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W C E P Verberk - One of the best experts on this subject based on the ideXlab platform.
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why polar gigantism and palaeozoic gigantism are not equivalent effects of Oxygen and temperature on the body size of ectotherms
Functional Ecology, 2013Co-Authors: W C E P Verberk, David AtkinsonAbstract:Summary Organisms of gigantic proportions inhabited the world at a time of a hyperoxic prehistoric atmosphere (Palaeozoic gigantism). Extant giants are found in cold polar waters, with large quantities of dissolved Oxygen (polar gigantism). Oxygen is usually deemed central to explain such gigantism. Examples of one category of gigantism are often cited in support of the other, but novel insights into the bioavailability of Oxygen imply that they cannot be taken as equivalent manifestations of the effect of Oxygen on body size. Recently, the availability of Oxygen has been shown to be lower in cold waters, despite greater Oxygen solubility. Consequently, gigantism in cold, Oxygenated waters and gigantism in an Oxygen-pressurized world are fundamentally different: Palaeozoic gigantism likely arose because of greater Oxygen availability, while polar gigantism arises in spite of lower Oxygen availability. The traditional view of respiration focuses on meeting the challenge of extracting sufficient amounts of Oxygen, which essentially is a toxic gas. We present a broader perspective, which specifically includes risks of Oxygen Poisoning. We discuss how challenges pertaining to balancing Oxygen uptake capacity and risks of Oxygen Poisoning are very different for animals breathing either air or water. We propose a novel explanation for polar gigantism in aquatic ectotherms, arguing that their larger body size represents a respiratory advantage that helps to overcome the larger viscous forces in water. Being large helps organisms to balance the opposing risks of asphyxiation and Poisoning, especially in colder, more viscous, water. This results in a selection for larger sizes, with polar gigantism as the extreme manifestation. Hence, a larger size provides respiratory benefits to water-breathing ectotherms, but not terrestrial ectotherms. This can explain why clines in body size across temperature and latitude are stronger in aquatic ectotherms.
Martin Muhler - One of the best experts on this subject based on the ideXlab platform.
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the influence of Oxygen Poisoning on a multiply promoted iron catalyst used for ammonia synthesis a temperature programmed desorption and reaction study
Studies in Surface Science and Catalysis, 1997Co-Authors: F Rosowski, Martin MuhlerAbstract:A multiply promoted iron catalyst used for ammonia synthesis was studied in a microreactor flow system equipped with a calibrated mass spectrometer. By feeding synthesis gas with about 5 ppm of Oxygenic compound at 603 K, the effluent ammonia concentration was decreased by a factor of 4. It was possible to regenrate the catalyst at 723 K by feeding purified synthesis gas indicating reversible Poisoning. The temperature-programmed desorption of N 2 (N 2 TPD) and the temperature-programmed surface reaction (TPSR) of adsorbed atomic nitrogen with H 2 werer studied in the active and in the poisoned state. The activation energy of N 2 desorption was found to increase from 146 kJ/mol to 174 kJ/mol due to Oxygen Poisoning in good agreement with values observed for potassium-promoted and potassium-free catalysts, respectively. The TPSR experiments in the poisoned state revealed that the onset temperature of NH 3 formation was shifted by 10 K to higher temperatures, and that the peak shape resembled potassium-free catalysts. These effects indicate that Oxygen Poisoning mainly affects potassium-promoted sites thus transforming the catalyst from the promoted state with an Oxygen-deficient K+O coadsorbate layer into an essentially unpromoted state with an Oxygen-saturated K+O coadsorbate layer.
David Atkinson - One of the best experts on this subject based on the ideXlab platform.
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why polar gigantism and palaeozoic gigantism are not equivalent effects of Oxygen and temperature on the body size of ectotherms
Functional Ecology, 2013Co-Authors: W C E P Verberk, David AtkinsonAbstract:Summary Organisms of gigantic proportions inhabited the world at a time of a hyperoxic prehistoric atmosphere (Palaeozoic gigantism). Extant giants are found in cold polar waters, with large quantities of dissolved Oxygen (polar gigantism). Oxygen is usually deemed central to explain such gigantism. Examples of one category of gigantism are often cited in support of the other, but novel insights into the bioavailability of Oxygen imply that they cannot be taken as equivalent manifestations of the effect of Oxygen on body size. Recently, the availability of Oxygen has been shown to be lower in cold waters, despite greater Oxygen solubility. Consequently, gigantism in cold, Oxygenated waters and gigantism in an Oxygen-pressurized world are fundamentally different: Palaeozoic gigantism likely arose because of greater Oxygen availability, while polar gigantism arises in spite of lower Oxygen availability. The traditional view of respiration focuses on meeting the challenge of extracting sufficient amounts of Oxygen, which essentially is a toxic gas. We present a broader perspective, which specifically includes risks of Oxygen Poisoning. We discuss how challenges pertaining to balancing Oxygen uptake capacity and risks of Oxygen Poisoning are very different for animals breathing either air or water. We propose a novel explanation for polar gigantism in aquatic ectotherms, arguing that their larger body size represents a respiratory advantage that helps to overcome the larger viscous forces in water. Being large helps organisms to balance the opposing risks of asphyxiation and Poisoning, especially in colder, more viscous, water. This results in a selection for larger sizes, with polar gigantism as the extreme manifestation. Hence, a larger size provides respiratory benefits to water-breathing ectotherms, but not terrestrial ectotherms. This can explain why clines in body size across temperature and latitude are stronger in aquatic ectotherms.
P Isnard - One of the best experts on this subject based on the ideXlab platform.
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catalytic wet air oxidation of acetic acid on carbon supported ruthenium catalysts
Journal of Catalysis, 1997Co-Authors: Pierre Gallezot, Stephane Chaumet, Alain Perrard, P IsnardAbstract:Ruthenium catalysts prepared by ion exchange of active carbons and high-surface-area graphites are active for the wet air oxidation of aqueous solutions of acetic acid (5–20 g/liter). A total conversion into CO2can be achieved between 448 and 473 K using air as oxidizing agent. No leaching of ruthenium can be detected which indicates that the reaction proceeds on the heterogeneous catalysts. For the same particle size (1 nm), graphite-supported ruthenium catalysts are much more active (up to 0.4 mol h−1gRu−1at 473 K in a stirred batch reactor pressurized with air at 10 MPa) than active carbon-supported catalysts. The lower activities of the latters could be due to internal diffusion limitation since the 1-nm Ru particles are located inside the micropores. However, graphite-supported catalysts might be intrinsically more active because of an electron transfer from graphite to metal particles which would increase the resistance of ruthenium to Oxygen Poisoning. It was also shown that the activity of ruthenium is particle size dependent: the smaller the sizes, the lower the activities. This effect could be interpreted by the higher adsorption energy of Oxygen on the small particles which produces a Poisoning of the metal surface. From measurements of the reaction rates on the Ru/HSAG graphite catalyst at different temperatures, pressures, and acetic acid concentrations, it was established that the reaction orders were zero and 0.65 with respect to the concentration and Oxygen pressure, respectively; the activation energy of the reaction was 100.5 kJ mol−1. An equation describing the reaction kinetics was proposed.
Carl W. White - One of the best experts on this subject based on the ideXlab platform.
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aconitase is a sensitive and critical target of Oxygen Poisoning in cultured mammalian cells and in rat lungs
Proceedings of the National Academy of Sciences of the United States of America, 1994Co-Authors: Paul R. Gardner, Deedee H Nguyen, Carl W. WhiteAbstract:The effect of hyperoxia on activity of the superoxide-sensitive citric acid cycle enzyme aconitase was measured in cultured human epithelial-like A549 cells and in rat lungs. Rapid and progressive loss of > 80% of the aconitase activity in A549 cells was seen during a 24-hr exposure to a PO2 of 600 mmHg (1 mmHg = 133 Pa). Inhibition of mitochondrial respiratory capacity correlated with loss of aconitase activity in A549 cells exposed to hyperoxia, and this effect could be mimicked by fluoroacetate (or fluorocitrate), a metabolic poison of aconitase. Exposure of rats to an atmospheric PO2 of 760 mmHg or 635 mmHg for 24 hr caused respective 73% and 61% decreases in total lung aconitase activity. We propose that early inactivation of aconitase and inhibition of the energy-producing and biosynthetic reactions of the citric acid cycle contribute to the sequelae of lung damage and edema seen during exposure to hyperoxia.
