Power Efficient High Temperature Asynchronous Microcontroller Design

There is an increasing demand for dependable and efficient digital circuitry capable of operating in high temperature environments. Extreme temperatures have adverse effects on traditional silicon synchronous systems because of the changes in delay and setup and hold times caused by the variances in each device’s threshold voltage. This dissertation focuses on the design of the major functionality of an asynchronous 8051 microcontroller in Raytheon’s high temperature Silicon Carbide process, rated for operation over 300ºC. The microcontroller is designed in NULL Convention Logic, for which the traditional bus architecture used for data transfer would consume a large amount of power. To make the design more power efficient, the bus architecture has been replaced with a more complex yet efficient MUX-based data transfer scheme. This change in the design architecture also allows for improved internal data transfer rates leading to an increase in overall circuit performance. Simulation results show that the designed Silicon Carbide microcontroller framework successful executes 8051 ISA instructions. Results from the MUX-based architecture show an overall decrease in power consumption of over two orders of magnitude when compared with its bus architecture counterpart. Also, the increased internal data transfer rates resulted in an overall performance improvement of 22.8%

Selection and Culture of Landscape Plants in Utah - A Guide for High Mountain Valleys

What traveler, driving across Utah, has not marveled at its diversity of geography, climate and vegetation? From Joshua-trees in the Mojave Desert, to alpine meadows, to pinion-juniper forests set against the red sandstone of the Colorado Plateau, it is truly a state of contrasts

Highly Sensitive HBsAg, Anti-HBc and Anti HBsAg Titres in Early Diagnosis of HBV Reactivation in Anti-HBc-Positive Onco-Haematological Patients

The role of novel HBV markers in predicting Hepatitis B virus reactivation (HBV-R) in HBsAg-negative/anti-HBc-positive oncohaematological patients was examined. One hundred and seven HBsAg-negative/anti-HBc-positive oncohaematological patients, receiving anti-HBV prophylaxis for >18 months, were included. At baseline, all patients had undetectable HBV DNA, and 67.3% were anti-HBs positive. HBV-R occurred in 17 (15.9%) patients: 6 during and 11 after the prophylaxis period. At HBV-R, the median (IQR) HBV-DNA was 44 (27-40509) IU/mL, and the alanine aminotransferase upper limit of normal (ULN) was 44% (median (IQR): 81 (49-541) U/L). An anti-HBc > 3 cut-off index (COI) plus anti-HBs persistently/declining to <50 mIU/mL was predictive for HBV-R (OR (95% CI): 9.1 (2.7-30.2); 63% of patients with vs. 15% without this combination experienced HBV-R (p < 0.001)). The detection of highly sensitive (HS) HBsAg and/or HBV-DNA confirmed at >2 time points, also predicts HBV-R (OR (95% CI): 13.8 (3.6-52.6); 50% of positive vs. 7% of negative patients to these markers experienced HBV-R (p = 0.001)). HS-HBs and anti-HBc titration proved to be useful early markers of HBV-R. The use of these markers demonstrated that HBV-R frequently occurs in oncohaematological patients with signs of resolved HBV infection, raising issues of proper HBV-R monitoring

Human Dectin-1 Deficiency Impairs Macrophage-Mediated Defense Against Phaeohyphomycosis

Subcutaneous phaeohyphomycosis typically affects immunocompetent individuals following traumatic inoculation. Severe or disseminated infection can occur in CARD9 deficiency or after transplantation, but the mechanisms protecting against phaeohyphomycosis remain unclear. We evaluated a patient with progressive, refractory Corynespora cassiicola phaeohyphomycosis and found that he carried biallelic deleterious mutations in CLEC7A encoding the CARD9-coupled, β-glucan-binding receptor, Dectin-1. The patient\u27s PBMCs failed to produce TNF-α and IL-1β in response to β-glucan and/or C. cassiicola. To confirm the cellular and molecular requirements for immunity against C. cassiicola, we developed a mouse model of this infection. Mouse macrophages required Dectin-1 and CARD9 for IL-1β and TNF-α production, which enhanced fungal killing in an interdependent manner. Deficiency of either Dectin-1 or CARD9 was associated with more severe fungal disease, recapitulating the human observation. Because these data implicated impaired Dectin-1 responses in susceptibility to phaeohyphomycosis, we evaluated 17 additional unrelated patients with severe forms of the infection. We found that 12 out of 17 carried deleterious CLEC7A mutations associated with an altered Dectin-1 extracellular C-terminal domain and impaired Dectin-1-dependent cytokine production. Thus, we show that Dectin-1 and CARD9 promote protective TNF-α- and IL-1β-mediated macrophage defense against C. cassiicola. More broadly, we demonstrate that human Dectin-1 deficiency may contribute to susceptibility to severe phaeohyphomycosis by certain dematiaceous fungi