48 research outputs found
Characterizing common cause closedness of quantum probability theories
We prove new results on common cause closedness of quantum probability
spaces, where by a quantum probability space is meant the projection lattice of
a non-commutative von Neumann algebra together with a countably additive
probability measure on the lattice. Common cause closedness is the feature that
for every correlation between a pair of commuting projections there exists in
the lattice a third projection commuting with both of the correlated
projections and which is a Reichenbachian common cause of the correlation. The
main result we prove is that a quantum probability space is common cause closed
if and only if it has at most one measure theoretic atom. This result improves
earlier ones published in Z. GyenisZ and M. Redei Erkenntnis 79 (2014) 435-451.
The result is discussed from the perspective of status of the Common Cause
Principle. Open problems on common cause closedness of general probability
spaces are formulated, where is an
orthomodular bounded lattice and is a probability measure on
.Comment: Submitted for publicatio
Reconstructing Bohr's Reply to EPR in Algebraic Quantum Theory
Halvorson and Clifton have given a mathematical reconstruction of Bohr's
reply to Einstein, Podolsky and Rosen (EPR), and argued that this reply is
dictated by the two requirements of classicality and objectivity for the
description of experimental data, by proving consistency between their
objectivity requirement and a contextualized version of the EPR reality
criterion which had been introduced by Howard in his earlier analysis of Bohr's
reply. In the present paper, we generalize the above consistency theorem, with
a rather elementary proof, to a general formulation of EPR states applicable to
both non-relativistic quantum mechanics and algebraic quantum field theory; and
we clarify the elements of reality in EPR states in terms of Bohr's
requirements of classicality and objectivity, in a general formulation of
algebraic quantum theory.Comment: 13 pages, Late
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Influence of muscle fiber type composition on early fat accumulation under high-fat diet challenge
Objective: To investigate whether differences in muscle fiber types affect early-stage fat accumulation, under high fat diet challenge in mice. Methods: Twelve healthy male C57BL/6 mice experienced with short-term (6 weeks) diet treatment for the evaluation of early pattern changes in muscular fat. The mice were randomly divided into two groups: high fat diet (n = 8) and normal control diet (n = 4). Extra- and intra-myocellular lipid (EMCL and IMCL) in lumbar muscles (type I fiber predominant) and tibialis anterior (TA) muscle (type II fiber predominant) were determined using magnetic resonance spectroscopy (MRS). Correlation of EMCL, IMCL and their ratio between TA and lumbar muscles was evaluated. Results: EMCL increased greatly in both muscle types after high fat diet. IMCL in TA and lumbar muscles increased to a much lower extent, with a slightly greater increase in TA muscles. EMCLs in the 2 muscles were positively correlated (r = 0.84, p = 0.01), but IMCLs showed a negative relationship (r = -0.84, p = 0.01). In lumbar muscles, high fat diet significantly decreased type I fiber while it increased type II fiber (all p≤0.001). In TA muscle, there was no significant fiber type shifting (p>0.05). Conclusions: Under short-time high fat diet challenge, lipid tends to initially accumulate extra-cellularly. In addition, compared to type II dominant muscle, Type I dominant muscle was less susceptible to IMCL accumulation but more to fiber type shifting. These phenomena might reflect compensative responses of skeletal muscle to dietary lipid overload in order to regulate metabolic homeostasis
Histone H3.3 sub-variant H3mm7 is required for normal skeletal muscle regeneration
Regulation of gene expression requires selective incorporation of histone H3 variant H3.3 into chromatin. Histone H3.3 has several subsidiary variants but their functions are unclear. Here we characterize the function of histone H3.3 sub-variant, H3mm7, which is expressed in skeletal muscle satellite cells. H3mm7 knockout mice demonstrate an essential role of H3mm7 in skeletal muscle regeneration. Chromatin analysis reveals that H3mm7 facilitates transcription by forming an open chromatin structure around promoter regions including those of myogenic genes. The crystal structure of the nucleosome containing H3mm7 reveals that, unlike the S57 residue of other H3 proteins, the H3mm7-specific A57 residue cannot form a hydrogen bond with the R40 residue of the cognate H4 molecule. Consequently, the H3mm7 nucleosome is unstable in vitro and exhibited higher mobility in vivo compared with the H3.3 nucleosome. We conclude that the unstable H3mm7 nucleosome may be required for proper skeletal muscle differentiation
ATM mediates pRBfunction to control DNMT1 protein stability and DNA methylation
The retinoblastoma tumor suppressor gene (RB) product has been implicated in epigenetic control of gene expression owing to its ability to physically bind to many chromatin modifiers. However, the biological and clinical significance of this activity was not well elucidated. To address this, we performed genetic and epigenetic analyses in an Rb-deficient mouse thyroid C cell tumor model. Here we report that the genetic interaction of Rb and ATM regulates DNMT1 protein stability and hence controls the DNA methylation status in the promoters of at least the Ink4a, Shc2, FoxO6, and Noggin genes. Furthermore, we demonstrate that inactivation of pRB promotes Tip60 (acetyltransferase)-dependent ATM activation; allows activated ATM to physically bind to DNMT1, forming a complex with Tip60 and UHRF1 (E3 ligase); and consequently accelerates DNMT1 ubiquitination driven by Tip60-dependent acetylation. Our results indicate that inactivation of the pRB pathway in coordination with aberration in the DNA damage response deregulates DNMT1 stability, leading to an abnormal DNA methylation pattern and malignant progression