Transportation Energy Pathways LDRD.

This report presents a system dynamics based model of the supply-demand interactions between the USlight-duty vehicle (LDV) fleet, its fuels, and the corresponding primary energy sources through the year2050. An important capability of our model is the ability to conduct parametric analyses. Others have reliedupon scenario-based analysis, where one discrete set of values is assigned to the input variables and used togenerate one possible realization of the future. While these scenarios can be illustrative of dominant trendsand tradeoffs under certain circumstances, changes in input values or assumptions can have a significantimpact on results, especially when output metrics are associated with projections far into the future. Thistype of uncertainty can be addressed by using a parametric study to examine a range of values for the inputvariables, offering a richer source of data to an analyst.The parametric analysis featured here focuses on a trade space exploration, with emphasis on factors thatinfluence the adoption rates of electric vehicles (EVs), the reduction of GHG emissions, and the reduction ofpetroleum consumption within the US LDV fleet. The underlying model emphasizes competition between13 different types of powertrains, including conventional internal combustion engine (ICE) vehicles, flex-fuel vehicles (FFVs), conventional hybrids(HEVs), plug-in hybrids (PHEVs), and battery electric vehicles(BEVs).We find that many factors contribute to the adoption rates of EVs. These include the pace of technologicaldevelopment for the electric powertrain, battery performance, as well as the efficiency improvements inconventional vehicles. Policy initiatives can also have a dramatic impact on the degree of EV adoption. Theconsumer effective payback period, in particular, can significantly increase the market penetration rates ifextended towards the vehicle lifetime.Widespread EV adoption can have noticeable impact on petroleum consumption and greenhouse gas(GHG) emission by the LDV fleet. However, EVs alone cannot drive compliance with the most aggressiveGHG emission reduction targets, even as the current electricity source mix shifts away from coal and towardsnatural gas. Since ICEs will comprise the majority of the LDV fleet for up to forty years, conventional vehicleefficiency improvements have the greatest potential for reductions in LDV GHG emissions over this time.These findings seem robust even if global oil prices rise to two to three times current projections. Thus,investment in improving the internal combustion engine might be the cheapest, lowest risk avenue towardsmeeting ambitious GHG emission and petroleum consumption reduction targets out to 2050.3 AcknowledgmentThe authors would like to thank Dr. Andrew Lutz, Dr. Benjamin Wu, Prof. Joan Ogden and Dr. ChristopherYang for their suggestions over the course of this project. This work was funded by the Laboratory DirectedResearch and Development program at Sandia National Laboratories.

Mitochondrial Genetic Background Modulates Bioenergetics and Susceptibility to Acute Cardiac Volume Overload

Dysfunctional bioenergetics has emerged as a key feature in many chronic pathologies such as diabetes and cardiovascular disease. This has led to the mitochondrial paradigm in which it has been proposed that mtDNA sequence variation contributes to disease susceptibility. In the present study we show a novel animal model of mtDNA polymorphisms, the MNX (mitochondrial–nuclear exchange) mouse, in which the mtDNA from the C3H/HeN mouse has been inserted on to the C57/BL6 nuclear background and vice versa to test this concept. Our data show a major contribution of the C57/BL6 mtDNA to the susceptibility to the pathological stress of cardiac volume overload which is independent of the nuclear background. Mitochondria harbouring the C57/BL6J mtDNA generate more ROS (reactive oxygen species) and have a higher mitochondrial membrane potential relative to those with C3H/HeN mtDNA, independent of nuclear background. We propose this is the primary mechanism associated with increased bioenergetic dysfunction in response to volume overload. In summary, these studies support the ‘mitochondrial paradigm’ for the development of disease susceptibility, and show that the mtDNA modulates cellular bioenergetics, mitochondrial ROS generation and susceptibility to cardiac stress

Developmental exposure to second-hand smoke increases adult atherogenesis and alters mitochondrial DNA copy number and deletions in apoE(-/-) mice.

Cardiovascular disease is a major cause of morbidity and mortality in the United States. While many studies have focused upon the effects of adult second-hand smoke exposure on cardiovascular disease development, disease development occurs over decades and is likely influenced by childhood exposure. The impacts of in utero versus neonatal second-hand smoke exposure on adult atherosclerotic disease development are not known. The objective of the current study was to determine the effects of in utero versus neonatal exposure to a low dose (1 mg/m(3) total suspended particulate) of second-hand smoke on adult atherosclerotic lesion development using the apolipoprotein E null mouse model. Consequently, apolipoprotein E null mice were exposed to either filtered air or second-hand smoke: (i) in utero from gestation days 1-19, or (ii) from birth until 3 weeks of age (neonatal). Subsequently, all animals were exposed to filtered air and sacrificed at 12-14 weeks of age. Oil red-O staining of whole aortas, measures of mitochondrial damage, and oxidative stress were performed. Results show that both in utero and neonatal second-hand smoke exposure significantly increased adult atherogenesis in mice compared to filtered air controls. These changes were associated with changes in aconitase and mitochondrial superoxide dismutase activities consistent with increased oxidative stress in the aorta, changes in mitochondrial DNA copy number and deletion levels. These studies show that in utero or neonatal exposure to second-hand smoke significantly influences adult atherosclerotic lesion development and results in significant alterations to the mitochondrion and its genome that may contribute to atherogenesis