DISPATCH: A Numerical Simulation Framework for the Exa-scale Era. I. Fundamentals

We introduce a high-performance simulation framework that permits the semi-independent, task-based solution of sets of partial differential equations, typically manifesting as updates to a collection of `patches' in space-time. A hybrid MPI/OpenMP execution model is adopted, where work tasks are controlled by a rank-local `dispatcher' which selects, from a set of tasks generally much larger than the number of physical cores (or hardware threads), tasks that are ready for updating. The definition of a task can vary, for example, with some solving the equations of ideal magnetohydrodynamics (MHD), others non-ideal MHD, radiative transfer, or particle motion, and yet others applying particle-in-cell (PIC) methods. Tasks do not have to be grid-based, while tasks that are, may use either Cartesian or orthogonal curvilinear meshes. Patches may be stationary or moving. Mesh refinement can be static or dynamic. A feature of decisive importance for the overall performance of the framework is that time steps are determined and applied locally; this allows potentially large reductions in the total number of updates required in cases when the signal speed varies greatly across the computational domain, and therefore a corresponding reduction in computing time. Another feature is a load balancing algorithm that operates `locally' and aims to simultaneously minimise load and communication imbalance. The framework generally relies on already existing solvers, whose performance is augmented when run under the framework, due to more efficient cache usage, vectorisation, local time-stepping, plus near-linear and, in principle, unlimited OpenMP and MPI scaling.Comment: 17 pages, 8 figures. Accepted by MNRA

Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves.

Schwann cells respond to nerve injury by cellular reprogramming that generates cells specialized for promoting regeneration and repair. These repair cells clear redundant myelin, attract macrophages, support survival of damaged neurons, encourage axonal growth, and guide axons back to their targets. There are interesting parallels between this response and that found in other tissues. At the cellular level, many other tissues also react to injury by cellular reprogramming, generating cells specialized to promote tissue homeostasis and repair. And at the molecular level, a common feature possessed by Schwann cells and many other cells is the injury-induced activation of genes associated with epithelial-mesenchymal transitions and stemness, differentiation states that are linked to cellular plasticity and that help injury-induced tissue remodeling. The number of signaling systems regulating Schwann cell plasticity is rapidly increasing. Importantly, this includes mechanisms that are crucial for the generation of functional repair Schwann cells and nerve regeneration, although they have no or a minor role elsewhere in the Schwann cell lineage. This encourages the view that selective tools can be developed to control these particular cells, amplify their repair supportive functions and prevent their deterioration. In this review, we discuss the emerging similarities between the injury response seen in nerves and in other tissues and survey the transcription factors, epigenetic mechanisms, and signaling cascades that control repair Schwann cells, with emphasis on systems that selectively regulate the Schwann cell injury response.Wellcome Trust, Medical Research Council, European Research Counci