Correlation of preoperative CT imaging shift parameters of the lateral plateau with lateral meniscal injury in Schatzker IV-C tibial plateau fractures.

BACKGROUND: Schatzker IV-C is a high-energy tibial plateau fracture often accompanied by lateral meniscus injuries. While imaging examinations are routine preoperative measurements, the correlation between CT imaging shift parameters of the lateral plateau and lateral meniscal injury in Schatzker IV-C fractures remains uncovered. METHODS: This retrospective study enrolled a total of 60 patients with Schatzker IV-C tibial plateau fractures at the First People's Hospital of Hefei. Prior to surgery, CT imaging was used to measure the numerical values of lateral plateau depression (LPD) and lateral plateau widening (LPW). The degree of lateral meniscus injury was confirmed based on intraoperative direct vision, with patients being classified into meniscus injury and non-meniscus injury groups. Dichotomous logistic regression was employed to evaluate the correlation between LPD, LPW, and lateral meniscus injury, while the optimal cut-off points for predicting lateral meniscal injury with LPD and LPW were determined using receiver operator characteristic (ROC) curves. RESULTS: The meniscus injury group exhibited a mean LPD of 15.3 ± 3.5 mm, which was significantly higher than the non-meniscus injury group's mean LPD of 8.4 ± 3.4 mm (P < 0.05). Similarly, the meniscus injury group had a larger mean LPW of 9.4 ± 1.8 mm compared to the non-meniscus injury group's mean LPW of 6.9 ± 0.9 mm (P < 0.05). The optimal cut-off points for predicting lateral meniscal injury were determined to be 8.40 mm for LPD (with a sensitivity of 95%, specificity of 85%, and AUC of 0.898) and 7.90 mm for LPW (with a sensitivity of 75%, specificity of 90%, and AUC of 0.897). CONCLUSIONS: Patients with Schatzker IV-C tibial plateau fractures are at a significantly higher risk of lateral meniscal injury when the LPD exceeds 8.40 mm and/or the LPW exceeds 7.90 mm. Our results may provide novel reference metrics for the early diagnosis of lateral meniscal injury in Schatzker IV-C tibial plateau fracture patients when the MRI examination is not available.

Prognostic Values of COL4As Transcriptional Expressions in Clear Cell Renal Cell Carcinoma Patients.

OBJECTIVE: The COL4A family genes (COL4As) are a set of extracellular matrix-related genes that have been proved a tight relationship among various cancers. However, the functional role of different COL4As (COL4A1/2/3/4/5/6) in clear cell renal cell carcinoma (ccRCC) is unclear. METHODS: We obtained the data from online open-access databases including ONCOMINE, UALCAN, GEPIA, Cancer Genome Atlas (TCGA), cBioPortal, METASCAPE, STRING, TIMER, GSCALite, MEXPRESS, and TISIDB to explore the correlation between COL4As expression and genome-wide difference, progression, prognosis, genetic mutation, functional enrichment, tumor immune microenvironment, and methylation in ccRCC patients. RESULTS: The significantly higher COL4A1/2 expression and lower COL4A3/4/5/6 expression were observed in ccRCC tissues than in normal kidney tissues. Transcriptomic levels of COL4A1/2/3/4 were significantly correlated with tumor grade and stage. The higher expression levels of COL4A1/2/3/4 were accompanied by a longer overall survival time (OS); the higher expression levels of COL4A3/4 with lower expression levels of COL4A5 were associated with a longer disease-free time (DFS). Univariate/multivariate regression model analysis showed that COL4A4 could be a potential independent biomarker for ccRCC prognosis. And a high mutation rate (29%) of COL4As was observed in ccRCC patients. However, there were no relationships between mutation rates of COL4As and OS, DFS in ccRCC patients (p>0.05). Besides, we founded that the COL4As expressions were significant associated with the infiltration of the immune cells, tumor-infiltrating lymphocytes, three immunomodulators (immunoinhibitory, immunostimulator, MHC molecule), chemokines, and receptors. CONCLUSION: The results suggested that the transcript levels of COL4As could act as potential indicators for early disease progression. The expression of COL4A4 could contribute directly to disease prognosis. Besides, COL4A1/2/3/4 widely participated in tumor immunity. However, further studies are needed to confirm their clinical values in the ccRCC patients.

Multimolecular characteristics of cell-death related hub genes in human cancers: a comprehensive pan-cancer analysis.

Failure of the normal process of cell death pathways contributes to the defection of immune systems and the occurrence of cancers. The key genes, the multimolecular mechanisms, and the immune functions of these genes in pan-cancers remain unclear. Using online databases of The Cancer Genome Atlas, GEPIA2, TISIDB, HPA, Kaplan-Meier Plotter, PrognoScan, cBioPortal, GSCALite, TIMER, and Sangerbox, we identified the key genes from the six primary cell death-related pathways and performed a comprehensive analysis to investigate the multimolecular characteristics and immunological functions of the hub genes in 33 human cancers. We identified five hub genes in the six primary cell death-related pathways (JUN, NFKB1, CASP3, PARP1, and TP53). We found that CASP3, PARP1, and TP53 were overexpressed in 28, 23, and 27 cancers. The expression of the five genes was associated with the development and prognosis of many cancers. Particularly, JUN, NFKB1, CASP3, and TP53 have prognostic values in Brain Lower Grade Glioma (LGG), while PARP1 and CASP3 could predict the survival outcomes in Adrenocortical carcinoma (ACC). In addition, an extensive association between five genes' expression, DNA methylation, and tumor-immune system interactions was noticed. The five cell death-related hub genes could function as potential biomarkers for various cancers, particularly LGG and ACC. The immunological function analysis of the five genes also proposes new targets for developing immunosuppressants and improving the immunotherapy efficacy of cancers. However, further extensive clinical and experimental research are required to validate their clinical values.

Bioinformatics Analysis Identified Five Widely Expressed Genes Associated with Prognosis in Sarcoma.

Background: Human sarcomas (SARC) are a group of malignant tumors that originated from mesenchymal lineages with more than 60 subtypes. However, potential biomarkers for the diagnosis and prognosis of SARC remain to be investigated. Methods: We obtained three GSE raw matrix files (GSE39262, GSE21122, GSE48418) that related to various subtypes of sarcoma from the public GEO database and explored the widely differential expression genes in three obtained GSE files. Then common differential expression genes (CDGEs) were identified. We analyzed the correlation between the expression of the top five interacted genes of CDEGs and genome-wide differences, prognosis, genetic mutation, functional enrichment, immune infiltration, immune checkpoint, and marker genes' expression of N6-methyladenosine (m6A) modification in SARC patients. Besides, a prognostic nomogram was constructed to predict the survival of SARC patients. Results: Among the three GSE files, 42 CDGEs were identified, and the top five interacted genes were ASPM, CCNB2, PRC1, AURKA, and SCM2. The expression levels of the five genes were higher in the SARC group than that in the normal group. The transcriptional level of CCNB2, PRC, and SCM2 was correlated to the worse survival of SARC. The constructed nomogram that combined CNB2, PRC1, and SCM2 showed a fairly good incredibility in predicting the survival of SARC (C-index: 0.711). Furthermore, the five genes were widely involved in immune infiltration, immune checkpoint, and m6A modification. In addition, we found a minor survival-related mutation rate (9%) of the five identified genes in SARC patients (p < 0.05). Conclusion: The results suggested the five identified genes widely participated in the prognosis, immune infiltration, immune checkpoint, and m6A modification of SARC patients. This study provided a theoretical basis for the research about the correlation between the level of five identified genes and sarcoma, but the further mechanism needs to be verified by experiments.

Bone marrow mesenchymal stem cells-derived exosomes suppress miRNA-5189-3p to increase fibroblast-like synoviocyte apoptosis via the BATF2/JAK2/STAT3 signaling pathway.

Ankylosing spondylitis (AS) is characterized by inflammation of the sacroiliac joint and the attachment point of the spine. Herein, we aimed to investigate the effect of bone marrow mesenchymal stem cells (BMSCs)-derived exosomes on apoptosis of fibroblast-like synoviocytes (FLSs) and explored its molecular mechanism. Exosomes were isolated from BMSCs and verified by transmission electron microscope and nanoparticle tracking analysis. FLSs were isolated and co-incubated with BMSC exosomes. Cell apoptosis was assessed using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling analysis and flow cytometry. The results showed that BMSC exosomes increased apoptosis of FLSs. MiR-5189-3p was downregulated, while basic leucine zipper transcription factor ATF-like 2 (BATF2) was upregulated in FLSs by treatment of BMSC exosomes. As a direct target of miR-5189-3p, BATF2 inactivates the JAK2/STAT3 pathway. MiR-5189-3p suppressed apoptosis of FLSs and BATF2 exerted an opposite effect. In conclusion, BMSCs-derived exosomes suppress miR-5189-3p to facilitate the apoptosis of FLSs via the BATF2/JAK2/STAT3 signaling pathway, which facilitates the understanding of the therapeutic effect of BMSCs on AS and the underlying molecular mechanism.

Prognostic Values of E2F1/2 Transcriptional Expressions in Chromophobe Renal Cell Carcinoma Patients: Evidence from Bioinformatics Analysis.

BACKGROUND: Numerous studies on the E2F transcription factors have led to increasing insights that E2Fs could be an important driver of the formation and progression of many human cancers. Little is known about the function of distinct E2Fs in chromophobe renal cell carcinoma (chRCC). METHODS: We utilized the UALCAN, GEPIA, Cancer Genome Atlas (TCGA) database, cBioPortal, Metascape, STRING, Cytoscape, GeneMANIA, TIMER, TISIDB, GSCALite, and MEXPRESS databases to investigate the transcription level, genetic alteration, methylation, and biological function of E2Fs in chRCC patients, and its association with the occurrence, progress, prognosis, and immune cell infiltration in patients with chRCC. RESULTS: We found that E2F1/2/4/7/8 were more expressed in chRCC tissues than in normal tissues, while the expression of E2F5/6 was lower in the former than in the latter, and the expression levels of E2F1/2/4/5/6//7/8 were also associated with the histological parameters of chRCC, including T-stage and N-stage. Higher expression of E2F1/2/7/8 was found to be significantly correlated with worse overall survival (OS) in chRCC patients. Cox regression and time-dependent ROC analysis further suggested that E2F1/2 could be the potential independent biomarkers for chRCC prognosis. Besides, a moderate mutation rate of E2Fs (34%) was noticed in chRCC, and the genetic mutations in E2Fs were associated with poor survival of chRCC patients. We noticed that the expression of E2Fs was statistically correlated with the immune cell infiltration in chRCC. Moreover, we also found that the expression of E2F1 was significantly correlated with tumor-infiltrating lymphocytes and immunomodulators, E2F7 expression was associated with MHC molecules, and the expression of E2F1/8 was correlated to their methylation levels. CONCLUSION: Our results provide novel insights for selecting the prognostic biomarkers for chRCC and suggest that E2F1/2 could act as potential prognostic biomarkers for the survival of chRCC patients. However, more in-depth experiments are required to identify the underlying mechanisms and verify the clinical value of E2F1/2 in the prognosis of chRCC.