Photo Inactivation of Streptococcus mutans Biofilm by Violet-Blue light

Among various preventive approaches, non-invasive phototherapy/photodynamic therapy is one of the methods used to control oral biofilm. Studies indicate that light at specific wavelengths has a potent antibacterial effect. The objective of this study was to determine the effectiveness of violet-blue light at 380-440 nm to inhibit biofilm formation of Streptococcus mutans or kill S. mutans. S. mutans UA159 biofilm cells were grown for 12-16 h in 96-well flat-bottom microtiter plates using tryptic soy broth (TSB) or TSB with 1 % sucrose (TSBS). Biofilm was irradiated with violet-blue light for 5 min. After exposure, plates were re-incubated at 37 °C for either 2 or 6 h to allow the bacteria to recover. A crystal violet biofilm assay was used to determine relative densities of the biofilm cells grown in TSB, but not in TSBS, exposed to violet-blue light. The results indicated a statistically significant (P < 0.05) decrease compared to the non-treated groups after the 2 or 6 h recovery period. Growth rates of planktonic and biofilm cells indicated a significant reduction in the growth rate of the violet-blue light-treated groups grown in TSB and TSBS. Biofilm viability assays confirmed a statistically significant difference between violet-blue light-treated and non-treated groups in TSB and TSBS. Visible violet-blue light of the electromagnetic spectrum has the ability to inhibit S. mutans growth and reduce the formation of S. mutans biofilm. This in vitro study demonstrated that violet-blue light has the capacity to inhibit S. mutans biofilm formation. Potential clinical applications of light therapy in the future remain bright in preventing the development and progression of dental caries

Photoinhibition of Streptococcus mutans Biofilm-Induced Lesions in Human Dentin by Violet-Blue Light

This in vitro study determined the effectiveness of violet-blue light on Streptococcus mutans (UA159) biofilm induced dentinal lesions. Biofilm was formed on human dentin specimens in a 96-well microtiter plate and incubated for 13 h in the presence of tryptic soy broth (TSB) or TSB supplemented with 1% sucrose (TSBS). Violet-blue light (405 nm) from quantitative light-induced fluorescence (QLFTM) was used to irradiate the biofilm. Supernatant liquid was removed, and the biofilm was irradiated continuously with QLF for 5 min twice daily with an interval of 6 h for 5 d, except with one treatment on the final day. Colony forming units (CFU) of the treated biofilm, changes in fluorescence (∆F; QLF-Digital BiluminatorTM), lesion depth (L), and integrated mineral loss (∆Z; both transverse microradiography) were quantified at the end of the fifth day. Statistical analysis used analysis of variance (ANOVA), testing at a 5% significance level. In the violet-blue light irradiated groups, there was a significant reduction (p < 0.05) of bacterial viability (CFU) of S. mutans with TSB and TSBS. Violet-blue light irradiation resulted in the reduction of ∆F and L of the dentinal surface with TSBS. These results indicate that violet-blue light has the capacity to reduce S. mutans cell numbers

LINC01605 Is a Novel Target of Mutant p53 in Breast and Ovarian Cancer Cell Lines

TP53 is the most frequently mutated gene in human cancers. Most TP53 genomic alterations are missense mutations, which cause a loss of its tumour suppressor functions while providing mutant p53 (mut_p53) with oncogenic features (gain-of-function). Loss of p53 tumour suppressor functions alters the transcription of both protein-coding and non-protein-coding genes. Gain-of-function of mut_p53 triggers modification in gene expression as well; however, the impact of mut_p53 on the transcription of the non-protein-coding genes and whether these non-protein-coding genes affect oncogenic properties of cancer cell lines are not fully explored. In this study, we suggested that LINC01605 (also known as lincDUSP) is a long non-coding RNA regulated by mut_p53 and proved that mut_p53 directly regulates LINC01605 by binding to an enhancer region downstream of the LINC01605 locus. We also showed that the loss or downregulation of LINC01605 impairs cell migration in a breast cancer cell line. Eventually, by performing a combined analysis of RNA-seq data generated in mut_TP53-silenced and LINC01605 knockout cells, we showed that LINC01605 and mut_p53 share common gene pathways. Overall, our findings underline the importance of ncRNAs in the mut_p53 network in breast and ovarian cancer cell lines and in particular the importance of LINC01605 in mut_p53 pro-migratory pathways

Managing carious lesions:consensus recommendations on carious tissue removal

The International Caries Consensus Collaboration undertook a consensus process and here presents clinical recommendations for carious tissue removal and managing cavitated carious lesions, including restoration, based on texture of demineralized dentine. Dentists should manage the disease dental caries and control activity of existing cavitated lesions to preserve hard tissues and retain teeth long-term. Entering the restorative cycle should be avoided as far as possible. Controlling the disease in cavitated carious lesions should be attempted using methods which are aimed at biofilm removal or control first. Only when cavitated carious lesions either are noncleansable or can no longer be sealed are restorative interventions indicated. When a restoration is indicated, the priorities are as follows: preserving healthy and remineralizable tissue, achieving a restorative seal, maintaining pulpal health, and maximizing restoration success. Carious tissue is removed purely to create conditions for long-lasting restorations. Bacterially contaminated or demineralized tissues close to the pulp do not need to be removed. In deeper lesions in teeth with sensible (vital) pulps, preserving pulpal health should be prioritized, while in shallow or moderately deep lesions, restoration longevity becomes more important. For teeth with shallow or moderately deep cavitated lesions, carious tissue removal is performed according toselective removal to firm dentine.In deep cavitated lesions in primary or permanent teeth,selective removal to soft dentineshould be performed, although in permanent teeth,stepwise removalis an option. The evidence and, therefore, these recommendations support less invasive carious lesion management, delaying entry to, and slowing down, the restorative cycle by preserving tooth tissue and retaining teeth long-term.status: publishe

Managing carious lesions:consensus recommendations on terminology

published_or_final_versio

Method for characterization of the enzyme profile and the determination of CBH I (Cel 7a) core protein in <i>Trichoderma reesei</i> cellulase preparations

Fast protein liquid chromatography (FPLC) was used to characterize a commercial cellulase preparation (Celluclast 1.5L, Novozymes) in relation to its protein profile and activity against hydroxyethylcellulose (HEC) and other substrates. Co-elution of CBHII (Cel 6A) with other enzyme components of the cellulase system was characterized by immunochemical assays using monoclonal antibodies, whereas the occurrence of EGII (Cel 5A) was assessed based on its ability to cleave the heterosidic bond of 4-methylumbellyferyl-β-d-cellotrioside (MUmbG3). The main cellulase constituents of Celluclast 1.5L were pooled into six fractions containing EGII (Cel 5A) and EGIII (Cel 12A) (F1), EGII and CBHII (Cel 6A) (F2), CBHII and EGI (Cel 7B) (F3), EGI (F4), and CBHI (Cel 7A) (F5). The occurrence of CBHI core protein within the CBHI fraction of the FPLC profile was determined by hydrophobic interaction chromatography. Using this method, we were able to demonstrate that the batch of Celluclast 1.5L used in this study contained 10.9–18.8% of CBHI as its corresponding free core protein