Does support for democracy matter? : a cross-national study of regime preferences and system change

Includes bibliographical references (leaves 54-55).Using survey data from the third World Values Survey and democracy scores from Freedom House, I outline and test a supply and demand model of democratic change and stability. While "support for democracy" is a common concept in political science, the only empirical studies of the relationship between these regime preferences and democracy (Inglehart, 2003; Inglehart & Welzel, 2003; Welzel, Inglehart and Klingemann 2003) do not control for reciprocal causation and use poorly conceptualised and measured variables. They claim that deeply-rooted cultural orientations called "self-expression values" are a better measure of implicit support for democracy than overt expressions of regime preference. However, I find that once I control for the possibility that democracy is exogenous, there is little difference between the explanatory power of cultural values versus overtly expressed preferences. Furthermore, I argue that popular regime preferences (or demand) affect the change in the level of democracy, but do so only in relation to its current supply. "Net demand" is the driver of system change rather than absolute levels of popular support for democracy

The Emotional Logic of Participation in Intergroup Violence

Existing theories of intergroup violence focus on the motives of group or leaders. But why do thousands of people choose to take part given the dangers and risks? This dissertation develops a model, the entitlement-blame-anger model, to explain participation in intergroup violence. According to this model, participation is motivated by emotional reactions of intergroup anger. Anger is useful in this respect because it shapes both the preference for confrontation and beliefs about the risks of taking part. Intergroup anger, in turn, is triggered by appraisals that the outgroup are to blame for some harm suffered by the ingroup. Blame and anger are then rooted in evaluations of group endowments and group entitlements. These are widely-shared beliefs concerning who gets what and who deserves what in a given society. Thus, when group endowments and group entitlements are incongruent, either because the outgroup are enjoying resources to which they are not entitled, or the ingroup getting less than their share, the outgroup is blamed, anger is experienced and large numbers of ingroup members may become willing to take part in violence directed at that group. The theoretical model is tested using an original survey dataset collected from a representative sample of 497 residents of of Alexandra, in Johannesburg, South Africa, where a national wave of attacks against immigrants began in 2008, and where intergroup tensions remain. Analysis of the survey data shows that each of the links in the model - from group entitlement violations to blame, blame to anger, and anger to participation intentions - is supported, even controlling for possible confounds such as previous participation in violence, the influence of peers and leaders, and exposure to material competition with the outgroup. A few other factors also emerge as important determinants of participation in intergroup violence. Support for violence increases both the desire to participate and the intensity of intergroup anger. Here is also some evidence of an instrumental pathway to participation: street traders, who compete with foreign traders for customers, show an increased likelihood of taking part in future violence, but only when they are also exposed to the social pressures produced by attendance at community policing meetings. Hearing friends and acquaintances blame the outgroup increases an individual\u27s own level of outgroup blame. Hearing leaders blame the outgroup, in contrast, increases the level of intergroup anger. Finally, authoritarian values also result in greater blame of the outgroup, but only when coupled with perceived violations of group entitlements

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

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

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele