Asymmetric electron occupation of transition metals for the oxygen evolution reaction via a ligand-metal synergistic strategy.

The performance of two-dimensional transition-metal (oxy)hydroxides (TMOOHs) for the electrocatalytic oxygen evolution reaction (OER), as well as their large-scale practical applications, are severely limited by the sluggish kinetics of the four-electron OER process. Herein, using a symmetry-breaking strategy, we simulated a complex catalyst composed of a single Co atom and a 1,10-phenanthroline (phen) ligand on CoOOH through density functional theory studies, which exhibits excellent OER performance. The active site Co undergoes a valence oscillation between +2, +3 and even high valence +4 oxidation states during the catalytic process, resulting from the distorted coordination effect after the ligand modification. The induced asymmetry in the electronic states of surrounding nitrogen and oxygen atoms modulates the eg occupation of Co-3d orbitals, which should be of benefit to reduce the overpotential in the OER process. By studying similar catalytic systems, the prominent role of ligands in creating asymmetric electronic structures and in modulating the valence of the active site and the OER performance was reconfirmed. This study provides a new dimension for optimizing the electrocatalytic performance of various TM-ligand complexes.

Aqueous Electroreduction of Nitric Oxide to Ammonia at Low Concentration via Vacancy Engineered FeOCl.

Electroreduction of nitric oxide (NO) to NH3 (NORR) has gained extensive attention for the sake of low carbon emission and air pollutant treatment. Unfortunately, NORR is greatly hindered by its sluggish kinetics, especially under low concentrations of NO. Herein, we developed a chlorine (Cl) vacancy strategy to overcome this limitation over FeOCl nanosheets (FeOCl-VCl ). Density functional theory (DFT) calculations revealed that the Cl vacancy resulted in defective Fe with sharp d-states characteristics in FeOCl-VCl to enhance the absorption and activation of NO. In situ X-ray absorption near-edge structure (XANES) and attenuated total reflection-infrared spectroscopy (ATR-IR) verified the lower average oxidation state of defective Fe to enhance the electron transfer for NO adsorption/activation and facilitate the generation of key NHO and NHx intermediates. As a result, the FeOCl-VCl exhibited superior NORR activities with the NH3 Faradaic efficiency up to 91.1 % while maintaining a high NH3 yield rate of 455.4 µg cm-2 h-1 under 1.0 vol % NO concentration, competitive with those of previously reported literatures under higher NO concentration. Further, the assembled Zn-NO battery utilizing FeOCl-VCl as cathode delivered a record peak power density of 6.2 mW cm-2 , offering a new route for simultaneous NO removal, NH3 production, and energy supply.

Achieving Stable Lithium Metal Anode at 50 mA cm-2 Current Density by LiCl Enriched SEI.

Lithium metal batteries are intensively studied due to the potential to bring up breakthroughs in high energy density devices. However, the inevitable growth of dendrites will cause the rapid failure of battery especially under high current density. Herein, the utilization of tetrachloroethylene (C2 Cl4 ) is reported as the electrolyte additive to induce the formation of the LiCl-rich solid electrolyte interphase (SEI). Because of the lower Li ion diffusion barrier of LiCl, such SEI layer can supply sufficient pathway for rapid Li ion transport, alleviate the concentration polarization at the interface and inhibit the growth of Li dendrites. Meanwhile, the C2 Cl4 can be continuously replenished during the cycle to ensure the stability of the SEI layer. With the aid of C2 Cl4 -based electrolyte, the Li metal electrodes can maintain stable for >300 h under high current density of 50 mA cm-2 with areal capacity of 5 mAh cm-2 , broadening the compatibility of lithium metal anode toward practical application scenarios.

Single Nickel Atom Catalysts Enable Fast Polysulfide Redox for Safe and Long-Cycle Lithium-Sulfur Batteries.

Lithium-sulfur (Li-S) batteries have attracted great interest due to their low cost, high theoretical energy density, and environmental friendliness. However, the sluggish conversion of lithium polysulfides (LiPS) to S and Li2 S during the charge/discharge process leads to unsatisfactory rate performance of lower to 0.1 C (1 C = 1675 mA g-1 ) especially for Li-S pouch batteries, thus hindering their practical applications in high power batteries. Here, well-defined and monodispersed Ni single-atom catalysts (SACs) embedded in highly porous nitrogen-doped graphitic carbons (NiSA-N-PGC) are designed and synthesized to form Ni-N4 catalytic sites at the atomic level. When serving as a bifunctional electrocatalyst, the Ni-N4 catalytic sites cannot only promote the interfacial conversion redox of LiPS by accelerating the transformation kinetics, but also suppress the undesirable shuttle effect by immobilizing LiPS. These findings are verified by both experimental results and DFT theoretical calculations. Furthermore, Li ions show low diffusion barrier on the surface of Ni-N4 sites, resulting in enhanced areal capacity of batteries. As a result, the Li-S battery delivers stable cycling life of more than 600 cycles with 0.069% capacity decay per cycle at a rate of 0.5 C. More importantly, the Li-S pouch cells with NiSA-N-PGC show an initial capacity of 1299 mAh g-1 at a rate of 0.2 C even with high sulfur loading of 6 mg cm-2 . This work opens up an avenue for developing single-atom catalysts to accelerate the kinetic conversion of LiPS for highly stable Li-S batteries.

Construction of stable MoxSy/CeO2 heterostructures for the electrocatalytic hydrogen evolution reaction.

The unique structures of polynuclear MoxSy clusters make it possible to maximize the number of their active sites and for them to be good candidates for HER catalysts. An appropriate support is highly necessary not only to avoid the desorption of MoxSy clusters in a working environment, but also to improve their HER activity. Our work here shows that the CeO2 support could provide strong support for interaction with various MoxSy clusters and the formed MoxSy/CeO2 hetero-structures also have modest ΔGH* for the HER. The electronic features of MoxSy clusters are regulated by the CeO2 support, which leads to charge redistribution on edge atoms and plays a key role in H adsorption. Our studies provide instructive predictions on efficient candidates of molybdenum-sulfur based catalysts for the HER.

Activity Trends and Mechanisms in Peroxymonosulfate-Assisted Catalytic Production of Singlet Oxygen over Atomic Metal-N-C Catalysts.

We synthesized a series of carbon-supported atomic metal-N-C catalysts (M-SACs: M=Mn, Fe, Co, Ni, Cu) with similar structural and physicochemical properties to uncover their catalytic activity trends and mechanisms. The peroxymonosulfate (PMS) catalytic activity trends are Fe-SAC>Co-SAC>Mn-SAC>Ni-SAC>Cu-SAC, and Fe-SAC displays the best single-site kinetic value (1.65×105  min-1 mol-1 ) compared to the other metal-N-C species. First-principles calculations indicate that the most reasonable reaction pathway for 1 O2 production is PMS→OH*→O*→1 O2 ; M-SACs that exhibit moderate and near-average Gibbs free energies in each reaction step have a better catalytic activity, which is the key for the outstanding performance of Fe-SACs. This study gives the atomic-scale understanding of fundamental catalytic trends and mechanisms of PMS-assisted reactive oxygen species production via M-SACs, thus providing guidance for developing M-SACs for catalytic organic pollutant degradation.

LCK inhibitor attenuates atherosclerosis in ApoE-/- mice via regulating T cell differentiation and reverse cholesterol transport.

Lots of studies demonstrated that CD4+ T cells regulate the development of atherosclerosis (AS). Previously, we reported that LCK, a key molecule in activation of T cell receptor (TCR) signalling and T cells, adversely affects reverse cholesterol transport (RCT), which ameliorates AS in vitro. To investigate the effect of LCK on AS in vivo, we injected the LCK inhibitor, PP2, into ApoE-/- mice fed a chow diet or a high-fat diet (HFD). Although, AS plaques were not affected by PP2 in chow diet-fed mice, PP2 significantly reduced the lesion percentage and necrotic core areas in HFD-fed mice. We further analysed the plaque contents and found that the accumulation of lipids and macrophages were decreased, while the contents of collagen and smooth muscle cells were increased by the LCK inhibitor. Thus, inhibiting LCK enhanced the plaque stability. We also found the LCK inhibitor improved cholesterol efflux capacity of HDL and up-regulated RCT regulatory proteins in the spleen. Moreover, inhibiting LCK regulated differentiation of T cells by increasing regulatory T (Treg) cells and decreasing the number of T helper 1 (Th1) cells in the aorta, thymus and spleen. Consistent with these results, infiltration of CD4+ T cells in plaques, secretion of pro-atherosclerotic cytokines, INF-γ and TNF-α synthesized mostly by Th1 cells, and the activation of PI3K/AKT/mTOR signalling were inhibited by the LCK inhibitor. Moreover, the effect of LCK inhibitor on the ratio of Th1 to Treg cells were compromised by activation of mTOR. Together, these data indicate that inhibiting LCK in TCR signalling attenuated the development of AS and promoted plaque stability. Improving RCT by upregulating RCT regulatory proteins and decreasing the Th1/Treg ratio by inhibiting PI3K/AKT/mTOR signalling may contribute to the anti-atherosclerotic effects of LCK inhibition.

