Cylindromatosis lysine 63 deubiquitinase (CYLD) suppress TLR3-mediated CCL5 expression in human renal proximal tubular epithelial cells.

BACKGROUND: One of the causes of tubulointerstitial nephritis is viral infection, with innate immune responses affecting its pathogenesis. Toll-like receptor 3 (TLR3) recognizes viral infections and acts antivirally by activating signaling to produce inflammatory cytokines/chemokines, including C-C motif chemokine ligand 5 (CCL5) and interferon-ß (IFN-ß). Although cylindromatosis lysine 63 deubiquitinase (CYLD) is known to be associated with tubulointerstitial nephritis and renal function, its role in the antiviral innate immune response in tubular epithelial cells remains unknown. In this study, we investigated the association between CYLD and TLR3-mediated CCL5 production in cultured human renal proximal tubular epithelial cells (hRPTECs). METHODS AND RESULTS: Polyinosinic-polycytidylic acid (poly IC), a synthetic TLR3 ligand, was used to stimulate hRPTECs. mRNA expression was measured using reverse transcription-quantitative polymerase chain reaction. Protein expression was assayed using western blotting or an enzyme-linked immunosorbent assay. Knockdown of IFN-ß, nuclear factor-kappa B (NF-κB) p65, and CYLD was performed by transfecting cells with specific small interfering RNAs. The intracellular localization of CYLD in hRPTECs was analyzed using immunofluorescence. Poly IC induced CCL5 expression in a time- and concentration-dependent manner, and knockdown of either IFN-ß or p65 reduced poly IC-induced CCL5 expression. CYLD knockdown increased the poly IC-induced CCL5, phosphorylated IκB kinase α/ß (IKK complex), and phosphorylated p65 expression. The CYLD protein was localized in the cytoplasm, and poly IC did not alter its expression. CONCLUSION: CYLD may prevent excessive inflammation due to an antiviral innate immune response by suppressing IKK complex and NF-κB activation downstream of TLR3 in hRPTECs.

Toll-Like Receptor 7-Expressed Macrophages Are Involved in the Pathogenesis of Esophageal Achalasia and Esophagogastric Junction Outflow Obstruction.

INTRODUCTION: Esophageal achalasia is a typical esophageal motility disorder (EMD). Although viral infections have been hypothesized to play a role in the pathogenesis of esophageal achalasia, its etiology remains unclear. This study used esophageal muscle layer specimens collected during per-oral endoscopic myotomy (POEM) procedures to investigate the association between esophageal achalasia and esophagogastric junction outflow obstruction (EGJOO) and pattern recognition receptors. METHODS: Patients with esophageal achalasia and EGJOO who underwent POEM were allocated to the EMD group. Biopsies of the inner circular muscle were conducted during the POEM procedure. The control group comprised individuals diagnosed with esophageal squamous cell carcinoma who underwent surgical resection. Expression of pattern recognition receptors, including Toll-like receptor (TLR) 7, was examined by polymerase chain reaction. Immunohistochemical staining was performed to determine TLR7 expression sites in the esophageal muscle layer, and the relationship between TLR7 mRNA expression and clinical score was investigated. RESULTS: Our analysis revealed a notable upregulation of TLR7 mRNA levels within the muscle layer of esophageal achalasia and EGJOO, in contrast to those of control specimens. In contrast, the correlation between TLR7 and clinical score was not significant. Immunohistochemical staining revealed increased numbers of TLR7-expressing macrophages between the muscle layers. CONCLUSIONS: TLR7-expressing macrophages are involved in the innate immune response underlying esophageal achalasia and EGJOO. This result will lead to the elucidation of new pathogenetic mechanisms and the development of novel therapeutic targets.

Mixed anion control of enhanced negative thermal expansion in the oxysulfide of PbTiO3.

The rare physical property of negative thermal expansion (NTE) is intriguing because materials with a large NTE over a wide temperature range can serve as high-performance thermal expansion compensators. However, the applications of NTE are hindered by the fact that most of the available NTE materials show small magnitudes of NTE, and/or NTE occurs only in a narrow temperature range. Herein, for the first time, we investigated the effect of anion substitution instead of general Pb/Ti-site substitutions on the thermal expansion properties of a typical ferroelectric NTE material, PbTiO3. Intriguingly, the substitution of S for O in PbTiO3 further increases the tetragonality of PbTiO3. Consequently, an unusually enhanced NTE with an average volumetric coefficient of thermal expansion of V = -2.50 × 10-5 K-1 was achieved over a wide temperature range (300-790 K), which is in contrast to that of pristine PbTiO3 (V = -1.99 × 10-5 K-1, RT-763 K). The intensified NTE is attributed to the enhanced hybridization between Pb/Ti and O/S atoms by the substitution of S, as evidenced by our theoretical investigations. We therefore demonstrate a new technique for introducing mixed anions to achieve a large NTE over a wide temperature range in PbTiO3-based ferroelectrics.

Expression of ISG60 is induced by TLR3 signaling in BEAS­2B bronchial epithelial cells: Possible involvement in CXCL10 expression.

Viral infections in the respiratory tract are common, and, in recent years, severe acute respiratory syndrome coronavirus 2 outbreaks have highlighted the effect of viral infections on antiviral innate immune and inflammatory reactions. Specific treatments for numerous viral respiratory infections have not yet been established and they are mainly treated symptomatically. Therefore, understanding the details of the innate immune system underlying the airway epithelium is crucial for the development of new therapies. The present study aimed to investigate the function and expression of interferon (IFN)­stimulated gene (ISG)60 in non­cancerous bronchial epithelial BEAS­2B cells exposed to a Toll­like receptor 3 agonist. BEAS­2B cells were treated with a synthetic TLR3 ligand, polyinosinic­polycytidylic acid (poly IC). The mRNA and protein expression levels of ISG60 were analyzed using reverse transcription­quantitative PCR and western blotting, respectively. The levels of C­X­C motif chemokine ligand 10 (CXCL10) were examined using an enzyme­linked immunosorbent assay, and the effects of knockdown of IFN­ß, ISG60 and ISG56 were examined using specific small interfering RNAs. Notably, ISG60 expression was increased in proportion to poly IC concentration, and recombinant human IFN­ß also induced ISG60 expression. By contrast, knockdown of IFN­ß and ISG56 decreased ISG60 expression, and ISG60 knockdown reduced CXCL10 and ISG56 expression. These findings suggested that ISG60 is partly implicated in CXCL10 expression and that ISG60 may serve a role in the innate immune response of bronchial epithelial cells. The present study highlights ISG60 as a potential target for new therapeutic strategies against viral infections in the airway.

Interferon-stimulated gene 56 positively regulates Toll-like receptor 3-mediated CXCL10 expression in human renal proximal tubular epithelial cells.

Viral infections in tubular epithelial cells lead to the production of inflammatory cytokines by innate immunity, causing tubulointerstitial nephritis. TLR3 recognizes viral infections and acts via the activation of interferon (IFN)/IFN-stimulated genes (ISGs). This study investigates the role of ISG56, a representative ISG, in TLR3 signaling in cultured human renal proximal tubular epithelial cells (hRPTECs). To this end, hRPTECs were stimulated by a synthetic TLR3 ligand, polyinosinic-polycytidylic acid (poly IC), recombinant human interferon-ß [r(h)IFN-ß] or Japanese encephalitis virus (JEV) infection and assayed for inflammatory cytokine mRNA expression by RT-qPCR, and protein expression via western blotting or ELISA. ISG56 was expressed by poly IC or r(h)IFN-ß and IFN-ß knockdown reduced poly IC-induced expression of ISG56 and CXCL10. Moreover, ISG56 knockdown reduced poly IC- or r(h)IFN-ß-induced expression of CXCL10 at the same time as increasing JEV growth and reducing CXCL10 expression induced by JEV infection. Overall, TLR3 signaling induced IFN-ß-dependent expression of ISG56 and CXCL10. We show that ISG56 possibly plays a critical role in antiviral immunity of hRPTECs by positive regulation of IFN-ß-mediated CXCL10 expression downstream of TLR3.

