Correlation between C7-T1 Intervertebral Foramen Area and Sagittal Parameters in Patients with Cervical Spondylotic Myelopathy.

OBJECTIVE: Cervical spondylotic myelopathy (CSM) is an incomplete spinal cord injury characterized with pain and stiffness in the neck and motor and sensory dysfunction. This study aims to determine whether C7-T1 intervertebral foramen area could be used as a parameter to evaluate the sagittal curvature of cervical spine. METHODS: Patients with clinical manifestations of spinal cord compression were hospitalized in our hospital from September 2018 to August 2019. All patients were diagnosed with CSM by nuclear magnetic imaging and other imaging methods. C2-C7 Cobb angle and T1 slop (T1S) were measured on the sagittal, T2-weighted magnetic resonance image of cervical spine, and C7-T1 intervertebral foramen area were measured using oblique cervical spine X-rays. Patients were divided into two groups according to the value of C2-C7 Cobb angle, including lordosis group (C2-C7 Cobb angle >10°, n = 45) and straight group (C2-7 Cobb angle ≤10°, n = 55). The reliability of the data was evaluated by intraclass correlation coefficient (ICC), and the correlation of the imaging parameters was analyzed by Pearson correlation. RESULTS: A total of 100 patients diagnosed with CSM hospitalized in our department were included. The ICC of the cervical parameters was 0.73. C7-T1 intervertebral foramen area was 40.69 ± 11.44 and 39.95 ± 10.94 mm2 in lordosis and straight group, respectively. The results showed that C7-T1 intervertebral foramen area was positively correlated with both C2-C7 Cobb angle (r = 0.23, p = 0.02) and T1S (r = 0.21, p = 0.03). In lordosis group, there was a positive correlation between C7 and T1 intervertebral foramen area and C2-C7 Cobb angle (r = 0.69, p < 0.01) and T1S (r = 0.34, p = 0.02). However, in straight group, C7-T1 intervertebral foramen area was not correlated with either C2-C7 Cobb angle or T1S. CONCLUSION: C7-T1 intervertebral foramen area measured by oblique X-ray could be an effective method to evaluate the sagittal balance of cervical vertebrae for CSM patients with cervical lordosis.

High expression of HOXA4 in patients with glioma indicates unfavorable clinical outcomes.

HOXA4 is a novel oncogene that has been observed in many kinds of tumors, but its role during glioma carcinogenesis and its clinical significance in diagnosing and prognosis human glioma remains unknown. In the present study, the Chinese Glioma Atlas (CGGA)-RNA sequencing database, CGGA microarray, and The Cancer Genome Atlas (TCGA)-RNA seq data from 1674 glioma patients were obtained from online databases and analyzed using quantitative reverse transcription-polymerase chain reaction (RT-qPCR) to detect changes in the expression level of HOXA4 and characterize the relationship between HOXA4 and the clinical characteristics and prognosis of patients with glioma. Gene set enrichment analysis (GSEA) was used to reveal how HOXA4 regulates tumor-related pathways. HOXA4 mRNA levels in glioma tissue were higher than those in adjacent brain tissue. HOXA4 expression was also closely related to the clinical and molecular characteristics of gliomas, such as tumor grade and isocitrate dehydrogenase (IDH) mutation. Functional enrichment analysis revealed that HOXA4 could regulate cancer-related signal pathways, such as Cell cycle, Cell adhesion molecules cams, and JAK/STAT signaling pathway. Results of in vitro experiments confirmed that knockdown of HOXA4 blocks the cell cycle pathway and inhibits the proliferation, invasion and chemotherapy resistance in gliomas. We concluded that HOXA4 was an independent risk factor for glioma and may have clinical diagnostic potential. Meanwhile, our findings revealed that HOXA4 could be used as a biomarker for glioma diagnosis and treatment.

The Association Between Sagittal Spinopelvic Alignment and Persistent Low Back Pain After Posterior Lumbar Interbody Fusion for Treatment of Mild L5-S1 Spondylolisthesis: A Retrospective Study.

Introduction: The aim of this study was to explore the association between sagittal spinopelvic alignment and persistent low back pain (PLBP) following posterior decompression and instrumented fusion for mild L5-S1 spondylolisthesis. Methods: By retrieving medical records from January 2015 to April 2020, 200 patients following PLIF for mild L5-S1 spondylolisthesis were retrospectively reviewed. Patients were divided into two groups: PLBP group and non-PLBP group. The baseline characteristics and radiographic parameters were analyzed and compared between groups. Results: The PLBP group comprised 26 patients, and the non-PLBP group comprised 174 patients. No significant differences in preoperative spinopelvic parameters were found between the two groups (p > 0.05). There were statistically significant differences between the preoperative and postoperative variations of LL, SL, LSA, SD, and HOD spinopelvic parameters, regardless of group (p < 0.05). Postoperative PT and SS differed significantly between the PLBP group and non-PLBP group (p < 0.05). In the PLBP group, there were no significant differences between preoperative and postoperative PT; the same applied to SS. However, significant differences were found for the variations in preoperative and postoperative PT and SS between the two groups. The ΔPT was found as an independent risk factor for postoperative PLBP. Conclusion: Patients with mild L5-S1 spondylolisthesis with PLBP after posterior lumbar spinal fusion had decreased SS and increased PT.

Cysteine cathepsin C: a novel potential biomarker for the diagnosis and prognosis of glioma.

BACKGROUND: Cysteine cathepsin C encoded by the CTSC gene is an important member of the cysteine cathepsin family that plays a key role regulation of many types of tumors. However, whether CTSC is involved in the pathological process of glioma has not yet been reported. We comprehensively analyzed data from multiple databases and for the first time revealed a role and specific mechanism of action of CTSC in glioma, identifying it as a novel and efficient biomarker for the diagnosis and treatment of this brain tumor. METHODS: The expression of CTSC in glioma and its relationship with clinical characteristics and prognosis of patients with glioma were analyzed at different levels by using clinical sample information from several databases. CTSC expression levels in glioma and normal brain tissues, as well as in glioma cells and normal brain cells, was validated by real-time quantitative polymerase chain reaction (RT-qPCR). Gene set enrichment analysis (GSEA) was used to reveal the signaling pathways that CTSC may participate in. The connectivity map was used to reveal small molecules that may inhibit CTSC expression in glioma, and the putative effect of these compounds was verified by RT-qPCR. RESULTS: Our analyses showed that the expression of CTSC in glioma was higher than that in non-cancerous cells. GSEA showed that CTSC expression may regulate the malignant development of glioma through Toll-like receptor signaling pathways, pathways in cancer, and extracellular matrix receptor interaction signaling pathways. And we proved piperlongumine and scopoletin could inhibit CTSC expression in glioma cells. CONCLUSIONS: CTSC may serve as an efficient molecular target for the diagnosis and therapy of glioma, thereby improving the poor prognosis of patients with glioma.

Circ_0016347 modulates proliferation, migration, invasion, cell cycle, and apoptosis of osteosarcoma cells via the miR-661/IL6R axis.

BACKGROUND: Osteosarcoma is a common primary bone tumour in children and adolescents. Circular RNAs (circRNAs) exert vital functions in human diseases, including osteosarcoma. Therefore, we explored the role of circ_0016347 in osteosarcoma. METHODS: The real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of circ_0016347, microRNA-661 (miR-661), and Interleukin-6 receptor (IL6R) in osteosarcoma tissues and cells. The proliferation of osteosarcoma cells was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT) and EdU experiments. The migration and invasion were determined by transwell assay. The cell cycle distribution and apoptosis were assessed by flow cytometry assay. The association relationships among circ_0016347, miR-661, and IL6R were analyzed by dual-luciferase reporter assays. The western blot assay was employed to assay the protein expression. A xenograft experiment was established to clarify the functional role of circ_0016347 inhibition in vivo. RESULTS: Circ_0016347 was obviously overexpressed in osteosarcoma tissues and cells compared with control groups. The suppression of circ_0016347 impeded proliferation, migration, invasion, and cell cycle and induced apoptosis in osteosarcoma cells, which was overturned by knockdown of miR-661. Consistently, circ_0016347 knockdown repressed tumour growth in vivo. Moreover, miR-661 directly targeted and inhibited IL6R, and the upregulation of IL6R reversed miR-661-induced effects on osteosarcoma cells. Furthermore, circ_0016347 could regulate IL6R expression through miR-661. Inhibition of circ_0016347 also inactivated the Janus kinase 2 (JAK2)/Transcription 3 (STAT3) signalling pathway in osteosarcoma cells by IL6R. CONCLUSION: Circ_0016347 functioned as an oncogene in osteosarcoma at least in part by the miR-661/IL6R axis and JAK2/STAT3 signalling pathway.

ITGB3BP is a potential biomarker associated with poor prognosis of glioma.

Despite the growing recognition of ITGB3BP as an essential feature of various cancers, the relationship between ITGB3BP and glioma remains unclear. The main aim of this study was to determine the prognostic and diagnostic value of ITGB3BP in glioma. RNA-Seq and microarray data from 2222 glioma patients were included, and we found that the expression level of ITGB3BP in glioma tissues was significantly higher than that in normal brain tissues. Moreover, ITGB3BP can be considered an independent risk factor for poor prognosis and has great predictive value for the prognosis of glioma. Gene Set Enrichment Analysis results showed that ITGB3BP contributes to the poor prognosis of glioma by activating tumour-related signalling pathways. Some small-molecule drugs were identified, such as hexestrol, which may specifically inhibit ITGB3BP and be useful in the treatment of glioma. The TIMER database analysis results revealed a correlation between the expression of ITGB3BP and the infiltration of various immune cells in glioma. Our findings provide the first evidence that the up-regulation of ITGB3BP correlates with poor prognosis in human glioma. Thus, ITGB3BP is a potential new biomarker that can be used for the clinical diagnosis and treatment of glioma.

Expression and clinical significance of TIMELESS in glioma.

In recent years, studies have shown that TIMELESS, as an oncogene, is involved in progression of cancers. However, its relationship with prognosis in glioma patients is rarely reported. Our purpose was to explore the role of TIMELESS in glioma. Based on 1814 glioma samples from multiple databases such as The Cancer Genome Atlas (TCGA), The Chinese Glioma Genome Atlas (CGGA), and The Gene Expression Omnibus (GEO), we use a variety of bioinformatics methods to verify the mechanism of action of TIMELESS in glioma from mRNA to protein, from appearance to mechanism analysis, from clinical features to prognosis. Then, the connectivity map (CMap) tool was used to predict drugs that inhibit the expression of TIMELESS. First, we found TIMELESS is highly expressed in glioma at mRNA and protein levels. Second, TIMELESS is an independent risk factor in prognosis and has suitable clinical diagnostic value in glioma. It was also positively correlated with World Health Organization (WHO) grade, age, and histology, and negatively correlated with isocitrate dehydrogenase (IDH) 1 mutation and 1p19q codeletion. Third, base excision, cell cycle, and mismatch repair pathway were activated by TIMELESS in glioma. We predict small molecules to inhibit TIMELESS such as 8-azaguanine, gw8510, 6-thioguanosine, and ursodeoxycholic acid. This study is the first comprehensive analysis of TIMELESS, revealing a relationship between this novel oncogene, clinical characteristics of patients with glioma, and a mechanism leading to poor prognosis. It also provides a biomarker for diagnosis and treatment of glioma and reveal the pathologic progress of glioma at the genetic level.

Expression and clinical significance of UBE2V1 in cervical cancer.

The majority of cervical cancer (CC) patients are caused by the high-risk human papillomavirus (HPV) infection Although they are preventable and controllable, the mortality rate is still high. It is essential to identify the biomarkers for early screening and diagnosis of CC to improve the prognosis of patients with CC. The conjugating enzyme 2 (E2) family members are the key components of ubiquitin protease system. However, the role of E2 family in CC remains unclear. We aimed to investigate the role of UBE2V1, a ubiquitin binding E2 enzyme variant protein (ube2v) without conserved cysteine residues required for E2s catalytic activity in CC. In this study, we first studied the expression of UBE2V1 in CC by real time quantitative PCR (RT-qPCR), and then, the clinical information of 191 CC patients in TCGA database was retrieved to explore the relationship between the expression of UBE2V1 and the occurrence and development of CC by examining the translational profile and methylation, the high expression of UBE2V1 was well correlated to the poor prognosis of patients, indicating that UBE2V1 is an independent risk factor for the prognosis of CC patients. The expression of UBE2V1 was also correlated with clinical stages, tumor grades and TNM stages of CC. In addition, the expression of UBE2V1 was slightly negatively correlated with the methylation at the multiple methylation sites. our study revealed the relationship between UBE2V1 and the occurrence and development of CC from the level of transcriptional profile and DNA methylation. UBE2V1 is a novel candidate biomarker for the diagnosis, screening and prognosis of CC.

ESPL1 Is a Novel Prognostic Biomarker Associated With the Malignant Features of Glioma.

Research has confirmed that extra spindle pole bodies-like 1 (ESPL1), an etiological factor, promotes the malignant progression of cancers. However, the relationship between ESPL1 and glioma has not yet been demonstrated. The purpose of this study was to reveal the potential mechanisms of ESPL1-mediated malignant glioma progression. Gene expression data and detailed clinical information of glioma cases were obtained from multiple public databases. Subsequently, a series of bioinformatics analyses were used to elucidate the effects of ESPL1 on glioma. The results demonstrated that the mRNA and protein levels of ESPL1 in glioma were higher than those in normal brain tissues. In addition, ESPL1 expression was considerably associated with the clinical and pathological features of gliomas, such as World Health Organization grade, histology, and 1p19q co-deletion status. Importantly, ESPL1 reduced the overall survival (OS) of glioma patients and had prognostic value for gliomas. Gene set enrichment analysis (GSEA) indirectly revealed that ESPL1 regulates the activation of cancer-related pathways, such as the cell cycle and base excision repair pathways. In addition, we used the Connectivity Map (CMap) database to screen three molecular drugs that inhibit ESPL1: thioguanosine, antimycin A, and zidovudine. Finally, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of ESPL1 in glioma cell lines. This study plays an important role in revealing the etiology of glioma by revealing the function of ESPL1, providing a potential molecular marker for the diagnosis and treatment of glioma, especially low-grade glioma.

Significantly high expression of NUP37 leads to poor prognosis of glioma patients by promoting the proliferation of glioma cells.

BACKGROUND: The carcinogenic effect of NUP37 has been reported recently in a variety of tumors, but its research in the field of glioma has not been paid attention. The main purpose of this study is to reveal the relationship between NUP37 and prognosis or clinical characteristics of glioma patients. METHODS: First, as a retrospective study, this study included thousands of tissue samples based on a variety of public databases and clinicopathological tissues. Second, a series of bioinformatics analysis methods were used to analyze the NUP37 and glioma samples from multiple databases such as the CGGA, TCGA, GEO, HPA, and GEPIA. Third, to analyze the relationship between the expression level of NUP37 in tumor tissues and cells and a variety of clinical prognostic molecular characteristics, whether it can be an independent risk factor leading to poor prognosis in glioma and whether it has clinical diagnostic value; GSEA was used to analyze the cancer-related signaling pathways that may be activated by high expression of NUP37. Fifth, CMap was used to analyze small molecule drugs that may inhibit NUP37 expression. Finally, the meta-analysis of thousands of tissue samples from seven datasets and cell proliferation and migration experiments confirmed that NUP37 has a malignant effect on glioma. RESULTS: NUP37 is highly expressed in glioma patient tissues and glioma cells, significantly correlates with reduced overall survival, and may serve as an independent prognostic factor with some diagnostic value. Silencing NUP37 suppresses malignant biological behaviors of glioma cells. 4 small molecule drugs that had potential targeting inhibitory effects on NUP37 overexpression. CONCLUSIONS: This study demonstrates for the first time a malignant role of NUP37 in glioma and provides a vision to unravel the complex pathological mechanisms of glioma and a potentially valuable biomarker for implementing individualized diagnosis and treatment of glioma.

GNG5 is a novel oncogene associated with cell migration, proliferation, and poor prognosis in glioma.

BACKGROUND: Although many biomarkers have been reported for detecting glioma, the prognosis for the disease remains poor, and therefore, new biomarkers need to be identified. GNG5, which is part of the G-protein family, has been associated with different malignant tumors, though the role of GNG5 in glioma has not been studied. Therefore, we aimed to identify the relationship between GNG5 and glioma prognosis and identify a new biomarker for the diagnosis and treatment of gliomas. METHODS: We used data on more than a thousand gliomas from multiple databases and clinical data to determine the expression of GNG5 in glioma. Based on clinical data and CGGA database, we identified the correlation between GNG5 and multiple molecular and clinical features and prognosis using various analytical methods. Co-expression analysis and GSEA were performed to detect GNG5-related genes in glioma and possible signaling pathways involved. ESTIMATE, ssGSEA, and TIMER were used to detect the relationship between GNG5 and the immune microenvironment. Functional experiments were performed to explore the function of GNG5 in glioma cells. RESULTS: GNG5 is highly expressed in gliomas, and its expression level is positively correlated with pathological grade, histological type, age, and tumor recurrence and negatively correlated with isocitrate dehydrogenase mutation, 1p/19 co-deletion, and chemotherapy. Moreover, GNG5 as an independent risk factor was negatively correlated with the overall survival time. GSEA revealed the potential signaling pathways involved in GNG5 function in gliomas, including cell adhesion molecules signaling pathway. The ssGSEA, ESTIMATE, and TIMER based analysis indicated a correlation between GNG5 expression and various immune cells in glioma. In vivo and in vitro experiments showed that GNG5 could participate in glioma cell proliferation and migration. CONCLUSIONS: Based on the large data platform and the use of different databases to corroborate results obtained using various datasets, as well as in vitro and in vivo experiments, our study reveals for the first time that GNG5, as an oncogene, is overexpressed in gliomas and can inhibit the proliferation and migration of glioma cells and lead to poor prognosis of patients. Thus, GNG5 is a potential novel biomarker for the clinical diagnosis and treatment of gliomas.

CircPRDM2 Contributes to Doxorubicin Resistance of Osteosarcoma by Elevating EZH2 via Sponging miR-760.

