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 data sets from Rehder (2014) on comparative judgments, and from Rehder & 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

TARP as immunotherapeutic target in AML expressed in the LSC compartment

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Lessons for Employing Participatory Design When Developing Care for Young People with Cancer: A Qualitative Multiple-Case Study

Purpose: Participatory design (PD) is a collective creative design process involving designers and nondesigners. There is limited reporting on the experience of using PD for adolescent and young adult (AYA) care. This study summarizes lessons from employing PD to develop care for AYAs with cancer. Methods: A qualitative multiple-case study method was conducted of three PD processes addressing food (FfC), intimacy and sexuality (I&S), and integrative medicine (IM) in caring for AYAs with cancer. Results: Local key stakeholders, who were exposed to a problem and had not been successful at solving it individually, were recruited to ‘‘dream’’ together. Through this synergy, a shared understanding of the problem and a joint mission emerged to find a solution. PD tools were used to develop a problem definition. An open mind and explorative research helped to understand the problems, and stakeholders were managed such that idea-sharing and learning were enabled. Designers translated ideas into prototypes. The PD process was prolonged due to the hierarchical hospital environment, business considerations, and additionally required evidence. The FfC program produced an effective new food service for the whole hospital. The I&S initiative developed a podcast, two articles, and a prototype website. The IM project developed a pilot study. Conclusions: For a PD process to successfully develop care for AYAs, one needs to use designers and skilled people, PD tools, and an open-ended approach to visualize an

Phenotypes induced by NM causing α-skeletal muscle actin mutants in fibroblasts, Sol 8 myoblasts and myotubes

<p>Abstract</p> <p>Background</p> <p>Nemaline myopathy is a neuromuscular disorder characterized by the presence of nemaline bodies in patient muscles. 20% of the cases are associated with α-skeletal muscle actin mutations. We previously showed that actin mutations can cause four different biochemical phenotypes and that expression of NM associated actin mutants in fibroblasts, myoblasts and myotubes induces a range of cellular defects.</p> <p>Findings</p> <p>We conducted the same biochemical experiments for twelve new actin mutants associated with nemaline myopathy. We observed folding and polymerization defects. Immunostainings of these and eight other mutants in transfected cells revealed typical cellular defects such as nemaline rods or aggregates, decreased incorporation in F-actin structures, membrane blebbing, the formation of thickened actin fibres and cell membrane blebbing in myotubes.</p> <p>Conclusion</p> <p>Our results confirm that NM associated α-actin mutations induce a range of defects at the biochemical level as well as in cultured fibroblasts and muscle cells.</p

Comparison of digital PCR platforms and semi-nested qPCR as a tool to determine the size of the HIV reservoir

HIV persists in latently infected cells of patients on antiretroviral therapy (ART). This persistent proviral DNA reservoir is an important predictor of viral rebound upon therapy failure or interruption and forms a major obstacle towards cure. Accurate quantification of the low levels of persisting HIV DNA may aid patient monitoring and cure research. Digital PCR is a promising tool that enables direct absolute quantification with high sensitivity. With recent technological advances, several platforms are available to implement digital PCR in a clinical setting. Here, we compared two digital PCR platforms, the Quantstudio 3D (Life Technologies) and the QX100 (Bio-Rad) with a semi-nested qPCR on serial HIV DNA dilutions and DNA isolated from PBMCs of ART-suppressed patients. All three methods were able to detect target to the lowest levels of 2.5 HIV DNA copies. The QX100 excelled in having the least bias and highest precision, efficiency and quantitative linearity. Patient sample quantifications by the QX100 and semi-nested qPCR were highly agreeable by Bland-Altman analysis (0.01 ± 0.32 log10). Due to the observation of false-positive signals with current digital PCR platforms however, semi-nested qPCR may still be preferred in a setup of low quantity detection to discriminate between presence or absence of HIV DNA

CD32+CD4+memory T cells are enriched for total HIV-1 DNA in tissues from humanized mice

CD32 has raised conflicting results as a putative marker of the HIV-1 reservoir. We measured CD32 expression in tissues from viremic and virally suppressed humanized mice treated relatively early or late after HIV-1 infection with combined antiretroviral therapy. CD32 was expressed in a small fraction of the memory CD4(+) T-cell subsets from different tissues in viremic and aviremic mice, regardless of treatment initiation time. CD32(+) memory CD4(+) T cells were enriched in cell associated (CA) HIV-1 DNA but not in CA HIV-1 RNA as compared to the CD32(-) CD4(+) fraction. Using multidimensional reduction analysis, several memory CD4(+)CD32(+) T-cell clusters were identified expressing HLA-DR, TIGIT, or PD-1. Importantly, although tissue-resident CD32(+)CD4(+) memory cells were enriched with translation-competent reservoirs, most of it was detected in memory CD32-CD4(+) T cells. Our findings support that CD32 labels highly activated/exhausted memory CD4(+) T-cell subsets that contain only a small proportion of the translation-competent reservoir