Role of extracellular DNA in Enterococcus faecalis biofilm formation and its susceptibility to sodium hypochlorite Objective: This study investigated the role of extracellular deoxyribonucleic acid (eDNA) on Enterococcus faecalis (E. faecalis) biofilm and the susceptibility of E. faecalis to sodium hypochlorite (NaOCl). Methodology: E. faecalis biofilm was formed in bovine tooth specimens and the biofilm was cultured with or without deoxyribonuclease (DNase), an inhibitor of eDNA. Then, the role of eDNA in E. faecalis growth and biofilm formation was investigated using colony forming unit (CFUs) counting, eDNA level assay, crystal violet staining, confocal laser scanning microscopy, and scanning electron microscopy.The susceptibility of E. faecalis biofilm to low (0.5%) or high (5%) NaOCl concentrations was also analyzed by CFU counting. Results: CFUs and biofilm formation decreased significantly with DNase treatment (p<0.05). The microstructure of DNase-treated biofilms exhibited less structured features when compared to the control. The volume of exopolysaccharides in the DNase-treated biofilm was significantly lower than that of control (p<0.05).Moreover, the CFUs, eDNA level, biofilm formation, and exopolysaccharides volume were lower when the biofilm was treated with DNase de novo when compared to when DNase was applied to matured biofilm (p<0.05). E. faecalis in the biofilm was more susceptible to NaOCl when it was cultured with DNase (p<0.05). Furthermore, 0.5% NaOCl combined with DNase treatment was as efficient as 5% NaOCl alone regarding susceptibility (p>0.05). Conclusions:Inhibition of eDNA leads to decrease of E. faecalis biofilm formation and increase of susceptibility of E. faecalis to NaOCl even at low concentrations. Therefore, our results suggest that inhibition of eDNA would be beneficial in facilitating the efficacy of NaOCl and reducing its concentration.
Background/Aims: To reduce the cancer burden, the Korean government initiated the National Cancer Control Plan including the National Liver Cancer Screening Program (NLCSP). Ultrasonography examinations and α-fetoprotein tests at six-month intervals are currently offered for high-risk individuals. High-risk individuals are identified by reviewing the National Health Insurance Service claims data for medical use for the past two years using International Classification of Diseases Codes for specific liver disease. We surveyed the attitudes and opinions towards the NLCSP to understand the issues surrounding the NLCSP in Korea. Methods: Altogether, 90 Korean Liver Cancer Association members participated in online and offline surveys between November and December 2019. Results: Approximately one-quarter (27%) of the survey participants rated the NLCSP as very contributing and about two-thirds (68%) as contributing to some extent toward reducing hepatocellular carcinoma (HCC)-related deaths in Korea. Most (87.8%) responded that the current process of identifying high-risk individuals needs improvement. Many (78.9%) were concerned that the current process identifies individuals who use medical services and paradoxically misses those who do not. When asked for the foremost priority for improvement, solving 'duplication issues between the NLCSP and private clinic HCC screening practices' was the most commonly selected choice (23.3%). Conclusions: The survey participants positively rated the role of the NLCSP in reducing liver cancer deaths. However, many participants rated the NCLSP as needing improvement in all areas. This survey can be a relevant resource for future health policy decisions regarding the NLCSP in Korea.
PurposeOxaliplatin is a third-generation platinum compound, and it has no nephrotoxicity and has reduced bone marrow toxicity. Cancer cells that are resistant to cisplatin are sensitive to oxaliplatin. Oxaliplatin is used widely for the treatment of colon cancers. Recently, oxaliplatin was reported to inhibit the expression of survivin, which protects cell apoptosis. However, there are no reports on the expressions of survivin variants and the changes in intracellular localization of survivin in cancer cells. We studied the expression of survivin caused by oxaliplatin in HCT116 colon cancer cells, and we observed the localization of survivin in the mitotic phase.MethodsWe treated the HCT116 colon cancer cells with 2.0 µM of oxaliplatin, and we studied the expressions of survivin protein, and survivin mRNA variants, as well as the changes in intracellular localization, by using the Western blot method, RT-PCR, immunocytochemistry, and flowcytometry.ResultsOxaliplatin inhibits the expression of the survivin protein and survivin mRNA in HCT116 colon cancer cells. The expression of the survivin-2B variants, which have no antiapoptotic activity but control cell mitosis by localization on a microtubule, is reduced continuously 2 days after treatment with oxaliplatin. In immunocytochemistry, expression of survivin in the cytoplasm is reduced and especially is not expressed in microtubules and contractile rings.ConclusionOne of the mechanisms of oxaliplatin is to inhibit the expression of and to change the localization of survivin. Based on these results, we suggest that changes in the expression of survivin variants and in their localization are two effects of oxaliplatin.
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