SULT2B1b inhibits reverse cholesterol transport and promotes cholesterol accumulation and inflammation in lymphocytes from AMI patients with low LDL-C levels.

The current main treatment for coronary artery disease (CAD) is to reduce low-density lipoprotein cholesterol (LDL-C) by statins, which could decrease the incidence of major adverse cardiovascular events (MACEs) by 30%. However, many residual risks still remain. To clarify the mechanism involved, we studied patients with acute myocardial infarction (AMI) with low LDL-C levels. Lymphocytes were isolated, and it was found that despite no difference in plasma LDL-C level, the lymphocyte cholesterol content was higher in AMI patient than those in non-CAD patients; thus, the decrease in intracellular cholesterol content was inconsistent with that in the plasma. Additionally, [3H]-cholesterol efflux rates were lower and mRNA levels of the inflammatory factors tumour necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) higher in AMI lymphocytes. It was found that sulphotransferase 2B1b (SULT2B1b) expression was higher in AMI lymphocytes. Further research using Jurkat T lymphocytes confirmed that SULT2B1b knockdown increased cholesterol efflux capacity and decreased mRNA levels of TNF-α and IFN-γ by increasing liver X receptor (LXR)-ß levels. Furthermore, the degree of CpG island methylation in the SULT2B1b promoter was reduced in cells from AMI patients. In conclusion, SULT2B1b up-regulation due to hypomethylation of its promoter promotes cholesterol accumulation and inflammation by inhibiting LXR-ß in lymphocytes of AMI patients with low LDL-C levels. Therefore, reducing intracellular cholesterol is also important as plasma cholesterol levels. Therapeutic approaches to decrease SULT2B1b expression might be potentially beneficial for CAD prevention by decreasing intracellular cholesterol.

Association of short-term exposure to sulfur dioxide and hospitalization for ischemic and hemorrhagic stroke in Guangzhou, China.

BACKGROUND: In developing countries, ambient sulfur dioxide (SO2) is a serious air pollutant concern, but there is no enough and consistent epidemiological evidence about its health effects on stroke hospitalization. METHODS: We collected the daily air pollution data, meteorological data and number of daily hospital admissions for ischemic and hemorrhagic stroke, in Guangzhou from January 1st 2009 to December 31st 2014. Then we applied generalized additive model with a quasi-Poisson link to assess the relationship between short-term SO2 exposure and the total number of hospital admissions for ischemic and hemorrhagic stroke. In addition, we evaluated the effect of ambient SO2 by age (< 65 years and ≥ 65 years). RESULTS: During the study period, a 24-h mean concentration of ambient SO2 of 27.82 µg/m3, a total of 58,473 ischemic stroke and 9167 hemorrhagic stroke hospital admissions hospital were recorded. Ambient SO2 was found to increase the risk for both ischemic and hemorrhagic stroke hospital admission in single pollutant model. The maximum value of percentage changes for ischemic and hemorrhagic stroke occurred in lag 0 day and lag 1 day, per 10 µg/m3 increase in SO2 concentrations was corresponded to a 1.27% (95% confidence interval (CI), 0.42-2.12%) and 1.55% (95%CI, 0.02-3.11%) increased risk, respectively. The association between SO2 and ischemic stroke hospitalization was robust to two pollutant model, but for hemorrhagic stroke it's partially weakened after adjusting for co-pollutants. The effect of ambient SO2 on ischemic stroke appeared to be greater for people < 65 years old, but null effect on hemorrhagic stroke was identified for both age groups. CONCLUSIONS: We found short-term exposure to ambient SO2 may significantly increase the risks of hospitalization for ischemic stroke. The findings may contribute to a better understanding of the health effects of low-levels of SO2.

