The PHENIX Experiment at RHIC

The physics emphases of the PHENIX collaboration and the design and current status of the PHENIX detector are discussed. The plan of the collaboration for making the most effective use of the available luminosity in the first years of RHIC operation is also presented.Comment: 5 pages, 1 figure. Further details of the PHENIX physics program available at http://www.rhic.bnl.gov/phenix

Review Section : Nature/Nurture Revisited I

Biologically oriented approaches to the study of human conflict have thus far been limited largely to the study of aggression. A sample of the literature on this topic is reviewed, drawing upon four major approaches: comparative psychology, ethology (including some popularized accounts), evolutionary-based theories, and several areas of human physiology. More sophisticated relationships between so-called "innate" and "acquired" determinants of behavior are discussed, along with the proper relevance of animal behavior studies for human behavior. Unless contained in a comprehensive theory which includes social and psychological variables, biolog ically oriented theories (although often valid within their domain) offer at best severely limited and at worst highly misleading explanations of complex social conflicts. The review concludes with a list of several positive contributions of these biological approaches and suggests that social scientists must become more knowledgeable about them.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68270/2/10.1177_002200277401800206.pd

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