Law, Biology, and Property: A New Theory of the Endowment Effect

Recent work at the intersection of law and behavioral biology has suggested numerous contexts in which legal thinking could benefit by integrating knowledge from behavioral biology. In one of those contexts, behavioral biology may help to provide theoretical foundation for, and potentially increased predictive power concerning, various psychological traits relevant to law. This Article describes an experiment that explores that context. The paradoxical psychological bias known as the endowment effect puzzles economists, skews market behavior, impedes efficient exchange of goods and rights, and thereby poses important problems for law. Although the effect is known to vary widely, there are at present no satisfying explanations for why it manifests when and how it does. Drawing on evolutionary biology, this Article provides a new theory of the endowment effect. Briefly, we hypothesize that the endowment effect is an evolved propensity of humans and, further, that the degree to which an item is evolutionarily relevant will affect the strength of the endowment effect. The theory generates a novel combination of three predictions. These are: (1) the effect is likely to be observable in many other species, including close primate relatives; (2) the prevalence of the effect in other species is likely to vary across items; and (3)the prevalence of the endowment effect will increase or decrease, respectively, with the increasing or decreasing evolutionary salience of the item in question. The authors tested these predictions in a chimpanzee (Pan troglodytes) experiment, recently published in Current Biology. The data, further explored here, are consistent with each of the three predictions. Consequently, this theory may explain why the endowment effect exists in humans and other species. It may also help both to predict and to explain some of the variability in the effect when it does manifest. And, more broadly, the results of the experiment suggest that combining life science and social science perspectives could lead to a more coherent framework for understanding the wider variety of other cognitive heuristics and biases relevant to law

Using an Evolutionary Approach to Improve Predictive Ability in Social Sciences: Property, the Endowment Effect, and Law

From the perspective of other disciplines, evolutionary approaches more often provide explanation and coherence than they help to solve discrete problems. We believe that more examples of the latter sort will help both with disciplinary synthesis and with the advance of knowledge. Here we describe a 20-year arc of research to demonstrate the problem-solving utility of an evolutionary perspective by focusing, as a case study, on a particular cognitive bias – the endowment effect – that has implications for law. Legal systems often assume that humans make decisions that are substantively rational, consistent, and aimed at maximizing their own wellbeing. But prevalent cognitive biases disrupt this, showing that humans consistently make decisions that seem to violate rationality and/or their own best interests. And despite decades of research, there has been little progress in understanding why these biases exist. We are among the scholars who have converged on the idea that many cognitive biases may have evolved as adaptations to pre-modern conditions, the evolutionarily sudden changes from which often leave them mis-matched to current conditions, prompting us to situationally irrational outcomes. Here, we discuss our data testing hypotheses derived from this perspective in both humans and nonhuman primates and consider how it has advanced our understanding of both the endowment effect narrowly and cognitive biases generally – including those relevant to law and policy

Law, Biology, and Property: A New Theory of the Endowment Effect

Recent work at the intersection of law and behavioral biology has suggested numerous contexts in which legal thinking could benefit by integrating knowledge from behavioral biology. In one of those contexts, behavioral biology may help to provide theoretical foundation for, and potentially increased predictive power concerning, various psychological traits relevant to law. This Article describes an experiment that explores that context. The paradoxical psychological bias known as the endowment effect puzzles economists, skews market behavior, impedes efficient exchange of goods and rights, and thereby poses important problems for law. Although the effect is known to vary widely, there are at present no satisfying explanations for why it manifests when and how it does. Drawing on evolutionary biology, this Article provides a new theory of the endowment effect. Briefly, we hypothesize that the endowment effect is an evolved propensity of humans and, further, that the degree to which an item is evolutionarily relevant will affect the strength of the endowment effect. The theory generates a novel combination of three predictions. These are: (1) the effect is likely to be observable in many other species, including close primate relatives; (2) the prevalence of the effect in other species is likely to vary across items; and (3) the prevalence of the endowment effect will increase or decrease, respectively, with the increasing or decreasing evolutionary salience of the item in question. The authors tested these predictions in a chimpanzee (Pan troglodytes) experiment, recently published in Current Biology. The data, further explored here, are consistent with each of the three predictions. Consequently, this theory may explain why the endowment effect exists in humans and other species. It may also help both to predict and to explain some of the variability in the effect when it does manifest. And, more broadly, the results of the experiment suggest that combining life science and social science perspectives could lead to a more coherent framework for understanding the wider variety of other cognitive heuristics and biases relevant to law

The 5'-3' exoribonuclease Pacman (Xrn1) regulates expression of the heat shock protein Hsp67Bc and the microRNA miR-277-3p in Drosophila wing imaginal discs