Highly Selective Electrochemical Reduction of CO2 to Alcohols on an FeP Nanoarray.

Electrochemical reduction of CO2 into various chemicals and fuels provides an attractive pathway for environmental and energy sustainability. It is now shown that a FeP nanoarray on Ti mesh (FeP NA/TM) acts as an efficient 3D catalyst electrode for the CO2 reduction reaction to convert CO2 into alcohols with high selectivity. In 0.5 m KHCO3 , such FeP NA/TM is capable of achieving a high Faradaic efficiency (FE CH 3 OH ) up to 80.2 %, with a total FE CH 3 OH + C 2 H 5 OH of 94.3 % at -0.20 V vs. reversible hydrogen electrode. Density functional theory calculations reveal that the FeP(211) surface significantly promotes the adsorption and reduction of CO2 toward CH3 OH owing to the synergistic effect of two adjacent Fe atoms, and the potential-determining step is the hydrogenation process of *CO.

Greatly Improving Electrochemical N2 Reduction over TiO2 Nanoparticles by Iron Doping.

Titanium-based catalysts are needed to achieve electrocatalytic N2 reduction to NH3 with a large NH3 yield and a high Faradaic efficiency (FE). One of the cheapest and most abundant metals on earth, iron, is an effective dopant for greatly improving the nitrogen reduction reaction (NRR) performance of TiO2 nanoparticles in ambient N2 -to-NH3 conversion. In 0.5 m LiClO4 , Fe-doped TiO2 catalyst attains a high FE of 25.6 % and a large NH3 yield of 25.47 µg h-1 mgcat -1 at -0.40 V versus a reversible hydrogen electrode. This performance compares favorably to those of all previously reported titanium- and iron-based NRR electrocatalysts in aqueous media. The catalytic mechanism is further probed with theoretical calculations.

Bimetal Metaphosphate/Molybdenum Oxide Heterostructure Nanowires for Boosting Overall Freshwater/Seawater Splitting at High Current Densities.

Exploring excellent non-noble bifunctional electrocatalysts for freshwater/seawater splitting at high current densities has attracted extensive interest owing to strong anodic oxidation and severe chloride corrosion challenges. Herein, hierarchical bimetal Ni-Co metaphosphate/molybdenum oxide heterostructure nanowires (NiCoMoPO) are rationally designed and fabricated to efficiently boost oxygen evolution reaction (OER) and hydrogen evolution reaction (HER) in alkaline freshwater/seawater, where the favorable electronic structure from heterostructures, signified by X-ray absorption spectra, endows NiCoMoPO with the enhanced intrinsic activity, while its hierarchical nanowire structure and heterostructures provide abundant active sites. Additionally, the PO3 - improves the chloride-corrosion resistance and efficiently facilitates the OER kinetics verified by theoretical and experimental studies. Therefore, NiCoMoPO drives 1000 mA cm-2 at low overpotentials of 467 and 442 mV for OER and HER in alkaline freshwater respectively, as well as a small cell voltage of 2.135 V for overall freshwater splitting with robust durability of 300 h. Impressively, due to the strong corrosion resistance, at 500 mA cm-2 of overall seawater splitting, NiCoMoPO maintains almost 2.096 V for 1200 h, indicating promising practical applications. This work sheds light on the rational design and fabrication of outstanding electrocatalysts at high current densities of seawater/freshwater splitting.

Enhancing Lithium-Sulfur Battery Performance with MXene: Specialized Structures and Innovative Designs.

Established in 1962, lithium-sulfur (Li-S) batteries boast a longer history than commonly utilized lithium-ion batteries counterparts such as LiCoO2 (LCO) and LiFePO4 (LFP) series, yet they have been slow to achieve commercialization. This delay, significantly impacting loading capacity and cycle life, stems from the long-criticized low conductivity of the cathode and its byproducts, alongside challenges related to the shuttle effect, and volume expansion. Strategies to improve the electrochemical performance of Li-S batteries involve improving the conductivity of the sulfur cathode, employing an adamantane framework as the sulfur host, and incorporating catalysts to promote the transformation of lithium polysulfides (LiPSs). 2D MXene and its derived materials can achieve almost all of the above functions due to their numerous active sites, external groups, and ease of synthesis and modification. This review comprehensively summarizes the functionalization advantages of MXene-based materials in Li-S batteries, including high-speed ionic conduction, structural diversity, shuttle effect inhibition, dendrite suppression, and catalytic activity from fundamental principles to practical applications. The classification of usage methods is also discussed. Finally, leveraging the research progress of MXene, the potential and prospects for its novel application in the Li-S field are proposed.

Reducing SULT2B1 promotes the interaction of LncRNAgga3-204 with SMAD4 to inhibit the macrophage inflammatory response and delay atherosclerosis progression.

Inflammation is a crucial pathophysiological mechanism in atherosclerosis (AS). This study aims to investigate the impact of sulfotransferase family 2b member 1 (SULT2B1) on the inflammatory response of macrophages and the progression of AS. Here, we reported that SULT2B1 expression increased with the progression of AS. In AS model mice, knockdown of Sult2b1 led to remission of AS and reduced inflammation levels. Further exploration of the downstream molecular mechanisms of SULT2B1 revealed that suppressing Sult2b1 in macrophages resulted in decreased levels of 25HC3S in the nucleus, elevated expression of Lxr, and increased the transcription of Lncgga3-204. In vivo, knockdown of Lncgga3-204 aggravated the inflammatory response and AS progression, while the simultaneous knockdown of both Sult2b1 and Lncgga3-204 exacerbated AS and the inflammatory response compared with knockdown of Sult2b1 alone. Increased binding of Lncgga3-204 to SMAD4 in response to oxidized-low density lipoprotein (ox-LDL) stimulation facilitated SMAD4 entry into the nucleus and regulated Smad7 transcription, which elevated SMAD7 expression, suppressed NF-κB entry into the nucleus, and ultimately attenuated the macrophage inflammatory response. Finally, we identified the presence of a single nucleotide polymorphism (SNP), rs2665580, in the SULT2B1 promoter region in monocytes from coronary artery disease (CAD) patients. The predominant GG/AG/AA genotypes were observed in the Asian population. Elevated SULT2B1 expression in monocytes with GG corresponded to elevated inflammatory factor levels and more unstable coronary plaques. To summarize, our study demonstrated that the critical role of SULT2B1/Lncgga3-204/SMAD4/NF-κB in AS progression. SULT2B1 serves as a novel biomarker indicating inflammatory status, thereby offering insights into potential therapeutic strategies for AS.

Aqueous alternating electrolysis prolongs electrode lifespans under harsh operation conditions.

It is vital to explore effective ways for prolonging electrode lifespans under harsh electrolysis conditions, such as high current densities, acid environment, and impure water source. Here we report alternating electrolysis approaches that realize promptly and regularly repair/maintenance and concurrent bubble evolution. Electrode lifespans are improved by co-action of Fe group elemental ions and alkali metal cations, especially a unique Co2+-Na+ combo. A commercial Ni foam sustains ampere-level current densities alternatingly during continuous electrolysis for 93.8 h in an acidic solution, whereas such a Ni foam is completely dissolved in ~2 h for conventional electrolysis conditions. The work not only explores an alternating electrolysis-based system, alkali metal cation-based catalytic systems, and alkali metal cation-based electrodeposition techniques, and beyond, but demonstrates the possibility of prolonged electrolysis by repeated deposition-dissolution processes. With enough adjustable experimental variables, the upper improvement limit in the electrode lifespan would be high.

Proline/serine-rich coiled-coil protein 1 inhibits macrophage inflammation and delays atherosclerotic progression by binding to Annexin A2.

