What are the differences in paraspinal muscle morphometry among degenerative spondylolisthesis patients, isthmic spondylolisthesis patients, and healthy individuals? A propensity score matching analysis.

PURPOSE: To compare the morphometry of paraspinal muscles in patients with degenerative spondylolisthesis (DS), isthmic spondylolisthesis (IS), and healthy individuals. METHODS: Thirty-seven pairs of DS patients were selected using propensity score matching with IS patients, while 37 healthy individuals matched for age, sex, and BMI were selected as controls. The relative cross-sectional area (rCSA), and relative functional cross-sectional area (rfCSA) of paraspinal muscles were measured, and the degree of fatty infiltration (FI) was calculated. Based on occupational differences, the patients were also divided into worker and farmer groups, and the same measurements were taken on them. RESULTS: At the L3/L4 level, the multifidus (MF) FI was greater in the DS and IS groups than in the control group, the erector spinae (ES) rfCSA was higher in the IS group than in the DS and control groups. At the L4/L5 level, MF rfCSA was smaller in the DS and IS groups than in the control group; ES rfCSA was higher in the IS group than in the DS and control groups. At the L5/S1 level, MF rfCSA was smaller in the DS and IS groups than in the control group; ES rfCSA was higher in the IS group than in the DS group. At the L3/L4, L4/L5 level, MF rfCSA were higher in the worker group than in the farmer group (p < 0.05). CONCLUSION: The morphological changes in paraspinal muscles in patients with DS were dominated by selective atrophy of the MF, while in patients with IS, the morphological changes in paraspinal muscle showed selective atrophy of the MF accompanied by compensatory hypertrophy of the ES. The surgeon should consider the morphological differences in paraspinal muscle between different types of lumbar spondylolisthesis when establishing the appropriate surgical program.

Optimized LNS-FAID of LDPC codes: a hybrid precision decoding approach for 50G-PON.

Efficient error correction in high-speed communication networks, such as the 50G passive optical network (50G-PON), is paramount. This Letter focuses on optimizing a layered non-surjective finite alphabet iterative decoder (LNS-FAID) for 50G-PON, with an emphasis on high-throughput and low-power consumption. We propose using a distinct lookup table (LUT) for each iteration to enhance decoding performance and lower error floors. Additionally, we improve the 2-bit LNS-FAID architecture by adding operational states and a sign backtracking (SBT) strategy. This paper also introduces a hybrid precision model that merges 3-bit and 2-bit LNS-FAIDs, which balances error correction with computational efficiency. Our simulation results show that these approaches significantly improve the performance of the LDPC code in 50G-PON.

Hispolon inhibits neuronal ferroptosis by promoting the expression of Nrf-2.

Research has shown that neuronal ferroptosis is associated with various central nervous system diseases, including Parkinson's disease, acute brain injury, and spinal cord injury. Inhibiting neuronal ferroptosis can greatly alleviate the progression of these diseases. However, there is currently a lack of effective drugs to inhibit neuronal ferroptosis. In this study, we pretreated neuronal cells with Hispolon and subsequently induced a neuronal ferroptosis model using Erastin. We further assessed the changes in the protein expression levels of SLC7A11, GPX4, ACSL4, Nrf-2, and HO-1 using Western blot and immunofluorescence techniques. Additionally, we measured the intracellular levels of Fe2+, GSH, and MDA using relevant assay kits. The research findings revealed that after Hispolon treatment, the expression of the pro-ferroptosis protein ACSL4 decreased, while the expression of the ferroptosis-regulating proteins GPX4 and SLC7A11 increased. Moreover, the use of an Nrf-2-specific inhibitor was able to reverse the effects of Hispolon as mentioned above. In this study, we discovered that Hispolon can promote the expression of Nrf-2 and inhibit the occurrence of neuronal ferroptosis induced by Erastin.

LINC02532 by Mediating miR-541-3p/HMGA1 Axis Exerts a Tumor Promoter in Breast cancer.

