Multi-omics analysis of macrophage-associated receptor and ligand reveals a strong prognostic signature and subtypes in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a significant contributor to morbidity and mortality worldwide. The interaction between receptors and ligands is the primary mode of intercellular signaling and plays a vital role in the progression of HCC. This study aimed to identify the macrophage-related receptor ligand marker genes associated with HCC and further explored the molecular immune mechanisms attributed to altered biomarkers. Single-cell RNA sequencing data containing primary and recurrent samples were downloaded from the China National GeneBank. Cell types were first identified to explore differences between immune cells from different sample sources. CellChat analysis was used to infer and analyze intercellular communication networks quantitatively. Three molecular subtypes were constructed based on the screened twenty macrophage-associated receptor ligand genes. Bulk RNA-Seq data were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. After the screening, the minor absolute shrinkage and selection operator (LASSO) regression model was employed to identify key markers. After collecting peripheral blood and clinical information from patients, an enzyme-linked immunosorbent assay (ELISA) was used to detect the correlation between key markers and IL-10, one of the macrophage markers. After developing a new HCC risk adjustment model and conducting analysis, it was found that there were significant differences in immune status and gene mutations between the high-risk and low-risk groups of patients based on macrophage-associated receptor and ligand genes. This study identified SPP1, ANGPT2, and NCL as key biological targets for HCC. The drug-gene interaction network analysis identified wortmannin, ribavirin, and tarnafloxin as potential therapeutic drugs for the three key markers. In a clinical cohort study, patients with immune checkpoint inhibitor (ICI) resistance had significantly higher expression levels of OPN, ANGPT2, NCL, and IL-10 than patients with ICI-responsiveness. These three key markers were positively correlated with the expression level of IL-10. The signature based on macrophage-associated receptor and ligand genes can accurately predict the prognosis of patients with HCC and the sensitivity to immunotherapy. These results may help guide the development of targeted prevention and personalized treatment of HCC.

Stem cell therapy with CRISPR/Cas9-mediated MALAT1 delivery modulates miR-142 and rescues wound healing in rats with age-associated diabetic foot ulcers.

BACKGROUND: Diabetic foot ulcer (DFU) is a serious diabetes complication, significantly impacting the quality of life, particularly in the elderly. Age-associated DFUs pose additional challenges due to impaired healing mechanisms. Our study aims to explore the role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) as a miR-142 sponge in repairing diabetic rat foot ulcer tissue under age-associated diabetes, offering a new theoretical basis and therapeutic target for preventing and treating diabetic vascular disease in the elderly. METHODS: Using qPCR, we analyzed MALAT1 and miR-142 expression in EPCs and hUC-MSCs. Targetscan predicted potential interaction targets for MALAT1 and miR-142, confirmed by dual luciferase reporter gene assay. An age-associated diabetic rat model was established using Streptozotocin (STZ) injection. Hypoxia, apoptosis, and angiogenesis-related proteins were assessed through Western Blot. In vitro, miR-142 inhibition and MALAT1 overexpression promoted foot ulcer healing in diabetic rats. RESULTS: MALAT1 acted as a miR-142 sponge, downregulated in hUC-MSCs under high glucose, relevant to age-associated diabetic foot ulcers. MiR-142 negatively regulated SIRT1 and Nrf2. In vitro experiments demonstrated potential significance for age-related DFU treatment. CONCLUSIONS: MALAT1 in human umbilical cord mesenchymal stem cells expedited foot ulcer healing in diabetic rats, particularly in age-associated diabetes, through miR-142 sponge activity. These findings offer insights for novel therapeutic strategies targeting elderly diabetic foot ulcers, emphasizing exogenous stem cell transplantation's potential in effective DFU treatment for the elderly.

Tumor-derived exosomes promote macrophages M2 polarization through miR-1-3p and regulate the progression of liver cancer.

