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As workforces become increasingly mobile with laptops, smartphones and other handheld devices, the potential for vulnerability increases massively.
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This potential for higher vulnerability is discussed due to their higher lifetime exposure (they start mobile phone use at an earlier age and use mobile phones more frequently than today's adults), their still developing nervous system and a greater conductivity of their brain tissue [ 8- 10].
Despite the prevalence of exaggerated advertised reference prices (ARPs) in retail ads and the potential for consumer vulnerability to false reference prices, research identifying boundary conditions to the effectiveness of exaggerated ARPs is scarce.
Our findings also highlight the potential for differential vulnerability of tropical tree species to the deleterious consequences of forest fragmentation.
First, our results highlight the potential for differential vulnerability of species to inbreeding, genetic drift and pollen limitation as a result of habitat fragmentation [15], [59], [60].
Possibilities include potential for plaque vulnerability, arrhythmogenesis, rapid occlusive thrombosis, mediation or repair of vessel walls, and regulation of signaling between the vascular endothelium and circulating blood cells.
We have also demonstrated the therapeutic potential of anti-IL-1 approaches for treating acute injury to the brain [ 7– 9]; however, a limitation of such an approach is the potential for increasing vulnerability to infection through systemic suppression of innate immunity.
By adding connectivity to devices, we greatly expand the potential for security vulnerabilities— with more connectivity comes more security problems.
Not only are many settlements built on risk-prone land, but settlements and dwellings are frequently poorly designed and constructed, suggesting the potential for continued exposure and vulnerability to floods and other hazards.
The end of a long unbeaten run brings perspective, but it also holds the potential for previously unseen vulnerability.
The epigenetic mechanisms involved in the dynamics of female stress responses across the lifespan along with the potential for prenatal male vulnerability warrant further investigation.
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