The misasandry myth: An inaccurate stereotype about feminists' attitudes toward men

In six studies, we examined the accuracy and underpinnings of the damaging stereotype that feminists harbor negative attitudes toward men. In Study 1 (n = 1,664), feminist and nonfeminist women displayed similarly positive attitudes toward men. Study 2 (n = 3,892) replicated these results in non-WEIRD countries and among male participants. Study 3 (n = 198) extended them to implicit attitudes. Investigating the mechanisms underlying feminists’ actual and perceived attitudes, Studies 4 (n = 2,092) and 5 (nationally representative UK sample, n = 1,953) showed that feminists (vs. nonfeminists) perceived men as more threatening, but also more similar, to women. Participants also underestimated feminists’ warmth toward men, an error associated with hostile sexism and a misperception that feminists see men and women as dissimilar. Random-effects meta-analyses of all data (Study 6, n = 9,799) showed that feminists’ attitudes toward men were positive in absolute terms and did not differ significantly from nonfeminists'. An important comparative benchmark was established in Study 6, which showed that feminist women's attitudes toward men were no more negative than men's attitudes toward men. We term the focal stereotype the misandry myth in light of the evidence that it is false and widespread, and discuss its implications for the movement

The Misandry Myth : An Inaccurate Stereotype About Feminists’ Attitudes Toward Men

In six studies, we examined the accuracy and underpinnings of the damaging stereotype that feminists harbor negative attitudes toward men. In Study 1 (n = 1,664), feminist and nonfeminist women displayed similarly positive attitudes toward men. Study 2 (n = 3,892) replicated these results in non-WEIRD countries and among male participants. Study 3 (n = 198) extended them to implicit attitudes. Investigating the mechanisms underlying feminists’ actual and perceived attitudes, Studies 4 (n = 2,092) and 5 (nationally representative UK sample, n = 1,953) showed that feminists (vs. nonfeminists) perceived men as more threatening, but also more similar, to women. Participants also underestimated feminists’ warmth toward men, an error associated with hostile sexism and a misperception that feminists see men and women as dissimilar. Random-effects meta-analyses of all data (Study 6, n = 9,799) showed that feminists’ attitudes toward men were positive in absolute terms and did not differ significantly from nonfeminists'. An important comparative benchmark was established in Study 6, which showed that feminist women's attitudes toward men were no more negative than men's attitudes toward men. We term the focal stereotype the misandry myth in light of the evidence that it is false and widespread, and discuss its implications for the movement

Empathy: Gender effects in brain and behavior

Evidence suggests that there are differences in the capacity for empathy between males and females. However, how deep do these differences go? Stereotypically, females are portrayed as more nurturing and empathetic, while males are portrayed as less emotional and more cognitive. Some authors suggest that observed gender differences might be largely due to cultural expectations about gender roles. However, empathy has both evolutionary and developmental precursors, and can be studied using implicit measures, aspects that can help elucidate the respective roles of culture and biology. This article reviews evidence from ethology, social psychology, economics, and neuroscience to show that there are fundamental differences in implicit measures of empathy, with parallels in development and evolution. Studies in nonhuman animals and younger human populations (infants/children) offer converging evidence that sex differences in empathy have phylogenetic and ontogenetic roots in biology and are not merely cultural byproducts driven by socialization. We review how these differences may have arisen in response to males’ and females’ different roles throughout evolution. Examinations of the neurobiological underpinnings of empathy reveal important quantitative gender differences in the basic networks involved in affective and cognitive forms of empathy, as well as a qualitative divergence between the sexes in how emotional information is integrated to support decision making processes. Finally, the study of gender differences in empathy can be improved by designing studies with greater statistical power and considering variables implicit in gender (e.g., sexual preference, prenatal hormone exposure). These improvements may also help uncover the nature of neurodevelopmental and psychiatric disorders in which one sex is more vulnerable to compromised social competence associated with impaired empathy

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease