Work-Function-Tunable Electron Transport Layer of Molecule-Capped Metal Oxide for a High-Efficiency and Stable p-i-n Perovskite Solar Cell.

The composite electron transporting layer (ETL) of metal oxide with [6,6]-phenyl-C61-butyric acid methyl ester (PCBM) prevents perovskite from metal electrode erosion and increases p-i-n perovskite solar cell (PVSC) stability. Although the oxide exhibits protective function, an additional work function modifier is still needed for good device performance. Usually, complicated multistep synthesis is employed to have a highly crystalline film that increases manufacturing cost and inhibits scalability. We report a facile synthesis of a novel organic-molecule-capped metal oxide nanoparticle film for the composite ETL. The nanoparticle film not only has a dual function of electron transport and protection but also exhibits work function tunability. Solvothermal-prepared SnO2 nanoparticles are capped with tetrabutylammonium hydroxide (TBAOH) through ligand exchange. The resulting TBAOH-SnO2 nanoparticles disperse well in ethanol and form a uniform film on PCBM. The power conversion efficiency of the device dramatically increases from 14.91 to 18.77% using this layer because of reduced charge accumulation and aligned band structure. The PVSC thermal stability is significantly enhanced by adopting this layer, which prevents migration of I- and Ag. The ligand exchange method extends to other metal oxides, such as TiO2, ITO, and CeO2, demonstrating its broad applicability. These results provide a cornerstone for large-scale manufacture of high-performance and stable PVSCs.

Enterovirus 71 virion-associated galectin-1 facilitates viral replication and stability.

Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal brain stem encephalitis complicated with pulmonary edema. Several severe EV71 endemics have occurred in Asia-Pacific region, including Taiwan, and have become a serious threat to children's health. EV71 infection is initiated by the attachment of the virion to the target cell surface. Although this process relies primarily upon interaction between viruses and cell surface receptors, soluble factors may also influence the binding of EV71 to host cells. Galectin-1 has been reported to participate in several virus infections, but is not addressed in EV71. In this study, we found that the serum levels of galectin-1 in EV71-infected children were higher than those in non-infected people. In EV71 infected cells, galectin-1 was found to be associated with the EV71 VP1 and VP3 via carbohydrate residues and subsequently released and bound to another cell surface along with the virus. EV71 propagated from galectin-1 knockdown SK-N-SH cells exhibited lower infectivity in cultured cells and less pathogenicity in mice than the virus propagated from parental cells. In addition, this galectin-1-free EV71 virus was sensitive to high temperature and lost its viability after long-term storage, which could be restored following supplement of recombinant galectin-1. Taken together, our findings uncover a new role of galectin-1 in facilitating EV71 virus infection.

Targeting NFKB by autophagy to polarize hepatoma-associated macrophage differentiation.

Tumor-associated macrophages (TAMs) have been linked to promoting tumor progression by stimulating angiogenesis, cell growth and inflammation. NFKB activity in TAMs may mediate inflammation-associated tumor formation. However, most isolated TAMs from established tumors express a M2 phenotype with less NFKB activation and show a strong immunosuppressive phenomenon. How tumors affect the dynamic of NFKB activity in TAMs, and hence maintain their pro-tumor M2 phenotype is still poorly understood. We recently found that hepatoma-derived toll-like receptor 2 (TLR2)-related ligands are capable of stimulating M2 macrophage differentiation via controlling NFKB RELA/p65 protein homeostasis by selective autophagy. TLR2 signal induces NFKB RELA cytosolic ubiquitination and leads to its degradation by SQSTM1/p62-mediated autophagy. Inhibition of autophagy will rescue NFKB activity and shape the phenotype of hepatoma-polarized M2 macrophages. This suggests that autophagy might play a role in manipulating TAM functions and tumor-associated immune responses. Our study also demonstrates that autophagy can directly control a transcriptional factor in addition to its regulatory molecules. This finding uncovers a new role of autophagy in controlling cellular functions.