Notch signaling during human T cell development

Notch signaling is critical during multiple stages of T cell development in both mouse and human. Evidence has emerged in recent years that this pathway might regulate T-lineage differentiation differently between both species. Here, we review our current understanding of how Notch signaling is activated and used during human T cell development. First, we set the stage by describing the developmental steps that make up human T cell development before describing the expression profiles of Notch receptors, ligands, and target genes during this process. To delineate stage-specific roles for Notch signaling during human T cell development, we subsequently try to interpret the functional Notch studies that have been performed in light of these expression profiles and compare this to its suggested role in the mouse

HIV infection of non-dividing cells: a divisive problem

Understanding how lentiviruses can infect terminally differentiated, non-dividing cells has proven a very complex and controversial problem. It is, however, a problem worth investigating, for it is central to HIV-1 transmission and AIDS pathogenesis. Here I shall attempt to summarise what is our current understanding for HIV-1 infection of non-dividing cells. In some cases I shall also attempt to make sense of controversies in the field and advance one or two modest proposals

Gender differences in the use of cardiovascular interventions in HIV-positive persons; the D:A:D Study

Peer reviewe

A quantum probability account of individual differences in causal reasoning

We use quantum probability (QP) theory to investigate individual differences in causal reasoning. By analyzing datasets from Rehder (2014) on comparative judgments, and from Rehder and Waldmann (2016) on absolute judgments, we show that a QP model can both account for individual differences in causal judgments, and why these judgments sometimes violate the properties of causal Bayes nets. We implement this and previously proposed models of causal reasoning (including classical probability models) within the same hierarchical Bayesian inferential framework to provide a detailed comparison between these models, including computing Bayes factors. Analysis of the inferred parameters of the QP model illustrates how these can be interpreted in terms of putative cognitive mechanisms of causal reasoning. Additionally, we implement a latent classification mechanism that identifies subcategories of reasoners based on properties of the inferred cognitive process, rather than post hoc clustering. The QP model also provides a parsimonious explanation for aggregate behavior, which alternatively can only be explained by a mixture of multiple existing models. Investigating individual differences through the lens of a QP model reveals simple but strong alternatives to existing explanations for the dichotomies often observed in how people make causal inferences. These alternative explanations arise from the cognitive interpretation of the parameters and structure of the quantum probability model