Implementing Risk-Limiting Post-Election Audits in California

Risk-limiting post-election audits limit the chance of certifying an electoral outcome if the outcome is not what a full hand count would show. Building on previous work, we report on pilot risk-limiting audits in four elections during 2008 in three California counties: one during the February 2008 Primary Election in Marin County and three during the November 2008 General Elections in Marin, Santa Cruz and Yolo Counties. We explain what makes an audit risk-limiting and how existing and proposed laws fall short. We discuss the differences among our four pilot audits. We identify challenges to practical, efficient risk-limiting audits and conclude that current approaches are too complex to be used routinely on a large scale. One important logistical bottleneck is the difficulty of exporting data from commercial election management systems in a format amenable to audit calculations. Finally, we propose a bare-bones risk-limiting audit that is less efficient than these pilot audits, but avoids many practical problems

Multiple novel prostate cancer susceptibility signals identified by fine-mapping of known risk loci among Europeans

Genome-wide association studies (GWAS) have identified numerous common prostate cancer (PrCa) susceptibility loci. We have fine-mapped 64 GWAS regions known at the conclusion of the iCOGS study using large-scale genotyping and imputation in 25 723 PrCa cases and 26 274 controls of European ancestry. We detected evidence for multiple independent signals at 16 regions, 12 of which contained additional newly identified significant associations. A single signal comprising a spectrum of correlated variation was observed at 39 regions; 35 of which are now described by a novel more significantly associated lead SNP, while the originally reported variant remained as the lead SNP only in 4 regions. We also confirmed two association signals in Europeans that had been previously reported only in East-Asian GWAS. Based on statistical evidence and linkage disequilibrium (LD) structure, we have curated and narrowed down the list of the most likely candidate causal variants for each region. Functional annotation using data from ENCODE filtered for PrCa cell lines and eQTL analysis demonstrated significant enrichment for overlap with bio-features within this set. By incorporating the novel risk variants identified here alongside the refined data for existing association signals, we estimate that these loci now explain ∼38.9% of the familial relative risk of PrCa, an 8.9% improvement over the previously reported GWAS tag SNPs. This suggests that a significant fraction of the heritability of PrCa may have been hidden during the discovery phase of GWAS, in particular due to the presence of multiple independent signals within the same regio