While many studies suggest evidence for the health benefits of nature, there is currently no standardized method to measure time spent in nature or nature contact, nor agreement on how best to define nature contact in research. The purpose of this review is to summarize how nature contact has been measured in recent health research and provide insight into current metrics of exposure to nature at individual and population scales. The most common methods include surrounding greenness, questionnaires, and global positioning systems (GPS) tracking. Several national-level surveys exist, though these are limited by their cross-sectional design, often measuring only a single component of time spent in nature, and poor links to measures of health. In future research, exposure assessment combining the quantifying (e.g., time spent in nature and frequency of visits to nature) and qualifying (e.g., greenness by the normalized difference of vegetation index (NDVI) and ratings on perception by individuals) aspects of current methods and leveraging innovative methods (e.g., experience sampling methods, ecological momentary assessment) will provide a more comprehensive understanding of the health effects of nature exposure and inform health policy and urban planning.

Ruthenium complexes are often investigated as potential replacements for platinum-based chemotherapeutics in hopes of identifying systems with improved tolerability in vivo and reduced susceptibility to cellular resistance mechanisms. Inspired by phenanthriplatin, a non-traditional platinum agent that contains only one labile ligand, monofunctional ruthenium polypyridyl agents have been developed, but until now, few demonstrated promising anticancer activity. Here we introduce a potent new scaffold, based on [Ru(tpy)(dip)Cl]Cl (tpy = 2,2':6',2''-terpyridine and dip = 4,7-diphenyl-1,10-phenanthroline) in pursuit of effective Ru(ii)-based monofunctional agents. Notably, the extension of the terpyridine at the 4' position with an aromatic ring resulted in a molecule that was cytotoxic in several cancer cell lines with sub-micromolar IC₅₀ values, induced ribosome biogenesis stress, and exhibited minimal zebrafish embryo toxicity. This study demonstrates the successful design of a Ru(ii) agent that mimics many of the biological effects and phenotypes seen with phenanthriplatin, despite numerous differences in both the ligands and metal center structure.

Organ-specific functions of tissue-resident macrophages in the steady-state heart are unknown. Here, we show that cardiac macrophages facilitate electrical conduction through the distal atrioventricular node, where conducting cells densely intersperse with elongated macrophages expressing connexin 43. When coupled to spontaneously beating cardiomyocytes via connexin-43-containing gap junctions, cardiac macrophages have a negative resting membrane potential and depolarize in synchrony with cardiomyocytes. Conversely, macrophages render the resting membrane potential of cardiomyocytes more positive and, according to computational modeling, accelerate their repolarization. Photostimulation of channelrhodopsin-2-expressing macrophages improves atrioventricular conduction, whereas conditional deletion of connexin 43 in macrophages and congenital lack of macrophages delay atrioventricular conduction. In the Cd11b^DTR mouse, macrophage ablation induces progressive atrioventricular block. These observations implicate macrophages in normal and aberrant cardiac conduction.