MicroRNA alteration in cerebrospinal fluid from comatose patients with traumatic brain injury after right median nerve stimulation.

Electrical stimulation of the right median nerve can aid coma arousal after traumatic brain injury (TBI). This study aimed to confirm the efficacy further and explore possible mechanisms of right median nerve electrical stimulation (RMNS). Five comatose patients after severe TBI from May to September 2020 in the Tianjin Medical University General Hospital received RMNS for 2 weeks besides standard management. After the 2-week treatment, the mean Glasgow Coma Scale (GCS) and neurophysiological examination were used. We then investigated the alterations in microRNA (miRNA) expression in cerebrospinal fluid (CSF) by high-throughput whole transcriptome sequencing, analyzed the data by Gene Ontology (GO) and pathway analysis, and constructed the miRNA-target gene network. Patient awareness and brain function showed a more rapid increase after treatment. We also found 38 differently expressed miRNAs, 34 of which were upregulated and 4 downregulated. GO analysis showed a relation of these differentially expressed miRNAs with neuronal growth, repair, and neural signal transmission. The most highly correlated pathways were primarily associated with the tumor necrosis factor (TNF) signaling pathway and dopaminergic synapse. The application of RMNS effectively promoted early awakening in comatose patients with severe TBI. Moreover, differentially expressed miRNAs might reduce neuronal apoptosis and increase dopamine levels by regulating target gene expression, thus participating in the specific biological process after arousal therapy. Our study provided novel targets for further research on the molecular mechanisms of RMNS arousal treatment and a new way to treat neurotraumatic diseases.

Multidisciplinary rehabilitation for adults with neuromyelitis optica spectrum disorders: A pilot study.

OBJECTIVE: To provide detailed data on the effects of multidisciplinary rehabilitation for patients with neuromyelitis optica spectrum disorder with moderate to severe disability. DESIGN: A pilot randomized control study. SUBJECTS/PATIENTS: A total of 39 patients with neuromyelitis optica spectrum disorder were randomized into intervention or control groups. METHODS: The intervention group received multidisciplinary rehabilitation 5 times/week for 4 weeks in a hospital, and the patients were guided to continue community- or home-based rehabilitation for 3 months. The control group did not receive any specific rehabilitation intervention. Disability was assessed using the Extended Disability Status Scale (EDSS) and Functional Systems (FS) scores after 4 weeks of rehabilitation and 3 months of follow-up. RESULTS: The mean EDSS score was 7.5 at admission for both groups. Improvements (p<0.05) in the EDSS score and domains of bowel, bladder and motor functions (pyramidal and walking function) were noted in the multidisciplinary rehabilitation group after 4 weeks. After 3 months, the patients in the usual care group showed improvement in EDSS score and walking ability score; however, no significant changes in other variables were noted. CONCLUSION: These results suggest that multidisciplinary rehabilitation potentially promotes motor functional recovery in patients with neuromyelitis optica spectrum disorders.

Overexpression of lncRNA TCTN2 protects neurons from apoptosis by enhancing cell autophagy in spinal cord injury.

Neuronal apoptosis is the main pathological feature of spinal cord injury (SCI), while autophagy contributes to ameliorating neuronal damage via inhibition of apoptosis. Here, we investigated the role of tectonic family member 2 (TCTN2) long non-coding RNA on apoptosis and autophagy in SCI. TCTN2 was down-regulated in the spinal cord tissues of a rat model of SCI and in oxygen-glucose deprivation-induced hypoxic SY-SH-5Y cells, while microRNA-216b (miR-216b) was up-regulated. Overexpression of TCTN2 reduced neuron apoptosis by inducing autophagy, and TCTN2 was observed to negatively regulate miR-216b. Furthermore, TCTN2 promoted autophagy to repress apoptosis through the miR-216b-Beclin-1 pathway, and overexpression of TCTN2 improved neurological function in the SCI rat model. In summary, our data suggest that TCTN2 enhances autophagy by targeting the miR-216b-Beclin-1 pathway, thereby ameliorating neuronal apoptosis and relieving spinal cord injury.

Hypoxia training attenuates left ventricular remodeling in rabbit with myocardial infarction.

OBJECTIVE: Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myocardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. METHODS: ADULT MALE RABBITS WERE RANDOMLY DIVIDED INTO THREE GROUPS: group SO (sham operated), group MI (myocardial infarction only) and group MI-HT (myocardial infarction plus hypoxia training). Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber (having equivalent condition at an altitude of 4000 m, FiO214.9%) for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor (VEGF) in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were assessed by echocardiography. RESULTS: After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI (130.27 ± 18.58 pg/mL, P < 0.01) and MI-HT (181.93 ± 20.29 pg/mL, P < 0.01) were significantly increased. Infarct size in Group MI-HT (29.67% ± 7.73%) was deceased remarkably, while its capillary density (816.0 ± 122.2/mm(2)) was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic (15.86 ± 1.09 mm, P < 0.05) and end-systolic dimensions (12.10 ± 1.20 mm, P < 0.01) significantly and improved left ventricular ejection fraction (54.39 ± 12.74 mm, P < 0.05). CONCLUSION: Hypoxia training may improve left ventricular function and reduce remodeling via angiogenesis in rabbits with MI.

Comparison of the reaction time of wrist flexion and extension between patients with stroke and age-matched healthy subjects and correlation with clinical measures.

BACKGROUND: Brain injury had an effect on reaction time (RT) and brain-injured patients were normally significantly slower than normal controls. The RT of the paretic upper limb (UL) in patients with stroke was slower than in a control group. The present study was designed to compare the RTs of the unaffected and affected sides in stroke survivors and those of normal subjects. This study also explores the relationships among wrist flexion and extension RTs in the affected side and the motor deficits of the UL as measured by clinical Composite Spasticity Index (CSI), Associated Reaction Rating Score (ARRS), and Wolf Motor Function Test (WMFT) scores. METHODS: Ninety-eight hemiparetic stroke survivors and 20 normal subjects participated in the study. Abnormal muscle tone was measured by CSI. Associated reaction was measured by ARRS. Motor function was measured by WMFT. The subject was asked to flex or extend the affected and non-affected wrists as fast as possible, following an auditory "go" signal. An electrogoniometer attached to the wrist measured wrist flexion and extension angle. RT was defined as the time from the "go" signal to a change in wrist angle denoting movement onset. Clinical assessments and RT were conducted within one day. Differences in the variables between normal subjects and the unaffected sides of the stroke patients were analyzed using analysis of variance. Correlations were assessed by computing Spearman's correlation coefficient. The significance level was set at 5%. RESULTS: RTs of wrist flexion and extension in the stroke survivors' affected hands were significantly longer than those in normal subjects and their unaffected hands (P < 0.01 for both). The wrist flexion RT moderately correlated with CSI (ρ = 0.412, P < 0.001) and ARRS (ρ = 0.341, P < 0.001) and with WMFT functional ability (negatively; ρ = -0.531, P < 0.001) and time score (ρ = 0.504, P < 0.001). Similarly, the wrist extension RT moderately correlated with CSI (ρ = 0.429, P < 0.001), ARRS (ρ = 0.374, P < 0.001), and with WMFT functional ability (negatively; ρ = -0.531, P < 0.001) and time score (ρ = 0.486, P < 0.001). CONCLUSIONS: RTs of wrist flexion and extension on the stroke survivors' affected sides were significantly longer than those on the unaffected sides and those of normal subjects. The wrist flexion and extension RTs moderately correlated with CSI and ARRS and inversely with motor functional performance of the UL in patients with stroke.