Towards improved socio-economic assessments of ocean acidification’s impacts

Ocean acidification is increasingly recognized as a component of global change that could have a wide range of impacts on marine organisms, the ecosystems they live in, and the goods and services they provide humankind. Assessment of these potential socio-economic impacts requires integrated efforts between biologists, chemists, oceanographers, economists and social scientists. But because ocean acidification is a new research area, significant knowledge gaps are preventing economists from estimating its welfare impacts. For instance, economic data on the impact of ocean acidification on significant markets such as fisheries, aquaculture and tourism are very limited (if not non-existent), and non-market valuation studies on this topic are not yet available. Our paper summarizes the current understanding of future OA impacts and sets out what further information is required for economists to assess socio-economic impacts of ocean acidification. Our aim is to provide clear directions for multidisciplinary collaborative research.

Estimating the economic loss of recent North Atlantic fisheries management

It is accepted that world’s fisheries are not generally exploited at their biological or their economic optimum. Most fisheries assessments focus on the biological capacity of fish stocks to respond to harvesting and few have attempted to estimate the economic efficiency at which ecosystems are exploited. The latter is important as fisheries contribute considerably to the economic development of many coastal communities. Here we estimate the overall potential economic rent for the fishing industry in the North Atlantic to be B€ 12.85, compared to current estimated profits of B€ 0.63. The difference between the potential and the net profits obtained from North Atlantic fisheries is therefore B€ 12.22. In order to increase the profits of North Atlantic fisheries to a maximum, total fish biomass would have to be rebuilt to 108 Mt (2.4 times more than present) by reducing current total fishing effort by 53%. Stochastic simulations were undertaken to estimate the uncertainty associated with the aggregate bioeconomic model that we use and we estimate the economic loss NA fisheries in a range of 2.5 and 32 billion of euro. We provide economic justification for maintaining or restoring fish stocks to above their MSY biomass levels. Our conclusions are consistent with similar global scale studies.

Fast and frugal models of clinical judgement in novice and expert physicians

Our objective was to study whether “compensatory” models provide better descriptions of clinical judgment than fast and frugal models, according to expertise and experience. Fifty practitioners appraised 60 vignettes describing a child with an exacerbation of asthma and rated their propensities to admit the child. Linear logistic (LL) models of their judgments were compared with a matching heuristic (MH) model that searched available cues in order of importance for a critical value indicating an admission decision. There was a small difference between the 2 models in the proportion of patients allocated correctly (admit or not-admit decisions), 91.2% and 87.8%, respectively. The proportion allocated correctly by the LL model was lower for consultants than juniors, whereas the MH model performed equally well for both. In this vignette study, neither model provided any better description of judgments made by consultants or by pediatricians compared to other grades and specialties.

IMPACT OF RNA VIRUSES ON THE REGULATION OF IL-23 IN MOUSE AND HUMAN MODELS OF INFECTION.

Interluekin-23 (IL-23) is a pro-inflammatory cytokine critical to the regulation of innate and adaptive immune responses. The main role for this cytokine is in the proliferation and differentiation of the IL-17 producing CD4 T helper cell, Th17. Virus infection deregulates IL-23 expression and function, but little is known about the mechanism behind this phenomena. Here, I demonstrate a reduction of Toll like receptor (TLR) ligand-induced IL-23 expression in lymphocytic choriomeningitis virus (LCMV)-infected bone marrow-derived dendritic cells (BMDCs), indicating that a function of these cells is disrupted during virus infection. I propose a mechanism of TLR ligand-induced IL-23 expression inhibition upon LCMV infection via the deactivation of p38, AP-1, and NF-κB. Further analysis revealed a direct relationship between LCMV infection with the IL-10 and SOCS3 expression. To understand IL-23 function, I characterized IL-23-induced JAK/STAT signalling pathway and IL-23 receptor expression on human CD4 T cells. My results demonstrate that IL-23 induces activation of p-JAK2, p-Tyk2, p-STAT1, p-STAT3, and p-STAT4 in CD4 T cells. For the first time I show that IL-23 alone induces the expression of its own receptor components, IL-12Rβ1 and IL-23Rα, in CD4 T cells. Blocking JAK2, STAT1, and STAT3 activation with specific inhibitors detrimentally effected expression of IL-23 receptor demonstrating that activation of JAK/STAT signalling is important for IL-23 receptor expression. I also addressed the effect of viral infection on IL-23 function and receptor expression in CD4 T cells using cells isolated from HIV positive individuals. These studies were based on earlier reports that the expression of IL-23 and the IL-23 receptor are impaired during HIV infection. I demonstrate that the phosphorylation of JAK2, STAT1, and STAT3 induced by IL-23, as well as IL-23 receptor expression are deregulated in CD4 T cells isolated from HIV positive individuals. This study has furthered the understanding of how the expression and function of IL-23 is regulated during viral infections.