The newly discovered LINC02532 is abnormally expressed in a variety of cancers and promotes cancer progression. The research proposed to discover the biological and molecular mechanisms of LINC02532 in breast cancer (BCa). In the resected BCa tissue samples and adjacent normal tissues, LINC02532, miR-541-3p, and High Mobility Group A1 (HMGA1) levels were determined. Cell function experiments were carried out on the premise of cell transfection with relevant plasmids. Based on that, the influence of LINC02532, miR-541-3p, and HMGA1 on MCF-7 cell activities (proliferation, migration, invasion, cell cycle, and apoptosis) was determined, as well as on EMT. Additionally, animal experiments were allowed to support cell experimental conclusions on LINC02532. Finally, the mechanistic network of LINC02532, miR-541-3p, and HMGA1 was identified. It was BCa tissues highly expressing LINC02532 and HMGA1, while lowly expressing miR-541-3p. Functionally, LINC02532 depletion repressed the activities and EMT process of MCF-7 cells. Silencing LINC02532 delayed tumor growth in mice. In terms of mechanism, LINC02532 mainly existed in the cytoplasm and could mediate HMGA1 expression by absorbing miR-541-3p. The findings offer new insights into the molecular mechanisms of LINC02532 in BCa and, more importantly, new strategies for the clinical treatment of BCa.

Entropy Minimization Versus Diversity Maximization for Domain Adaptation.

Entropy minimization has been widely used in unsupervised domain adaptation (UDA). However, existing works reveal that the use of entropy-minimization-only may lead to collapsed trivial solutions for UDA. In this article, we try to seek possible close-to-ideal UDA solutions by focusing on some intuitive properties of the ideal domain adaptation solution. In particular, we propose to introduce diversity maximization for further regulating entropy minimization. In order to achieve the possible minimum target risk for UDA, we show that diversity maximization should be elaborately balanced with entropy minimization, the degree of which can be finely controlled with the use of deep embedded validation in an unsupervised manner. The proposed minimal-entropy diversity maximization (MEDM) can be directly implemented by stochastic gradient descent without the use of adversarial learning. Empirical evidence demonstrates that MEDM outperforms the state-of-the-art methods on four popular domain adaptation datasets.

MiR-574-5p promotes cell proliferation by negatively regulating small C-terminal domain phosphatase 1 in esophageal squamous cell carcinoma.

Objectives: Esophageal cancer is one of the most common cancers with high incidence and mortality rates, especially in China. MicroRNA (miRNA) can be used as a prognostic marker for various human cancers. This study aims to detect suitable miRNA markers for esophageal squamous cell carcinoma (ESCC). Materials and Methods: Our previous gene expression data of ESCC cells and the data from GSE43732 and GSE112840 were analyzed. The expression of miR-574-5p in ESCC patients and controls was analyzed by real-time quantitative PCR. The effect of miR-574-5p on proliferation was detected by real-time cell analysis (RTCA) and EdU proliferation assay after cell transfections. The target gene small C-terminal domain phosphatase 1 (CTDSP1) of miR-574-5p was validated by luciferase reporter assay and western blotting. Results: In the current study, the bioinformatics analysis found miR-574-5p up-regulated in ESCC. The qPCR assay of 26 ESCC and 13 adjacent/ normal tissues confirmed these results. We further demonstrated that miR-574-5p overexpression promoted cell proliferation. Then the dual-luciferase reporter assay and the rescue experiment suggested that CTDSP1 was a direct target of miR-574-5p. Conclusion: MiR-574-5p played an oncological role in ESCC by interacting and negatively regulating CTDSP1. These results provided a deeper understanding of the effect of miR-574-5p on ESCC.

CRC-Aided Adaptive BP Decoding of PAC Codes.

Although long polar codes with successive cancellation decoding can asymptotically achieve channel capacity, the performance of short blocklength polar codes is far from optimal. Recently, Arikan proposed employing a convolutional pre-transformation before the polarization network, called polarization-adjusted convolutional (PAC) codes. In this paper, we focus on improving the performance of short PAC codes concatenated with a cyclic redundancy check (CRC) outer code, CRC-PAC codes, since error detection capability is essential in practical applications, such as the polar coding scheme for the control channel. We propose an enhanced adaptive belief propagation (ABP) decoding algorithm with the assistance of CRC bits for PAC codes. We also derive joint parity-check matrices of CRC-PAC codes suitable for iterative BP decoding. The proposed CRC-aided ABP (CA-ABP) decoding can effectively improve error performance when partial CRC bits are used in the decoding. Meanwhile, the error detection ability can still be guaranteed by the remaining CRC bits and adaptive decoding parameters. Moreover, compared with the conventional CRC-aided list (CA-List) decoding, our proposed scheme can significantly reduce computational complexity, to achieve a better trade-off between the performance and complexity for short PAC codes.

PCQNet: A Trainable Feedback Scheme of Precoder for the Uplink Multi-User MIMO Systems.

