Downscale: An R package for downscaling species occupancy from coarse-grain data to predict occupancy at fine-grain sizes

The geographical area occupied by a species is a valuable measure for assessing its conservation status. Coarse-grained occupancy maps are available for many taxa, e.g., as atlases, but often at spatial resolutions too coarse for conservation use. However, mapping occupancy at fine spatial resolution across the entire extent of the species’ distribution is often prohibitively expensive for the majority of species. Occupancy downscaling is a technique to estimate finer scale occupancy from coarse scale maps, by using the occupancy-area relationship (OAR) which reflects how the proportion of area occupied increases with spatial grain size. Models that describe the OAR are fitted to observed occupancies at the available coarse-grain sizes and then extrapolated to predict occupancy at the finer grain sizes required. The downscale package in the R programming environment provides users with easy-to-use functions for downscaling occupancy with ten published models. First, upgrain calculates occupancy for multiple grain sizes larger than the input data. Normal methods for aggregating raster data increase the extent of the focal area as grain size increases which is undesirable, so the function fixes the extent for all grain sizes, assigning unsampled cells as absences. Four suggested methods are provided to enable this and upgrain.threshold provides diagnostic plots that allow the user to explore the inherent trade-off between making assumptions about unsampled locations and discarding information from sampled locations. downscale fits nine possible models to the data generated from upgrain. hui.downscale fits the special case of the Hui model. predict and plot extrapolate the fitted models to predict and plot occupancy at finer grain sizes. Finally, ensemble.downscale simultaneously fits two or more of the downscaling models and calculates mean predicted occupancy across all selected models. Here we describe the package and apply the functions to atlas data of a hypothetical UK species

Matrix composition mediates effects of habitat fragmentation: a modelling study

Context Habitat loss has clear negative effects on biodiversity, but whether fragmentation per se (FPS), excluding habitat loss does is debatable. A contribution to this debate may be that many fragmentation studies tend to use landscapes of fragmented focal-habitat and a single vastly different species-poor intervening land cover (the matrix). Objectives How does matrix composition influence the effect of FPS on biodiversity?. Methods Using an individual-based model to investigate the effect of different configurations of the matrix on the relationship between FPS and biodiversity of the focal-habitat. We manipulated the number and quality of land cover types in the matrix, and their similarity to the focal-habitat. Results Extremely different matrix, caused an order of magnitude stronger effect of FPS on alpha- and gamma-diversity and beta-diversity to decline. Low FPS led to high gamma-diversity. Increasing FPS caused a dramatic decline to low diversity. In contrast landscapes with a more similar matrix had lower diversity under low FPS declining little with increasing FPS. Having few matrix types caused beta-diversity to decline in general compared to landscapes with a larger numbers. Conclusions The effects of FPS on biodiversity may change depending on the number of matrix types and their similarity to the focal-habitat. We recommend that fragmentation studies should consider a greater variety of landscapes to help assess in which cases FPS does not have a negative impact and allow better predictions of the impacts of fragmentation. We show the importance of having a diversity of matrix land cover types and improving the hospitability of the matrix for species dependent on the focal-habitat

Genetic determinants of risk in pulmonary arterial hypertension: international genome-wide association studies and meta-analysis

Background Rare genetic variants cause pulmonary arterial hypertension, but the contribution of common genetic variation to disease risk and natural history is poorly characterised. We tested for genome-wide association for pulmonary arterial hypertension in large international cohorts and assessed the contribution of associated regions to outcomes. Methods We did two separate genome-wide association studies (GWAS) and a meta-analysis of pulmonary arterial hypertension. These GWAS used data from four international case-control studies across 11744 individuals with European ancestry (including 2085 patients). One GWAS used genotypes from 5895 whole-genome sequences and the other GWAS used genotyping array data from an additional 5849 individuals. Cross-validation of loci reaching genome-wide significance was sought by meta-analysis. Conditional analysis corrected for the most significant variants at each locus was used to resolve signals for multiple associations. We functionally annotated associated variants and tested associations with duration of survival. All-cause mortality was the primary endpoint in survival analyses. Findings A locus near SOX17 (rs10103692, odds ratio 1·80 [95% CI 1·55–2·08], p=5·13×10– ¹⁵) and a second locus in HLA-DPA1 and HLA-DPB1 (collectively referred to as HLA-DPA1/DPB1 here; rs2856830, 1·56 [1·42–1·71], p=7·65×10– ²⁰) within the class II MHC region were associated with pulmonary arterial hypertension. The SOX17 locus had two independent signals associated with pulmonary arterial hypertension (rs13266183, 1·36 [1·25–1·48], p=1·69×10– ¹²; and rs10103692). Functional and epigenomic data indicate that the risk variants near SOX17 alter gene regulation via an enhancer active in endothelial cells. Pulmonary arterial hypertension risk variants determined haplotype-specific enhancer activity, and CRISPR-mediated inhibition of the enhancer reduced SOX17 expression. The HLA-DPA1/DPB1 rs2856830 genotype was strongly associated with survival. Median survival from diagnosis in patients with pulmonary arterial hypertension with the C/C homozygous genotype was double (13·50 years [95% CI 12·07 to >13·50]) that of those with the T/T genotype (6·97 years [6·02–8·05]), despite similar baseline disease severity. Interpretation This is the first study to report that common genetic variation at loci in an enhancer near SOX17 and in HLA-DPA1/DPB1 is associated with pulmonary arterial hypertension. Impairment of SOX17 function might be more common in pulmonary arterial hypertension than suggested by rare mutations in SOX17. Further studies are needed to confirm the association between HLA typing or rs2856830 genotyping and survival, and to determine whether HLA typing or rs2856830 genotyping improves risk stratification in clinical practice or trials. Funding UK NIHR, BHF, UK MRC, Dinosaur Trust, NIH/NHLBI, ERS, EMBO, Wellcome Trust, EU, AHA, ACClinPharm, Netherlands CVRI, Dutch Heart Foundation, Dutch Federation of UMC, Netherlands OHRD and RNAS, German DFG, German BMBF, APH Paris, INSERM, Université Paris-Sud, and French ANR

Measuring β-diversity with species abundance data

1. In 2003, 24 presence–absence β-diversity metrics were reviewed and a number of trade-offs and redundancies identified. We present a parallel investigation into the performance of abundance-based metrics of β-diversity. 2. β-diversity is a multi-faceted concept, central to spatial ecology. There are multiple metrics available to quantify it: the choice of metric is an important decision. 3. We test 16 conceptual properties and two sampling properties of a β-diversity metric: metrics should be 1) independent of α-diversity and 2) cumulative along a gradient of species turnover. Similarity should be 3) probabilistic when assemblages are independently and identically distributed. Metrics should have 4) a minimum of zero and increase monotonically with the degree of 5) species turnover, 6) decoupling of species ranks and 7) evenness differences. However, complete species turnover should always generate greater values of β than extreme 8) rank shifts or 9) evenness differences. Metrics should 10) have a fixed upper limit, 11) symmetry (βA,B = βB,A), 12) double-zero asymmetry for double absences and double presences and 13) not decrease in a series of nested assemblages. Additionally, metrics should be independent of 14) species replication 15) the units of abundance and 16) differences in total abundance between sampling units. When samples are used to infer β-diversity, metrics should be 1) independent of sample sizes and 2) independent of unequal sample sizes. We test 29 metrics for these properties and five ‘personality’ properties. 4. Thirteen metrics were outperformed or equalled across all conceptual and sampling properties. Differences in sensitivity to species’ abundance lead to a performance trade-off between sample size bias and the ability to detect turnover among rare species. In general, abundance-based metrics are substantially less biased in the face of undersampling, although the presence–absence metric, βsim, performed well overall. Only βBaselga R turn, βBaselga B-C turn and βsim measured purely species turnover and were independent of nestedness. Among the other metrics, sensitivity to nestedness varied >4-fold. 5. Our results indicate large amounts of redundancy among existing β-diversity metrics, whilst the estimation of unseen shared and unshared species is lacking and should be addressed in the design of new abundance-based metrics

Exercise intensity and postprandial health outcomes in adolescents

The final publication is available at Springer via http://dx.doi.org/10.1007/s00421-014-3074-8© 2014, Springer-Verlag Berlin Heidelberg. Method: Twenty adolescents (10 male, 14.3 ± 0.3 years) completed three 1-day trials: (1) rest (CON); (2) 8 × 1 min cycling at 90 % peak power with 75 s recovery (HIIE); (3) cycling at 90 % of the gas exchange threshold (MIE), 1 h before consuming a high-fat milkshake (1.50 g fat and 80 kJ kg⁻¹). Postprandial TAG, SBP and fat oxidation were assessed over 4 h Results : Compared to CON, the incremental area under the curve for TAG (IAUC-TAG) was not significantly lowered in HIIE [P = 0.22, effect size (ES) = 0.24] or MIE (P = 0.65, ES = 0.04) for boys. For girls, HIIE and MIE lowered IAUC-TAG by 34 % (P = 0.02, ES = 0.58) and 38 % (P = 0.09, ES = 0.73), respectively, with no difference between HIIE and MIE (P = 0.74, ES = 0.14). Changes in TAG were not related to energy expenditure during exercise or postprandial fat oxidation. Postprandial SBP (total-AUC pooled for both sexes) was lower in HIIE compared to CON (P = 0.01, ES = 0.68) and MIE (P = 0.02, ES = 0.60), with no difference between MIE and CON (P = 0.45, ES = 0.14). Purpose: The effect of exercise intensity and sex on postprandial risk factors for cardiovascular disease in adolescents is unknown. We examined the effect of a single bout of work-matched high-intensity interval exercise (HIIE) and moderate-intensity exercise (MIE) on postprandial triacylglycerol (TAG) and systolic blood pressure (SBP) in adolescents. Conclusion: A single bout of HIIE and MIE, performed 1 h before an HFM, can meaningfully attenuate IAUC-TAG in girls but not boys. Additionally, HIIE, but not MIE, may lower postprandial SBP in normotensive adolescents