Repair mechanism of astrocytes and non-astrocytes in spinal cord injury

BACKGROUND Spinal cord injury(SCI)is a destructive disease that incurs huge personal and social costs,and there is no effective treatment.Although the pathogenesis and treatment mechanism of SCI has always been a strong scientific focus,the pathogenesis of SCI is still under investigation.AIM To determine the key genes based on the modularization of in-depth analysis,in order to identify the repair mechanism of astrocytes and non-astrocytes in SCI.METHODS Firstly,the differences between injured and non-injured spinal cord of astrocyte(HA),injured and non-injured spinal cord of non-astrocyte(FLOW),injured spinal cord of non-injured astrocyte(HA)and non-injured spinal cord of nonastrocyte(FLOW),and non-injured spinal cord of astrocyte(HA)and nonastrocyte(FLOW)were analyzed.The total number of differentially expressed genes was obtained by merging the four groups of differential results.Secondly,the genes were co-expressed and clustered.Then,the enrichment of GO function and KEGG pathway of module genes was analyzed.Finally,non-coding RNA,transcription factors and drugs that regulate module genes were predicted using hypergeometric tests.RESULTS In summary,we obtained 19 expression modules involving 5216 differentially expressed genes.Among them,miR-494,XIST and other genes were differentially expressed in SCI patients,and played an active regulatory role in dysfunction module,and these genes were recognized as the driving genes of SCI.Enrichment results showed that module genes were significantly involved in the biological processes of inflammation,oxidation and apoptosis.Signal pathways such as NF-kappa B/A20,AMPK and MAPK were significantly regulated.In addition,non-coding RNA pivot(including miR-136-5p and let-7d-5p,etc.)and transcription factor pivot(including NFKB1,MYC,etc.)were identified as significant regulatory dysfunction modules.CONCLUSION Overall,this study uncovered a co-expression network of key genes involved in astrocyte and non-astrocyte regulation in SCI.These findings helped to reveal the core dysfunction modules,potential regulatory factors and driving genes of the disease,and to improve our understanding of its pathogenesis.

Spinal Cord Kinking in Thoracic Myelopathy Caused by Ossification of the Ligamentum Flavum

Background：Ossification of the ligamentum flavum （OLF） is being increasingly recognized as a cause of thoracic myelopathy.This study was to describe a rare clinical entity of spinal cord kinking （SK） in thoracic myelopathy secondary to OLF.Methods：The data of 95 patients with thoracic myelopathy secondary to OLF were analyzed retrospectively.The incidence and location of SK were determined using preoperative magnetic resonance imaging （MRI）.The clinical presentation and radiological characteristics in patients with SK were analyzed.Posterior en bloc laminectomy with OLF was performed,and the surgical results were evaluated.Results：SK was found in seven patients （7.4％） based on preoperative MRI.The patients included one male and six females with an average age of 55.6 years （range,48-64 years）.Five patients presented with radiculomyelopathy and two presented with typical thoracic myelopathy of spastic paraparesis.In all cases,the kinking was located just above the end of the spinal cord where the conus medullaris （CM） was compressed by the OLF.The degree of SK varied from mild to severe.The tip of the CM was located between the upper third of T1 1 to the lower third of L 1,above the lower edge of L 1.With an average follow-up of 30.4 months,the modified Japanese Orthopedic Association score significantly improved from 5.7 ± 1.8 preoperatively to 8.9 ± 1.4 postoperatively （t =12.05;P ＜ 0.0001） with an improvement rate of 63.1 ± 12.3％.Conclusions：SK is a rare radiological phenomenon.It is typically located at the thoracolumbar junction,where the CM is compressed by the OLF.Our findings indicate that these patients may benefit from a posterior decompressive procedure.