Multi-user multiple-input multiple-output (MU-MIMO) technology can significantly improve the spectral and energy efficiencies of wireless networks. In the uplink MU-MIMO systems, the optimal precoder design at the base station utilizes the Lagrange multipliers method and the centralized iterative algorithm to minimize the mean squared error (MSE) of all users under the power constraint. The precoding matrices need to be fed back to the user equipment to explore the potential benefits of the joint transceiver design. We propose a CNN-based compression network named PCQNet to minimize the feedback overhead. We first illustrate the effect of the trainable compression ratios and feedback bits on the MSE between the original precoding matrices and the recovered ones. We then evaluate the block error rates as the performance measure of the centralized implementation with an optimal minimum mean-squared error (MMSE) transceiver. Numerical results show that the proposed PCQNet achieves near-optimal performance compared with other quantized feedback schemes and significantly reduces the feedback overhead with negligible performance degradation.

LINC00092 Suppresses the Malignant Progression of Breast Invasive Ductal Carcinoma Through Modulating SFRP1 Expression by Sponging miR-1827.

Breast invasive ductal carcinoma (IDC) is a most common kind of breast cancer (BC), yet to date the corresponding effective therapies are limited. Extensive evidence has indicated that lncRNAs are involved in multiple cancers, and the potential mechanism of lncRNAs, such as LINC00092, mentioned in IDC remains elusive. IDC clinical samples from TCGA database were used to analyze the expression levels of LINC00092, miR-1827 and SFRP1. Kaplan-Meier method was applied to plot the overall survival curves. KEGG and GO were employed to screen the pathway that LINC00092 participated in. Pearson's correlation analysis determined the relationship between LINC00092 and SFRP1. Bioinformatics analysis and dual-luciferase reporter assay examined the association among LINC00092, miR-1827, and SFRP1. Cell counting kit-8, colony formation and transwell assays were performed to detect cell viability, colony formation, and migration and invasion, respectively. Quantitative reverse-transcription polymerase chain reaction and western blot were utilized to investigate the expression at RNA and protein levels. LINC00092 expression was down-regulated in IDC tissues and cells, which was correlated with poor prognosis. Down-regulated LINC00092 facilitated cell proliferation, colony formation, and cell migration and invasion, while up-regulated LINC00092 inhibited cell malignant behaviors. LINC00092/SFRP1 physically bound to miR-1827 in IDC. SFRP1 expression was proportional to LINC00092 expression and inversely proportional to miR-1827 expression. The inhibitory effects of LINC00092 on cell aggressive behaviors were partially regulated by miR-1827/SFRP1. In summary, our results indicated that overexpression of LINC00092 inhibited the development of IDC through modulating miR-1827/SFRP1 axis, suggesting new therapeutic targets to treat IDC.

An enzyme-responsive Gp1a-hydrogel for skin wound healing.

Faster recovery and fewer scars are ideal wound healing. We have demonstrated that the cannabinoid receptor 2 (CB2) agonist Gp1a is beneficial to skin wound healing, which inhibits inflammation and fibrogenesis while promoting re-epithelialization. However, the systemic administration is imprecise and overqualified for a local skin wound. Herein, we prepared Gp1a-gel using triglycerol monostearate (Tm) hydrogel and detected whether the Gp1a-gel worked effectively on mouse skin excision wounds. The results showed that Gp1a-gel might sustainably increase the CB2 for at least 8 days. It decreased inflammation and fibrogenesis while promoting wound enclosure and re-epithelialization. These results suggested Gp1a-gel may utilize as a potential formulation strategy to treat the skin wound.

Protective role of histone deacetylase 4 from ultraviolet radiation-induced DNA lesions.

Ultraviolet B (UVB) exposure is a core factor that leads to skin disease or carcinogenesis through the insufficient repair of DNA lesions. UVB-induced DNA lesions are mainly removed by the nucleotide excision repair (NER) mechanism. The expression of histone deacetylase 4 (HDAC4) is altered in the skin upon UVB exposure, indicating its possible implication in UVB-induced DNA lesions repair. Here, we investigated the role of HDAC4 in the NER removal of the main classes of UVB-induced DNA lesions consisting of cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs). We found that UVB irradiation increased HDAC4 expression at both the mRNA and protein levels. HDAC4 interacted with NER factor XPC, which played an important role in effectively removing the UVB-induced DNA lesions. This study provides an understanding of the HDAC4 function in DNA repair, which will allow the development of efficient strategies to protect the skin from UVR-induced diseases.

