OBJECTIVE: There were previous reports of redundant nerve roots (RNRs) focused on their clinical significance and pathogenesis. In this study, we investigated the significant radiologic findings that correlate with RNRs occurrence. These relations would provide an advanced clue for clinical significance and pathogenesis of RNRs. METHODS: Retrospective research was performed with data from 126 patients who underwent surgery for central lumbar spinal stenosis (LSS). Finally, 106 patients with common denominators (inter-observer accuracy : 84%) were included on this study. We divided the patients into two groups by MRI, patients with RNRs and those with no RNRs (NRNRs). Comparative analyses were performed with clinical and radiologic parameters. RESULTS: RNRs were found in 45 patients (42%) with central LSS. There were no statistically significant differences between the two groups in severity of symptoms. On the other hand, we found statistically significant differences in duration of symptom and number of level included (p<0.05). In the maximal stenotic level, ligamentum flavum (LF) thickness, LF cross-sectional area (CSA), dural sac CSA, and segmental angulation are significantly different in RNRs group compared to NRNRs group (p<0.05). CONCLUSION: RNRs patients showed clinically longer duration of symptoms and multiple levels included. We also confirmed that wide segmental angulation and LF hypertrophy play a major role of the development of RNRs in central LSS. Together, our results suggest that wide motion in long period contribute to LF hypertrophy, and it might be the key factor of RNRs formation in central LSS.
Hand ; Humans ; Hypertrophy ; Ligamentum Flavum ; Retrospective Studies ; Spinal Stenosis

Purpose: One of the novel cell sources of cell-based liver regenerative medicine is human chemically-derived hepatic progenitors (hCdHs). We previously established this cell by direct hepatocyte reprogramming with a combination of small molecules (hepatocyte growth factor, A83-01, CHIR99021). However, there have been several issues concerning the cell’s stability and maintenance, namely the occurrences of epithelial-mesenchymal transition (EMT) that develop fibrotic phenotypes, resulting in the loss of hepatic progenitor characteristics. These hepatic progenitor attributes are thought to be regulated by SOX9, a transcription factor essential for hepatic progenitor cells and cholangiocytes. Methods: To suppress the fibrotic phenotype and improve our long-term hCdHs culture technology, we utilized the epigenetic modulating drugs DNA methyltransferase inhibitor (5-azacytidine) and histone deacetylase inhibitor (sodium butyrate) that have been reported to suppress and revert hepatic fibrosis. To confirm the essential role of SOX9 to our cell, we used clustered regularly interspaced short palindromic repeats-interference (CRISPRi) to repress the SOX9 expression. Results: The treatment of only 5-azacytidine significantly reduces the fibrosis/mesenchymal marker and EMT-related transcription factor expression level in the early passages. Interestingly, this treatment also increased the hepatic progenitor markers expression, even during the reprogramming phase. Then, we confirmed the essential role of SOX9 by repressing the SOX9 expression with CRISPRi which resulted in the downregulation of several essential hepatic progenitor cell markers. Conclusion These results highlight the capacity of 5-azacytidine to inhibit EMT-driven hepatic fibrosis and the significance of SOX9 on hepatic progenitor cell stemness properties.