Circ_0000069 promotes the development of hepatocellular carcinoma by regulating CCL25.

BACKGROUND: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths globally, influenced by aberrant circRNA expression. Investigating circRNA-miRNA-mRNA interactions can unveil underlying mechanisms of HCC and identify potential therapeutic targets. METHODS: In this study, we conducted differential analyses of mRNAs, miRNAs, and circRNAs, and established their relationships using various databases such as miRanda, miRDB, and miTarBase. Additionally, functional enrichment and immune infiltration analyses were performed to evaluate the roles of key genes. We also conducted qPCR assays and western blotting (WB) to examine the expression levels of circRNA, CCL25, and MAP2K1 in both HCC cells and clinical samples. Furthermore, we utilized overexpression and knockdown techniques for circ_0000069 and conducted wound healing, transwell invasion assays, and a tumorigenesis experiment to assess the migratory and invasive abilities of HCC cells. RESULTS: Our findings revealed significant differential expression of 612 upregulated genes and 1173 downregulated genes in HCC samples compared to normal liver tissue. Additionally, 429 upregulated circRNAs and 453 downregulated circRNAs were identified. Significantly, circ_0000069 exhibited upregulation in HCC tissues and cell lines. The overexpression of circ_0000069 notably increased the invasion and migration capacity of Huh7 cells, whereas the downregulation of circ_0000069 reduced this capability in HepG2 cells. Furthermore, this effect was counteracted by CCL25 silencing or overexpression, separately. Animal studies further confirmed that the overexpression of hsa_circ_0000069 facilitated tumor growth in xenografted nude mice, while the inhibition of CCL25 attenuated this effect. CONCLUSION: Circ_0000069 appears to promote HCC progression by regulating CCL25, suggesting that both circ_0000069 and CCL25 can serve as potential therapeutic targets.

miR-10b-5p promotes tumor growth by regulating cell metabolism in liver cancer via targeting SLC38A2.

Metabolic reprogramming plays a critical role in hepatocarcinogenesis. However, the mechanisms regulating metabolic reprogramming in primary liver cancer (PLC) are unknown. Differentially expressed miRNAs between PLC and normal tissues were identified using bioinformatic analysis. RT-qPCR was used to determine miR-10b-5p and SCL38A2 expression levels. IHC, WB, and TUNEL assays were used to assess the proliferation and apoptosis of the tissues. The proliferation, migration, invasion, and apoptosis of PLC cells were determined using the CCK-8 assay, Transwell assay, and flow cytometry. The interaction between miR-10b-5p and SLC38A2 was determined using dual-luciferase reporter assay. A PLC xenograft model in BALB/c nude mice was established, and tumorigenicity and SLC38A2 expression were estimated. Finally, liquid chromatography - mass spectrometry (LC-MS) untargeted metabolomics was used to analyze the metabolic profiles of xenograft PLC tissues in nude mice. miR-10b-5p was a key molecule in the regulation of PLC. Compared with para-carcinoma tissues, miR-10b-5p expression was increased in tumor tissues. miR-10b-5p facilitated proliferation, migration, and invasion of PLC cells. Mechanistically, miR-10b-5p targeted SLC38A2 to promote PLC tumor growth. Additionally, miR-10b-5p altered the metabolic features of PLC in vivo. Overexpression of miR-10b-5p resulted in remarkably higher amounts of lumichrome, folic acid, octanoylcarnitine, and Beta-Nicotinamide adenine dinucleotide, but lower levels of 2-methylpropanal, glycyl-leucine, and 2-hydroxycaproic acid. miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment.

CircCDK17 promotes the proliferation and metastasis of ovarian cancer cells by sponging miR-22-3p to regulate CD147 expression.

Ovarian cancer (OC) is a common malignancy in women of reproductive age. Circular RNAs (circRNAs) are emerging players in OC progression. We investigated the function and mechanism of circular RNA hsa_circ_0027803 (circCDK17) in OC pathogenesis. Real­time PCR (RT-qPCR) and western blot were utilized for gene and protein expression analysis, respectively. Cell counting kit­8 (CCK-8), EdU and Transwell assays investigated OC cell proliferation, migration and invasion. The associations between circCDK17, miR-22-3p and CD147 were examined by dual-luciferase reporter and RNA-protein immunoprecipitation (RIP) assays. The in vivo model of OC nude mice was constructed to explore the role of circCDK17. CircCDK17 was increased in OC tissue and cells, and patients with higher expression of circCDK17 had a shorter survival. CircCDK17 downregulation inhibited OC cell proliferation, migration and invasion, and reduced epithelial-mesenchymal transition (EMT)-related markers. In vivo experiments showed that circCDK17 silencing inhibited OC tumor growth and metastasis. CircCDK17 depletion reduced CD147 level via sponging miR-22-3p. MiR-22-3p knockdown overturned effect of circCDK17 depletion on OC cell proliferation, migration and invasion. Meanwhile, overexpressed CD147 restored functions of circCDK17 downregulation on OC development. CircCDK17 is an important molecule that regulates OC pathogenic process through miR-22-3p/CD147.

E2F1-mediated KDM4A-AS1 up-regulation promotes EMT of hepatocellular carcinoma cells by recruiting ILF3 to stabilize AURKA mRNA.

Hepatocellular carcinoma (HCC) is a gastrointestinal tumor with high clinical incidence. Long non-coding RNAs (lncRNAs) play vital roles in modulating the growth and epithelial-mesenchymal transition (EMT) of HCC. However, the underlying mechanism of lncRNA KDM4A antisense RNA 1 (KDM4A-AS1) in HCC remains elusive. In our study, the role of KDM4A-AS1 in HCC was systematically investigated. The levels of KDM4A-AS1, interleukin enhancer-binding factor 3 (ILF3), Aurora kinase A (AURKA), and E2F transcription factor 1 (E2F1) were determined by RT-qPCR or western blot. ChIP and dual luciferase reporter experiments were performed to detect the binding relationship between E2F1 and KDM4A-AS1 promoter sequence. RIP and RNA-pull down confirmed the interaction of ILF3 with KDM4A-AS1/AURKA. Cellular functions were analyzed by MTT, flow cytometry, wound healing and transwell assays. IHC was performed to detect Ki67 in vivo. We found that KDM4A-AS1 was increased in HCC tissues and cells. Elevated KDM4A-AS1 level was correlated to poor prognosis of HCC. Knockdown of KDM4A-AS1 inhibited the proliferation, migration, invasion and EMT of HCC cells. ILF3 bound to KDM4A-AS1 and AURKA. KDM4A-AS1 maintained the stability of AURKA mRNA by recruiting ILF3. E2F1 transcriptionally activated KDM4A-AS1. Overexpressed KDM4A-AS1 reversed the contribution of E2F1 depletion to AURKA expression and EMT in HCC cells. KDM4A-AS1 promoted tumor formation in vivo through the PI3K/AKT pathway. These results revealed that E2F1 transcriptionally activated KDM4A-AS1 to regulate HCC progression via the PI3K/AKT pathway. E2F1 and KDM4A-AS1 may serve as good prognostic targets for HCC treatment.

MiR-1-3p enhances the sensitivity of ovarian cancer cells to ferroptosis by targeting FZD7. / MiR-1-3p通过靶向FZD7增强卵巢癌细胞对铁死亡的敏感性.

OBJECTIVES: Frizzled 7 (FZD7) is abnormally expressed and activated in a variety of cancers. In ovarian cancer, overexpression of FZD7 reduces the sensitivity of platinum-resistant ovarian cancer cells to ferroptosis, thereby allowing cancer cells to survive. However, whether FZD7 inhibits ferroptosis in ovarian cancer cells and its mechanisms are remain unclear. This study aims to explore the effects of FZD7 and its upstream regulator miR-1-3p on ferroptosis in ovarian cancer cells are evaluated to clarify the molecular mechanism for miR-1-3p and FZD7's involvement in ferroptosis in ovarian cancer cells. METHODS: Human ovarian cancer cell lines HO8910 and SKOV3 were used as the research subjects. In the first part of the experiment, human ovarian cancer cells were transfected with blank plasmid and FZD7 overexpression plasmid, respectively; in the second and third parts, human ovarian cancer cells were transfected with miR-1-3p mimics negative control, miR-1-3p mimics, miR-1-3p inhibitors negative control, and miR-1-3p inhibitors, respectively; in the fourth part of the experiment, human ovarian cancer cells were transfected with miR-1-3p mimics and miR-1-3p mimics+FZD7 overexpression plasmid, respectively, and normal cultured cells were set as the control group. The human ovarian cancer cell ferroptosis model was established by incubating human ovarian cancer cells with different treatments with ferroptosis inducer Erastin or RSL3. Real-time RT-PCR was used to detect the mRNA expression levels of FZD7 and miR-1-3p; Western blotting was used to detect the protein expression levels of FZD7; CCK-8 assay was used to detect the cell viability; lipid peroxidation colorimetric assay kit was used to detect the level of intracellular MDA; and iron assay kit was used to detect the level of intracellular Fe2+. Dual-luciferase assay was used to detect the targeting relationship between miR-1-3p and FZD7. RESULTS: Overexpression of FZD7 increased the cell viability of human ovarian cancer cell lines HO8910 or SKOV3 (P<0.05, P<0.01, or P<0.001) and decreased the intracellular MDA levels (P<0.01) in Erastin-treated or RSL3-treated ovarian cancer cells. FZD7 was a direct target of miR-1-3p, which inhibited the expression of FZD7 (P<0.01) by binding to the 3'-untranslated region (3'UTR) site of FZD7. MiR-1-3p mimics decreased the cell viability of human ovarian cancer cell lines HO8910 or SKOV3 (P<0.05, P<0.01, or P<0.001) and increased the intracellular MDA levels (P<0.01) in Erastin-treated or RSL3-treated ovarian cancer cells; while miR-1-3p inhibitors significantly increased the cell viability of human ovarian cancer cell lines HO8910 or SKOV3 (P<0.05, P<0.01, or P<0.001) and decreased the intracellular MDA levels (P<0.01) in Erastin-treated or RSL3-treated ovarian cancer cells. The effect of miR-1-3p mimics on enhancing the sensitivity of human ovarian cancer cells to Erastin-induced or RSL3-induced ferroptosis was abrogated by overexpression of FZD7(P<0.05 or P<0.01). CONCLUSIONS: MiR-1-3p enhances the sensitivity of ovarian cancer cells to ferroptosis by targeting FZD7.

