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Abstract Communication by rare, binary spikes is a key factor for the energy efficiency of biological brains. However, it is harder to train biologically-inspired spiking neural networks than artificial neural networks. This is puzzling given that theoretical results provide exact mapping algorithms from artificial to spiking neural networks with time-to-first-spike coding. In this paper we analyze in theory and simulation the learning dynamics of time-to-first-spike-networks and identify a specific instance of the vanishing-or-exploding gradient problem. While two choices of spiking neural network mappings solve this problem at initialization, only the one with a constant slope of the neuron membrane potential at threshold guarantees the equivalence of the training trajectory between spiking and artificial neural networks with rectified linear units. For specific image classification architectures comprising feed-forward dense or convolutional layers, we demonstrate that deep spiking neural network models can be effectively trained from scratch on MNIST and Fashion-MNIST datasets, or fine-tuned on large-scale datasets, such as CIFAR10, CIFAR100 and PLACES365, to achieve the exact same performance as that of artificial neural networks, surpassing previous spiking neural networks. Our approach accomplishes high-performance classification with less than 0.3 spikes per neuron, lending itself for an energy-efficient implementation. We also show that fine-tuning spiking neural networks with our robust gradient descent algorithm enables their optimization for hardware implementations with low latency and resilience to noise and quantization.

Optical identification is often done with spatial or temporal visual pattern recognition and localization. Temporal pattern recognition, depending on the technology, involves a trade-off between communication frequency, range, and accurate tracking. We propose a solution with light-emitting beacons that improves this trade-off by exploiting fast event-based cameras and, for tracking, sparse neuromorphic optical flow computed with spiking neurons. The system is embedded in a simulated drone and evaluated in an asset monitoring use case. It is robust to relative movements and enables simultaneous communication with, and tracking of, multiple moving beacons. Finally, in a hardware lab prototype, we demonstrate for the first time beacon tracking performed simultaneously with state-of-the-art frequency communication in the kHz range.

Abstract Visual oddity task was conceived to study universal ethnic-independent analytic intelligence of humans from a perspective of comprehension of spatial concepts. Advancements in artificial intelligence led to important breakthroughs, yet excelling at such abstract tasks remains challenging. Current approaches typically resort to non-biologically-plausible architectures with ever-growing models consuming substantially more energy than the brain. Motivated by the brain’s efficiency and reasoning capabilities, we present a biologically inspired system that receives inputs from synthetic eye movements – reminiscent of saccades, and processes them with neuronal units incorporating dynamics of neocortical neurons. We introduce a procedurally generated visual oddity dataset to train an architecture extending conventional relational networks and our proposed system. We demonstrate that both approaches are capable of abstract problem-solving at high accuracy, and we uncover that both share the same essential underlying mechanism of reasoning in seemingly unrelated aspects of their architectures. Finally, we show that the biologically inspired network achieves superior accuracy, learns faster and requires fewer parameters than the conventional network.

Tasks involving continual learning and adaptation to real-time scenarios remain challenging for artificial neural networks in contrast to real brain. The authors propose here a brain-inspired optimizer based on mechanisms of synaptic integration and strength regulation for improved performance of both artificial and spiking neural networks.

Abstract Background Genomic rearrangements exert a heavy influence on the molecular landscape of cancer. New analytical approaches integrating somatic structural variants (SSVs) with altered gene features represent a framework by which we can assign global significance to a core set of genes, analogous to established methods that identify genes non-randomly targeted by somatic mutation or copy number alteration. While recent studies have defined broad patterns of association involving gene transcription and nearby SSV breakpoints, global alterations in DNA methylation in the context of SSVs remain largely unexplored. Results By data integration of whole genome sequencing, RNA sequencing, and DNA methylation arrays from more than 1400 human cancers, we identify hundreds of genes and associated CpG islands (CGIs) for which the nearby presence of a somatic structural variant (SSV) breakpoint is recurrently associated with altered expression or DNA methylation, respectively, independently of copy number alterations. CGIs with SSV-associated increased methylation are predominantly promoter-associated, while CGIs with SSV-associated decreased methylation are enriched for gene body CGIs. Rearrangement of genomic regions normally having higher or lower methylation is often involved in SSV-associated CGI methylation alterations. Across cancers, the overall structural variation burden is associated with a global decrease in methylation, increased expression in methyltransferase genes and DNA damage response genes, and decreased immune cell infiltration. Conclusion Genomic rearrangement appears to have a major role in shaping the cancer DNA methylome, to be considered alongside commonly accepted mechanisms including histone modifications and disruption of DNA methyltransferases.

Summary: A systematic cataloging of genes affected by genomic rearrangement, using multiple patient cohorts and cancer types, can provide insight into cancer-relevant alterations outside of exomes. By integrative analysis of whole-genome sequencing (predominantly low pass) and gene expression data from 1,448 cancers involving 18 histopathological types in The Cancer Genome Atlas, we identified hundreds of genes for which the nearby presence (within 100 kb) of a somatic structural variant (SV) breakpoint is associated with altered expression. While genomic rearrangements are associated with widespread copy-number alteration (CNA) patterns, approximately 1,100 genes—including overexpressed cancer driver genes (e.g., TERT, ERBB2, CDK12, CDK4) and underexpressed tumor suppressors (e.g., TP53, RB1, PTEN, STK11)—show SV-associated deregulation independent of CNA. SVs associated with the disruption of topologically associated domains, enhancer hijacking, or fusion transcripts are implicated in gene upregulation. For cancer-relevant pathways, SVs considerably expand our understanding of how genes are affected beyond point mutation or CNA. : Zhang et al. analyzed over 1,400 cancers by high- or low-pass whole-genome sequencing, focusing on patterns of structural variation. They saw a widespread impact of somatic structural variants on gene expression patterns, independent of copy-number alterations, involving key oncogenes and tumor suppressor genes. Keywords: cancer, structural variation, genomic rearrangement, whole genome sequencing, pan-cancer, TCGA