Anion Modulation of Ag-Imidazole Cuboctahedral Cage Microenvironments for Efficient Electrocatalytic CO2 Reduction.

How to achieve CO2 electroreduction in high efficiency is a current challenge with the mechanism not well understood yet. The metal-organic cages with multiple metal sites, tunable active centers, and well-defined microenvironments may provide a promising catalyst model. Here, we report self-assembly of Ag4L4 type cuboctahedral cages from coordination dynamic Ag+ ion and triangular imidazolyl ligand 1,3,5-tris(1-benzylbenzimidazol-2-yl) benzene (Ag-MOC-X, X= NO3, ClO4, BF4) via anion template effect. Notably, Ag-MOC-NO3 achieves the highest CO faradaic efficiency in pH-universal electrolytes of 86.1%(acidic), 94.1%(neutral) and 95.3% (alkaline), much higher than those of Ag-MOC-ClO4 and Ag-MOC-BF4 with just different counter anions. In situ attenuated total reflection Fourier transform infrared spectroscopy observes formation of vital intermediate *COOH for CO2-to-CO conversion. The density functional theory calculations suggest that the adsorption of CO2 on unsaturated Ag-site is stabilized by C-H⋅⋅⋅O hydrogen-bonding of CO2 in a microenvironment surrounded by three benzimidazole rings, and the activation of CO2 is dependent on the coordination dynamics of Ag-centers modulated by the hosted anions through Ag⋅⋅⋅X interactions. This work offers a supramolecular electrocatalytic strategy based on Ag-coordination geometry and host-guest interaction regulation of MOCs as high-efficient electrocatalysts for CO2 reduction to CO which is a key intermediate in chemical industry process.

Corrigendum to "Controlled Release of Interleukin-1 Receptor Antagonist from Hyaluronic Acid-Chitosan Microspheres Attenuates Interleukin-1ß-Induced Inflammation and Apoptosis in Chondrocytes".

[This corrects the article DOI: 10.1155/2016/6290957.].

Controlled Release of Interleukin-1 Receptor Antagonist from Hyaluronic Acid-Chitosan Microspheres Attenuates Interleukin-1ß-Induced Inflammation and Apoptosis in Chondrocytes.

This paper investigates the protective effect of interleukin-1 receptor antagonist (IL-1Ra) released from hyaluronic acid chitosan (HA-CS) microspheres in a controlled manner on IL-1ß-induced inflammation and apoptosis in chondrocytes. The IL-1Ra release kinetics was characterized by an initial burst release, which was reduced to a linear release over eight days. Chondrocytes were stimulated with 10 ng/ml IL-1ß and subsequently incubated with HA-CS-IL-1Ra microspheres. The cell viability was decreased by IL-1ß, which was attenuated by HA-CS-IL-1Ra microspheres as indicated by an MTT assay. ELISA showed that HA-CS-IL-1Ra microspheres inhibited IL-1ß-induced inflammation by attenuating increases in NO2- and prostaglandin E2 levels as well as increase in glycosaminoglycan release. A terminal deoxyribonucleotide transferase deoxyuridine triphosphate nick-end labeling assay revealed that the IL-1ß-induced chondrocyte apoptosis was decreased by HA-CS-IL-1Ra microspheres. Moreover, HA-CS-IL-1Ra microspheres blocked IL-1ß-induced chondrocyte apoptosis by increasing B-cell lymphoma 2 (Bcl-2) and decreasing Bcl-2-associated X protein and caspase-3 expressions at mRNA and protein levels, as indicated by reverse-transcription quantitative polymerase chain reaction and western blot analysis, respectively. The results of the present study indicated that HA-CS-IL-1Ra microspheres as a controlled release system of IL-1Ra possess potential anti-inflammatory and antiapoptotic properties in rat chondrocytes due to their ability to regulate inflammatory factors and apoptosis associated genes.