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Efforts have been made in the past to enhance building exposure models on a regional scale with increasing spatial resolutions by integrating different data sources. This work follows a similar path and focuses on the downscaling of the existing SARA exposure model that was proposed for the residential building stock of the communes of Valparaiso and Vina del Mar (Chile). Although this model allowed great progress in harmonising building classes and characterising their differential physical vulnerabilities, it is now outdated, and in any case, it is spatially aggregated over large administrative units. Hence, to more accurately consider the impact of future earthquakes on these cities, it is necessary to employ more reliable exposure models. For such a purpose, we propose updating this existing model through a Bayesian approach by integrating ancillary data that has been made increasingly available from Volunteering Geo-Information (VGI) activities. Its spatial representation is also optimised in higher resolution aggregation units that avoid the inconvenience of having incomplete building-by-building footprints. A worst-case earthquake scenario is presented to calculate direct economic losses and highlight the degree of uncertainty imposed by exposure models in comparison with other parameters used to generate the seismic ground motions within a sensitivity analysis. This example study shows the great potential of using increasingly available VGI to update worldwide building exposure models as well as its importance in scenario-based seismic risk assessment.
Epigenetic modifications are a mechanism conveying environmental information to subsequent generations via parental germ lines. Research on epigenetic responses to environmental changes in wild mammals has been widely neglected, as well as studies that compare responses to changes in different environmental factors. Here, we focused on the transmission of DNA methylation changes to naive male offspring after paternal exposure to either diet (~40% less protein) or temperature increase (10 °C increased temperature). Because both experiments focused on the liver as the main metabolic and thermoregulation organ, we were able to decipher if epigenetic changes differed in response to different environmental changes. Reduced representation bisulfite sequencing (RRBS) revealed differentially methylated regions (DMRs) in annotated genomic regions in sons sired before (control) and after the fathers’ treatments. We detected both a highly specific epigenetic response dependent on the environmental factor that had changed that was reflected in genes involved in specific metabolic pathways, and a more general response to changes in outer stimuli reflected by epigenetic modifications in a small subset of genes shared between both responses. Our results indicated that fathers prepared their offspring for specific environmental changes by paternally inherited epigenetic modifications, suggesting a strong paternal contribution to adaptive processes.
Epigenetic modifications, of which DNA methylation is the most stable, are a mechanism conveying environmental information to subsequent generations via parental germ lines. The paternal contribution to adaptive processes in the offspring might be crucial, but has been widely neglected in comparison to the maternal one. To address the paternal impact on the offspring’s adaptability to changes in diet composition, we investigated if low protein diet (LPD) in F0 males caused epigenetic alterations in their subsequently sired sons. We therefore fed F0 male Wild guinea pigs with a diet lowered in protein content (LPD) and investigated DNA methylation in sons sired before and after their father’s LPD treatment in both, liver and testis tissues. Our results point to a ‘heritable epigenetic response’ of the sons to the fathers’ dietary change. Because we detected methylation changes also in the testis tissue, they are likely to be transmitted to the F2 generation. Gene-network analyses of differentially methylated genes in liver identified main metabolic pathways indicating a metabolic reprogramming (‘metabolic shift’). Epigenetic mechanisms, allowing an immediate and inherited adaptation may thus be important for the survival of species in the context of a persistently changing environment, such as climate change.
Climate change is expected to exacerbate the current threats to freshwater ecosystems, yet multifaceted studies on the potential impacts of climate change on freshwater biodiversity at scales that inform management planning are lacking. The aim of this study was to fill this void through the development of a novel framework for assessing climate change vulnerability tailored to freshwater ecosystems. The three dimensions of climate change vulnerability are as follows: (i) exposure to climate change, (ii) sensitivity to altered environmental conditions and (iii) resilience potential. Our vulnerability framework includes 1685 freshwater species of plants, fishes, molluscs, odonates, amphibians, crayfish and turtles alongside key features within and between catchments, such as topography and connectivity. Several methodologies were used to combine these dimensions across a variety of future climate change models and scenarios. The resulting indices were overlaid to assess the vulnerability of European freshwater ecosystems at the catchment scale (18 783 catchments). The Balkan Lakes Ohrid and Prespa and Mediterranean islands emerge as most vulnerable to climate change. For the 2030s, we showed a consensus among the applied methods whereby up to 573 lake and river catchments are highly vulnerable to climate change. The anthropogenic disruption of hydrological habitat connectivity by dams is the major factor reducing climate change resilience. A gap analysis demonstrated that the current European protected area network covers <25% of the most vulnerable catchments. Practical steps need to be taken to ensure the persistence of freshwater biodiversity under climate change. Priority should be placed on enhancing stakeholder cooperation at the major basin scale towards preventing further degradation of freshwater ecosystems and maintaining connectivity among catchments. The catchments identified as most vulnerable to climate change provide preliminary targets for development of climate change conservation management and mitigation strategies.
Flood risk analyses are often estimated assuming the same flood intensity along the river reach under study, i.e. discharges are calculated for a number of return periods T, e.g. 10 or 100 years, at several streamflow gauges. T-year discharges are regionalised and then transferred into T-year water levels, inundated areas and impacts. This approach assumes that (1) flood scenarios are homogeneous throughout a river basin, and (2) the T-year damage corresponds to the T-year discharge. Using a reach at the river Rhine, this homogeneous approach is compared with an approach that is based on four flood types with different spatial discharge patterns. For each type, a regression model was created and used in a Monte-Carlo framework to derive heterogeneous scenarios. Per scenario, four cumulative impact indicators were calculated: (1) the total inundated area, (2) the exposed settlement and industrial areas, (3) the exposed population and 4) the potential building loss. Their frequency curves were used to establish a ranking of eight past flood events according to their severity. The investigation revealed that the two assumptions of the homogeneous approach do not hold. It tends to overestimate event probabilities in large areas. Therefore, the generation of heterogeneous scenarios should receive more attention.
The toxicologically most relevant mercury (Hg) species for human exposure is methylmercury (MeHg). Thiomersal is a common preservative used in some vaccine formulations. The aim of this study is to get further mechanistic insight into the yet not fully understood neurotoxic modes of action of organic Hg species. Mercury species investigated include MeHgCl and thiomersal. Additionally HgCl2 was studied, since in the brain mercuric Hg can be formed by dealkylation of the organic species. As a cellular system astrocytes were used. In vivo astrocytes provide the environment necessary for neuronal function. In the present study, cytotoxic effects of the respective mercuricals increased with rising alkylation level and correlated with their cellular bioavailability. Further experiments revealed for all species at subcytotoxic concentrations no induction of DNA strand breaks, whereas all species massively increased H2O2-induced DNA strand breaks. This co-genotoxic effect is likely due to a disturbance of the cellular DNA damage response. Thus, at nanomolar, sub-cytotoxic concentrations, all three mercury species strongly disturbed poly(ADP-ribosyl)ation, a signalling reaction induced by DNA strand breaks. Interestingly, the molecular mechanism behind this inhibition seems to be different for the species. Since chronic PARP-1 inhibition is also discussed to sacrifice neurogenesis and learning abilities, further experiments on neurons and in vivo studies could be helpful to clarify whether the inhibition of poly(ADP-ribosyl)ation contributes to organic Hg induced neurotoxicity.