Simonhovgaard9793

Gender- and age-related temporal differences were negligible. Variability in HGS declined substantially over time (ratio of CVs [95%CI] 0.88 [0.86-0.90]), with declines 1.9-fold larger in women compared to men and 1.7-fold larger in 70- to 79-year-olds compared to 60- to 69-year-olds. CONCLUSIONS there has been a small, progressive improvement in mean HGS for older Japanese adults since 1998, which is suggestive of a corresponding improvement in strength capacity. The substantial decline in variability indicates that the improvement in mean HGS was not uniform across the population. © The Author(s) 2020. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For permissions, please email journals.permissions@oup.com.BACKGROUND older workers experiencing chronic health conditions (CHCs) are more likely to retire early. The different pathways through which CHCs stimulate retirement preferences, however, remain largely unexplored. OBJECTIVE we present a more comprehensive model in which we test the different pathways through which four specific CHCs-arthritis, cardiovascular disease, sleep disorders and psychological disorders-influence early retirement preferences. We hypothesize that the association between CHCs and early retirement preferences is differentially mediated by subjective life expectancy (SLE), perceived health-related work limitations (HRWL) and vitality. METHODS we collected data from 5,696 wage-employed older workers (60 to 64 years) in the Netherlands in 2015. Regression models were estimated to examine the associations between CHCs and early retirement preferences. Mediation analysis with the Karlson, Holm and Breen method was used to examine potential mediation pathways. RESULTS SLE, HRWL and vitality mediated the association between CHCs and older workers' early retirement preferences. The dominant mediator differed depending on the CHC. Severe HRWL predominantly guided the retirement preferences of older workers with arthritis and cardiovascular disease. Lower vitality mainly mediated retirement preferences of older workers with sleep and psychological disorders. Lower SLE was a significant mediation pathway for older workers with cardiovascular diseases. CONCLUSIONS HRWL and vitality play a major role in determining retirement preferences of older workers experiencing CHCs. Since both mediators are modifiable, targeted interventions may not only extend older workers' working lives, but also improve the quality of their working lives. © The Author(s) 2020. Published by Oxford University Press on behalf of the British Geriatrics Society.It has been reported that abnormal epigenetic modification is associated with the occurrence of Parkinson's disease (PD). Here, we found that a Ten-Eleven Translocation 2 (TET2), a staff of the DNA hydroxylases family, was increased in dopaminergic neurons in vitro and in vivo. Genome-wide mapping of DNA 5-hmC-sequencing has revealed an aberrant epigenome 5-hydroxymethylcytosine (5-hmC) landscape in 1-Methyl-4-phenylpyridinium iodide (MPP+)-induced SH-SY5Y cells. Onametostat in vivo The TET family of DNA hydroxylases could reverse DNA methylation by oxidization of 5-methylcytosine (5-mC) to 5-hmC. However, the relationship between modification of DNA hydroxymethylation and the pathogenesis of PD is not clear. According to the results of 5-hmC-sequencing studies, 5-hmC was associated with gene-rich regions in the genomes related to cell cycle, especially gene cyclin dependent kinase inhibitor 2A (Cdkn2A). Downregulation of TET2 expression could significantly rescue MPP+-stimulated SH-SY5Y cell damage and cell cycle arrest. Meanwhile, knockdown of Tet2 expression in the substantia nigra pars compacta of MPTP-induced PD mice, resulted in attenuated MPTP-induced motor deficits and dopaminergic neuronal injury via p16 suppression. In this study, we demonstrated a critical function of TET2 in PD development via the CDKN2A activity-dependent epigenetic pathway, suggesting a potential new strategy for epigenetic therapy. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email journals.permissions@oup.com.Sleep exerts modulatory effects on the cerebral cortex. Whether sleep modulates local connectivity in the cortex or only individual neural activity, however, is poorly understood. Here we investigated functional connectivity, that is, covarying activity between neurons, during spontaneous sleep-wake states and during and after sleep deprivation using calcium imaging of identified excitatory/inhibitory neurons in the motor cortex. Functional connectivity was estimated with a statistical learning approach glasso and quantified by "the probability of establishing connectivity (sparse/dense)" and "the strength of the established connectivity (weak/strong)." Local cortical connectivity was sparse in non-rapid eye movement (NREM) sleep and dense in REM sleep, which was similar in both excitatory and inhibitory neurons. The overall mean strength of the connectivity did not differ largely across spontaneous sleep-wake states. Sleep deprivation induced strong excitatory/inhibitory and dense inhibitory, but not excitatory, connectivity. Subsequent NREM sleep after sleep deprivation exhibited weak excitatory/inhibitory, sparse excitatory, and dense inhibitory connectivity. These findings indicate that sleep-wake states modulate local cortical connectivity, and the modulation is large and compensatory for stability of local circuits during the homeostatic control of sleep, which contributes to plastic changes in neural information flow. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For permissions, please e-mail journals.permission@oup.com.The Multiprotein Bridging Factor 1 (MBF1) proteins are transcription co-factors whose molecular function is to form a bridge between transcription factors and the basal machinery of transcription. MBF1s are present in most archaea and all eukaryotes, and numerous reports show that they are involved in developmental processes and in stress responses. In this review we summarize almost three decades of research on the plant MBF1 family, which has mainly focused on their role in abiotic stress responses, in particular the heat stress response. However, despite the amount of information available, there are still many questions that remain about how plant MBF1 genes, transcripts, and proteins respond to stress, and how they in turn modulate stress response transcriptional pathways. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Experimental Biology. All rights reserved. For permissions, please email journals.permissions@oup.com.