Statistical Epistemic Logic

We introduce a modal logic for describing statistical knowledge, which we call statistical epistemic logic. We propose a Kripke model dealing with probability distributions and stochastic assignments, and show a stochastic semantics for the logic. To our knowledge, this is the first semantics for modal logic that can express the statistical knowledge dependent on non-deterministic inputs and the statistical significance of observed results. By using statistical epistemic logic, we express a notion of statistical secrecy with a confidence level. We also show that this logic is useful to formalize statistical hypothesis testing and differential privacy in a simple and abstract manner

Specific Loss of Histone H3 Lysine 9 Trimethylation and HP1γ/Cohesin Binding at D4Z4 Repeats Is Associated with Facioscapulohumeral Dystrophy (FSHD)

Facioscapulohumeral dystrophy (FSHD) is an autosomal dominant muscular dystrophy in which no mutation of pathogenic gene(s) has been identified. Instead, the disease is, in most cases, genetically linked to a contraction in the number of 3.3 kb D4Z4 repeats on chromosome 4q. How contraction of the 4qter D4Z4 repeats causes muscular dystrophy is not understood. In addition, a smaller group of FSHD cases are not associated with D4Z4 repeat contraction (termed “phenotypic” FSHD), and their etiology remains undefined. We carried out chromatin immunoprecipitation analysis using D4Z4–specific PCR primers to examine the D4Z4 chromatin structure in normal and patient cells as well as in small interfering RNA (siRNA)–treated cells. We found that SUV39H1–mediated H3K9 trimethylation at D4Z4 seen in normal cells is lost in FSHD. Furthermore, the loss of this histone modification occurs not only at the contracted 4q D4Z4 allele, but also at the genetically intact D4Z4 alleles on both chromosomes 4q and 10q, providing the first evidence that the genetic change (contraction) of one 4qD4Z4 allele spreads its effect to other genomic regions. Importantly, this epigenetic change was also observed in the phenotypic FSHD cases with no D4Z4 contraction, but not in other types of muscular dystrophies tested. We found that HP1γ and cohesin are co-recruited to D4Z4 in an H3K9me3–dependent and cell type–specific manner, which is disrupted in FSHD. The results indicate that cohesin plays an active role in HP1 recruitment and is involved in cell type–specific D4Z4 chromatin regulation. Taken together, we identified the loss of both histone H3K9 trimethylation and HP1γ/cohesin binding at D4Z4 to be a faithful marker for the FSHD phenotype. Based on these results, we propose a new model in which the epigenetic change initiated at 4q D4Z4 spreads its effect to other genomic regions, which compromises muscle-specific gene regulation leading to FSHD pathogenesis

Brain Tumor Epidemiology – A Hub within Multidisciplinary Neuro-oncology. Report on the 15th Brain Tumor Epidemiology Consortium (BTEC) Annual Meeting, Vienna, 2014

The Brain Tumor Epidemiology Consortium (BTEC) is an open scientific forum, which fosters the development of multi-center, international and inter-disciplinary collaborations. BTEC aims to develop a better understanding of the etiology, outcomes, and prevention of brain tumors (http://epi.grants.cancer.govibtec/). The 15th annual Brain Tumor Epidemiology Consortium Meeting, hosted by the Austrian Societies of Neuropathology and Neuro-oncology, was held on September 9 - 11, 2014 in Vienna, Austria. The meeting focused on the central role of brain tumor epidemiology within multidisciplinary neuro-oncology. Knowledge of disease incidence, outcomes, as well as risk factors is fundamental to all fields involved in research and treatment of patients with brain tumors; thus, epidemiology constitutes an important link between disciplines, indeed the very hub. This was reflected by the scientific program, which included various sessions linking brain tumor epidemiology with clinical neuro-oncology, tissue-based research, and cancer registration. Renowned experts from Europe and the United States contributed their personal perspectives stimulating further group discussions. Several concrete action plans evolved for the group to move forward until next year's meeting, which will be held at the Mayo Clinic at Rochester, MN, USA

Toward a Formal Model for Group Polarization in Social Networks

International audienceIn this paper we develop a preliminary model for social networks , and a measure of the level of polarization in these social networks, based on Esteban and Ray's classic measure of polarization for economic situations. Our model includes information about each agent's quantitative strength of belief in a proposition of interest and a representation of the strength of each agent's influence on every other agent. We consider how the model changes over time as agents interact and communicate, and include several different options for belief update, including rational belief update and update taking into account irrational responses such as confirmation bias and the backfire effect. Under various scenarios, we consider the evolution of polarization over time, and the implications of these results for real world social networks

Logic and probabilistic update

This chapter surveys recent work on probabilistic extensions of epistemic and dynamic-epistemic logics (the latter include the basic system of public announcement logic as well as the full product update logic). It emphasizes the importance of higher-order information as a distinguishing feature of these logics. This becomes particularly clear in the dynamic setting: Although there exists a clear relationship between usual Bayesian conditionalization and public announcement, the probabilistic effects of the latter are in general more difficult to describe, because of the subtleties involved in higher-order information. Finally, the chapter discusses some applications of probabilistic dynamic epistemic logic, such as the Lockean thesis in formal epistemology and Aumann’s agreement theorem in game theory