BACKGROUND: Atherosclerosis (AS), the main pathological basis of life-threatening cardiovascular disease, is essentially caused by chronic macrophage inflammation. Overexpression of proline/serine-rich coiled-coil protein 1 (PSRC1) reduces macrophage inflammatory responses and delays AS development. However, the exact mechanism of PSRC1 is unclear. METHODS: Proteins interacting with PSRC1 were screened by proteomics in RAW264.7 cells, followed by RT-qPCR, immunoprecipitation and immunofluorescence to explore the specific mechanistic pathways affecting inflammation. CRISPR-Cas9 constructs for PSRC1-/- ApoE-/- (DKO) mice and high-fat diet-fed ApoE-/- and DKO mice were used for AS models for in vivo experiments. Upstream transcription factors of PSRC1 were predicted by ATAC-seq, ChIP-seq and UCSC, and the regulatory mechanism was verified by ChIP-qPCR and dual luciferase assays. Peripheral blood serum and monocytes were collected from coronary artery disease (CAD) patients and non-CAD patients. RESULTS: Increased binding of ANXA2 to PSRC1 in macrophages under oxidized low-density lipoprotein stimulation and decreased release of ANXA2 to the extracellular compartment were observed. Knockdown of ANXA2 in AS model mice delayed AS progression. Knockdown of ANXA2 in DKO mice reversed the AS-promoting effect of PSRC1 knockdown. Mechanistically, ANXA2 promotes STAT3 phosphorylation, which in turn promotes inflammatory responses. In addition, SP1 is a PSRC1 upstream repressive transcription factor, and the SP1 inhibitor mithramycin (Mith) elevated PSRC1 expression and exerted anti-AS effects in AS model mice. Patients with CAD had considerably greater serum levels of ANXA2 than those without CAD, and Mith reduced the secretion of ANXA2 in peripheral blood monocytes of CAD patients. CONCLUSION: In macrophages, PSRC1 can interact with ANXA2 to inhibit its extracellular release and delay AS development. SP1 is an upstream transcription factor of PSRC1 and inhibits the transcription of PSRC1. The SP1 inhibitor Mith can elevate PSRC1 levels and slow AS progression while reducing ANXA2 release from monocytes in CAD patients. Mith is expected to be a new agent for AS treatment.

Phenotypic Changes of Peripheral γδ T Cell and Its Subsets in Patients With Coronary Artery Disease.

Coronary atherosclerotic heart disease (CAD) is a chronic inflammatory cardiovascular disease with high morbidity and mortality. Growing data indicate that many immune cells are involved in the development of atherosclerosis. However, the immunological roles of γδ T cells in the initiation and progression of CAD are not fully understood. Here, we used flow cytometry to determine phenotypical changes of γδ T cells and their subpopulations in peripheral blood samples collected from 37 CAD patients. The Pearson correlation coefficient was used to analyze the relationship between the clinical parameter (serum LDL-C level) and the changes of immunophenotypes of γδ T cells. Our results demonstrated that the frequencies and absolute numbers of total γδ T cells and Vδ2+ T cells were significantly decreased in CAD patients when compared to healthy individuals. However, the proportion of Vδ1+ T cells was much lower in CAD patients than that of healthy individuals. Most importantly, a significant alteration of the Vδ1/Vδ2 ratio was found in CAD patients. In addition, a series of surface markers that are associated with costimulatory signals (CD28, CD40L, CD80, CD86), activation levels (CD69, CD25, HLA-DR), activating NK cell receptors (NKp30, NKp46, NKG2D) and inhibitory receptors (PD-1, CTLA-4, PD-1, Tim-3) were determined and then analyzed in the total γδ T cells, Vδ2+T cells and Vδ2-T cells of CAD patients and healthy individuals. The data demonstrated that immunological activities of total γδ T cells, Vδ2+T cells, and Vδ2-T cells of CAD patients were much lower than those in healthy individuals. Moreover, we found that there were positive correlations between the serum LDL-C levels and frequencies of CD3+γδ+ T cells, CD69+Vδ2+T cells, NKG2D+Vδ2+T cells, and NKp46+Vδ2+T cells. By contrast, there was an inverse correlation between the levels of serum LDL-C and the frequencies of CD69+Vδ2-T cells and NKp46+Vδ2-T cells. Accordingly, these findings could help us to better understand the roles of γδ T cells in the CAD, and shed light on the development of novel diagnostic techniques and therapeutic strategies by targeting γδ T cells for CAD patients.

