Addressing the urban heat islands effect: A cross-country assessment of the role of green infrastructure

© 2021 by the authors. Licensee MDPI, Basel, Switzerland. The Urban Heat Islands (UHI) effect is a microclimatic phenomenon that especially affects urban areas. It is associated with significant temperature increases in the local microclimate, and may amplify heat waves. Due to their intensity, UHI causes not only thermal discomfort, but also reductions in the levels of life quality. This paper reviews the important role of green infrastructure as a means through which the intensity of UHI may be reduced, along with their negative impact on human comfort and wellbeing. Apart from a comprehensive review of the available literature, the paper reports on an analysis of case studies in a set of 14 cities in 13 countries representing various geographical regions and climate zones. The results obtained suggest that whereas UHI is a common phenomenon, green infrastructure in urban areas may under some conditions ameliorate their impacts. In addition, the study revealed that the scope and impacts of UHI are not uniform: depending on peculiarities of urban morphologies, they pose different challenges linked to the microclimate peculiar to each city. The implications of this paper are threefold. Firstly, it reiterates the complex interrelations of UHIs, heat waves and climate change. Secondly, it outlines the fact that keeping and increasing urban green resources leads to additional various benefits that may directly or indirectly reduce the impacts of UHI. Finally, the paper reiterates the need for city planners to pay more attention to possible UHI effects when initiating new building projects or when adjusting current ones

Phylogenetic Detection of Recombination with a Bayesian Prior on the Distance between Trees

Genomic regions participating in recombination events may support distinct topologies, and phylogenetic analyses should incorporate this heterogeneity. Existing phylogenetic methods for recombination detection are challenged by the enormous number of possible topologies, even for a moderate number of taxa. If, however, the detection analysis is conducted independently between each putative recombinant sequence and a set of reference parentals, potential recombinations between the recombinants are neglected. In this context, a recombination hotspot can be inferred in phylogenetic analyses if we observe several consecutive breakpoints. We developed a distance measure between unrooted topologies that closely resembles the number of recombinations. By introducing a prior distribution on these recombination distances, a Bayesian hierarchical model was devised to detect phylogenetic inconsistencies occurring due to recombinations. This model relaxes the assumption of known parental sequences, still common in HIV analysis, allowing the entire dataset to be analyzed at once. On simulated datasets with up to 16 taxa, our method correctly detected recombination breakpoints and the number of recombination events for each breakpoint. The procedure is robust to rate and transition∶transversion heterogeneities for simulations with and without recombination. This recombination distance is related to recombination hotspots. Applying this procedure to a genomic HIV-1 dataset, we found evidence for hotspots and de novo recombination

Myosin II Motor Proteins with Different Functions Determine the Fate of Lamellipodia Extension during Cell Spreading

Non-muscle cells express multiple myosin-II motor proteins myosin IIA, myosin IIB and myosin IIC transcribed from different loci in the human genome. Due to a significant homology in their sequences, these ubiquitously expressed myosin II motor proteins are believed to have overlapping cellular functions, but the mechanistic details are not elucidated. The present study uncovered a mechanism that coordinates the distinctly localized myosin IIA and myosin IIB with unexpected opposite mechanical roles in maneuvering lamellipodia extension, a critical step in the initiation of cell invasion, spreading, and migration. Myosin IIB motor protein by localizing at the front drives lamellipodia extension during cell spreading. On the other hand, myosin IIA localizes next to myosin IIB and attenuates or retracts lamellipodia extension. Myosin IIA and IIB increase cell adhesion by regulating focal contacts formation in the spreading margins and central part of the spreading cell, respectively. Spreading cells expressing both myosin IIA and myosin IIB motor proteins display an organized actin network consisting of retrograde filaments, arcs and central filaments attached to focal contacts. This organized actin network especially arcs and focal contacts formation in the spreading margins were lost in myosin IIÂ cells. Surprisingly, myosin IIB̂ cells displayed long parallel actin filaments connected to focal contacts in the spreading margins. Thus, with different roles in the regulation of the actin network and focal contacts formation, both myosin IIA and IIB determine the fate of lamellipodia extension during cell spreading