Efforts to mitigate the impacts of climate change will require deep reductions in anthropogenic CO2 emissions on the scale of gigatonnes per year. CO2 capture and utilization and/or storage technologies are a class of approaches that can substantially reduce CO2 emissions. Even though examples of this approach, such as CO2-enhanced oil recovery, are already being practiced on a scale >0.05 Gt/year, little attention has been focused on the supply of CO2 for these projects. Here, facility-scale data newly collected by the U.S. Environmental Protection Agency was processed to produce the first comprehensive map of CO2 sources from industrial sectors currently supplying CO2 in the United States. Collectively these sources produce 0.16 Gt/year, but the data reveal the presence of large areas without access to CO2 at an industrially relevant scale (>25 kt/year). Even though some facilities with the capability to capture CO2 are not doing so and in some regions pipeline networks are being built to link CO2 sources and sinks, much of the country exists in "CO2 deserts". A life cycle analysis of the sources reveals that the predominant source of CO2, dedicated wells, has the largest carbon footprint further confounding prospects for rational carbon management strategies.

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Macrophages play critical roles in renal fibrosis. However, macrophages exhibit ontogenic and functional heterogeneities, and which population of macrophages contributes to renal fibrosis and the underlying mechanisms remain unclear. In this study, we genetically targeted Notch signaling by disrupting the transcription factor recombination signal binding protein-Jκ (RBP-J), to reveal its role in regulation of macrophages during the unilateral ureteral obstruction (UUO)-induced murine renal fibrosis. Myeloid-specific disruption of RBP-J attenuated renal fibrosis with reduced extracellular matrix deposition and myofibroblast activation, as well as attenuated epithelial-mesenchymal transition, likely owing to the reduced expression of TGF-β. Meanwhile, RBP-J deletion significantly hampered macrophage infiltration and activation in fibrotic kidney, although their proliferation appeared unaltered. By using macrophage clearance experiment, we found that kidney resident macrophages made negligible contribution, but bone marrow (BM)-derived macrophages played a major role in renal fibrogenesis. Further mechanistic analyses showed that Notch blockade reduced monocyte emigration from BM by down-regulating CCR2 expression. Finally, we found that myeloid-specific Notch activation aggravated renal fibrosis, which was mediated by CCR2 macrophages infiltration. In summary, our data have unveiled that myeloid-specific targeting of Notch could ameliorate renal fibrosis by regulating BM-derived macrophages recruitment and activation, providing a novel strategy for intervention of this disease.