State of health estimation for lithium-ion batteries under arbitrary usage using data-driven multi-model fusion

Accurately estimating the state of health (SoH) of batteries is indispensable for the safety, reliability, and optimal energy and power management of electric vehicles. However, from a data-driven perspective, complications, such as dynamic vehicle operating conditions, stochastic user behaviors, and cell-to-cell variations, make the estimation task challenging. This work develops a data-driven multi-model fusion method for SoH estimation under arbitrary usage profiles. All possible operating conditions are categorized into six scenarios. For each scenario, an appropriate feature set is extracted to indicate the SoH. Based on the obtained features, four machine learning algorithms are applied individually to train SoH estimation models using time-series data. In addition to the estimates at the current time step, a histogram data-based and online adaptive model is taken from previous work for predicting the next-step SoH. Then, a Kalman filter is applied to systematically fuse the results of all the estimation and prediction models. Experimental data collected from different types of batteries operated under diverse profiles verify the effectiveness and practicability of the developed method, as well as its superiority over individual models

A machine learning-based framework for online prediction of battery ageing trajectory and lifetime using histogram data

Accurately predicting batteries’ ageing trajectory and remaining useful life is not only required to ensure safe and reliable operation of electric vehicles (EVs) but is also the fundamental step towards health-conscious use and residual value assessment of the battery. The non-linearity, wide range of operating conditions, and cell to cell variations make battery health prediction challenging. This paper proposes a prediction framework that is based on a combination of global models offline developed by different machine learning methods and cell individualised models that are online adapted. For any format of raw data collected under diverse operating conditions, statistic properties of histograms can be still extracted and used as features to learn battery ageing. Our framework is trained and tested on three large datasets, one being retrieved from 7296 plug-in hybrid EVs. While the best global models achieve 0.93% mean absolute percentage error (MAPE) on laboratory data and 1.41% MAPE on the real-world fleet data, the adaptation algorithm further reduced the errors by up to 13.7%, all requiring low computational power and memory. Overall, this work proves the feasibility and benefits of using histogram data and also highlights how online adaptation can be used to improve predictions

Artificial intelligence based automatic quantification of epicardial adipose tissue suitable for large scale population studies

To develop a fully automatic model capable of reliably quantifying epicardial adipose tissue (EAT) volumes and attenuation in large scale population studies to investigate their relation to markers of cardiometabolic risk. Non-contrast cardiac CT images from the SCAPIS study were used to train and test a convolutional neural network based model to quantify EAT by: segmenting the pericardium, suppressing noise-induced artifacts in the heart chambers, and, if image sets were incomplete, imputing missing EAT volumes. The model achieved a mean Dice coefficient of 0.90 when tested against expert manual segmentations on 25 image sets. Tested on 1400 image sets, the model successfully segmented 99.4% of the cases. Automatic imputation of missing EAT volumes had an error of less than 3.1% with up to 20% of the slices in image sets missing. The most important predictors of EAT volumes were weight and waist, while EAT attenuation was predicted mainly by EAT volume. A model with excellent performance, capable of fully automatic handling of the most common challenges in large scale EAT quantification has been developed. In studies of the importance of EAT in disease development, the strong co-variation with anthropometric measures needs to be carefully considered

A panel of CSF proteins separates genetic frontotemporal dementia from presymptomatic mutation carriers: a GENFI study.

BACKGROUND: A detailed understanding of the pathological processes involved in genetic frontotemporal dementia is critical in order to provide the patients with an optimal future treatment. Protein levels in CSF have the potential to reflect different pathophysiological processes in the brain. We aimed to identify and evaluate panels of CSF proteins with potential to separate symptomatic individuals from individuals without clinical symptoms (unaffected), as well as presymptomatic individuals from mutation non-carriers. METHODS: A multiplexed antibody-based suspension bead array was used to analyse levels of 111 proteins in CSF samples from 221 individuals from families with genetic frontotemporal dementia. The data was explored using LASSO and Random forest. RESULTS: When comparing affected individuals with unaffected individuals, 14 proteins were identified as potentially important for the separation. Among these, four were identified as most important, namely neurofilament medium polypeptide (NEFM), neuronal pentraxin 2 (NPTX2), neurosecretory protein VGF (VGF) and aquaporin 4 (AQP4). The combined profile of these four proteins successfully separated the two groups, with higher levels of NEFM and AQP4 and lower levels of NPTX2 in affected compared to unaffected individuals. VGF contributed to the models, but the levels were not significantly lower in affected individuals. Next, when comparing presymptomatic GRN and C9orf72 mutation carriers in proximity to symptom onset with mutation non-carriers, six proteins were identified with a potential to contribute to a separation, including progranulin (GRN). CONCLUSION: In conclusion, we have identified several proteins with the combined potential to separate affected individuals from unaffected individuals, as well as proteins with potential to contribute to the separation between presymptomatic individuals and mutation non-carriers. Further studies are needed to continue the investigation of these proteins and their potential association to the pathophysiological mechanisms in genetic FTD