The activity evidence of Ti defect towards electrocatalytic N2reduction.

Electrochemical N2reduction reaction (NRR) for NH3synthesis, which usually needs highly-efficient electrocatalysts for N2activation, is a carbon-neutral alternation compared to the traditional Haber-Bosch process. Although Ti-based compounds is widely used as electrocatalysts, what Ti defect affects NRR activity is still illusive. In this work, our systematic density functional calculations on Ti defect-decorated titanium oxide disclose that the unsaturated-Ti with the orbital splitting of defect electron states is the necessary feature for N2binding and activation, which can be further enhanced by increasing the splitting degree. The bonding/antibonding orbital population and projected density of states indicate that the nature of N2binding and activation on Ti-defect site is attributed to the elimination of the bonding orbital population in the conduction bands and the formation of*πback-bonding in the valence bands. For the whole NRR process, the synergy of Ti-defect and oxygen vacancy (VO) promotes N2reduction, and the required maximum energy input scales quite well with the adsorption strength of*NNH. Finally, the formed volcano shape successfully predicts new candidate catalysts for ammonia synthesis, such as TiO2combined VOwith Ti interstitial or H atom. This work provides disclosure of the key elements on the rational design of Ti-based nanomaterial electrocatalysts for artificial N2fixation.

Reduced SULT2B1b expression alleviates ox-LDL-induced inflammation by upregulating miR-148-3P via inhibiting the IKKß/NF-κB pathway in macrophages.

Atherosclerosis is a lipid-driven chronic inflammatory disease in which lipid-laden macrophage foam cells lead to inflamed lesions in arteries. Previous studies have proven that sulfotransferase 2B1b (SULT2B1b) has several roles in the regulation of lipid metabolism and the inflammatory response. However, little is known about the functions of SULT2B1b in ox-LDL-induced inflammation in macrophages. In this study, after treatment with either ox-LDL alone or combined with transfection of siRNAs targeting SULT2B1b, IL-6, TNF-α, NF-κB, IKKß and IκB mRNA and protein expression were determined in Raw264.7 cells by real-time PCR and Western blot, respectively. The proliferative capacity was determined by EdU staining and Cell Counting Kit-8. Our data demonstrated that SULT2B1b knockdown could reduce phosphorylated NF-κB levels and downregulate IKKß protein levels. Additionally, IκB levels were increased and the proliferation of ox-LDL stimulated cells was inhibited after SULT2B1b silencing. Downregulation of SULT2B1b expression was found to upregulate miR-148a-3p expression by microarray assay, while IKKß was a miR-148a-3p target gene. Our study suggests that SULT2B1b knockdown could promote miR148a-3p expression and inhibit activation of the IKKß/NF-κB signalling pathway, which suppressed the inflammatory response in macrophages. Therefore, targeting the SULT2B1b gene might be potentially beneficial for atherosclerosis prevention by decreasing the inflammatory response.

[Serum annexin A2 level is significantly elevated in patients with coronary heart disease].

OBJECTIVE: To analyze the correlation of annexin A2 with coronary atherosclerotic heart disease (CAD) and the severity of CAD. METHODS: We collected data from a total of 200 inpatients admitted in our department between August, 2017 and August, 2019. According to the. RESULTS: of coronary angiography, the patients were divided into CAD group (n=150) and non-CAD (n=50), and the CAD patients was further divided, according to their clinical stability, into stable angina (SAP) group and acute coronary syndrome (ACS) group. Serum levels of annexin A2, MPO and PON1 were detected in all these patients, and their correlations with CAD, disease severity, and degree of coronary artery stenosis were analyzed.ResultsThe levels of annexin A2 and MPO were significantly higher in CAD patients than in non-CAD patients (P < 0.05). Among the CAD patients, those with ACS had significantly higher levels of annexin A2 (P < 0.05) and lower levels of PON-1 (P < 0.05) than those with SAP, but annexin A2 level was not significantly correlated with coronary lesion count, Gensini score, or the co-morbidity of diabetes. CONCLUSIONS: Annexin A2 is significantly elevated in patients with CAD, especially in those with ACS, and can be used as a predictor of clinical instability.