An Event Structure Model for Probabilistic Concurrent Kleene Algebra

We give a new true-concurrent model for probabilistic concurrent Kleene algebra. The model is based on probabilistic event structures, which combines ideas from Katoen's work on probabilistic concurrency and Varacca's probabilistic prime event structures. The event structures are compared with a true-concurrent version of Segala's probabilistic simulation. Finally, the algebraic properties of the model are summarised to the extent that they can be used to derive techniques such as probabilistic rely/guarantee inference rules.Comment: Submitted and accepted for LPAR19 (2013

Reverse Bisimulations on Stable Configuration Structures

The relationships between various equivalences on configuration structures, including interleaving bisimulation (IB), step bisimulation (SB) and hereditary history-preserving (HH) bisimulation, have been investigated by van Glabbeek and Goltz (and later Fecher). Since HH bisimulation may be characterised by the use of reverse as well as forward transitions, it is of interest to investigate forms of IB and SB where both forward and reverse transitions are allowed. We give various characterisations of reverse SB, showing that forward steps do not add extra power. We strengthen Bednarczyk's result that, in the absence of auto-concurrency, reverse IB is as strong as HH bisimulation, by showing that we need only exclude auto-concurrent events at the same depth in the configuration

A Logic with Reverse Modalities for History-preserving Bisimulations

We introduce event identifier logic (EIL) which extends Hennessy-Milner logic by the addition of (1) reverse as well as forward modalities, and (2) identifiers to keep track of events. We show that this logic corresponds to hereditary history-preserving (HH) bisimulation equivalence within a particular true-concurrency model, namely stable configuration structures. We furthermore show how natural sublogics of EIL correspond to coarser equivalences. In particular we provide logical characterisations of weak history-preserving (WH) and history-preserving (H) bisimulation. Logics corresponding to HH and H bisimulation have been given previously, but not to WH bisimulation (when autoconcurrency is allowed), as far as we are aware. We also present characteristic formulas which characterise individual structures with respect to history-preserving equivalences.Comment: In Proceedings EXPRESS 2011, arXiv:1108.407

CNTNAP4 signaling regulates osteosarcoma disease progression

Abstract Improved treatment strategies for sarcoma rely on clarification of the molecular mediators of disease progression. Recently, we reported that the secreted glycoprotein NELL-1 modulates osteosarcoma (OS) disease progression in part via altering the sarcomatous extracellular matrix (ECM) and cell-ECM interactions. Of known NELL-1 interactor proteins, Contactin-associated protein-like 4 (Cntnap4) encodes a member of the neurexin superfamily of transmembrane molecules best known for its presynaptic functions in the central nervous system. Here, CRISPR/Cas9 gene deletion of CNTNAP4 reduced OS tumor growth, sarcoma-associated angiogenesis, and pulmonary metastases. CNTNAP4 knockout (KO) in OS tumor cells largely phenocopied the effects of NELL-1 KO, including reductions in sarcoma cell attachment, migration, and invasion. Further, CNTNAP4 KO cells were found to be unresponsive to the effects of NELL-1 treatment. Transcriptomic analysis combined with protein phospho-array demonstrated notable reductions in the MAPK/ERK signaling cascade with CNTNAP4 deletion, and the ERK1/2 agonist isoproterenol restored cell functions among CNTNAP4 KO tumor cells. Finally, human primary cells and tissues in combination with sequencing datasets confirmed the significance of CNTNAP4 signaling in human sarcomas. In summary, our findings demonstrate the biological importance of NELL-1/CNTNAP4 signaling axis in disease progression of human sarcomas and suggest that targeting the NELL-1/CNTNAP4 signaling pathway represents a strategy with potential therapeutic benefit in sarcoma patients

Schedulers and finishers : on generating the behaviours of an event structure

It is well known that every trace of a transition system can be generated using a scheduler. However, this basic completeness result does not hold in event structure models. The reason for this failure is that, according to its standard definition, a scheduler chooses which action to schedule and, at the same time, finishes the one scheduled last. Thus, scheduled events will never be able to overlap. We propose to separate scheduling from finishing and introduce the dual notion of finishers which, together with schedulers, are enough to regain completeness back. We then investigate all possible interactions between schedulers and finishers, concluding that simple alternating interactions are enough to express complex ones. Finally, we show how finishers can be used to filter behaviours to the extent to which they capture intrinsic system characteristics.18 page(s