36 research outputs found

    Live reptile smuggling is predicted by trends in the legal exotic pet trade

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    ACKNOWLEDGMENTS This research was funded by the Centre for Invasive Species Solutions (Project PO1-I-002). PG-D was partially supported by NERC grant NE/S011641/1 under the Newton Latam program. The authors acknowledge the Indigenous Traditional Owners of the land on which the University of Adelaide is built—the Kaurna people of the Adelaide Plains. We thank Jacob Maher and Talia Wittmann for sharing Australian zoo keeping data.Peer reviewedPublisher PD

    Drivers of the Australian native pet trade : the role of species traits, socioeconomic attributes and regulatory systems

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    Acknowledgements We acknowledge that the land on which we conducted our research is the traditional land of the Kaurna people of the Adelaide Plains. We pay our respects to Kaurna elders past, present and emerging. We thank the South Australian Department for the Environment and Water for recording and facilitating access to all permit data used in our analysis. This research was funded by the Centre for Invasive Species Solutions (Project P01-I-002). PC was supported by an Australian Research Council Discovery grant (DP210103050). PG-D was supported by the NERC grant NE/S011641/1 under the Newton LATAM funding programme.Peer reviewedPublisher PD

    A Snapshot of Online Wildlife Trade : Australian e-commerce trade of native and non-native pets  

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    Funding This project was funded by the Centre for Invasive Species Solutions (Project PO1-I-001). Adam Toomes was additionally supported by the FJ Sandoz PhD Scholarship. Pablo GarcíaDíaz was funded by NERC grants NE/S011641/1 (Newton LATAM programme) and 2022GCBCCONTAIN.Peer reviewedPublisher PD

    Scientists' warning to humanity on illegal or unsustainable wildlife trade

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    Illegal or unsustainable wildlife trade is growing at a global level, threatening the traded species and coexisting biota, and promoting the spread of invasive species. From the loss of ecosystem services to diseases transmitted from wildlife to humans, or connections with major organized crime networks and disruption of local to global economies, its ramifications are pervading our daily lives and perniciously affecting our well-being. Here we build on the manifesto 'World Scientists' Warning to Humanity, issued by the Alliance of World Scientists. As a group of researchers deeply concerned about the consequences of illegal or unsustainable wildlife trade, we review and highlight how these can negatively impact species, ecosystems, and society. We appeal for urgent action to close key knowledge gaps and regulate wildlife trade more stringently.Peer reviewe

    Hundreds of variants clustered in genomic loci and biological pathways affect human height

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    Most common human traits and diseases have a polygenic pattern of inheritance: DNA sequence variants at many genetic loci influence the phenotype. Genome-wide association (GWA) studies have identified more than 600 variants associated with human traits, but these typically explain small fractions of phenotypic variation, raising questions about the use of further studies. Here, using 183,727 individuals, we show that hundreds of genetic variants, in at least 180 loci, influence adult height, a highly heritable and classic polygenic trait. The large number of loci reveals patterns with important implications for genetic studies of common human diseases and traits. First, the 180 loci are not random, but instead are enriched for genes that are connected in biological pathways (P = 0.016) and that underlie skeletal growth defects (P < 0.001). Second, the likely causal gene is often located near the most strongly associated variant: in 13 of 21 loci containing a known skeletal growth gene, that gene was closest to the associated variant. Third, at least 19 loci have multiple independently associated variants, suggesting that allelic heterogeneity is a frequent feature of polygenic traits, that comprehensive explorations of already-discovered loci should discover additional variants and that an appreciable fraction of associated loci may have been identified. Fourth, associated variants are enriched for likely functional effects on genes, being over-represented among variants that alter amino-acid structure of proteins and expression levels of nearby genes. Our data explain approximately 10% of the phenotypic variation in height, and we estimate that unidentified common variants of similar effect sizes would increase this figure to approximately 16% of phenotypic variation (approximately 20% of heritable variation). Although additional approaches are needed to dissect the genetic architecture of polygenic human traits fully, our findings indicate that GWA studies can identify large numbers of loci that implicate biologically relevant genes and pathways.

    Scientists' warning to humanity on illegal or unsustainable wildlife trade

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    Illegal or unsustainable wildlife trade is growing at a global level, threatening the traded species and coexisting biota, and promoting the spread of invasive species. From the loss of ecosystem services to diseases transmitted from wildlife to humans, or connections with major organized crime networks and disruption of local to global economies, its ramifications are pervading our daily lives and perniciously affecting our well-being. Here we build on the manifesto ‘World Scientists’ Warning to Humanity, issued by the Alliance of World Scientists. As a group of researchers deeply concerned about the consequences of illegal or unsustainable wildlife trade, we review and highlight how these can negatively impact species, ecosystems, and society. We appeal for urgent action to close key knowledge gaps and regulate wildlife trade more stringently.</p

    Challenges and perspectives on tackling illegal or unsustainable wildlife trade

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    Illegal or unsustainable wildlife trade (IUWT) currently presents one of the most high-profile conservation challenges. There is no “one-size-fits-all” strategy, and a variety of disciplines and actors are needed for any counteractive approach to work effectively. Here, we detail common challenges faced when tackling IUWT, and we describe some available tools and technologies to curb and track IUWT (e.g. bans, quotas, protected areas, certification, captive-breeding and propagation, education and awareness). We discuss gaps to be filled in regulation, enforcement, engagement and knowledge about wildlife trade, and propose practical solutions to regulate and curb IUWT, paving the road for immediate action

    Abdominal aortic aneurysm is associated with a variant in low-density lipoprotein receptor-related protein 1

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    Abdominal aortic aneurysm (AAA) is a common cause of morbidity and mortality and has a significant heritability. We carried out a genome-wide association discovery study of 1866 patients with AAA and 5435 controls and replication of promising signals (lead SNP with a p value &lt; 1 × 10-5) in 2871 additional cases and 32,687 controls and performed further follow-up in 1491 AAA and 11,060 controls. In the discovery study, nine loci demonstrated association with AAA (p &lt; 1 × 10-5). In the replication sample, the lead SNP at one of these loci, rs1466535, located within intron 1 of low-density-lipoprotein receptor-related protein 1 (LRP1) demonstrated significant association (p = 0.0042). We confirmed the association of rs1466535 and AAA in our follow-up study (p = 0.035). In a combined analysis (6228 AAA and 49182 controls), rs1466535 had a consistent effect size and direction in all sample sets (combined p = 4.52 × 10-10, odds ratio 1.15 [1.10-1.21]). No associations were seen for either rs1466535 or the 12q13.3 locus in independent association studies of coronary artery disease, blood pressure, diabetes, or hyperlipidaemia, suggesting that this locus is specific to AAA. Gene-expression studies demonstrated a trend toward increased LRP1 expression for the rs1466535 CC genotype in arterial tissues; there was a significant (p = 0.029) 1.19-fold (1.04-1.36) increase in LRP1 expression in CC homozygotes compared to TT homozygotes in aortic adventitia. Functional studies demonstrated that rs1466535 might alter a SREBP-1 binding site and influence enhancer activity at the locus. In conclusion, this study has identified a biologically plausible genetic variant associated specifically with AAA, and we suggest that this variant has a possible functional role in LRP1 expression

    Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes.

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    OBJECTIVE: Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS: We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS: Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10(-4)), improved β-cell function (P = 1.1 × 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS: We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis

    A genome-wide association search for type 2 diabetes genes in African Americans.

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    African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n = 550 independent loci) were genotyped in a replication cohort and 122 SNPs (n = 98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5×10(-8)). SNP rs7560163 (P = 7.0×10(-9), OR (95% CI) = 0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5×10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations
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