Electronic Activation during Nanoparticle Exsolution for Enhanced Activity at Elevated Temperature.

Nanoparticle (NP) exsolution from perovskite-based oxides matrix upon reduction has emerged as an ideal platform for designing highly active catalysts for energy and environmental applications. However, the mechanism of how the material characteristics impacts the activity is still ambiguous. In this work, taking Pr0.4Sr0.6Co0.2Fe0.7Nb0.1O3 thin film as the model system, we demonstrate the critical impact of the exsolution process on the local surface electronic structure. Combining advanced microscopic and spectroscopic techniques, particularly scanning tunneling microscopy/spectroscopy and synchrotron-based near ambient X-ray photoelectron spectroscopy, we find that the band gaps of both the oxide matrix and exsolved NP decrease during exsolution. Such changes are attributed to the defect state within the forbidden band introduced by oxygen vacancies and the charge transfer across the NP/matrix interface. Both the electronic activations of oxide matrix and the exsolved NP phase lead to good electrocatalytic activity toward the fuel oxidation reaction at elevated temperature.

Activating Lattice Oxygen in Perovskite Oxide by B-Site Cation Doping for Modulated Stability and Activity at Elevated Temperatures.

Doping perovskite oxide with different cations is used to improve its electro-catalytic performance for various energy and environment devices. In this work, an activated lattice oxygen activity in Pr0.4 Sr0.6 Cox Fe0.9- x Nb0.1 O3- δ (PSCxFN, x = 0, 0.2, 0.7) thin film model system by B-site cation doping is reported. As Co doping level increases, PSCxFN thin films exhibit higher concentration of oxygen vacancies ( V o • • ) as revealed by X-ray diffraction and synchrotron-based X-ray photoelectron spectroscopy. Density functional theory calculation results suggest that Co doping leads to more distortion in FeO octahedra and weaker metaloxygen bonds caused by the increase of antibonding state, thereby lowering V o • • formation energy. As a consequence, PSCxFN thin film with higher Co-doping level presents larger amount of exsolved particles on the surface. Both the facilitated V o • • formation and B-site cation exsolution lead to the enhanced hydrogen oxidation reaction (HOR) activity. Excessive Co doping until 70%, nevertheless, results in partial decomposition of thin film and degrades the stability. Pr0.4 Sr0.6 (Co0.2 Fe0.7 Nb0.1 )O3 with moderate Co doping level displays both good HOR activity and stability. This work clarifies the critical role of B-site cation doping in determining the V o • • formation process, the surface activity, and structure stability of perovskite oxides.

Enhancing the Intrinsic Activity and Stability of Perovskite Cobaltite at Elevated Temperature Through Surface Stress.

Perovskite-based oxides attract great attention as catalysts for energy and environmental devices. Nanostructure engineering is demonstrated as an effective approach for improving the catalytic activity of the materials. The mechanism for the enhancement, nevertheless, is still not fully understood. In this study, it is demonstrated that compressive strain can be introduced into freestanding perovskite cobaltite La0.8 Sr0.2 CoO3- δ (LSC) nanofibers with sufficient small size. Crystal structure analysis suggests that the LSC fiber is characterized by compressive strain along the ab plane and less distorted CoO6 octahedron compared to the bulk powder sample. Accompanied by such structural changes, the nanofiber shows significantly higher oxygen reduction reaction (ORR) activity and better stability at elevated temperature, which is attributed to the higher oxygen vacancy concentration and suppressed Sr segregation in the LSC nanofibers. First-principle calculations further suggest that the compressive strain in LSC nanofibers effectively shortens the distance between the Co 3d and O 2p band center and lowers the oxygen vacancy formation energy. The results clarify the critical role of surface stress in determining the intrinsic activity of perovskite oxide nanomaterials. The results of this work can help guide the design of highly active and durable perovskite catalysts via nanostructure engineering.

Use of cell free DNA as a prognostic biomarker in non-small cell lung cancer patients with bone metastasis.

BACKGROUND: Non-small cell lung cancer (NSCLC) is difficult to treat when metastasis has occurred. This study explores the use of cell-free DNA in the clinical management of NSCLC patients who have Kirsten rat sarcoma viral oncogene homolog (KRAS)-positive mutations and as a marker for prognosis. METHODS: Peripheral blood collected from advanced NSCLC patients was examined with digital droplet polymerase chain reaction and ultraviolet spectrometry. KRAS mutations were analyzed and quantitated. The specificity and sensitivity of the proposed assay was computed by associating the results with tumor tissue specimens. Comparison against different sub-groups of patients with different metastatic sites and healthy volunteers were made. Patients were subsequently followed up and survival analysis was conducted. RESULTS: Among the 186 patients recruited, 150 had concordant KRAS mutational profiles using cell-free DNA with tumor tissues. The assay sensitivity and specificity were 80.6% and 100%, respectively. For the 150 patients with concordant results, the range of cell-free DNA quantities in peripheral blood was 5.3 to 115 ng. Among the patient groups with different metastatic sites, we observed that patients with bone metastasis had higher concentrations of cell-free DNA. Survival analysis showed that these patients had worse survival outcome. Patients with higher KRAS counts in peripheral blood also had worse outcome. CONCLUSION: The use of cell-free DNA presents opportunities for risk stratification of patients and possibly aids in the clinical management of the disease. In the current study for NSCLC, patients with bone metastases showed higher cell-free DNA concentrations. Quantitating the concentrations of cell-free DNA presents a noninvasive biomarker capable of prognostic utility.

Protective effects of liraglutide on glomerular podocytes in obese mice by inhibiting the inflammatory factor TNF-α-mediated NF-κB and MAPK pathway.

OBJECTIVE: To evaluate the protective effects of Glucagon-like peptide-1(GLP-1) receptor agonist (liraglutide) on glomerular podocytes of obese mice, and explore the possible underlying mechanism. METHODS: Twelve of the thirty-four healthy and clean male mice were randomly selected as the normal control group. The remaining twenty-two mice were included in the high-fat diet (HFD) feeding group. After twelve weeks of high-fat diet and normal diet, two mice each from the HFD feeding group and the normal control group were randomly selected and sacrificed to suggested that the modeling was successful in the HFD feeding group. Then, twenty mice were randomly divided into HFD + liraglutide group (liraglutide group, n = 10) and HFD group (n = 10). The morphology and the structure of glomerular podocytes were observed using electron microscopy. Podocyte foot process diameter, glomerular basement membrane thickness were measured. ELISA was performed to determine the serum tumor necrosis factor α (TNF-α) level. The expression levels of TNF-α protein and nuclear factor-kappa B (NF-κB) in kidney tissues, extracellularsignal regulating kinase(ERK), c-Jun N-terminal kinase (JNK) and p38MAPK in the mitogenactivated protein kinases(MAPK) pathway were detected by western blotting. RESULTS: HFD-feeding caused significant renal injury, podocyte pathological changes, podocyte foot process diameter and glomerular basement membrane thickness were significantly increased compared with the control group. Liraglutide injection significantly alleviated HFD-induced effects on renal functions and podocyte morphology, as 24 h urine protein, urinary albumin and podocyte histomorphology. Moreover, HFD-induced Inflammatory reaction were obviously attenuated by Liraglutide administration, so did the HFD-induced activation of TNF-α-mediated NF-κB and MAPK pathways. CONCLUSION: Liraglutide reduced urinary albumin excretion in obesity-related glomerulopathy model mice, and improved podocyte morphology and structural damage. The mechanism may be partly related to the inhibition of TNF-α-mediated NF-κB and MAPK pathways.