bioRxiv ScienceSearch

bioRxiv · 10.1101/2021.01.13.426509

Fatigue, Alertness and Risk Prediction for Shift Workers

Abstract

Executive summaryO_LIThis report describes the principal outcomes of an Impact Acceleration Account project (grant number EP/I000992/1) between the University of Surrey and Transport for London carried out between Oct. 2019 and Mar. 2020. C_LIO_LIThe aim of the project was to compare the Health and Safety Executive (HSE) Fatigue Risk tool with SAFTE and other more recent models of fatigue, where fatigue here primarily means a reduced ability to function effectively and efficiently as a result of inadequate sleep. C_LIO_LIWe have not sought to discuss the useability of the HSE Fatigue Risk tool or SAFTE since this has been discussed comprehensively elsewhere (e.g. [1, 2]). We have instead focussed on the fundamental principles underlying the models. C_LIO_LIAll current biomathematical models have limitations and make asumptions that are not always evident from the accompanying documentation. Since full details of the HSE Fatigue Risk tool and the SAFTE model are not publicly available, Sections 1 and 2 give a mathematical description of the equations that we believe underlie each of these models. C_LIO_LIA comparison of predictions made by our versions of the HSE and SAFTE equations for one particular shift schedule of relevance to the UK and global tunnelling and construction industries is shown in Section 3. In this comparison, we use data collected durings TfLs Crossrail project by Dragados1. Essentially, both models give broadly the same message for the schedule we looked at, but the ability to display fatigue as it develops within a shift is a strength of SAFTE. C_LIO_LIA summary of the strengths and limitations of the use of these kind of scheduling tools is given in the final Section 4. Limitations include: O_LIModels do not describe fatigue during times when people are not in shift (e.g. driving home). However, they could readily be extended to do so. C_LIO_LIModels assume people start well-rested. This is not always a good assumption and can lead to an under-estimate of fatigue. C_LIO_LIMost models are currently based on population averages, but there are large individual different. It would be possible to further develop models to include uncertainty in fatigue predictions associated with individual differences. C_LIO_LIFew mdels include the light environment, which is important both to promote short-term alertness and facilitate circadian alignment. C_LIO_LIModels are not transparent, which makes them hard to independently validate. C_LIO_LIIt is hard to relate the outputs of current models to measureable outcomes in the field. C_LI C_LIO_LIWe also discuss briefly recent developments in mathematical modelling of fatigue and possible future directions. These include O_LIGuidance on scheduling and education on sleep and fatigue should be considered at least as important as current biomathematical models. C_LIO_LIOnly by analysing and integrating high quality individual data on sleep, fatigue, performance, near misses, accidents, actual shift patterns with models can we develop better models and management systems to reduce fatigue and associated risks. Wearables combined with apps present a great opportunity to collect data at scale but need to be used appropriately. C_LIO_LIThe importance of making time for sleep is not always recognised. Education, early diagnosis of sleep disorders such as sleep apnea, and self-monitoring all have a role to play in reducing fatigue-related risk in the work-place. C_LI C_LIO_LISection 3 and Section 4 may be understood without reading the intermediate more mathematical sections. C_LI

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Creator, S. F., Coutts, L. V., Phillips, R., Turner, R., Dijk, D.-J., Skeldon, A. C.. 2021-01-15. Fatigue, Alertness and Risk Prediction for Shift Workers. https://doi.org/10.1101/2021.01.13.426509

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience