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Additional file 2. Figure S1. Construction of mBMSCs/BCP bone tissue grafts. A mBMSCs labeled with GFP (green fluorescence) were co-cultured with BCP for 7 days. B left panel: immunofluorescence staining showing the mBMSCs (green) stained with DAPI (blue) in BCP 7 days after co-culture, scale bar, 100 μm; right panel showed the magnification in the box of left panel, scale bar, 50 μm. C The graft dissected from the skull periosteum of C57BL/6 mice at 1 month after operation, showing the grafts were integrated with the skull of mice, scale bar, 1 mm.

Additional file 1. Table S1 Primer sequence of the target genes.

Additional file 3. Figure S2. LLLT promotes cell proliferation and ROS in the co-culture of hBMSCs and HUVECs. A Bright-field image of hBMSCs, HUVECs, co-culture of hBMSCs and HUVECs, scale bar, 100 μm. B, C LLLT on cell proliferation of co-culture of hBMSCs and HUVECs for 1-5 days was investigated by CCK8 assay, showing LLLT at the dose of 100 mW 3 min (4.5 J/cm2) was better than others. D The ROS assay and ALP staining was performed to detect the effects of LLLT on the ROS level and the osteogenic ability in co-culture system at 5 days. E Quantitative analysis of the effects of different doses of LLLT on the ROS level at 5 days in the co-culture system. To sum up, the effect of LLLT at the dose of 100 mW 3 min (4.5 J/cm2) was better than others.

The aim of this study was to carry out the comparative analysis of the brushing force following various brushing techniques by toothbrush mounted pressure sensing unit. The study group consisted of 10 dental hygienist participants. The brushing forces (on buccal area of each first molar) were monitored on 8 different kinds of brushing techniques; Fones, Bass, Rolling, Scrub, Charters, stillman, Modified bass and Modified stillman. In Bass, Charters, Fones and Scrub method, force distributions showed a small gap of maximum and minimum value (Max/Min) while a big difference was noted in Modified bass, Modified stillman, Rolling and Stillman methods. Especially, the biggest difference of Max/Min value was observed in the area of lower left first molar. In conclusion, highly delicate manual skill is needed in showing big error range of force distribution. It means that careful force needs to be focused during toothbrushing instruction when a delicate manual skill was carried out.

One of the theories regarding oral carcinogenesis is that the tumor growth is initiated from cancer stem cells (CSCs) that self-renew and give rise to differentiated tumor cells, like stem cells do in normal tissues. The most common methods of CSC identification are based on CSC marker expression in carcinogenesis. This study examined the expression of CD133 and CD44, the most commonly used CSC biomarkers in oral squamous cell sarcoma (SCC), with the goal of identifying molecular biomarkers whose expression is associated with the multistep oral carcinogenesis. The expression of CD133, CD44, proliferating cell nuclear antigen (PCNA), and Cytokeratin (CK) was examined by Western blot analysis and confirmed by immunohistochemistry in a 4-nitroquinoline 1-oxide-induced rat tongue carcinogenesis model. Also, the expression of aldehyde dehydrogenase 1 (ALDH1), OCT-4 and Nanog were investigated for alteration of cancer cell stemness by Western blot. Along with the progress of multistep carcinogenesis, there were slight increases of CD133 and CD44 expression in the dysplasia group compared with normal rats. However, CD133 protein level was significantly overexpressed in SCC. The expression of PCNA and CK were low in normal group, but sequentially increased in SCC. ALDH1, Nanog and OCT-4 expression were significantly increased according to SCC grade during carcinogenesis. The findings indicate that CD133 is useful in identifying oral CSCs, which suggests that CD133 may serve as a predictor to identify CSCs with a high risk of oral cancer development.

Papain was first used as the catalyst for the synthesis of 5-benzylidene rhodanine derivative through the condensation reaction of 4-nitrobenzaldehyde and rhodanine. The result showed that the yield could be up to 86% by optimizing the reaction conditions.

Background Photodynamic therapy (PDT) is an anticancer treatment that generates excessive reactive oxygen species after photosensitizer treatments following specific wavelength irradiation. In another reports, PDT was regulated with autophagic cell death and apoptotic cell death. However, the mechanism of PDT resistance in PDT-stimulated cell death is unclear. In this study, we determined PDT resistance by autophagy and apoptosis in HP-PDT-treated oral cancer cells. Materials & Methods Cells were treated hematoporphyrin and then irradiation with or without inhibitor. Cell lysates were checked protein expression with specific antibody. PDT resistance cells were generated with PDT repeated treatments. Results In HP-PDT, PDT induced autophagy through mTOR, ATG5, and LC3 in dose-dependent manners. Also, PDT at high dose induced apoptosis through caspase activation and PARP-1. Moreover, PARP-1 inhibitor protected cells against HP-PDT-induced cell death, but not by caspase inhibitor. At low dose of HP, autophagy inhibitor partially protected from HP-PDT-induced cell death. In autophagy phases, at low doses, HP-PDT regulated autophagic cell death through the inhibition of LC3II. Although autophagy inhibitor did not alter cell death directly, autophagy has associated with HP-PDT-induced apoptotic cell death by PARP-1 regulation. Conclusion Taken together, HP-PDT induces apoptotic cell death with autophagy in oral cancer cells. PDT resistance is related to autophagy by PARP-1 regulation in oral cancer cells.