Reciprocity as a foundation of financial economics

This paper argues that the subsistence of the fundamental theorem of contemporary financial mathematics is the ethical concept ‘reciprocity’. The argument is based on identifying an equivalence between the contemporary, and ostensibly ‘value neutral’, Fundamental Theory of Asset Pricing with theories of mathematical probability that emerged in the seventeenth century in the context of the ethical assessment of commercial contracts in a framework of Aristotelian ethics. This observation, the main claim of the paper, is justified on the basis of results from the Ultimatum Game and is analysed within a framework of Pragmatic philosophy. The analysis leads to the explanatory hypothesis that markets are centres of communicative action with reciprocity as a rule of discourse. The purpose of the paper is to reorientate financial economics to emphasise the objectives of cooperation and social cohesion and to this end, we offer specific policy advice

Moving in the anthropocene: global reductions in terrestrial mammalian movements

Animal movement is fundamental for ecosystem functioning and species survival, yet the effects of the anthropogenic footprint on animal movements have not been estimated across species. Using a unique GPS-tracking database of 803 individuals across 57 species, we found that movements of mammals in areas with a comparatively high human footprint were on average one-half to one-third the extent of their movements in areas with a low human footprint. We attribute this reduction to behavioral changes of individual animals and to the exclusion of species with long-range movements from areas with higher human impact. Global loss of vagility alters a key ecological trait of animals that affects not only population persistence but also ecosystem processes such as predator-prey interactions, nutrient cycling, and disease transmission

1012-P: Neighborhood Disadvantage, Childhood Opportunity Index, and Glycemic Control for Children with Type 1 Diabetes?

Background: Disparities in outcomes for children with type 1 diabetes (T1DM) are associated with poverty and race. However, little is known regarding the impact of systemic racism. Objective: This aim of this study is to determine if neighborhood concentrated disadvantage index (NCDI) or Childhood Opportunity Index (COI) are associated with HbA1c and diabetes ketoacidosis (DKA) in children ≤ 18 years of age with type 1 diabetes. Methods: The retrospective secondary data analysis included data from children ≤ 18 years of age with a diagnosis of T1DM for ≥ 6 months seen in 2017 who reside in Kentucky (n=675) . NCDI scores were calculated based on the NIH PhenX Toolkit protocol. The tool was developed from a principal components analysis of six variables at the census tract level. COI was obtained from diversitydatakids.org. Univariate analyses were performed using Kruskal-Wallis test or Pearson’s correlation. Multiple linear regression analysis was conducted to to evaluate HbA1C and multivariate Poisson model was used for DKA. Results: Prior to controlling for age, race, and insurance type, NCDI (p&amp;lt;0.001) and COI (p&amp;lt; 0.001) were significant predictors for HbA1c. For every 1 unit increase in COI, the predicted value of AIc level decreased by 8.66 (p=0.0004) . NCDI and COI were not significant when controlling for age, race, and insurance. NCDI and COI were not significant predictors of DKA episodes. Conclusions: This study identified NCDI and COI as predictors of HbA1c in children and adolescents with T1DM only in univariate analysis. While NCDI and COI have been shown to correlate with structural racism, these findings suggest that more research is needed in larger and more diverse samples to disentangle the complex relationships among race, racism, and poverty. Understanding the mechanisms through which racism impacts outcomes for children with T1DM is essential to improving health equity. Disclosure M.B.Coriell: None. K.S.Jawad: None. Y.B.Feygin: None. S.Watson: None. M.D.Stevenson: None. B.A.Wattles: Research Support; Merck &amp; Co., Inc. V.F.Jones: None. J.Porter: None. D.W.Davis: None. </jats:sec