TY  - GEN
A1  - Shan, Yuli
A1  - Guan, Dabo
A1  - Hubacek, Klaus
A1  - Zheng, Bo
A1  - Davis, Steven J.
A1  - Jia, Lichao
A1  - Liu, Jianghua
A1  - Liu, Zhu
A1  - Fromer, Neil
A1  - Mi, Zhifu
A1  - Meng, Jing
A1  - Deng, Xiangzheng
A1  - Li, Yuan
A1  - Lin, Jintai
A1  - Schroeder, Heike
A1  - Weisz, Helga
A1  - Schellnhuber, Hans Joachim
T1  - City-level climate change mitigation in China
T2  - Postprints der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe
N2  - As national efforts to reduce CO2 emissions intensify, policy-makers need increasingly specific, subnational information about the sources of CO2 and the potential reductions and economic implications of different possible policies. This is particularly true in China, a large and economically diverse country that has rapidly industrialized and urbanized and that has pledged under the Paris Agreement that its emissions will peak by 2030. We present new, city level estimates of CO2 emissions for 182 Chinese cities, decomposed into 17 different fossil fuels, 46 socioeconomic sectors, and 7 industrial processes. We find that more affluent cities have systematically lower emissions per unit of gross domestic product (GDP), supported by imports from less affluent, industrial cities located nearby. In turn, clusters of industrial cities are supported by nearby centers of coal or oil extraction. Whereas policies directly targeting manufacturing and electric power infrastructure would drastically undermine the GDP of industrial cities, consumption based policies might allow emission reductions to be subsidized by those with greater ability to pay. In particular, sector based analysis of each city suggests that technological improvements could be a practical and effective means of reducing emissions while maintaining growth and the current economic structure and energy system. We explore city-level emission reductions under three scenarios of technological progress to show that substantial reductions (up to 31%) are possible by updating a disproportionately small fraction of existing infrastructure.
T3  - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 1096 
KW  - carbon-dioxide emissions
KW  - fired power plants
KW  - co2 emissions
KW  - energy use
KW  - cluster analysis
KW  - uncertainties
KW  - urbanization
KW  - methodology
KW  - combustion
KW  - inventory
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-471541
SN  - 1866-8372
IS  - 1096
ER  - 
TY  - JOUR
A1  - Renz, Marc
A1  - Otten, Cecile
A1  - Faurobert, Eva
A1  - Rudolph, Franziska
A1  - Zhu, Yuan
A1  - Boulday, Gwenola
A1  - Duchene, Johan
A1  - Mickoleit, Michaela
A1  - Dietrich, Ann-Christin
A1  - Ramspacher, Caroline
A1  - Steed, Emily
A1  - Manet-Dupe, Sandra
A1  - Benz, Alexander
A1  - Hassel, David
A1  - Vermot, Julien
A1  - Huisken, Jan
A1  - Tournier-Lasserve, Elisabeth
A1  - Felbor, Ute
A1  - Sure, Ulrich
A1  - Albiges-Rizo, Corinne
A1  - Abdelilah-Seyfried, Salim
T1  - Regulation of beta 1 Integrin-Klf2-Mediated angiogenesis by CCM proteins
JF  - Developmental cell
N2  - Mechanotransduction pathways are activated in response to biophysical stimuli during the development or homeostasis of organs and tissues. In zebrafish, the blood-flow-sensitive transcription factor Klf2a promotes VEGF-dependent angiogenesis. However, the means by which the Klf2a mechanotransduction pathway is regulated to prevent continuous angiogenesis remain unknown. Here we report that the upregulation of klf2 mRNA causes enhanced egfl7 expression and angiogenesis signaling, which underlies cardiovascular defects associated with the loss of cerebral cavernous malformation (CCM) proteins in the zebrafish embryo. Using CCM-protein-depleted human umbilical vein endothelial cells, we show that the misexpression of KLF2 mRNA requires the extracellular matrix-binding receptor beta 1 integrin and occurs in the absence of blood flow. Downregulation of beta 1 integrin rescues ccm mutant cardiovascular malformations in zebrafish. Our work reveals a beta 1 integrin-Klf2-Egfl7-signaling pathway that is tightly regulated by CCM proteins. This regulation prevents angiogenic overgrowth and ensures the quiescence of endothelial cells.
Y1  - 2015
U6  - https://doi.org/10.1016/j.devcel.2014.12.016
SN  - 1534-5807
SN  - 1878-1551
VL  - 32
IS  - 2
SP  - 181
EP  - 190
PB  - Cell Press
CY  - Cambridge
ER  -