39 research outputs found

    Silicon carbide semiconductor technology for high temperature and radiation environments

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    Viewgraphs on silicon carbide semiconductor technology and its potential for enabling electronic devices to function in high temperature and high radiation environments are presented. Topics covered include silicon carbide; sublimation growth of 6H-SiC boules; SiC chemical vapor deposition reaction system; 6H silicon carbide p-n junction diode; silicon carbide MOSFET; and silicon carbide JFET radiation response

    Silicon carbide, a semiconductor for space power electronics

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    After many years of promise as a high temperature semiconductor, silicon carbide (SiC) is finally emerging as a useful electronic material. Recent significant progress that has led to this emergence has been in the areas of crystal growth and device fabrication technology. High quality single-crystal SiC wafers, up to 25 mm in diameter, can now be produced routinely from boules grown by a high temperature (2700 K) sublimation process. Device fabrication processes, including chemical vapor deposition (CVD), in situ doping during CVD, reactive ion etching, oxidation, metallization, etc. have been used to fabricate p-n junction diodes and MOSFETs. The diode was operated to 870 K and the MOSFET to 770 K

    High-temperature electronics

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    To meet the needs of the aerospace propulsion and space power communities, the high temperature electronics program at the Lewis Research Center is developing silicon carbide (SiC) as a high temperature semiconductor material. This program supports a major element of the Center's mission - to perform basic and developmental research aimed at improving aerospace propulsion systems. Research is focused on developing the crystal growth, characterization, and device fabrication technologies necessary to produce a family of SiC devices

    Silicon carbide, an emerging high temperature semiconductor

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    In recent years, the aerospace propulsion and space power communities have expressed a growing need for electronic devices that are capable of sustained high temperature operation. Applications for high temperature electronic devices include development instrumentation within engines, engine control, and condition monitoring systems, and power conditioning and control systems for space platforms and satellites. Other earth-based applications include deep-well drilling instrumentation, nuclear reactor instrumentation and control, and automotive sensors. To meet the needs of these applications, the High Temperature Electronics Program at the Lewis Research Center is developing silicon carbide (SiC) as a high temperature semiconductor material. Research is focussed on developing the crystal growth, characterization, and device fabrication technologies necessary to produce a family of silicon carbide electronic devices and integrated sensors. The progress made in developing silicon carbide is presented, and the challenges that lie ahead are discussed

    Development of silicon carbide semiconductor devices for high temperature applications

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    The semiconducting properties of electronic grade silicon carbide crystals, such as wide energy bandgap, make it particularly attractive for high temperature applications. Applications for high temperature electronic devices include instrumentation for engines under development, engine control and condition monitoring systems, and power conditioning and control systems for space platforms and satellites. Discrete prototype SiC devices were fabricated and tested at elevated temperatures. Grown p-n junction diodes demonstrated very good rectification characteristics at 870 K. A depletion-mode metal-oxide-semiconductor field-effect transistor was also successfully fabricated and tested at 770 K. While optimization of SiC fabrication processes remain, it is believed that SiC is an enabling high temperature electronic technology

    Advances in silicon carbide Chemical Vapor Deposition (CVD) for semiconductor device fabrication

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    Improved SiC chemical vapor deposition films of both 3C and 6H polytypes were grown on vicinal (0001) 6H-SiC wafers cut from single-crystal boules. These films were produced from silane and propane in hydrogen at one atmosphere at a temperature of 1725 K. Among the more important factors which affected the structure and morphology of the grown films were the tilt angle of the substrate, the polarity of the growth surface, and the pregrowth surface treatment of the substrate. With proper pregrowth surface treatment, 6H films were grown on 6H substrates with tilt angles as small as 0.1 degrees. In addition, 3C could be induced to grow within selected regions on a 6H substrate. The polarity of the substrate was a large factor in the incorporation of dopants during epitaxial growth. A new growth model is discussed which explains the control of SiC polytype in epitaxial growth on vicinal (0001) SiC substrates

    The Actin-Binding Protein Capulet Genetically Interacts with the Microtubule Motor Kinesin to Maintain Neuronal Dendrite Homeostasis

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    BACKGROUND: Neurons require precise cytoskeletal regulation within neurites, containing microtubule tracks for cargo transport in axons and dendrites or within synapses containing organized actin. Due to the unique architecture and specialized function of neurons, neurons are particularly susceptible to perturbation of the cytoskeleton. Numerous actin-binding proteins help maintain proper cytoskeletal regulation. METHODOLOGY/PRINCIPAL FINDINGS: From a Drosophila forward genetic screen, we identified a mutation in capulet--encoding a conserved actin-binding protein--that causes abnormal aggregates of actin within dendrites. Through interaction studies, we demonstrate that simultaneous genetic inactivation of capulet and kinesin heavy chain, a microtubule motor protein, produces elongate cofilin-actin rods within dendrites but not axons. These rods resemble actin-rich structures induced in both mammalian neurodegenerative and Drosophila Alzheimer's models, but have not previously been identified by loss of function mutations in vivo. We further demonstrate that mitochondria, which are transported by Kinesin, have impaired distribution along dendrites in a capulet mutant. While Capulet and Cofilin may biochemically cooperate in certain circumstances, in neuronal dendrites they genetically antagonize each other. CONCLUSIONS/SIGNIFICANCE: The present study is the first molecularly defined loss of function demonstration of actin-cofilin rods in vivo. This study suggests that simultaneous, seemingly minor perturbations in neuronal dendrites can synergize producing severe abnormalities affecting actin, microtubules and mitochondria/energy availability in dendrites. Additionally, as >90% of Alzheimer's and Parkinson's cases are sporadic this study suggests mechanisms by which multiple mutations together may contribute to neurodegeneration instead of reliance on single mutations to produce disease

    Anti-α-Internexin Autoantibody from Neuropsychiatric Lupus Induce Cognitive Damage via Inhibiting Axonal Elongation and Promote Neuron Apoptosis

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    Neuropsychiatric systemic lupus erythematosus (NPSLE) is a major complication for lupus patients, which often leads to cognitive disturbances and memory loss and contributes to a significant patient morbidity and mortality. The presence of anti-neuronal autoantibodies (aAbs) has been identified; as examples, anti-NMDA receptors and anti-Ribsomal P aAbs have been linked to certain pathophysiological features of NPSLE.In the current study, we used a proteomic approach to identify an intermediate neurofilament alpha-internexin (INA) as a pathogenetically relevant autoantigen in NPSLE. The significance of this finding was then validated in an expanded of a cohort of NPSLE patients (n = 67) and controls (n = 270) by demonstrating that high titers of anti-INA aAb was found in both the serum and cerebrospinal fluid (CSF) of ∼50% NPSLE. Subsequently, a murine model was developed by INA immunization that resulted in pronounced cognitive dysfunction that mimicked features of NPSLE. Histopathology in affected animals displayed cortical and hippocampal neuron apoptosis. In vitro studies further demonstrated that anti-INA Ab mediated neuronal damage via inhibiting axonal elongation and eventually driving the cells to apoptosis.Taken together, this study identified a novel anti-neurofilament aAb in NPSLE, and established a hitherto undescribed mechanism of aAb-mediated neuron damage that could have relevance to the pathophysiology of NPSLE
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