Constructing a holistic approach to disaster risk reduction: the significance of focusing on vulnerability reduction

As a result of the increase in natural disaster losses, policy‐makers, practitioners, and members of the research community around the world are seeking effective and efficient means of overcoming or minimising them. Although various theoretical constructs are beneficial to understanding the disaster phenomenon and the means of minimising losses, the disaster risk management process becomes less effective if theory and practice are set apart from one another. Consequently, this paper seeks to establish a relationship between two theoretical constructs, ‘disaster risk reduction (DRR)’ and ‘vulnerability reduction’, and to develop a holistic approach to DRR with particular reference to improving its applicability in practical settings. It is based on a literature review and on an overall understanding gained through two case studies of post‐disaster infrastructure reconstruction projects in Sri Lanka and three expert interviews in Sri Lanka and the United Kingdom.     

Prenatal exposure to environmental pro-oxidants induces mitochondria-mediated epigenetic changes: a cross-sectional pilot study

Mitochondria play a central role in maintaining cellular and metabolic homeostasis during vital development cycles of foetal growth. Optimal mitochondrial functions are important not only to sustain adequate energy production but also for regulated epigenetic programming. However, these organelles are subtle targets of environmental exposures, and any perturbance in the defined mitochondrial machinery during the developmental stage can lead to the re-programming of the foetal epigenetic landscape. As these modifications can be transferred to subsequent generations, we herein performed a cross-sectional study to have an in-depth understanding of this intricate phenomenon. The study was conducted with two arms: whereas the first group consisted of in utero pro-oxidant exposed individuals and the second group included controls. Our results showed higher levels of oxidative mtDNA damage and associated integrated stress response among the exposed individuals. These disturbances were found to be closely related to the observed discrepancies in mitochondrial biogenesis. The exposed group showed mtDNA hypermethylation and changes in allied mitochondrial functioning. Altered expression of mitomiRs and their respective target genes in the exposed group indicated the possibilities of a disturbed mitochondrial-nuclear cross talk. This was further confirmed by the modified activity of the mitochondrial stress regulators and pro-inflammatory mediators among the exposed group. Importantly, the disturbed DNMT functioning, hypermethylation of nuclear DNA, and higher degree of post-translational histone modifications established the existence of aberrant epigenetic modifications in the exposed individuals. Overall, our results demonstrate the first molecular insights of in utero pro-oxidant exposure associated changes in the mitochondrial-epigenetic axis. Although, our study might not cement an exposure-response relationship for any particular environmental pro-oxidant, but suffice to establish a dogma of mito-epigenetic reprogramming at intrauterine milieu with chronic illness, a hitherto unreported interaction.

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Designing a community-based insurance scheme to reduce human–wildlife conflict

Environment, Development and Sustainability - Globally, human–wildlife conflict (HWC) is a burning issue, which the conservationists have attempted to address through various conservation...