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Bacterial diversity alteration shows biomarkers associated with contamination within soil-river-lake procession.
Overall or all-cause mortality is a key measure of health in a population. Multiple epigenome-wide association studies have been conducted on all-cause mortality with limited significant findings and low replication. In order to elucidate the co-regulated DNA methylation patterns associated with all-cause mortality, we conducted a weighted DNA methylation co-regulation network analysis on whole-blood samples of 1,425 older individuals from the Lothian Birth Cohorts of 1921 and 1936. Our network-based analysis defined coregulated DNA methylation patterns in gene promoters into clusters or modules whose correlation with all-cause mortality was assessed by survival analysis. We found two significant modules or gene clusters associated with all-cause mortality in LBC1921 based on their eigengenes; one negatively correlated (p=8.14E-03, 698 genes) and one positively correlated (p=4.26E-02, 1431 genes) with the risk of death. The two modules were replicated in LBC1936 with the same directions of correlation (p=6.35E-02 and p=3.64E-02, respectively). Furthermore, the modules revealed 32 genes associated with all-cause mortality (FDR less then 0.05) linked to various diseases, including cancer and diabetes. Additionally, we performed pathway analysis and found 22 pathways (FDR less then 0.05), including a pathway for taste transduction, which has been shown to be associated with poor prognosis in acutely hospitalized patients and several pathways were linked to different types of cancer. The results from our network analysis show that DNA methylation of multiple genes could have been co-regulated in an association with the overall risk of death. The identified epigenetic markers might help with our understanding of the molecular basis of all-cause mortality and general health. © The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail [email protected] restorative function of sleep has been linked to a net reduction in synaptic strength. The slope of slow waves, a major characteristic of non-rapid eye movement (NREM) sleep, has been shown to directly reflect synaptic strength, when accounting for amplitude changes across the night. In this study, we aimed to investigate overnight slope changes in the course of development in an age-, amplitude-, and region-dependent manner. All-night high-density electroencephalography data was analyzed in a cross-sectional population of 60 healthy subjects in the age range of 8 to 29 years. To control for amplitude changes across the night, we matched slow waves from the first and the last hour of NREM sleep according to their amplitude. We found a reduction of slow wave slopes from the first to the last hour of NREM sleep across all investigated ages, amplitudes, and most brain regions. The overnight slope change was largest in children and decreased towards early adulthood. A topographical analysis revealed regional differences in slope change. Specifically, for small amplitude waves the decrease was smallest in an occipital area, whereas for large amplitude waves, the decrease was smallest in a central area. The larger slope decrease in children might be indicative of a boosted renormalization of synapses during sleep in childhood, which, in turn, might be related to increased plasticity during brain maturation. Regional differences in the extent of slow wave slope reduction may reflect a "smart" down-selection process or, alternatively, indicate amplitude-dependent differences in the generation of slow waves. © Sleep Research Society 2020. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please e-mail [email protected] of offspring life-course health by maternal nutrition and stress are well studied. At postnatal day 850, we evaluated male and female steroid levels and metabolism in aged offspring of primigravid sister rats bred at 70, 90, 150- or 300-days' life. At 850 days life, male offspring corticosterone was similar regardless of maternal age. Female corticosterone was highest in offspring of 70- and 300-day mothers. Serum dehydroepiandrosteronecorticosterone was lowest in both sexes of offspring of 70- and 300-day mothers. Male and female fat depots were smaller in offspring of 150 than 70- and 90-day mothers. Insulin, glucose and homeostatic model assessment were similar in all male offspring but higher in female offspring of 70-day mothers than other ages. We conclude, maternal age affects offspring aging in an offspring sex dependent manner and merits consideration in designing and interpreting programming studies. © The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail [email protected] The present study investigated the effects of microvascular endothelial cells (MECs) on the chemotaxis, adhesion and proliferation of bone marrow hematopoietic stem cells (HSCs) ex vivo. METHODS AND RESULTS MECs were collected from the lung tissue of C57BL/6 mice, and HSCs were isolated with immunomagnetic beads from bone marrow of GFP mice. MECs and HSCs were co-cultured with or without having direct cell-cell contact in Transwell device for the measurement of chemotaxis and adhesion of MECs to HSCs. Liraglutide nmr Experimental results indicate that the penetration rate of HSCs from the Transwell upper chamber to lower chamber in 'co-culture' group was significantly higher than that of 'HSC single culture' group. Also, the HSCs in co-culture group were all adherent at 24 h, and the co-culture group with direct cell-cell contact had highest proliferation rate. The HSC number was positively correlated with vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1) levels in supernatants of the culture. CONCLUSIONS Our study reports that MECs enhance the chemotaxis, adhesion and proliferation of HSCs, which might be related to cytokines SDF-1 and VEGF secreted by MECs, and thus MECs enhance the HSC proliferation through cell-cell contact. The present study revealed the effect of MECs on HSCs, and provided a basis and direction for effective expansion of HSCs ex vivo. © 2020 The Author(s).
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