Background Traditional assessments of minimally invasive spine surgery (MISS) often rely on superficial metrics like incision length and overt blood loss (OBL), neglecting systemic stress and hidden blood loss (HBL). Objective To evaluate the perioperative hidden trauma, muscle injury, and HBL of endoscopic dual-zone decompression (DZD) compared with transforaminal lumbar interbody fusion (TLIF) in elderly patients with degenerative lumbar spinal stenosis (DLSS). Methods A retrospective, multicenter cohort study was conducted on 432 elderly patients with DLSS from January 2024 to December 2025. Patients were divided into the DZD group (n = 220) and the TLIF group (n = 212). Propensity matching verified homogeneous baselines across 12 variables (P > 0.10). Total blood loss (TBL) and HBL were derived utilizing the Nadler and Gross equations. Systemic inflammatory dynamics (Interleukin-6 [IL-6], Tumor Necrosis Factor-α [TNF-α]) and multifidus muscle damage (Creatine Kinase [CK]) were tracked longitudinally at preoperative (T0), postoperative 24h (T1), 72h (T2), and 7 days (T3). Results OBL was significantly lower in the DZD group than in the TLIF group (45.2 ± 12.4 mL vs. 412.8 ± 85.4 mL, P < 0.001). However, HBL accounted for 79.31 ± 6.42% of TBL in the DZD group, which was significantly higher than the 53.33 ± 5.18% observed in the TLIF group (P < 0.001). Repeated-measures ANOVA revealed significant group × time interaction effects for IL-6, TNF-α, and CK (P < 0.001). Serum CK in the DZD group experienced a mild elevation at T1 (124.2 ± 32.5 U/L) and completely reverted to baseline at T3 (86.2 ± 15.4 U/L), whereas the TLIF group exhibited severe, prolonged muscle destruction (P < 0.001). Conclusion Although endoscopic DZD demonstrates a paradoxically higher proportion of hidden blood loss due to hydrostatic containment intraoperatively, it significantly mitigates systemic inflammatory responses and preserves the structural integrity of the posterior tension band compared to open surgery.

Background: Spinal cord injury (SCI) leads to permanent sensory and motor function loss, characterized by inflammation and neuronal loss. A promising therapeutic strategy involves delivering anti-inflammatory and neuroregenerative agents tailored to these phases. Methods: GelMA-AFN hydrogel microspheres were prepared by a UV-crosslinked microfluidic chip. Immunofluorescence was performed to assess the effect of GelMA-AFN on apoptosis, axonal growth in dorsal root ganglion (DRG) neurons. Immunohistochemistry, flow cytometry, electrophysiology, RNA-seq, and behavioral testing were used to evaluate histological and functional recovery in a rat SCI model. Results: In this study, we developed GelMA-AFN with a dual-layer structure and an mean diameter of 50 µm. The outer layer, containing low-concentration gelatin methacryloyl (GelMA, 5%) and annexin A1 (ANXA1), provided sustained ANXA1 released for up to 7 days, while the inner layer, with high-concentration GelMA (10%), nanoclay, fibronectin (FN), and nerve growth factor (NGF), releases FN and NGF over 6 weeks. In vitro, GelMA-AFN inhibits neuronal apoptosis, promoted axonal growth, and enhances survival under oxidative stress. In vivo, it reduced early inflammation by limiting neutrophil recruitment and promoting macrophage M2 polarization. Eight weeks post-SCI in a rat model, GelMA-AFN enhanced axonal extension, myelin regeneration, beneficial ECM deposition, and reduced glial scar formation, leading to significant neural electrical signal conduction and motor function recovery. mRNA-seq analysis confirmed GelMA-AFN upregulates genes associated with anti-inflammatory responses and axonal extension while downregulating pro-inflammatory genes. Conclusion: These results suggest GelMA-AFN as a promising therapeutic approach for SCI by providing spatiotemporal delivery aligned with the injury's dynamic stages.

