13 research outputs found

    Origin and Evolution of Prebiotic Organic Matter as Inferred from the Tagish Lake Meteorite

    Get PDF
    The complex suite of organic materials in carbonaceous chondrite meteorites probably originally formed in the interstellar medium and/or the solar protoplanetary disk, but was subsequently modified in the meteorites' asteroidal parent bodies. The mechanisms of formation and modification are still very poorly understood. We carried out a systematic study of variations in the mineralogy, petrology, and soluble and insoluble organic matter in distinct fragments of the Tagish Lake meteorite. The variations correlate with indicators of parent body aqueous alteration and at least some molecules of pre-biotic importance formed during the alteration

    Best practices for using drones in seabird monitoring and research

    Get PDF
    Over the past decade, drones have become increasingly popular in environmental biology and have been used to study wildlife on all continents. Drones have become of global importance for surveying breeding seabirds by providing opportunities to transform monitoring techniques and allow new research on some of the most threatened birds. However, such fast-changing and increasingly available technology presents challenges to regulators responding to requests to carry out surveys and to researchers ensuring their work follows best practice and meets legal and ethical standards. Following a workshop convened at the 14th International Seabird Group Conference and a subsequent literature search, we collate information from over 100 studies and present a framework to ensure drone-seabird surveys are safe, effective, and within the law. The framework comprises eight steps: (1) Objectives and Feasibility; (2) Technology and Training; (3) Site Assessment and Permission; (4) Disturbance Mitigation; (5) Pre-deployment Checks; (6) Flying; (7) Data Handling and Analysis; and (8) Reporting. The audience is wide-ranging with sections having relevance for different users, including prospective and experienced drone-seabird pilots, landowners, and licensors. Regulations vary between countries and are frequently changing, but common principles exist. Taking-off, landing, and conducting in-flight changes in altitude and speed at ≥ 50 m from the study area, and flying at ≥ 50 m above ground-nesting seabirds/horizontal distance from vertical colonies, should have limited disturbance impact on many seabird species; however, surveys should stop if disturbance occurs. Compared to automated methods, manual or semi-automated image analyses are, at present, more suitable for infrequent drone surveys and surveys of relatively small colonies. When deciding if drone-seabird surveys are an appropriate monitoring method long-term, the cost, risks, and results obtained should be compared to traditional field monitoring where possible. Accurate and timely reporting of surveys is essential to developing adaptive guidelines for this increasingly common technology

    Best practices for using drones in seabird monitoring and research

    Get PDF
    Over the past decade, drones have become increasingly popular in environmental biology and have been used to study wildlife on all continents. Drones have become of global importance for surveying breeding seabirds by providing opportunities to transform monitoring techniques and allow new research on some of the most threatened birds. However, such fast-changing and increasingly available technology presents challenges to regulators responding to requests to carry out surveys and to researchers ensuring their work follows best practice and meets legal and ethical standards. Following a workshop convened at the 14th International Seabird Group Conference and a subsequent literature search, we collate information from over 100 studies and present a framework to ensure drone-seabird surveys are safe, effective, and within the law. The framework comprises eight steps: (1) Objectives and Feasibility; (2) Technology and Training; (3) Site Assessment and Permission; (4) Disturbance Mitigation; (5) Pre-deployment Checks; (6) Flying; (7) Data Handling and Analysis; and (8) Reporting. The audience is wide-ranging with sections having relevance for different users, including prospective and experienced drone-seabird pilots, landowners, and licensors. Regulations vary between countries and are frequently changing, but common principles exist. Taking-off, landing, and conducting in-flight changes in altitude and speed at ≥ 50 m from the study area, and flying at ≥ 50 m above ground-nesting seabirds/horizontal distance from vertical colonies, should have limited disturbance impact on many seabird species; however, surveys should stop if disturbance occurs. Compared to automated methods, manual or semi-automated image analyses are, at present, more suitable for infrequent drone surveys and surveys of relatively small colonies. When deciding if drone-seabird surveys are an appropriate monitoring method long-term, the cost, risks, and results obtained should be compared to traditional field monitoring where possible. Accurate and timely reporting of surveys is essential to developing adaptive guidelines for this increasingly common technology

    Effects of environmental Bisphenol A exposures on germ cell development and Leydig cell function in the human fetal testis

    Get PDF
    <div><p>Background</p><p>Using an organotypic culture system termed human Fetal Testis Assay (hFeTA) we previously showed that 0.01 μM BPA decreases basal, but not LH-stimulated, testosterone secreted by the first trimester human fetal testis. The present study was conducted to determine the potential for a long-term antiandrogenic effect of BPA using a xenograft model, and also to study the effect of BPA on germ cell development using both the hFETA and xenograft models.</p><p>Methods</p><p>Using the hFeTA system, first trimester testes were cultured for 3 days with 0.01 to 10 μM BPA. For xenografts, adult castrate male nude mice were injected with hCG and grafted with first trimester testes. Host mice received 10 μM BPA (~ 500 μg/kg/day) in their drinking water for 5 weeks. Plasma levels of total and unconjugated BPA were 0.10 μM and 0.038 μM respectively. Mice grafted with second trimester testes received 0.5 and 50 μg/kg/day BPA by oral gavage for 5 weeks.</p><p>Results</p><p>With first trimester human testes, using the hFeTA model, 10 μM BPA increased germ cell apoptosis. In xenografts, germ cell density was also reduced by BPA exposure. Importantly, BPA exposure significantly decreased the percentage of germ cells expressing the pluripotency marker AP-2γ, whilst the percentage of those expressing the pre-spermatogonial marker MAGE-A4 significantly increased. BPA exposure did not affect hCG-stimulated androgen production in first and second trimester xenografts as evaluated by both plasma testosterone level and seminal vesicle weight in host mice.</p><p>Conclusions</p><p>Exposure to BPA at environmentally relevant concentrations impairs germ cell development in first trimester human fetal testis, whilst gonadotrophin-stimulated testosterone production was unaffected in both first and second trimester testis. Studies using first trimester human fetal testis demonstrate the complementarity of the FeTA and xenograft models for determining the respective short-term and long term effects of environmental exposures.</p></div

    Effect of BPA exposure on germ cell differentiation in first trimester human fetal testis xenografts.

    No full text
    <p>Human fetal testes (9.1–11.3 GW) were xenografted into castrate Nude (host) mice. Host mice received vehicle (Control) or 10μM BPA in the drinking water for five weeks. (A) Histological sections of testes after immunostaining for AP-2γ (gonocytes). Positive (red arrows) and negative (black arrows) germ cells can be identified. Scale bar: 60 μm. (B) Quantification of AP-2γ-positive cells displayed as mean ± SEM (n = 9) on the left panel and as individual values with a line drawn between the control and the corresponding BPA-treated testis from the same fetus on the right panel. (C) Histological sections of testes after immunostaining for MAGE-A4 (prespermatogonia). Positive (red arrows) and negative (black arrows) germ cells can be identified. Scale bar: 60 μm. (D) Quantification of MAGE-A4-positive cells displayed as mean ± SEM (n = 8) on the left part and as individual values with a line drawn between the control and the corresponding BPA-treated testis from the same fetus on the right part. Data analyzed using the Wilcoxon paired-test. *p<0.05, **p<0.01.</p

    Effect of BPA exposure on plasma BPA concentration in xenografted mice.

    No full text
    <p>Plasma levels of BPA were quantified by gas chromatography coupled to tandem mass spectrometry (GC-MS/MS) from castrated Nude male mice xenografted with first trimester human fetal testis (9.1–11.3 GW, mean 10.2 ± 0.2 GW; n = 6–7) and exposed to vehicle (Control) or BPA (10 μM in the drinking water) for five weeks. For each fetus, all the pieces from one testis were grafted in a control mouse and all the pieces from the contralateral testis were grafted in a BPA-treated mouse. Statistical analysis was performed using the Mann-Whitney test. *p<0.05, **p<0.01.</p

    Effect of BPA exposure on germ cell apoptosis and proliferation in first trimester human fetal testes cultured using the FeTA system.

    No full text
    <p>Human fetal testes (6–12 GW, mean 8.7 ± 0.6 GW) were cultured using the ex vivo <u>h</u>uman <u>Fe</u>tal <u>T</u>estis <u>A</u>ssay system (hFeTA). After 24 hours in control medium, explants were cultured with 100 ng/mL of LH for the 3 subsequent days in the presence of ethanol vehicle (control explants) or BPA at concentrations ranging from 0.01 to 10 μM. Control and BPA-treated explants were paired samples from the same testis. (A) Histological sections after labeling with anti-cleaved caspase-3 antibody (brown) and anti-AMH antibody (green). Positive (red arrows) and negative (black arrows) germ cells can be identified. Scale bar: 10 μm. (B) Quantification of cleaved caspase-3 positive cells (mean ± SEM; n = 4–8). (C) Histological sections after labeling with anti-Ki-67 antibody (brown) and anti-AMH antibody (green). Positive (red arrows) and negative (black arrows) germ cells can be identified. Scale bar: 50 μm. (D) Quantification of Ki67 positive gonocytes (mean ± SEM; n = 4–8).</p

    Effect of BPA exposure on germ cell density in first trimester human fetal testis xenografts.

    No full text
    <p>Human fetal testes (9.1–11.3 GW) were xenografted into castrate Nude (host) mice. Host mice received vehicle (Control) or 10μM BPA in the drinking water for five weeks. (A) Histological sections after haematoxylin-eosin-saffron staining. Germ cells (black arrow) can be easily identified. Scale bar: 20 μm. (B) Quantification of germ cell density displayed as mean ± SEM (n = 9) on the left panel and as individual values with a line drawn between the control and the corresponding BPA-treated testis from the same fetus on the right panel. Data analyzed using the Wilcoxon paired-test. *p<0.05 compared with control condition.</p

    Effect of BPA exposure on plasma testosterone level and seminal vesicle weight in the host mice xenografted with first trimester human testes and on steroidogenic genes expression in the xenografts.

    No full text
    <p>Human fetal testes (9.1–11.3 GW) were xenografted into castrate Nude (host) mice. Host mice received vehicle (Control) or 10 μM BPA in the drinking water for five weeks. (A) seminal vesicle weight displayed as mean ± SEM (n = 6) on the left panel and as individual values with a line drawn between the control and the corresponding BPA-exposed testis from the same fetus on the right panel. B) plasma testosterone concentration in host mice displayed as mean ± SEM (n = 6) on the left panel and as individual values with a line drawn between the control and the corresponding BPA-exposed testis from the same fetus on the right panel. C) Expression of key genes in the steroidogenic pathway (STAR, CYP11A1, CYP17A1 and CYP19) using quantitative RT-PCR standardized to either β-ACTIN (ACTIN) or RPLP0 or CYPA as endogenous control. Results are presented as a percentage of the control value (mean ± SEM; n = 4). Data analyzed by Wilcoxon test. No significant difference between BPA-treated and control mice were identified.</p
    corecore