Impact of nanoceria shape on degradation of diethyl paraoxon: Synthesis, catalytic mechanism, and water remediation application.

A series of nanomaterials have been demonstrated to be powerful for direct degradation of diethyl paraoxon (EP) to diethyl phosphate and 4-nitrophenol in aqueous solution. However, comparison of catalytic activity of different nanomaterials toward EP is rarely explored. In the present study, four different morphological nanoceria (cubes, rods, polyhedral, and spheres) were synthesized, characterized, and evaluated as a catalyst for the degradation of EP in comparison to other commercially available nanomaterials. Among the tested nanoceria, the cerium dioxide (CeO2) nanopolyhedra possess the best catalytic activity toward the hydrolysis of EP owing to their abundant oxygen vacancy sites, optimal ratio of Ce(III) to Ce(IV), and specific exposed facets. Under the conditions of 0.2 M NH3/NH4Cl buffer and 25 °C, the CeO2 nanopolyhedra catalyzed the reduction of EP to 4-nitrophenol with a >99% conversion at pH 8.0 for 50 h, at pH 10.0 for 12 h, and at pH 12.0 for 2.5 h. The catalytic degradation of nearly 100% EP in NH3/NH4Cl buffer (pH 10.0) at 25 °C is in the decreasing order of CeO2 nanopolyhedra > CeO2 nanorods > ZnO nanospheres (NSs) > CeO2 nanocubes > TiO2 NSs > CeO2 NSs > Fe3O4 NSs ~ Co3O4 NSs ~ control experiment. The mechanism for the degradation of EP was confirmed by monitoring catalytic kinetics of the CeO2 nanopolyhedra in the presence of EP, dimethyl paraoxon, 4-nitrophenyl phosphate, and parathion. The nanocomposites were simply fabricated by electrostatic self-assembly of the CeO2 nanopolyhedra and poly(diallyldimethylammonium chloride)-capped gold nanoparticles (PDDA-AuNPs). The resultant nanocomposites still efficiently catalyzed NaBH4-mediated reduction of 4-nitrophenol to 4-aminophenol with a normalized rate constant of 6.68 ± 0.72 s-1 g-1 and a chemoselectivity of >99%. In confirmation of the robustness and applicability of the as-prepared nanocomposites, they were further used to catalyze the degradation of EP to 4-amionphenol in river water and seawater.

Inhibition of catalytic activity of fibrinogen-stabilized gold nanoparticles via thrombin-induced inclusion of nanoparticle into fibrin: Application for thrombin sensing with more than 104-fold selectivity.

Citrate-capped gold nanoparticles (AuNPs) modified with thrombin-binding aptamer are often implemented for colorimetric, fluorescent, and electrochemical detection of thrombin in an aqueous solution. However, researchers have rarely explored the application of fibrinogen-modified AuNPs (F-AuNPs) for thrombin sensing. We present a simple, inexpensive, sensitive, and selective probe for colorimetric assay of thrombin through combining thrombin-induced inclusion of F-AuNPs into Fibrin and F-AuNPs-catalyzed reduction of 4-nitrophenol with an excess amount of NaBH4. Considering that fibrinogen stabilized citrate-capped AuNPs against a high-ionic-strength buffer, F-AuNPs efficiently catalyzed the NaBH4-mediated decrease of yellow 4-nitrophenol to colorless 4-aminophenol. The presence of thrombin converted fibrinogen into fibrin on the nanoparticle surface, leading to the inclusion of nanoparticles into fibrin. The formation of fibrin inhibited that the AuNPs catalyzed the NaBH4-mediated reduction of 4-nitrophenol. Consequently, the color of the solution gradually varied from colorless to yellow with increasing thrombin concentration. The proposed system was shown to be accurate in the quantification of small differences in the concentration of human thrombin over the range of 4-60 pM. The lowest detectable concentration of human thrombin by the naked eye was as low as 16 pM. We demonstrated the practical application of the proposed system in quantifying 1-15 nM human thrombin in human plasma.

Retrospective analysis of 18 cases of antithyroid drug (ATD)-induced agranulocytosis.

In this study, we retrospectively analyzed 18 patients in whom antithyroid drug (ATD)-induced agranulocytosis developed during treatment of Graves' disease. All patients were more than 20 years of age, and we saw no correlation between age and the development of agranulocytosis. In 17 of 18 patients, ATD-induced agranulocytosis developed within 2 to 12 weeks of starting ATD treatment. Development of agranulocytosis was related to the dose of ATD. In some patients, agranulocytosis developed abruptly, and even weekly routine WBC and granulocyte counts failed to predict all case occurrences. Fever and sore throat were the earliest symptoms of agranulocytosis; patients who developed either of these symptoms were closely monitored immediately with WBC and granulocyte count examinations. In this series of patients, treatment with granulocyte-macrophage colony stimulating factor (GM-CSF) increased the granulocyte counts, whereas the effectiveness of glucocorticoid treatment was not confirmed.