156 research outputs found

    Semisimple stable and superstable groups

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    Growth and Decay in Life-Like Cellular Automata

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    We propose a four-way classification of two-dimensional semi-totalistic cellular automata that is different than Wolfram's, based on two questions with yes-or-no answers: do there exist patterns that eventually escape any finite bounding box placed around them? And do there exist patterns that die out completely? If both of these conditions are true, then a cellular automaton rule is likely to support spaceships, small patterns that move and that form the building blocks of many of the more complex patterns that are known for Life. If one or both of these conditions is not true, then there may still be phenomena of interest supported by the given cellular automaton rule, but we will have to look harder for them. Although our classification is very crude, we argue that it is more objective than Wolfram's (due to the greater ease of determining a rigorous answer to these questions), more predictive (as we can classify large groups of rules without observing them individually), and more accurate in focusing attention on rules likely to support patterns with complex behavior. We support these assertions by surveying a number of known cellular automaton rules.Comment: 30 pages, 23 figure

    New insights into the genetic etiology of Alzheimer's disease and related dementias

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    Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele
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