Dataset Information

Distributions of observed death tolls govern sensitivity to human fatalities.

ABSTRACT: How we react to humanitarian crises, epidemics, and other tragic events involving the loss of human lives depends largely on the extent to which we are moved by the size of their associated death tolls. Many studies have demonstrated that people generally exhibit a diminishing sensitivity to the number of human fatalities and, equivalently, a preference for risky (vs. sure) alternatives in decisions under risk involving human losses. However, the reason for this tendency remains unknown. Here we show that the distributions of event-related death tolls that people observe govern their evaluations of, and risk preferences concerning, human fatalities. In particular, we show that our diminishing sensitivity to human fatalities follows from the fact that these death tolls are approximately power-law distributed. We further show that, by manipulating the distribution of mortality-related events that people observe, we can alter their risk preferences in decisions involving fatalities. Finally, we show that the tendency to be risk-seeking in mortality-related decisions is lower in countries in which high-mortality events are more frequently observed. Our results support a model of magnitude evaluation based on memory sampling and relative judgment. This model departs from the utility-based approaches typically encountered in psychology and economics in that it does not rely on stable, underlying value representations to explain valuation and choice, or on choice behavior to derive value functions. Instead, preferences concerning human fatalities emerge spontaneously from the distributions of sampled events and the relative nature of the evaluation process.

SUBMITTER: Olivola CY

PROVIDER: S-EPMC2799776 | biostudies-literature | 2009 Dec

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Distributions of observed death tolls govern sensitivity to human fatalities.

Olivola Christopher Y CY Sagara Namika N

Proceedings of the National Academy of Sciences of the United States of America 20091215 52

How we react to humanitarian crises, epidemics, and other tragic events involving the loss of human lives depends largely on the extent to which we are moved by the size of their associated death tolls. Many studies have demonstrated that people generally exhibit a diminishing sensitivity to the number of human fatalities and, equivalently, a preference for risky (vs. sure) alternatives in decisions under risk involving human losses. However, the reason for this tendency remains unknown. Here we ...[more]

PMID: 20018778

Similar Datasets

Project description:Psychopathology is a risk factor for accelerated biological aging and early mortality. We examined associations between broad underlying dimensions of psychopathology (reflecting internalizing and externalizing psychiatric symptoms), PTSD, and age-adjusted GrimAge ("GrimAge residuals"), a DNA methylation biomarker of mortality risk relative to age. We also examined neurobiological correlates of GrimAge residuals, including neurocognitive functioning, blood-based biomarkers (of inflammation, neuropathology, metabolic disease), and cortical thickness. Data from two independent trauma-exposed military cohorts (n = 647 [62.9% male, Mage = 52], n = 434 [90% male, Mage = 32]) were evaluated using linear regression models to test associations between GrimAge residuals, psychopathology, and health correlates. Externalizing psychopathology significantly predicted GrimAge residuals in both cohorts (ps < 0.028). PTSD predicted GrimAge residuals in the younger (p = 0.001) but not the older cohort. GrimAge residuals were associated with several neurobiological variables available in the younger cohort, including cognitive disinhibition (padj = 0.021), poorer memory recall (padj = 0.023), cardiometabolic pathology (padj < 0.001), oxidative stress (padj = 0.003), astrocyte damage (padj = 0.021), inflammation (C-reactive protein: padj < 0.001; IL-6: padj < 0.001), and immune functioning (padj < 0.001). A subset of inflammatory and neuropathology analytes were available in the older cohort and showed associations with GrimAge residuals (IL-6: padj < 0.001; TNF-α: padj < 0.001). GrimAge residuals were also associated with reduced cortical thickness in right lateral orbitofrontal cortex (padj = 0.018) and left fusiform gyrus (padj = 0.030), which are related to emotion regulation and facial recognition, respectively. Psychopathology may be a common risk factor for elevated mortality risk. GrimAge could help identify those at risk for adverse health outcomes and allow for early disease identification and treatment.