Modifications of the charge-discharge behaviour of Fe2(MoO4)3 in all-solid-state lithium-ion batteries.

The solidification of lithium-ion batteries (LIBs) by replacing liquid electrolytes with solid electrolytes enables the development of a new class of LIBs, namely all-solid-state lithium-ion batteries (ASSLIBs), with improved safety and energy density. Such battery solidification can greatly influence the properties of battery components, as exemplified by a recent report suggesting that the (dis)charge behaviour of Fe2(MoO4)3 (FMO), a promising two-phase electrode material, differs on solid electrolytes compared to liquid electrolytes. However, its underlying mechanism remains unclear. Here we examined the (de)lithiation behaviour of FMO thin films on solid electrolytes using operando synchrotron X-ray diffraction (XRD) to gain insights into the influence of the solidification on the (dis)charge mechanism of electrode materials. The XRD results revealed that FMO on solid electrolytes exhibits a monotonic peak shift over a wide capacity range, accompanied by a temporary peak broadening. This suggests that FMO possesses an expanded solid-solution reaction region and a narrower two-phase reaction region in solidified batteries compared to liquid-based LIBs. The altered (dis)charge behavior was suggested to be thermodynamically driven, as it remained largely unchanged with varying rates and under open circuit conditions. Qualitative analysis considering stress-induced variations in Gibbs free energy curves demonstrated that external stress, potentially caused by the constraint of chemo-mechanical expansion, can thermodynamically narrow the two-phase region when the chemical expansion coefficients of the two phases of FMO differ. These findings highlight the significant impact of the battery solidification on electrode material properties, emphasizing the importance of considering these unique issues in the design of ASSLIBs.

High-throughput and high-resolution powder X-ray diffractometer consisting of six sets of 2D CdTe detectors with variable sample-to-detector distance and innovative automation system.

The demand for powder X-ray diffraction analysis continues to increase in a variety of scientific fields, as the excellent beam quality of high-brightness synchrotron light sources enables the acquisition of high-quality measurement data with high intensity and angular resolution. Synchrotron powder diffraction has enabled the rapid measurement of many samples and various in situ/operando experiments in nonambient sample environments. To meet the demands for even higher throughput measurements using high-energy X-rays at SPring-8, a high-throughput and high-resolution powder diffraction system has been developed. This system is combined with six sets of two-dimensional (2D) CdTe detectors for high-energy X-rays, and various automation systems, including a system for automatic switching among large sample environmental equipment, have been developed in the third experimental hutch of the insertion device beamline BL13XU at SPring-8. In this diffractometer system, high-brilliance and high-energy X-rays ranging from 16 to 72 keV are available. The powder diffraction data measured under ambient and various nonambient conditions can be analysed using Rietveld refinement and the pair distribution function. Using the 2D CdTe detectors with variable sample-to-detector distance, three types of scan modes have been established: standard, single-step and high-resolution. A major feature is the ability to measure a whole powder pattern with millisecond resolution. Equally important, this system can measure powder diffraction data with high Q exceeding 30 Å-1 within several tens of seconds. This capability is expected to contribute significantly to new research avenues using machine learning and artificial intelligence by utilizing the large amount of data obtained from high-throughput measurements.

TLR3 signaling-induced interferon-stimulated gene 56 plays a role in the pathogenesis of rheumatoid arthritis.

Rheumatoid fibroblast-like synoviocytes (RFLS) have an important role in the inflammatory pathogenesis of rheumatoid arthritis (RA). Toll-like receptor 3 (TLR3) is upregulated in RFLS; its activation leads to the production of interferon-ß (IFN-ß), a type I IFN. IFN-stimulated gene 56 (ISG56) is induced by IFN and is involved in innate immune responses; however, its role in RA remains unknown. Therefore, the purpose of this study was to investigate the role of TLR3-induced ISG56 in human RFLS. RFLS were treated with polyinosinic-polycytidylic acid (poly I:C), which served as a TLR3 ligand. ISG56, melanoma differentiation-associated gene 5 (MDA5), and C-X-C motif chemokine ligand 10 (CXCL10) expression were measured using quantitative reverse transcription-polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay. Using immunohistochemistry, we found that ISG56 was expressed in synovial tissues of patients with RA and osteoarthritis. Under poly I:C treatment, ISG56 was upregulated in RFLS. In addition, we found that the type I IFN-neutralizing antibody mixture suppressed ISG56 expression. ISG56 knockdown decreased CXCL10 expression and MDA5 knockdown decreased ISG56 expression. In addition, we found that ISG56 was strongly expressed in the synovial cells of patients with RA. TLR3 signaling induced ISG56 expression in RFLS and type I IFN was involved in ISG56 expression. ISG56 was also found to be associated with CXCL10 expression, suggesting that ISG56 may be involved in TLR3/type I IFN/CXCL10 axis, and play a role in RA synovial inflammation.

First synthesis of RuSn solid-solution alloy nanoparticles and their enhanced hydrogen evolution reaction activity.

Solid-solution alloys based on platinum group metals and p-block metals have attracted much attention due to their promising potential as materials with a continuously fine-tunable electronic structure. Here, we report on the first synthesis of novel solid-solution RuSn alloy nanoparticles (NPs) by electrochemical cyclic voltammetry sweeping of RuSn@SnOx NPs. High-angle annular dark-field scanning transmission electron microscopy and energy-dispersive X-ray spectroscopy maps confirmed the random and homogeneous distribution of Ru and Sn elements in the alloy NPs. Compared with monometallic Ru NPs, the RuSn alloy NPs showed improved hydrogen evolution reaction (HER) performance. The overpotentials of Ru0.94Sn0.06 NPs/C and Ru0.87Sn0.13 NPs/C to achieve a current density of 10 mA cm-2 were 43.41 and 33.19 mV, respectively, which are lower than those of monometallic Ru NPs/C (53.53 mV) and commercial Pt NPs/C (55.77 mV). The valence-band structures of the NPs investigated by hard X-ray photoelectron spectroscopy demonstrated that the d-band centre of RuSn NPs shifted downward compared with that of Ru NPs. X-ray photoelectron spectroscopy and X-ray absorption near-edge structure analyses indicated that in the RuSn alloy NPs, charge transfer occurs from Sn to Ru, which was considered to result in a downward shift of the d-band centre in RuSn NPs and to regulate the adsorption energy of intermediate Hads effectively, and thus enable the RuSn solid-solution alloy NPs to exhibit excellent HER catalytic properties.

Polymorphism of Two-Dimensional Semiconducting Coordination Polymers: Impact of a Lead-Sulfur Network on Photoconductivity.

Sulfur-coordinated coordination polymers (S-CPs) have unique optoelectrical properties that originate from infinite M-S bond networks. In this study, we synthesized and characterized two polymorphs of a two-dimensional (2D) Pb(II) S-CP with a formula of [Pb(tzdt)(OAc)] (Htzdt=1,3-thiazolidine-2-thione, OAc=acetate). Our findings revealed that the thermodynamic product (KGF-26) possesses quasi-2D (-Pb-S-)n layers with weak nonbonded Pb-S bonds, whereas the kinetic product (KGF-27) has intrinsic 2D (-Pb-S-)n layers with Pb-S bonds. The results of time-resolved microwave conductivity measurements and first-principles calculations confirmed that KGF-27 exhibits higher photoconductivity than KGF-26, which establishes that the inorganic (-Pb-S-)n networks with Pb-S bonds are crucial for achieving high photoconductivity. This is the first experimental demonstration of the impact of the (-M-S-)n networks in S-CPs on photoconductivity through the comparison of crystal polymorphisms.

Resiquimod Induces C-C Motif Chemokine Ligand 2 Via Nuclear Factor-Kappa B in SH-SY5Y Human Neuroblastoma Cells.

Toll-like receptor (TLR) 7 plays an important role in recognizing virus-derived nucleic acids. TLR7 signaling in astrocytes and microglia is critical for activating immune responses against neurotrophic viruses. Neurons express TLR7, similar to glial cells; however, the role of neuronal TLR7 has not yet been fully elucidated. This study sought to determine whether resiquimod, the TLR7/8 agonist, induces the expression of inflammatory chemokines in SH-SY5Y human neuroblastoma cells. Immunofluorescence microscopy revealed that TLR7 was constitutively expressed in SH-SY5Y cells. Stimulation with resiquimod induced C-C motif chemokine ligand 2 (CCL2) expression, accompanied by the activation of nuclear factor-kappa B (NF-κB) in SH-SY5Y cells. Resiquimod increased mRNA levels of C-X-C motif chemokine ligand 8 (CXCL8) and CXCL10, while the increase was slight at the protein level. Knockdown of NF-κB p65 eliminated resiquimod-induced CCL2 production. This study provides novel evidence that resiquimod has promising therapeutic potential against central nervous system viral infections through its immunostimulatory effects on neurons.

TMEM2 suppresses TLR3-mediated IFN-ß/ISG56/CXCL10 expression in BEAS-2B bronchial epithelial cells.

BACKGROUND: Bronchial epithelial cells are at the front line of viral infections. Toll-like receptor 3 (TLR3) cascade causes the expression of interferon (IFN)-ß and IFN-stimulated genes (ISGs), which in turn induce an antiviral response. Members of the transmembrane protein (TMEM) family are expressed in various cell types. Although the prognostic value of TMEM2 in various cancers has been reported, its association with infectious diseases remains unknown. In this study, we investigated the effects of TMEM2 on antiviral immunity in BEAS-2B bronchial epithelial cells. METHODS AND RESULTS: TMEM2 protein was found in the cytoplasm of normal human bronchial epithelial cells and differed between organs using immunohistochemistry. Cultured BEAS-2B cells were transfected with TMEM2 siRNA, followed by administration of TLR3 ligand polyinosinic-polycytidylic acid (poly IC) or recombinant human (r(h)) IFN-ß. The expression of TMEM2, IFN-ß, ISG56, C-X-C motif chemokine ligand 10 (CXCL10) and hyaluronan were evaluated appropriately by western blotting, quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. TMEM2 expression was not altered by poly IC stimulation. Knockdown of TMEM2 increased poly IC-induced expression of IFN-ß, CXCL10, and ISG56, while IFN-ß-induced expression of ISG56 and CXCL10 were not changed by TMEM2 knockdown. The hyaluronan concentration in the medium was decreased by either TMEM2 knockdown or poly IC, but additive or synergistic effects were not observed. CONCLUSIONS: TMEM2 knockdown enhanced TLR3-mediated IFN-ß, CXCL10, and ISG56 expression in BEAS-2B cells. This implies that TMEM2 suppresses antiviral immune responses and prevents tissue injury in bronchial epithelial cells.

The inhibitory effect of DIF-3 on polyinosinic-polycytidylic acid-induced innate immunity activation in human cerebral microvascular endothelial cells.

For the treatment and prevention of autoinflammatory diseases, it is essential to develop the drug, regulating the innate immune system. Although differentiation-inducing factor (DIF) derivatives, extracted from the cellular slime mold, Dictyostelium discoideum, exhibit immunomodulatory effects, their effects on the regulation of innate immunity in brain are unknown. In this study, we used the human cerebral microvascular endothelial cell line, hCMEC/D3, to investigate the effects of DIF derivatives on the generation of C-X-C motif chemokine (CXCL) 10 and interferon (IFN)-ß induced by polyinosinic-polycytidylic acid (poly IC). DIF-3 (1-10 µM), but not DIF-1 and DIF-2, dose-dependently inhibited the biosynthesis of not only CXCL10 but also CXCL16 and C-C motif chemokine 2 induced by poly IC. DIF-3 also strongly decreased IFN-ß mRNA expression and protein release from the cells induced by poly IC through the prohibition of p65, a subtype of NF-ĸB, not interferon regulatory transcription factor 3 phosphorylation. In the docking simulation study, we confirmed that DIF-3 had a high affinity to p65. These results suggest that DIF-3 regulates the innate immune system by inhibiting TLR3/IFN-ß signaling axis through the NF-ĸB phosphorylation inhibition.

