Luminescent Liquid Crystals Based on Carbonized Polymer Dots and Their Polarized Luminescence Application.

Traditional luminescent liquid crystals (LLCs) suffer from fluorescence quenching caused by aggregation, which greatly limits their further application. In this work, a kind of novel LLCs (named carbonized polymer dot liquid crystals (CPD-LCs)) are designed and successfully synthesized through grafting the rod-shaped liquid crystal (LC) molecules of 4'-cyano-4-(4″-bromohexyloxy) biphenyl on the surface of CPDs. The peripheral LC molecules not only increase the distance between different CPDs to prevent them from aggregating and reduce intermolecular energy resonance transfer but also make this LLC have an ordered arrangement. Thus, the obtained CPD-LCs show good LC property and excellent high luminous efficiency with an absolute photoluminescence quantum yield of 14.52% in the aggregated state. Furthermore, this kind of CPD-LC is used to fabricate linearly polarized devices. The resultant linearly polarized dichroic ratio (N) and polarization ratio (ρ) are 2.59 and 0.44, respectively. Clearly, this type of CPD-LC shows promising applications for optical devices.

Association between COX-2 -1195G>A polymorphism and gastrointestinal cancer risk: A meta-analysis.

AIM: To perform a meta-analysis to investigate the association between cyclooxygenase-2 (COX-2) -1195G>A gene polymorphism and gastrointestinal cancers. METHODS: Publications related to the COX-2 -1195G>A gene polymorphism and gastrointestinal cancers published before July 2016 were retrieved from PubMed, EMBASE, Web of Science, China Biological Medicine Database, China National Knowledge Infrastructure, and CQVIP Database. Meta-analysis was performed using Stata11.0 software. The strength of the association was evaluated by calculating the combined odds ratios (ORs) and the corresponding 95%CIs. The retrieved publications were excluded or included one by one for sensitivity analysis. In addition, the funnel plot, Begg's rank correlation test, and Egger's linear regression method were applied to analyse whether the included publications had publication bias. RESULTS: A total of 24 publications related to the COX-2 -1195G>A gene polymorphism were included, including 28 studies involving 11043 cases and 18008 controls. The meta-analysis results showed that the COX-2 -1195G>A gene polymorphism significantly correlated with an increased risk of gastrointestinal cancers, particularly gastric cancer (A vs G: OR = 1.35; AA/AG vs GG: OR = 1.54; AA vs GG/AG: OR = 1.43; AA vs GG: OR = 1.80; AG vs GG: OR = 1.35). Compared to the Caucasian population in America and Europe, the COX-2 -1195G>A gene polymorphism in the Asian population (A vs G: OR = 1.30; AA/AG vs GG: OR = 1.50; AA vs GG/AG: OR = 1.35; AA vs GG: OR = 1.71; AG vs GG: OR = 1.37) significantly increased gastrointestinal cancer risk. The sensitivity analysis (P < 0.05) and the false positive report probability (P < 0.2) confirmed the reliability of the results. CONCLUSION: The results showed that the COX-2 -1195G>A gene polymorphism might be a potential risk factor for gastrointestinal cancers. Further validation by a large homogeneous study is warranted.

ATG4A promotes tumor metastasis by inducing the epithelial-mesenchymal transition and stem-like properties in gastric cells.

The metastasis of tumor cells to distant organs is an ominous feature of gastric cancer. However, the molecular mechanisms underlying the invasion and metastasis of gastric cancer cells remain elusive. In this study, we found that the expression of ATG4A, an autophagy-regulating molecule, was significantly increased in gastric cancer tissues and was significantlycorrelated with the gastric cancer differentiation degree, tumor invasion and lymph node metastasis. ATG4A over-expression significantly promoted gastric cancer cell migration and invasion in vitro and metastasis in vivo, as well as promoted gastric cancer cell stem-like properties and the epithelial-mesenchymal transition (EMT) phenotype. By contrast, ATG4A knockdown inhibited the migration, invasion and metastasis of cancer cells, as well as the stem-like properties and EMT phenotype. Mechanistically, ATG4A promotes gastric cancer cell stem-like properties and the EMT phenotype through the activation of Notch signaling not via autophagy, and using the Notch signaling inhibitor DAPT attenuated the effects of ATG4A on gastric cancer cells. Taken together, these findings demonstrated that ATG4A promotes the metastasis of gastric cancer cells via the Notch signaling pathway, which is an autophagy-independent mechanism.

Increased chemokine receptor IL-17RA expression is associated with poor survival in gastric cancer patients.

BACKGROUND: Previous researchers have identified that the chemokine interleukin-17 (IL-17) was associated with survival time of patients with gastric cancer, but the roles of its receptors (IL-17R) in gastric cancer remain unknown. Our studies were designed to clarify the function of IL-17RA and to explore their potential role in gastric cancer. MATERIALS AND METHODS: The expression of IL-17RA was determined in primary gastric cancer tissues (n=101) using Real-time RT-PCR, immunohistochemistry, and western blotting. To investigate the functional significance of IL-17RA expression, IL-17RA expression and clinical parameters, multivariate survival was analyzed in patients with gastric cancer. RESULTS: IL-17RA was overexpression in gastric cancer tissues compared with adjacent normal tissues (P<0.05). The elevated expression level of IL-17RA was observed correlated significantly with tumor progression (P=0.003), Lymphatic invasion (P=0.019), lymphoid nodal status (P=0.001), distant metastasis (P<0.001) of gastric cancer patients, TNM stage (P=0.0013) and was one of the independent prognostic factors for patient's overall survival. CONCLUSIONS: These results demonstrated that the expression of IL-17RA plays an important role in gastric cancer progression, migration and prognosis of gastric cancer. The IL-17-IL-17RA signaling mechanism may be a potential novel target.

A meta-analysis: The association between interleukin-17 pathway gene polymorphism and gastrointestinal diseases.

BACKGROUND: A number of studies have been conducted to investigate associations between genetic polymorphisms in interleukin-17 (IL-17) pathway and the risk of gastrointestinal diseases. Results, however, have been inconclusive. We aimed to evaluate these associations through a meta-analysis. METHODS: We searched electronic databases (PubMed, Embase, Web of Science, CBM and CNKI) to identify papers, published before October 2014, on associations between polymorphisms in the IL-17 pathway genes (rs2275913, rs763780, rs3748067, rs3819025, rs9382084, rs12203582 and rs8193036) and the risk of gastrointestinal diseases. We estimated the strength of candidate associations through calculating pooled odds ratios (ORs) and 95% confidence intervals (CIs). A test of heterogeneity, a false-positive report probability (FPRP) test, sensitivity analyses and examination for bias were further conducted to evaluate cumulative evidence of these associations. RESULTS: We identified 25 eligible case-control studies retrieved from 16 articles involved in a total of 4507 cases and 5733 controls. Of them, IL-17 (-197G/A) polymorphism (rs2275913) was statistically significantly associated with risk of gastrointestinal diseases, especially for gastrointestinal malignancy and gastroduodenal diseases. Based on heterogeneity (P<0.05) and FPRP (P<0.2) identified in this study, we graded cumulative epidemiological evidence of an association with gastrointestinal diseases for this polymorphism. However, IL-17 (7488T/C) polymorphism (rs763780) did not show significant associations with gastrointestinal diseases either individually or overall (P>0.05). CONCLUSION: Our study provides moderate evidence that IL-17 (-197G/A) polymorphism may be a potential risk factor for gastrointestinal diseases, particularly for malignancy. Further validation of this association in a large homogeneous study is warranted.