Degradation in AlGaN/GaN heterojunction field effect transistors upon electrical stress: Effects of field and temperature

AlGaN/GaN heterojunction field effect transistors (HFETs) with 2 μm gate length were subjected to on-state-high-field (high drain bias and drain current) and reverse-gate-bias (no drain currentand reverse gate bias) stress at room and elevated temperatures for up to 10 h. The resulting degradation of the HFETs was studied by direct current and uniquely phase noise before and after stress. A series of drain and gate voltages was applied during the on-state-high-field and reverse-gate-bias stress conditions, respectively, to examine the effect of electric field on degradation of the HFET devices passivated with SiNx. The degradation behaviors under these two types of stress conditions were analyzed and compared. In order to isolate the effect of self-heating/temperature on device degradation, stress experiments were conducted at base plate temperatures up to 150 °C. It was found that the electric field induced by reverse-gate-bias mainly generated trap(s), most likely in the AlGaN barrier, which initially were manifested as generation-recombination (G-R) peak(s) in the phase noise spectra near 103 Hz. Meanwhileelectric field induced by on-state-high-field stress mainly generated hot-electron and hot-phonon effects, which result in a nearly frequency independent increase of noise spectra. The external base plate temperatures promote trap generation as evidenced by increased G-R peak intensities

Anisotropy of free-carrier absorption and diffusivity in m-plane GaN

Polarization-dependent free-carrier absorption (FCA) in bulk m-plane GaN at 1053 nm revealed approximately 6 times stronger hole-related absorption for E⊥c than for E||c probe polarization both at low and high carrier injection levels. In contrast, FCA at 527 nm was found isotropic at low injection levels due to electron resonant transitions between the upper and lower conduction bands, whereas the anisotropic impact of holes was present only at high injection levels by temporarily blocking electron transitions. Carrier transport was also found to be anisotropic under two-photon excitation, with a ratio of 1.17 for diffusivity perpendicular and parallel to the c-axis

The effect of stair case electron injector design on electron overflow in InGaN light emitting diodes

Effect of two-layer (In0.04Ga0.96N and In0.08Ga0.92N) staircase electron injector (SEI) on quantum efficiency of light-emitting-diodes (LEDs) in the context of active regions composed of single and quad 3 nm double heterostructures (DHs) is reported. The experiments were augmented with the first order model calculations of electron overflow percentile. Increasing the two-layer SEI thickness from 4 + 4 nm up to 20 + 20 nm substantially reduced, if not totally eliminated, the electron overflow in single DH LEDs at low injections without degrading the material quality evidenced by the high optical efficiency observed at 15K and room temperature. The improvement in quad 3 nm DH LEDs with increasing SEI thickness is not so pronounced as the influence of SEI is less for thicker active regions, which in and of themselves necessarily thermalize the carriers. (C) 2013 AIP Publishing LLC

Heisenberg Picture Approach to the Stability of Quantum Markov Systems

Quantum Markovian systems, modeled as unitary dilations in the quantum stochastic calculus of Hudson and Parthasarathy, have become standard in current quantum technological applications. This paper investigates the stability theory of such systems. Lyapunov-type conditions in the Heisenberg picture are derived in order to stabilize the evolution of system operators as well as the underlying dynamics of the quantum states. In particular, using the quantum Markov semigroup associated with this quantum stochastic differential equation, we derive sufficient conditions for the existence and stability of a unique and faithful invariant quantum state. Furthermore, this paper proves the quantum invariance principle, which extends the LaSalle invariance principle to quantum systems in the Heisenberg picture. These results are formulated in terms of algebraic constraints suitable for engineering quantum systems that are used in coherent feedback networks

To respond or not to respond - a personal perspective of intestinal tolerance

For many years, the intestine was one of the poor relations of the immunology world, being a realm inhabited mostly by specialists and those interested in unusual phenomena. However, this has changed dramatically in recent years with the realization of how important the microbiota is in shaping immune function throughout the body, and almost every major immunology institution now includes the intestine as an area of interest. One of the most important aspects of the intestinal immune system is how it discriminates carefully between harmless and harmful antigens, in particular, its ability to generate active tolerance to materials such as commensal bacteria and food proteins. This phenomenon has been recognized for more than 100 years, and it is essential for preventing inflammatory disease in the intestine, but its basis remains enigmatic. Here, I discuss the progress that has been made in understanding oral tolerance during my 40 years in the field and highlight the topics that will be the focus of future research

Innate Immune Activation in Intestinal Homeostasis

Loss of intestinal immune regulation leading to aberrant immune responses to the commensal microbiota are believed to precipitate the chronic inflammation observed in the gastrointestinal tract of patients with inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis. Innate immune receptors that recognize conserved components derived from the microbiota are widely expressed by both epithelial cells and leucocytes of the gastrointestinal tract and play a key role in host protection from infectious pathogens; yet precisely how pathogenic and commensal microbes are distinguished is not understood. Furthermore, aberrant innate immune activation may also drive intestinal pathology, as patients with IBD exhibit extensive infiltration of innate immune cells to the inflamed intestine, and polymorphisms in many innate immunity genes influence susceptibility to IBD. Thus, a balanced interaction between the microbiota and innate immune activation is required to maintain a healthy mutualistic relationship between the microbiota and the host, which when disturbed can result in intestinal inflammation

Homeostatic Regulation of Salmonella-Induced Mucosal Inflammation and Injury by IL-23

IL-12 and IL-23 regulate innate and adaptive immunity to microbial pathogens through influencing the expression of IFN-γ, IL-17, and IL-22. Herein we define the roles of IL-12 and IL-23 in regulating host resistance and intestinal inflammation during acute Salmonella infection. We find that IL-23 alone is dispensable for protection against systemic spread of bacteria, but synergizes with IL-12 for optimal protection. IL-12 promotes the production of IFN-γ by NK cells, which is required for resistance against Salmonella and also for induction of intestinal inflammation and epithelial injury. In contrast, IL-23 controls the severity of inflammation by inhibiting IL-12A expression, reducing IFN-γ and preventing excessive mucosal injury. Our studies demonstrate that IL-23 is a homeostatic regulator of IL-12-dependent, IFN-γ-mediated intestinal inflammation

Low-level regulatory T-cell activity is essential for functional type-2 effector immunity to expel gastrointestinal helminths

Helminth infection is frequently associated with the expansion of regulatory T cells (Tregs) and suppression of immune responses to bystander antigens. We show that infection of mice with the chronic gastrointestinal helminth Heligmosomoides polygyrus drives rapid polyclonal expansion of Foxp3(+)Helios(+)CD4(+) thymic (t)Tregs in the lamina propria and mesenteric lymph nodes while Foxp3(+)Helios(-)CD4(+) peripheral (p)Treg expand more slowly. Notably, in partially resistant BALB/c mice parasite survival positively correlates with Foxp3(+)Helios(+)CD4(+) tTreg numbers. Boosting of Foxp3(+)Helios(+)CD4(+) tTreg populations by administration of recombinant interleukin-2 (rIL-2):anti-IL-2 (IL-2C) complex increased worm persistence by diminishing type-2 responsiveness in vivo, including suppression of alternatively activated macrophage and granulomatous responses at the sites of infection. IL-2C also increased innate lymphoid cell (ILC) numbers, indicating that Treg functions dominate over ILC effects in this setting. Surprisingly, complete removal of Tregs in transgenic Foxp3-DTR mice also resulted in increased worm burdens, with "immunological chaos" evident in high levels of the pro-inflammatory cytokines IL-6 and interferon-γ. In contrast, worm clearance could be induced by anti-CD25 antibody-mediated partial depletion of early Treg, alongside increased T helper type 2 responses and without incurring pathology. These findings highlight the overarching importance of the early Treg response to infection and the non-linear association between inflammation and the prevailing Treg frequency

Barrier Tissue Macrophages: Functional Adaptation to Environmental Challenges

Macrophages are found throughout the body, where they have crucial roles in tissue development, homeostasis and remodeling, as well as being sentinels of the innate immune system that can contribute to protective immunity and inflammation. Barrier tissues, such as the intestine, lung, skin and liver, are exposed constantly to the outside world, which places special demands on resident cell populations such as macrophages. Here we review the mounting evidence that although macrophages in different barrier tissues may be derived from distinct progenitors, their highly specific properties are shaped by the local environment, which allows them to adapt precisely to the needs of their anatomical niche. We discuss the properties of macrophages in steady-state barrier tissues, outline the factors that shape their differentiation and behavior and describe how macrophages change during protective immunity and inflammation

Malaria in Africa: Vector Species' Niche Models and Relative Risk Maps

A central theoretical goal of epidemiology is the construction of spatial models of disease prevalence and risk, including maps for the potential spread of infectious disease. We provide three continent-wide maps representing the relative risk of malaria in Africa based on ecological niche models of vector species and risk analysis at a spatial resolution of 1 arc-minute (9 185 275 cells of approximately 4 sq km). Using a maximum entropy method we construct niche models for 10 malaria vector species based on species occurrence records since 1980, 19 climatic variables, altitude, and land cover data (in 14 classes). For seven vectors (Anopheles coustani, A. funestus, A. melas, A. merus, A. moucheti, A. nili, and A. paludis) these are the first published niche models. We predict that Central Africa has poor habitat for both A. arabiensis and A. gambiae, and that A. quadriannulatus and A. arabiensis have restricted habitats in Southern Africa as claimed by field experts in criticism of previous models. The results of the niche models are incorporated into three relative risk models which assume different ecological interactions between vector species. The “additive” model assumes no interaction; the “minimax” model assumes maximum relative risk due to any vector in a cell; and the “competitive exclusion” model assumes the relative risk that arises from the most suitable vector for a cell. All models include variable anthrophilicity of vectors and spatial variation in human population density. Relative risk maps are produced from these models. All models predict that human population density is the critical factor determining malaria risk. Our method of constructing relative risk maps is equally general. We discuss the limits of the relative risk maps reported here, and the additional data that are required for their improvement. The protocol developed here can be used for any other vector-borne disease