Surface Composition and Lattice Ordering-Controlled Activity and Durability of CuPt Electrocatalysts for Oxygen Reduction Reaction

We report the enhanced activity and stability of CuPt bimetallic tubular electrocatalysts through potential cycling in acidic electrolyte. A series of CuPt tubular electrocatalysts with sequential increased lattice ordering and surface atomic fraction of Pt were designed and synthesized by thermal annealing to reveal their improved electrocatalytic properties. These low-Pt-content electrocatalysts with Pt shell are formed through the thermal annealing and following potential cycling treatment. The catalysts (C1) with a low atomic fraction of Pt on the surface and low lattice ordering in the bulk are treated in acidic electrolyte, resulting in the formation of a Pt shell with relatively low activity and stability. However, the catalysts (C2) with a Pt-rich surface and high lattice ordering have a highly enhanced electrochemical surface area after potential cycling via surface roughing. The rough Pt shell of the C2 catalysts is achieved by leaching of surface Cu and the concomitant morphology restructuring. The C2 Pt surface demonstrated highly improved specific and mass activities of 0.8 mA cm_Pt^–2 and 0.232 A mg_Pt^–1 at 0.9 V for oxygen reduction reaction (ORR), and after 10 000 cycles, the C2 catalysts display almost no loss of the initial electrochemical active surface area (ECSA). Meanwhile, the stability of these CuPt catalysts shows regular change. Moreover, after a long-term stability measurement, the ECSA of C2 catalysts can be restored to the initial value after another potential cycling treatment, and thus, this kind of electrocatalyst may be developed as next-generation restorable cathode fuel cell catalysts

Scalable Bromide-Triggered Synthesis of Pd@Pt Core–Shell Ultrathin Nanowires with Enhanced Electrocatalytic Performance toward Oxygen Reduction Reaction

This article reports a novel scalable method to prepare ultrathin and uniform Pd@Pt nanowires (NWs) with controllable composition and shell thickness, high aspect ratio, and smooth surface, triggered by bromide ions via a galvanic replacement reaction between PtCl₆^2– and Pd NWs. It was found that bromide ions played a vital role in initiating and promoting the galvanic reaction. The bromide ions served as capping and oxidized etching agents, counterbalancing the Pt deposition and Pd etching on the surface to give final Pd@Pt core–shell nanostructures. Such a counterbalance and the formation PtBr₆^2– with lower redox potential could lower the reaction rate and be responsible for full coverage of a smooth Pt shell. The full coverage of Pt deposited on Pd NWs is important for the enhancement of the activity and stability, which depend strongly on the Pt content and Pt shell thickness. Significantly, the Pd@Pt NWs with Pt content of 21.2% (atomic ratio) exhibited the highest mass activity (810 mA mg^–1_Pt) and specific activity (0.4 mA cm^–2). Interestingly, the mass activity (1560 mA mg^–1_Pt) and specific activity (0.98 mA cm^–2) of Pd@Pt (21.2%) NWs increased to 2.45 and 1.95 times the initial values after 60k cycles tests, 8.5 and 9.0 times greater than those of Pt/C catalysts. In addition, these ultrathin NW electrocatalysts with large aspect ratio are easy to form into a freestanding film, which improves the mass transport, electrical conductivity, and structure stability

Effects of melatonin on the expression of hepatic antioxidant enzymes.

<p>Mice were treated as Materials and Methods. Liver samples were collected at 4 h after APAP. The expression of hepatic antioxidant enzymes were detected using real-time RT-PCR. (A) SOD1; (B) Catalase; (C) GSHRd; (D) GSHPx1. All data were expressed as means ± SEM (n = 6). *<i>P</i><0.05, **<i>P</i><0.01 as compared with the control. ‡ <i>P</i><0.05, ‡‡ <i>P</i><0.01 as compared with APAP group.</p

Melatonin protects against APAP-induced hepatocyte death.

