To what extent can the harms of misinformation be mitigated by relying on nudges? Prior research has demonstrated that non-intrusive ‘accuracy nudges’ can reduce the sharing of misinformation. We investigate an alternative approach. Rather than subtly reminding people about accuracy, our intervention, indebted to research on the bystander effect, explicitly appeals to individuals' capacity to help solve the misinformation challenge. Our results are mixed. On the one hand, our intervention reduces the willingness to share and believe in misinformation fact-checked as false. On the other hand, it also reduces participants' willingness to share information that has been fact-checked as true and innocuous, as well as non-fact-checked information. Experiment 1 offers proof of concept; Experiment 2 tests our intervention with a more realistic mix of true and false social media posts; Experiment 3 tests our interventions alongside an accuracy nudge. The effectiveness of our intervention at reducing willingness to share misinformation remains consistent across experiments; meta-analysis reveals that our treatment reduced willingness to share false content across experiments by 20% of a scale point on a six-point scale. We do not observe the accuracy nudge reducing willingness to share false content. Taken together, these results highlight the advantages and disadvantages of accuracy nudges and our more confrontational approach.

Research has shown that people perceive themselves as less biased than others, and as better than average in many favorable characteristics. We suggest that these types of biased perceptions regarding intentions and behavior of others may directly affect people’s decisions. In the current research we focus on possible influences in the context of helping behavior. In four experiments we found that, people believe that others, compared to themselves, are less inclined to help and cooperate, are less aware of the number of bystanders and more influenced by the “proportion dominance” bias and by the “identifiable victim effect.” We demonstrate that these perceptions are naïve and unrealistic by showing that decisions from both self and others’ perspectives are equally biased. Finally, we show how the perspective from which a decision is made (self vs. others) may affect private as well as public decisions in ways that might not be in the best interest of the decision maker and the public.

L’AEN (Agence pour l’énergie nucléaire) a organisé un atelier « Sciences and values in radiological protection » afin d’identifier les voies possibles d’intégration en radioprotection de certains résultats du domaine de la recherche sur les effets biologiques et sur la santé des rayonnements ionisants. Trois thèmes d’actualité ont été développés : les effets non ciblés, la radiosensibilité individuelle et les maladies cardio-vasculaires. À l’issue de ces journées, des recommandations ont été émises envers les scientifiques, les radioprotectionnistes et les parties prenantes.

Nous présentons à travers l'historique du Laboratoire de Microanalyses Nucléaires Alain Chambaudet (LMN-AC) les différentes thématiques de recherche entrant dans le cadre de la dosimétrie des rayonnements ionisants et de la radiophysique.

In this paper our current knowledge of the mechanisms underlying the induction of bystander effects by low dose low LET ionizing radiation is reviewed in the context of relevance to radiation protection issues. The question of how bystander effects may be related to observed adaptive responses, systemic genomic instability or other effects of low doses exposures is also considered. Bystander effects appear to be the result of a generalized stress response in tissues or cells. The signals may be produced by all exposed cells, but the response may require additional system parameters to exist in order to be expressed. The major response involving low LET radiation exposure discussed in the existing literature is a death response. This can manifest as apoptotic cell death, terminal differentiation, reproductive cell death or necrosis. While a death response might appear to be adverse, the position is argued in this paper, that it can in fact be protective and remove damaged cells from the reproducing population. Since many cell populations carry damaged cells without being exposed to radiation (so-called “background damage”), it is possible that low dose radiation exposures cause removal of cells damaged by agents other than the test dose of radiation. This mechanism would lead to the production of “u- or n-shaped” dose response curves. In this scenario, the level of harmful or beneficial response will be related to the background damage carried by the cell population and the genetic program determining response to damage. This model may be particularly important when attempting to predict the consequences of mixed exposures involving radiation and other environmental stressors on biota.

Evidence has emerged over the past decade for the existence of two cellular phenomenons which challenge the standard paradigms for the induction of biological effects by ionizing radiation. In both cases, important genetic changes arise in cells that in themselves receive no radiation exposure. In the first, radiation induces a type of transmissible genomic instability in cells that leads to a persistent enhancement in the rate at which genetic alterations including mutations and chromosomal aberrations arise in the descendents of the original irradiated cell after many generations of replication. In the bystander effect, damage signals are transmitted from irradiated to non-irradiated cells in the population, leading to the occurrence of biologic effects in these “bystander” cells. In this review, our current knowledge concerning these two phenomena is described and their potential impact on the estimation of risks of low level radiation exposure discussed.