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The increasingly stringent emission regulations make it urgent to get a fundamental understanding on the catalytic behaviors of rhodium, the most efficient component in three-way catalysts (TWCs) to convert NOx into N2. Herein, the catalytic conversion of NO and CO into N2 and CO2 by gas-phase rhodium-aluminum oxide species (RhAlO0–3 and RhAl2O1–4) was identified by mass spectrometry and quantum chemical calculations. This finding represents a significant step in the field of gas-phase catalysis, given that only elementary reactions for this conversion are commonly observed because it is extremely challenging to rupture the strong N–O bond and couple the N–N bond as well as drive the resulting product to oxidize CO. It emphasized that a polarized Rh–Al bond in gas-phase species is indispensable and the RhAlO0,1 and RhAl2O1,2 species with direct Rh–Al bonding can be involved in catalytic NO reduction by CO.

Fundamental understanding of the nature of active sites in real-life water gas shift (WGS) catalysts that can convert CO and H2O into CO2 and H2 is crucial to engineer related catalysts performing under ambient conditions. Herein, we identified that the WGS reaction can be, in principle, catalyzed by rhodium-manganese oxide clusters Rh2MnO1,2- in the gas phase at room temperature. This is the first example of the construction of such a potential catalysis in cluster science because it is challenging to discover clusters that can abstract the oxygen from H2O and then supply the anchored oxygen to oxidize CO. The WGS reaction was characterized by mass spectrometry, photoelectron spectroscopy, and quantum-chemical calculations. The coordinated oxygen in Rh2MnO1,2- is paramount for the generation of an electron-rich Mn+-Rh- bond that is critical to capture and reduce H2O and giving rise to a polarized Rh+-Rh- bond that functions as the real redox center to drive the WGS reaction.

Gas-phase studies on catalytic CO oxidation by O2 mediated with gold-containing heteronuclear metal oxide clusters are vital to obtain the structure-reactivity relationship of supported gold catalysts, while it is challenging to trigger the reactivity of clusters with closed-shell electronic structure in O2 activation. Herein, we identified that CO oxidation by O2 can be catalyzed by the AuTi2 O4-6- clusters, among which AuTi2 O4- with closed-shell electronic structure can effectively activate O2 . The reactions were characterized by mass spectrometry and quantum chemical calculations. Theoretical calculations showed that in the initial stage of O2 activation, the Ti2 O4 moiety in AuTi2 O4- contributes dominantly to activate O2 into superoxide (O2- ⋅) without participation of the Au atom. In subsequent steps, the intimate charge transfer interaction between Au and the Ti2 O4 moiety drives the direct dissociation of the O2- ⋅ unit.

Cleavage of the triple N≡N bond by metal clusters is of fundamental interest and practical importance in nitrogen fixation. Previous studies of N≡N bond cleavage by gas-phase metal clusters emphasized the importance of the dinuclear metal centers. Herein, the dissociative adsorption of N2 and subsequent C-N coupling on trinuclear carbide cluster anions V3C4- under thermal collision conditions have been characterized by employing mass spectrometry (collision induced dissociation), cryogenic photoelectron imaging spectroscopy, and quantum chemistry calculations. A theoretical analysis identified a crucial adsorption intermediate with N2 bonded with the V3 metal core in the end-on/side-on/side-on (ESS) mode, which most likely enables the facile cleavage of the N≡N bond. Such a vital N2 coordination in the ESS mode is a result of symmetry-matched interactions between the occupied orbitals of the metal core and both of the two empty π* orbitals of N2. Furthermore, carbon ligands also play a considerable role in enhancing the reactivity of the metal core toward N2. This study strongly suggests a new mechanism of N≡N bond cleavage by gas-phase metal clusters.

Adverse cardiac remodeling after myocardial infarction (MI) is associated with extremely high mortality rates worldwide. Although optimized medical therapy, Preservation of lusitropic and inotropic function and protection against adverse remodeling in ventricular structure remain relatively frequent. This study demonstrated that Andrographolide (Andr) significantly ameliorated adverse cardiac remodeling induced by myocardial infarction and improves contractile function in mice with LAD ligation compared with the control group. Briefly, Andr markedly attenuated cardiac fibrosis and relieved inflammation after myocardial infarction. Specifically, Andr significantly blocked oxidative stress and the nuclear translocation of p-P65 following myocardial infarction. At the mechanistic level, antioxidant effect of Andr was achieved through strengthening antioxidative stress capacity and attributed to the activation of Nrf2/HO-1 Signaling. Consistently, H9C2 administrated with Andr showed a decreased oxidative stress caused by hypoxia precondition, but treatment with specific Nrf2 inhibitor (ML385) or the silence of Nrf2 blunted the activation of Nrf2/HO-1 Signaling and removed the protective effects of Andr in vitro. Thus, we suggest that Andr alleviates adverse cardiac remodeling following myocardial infarction through enhancing Nrf2 signaling pathway.

