BackgroundThe aim of this study was to explore the diagnostic value of sagittal measurement of thoracic inlet parameters for degenerative cervical spondylolisthesis (DCS).Material/MethodsWe initially included 65 patients with DCS and the same number of health people as the control group by using cervical radiograph evaluations. We analyzed the x-ray and computer tomographic (CT) data in prone and standing position at the same time. Measurement of cervical sagittal parameters was carried out in a standardized supine position. Multivariate logistic regression analysis was performed to evaluate these parameters as a diagnostic index for DCS.ResultsThere were 60 cases enrolled in the DCS group, and 62 cases included in the control group. The T1 slope and thoracic inlet angle (TIA) were significantly greater for the DCS group compared to the control group (24.33±2.85º versus 19.59±2.04º, p=0.00; 76.11±9.82º versus 72.86±7.31º, p=0.03, respectively). We observed no significant difference for the results of the neck tilt (NT), C2–C7 angle in the control and the DSC group (p>0.05). Logistic regression analysis and receiver operating characteristic (ROC) curve revealed that preoperative T1 slope of more than 22.0º showed significantly diagnostic value for the DCS group (p<0.05).ConclusionsPatients with preoperative sagittal imbalance of thoracic inlet have a statistically significant increased risk of DCS. T1 slope of more than 22.0º showed significantly diagnostic value for the incidence of DCS.
An odontogenic keratocyst (OKC) is a common oral cyst arising from the odontogenic epithelium, which has the characteristics of a tumor. Previous studies have demonstrated that M2-polarized macrophages and angiogenesis have important roles in the progression of OKCs. As transforming growth factor (TGF)-β1 is important in growth and developmental processes, and early studies have indicated that TGF-β1 is upregulated in OKCs, the present study aimed to investigate the expression levels of TGF-β1 as a first step. Flow cytometric analysis suggested that TGF-β1 induced M2-polarization of macrophages in a dose-dependent manner. Expression levels of cyclooxygenase (COX)-1 and-2 were measured after treatment of M2 macrophages with TGF-β1 and OKC homogenate supernatant. COX-2 expression was influenced by TGF-β1 in a concentration-dependent manner and in OKC induction. In addition, inhibition of COX-2 resulted in the induction of M2-polarization of macrophages via TGF-β1 and OKC disruption. Because the extracellular matrix (ECM) is altered in individuals with chronic diseases, the present study analyzed the expression of matrix metalloproteinase (MMP)-9, which is able to degrade the ECM. The present study observed a decrease in MMP-9 activity following treatment with TGF-β1 and OKC homogenate supernatant. Additionally, the present study analyzed tube formation caused by OKC with or without a COX-2 inhibitor. The results of the present study suggested that angiogenesis increased following treatment with OKC homogenate supernatant but decreased after treatment with a COX-2 inhibitor. These findings indicated that the TGF-β1/COX-2 pathway may have an important role in the progression of OKC.
Polylactic acid nanoparticles (PLA-NPs) not only have the characteristics of NPs, but also can be used as drug carriers. In this experiment, PLA-NPs were used as nano-carriers to construct nano-drugs carrying cucurbitacin B and long non-coding RNA (lncRNA) cancer susceptibility candidate 2c (CASC2c) (lncRNA CASC2C), to intervene oral cancer cells followed by analysis of their effect on cell progression. CuB-PLA-NPs and CuB-PLANPs-CASC2c were prepared, and properties of two NPs and in vitro drug release were analyzed. Oral cancer cells were treated with CuB-PLA-NPs or CuB-PLA-NPs-CASC2c. MTT was used to detect cell proliferation under intervention of 3.125, 6.25, 12.5, 25, 50, and 100 μmol/L drug concentrations. AnnexinV/PI staining method detected cell apoptosis, and Transwell assay detected cell migration and invasion. Moreover, RT-qPCR was applied to detect expressions of CASC2C, STAT3, MMP-2, and VEGF. CuB-PLA-NPs were milky white granular, and there was no adhesion between NPs with in vitro drug release of 90% and short release time. The CuB-PLA-NPs-CASC2c (size of 200 nm) had the release rate of 62%, with long release time. The proliferation inhibition rate was increased with increased drug concentration (P < 0.05). Experimental group showed higher proliferation inhibition rate than blank and control groups (P < 0.05). Treatment with CuB-PLA-NPs-CASC2c resulted in increased apoptosis rate (90%) (P < 0.05) and decreased both cell migration rate [(49.78±33.79)%] and invasion rate [(10.24±8.79)%] (P < 0.05). Additionally, CASC2c expression (57.34±3.21) was higher in experiment group, but expressions of STAT3 (29.78±4.21), MMP-2 (10.96±291), and VEGF (29.41±4.01) all decreased (P < 0.05). CuB-PLA-NPs-CASC2c inhibited oral cancer cell migration and invasion and further increased apoptosis. The high expression status of CASC2c in oral cancer cells negatively regulates the STAT3 signaling pathway, and further inhibits expression of MMP-2 and VEGF, thus inhibiting the formation of new blood vessels.
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