In China, non-litigation methods constitute the primary approach for resolving medical disputes. However, the empirical estimation of compensation amounts in the absence of medical appraisal support often leads to significant discrepancies in outcomes. This study discuss factors influencing hospital compensation costs in non-litigation medical disputes, providing scientific evidence to facilitate rational assessment of compensation amounts. The records of 131 cases of medical dispute compensation in a tertiary general hospital were examined from 2018 to 2022. The aim was to identify factors that could impact the costs associated with these compensation events. Various information was collected and organized, including patient details, information about the doctors involved, and details about the dispute events. All this information was recorded in an Excel file. To analyze the relationship between these factors and the compensation costs, statistical analysis software was utilized. Correlation analysis using Pearson's correlation, independent sample t-tests, analysis of variance, and other methods were performed. Additionally, multiple linear regression analysis was used to determine the influencing factors associated with the correlation. The results of the correlation analysis indicated a significant correlation between 3 factors (personal injury outcome, dispute resolution time in months, and degree of responsibility in settlement) and the costs of dispute compensation (P < .05). Additionally, the multiple linear regression analysis confirmed that these 3 factors were significant in influencing the dispute compensation costs (P < .05). The compensation costs for medical disputes between doctors and patients that do not involve litigation, are influenced by several important factors. These include the outcome of the personal injury, the time taken to resolve the dispute (measured in months), and the level of responsibility assigned in the settlement.

PURPOSE:Discitis is a severe suppurative infection of the intervertebral disc (IVD) posing significant clinical challenges. This study evaluated the therapeutic efficacy of ozonated water (OW) in a rat model of Staphylococcus aureus-induced discitis and elucidated its underlying mechanisms, focusing on NF-κB signaling, extracellular matrix homeostasis, and nucleus pulposus (NP) cell apoptosis. METHODS:A rat tail coccygeal IVD discitis model was established by injecting S. aureus (102 cfu) into the disc space. From day 3 post-infection, animals received transdiscal lavage with normal saline, levofloxacin (5 mg/mL), or OW (30 μg/mL) three times daily until day 9. In vitro, NP cells were stimulated with S. aureus Protein A (SpA, 1 μg/mL). Antibacterial activity, extracellular matrix metabolism, inflammatory cytokine expression, NF-κB p65 signaling, and apoptosis were evaluated by bacterial culture, Western blotting, immunohistochemistry, TUNEL assay, and flow cytometry. RESULTS:OW significantly alleviated tail swelling and IVD structural damage. OW demonstrated potent antibacterial activity against S. aureus, disrupting bacterial membrane integrity. OW attenuated extracellular matrix degradation by upregulating collagen II and aggrecan while downregulating MMP3 and MMP9, and suppressed inflammatory responses (IL-1β, IL-6, TNF-α, Cox2) by inhibiting NF-κB p65 phosphorylation and nuclear translocation. OW also reduced NP cell apoptosis, evidenced by decreased TUNEL-positive rate, elevated Bcl-2/Bax ratio, and reduced Cleaved caspase-3. CONCLUSIONS:OW attenuates S. aureus-induced discitis through direct antibacterial action, suppression of NF-κB-mediated inflammation, protection against NP cell apoptosis, and preservation of extracellular matrix integrity, highlighting its promise as a novel lavage strategy for discitis management.

Cartilage degradation, inflammation, and pyroptosis are key drivers of Osteoarthritis (OA) pathogenesis, contributing to chondrocyte impairment. However, the therapeutic potential of KLK8, a cartilage-associated protease, remains unexplored in OA. KLK8 expression was detected in meniscal/ligamentous injury (MLI)-induced OA mouse models and human OA cartilage tissues. KLK8 expression in chondrocytes stimulated with interleukin-1β (IL-1β) was also detected and quantified. Small interfering RNA (siRNA) was used to inhibit KLK8 in IL-1β-stimulated chondrocytes and its influence on the expression of cartilage catabolic factor and inflammatory factors expression were examined. The mechanism through which KLK8 regulates NF-κB activity was investigated. Chondrocyte pyroptosis were also measured. MLI-induced OA in mice were used to investigate KLK8's in vivo therapeutic potential. KLK8 expression was significantly upregulated in articular cartilage from OA patients and mice models. IL-1β stimulation increased KLK8 levels in chondrocytes in vitro. Functional assays showed that KLK8 knockdown attenuated IL-1β-induced inflammatory responses and extracellular matrix degradation in chondrocytes. KLK8 directly interacts with IκBα to promote its cytoplasmic degradation, which leads to p65 release, nuclear translocation and extended nuclear retention, thus enhancing NF-κB activity in IL-1β-stimulated chondrocytes. Furthermore, the levels of NLRP3, ASC and cleaved Caspase-1 were decreased after IL-1β stimulation in KLK8-deficient chondrocyte, indicating a stimulatory effect on NLRP3 inflammasome activation. Flow cytometry showed reduced chondrocyte pyroptosis after KLK8 knockdown, and ELISA detected decreased TNF-α, IL-6, and IL-18 levels, indicating KLK8 regulates chondrocyte pyroptosis. In vivo, KLK8 knockdown mitigated OA progression and reduced the expression of NLRP3, MMP13, COL2A1, and IL-18 in OA mice. These findings indicate that KLK8 promotes cartilage degradation, inflammation and pyroptosis via activating the NF-κB and NLRP3 inflammasome pathways. In vivo, KLK8 inhibition significantly alleviates OA progression, highlighting KLK8 as a potential therapeutic target for OA.

Secondary spinal cord injury (SCI) involves neuroinflammatory mechanisms such as microglial pyroptosis, which aggravates neural impairment via NLRP3 inflammasome activation. Although liraglutide (Lr) is commonly used for managing blood glucose, it also exhibits anti-inflammatory effects. Previous studies from our group have shown that glucagon-like peptide-1 receptor (GLP-1R) activation in microglia attenuates neuroinflammation and promotes functional recovery after SCI, the precise mechanism linking GLP-1R to the inhibition of pyroptosis remained unclear. Here, we report that high-dose Lr (independent of its metabolic effects) significantly improves functional and histological outcomes in a murine SCI model, and these benefits are abolished in GLP-1R-/- mice. In vitro, RNA sequencing, combined with pharmacological and genetic approaches, revealed that Lr, via the PI3K/Akt/transcription factor EB (TFEB) axis, by upregulates Fanconi anemia complementation group C (FANCC) to suppress pyroptosis. Crucially, FANCC knockdown both elevated p38 phosphorylation and blocked the anti-pyroptotic effect of Lr, thereby establishing FANCC as an essential downstream mediator. This signaling cascade culminates in the inhibition of p38-dependent NLRP3 inflammasome activation. Collectively, our work defines a novel GLP-1R/PI3K/Akt/TFEB/FANCC/p38 pathway through which Lr alleviates secondary SCI, identifying FANCC as a pivotal neuroprotective node and supporting the translational potential of GLP-1R modulation in SCI.

The formation of foamy cells (FMMs) by excessive engulfment of myelin debris (MD) causes secondary neuroinflammation and chronic neuropathies after traumatic spinal cord injury (SCI). It is unclear what the function and mechanism of retinoid X receptor (RXR) α are in FMMs-induced neuroinflammation and neural improvement post SCI. The present study aims to investigate the effects and underlying mechanisms of RXRα activation on FMMs and SCI mice. We established an in vitro FMMs model by MD stimulation and an in vivo SCI model in mice. Using an agonist 2, 4-Di-tert-butylphenol (2, 4-DTBP), we activated RXRα and examined the inflammation levels by PCR, WB, and Immunofluorescence (IF), then detected lipid accumulation by BODIPY and Oil red O staining, and determined secondary neuropathies using IF and histological staining. The locomotor function recovery was assessed using motor evoked potential (MEP), Basso Mouse Scale (BMS), as well as footprint assay. Activation of RXRα by 2, 4-DTBP reduced the expression of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α and the levels of inflammatory mediators iNOS and COX-2. Besides, treatment with 2, 4-DTBP increased the expression of cholesterol efflux channels including Abca1, Abcg1, Apoe, and caused a marked decrease in intracellular cholesterol and lipid accumulation. Blocking the RXRα-induced cholesterol efflux caused an increase in cholesterol and FMMs, reversing the prior decrease, and exacerbated the degree of neuroinflammation. Also, administration of 2, 4-DTBP improved the neuropathies and locomotor function recovery after SCI.Taken together, activation of RXRα decreased the formation of FMMs by promoting cholesterol efflux and inhibited neuroinflammation by inhibition of p38 and NF-κB signaling after SCI. It is a promising target for mitigating FMMs-induced neuroinflammation and locomotor dysfunction.

Spinal cord injury (SCI) is a debilitating and destructive disorder of the central nervous system (CNS), resulting in severe sensory and motor deficits. Secondary injury mechanisms, including neuroinflammation and oxidative stress, play critical roles in disease progression. Pharmacological interventions with anti-inflammatory and antioxidant agents have shown promise as therapeutic strategies for SCI. Hyperoside (HYP), a bioactive flavonoid derived from traditional Chinese medicinal herbs, exhibits potent anti-inflammatory and antioxidant properties. This study aimed to investigate whether HYP mitigates secondary injury and promote functional recovery after SCI. We evaluated neuroinflammation and oxidative stress using western blot (WB), immunofluorescence staining, and quantitative real-time PCR in both in vitro and in vivo models. SCI mice were treated with HYP (10 mg/kg or 50 mg/kg) via intraperitoneal injection. Functional recovery was assessed using the Basso Mouse Scale score and swimming tests. Histopathological changes were examined through Hematoxylin and Eosin, Nissl, and Luxol Fast Blue staining. HYP treatment significantly reduced the expression of pro-inflammatory mediators (IL-1β, IL-6, TNF-α, iNOS, and COX-2) and oxidative stress-related markers (NOX1, NOX2, and NOX4). Furthermore, HYP enhanced the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway and upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in LPS-insulted macrophages. Administration of HYP attenuated tissue damage, reduced demyelination, preserved neuronal structure, and promoted functional recovery following SCI. In vitro, these protective effects were mediated through the suppression of macrophage-driven neuroinflammation and oxidative stress via activation of the PI3K/ AKT and Nrf2/HO-1 signaling pathways. In conclusion, our findings demonstrate that HYP confers neuroprotection by alleviating neural tissue damage and facilitating locomotor recovery after SCI, highlighting its potential as a therapeutic agent for SCI treatment.

The thoracolumbar and lumbar spine is mainly involved in T11 to L5, which is the transition from the relatively fixed thoracic vertebrae to the more mobile lumbar vertebrae, where the main stress of the trunk is concentrated.This study aims to perform a detailed morphometric analysis of the thoracolumbar and lumbar region using high-resolution CT scans to define safe working zones for the transdiaphragmatic and transpsoas approaches. Patients who underwent CT examination from February 2024 through September 2024 were from our database. Measurements were performed from T10-T11,T11-T12,T12-L1,L1-L2,L2-L3,L3-L4 and L4-L5 disc levels and were determined using the PACS software computer digitizer and SYNGO System. Using this data, one surgeon carried out measurements of the lower vertebral endplate at each level (sagittal and transversal), position of muscle attachment area, position of the nerve roots, position of the retroperitoneal vessels.The safe zone is defined as the region between retroperitoneal vessels (including arteries and veins) and nerve roots. Its superior boundary is demarcated by the horizontal plane of the most inferior vessel border, while the inferior boundary corresponds to the horizontal plane of the most superior nerve root border. In all subjects, the transverse diameters demonstrated a progressive increase across the T10–T11 to L4–L5 spinal segments. Sagittal diameters exhibited a similar ascending trend from T10–T11 to L2–L3, followed by a gradual reduction from L2–L3 to L4–L5. Notably, the smallest sagittal diameter was recorded at T10–T11, while the maximum value peaked at L2–L3.The projection of nerve roots is identical on both sides. The nerve-vertebral overlap height progressively decreased from T10/T11 to L1/L2, then progressively increased from L1/L2 to L4/L5, with the maximal overlap observed at L4/L5 and the minimal at L1/L2.The vascular-vertebral overlap height progressively decreased from T10/T11 to L1/L2, then progressively increased from L1/L2 to L4/L5, with the maximal overlap observed at T10/T11 and the minimal at L1/L2.No diaphragmatic attachments were observed bilaterally at the T10-T11 level. Partial bilateral diaphragmatic attachments with craniocaudal elevation were identified at T11/T12 in 28.3

A 51-year-old female with a 10-year history of progressive low back pain presented with a 9 ! 15 mm circular tumor adjacent to L1 on preoperative magnetic resonance imaging. The lesion was successfully removed by T12–L2 laminectomy and nail–rod fixation. Histopathological examination diagnosedmature intramedullary cystic teratoma. At 6-month follow-up, right lower limb numbness and pain were reduced. Cite this article as: Li H, Liu X, Zhang Q. A rare case of a mature intramedullary cystic teratoma in an adult female: A case report and literature review. Acta Orthop Traumatol Turc., 2025;59(2):129-132.

This study aimed to compare the predictive performance of CT-derived Hounsfield units (HU) and MRI-based vertebral bone quality (VBQ) scores for pedicle screw loosening (PSL) following single-level lumbar spinal fusion in patients with various types of degenerative lumbar disorders. A retrospective analysis was conducted on patients who underwent transforaminal lumbar interbody fusion (TLIF) at our institution between April 2021 and December 2023. PSL was identified on lumbar X-ray obtained at 12-month follow-up, defined as a radiolucent zone of ≥ 1 mm around the pedicle screw. VBQ score and HU value were measured using preoperative MRI and CT, respectively. Receiver operating characteristic (ROC) curve analysis was performed to evaluate and compare the predictive capabilities of HU and VBQ for PSL. Across all patients (n = 154), the area under the curve (AUC) of the VBQ score (AUC = 0.807; 95

Spinal cord injury (SCI) is a devastating condition characterized by the accumulation of myelin debris (MD), persistent neuroinflammation, and impaired neural regeneration. Although macrophages are pivotal for MD clearance, the impact of excessive MD phagocytosis on macrophage phenotype and function remains poorly understood. Building upon our prior evidence that exendin-4 (Ex-4), a glucagon-like peptide-1 receptor (GLP-1R) agonist, mitigates microglia-driven neuroinflammation post-SCI, this study elucidates the therapeutic efficacy and underlying mechanisms of Ex-4 in alleviating macrophage senescence, restoring efferocytotic capacity, and facilitating neural repair. Employing a T10 contusive SCI model in male C57BL/6 mice, in vivo administration of Ex-4 was combined with macrophage-specific knockdown of growth arrest-specific 6 (Gas6) via AAV-shRNA. Complementary in vitro assays involved bone marrow-derived macrophages (BMDMs) challenged with MD in the presence or absence of Ex-4 or AMP-activated protein kinase (AMPK) inhibition. Cellular senescence and efferocytosis were comprehensively assessed through live-cell imaging, immunofluorescence, senescence-associated β-galactosidase staining, quantitative PCR, and western blotting. Molecular docking and dynamics simulations elucidated GLP-1R–AMPK interactions, corroborated by in vivo validation. Results demonstrate that MD-engulfing macrophages exhibit foam cell-like morphology and upregulated senescence markers, including increased β-galactosidase activity and senescence-associated secretory phenotype, concomitant with diminished efferocytosis via downregulation of the Axl receptor. Senescent macrophages were shown to exacerbate neuronal apoptosis and astrocytic scar formation in co-culture systems. Ex-4 treatment significantly attenuated macrophage senescence, restored efferocytotic function, and reduced neuronal injury and astrocyte activation, effects contingent upon AMPK/Gas6/Axl pathway activation and abrogated by Gas6 knockdown. In vivo, Ex-4 administration enhanced remyelination, axonal regeneration, and functional recovery, while attenuating glial scar formation following SCI. Collectively, these findings identify macrophage senescence induced by excessive MD phagocytosis as a novel pathological contributor to SCI progression and establish Ex-4 as a promising therapeutic agent that restores macrophage homeostasis and promotes neural repair via GLP-1R/AMPK/Gas6/Axl signaling.

Background: This study aimed to evaluate the risk factors for machine learning (ML) algorithms in predicting postoperative surgical site infection (SSI) following spine surgery. Methods: This prospective cohort study included 986 patients who underwent spine surgery at Taizhou People's Hospital Affiliated to Nanjing Medical University from January 2015 to October 2022. Supervised ML algorithms included support vector machine, logistic regression, random forest, XGboost, decision tree, k -nearest neighbour, and na & imath;ve Bayes (NB), which were tested and trained to develop a predicting model. The ML model performance was evaluated from the test dataset. We gradually analysed their accuracy, sensitivity, and specificity, as well as the positive predictive value, negative predictive value, and area under the curve. Results: The rate of SSI was 9.33%. Using a backward stepwise approach, we identified that the remarkable risk factors predicting SSI in the multi-variate Cox regression analysis were age, body mass index, smoking, cerebrospinal fluid leakage, drain duration and preoperative albumin level. Compared with other ML algorithms, the NB model had the highest performance in seven ML models, with an average area under the curve of 0.95, sensitivity of 0.78, specificity of 0.88, and accuracy of 0.87. Conclusions: The NB model in the ML algorithm had excellent calibration and accurately predicted the risk of SSI compared with the existing models, and might serve as an important tool for the early detection and treatment of SSI following spinal infection. (c) 2023 The Author(s). Published by Elsevier Ltd on behalf of The Healthcare Infection Society. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

AbstractBackgroundSpinal cord injury (SCI)‐induced neuroinflammation and oxidative stress (OS) are crucial events causing neurological dysfunction. Aconitate decarboxylase 1 (ACOD1) and its metabolite itaconate (Ita) inhibit inflammation and OS by promoting alkylation of Keap1 to induce Nrf2 expression; however, it is unclear whether there is another pathway regulating their effects in inflammation‐activated microglia after SCI.MethodsAdult male C57BL/6 ACOD1−/− mice and their wild‐type (WT) littermates were subjected to a moderate thoracic spinal cord contusion. The degree of neuroinflammation and OS in the injured spinal cord were assessed using qPCR, western blot, flow cytometry, immunofluorescence, and trans‐well assay. We then employed immunoprecipitation‐western blot, chromatin immunoprecipitation (ChIP)‐PCR, dual‐luciferase assay, and immunofluorescence‐confocal imaging to examine the molecular mechanisms of ACOD1. Finally, the locomotor function was evaluated with the Basso Mouse Scale and footprint assay.ResultsBoth in vitro and in vivo, microglia with transcriptional blockage of ACOD1 exhibited more severe levels of neuroinflammation and OS, in which the expression of p62/Keap1/Nrf2 was down‐regulated. Furthermore, silencing ACOD1 exacerbated neurological dysfunction in SCI mice. Administration of exogenous Ita or 4‐octyl itaconate reduced p62 phosphorylation. Besides, ACOD1 was capable of interacting with phosphorylated p62 to enhance Nrf2 activation, which in turn further promoted transcription of ACOD1.ConclusionsHere, we identified an unreported ACOD1‐p62‐Nrf2‐ACOD1 feedback loop exerting anti‐inflammatory and anti‐OS in inflammatory microglia, and demonstrated the neuroprotective role of ACOD1 after SCI, which was different from that of endogenous and exogenous Ita. The present study extends the functions of ACOD1 and uncovers marked property differences between endogenous and exogenous Ita.Key points ACOD1 attenuated neuroinflammation and oxidative stress after spinal cord injury. ACOD1, not itaconate, interacted with p‐p62 to facilitate Nrf2 expression and nuclear translocation. Nrf2 was capable of promoting ACOD1 transcription in microglia.

BACKGROUND:Following spinal cord injury (SCI), the inflammatory storm initiated by microglia/macrophages poses a significant impediment to the recovery process. Exosomes play a crucial role in the transport of miRNAs, facilitating essential cellular communication through the transfer of genetic material. However, the miRNAs from iPSC-NSCs-Exos and their potential mechanisms leading to repair after SCI remain unclear. This study aims to explore the role of iPSC-NSCs-Exos in microglia/macrophage pyroptosis and reveal their potential mechanisms. METHODS:iPSC-NSCs-Exos were characterized and identified using transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. A mouse SCI model and a series of in vivo and in vitro experiments were conducted to investigate the therapeutic effects of iPSC-NSCs-Exos. Subsequently, miRNA microarray analysis and rescue experiments were performed to confirm the role of miRNAs in iPSC-NSCs-Exos in SCI. Mechanistic studies were carried out using Western blot, luciferase activity assays, and RNA-ChIP. RESULTS:Our findings revealed that iPSC-NSCs-derived exosomes inhibited microglia/macrophage pyroptosis at 7 days post-SCI, maintaining myelin integrity and promoting axonal growth, ultimately improving mice motor function. The miRNA microarray showed let-7b-5p to be highly enriched in iPSC-NSCs-Exos, and LRIG3 was identified as the target gene of let-7b-5p. Through a series of rescue experiments, we uncovered the connection between iPSC-NSCs and microglia/macrophages, revealing a novel target for treating SCI. CONCLUSION:In conclusion, we discovered that iPSC-NSCs-derived exosomes can package and deliver let-7b-5p, regulating the expression of LRIG3 to ameliorate microglia/macrophage pyroptosis and enhance motor function in mice after SCI. This highlights the potential of combined therapy with iPSC-NSCs-Exos and let-7b-5p in promoting functional recovery and limiting inflammation following SCI.

Background Mechanical spinal cord injury (SCI) is a deteriorative neurological disorder, causing secondary neuroinflammation and neuropathy. ADAM8 is thought to be an extracellular metalloproteinase, which regulates proteolysis and cell adherence, but whether its intracellular region is involved in regulating neuroinflammation in microglia after SCI is unclear.Methods Using animal tissue RNA-Seq and clinical blood sample examinations, we found that a specific up-regulation of ADAM8 in microglia was associated with inflammation after SCI. In vitro, microglia stimulated by HMGB1, the tail region of ADAM8, promoted microglial inflammation, migration and proliferation by directly interacting with ERKs and Fra-1 to promote activation, then further activated Map3k4/JNKs/p38. Using SCI mice, we used BK-1361, a specific inhibitor of ADAM8, to treat these mice.Results The results showed that administration of BK-1361 attenuated the level of neuroinflammation and reduced microglial activation and recruitment by inhibiting the ADAM8/Fra-1 axis. Furthermore, treatment with BK-1361 alleviated glial scar formation, and also preserved myelin and axonal structures. The locomotor recovery of SCI mice treated with BK-1361 was therefore better than those without treatment.Conclusions Taken together, the results showed that ADAM8 was a critical molecule, which positively regulated neuroinflammatory development and secondary pathogenesis by promoting microglial activation and migration. Mechanically, ADAM8 formed a complex with ERK and Fra-1 to further activate the Map3k4/JNK/p38 axis in microglia. Inhibition of ADAM8 by treatment with BK-1361 decreased the levels of neuroinflammation, glial formation, and neurohistological loss, leading to favorable improvement in locomotor functional recovery in SCI mice.

The purpose of this study was to analyze the impact of implementing a driver's license-type scoring system on the quality management of hospital medical records. We collected relevant medical record quality control data before (from April to November 2021) and after (from April to November 2022) the use of the driver's license-type scoring management in the medical record quality management of a Grade-A tertiary general hospital in a prefecture-level city ("R Hospital" for short). We evaluated the impact by statistically analyzing the data using the chi(2) test and t test with the SPSSAU online statistical analysis software. Compared with before the implementation of the new system, the filling rate of discharge medical records within 2 days, logical rate of day diagnosis and treatment medical records, logical rate of day surgery medical records, and clinical tumor-node-metastasis staging evaluation rate before tumor treatment significantly increased, and the difference was statistically significant (P < .05); the rate of errors or omissions on the first page of inpatient medical records significantly decreased, and the difference between before and after implementation of the new system was statistically significant (P < .05). We found that the driver's license-type scoring management adapted for use in the quality management of hospital medical records was effective in regulating the medical record writing behavior of physicians and improved the quality of medical records, thus meriting wide promotion.

Background: Spinal cord injury (SCI)-induced neuroinflammation and oxidative stress (OS) are crucial events causing terrible neurological dysfunction. Aconitate decarboxylase 1 (ACOD1) and its metabolite itaconate (Ita) inhibit inflammation and OS by promoting alkylation of Keap1 and releasing Nrf2; however, it is unclear whether there is another pathway regulating their effects in inflammation-activated microglia after SCI.Methods: Adult male C57BL/6 ACOD1-/- mice and their wildtype (WT) littermates were subjected to a moderate thoracic spinal cord contusion. Degree of neuroinflammation and OS in the injured spinal cord were assessed using qPCR technique, western blot, oxidization determination, immunofluorescence, and trans-well assay. We then employed immunoprecipitation-western blot, chromatin immunoprecipitation (ChIP)-PCR, dual-luciferase assay, and immunofluorescence-confocal imaging to examine the molecular mechanisms of ACOD1. Locomotor function was evaluated with the Basso Mouse Scale and footprint assay.Findings: Both in vitro and in vivo, microglia with transcriptional blockage of ACOD1 exhibited more severe levels of neuroinflammation and OS, in which the expression of p62/Keap1/Nrf2 pathway was down-regulated; deficiency of ACOD1 exacerbated dysfunction of neurohistology and neuroethology in the SCI mice. Supplement of exogenous Ita or 4-octyl itaconate instead reduced p62 phosphorylation and inhibited autophagy. Besides, ACOD1 was capable of interacting with p-p62 and enhanced Nrf2 activation, further endonuclear Nrf2 promoted transcription of ACOD1 gene.Interpretation: Here we identified an unreported ACOD1-p62-Nrf2-ACOD1 feedback loop exerting the anti-inflammation and anti-OS effects in inflammatory microglia, and demonstrated the neuroprotective role of ACOD1 after SCI rather than exogenous Ita. The present study extends the functions of ACOD1 and uncovers marked property differences between endogenous and exogenous Ita.Funding: The study was supported by the Natural Science Foundation of Jiangsu Province (Grant No. SBK2022022488), the Chinese Traditional Medicine Technology Development Project of Taizhou City (Grant No. TZ202208), the 2022 Lifting Project for Young Scientific and Technological Talents Funded by Jiangsu Association of Science and Technology (Grant No. TJ-2022-033), and the China Postdoctoral Science Foundation (CPSF; Grant No. 2022M721680).Declaration of Interest: The authors declare that they have no competing interests.Ethical Approval: The project was approved by the Ethics Committee of Taizhou People’s Hospital of Nanjing Medical University and the procedure was obeyed by the guidelines of the National Institutes of Health Animal Laboratory Animal Care and Use Guidelines.

Backgroud: Many far lateral lumbar disc herniation (FLLDH) classifications utilize image technology to describe the size, shape, and location of disc herniation. However, these approaches are fail in illustrating the spatial relationship between disc herniation and nerve roots. Their utility in offering guidance for the clinical execution of percutaneous transforaminal endoscopic discectomy (PTED) is limited and isgenerally more suited for open surgery. The aim of this study was to propose a clinical classification for FLLDH based on three-dimensional double-echo steady-state (3D-DESS) imaging technology and to provide guidance with precise cannula placement and surgical operation for PTED. Methods: A retrospective analysis was conducted on the images of 178 FLLDH patients diagnosed by 3D-DESS. Based on the positional relationship between nerve roots and disc herniation, FLLDH patients were classified into 3 types: type I, axillary tennis type; type II, axillary elevated type; and type III, shoulder type. Among these, 68 patients underwent PTED treatment. The clinical results were assessed using the Visual Analog Scale (VAS) leg pain score, the Oswestry Disability Index (ODI) score, and the modified Macnab criteria. Results: The average age of the patients was 61.29 ± 11.60 years, with a male/female ratio of 42:26. According to the 3D-DESS classification, there were I=25, II=40 and III=3. The average operation time was 66.91 ± 18.87 minutes, the average follow-up was 24.27±4.66 months, and the recurrence rate was 6%. The VAS leg pain score improved from 7.63 ± 0.91 to 0.69 ± 1.37. The ODI score improved from 51.27 ± 9.09 to 3.87 ± 5.75. The modified Macnab criteria results showed that 35 patients (51%) were excellent, 25 patients (37%) were good, 4 patients (6%) were fair and 4 patients (6%) were poor. No complications, such as infection or nerve or vascular injury, occurred in the patients. Conclusions: Using 3D-DESS to classify FLLDH patients can provide clinical guidance with precise puncture and treatment for PTED. It helps operators remove disc herniation, decompress nerve roots, shorten operation time, and improve the success rate of PTED.

Introduction:Pedicle screw fixation (PSF) has been the standard therapy for the treatment of various spinal diseases. Although complications are identified regularly, iatrogenic vascular injury is one of the rare but life-threatening complications. In this literature, we describe the first case of inferior vena cava (IVC) injury during pedicle screw removal.Case description:A 31-year-old man was treated by percutaneous pedicle screw fixation for an L1 compression fracture. After a year, the fracture healed well and hardware removal surgery was performed. During the procedure, the hardware on the right was removed unremarkably except for the L2 pedicle screw which slipped into the retroperitoneum because of the improper technique. The CT angiogram revealed the screw had breached the anterior cortex of the L2 vertebral body and penetrated the IVC. After multidisciplinary cooperation, the defect of IVC was reconstructed and the L2 screw was removed from the posterior approach in the end.Result:The patient recovered well and was discharged after 3 weeks without further events. The removal of the contralateral implants was unremarkable at 7 months postoperatively. At the 3-year follow-up, the patient returned to his normal daily activity without any complaints.Conclusion:Although pedicle screw removal is a rather simple procedure, severe complications may have occurred from this procedure. Surgeons should keep vigilant to avoid the complication noted in this case.

Abstract Background Spinal cord injury (SCI) is a troublesome and destructive disease in the central nervous system (CNS) that leads to severe sensory and locomotor damage. Neuro-inflammation and oxidative stress are secondary injuries after SCI, and treating SCI to with the anti-inflammatory and antioxidant drug is an effective treatment method. Hyperoside (HYP), a Chinese medicinal herb, has been demonstrated to have anti-inflammmation and anti-oxidative pharmacological effects. Objective In order to explore whether HYP can alleviate the secondary injury and promote the recovery of motor function after SCI. Methods Neuro-inflammation and oxidative stress were detected by western blotting (WB), immunofluorescence (IF) staining, and Real-time quantitative reverse-transcription PCR (qRT-PCR) both in vitro and in vivo. HYP (10 mg/kg, 50 mg/kg) were intraperitoneally injected into SCI mice in vivo. Basso mouse scale scores and swimming test were performed to evaluate locomotor function recovery of SCI mice. Morphology were assessed by Hematoxylin-eosin, Nissl, and Luxol Fast Blue staining following SCI. Results HYP decreased the level of pro-inflammatory mediators (IL-1β, IL-6, TNF-α, iNOS and COX-2) and oxidative stress-related indicators (NOX1, NOX2 and NOX4). Phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) expression were increased by treating with HYP. Additionally, HYP upregulated transcription factor nuclear factor E2-related factor 2 (Nrf2) and Heme oxygenase 1 (HO-1). HYP administration decreased tissue deficiency, alleviated demyelination, protected neural structure and function, and promoted locomotor recovery post SCI. Conclusion HYP mitigated macrophage-mediated neuroinflammation and oxidative stress by activating the PI3K/AKT and Nrf2/HO-1 signaling pathway post SCI. This research revealed that HYP contributed a neuroprotective effect to reduce nervous tissue damage and promoting locomotor recovery after SCI.

Abstract Background: To describe a rare case of mature intramedullary cystic teratoma. Case presentation: A 51-year-old female with a 10-year history of progressive low back pain presented with a 9 × 15 mm circular tumor adjacent to L1 on preoperative magnetic resonance imaging (MRI). The lesion was successfully removed by T12–L2 laminectomy and nail–rod fixation, and the diagnosis was subsequently confirmed by histopathological examination. At 6-month follow-up, right lower limb numbness and pain were reduced. Conclusions: Mature intramedullary cystic teratoma size, morphology, and location relative to peripheral nerves can be revealed by MRI for preoperative planning. Surgical resection with nail–rod fixation is the best treatment for multilevel lesions.