This paper presents a case study where a model predictive control (MPC) logic is developed for energy flexible operation of a space heating system in an educational building. A Long Short-Term Memory Neural Network (LSTM) surrogate model is trained on the output of an EnergyPlus building simulation model. This LSTM model is used within an MPC framework where a genetic algorithm is used to optimize setpoint sequences. The EnergyPlus model is used to validate the performance of the control logic. The MPC approach leads to a substantial reduction in energy consumption (7%) and energy costs (13%) with improved comfort performance. Additional energy costs savings are possible (7–16%) if a sacrifice in indoor thermal comfort is accepted. The presented method is useful for developing MPC systems in the design stages where measured data is typically not available. Additionally, this study illustrates that LSTM models are promising for MPC for buildings.
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Reliability is a constraint of low-power wireless connectivity, commonly addressed by the deployment of mesh topology. Accordingly, power consumption becomes a major concern during the design and implementation of such networks. Thus, a mono-objective optimization was implemented in this work to decrease the total amount of power consumed by a low-power wireless mesh network based on Thread protocol. Using a genetic algorithm, the optimization procedure takes into account a pre-defined connectivity matrix, in which the possible distances between all network devices are considered. The experimental proof-of-concept shows that a mean gain of 26.45 dB is achievable in a specific scenario. Through our experimental results, we conclude that the Thread mesh protocol has much leeway to meet the low-power consumption requirement of wireless sensor networks.
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Humanitarian logistics is regarded as a key area for improved disaster management efficiency and effectiveness. In this study, a multi-objective integrated logistic model is proposed to locate disaster relief centers while taking into account network costs and responsiveness. Because this location problem is NP-hard, we present a genetic approach to solve the proposed model.
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Huntington’s disease (HD) and various spinocerebellar ataxias (SCA) are autosomal dominantly inherited neurodegenerative disorders caused by a CAG repeat expansion in the disease-related gene1. The impact of HD and SCA on families and individuals is enormous and far reaching, as patients typically display first symptoms during midlife. HD is characterized by unwanted choreatic movements, behavioral and psychiatric disturbances and dementia. SCAs are mainly characterized by ataxia but also other symptoms including cognitive deficits, similarly affecting quality of life and leading to disability. These problems worsen as the disease progresses and affected individuals are no longer able to work, drive, or care for themselves. It places an enormous burden on their family and caregivers, and patients will require intensive nursing home care when disease progresses, and lifespan is reduced. Although the clinical and pathological phenotypes are distinct for each CAG repeat expansion disorder, it is thought that similar molecular mechanisms underlie the effect of expanded CAG repeats in different genes. The predicted Age of Onset (AO) for both HD, SCA1 and SCA3 (and 5 other CAG-repeat diseases) is based on the polyQ expansion, but the CAG/polyQ determines the AO only for 50% (see figure below). A large variety on AO is observed, especially for the most common range between 40 and 50 repeats11,12. Large differences in onset, especially in the range 40-50 CAGs not only imply that current individual predictions for AO are imprecise (affecting important life decisions that patients need to make and also hampering assessment of potential onset-delaying intervention) but also do offer optimism that (patient-related) factors exist that can delay the onset of disease.To address both items, we need to generate a better model, based on patient-derived cells that generates parameters that not only mirror the CAG-repeat length dependency of these diseases, but that also better predicts inter-patient variations in disease susceptibility and effectiveness of interventions. Hereto, we will use a staggered project design as explained in 5.1, in which we first will determine which cellular and molecular determinants (referred to as landscapes) in isogenic iPSC models are associated with increased CAG repeat lengths using deep-learning algorithms (DLA) (WP1). Hereto, we will use a well characterized control cell line in which we modify the CAG repeat length in the endogenous ataxin-1, Ataxin-3 and Huntingtin gene from wildtype Q repeats to intermediate to adult onset and juvenile polyQ repeats. We will next expand the model with cells from the 3 (SCA1, SCA3, and HD) existing and new cohorts of early-onset, adult-onset and late-onset/intermediate repeat patients for which, besides accurate AO information, also clinical parameters (MRI scans, liquor markers etc) will be (made) available. This will be used for validation and to fine-tune the molecular landscapes (again using DLA) towards the best prediction of individual patient related clinical markers and AO (WP3). The same models and (most relevant) landscapes will also be used for evaluations of novel mutant protein lowering strategies as will emerge from WP4.This overall development process of landscape prediction is an iterative process that involves (a) data processing (WP5) (b) unsupervised data exploration and dimensionality reduction to find patterns in data and create “labels” for similarity and (c) development of data supervised Deep Learning (DL) models for landscape prediction based on the labels from previous step. Each iteration starts with data that is generated and deployed according to FAIR principles, and the developed deep learning system will be instrumental to connect these WPs. Insights in algorithm sensitivity from the predictive models will form the basis for discussion with field experts on the distinction and phenotypic consequences. While full development of accurate diagnostics might go beyond the timespan of the 5 year project, ideally our final landscapes can be used for new genetic counselling: when somebody is positive for the gene, can we use his/her cells, feed it into the generated cell-based model and better predict the AO and severity? While this will answer questions from clinicians and patient communities, it will also generate new ones, which is why we will study the ethical implications of such improved diagnostics in advance (WP6).
