A Core-Shell-Structured Silver Nanowire/Nitrogen-Doped Carbon Catalyst for Enhanced and Multifunctional Electrofixation of CO2.

Numerous catalysts have been successfully introduced for CO2 fixation in aqueous or organic systems. However, a single catalyst showing activity in both solvent types is still rare, to the best of our knowledge. We developed a core-shell-structured AgNW/NC700 composite using a Ag nanowire (NW) core encapsulated by a N-doped carbon (NC) shell at 700 °C. Through control experiments and density functional theory calculations, it was confirmed that Ag nanowires acted as the active sites for CO2 fixation and the uniformly coating of N-doped carbon created a CO2 -rich environment around the Ag nanowires, which could significantly improve the catalytic activity of Ag nanowires for electrochemical CO2 fixation. Under mild conditions, up to 96 % faradaic efficiency of CO, 95 % yield of Ibuprofen and 92 % yield of propylene carbonate could be obtained in the electrochemical CO2 direct reduction, carboxylation and cycloaddition, respectively, using the same AgNWs/NC700 catalyst. These results might provide an alternative strategy for efficient electrochemical fixation of CO2 .

Platinum/nitrogen-doped carbon/carbon cloth: a bifunctional catalyst for the electrochemical reduction and carboxylation of CO2 with excellent efficiency.

A novel Pt-NP@NCNF@CC composite was prepared by the electrospinning technique. It is a highly efficient and binder-free catalyst for the direct reduction and carboxylation of CO2 with halides. Formate with 91% Faradaic efficiency and 2-phenylpropionic acid with 99% yield could be obtained, respectively. Moreover, this catalyst has excellent stability and reusability.

Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF-κB, PPAR-γ and Bcl-2 in rats with myocardial infarction injury.

Curcumin is a natural polyphenol with powerful antioxidant and anti-inflammatory properties. The present study evaluated the protective effect of curcumin on myocardial injury in rats as well as the mechanisms underlying these effects, and examined the expression of nuclear factor-κB (NF-κB), peroxisome proliferator-activated receptor-γ (PPAR-γ) and B-cell leukemia/lymphoma-2 (Bcl-2) following myocardial infarction. A rat model of myocardial infarction was successfully established. Hematoxylin and eosin staining showed cellular atrophy and hyperchromatic cytoplasm in the myocardial infarction area. The myocardial cells displayed lysis and breakage of cardiac muscle fibers, karyopyknosis and karyorrhexis associated with infiltration of inflammatory cells and proliferation of fibrous tissue. Curcumin treatment at a dosage of 150 mg/kg/body weight resulted in an increase in surviving cells, fewer apoptotic cells, decreased proliferation of fibrous tissue and reduced infiltration of inflammatory cells, though necrosis was still present compared with the rats without curcumin treatment. The immunohistochemical assay demonstrated that curcumin treatment inhibited the expression of NF-κB, but increased the expression of PPAR-γ. The results of the reverse transcription-polymerase chain reaction indicated that curcumin treatment significantly increased the mRNA expression levels of Bcl-2 (P<0.01). Therefore, curcumin antagonizes cardiomyocyte apoptosis and inhibits inflammatory cell infiltration following myocardial infarction, which may be associated with its inhibitory effects on the expression of NF-κB, and activating effects on the expression of PPAR-γ and Bcl-2 in myocardial cells. Curcumin may be useful in clinical practice for saving more living heart muscle in the area of myocardial infarction and improving cardiac function following the elective opening of obstructed coronary arteries.

Expression of Kin17 promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

Kin17 protein is ubiquitously expressed in mammals and is correlated with vital biological functions. However, little is known about the role of Kin17 in the proliferation of hepatocellular carcinoma cells. The aim of the present study was to investigate whether the upregulation of Kin17 can promote the growth of hepatocellular carcinoma cells. A series of assays was performed to study the effect of Kin17 in the proliferation of hepatocellular carcinoma cells in vitro and in vivo. The western blotting results revealed that Kin17 expression was increased in hepatocellular carcinoma tissues compared with that of the corresponding normal tissues. Moreover, ectopic upregulation of Kin17 expression promoted the growth of hepatocellular carcinoma cells in vitro and in vivo. These results indicated that Kin17 is involved in the tumorigenesis of hepatocellular carcinoma, and that Kin17 has the potential to serve as a therapeutic target for hepatocellular carcinoma.