Project description:Epithelial tissues (epithelia) remove excess cells through extrusion, preventing the accumulation of unnecessary or pathological cells. The extrusion process can be triggered by apoptotic signalling, oncogenic transformation and overcrowding of cells. Despite the important linkage of cell extrusion to developmental, homeostatic and pathological processes such as cancer metastasis, its underlying mechanism and connections to the intrinsic mechanics of the epithelium are largely unexplored. We approach this problem by modelling the epithelium as an active nematic liquid crystal (that has a long range directional order), and comparing numerical simulations to strain rate and stress measurements within monolayers of MDCK (Madin Darby canine kidney) cells. Here we show that apoptotic cell extrusion is provoked by singularities in cell alignments in the form of comet-shaped topological defects. We find a universal correlation between extrusion sites and positions of nematic defects in the cell orientation field in different epithelium types. The results confirm the active nematic nature of epithelia, and demonstrate that defect-induced isotropic stresses are the primary precursors of mechanotransductive responses in cells, including YAP (Yes-associated protein) transcription factor activity, caspase-3-mediated cell death, and extrusions. Importantly, the defect-driven extrusion mechanism depends on intercellular junctions, because the weakening of cell-cell interactions in an ?-catenin knockdown monolayer reduces the defect size and increases both the number of defects and extrusion rates, as is also predicted by our model. We further demonstrate the ability to control extrusion hotspots by geometrically inducing defects through microcontact printing of patterned monolayers. On the basis of these results, we propose a mechanism for apoptotic cell extrusion: spontaneously formed topological defects in epithelia govern cell fate. This will be important in predicting extrusion hotspots and dynamics in vivo, with potential applications to tissue regeneration and the suppression of metastasis. Moreover, we anticipate that the analogy between the epithelium and active nematic liquid crystals will trigger further investigations of the link between cellular processes and the material properties of epithelia.

Project description:A species sensitivity distribution (SSD) is a cumulative distribution function of toxicity endpoints for a receptor group. A key assumption when deriving an SSD is that the toxicity data points are independent and identically distributed (iid). This assumption is tenuous, however, because closely related species are more likely to have similar sensitivities than are distantly related species. When the response of 1 species can be partially predicted by the response of another species, there is a dependency or autocorrelation in the data set. To date, phylogenetic relationships and the resulting dependencies in input data sets have been ignored in deriving SSDs. In this paper, we explore the importance of the phylogenetic signal in deriving SSDs using a case studies approach. The case studies involved toxicity data sets for aquatic autotrophs exposed to atrazine and aquatic and avian species exposed to chlorpyrifos. Full and partial data sets were included to explore the influences of differing phylogenetic signal strength and sample size. The phylogenetic signal was significant for some toxicity data sets (i.e., most chlorpyrifos data sets) but not for others (i.e., the atrazine data sets, the chlorpyrifos data sets for all insects, crustaceans, and birds). When a significant phylogenetic signal did occur, effective sample size was reduced. The reduction was large when the signal was strong. In spite of the reduced effective sample sizes, significant phylogenetic signals had little impact on fitted SSDs, even in the tails (e.g., hazardous concentration for 5th percentile species [HC5]). The lack of a phylogenetic signal impact occurred even when we artificially reduced original sample size and increased strength of the phylogenetic signal. We conclude that it is good statistical practice to account for the phylogenetic signal when deriving SSDs because most toxicity data sets do not meet the independence assumption. That said, SSDs and HC5s are robust to deviations from the independence assumption. Integr Environ Assess Manag 2019;00:1-13. © 2019 The Authors. Integrated Environmental Assessment and Management published by Wiley Periodicals, Inc. on behalf of Society of Environmental Toxicology & Chemistry (SETAC).

Dataset Information

Distributions of observed death tolls govern sensitivity to human fatalities.

Publications

Distributions of observed death tolls govern sensitivity to human fatalities.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets