Towards a Formulation of Quantum Theory as a Causally Neutral Theory of Bayesian Inference

Quantum theory can be viewed as a generalization of classical probability theory, but the analogy as it has been developed so far is not complete. Whereas the manner in which inferences are made in classical probability theory is independent of the causal relation that holds between the conditioned variable and the conditioning variable, in the conventional quantum formalism, there is a significant difference between how one treats experiments involving two systems at a single time and those involving a single system at two times. In this article, we develop the formalism of quantum conditional states, which provides a unified description of these two sorts of experiment. In addition, concepts that are distinct in the conventional formalism become unified: channels, sets of states, and positive operator valued measures are all seen to be instances of conditional states; the action of a channel on a state, ensemble averaging, the Born rule, the composition of channels, and nonselective state-update rules are all seen to be instances of belief propagation. Using a quantum generalization of Bayes' theorem and the associated notion of Bayesian conditioning, we also show that the remote steering of quantum states can be described within our formalism as a mere updating of beliefs about one system given new information about another, and retrodictive inferences can be expressed using the same belief propagation rule as is used for predictive inferences. Finally, we show that previous arguments for interpreting the projection postulate as a quantum generalization of Bayesian conditioning are based on a misleading analogy and that it is best understood as a combination of belief propagation (corresponding to the nonselective state-update map) and conditioning on the measurement outcome.Comment: v1 43 pages, revTeX4. v2 42 pages, edited for clarity, added references and corrected minor errors, submitted to Phys. Rev. A. v3 41 pages, improved figures, added two new figures, added extra explanation in response to referee comments, minor rewrites for readability. v4 44 pages, added "towards" to title, rewritten abstract, rewritten introduction with new table

Nitric oxide inhibits the accumulation of CD4+CD44hiTbet+CD69lo T cells in mycobacterial infection

Animals lacking the inducible nitric oxide synthase gene (nos2-/-) are less susceptible to Mycobacterium avium strain 25291 and lack nitric oxide-mediated immunomodulation of CD4+ T cells. Here we show that the absence of nos2 results in increased accumulation of neutrophils and both CD4+ and CD8+ T cells within the M. avium containing granuloma. Examination of the T-cell phenotype in M. avium infected mice demonstrated that CD4+CD44hi effector T cells expressing the Th1 transcriptional regulator T-bet (T-bet+) were specifically reduced by the presence of nitric oxide. Importantly, the T-bet+ effector population could be separated into CD69hi and CD69lo populations, with the CD69lo population only able to accumulate during chronic infection within infected nos2-/- mice. Transcriptomic comparison between CD4+CD44hiCD69hi and CD4+CD44hiCD69lo populations revealed that CD4+CD44hiCD69lo cells had higher expression of the integrin itgb1/itga4 (VLA-4, CD49d/CD29). Inhibition of Nos2 activity allowed increased accumulation of the CD4+CD44hiT-bet+CD69lo population in WT mice as well as increased expression of VLA-4. These data support the hypothesis that effector T cells in mycobacterial granulomata are not a uniform effector population but exist in distinct subsets with differential susceptibility to the regulatory effects of nitric oxide

Dynamic scaling for 2D superconductors, Josephson junction arrays and superfluids

The value of the dynamic critical exponent $z$ is studied for two-dimensional superconducting, superfluid, and Josephson Junction array systems in zero magnetic field via the Fisher-Fisher-Huse dynamic scaling. We find $z\simeq5.6\pm0.3$, a relatively large value indicative of non-diffusive dynamics. Universality of the scaling function is tested and confirmed for the thinnest samples. We discuss the validity of the dynamic scaling analysis as well as the previous studies of the Kosterlitz-Thouless-Berezinskii transition in these systems, the results of which seem to be consistent with simple diffusion ($z=2$). Further studies are discussed and encouraged.Comment: 19 pages in two-column RevTex, 8 embedded EPS figure

Transcriptional regulatory networks underlying gene expression changes in Huntington's disease

Abstract Transcriptional changes occur presymptomatically and throughout Huntington's disease (HD), motivating the study of transcriptional regulatory networks (TRNs) in HD. We reconstructed a genome‐scale model for the target genes of 718 transcription factors (TFs) in the mouse striatum by integrating a model of genomic binding sites with transcriptome profiling of striatal tissue from HD mouse models. We identified 48 differentially expressed TF‐target gene modules associated with age‐ and CAG repeat length‐dependent gene expression changes in Htt CAG knock‐in mouse striatum and replicated many of these associations in independent transcriptomic and proteomic datasets. Thirteen of 48 of these predicted TF‐target gene modules were also differentially expressed in striatal tissue from human disease. We experimentally validated a specific model prediction that SMAD3 regulates HD‐related gene expression changes using chromatin immunoprecipitation and deep sequencing (ChIP‐seq) of mouse striatum. We found CAG repeat length‐dependent changes in the genomic occupancy of SMAD3 and confirmed our model's prediction that many SMAD3 target genes are downregulated early in HD

Highlights of children with Cancer UK’s workshop on drug delivery in paediatric brain tumours

The first Workshop on Drug Delivery in Paediatric Brain Tumours was hosted in London by the charity Children with Cancer UK. The goals of the workshop were to break down the barriers to treating central nervous system (CNS) tumours in children, leading to new collaborations and further innovations in this under-represented and emotive field. These barriers include the physical delivery challenges presented by the blood–brain barrier, the underpinning reasons for the intractability of CNS cancers, and the practical difficulties of delivering cancer treatment to the brains of children. Novel techniques for overcoming these problems were discussed, new models brought forth, and experiences compared

Mycobacterium tuberculosis infection induces il12rb1 splicing to generate a novel IL-12Rβ1 isoform that enhances DC migration

RNA splicing is an increasingly recognized regulator of immunity. Here, we demonstrate that after Mycobacterium tuberculosis infection (mRNA) il12rb1 is spliced by dendritic cells (DCs) to form an alternative (mRNA) il12rb1Deltatm that encodes the protein IL-12Rbeta1DeltaTM. Compared with IL-12Rbeta1, IL-12Rbeta1DeltaTM contains an altered C-terminal sequence and lacks a transmembrane domain. Expression of IL-12Rbeta1DeltaTM occurs in CD11c(+) cells in the lungs during M. tuberculosis infection. Selective reconstitution of il12rb1(-/-) DCs with (mRNA) il12rb1 and/or (mRNA) il12rb1Deltatm demonstrates that IL-12Rbeta1DeltaTM augments IL-12Rbeta1-dependent DC migration and activation of M. tuberculosis-specific T cells. It cannot mediate these activities independently of IL12Rbeta1. We hypothesize that M. tuberculosis-exposed DCs express IL-12Rbeta1DeltaTM to enhance IL-12Rbeta1-dependent migration and promote M. tuberculosis-specific T cell activation. IL-12Rbeta1DeltaTM thus represents a novel positive-regulator of IL12Rbeta1-dependent DC function and of the immune response to M. tuberculosis.This work was supported by the Trudeau Institute and the National Institutes of Health (AI067723 to A. M. Cooper; AI49823 to D. L. Woodland [trainee: R. T. Robinson] and AI084397 to R. T. Robinson)

Rapid Evolution of Enormous, Multichromosomal Genomes in Flowering Plant Mitochondria with Exceptionally High Mutation Rates

A pair of species within the genus Silene have evolved the largest known mitochondrial genomes, coinciding with extreme changes in mutation rate, recombination activity, and genome structure