Data-driven approach for highlighting priority areas for protection in marine areas beyond national jurisdiction

One of the aims of the United Nations (UN) negotiations on the conservation and sustainable use of marine biodiversity in areas beyond national jurisdiction (ABNJ) is to develop a legal process for the establishment of area-based management tools, including marine protected areas, in ABNJ. Here we use a conservation planning algorithm to integrate 55 global data layers on ABNJ species diversity, habitat heterogeneity, benthic features, productivity, and fishing as a means for highlighting priority regions in ABNJ to be considered for spatial protection. We also include information on forecasted species distributions under climate change. We found that parameterizing the planning algorithm to protect at least 30% of these key ABNJ conservation features, while avoiding areas of high fishing effort, yielded a solution that highlights 52,545,634 km2 (23.7%) of ABNJ as high priority regions for protection. Instructing the planning model to avoid ABNJ areas with high fishing effort resulted in relatively minor shifts in the planning solution, when compared to a separate model that did not consider fishing effort. Integrating information on climate change had a similarly minor influence on the planning solution, suggesting that climate-informed ABNJ protected areas may be able to protect biodiversity now and in the future. This globally standardized, data-driven process for identifying priority ABNJ regions for protection serves as a valuable complement to other expert-driven processes underway to highlight ecologically or biologically significant ABNJ regions. Both the outputs and methods exhibited in this analysis can additively inform UN decision-making concerning establishment of ABNJ protected areas

Podocyte specific knock out of selenoproteins does not enhance nephropathy in streptozotocin diabetic C57BL/6 mice

<p>Abstract</p> <p>Background</p> <p>Selenoproteins contain selenocysteine (Sec), commonly considered the 21^stgenetically encoded amino acid. Many selenoproteins, such as the glutathione peroxidases and thioredoxin reductases, protect cells against oxidative stress by functioning as antioxidants and/or through their roles in the maintenance of intracellular redox balance. Since oxidative stress has been implicated in the pathogenesis of diabetic nephropathy, we hypothesized that selenoproteins protect against this complication of diabetes.</p> <p>Methods</p> <p>C57BL/6 mice that have a podocyte-specific inability to incorporate Sec into proteins (denoted in this paper as PodoTrsp^-/-) and control mice were made diabetic by intraperitoneal injection of streptozotocin, or were injected with vehicle. Blood glucose, body weight, microalbuminuria, glomerular mesangial matrix expansion, and immunohistochemical markers of oxidative stress were assessed.</p> <p>Results</p> <p>After 3 and 6 months of diabetes, control and PodoTrsp^-/-mice had similar levels of blood glucose. There were no differences in urinary albumin/creatinine ratios. Periodic acid-Schiff staining to examine mesangial matrix expansion also demonstrated no difference between control and PodoTrsp^-/-mice after 6 months of diabetes, and there were no differences in immunohistochemical stainings for nitrotyrosine or NAD(P)H dehydrogenase, quinone 1.</p> <p>Conclusion</p> <p>Loss of podocyte selenoproteins in streptozotocin diabetic C57BL/6 mice does not lead to increased oxidative stress as assessed by nitrotyrosine and NAD(P)H dehydrogenase, quinone 1 immunostaining, nor does it lead to worsening nephropathy.</p

Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk

BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat