4-Methylumbelliferone Attenuates Macrophage Invasion and Myocardial Remodeling in Pressure-Overloaded Mouse Hearts.

[Figure: see text].

Portable PSG for sleep stage monitoring in sports: Assessment of SOMNOwatch plus EEG.

Current sport-scientific studies mostly neglect the assessment of sleep architecture, although the distribution of different sleep stages is considered an essential component influencing an athlete's recovery and performance capabilities. A mobile, self-applied tool like the SOMNOwatch plus EEG might serve as an economical and time-friendly alternative to activity-based devices. However, self-application of SOMNOwatch plus EEG has not been validated against conventional polysomnography (PSG) yet. For evaluation purposes, 25 participants (15 female, 10 male; M age = 22.92 ± 2.03 years) slept in a sleep laboratory on two consecutive nights wearing both, conventional PSG and SOMNOwatch plus EEG electrodes. Sleep parameters and sleep stages were compared using paired t-tests and Bland-Altman plots. No significant differences were found between the recordings for Sleep Onset Latency, stages N1 to N3 as well as Rapid Eye Movement stage. Significant differences (Bias [95%-confidence interval]) were present between Total Sleep Time (9.95 min [-29.18, 49.08], d = 0.14), Total Wake Time (-13.12 min [-47.25, 23.85], d = -0.28), Wake after Sleep Onset (-11.70 min [-47.25, 23.85], d = -0.34) and Sleep Efficiency (2.18% [-7.98, 12.34], d = 0.02) with small effect sizes. Overall, SOMNOwatch plus EEG can be considered a valid and practical self-applied method for the examination of sleep. In sport-scientific research, it is a promising tool to assess sleep architecture in athletes; nonetheless, it cannot replace in-lab PSG for all clinical or scientific purposes.

Deficiency of the clock gene Bmal1 affects neural progenitor cell migration.

We demonstrate the impact of a disrupted molecular clock in Bmal1-deficient (Bmal1-/-) mice on migration of neural progenitor cells (NPCs). Proliferation of NPCs in rostral migratory stream (RMS) was reduced in Bmal1-/- mice, consistent with our earlier studies on adult neurogenesis in hippocampus. However, a significantly higher number of NPCs from Bmal1-/- mice reached the olfactory bulb as compared to wild-type littermates (Bmal1+/+ mice), indicating a higher migration velocity in Bmal1-/- mice. In isolated NPCs from Bmal1-/- mice, not only migration velocity and expression pattern of genes involved in detoxification of reactive oxygen species were affected, but also RNA oxidation of catalase was increased and catalase protein levels were decreased. Bmal1+/+ migration phenotype could be restored by treatment with catalase, while treatment of NPCs from Bmal1+/+ mice with hydrogen peroxide mimicked Bmal1-/- migration phenotype. Thus, we conclude that Bmal1 deficiency affects NPC migration as a consequence of dysregulated detoxification of reactive oxygen species.