34 research outputs found

    Threshold effects of habitat fragmentation on fish diversity at landscapes scales

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    Habitat fragmentation involves habitat loss concomitant with changes in spatial configuration, confounding mechanistic drivers of biodiversity change associated with habitat disturbance. Studies attempting to isolate the effects of altered habitat configuration on associated communities have reported variable results. This variability may be explained in part by the fragmentation threshold hypothesis, which predicts that the effects of habitat configuration may only manifest at low levels of remnant habitat area. To separate the effects of habitat area and configuration on biodiversity, we surveyed fish communities in seagrass landscapes spanning a range of total seagrass area (2-74% cover within 16 000-m2 landscapes) and spatial configurations (1-75 discrete patches). We also measured variation in fine-scale seagrass variables, which are known to affect faunal community composition and may covary with landscape-scale features. We found that species richness decreased and the community structure shifted with increasing patch number within the landscape, but only when seagrass area was low (<25% cover). This pattern was driven by an absence of epibenthic species in low-seagrass-area, highly patchy landscapes. Additional tests corroborated that low movement rates among patches may underlie loss of vulnerable taxa. Fine-scale seagrass biomass was generally unimportant in predicting fish community composition. As such, we present empirical support for the fragmentation threshold hypothesis and we suggest that poor matrix quality and low dispersal ability for sensitive taxa in our system may explain why our results support the hypothesis, while previous empirical work has largely failed to match predictions

    A Germline Variant at 8q24 Contributes to Familial Clustering of Prostate Cancer in Men of African Ancestry

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    Although men of African ancestry have a high risk of prostate cancer (PCa), no genes or mutations have been identified that contribute to familial clustering of PCa in this population. We investigated whether the African ancestry–specific PCa risk variant at 8q24, rs72725854, is enriched in men with a PCa family history in 9052 cases, 143 cases from high-risk families, and 8595 controls of African ancestry. We found the risk allele to be significantly associated with earlier age at diagnosis, more aggressive disease, and enriched in men with a PCa family history (32% of high-risk familial cases carried the variant vs 23% of cases without a family history and 12% of controls). For cases with two or more first-degree relatives with PCa who had at least one family member diagnosed at age <60 yr, the odds ratios for TA heterozygotes and TT homozygotes were 3.92 (95% confidence interval [CI] = 2.13–7.22) and 33.41 (95% CI = 10.86–102.84), respectively. Among men with a PCa family history, the absolute risk by age 60 yr reached 21% (95% CI = 17–25%) for TA heterozygotes and 38% (95% CI = 13–65%) for TT homozygotes. We estimate that in men of African ancestry, rs72725854 accounts for 32% of the total familial risk explained by all known PCa risk variants. Patient summary: We found that rs72725854, an African ancestry–specific risk variant, is more common in men with a family history of prostate cancer and in those diagnosed with prostate cancer at younger ages. Men of African ancestry may benefit from the knowledge of their carrier status for this genetic risk variant to guide decisions about prostate cancer screening. © 2020 The AuthorsThe African ancestry–specific prostate cancer risk variant at 8q24, rs72725854, is enriched in men diagnosed at younger ages and men with a prostate cancer family history. Carriers of this risk allele would benefit from regular and earlier prostate cancer screening

    Genome-wide association study identifies two susceptibility loci for osteosarcoma

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    Osteosarcoma is the most common primary bone malignancy of adolescents and young adults. To better understand the genetic etiology of osteosarcoma, we performed a multistage genome-wide association study consisting of 941 individuals with osteosarcoma (cases) and 3,291 cancer-free adult controls of European ancestry. Two loci achieved genome-wide significance: a locus in the GRM4 gene at 6p21.3 (encoding glutamate receptor metabotropic 4; rs1906953; P = 8.1 × 10⁻⁹) and a locus in the gene desert at 2p25.2 (rs7591996 and rs10208273; P = 1.0 × 10⁻⁸ and 2.9 × 10⁻⁷, respectively). These two loci warrant further exploration to uncover the biological mechanisms underlying susceptibility to osteosarcoma
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