Prevention of ATP binding cassette transporter A1 (ABCA1)-dependent cholesterol efflux leads to lipid accumulation in macrophages and atherosclerosis development. C1q tumor necrosis factor-related protein 1 (CTRP1), a conserved paralog of adiponectin, has been shown to aggravate atherosclerosis via its pro-inflammatory property. However, very little is known about its effects on ABCA1 expression and macrophage lipid accumulation. In the current studies, we found that CTRP1 down-regulated ABCA1 expression, inhibited cholesterol efflux to apoA-I and promoted lipid accumulation in THP-1 macrophage-derived foam cells. Forkhead box O1 (FoxO1), a transcriptional repressor of ABCA1, was identified as a direct target of miR-424-5p. Mechanistically, CTRP1 attenuated miR-424-5p levels and then augmented FoxO1 expression in the nucleus, which led to down-regulation of ABCA1 expression and inhibition of cholesterol efflux. In conclusion, these findings suggest that CTRP1 restrains cholesterol efflux and facilitates macrophage lipid accumulation through the miR-424-5p/FoxO1/ABCA1 signaling pathway, thereby providing a novel mechanistical insight into its pro-atherosclerotic action. This article is protected by copyright. All rights reserved.

Understanding the heterogeneous oxidation of isoprene is crucial to discover the missing sink of the atmospheric isoprene. Iron oxide nanoparticles dominate the most abundant type of anthropogenic ...

Doped metal oxide catalysts have important applications in heterogeneous catalysis, whereas the fundamental effects of doping on the reactivity of catalysts are elusive. Herein, benefiting from the study of a series of atomic clusters MVO5– (M = V–Zn) in catalytic CO oxidation by molecular O2 under thermal collision conditions, the crucial effects of doping on the electronic structure and then the catalytic reactivity of MVO5– were successfully rationalized by using mass spectrometry and theoretical calculations. We defined the energy gap of active orbitals that are closely related to electron transfer in MVO5– during CO oxidation. It was discovered that such an energy gap can modulate reaction thermodynamics, whereas the orbital overlap of MVO5– with CO controls the kinetics. The doped clusters MVO5– (M = Cr–Zn) have reduced energy gaps than that in host V2O5–, and doping can modify the orbital overlap of MVO5– (M = Cr–Zn) with CO. Only the MnVO5– and ZnVO5– clusters that have rational energy gaps and pr...

Oxidation of CO by gas-phase atomic clusters is being actively studied to understand the molecular-level mechanisms of heterogeneous CO oxidation over related catalytic surfaces. However, it is experimentally challenging to study CO oxidation by neutral heteronuclear metal oxide clusters because of the difficulty of cluster ionization and detection without fragmentation. Herein, the neutral AuVO $_{2-4}$ clusters were experimentally generated and their reactions with CO and O $_2$ were studied. The experimental results showed that CO adsorption is the dominant channel on the interactions of AuVO $_4$ and AuVO $_3$ with CO, and AuVO $_2$ can pick up an O $_2$ molecule to generate AuVO $_4$ . Theoretical studies indicated that the oxidation of the trapped CO in AuVO $_{3,4}$ CO into CO $_2$ is exothermic while the reaction barriers have to be overcome at the elevated temperatures. A catalytic cycle for CO oxidation by AuVO $_{2-4}$ is proposed.

The thermal reaction of diatomic gold boride cation AuB+ with methane has been studied by using state-of-the-art mass spectrometry in conjunction with density functional theory calculations. The AuB+ ion can activate a methane molecule to produce exclusively the free hydrogen atom, an important intermediate in hydrocarbon transformation. This result is different from the reactivity of AuC+ and CuB+ counterparts with methane in previous studies. The AuC+ cation mainly transforms methane into ethylene. The CuB+ reaction system principally generates the free hydrogen atoms, but it also gives rise a portion of ethylene-like product H2B−CH2. The B atom of AuB+ is the active site to activate methane. The strong relativistic effect on gold plays an important role for the product selectivity. The mechanistic insights obtained from this study provide guidance for rational design of active sites with high product selectivity toward methane activation.

Oxide supported gold catalysts (e.g., Au/TiO2) are of great significance in heterogeneous catalysis owing to their extraordinary catalytic activity. Study of heteronuclear metal oxide clusters (HMOCs, e.g., Au xTi yO z q) is an important way to uncover the molecular-level mechanisms of gold catalysis in the related heterogeneous catalytic systems. However, the current studies of HMOCs are focused on charged clusters with little attention paid to neutral species. The reactivity study of neutral HMOCs is vital to have a comprehensive understanding of heterogeneous catalysis, but it is experimentally challenging because of the difficulty of cluster ionization and detection without fragmentation. Herein, benefiting from a homemade time-of-flight mass spectrometer coupled with a vacuum ultraviolet laser system, the reactivity of neutral Au1-doped titanium oxide clusters AuTi2O3-6 in catalytic CO oxidation by O2 has been successfully identified. The mechanistic details of the catalysis have been elucidated by quantum chemistry calculations. The crucial roles of the mobile AuCO species that can facilitate not only the process of CO oxidation but also the process of O2 activation have been discovered in the cluster catalysis. The fascinating results are of substantial importance to understand the mechanisms of CO oxidation over Au/TiO2, one type of the best studied gold catalysts.

Cationic gold has been frequently identified as a suitable reactive species for activating methane in condensed-phase studies. However, it is far from clear how the coordination site manipulates the activity of such species. Herein, by anchoring AuI on silicon oxide cluster supports of variable sizes, the site-specific methane activation by AuI -Ox has been clarified by mass spectrometry in conjunction with quantum chemistry calculations. An unexpected mechanistic switch in C-H activation was identified for the cluster anions Au(SiO2 )n O- (n=1-3) that selectively activate one of the four C-H bonds of methane with different reaction efficiencies: a low efficiency was observed for the two-fold-coordinated gold ion (AuI, 2f ), which was anchored on an AuSiO3- or AuSi2 O5- cluster, through an oxidative addition mechanism (a homolytic process), and high efficiency was observed for the one-fold-coordinated gold ion (AuI, 1f ), which was supported on an AuSi3 O7- cluster, through Lewis acid/base pairs mechanism (AuI, 1f ⋅⋅⋅O2- , a heterolytic process). Fine regulation of the 5d orbital level of the Au atom by the oxygen ligands accounted for the mechanistic difference between AuI, 2f and AuI, 1f species. The mechanistic understanding of the reactivity of AuI -Ox at a strictly molecular level can be used to clarify the dissimilar activity of gold anchored on different oxide supports.

Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE−/− mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE−/− mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.

C1q tumor necrosis factor-related protein 12 (CTRP12), a conserved paralog of adiponectin, is closely associated with cardiovascular disease. However, little is known about its role in atherogenesis. The aim of this study was to examine the influence of CTRP12 on atherosclerosis and explore the underlying mechanisms. Our results showed that lentivirus-mediated CTRP12 overexpression inhibited lipid accumulation and inflammatory response in lipid-laden macrophages. Mechanistically, CTRP12 decreased miR-155-5p levels and then increased its target gene liver X receptor α (LXRα) expression, which increased ATP binding cassette transporter A1 (ABCA1)- and ABCG1-dependent cholesterol efflux and promoted macrophage polarization to the M2 phenotype. Injection of lentiviral vector expressing CTRP12 decreased atherosclerotic lesion area, elevated plasma high-density lipoprotein cholesterol levels, promoted reverse cholesterol transport (RCT), and alleviated inflammatory response in apolipoprotein E-deficient (apoE−/−) mice fed a Western diet. Similar to the findings of in vitro experiments, CTRP12 overexpression diminished miR-155-5p levels but increased LXRα, ABCA1, and ABCG1 expression in the aortas of apoE−/− mice. Taken together, these results suggest that CTRP12 protects against atherosclerosis by enhancing RCT efficiency and mitigating vascular inflammation via the miR-155-5p/LXRα pathway. Stimulating CTRP12 production could be a novel approach for reducing atherosclerosis.

Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms. Our results showed that administration of BCA promoted reverse cholesterol transport (RCT), improved plasma lipid profile, and decreased serum proinflammatory cytokine levels and atherosclerotic lesion area in apoE-/- mice fed a Western diet. In THP-1 macrophage-derived foam cells, treatment with BCA upregulated ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 expression and facilitated subsequent cholesterol efflux and diminished intracellular cholesterol contents by activating the peroxisome proliferator-activated receptor γ (PPARγ)/liver X receptor α (LXRα) and PPARγ/heme oxygenase 1 (HO-1) pathways. BCA also activated these two signaling pathways to inhibit the secretion of proinflammatory cytokines. Taken together, these findings suggest that BCA is protective against atherosclerosis by inhibiting lipid accumulation and inflammatory response through the PPARγ/LXRα and PPARγ/HO-1 pathways. BCA may be an attractive drug for the prevention and treatment of atherosclerotic cardiovascular disease.

The use of CH4 and CO2 to produce value-added chemicals via direct C-C coupling is a challenging chemistry problem because of the inertness of these two molecules. Herein, mass spectrometric experiments and high-level quantum-chemical calculations have identified the first diatomic species (CuB+ ) that can couple CH4 with CO2 under thermal collision conditions to produce ketene (H2 C=C=O), an important intermediate in synthetic chemistry. The order to feed the reactants (CH4 and CO2 ) is important and CH4 should be firstly fed to produce the C2 product. Molecular-level mechanisms including control of product selectivity have been revealed for coupling of CH4 with CO2 under mild conditions.

