Can we explain regional abundance and road‐kill patterns with variables derived from local‐scale road‐kill models? Evaluating transferability with the European polecat

Aim We evaluated the transferability of variables previously found to have a significant effect on European polecat Mustela putorius road‐kills at a local scale (i.e. 50 m around location points) when we extrapolate them to a large scale [Universal Transverse Mercator (UTM) 100 km²] in a neighbouring area. Location Andalusia, south Spain. We carried out our study in 821 of the 985 UTM 100 km² cells included in this region. Methods The units of the different variables were adapted to the new scale. We used data from the Spanish Atlas survey to obtain the abundance of the different species and GIS data for the rest of the variables. We controlled the spatial autocorrelation by incorporating spatial filters obtained with Spatial Eigenvector Mapping into multiple regression analyses. We used AIC criteria and the best subset procedure to investigate the relationship between the selected variables and species abundance, and road‐kill occurrence. Results The best subset procedure provided two models that explained 40% of variation in polecat abundance and eleven models that explained around 25% of variation in road‐kills. The main explanatory factor for polecat abundance was the abundance of other carnivores, whereas polecat abundance was the main factor for road‐kills. In both cases, rabbit abundance was the second most important explanatory variable. Main Conclusions Our findings highlight the possibility of partially explaining the abundance and road‐kill patterns at a large scale based on significant variables from local‐scale models. Mitigation measures to reduce polecat fatalities should combine actions at different scales. Routes that cross carnivore hotspots, including those of polecats, and areas with important populations of rabbits, should be avoided during road planning. When these routes are unavoidable, local‐scale mitigation measures must be implemented.     

Lessons from a kill

During their colonization by Polynesians and later by Europeans, the Hawaiian islands suffered a massive loss of species. All the extinctions are indirectly attributable to human impact. Nonetheless, it has proved extremely difficult to specify which of several possible mechanisms caused each particular extinction. This seems to admit defeat in the battle to understand past extinctions. Such understanding could guide our efforts to protect species that are now threatened with extinction. Will it be easier to understand the causes of future extinctions? Surveys of future extinctions stress habitat destruction as the simple and dominant mechanism. This contrasts to its secondary (and generally confused) role in past extinctions. I argue that this contrast between the complexity of the past and the apparent simplicity of the future arises because extinction mechanisms are inherently synergistic. Once extensive species losses begin, it may be impossible to separate the mechanisms and thus manage an individual species as if its decline had a single cause.     

A view to kill

Genome and proteome data from Hydra magnipapillata have opened the way for the molecular analysis of an ancient nervous system, which includes stinging cells, an unusual neurosensory and neurosecretory cell type. They hold some surprises for the mechanisms and evolution of sensory transduction that could not have been anticipated from what has been learned from flies and vertebrates. Research in BMC Biology now implicates the ancient opsin-mediated transduction pathway in the neuronal control of stinging cell discharge.     

Bax: Addressed to kill

The pro-apoptototic protein Bax (Bcl-2 Associated protein X) plays a central role in the mitochondria-dependent apoptotic pathway. In healthy mammalian cells, Bax is essentially cytosolic and inactive. Following a death signal, the protein is translocated to the outer mitochondrial membrane, where it promotes a permeabilization that favors the release of different apoptogenic factors, such as cytochrome c. The regulation of Bax translocation is associated to conformational changes that are under the control of different factors. The evidences showing the involvement of different Bax domains in its mitochondrial localization are presented. The interactions between Bax and its different partners are described in relation to their ability to promote (or prevent) Bax conformational changes leading to mitochondrial addressing and to the acquisition of the capacity to permeabilize the outer mitochondrial membrane.     

Does austerity really kill?

A growing body of the literature has argued that austerity has been bad for health, though without directly measuring austerity. This paper explicitly distinguishes the association of mortality with macroeconomic fluctuations from that with fiscal policy measures, using data for 28 European Union (EU) countries covering the period 1991–2013. The main results present a nuanced, complex picture about the mortality impact of fiscal policies. We confirm the mortality decreasing (increasing) effect of recessions (booms), with the exception of suicide mortality, which shows the opposite effects. Austerity regimes are associated with an increase in all-cause mortality (0.7%). At the same time, fiscal stimuli tend to significantly increase death rates due to cirrhosis or chronic liver disease (3%) and those due to vehicle accidents (4.3%). Our results are sensitive to the set of countries included: when excluding the Baltics, Romania and Hungary, austerity policies turn out to significantly increase suicide-related mortality (2.8%), while the effect on all-cause mortality remains unaffected (0.7%). Overall, however it appears that the austerity-increasing effects are mostly compensated by the (mostly) mortality-decreasing effects of recessions. A notable exception appears to be suicides, which receive a ‘double-boost’ from both recessions and austerity.