<p>Mice were treated as Materials and Methods. Liver samples were collected at 4 h after APAP administration. Hepatocyte death was determined using TUNEL assay. Representative photomicrographs of liver section from mice treated with saline (A as control), APAP alone (B), melatonin alone (C), and combination of APAP and melatonin (D) are shown. (E) TUNEL+ cells were analyzed. All data were expressed as means ± SEM (n = 6). **<i>P</i><0.01 as compared with the control. ‡‡ <i>P</i><0.01 as compared with APAP group.</p

Melatonin attenuates APAP-induced acute liver injury.

<p>Mice were treated as Materials and Methods. Liver samples were collected at 4 h after APAP administration. Representative photomicrographs of liver histology from mice treated with saline (A as control), APAP alone (B), melatonin alone (C), and combination of APAP and melatonin (D) are shown (H & E, magnification: 100×). (E) Sera were collected at 4 h after APAP administration. Serum ALT was measured. All data were expressed as means ± SEM (n = 6). **<i>P</i><0.01 as compared with the control. ‡‡ <i>P</i><0.01 as compared with APAP group.</p

Effects of melatonin on APAP-induced release of cytochromec and AIF translocation.

<p>Mice were treated as Materials and Methods. Liver samples were collected at 4 h after APAP administration. Nuclear translocation of AIF was analyzed using immunohistochemistry. Representative photomicrographs of liver histology from mice treated with saline (A as control), melatonin alone (B), APAP alone (C) and melatonin+APAP (D) are shown. Original magnification: 200×.(E) Cyt c in cytosol was detected by immunoblots. All experiments were repeated for four times. All data were expressed as means ± SEM (n = 4). **<i>P</i><0.01 as compared with the control. ‡‡ <i>P</i><0.01 as compared with APAP group.</p

Primers for real-time RT-PCR.

<p>Primers for real-time RT-PCR.</p

Effects of melatonin on APAP-induced hepatic GSH depletion.

<p>Mice were treated as Materials and Methods. Liver samples were collected at 4 h after APAP. Hepatic GSH and GSSG contents were detected. (A) GSH; (B) GSSG; (C) GSSG/GSH. All data were expressed as means ± SEM (n = 6). **<i>P</i><0.01 as compared with the control.</p

Melatonin attenuates APAP-induced hepatic RIP1 activation and JNK phosphorylation.

<p>Mice were treated as Materials and Methods. Liver samples were collected at 1 h after APAP administration. (A) Hepatic RIP1 was detected by immunoblots. (B) All mice except controls were i.p. injected with APAP (300 mg/kg). In melatonin+APAP group, mice were i.p. injected with different doses of melatonin (1.25, 5, 20 mg/kg) 30 min before APAP (300 mg/kg, i.p.). Liver samples were collected at 4 h after APAP administration. Hepatic phosphorylated JNK was detected by immunoblots. All experiments were repeated for four times. Quantitative analyses of scanning densitometry on four different samples were performed. All data were expressed as means±SEM (n = 4). **<i>P</i><0.01 as compared with the control. ‡‡ <i>P</i><0.01 as compared with APAP group.</p

Microporous Luminescent Metal–Organic Framework for a Sensitive and Selective Fluorescence Sensing of Toxic Mycotoxin in Moldy Sugarcane

Food contamination by toxic mycotoxins not only causes a considerable loss in economy, but importantly poses a huge threat to human health through accidental ingestion. Hence, it is an ongoing and imperative need to develop a convenient, cost-effective method for the detection of the mycotoxin-infected agricultural commodities. To this end, we herein fabricated a novel metal–organic framework-derived composite material that displays a strong solid-state emission in the visible region, by attaching a frequently used fluorescent label, fluorescein isothiocyanate (FITC), via guest adsorption. Significantly, owing to the inherent pH-responsive conformational changes of FITC, the resulting composite material provides, to the best of our knowledge, the first example of the sensitive and selective fluorescence sensing toward 3-nitropropionic acid, which, as a major naturally occurring mycotoxin in moldy sugarcane, has been closely linked to poisoning episodes in human beings and animals