The low-temperature NO2 removal by tailoring metal node in porphyrin-based metal-organic frameworks.

Nitrogen dioxide (NO2) is the most toxic and prevalent form of nitrogen oxides (NOx) pollutant and its removal from ambient air is a pressing challenge. The state-of-the-art deNOx technologies such as selective catalytic reduction (SCR) can only work at elevated temperatures (>250-300 °C), but ineffective for the NOx removal under ambient conditions. The adsorptive removal of NO2 is an alternative approach to SCR, whose success depends on the design of stable adsorbents capable of selectively capturing NO2 with a highly reversible capacity. Here we synthesized and developed five porphyrin-based metal-organic frameworks (PMOFs) as robust ambient NO2 adsorbents, including three aluminum-based (Al-PMOF) isostructures, and two zirconium-based (Zr-PMOFs) isostructures. Of them, Al-PMOF stands out to be the most promising candidate by showing the highest NO2 adsorption capacity (1.85 mmol/g), high stability, and good regenerability (retaining 87% capacity after five cycles of adsorption) at dry conditions. The NO2 adsorption capacity of Al-PMOF was approximately doubled (3.61 mmol/g) at wet conditions. In situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) revealed the NO2 adsorption mechanism - the hydrogen bonding occurs between bridging hydroxyl (-OH) (attached to the metal node) and NO2 molecules. Our work demonstrates that PMOFs are promising NO2 adsorbents and will provide guidance for designing robust and reusable adsorbents for efficiently removing NO2 at ambient temperature.

Enhancing levoglucosan production from waste biomass pyrolysis by Fenton pretreatment.

Levoglucosan is served as a significant versatile product to generate high value-added chemicals and pharmaceutical additives. Levoglucosan was predominately produced from pyrolysate of cellulose. However, the direct fast pyrolysis of waste biomass produces a small quantity of levoglucosan in comparison with the theoretical value of cellulose. This study explored Fenton pretreatment as a possible route to enhance levoglucosan yield during the fast pyrolysis of the waste corncob. The experimental results showed that different Fenton pretreated conditions and pyrolytic temperatures played vital roles in the formation of levoglucosan. The levoglucosan yield from fast pyrolysis at 500 °C of corncob pretreated by Fenton reaction of 14 mL/g H2O2 and 16 mM FeSO4 was about 95% higher than that of the untreated corncob. Additionally, Fenton pretreated corncob was capable of obtaining the levoglucosan at a low pyrolytic temperature (300 °C). It was mainly attributed to the effective disrupting of biomass structures and the selective degradation of lignin and hemicellulose during pretreatment. Furthermore, the powerful removal of alkali and alkaline earth metals during Fenton pretreatment was beneficial to increasing the levoglucosan yield. These findings demonstrate that Fenton pretreatment can provide a novel effective method to enhance levoglucosan yield during biomass fast pyrolysis.

Atorvastatin reduces alcohol-induced endoplasmic reticulum stress in AC16 cardiomyocytes.

OBJECTIVES: To investigate the effects of atorvastatin on the ultrastructure and lipid metabolism of AC16 cardiomyocytes in response to alcohol-induced endoplasmic reticulum stress (ERS). DESIGN: The expression of the ERS-related factor GRP78 in the established ERS model was determined by western blotting. Alcohol-exposed cardiomyocytes were treated with various concentrations of atorvastatin, and GRP78 expression was measured. Cardiomyocyte ultrastructure was observed and SREBP-1c and triglyceride (TG) levels were evaluated. RESULTS: Exposure to ethanol for 0, 12, 24, and 48 h significantly affected GRP78 expression (0.19 ± 0.02, 0.27 ± 0.03, 0.39 ± 0.01, and 0.64 ± 0.02, respectively). GRP78 expression in the 1, 10, and 100 µmol L-1 atorvastatin-treated groups was 0.50 ± 0.04, 0.38 ± 0.03, and 0.24 ± 0.01, respectively, and significantly different from control group expression (0.19 ± 0.02); the expression in the alcohol group was 0.64 ± 0.02. Alcohol-treated AC16 cells had significantly larger and fewer mitochondria and disorganized cristae, often replaced by vacuoles. These aberrations decreased with increasing atorvastatin concentrations. SREBP-1c expression also differed significantly among all atorvastatin-treated and control groups (0.47 ± 0.04, 0.39 ± 0.03, and 0.31 ± 0.02; normal 0.25 ± 0.02; alcohol 0.56 ± 0.03). TG expression differed significantly between the 10 and 100 µmol L-1 groups (26.84 ± 1.63, 23.11 ± 2.05) and the alcohol group (36.35 ± 2.41). CONCLUSIONS: Atorvastatin inhibited the expression of the ERS-related factor GRP78 in response to alcohol exposure, improved cell morphology, and enhanced lipid metabolism in a cellular model of alcoholic cardiomyopathy.