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Basal plane slip is the most frequently observed deformation mechanism in 4H-type silicon carbon (4H-SiC) single crystals grown by the physical vapor transport (PVT) method. However, it was recently reported that dislocations in such crystals can also glide in prismatic slip systems. In this study, we observed nonuniform distributions of three sets of prismatic dislocations in a commercial 4H-SiC substrate wafer. The nonuniformity is a result of the distribution of resolved shear stress on each prismatic slip system caused by radial thermal gradients in the growing crystal boule. A radial thermal model has been developed to estimate the thermal stress across the entire area of the crystal boule during PVT growth. The model results show excellent agreement with the observations, confirming that radial thermal gradients play a key role in activating prismatic slip in 4H-SiC during bulk growth.

The commercial availability of high quality 150 mm 4H SiC wafers has aided in the growth of SiC power device fabrication. The progress of 150 mm 4H SiC wafer development at Dow Corning is reviewed. Defect densities compare well to those typical for 100 mm wafers, with even lower threading screw dislocation densities observed in 150 mm wafers. Resistivity data shows a comparable range from 0.012 – 0.025 ohm.cm, and excellent shape control is highlighted for wafer thicknesses of 350 μm and 500 μm.

Efforts to develop 150 mm 4H SiC bare wafer and epitaxial substrates for power electronic device applications have resulted in quality improvements, such that key metrics match or outperform 100 mm substrates. Total dislocation densities and threading screw dislocation densities measured for 150 mm wafers were ~4100 cm-2 and ~100 cm-2, respectively, compared with values of ~5900 cm-2 and ~300 cm-2 measured for 100 mm wafers. While median basal plane dislocation counts in 150 mm samples exceed those of the smaller platform, a nearly 45% reduction was realized, resulting in a median density of ~3900 cm-2. Epilayers grown on 150 mm substrates likewise exhibit quality metrics that are comparable to 100 mm samples, with median thickness and doping sigma/mean values of 1.1% and 4.4%, respectively.

Synchrotron white beam X-ray topography studies carried out on 4H-SiC wafers characterized by locally varying doping concentrations reveals the presence of overlapping Shockley stacking faults generated from residual surface scratches in regions of higher doping concentrations after the wafers have been subjected to heat treatment. The fault generation process is driven by the fact that in regions of higher doping concentrations, a faulted crystal containing double Shockley faults is more stable than perfect 4H–SiC crystal at the high temperatures (>1000 °C) that the wafers are subject to during heat treatment. We have developed a model for the formation mechanism of the rhombus shaped stacking faults, and experimentally verified it by characterizing the configuration of the bounding partials of the stacking faults on both surfaces. Using high resolution transmission electron microscopy, we have verified that the enclosed stacking fault is a double Shockley type.

The flatness of a silicon carbide wafer in terms of bow and warp is the result of the combination of factors both material and process related. Sub-surface damage (SSD) from the wafering process steps can be considered as a thin film under compressive stress on the wafer surface. SSD is generally decreased with each subsequent processing step after the multiwire saw. Single-sided process steps can produce very different levels of SSD on opposing wafer surfaces, leading to high bow and warp values. The present study investigates the effects of SSD on wafer flatness at various process steps as well as methods to minimize shape effects due to SSD during and after processing.

Understanding the growth and propagation of defects in SiC remains of interest in an effort to continue to improve device performance. A post-growth boule heat-treatment revealed to form micropipe pairs from apparent single screw dislocations is reviewed. In the treated samples almost no 1c threading screw dislocations were found. Instead, micropipe pairs were observed in similar densities to 1c threading screw dislocations in non-heat treated samples. It is hypothesized that the elevated temperatures allowed for enhanced dislocation mobility, enabling the transition.

