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. Electronic supplementary material The online version of this article (10.1007/s00429-018-1775-1) contains supplementary material, which is available to authorized users.

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, selfapplied 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.

Cardiac wall stress induces local and systemic inflammatory responses that are increasingly recognized as key modulators of extracellular matrix remodeling. Hyaluronic acid interacts with immune cells and mesenchymal cells thereby modulating profibrotic signals. Here we tested the hypothesis that 4-methylumbelliferone (4-MU), an inhibitor of hyaluronic acid synthesis, would attenuate inflammation and extracellular matrix remodeling of pressure-overloaded myocardium in C57BL/6J male mice fed with 4-MU and subjected to TAC (transverse aortic constriction) surgery. Flow cytometry of immune cells showed TAC-induced leukocytosis due to an increase of neutrophils and monocytes. 4-MU strongly attenuated both circulating and cardiac leukocyte numbers 3 days after TAC. In the hearts, 4-MU reduced the number of CCR2 − resident macrophages. At later time points, 4-MU also prevented the infiltration of heart tissue by bone marrow-derived circulating monocytes leading to reduced cardiac macrophage counts even 7 weeks after TAC. The long-term attenuation of macrophage-driven inflammation was associated with less myocardial fibrosis in 4-MU-treated compared with untreated mice. Unexpectedly, 4-MU also reduced the development of left ventricular hypertrophy and increased cardiac output after TAC without affecting blood pressure. The data demonstrate that 4-MU reduces both resident and invading cardiac macrophages and may be a promising agent to alleviate pressure-overload induced myocardial damage.