60 research outputs found

    Advancing Monitoring Infrastructure for Oregon’s Native Freshwater Turtles with Citizen Science Platforms

    Get PDF
    Monitoring is a core component of conservation plans as well as an opportunity for local stakeholders to contribute. Our objective was to advance monitoring infrastructure for the protection of native, threatened freshwater turtles in the Pacific Northwest through the creation of a citizen science application. This was done by researching previous designs of citizen science projects over the past ten years and improving the platform based on recommendations by practitioners. Current platforms can be improved by better crediting the work of citizen scientists, improving communication between scientists and users, building in flexibility for scientists, and accommodating for disabilities through ergonomic design. This set the framework to design and build a new multi-platform monitoring application. The final product is a mobile and web application that embodies these concepts and is ready for user-testing in the summer, providing scientists with critical data to help monitor multiple species of conservation concern, while engaging the public in this important task

    Status and Trends of Phragmites australis invasion within constructed wetlands in Virginia

    Get PDF
    Part I. Field GPS Mapping of P. australis Populations. Kirk J. Havens, Harry Berquist, and Walter I. Priest, Ill Part II. Evaluating the Use of Multispectral Imagery for Identifying and Quantifying P. australis Populations in Created Wetlands. James E. Perry and John Anderson Part Ill. A Summary of Methods for Controlling Phragmites australis. Libby Norris, James E. Perry, and Kirk J. Haven

    BMPR2 expression is suppressed by signaling through the estrogen receptor

    Get PDF
    <p>Abstract</p> <p>Background</p> <p>Studies in multiple organ systems have shown cross-talk between signaling through the bone morphogenetic protein receptor type 2 (BMPR2) and estrogen pathways. In humans, pulmonary arterial hypertension (PAH) has a female predominance, and is associated with decreased BMPR2 expression. The goal of this study was to determine if estrogens suppress BMPR2 expression.</p> <p>Methods</p> <p>A variety of techniques were utilized across several model platforms to evaluate the relationship between estrogens and BMPR2 gene expression. We used quantitative RT-PCR, gel mobility shift, and luciferase activity assays in human samples, live mice, and cell culture.</p> <p>Results</p> <p>BMPR2 expression is reduced in lymphocytes from female patients compared with male patients, and in whole lungs from female mice compared with male mice. There is an evolutionarily conserved estrogen receptor binding site in the BMPR2 promoter, which binds estrogen receptor by gel-shift assay. Increased exogenous estrogen decreases BMPR2 expression in cell culture, particularly when induced to proliferate. Transfection of increasing quantities of estrogen receptor alpha correlates strongly with decreasing expression of BMPR2.</p> <p>Conclusions</p> <p>BMPR2 gene expression is reduced in females compared to males in live humans and in mice, likely through direct estrogen receptor alpha binding to the BMPR2 promoter. This reduced BMPR2 expression may contribute to the increased prevalence of PAH in females.</p

    The James Webb Space Telescope Mission

    Full text link
    Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least 4m4m. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the 6.5m6.5m James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

    The FANCM:p.Arg658* truncating variant is associated with risk of triple-negative breast cancer

