Tree cavity use by Chimney Swifts: implications for forestry and population recovery

Chimney Swifts used at least 13 different deciduous and coniferous tree species. All of the trees were greater than 0.5 m diameter at breast height (DBH) and were described as hollow or having cavities. Nest or roost tree height was 12.7 ± 7.0 m (mean ± SD; range: 3.6-28.0 m; n = 25) and DBH was 1.0 m ± 0.5 m (range 0.5-2.1 m; n = 21). According to our description of used trees, the number of suitably hollow Chimney Swift nest or roost trees may be two to three times higher, although still rare, in most unlogged compared to logged hardwood forests. Whether the current total supply of suitable nest or roost trees is sufficient to carry the anticipated increase in use by Chimney Swifts as chimney habitat is modified or deteriorates is unknown. Monitoring the frequency of use of tree cavities by nesting and roosting Chimney Swifts over time, and more robustly quantifying the availability of suitable tree cavities in different forest types for nesting and roosting Chimney Swifts, particularly in unlogged versus logged forests, are fruitful areas for future research. . D'après la description des arbres occupés, le nombre d'arbres creux convenables pour la nidification ou le repos du Martinet ramoneur pourrait être de 2 à 3 fois plus élevé -quoique ces arbres sont quand même rares -dans la plupart des forêts de feuillus non-récoltées, comparativement aux forêts récoltées. Nous ne savons pas si la quantité actuelle d'arbres propices est suffisante pour satisfaire l'utilisation accrue anticipée par les Martinets ramoneurs vu la détérioration ou la destruction des cheminées. Le suivi temporel de la fréquence d'utilisation des cavités d'arbres par les martinets pour y nicher ou y dormir et une meilleure quantification de la disponibilité de cavités d'arbres propices dans différents types de forêts, en particulier les forêts intactes versus récoltées, sont des avenues de recherche prometteuses. Utilisation de cavités d'arbres par le Martinet ramoneur : incidence sur les plans de l'exploitation forestière et du rétablissement des population

Height, selected genetic markers and prostate cancer risk:Results from the PRACTICAL consortium

Background: Evidence on height and prostate cancer risk is mixed, however, recent studies with large data sets support a possible role for its association with the risk of aggressive prostate cancer. Methods: We analysed data from the PRACTICAL consortium consisting of 6207 prostate cancer cases and 6016 controls and a subset of high grade cases (2480 cases). We explored height, polymorphisms in genes related to growth processes as main effects and their possible interactions. Results: The results suggest that height is associated with high-grade prostate cancer risk. Men with height 4180cm are at a 22% increased risk as compared to men with height o173cm (OR 1.22, 95% CI 1.01–1.48). Genetic variants in the growth pathway gene showed an association with prostate cancer risk. The aggregate scores of the selected variants identified a significantly increased risk of overall prostate cancer and high-grade prostate cancer by 13% and 15%, respectively, in the highest score group as compared to lowest score group. Conclusions: There was no evidence of gene-environment interaction between height and the selected candidate SNPs. Our findings suggest a role of height in high-grade prostate cancer. The effect of genetic variants in the genes related to growth is seen in all cases and high-grade prostate cancer. There is no interaction between these two exposures.</p

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe

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

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation

Although genome-wide association studies have identified over 100 risk loci that explain ∼33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa

Tree cavity use by Chimney Swifts: implications for forestry and population recovery

The Chimney Swift (Chaetura pelagica) is an aerial insectivore and a cavity-nesting/roosting specialist designated as threatened in several jurisdictions. As the occurrence of suitable chimneys declines, Chimney Swifts may increasingly nest and roost in tree cavities. It is therefore important to identify characteristics of suitable nest or roost trees and assess their frequency of occurrence. We reviewed 59 historic and modern records of trees used by Chimney Swifts to understand characteristics of suitable nest or roost trees. Chimney Swifts used at least 13 different deciduous and coniferous tree species. All of the trees were greater than 0.5 m diameter at breast height (DBH) and were described as hollow or having cavities. Nest or roost tree height was 12.7 ± 7.0 m (mean ± SD; range: 3.6-28.0 m; n = 25) and DBH was 1.0 m ± 0.5 m (range 0.5-2.1 m; n = 21). According to our description of used trees, the number of suitably hollow Chimney Swift nest or roost trees may be two to three times higher, although still rare, in most unlogged compared to logged hardwood forests. Whether the current total supply of suitable nest or roost trees is sufficient to carry the anticipated increase in use by Chimney Swifts as chimney habitat is modified or deteriorates is unknown. Monitoring the frequency of use of tree cavities by nesting and roosting Chimney Swifts over time, and more robustly quantifying the availability of suitable tree cavities in different forest types for nesting and roosting Chimney Swifts, particularly in unlogged versus logged forests, are fruitful areas for future research

Height, selected genetic markers and prostate cancer risk: results from the PRACTICAL consortium

Background: Evidence on height and prostate cancer risk is mixed, however, recent studies with large data sets support a possible role for its association with the risk of aggressive prostate cancer. Methods: We analysed data from the PRACTICAL consortium consisting of 6207 prostate cancer cases and 6016 controls and a subset of high grade cases (2480 cases). We explored height, polymorphisms in genes related to growth processes as main effects and their possible interactions. Results: The results suggest that height is associated with high-grade prostate cancer risk. Men with height 4180cm are at a 22% increased risk as compared to men with height o173cm (OR 1.22, 95% CI 1.01–1.48). Genetic variants in the growth pathway gene showed an association with prostate cancer risk. The aggregate scores of the selected variants identified a significantly increased risk of overall prostate cancer and high-grade prostate cancer by 13% and 15%, respectively, in the highest score group as compared to lowest score group. Conclusions: There was no evidence of gene-environment interaction between height and the selected candidate SNPs. Our findings suggest a role of height in high-grade prostate cancer. The effect of genetic variants in the genes related to growth is seen in all cases and high-grade prostate cancer. There is no interaction between these two exposures.</p