Intimate partner violence, interpersonal aggression, and life history strategy

We integrate life history (LH) theory with "hot/cool" systems theory of self-regulation to predict sexually and socially coercive behaviors, including intimate partner violence (IPV) and interpersonal aggression (IPA). LH theory predicts that a variety of traits form LH strategies: adaptively coordinated behavioral clusters arrayed on a continuum from slow to fast. We test structural models examining 2 propositions: (a) "hot" cognitive processes, promoted by faster LH strategies, increase the likelihood of sexually/socially coercive behaviors that make up IPV and IPA; (b) "cool" cognitive processes, promoted by slower LH strategies, buffer against the likelihood of sexually/socially coercive behaviors that make up IPV and IPA. We present single and multisample structural equations models (SEMs and MSEMs) testing hypothesized causal relations among these theoretically specified predictors with IPV and IPA. Study 1 develops a Structural Equation Model for IPV; Study 2 extends the model to IPA using MSEM and provides 5 cross-cultural constructive replications of the findings. Integrating LH theory and hot/cool systems analysis of cognitive processes is a promising and productive heuristic for future research on IPV and IPA perpetration and victimization. </p

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

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

Universal and Local Understanding of Poverty in Peru

The purpose of this survey of the literature on poverty in Peru is to contribute to universal and interdisciplinary understanding, while at the same time giving due weight to discipline-specific contributions. The first three sections review relevant literature on Peru by economists, social anthropologists and sociologists. The strict positivism of much economic literature renders it susceptible to neglect power relations and assume a benign and universal process of modernization. Anthropologists have revealed the importance of local cultural identity, but at the risk of downplaying universal dimensions of well-being. Sociologists struggle to reconcile a universal analysis of class structure with renewed emphasis on individual and collective agency in adversity. The last section puts forward an integrating theoretical framework centred on the concepts of inclusion and exclusion. In contrast to the ‘tragic optimism’ of Sender this theory of social exclusion can best be summed up as ‘constructive pessimism’