Search

Higher static magnetic field (SMF) enables higher imaging capability in magnetic resonance imaging (MRI), which encourages the development of ultra-high field MRIs above 20 T with a prerequisite for safety issues. However, animal tests of ≥ 20 T SMF exposure are very limited. The objective of the current study is to evaluate mice behaviour consequences of 3.5-23.0 T SMF exposure.We systematically examined 112 mice for their short- and long-term behaviour responses to a 2-h exposure of 3.5-23.0 T SMFs. Locomotor activity and cognitive functions were measured by five behaviour tests, including balance beam, open field, elevated plus maze, three-chamber social recognition, and Morris water maze tests.Besides the transient short-term impairment of the sense of balance and locomotor activity, the 3.5-23.0 T SMFs did not have long-term negative effects on mice locomotion, anxiety level, social behaviour, or memory. In contrast, we observed anxiolytic effects and positive effects on social and spatial memory of SMFs, which is likely correlated with the significantly increased CaMKII level in the hippocampus region of high SMF-treated mice.Our study showed that the short exposures to high-field SMFs up to 23.0 T have negligible side effects on healthy mice and may even have beneficial outcomes in mice mood and memory, which is pertinent to the future medical application of ultra-high field SMFs in MRIs and beyond.• Short-term exposure to magnetic fields up to 23.0 T is safe for mice. • High-field static magnetic field exposure transiently reduced mice locomotion. • High-field static magnetic field enhances memory while reduces the anxiety level.

During development, melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) become light sensitive much earlier than rods and cones. IpRGCs project to many subcortical areas, whereas physiological functions of these projections are yet to be fully elucidated. Here, we found that ipRGC-mediated light sensation promotes synaptogenesis of pyramidal neurons in various cortices and the hippocampus. This phenomenon depends on activation of ipRGCs and is mediated by the release of oxytocin from the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) into cerebral-spinal fluid. We further characterized a direct connection between ipRGCs and oxytocin neurons in the SON and mutual projections between oxytocin neurons in the SON and PVN. Moreover, we showed that the lack of ipRGC-mediated, light-promoted early cortical synaptogenesis compromised learning ability in adult mice. Our results highlight the importance of light sensation early in life on the development of learning ability and therefore call attention to suitable light environment for infant care.

Introduction There have been problems with low qualification operator-related complications and failures of transurethral seminal vesiculoscopy (TSV) in China. Aim To study the guiding role of seminal tract anatomical study (STAS) in TSV. Material and methods We performed STAS to study the structure, morphology, duct trajectory, and anatomical relationships between the seminal vesicles and the adjacent tissue in pelvic specimens from 12 adult cadavers. Then the surgical effects and complications of 82 cases of TSV performed by 3 doctors were retrospectively studied to compare the difference between the two groups of before and after the anatomical study. Results The anatomical studies of the 12 adult cadaveric pelvis specimens identified the lengths and widths of the right- and left-side seminal vesicles and tracts. The TSV can treat lesions located in the distal seminal tract and vesicle, but proximal lesions cannot be reached, which is an anatomical limitation of this technique. There were significant differences in the surgical times and the surgical validity rates between the 2 groups. Conclusions Our anatomical study of the seminal tract and seminal vesicles is valuable for guiding TSV in clinical practice.

Although recent studies have found that HO-1 plays an important role in neuronal survival, little is known about the precise mechanisms occurring during cerebral ischemia/reperfusion (I/R). Therefore, the aim of this study was to investigate the neuroprotective mechanisms of HO-1 against ischemic brain injury induced by cerebral I/R and to explore whether the BDNF-TrkB-PI3K/Akt signaling pathway contributed to the protection provided by HO-1. Over-expressed HO-1 plasmids were employed to induce the overexpression of HO-1 through hippocampi CA1 injection 5 days before the cerebral I/R animal model was induced by four-vessel occlusion for 15 min transient ischemia and followed by reperfusion in Sprague-Dawley rats. Immunoblotting was carried out to examine the expression of the related proteins, and HE-staining was used to detect the percentage of living neurons in the hippocampal CA1 region. The results showed that over-expressed HO-1 could significantly protect neurons against cerebral I/R. Furthermore, the protein expression of BDNF, TrkB and p-Akt also increased in the rats treated with over-expressed HO-1 plasmids. However, treatment with tropomyosin receptor kinase B (TrkB) receptor antagonist (K252a) reversed the HO-1-induced increase in BDNF and p-Akt protein levels and decreased the level of cleaved caspase-3 protein in I/R rats. In summary, our results imply that HO-1 can decrease cell apoptosis in the I/R rat brain and that the mechanism may be related to the activation of the BDNF-TrkB-PI3K/Akt signaling pathway.