Hepatic carcinoma is one of the most life-threatening malignancies in the world. In the clinic, it is urgent to establish a clear mechanism of hepatic carcinoma development as the basis for intervention and treatment. The purpose of this study was to explore the regulatory effect of tumor-derived exosomes on the progression of hepatocellular carcinoma.qPCR was used to detect the expression of miR-1-3p. CCk-8 and EdU staining were used to detect the proliferation and activity of hepatocellular carcinoma cells under different conditions. Transwell assay was used to detect migration and invasion of hepatocellular carcinoma cells. The morphology and size of exosomes were detected by transmission electron microscope and nanoparticle tracking analysis. Western blot was used to detect the expression of markers of exosomes. Immunofluorescence staining was used to explore the location of exosomes in hepatocellular carcinoma cells.The results showed that the expression of miR-1-3p was significantly reduced in hepatocellular carcinoma cells, and the exosomes transfected with miR-1-3p could enter macrophages and express miR-1-3p in large quantities. Macrophages polarized to M2 type under the action of miR-1-3p. Polarized M2 macrophages further down-regulated the proliferation, migration and invasion of Huh-7 cells.In summary, miR-1-3p can enter macrophages through exosomes and affect their polarization, thus affecting the growth of hepatic carcinoma cells. miR-1-3p may be a potentially effective target for regulating liver cancer progression.

Integration of Multimodal Computed Tomography Radiomic Features of Primary Tumors and the Spleen to Predict Early Recurrence in Patients with Postoperative Adjuvant Transarterial Chemoembolization.

Background: Hepatocellular carcinoma (HCC) is one of the most lethal malignancies in the world. Patients with HCC choose postoperative adjuvant transarterial chemoembolization (PA-TACE) after surgical resection to reduce the risk of recurrence. However, many of them have recurrence within a short period. Methods: In this retrospective analysis, a total of 173 patients who underwent PA-TACE between September 2016 and March 2020 were recruited. Radiomic features were derived from the arterial and venous phases of each patient. Early recurrence (ER)-related radiomics features of HCC and the spleen were selected to build two rad-scores using the least absolute shrinkage and selection operator (LASSO) Cox regression analysis. Logistic regression was applied to establish the Radiation (Rad)_score by combining the two regions. We constructed a nomogram containing clinical information and dual-region rad-scores, which was evaluated in terms of discrimination, calibration, and clinical usefulness. Results: All three radiological scores showed good performance for ER prediction. The combined Rad_score performed the best, with an area under the curve (AUC) of 0.853 (95% confidence interval [CI], 0.783-0.908) in the training set and 0.929 (95% CI, 0.789-0.988) in the validation set. Multivariate analysis identified total bilirubin (TBIL) and the combined Rad_score as independent prognostic factors for ER. The nomogram was found to be clinically valuable, as determined by the decision curves (DCA) and clinical impact curves (CIC). Conclusion: A multimodal dual-region radiomics model combining HCC and the spleen is an independent prognostic tool for ER. The combination of dual-region radiomics features and clinicopathological factors has a good clinical application value.

Uterine artery embolization combined with ultrasound-guided dilation and curettage for the treatment of cesarean scar pregnancy: Efficacy and 5-8-year follow-up study.

Objective: To evaluate the efficacy and safety of uterine artery embolization (UAE) combined with dilation and curettage (D&C) using ultrasound as a treatment for cesarean scar pregnancy (CSP) and assess its effect on ovarian and reproductive function. Methods: A total of 54 patients with uterine CSP between January 2011 and December 2015 were included in this retrospective study. The patients were treated with UAE combined with D&C using ultrasound for the treatment of CSP and followed up for 5-8 years. Their medical records, medical histories, clinical manifestations, treatment courses, and treatment results were analyzed. Results: The 54 patients were initially treated without severe complications. ß-Human chorionic gonadotropin (ß-hCG) normalization took 36.11 â€‹± â€‹10.73 days (range, 25-84 days), length of hospitalization was 6.6 â€‹± â€‹1.5 days (range, 4-10 days), and total blood loss was 18.48 â€‹± â€‹8.41 â€‹mL (range, 5-33 â€‹mL). All patients resumed normal menstruation after 33.48 â€‹± â€‹8.71 days (range, 26-70 days). At the 5-8-year follow-up after UAE combined with D&C by ultrasound for the treatment of uterine CSP, the menstrual volume in 32 (59.3%) patients decreased versus before the operation. Compared with pretreatment, the menstrual cycle was prolonged in two (3.7%) cases, shortened in 10 (18.5%) cases, irregular in one (1.9%) case, and unchanged in 39 (72.2%) cases. Three patients conceived naturally and successfully gave birth to healthy children. Seven (12.96%) patients with accidental natural pregnancies chose induced abortion with no significant change in their sex lives. Conclusion: UAE combined with D&C using ultrasound for the treatment of uterine CSP is safe and effective and may not affect the fertility of patients aged <40 years. However, menstrual volume may be reduced in some patients.

Hypoxic ADSC-derived exosomes enhance wound healing in diabetic mice via delivery of circ-Snhg11 and induction of M2-like macrophage polarization.

Diabetes mellitus is a major cause of blindness and chronic ulcers in the working age population worldwide. Former research have found that differentially expressed circular RNAs (circRNAs) are associated with hyperglycemia (HG)-induced endothelial cell damage. And adipose-derived stem cells (ADSCs)-exosome transplant have more therapeutic effect to enhance wound healing in diabetic mice by delivery circRNA. The current investigation employed high-throughput sequencing to identify circRNAs that are abnormally expressed in endothelial progenitor cells (EPCs) under HG conditions. The regulatory mechanism and predicted targets of one differentially expressed circRNA, circ-Snhg11, were investigated utilizing bioinformatics analyses, luciferase reporter assays, angiogenic differentiation assays, flow cytometric apoptosis analysis, and RT-qPCR. The result show that circ-Snhg11 expression decreased in EPCs under HG conditions and that overexpression of circ-Snhg11 suppressed HG-induced endothelial cell damage and M1-like macrophage polarization. miR-144-3p and HIF-1α were identified as downstream targets of circ-Snhg11, which was further verified by luciferase reporter analysis. miR-144-3p overexpression or HIF-1α inhibition reversed circ-Snhg11 protective effect on HG-induced endothelial cell dysfunction, as evidenced by increased apoptosis, abnormal vascular differentiation, and secretion of inflammatory factors. In addition, miR-144-3p overexpression or inhibition of HIF-1α reversed protective effect regarding circ-Snhg11 on M2-like macrophage polarization under HG conditions. These findings suggest that circ-Snhg11 promotes HIF-1α expression through miR-144-3p sponging. Our data demonstrate that circ-Snhg11 overexpression exosome from ADSCs suppresses HG-induced endothelial cell damage and induces M2-like macrophage polarization via the miR-144-3p/HIF-1α axis.

A 3D multi-modal intelligent intervention system using electromagnetic navigation for real-time positioning and ultrasound images: a prospective randomized controlled trial.

Background: Anesthesia, nerve block, therapeutic injections, and biopsies all require an acupuncture intervention. However, traditional two-dimensional (2D) ultrasound-guided needle puncture is often challenging and therefore requires the use of three-dimensional (3D) ultrasound images to accurately identify and evaluate the patient's anatomical structure. Methods: In this study, a 3D multi-modal intelligent intervention system using electromagnetic navigation for real-time positioning and ultrasound images was described. A total of 190 cases requiring puncture were randomly divided into control (conventional 2D ultrasound instrument) and experimental (novel 3D ultrasound imedis9000) groups. The advantages and disadvantages of the two puncture methods were prospectively analyzed in the 190 cases, and the feasibility of electromagnetic navigation real-time positioning was compared to ultrasound imaging. Results: This study included 190 cases from two centers that required puncture treatment and were randomly assigned to the control (conventional 2D ultrasound instrument; n=95) or the experimental (novel 3D ultrasound imedis9000; n=95) groups. Percutaneous vascular puncture, percutaneous biopsy, percutaneous bile duct puncture, thoracic paravertebral nerve block, and sciatic nerve block operations were performed separately. The results indicated that the puncture time and number of trials in the experimental group were significantly lower than those in the control group. No significant difference was identified in the basic vital signs between the two groups before and after surgery. The success rate of the novel 3D ultrasound imedis9000 was 100%, and the success rate of the conventional 2D ultrasound instrument was 95.7%. Furthermore, the results also showed that the novel 3D ultrasound imedis9000 and the matching coaxial positioning channel puncture needle had low pain, good toughness and strength, and great convenience. Conclusions: The new 3D multi-modal intelligent intervention system using electromagnetic navigation real-time positioning and ultrasound images has significant advantages compared with conventional 2D ultrasound in terms of puncture time, number of trials, operation difficulty, and convenience, and is worthy of further promotion and use in clinics. Trial Registration: Beijing Municipal Drug Administration, 20190015.

Molecular subtypes, prognostic and immunotherapeutic relevant gene signatures mediated by DNA methylation regulators in hepatocellular carcinoma.

Growing evidence has revealed the crucial role of epigenetics in tumor progression and immune response. However, the molecular subtypes and their microenvironment characterization mediated by DNA methylation regulators in hepatocellular carcinoma remain little known. In this study, we comprehensively integrated the transcriptome profiling of twenty DNA methylation regulators in hepatocellular carcinoma. Consensus clustering was used to identify distinct methylation regulator-related molecular subtypes. The prognostic DMS signature was constructed using principal components analysis. Most regulators experienced a low genomic variation, but we found a remarkably difference in mRNA expression of these regulators between normal and tumor tissues. Three distinct methylation regulator-related molecular subtypes were successfully identified according to the expression of 20 regulators, which had substantially different biological characteristics and prognosis. The classic carcinogenic pathways and stromal activity including TGF-beta, p53 and WNT signaling pathway were significantly activated in subtype B, leading to a survival inferiority in subtype B compared to other two subtypes. Further analysis demonstrated the constructed DMS signature was an independent predictive biomarker in patient prognosis. Two anti-checkpoint immunotherapy cohorts demonstrated patients with high DMS presented significantly improved treatment advantages and enhanced responses especially the survival prolonged. Generally, the high DMS groups improved more than 15% clinical response to immunotherapy than low DMS groups. In conclusion, this study identified three DNA methylation regulator-related subtypes with distinct clinical, molecular and biological characteristics, and constructed a prognostic and immunotherapeutic relevant gene signature. It might help to promote individualized immunotherapy for hepatocellular carcinoma from the perspective DNA methylation regulators.

Prognostic nomogram for hepatocellular carcinoma patients after transarterial chemoembolization based on des-γ-carboxy prothrombin reactivity and modified Response Evaluation Criteria in Solid Tumors.

AIMS: The aim of this study was to construct a nomogram that will predict the overall survival (OS) of hepatocellular carcinoma (HCC) patients after transarterial chemoembolization (TACE). MATERIALS AND METHODS: Imaging data, clinical characteristics, and serum des-γ-carboxy prothrombin (DCP) levels of 93 HCC patients treated with TACE were collected. Lasso regression, random forest, and other methods were used to screen the OS-related variables and construct the Cox prognosis model. The model was visualized by nomogram, and the net benefit of the clinical decision was assessed by decision curve analysis (DCA). RESULTS: It was found that DCP level after TACE was an important predictor of OS in HCC patients. The OS of the patients with lower serum DCP levels after TACE was significantly better than the group with higher levels (P = 0.003). The Cox prognostic model was constructed using four predictors including DCP reactivity (P = 0.001), modified Response Evaluation Criteria in Solid Tumors (mRECIST, P = 0.005), Child-Pugh class (P = 0.018), and portal vein thrombosis (P = 0.039). The C-index of the nomogram for OS of patients after TACE was 0.813. The clinical decision-making net benefits based on the nomogram were better than the decision-making based on the TNM stage system. CONCLUSION: DCP reactivity and mRECIST are the key predictors of prognosis in HCC patients that received TACE as their initial treatment. The nomogram constructed with these two indicators as the core could predict the OS of HCC patients after TACE and help in clinical decision-making.

Epigenetic age acceleration of early stage hepatocellular carcinoma tightly associated with hepatitis B virus load, immunoactivation, and improved survival.

Properly stratifying high-risk individuals with early stage hepatocellular carcinoma (HCC) is essential to identify patients in which the potentially therapies can be offered. To this context, we systematically investigated the prognostic value of epigenetic clock with early stage HCC as well as the association with other molecular characteristics.We computed DNA methylation (DNAm) age of 256 early stage HCC patients and 50 normal samples from TCGA by Horvath clock model. The characteristics of two DNAm age subgroups were differentiated regarding HBV expression, pathway activity, epigenomic, and genomic alteration. Cox regression and restricted cubic spline (RCS) analysis were utilized to evaluate the prognostic value of epigenetic acceleration.DNAm age was significantly associated with chronological age in normal tissue but largely disrupted in tumors (P< .001), and showed significant negative correlation with HBV expression (P< .05). We identified two DNAm age groups (DNAmAge-ACC and DNAmAge-DEC), and the former presented with an immunoactive phenotype (all FDRs<0.05 in enrichment analysis), CpG island hypermethylation (P< .001), and lower mutation burden (P= .018). Every 10-year increase in DNAm age was associated with a 18% decrease in fatality after adjustment for major clinical variables; DNAmAge-ACC had 50% lower mortality risk than DNAmAge-DEC (HR: 0.50, 95% CI: 0.27-0.94, P= .03). RCS revealed the fatality risk significantly decreased as epigenetic age accelerated (P = .04). Conclusions.In summary, we highlighted the prognostic value of epigenetic age acceleration for early stage HCC; better prognosis, relatively lower HBV load, and higher enrichment of immune signatures were tightly associated with epigenetic age accelerated tumors.

