Boosting electrochemical CO2 reduction via valence state and oxygen vacancy controllable Bi-Sn/CeO2 nanorod.

Electrocatalytic CO2 reduction reaction (CO2RR) to produce formate has been recognized as one of the most efficient strategies to convert CO2 to energy-rich products and store renewable energy compared with other methods such as biological reduction, thermal catalytic reduction, and photocatalytic reduction. Developing an efficient catalyst is crucial to enhance the formate Faradaic efficiency (FEformate) and retard the competing H2 evolution reaction. The combination of Sn and Bi has been demonstrated to be effective in inhibiting the evolution of H2 and the generation of CO, promoting the formation of formate. Herein, we design Bi- and Sn-anchored CeO2 nanorods catalysts with the valence state and oxygen vacancy (Vo) concentration controllable for CO2RR by reduction treatment at different environments. The m-Bi1Sn2Ox/CeO2 with moderate H2 composition reduction and suitable Sn/Bi molar ratio achieves a remarkable FEformate of 87.7% at -1.18 V vs. RHE compared with other catalysts. Additionally, the selectivity of formate was maintained over 20 h with an outstanding FEformate of above 80% in 0.5 M KHCO3 electrolyte. The outstanding CO2RR performance was attributed to the highest surface Sn2+ concentration which improves the formate selectivity. Further, the electron delocalization effect between Bi, Sn, and CeO2 tunes electronic structure and Vo concentration, promoting the CO2 adsorption and activation as well as facilitating the formation of key intermediates HCOO* as evidenced by the in-situ Attenuated Total Reflectance-Fourier Transform Infrared measurements and Density Functional Theory calculations. This work provides an interesting measure for the rational design of efficient CO2RR catalysts via valence state and Vo concentration control.

Semi-industrial scale (30 m3) fed-batch fermentation for the production of D-lactate by Escherichia coli strain HBUT-D15.

D(-)-lactic acid is needed for manufacturing of stereo-complex poly-lactic acid polymer. Large scale D-lactic acid fermentation, however, has yet to be demonstrated. A genetically engineered Escherichia coli strain, HBUT-D, was adaptively evolved in a 15% calcium lactate medium for improved lactate tolerance. The resulting strain, HBUT-D15, was tested at a lab scale (7 L) by fed-batch fermentation with up to 200 g L-1 of glucose, producing 184-191 g L-1 of D-lactic acid, with a volumetric productivity of 4.38 g L-1 h-1, a yield of 92%, and an optical purity of 99.9%. The HBUT-D15 was then evaluated at a semi-industrial scale (30 m3) via fed-batch fermentation with up to 160 g L-1 of glucose, producing 146-150 g L-1 of D-lactic acid, with a volumetric productivity of 3.95-4.29 g L-1 h-1, a yield of 91-94%, and an optical purity of 99.8%. These results are comparable to that of current industrial scale L(+)-lactic acid fermentation.

Ultrasound-guided radiofrequency ablation enhances natural killer-mediated antitumor immunity against liver cancer.

For patients with liver cancer who are not sufficiently fit for surgical resection, radiofrequency ablation (RFA) is an effective and low risk treatment modality; however, the mechanism underlying this procedure is not fully understood. In the present study, a series of experiments were conducted, which demonstrated that RFA therapy stimulates innate antitumor immunity via directly enhancing natural killer (NK) cell cytotoxicity, thus achieving a favorable outcome for patients with liver tumors. It was determined that the percentage of NK cells within the peripheral blood of the rabbits in the RFA treatment groups were significantly higher, compared with the control groups. The levels of interferon-γ and tumor necrosis factor-α in NK cells were also significantly upregulated following thermal coagulation induced via RFA. In addition, RFA enhanced the NK cell receptor, NK group 2D (NKG2D), expression and NK cell antitumor cytotoxicity in hepatic cancer cells. The results indicated that the RFA treatment could effectively eliminate liver tumors via enhancing NK-mediated antitumor activity and NKG2D expression.