In this study, we seek to highlight a potentially fundamental shift in how dynamic stressor-strain relationships should be conceptualized over time. Specifically, we provide an integrated empirical test of adaptation and role theory within a longitudinal framework. Data were collected at 3 time points, with a 6-week lag between time points, from 534 respondents. Using latent change modeling, results supported within-person adaptation to changes in job satisfaction and role conflict. Specifically, over the 12-week course of the study, changes in role clarity tended to be maintained, whereas changes in job satisfaction and role conflict tended to be fleeting and reverse themselves. Theoretical implications and future directions are discussed. (PsycINFO Database Record

The present study utilizes meta-analytic techniques to examine the literature on sleep and work performance. In line with previous meta-analytic research, results indicate that sleep and work performance have a positive relationship. However, more importantly, results from moderator analyses reveal that the type of sleep measurement (sleep quantity and sleep quality), work performance measurement (task performance, organizational citizenship behavior, and counterproductive work behavior), analysis method (between-person and within-person), sleep report source (self-report, other report, and objective), sleep recall window (day, week/month, and more than 1 month), and study setting (field and laboratory) differentially influence the strength of the sleep-work performance relationship. Furthermore, meta-analytic SEM results indicate that certain mediators (affect, job attitudes, and cognitive resources) provide stronger explanations (i.e., stronger indirect effects) for the relationship between sleep and work performance, depending on the specific type of performance being examined. In general, results highlight the importance of construct operationalization and methodology decisions when conducting sleep-work performance research and provide greater insight into explanations for the relationship between sleep and work performance. Research implications, practical implications, potential limitations, and future directions are also discussed.

Background Background: Investigating early white matter (WM) change in Huntington's disease (HD) can improve our understanding of the way in which disease spreads from the striatum. Objectives Objectives: We provide a detailed characterization of pathology-related WM change in HD. We first examined WM microstructure using diffusion-weighted imaging and then investigated both underlying biological properties of WM and products of WM damage including iron, myelin plus neurofilament light, a biofluid marker of axonal degeneration-in parallel with the mutant huntingtin protein. MethodsMethods: We examined WM change in HD gene carriers from the HD-CSFcohort, baseline visit. We used standard-diffusion magnetic resonance imaging to measure metrics including fractional anisotropy, a marker of WM integrity, and diffusivity; a novel diffusion model (neurite orientation dispersion and density imaging) to measure axonal density and organization; T1-weighted and T2-weighted structural magnetic resonance imaging images to derive proxy iron content and myelin-contrast measures; and biofluid concentrations of neurofilament light (in cerebrospinal fluid (CSF) and plasma) and mutant huntingtin protein (in CSF). ResultsResults: HD gene carriers displayed reduced fractional anisotropy and increased diffusivity when compared with controls, both of which were also associated with disease progression, CSF, and mutant huntingtin protein levels. HD gene carriers also displayed proxy measures of reduced myelin contrast and iron in the striatum. Conclusion Conclusion: Collectively, these findings present a more complete characterization of HD-related microstructural brain changes. The correlation between reduced fractional anisotropy, increased axonal orientation, and biofluid markers suggest that axonal breakdown is associated with increased WM degeneration, whereas higher quantitative T2 signal and lower myelin-contrast may indicate a process of demyelination limited to the striatum.The ongoing development of novel therapeutics to treat Huntington's disease (HD) necessitates improved characterization of HD-related brain changes. HD is a progressive neurodegenerative disorder characterized by a motor, cognitive, and neuropsychiatric phenotype and caused by CAG expansions in the huntingtin gene (HTT). Given the certainty of onset in those that inherit the gene combined with genetic testing, we can examine brain changes from the earliest, presymptomatic disease stages.Magnetic resonance imaging (MRI) measures of neuronal atrophy have characterized macrostructural brain changes associated with HD progression. 1,2 Neurodegeneration primarily originates in the striatum, extending to white matter (WM) and finally the cortex. 1,3 However, although a robust marker of disease progression, macrostructural changes provide limited descriptions of pathological mechanisms underlying HD. Investigating early WM microstructural changes in HD can improve our understanding of WM organization

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