Biology subjects

Bennett, A. J.

Publications and source records attributed to Bennett, A. J..

4 recordsLinked to original sources

bioRxiv2018

Where do animals covered by the US Animal Welfare Act live? Analysis of USDA licensed and registered entities

Nonhuman animals are housed in captivity for a range of purposes in the US and other countries. The regulation, oversight, and public transparency of decisions related to the care and use of those animals varies by species and activity. The goals of this paper are 1) to provide a concise and accessible summary of the number and types of facilities either registered or licensed by the USDA and overseen by the federal agency; and 2) to provide concise comparisons of the relative proportion of different types of use of nonhuman animals that fall under the AWA (Animal Welfare Act). Analysis of the publicly-available list of USDA certificate holders produced descriptive data for each state and the US overall. Licensed exhibitors (N=2,640; 33% of total) and breeders (N=2,701; 34% of total) comprise two-thirds of the 8,002 USDA certificate holders. Registered research facilities (N=1,110) account for 14% of the total USDA certificates. The final 19% consists of licensed dealers (N=763; 9%) and registered carriers or interim handlers (N=788; 10%). The number and distribution of types of certificates varies across states. The largest number of exhibitors and dealers are in Florida, while the largest number of breeders are in Missouri. California has the largest number of research registered facilities. Finally, a comparison of the estimated number of animals in the US that are pets, used in agriculture, exhibition, and research suggests that animals in research are between 0.07-2.3% of the total. The comparison also highlights areas in which public information about captive animals in the US is uneven or missing altogether. Together, the current report provides a concise view of basic information and data relevant to public consideration and policy decisions about animals housed in the set of captive settings to which the AWA applies.

zoology↗

bioRxiv2018

A Model Quantitative Assessment Tool for Nonhuman Primate Environmental Enrichment Plans

The housing and care of captive nonhuman primates (NHP) typically meets federal regulations and standards as well as guidelines by private accreditation organizations. There is, however, a gap between such policy, common practices, and the findings of a large empirical research literature on the effects of environmental enrichment (EE), particularly with respect to the degree to which different enrichment strategies lead to a demonstrable improvement of the animals psychological wellbeing. Assessment tools to guide decisions about selection and refinement of EE practices are largely missing and our companion paper offers a theoretically grounded qualitative approach to the categorization and assessment of sensory, motor, and cognitive (SMC) EE strategies. Here, we propose and illustrate a model for quantitative assessment of enrichment practices using a sample of research facility, zoo, and sanctuary NHP environmental enrichment plans (EEP). Our scoring technique provides a means for comparing the efficacy of different strategies across facilities and allows for the selection of priority areas for improvement. Overall, our assessment tool provides a framework that has several advantages. It is inherently flexible. It can be tailored to fit a range of species. It can readily be adapted to accommodate new evidence about a specific EE strategy, or new EE strategies, or both. Because a scientifically valid evidence-based framework drives priority, our method is readily adaptable to different types of facilities and is more likely to lead to longer-term benefits, both in terms of the enhancement of psychological wellbeing of captive NHP, and with respect to the judicious use of limited resources.\n\nAcronyms

animal behavior and cognition↗

bioRxiv2018

Fine-mapping of an expanded set of type 2 diabetes loci to single-variant resolution using high-density imputation and islet-specific epigenome maps

We aggregated genome-wide genotyping data from 32 European-descent GWAS (74,124 T2D cases, 824,006 controls) imputed to high-density reference panels of >30,000 sequenced haplotypes. Analysis of {small tilde}27M variants ({small tilde}21M with minor allele frequency [MAF]<5%), identified 243 genome-wide significant loci (p<5x10-8; MAF 0.02%-50%; odds ratio [OR] 1.04-8.05), 135 not previously-implicated in T2D-predisposition. Conditional analyses revealed 160 additional distinct association signals (p<10-5) within the identified loci. The combined set of 403 T2D-risk signals includes 56 low-frequency (0.5%[≤]MAF<5%) and 24 rare (MAF<0.5%) index SNPs at 60 loci, including 14 with estimated allelic OR>2. Forty-one of the signals displayed effect-size heterogeneity between BMI-unadjusted and adjusted analyses. Increased sample size and improved imputation led to substantially more precise localisation of causal variants than previously attained: at 51 signals, the lead variant after fine-mapping accounted for >80% posterior probability of association (PPA) and at 18 of these, PPA exceeded 99%. Integration with islet regulatory annotations enriched for T2D association further reduced median credible set size (from 42 variants to 32) and extended the number of index variants with PPA>80% to 73. Although most signals mapped to regulatory sequence, we identified 18 genes as human validated therapeutic targets through coding variants that are causal for disease. Genome wide chip heritability accounted for 18% of T2D-risk, and individuals in the 2.5% extremes of a polygenic risk score generated from the GWAS data differed >9-fold in risk. Our observations highlight how increases in sample size and variant diversity deliver enhanced discovery and single-variant resolution of causal T2D-risk alleles, and the consequent impact on mechanistic insights and clinical translation.

genomics↗

bioRxiv2017

Integration of human pancreatic islet genomic data refines regulatory mechanisms at Type 2 Diabetes susceptibility loci

Human genetic studies have emphasised the dominant contribution of pancreatic islet dysfunction to development of Type 2 Diabetes (T2D). However, limited annotation of the islet epigenome has constrained efforts to define the molecular mechanisms mediating the, largely regulatory, signals revealed by Genome-Wide Association Studies (GWAS). We characterised patterns of chromatin accessibility (ATAC-seq, n=17) and DNA methylation (whole-genome bisulphite sequencing, n=10) in human islets, generating high-resolution chromatin state maps through integration with established ChIP-seq marks. We found enrichment of GWAS signals for T2D and fasting glucose was concentrated in subsets of islet enhancers characterised by open chromatin and hypomethylation, with the former annotation predominant. At several loci (including CDC123, ADCY5, KLHDC5) the combination of fine-mapping genetic data and chromatin state enrichment maps, supplemented by allelic imbalance in chromatin accessibility pinpointed likely causal variants. The combination of increasingly-precise genetic and islet epigenomic information accelerates definition of causal mechanisms implicated in T2D pathogenesis.

genomics↗