468 research outputs found

    Shared memory for a fault-tolerant computer

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    A system is described for sharing a memory in a fault-tolerant computer. The memory is under the direct control and monitoring of error detecting and error diagnostic units in the fault-tolerant computer. This computer verifies that data to and from the memory is legally encoded and verifies that words read from the memory at a desired address are, in fact, actually delivered from that desired address. The means are provided for a second processor, which is independent of the direct control and monitoring of the error checking and diagnostic units of the fault-tolerant computer, and to share the memory of the fault-tolerant computer. Circuitry is included to verify that: (1) the processor has properly accessed a desired memory location in the memory; (2) a data word read-out from the memory is properly coded; and (3) no inactive memory was erroneously outputting data onto the shared memory bus

    Size Distribution of Sediment as Affected by Surface Residue and Slope Length

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    Runoff samples for determination of size distribution of sediment were collected under simulated rainfall conditions at selected downslope distances on plots covered with sorghum and soybean residue at rates ranging from 0.00 to 6.73 t/ha . The effects of surface residue and slope length on size distribution of sediment were evaluated. Substantial movement of sediment in the form of aggregates was found for each of the residue treatments. Significant differences in size distribution of sediment occurred between residue treatments. For a given residue rate, differences in sediment size distribution were found between sorghum and soybean residue. Size distribution of sediment was also determined to be significantly different at selected downslope distances

    Runoff and Erosion as Affected by Sorghum and Soybean Residue

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    A rainfall simulator was used to measure the effects of varying rates of sorghum and soybean residue on runoff and erosion. In general, increased surface cover caused reduced runoff, sediment concentration and soil loss. Substantial reductions in erosion resulted from the use of small amounts of crop residue. Regression equations were obtained which related surface cover to residue mass. Equations describing relative runoff, sediment concentration and soil loss as a function of surface cover were also developed. Runoff, sediment concentration and soil loss were all found to be highly correlated to surface cover

    Size Distribution of Sediment as Affected by Corn Residue

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    Size distribution of sediment was measured under simulated rainfall conditions at selected downslope distances on plots with corn residue rates ranging from 0.00 to 6.73 t/ha. The formation of rills caused increases in the percentage of larger sized sediment material. Greater surface cover usually resulted in an increase in the percentage of smaller sized sediment. Considerable variation in the size of sediment from both rill and interrill areas was found with downslope distance. On interrill regions, the presence of residue served to reduce sediment size along the entire plot length. Transport of aggregated sediment occurred on each of the residue treatments

    A Simplified Equation for Modeling Sediment Transport Capacity

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    Sediment transport capacity for shallow overland flow was represented as a quadratic function of downslope distance using the assumption of a linear increase in overland flow discharge with downslope distance and an approximation to the Yalin equation for sediment transport capacity. The simplified equation for sediment transport applies to complex topography having uniform soil and management characteristics. The simplified equation accurately approximated the Yalin equation when calibrated using the average of the hydraulic shear stresses at the end of a constant slope reference profile and the end of the actual profile. The simplified equation is useful in deriving closed-form solutions to the governing erosion equations for steady state conditions and reduces the computational time when numerical solutions are required

    A Simplified Equation for Modeling Sediment Transport Capacity

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    Sediment transport capacity for shallow overland flow was represented as a quadratic function of downslope distance using the assumption of a linear increase in overland flow discharge with downslope distance and an approximation to the Yalin equation for sediment transport capacity. The simplified equation for sediment transport applies to complex topography having uniform soil and management characteristics. The simplified equation accurately approximated the Yalin equation when calibrated using the average of the hydraulic shear stresses at the end of a constant slope reference profile and the end of the actual profile. The simplified equation is useful in deriving closed-form solutions to the governing erosion equations for steady state conditions and reduces the computational time when numerical solutions are required

    Neurotoxin-mediated potent activation of the axon degeneration regulator SARM1

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    Axon loss underlies symptom onset and progression in many neurodegenerative disorders. Axon degeneration in injury and disease is promoted by activation of the nicotinamide adenine dinucleotide (NAD)-consuming enzyme SARM1. Here, we report a novel activator of SARM1, a metabolite of the pesticide and neurotoxin vacor. Removal of SARM1 completely rescues mouse neurons from vacor-induced neuron and axon death in vitro and in vivo. We present the crystal structure the Drosophila SARM1 regulatory domain complexed with this activator, the vacor metabolite VMN, which as the most potent activator yet know is likely to support drug development for human SARM1 and NMNAT2 disorders. This study indicates the mechanism of neurotoxicity and pesticide action by vacor, raises important questions about other pyridines in wider use today, provides important new tools for drug discovery, and demonstrates that removing SARM1 can robustly block programmed axon death induced by toxicity as well as genetic mutation

    Reciprocity as a foundation of financial economics

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    This paper argues that the subsistence of the fundamental theorem of contemporary financial mathematics is the ethical concept ‘reciprocity’. The argument is based on identifying an equivalence between the contemporary, and ostensibly ‘value neutral’, Fundamental Theory of Asset Pricing with theories of mathematical probability that emerged in the seventeenth century in the context of the ethical assessment of commercial contracts in a framework of Aristotelian ethics. This observation, the main claim of the paper, is justified on the basis of results from the Ultimatum Game and is analysed within a framework of Pragmatic philosophy. The analysis leads to the explanatory hypothesis that markets are centres of communicative action with reciprocity as a rule of discourse. The purpose of the paper is to reorientate financial economics to emphasise the objectives of cooperation and social cohesion and to this end, we offer specific policy advice

    Two step activation of FOXO3 by AMPK generates a coherent feed-forward loop determining excitotoxic cell fate

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    Cerebral ischemia and excitotoxic injury induce transient or permanent bioenergetic failure, and may result in neuronal apoptosis or necrosis. We have previously shown that ATP depletion and activation of AMP-activated protein kinase (AMPK) during excitotoxic injury induces neuronal apoptosis by transcription of the proapoptotic BH3 only protein, Bim. AMPK, however, also exerts pro-survival functions in neurons. The molecular switches that determine these differential outcomes are not well understood. Using an approach combining biochemistry, single cell imaging and computational modeling, we here demonstrate that excitotoxic injury activated the bim promoter in a FOXO3-dependent manner. The activation of AMPK reduced AKT activation, and led to dephosphorylation and nuclear translocation of FOXO3. Subsequent mutation studies indicated that bim gene activation during excitotoxic injury required direct FOXO3 phosphorylation by AMPK in the nucleus as a second activation step. Inhibition of this phosphorylation prevented Bim expression and protected neurons against excitotoxic and oxygen/glucose deprivation-induced injury. Systems analysis and computational modeling revealed that these two activation steps defined a coherent feedforward loop; a network motif capable of filtering any effects of short-term AMPK activation on bim gene induction. This may prevent unwanted AMPK-mediated Bim expression and apoptosis during transient or physiological bioenergetic stress
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