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For small Pt nanoparticles (NPs), catalytic activity is, as observed, adversely affected by size in the 1-3 nm range. We elucidate, via first-principles-based thermodynamics, the operation H* distribution and cyclic voltammetry (CV) during the hydrogen evolution reaction (HER) across the electrochemical potential, including the underpotential region (U ≤ 0) that is difficult to assess in experiment. We consider multiple adsorption sites on a 1 nm Pt NP model and show that the characteristic CV peaks from different H* species correspond well to experiment. We next quantify the activity contribution from each H* species to explain the adverse effect of size. From the resolved CV peaks at the standard hydrogen electrode potential (U = 0), we first deduce that the active species for the HER are the partially covered (100)-facet bridge sites and the (111)-facet hollow sites. Upon evaluation of the reaction barriers at operation H* distribution and microkinetic modeling of the exchange current, we find that the nearest-neighbor (100)-facet bridge site pairs have the lowest activation energy and contribute to ∼75% of the NP activity. Edge bridge sites (fully covered by H*) per se are not active; however, they react with neighboring (100)-facet H* to account for ∼18% of the activity, whereas (111)-facet hollow sites contribute little. Extrapolating the relative contributions to larger NPs in which the ratio of facet-to-edge sites increases, we show that the adverse size effect of Pt NP HER activity kicks in for sizes below 2 nm. KeywordsMaterials Science and Engineering, first-principles, cluster expansion, adsorption isotherm, hydrogen evolution, hydrogen oxidation, cyclic voltammetry, catalysis, platinum, electrochemistry ABSTRACT: For small Pt nanoparticles (NPs), catalytic activity is, as observed, adversely affected by size in the 1−3 nm range. We elucidate, via first-principlesbased thermodynamics, the operation H* distribution and cyclic voltammetry (CV) during the hydrogen evolution reaction (HER) across the electrochemical potential, including the underpotential region (U ≤ 0) that is difficult to assess in experiment. We consider multiple adsorption sites on a 1 nm Pt NP model and show that the characteristic CV peaks from different H* species correspond well to experiment. We next quantify the activity contribution from each H* species to explain the adverse effect of size. From the resolved CV peaks at the standard hydrogen electrode potential (U = 0), we first deduce that the active species for the HER are the partially covered (100)-facet bridge sites and the (111)-facet hollow sites. Upon evaluation of the reaction barriers at operation H* distribution and microkinetic modeling of the exchange current, we find that the nearest-neighbor (100)-facet bridge site pairs have the lowest activation energy and contribute to ∼75% of the NP activity. Edge bridge sites (fully covered by H*) per se are not active; however, they react with neighboring (100)-facet H* to account for ∼18% of the activity, wherea...

The characterization of nanometer-scale interactions between carbon-containing substrates and alumina surfaces is of paramount importance to industrial and academic catalysis applications, but it is also very challenging. Here, we demonstrate that dynamic nuclear polarization surface-enhanced NMR spectroscopy (DNP SENS) allows the unambiguous description of the coordination geometries and conformations of the substrates at the alumina surface through high-resolution measurements of C-Al distances. We apply this new technique to elucidate the molecular-level geometry of C-enriched methionine and natural abundance poly(vinyl alcohol) adsorbed on γ-AlO-supported Pd catalysts, and we support these results with element-specific X-ray absorption near-edge measurements. This work clearly demonstrates a surprising bimodal coordination of methionine at the Pd-AlO interface.

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We show that the noncrystalline-to-crystalline transition of supported Pt nanoparticles (NPs) in the subnanometer to nanometer size range is statistical in nature, and strongly affected by particle size, support, and adsorbates (here we use H2). Unlike in the bulk, a noncrystalline phase exists and is stable in small NPs, reflecting a general mesoscopic feature. Observations of >3000 particles by high-resolution transmission electron microscopy show a noncrystalline-to-crystalline transition zone that is nonabrupt; there is a size regime where disordered and ordered NPs coexist. The NP size at which this transition occurs is strongly dependent on both the adsorbate and the support, and this effect is general for late 5d transition metals. All results are reconciled via a statistical description of particle-support-adsorbate interactions.

The objective of the present study was to investigate whether pretreatment with single low loading dose of tongxinluo (TXL), a traditional Chinese medicine, 1 h before myocardial ischemia could attenuate no-reflow and ischemia-reperfusion injury by regulating endothelial nitric oxide synthase (eNOS) via the PKA pathway. In a 90-min ischemia and 3-h reperfusion model, minipigs were randomly assigned to the following groups: sham, control, TXL (0.05 g/kg, gavaged 1 h before ischemia), TXL + H-89 (a PKA inhibitor, intravenously infused at a dose of 1.0 μg·kg(-1)·min(-1) 30 min before ischemia), and TXL + N(ω)-nitro-L-arginine (L-NNA; an eNOS inhibitor, intravenously administered at a dose of 10 mg/kg 30 min before ischemia). TXL decreased creatine kinase (CK) activity (P < 0.05) and reduced the no-reflow area from 48.6% to 9.5% and infarct size from 78.5% to 59.2% (P < 0.05), whereas these effects of TXL were partially abolished by H-89 and completely reversed by L-NNA. TXL elevated PKA activity and the expression of PKA, Thr(198) phosphorylated PKA, Ser(1179) phosphorylated eNOS, and Ser(635) phosphorylated eNOS in the ischemic myocardium. H-89 repressed the TXL-induced enhancement of PKA activity and phosphorylation of eNOS at Ser(635), and L-NNA counteracted the phosphorylation of eNOS at Ser(1179) and Ser(635) without an apparent influence on PKA activity. In conclusion, pretreatment with a single low loading dose of TXL 1 h before ischemia reduces myocardial no-reflow and ischemia-reperfusion injury by upregulating the phosphorylation of eNOS at Ser(1179) and Ser(635), and this effect is partially mediated by the PKA pathway.

Bone marrow released by microfracture or full-thickness cartilage defect can initiate the in situ cartilage repair. However, it can only repair small cartilage defects (<2 cm 2 ). This study aimed to investigate whether autologous platelet-rich plasma (PRP) transplantation in collagen matrix can improve the in situ bone marrow-initiated cartilage repair. Full-thickness cartilage defects (diameter 4 mm, thickness 3 mm) in the patellar grooves of male New Zealand White rabbits were chosen as a model of in situ cartilage repair. They were treated with bilayer collagen scaffold (group II), PRP and bilayer collagen scaffold (group III), and untreated (group I), respectively (n = 11). The rabbits were sacrificed at 6 and 12 weeks after operation. The repaired tissues were processed for histology and for mechanical test. The results showed that at both 6 and 12 weeks, group III had the largest amounts of cartilage tissue, which restored a larger surface area of the cartilage defects. Moreover, group III had higher histological scores and more glycosaminoglycans (GAGs) content than those in the other two groups (p < 0.05). The Young's modulus of the repaired tissue in group II and group III was higher than that of group I (p < 0.05). Autologous PRP and bilayer collagen matrix stimulated the formation of cartilage tissues. The findings implicated that the combination of PRP with collagen matrix may repair larger cartilage defects that currently require complex autologous chondrocyte implantation (ACI) or osteochondral grafting.

MicroRNAs have been implicated in the regulation of several cellular signaling pathways of colorectal cancer (CRC) cells. Although emerging evidence proves that microRNA (miR)-106a is expressed highly in primary tumor and stool samples of CRC patients; whether or not miR-106a mediates cancer metastasis is unknown. We show here that miR-106a is highly expressed in metastatic CRC cells, and regulates cancer cell migration and invasion positively in vitro and in vivo. These phenotypes do not involve confounding influences on cancer cell proliferation. MiR-106a inhibits the expression of transforming growth factor-β receptor 2 (TGFBR2), leading to increased CRC cell migration and invasion. Importantly, miR-106a expression levels in primary CRCs are correlated with clinical cancer progression. These observations indicate that miR-106a inhibits the anti-metastatic target directly and results in CRC cell migration and invasion.