13 research outputs found
Perovskite Chromates Cathode with Exsolved Iron Nanoparticles for Direct High-Temperature Steam Electrolysis
Recently, composite cathodes based
on doped lanthanum chromates have been widely employed for direct
steam electrolysis. However, this approach limits the electrode performances
and Faraday efficiency due to insufficient electrocatalytic activity.
This study addresses the drawbacks and reports an improved electrocatalytic
activity and Faraday efficiency of composite cathode with a reversibly
exsolved iron nanoparticles anchored on the surface of doped lanthanum
chromates. A-site deficient and B-site excess (La<sub>0.75</sub>Sr<sub>0.25</sub>)<sub>0.85</sub>(Cr<sub>0.5</sub>Fe<sub>0.5</sub>)<sub>0.85</sub>Fe<sub>0.15</sub>O<sub>3−δ</sub> (LSCrFF)
was designed as the parent material to anchor the exsolved iron nanoparticles
on the surface of perovskite chromate (La<sub>0.75</sub>Sr<sub>0.25</sub>)Â(Cr<sub>0.5</sub>Fe<sub>0.5</sub>)ÂO<sub>3‑δ</sub> (LSCrF)
via high-temperature reduction. The electrical properties of LSCrF
and Fe/LSCrF were systematically investigated and correlated with
electrochemical performance of the composite electrodes in symmetrical
cells and electrolysis cells. The iron nanoparticles significantly
improve the electrical conductivity of LSCrF from 1.80 to 6.35 S cm<sup>–1</sup> for Fe/LSCrF at 800 °C and Po<sub>2</sub> of
10<sup>–15</sup> atm. The polarization resistance, <i>R</i><sub>p</sub>, of the symmetrical cells was accordingly
enhanced from 4.26 Ω cm<sup>2</sup> with LSCrF to 2.58 Ω
cm<sup>2</sup> with Fe/LSCrF in hydrogen atmosphere at 800 °C.
The Faraday efficiency for the direct steam electrolysis showed a
marked increase of 89.3% with LSCrFF cathode at 800 °C and 1.8
V as opposed to 76.7% with the cathodes based on LSCrF. The synergetic
effect of catalytic-active iron nanoparticles and redox-stable LSCrF
substrate produced improved performances and excellent stability for
the direct steam electrolysis without a flow of reducing gas over
the composite cathodes
IL-17A-depleted A549 cells prevent tumor metastasis-induced bone destruction <i>in vivo</i>.
(A) X-ray images of the tibias of mice at 4 weeks after A549 cell-injection. (B) Quantitative analysis of osteolytic bone destruction. (C) Hematoxylin and eosin (HE) and (D) TRAP staining of one representative tibia from each group. (E) Quantitative analysis of osteoclast numbers in bone metastases of A549 cells. Data are expressed as number of osteoclasts/mm at the tumor-bone interface and the mean ± SD. Arrows indicate osteoclasts; # tumor mass. **p < 0.01. Scale bar, 50 μm.</p
Conditioned medium (CM) from IL-17A-depleted A549 cells inhibits osteoclast differentiation by promoting CASP3 expression.
(A) RAW 264.7 cells were cultured in A549-CM or A549-si-CM in the presence of RANKL for 24 h. (A) Apoptosis-related proteins were detected via western blotting, and (B) protein expression was normalized against β-actin. (C) RAW 264.7 cells were cultured in A549-si-CM with or without Z-DEVD-FMK (a CASP3 inhibitor) in the presence of RANKL for 5 days. (D) Quantitative analysis of TRAP-positive multinucleated (≥3 nuclei) RAW264.7 cells. Data represent the mean ± SD of experiments performed independently in triplicate. *p < 0.05, **p < 0.01. Scale bar, 100 μm.</p
Expression of apoptosis-related mRNA after treatment with A549-CM and A549-si-CM.
Expression of apoptosis-related mRNA after treatment with A549-CM and A549-si-CM.</p
Sequences of primers used in RT-PCR analysis.
Osteoclasts are crucial in the events leading to bone metastasis of lung cancer. Interleukin-17A (IL-17A) affects osteogenesis by regulating the survival of osteoclast precursors (OCPs) and is enriched in lung cancer cells. However, how factors derived from tumor cells that metastasize to bone affect osteoclastogenesis remains poorly understood. We examined whether IL-17A derived from lung cancer cells affects osteoclast differentiation by regulating OCP apoptosis. IL-17A expression was inhibited in A549 non-small cell lung cancer cells using RNA interference. Compared with conditioned medium (CM) from A549 cells (A549-CM), CM from IL-17A-deficient A549 cells (A549-si-CM) suppressed osteoclastogenesis. The mRNA expression of osteoclast-specific genes was downregulated following A549-si-CM treatment. Furthermore, A549-si-CM promoted osteoclast precursor apoptosis at an early stage of osteoclastogenesis, which was related to the promotion of caspase-3 expression by A549-si-CM during osteoclast differentiation. In vivo experiments also showed that inhibition of IL-17A expression in A549 cells reduced osteoclast activation and bone tissue destruction. Collectively, our results indicate that IL-17A deficiency inhibits lung cancer-induced osteoclast differentiation by promoting apoptosis of osteoclast precursors in the early stage of osteoclast formation and that IL-17A is a potential therapeutic target for cancer-associated bone resorption in patients with lung cancer.</div
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Osteoclasts are crucial in the events leading to bone metastasis of lung cancer. Interleukin-17A (IL-17A) affects osteogenesis by regulating the survival of osteoclast precursors (OCPs) and is enriched in lung cancer cells. However, how factors derived from tumor cells that metastasize to bone affect osteoclastogenesis remains poorly understood. We examined whether IL-17A derived from lung cancer cells affects osteoclast differentiation by regulating OCP apoptosis. IL-17A expression was inhibited in A549 non-small cell lung cancer cells using RNA interference. Compared with conditioned medium (CM) from A549 cells (A549-CM), CM from IL-17A-deficient A549 cells (A549-si-CM) suppressed osteoclastogenesis. The mRNA expression of osteoclast-specific genes was downregulated following A549-si-CM treatment. Furthermore, A549-si-CM promoted osteoclast precursor apoptosis at an early stage of osteoclastogenesis, which was related to the promotion of caspase-3 expression by A549-si-CM during osteoclast differentiation. In vivo experiments also showed that inhibition of IL-17A expression in A549 cells reduced osteoclast activation and bone tissue destruction. Collectively, our results indicate that IL-17A deficiency inhibits lung cancer-induced osteoclast differentiation by promoting apoptosis of osteoclast precursors in the early stage of osteoclast formation and that IL-17A is a potential therapeutic target for cancer-associated bone resorption in patients with lung cancer.</div
Effects of siRNA-mediated IL-17A silencing in A549 cells.
Effects of siRNA-mediated IL-17A silencing in A549 cells.</p
Conditioned medium (CM) from IL-17A-depleted A549 cells suppresses RANKL-induced osteoclastogenesis and the expression of osteoclast-related genes.
(A) RAW 264.7 cells were cultured with CM from A549 cells transfected with siRNA against IL-17A (A549-si-CM), a negative control (A549-snc-CM), or from untransfected cells (A549-CM) in the presence of RANKL for 5 days. (B) Quantitative analysis of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated (≥3 nuclei) RAW264.7 cells cultured in CM. (C) Transcript levels of c-Fos, NFATC-1, TRAP, and CatK in cells treated with A549-si-CM, A549-snc-CM, or A549-CM in the presence of RANKL for 48 h. Data represent the fold-changes in target gene expression normalized to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and are expressed as a percentage of the levels in cells treated with A549-CM, which was set to 100%. (D) RAW 264.7 cells were cultured in A549-CM with or without secukinumab (an IL-17A monoclonal antibody) in the presence of RANKL for 5 days. (E) Quantitative analysis of TRAP-positive multinucleated (≥3 nuclei) RAW264.7 cells cultured in A549-CM with or without secukinumab. (F) RAW 264.7 cells were cultured in A549-si-CM with or without IL-17A (1 ng/mL) in the presence of RANKL for 5 days. (G) Quantitative analysis of TRAP-positive multinucleated (≥3 nuclei) RAW264.7 cells cultured in A549-si-CM with or without IL-17A. Values represent the mean ± standard deviation (SD) of experiments performed independently in triplicate. CTR-N, control group treated without RANKL; CTR-R, control group treated with RANKL. *P < 0.05, **p < 0.01, ***p < 0.001. Scale bar, 100 μm.</p
Conditioned medium (CM) from IL-17A-depleted A549 cells promotes osteoclast precursor (OCP) apoptosis at an early stage of osteoclast differentiation.
(A) RAW 264.7 cells were cultured in A549-CM or A549-si-CM in the presence of RANKL for 5 days. A549-si-CM was added to the culture medium on the first (D1) and third days (D3), respectively. (B) Quantitative analysis of TRAP-positive multinucleated (≥3 nuclei) RAW264.7 cells. (C) Annexin V-FITC/PI staining was performed to label apoptotic cells. The percentages of apoptotic cells (Annexin V+) were counted using flow cytometry, and (D) Q2 and Q3 quadrants indicated increased apoptosis after A549-si-CM treatment on the first day. Cells treated with A549-CM were used as controls. Data are presented as the mean ± SD from three independent experiments. *p < 0.05, ***p<0.001. Scale bar, 100 μm.</p
Truncated Cross Effect Dynamic Nuclear Polarization: An Overhauser Effect Doppelgänger
The
discovery of a truncated cross-effect (CE) in dynamic nuclear
polarization (DNP) NMR that has the features of an Overhauser-effect
DNP (OE-DNP) is reported here. The apparent OE-DNP, where minimal
μw power achieved optimum enhancement, was observed when doping
Trityl-OX063 with a pyrroline nitroxide radical that possesses electron-withdrawing
tetracarboxylate substituents (tetracarboxylate-ester-pyrroline or
TCP) in vitrified water/glycerol at 6.9 T and at 3.3 to 85 K, in apparent
contradiction to expectations. While the observations are fully consistent
with OE-DNP, we discover that a truncated cross-effect (<i>t</i>CE) is the underlying mechanism, owing to TCP’s shortened
T<sub>1e</sub>. We take this observation as a guideline and demonstrate
that a crossover from CE to <i>t</i>CE can be replicated
by simulating the CE of a narrow-line (Trityl-OX063) and a broad-line
(TCP) radical pair, with a significantly shortened T<sub>1e</sub> of
the broad-line radical