15 Years of Evolution of Non-Invasive EEG-Based Methods for Restoring Hand &Arm Function with Motor Neuroprosthetics in Individuals with High Spinal Cord Injury: A Review of Graz BCI Research

Patients who suffer from a high spinal cord injury have severe motor disabilities in the lower as well as in the upper extremities. Thus they rely on the help of other people in everyday life. Restoring the function of the upper limbs, especially the grasp function can help them to gain some independence. Using EEG-based neuroprosthetics is a way to help tetraplegic people restore different grasp types as well as moving the arm and the elbow. In this work an overview of non-invasive EEG-based methods for restoring the hand and arm function with the use of neuroprosthetics in individuals with high spinal cord injury is given. Since the Graz BCI group is leading in this area of non-invasive research mainly, the work of this group is represented.

On Similarities and Differences of Invasive and Non-Invasive Electrical Brain Signals in Brain-Computer Interfacing

We perceive that some Brain-Computer Interface (BCI) researchers believe in totally different origins of invasive and non-invasive electrical BCI signals. Based on available literature we argue, however, that although invasive and non-invasive BCI signals are different, the underlying origin of electrical BCIs signals is the same.

Apoptosis inhibitory effect of anti-miR-146b on hippocampal neurons of OGD/R-induced injury

Objective:To construct a cellular model of oxygen-glucose deprivation and reoxygenation (OGD/R)-induced injury in hippocampal neuronsin vitro, and to explore the inhibitory effect of anti-miR-146b on the apoptosis of hippocampal neurons of ischemic/reperfusion injury. Methods: Primary rat hippocampal neurons were cultured, and oxygen-glucose deprivation and reoxygenation (OGD/R) were constructed. The anti-miR-146b lentivirus was used to transfect the hippocampal neurons, and the cells were divided into the normal group, the OGD/R group and the OGD/R + anti-miR-146b group. Real time fluorescence quantitative PCR (qRT-PCR) was used to detect the mRNA expression of miR-146b, KLF7, Caspase-3, Bcl-2 and Bax in each group. Cell viability was detected by CCK8 assay, and apoptosis was detected by Hoechst33342/PI double staining.Results: Compared with the normal group, the cell morphology of the OGD/R group and the OGD/R + anti-miR-146b group was damaged, the cell activity was decreased, and the cell apoptosis rate was increased significantly (P<0.05). However, Compared with OGD/R group, the cell morphology of the OGD/R + KLF7 group was improved, the cell activity was increased, and the apoptosis rate was decreased significantly (P<0.05). Compared with the normal group, the mRNA expression levels of miR-146b, KLF7, Caspase-3, Bax and Bcl-2 in the OGD/R group and the OGD/R + KLF7 group was increased (P<0.05). Compared with the OGD/R group, the mRNA expression of KLF7, Bcl-2 were increased in the OGD/R + KLF7 group significantly, however, the mRNA expression of miR-146b, Caspase-3, Bax were decreased significantly (P<0.05).Conclusion:Anti-miR-146b play protective effect on hippocampal neurons of OGD/R-induced injury. The mechanism may be related to upregulation of KLF7 signaling pathway, downregulation expression of Caspase-3 and Bax, upregulation expression of Bcl-2, and inhibition of apoptosis induced by OGD/R.

Chx10+V2a interneurons in spinal motor regulation and spinal cord injury

Chx10-expressing V2 a(Chx10+V2 a) spinal interneurons play a large role in the excitatory drive of motoneurons. Chemogenetic ablation studies have demonstrated the essential nature of Chx10+V2 a interneurons in the regulation of locomotor initiation, maintenance, alternation, speed, and rhythmicity. The role of Chx10+V2 a interneurons in locomotion and autonomic nervous system regulation is thought to be robust, but their precise role in spinal motor regulation and spinal cord injury have not been fully explored. The present paper reviews the origin, characteristics, and functional roles of Chx10+V2 a interneurons with an emphasis on their involvement in the pathogenesis of spinal cord injury. The diverse functional properties of these cells have only been substantiated by and are due in large part to their integration in a variety of diverse spinal circuits. Chx10+V2 a interneurons play an integral role in conferring locomotion, which integrates various corticospinal, mechanosensory, and interneuron pathways. Moreover, accumulating evidence suggests that Chx10+V2 a interneurons also play an important role in rhythmic patterning maintenance, leftright alternation of central pattern generation, and locomotor pattern generation in higher order mammals, likely conferring complex locomotion. Consequently, the latest research has focused on postinjury transplantation and noninvasive stimulation of Chx10+V2 a interneurons as a therapeutic strategy, particularly in spinal cord injury. Finally, we review the latest preclinical study advances in laboratory derivation and stimulation/transplantation of these cells as a strategy for the treatment of spinal cord injury. The evidence supports that the Chx10+V2 a interneurons act as a new therapeutic target for spinal cord injury. Future optimization strategies should focus on the viability, maturity, and functional integration of Chx10+V2 a interneurons transplanted in spinal cord injury foci.

Krüppel-like factor 7 attenuates hippocampal neuronal injury after traumatic brain injury

Our previous study has shown that the transcription factor Krüppel-like factor 7(KLF7) promotes peripheral nerve regeneration and motor function recovery after spinal cord injury.KLF7 also participates in traumatic brain injury,but its regulatory mechanisms remain poorly understood.In the present study,an HT22 cell model of traumatic brain injury was established by stretch injury and oxygenglucose deprivation.These cells were then transfected with an adeno-associated virus carrying KLF7(AAV-KLF7).The results revealed that,after stretch injury and oxygen-glucose deprivation,KLF7 greatly reduced apoptosis,activated caspase-3 and lactate dehydrogenase,downregulated the expression of the apoptotic markers B-cell lymphoma 2(Bcl-2)-associated X protein(Bax) and cleaved caspase-3,and increased the expression of βIII-tubulin and the antiapoptotic marker Bcl-2.Furthermore,KLF7 overexpression upregulated Janus kinase 2(JAK2) and signal transducer and activator of transcription 3(STAT3) phosphorylation in HT22 cells treated by stretch injury and oxygenglucose deprivation.Immunoprecipitation assays revealed that KLF7 directly participated in the phosphorylation of STAT3.In addition,treatment with AG490,a selective inhibitor of JAK2/STAT3,weakened the protective effects of KLF7.A mouse controlled cortical impact model of traumatic brain injury was then established.At 30 minutes before modeling,AAV-KLF7 was injected into the ipsilateral lateral ventricle.The protein and m RNA levels of KLF7 in the hippocampus were increased at 1 day after injury and recovered to normal levels at 3 days after injury.KLF7 reduced ipsilateral hippocampal atrophy,decreased the injured cortex volume,downregulated Bax and cleaved caspase-3 expression,and increased the number of 5-bromo-2'-deoxyuridine-positive neurons and Bcl-2 protein expression.Moreover,KLF7 transfection greatly enhanced the phosphorylation of JAK2 and STAT3 in the ipsilateral hippocampus.These results suggest that KLF7 may protect hippocampal neurons after traumatic brain injury through activation of the JAK2/STAT3 signaling pathway.The study was approved by the Institutional Review Board of Mudanjiang Medical University,China(approval No.mdjyxy-2018-0012) on March 6,2018.