Feature Extraction Methods for Neural Networks in the Classification of Structural Health Anomalies

Failure of large complex structures such as buildings and bridges can have monumental repercussions such as human mortality, environmental destruction and economic consequences. It is therefore paramount that detection of structural damage or anomalies are identified and managed early. This highlights the need to develop automated Structural Health Monitoring (SHM) systems that can continuously allow the safety status of structures to be determined, even in the worst and most isolated conditions, to ultimately help prevent destruction and save lives. Signal processing is a crucial step to detecting structural anomalies and recent work demonstrates the opportunities for neural networks, however the encoding of data for SHM requires the extraction of features due to often, noisy data. This paper focuses on feature extraction methods for artificial neural networks (ANNs) and spiking neural networks (SNNs) and aims to identify bespoke features which enable SNNs to encode data and perform the classification of anomalies. Results show that extraction of particular features in large real-world applications improve the classification accuracy of SNNs

Mathematical modeling of PI3K/Akt pathway in microglia

The motility of microglia involves intracellular signaling pathways that are predominantly controlled by changes in cytosolic Ca2+ and activation of PI3K/Akt (phosphoinositide-3-kinase/protein kinase B). In this letter, we develop a novel biophysical model for cytosolic Ca2+ activation of the PI3K/Akt pathway in microglia where Ca2+ influx is mediated by both P2Y purinergic receptors (P2YR) and P2X purinergic receptors (P2XR). The model parameters are estimated by employing optimization techniques to fit the model to phosphorylated Akt (pAkt) experimental modeling/in vitro data. The integrated model supports the hypothesis that Ca2+ influx via P2YR and P2XR can explain the experimentally reported biphasic transient responses in measuring pAkt levels. Our predictions reveal new quantitative insights into P2Rs on how they regulate Ca2+ and Akt in terms of physiological interactions and transient responses. It is shown that the upregulation of P2X receptors through a repetitive application of agonist results in a continual increase in the baseline [Ca2+], which causes the biphasic response to become a monophasic response which prolongs elevated levels of pAkt