BACKGROUND: Circular RNAs (circRNAs) are implicated in the chemoresistance of human cancers. However, the functions of circRNA PR/SET domain 2 (circPRDM2) in the resistance of osteosarcoma (OS) to doxorubicin (DXR) are unknown. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) assay was conducted to determine the levels of circPRDM2, microRNA-760 (miR-760) and enhancer of zeste homolog 2 (EZH2). RNase R assay was used to analyze the characteristics of circPRDM2. IC50 of DXR was estimated by Cell Counting Kit-8 (CCK-8) assay. Colony formation assay was performed for cell colony formation ability. Wound-healing assay and transwell assay were utilized for cell migration and invasion. Flow cytometry analysis was conducted for cell apoptosis. Western blot assay was employed for protein levels. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay were adopted to analyze the relationships among circPRDM2, miR-760 and EZH2. Murine xenograft model assay was utilized to explore DXR resistance in vivo. RESULTS: CircPRDM2 level was enhanced in DXR-resistant OS tissues and cells. CircPRDM2 deficiency inhibited IC50 of DXR, colony formation, migration and invasion and facilitated apoptosis in DXR-resistant OS cells in vitro. CircPRDM2 was identified as the sponge for miR-760. MiR-760 inhibition reversed the inhibitory effects of circPRDM2 knockdown on DXR resistance and cell progression in DXR-resistant OS cells. Moreover, EZH2 was identified as the target gene of miR-760 and EZH2 overexpression abolished miR-760-mediated impacts on DXR sensitivity and malignant behaviors in DXR-resistant OS cells. Also, circPRDM2 silencing improved DXR sensitivity in vivo. CONCLUSION: Our study demonstrated the role of circPRDM2/miR-760/EZH2 axis in enhancing DXR resistance.

Overexpressed XRCC2 as an independent risk factor for poor prognosis in glioma patients.

BACKGROUND: XRCC2, a homologous recombination-related gene, has been reported to be associated with a variety of cancers. However, its role in glioma has not been reported. This study aimed to find out the role of XRCC2 in glioma and reveal in which glioma-specific biological processes is XRCC2 involved based on thousands of glioma samples, thereby, providing a new perspective in the treatment and prognostic evaluation of glioma. METHODS: The expression characteristics of XRCC2 in thousands of glioma samples from CGGA and TCGA databases were comprehensively analyzed. Wilcox or Kruskal test was used to analyze the expression pattern of XRCC2 in gliomas with different clinical and molecular features. The effect of XRCC2 on the prognosis of glioma patients was explored by Kaplan-Meier and Cox regression. Gene set enrichment analysis (GSEA) revealed the possible cellular mechanisms involved in XRCC2 in glioma. Connectivity map (CMap) was used to screen small molecule drugs targeting XRCC2 and the expression levels of XRCC2 were verified in glioma cells and tissues by RT-qPCR and immunohistochemical staining. RESULTS: We found the overexpression of XRCC2 in glioma. Moreover, the overexpressed XRCC2 was associated with a variety of clinical features related to prognosis. Cox and meta-analyses showed that XRCC2 is an independent risk factor for the poor prognosis of glioma. Furthermore, the results of GSEA indicated that overexpressed XRCC2 could promote malignant progression through involved signaling pathways, such as in the cell cycle. Finally, doxazosin, quinostatin, canavanine, and chrysin were identified to exert anti-glioma effects by targeting XRCC2. CONCLUSIONS: This study analyzed the expression pattern of XRCC2 in gliomas and its relationship with prognosis using multiple datasets. This is the first study to show that XRCC2, a novel oncogene, is significantly overexpressed in glioma and can lead to poor prognosis in glioma patients. XRCC2 could serve as a new biomarker for glioma diagnosis, treatment, and prognosis evaluation, thus bringing new insight into the management of glioma.

Interleukin-1 receptor-associated kinase 4 as a potential biomarker: Overexpression predicts poor prognosis in patients with glioma.

The undetectable onset of glioma and the difficulty of surgery lead to a poor prognosis. Appropriate biomarkers for diagnosis and treatment need to be identified. Interleukin-1 receptor-associated kinase 4 (IRAK4) is involved in the initiation and progression of cancer. However, up until now, no report has revealed the relationship between IRAK4 and glioma. The present study aimed to examine the expression of IRAK4 in glioma, and to determine if there was a relationship between IRAK4 expression and clinical outcomes or survival prognosis. Thousands of glioma tissue samples and corresponding clinical information were obtained from various databases. Then a series of bioinformatics methods were used to reveal the role of IRAK4 in glioma. Finally, reverse transcription-quantitative PCR technology was used to verify the bioinformatics results. The study found that the expression of IRAK4 was significantly increased in glioma compared with the control brain tissue samples, and IRAK4, as an independent prognostic factor, shortened the overall survival time of patients with glioma. Gene Set Enrichment Analysis showed that IRAK4 promoted the activation of cell signalling pathways, such as NOD-like and Toll-like receptor signalling pathways. Co-expression analysis showed that the expression of IRAK4 was correlated with CMTM6, MOB1A and other genes. The present study demonstrated the role of IRAK4 as an oncogene in the pathological process of glioma for the first time, and highlights the potential of IRAK4 as a biomarker for prognostic evaluation and treatment of glioma.

