No abstract

Spinal cord injury (SCI), following explosive oxidative stress, causes an abrupt and irreversible pathological deterioration of the central nervous system. Thus, preventing secondary injuries caused by reactive oxygen species (ROS), as well as monitoring and assessing the recovery from SCI are critical for the emergency treatment of SCI. Herein, an emergency treatment strategy is developed for SCI based on the selenium (Se) matrix antioxidant system to effectively inhibit oxidative stress‐induced damage and simultaneously real‐time evaluate the severity of SCI using a reversible dual‐photoacoustic signal (680 and 750 nm). Within the emergency treatment and photoacoustic severity assessment (ETPSA) strategy, the designed Se loaded boron dipyrromethene dye with a double hydroxyl group (Se@BDP‐DOH) is simultaneously used as a sensitive reporter group and an excellent antioxidant for effectively eliminating explosive oxidative stress. Se@BDP‐DOH is found to promote the recovery of both spinal cord tissue and locomotor function in mice with SCI. Furthermore, ETPSA strategy synergistically enhanced ROS consumption via the caveolin 1 (Cav 1)‐related pathways, as confirmed upon treatment with Cav 1 siRNA. Therefore, the ETPSA strategy is a potential tool for improving emergency treatment and photoacoustic assessment of SCI.

Background The aim of this study was to analyze the effect of unilateral K-rod dynamic internal fixation on paraspinal muscles for lumbar degenerative diseases. Methods This study retrospectively collected 52 patients who underwent lumbar surgery with the K-rod group or PLIF. The operation time, intraoperative blood loss, postoperative drainage volume, postoperative exercise time were compared in the two groups. The visual analog scale (VAS) score and the oswestry dysfunction index (ODI) were employed to evaluate the clinical outcomes. The functional cross-sectional area (FCSA) of the paraspinal muscles and paraspinal muscles fat infiltration were measured to assess on the paraspinal muscles. Results As compared with the PLIF group, the operation time, the postoperative time in the field, and the average postoperative hospital stay in the K-rod internal fixation group were significantly shortened. At the last follow-up, both the groups showed significant improvement in the VAS score and ODI. The FCSA atrophy of the upper and lower adjacent segments (UAS and LAS) of the K-rod internal group was significantly less than that of the PLIF group. The extent of increase in the fatty infiltration of the paraspinal muscles in the K-rod group was significantly lesser than that in the PLIF group. The postoperative low back pain of the two groups of patients was significantly positively correlated with the FCSA atrophy. Conclusions As compared to PLIF, the posterior lumbar unilateral K-rod dynamic internal fixation showed significantly lesser paraspinal muscle atrophy and fatty infiltration, which were significantly positively correlated with postoperative low back pain.

The maintenance of appropriate endoplasmic reticulum (ER) homeostasis is critical to effective spinal cord injury (SCI) repair. In previous reports, protein disulfide isomerase A6 (PDIA6) demonstrated to serve as a reversible functional modulator of ER stress responses, while spastin can coordinate ER organization through the modulation of the dynamic microtubule network surrounding this organelle. While both PDIA6 and spastin are thus important regulators of the ER, whether they interact with one another for SCI repair still needs to be determined. Here a proteomics analysis identified PDIA6 as being related to SCI repair, and protein interaction mass spectrometry further confirmed the ability of PDIA6 and spastin to interact with one another. Pull-down and co-immunoprecipitation assays were further performed to validate and characterize the interactions between these two proteins. The RNAi-based knockdown of PDIA6 in COS-7 cells inhibited the activity of spastin-dependent microtubule severing. PDIA6 was also found to promote injured neuron repair, while spastin knockdown reversed this reparative activity. Together, these results thus confirm that PDIA6 and spastin function together as critical mediators of nerve repair, highlighting their potential value as validated targets for efforts to promote SCI repair.