    Get PDF
    Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PALB2, ATM, and CHEK2 are associated with breast cancer risk. FANCM, which encodes for a DNA translocase, has been proposed as a breast cancer predisposition gene, with greater effects for the ER-negative and triple-negative breast cancer (TNBC) subtypes. We tested the three recurrent protein-truncating variants FANCM:p.Arg658*, p.Gln1701*, and p.Arg1931* for association with breast cancer risk in 67,112 cases, 53,766 controls, and 26,662 carriers of pathogenic variants of BRCA1 or BRCA2. These three variants were also studied functionally by measuring survival and chromosome fragility in FANCM (-/-) patient-derived immortalized fibroblasts treated with diepoxybutane or olaparib. We observed that FANCM:p.Arg658* was associated with increased risk of ER-negative disease and TNBC (OR = 2.44, P = 0.034 and OR = 3.79; P = 0.009, respectively). In a country-restricted analysis, we confirmed the associations detected for FANCM:p.Arg658* and found that also FANCM:p.Arg1931* was associated with ER-negative breast cancer risk (OR = 1.96; P = 0.006). The functional results indicated that all three variants were deleterious affecting cell survival and chromosome stability with FANCM:p.Arg658* causing more severe phenotypes. In conclusion, we confirmed that the two rare FANCM deleterious variants p.Arg658* and p.Arg1931* are risk factors for ER-negative and TNBC subtypes. Overall our data suggest that the effect of truncating variants on breast cancer risk may depend on their position in the gene. Cell sensitivity to olaparib exposure, identifies a possible therapeutic option to treat FANCM-associated tumors

    To \u27Die Hel\u27 and back. Expeditions of the Phylogeny of World Tachinidae Project. Part I: Western Cape, South Africa

    Get PDF
    The “Phylogeny of World Tachinidae” project kicked off with an operational meeting in June 2012 at the Canadian National Collection of Insects (CNC) in Ottawa. Goals were discussed, work plans prepared, and of course the destinations and timing of major field expeditions were debated. During our three years of National Science Foundation funding we hope to gather fresh material for molecular analysis from all biogeographic regions of the world

    To \u27Die Hel\u27 and back. Expeditions of the Phylogeny of World Tachinidae Project. Part I: Western Cape, South Africa

    No full text
    The “Phylogeny of World Tachinidae” project kicked off with an operational meeting in June 2012 at the Canadian National Collection of Insects (CNC) in Ottawa. Goals were discussed, work plans prepared, and of course the destinations and timing of major field expeditions were debated. During our three years of National Science Foundation funding we hope to gather fresh material for molecular analysis from all biogeographic regions of the world

    Novel mutations of the growth hormone 1 (GH1) gene disclosed by modulation of the clinical selection criteria for individuals with short stature

    No full text
    Subtle mutations in the growth hormone 1 (GH1) gene have been regarded as a comparatively rare cause of short stature. Such lesions were sought in a group of 41 individuals selected for short stature, reduced height velocity, and bone age delay; a group of 11 individuals with short stature and idiopathic growth hormone deficiency (IGHD); and a group of 154 controls. Heterozygous mutations were identified in all three groups but disproportionately in the individuals with short stature, both with (odds ratio 25.2; 95% CI, 5.1–132.2) and without (odds ratio 3.6; 95% CI, 1.0–12.9) IGHD. Twenty-four novel GH1 gene lesions were found. Thirteen novel missense mutations were characterized by assaying the signal transduction activity of in vitro expressed variants; six (T27I, K41R, N47D, S71F, S108R, and T175A) exhibited a reduced ability to activate the JAK/STAT pathway. Molecular modeling suggested that both K41R and T175A might compromise GH receptor binding. Seven GH variants (R16C, K41R, S71F, E74K, Q91L, S108C, and a functional polymorphism, V110I) manifested reduced secretion in rat pituitary cells after allowance had been made for the level of expression attributable to the associated GH1 proximal promoter haplotype. A further leader peptide variant (L-11P) was not secreted. Eleven novel mutations in the GH1 gene promoter were assessed by reporter gene assay but only two, including a GH2 gene-templated gene conversion, were found to be associated with a significantly reduced level of expression. Finally, a novel intron 2 acceptor splice-site mutation, detected in a family with autosomal dominant type II IGHD, was shown to lead to the skipping of exon 3 from the GH1 transcript. A total of 15 novel GH1 gene mutations were thus considered to be of probable phenotypic significance. Such lesions are more prevalent than previously recognized and although most may be insufficient on their own to account for the observed clinical phenotype, they are nevertheless likely to play a contributory role in the etiology of short stature
    • 

    corecore