Abnormal expression of HOXD11 promotes the malignant behavior of glioma cells and leads to poor prognosis of glioma patients.

BACKGROUND: Homeobox D11 (HOXD11) plays an important role in a variety of cancers, but its precise role in gliomas remains unclear. This study aimed to explore the relationship between HOXD11 and gliomas by combining bioinformatics methods with basic experimental validation. MATERIALS AND METHODS: Obtain gene expression information and clinical information of glioma and non-tumor brain tissue samples from multiple public databases such as TCGA (666 glioma samples), CGGA (749 glioma samples), GEPIA(163 glioblastoma samples and 207 normal control samples), GEO (GSE4290 and GSE15824). Nine cases of glioma tissue and five cases of normal control brain tissue were collected from the clinical department of Henan Provincial People's Hospital for further verification. A series of bioinformatic analysis methods were used to confirm the relationship between HOXD11 expression and overall survival and clinical molecular characteristics of patients with glioma. RT-qPCR was used to verify the change of expression level of HOXD11 in glioma cells and tissues. MTT assay, colony formation assay, wound-healing assay, immunofluorescence staining, flow cytometry and western blotting were used to detect the effect of HOXD11 on the biological behavior of glioma cell line U251. RESULTS: The high expression of HOXD11 was significantly related to age, World Health Organization (WHO) grade, chemotherapy status, histological type, and even 1p19q codeletion data and isocitrate dehydrogenase (IDH) mutation. HOXD11, as an independent risk factor, reduces the overall survival of glioma patients and has diagnostic value for the prognosis of glioma. Gene Set Enrichment Analysis (GSEA) showed that HOXD11 was significantly enriched in cell signaling pathway such as cell cycle, DNA replication and so on. Finally, we confirmed that the knockout of HOXD11 can inhibit the proliferation and invasion of U251 glioma cells, and change the biological behavior of tumor cells by preventing the progression of cell cycle. CONCLUSIONS: HOXD11 may be used as a candidate biomarker for the clinical application of targeted drug and prognostic assessment treatment of glioma. In addition, This study will help to explore the pathological mechanism of glioma.

ELK3: A New Molecular Marker for the Diagnosis and Prognosis of Glioma.

ETS transcription factor ELK3 (ELK3), a novel oncogene, affects pathological processes and progression of many cancers in human tissues. However, it remains unclear whether ELK3, as a key gene, affects the pathological process of gliomas and the prognosis of patients with gliomas. This study aimed to comprehensively and systematically reveal the correlation between ELK3 and the malignant progression of gliomas by analyzing clinical sample information stored in multiple databases. We revealed the putative mechanism of ELK3 involvement in malignant gliomas progression and identified a new and efficient biomarker for glioma diagnosis and targeted therapy. Based on the sample data from multiple databases and real-time quantitative polymerase chain reaction (RT-qPCR), the abnormally high expression of ELK3 in gliomas was confirmed. Kaplan-Meier and Cox regression analyses demonstrated that a high ELK3 expression was markedly associated with low patient survival and served as an independent biomarker of gliomas. Wilcox and Kruskal-Wallis tests revealed that expression of ELK3 was positively correlated with several clinical characteristics of patients with gliomas, such as age, WHO classification, and recurrence. Moreover, Cell Counting Kit-8 (CCK-8), immunofluorescence, and wound healing assays confirmed that ELK3 overexpression markedly promoted the proliferation and migration of glioma cells. Finally, gene set enrichment analysis (GSEA) and western blotting confirmed that overexpression of ELK3 regulated the JAK-STAT signaling pathway and upregulate the expression of signal transducer and activator of transcription 3 (STAT3) and phosphorylated STAT3 (P-STAT3) to promote the malignant transition of gliomas. Therefore, ELK3 may serve as an efficient biomarker for the diagnosis and prognosis of gliomas and it can also be used as a therapeutic target to improve the poor prognosis of patients with gliomas.

Correlation between C7 slope and cervical lordosis in patients after expansive open-door laminoplasty.

