Cities’ role in mitigating United States food system greenhouse gas emissions

Current trends of urbanization, population growth, and economic development have made cities a focal point for mitigating global greenhouse gas (GHG) emissions. The substantial contribution of food consumption to climate change necessitates urban action to reduce the carbon intensity of the food system. While food system GHG mitigation strategies often focus on production, we argue that urban influence dominates this sector’s emissions and that consumers in cities must be the primary drivers of mitigation. We quantify life cycle GHG emissions of the United States food system through data collected from literature and government sources producing an estimated total of 3800 kg CO2e/capita in 2010, with cities directly influencing approximately two-thirds of food sector GHG emissions. We then assess the potential for cities to reduce emissions through selected measures; examples include up-scaling urban agriculture and home delivery of grocery options, which each may achieve emissions reductions on the order of 0.4 and ∼1% of this total, respectively. Meanwhile, changes in waste management practices and reduction of postdistribution food waste by 50% reduce total food sector emissions by 5 and 11%, respectively. Consideration of the scale of benefits achievable through policy goals can enable cities to formulate strategies that will assist in achieving deep long-term GHG emissions targets

Studies on the lifespan extension by low levels of reactive oxygen species in C. elegans

MasterFor the last two decades, many molecules and pathways that regulate life span in various organisms have been identified. Among these, reduced mitochondrial respiration has been shown to extend the lifespan of various species including C. elegans, Drosophila and mice. Although several recent studies identified genes that are required for this lifespan extension, underlying molecular mechanism are still poorly understood. Our group previously proposed that the inhibition of the respiration lengthens the lifespan of C. elegans through increasing the level of reactive oxygen species (ROS). We showed that the elevated ROS stabilize hypoxia inducible factor (HIF-1), a longevity-promoting transcription factor required for the responses to low oxygen conditions. Our findings challenged the oxidative stress theory of aging that reactive oxygen species (ROS) are byproducts of mitochondrial respiration and main determinants of aging through damaging molecules such as - DNA, proteins and lipids. In this thesis, I focused on further elucidation of the molecular mechanisms by which ROS promote the long lifespan of C. elegans. First, since dietary restriction is a well known evolutionarily conserved longevity mechanism, therefore I examined whether ROS treatment mimicked dietary restriction by reducing the feeding of C. elegans and found that it did not. Second, I tested whether the ROS treatment increased lifespan by enhancing innate immune response and found that it did not. I examined which longevity genes are required for the ROS- induced lifespan extension by using mutations in hsf-1/heat shock factor 1, aak-2/AMP kinase, and sir-2.1/sirtuin. I found that aak-2 is required for this lifespan extension similar to hif-1. Since mice with reduced respiration mutation live long as well as C. elegans, it will be important to examine how inhibition of mitochondrial respiration increases lifespan and I believe my study will shed light on elucidating the molecular mechanisms