35 research outputs found

    Optimization of thermal insulation thickness pertaining to embodied and operational GHG emissions in cold climates – Future and present cases

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    Determining the optimal insulation thickness is useful for designing zero-emission buildings (ZEB) to minimize the environmental impacts. The energy required to heat buildings in cold climates is relatively high. Substantial reductions in the total energy usage of a building can be achieved by reducing the U-value of the external surfaces. Increasing the insulation thickness reduces the operational CO2 emissions, although simultaneously increases the embodied CO2 emissions from materials. To mitigate climate change, Norway and Denmark are trending towards stricter regulations to limit energy use in buildings. However, these countries have no current regulations in the building codes for limit embodied CO2 emissions from materials. This study analyzes the influence of the energy emission factor and future climate change (scenarios?) on the optimal insulation thickness. We used three independent models for case studies in Greenland and Norway. The differences between the case studies highlight the influence of model parameter choices, such as indoor climate, energy emission factor and material emissions, whereas the similarities may be used to analyze the problem from a broader perspective. The results show that optimal insulation thickness calculations are most valuable for case studies in which the energy emission factor is low. Considering energy emission factors above 25–30 g CO2eq/kWh, operational emissions dominated the calculation results in all case studies.publishedVersio

    Simvastatin effects on skeletal muscle:relation to decreased mitochondrial function and glucose intolerance

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    ObjectivesGlucose tolerance and skeletal muscle coenzyme Q10 (Q10) content, mitochondrial density, and mitochondrial oxidative phosphorylation (OXPHOS) capacity were measured in simvastatin-treated patients (n = 10) and in well-matched control subjects (n = 9).BackgroundA prevalent side effect of statin therapy is muscle pain, and yet the basic mechanism behind it remains unknown. We hypothesize that a statin-induced reduction in muscle Q10 may attenuate mitochondrial OXPHOS capacity, which may be an underlying mechanism.MethodsPlasma glucose and insulin concentrations were measured during an oral glucose tolerance test. Mitochondrial OXPHOS capacity was measured in permeabilized muscle fibers by high-resolution respirometry in a cross-sectional design. Mitochondrial content (estimated by citrate synthase [CS] activity, cardiolipin content, and voltage-dependent anion channel [VDAC] content) as well as Q10 content was determined.ResultsSimvastatin-treated patients had an impaired glucose tolerance and displayed a decreased insulin sensitivity index. Regarding mitochondrial studies, Q10 content was reduced (p = 0.05), whereas mitochondrial content was similar between the groups. OXPHOS capacity was comparable between groups when complex I– and complex II–linked substrates were used alone, but when complex I + II–linked substrates were used (eliciting convergent electron input into the Q intersection [maximal ex vivo OXPHOS capacity]), a decreased (p < 0.01) capacity was observed in the patients compared with the control subjects.ConclusionsThese simvastatin-treated patients were glucose intolerant. A decreased Q10 content was accompanied by a decreased maximal OXPHOS capacity in the simvastatin-treated patients. It is plausible that this finding partly explains the muscle pain and exercise intolerance that many patients experience with their statin treatment
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