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Platinum is a much used catalyst that, in petrochemical processes, is often alloyed with other metals to improve catalytic activity, selectivity and longevity 1 – 5 . Such catalysts are usually prepared in the form of metallic nanoparticles supported on porous solids, and their production involves reducing metal precursor compounds under a H 2 flow at high temperatures 6 . The method works well when using easily reducible late transition metals, but Pt alloy formation with rare-earth elements through the H 2 reduction route is almost impossible owing to the low chemical potential of rare-earth element oxides 6 . Here we use as support a mesoporous zeolite that has pore walls with surface framework defects (called ‘silanol nests’) and show that the zeolite enables alloy formation between Pt and rare-earth elements. We find that the silanol nests enable the rare-earth elements to exist as single atomic species with a substantially higher chemical potential compared with that of the bulk oxide, making it possible for them to diffuse onto Pt. High-resolution transmission electron microscopy and hydrogen chemisorption measurements indicate that the resultant bimetallic nanoparticles supported on the mesoporous zeolite are intermetallic compounds, which we find to be stable, highly active and selective catalysts for the propane dehydrogenation reaction. When used with late transition metals, the same preparation strategy produces Pt alloy catalysts that incorporate an unusually large amount of the second metal and, in the case of the PtCo alloy, show high catalytic activity and selectivity in the preferential oxidation of carbon monoxide in H 2 . Alloy nanoparticles of platinum and rare-earth elements are formed using zeolites with pore-wall defects, producing stable, highly active and selective catalysts for the propane dehydrogenation reaction.

Mechanically tough and self-healable polymeric materials have found widespread applications in a sustainable future. However, coherent strategies for mechanically tough self-healing polymers are still lacking due to a trade-off relationship between mechanical robustness and viscoelasticity. Here, we disclose a toughening strategy for self-healing elastomers crosslinked by metal–ligand coordination. Emphasis was placed on the effects of counter anions on the dynamic mechanical behaviors of polymer networks. As the coordinating ability of the counter anion increases, the binding of the anion leads to slower dynamics, thus limiting the stretchability and increasing the stiffness. Additionally, multimodal anions that can have diverse coordination modes provide unexpected dynamicity. By simply mixing multimodal and non-coordinating anions, we found a significant synergistic effect on mechanical toughness ( > 3 fold) and self-healing efficiency, which provides new insights into the design of coordination-based tough self-healing polymers. The trade-off relationship between mechanical robustness and viscoelasticity limits the strategies to produce mechanically tough self-healing polymers. Here the authors, introduce a strengthening strategy for self-healing polymers cross-linked by metal-ligand coordination using mixed counter anion dynamics.

The economic crisis of 2008-2010 stimulated an already growing sociological interest in finance. Before the crisis, disintermediation and securitization changed how the U.S. financial system operated, as bank operations shifted from the traditional originate-and-hold model to originate-and-distribute. During the 1980s and 1990s, the overall size and profitability of the financial system grew as deregulation unleashed financial innovation and reorganization. Global shifts toward capital market integration and liberalization created greater global interdependence. Households in the years before the crisis also altered their relationship to the financial system, increasing debt loads and overall exposure to the stock market. Research reveals the importance of politics for many financial market developments, various implications for corporate governance, the continuing significance of social factors within finance, and the role of theoretical and material devices in shaping financial practices. Key directions for future research focus on finance in relation to social inequality, informal sectors, valuation, and social networks.

A cobalt-silica hybrid nanocatalyst bearing small cobalt particles of diameter ~5 nm was prepared through a hydrothermal reaction and hydrogen reduction. The resulting material showed very high CO conversion (>82%) and high hydrocarbon productivity (~1.0 g HC ·g −1 cat ·h −1 ) with high activity (~8.5 × 10 −5 mol CO ·g Co −1 ·s −1 ) in the Fischer–Tropsch synthesis reaction.

NaA zeolite (Si/Al = 1.00) has been commercially applied for capturing radioactive 90Sr 2+ because of its high surface charge density, effectively stabilizing the multivalent cation. However, owing to its narrow micropore opening (4.0 Å), large micron-sized crystallites, and bulkiness of hydrated Sr 2+, the Sr 2+ exchange over NaA has been limited by very slow kinetics. In this study, we synthesized nanocrystalline low-silica X by minimizing a water content in a synthesis gel and utilizing a methyl cellulose hydrogel as a crystal growth inhibitor. The resulting zeolite exhibited high crystallinity and Al-rich framework (Si/Al of approximately 1.00) with the sole presence of tetrahedral Al sites, which are capable of high Sr 2+ uptake and ion selectivity. Meanwhile, the zeolite with a FAU topology has a much larger micropore opening size (7.4 Å) and a much smaller crystallite size (~340 nm) than NaA, which enable significantly enhanced ion-exchange kinetics. Compared to conventional NaA, the nanocrystalline low-silica X exhibited remarkably increased Sr 2+-exchange kinetics (> 18-fold larger rate constant) in batch experiments. Although both the nanocrystalline low-silica X and NaA exhibited comparable Sr 2+ capacities under equilibrated conditions, the former demonstrated a 5.5-fold larger breakthrough volume than NaA under dynamic conditions, attributed to its significantly faster Sr 2+-exchange kinetics.

Breast cancer stem cells (BCSCs) are a small subpopulation of breast cancer cells that have been proposed to be a primary cause of failure of therapies, including ionizing radiation (IR). Their embryonic stem-like signature is associated with poor clinical outcome. In the present study, the function of octamer-binding transcription factor 4 (Oct4), an embryonic stem cell factor, in the resistance of BCSCs to IR was investigated. Mammosphere cells exhibited increased expression of stemness-associated genes, including Oct4 and sex-determining region Y-box 2 (Sox2), and were more resistant to IR compared with serum-cultured monolayer cells. IR-resistant MCF7 cells also exhibited significantly increased expression of Oct4. To investigate the possible involvement of Oct4 in IR resistance of breast cancer cells, cells were transfected with Oct4. Ectopic expression of Oct4 increased the clonogenic survival of MCF7 cells following IR, which was reversed by treatment with small interfering RNA (siRNA) targeting Oct4. Oct4 expression decreased phosphorylated histone H2AX (γ-H2AX) focus formation and suppressed IR-induced premature senescence in these cells. Mammosphere, IR-resistant and Oct4-overexpressing MCF7 cells exhibited enhanced phosphorylation of signal transducer and activation of transcription 3 (STAT3) (Tyr705) and inhibitor of nuclear factor κB (NF-κB), and blockade of these pathways with siRNA against STAT3 and/or specific inhibitors of STAT3 and NF-κB significantly increased IR-induced senescence. Secretome analysis revealed that Oct4 upregulated interleukin 24 (IL-24) expression through STAT3 and NF-κB signaling, and siRNA against IL-24 increased IR-induced senescence, whereas recombinant human IL-24 suppressed it. The results of the present study indicated that Oct4 confers IR resistance on breast cancer cells by suppressing IR-induced premature senescence through STAT3- and NF-κB-mediated IL-24 production.

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a common and serious postoperative complication of cardiac surgery requiring cardiopulmonary bypass (CPB), and it is the second most common cause of AKI in the intensive care unit. Although the complication has been associated with the use of CPB, the etiology is likely multifactorial and related to intraoperative and early postoperative management including pharmacologic therapy. To date, very little evidence from randomized trials supporting specific interventions to protect from or prevent AKI in broad cardiac surgery populations has been found. The definition of AKI employed by investigators influences not only the incidence of CSA-AKI, but also the identification of risk variables. The advent of novel biomarkers of kidney injury has the potential to facilitate the subclinical diagnosis of CSA-AKI, the assessment of its severity and prognosis, and the early institution of interventions to prevent or reduce kidney damage. Further studies are needed to determine how to optimize cardiac surgical procedures, CPB parameters, and intraoperative and early postoperative blood pressure and renal blood flow to reduce the risk of CSA-AKI. No pharmacologic strategy has demonstrated clear efficacy in the prevention of CSA-AKI; however, some agents, such as the natriuretic peptide nesiritide and the dopamine agonist fenoldopam, have shown promising results in renoprotection. It remains unclear whether CSA-AKI patients can benefit from the early institution of such pharmacologic agents or the early initiation of renal replacement therapy.

Rheumatoid arthritis (RA) and antisynthetase syndrome (ASS) are distinct clinical syndromes, and their co-occurrence is rarely encountered. The authors report the case of a 56-year-old female patient with RA of 3 years duration who suddenly developed ASS, and include a review of the literature. The patient was diagnosed with ASS based on; positivity for anti-histidyl-tRNA synthetase (Jo-1) antibody, interstitial lung disease, polyarthritis, and mechanic’s hands. High-dose corticosteroid and pulse intravenous cyclophosphamide were used to control the ASS. This case demonstrates that ASS should be considered during clinical presentations due to its potential overlap with RA.

Dermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM) with typical cutaneous manifestations. It has been proposed that DM may be caused by autoimmune responses to viral infections, and previous studies have also shown that an association between DM and malignancy. However, chronic hepatitis B virus (HBV) infection associated with DM and hepatocellular carcinoma (HCC) is rarely encountered. The authors report a case of DM and HCC in a patient with a HBV infection. A 58-year-old man presented erythematous skin rashes on a sun-exposed area of 2 year’s duration, and recent proximal muscle weakness. His medical history revealed that he had a chronic HBV infection. A diagnosis of DM relies on proximal muscle weakness, elevated muscle enzymes, myopathic changes (demonstrated by electromyography), muscle biopsy evidence of myositis, and its characteristic cutaneous findings. A Liver mass in the left lobe visualized by abdominal computed tomography was confirmed histologically as HCC. This case suggests that DM associated with HCC might be caused by a HBV infection.

Breast cancer stem cells (BCSCs) are a small subpopulation of breast cancer cells that have been proposed to be a primary cause of failure of therapies, including ionizing radiation (IR). Their embryonic stem-like signature is associated with poor clinical outcome. In the present study, the function of octamer-binding transcription factor 4 (Oct4), an embryonic stem cell factor, in the resistance of BCSCs to IR was investigated. Mammosphere cells exhibited increased expression of sternness-associated genes, including Oct4 and sex-determining region Y-box 2 (Sox2), and were more resistant to IR compared with serum-cultured monolayer cells. IR-resistant MCF7 cells also exhibited significantly increased expression of Oct4. To investigate the possible involvement of Oct4 in IR resistance of breast cancer cells, cells were transfected with Oct4. Ectopic expression of Oct4 increased the clonogenic survival of MCF7 cells following IR, which was reversed by treatment with small interfering RNA (siRNA) targeting Oct4. Oct4 expression decreased phosphorylated histone H2AX ([gamma]-H2AX) focus formation and suppressed IR-induced premature senescence in these cells. Mammosphere, IR-resistant and Oct4-overexpressing MCF7 cells exhibited enhanced phosphorylation of signal transducer and activation of transcription 3 (STAT3) ([Tyr.sup.705]) and inhibitor of nuclear factor [kappa]B (NF-[kappa]B), and blockade of these pathways with siRNA against STAT3 and/or specific inhibitors of STAT3 and NF-[kappa]B significantly increased IR-induced senescence. Secretome analysis revealed that Oct4 upregulated interleukin 24 (IL-24) expression through STAT3 and NF-[kappa]B signaling, and siRNA against IL-24 increased IR-induced senescence, whereas recombinant human IL-24 suppressed it. The results of the present study indicated that Oct4 confers IR resistance on breast cancer cells by suppressing IR-induced premature senescence through STAT3- and NF-[kappa]B-mediated IL-24 production.