National Natural Science Foundation of China.

The preliminary results demonstrate good flexibility and efficacy of the Willis covered stent in the treatment of DICA aneurysms in selected patients; longer follow-up and expanded clinical trials are needed.

Quantum dots (QDs) have been widely used as fluorescent probes in cell-targeted imaging. However, nonspecific binding to cellular membranes has been a major challenge. In this study, a new approach is developed for effective reduction of nonspecific binding by bovine serum albumin (BSA)-coated QDs in cell targeting. The experimental results show efficient transfer of hydrophobic QDs from organic to aqueous phase in the presence of BSA aqueous solution under ultrasonication. This ultrasonication-based approach is facile, rapid, and efficient. Stabilization of QDs is mainly achieved by multiple mercapto groups in BSA macromolecules as multidentate ligands and partially by hydrophobic interaction between BSA and pending fatty ligands on QDs. The water solubility of QDs is enhanced by the surface amino and carboxyl groups, which also provide reaction sites for conjugation of targeting ligands. The BSA-coated QDs, with an overwhelming majority of hydrodynamic diameter size of ca. 18 nm, are colloidally stable under both acidic and basic conditions and found to exhibit strong fluorescent intensities. The nonspecific cellular binding is effectively reduced by BSA-coated QDs, compared with the mercaptopropionic acid (MPA)-coated CdTe QDs. BSA-coated QDs are further functionalized with cyclic Arg-Gly-Asp (cRGD) peptide. The cell assays indicate their high target-selectivity in integrin α(v)β(3)-expressed cell imaging.

Epithelial–mesenchymal transition (EMT) and Notch signaling are important for the growth and invasion of pancreatic cancer, which is a leading cause of cancer-related deaths worldwide. miR-34a has been shown to play pivotal roles in the progression of several types of cancer. However, little is known about the regulatory mechanisms of miR-34a in pancreatic cancer processes. The aim of this study was to determine whether miR-34a has negative effects on pancreatic cancer and whether these effects are related to EMT and Notch signaling. In vitro, we demonstrated that miR-34a inhibited, while miR-34a inhibitors enhanced, migration and invasion of pancreatic cancer cell lines (PANC-1 and SW-1990).These effects were reversed by Snail1 overexpression or Snail1 shRNA. Furthermore, the anti-apoptotic effects of the miR-34a inhibitors in pancreatic cancer cells were abrogated by Notch1 shRNA. Luciferase reporter assays revealed that the Snail1 and Notch1 genes were direct targets of miR-34a. In vivo, we also demonstrated that miR-34a inhibited pancreatic cancer growth by decreasing Snail1 and Notch1 expression. Therefore, our results indicate that miR-34a inhibits pancreatic cancer progression by post-transcriptionally regulating Snail1 and Notch1 expression.