Purpose of the article: To investigate the correlation between C7 slope and cervical lordosis in patients after expansive open-door laminoplasty (EOLP).Material and methods: We retrospectively analyzed 57 patients who underwent EOLP between June 2013 and January 2017 in the Department of Spinal Surgery of our hospital. The operation time, intraoperative blood loss and follow-up time were recorded. The C7 slope, C2-7 sagittal vertical axis, and C2-7 Cobb angle were measured anteroposterior radiograph of the cervical spine preoperatively and postoperatively. All patients were divided into two groups according to the preoperative C7 slope (C7 slope ≤20° group and C7 slope >20° group).Results: The amount of intraoperative bleeding was 220.2 ± 180.9ml, and the operation time was 143.4 ± 51.2min. The average follow-up time was 24.9 ± 10.3months (range12-48 months). The C2-7 Cobb angle was 13.49 ± 10.46°at the final follow-up, which was significantly lower than that preoperatively (p = .026). But, The C7 slope and C2-7 sagittal vertical axis showed no significant difference between preoperatively and postoperatively. Preoperative and postoperative C7 slope and C2-7 Cobb angle were positively correlated to age and significant difference was observed. In the group of C7 slope >20°, significant difference was observed in term of the change of the C2-7 Cobb angle and C2-7SVA postoperatively (p = .009 and p= .020). However, there was no statistically significant difference detected in these two parameters in the group of C7 slope ≤20°.Conclusion: This study indicated that C7 slope could be used as an indicator of the change in the curvature of the cervical spine after EOLP. The loss of cervical curvature after surgery was prone to occur when C7 slope was greater than 20°, which should be noted in clinical practice.

[Correlation analysis of preoperative T 1 slope in MRI and physiological curvature loss after expansive open-door laminoplasty].

Objective: To investigate whether preoperative T 1 slope (T 1S) in MRI can predict the changes of cervical curvature after expansive open-door laminoplasty (EOLP) in patients with cervical spondylotic myelopathy, so as to make up for the shortcomings of difficult measurement in X-ray film. Methods: The clinical data of 36 patients with cervical spondylotic myelopathy who underwent EOLP were retrospectively analysed. There were 21 males and 15 females with an average age of 55.8 years (range, 37-73 years) and an average follow-up time of 14.3 months (range, 12-24 months). The preoperative X-ray films at dynamic position, CT, and MRI of cervical spine before operation, and the anteroposterior and lateral X-ray films at last follow-up were taken out to measure the following sagittal parameters. The parameters included C 2-C 7 Cobb angle and C 2-C 7 sagittal vertical axis (C 2-C 7 SVA) in all patients before operation and at last follow-up; preoperative T 1S were measured in MRI, and the patients were divided into larger T 1S group (T 1S>19°, group A) and small T 1S group (T 1S≤19°, group B) according to the median of T 1S, and the preoperative T 1S, C 2-C 7 Cobb angle, C 2-C 7 SVA, and the C 2-C 7 Cobb angle and C 2-C 7 SVA at last follow-up, difference in axial distance (the difference of C 2-C 7 SVA before and after operation), postoperative curvature loss (the difference of C 2-C 7 Cobb angle before and after operation), the number of patients whose curvature loss was more than 5° after operation, and the number of patients whose kyphosis changed (C 2-C 7 Cobb angle was less than 0° after operation). Results: The C 2-C 7 Cobb angle at last follow-up was significantly decreased when compared with preoperative value ( t=8.000, P=0.000), but there was no significant difference in C 2-C 7 SVA between pre- and post-operation ( t=-1.842, P=0.074). The preoperative T 1S was (19.69±3.39)°; there were 17 cases in group A and 19 cases in group B with no significant difference in gender and age between 2 groups ( P>0.05). The preoperative C 2-C 7 Cobb angle in group B was significantly lower than that in group A ( t=-2.150, P=0.039), while there was no significant difference in preoperative C 2-C 7 SVA between 2 groups ( t=0.206, P=0.838). At last follow-up, except for the curvature loss after operation in group B was significantly lower than that in group A ( t=-2.723, P=0.010), there was no significant difference in the other indicators between 2 groups ( P>0.05). Conclusion: Preoperative larger T 1S (T 1S>19°) in MRI had a larger preoperative lordosis angle, but more postoperative physiological curvature was lost; preoperative T 1S in MRI can not predict postoperative curvature loss, but preoperative larger T 1S may be more prone to kyphosis.

[Analysis of cervical sagittal parameters on MRI in patients with cervical spondylotic myelopathy].