Pacman/Xrn1 is a highly conserved exoribonuclease known to play a critical role in gene regulatory events such as control of mRNA stability, RNA interference and regulation via miRNAs. Although Pacman has been well studied in Drosophila tissue culture cells, the biologically relevant cellular pathways controlled by Pacman in natural tissues are unknown. This study shows that a hypomorphic mutation in pacman (pcm5) results in smaller wing imaginal discs. These tissues, found in the larva, are known to grow and differentiate to form wing and thorax structures in the adult fly. Using microarray analysis, followed by quantitative RT-PCR, we show that eight mRNAs were increased in level by >2 fold in the pcm5 mutant wing discs compared to the control. The levels of pre mRNAs were tested for five of these mRNAs; four did not increase in the pcm5 mutant, showing that they are regulated at the post-transcriptional level and therefore could be directly affected by Pacman. These transcripts include one that encodes the heat-shock protein Hsp67Bc, which is upregulated 11.9-fold at the post-transcriptional level and 2.3-fold at the protein level. One miRNA, miR-277-3p, is 5.6-fold downregulated at the post-transcriptional level in mutant discs, suggesting that Pacman affects its processing in this tissue. Together, these data show that a relatively small number of mRNAs and miRNAs substantially change in abundance in pacman mutant wing imaginal discs. Since Hsp67Bc is known to regulate autophagy and protein synthesis, it is possible that Pacman may control the growth of wing imaginal discs by regulating these processes

RNA-seq reveals post-transcriptional regulation of Drosophila insulin-like peptide dilp8 and the neuropeptide-like precursor Nplp2 by the exoribonuclease Pacman/XRN1

Ribonucleases are critically important in many cellular and developmental processes and defects in their expression are associated with human disease. Pacman/XRN1 is a highly conserved cytoplasmic exoribonuclease which degrades RNAs in a 5' - 3' direction. In Drosophila, null mutations in pacman result in small imaginal discs, a delay in onset of pupariation and lethality during the early pupal stage. In this paper, we have used RNA-seq in a genome-wide search for mRNAs misregulated in pacman null wing imaginal discs. Only 4.2% of genes are misregulated ±>2-fold in pacman null mutants compared to controls, in line with previous work showing that Pacman has specificity for particular mRNAs. Further analysis of the most upregulated mRNAs showed that Pacman post-transcriptionally regulates the expression of the secreted insulin-like peptide Dilp8. Dilp8 is related to human IGF-1, and has been shown to co-ordinate tissue growth with developmental timing in Drosophila. The increased expression of Dilp8 is consistent with the developmental delay seen in pacman null mutants. Our analysis, together with our previous results, show that the normal role of this exoribonuclease in imaginal discs is to suppress the expression of transcripts that are crucial in apoptosis and growth control during normal development

An indigenous approach to explore health-related experiences among Māori parents: the Pukapuka Hauora asthma study.

Published onlineJournal ArticleResearch Support, Non-U.S. Gov'tBACKGROUND: The prevalence of asthma for Indigenous New Zealand Māori is amongst the highest in the world. Recent evidence shows ethnic differences in asthma symptom prevalence in New Zealand have widened, with asthma symptoms and hospitalisation rates consistently higher for Māori across all age-groups, especially children and adolescents. This paper: outlines our qualitative, longitudinal research exploring the practical issues Māori children and their families face trying to achieve optimum asthma outcomes; details the research methods used within this study; and discusses the process evaluation findings of the features that made this approach successful in engaging and retaining participants in the study. METHODS: Thirty-two Māori families were recruited using a Kaupapa Māori (Māori way) Research approach. Each participated in a series of four in-depth interviews that were carried out at seasonal intervals over the course of one year. Families also took part in an interviewer-administered questionnaire and participated in a Photovoice exercise. All interviews were digitally recorded, transcribed verbatim and independently coded by two researchers. The research team then conducted the analysis and theme development. The questionnaires were analysed separately, with explanations for findings explored within the qualitative data. RESULTS: The methodology produced a 100 percent retention rate of the participating families over the course of the follow-up. This was attributed to the research collaboration, the respectful research relationships established with families, and the families' judgement that the methods used enabled them to tell their stories. The acceptability of the methodology will add to the validity and trustworthiness of the findings. CONCLUSION: Given the extent and persistence of ethnic disparities in childhood asthma management, it is imperative that an indigenous approach be taken to understanding the core issues facing Māori families. By conducting community-partnership research underpinned by an indigenous methodology, and employing a range of appropriate methods, we have successfully recruited and retained a cohort of Māori families with experiences of childhood asthma. We aim to make their voices heard in order to develop a series of culturally relevant interventions aimed at remediating these disparities.Health Research Council of New ZealandNIH

The roles of the exoribonucleases DIS3L2 and XRN1 in disease

RNA degradation is a vital post-transcriptional process which ensures that transcripts are maintained at the correct level within the cell. DIS3L2 and XRN1 are conserved exoribonucleases which are critical for the degradation of cytoplasmic RNAs. Although the molecular mechanisms of RNA degradation by DIS3L2 and XRN1 have been well studied, less is known about their specific roles in development of multicellular organisms or human disease. This review focusses on the roles of DIS3L2 and XRN1 in the pathogenesis of human disease, particularly in relation to phenotypes seen in model organisms. The known diseases associated with loss of activity of DIS3L2 and XRN1 are discussed, together with possible mechanisms and cellular pathways leading to these disease conditions