Multi-domain wavelet boundary element method for calculating two-dimensional stress intensity factors.

In order to improve the accuracy of stress intensity factors (SIFs) calculated by traditional boundary element methods (BEM), the multi-domain wavelet boundary element method (WBEM) is proposed. Firstly, by adjusting the nodes of the B-spline wavelet element on the interval, crack-tip elements are constructed. Since B-spline wavelet on the interval (BSWI) has excellent compact support characteristics and is particularly suitable for describing solution domains with large gradient changes, the constructed crack-tip can reduce the numerical oscillation effect near the crack tip. Secondly, the crack-tip elements are implemented into WBEM. And the combination of WBEM and multi-domain technology can effectively handle interface cracks. Thirdly, the crack problem solving strategy based on multi-domain WBEM can directly evaluate the SIFs of cracks. Finally, several numerical examples involving homogeneous media and bi-material models are given to verify that the proposed method is simple and highly accurate.

lncRNA CASC2/miR­18a­5p axis regulates the malignant potential of nasopharyngeal carcinoma by targeting RBBP8.

Nasopharyngeal carcinoma (NPC) is a prevalent head and neck tumor which has a high mortality rate in Southeast Asia, especially in Southern China. Cancer susceptibility candidate 2 (CASC2) is a newly identified long non­coding RNA (lncRNA) that has been found to play a suppressive role in several types of tumors. However, the expression and functional role of CASC2 in NPC are still unclear. In the present study, using NPC tissues, cells and transplanted mice, we investigated the mechanism of CASC2­mediated regulation of NPC. We showed that the CASC2 level is reduced in NPC tissues and cells. CASC2 downregulation promoted proliferation and inhibited apoptotic cell death in NPC cells. In contrast, CASC2 upregulation inhibited proliferation and increased apoptosis. There were putative binding sites of microRNA (miR)­18a­5p in the promoter of CASC2. The level of miR­18a­5p was upregulated in NPC tissues and cells. We further confirmed that CASC2 could directly bind with miR­18a­5p and inhibit miR­18a­5p expression, using reporter gene and RNA immunoprecipitation assays. miR­18a­5p suppressed CASC2 upregulation­mediated decrease in proliferation and increase in apoptotic cell death. Bioinformatics predicted the putative binding site of miR­18a­5p in the 3' untranslated region of C­terminal binding protein interacting protein (CtIP)/RBBP8. It was further confirmed that miR­18a­5p could directly bind with RBBP8 and inhibit RBBP8 expression. Downregulation of RBBP8 inhibited the anti­miR­18a­5p­mediated increase in apoptosis and decrease in proliferation. Downregulation of CASC2 increased tumor growth, increased the level of miR­18a­5p and decreased RBBP8 expression in vivo. In summary, CASC2 regulates NPC malignancy through modulation of RBBP8 via sponging miR­18a­5p. Our findings highlight the CASC2/miR­18a­5p/RBBP8 axis in NPC pathogenesis and provide new biomarkers and potential targets for the therapy of NPC.

Interactions of Bromocarbazoles with Human Serum Albumin Using Spectroscopic Methods.

The 1,3,6,8-tetrabromocarbazole and 3-bromocarbazole have attracted great attention in the ecotoxicology field recently as hazardous environmental contaminants. In this study, the quenching mechanism of these two substances binding with human serum albumin (HSA) has been investigated with spectroscopic methods. Through fluorescence quenching and binding site experiments with steady-state fluorescence and UV-Vis spectra, the intrinsic fluorescence of HSA quenched by 1,3,6,8-tetrabromocarbazole and 3-bromocarbazole both in static process, are activated by binding to site II (subdomain IIIA) of the HSA. In addition, it was not only found that the conformation and secondary structure of the proteins changes, but also that their spontaneous binding processes were driven by electrostatic interactions as well as hydrophobic forces for HSA-1,3,6,8-tetrabromocarbazole, and by typical hydrophobic forces for HSA-3-bromocarbazole. The above studies are beneficial to enhance our understanding of the ecotoxicology and environmental behaviors of halogenated carbazoles.

MicoRNA-451 is a novel tumor suppressor via targeting c-myc in head and neck squamous cell carcinomas.

