Recent experimental observations and theoretical advances have indicated that the homeostatic equilibrium for sleep/wake regulation--and thereby sensitivity to neurobehavioral impairment from sleep loss--is modulated by prior sleep/wake history. This phenomenon was predicted by a biomathematical model developed to explain changes in neurobehavioral performance across days in laboratory studies of total sleep deprivation and sustained sleep restriction. The present paper focuses on the dynamics of neurobehavioral performance within days in this biomathematical model of fatigue. Without increasing the number of model parameters, the model was updated by incorporating time-dependence in the amplitude of the circadian modulation of performance. The updated model was calibrated using a large dataset from three laboratory experiments on psychomotor vigilance test (PVT) performance, under conditions of sleep loss and circadian misalignment; and validated using another large dataset from three different laboratory experiments. The time-dependence of circadian amplitude resulted in improved goodness-of-fit in night shift schedules, nap sleep scenarios, and recovery from prior sleep loss. The updated model predicts that the homeostatic equilibrium for sleep/wake regulation--and thus sensitivity to sleep loss--depends not only on the duration but also on the circadian timing of prior sleep. This novel theoretical insight has important implications for predicting operator alertness during work schedules involving circadian misalignment such as night shift work.
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http://dx.doi.org/10.5665/sleep.3246 | DOI Listing |
Sci Rep
December 2024
Institute for Medical Informatics, Statistics and Epidemiology (IMISE), University of Leipzig, 04107, Leipzig, Germany.
When infected with SARS-CoV-2, Syrian hamsters (Mesocricetus auratus) develop moderate disease severity presenting key features of human COVID-19. We here develop a biomathematical model of the disease course by translating known biological mechanisms of virus-host interactions and immune responses into ordinary differential equations. We explicitly describe the dynamics of virus population, affected alveolar epithelial cells, and involved relevant immune cells comprising for example CD4+ T cells, CD8+ T cells, macrophages, natural killer cells and B cells.
View Article and Find Full Text PDFPLoS One
December 2024
Facultad de Ingeniería, Universidad de San Buenaventura, Cali, Colombia.
The Covid-19 pandemic has challenged both the scientific community and government authorities in Colombia. Both sectors are collaborating to understand the transmission and spread of the virus and to establish control strategies. This study proposes a biomathematical model with difference equations to analyze the transmission of Covid-19 in Santiago de Cali from March 2020 to June 2022.
View Article and Find Full Text PDFClin Transl Med
October 2024
Cardiovascular Research Unit, Department of Precision Health, Luxembourg Institute of Health, Strassen, Luxembourg.
J Theor Biol
August 2024
Sleep and Performance Research Center, Washington State University, 412 E. Spokane Falls Blvd., Spokane, WA 99202-2131, USA; Department of Translational Medicine and Physiology, Washington State University Health Sciences Spokane, 412 E. Spokane Falls Blvd., Spokane, WA 99202, USA. Electronic address:
Biomathematical models of fatigue capture the physiology of sleep/wake regulation and circadian rhythmicity to predict changes in neurobehavioral functioning over time. We used a biomathematical model of fatigue linked to the adenosinergic neuromodulator/receptor system in the brain as a framework to predict sleep inertia, that is, the transient neurobehavioral impairment experienced immediately after awakening. Based on evidence of an adenosinergic basis for sleep inertia, we expanded the biomathematical model with novel differential equations to predict the propensity for sleep inertia during sleep and its manifestation after awakening.
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