Submillisecond in situ X-ray diffraction measurement system with changing temperature and pressure using diamond anvil cells at BL10XU/SPring-8.

Recently, there has been a high demand for elucidating kinetics and visualizing reaction processes under extreme dynamic conditions, such as chemical reactions under meteorite impact conditions, structural changes under nonequilibrium conditions, and in situ observations of dynamic changes. To accelerate material science studies and Earth science fields under dynamic conditions, a submillisecond in situ X-ray diffraction measurement system has been developed using a diamond anvil cell to observe reaction processes under rapidly changing pressure and temperature conditions replicating extreme dynamic conditions. The development and measurements were performed at the high-pressure beamline BL10XU/SPring-8 by synchronizing a high-speed hybrid pixel array detector, laser heating and temperature measurement system, and gas-pressure control system that enables remote and rapid pressure changes using the diamond anvil cell. The synchronized system enabled momentary heating and rapid cooling experiments up to 5000 K via laser heating as well as the visualization of structural changes in high-pressure samples under extreme dynamic conditions during high-speed pressure changes.

A Three-Dimensionally Extended Metal-Organic Ladder Compound Exhibiting Proton Conduction.

Ladder systems situated in the dimensional crossover region have attracted much attention because their electronic states and physical properties depend strongly on the electronic correlations among the constituent legs. Generally, two-/three-legged transition metal-oxide ladder compounds are studied as representative ladder systems, but two-/three-dimensional (2D/3D) extensions based on such ladder systems with a few numbers of legs are difficult because of the extreme synthesis conditions. Here, for the first time, we report the successful creation of a 3D extended two-legged ladder compound, [Pt(en)(dpye)I]2(NO3)4 ⋅ 2H2O (en=ethylenediamine; dpye=1,2-Di(4-pyridyl)ethane), which is obtained by simple oxidative polymerization of a small Pt macrocyclic complex using elemental I2. The unique 3D extended lattice consists of 1D mixed-valence halogen-bridged metal chains (⋅⋅⋅Pt-I-Pt-I⋅⋅⋅) and helically arranged macrocyclic units as the constituent legs and rungs, as confirmed by single-crystal X-ray diffraction. Diffuse X-ray scattering analyses and optical measurements revealed that the out-of-phase mixed-valence Pt2+/Pt4+ arrangement arises from the weak interchain correlation among adjacent legs. In addition, this compound shows an increase in proton conductivity by a factor of up to 1000, depending on humidity.

Possible involvement of DExD/H box helicase 60 in synovial inflammation of rheumatoid arthritis: role of toll-like receptor 3 signaling.

BACKGROUND: Innate immunity is known to be implicated in the etiology of synovitis in rheumatoid arthritis (RA). However, details of the molecular mechanisms have not been fully clarified. DExD/H-box helicase 60 (DDX60), a putative RNA helicase, is of consequence in anti-viral innate immune reactions followed by inflammation. Although DDX60 is involved in the pathogenesis of autoimmune diseases such as systemic lupus nephritis, the role of DDX60 in RA has not been elucidated. The objective of this study was to examine the expression and the role of DDX60 in RA synovial inflammation. METHODS AND RESULTS: DDX60 protein expression was investigated by immunohistochemistry in synovial tissues resected from 4 RA and 4 osteoarthritis (OA) patients. We found that synovial DDX60 expression was more intense in RA than in OA. Treatment of human rheumatoid fibroblast-like synoviocytes in culture with polyinosinic-polycytidylic acid, a Toll-like receptor 3 (TLR3) ligand, increased DDX60 protein and mRNA expression. A knockdown experiment of DDX60 using RNA interference revealed a decrease in the expression of poly IC-induced C-X-C motif chemokine ligand 10 (CXCL10) which induces lymphocyte chemotaxis. CONCLUSIONS: The synovial DDX60 was more expressed in RA patients than in OA. In human RFLS, DDX60 stimulated by TLR3 signaling affected CXCL10 expression. DDX60 may contribute to synovial inflammation in RA.

