Taking Stock of Built Environment Stock Studies: Progress and Prospects.

Built environment stocks (buildings and infrastructures) play multiple roles in our socio-economic metabolism: they serve as the backbone of modern societies and human well-being, drive the material cycles throughout the economy, entail temporal and spatial lock-ins on energy use and emissions, and represent an extensive reservoir of secondary materials. This review aims at providing a comprehensive and critical review of the state of the art, progress, and prospects of built environment stocks research which has boomed in the past decades. We included 249 publications published from 1985 to 2018, conducted a bibliometric analysis, and assessed the studies by key characteristics including typology of stocks (status of stock and end-use category), type of measurement (object and unit), spatial boundary and level of resolution, and temporal scope. We also highlighted the strengths and weaknesses of different estimation approaches. A comparability analysis of existing studies shows a clearly higher level of stocks per capita and per area in developed countries and cities, confirming the role of urbanization and industrialization in built environment stock growth. However, more spatially refined case studies (e.g., on developing cities and nonresidential buildings) and standardization and improvement of methodology (e.g., with geographic information system and architectural knowledge) and data (e.g., on material intensity and lifetime) would be urgently needed to reveal more robust conclusions on the patterns, drivers, and implications of built environment stocks. Such advanced knowledge on built environment stocks could foster societal and policy agendas such as urban sustainability, circular economy, climate change, and United Nations 2030 Sustainable Development Goals.

Intravenous adenosine protects the myocardium primarily by activation of a neurogenic pathway.

Endogenous adenosine is a trigger for ischemic myocardial preconditioning (IPC). Although intravascular administration of adenosine has been used to further unravel the mechanism of protection by IPC, it is questionable whether adenosine and IPC employ the same signaling pathways to exert cardioprotection. We therefore investigated whether the active metabolic barrier of the endothelium prevents an increase in myocardial interstitial adenosine concentrations by intravenous adenosine, using microdialysis, and also the role of NO and activation of a neurogenic pathway in the cardioprotection by adenosine. In pentobarbital-anesthetized rats, area at risk and infarct size (IS) were determined 120 min after a 60-min coronary artery occlusion (CAO), using trypan blue and nitro-blue-tetrazolium staining, respectively. IPC with a single 15-min CAO and a 15-min adenosine infusion (ADO, 200 microg min(-1) i.v.) limited IS to the same extent (IS = 41 +/- 6% and IS = 40 +/- 4%, respectively) compared to control rats (IS = 63 +/- 3%, both P < 0.05). However, IPC increased myocardial interstitial adenosine levels seven-fold from 4.3 +/- 0.7 to 27.1 +/- 10.0 microM (P < 0.05), while ADO had no effect on interstitial adenosine (4.1 +/- 1.2 microM), or any of the other purines. The NO synthase inhibitor N(omega)-nitro-L-arginine (LNNA), which did not affect IS (IS = 62 +/- 3%), attenuated the protection by ADO (IS = 56 +/- 3%; P < 0.05 vs ADO, P = NS vs LNNA). The ganglion blocker hexamethonium, which had also no effect on IS (IS = 66 +/- 3%), blunted the protection by ADO (IS = 55 +/- 4%; P < 0.05 vs ADO and vs hexamethonium). These observations demonstrate that cardioprotection by ADO is dependent on NO, and is primarily mediated by activation of a neurogenic pathway.