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Abstract: In this paper, a new robust C 0 triangular element is proposed for the fourth order elliptic singular perturbation problem with double set parameter method and bubble function technique, and a general convergence theorem for C 0 nonconforming elements is presented. The convergence of the new element is proved in the energy norm uniformly with respect to the perturbation parameter. Numerical experiments are also carried out to demonstrate the efficiency of the new element. [ABSTRACT FROM AUTHOR]

Objective: To examine the expression of Twist1 in cervical cancer and to explore its biological function in the progression of cervical cancer.
, Methods: The expressions of Twist1 in 32 cervical cancers and matched normal tissues were examined by immunohistochemistry (IHC). Cell invasive ability and the expression of invasion-related genes were determined in RNAi-based Twist1-silencing HeLa cells. The relationship between Twist1 and microRNA-33a (miR-33a) in cervical cancer was studied by Pearson correlation analysis, and the roles of miR-33a in regulation of Twist1 and cell invasiveness were studied.
, Results: The positive expression rate of Twist1 was 75.0% (24/32) and 21.9% (7/32) in the cervical cancer and the matched normal tissues, respectively, with significant difference between them (P<0.05). Twist1 shRNA significantly decreased the invasiveness of HeLa cells (P<0.05). Compared with the matched normal tissues, the expression of miR-33a was increased in the cervical cancer tissues, which was negatively correlated with Twist1 (r=-0.661, P<0.05). Overexpression of miR-33a could significantly suppress Twist1 expression as well as cell invasiveness (P<0.05).
, Conclusion: Twist1 is critical for the invasiveness of cervical cancer cells; miR-33a, as a tumor suppressor gene, functions as an upstream regulator of Twist1 and is involved in the invasiveness of cervical cancer cell.

Objective: The objective of the present study was to explore the major risk factors of surgical complications using the Clavien-Dindo classification., Methods: The case-control design was used. A total of 1049 patients who underwent radical gastrectomy in Hunan Cancer Hospital between October 2010 and August 2014 were retrospectively analyzed, including 122 patients (11.6%) with complications and 927 patients (88.4%) with no complications. Risk factors were evaluated., Results: Following radical gastrectomy, 122 patients (11.6%) experienced a total of 151 complications. The incidence of Stages II, IIIa, IIIb, IVa, IVb and V complications was 9.6% (n = 101), 2.5% (n = 26), 1.0% (n = 11), 0.8% (n = 8), 0% (n = 0), and 0.5% (n = 5), respectively. The incidence of severe complications (Stage ≥ IIIa) was 4.8% (n = 50). Multivariate analysis showed that combined resection (Odds Ratio [OR] = 3.36, 95% confidence interval [CI]: 1.71~6.60, P < 0.01), perioperative blood transfusion (OR = 2.13, 95% CI: 1.38-3.29, P < 0.01), and BMI ≥ 25 kg/m(2) (OR = 1.98, 95% CI: 1.16-3.40, P = 0.01) were independent risk factors of complications., Conclusions: Combined resection, perioperative blood transfusion, and BMI ≥ 25 kg/m(2) are positively correlated with complications.

Toll-like receptor 3 (TLR3), a member of the pathogen recognition receptors, is widely expressed in various cells and has been shown to activate immune signaling pathways by recognizing viral double-stranded RNA. Recently, it was reported that the activation of TLR3 induced apoptosis in some cells, but the detailed molecular mechanism is not fully understood. In this study, we found that in endothelial cells polyinosinic-polycytidylic acid (poly(I-C)) induced dose- and time-dependent cell apoptosis, which was elicited by TLR3 activation, as TLR3 neutralization and down-regulation repressed the apoptosis. Poly(I-C) induced the activation of both caspases 8 and 9, indicating that TLR3 triggered the signaling of both the extrinsic and intrinsic apoptotic pathways. Poly(I-C) up-regulated tumor necrosis factor-related apoptosis-inducing ligand and its receptors, death receptors 4/5, resulting in initiating the extrinsic pathway. Furthermore, poly(I-C) down-regulated anti-apoptotic protein, B cell lymphoma 2 (Bcl-2), and up-regulated Noxa, a key Bcl-2 homology 3-only antagonist of Bcl-2, leading to the priming of the intrinsic pathway. A p53-related protein, the transactivating p63 isoform α (TAp63α), was induced by TLR3 activation and contributed to the activation of both the intrinsic and extrinsic apoptotic pathways. Both the cells deficient in p63 gene expression by RNA interference and cells that overexpressed the N-terminally truncated p63 isoform α (ΔNp63α), a dominant-negative variant of TAp63α, by gene transfection, survived TLR3 activation. Taken together, TAp63α is a crucial regulator downstream of TLR3 to induce cell death via death receptors and mitochondria.

Toll-like receptor 3 (TLR3), a receptor for viral double strain RNA (dsRNA), mediates anti-viral immune response by activating the innate immunity and cross-priming CD8(+) T cells. TLR3 agonists can directly trigger apoptosis in human cancer cells, and have been used as adjuvants to treat cancer patients with the aim of inducing an IFN-dependent immune response. In this study, we examined the effect of TLR3 activation on the metastasis of nasopharyngeal carcinoma (NPC). We found that NPC cells expressed TLR3 gene transcript and protein. TLR3 activation downregulated the expression of chemokine receptor CXCR4 in a dose-dependent manner, and inhibited cell migration in response to CXCR4 ligand stromal cell-derived factor-1alpha (SDF-1alpha) in chemotaxis assays. Furthermore, TLR3 activation significantly reduced the capacity of NPC cells to form metastasis in draining lymph nodes when injected in athymic mice. The anti-metastasis activity of endogenous human TLR3 expression in cancer cells reveals a novel aspect of the multiple-faced TLR biology, which may open new clinical prospects for using TLR3 agonists to control cancer metastasis in selected cancers.

Objective: To determine the effect of gamma-aminobutyric acid(GABA) on proliferation and malignant phenotypes of hepatocellular carcinoma cell line HepG-2., Methods: HepG-2 cells were cultured by routine method, and then treated with different concentrations of GABA. The proliferation of HepG-2 cells was measured through MTT, doubling time and cell cycles by flow cytometry. The malignant phenotypes were investigated by soft agar colony formation assay., Results: Compared with the control group, GABA efficiently stimulated the proliferation of HepG-2 cells in a dose-dependent manner and affected the distribution of cell cycles of HepG-2 cells. The doubling time of the control group and the GABA-treated group were 39.0, 30.6, 30.0, 27.3, 26.6, and 38.2 h, respectively. The colony formation rates were 3.2%, 4.2%, 5.4%, 6.6%,6.5%, and 3.5%, respectively. Tumorigenicity testing showed that the average weights of tumor was 1.382 g, and 0.285 g for the 2 groups. The difference between the control group and the GABA-treated groups was significant (P<0.01)., Conclusion: GABA can enhance the proliferation and malignant phenotypes of HepG-2 cells.