Collaboration Through NEPA: Achieving a Social License to Operate On Federal Public Lands

As demand and consumption of natural gas increases, so will drilling operations to extract the natural gas on federal public lands. Fueled by the shale gas revolution, natural gas drilling operations are now frequently taking place, not only in the highly documented urban settings, but also on federal public lands with high conservation value. The phenomenon of increased drilling in sensitive locations, both urban and remote, has sparked increased public opposition, requiring oil and gas producers to reconsider how they engage the public. Oil and gas producers have increasingly deployed the concept of a social license to operate to gain support from the public and the communities in which they operate. A social license to operate is a voluntary license granted by communities, obligating companies to go above and beyond the requirements of their legal license to operate. While natural gas developers have increasingly sought to achieve a social license to operate in urban settings, such as the Colorado Front Range, there has been little use of this approach by operators drilling on federal public land. We advocate for the use of increased collaboration with affected stakeholders and communities through the NEPA process as a means to achieve a social license to operate on federal public land

Collaboration Through NEPA: Achieving a Social License to Operate On Federal Public Lands

As demand and consumption of natural gas increases, so will drilling operations to extract the natural gas on federal public lands. Fueled by the shale gas revolution, natural gas drilling operations are now frequently taking place, not only in the highly documented urban settings, but also on federal public lands with high conservation value. The phenomenon of increased drilling in sensitive locations, both urban and remote, has sparked increased public opposition, requiring oil and gas producers to reconsider how they engage the public. Oil and gas producers have increasingly deployed the concept of a social license to operate to gain support from the public and the communities in which they operate. A social license to operate is a voluntary license granted by communities, obligating companies to go above and beyond the requirements of their legal license to operate. While natural gas developers have increasingly sought to achieve a social license to operate in urban settings, such as the Colorado Front Range, there has been little use of this approach by operators drilling on federal public land. We advocate for the use of increased collaboration with affected stakeholders and communities through the NEPA process as a means to achieve a social license to operate on federal public land

The tribulations of trials: Lessons learnt recruiting 777 older adults into REtirement in ACTion (REACT), a trial of a community, group-based active ageing intervention targeting mobility disability

© The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. BACKGROUND: Challenges of recruitment to randomized controlled trials (RCTs) and successful strategies to overcome them should be clearly reported to improve recruitment into future trials. REtirement in ACTion (REACT) is a United Kingdom-based multicenter RCT recruiting older adults at high risk of mobility disability to a 12-month group-based exercise and behavior maintenance program or to a minimal Healthy Aging control intervention. METHODS: The recruitment target was 768 adults, aged 65 years and older scoring 4-9 on the Short Physical Performance Battery (SPPB). Recruitment methods include the following: (a) invitations mailed by general practitioners (GPs); (b) invitations distributed via third-sector organizations; and (c) public relations (PR) campaign. Yields, efficiency, and costs were calculated. RESULTS: The study recruited 777 (33.9% men) community-dwelling, older adults (mean age 77.55 years (SD 6.79), mean SPPB score 7.37 (SD 1.56)), 95.11% white (n = 739) and broadly representative of UK quintiles of deprivation. Over a 20-month recruitment period, 25,559 invitations were issued. Eighty-eight percent of the participants were recruited via GP invitations, 5.4% via the PR campaign, 3% via word-of-mouth, and 2.5% via third-sector organizations. Mean recruitment cost per participant was £78.47, with an extra £26.54 per recruit paid to GPs to cover research costs. CONCLUSIONS: REACT successfully recruited to target. Response rates were lower than initially predicted and recruitment timescales required adjustment. Written invitations from GPs were the most efficient method for recruiting older adults at risk of mobility disability. Targeted efforts could achieve more ethnically diverse cohorts. All trials should be required to provide recruitment data to enable evidence-based planning of future trials

A community-based physical activity intervention to prevent mobility-related disability for retired older people (REtirement in ACTion (REACT)): Study protocol for a randomised controlled trial

© 2018 The Author(s). Background: The REtirement in ACTion (REACT) study is a multi-centre, pragmatic, two-arm, parallel-group randomised controlled trial (RCT) with an internal pilot phase. It aims to test the effectiveness and cost-effectiveness of a community, group-based physical activity intervention for reducing, or reversing, the progression of functional limitations in older people who are at high risk of mobility-related disability. Methods/design: A sample of 768 sedentary, community-dwelling, older people aged 65 years and over with functional limitations, but who are still ambulatory (scores between 4 and 9 out of 12 in the Short Physical Performance Battery test (SPPB)) will be randomised to receive either the REACT intervention, delivered over a period of 12 months by trained facilitators, or a minimal control intervention. The REACT study incorporates comprehensive process and economic evaluation and a nested sub-study which will test the hypothesis that the REACT intervention will slow the rate of brain atrophy and of decline in cognitive function assessed using magnetic resonance imaging (MRI). Outcome data will be collected at baseline, 6, 12 and 24 months for the main study, with MRI sub-study data collected at baseline, 6 and 12 months. The primary outcome analysis (SPPB score at 24 months) will be undertaken blinded to group allocation. Primary comparative analyses will be on an intention-to-treat (ITT) basis with due emphasis placed on confidence intervals. Discussion: REACT represents the first large-scale, pragmatic, community-based trial in the UK to target the non-disabled but high-risk segment of the older population with an intervention to reduce mobility-related disability. A programme that can successfully engage this population in sufficient activity to improve strength, aerobic capacity, coordination and balance would have a major impact on sustaining health and independence. REACT is also the first study of its kind to conduct a full economic and comprehensive process evaluation alongside the RCT. If effective and cost-effective, the REACT intervention has strong potential to be implemented widely in the UK and elsewhere

PRC2 is required for extensive reorganization of H3K27me3 during epigenetic reprogramming in mouse fetal germ cells

BACKGROUND: Defining how epigenetic information is established in the germline during fetal development is key to understanding how epigenetic information is inherited and impacts on evolution and human health and disease. RESULTS: Here, we show that Polycomb Repressive Complex 2 is transiently localized in the nucleus of mouse fetal germ cells, while DNA methylation is removed from the germline. This coincides with significant enrichment of trimethylated lysine 27 on histone 3 near the nuclear lamina that is dependent on activity of the essential PRC2 catalytic proteins, Enhancer of Zeste 1 and/or 2. CONCLUSIONS: Combined, these data reveal a role for Polycomb Repressive Complex 2 and trimethylated lysine 27 on histone 3 during germline epigenetic programming that we speculate is required to repress target sequences while DNA methylation is removed. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s13072-017-0113-9) contains supplementary material, which is available to authorized users

Reduced PRC2 function alters male germline epigenetic programming and paternal inheritance

Abstract Background Defining the mechanisms that establish and regulate the transmission of epigenetic information from parent to offspring is critical for understanding disease heredity. Currently, the molecular pathways that regulate epigenetic information in the germline and its transmission to offspring are poorly understood. Results Here we provide evidence that Polycomb Repressive Complex 2 (PRC2) regulates paternal inheritance. Reduced PRC2 function in mice resulted in male sub-fertility and altered epigenetic and transcriptional control of retrotransposed elements in foetal male germ cells. Males with reduced PRC2 function produced offspring that over-expressed retrotransposed pseudogenes and had altered preimplantation embryo cleavage rates and cell cycle control. Conclusion This study reveals a novel role for the histone-modifying complex, PRC2, in paternal intergenerational transmission of epigenetic effects on offspring, with important implications for understanding disease inheritance

Loss of maternal EED results in postnatal overgrowth

Background: Investigating how epigenetic information is transmitted through the mammalian germline is the key to understanding how this information impacts on health and disease susceptibility in offspring. EED is essential for regulating the repressive histone modification, histone 3 lysine 27 tri-methylation (H3K27me3) at many developmental genes. Results: In this study, we used oocyte-specific Zp3-Cre recombinase (Zp3Cre) to delete Eed specifically in mouse growing oocytes, permitting the study of EED function in oocytes and the impact of depleting EED in oocytes on outcomes in offspring. As EED deletion occurred only in growing oocytes and females were mated to normal wild type males, this model allowed the study of oocyte programming without confounding factors such as altered in utero environment. Loss of EED from growing oocytes resulted in a significant overgrowth phenotype that persisted into adult life. Significantly, this involved increased adiposity (total fat) and bone mineral density in offspring. Similar overgrowth occurs in humans with Cohen-Gibson (OMIM 617561) and Weaver (OMIM 277590) syndromes, that result from de novo germline mutations in EED or its co-factor EZH2, respectively. Consistent with a role for EZH2 in human oocytes, we demonstrate that de novo germline mutations in EZH2 occurred in the maternal germline in some cases of Weaver syndrome. However, deletion of Ezh2 in mouse oocytes resulted in a distinct phenotype compared to that resulting from oocyte-specific deletion of Eed. Conclusions: This study provides novel evidence that altering EED-dependent oocyte programming leads to compromised offspring growth and development in the next generation.Medicine, Faculty ofOther UBCNon UBCMedical Genetics, Department ofReviewedFacult