OBJECTIVE: Head and neck squamous cell carcinoma (HNSCC) represents as a common malignancy with increasing incidence in the worldwide. The fact of its poor survival rate urgently requires developing efficient predictive biomarkers for clinical use. MicroRNAs (miRNAs) recently represent as a novel direction for early diagnosis and prognosis prediction in HNSCC therapy. In this study, we comprehensively investigated the function and putative target of miRNA-451 in vitro. METHODS: The expression of miRNA-451 was detected in HNSCC tissues and cell lines by real-time PCR. Forced expression or inhibition of miRNA-451 was done by transient transfection of mimics or inhibitor of miRNA-451 into indicated cells, respectively. Cell proliferation was evaluated by cell counting and crystal staining. Afterwards, we perform western blot to verify the expression of the miRNA-451 predicted target, c-myc, after miRNA-451 was overexpressed. RESULTS: We showed that miRNA-451 was downregulated in paired HNSCC tissues as well as in cell lines. And overexpression of miRNA-451 in cells with low endogenous expression of miRNA-451 accelerated proliferation. To the contrast, knockdown of miRNA-451 in cells with high levels of miRNA-451 significantly reduced cell growth rate. Furthermore, we used bioinformatics and cellular methods to predict and prove that c-myc was targeted by miRNA-451, since forced expression of miRNA-451 leaded to decreased c-myc protein expression in HNSCC cells. CONCLUSION: Our findings identify miRNA-451 as a potential biomarker and suggest a key role of miRNA-451-c-myc pathway in HNSCC cell transformation, which could represent a novel therapeutic strategy in HNSCC treatment.

[Tumor suppressive effect and relative mechanisms of tea polyphenol on nasopharyngeal carcinoma cells].

OBJECTIVE: To investigate the effect and mechanism of tea polyphenol (TP) on the proliferation, apoptosis, migration and invasion of nasopharyngeal carcinoma(NPC) cell line HONEl. METHOD: After treated with different concentration of tea polyphenol, CCK-8 assay, fluorescent staining, cell scratching assay and transwell assay were applied to detect the effect of tea polyphenol on the HONE1 cells. Furthermore, the expression of protein VEGF was investigated by flow cytometry assay. RESULT: It was found that tea polyphenol could inhibit NPC cell proliferation significantly in a dose-dependent manner, however, little impact was observed in normal nasopharyngeal epithelial cell line NP69. Furthermore, it was demonstrated by fluorescent staining assay that tea polyphenol could induce NPC cell apoptosis, and cell scratching assay and transwell assay showed that tea polyphenol could inhibit cell migration and invasion. CONCLUSION: Tea polyphenol can significantly inhibit cell proliferation, induce cell apoptosis and decreased the migration and invasion ability of NPC cells in vitro. Tea polyphenol might be a tumor suppressor of NPC cells.

[Studies progress in preventing xerostomia after radiotherapy of nasopharyngeal carcinoma].

Radiotherapy is the main way to treat the Nasopharyngeal Carcinoma. But there are a lot of serious complications, the most common one of then is radioactive xerostomia. It seriously affect the patients's quality of life, even make patients change or stop their radiotherapy. It is extremely important to prevent and treat xerostomia caused by radiotherapy.

[Advances on the anti-tumor and anti-radiation effect of tea polyphenols in nasopharyngeal carcinoma].

NPC is a high incidence of malignant tumors of the head and neck, and is currently used mainly radiotherapy based, supplemented by a comprehensive treatment of chemotherapy, radiotherapy and chemotherapy, which have serious complications and serious impact on the treatment of patients and quality of life. Polyphenols are the main component of tea. Studies have shown that tea polyphenols have a significant anti-tumor effect of im proving the effect of radiotherapy and chemotherapy, reducing radiation damage, reducing conventional chemo therapy drugs IC50 and reducing the complications of chemotherapy. Tea polyphenols in the treatment of nasopharyngeal carcinoma has also made great progress. It has a strong inhibition of nasopharyngeal carcinoma cells, and can greatly reduce the occurrence of xerostomia after radiotherapy, which is of important clinical research value.