Knockdown of Ror2 suppresses TNF­α­induced inflammation and apoptosis in vascular endothelial cells.

Wnt family member 5a (Wnt5a) is a noncanonical member of the Wnt family that is highly expressed in atherosclerosis. Studies have shown that Wnt5a/receptor tyrosine kinase­like orphan receptors 2 (Ror2) signaling can participate in the formation of foam cells; however, the role of Ror2 in vascular endothelial cells during atherosclerotic injury is unknown. Therefore, the present study aimed to investigate the role of Ror2 in tumor necrosis factor (TNF)­α­induced vascular endothelial cell injury and investigate whether it could be regulated by Wnt5a. Human umbilical vein endothelial cells were transfected with short hairpin RNA specific against Ror2 in the absence or presence of TNF­α. The alteration of inflammatory cytokine levels was detected, and the expression of adhesion molecules was assessed. Western blot and flow cytometry analyses were used to detect the activation of nuclear factor­κB (NF­κB) signaling and cell apoptosis. The interaction between Ror2 and Wnt5a was confirmed by immunoprecipitation. Ror2 was upregulated upon TNF­α stimulation. Knockdown of Ror2 inhibited the TNF­α­induced release of inflammatory cytokines, the expression of intercellular adhesion molecule­1 and vascular cell adhesion molecule­1 and the activation of NF­κB signaling. Furthermore, cell apoptosis induced by TNF­α was rescued by Ror2 silencing. In addition, Wnt5a expression was increased by TNF­α, and Ror2 could bind to Wnt5a, the knockdown of which could downregulate the levels of Ror2. In conclusion, it was demonstrated that Ror2 was upregulated upon TNF­α stimuli, and interference of Ror2 regulated by Wnt5a could suppress TNF­α­induced inflammation and apoptosis in vascular endothelial cells.

Role and effect of vein-transplanted human umbilical cord mesenchymal stem cells in the repair of diabetic foot ulcers in rats.

Diabetic foot ulcer (DFU) is one of diabetic complications, which is frequently present and tormented in diabetes mellitus. Most multipotent mesenchymal stromal cells (MSCs) are capable of immune evasion, providing an allogeneic, ready-to-use, cell product option for therapeutic applications. The beneficial effect of MSCs for the treatment of a variety of traumatic injuries, such as open wounds, has been extensively explored. In this study, a rat DFU model was used to simulate the pathophysiology of clinical patients and to investigate the localization of human umbilical cord mesenchymal stem cells (hUC-MSCs) after intravenous transplantation and its role in DFU healing, so as to evaluate the potential of hUC-MSCs in the treatment of DFU. The diabetic rat model was established by streptozotocin injection, which was used to create full-thickness foot dorsal skin wounds to mimic DFU by a 6-mm skin biopsy punch and a Westcott scissor. The hUC-MSCs were transplanted through femoral vein, and the ulcer cicatrization situation and the fate of hUC-MSCs were evaluated. Our data suggest that intravenously transplantated hUC-MSCs have the ability to migrate and locate to the wound tissue and are helpful to wound healing in DFU rats, partly by regulating inflammation, trans-differentiation and providing growth factors that promote angiogenesis, cell proliferation and collagen deposition. Herein, we demonstrate that hUC-MSC transplantation is able to accelerate DFU healing in rats and transplantation of exogenous stem cells may be a potential strategy for clinical application in DFUs.

Exosomes derived from mmu_circ_0000250-modified adipose-derived mesenchymal stem cells promote wound healing in diabetic mice by inducing miR-128-3p/SIRT1-mediated autophagy.

More and more evidence advises that circular RNAs (circRNAs) function critically in regulating different disease microenvironments. Our previous study found that autotransplantation of adipose-derived mesenchymal stem cells (ADSCs) promotes diabetes wound healing. Exosomes derived in ADSCs play an important regulatory role. This study aimed to characterize if mmu_circ_0000250 played a role in ADSC-exosome-mediated full-thickness skin wound repair in diabetic rats. Endothelial progenitor cells (EPCs) were selected to study the therapeutic mechanism of exosomes in high-glucose (HG)-induced cell damage and dysfunction. Analysis and luciferase reporter assay were utilized to explore the interaction among mmu_circ_0000250, miRNA (miR)-128-3p, and sirtuin (SIRT)1. The diabetic rats were used to confirm the therapeutic effect of mmu_circ_0000250 against exosome-mediated wound healing. Exosomes containing a high concentration of mmu_circ_0000250 had a greater therapeutic effect on restoration of the function of EPCs by promotion autophagy activation under HG conditions. Expression of mmu_circ_0000250 promoted SIRT1 expression by miR-128-3p adsorption, which was confirmed via luciferase reporter assay and bioinformatics analysis. In vivo, exosomes containing a high concentration of mmu_circ_0000250 had a more therapeutic effect on wound healing when compared with wild-type exosomes from ADSCs. Immunohistochemistry and immunofluorescence detection showed that mmu_circ_0000250 increased angiopoiesis with exosome treatment in wound skin and suppressed apoptosis by autophagy activation. In conclusion, we verified that mmu_circ_0000250 enhanced the therapeutic effect of ADSC-exosomes to promote wound healing in diabetes by absorption of miR-128-3p and upregulation of SIRT1. Therefore, these findings advocate targeting the mmu_circ_0000250/miR-128-3p/SIRT1 axis as a candidate therapeutic option for diabetic ulcers.

miR-221-3p and miR-15b-5p promote cell proliferation and invasion by targeting Axin2 in liver cancer.

Globally, liver cancer has the third highest mortality rate among all types of cancer due to the invasive and metastatic capacities of liver tumor cells. MicroRNA (miR) is a class of non-coding RNAs that participate in the development of liver cancer. The aim of the present study was to explore the molecular mechanisms by which miR-221-3p and miR-15b-5p promote the proliferation and invasion of liver cancer cells through targeting axis formation inhibitor 2 (Axin2) and to identify suitable targets for the treatment of liver cancer. The expression levels of miR-221-3p and miR-15b-5p were determined in liver cancer tissues and cells by quantitative PCR, and the association between miR-221-3p, miR-15b-5p and Axin2 expression in liver cancer cells was analyzed using cell transfection. The results demonstrated that miR-221-3p and miR-15b-5p levels were upregulated in liver cancer tissues and cell lines, and results from predictive bioinformatic analysis and identification revealed that Axin2 was the common target gene of miR-221-3p and miR-15b-5p. miR-221-3p and miR-15b-5p may be used as prognostic indicators for liver cancer. The miR-221-3p/miR-15b-5p-Axin2 axis may serve as a therapeutic target in patients with liver cancer.

Effects of bone cement on intervertebral disc degeneration.

Percutaneous vertebroplasty (PVP) is popular for the treatment of intractable pain due to vertebral collapse from various lesions, intervertebral disk leakage of cement is a frequent complication. The aim of this study was to determine whether bone cement causes disc degeneration, and to evaluate the degree of intervertebral disc degeneration (IDD) according to the time period following cement injection, and the type and volume of cement injected. Sixteen dogs were randomly divided into two groups that were sacrificed at 12 or 24 weeks following cement injection. Five intervertebral discs in each dog were studied, including one control untreated disc and four discs randomly injected with polymethylmethacrylate (PMMA) or calcium phosphate cement (CPC) in two quantities. Radiographic and magnetic resonance imaging (MRI) studies were performed prior to animal sacrifice. T2-weighted mid-sagittal images of the discs were qualitatively analyzed for evidence of degeneration by calculating the MRI index, and all harvested discs were studied histopathologically. IDD was not evident in control discs. Univariate analysis revealed significant differences in the MRI index and the histological grade of disc degeneration in terms of the time period following cement injection, as well as the type and volume of cement injected. Result indicate that direct contact with PMMA and CPC can lead to IDD. However, IDD induced by PMMA was more severe than that induced by CPC. The extent of IDD was found to correlate with the time period post-cement injection and the volume of cement injected into the disc. PMMA and CPC may lead to intervertebral disc degeneration. Intervertebral disc degeneration induced by PMMA is more serious than that of CPC. The degree of intervertebral disc degeneration is correlative to the time after operation and the doses of bone cement.