984 resultados para High Altitude Pollution Program (U.S.)
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The European Union (EU) was the frontrunner for the establishment of the world’s first multinational emissions trading scheme (ETS). Committed to combating climate change, the EU sought to overcome the multilateral paralysis within the International Civil Aviation Organization (ICAO) to mitigate aviation emissions. Unsuccessful in pushing for a global market-based measure (MBM) within the organisation, the EU was ready for take-off to include the sector in the EU emissions trading system (EU ETS). The geographical scope, however, including all flights from and to Europe in their entire trajectory, caused frictions with the international community about sovereignty issues. Ultimately, Climate Commissioner Connie Hedegaard announced a ‘stop-the-clock’ for international flights, a temporary derogation until the 2013 ICAO Assembly in order to find a global agreement. The ’stop-the-clock’ initiative provides ample opportunity to analyse EU leadership in curbing aviation emissions based on an analytical framework specifying different types of leadership. Its shows the global challenge to the EU’s claim of structural leadership on various levels in and beyond ICAO. The paper aims to analyse to what extent the EU is a global leader in mitigating aviation emissions and to identify the kind of EU leadership according to a threefold analytical framework. In addition, it will factor in the 'stop-the-clock' initiative and to what extent it altered the perception of EU leadership in the field. The paper comes to the conclusion that EU leadership in mitigating aviation emissions is not stalling. On the contrary, the EU, by pursuing the extension of the EU ETS, has put aviation emissions on everybody’s radar – and thus showed idea-based leadership. Proving the scheme’s feasibility further underlined EU leadership, in the form of directional leadership. The 'stop-the-clock' decision, however, already indicated what was later on confirmed in the 38th ICAO Assembly: Unilateral structural leadership of the EU in the field of aviation emissions is not credible at the moment.
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OBJECTIVE High altitude-related hypoxia induces pulmonary vasoconstriction. In Fontan patients without a contractile subpulmonary ventricle, an increase in pulmonary artery pressure is expected to decrease circulatory output and reduce exercise capacity. This study investigates the direct effects of short-term high altitude exposure on pulmonary blood flow (PBF) and exercise capacity in Fontan patients. METHODS 16 adult Fontan patients (mean age 28±7 years, 56% female) and 14 matched controls underwent cardiopulmonary exercise testing with measurement of PBF with a gas rebreathing system at 540 m (low altitude) and at 3454 m (high altitude) within 12 weeks. RESULTS PBF at rest and at exercise was higher in controls than in Fontan patients, both at low and high altitude. PBF increased twofold in Fontan patients and 2.8-fold in the control group during submaximal exercise, with no significant difference between low and high altitude (p=0.290). A reduction in peak oxygen uptake at high compared with low altitude was observed in Fontan patients (22.8±5.1 and 20.5±3.8 mL/min/kg, p<0.001) and the control group (35.0±7.4 and 29.1±6.5 mL/min/kg, p<0.001). The reduction in exercise capacity was less pronounced in Fontan patients compared with controls (9±12% vs 17±8%, p=0.005). No major adverse clinical event was observed. CONCLUSIONS Short-term high altitude exposure has no negative impact on PBF and exercise capacity in Fontan patients when compared with controls, and was clinically well tolerated. TRIAL REGISTRATION NUMBER NCT02237274: Results.
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Mode of access: Internet.
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Sample recipes: English roast turkey, Hot water sponge cake, Mustard pickles.
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Mode of access: Internet.
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References: p. 92.
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"United States Atomic Energy Commission Contract W-7405-Eng. 36"--Cover.
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Mode of access: Internet.
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Item 1038-A, 1038-B (microfiche).
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"ART-302-AX3204-1"--P. [4] of cover.
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Red blood cells (RBCs) are key players in systemic oxygen transport. RBCs respond to in vitro hypoxia through the so-called oxygen-dependent metabolic regulation, which involves the competitive binding of deoxyhemoglobin and glycolytic enzymes to the N-terminal cytosolic domain of band 3. This mechanism promotes the accumulation of 2,3-DPG, stabilizing the deoxygenated state of hemoglobin, and cytosol acidification, triggering oxygen off-loading through the Bohr effect. Despite in vitro studies, in vivo adaptations to hypoxia have not yet been completely elucidated. Within the framework of the AltitudeOmics study, erythrocytes were collected from 21 healthy volunteers at sea level, after exposure to high altitude (5260m) for 1, 7 and 16days, and following reascent after 7days at 1525m. UHPLC-MS metabolomics results were correlated to physiological and athletic performance parameters. Immediate metabolic adaptations were noted as early as a few hours from ascending to >5000m, and maintained for 16 days at high altitude. Consistent with the mechanisms elucidated in vitro, hypoxia promoted glycolysis and deregulated the pentose phosphate pathway, as well purine catabolism, glutathione homeostasis, arginine/nitric oxide and sulphur/H2S metabolism. Metabolic adaptations were preserved one week after descent, consistently with improved physical performances in comparison to the first ascendance, suggesting a mechanism of metabolic memory.