LncRNA KCNQ1OT1 accelerates ovarian cancer progression via miR-125b-5p/CD147 axis.

BACKGROUND: Ovarian cancer (OC) is one of the most common gynecological malignancies with a high incidence. Researches showed that lncRNA KCNQ1OT1 (KCNQ1OT1) was involved various tumors progression, including OC. However, the precise mechanism of KCNQ1OT1 in OC needs to be further clarified. OBJECTIVE: For investigate the underlying mechanism of KCNQ1OT1 regulating OC progression. METHODS: CCK-8 assay, colony formation assay, Transwell assay, Western blot and quantitative real-time PCR (qRT-PCR) were performed to examine viability, proliferation, migration and invasion, genes and proteins' level. To identify KCNQ1OT1 as a regulator of miR-125b-5p and miR-125b-5p as a regulator of CD147, we used miRNA target prediction algorithms, Pearson's correlation analysis and dual-luciferase reporter gene assay. RESULTS: KCNQ1OT1 was high expression and miR-125b-5p was low expression in OC, and KCNQ1OT1 was negatively correlated with that of miR-125b-5p in OC specimens. KCNQ1OT1 promoted OC cell proliferation and metastasis by binding to miR-125b-5p. miR-125b-5p targeted CD147, and which was negatively correlated with that of miR-125b-5p in OC specimens. KCNQ1OT1 was positively correlated with that of CD147 in OC specimens, and KCNQ1OT1 accelerated OC progression via miR-125b-5p/CD147 axis. CONCLUSION: KCNQ1OT1 accelerated OC progression via miR-125b-5p/CD147 axis indicating KCNQ1OT1 serve as a novel biomarker for OC treatment. Our research provides a new direction for OC treatment.

Identification of key snoRNAs serves as biomarkers for hepatocellular carcinoma by bioinformatics methods.

BACKGROUND: Hepatocellular carcinoma (HCC) is a common malignancy with high mortality and poor prognosis due to a lack of predictive markers. However, research on small nuclear RNAs (snoRNAs) in HCC were very little. This study aimed to identify a potential diagnostic and prognostic snoRNA signature for HCC. METHODS: HCC datasets from the cancer genome atlas (TCGA) and international cancer genome consortium (ICGC) cohorts were used. Differentially expressed snoRNA (DEs) were identified using the limma package. Based on the DEs, diagnostic and prognostic models were established by the least absolute shrinkage and selection operator (LASSO) regression and COX analysis, and Kaplan-Meier (K-M) survival analysis and receiver operating characteristic (ROC) curve analysis were conducted to evaluate the efficiency of signatures. Gene set enrichment analysis (GSEA) and gene set variation analysis (GSVA) were used to analyze the risk score and further explore the potential correlation between the risk groups and tumor immune status in TCGA. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to determine the functions of key snoRNAs. RESULTS: We constructed a 6-snoRNAs signature which could classify patients into high- or low-risk groups and found that patients in the high-risk group had a worse prognosis than those in the low-risk group and were significantly involved in p53 processes. Tumor immune status analysis revealed that CTLA4 and PDCD1 (PD1) were highly expressed in the high-risk group, which responded to PD1 inhibitor therapy. Additionally, a 25-snoRNAs diagnostic signature was constructed with an area under the curve (AUC) of 0.933 for distinguishing HCCs from normal controls. Finally, 3 key snoRNAs (SNORA11, SNORD124, and SNORD46) were identified with both diagnostic and prognostic efficacy, some of which were closely related to the spliceosome and Notch signaling pathways. CONCLUSIONS: Our study identified 6 snoRNAs that may serve as novel prognostic models and 3 key snoRNAs with both diagnostic and prognostic efficacy for HCC.

