra-SR [Ca2+] during ligand and voltage activation of RyR1 revealed a significant decrease in the SR[Ca2+]free in intact CASQ1 null fibers and a increase in the release and uptake kinetics consistent with a depletion of intra-SR Ca2+ buffering capacity. Taken together we have revealed that the genetic ablation of CASQ1 expression results in significant functional deficits consistent with a decrease in the slowly decaying component of SR Ca2+ release

Comparison of classical, stealth and super-stealth liposomes for intravenous delivery of lumefantrine: Formulation, characterization and pharmacodynamic study

Purpose: To develop and compare classical liposomes (CL), stealth liposomes (SL) and super-stealth liposomes (SSL) encapsulating lumefantrine for intravenous administration. Method: CL, SL or SSL were prepared by thin-layer evaporation method and evaluated for particle size, polydispersity index (PdI), encapsulation efficiency and short-term stability. Pharmacodynamic study using mice infected with Plasmodium berghei was also carried out. Results: The particle sizes (nm) and PDI of the liposomes were: CL (248 \ub1 44.89; 0.78 \ub1 0.02), SL (235.8 \ub1 45.18; 0.39 \ub1 0.06) and SSL (238.2 \ub1 23.0; 0.24 \ub1 0.04). Encapsulation efficiency was highest in SSL (66 %), followed by SL (44.4 %) and then by CL (42.5 %). SSL was the most stable after 72 h of storage. In vivo, lumefantrine produced significant reduction in parasitaemia after 7 days (p < 0.05) by SSL (68.3 \ub1 8.9 %) followed by CL (55.8 \ub1 15.2 %) and then SL (53.4 \ub1 14.9 %). Conclusion: SSL formulation of lumefantrine exhibits good physicochemical and pharmacodynamic potentials and should be further investigated in future studies for the treatment of malaria