Polymers via Reversible Addition-Fragmentation Chain Transfer Polymerization with High Thiol End-Group Fidelity for Effective Grafting-To Gold Nanoparticles.

End-group fidelity is the most important property for end-functional polymers. Compared to other controlled living polymerization methods, reversible addition-fragmentation chain transfer (RAFT) polymerization often yields polymers with a lower end-group fidelity, which greatly affects their applications. Herein, we report a staged-thermal-initiation RAFT polymerization for the synthesis of polymers with high thiol end-group fidelity and their high efficiencies for grafting to various gold nanoparticles (GNPs). We experimentally prove that the decrease of end-group fidelity with their molecular weight is caused by the gradual decomposition of the initiator rather than the degradation of chain-transfer agents. We show that the staged-thermal-initiation RAFT polymerization is more effective for synthesis of polymers with high thiol end-group fidelity. The grafting-to assays for various GNPs illustrate the positive correlation between the end-group fidelity of polymers and grafting-to efficiency. This work highlights the prospects for synthesis of high end-group fidelity polymers and their application in the preparation of nanoparticles-polymer hybrid materials.

Infectivity of Zika virus on primary cells support tree shrew as animal model.

Zika virus (ZIKV) is a mosquito-borne flavivirus that caused the public health emergency. Recently, we have proved a novel small animal tree shrew was susceptive to ZIKV infection and presented the most common rash symptoms as ZIKV patients. Here we further cultured the primary cells from different tissues of this animal to determine the tissue tropism of ZIKV infection in vitro. The results showed that the primary cells from tree shrew kidney, lung, liver, skin and aorta were permissive to ZIKV infection and could support viral replication by the detection of viral specific RNA intra- and extra-cells. In comparing, the skin fibroblast and vascular endothelial cells were highly permissive to ZIKV infection with high releasing of active virus particles in supernatants proved by its infectivity in established neonatal mouse model. The expressions of ZIKV envelop and nonstructural protein-1, and the effects and strong immune response of primary tree shrew cells were also detected followed by ZIKV infection. These findings provide powerful in vitro cell-level evidence to support tree shrew as animal model of ZIKV infection and may help to explain the rash manifestations in vivo.

Cinobufacin suppresses cell proliferation via miR-494 in BGC- 823 gastric cancer cells.

Cinobufacin is used clinically to treat patients with many solid malignant tumors. However, the mechanisms underlying action remain to be detailed. Our study focused on miRNAs involved in cinobufacin inhibition of GC cell proliferation. miRNA microarray analysis and real time PCR identified miR-494 as a significant cinobufacin- associated miRNA. In vivo, ectopic expression of miR-494 inhibited the proliferation and induced apoptosis of BGC-823 cells on CCK-8 and flow cytometry analysis. Further study verified BAG-1 (anti-apoptosis gene) to bea target of miR-494 by luciferase reporter assay and Western blotting. In summary, our study demonstrated that cinobufacin may inhibit the proliferation and promote the apoptosis of BGC-823 cells. Cinobufacin-associated miR-494 may indirectly be involved in cell proliferation and apoptosis by targeting BAG-1, pointing to use as a potential molecular target of cinobufacin in gastric cancer therapy.

Hsa-miR-181a-5p expression and effects on cell proliferation in gastric cancer.

PURPOSE: MicroRNAs (miRNAs) are small endogenous, non-coding, single-stranded RNAs (approximately 22 nt). Accumulating evidence has shown that aberrant miRNA expression is pronounced and correlated with gastric cancer genesis and progression. MATERIALS AND METHODS: Expression levels of miR-181a-5p in GC tissues and cell lines were assessed by qRT-PCR and tested for correlation with clinical features. In addition, effects of miR-181a-5p on GC cell growth were investigated. RESULTS: Our findings indicate that miR-181a-5p is upregulated in GC, in correlation with lymph node invasion, nerve invasion and vascular invasion (P<0.05). Enforced expression of miR-181a -5p promoted cell proliferation ability. CONCLUSIONS: This study suggested that increased miR-181a-5p is related to GC progression. MiR-181a-5p may represent a potential therapeutic target for GC.