Comparison of surgical resection and radiofrequency ablation for stages I and II elderly hepatocellular carcinoma patients (≥ 65 years): A SEER population-based propensity score matching's study.

Objectives: The treatment for hepatocellular carcinoma (HCC) remains controversial and limited in elderly patients. Therefore, we aimed to explore treatment choices for the elderly patients (≥ 65years) following surgical resection (SR) versus radiofrequency ablation (RFA) with HCC (single lesion less than 5 cm). Methods: We used SEER database to identify HCC patients who received treatment of SR/RFA. Kaplan-Meier method and Cox proportional hazards regression method were used to determine the prognostic factors associated with overall survival (OS) and disease-specific survival (DSS). In addition, RFA group and SR group patients were matched with 1:1 propensity score matching (PSM) for diagnosis age, sex, race, marital, American Joint Committee on Cancer (AJCC), grade, radiotherapy, and chemotherapy to decrease the possibility of selection bias. Conditional disease-specific survival (CS) was estimated using the life-table method. Results: A total of 794 patients who underwent SR and 811 patients who underwent RFA were confirmed from the SEER database. Surgery type was an independent risk factor for HCC. Survival analysis indicated that SR, races, AJCC I, no chemotherapy treatment, and grade I were cumulative risk factors that can significantly improve median survival for HCC (P < 0.05). After PSM analysis, only surgery type was significantly improved median survival of HCC patients (SR vs. RFA, HR: 0.644, 95% CI: 0.482-0.86; P < 0.001). For RFA group, the 2-, 3-, and 5-year CS rates were approximately 71%, 65%, and 62%, respectively, and corresponding to 82%, 80%, and 78% in the SR group. Conclusion: SR treatment can provide survival benefits for elderly patients of <5 cm single lesion HCC.

Biaxially Compressive Strain in Ni/Ru Core/Shell Nanoplates Boosts Li-CO2 Batteries.

Regulating surface strain of nanomaterials is an effective strategy to manipulate the activity of catalysts, yet not well recognized in rechargeable Li-CO2 batteries. Herein, biaxially compressive strained nickel/ruthenium core/shell hexagonal nanoplates (Ni/Ru HNPs) with lattice compression of ≈5.1% and ≈3.2% in the Ru {10-10} and (0002) facets are developed as advanced catalysts for Li-CO2 batteries. It is demonstrated that tuning the electronic structure of Ru shell through biaxially compressive strain engineering can boost the kinetically sluggish CO2 reduction and evolution reactions, thus achieving a high-performance Li-CO2 battery with low charge platform/overpotential (3.75 V/0.88 V) and ultralong cycling life (120 cycles at 200 mA g-1 with a fixed capacity of 1000 mAh g-1 ). Density functional theory calculations reveal that the biaxially compressive strain can downshift the d-band center of surface Ru atoms and thus weaken the binding of CO2 molecules, which is energetically beneficial for the nucleation and decomposition of Li2 CO3 crystals during the discharge and charge processes. This study confirms that strain engineering, though constructing a well-defined core/shell structure, is a promising strategy to improve the inherent catalytic activity of Ru-based materials in Li-CO2 batteries.

Histone Demethylase GASC1 Inhibitor Targeted GASC1 Gene to Inhibit the Malignant Transformation of Esophageal Cancer through the NOTCH-MAPK Signaling Pathway.

