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Periodic mesoporous organosilica (PMO) supported ionic liquids with high catalytic ability were prepared and tested in synthesis of 2‐oxazolidinones from the three‐component cycloaddition reactions of CO2, aryl amines and epoxide. The functionalized PMO material PMO@TZ‐ILSmCl4 revealed the most excellent catalytic performance than PMO@TZ‐ILLaCl4 during the catalytic synthesis of 2‐oxazolidinones. Different parameters such as catalyst loading, temperature, CO2 pressure and reaction time were also investigated. Good to excellent yields for 2‐oxazolidinones and stable reusability were reached in the CO2 cycloaddition under solvent‐ /ligand‐free conditions. This work provides a useful route to design novel and highly efficient catalytic systems for the transformation of CO2 into other valuable 2‐oxazolidinones. [ABSTRACT FROM AUTHOR]

A new methodology for the highly efficient and atom‐economic oxidation of alcohols and benzylic compounds to the corresponding aldehydes and ketones with environmental‐friendly hydrogen peroxide using a magnetic MOF nanocatalyst has been developed. We demonstrated that the resulting magnetic nanocomposite CoFe2O4@SiO2@MIL‐53(Fe) can show excellent catalytic performances in the highly selective oxidation at room temperature, based on a synergetic effect between iron sites and CoFe2O4@SiO2. The nanocatalyst offers simple operation for recovery and the recycling test showed that it could be reused for successive runs without significant degradation in catalytic activity. [ABSTRACT FROM AUTHOR]

Acute-phase inflammation plays a critical role in liver graft injury. Inflammasomes, multi-molecular complexes in the cytoplasm, are responsible for initiating inflammation. Here, we aimed to explore the role of inflammasomes in liver graft injury and further to investigate the regulatory mechanism. In a clinical liver transplant cohort, we found that intragraft expression of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 ( NLRP3) inflammasomes was significantly up-regulated post-transplantation. Importantly, overexpression of NLRP3 was strongly associated with poor liver function characterized by high levels of ALT, AST, and urea, as well as neutrophil infiltration after transplantation. The significant correlation between NLRP3 and IL-1β mRNA levels led us to focus on one of the associated upstream regulators, telomere-independent repressor activator protein 1 ( RAP1), which was further proved to be co-localized with NLRP3 in neutrophils. In the liver of a mouse model (hepatic ischaemia/reperfusion and hepatectomy model) and isolated neutrophils from RAP1−/− mice, the expression levels of NLRP3 and keratinocyte chemoattractant ( KC) were significantly down-regulated in contrast to those in wild types. The levels of ALT and AST, as well as the neutrophil infiltration, were also decreased by RAP1 deficiency. In our clinical validation, intragraft KC expression was associated with NLRP3 and co-localized with RAP1 in neutrophils. Furthermore, NLRP3 inflammasomes were up-regulated by recombinant KC in the isolated neutrophils and liver of the mouse model. Our data demonstrated that NLRP3 inflammasomes, activated by the RAP1/ KC axis, played a critical role in initiating inflammation during the early stage of liver graft injury. Targeting RAP1/ KC/ NLRP3 inflammasomes may offer a new therapeutic strategy against liver graft injury. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

The effects of radiation on the Ca2+ signaling system in HSY cells transfected with the Bcl‐2 or Bcl‐XL gene were studied. Bcl‐2 overexpression did not alter carbachol (CCh)‐elicited initial increase in cytosolic free Ca2+ concentrations ([Ca2+]i), but Bcl‐XL overexpression dramatically reduced this response. Exposure to 10 Gy γ‐ray did not alter basal [Ca2+]i. By contrast, the CCh‐stimulated initial [Ca2+]i increase was reduced at 0.5 and 4 h post‐irradiation in all cell types and remained decreased at 24 h in wild‐type and control‐transfected cells, but recovered in Bcl‐2‐ and Bcl‐XL‐transfectants. The formation of inositol 1,4,5‐trisphosphate (IP3) in response to CCh at 4‐h post‐irradiation was decreased in wild‐type and control‐transfected cells, but not in Bcl‐2 and Bcl‐XL transfectants. The capacity of the IP3‐sensitive Ca2+ store was significantly reduced by radiation in all cells except Bcl‐XL transfectants. Ca2+ influx after stimulation with CCh was suppressed by exposure to radiation in wild‐type and control‐transfected cells, but not in Bcl‐2‐ and Bcl‐XL‐transfectants. However, radiation enhanced Ca2+ influx activated by thapsigargin in all cell types. These results suggest that 1) radiation diminishes IP3 formation and Ca2+release in response to CCh, but potentiates the store‐operated Ca2+ influx; and 2) overexpression of Bcl‐2 or Bcl‐XL partially protects cells from radiation‐induced inhibition of Ca2+ signaling. [ABSTRACT FROM AUTHOR]