In this paper, we experiment with novelty-based variants of OpenAI-ES, the NS-ES and NSR-ES algorithms, and evaluate their effectiveness in training complex, transformer-based architectures designed for the problem of reinforcement learning such as Decision Transformers. We also test if we can accelerate the novelty-based training of these larger models by seeding the training by a pretrained models. By this, we build on our previous work, where we tested the ability of evolution strategies - specifically the aforementioned OpenAI-ES - to train the Decision Transformer architecture. The results were mixed. NS-ES showed progress, but it would clearly need many more iterations for it to yield interesting results. NSR-ES, on the other hand, proved quite capable of being straightforwardly used on larger models, since its performance appears as similar between the feed-forward model and Decision Transformer, as it was for the OpenAI-ES in our previous work.

The Wilson-Cowan model for metapopulation, a Neural Mass Network Model, treats different subcortical regions of the brain as connected nodes, with connections representing various types of structural, functional, or effective neuronal connectivity between these regions. Each region comprises interacting populations of excitatory and inhibitory cells, consistent with the standard Wilson-Cowan model. By incorporating stable attractors into such a metapopulation model's dynamics, we transform it into a learning algorithm capable of achieving high image and text classification accuracy. We test it on MNIST and Fashion MNIST, in combination with convolutional neural networks, on CIFAR-10 and TF-FLOWERS, and, in combination with a transformer architecture (BERT), on IMDB, always showing high classification accuracy. These numerical evaluations illustrate that minimal modifications to the Wilson-Cowan model for metapopulation can reveal unique and previously unobserved dynamics.

Epidemic spreading phenomena are ubiquitous in nature and society. Examples include the spreading of diseases, information, and computer viruses. Epidemics can spread by local spreading, where infected nodes can only infect a limited set of direct target nodes and global spreading, where an infected node can infect every other node. In reality, many epidemics spread using a hybrid mixture of both types of spreading. In this study we develop a theoretical framework for studying hybrid epidemics, and examine the optimum balance between spreading mechanisms in terms of achieving the maximum outbreak size. We show the existence of critically hybrid epidemics where neither spreading mechanism alone can cause a noticeable spread but a combination of the two spreading mechanisms would produce an enormous outbreak. Our results provide new strategies for maximising beneficial epidemics and estimating the worst outcome of damaging hybrid epidemics.