When helping is risky: the behavioral and neurobiological tradeoff of social and risk preferences

This is the final version. Available on open access from SAGE Publications via the DOI in this recordData availability: Methods and data for Study 1 can be accessed at https://dataverse.nl/dataset.xhtml?persistentId=doi:10.34894/9UIPH4; for Study 2, please contact dr. M.J. Crockett. The authors declare no conflict of interest.Helping other people can entail risks for the helper. For example, when treating infectious patients, medical volunteers risk their own health. In such situations, decisions to help should depend on the individual’s valuation of others’ well-being (social preferences) and the degree of personal risk the individual finds acceptable (risk preferences). We investigated how these distinct preferences are psychologically and neurobiologically integrated when helping is risky. We used incentivized decision-making tasks (Study 1; N = 292 adults) and manipulated dopamine and norepinephrine levels in the brain by administering methylphenidate, atomoxetine, or a placebo (Study 2; N = 154 adults). We found that social and risk preferences are independent drivers of risky helping. Methylphenidate increased risky helping by selectively altering risk preferences rather than social preferences. Atomoxetine influenced neither risk preferences nor social preferences and did not affect risky helping. This suggests that methylphenidate-altered dopamine concentrations affect helping decisions that entail a risk to the helper.Netherlands Science FoundationUniversity of AmsterdamWellcome TrustAcademy of Medical SciencesOxford Martin SchoolMedical Research Council (MRC)National Institute for Health Research (NIHR

Invasive group A streptococcal disease in The Netherlands:Evidence for a protective role of anti-exotoxin A antibodies

As part of a nationwide surveillance in The Netherlands during 1994-1997, 53 patients with invasive group A streptococcal (GAS) infections were evaluated for medical history, symptoms, and outcome. Patients' isolates were tested for the production of pyrogenic exotoxins A (SPE-A) and B (SPE-B). Acute-phase sera from all patients and convalescent sera from 12 patients were investigated for the presence of antibodies against SPE-A and SPE-B, Twenty-three patients developed toxic shock-like syndrome and 16 died, Absence of antibodies against SPE-A and/or SPE-B was a risk factor for developing invasive streptococcal disease. Toxic shock and mortality were associated with a lack of anti-SPE-A antibodies (