To compare the efficacy of robot‑assisted (RA) and conventional fluoroscopy‑guided percutaneous vertebroplasty (PVP) combined with pediculoplasty in the treatment symptomatic chronic thoracolumbar osteoporotic vertebral fracture (SCOVF) without neurological deficits. This retrospective analysis included a total of 120 patients, with 87 in RA group and 33 in conventional group. Parameters such as operation time, volume of bone cement injected, and first-attempt success rate of puncture were recorded. Additionally, assessments were made for vertebral body index (VBI), bisegmental Cobb angle, visual analogue scale (VAS) score, Oswestry dysfunction index (ODI) score, and the occurrence of bone cement leakage or displacement during follow-up. The success rate of puncture was higher in RA group than conventional group (95.4

This review article describes recent research advances in the relationship between spinal cord injury (SCI) and the gut microbiota and each other’s inflammatory response. SCI is a serious neurological disease that directly damages physiological function. Recent studies have shown that SCI significantly affected the composition and function of the gut microbiota, and even caused intestinal inflammation. The gut microbiota, a community of microorganisms inhabiting the intestinal tract, is closely related to the human health. Recent studies have indicated that the disordered gut microbiota was strongly associated with the progression of several diseases, including intestinal inflammation and SCI, in addition, some specific strains may be involved in the development of intestinal inflammation and secondary inflammatory after SCI. These strains promote intestinal inflammation through the production of inflammatory mediators and activation of immune cells. Intestinal inflammation, in turn, further exacerbate spinal cord pathology and secondary inflammatory. In summary, there is an intimate interaction between the intestinal microbiota, intestinal inflammation and SCI, secondary inflammation. An in-depth study of these interaction mechanisms presented here may aid in understanding of SCI occurrence and development and provide new ideas for future therapeutic strategies.

The optimal treatment strategy for atlantoaxial fracture-dislocation remains a focal point of clinical research and a subject of ongoing debate, with a paucity of definitive comparative clinical studies. With the increasing application of robot-assisted (RA) technology in spinal surgery, the present study aims to compare the clinical efficacy of traditional fluoroscopy-assisted freehand screw placement (FA) and robot-assisted screw placement in the treatment of atlantoaxial fracture-dislocation, providing a reference for clinical practice. This retrospective study analyzed the clinical data of 59 patients with atlantoaxial fracture-dislocation who underwent surgical treatment at Honghui Hospital in Xi'an from May 2023 to August 2024. Patients were divided into two groups based on the method of screw placement: the freehand group (n = 36) and the robot-assisted group (n = 23). Data on surgical time, intraoperative blood loss, postoperative hospital stay, and the incidence of complications, such as vascular, neural, and spinal cord injuries were collected. The accuracy of pedicle screw placement was evaluated using the Gertzbein and Robbins scoring system. Treatment outcomes were assessed using visual analog scale (VAS) scores for pain, Japanese Orthopaedic Association (JOA) scores for cervical spine function, and the incidence of postoperative complications. All 59 patients successfully underwent surgery, with significant postoperative improvement in symptoms. The study results demonstrated that the robotic-assisted group had significantly longer operative times (171.1 ± 23.6 min) and higher intraoperative blood loss (305.9 ± 53.7 ml) compared with the manual group (operative time: 109.9 ± 18.5 min; intraoperative blood loss: 185.0 ± 21.2 ml), with statistically significant differences between the two groups (P < 0.01). However, the robotic-assisted group exhibited significantly higher accuracy and safety in screw placement (96.5

Intervertebral disc degeneration (IDD) is a leading cause of low back pain, necessitating a comprehensive understanding of the molecular mechanisms driving disc degeneration to develop effective preventive and therapeutic strategies. Chondrocytes, as the predominant cellular constituents of the nucleus pulposus, are thought to play a pivotal role in the pathogenesis of IDD. In this study, we leveraged publicly available single-cell RNA sequencing (scRNA) data from the Gene Expression Omnibus (GEO) database for a comprehensive analysis. Employing unsupervised clustering methods, we successfully identified five distinct subtypes of chondrocytes and characterized two distinct terminal cell fates within the chondrocyte population. Through weighted gene co-expression network analysis (WGCNA), we identified RPL17, RPL13A, RPS18, and RPS24 as hub genes significantly associated with disc degeneration compared to control discs. Furthermore, our analysis of cell communication unveiled the activation of pro-inflammatory pathways in intervertebral disc degeneration. These findings shed light on the intricate complexity of chondrocyte involvement in the development of intervertebral disc degeneration and enhance our understanding of the role of chondrocyte niches within the nucleus pulposus during degenerative processes. Importantly, our study paves the way for potential targeted therapeutic approaches to address IDD. ### Competing Interest Statement The authors have declared no competing interest.