Low-Temperature Chiral Crystal Structure and Superconductivity in (Pt0.2Ir0.8)3Zr5.

We report the observation of superconductivity in (Pt0.2Ir0.8)3Zr5 with a chiral space group (P6122) at low temperatures. The bulk nature of the superconductivity at a transition temperature of 2.2 K was confirmed using specific heat measurements. We revealed that (Pt0.2Ir0.8)3Zr5 obeys the weak-coupling Bardeen-Cooper-Schrieffer model, and the dominant mechanism in the upper critical field is the orbital pair-breaking limit rather than the Pauli-Clogston limit. This indicates that the antisymmetric spin-orbit coupling caused by the chiral crystal structure does not significantly affect the superconductivity of (Pt0.2Ir0.8)3Zr5.

Denary High-Entropy Oxide Nanoparticles Synthesized by a Continuous Supercritical Hydrothermal Flow Process.

High-entropy oxide nanoparticles (HEO NPs) have been intensively studied because of their attractive properties, such as high stability and enhanced catalytic activity. In this work, for the first time, denary HEO NPs were successfully synthesized using a continuous supercritical hydrothermal flow process without calcination. Interestingly, this process allows the formation of HEO NPs on the order of seconds at a relatively lower temperature. The synthesized HEO NPs contained 10 metal elements, La, Ca, Sr, Ba, Fe, Mn, Co, Ru, Pd, and Ir, and had a perovskite-type structure. Atomic-resolution high-angle annular dark-field scanning transmission electron microscopy and energy-dispersive X-ray spectroscopy measurements revealed homogeneous dispersion of the 10 metal elements. The obtained HEO NPs also exhibited a higher catalytic activity for the CO oxidation reaction than that of the LaFeO3 NPs.

Generalised analytical method unravels framework-dependent kinetics of adsorption-induced structural transition in flexible metal-organic frameworks.

Flexible metal-organic frameworks (MOFs) exhibiting adsorption-induced structural transition can revolutionise adsorption separation processes, including CO2 separation, which has become increasingly important in recent years. However, the kinetics of this structural transition remains poorly understood despite being crucial to process design. Here, the CO2-induced gate opening of ELM-11 ([Cu(BF4)2(4,4'-bipyridine)2]n) is investigated by time-resolved in situ X-ray powder diffraction, and a theoretical kinetic model of this process is developed to gain atomistic insight into the transition dynamics. The thus-developed model consists of the differential pressure from the gate opening (indicating the ease of structural transition) and reaction model terms (indicating the transition propagation within the crystal). The reaction model of ELM-11 is an autocatalytic reaction with two pathways for CO2 penetration of the framework. Moreover, gas adsorption analyses of two other flexible MOFs with different flexibilities indicate that the kinetics of the adsorption-induced structural transition is highly dependent on framework structure.

Molybdenum-Ruthenium-Carbon Solid-Solution Alloy Nanoparticles: Can They Be Pseudo-Technetium Carbide?

Technetium (Tc), atomic number 43, is an element that humans cannot freely use even in the 21st century because Tc is radioactive and has no stable isotope. In this report, we present molybdenum-ruthenium-carbon solid-solution alloy (MoxRu1-xCy) nanoparticles (NPs) that are expected to have an electronic structure similar to that of technetium carbide (TcCy). MoxRu1-xCy NPs were synthesized by annealing under a helium/hydrogen atmosphere following thermal decomposition of metal precursors. The obtained NPs had a solid-solution structure in the whole composition range. MoxRu1-xCy with a cubic structure (down to 30 atom % Mo in the metal ratio) showed a superconducting state, and the transition temperature (Tc) increased with increasing Mo composition. The continuous change in Tc across that of TcCy indicates the continuous control of the electronic structure by solid-solution alloying, leading to pseudo-TcCy. Density functional theory calculations indicated that the synthesized Mo0.53Ru0.47C0.41 has a similar electronic structure to TcC0.41.