miR-92b has been reported to be dysregulated in many types of human cancers. However, the role of miR-92b in oral squamous cell carcinoma (OSCC) is unknown. The aim of the present study was to investigate the function and mechanism of miR-92b in human OSCC. Using quantitative reverse‑transcription PCR (qRT-PCR), we found that the miR-92b level in primary tumors (n=85) was significantly elevated compared with that in the adjacent normal tissues (p<0.001). A high level of miR-92b was significantly associated with a large tumor size (p=0.005), advanced tumor stage (p<0.001) and poorer prognosis (p=0.04). Functionally, miR-92b was shown to not only promote the proliferation of OSCC cells in MTT and colony formation and xenograft assays, but also to inhibit cell apoptosis in a flow cytometric assay. In western blotting and luciferase assay, NLK was identified as a direct and functional target of miR-92b. We also found that NLK was involved in miR-92b-induced cell proliferation, and its protein level was obviously downregulated in the miR-92b-overexpressing xenograft tumors. Finally, luciferase reporter assay and fluorescent immunostaining revealed that miR-92b activated the NF-κB signaling pathway, which may be responsible for the effects of miR-92b on cell proliferation. Taken together, our results indicate that miR-92b upregulation accelerates tumor growth and present a novel mechanism of miRNA‑mediated NF-κB activation in OSCC.
Background. gcrR gene acts as a negative regulator related to sucrose-dependent adherence in S. mutans. It is constructive to test the potential capacity of mutans with gcrR gene deficient in bacteria replacement therapy. Methods. In this study, we constructed the mutant by homologous recombination. The morphological characteristics of biofilms were analyzed by confocal laser scanning microscopy. S. mutans UA159 and the mutant MS-gcrR-def were inoculated, respectively, or together for competitive testing in vitro and in rat model. Results. Adhesion assay showed that the adhesion ability of the mutant increased relative to the wild type, especially in the early stage. MS-gcrR-def out-competed S. mutans UA159 in vitro biofilm, and correspondingly coinfection displayed significantly fewer caries in vivo. The former possessed both a lower level of acid production and a stronger colonization potential than S. mutans UA159. Conclusion. These findings demonstrate that MS-gcrR-def appears to be a good candidate for replacement therapy.
Some adhesives produce a pH below the critical pH of hydroxyapatite and may not be suitable for patients with natural teeth. None of the tested adhesives significantly affect S. mutans growth.
Objective: The influence of continuous renal replacement therapy (CRRT) on the steady-state plasma concentration of high-dose tigecycline was investigated in septic shock patients to provide references for drug dosing.Methods: In this prospective observational study, 17 septic shock patients presenting with severe infections needing a broad-spectrum antibiotic therapy with high-dose tigecycline (100 mg per 12 h) in the intensive care unit were included and divided into CRRT group (n = 6) or non-CRRT group (n = 11). The blood samples were collected and plasma drug concentration was determined by SHIMADZU LC-20A and SHIMADZU LCMS 8040. The steady-state plasma concentration was compared between groups using unpaired t-test. Furthermore, between-groups comparisons adjusted for baseline value was also done using multivariate linear regression model.Results: Peak concentration (Cmax) of tigecycline was increased in CRRT group compared to non-CRRT group, but there were no statistical differences (505.11 ± 143.84 vs. 406.29 ± 108.00 ng/mL, p-value: 0.129). Trough concentration (Cmin) of tigecycline was significantly higher in CRRT group than in non-CRRT group, with statistical differences (287.92 ± 41.91 vs. 174.79 ± 33.15 ng/mL, p-value: 0.000, adjusted p-value: 0.000). In safety, Cmin was reported to be a useful predictor of hepatotoxicity with a cut-off of 474.8 ng/mL. In our studies, Cmin of all patients in CRRT group was lower than 474.8 ng/mL.Conclusion: The plasma concentration of tigecycline was increased in septic shock patients with CRRT treatment and only Cmin shown statistical differences. No dose adjustment seems needed in the view of hepatotoxicity.Clinical Trial Registration:https://www.chictr.org.cn/, identifier ChiCTR2000037475.
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