Poleward bound: adapting to climate-driven species redistribution

One of the most pronounced effects of climate change on the world’s oceans is the (generally) poleward movement of species and fishery stocks in response to increasing water temperatures. In some regions, such redistributions are already causing dramatic shifts in marine socioecological systems, profoundly altering ecosystem structure and function, challenging domestic and international fisheries, and impacting on human communities. Such effects are expected to become increasingly widespread as waters continue to warm and species ranges continue to shift. Actions taken over the coming decade (2021–2030) can help us adapt to species redistributions and minimise negative impacts on ecosystems and human communities, achieving a more sustainable future in the face of ecosystem change. We describe key drivers related to climate-driven species redistributions that are likely to have a high impact and influence on whether a sustainable future is achievable by 2030. We posit two different futures—a ‘business as usual’ future and a technically achievable and more sustainable future, aligned with the Sustainable Development Goals. We then identify concrete actions that provide a pathway towards the more sustainable 2030 and that acknowledge and include Indigenous perspectives. Achieving this sustainable future will depend on improved monitoring and detection, and on adaptive, cooperative management to proactively respond to the challenge of species redistribution. We synthesise examples of such actions as the basis of a strategic approach to tackle this global-scale challenge for the benefit of humanity and ecosystems

Transcriptional mechanisms of addiction: role of ΔFosB

Regulation of gene expression is considered a plausible mechanism of drug addiction, given the stability of behavioural abnormalities that define an addicted state. Among many transcription factors known to influence the addiction process, one of the best characterized is ΔFosB, which is induced in the brain's reward regions by chronic exposure to virtually all drugs of abuse and mediates sensitized responses to drug exposure. Since ΔFosB is a highly stable protein, it represents a mechanism by which drugs produce lasting changes in gene expression long after the cessation of drug use. Studies are underway to explore the detailed molecular mechanisms by which ΔFosB regulates target genes and produces its behavioural effects. We are approaching this question using DNA expression arrays coupled with the analysis of chromatin remodelling—changes in the posttranslational modifications of histones at drug-regulated gene promoters—to identify genes that are regulated by drugs of abuse via the induction of ΔFosB and to gain insight into the detailed molecular mechanisms involved. Our findings establish chromatin remodelling as an important regulatory mechanism underlying drug-induced behavioural plasticity, and promise to reveal fundamentally new insight into how ΔFosB contributes to addiction by regulating the expression of specific target genes in brain reward pathways

Trajectories in the Evolution of Technology: A Multi-Level Study of Competition in Formula 1 Racing.

This paper explores the trajectories of three key technologies in Formula 1 racing at the component, firm and system levels of analysis. The purpose is to gain an understanding of the evolutionary forces that contribute to the emergence and survival of dominant designs. Based on archival data and contemporaneous accounts of the period 1967-1982, we develop a series of propositions specifying the evolutionary forces acting on technological trajectories within each level of analysis. The resulting framework leads to a set of predictions about relationships between technological transparency, co-evolution, and the emergence of dominant designs. Specifically, we argue that when the costs and difficulty associated with transferring component knowledge between firms is low (technological transparency is high), technologies tend to co-evolve across firms, leading to the development of complementary technologies and increasing the likelihood of industry dominance. Where transparency is low, however, technologies tend to co-evolve across functions within firms, leading to the development of competing technologies across firms, increasing the likelihood of a technology's dominance within the firm. The data and argument suggest that the forces acting on these two types of technological trajectories are self-reinforcing, so that as momentum builds behind a trajectory, it becomes more likely that its evolutionary path will end in either firm-or system-level dominance

Neurobiological mechanisms for opponent motivational processes in addiction

The conceptualization of drug addiction as a compulsive disorder with excessive drug intake and loss of control over intake requires motivational mechanisms. Opponent process as a motivational theory for the negative reinforcement of drug dependence has long required a neurobiological explanation. Key neurochemical elements involved in reward and stress within basal forebrain structures involving the ventral striatum and extended amygdala are hypothesized to be dysregulated in addiction to convey the opponent motivational processes that drive dependence. Specific neurochemical elements in these structures include not only decreases in reward neurotransmission such as dopamine and opioid peptides in the ventral striatum, but also recruitment of brain stress systems such as corticotropin-releasing factor (CRF), noradrenaline and dynorphin in the extended amygdala. Acute withdrawal from all major drugs of abuse produces increases in reward thresholds, anxiety-like responses and extracellular levels of CRF in the central nucleus of the amygdala. CRF receptor antagonists block excessive drug intake produced by dependence. A brain stress response system is hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence and to contribute to stress-induced relapse. The combination of loss of reward function and recruitment of brain stress systems provides a powerful neurochemical basis for the long hypothesized opponent motivational processes responsible for the negative reinforcement driving addiction