Objective: To analyse the correlation between cervical sagittal parameters of cervical spondylotic myelopathy in different sagittal curvature so as to find out representative cervical sagittal alignment parameters by measuring on MRI. Methods: A retrospective analysis was made on the clinical data of 88 patients with cervical spondylotic myelopathy between July 2015 and January 2016. The C 2-C 7 Cobb angle, T 1 slope (T 1S), and C 2-C 7 sagittal vertical axis (C 2-C 7 SVA) were measured on T2-weight MRI. According to C 2-C 7 Cobb angle, the patients were divided into lordosis group (≥10° Cobb angle, 48 cases) and straightened group (0-10° Cobb angle, 40 cases). Intraclass correlation coefficient (ICC) was used for the reliability of measured data, Pearson correlation analysis for correlation between cervical sagittal parameters. Results: ICC was 0.858-0.946, indicating good consistency of measurement parameters. The C 2-C 7 Cobb angle, T 1S, and C 2-C 7 SVA were (5.6±2.4)°, (22.2±6.7)°, and (10.2±5.4) mm in straightened group, and were (20.1±8.2)°, (23.4±8.9)°, and (8.2±4.6) mm in lordosis group respectively. There was no correlation between the 3 parameters in straighten group ( r=0.100, P=0.510 for T 1S and C 2-C 7 Cobb angle; r=-0.100, P=0.500 for T 1S and C 2-C 7 SVA; r=0.080, P=0.610 for C 2-C 7 Cobb angle and C 2-C 7 SVA). There was positive correlation between T 1S and C 2-C 7 Cobb angle ( r=0.540, P=0.000), negative correlation between T 1S and C 2-C 7 SVA ( r=-0.450, P=0.001), and no correlation between C 2-C 7 Cobb angle and C 2-C 7 SVA ( r=-0.003, P=0.980). Conclusion: For cervical spondylotic myelopathy in patients with cervical lordosis, only T 1S measurement on MRI can be used as the main parameter to judge the sagittal curvature, but in patients with straightened cervical Cobb angle, measurements of T 1S, C 2-C 7 Cobb angle, and C 2-C 7 SVA should be taken for the comprehensive evaluation of cervical sagittal curvature.

[EFFECT OF MEDIAL 1/3 ANATOMICAL ORIENTATION OF TIBIAL TUBERCLE ON ROTATIONAL ALIGNMENT OF Gemini MK-II TIBIAL COMPONENTS IN TOTAL KNEE ARTHROPLASTY].

OBJECTIVE: To investigate the effect of medial 1/3 anatomical orientation of the tibial tubercie on tne rotational alignment of Gemini MK-II tibial components in total knee arthroplasty (TKA). METHODS: Between March 2011 and December 2012, 61 cases (67 knees) of varus knee osteoarthritis underwent Gemini MK-II knee arthroplasty, and the clinical data were retrospectively analyzed. There were 12 males and 49 females, with an average age of 67.6 years (range, 50-82 years). The body mass index ranged from 20.9 to 33.7 kg/m2 (mean, 28.2 kg/m2). Unilateral TKA was performed in 55 cases and bilatepal TKA in 6 cases. The duration of knee osteoarthritis ranged from 2 to 30 years (mean, 12.1 years). According to radiographic changes, 56 knees were rated as Kellgren-Lawrence grade III and 11 knees as grade IV. During TKA, the tibial rotational alignment was determined by medial 1/3 anatomical orientation of the tibial tubercle. The anteroposterior and lateral X-ray films and CT scan were taken to measure the tibial rotational angle (TRA) at pre- and post-operation and to analyze the relative factors for TRA by Pearson correlation analysis. RESULTS: All the patients were followed up 18-41 months (mean, 20.5 months). The range of motion (ROM) significantly increased from (98.806±16.969)° preoperatively to (116.806±11.458) at last follow-up (t= -11.760, P=0.000). The knee society score (KSS) significantly increased from 111.239±20.344 to 160.522±17.872 at last follow-up (t= -27.271, P=0.000). The anatomical tibiofemoral angle (ATFA), posterior condylar angle (PCA), and TRA were all improved after TKA, showing significant differences when compared with preoperative ones (P<0.05). Rotational malalignment was observed in 11 knees (16.42%). before TKA, and in 14 knees (20.90%) at 1 week after TKA, showing no significant difference (χ2=0.443, P=0.506). There were 8 knees (11.94%) of internal rotation (>8°) and 6 knees (8.96%) of external rotation (>8°). The postoperative tibial prosthesis TRA had no correlation with the preoperative ATFA and tibial plateau TRA, the postoperative PCA and ATFA (r= -0.174, P=0.159; r=0.220, P=0.074; r=0.237, P=0.053; r= -0.095, P=0.442). CONCLUSION: In patients with varus knee osteoarthritis, medial 1/3 anatomical orientation of the tibial tubercle will contribute to the development of tibial rotational malalignment when TKA is performed by using Gemini MK-II tibial components.