Applying neuromorphic vision sensors to planetary landing tasks

Recently there has been an increasing interest in application of bio-mimetic controller s and neuromorphic vision sensor s to planetary landing tasks. Within this context, we present combined low-level (SPICE) and high-level (behavioral) simulations of a novel neuromorphic VLSI vision sensor in a realistic planetary landing scenar io. We use results from low level simulations to build an abstr act descr iption of the chip which can be used in higher level simulations which include closed-loop control of the cr aft

Rhythmic inhibition allows neural networks to search for maximally consistent states

Gamma-band rhythmic inhibition is a ubiquitous phenomenon in neural circuits yet its computational role still remains elusive. We show that a model of Gamma-band rhythmic inhibition allows networks of coupled cortical circuit motifs to search for network configurations that best reconcile external inputs with an internal consistency model encoded in the network connectivity. We show that Hebbian plasticity allows the networks to learn the consistency model by example. The search dynamics driven by rhythmic inhibition enable the described networks to solve difficult constraint satisfaction problems without making assumptions about the form of stochastic fluctuations in the network. We show that the search dynamics are well approximated by a stochastic sampling process. We use the described networks to reproduce perceptual multi-stability phenomena with switching times that are a good match to experimental data and show that they provide a general neural framework which can be used to model other 'perceptual inference' phenomena

Novel insights into the transport mechanism of the human amino acid transporter LAT1 (SLC7A5) : probing critical residues for substrate translocation

BACKGROUND: LAT1 (SLC7A5) is the transport competent unit of the heterodimer formed with the glycoprotein CD98 (SLC3A2). It catalyzes antiport of His and some neutral amino acids such as Ile, Leu, Val, Cys, Met, Gln and Phe thus being involved in amino acid metabolism. Interestingly, LAT1 is over-expressed in many human cancers that are characterized by increased demand of amino acids. Therefore LAT1 was recently acknowledged as a novel target for cancer therapy. However, knowledge on molecular mechanism of LAT1 transport is still scarce. METHODS: Combined approaches of bioinformatics, site-directed mutagenesis, chemical modification, and transport assay in proteoliposomes, have been adopted to unravel dark sides of human LAT1 structure/function relationships. RESULTS: It has been demonstrated that residues F252, S342, C335 are crucial for substrate recognition and C407 plays a minor role. C335 and C407 cannot be targeted by SH reagents. The transporter has a preferential dimeric structure and catalyzes an antiport reaction which follows a simultaneous random mechanism. CONCLUSIONS: Critical residues of the substrate binding site of LAT1 have been probed. This site is not freely accessible by molecules other than substrate. Similarly to LeuT, K+ has some regulatory properties on LAT1. GENERAL SIGNIFICANCE: The collected data represent a solid basis for deciphering molecular mechanism underlying LAT1 function

Event-based Classification with Recurrent Spiking Neural Networks on Low-end Micro-Controller Units

Due to its intrinsic sparsity both in time and space, event-based data is optimally suited for edge-computing applications that require low power and low latency. Time varying signals encoded with this data representation are best processed with Spiking Neural Networks (SNN). In particular, recurrent SNNs (RSNNs) can solve temporal tasks using a relatively low number of parameters, and therefore support their hardware implementation in resource-constrained computing architectures. These premises propel the need of exploring the properties of these kinds of structures on low-power processing systems to test their limits both in terms of computational accuracy and resource consumption, without having to resort to full-custom implementations. In this work, we implemented an RSNN model on a low-end, resource-constrained ARM-Cortex-M4-based Micro Controller Unit (MCU). We trained it on a down-sampled version of the N-MNIST event-based dataset for digit recognition as an example to assess its performance in the inference phase. With an accuracy of 97.2%, the implementation has an average energy consumption as low as 4.1μJ and a worst-case computational time of 150.4μs per time-step with an operating frequency of 180 MHz, so the deployment of RSNNs on MCU devices is a feasible option for small image vision real-time tasks

Mimicking human riboflavin responsive neuromuscular disorders by silencing flad-1 gene in C. elegans: Alteration of vitamin transport and cholinergic transmission

Riboflavin (Rf), or vitamin B2, is the precursor of FMN and FAD, redox cofactors of several dehydrogenases involved in energy metabolism, redox balance and other cell regulatory processes. FAD synthase, coded by FLAD1 gene in humans, is the last enzyme in the pathway converting Rf into FAD. Mutations in FLAD1 gene are responsible for neuromuscular disorders, in some cases treatable with Rf. In order to mimic these disorders, the Caenorhabditis elegans (C. elegans) gene orthologue of FLAD1 (flad-1) was silenced in a model strain hypersensitive to RNA interference in nervous system. Silencing flad-1 resulted in a significant decrease in total flavin content, paralleled by a decrease in the level of the FAD-dependent ETFDH protein and by a secondary transcriptional down-regulation of the Rf transporter 1 (rft-1) possibly responsible for the total flavin content decrease. Conversely an increased ETFDH mRNA content was found. These biochemical changes were accompanied by significant phenotypical changes, including impairments of fertility and locomotion due to altered cholinergic transmission, as indicated by the increased sensitivity to aldicarb. A proposal is made that neuronal acetylcholine production/release is affected by alteration of Rf homeostasis. Rf supplementation restored flavin content, increased rft-1 transcript levels and eliminated locomotion defects. In this aspect, C. elegans could provide a low-cost animal model to elucidate the molecular rationale for Rf therapy in human Rf responsive neuromuscular disorders and to screen other molecules with therapeutic potential

SLC1A5 (solute carrier family 1 (neutral amino acid transporter), member 5)

Review on human SLC1A5, with data on DNA/RNA, on the protein encoded and pathological and physiological implications

SLC6A14, a Pivotal Actor on Cancer Stage: When Function Meets Structure

SLC6A14 (ATB0,+) is a sodium- and chloride-dependent neutral and dibasic amino acid transporter that regulates the distribution of amino acids across cell membranes. The transporter is overexpressed in many human cancers characterized by an increased demand for amino acids; as such, it was recently acknowledged as a novel target for cancer therapy. The knowledge on the molecular mechanism of SLC6A14 transport is still limited, but some elegant studies on related transporters report the involvement of the 12 transmembrane \u3b1-helices in the transport mechanism, and describe structural rearrangements mediated by electrostatic interactions with some pivotal gating residues. In the present work, we constructed a SLC6A14 model in outward-facing conformation via homology modeling and used molecular dynamics simulations to predict amino acid residues critical for substrate recognition and translocation. We docked the proteinogenic amino acids and other known substrates in the SLC6A14 binding site to study both gating regions and the exposed residues involved in transport. Interestingly, some of these residues correspond to those previously identified in other LeuT-fold transporters; however, we could also identify a novel relevant residue with such function. For the first time, by combined approaches of molecular docking and molecular dynamics simulations, we highlight the potential role of these residues in neutral amino acid transport. This novel information unravels new aspects of the human SLC6A14 structure-function relationship and may have important outcomes for cancer treatment through the design of novel inhibitors of SLC6A14-mediated transport