1,757 research outputs found

    “There’s a Moment When All Old Things Become New Again”: The Canadian Oil and Gas Royalty – A Modern Rent Charge

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    While American law recognizes the oil and gas royalty as a real property interest, Canadian law, although based on the American experience, is not as clear. This Article argues that the oil and gas royalty, an integral part of the investment necessary to the operation of the Canadian oil and gas industry, represents a modern example of the rent charge, a proprietary interest in land with origins in medieval common law. The Article makes this claim for two reasons: one is pragmatic, the other theoretical-pedagogical. First, pragmatically, as the value of oil and gas rises precipitously in response to the global supply crunch created by the Russian invasion of Ukraine, exploration for and production of Canadian reserves will expand. Therefore, the owners of those oil and gas reserves will seek to ensure their share in the resulting revenue; recognition as a rent charge provides that security. And second, theoretically- pedagogically, while the oil and gas royalty may be representative of a dying industry in the midst of a world transitioning from fossil-fuel dependency into a clean renewable energy future, the analysis that demonstrates it to be a proprietary interest in land is valuable for what it reveals about real property: its ability to adapt to changing circumstances. Outlining this analytical method provides important guidance as to the flexibility and organic development of the law of real property in accommodating future novel legal relationships. In demonstrating this analysis, the Article provides a framework within which to consider the legal characterization of the oil and gas royalty interest in both Canadian and American law. But more importantly, the Article is prospective, providing a methodology capable of use in considering the proprietary status of new legal relationships which may emerge as part of a clean energy future

    Role of C-reactive protein in a murine model of vein graft disease

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    Abstract only availableC-reactive protein (CRP), an acute phase reactant plasma protein, plays a key role in modulating the innate immune system. Elevated plasma levels of CRP are independently associated with increased risk of thrombosis. In coronary artery bypass grafting (CABG), leg veins are grafted around a coronary artery in order to divert blood flow around blocked areas of the artery. However, vein grafts can develop thrombosis, intimal hyperplasia, and atherosclerosis leading to vein graft disease (VGD). Published studies suggest that increased plasma levels of CRP are a risk factor for developing VGD. Microparticles (MP), submicron cell fragment released from apoptotic cells, promote thrombosis by increasing available surface area for clotting factor assembly. As increased plasma CRP levels can cause vascular cells to apoptose and release MP, we studied the relationship between increased plasma CRP levels, vein graft intimal hyperplasia, and MP formation in the mouse. CRP transgenic and wild type (WT) mice were used to assess the effect of CRP on VGD. Vein grafts harvested from donor mice were grafted into recipient mice and one month after surgery vein grafts were excised and processed for analysis. Planemetry was performed to measure intimal hyperplasia and samples were stained with antibodies against CRP to view the levels of the protein in each graft. MPs were separated from mouse whole blood and quantified by flow cytometry. No significant difference in neointima formation was seen between groups. CRP immunostaining suggests that CRP present in vein grafts is primarily of systemic origin. There was no significant difference in MP concentration between groups, although there was a trend for higher concentrations in CRP-Tg mice. CRP does not significantly increase intimal hyperplasia in vein graft segments or plasma MP concentration. However, sample sizes were small and further studies need to be performed to elucidate.Life Sciences Undergraduate Research Opportunity Progra

    An Analysis of Mechanisms Underlying the Antifibrinolytic Properties of Radiographic Contrast Agents

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    Background: Radiographic contrast agents inhibit fibrinolysis, although by poorly defined pathways. The purpose of this study was to define specific mechanisms by which contrast agents inhibit clot lysis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47998/1/11239_2004_Article_397950.pd

    Induction of Heme Oxygenase-1 Expression Inhibits Platelet-Dependent Thrombosis

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    Heme oxygenase-1 (HO-1) plays a key role in protecting tissue from oxidative stress. Although some studies implicate HO-1 in modulating thrombosis after vascular injury, the impact of HO-1 on the rate of clot formation in vivo is poorly defined. This study examined the potential function of HO-1 in regulating platelet-dependent arterial thrombosis. Platelet-rich thrombi were induced in C57BL/6J mice by applying 10% ferric chloride to the exposed carotid artery. Mean occlusion time of wild-type mice (n = 10) was 14.6 ± 1.0 min versus 12.9 ± 0.6 min for HO-1-/- mice (n = 11, p = 0.17). However, after challenge with hemin, mean occlusion time was significantly longer in wild-type mice (16.3 ± 1.2 min, n = 15) than HO-1-/- mice (12.0 ± 1.0 min, n = 9; p = 0.021). Hemin administration induced an approximately twofold increase in oxidative stress, measured as plasma thiobarbituric acid reactive substances. Immunohistochemical analysis revealed that hemin induced a robust increase in HO-1 expression within the carotid arterial wall. Ex vivo blood clotting within a collagen-coated perfusion chamber was studied to determine whether the accelerated thrombosis observed in HO-1-/- mice was contributed to by effects on the blood itself. Under basal conditions, mean clot formation during perfusion of blood over collagen did not differ between wild-type mice and HO-1-/- mice. However, after hemin challenge, mean clot formation was significantly increased in HO-1-/- mice compared with wild-type controls. These results suggest that, under basal conditions, HO-1 does not exert a significant effect on platelet-dependent clot formation in vivo. However, under conditions that stimulate HO-1 production, platelet-dependent thrombus formation is inhibited by HO-1. Enhanced HO-1 expression in response to oxidative stress may represent an adaptive response mechanism to down-regulate platelet activation under prothrombotic conditions.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/63386/1/1523086041361677.pd

