Designing Smart Microcapsules with Natural Polyelectrolytes to Improve Self-Healing Performance for Water-Based Polyurethane Coatings.

Active anticorrosive organic coatings adopting microcapsules (MCs) have lately attracted extensive attention as they were proven to be effective to minimize metal corrosions and offer a long-lasting protection performance. Herein, a novel environmental-friendly active corrosion protection system was designed for aluminum alloy 2024 (AA2024) based on water-based polyurethane coatings with the addition of water and alkaline pH-responsive smart MCs, which is fabricated by utilizing 2-mercaptobenzothiazole (2-MBT) as an inhibitor, halloysite clay nanotubes (HNTs) as an inhibitor carrier, and the natural polyelectrolytes ε-poly-l-lysine (ε-PLL) and sodium alginate (SA) as layer-by-layer (LBL) encapsulation polyelectrolytes. Salt spray tests and electrochemical measurements prove that the scratched coatings with embedded MCs possess an excellent self-healing performance by forming an adsorption layer of released 2-MBT on the AA2024 surface, thereby providing over 90% inhibition efficiency within 6 days' immersion. The UV-vis spectrophotometer results further showed that the release of 2-MBT is a three-stage long-term process sensitive to water and alkaline pH value, while the outward release rate is both regulated by the solubility of 2-MBT and the SA layer. The fabricated MCs not only offer a great promise to provide an excellent self-healing performance but also shed light on the future design of advanced MCs on demand based on the LBL technique.

The long non-coding RNA LINC00473 contributes to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer.

Prostate cancer is a kind of male malignant tumor, which has brought tremendous health threat to men. Prostate cancer is difficult to be cured because of high incidence and metastasis rate. Thereby, it is of great urgency to elucidate the underlying molecular mechanism of prostate cancer for the treatment of this cancer. LINC00473 dysregulation has been observed in many cancers. However, the role of LINC00473 was unknown in prostate cancer. In the present study, we discovered that prostate cancer cells presented high expression of LINC00473, and LINC00473 inhibition limited cell proliferation and the expression of proteins in JAK-STAT3 signaling pathway. Additionally, LINC00473 acted as an up-stream factor for miR-195-5p to negatively modulate miR-195-5p expression. Moreover, SEPT2 interacted with miR-195-5p in prostate cancer and SEPT2 expression was positively modulated by LINC00473 and negatively regulated by miR-195-5p. Last, the inhibitory effect of LINC00473 knockdown on cell proliferation and expression of proteins of JAK-STAT3 signaling pathway was restored by SEPT2 overexpression. All in all, LINC00473 contributed to cell proliferation via JAK-STAT3 signaling pathway by regulating miR-195-5p/SEPT2 axis in prostate cancer, which provided a novel therapeutic tactic for prostate cancer patients.