A Novel Circular RNA hsa_circRPPH1_015 Exerts an Oncogenic Role in Breast Cancer by Impairing miRNA-326-Mediated ELK1 Inhibition.

Background: Breast cancer (BC) represents a heterogeneous disease with distinct subtypes and high tumor metastatic potentials. Recent researchers identify the implication of circular RNAs (circRNAs) in the initiation of BC. Herein, we uncover a novel circRNA hsa_circRPPH1_015 as a tumor promoter in BC. Methods: A total of 86 paired cancerous and non-cancerous tissues were surgically resected and collected from BC patients. Cell proliferation, colony formation, and cell invasion were examined by Edu staining, clone formation assays, propidium iodide (PI)-labeled flow cytometry, and Transwell invasion assays. PCNA, Ki67, MMP-2, MMP-9, Cyclin D1, and CDK4 expression was assayed using Western blot analysis. RNA pull-down, dual-luciferase reporter gene assay, and RNA binding protein immunoprecipitation (RIP) assay were performed to investigate the relationships among hsa_circRPPH1_015, microRNA-326 (miR-326), and ELK1. The tumor growth of human BC MCF-7 cells in vivo was evaluated in nude mice by subcutaneous xenografts of MCF-7 cells. Results: hsa_circRPPH1_015 expression was upregulated in BC tissues. Knockdown of hsa_circRPPH1_015 restrained the aggressive behavior of MCF-7. hsa_circRPPH1_015 could bind to miRNA-326 that negatively regulates ELK1. Elevation of miRNA-326 expression resulted in inhibition of cell proliferation, colony formation, and cell invasion of MCF-7. Disturbance of miRNA-326 or overexpression of ELK1 restored the proliferation and aggressiveness in hsa_circRPPH1_015-depleted MCF-7 cells. Tumor growth of MCF-7 cells in vivo was reduced in nude mice lack of endogenous hsa_circRPPH1_015 expression. Conclusion: Overall, the present study demonstrates that hsa_circRPPH1_015 was an oncogene and unfavorable prognostic factor in BC, providing an exquisite therapeutic target for BC.

ID4 Promotes Breast Cancer Chemotherapy Resistance via CBF1-MRP1 Pathway.

Chemo-resistance is considered a key problem in triple negative breast cancer (TNBC) chemotherapy and as such, an urgent need exists to identify its exact mechanisms. Inhibitor of DNA binding factor 4 (ID4) was reported to play diverse roles in different breast cancer molecular phenotypes. In addition, ID4 was associated with mammary carcinoma drug resistance however its functions and contributions remain insufficiently defined. The expression of ID4 in MCF-7, MCF-7/Adr and MDA-MB-231 breast cancer cell lines and patients' tissues were detected by RT-PCR, western blot and immunohistochemistry. Furthermore, TCGA database was applied to confirm these results. Edu and CCK8 assay were performed to detect the proliferation and drug resistance in breast cancer cell lines. Transwell and scratch migration assay were used to detected metastasis. Western blot, TCGA database, Immunoprecipitation (IP), Chromatin Immunoprecipitation (ChIP) and Luciferase reporter assay were used to investigate the tumor promotion mechanisms of ID4. In this study, we report that the expression levels of ID4 appeared to correlate with breast cancers subtype differentiation biomarkers (including ER, PR) and chemo-resistance related proteins (including MRP1, ABCG2, P-gp). Down-regulation of ID4 in MCF-7/Adr and MDA-MB-231 breast cancer cell lines significantly suppressed cell proliferation and invasion, however enhanced Adriamycin sensitivity. We further demonstrated that the oncogenic and chemo-resistant effects of ID4 could be mediated by binding to CBF1 promoter region though combination with MyoD1, and then the downstream target MRP1 could be activated. We reveal for the first time that ID4 performs its function via a CBF1-MRP1 signaling axis, and this finding provides a novel perspective to find potential therapeutic targets for breast cancer chemotherapy.

Akt inhibitor deguelin aggravates inflammation and fibrosis in myocarditis.

OBJECTIVES: Myocarditis is characterized by inflammatory cell infiltration in myocardial stroma. Attenuation of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß is a reliable mark for improving the prognosis. Protein kinase B (Akt) plays an important role in the development and progression of myocarditis. The specific role of the natural inhibitor of Akt, Deguelin, on myocarditis has not been reported. In this study, we used deguelin to investigate the effects of natural Akt inhibitor on myocarditis in experimental autoimmune myocarditis (EAM) rats. MATERIALS AND METHODS: EAM rat models were made by using Lewis rats and Deguelin was injected intraperitoneally on day 3, 6, 9, 12 and 15 after successful modeling. On day 18, rats were sacrificed and the heart weight (HW)/ body weight (BW) ratio were measured. The pathological changes, pathological scores and fibrosis area were evaluated after H.&E. and Masson's trichrome staining. The mRNA levels of TNF-α and IL-1ß were measured by RT-qPCR, while the protein expressions of TNF-α and IL-1ß were detected by immunohistochemical staining and Western bolt. The protein expressions of Akt, Akt1, phosphorylated (p-) Akt and nuclear factor (NF)-κB were detected by Western bolt. RESULTS: We found that the TNF-α and IL-1ß levels, inflammatory scores and fibrosis areas were markedly increased after 18 days deguelin administration. CONCLUSION: Akt inhibition with deguelin may aggravate myocarditis of EAM rats.

Reduction of PGRN increased fibrosis during skin wound healing in mice.

Progranulin (PGRN) is a multi-functional growth factor known to be involved in regulating of development, cell cycle progression, cell motility, tumorigenesis and angiogenesis. Research has revealed that PGRN is a crucial mediator of skin wound healing. Nonetheless, the role of PGRN in the fibrosis process of cutaneous wound healing has not been identified. In the present study, mice with excisional wounds were treated with si-m-PGRN or physiological saline. We observed the expression of PGRN in intact and post-injury skin by immunohistochemistry. Tissue sections of skin around the wound were performed by hematoxylin & eosin and masson's trichrome staining. After PGRN knockdown by siRNA, the expression of PGRN, collagen I (Col I), small mothers against decapentaplegic homolog 3 (Smad3), phosphorylated Smad3 (P-Smad3), transforming growth factor (TGF)-ß1 and TGF-ß receptor I (TßRI) were detected by real-time reverse transcription polymerase chain reaction (RT-qPCR) or Western blot. PGRN mRNA and protein expressions were increased after insult and remained above that of intact skin through day 20. Down-regulation of PGRN augmented fibrosis area, skin thickness and the expression of Col I. In addition, reduction of PGRN considerably increased the expression of TGF-ß1, TßRI, Smad3 and P-Smad3. These results indicate that PGRN knockdown enhances the fibrosis degree, probably via the TGF-ß/Smad signaling pathway.

Design of Tumor Microenvironment-Responsive Drug-Drug Micelle for Cancer Radiochemotherapy.

Concomitant radiochemotherapy is a major therapeutic strategy for treating malignant tumors. However, the greatest challenge is how to improve the therapeutic effect of radiochemotherapy to achieve the proper synergetic chemo-/radiotherapy for the tumor. In this study, ferrocenium (antitumor effect) and nitroimidazole (hypoxic cell radiosensitization) conjugates were synthesized to form amphiphilic ferrocenium-hexane-nitroimidazole (Fe-NI), which can self-assemble in aqueous solution. The Fe-NI micelles successfully encapsulate the hydrophobic chemotherapy drug doxorubicin (DOX) and are modified with hyaluronic acid (HA) by electrostatic interactions to form HA-Fe-NIs-DOX micelles. HA-Fe-NIs-DOX micelles rapidly release DOX under tumor hypoxia and a high glutathione (GSH) environment and achieve a synergetic chemo-/radiotherapy for the tumor based on the properties of nitroimidazoles and ferrocenes. The biodistribution results obtained in vivo reveal an effective accumulation in the tumor. The HA-Fe-NIs-DOX micelles show a significant radiosensitizing effect on the tumors, and the combination of chemotherapy and radiotherapy is realized for the treatment of tumor in vitro and in vivo. These findings illustrate that HA-Fe-NIs micelles are a promising candidate, which enhances the antitumor effects as a DOX delivery system, owing to the synergistic mechanisms of antitumor agents and chemo-/radiotherapy.

Risk Factors for Lower Limb Deep Vein Thrombosis in Patients With Single-Level Lumbar Fusion: A Prospective Study of 710 Cases.

Lower limb deep vein thrombosis (DVT) is not an uncommon postoperative complication of spinal fusion surgery. However, the related risk factors identified in previous studies remain controversial. This study aimed to investigate risk factors for lower limb DVT in patients with single-level lumbar fusion surgery. Between January 2010 and December 2016, a total of 710 patients undergoing lumbar fusion were recruited for this study, including 172 males and 538 females (aged 18-75 years). Deep vein thrombosis was detected by ultrasonography. Accordingly, patients were divided into the DVT group and the non-DVT group and compared in terms of operative data, underlying diseases, and biochemical data. Additionally, logistic regression analysis was performed to identify risk factors for lower limb DVT. The incidence of lower limb DVT was 11.8% (84 of 710 cases). Five patients were symptomatic, with lower limb pain and swelling. Two patients developed pulmonary embolism and 1 died. Binary logistic regression indicated that advanced age (P = .001, odds ratio [OR] = 2.86, 95% CI: 1.85-5.12), hypertension (P = .006, OR = 4.10, 95% CI: 1.09-2.30), and increased d-dimer (P < .001, OR = 3.49, 95% CI: 2.05-6.36) were risk factors for postoperative DVT. In conclusion, for patients with single-level lumbar fusion, advanced age, increased d-dimer, and hypertension may contribute to DVT development after spinal fusion surgery. Therefore, patients with these risk factors should be protected during the perioperative period.

MicroRNA-34a promotes MICB expression in hepatocytes.

MicroRNA-34a (miR-34a) behaves as a tumor suppressor by decreasing the expression of oncogenes involved in multiple carcinogenic pathways. Intravenous delivery of miR-34a mimics has been investigated in clinical trials as a potential treatment for advanced cancers; however, the effect of miR-34a on cancer immune surveillance is controversial. In the current study, we found that miR-34a plays a dual role in the regulation of major histocompatibility complex class I-related sequence B (MICB) protein, a ligand of the NKG2D receptor. MiR-34a could both induce and reduce MICB expression by upregulating ataxia telangiectasia and Rad3-related (ATR) protein kinase and downregulating the transcription factor E2F1, respectively. The net effect of miR-34a on MICB expression depended on endogenous E2F1 levels. Overexpression of miR-34a promoted MICB expression in hepatocytes and hepatocellular carcinoma (HCC) cells that have low E2F1 levels but not in HCC cells that have high E2F1 levels. In HCC patients, the expression of miR-34a and MICB showed positive correlation in paratumor liver tissues, which have low E2F1 levels, but not in HCC tissues, which have high E2F1 levels. We showed that miR-34a overexpression in non-transformed liver cells enhanced cytolysis and interferon-γ production by NK-92MI cells. Furthermore, higher miR-34a expression in tumor and paratumor tissues was associated with positive and negative outcomes, respectively, in HCC patients. Our findings suggest that miR-34a induces MICB expression in paratumor liver tissues, which may cause liver damage and serious cytokine release syndrome, thus disclosing potential side effects of systemic administration of miR-34a in anticancer therapy.

Anterior cervical discectomy and fusion versus hybrid surgery in multilevel cervical spondylotic myelopathy: A meta-analysis.

OBJECTIVE: A meta-analysis was performed to compare the radiographic and surgical outcomes between anterior cervical discectomy and fusion (ACDF) and hybrid surgery (HS, corpectomy combined with discectomy) in the treatment for multilevel cervical spondylotic myelopathy (mCSM). SUMMARY OF BACKGROUND DATA: Both ACDF and HS are used to treat mCSM, however, which one is better treatment for mCSM remains considerable controversy. METHODS: An extensive search of literature was searched in PubMed/Medline, Embase, the Cochrane library, CNKI, and WANFANG databases on ACDF versus HS treating mCSM from January 2011 to December 2017. The following variables were extracted: blood loss, operation time, fusion rate, Cobb angles of C2-C7, total complications, dysphagia, hoarseness, C5 palsy, infection, cerebral fluid leakage, epidural hematoma, and graft subsidence. Data analysis was conducted with RevMan 5.3 and STATA 12.0. RESULTS: A total of 4 studies including 669 patients were included in our study. The pooled analysis showed that there were no significant difference in the operation time, fusion rate, Cobb angles of C2-C7, dysphagia, hoarseness, C5 palsy, infection, cerebral fluid leakage, epidural hematoma, and graft subsidence. However, there were significant difference between 2 groups in blood loss [P < .00001, SMD = -30.29 (-45.06, -15.52); heterogeneity: P = .38, I = 0%= and total complications [P = .04, OR = 0.66 95%CI (0.44, 0.98); heterogeneity: P = .37, I = 4%]. CONCLUSIONS: Based on our meta-analysis, except for blood loss and total complications, both ACDF and hybrid surgery are effective options for the treatment of multilevel cervical spondylotic myelopathy.