    MT1-matrix metalloproteinase directs arterial wall invasion and neointima formation by vascular smooth muscle cells

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    During pathologic vessel remodeling, vascular smooth muscle cells (VSMCs) embedded within the collagen-rich matrix of the artery wall mobilize uncharacterized proteolytic systems to infiltrate the subendothelial space and generate neointimal lesions. Although the VSMC-derived serine proteinases, plasminogen activator and plasminogen, the cysteine proteinases, cathepsins L, S, and K, and the matrix metalloproteinases MMP-2 and MMP-9 have each been linked to pathologic matrix-remodeling states in vitro and in vivo, the role that these or other proteinases play in allowing VSMCs to negotiate the three-dimensional (3-D) cross-linked extracellular matrix of the arterial wall remains undefined. Herein, we demonstrate that VSMCs proteolytically remodel and invade collagenous barriers independently of plasmin, cathepsins L, S, or K, MMP-2, or MMP-9. Instead, we identify the membrane-anchored matrix metalloproteinase, MT1-MMP, as the key pericellular collagenolysin that controls the ability of VSMCs to degrade and infiltrate 3-D barriers of interstitial collagen, including the arterial wall. Furthermore, genetic deletion of the proteinase affords mice with a protected status against neointimal hyperplasia and lumen narrowing in vivo. These studies suggest that therapeutic interventions designed to target MT1-MMP could prove beneficial in a range of human vascular disease states associated with the destructive remodeling of the vessel wall extracellular matrix

    Prognostic value of the 6-gene OncoMasTR test in hormone receptor–positive HER2-negative early-stage breast cancer: Comparative analysis with standard clinicopathological factors

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    Aim: The aim of the study was to assess the prognostic performance of a 6-gene molecular score (OncoMasTR Molecular Score [OMm]) and a composite risk score (OncoMasTR Risk Score [OM]) and to conduct a within-patient comparison against four routinely used molecular and clinicopathological risk assessment tools: Oncotype DX Recurrence Score, Ki67, Nottingham Prognostic Index and Clinical Risk Category, based on the modified Adjuvant! Online definition and three risk factors: patient age, tumour size and grade. Methods: Biospecimens and clinicopathological information for 404 Irish women also previously enrolled in the Trial Assigning Individualized Options for Treatment [Rx] were provided by 11 participating hospitals, as the primary objective of an independent translational study. Gene expression measured via RT-qPCR was used to calculate OMm and OM. The prognostic value for distant recurrence-free survival (DRFS) and invasive disease-free survival (IDFS) was assessed using Cox proportional hazards models and Kaplan-Meier analysis. All statistical tests were two-sided ones. Results: OMm and OM (both with likelihood ratio statistic [LRS] P Discussion: Both OncoMasTR scores were significantly prognostic for DRFS and IDFS and provided additional prognostic information to the molecular and clinicopathological risk factors/tools assessed. OM was also the most accurate risk classification tool for identifying DR. A concise 6-gene signature with superior risk stratification was shown to increase prognosis reliability, which may help clinicians optimise treatment decisions. Trial registration: ClinicalTrials.gov NCT02050750 NCT00310180.</p

    Rapid SNP Discovery and Genetic Mapping Using Sequenced RAD Markers

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    Single nucleotide polymorphism (SNP) discovery and genotyping are essential to genetic mapping. There remains a need for a simple, inexpensive platform that allows high-density SNP discovery and genotyping in large populations. Here we describe the sequencing of restriction-site associated DNA (RAD) tags, which identified more than 13,000 SNPs, and mapped three traits in two model organisms, using less than half the capacity of one Illumina sequencing run. We demonstrated that different marker densities can be attained by choice of restriction enzyme. Furthermore, we developed a barcoding system for sample multiplexing and fine mapped the genetic basis of lateral plate armor loss in threespine stickleback by identifying recombinant breakpoints in F2 individuals. Barcoding also facilitated mapping of a second trait, a reduction of pelvic structure, by in silico re-sorting of individuals. To further demonstrate the ease of the RAD sequencing approach we identified polymorphic markers and mapped an induced mutation in Neurospora crassa. Sequencing of RAD markers is an integrated platform for SNP discovery and genotyping. This approach should be widely applicable to genetic mapping in a variety of organisms

    Nitrogen but not phosphorus addition affects symbiotic N2 fixation by legumes in natural and semi‑natural grasslands located on four continents

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    The amount of nitrogen (N) derived from symbiotic N2 fixation by legumes in grasslands might be affected by anthropogenic N and phosphorus (P) inputs, but the underlying mechanisms are not known. Methods We evaluated symbiotic N2 fixation in 17 natural and semi-natural grasslands on four continents that are subjected to the same full-factorial N and P addition experiment, using the 15N natural abundance method. Results N as well as combined N and P (NP) addition reduced aboveground legume biomass by 65% and 45%, respectively, compared to the control, whereas P addition had no significant impact. Addition of N and/or P had no significant effect on the symbiotic N2 fixation per unit legume biomass. In consequence, the amount of N fixed annually per grassland area was less than half in the N addition treatments compared to control and P addition, irrespective of whether the dominant legumes were annuals or perennials. Conclusion Our results reveal that N addition mainly impacts symbiotic N2 fixation via reduced biomass of legumes rather than changes in N2 fixation per unit legume biomass. The results show that soil N enrichment by anthropogenic activities significantly reduces N 2 fixation in grasslands, and these effects cannot be reversed by additional P amendment.EEA Santa CruzFil: Vázquez, Eduardo. University of Bayreuth. Department of Soil Ecology. Bayreuth Center of Ecology and Environmental Research (BayCEER); AlemaniaFil: Vázquez, Eduardo. Swedish University of Agricultural Sciences. Department of Soil and Environment; SueciaFil: Schleuss, Per‑Marten. University of Bayreuth. Department of Soil Ecology. Bayreuth Center of Ecology and Environmental Research (BayCEER); AlemaniaFil: Borer, Elizabeth T. University of Minnesota. Department of Ecology, Evolution, and Behavior; Estados UnidosFil: Bugalho, Miguel N. University of Lisbon. Centre for Applied Ecology “Prof. Baeta Neves” (CEABN-InBIO). School of Agriculture; Portugal.Fil: Caldeira, Maria. C. University of Lisbon. Forest Research Centre. School of Agriculture; Portugal.Fil: Eisenhauer, Nico. German Centre for Integrative Biodiversity Research; AlemaniaFil: Eisenhauer, Nico. Leipzig University. Institute of Biology; AlemaniaFil: Eskelinen, Anu. German Centre for Integrative Biodiversity Research; AlemaniaFil: Eskelinen, Anu. Physiological Diversity, Helmholtz Centrefor Environmental Research; AlemaniaFil: Eskelinen, Anu. University of Oulu. Ecology & Genetics; FinlandiaFil: Fay, Philip A. Grassland Soil and Water Research Laboratory (USDA-ARS); Estados UnidosFil: Haider, Sylvia. German Centre for Integrative Biodiversity Research; AlemaniaFil: Haider, Sylvia. Martin Luther University. Institute of Biology. Geobotany and Botanical Garden; AlemaniaFil: Jentsch, Anke. University of Bayreuth. Department of Soil Ecology. Bayreuth Center of Ecology and Environmental Research (BayCEER); AlemaniaFil: Kirkman, Kevin P. University of KwaZulu-Natal. School of Life Sciences; SudáfricaFil: McCulley, Rebecca L. University of Kentucky. Department of Plant and Soil Sciences; Estados UnidosFil: Peri, Pablo Luis. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Santa Cruz; Argentina.Fil: Peri, Pablo Luis. Universidad Nacional de la Patagonia Austral; Argentina.Fil: Peri, Pablo Luis. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Price, Jodi. Charles Sturt University. Institute for Land, Water and Society; Australia.Fil: Richards, Anna E. CSIRO Land and Water. Northern Territory; Australia.Fil: Risch, Anita C. Swiss Federal Institute for Forest, Snow and Landscape Research WSL; SuizaFil: Roscher, Christiane. German Centre for Integrative Biodiversity Research; AlemaniaFil: Roscher, Christiane. Physiological Diversity, Helmholtz Centre for Environmental Research; AlemaniaFil: Schütz, Martin. Swiss Federal Institute for Forest, Snow and Landscape Research WSL; SuizaFil: Seabloom, Eric William. University of Minnesota. Dept. of Ecology, Evolution, and Behavior; Estados UnidosFil: Standish, Rachel J. Murdoch University. Harry Butler Institute; Australia.Fil: Stevens, Carly J. Lancaster University. Lancaster Environment Centre; Reino UnidoFil: Tedder, Michelle J. University of KwaZulu-Natal. School of Life Sciences; SudáfricaFil: Virtanen, Risto. University of Oulu. Ecology & Genetics; Finlandia.Fil: Spohn, Marie. University of Bayreuth. Department of Soil Ecology. Bayreuth Center of Ecology and Environmental Research (BayCEER); AlemaniaFil: Spohn, Marie. Swedish University of Agricultural Sciences. Department of Soil and Environment; Sueci
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