The hydrogenation of carbon dioxide into value-added chemicals is of great importance for CO2 recycling. However, the underlying mechanism of CO2 hydrogenation remains elusive owing to the lack of experimental evidence for the formation of the C–H bond. Herein, the gas-phase reaction of copper hydride anion Cu2H2– with CO2 at variable temperatures (∼300–560 K) was investigated. Metal hydrides are the ideal models to study the nature of C–H bond formation in CO2 hydrogenation, while the related studies are scarcely reported, particularly for the hydrogenation reactions at temperatures above 300 K. The generation of formate (HCO2–) attached on product CuH2CO2– was identified by temperature-dependent mass spectrometric experiments and density functional theory calculations. Temperature played crucial roles to fine-tune the product selectivity, from Cu2H2CO2– that dominates the room-temperature reaction into CuH2CO2– at elevated temperatures. The nature behind the temperature-dependent product selectivity and...

Identification of molecular-level mechanisms of methane activation is very important in order to transform the most stable alkane molecule into value-added chemicals. Herein, by employing a homemade time-of-flight mass spectrometer coupled with a vacuum ultraviolet (VUV) laser system, the reactions of neutral heteronuclear metal oxide clusters AuxAlyOz (x = 1, 2) with CH4 have been investigated. The interesting channel of Au2Al2O3H+ production was observed for the interaction of a Au2Al2O3 cluster with CH4 after VUV ionization, suggesting that the methyl radical was generated. Combined with the theoretical calculations, this study proposes that VUV ionization of the neutral adsorption complex (Au2Al2O3CH4) creates an active cation (Au2Al2O3CH4+)* to induce C–H bond activation and the methyl radical formation. The photochemistry of this cluster study provides molecular-level insights into the interactions between methane and active sites in related photocatalytic processes.

Investigation on the reactivity of atomic clusters represents an important approach to discover new species to activate and transform methane, the most stable alkane molecule. While a few types of transition metal species have been found to be capable of cleaving the C–H bond of methane, methane activation by the transition metal boride species has not been explored yet. This study reports that vanadium boride cluster cations VBn+ (n = 3–6) can dehydrogenate methane under thermal collision conditions. The mechanistic details of the efficient reactions have been elucidated by quantum chemistry calculations on the VB3+ reaction system. Compared to the non-polar bare B3 cluster, the B3 moiety in VB3+ can be polarized by the V+ cation and thus its reactivity toward methane can be much enhanced. This study provides new insights into the rational design of boron-based catalysts for methane activation.

Novel chiral temperature-sensitive microgels based on N-isopropylacrylamide are reported in this paper. Such particles, poly (N-isopropylacrylamide-co-acrylic acid-L-phenylalanine ethyl ester)[ poly (NIPAM-co-ALPhe)], were prepared by free radical polymerization of NIPAM, chiral monomer ALPhe and crosslinker N,N,-methylene-bis (acrylamide). The microgels exhibit spherical shape and favorable monodispersity. Increasing the content of ALPhe units incorporated into the microgel network will increase the average diameter, but decrease the swelling ratios and the transition temperature of particles.

Poly(NIPAAm-co-AAc) hydrogels of different ratios were prepared by copolymerization and then modified with L-phenylalanine by amidation of carboxyl groups of acrylic acid. The structures of the hydrogels were identified by IR and the chiral separation experiments of hydrogels on D/L-phenylalanine were investigated. The results showed that the chiral hydrogels exhibited enantioselectivity for L-phenylalanine and the resolution capability increased with the rising of temperature and contents of L-phenylalanine groups.

A serious of poly(NIPA-co-NALPE) hydrogels containing chiral group (L-Phenylalanine ethyl ester) were prepared by copolymerization of N-isopropylacrylamide(NIPA) and acrylic acid derivatived L-Phenylalanine ethyl ester (NALPE) in ethanol with different feed ratios. The kinetics adsorption approach, isothermal adsorption and chiral separation experiment of hydrogels on D/L-phenylalanine were investigated, and the results showed that the chiral hydrogels exhibited enantioselectivity for D/L-phenylalanine and the absorption capability increased with the rising temperature and increasing contents of NALPE due to the temperature-sensitive NIPA molecular chains and the chiral monomer NALPE, respectively. Furthermore, the poly(NIPA-co-NALPE) hydrogels were also used to separate DL-alanine and DL-tartaric acid, which suggested that the gels are also applicable to other chiral molecules besides DL-phenylalanine and have potential applications in separation of chiral drugs.

In the title compound, C5H6N+·C8H4NO6 −, N—H...O and O—H...O hydrogen bonds stabilize the crystal structure.