Background:Probiotics have been demonstrated to repair spinal cord injuries (SCI) by improving gut microbiota dysbiosis; however, the specific mechanisms underlying their therapeutic effects on SCI remain incompletely elucidated. Objective:This study aims to investigate the therapeutic effects of probiotics and analyze the mechanisms of probiotic treatment for SCI through the gut-spinal cord axis. Methods:A rat model of SCI was established to evaluate the therapeutic effects of probiotics. Fecal samples were analyzed to assess gut microbiota composition and metabolite profiles, while differential gene expression in spinal cord tissue was examined. Results:Pathological assessments demonstrated that probiotic treatment facilitated structural restoration of the spinal cord tissue. Behavioral evaluations via the Basso Mouse Scale (BMS) and inclined plane tests revealed significant improvements in locomotor recovery after SCI. Metagenomic sequencing showed that probiotics enhanced gut microbiota diversity, particularly enriching the relative abundance of Bacillota (formerly Firmicutes) and Clostridia. Metabolite profiling identified an enrichment of key tryptophan metabolites, including 3-Indoleacetonitrile, Xanthoxic acid, Serotonin, and Tryptophanol. Transcriptomic analysis identified 468 upregulated and 173 downregulated genes in spinal cord tissues. Furthermore, gut microbiota, microbial metabolites and spinal cord gene expression were integrated to construct a "gut microbiota-tryptophan metabolites-signaling pathway network" using Cytoscape v.3.10.2. This network linked 19 microbial species (17 belonging to Bacillota and Clostridia, including seven Lactobacillus species) with tryptophan metabolites and downstream signaling pathways. Among these, tryptophan metabolites activated 17 genes predominantly involved in anti-inflammatory and neuroregenerative processes. Protein-level validation confirmed the neuroprotective and anti-inflammatory effects of probiotics. Conclusion:The "Gut microbiota-tryptophan metabolites-signaling pathway network" offers novel therapeutic targets for SCI injury treatment. Probiotics exert their effects by modulating gut microbiota and enhancing tryptophan metabolism, thereby influencing multiple signaling pathways in the spinal cord that can lead to anti-inflammatory and neuroprotective outcomes.

OBJECTIVE:This study aimed to compare the clinical outcomes of patients with AOSpine A3 or A4 thoracolumbar fractures presenting with neurological deficits treated with endoscopic decompression combined with percutaneous pedicle screws fixation (endoscopic minimally invasive surgery, EMIS) or conventional open surgery (OS). METHODS:Data of patients with AOSpine A3 or A4 thoracolumbar fractures with neurological deficits who were treated with EMIS or OS between June 2019 and July 2021 were extracted from the electronic database. Various clinical outcomes were compared between the 2 cohorts. RESULTS:Among the 231 patients who were followed up for more than 2 years, 107 were in the EMIS cohort and 124 were in the OS cohort. Compared with the OS cohort, the EMIS cohort had longer operative time (p<0.05), but the intraoperative blood loss, incision length and hospital stay were significantly reduced (p<0.05). At both postoperative and final follow-up assessments, the EMIS cohort demonstrated significantly better visual analogue scale and Oswestry Disability Index outcomes compared to the OS cohort (p<0.05). Both cohorts maintained similar correction of spinal canal erosion rate, percentage of anterior vertebral height and sagittal Cobb angle after surgery and at the last follow-up (p>0.05). According to American Spinal Injury Association classification, the 2 cohorts had similar neurological recovery at the last follow-up (p>0.05). CONCLUSION:In comparison to OS, EMIS treatment for AOSpine A3 or A4 thoracolumbar fractures with neurological deficits has shown comparable clinical efficacy while significantly reducing surgical trauma.

Background: Emerging research indicates that PCSK9 inhibitors, which originally developed for lowering LDL cholesterol, may positively impact bone skeletal system. By potentially enhancing bone density and strength, PCSK9 inhibitors offer a promising new avenue in bone disease management, signaling a significant shift in therapeutic strategies. Methods: This study employed a comprehensive approach involving the extraction of single- nucleotide polymorphisms (SNPs) from genome-wide association studies (GWAS), followed by rigorous quality checks. PCSK9 instrumental variables were utilized to evaluate the effect of cholesterol-lowering drugs on osteoporosis, osteoarthritis, and rheumatoid arthritis. Cross-Phenotype Association Analysis (CPASSOC) and colocalization analysis were conducted to identify overlapping genetic sites Results: Our analysis did not reveal a significant causal relationship between lower BMD and the predicted risk of FCHL. However, there was an observed association between an increased genetic risk of FCHL and reduced BMD, particularly in younger individuals (TB-BMD (age 15-30): OR = 0.922, 95% CI: 0.844-0.993, P = 0.032). PCSK9 inhibitors were found to increase BMD while reducing the risk of FCHL. Notably, rs998584 in the VEGFA gene emerged as a shared locus in both CPASSOC and colocalization analyses, with high expression in Adipo-CAR cells in the bone marrow. Conclusions: This study's cross-trait analysis uncovers a shared genetic basis between FCHL and BMD, elucidating the causal relationship between genetic predisposition to FCHL and the likelihood of reduced BMD. Our findings contribute to a more nuanced understanding of the genetic factors influencing bone health in European populations and highlight potential therapeutic targets for improving BMD in individuals with FCHL. ### Competing Interest Statement The authors have declared no competing interest. ### Funding Statement This work was supported by Special Support Project for High-level Talents of Shaanxi Province (2020), Shaanxi Provincial Key Research and Development Project (2020GXLH-Y-027), Scientific Research Project of Xi 'an Health Commission (2020qn16) and National Natural Science Foundation of China (NSFC, Grant code: 81830077). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: The study used ONLY openly available human data that were originally located at: https://gwas.mrcieu.ac.uk/ I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The datasets analyzed for this study can be found in the IEU OpenGWAS https://gwas.mrcieu.ac.uk/datasets/ and the GEO database https://www.ncbi.nlm.nih.gov/geo.

Spinal cord injury (SCI) leads to extensive neuronal loss and substantial neurological impairment within the spinal cord. The acute inflammatory response and the limited regenerative capacity of neurons are major barriers to neural repair. In this study, we developed bilayer hydrogel microspheres (PC-GEN) with a core-shell structure through droplet microfluidics. The shell layer, composed of PEG-4MAL hydrogels embedded with cerium oxide nanoparticles (CONPs), was released during the first week. The GelMA hydrogel core, containing spinal white matter extracellular matrix (swm-ECM) and nerve growth factor (NGF), provides sustained release for up to eight weeks. PC-GEN mitigates early inflammation during the acute phase by enhancing macrophage/microglia M2 polarization and reducing inflammatory cell infiltration. PC-GEN promoted axonal extension, myelin regeneration, and functional neural network reconstruction in the SCI rat model, resulting in substantial functional recovery. Notably, swm-ECM significantly improved the inhibitory microenvironment following SCI by increasing permissive ECM deposition and decreasing glial scar formation. Furthermore, mRNA-seq analysis confirmed that PC-GEN elevated the expression of genes associated with ECM proteins and neurogenesis, while simultaneously downregulating pro-inflammatory gene transcription. The sequential release of PC-GEN provides a biomimetic delivery strategy tailored to the dynamic pathological changes in SCI, positioning it as a promising therapeutic approach for SCI.

This study delved into the molecular mechanisms underlying mechanical stress-induced intervertebral disc degeneration (msi-IDD) through single-cell and high-throughput transcriptome sequencing in mouse models and patient samples. Results exhibited an upsurge in macrophage presence in msi-IDD intervertebral disc (IVD) tissues, with secreted phosphoprotein 1 (SPP1) identified as a pivotal driver exacerbating degeneration via the protein kinase RNA-like endoplasmic reticulum kinase/ activating transcription factor 4/ interleukin-10 (PERK/ATF4/IL-10) signaling axis. Inhibition of SPP1 demonstrated promising outcomes in mitigating msi-IDD progression in both in vitro and in vivo models. These findings underscore the therapeutic promise associated with the modulation of the PERK signaling pathway in IDD, shedding light on the pathogenesis of msi-IDD and proposing a promising avenue for intervention strategies.

To evaluate the clinical efficacy and safety of robot-assisted targeted co-ablation (CA) combined with percutaneous vertebroplasty (PVP) under local anesthesia for spinal metastases. This was a retrospective study of 43 patients with spinal metastases treated in our hospital from October 2022 to October 2023. Among the 43 patients, 18 underwent robot-assisted targeted CA combined with PVP (CA group) and 25 underwent PVP alone (PVP group). The visual analogue scale (VAS), the Oswestry Disability Index (ODI), and the Karnofsky Performance Status (KPS) were used to evaluate the intensity of pain, and the quality of life. There were no significant differences in the baseline data between the two groups (P > 0.05). The time of puncture channel establishment in the CA group was significantly shorter than that in the PVP group (11.33 ± 2.22 vs. 26.72 ± 4.20 min, P < 0.001). There were significantly improvements in VAS, ODI and KPS of two groups at each follow-up visit than before the operation (P > 0.05). However, at the 6 months follow-up, patients of the CA group had significantly lower VAS and ODI scores than the PVP group, and the KPS was higher (P < 0.05). The imaging examination performed at 6 months after the operation revealed that only one patient (5.6

Spinal cord injury (SCI) remains a severely disabling disorder that impacts millions globally by causing irreversible damage to the nervous system. Although cell - based therapies have shown notable progress, the post - injury microenvironment presents significant obstacles that hinder the survival and effectiveness of implanted cells, ultimately limiting sustained functional restoration. Exosomes have emerged as a promising cell - free therapeutic alternative due to their stability, low immunogenicity, and ability to carry bioactive molecules such as proteins, microRNAs, and lipids. These vesicles can modulate the injured microenvironment, support neuroprotection, and facilitate repair. This review begins by discussing the pathological alterations that disrupt the microenvironment following SCI. The review then outlines the process of exosome formation and highlights their structural features. Furthermore, the review delves into the diverse cellular sources of exosomes and evaluates their therapeutic relevance in the context of SCI. Special attention is given to the multifaceted roles exosomes play in neuroprotection, such as reinforcing the blood - spinal cord barrier, stimulating axonal regeneration, promoting new blood vessel formation, suppressing programmed cell death in neurons, and modulating inflammatory responses. The synergistic use of exosomes in combination with biomaterials is also explored, with the aim of optimizing their therapeutic potential. Lastly, the review addresses the key obstacles that must be overcome to bring exosome - based treatments into clinical application and offers perspectives on future advancements in this evolving field. In summary, exosomes offer a novel and promising avenue for SCI intervention, holding considerable promise as an alternative to traditional therapeutic approaches.

Background: While certain studies suggest a relationship between hyperlipidemia and bone metabolism, the exact nature of proprotein convertase subtilisin/kexin 9 inhibitors (PCSK9i, targeted by, eg, alirocumab), which were originally developed for lowering LDL cholesterol inhibitors, with bone disease is still unclear. This research endeavors to uncover the potential causal relationship between PCSK9i and several most popular bone diseases (osteoporosis (OP), osteoarthritis (OA), rheumatoid osteoarthritis (RA)) using Mendelian randomization (MR). Methods: This study employed a comprehensive approach involving the extraction of single-nucleotide polymorphisms (SNPs) from genome-wide association studies (GWAS), followed by rigorous quality checks. PCSK9i instrumental variables were utilized to evaluate the effect of cholesterol-lowering drugs on osteoporosis, osteoarthritis, and rheumatoid arthritis. Results: PCSK9i instrumental variables were validated using familial combined hyperlipidemia summary data. Our analysis did not reveal a significant causal relationship between PCSK9i and OP. However, there was an observed an increased Lumbar-spine bone mineral density (LS-BMD) with PCSK9i intaking (OR=1.157, 95% CI: 0.963 to 1.330, P=0.044). PCKS9i significantly increased genetic risk of knee OA (OR=1.136, 95% CI: 1.027 to 1.228, P=0.013), but not for hip OA. Genetic risk of seropositive RA was strongly reduced while consuming PCSK9i (OR=0.796, 95% CI: 0.580 to 0.964, P=0.020) and this effect is independent with LDL levels, while we don’t observe causal relationships with PCSK9i on seronegative RA. Conclusions: This study elucidates the causal relationship between PCSK9i and genetic predisposition to OP, OA, and RA. PCSK9i would benefit LS-BMD and protect the genetic risk of seropositive RA. Meanwhile, PCSK9i might be a risk factor for knee OA.

Spinal cord injury (SCI) is a life - altering neurological condition that carries significant global morbidity and mortality. It results in the disruption of motor and sensory pathways below the site of injury, often leading to permanent functional impairments and severely diminished quality of life. Despite decades of clinical and research efforts, current treatment options remain largely supportive, with limited success in promoting meaningful functional recovery or neural regeneration. In recent years, nanozymes have emerged as a promising frontier in the therapeutic landscape for SCI. These nanomaterial - based artificial enzymes offer several compelling advantages over their natural counterparts, including superior stability under physiological conditions, adjustable catalytic activity, cost - effective production, and prolonged shelf life. Unlike traditional therapeutic agents, nanozymes can be engineered to closely mimic the activity of key endogenous antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase. By scavenging reactive oxygen species and attenuating oxidative damage, nanozymes help preserve neuronal integrity and support the intrinsic repair processes of the central nervous system. This review provides a comprehensive overview of the pathophysiological mechanisms underlying SCI and examines the classification and catalytic principles governing nanozyme activity. We delve into the molecular pathways through which nanozymes exert their neuroprotective effects, particularly their roles in modulating oxidative stress and suppressing inflammatory responses following injury. Additionally, we explore the current challenges associated with nanozyme development, such as biocompatibility, targeted delivery, and long - term safety, and discuss future directions for optimizing their therapeutic potential in clinical applications. By synthesizing emerging insights into antioxidant nanozyme - based strategies, this review aims to contribute to the evolving landscape of SCI treatment and to highlight the transformative potential of nanozymes in advancing neuroregenerative medicine. These innovative agents represent a new horizon in SCI management, offering renewed hope for improving neurological outcomes and quality of life in affected individuals.

The antler is the only organ that can fully regenerate annually in mammals. However, the regulatory pattern and mechanism of gene expression and cell differentiation during this process remain largely unknown. Here, we obtain comprehensive assembly and gene annotation of the sika deer (Cervus nippon) genome. We construct, together with large-scale chromatin accessibility and gene expression data, gene regulatory networks involved in antler regeneration, identifying four transcription factors,MYC,KLF4,NFE2L2,andJDP2, with high regulatory activity across the whole regeneration process. Comparative studies and luciferase reporter assay suggest theMYCexpression driven by a cervid-specific regulatory element might be important for antler regenerative ability. We further develop a model called combinatorial TF Oriented Program (cTOP), which integrates single-cell data with bulk regulatory networks and findPRDM1,FOSL1,BACH1, andNFATC1as potential pivotal factors in antler stem cell activation and osteogenic differentiation. Additionally, we uncover interactions within and between cell programs and pathways during the regeneration process. These findings provide insights into the gene and cell regulatory mechanisms of antler regeneration, particularly in stem cell activation and differentiation.

To describe the clinical and radiographic outcomes of patients with severe post-tubercular kyphosis (PTK) in adults who underwent modified posterior vertebral column resection (mPVCR). A retrospective analysis was conducted on data from 22 patients with severe PTK who underwent surgical treatment. All patients received a one-stage mPVCR deformity correction. General information, radiological parameters including kyphosis angle (KA) and sagittal vertical axis (SVA), functional outcomes including America Spinal Injury Association (ASIA) grades, Oswestry Disability Index (ODI), Scoliosis Research Society-22 (SRS-22) scores, and complications were recorded. The mean age of the population was 33.6 ± 11.6 years (range: 18–59 years). The average operation time was 383.2 ± 53.8 min, and the mean intraoperative blood loss was 1652.3 ± 331.8 ml. Significant changes in KA (preoperative: 129.5 ± 17.3° vs. postoperative: 43.7 ± 7.6°; p < 0.001) and SVA (preoperative: 30.9 ± 7.5 mm vs. postoperative: 15.0 ± 4.1 mm; p < 0.001) were observed after the surgery. In addition, the mean SRS-22 scores improved following surgical correction, with the most significant improvement in the self-image domain. The overall complication rate was 36.4

Spinal cord injury (SCI) is a neurological disease characterized by the loss of motor and sensory function below the injury level. The pathogenesis of SCI is complex, involving the recruitment of various cells that play key roles in the injury area. Single-cell RNA sequencing (scRNA-seq) can analyze cell heterogeneity and inter-cell communication. Bulk RNA-seq offers advantages such as low cost, mature technology and high throughput. Joint analysis of bulk RNA-seq and scRNA-seqis more complementary for exploring the pathophysiology of diseases. In this study, we revealed changes in cell clusters and intercellular signaling after SCI through the scRNA-seq analysis. Bioinformatics analyses and experimental verification showed that macrophages increase rapidly and become the dominant cell type after SCI. The mTOR gene is the key molecule of M1 macrophage autophagy blockade and the PI3K-AKT-mTOR signaling pathway plays an important role in blockings macrophage autophagy.

Background : Manual placement of cervical pedicle screws is risky, and robot-assisted placement of atlantoaxial pedicle screws has not been reported. Case report : We describe a 74-year-old female patient with atlantoaxial fracture and dislocation combined with spinal cord injury caused by a car accident. The left lower limb muscle strength was grade 0, the right upper limb muscle strength was grade 1, and the right lower limb muscle strength was grade 2. Loss of sensation below the clavicle level, decreased superficial sensation in the extremities, loss of deep sensation in the left lower extremity, and incontinence were observed. We successfully placed atlas pedicle screws with the assistance of the Mazor X robot. One week after the operation, radiological imaging revealed that the reduction effect was good, the placement of the pedicle screws was satisfactory, the left upper limb and left lower limb muscle strength was level 2, the right upper limb and the muscle strength of the right lower limb were grade 3, and the sensory function was partially restored. No complications related to screw placement were found at the 3-month postoperative follow-up. Conclusions : Mazor X robot-assisted descending pedicle screw fixation of the atlas is feasible and safe.

Lumbar disc herniation (LDH) is a common degenerative disease of the lumbar spine, which is related to host genetic factors. Our study aimed to explore the association between MIR3142HG polymorphisms and LDH susceptibility. Six SNPs in MIR3142HG from 504 LDH patients and 500 healthy individuals were genotyped by the Agena MassARRAY platform. The relationship between SNPs and LDH susceptibility was evaluated with logistic regression analysis by calculating odds ratios (ORs) and 95% confidence intervals (CIs). The interactions between SNP and SNP were analyzed using the multifactor dimensionality reduction (MDR) method. Our study showed that rs7727115 was related to a decreased susceptibility to LDH. Rs2961920 and rs58747524 were significantly associated with an increased risk of LDH. Stratified analysis showed that rs7727115 reduced the risk of LDH in patients aged > 49 years. Rs17057846, rs2961920, and rs58747524 had a risk-increasing influence on patients aged > 49 years and women. Besides, rs7727115 decreased susceptibility in cases of disc prolapse, while rs2961920 and rs58747524 increased the risk. Rs2431689 increased susceptibility in patients with a single hernia, and rs58747524 correlated with an increased risk in cases of multiple hernias. Moreover, MDR analysis indicated that the combination of rs1582417, rs2431689, rs7727115, rs17057846, rs2961920, and rs58747524 was the best predictive model for LDH. Our study showed that MIR3142HG polymorphisms were significantly associated with LDH risk, which suggests that MIR3142HG polymorphisms play some potential roles in diagnosing LDH.