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Objective To explore the role of apoliprotein D (APOD) in the proliferation and migration of human dental pulp cells (DPCs) and to provide a basis for the use of APOD to promote pulp regeneration. Methods APOD ex⁃ pression in human dental pulp cells was inhibited by siRNA. The inhibition effect of APOD was confirmed by qPCR and Western blot. After APOD inhibition, colony formation experiments and CCK8 assays were employed to confirm the proliferation ability of dental pulp cells. Transwell assays were used to verify the cell migration ability after the inhibi⁃ tion of APOD expression. Results After inhibiting APOD expression, the colony formation rate in the si⁃apod group was reduced compared with the NC group, and the difference was statistically significant (t＝7.624, P＝0.002). The CCK8 experiment showed that the OD value in the si⁃apod group decreased at 3, 5 and 7 d compared with that in the NC group (P < 0.05). Transwell results showed that the number of cell divisions was 57.25 ± 4.03 in the si⁃apod group and 154.50 ± 8.39 in the NC group, and the difference was statistically significant (t＝10.45, P < 0.001). Conclusion Inhibition of APOD expression in dental pulp cells inhibits their proliferation and migration ability.

Objective To investigate the levels of the Twist and Vimentin proteins in oral squamous cell carcinoma (OSCC) and analyze the clinical significance of Twist and Vimentin. Methods Eighty⁃five samples of OSCC and fif⁃ teen samples of normal oral mucosa were collected. Immunohistochemistry (SP method) was used to detect the expres⁃ sion of proteins, including Twist and vimentin. The relationship among these proteins and clinical pathological parame⁃ ters was analyzed using SPSS statistical software. Results In the normal group, 13.3% (2/15) of samples were positive for the Twist protein; this value was significantly lower than that in OSCC group (80.0%, 66/85) (c2＝26.98, P < 0.001). The expression of Twist was associated with clinical stage (c2＝5.40, P＝0.02) and lymph node metastasis (c2＝8.35, P＝0.006), while no correlations were found between the expression of Twist and sex (c2＝0.23, P＝0.63), age (c2＝0.31, P＝0.58), location (c2＝1.46, P＝0.235) or degree of differentiation (c2＝1.52, P＝0.47). Additionally, 6.7% of samples (1/15) were positive for vimentin; this value was significantly lower than that in OSCC group (74.1%, 63/85) (c2＝20.71, P < 0.001). The expression of vimentin was associated with clinical stage (c2＝4.51, P＝0.034) and lymph node metastasis (c2＝6.75, P＝0.009), while no correlations were found between the expression of vimentin and sex (c2＝0.40, P＝0.53), age (c2＝0.17, P＝0.68), location (c2＝0.74， P＝0.39) or degree of differentiation (c2＝4.58, P＝ 0.10). Spearman correlation analyses showed that Twist protein expression was positively correlated with vimentin (r＝ 0.578, P＜0.05). Conclusion Our data demonstrate that in OSCC, Twist and vimentin levels were upregulated, and Twist protein expression was positively correlated with vimentin, which indicates that both Twist and vimentin may be involved in the occurrence of OSCC.

Background: Histone methylation is considered to play an important role in the occurrence and development of periodontitis. Plant homeodomain finger protein 8 (PHF8), a histone demethylase, has been shown to regulate inflammation and osteogenic differentiation of bone marrow stromal cells (BMSCs). This study aimed to detect the functions of PHF8 and TLR4 in osteogenic differentiation in an inflammatory environment induced by Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) METHODS: A periodontitis mouse model was established, and the mice were treated with TAK-242. Immunohistochemical staining was used to detect the expression of PHF8 in periodontal tissue. Periodontal ligament cells (PDLCs) were treated with mineralization induction medium supplemented with Pg-LPS and/or TAK-242, and a Cell Counting Kit-8 (CCK-8) assay was used to detect the proliferation of PDLCs. Real-time PCR and western blotting were used to detect the mRNA and protein expression levels, respectively, of PHF8, toll-like receptor 4 (TLR4) and the other osteogenic markers alkaline phosphatase (ALP), osteocalcin (OCN), Special AT-rich sequence-binding protein 2 (Satb2) and Runt-related transcription factor 2 (Runx2) RESULTS: Periodontitis reduced PHF8 expression in periodontal tissue, and TAK-242 partially reversed this downregulation. An in vitro experiment revealed that the mRNA and protein expression levels of PHF8 were significantly upregulated during the osteogenic differentiation of PDLCs. Alizarin red staining showed that the mineralized nodules of PDLCs in osteogenic induction group were more than those in control group. Real-time PCR and western blot results indicated that Pg-LPS inhibited PHF8 expression and upregulated TLR4 expression in PDLCs. TAK-242 inhibited TLR4 and partially reversed the inhibition of PHF8 expression and osteogenic differentiation induced by Pg-LPS in PDLCs CONCLUSION: PHF8 and TLR4 play important roles in periodontitis. Pg-LPS inhibits the expression of PHF8 via upregulation of TLR4 and might further inhibit the osteogenic differentiation of PDLCs. However, the specific mechanisms involved remain to be explored. [ABSTRACT FROM AUTHOR]

A novel fiber-end antireflection method for reducing the reflection noise in ultra-weak fiber Bragg grating (FBG) sensing systems is proposed in this study. The principle of fiber-end antireflection is analyzed and simulated theoretically, and then an antireflection structure is designed and fabricated. In this method, the fiber end is cut into an inclined surface and covered directly with an ellipsoid photosensitive ultraviolet (UV) glue drop, whose refractive index is similar to that of the fiber core. Under the online monitoring of the fiber-end reflection with the ultra-weak FBG interrogator, the refractive index of the glue drop is adjusted by controlling the UV curing time to achieve optimal reflection suppression. Results show that this method can reduce fiber-end reflection to less than −60 dB and effectively eliminate the influence of fiber-end reflection noise on the last sensor. The proposed method thus provides an excellent solution for the fiber-end processing of ultra-weak FBG sensing systems. [ABSTRACT FROM AUTHOR]