Deciphering the relationship between the active-site structure and CO 2 methanation mechanism over Ni-based catalysts faces great challenges. Herein, different distributions of frustrated Lewis pair (FLP) structures were precisely fabricated over Ni/ CeO 2 -nanorods, Ni/CeO 2 -nanocubes, and Ni/CeO 2 -nanooctahedra to make progress in this issue. Ni/CeO 2 -nanorods presented the highest possibility for FLP construction among these catalysts due to their CeO 2 (110) nature and the steric hindrance between the oxygen vacancy (O V ) and hydroxyl species (OH). Compared to other samples with fewer FLPs, FLPs-enriched Ni/CeO 2nanorods showed a significantly higher CO 2 conversion (84.2%) and a CH 4 productivity of up to 147.1 mmol g cat −1 h −1 with a higher CH 4 selectivity (97.8%) even at a temperature as low as 225 °C. As evidenced from systematical ex situ and in situ surface analysis results, this better low-temperature activity along with its acceptable stability was closely associated with the construction of catalytically active FLPs, which could effectively activate and convert CO 2 via the cooperation of O V and OH. Also, the in situ (Raman and diffuse-reflectance infrared Fourier transform spectroscopy) analysis combined with density functional theory calculations further demonstrated that the copromotion of the emerged CO* route and formate pathway was responsible for the promising low-temperature (≤225 °C) methanation performance over the FLP-enriched Ni/CeO 2 -nanorods. Such CO 2 activation by FLPs will potentially guide the design of CO 2 hydrogenation catalysts.

aIn this work, poly(lactic acid) and poly(butylene adipate-co-terephthalate) (PLA/PBAT 50/50) were meltblended in the presence of 4,4 0 -methylene diphenyl diisocyanate (MDI) which acted as a reactive chain extender. The mechanical properties, phase morphology, thermal behavior and crystalline structure of the blends were investigated. Fourier transform infrared measurements revealed that some remarkable chemical interaction had taken place between the two polymers and MDI. Upon increasing the content of MDI, the blends showed increased tensile strength and elongation at break. With the addition of 0-2 wt% MDI, the impact strength of PLA/PBAT-MDI blends increased from 7.0 kJ m À2 to 70.0 kJ m À2. A large shift towards each other in terms of the glass transition temperature was observed by DMA and DSC analysis. SEM micrographs showed not only a reduction in the PBAT phase size but also a significant increase in interfacial adhesion between the PLA and PBAT phases with increasing of MDI. Furthermore, the toughening mechanism of the oriented samples was confirmed by wide-angle X-ray diffraction (WAXD) and small-angle X-ray scattering (SAXS) images; it was possible for the smaller crystallites of blends to form during the course of chain extension.

ObjectiveThis study aims to figure out the mechanism of astragaloside IV (AS-IV) in the protection of podocyte apoptosis in diabetic nephropathy (DN) rats.Materials and methodsStreptozotocin (STZ) was used to induce diabetes in rats, and the diabetic rats were treated with 5 mg/kg/d of AS-IV for 12 weeks. Albuminuria level, relative TUG1 and TRAF5 levels, and TRAF5 and cleaved-caspase-3 protein levels were examined by ELISA, quantitative reverse transcription (qRT)-PCR, and Western blot analyses, respectively. The interaction between TUG1 and TRAF5 was confirmed by RNA pull-down and RNA precipitation. TUNEL assay was used to detect podocyte apoptosis.ResultsCompared with control rats, DN rats had higher albuminuria and TRAF5 levels and lower TUG1 level. AS-IV treatment attenuated albuminuria and TRAF5 levels and improved TUG1 level in DN rats. TUG1 was downregulated and TRAF5 was upregulated in high-glucose-treated MPC5 cells, and AS-IV ameliorated the TUG1 level. In addition, TUG1 interacted with TRAF5, and TUG1 overexpression promoted degradation of TRAF5 protein. Besides, AS-IV modulated TRAF5 expression through regulating TUG1. AS-IV decreased podocyte apoptosis via the TUG1/TRAF5 pathway. Finally, in vivo experiment proved that si-TUG1 abrogated the protective effect of AS-IV on DN.ConclusionAS-IV attenuated podocyte apoptosis and protected diabetic rats from DN via the lncRNA-TUG1/TRAF5 pathway.