This dissertation represents a systematic study of microstructure-mechanical property relationships of titanium-aluminum-niobium-molybdenum (Ti-Al-Nb-Mo) alloys and metal matrix composites (MMCs). The aspects investigated were the microstructures, elevated-temperature creep behavior, room-temperature and elevated-temperature tensile behavior, and the out-of-phase thermomechanical fatigue behavior. The specific alloy compositions investigated were: Ti-24Al-17Nb-0.66Mo (at.%) and Ti-24Al-17Nb-2.3Mo (at.%). The MMCs were reinforced with Ultra SCS-6 fibers and the specific compositions of the matrices were: Ti-24Al-17Nb-0.66Mo (at.%), Ti-24Al-17Nb-1.1Mo (at.%), and Ti-24Al-17Nb-2.3Mo (at.%). All of the materials were fabricated using a powder-metallurgy, tape casting technique. A subtransus heat-treatment produced microstructures containing a hexagonal close-packed a2 phase, orthorhombic (O) phase, and a body-centered cubic (BCC) phase. The higher Mo contents were shown to stabilize the BCC phase and result in an increase the O+BCC phase volume percent and a subsequent decrease in the a2 phase volume percent. The creep deformation behavior of the alloys and MMCs was the main focus of this dissertation. Creep experimentation was performed to understand the deformation mechanisms as a function of stress, temperature, and strain rate. Higher Mo contents significantly increased the creep resistance of the alloys, which was attributed to the decrease in the number of a2/a2 grain boundaries, increased O+BCC colony size, and Mo solid solution strengthening. This was one of the major findings of the work. In-situ tensile-creep experiments indicated that grain boundaries were the locus of deformation and cracking in each of the alloys investigated. MMC creep experimentation was performed with the fibers aligned perpendicular to the loading direction. Similar to alloy creep results, higher Mo contents increased the creep resistance of the MMCs. However, the creep resistance of the MMCs was significantly less than that of their respective alloy compositions. An effort was made to model the creep behavior of the MMCs based on the creep behavior of the alloys and fiber/matrix bond strength. The model predicted the secondary creep rates of the MMCs well for a condition assuming no bond strength between the fiber and matrix. The model predicts that the MMC will exhibit a secondary creep rate lower than that for the alloy when the applied creep stress is less than the fiber/matrix bond strength. However, no such transition was observed in the experimental data. Experimental testing and finite element modeling revealed that the interfacial bond strength between the matrix and the fiber was indeed very small, suggesting that the MMC creep resistance would not be greater than the matrix alloy under practical loading applications. Overall, the work performed in this dissertation helped fill the knowledge gap which exists for the physical and mechanical metallurgy effects of varying Mo additions in titanium aluminides.

A mouse study reveals that acetylcholine signalling networks have a role in the regulation of body weight homeostasis, with increased activity of cholinergic neurons decreasing food consumption through downstream hypothalamic targets. Cholinergic signalling influences feeding behaviour In studies of the neuronal control of feeding behaviour, most work has focused on the canonical circuits in the hypothalamus; here, Benjamin Arenkiel and colleagues examine the acetylcholine signalling network for a role in the regulation of body weight homeostasis. They find that increased activity of cholinergic neurons in the basal forebrain decreases food consumption, whereas impairment of this signalling leads to enhanced food intake. This influence on feeding behaviour occurs through downstream hypothalamic targets, linking cholinergic signalling to the hypothalamic control of food intake. Atypical food intake is a primary cause of obesity and other eating and metabolic disorders. Insight into the neural control of feeding has previously focused mainly on signalling mechanisms associated with the hypothalamus 1 , 2 , 3 , 4 , 5 , the major centre in the brain that regulates body weight homeostasis 6 , 7 . However, roles of non-canonical central nervous system signalling mechanisms in regulating feeding behaviour have been largely uncharacterized. Acetylcholine has long been proposed to influence feeding 8 , 9 , 10 owing in part to the functional similarity between acetylcholine and nicotine, a known appetite suppressant. Nicotine is an exogenous agonist for acetylcholine receptors, suggesting that endogenous cholinergic signalling may play a part in normal physiological regulation of feeding. However, it remains unclear how cholinergic neurons in the brain regulate food intake. Here we report that cholinergic neurons of the mouse basal forebrain potently influence food intake and body weight. Impairment of cholinergic signalling increases food intake and results in severe obesity, whereas enhanced cholinergic signalling decreases food consumption. We found that cholinergic circuits modulate appetite suppression on downstream targets in the hypothalamus. Together our data reveal the cholinergic basal forebrain as a major modulatory centre underlying feeding behaviour.

Here we present a standard developed by the Genomic Standards Consortium (GSC) for reporting marker gene sequences—the minimum information about a marker gene sequence (MIMARKS). We also introduce a system for describing the environment from which a biological sample originates. The 'environmental packages' apply to any genome sequence of known origin and can be used in combination with MIMARKS and other GSC checklists. Finally, to establish a unified standard for describing sequence data and to provide a single point of entry for the scientific community to access and learn about GSC checklists, we present the minimum information about any (x) sequence (MIxS). Adoption of MIxS will enhance our ability to analyze natural genetic diversity documented by massive DNA sequencing efforts from myriad ecosystems in our ever-changing biosphere.

The DNA-binding factor SATB1 is known as a chromatin organizer. Schultze and colleagues show regulation of SATB1 expression by the transcription factor Foxp3 is necessary to confer suppression of effector cell activity. Regulatory T cells (T reg cells) are essential for self-tolerance and immune homeostasis. Lack of effector T cell (T eff cell) function and gain of suppressive activity by T reg cells are dependent on the transcriptional program induced by Foxp3. Here we report that repression of SATB1, a genome organizer that regulates chromatin structure and gene expression, was crucial for the phenotype and function of T reg cells. Foxp3, acting as a transcriptional repressor, directly suppressed the SATB1 locus and indirectly suppressed it through the induction of microRNAs that bound the SATB1 3′ untranslated region. Release of SATB1 from the control of Foxp3 in T reg cells caused loss of suppressive function, establishment of transcriptional T eff cell programs and induction of T eff cell cytokines. Our data support the proposal that inhibition of SATB1-mediated modulation of global chromatin remodeling is pivotal for maintaining T reg cell functionality.