Objectification theory suggests that sexualization has significant dehumanizing consequences for how perceivers see women. To date, research has mostly documented how sexualized bodies in the mass media are objectified and dehumanized. The purpose of the present work was to test the novel cosmetics dehumanization hypothesis (CDH), that is, that subtler manifestations of sexualization, such as heavy makeup, might influence the way people attribute humanness-related traits to women. Across four experiments, 1000 participants (mostly from the United Kingdom and United States) were asked to evaluate women's faces with or without heavy makeup. Consistent with the CDH, results showed that faces with makeup were rated as less human while using complementary indicators of dehumanization: They were perceived as possessing less humanness, less agency, less experience (Experiment 1), less competence, less warmth, and less morality (Experiments 2-4) than faces without makeup. This pattern of results was observed for faces of both models (Experiments 1-2) and ordinary women (Experiments 3-4). In Experiment 4, we manipulated the part of the face that wore makeup (eye makeup vs. lipstick) and found that faces with eye makeup were attributed the least amount of warmth and competence. A meta-analysis based on Experiments 2-4 confirmed the robustness of the findings, which were not moderated by either participant gender or sexual orientation. Whereas prior studies suggested that a focus on faces may serve as an antidote for objectification and related dehumanization, the present set of experiments indicates that this strategy might not always be effective.
Recombinant human interferon-alpha (IFN-alpha) can induce a hematologic remission in patients with chronic myeloid leukemia. However, some patients are resistant and others develop late resistance to the IFN- alpha treatment. To understand the molecular mechanism of this resistance, we have analyzed the expression of 10 IFN-inducible genes in the cells of three resistant patients, two responsive patients, and six healthy controls. Northern blot hybridizations showed that all the genes were induced in in vitro IFN-alpha treated peripheral blood cells of the patients and healthy controls. These genes were also inducible in peripheral blood and bone marrow cells of two out of two resistant patients administered an injection of IFN-alpha. We conclude that the resistance to the IFN-alpha treatment of the chronic myeloid leukemia patients we studied is not due to (1) the absence of induction of any of the 10 IFN-inducible genes we studied, including the low-molecular- weight 2′-5′oligoadenylate synthetase; (2) the presence of an antagonist of IFN-alpha in the peripheral blood or bone marrow cells; and (3) the presence of neutralizing anti-IFN-alpha antibodies.
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