Modelling and analysis of spiking neural P systems with anti-spikes using Pnet lab

a b s t r a c t Petri Nets are promising methods for modelling and simulating biological systems. Spiking Neural P system with anti-spikes (SN PA systems) is a biologically inspired computing model that incorporates two types of objects called spikes and anti-spikes thus representing binary information in a natural way. In this paper, we propose a methodology to simulate SN PA systems using a Petri net tool called Pnet Lab. It provides a promising way for SN PA systems because of its parallel execution semantics and appropriateness to represent typical working processes of these systems. This enables us to verify system properties, system soundness and to simulate the dynamic behaviour

P Systems with Anti-Matter

After a short introduction to the area of membrane computing (a branch of natural computing), we introduce the concept of anti-matter in membrane computing. First we consider spiking neural P systems with anti-spikes, and then we show the power of anti-matter in cell-like P systems. As expected, the use of anti-matter objects and especially of matter/anti-matter annihilation rules, turns out to be rather powerful: computational completeness of P systems with anti-matter is obtained immediately, even without using catalysts. Finally, some open problems are formulated, too

Activation of the pro-resolving receptor Fpr2 attenuates inflammatory microglial activation

Poster number: P-T099 Theme: Neurodegenerative disorders & ageing Activation of the pro-resolving receptor Fpr2 reverses inflammatory microglial activation Authors: Edward S Wickstead - Life Science & Technology University of Westminster/Queen Mary University of London Inflammation is a major contributor to many neurodegenerative disease (Heneka et al. 2015). Microglia, as the resident immune cells of the brain and spinal cord, provide the first line of immunological defence, but can become deleterious when chronically activated, triggering extensive neuronal damage (Cunningham, 2013). Dampening or even reversing this activation may provide neuronal protection against chronic inflammatory damage. The aim of this study was to determine whether lipopolysaccharide (LPS)-induced inflammation could be abrogated through activation of the receptor Fpr2, known to play an important role in peripheral inflammatory resolution. Immortalised murine microglia (BV2 cell line) were stimulated with LPS (50ng/ml) for 1 hour prior to the treatment with one of two Fpr2 ligands, either Cpd43 or Quin-C1 (both 100nM), and production of nitric oxide (NO), tumour necrosis factor alpha (TNFα) and interleukin-10 (IL-10) were monitored after 24h and 48h. Treatment with either Fpr2 ligand significantly suppressed LPS-induced production of NO or TNFα after both 24h and 48h exposure, moreover Fpr2 ligand treatment significantly enhanced production of IL-10 48h post-LPS treatment. As we have previously shown Fpr2 to be coupled to a number of intracellular signaling pathways (Cooray et al. 2013), we investigated potential signaling responses. Western blot analysis revealed no activation of ERK1/2, but identified a rapid and potent activation of p38 MAP kinase in BV2 microglia following stimulation with Fpr2 ligands. Together, these data indicate the possibility of exploiting immunomodulatory strategies for the treatment of neurological diseases, and highlight in particular the important potential of resolution mechanisms as novel therapeutic targets in neuroinflammation. References Cooray SN et al. (2013). Proc Natl Acad Sci U S A 110: 18232-7. Cunningham C (2013). Glia 61: 71-90. Heneka MT et al. (2015). Lancet Neurol 14: 388-40