BackgroundThe recent Ebola virus disease (EVD) outbreak in West Africa has spread wider than any previous human EVD epidemic. While individual-level risk factors that contribute to the spread of EVD have been studied, the population-level attributes of subnational regions associated with outbreak severity have not yet been considered.MethodsTo investigate the area-level predictors of EVD dynamics, we integrated time series data on cumulative reported cases of EVD from the World Health Organization and covariate data from the Demographic and Health Surveys. We first estimated the early growth rates of epidemics in each second-level administrative district (ADM2) in Guinea, Sierra Leone and Liberia using exponential, logistic and polynomial growth models. We then evaluated how these growth rates, as well as epidemic size within ADM2s, were ecologically associated with several demographic and socio-economic characteristics of the ADM2, using bivariate correlations and multivariable regression models.ResultsThe polynomial growth model appeared to best fit the ADM2 epidemic curves, displaying the lowest residual standard error. Each outcome was associated with various regional characteristics in bivariate models, however in stepwise multivariable models only mean education levels were consistently associated with a worse local epidemic.DiscussionBy combining two common methods—estimation of epidemic parameters using mathematical models, and estimation of associations using ecological regression models—we identified some factors predicting rapid and severe EVD epidemics in West African subnational regions. While care should be taken interpreting such results as anything more than correlational, we suggest that our approach of using data sources that were publicly available in advance of the epidemic or in real-time provides an analytic framework that may assist countries in understanding the dynamics of future outbreaks as they occur.

Transitional-care-related factors are found to be associated with post-pancreatectomy readmission for dehydration and FTT. Using these results to identify high-risk patients and implement focused preventive measures combining efficient communication and optimal inpatient and outpatient management could potentially decrease readmission rates.

BackgroundAlthough genome-wide association studies (GWASs) have identified thousands of disease susceptibility regions, the underlying causal mechanism in these regions is not fully known. It is likely that the GWAS signal originates from one or many as yet unidentified causal variants.MethodsUsing next-generation sequencing, we characterized 12 breast cancer susceptibility regions identified by GWASs in 2288 breast cancer cases and 2323 controls across four populations of African American, European, Japanese, and Hispanic ancestry.ResultsAfter genotype calling and quality control, we identified 137,530 single-nucleotide variants (SNVs); of those, 87.2 % had a minor allele frequency (MAF) <0.005. For SNVs with MAF >0.005, we calculated the smallest number of SNVs needed to obtain a posterior probability set (PPS) such that there is 90 % probability that the causal SNV is included. We found that the PPS for two regions, 2q35 and 11q13, contained less than 5 % of the original SNVs, dramatically decreasing the number of potentially causal SNVs. However, we did not find strong evidence supporting a causal role for any individual SNV. In addition, there were no significant gene-based rare SNV associations after correcting for multiple testing.ConclusionsThis study illustrates some of the challenges faced in fine-mapping studies in the post-GWAS era, most importantly the large sample sizes needed to identify rare-variant associations or to distinguish the effects of strongly correlated common SNVs.Electronic supplementary materialThe online version of this article (doi:10.1186/s13058-016-0772-7) contains supplementary material, which is available to authorized users.