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- Creators: Department of Physics
- Member of: Programs and Communities
Warming associated with urban development will be exacerbated in future years by temperature increases due to climate change. The strategic implementation of urban green infrastructure (UGI) e.g. street trees, parks, green roofs and facades can help achieve temperature reductions in urban areas while delivering diverse additional benefits such as pollution reduction and biodiversity habitat. Although the greatest thermal benefits of UGI are achieved in climates with hot, dry summers, there is comparatively little information available for land managers to determine an appropriate strategy for UGI implementation under these climatic conditions. We present a framework for prioritisation and selection of UGI for cooling. The framework is supported by a review of the scientific literature examining the relationships between urban geometry, UGI and temperature mitigation which we used to develop guidelines for UGI implementation that maximises urban surface temperature cooling. We focus particularly on quantifying the cooling benefits of four types of UGI: green open spaces (primarily public parks), shade trees, green roofs, and vertical greening systems (green walls and facades) and demonstrate how the framework can be applied using a case study from Melbourne, Australia.
Cancer is sometimes depicted as a reversion to single cell behavior in cells adapted to live in a multicellular assembly. If this is the case, one would expect that mutation in cancer disrupts functional mechanisms that suppress cell-level traits detrimental to multicellularity. Such mechanisms should have evolved with or after the emergence of multicellularity. This leads to two related, but distinct hypotheses: 1) Somatic mutations in cancer will occur in genes that are younger than the emergence of multicellularity (1000 million years [MY]); and 2) genes that are frequently mutated in cancer and whose mutations are functionally important for the emergence of the cancer phenotype evolved within the past 1000 million years, and thus would exhibit an age distribution that is skewed to younger genes. In order to investigate these hypotheses we estimated the evolutionary ages of all human genes and then studied the probability of mutation and their biological function in relation to their age and genomic location for both normal germline and cancer contexts.
We observed that under a model of uniform random mutation across the genome, controlled for gene size, genes less than 500 MY were more frequently mutated in both cases. Paradoxically, causal genes, defined in the COSMIC Cancer Gene Census, were depleted in this age group. When we used functional enrichment analysis to explain this unexpected result we discovered that COSMIC genes with recessive disease phenotypes were enriched for DNA repair and cell cycle control. The non-mutated genes in these pathways are orthologous to those underlying stress-induced mutation in bacteria, which results in the clustering of single nucleotide variations. COSMIC genes were less common in regions where the probability of observing mutational clusters is high, although they are approximately 2-fold more likely to harbor mutational clusters compared to other human genes. Our results suggest this ancient mutational response to stress that evolved among prokaryotes was co-opted to maintain diversity in the germline and immune system, while the original phenotype is restored in cancer. Reversion to a stress-induced mutational response is a hallmark of cancer that allows for effectively searching “protected” genome space where genes causally implicated in cancer are located and underlies the high adaptive potential and concomitant therapeutic resistance that is characteristic of cancer.