The 2007 IEEE CEC simulated car racing competition

This paper describes the simulated car racing competition that was arranged as part of the 2007 IEEE Congress on Evolutionary Computation. Both the game that was used as the domain for the competition, the controllers submitted as entries to the competition and its results are presented. With this paper, we hope to provide some insight into the efficacy of various computational intelligence methods on a well-defined game task, as well as an example of one way of running a competition. In the process, we provide a set of reference results for those who wish to use the simplerace game to benchmark their own algorithms. The paper is co-authored by the organizers and participants of the competition. © 2008 Springer Science+Business Media, LLC

Rare variants in CFI, C3 and C9 are associated with high risk of advanced age-related macular degeneration

To define the role of rare variants in advanced age-related macular degeneration (AMD) risk, we sequenced the exons of 681 genes within AMD-associated loci and pathways in 2,493 cases and controls. We first tested each gene for increased or decreased burden of rare variants in cases compared to controls. We found that 7.8% of AMD cases compared to 2.3% of controls are carriers of rare missense CFI variants (OR=3.6, p=2×10(−8)). There was a predominance of dysfunctional variants in cases compared to controls. We then tested individual variants for association to disease. We observed significant association with rare missense alleles outside CFI. Genotyping in 5,115 independent samples confirmed associations to AMD with a K155Q allele in C3 (replication p=3.5×10(−5), OR=2.8; joint p=5.2×10(−9), OR=3.8) and a P167S allele in C9 (replication p=2.4×10(−5), OR=2.2; joint p=6.5×10(−7), OR=2.2). Finally, we show that the 155Q allele in C3 results in resistance to proteolytic inactivation by CFH and CFI. These results implicate loss of C3 protein regulation and excessive alternative complement activation in AMD pathogenesis, thus informing both the direction of effect and mechanistic underpinnings of this disorder