OBJECTIVE: Esophageal cancer is a common gastrointestinal tumor, with high incidence in our country. Histone demethylase 4 plays an important role in chromosome structural modification and gene expression regulation, becoming a new target for tumor treatment. GASC1 is an important member of the KDM4 family, closely related to the malignancy of tumors. METHODS: Constructing the short hairpin interfering RNA plasmid and blank control plasmid of gene KDM4C (also known as GASC1), transfecting them into human esophageal squamous cell carcinoma cell lines (KYSE-150 and KYSE-30, respectively), and screening the best treatment concentration based on cell viability. Cell cloning experiments analyzed the proliferation characteristics of each group of cells. Cell migration and scratch healing experiments analyzed the tumor's malignant metastasis and invasion capabilities. Immunofluorescence analysis was used to test the expression characteristics of protein GASC1. Western blot was used to analyze protein Notch1, HIF1A, Flt-1, c-myc, c-fos expression in each group of cell lines. RESULTS: In this experiment, caffeic acid and interfering RNA plasmids were added to regulate the expression level of GASC1 protein in each group. After that, a series of characterization methods were used to determine the positive correlation of the metastasis and proliferation ability of esophageal cancer cells with the expression level of GASC1 protein. The regulation of GASC1 protein was further proved by measuring the expression of each cancer-related protein. CONCLUSION: GASC1 gene plays a crucial role in the progression of esophageal cancer. By inhibiting the expression of GASC1 gene, pathways closely related to cancer development such as NOTCH and MAPK will also be inhibited, which may ultimately control the malignant development.

Insights into Antiperovskite Ni3 In1-x Cux N Multi-Crystalline Nanoplates and Bulk Cubic Particles as Efficient Electrocatalysts on Hydrogen Evolution Reaction.

Intrinsic hydrogen evolution reaction (HER) activity and the mechanism of antiperovskite Ni3 In1-x Cux N bulk cubic particles and multi-crystalline nanoplates are thoroughly investigated. Stoichiometric Ni3 In0.6 Cu0.4 N reaches the best HER performance, with an overpotential of 102 mV in its multi-crystalline nanoplates obtained from the LDH-derived method, and 143 mV in its bulk cubic particles from the citric method. DFT calculation reveals that Ni-In or Ni-Cu paired on the (100) plane serve as primary active sites. The Ni-Cu pair exhibits stronger OH* and H* affinity that correspondingly reduce OH* and H* adsorption free energy. Introducing specific amounts of the Ni-Cu pair, that is In:Cu = 0.6:0.4 in Ni3 In0.6 Cu0.4 N, can optimize OH* and H* adsorption free energy to facilitate water dissociation in the HER process, while avoiding OH* adsorption getting too strong to block active sites. Besides, Ni3 In0.6 Cu0.4 N turns the water adsorption step spontaneous, which may be attributed to the shifted d-band center and polarizing effect from surface In-Cu charge distribution. This work expands the scope for material design in an antiperovskite system by tailoring the chemical components and morphology for optimal reaction free energy and performance.

Boron-Functionalized Organic Framework as a High-Performance Metal-Free Catalyst for N2 Fixation.

Inspired by the recently synthesized covalent organic framework (COF) containing triquinoxalinylene and benzoquinone units (TQBQ) in the skeleton, we study the stability and properties of its two-dimensional analogue, TQBQCOF, and examine its potential for the synthesis of ammonia using first-principles calculations. We show that the TQBQCOF sheet is mechanically, dynamically, and thermally stable up to 1200 K. It is a semiconductor with a direct band gap of 2.70 eV. We further investigate the electrocatalytic reduction of N2to NH3on the Boron-functionalized TQBQCOF sheet (B/TQBQCOF). The rate-determining step of the catalytic pathways is found to be *N-N → *N-NH for the distal, alternating, and enzymatic catalytic mechanisms, with the corresponding overpotentials of 0.65, 0.65, and 0.07 V, respectively. The value of 0.07 V is the lowest required voltage among all of the N2 reduction catalysts reported so far, showing the potential of B/TQBQCOF as a metal-free catalyst to effectively reduce N2to NH3.

Genome-scale CRISPR-Cas9 knockout screening in hepatocellular carcinoma with lenvatinib resistance.

Lenvatinib is the first target drug approved for advanced hepatocellular carcinoma (HCC). However, the development of drug resistance is common, and the mechanisms of lenvatinib resistance and resistant targets in HCC are poorly understood. By using CRISPR/Cas9 library screening, we screened out two key resistance genes, neurofibromin 1(NF1), and dual specificity phosphatase 9 (DUSP9), as critical drivers for lenvatinib resistance in HCC. With RNAi knockdown and CRISPR/Cas9 knockout models, we further clarified the mechanisms by which NF1 loss reactivates the PI3K/AKT and MAPK/ERK signaling pathways, while DUSP9 loss activates the MAPK/ERK signaling pathways, thereby inactivating FOXO3, followed by degradation of FOXO3, finally induced lenvatinib resistance. We also screened out trametinib, a small molecule pathway inhibitor for MEK, that can be used to reverse resistance induced by NF1 and DUSP9 loss in HCC cells. Trametinib was still able to halt HCC growth even when NF1 was knocked out in mice. Collectively, the findings indicate that NF1 and DUSP9 takes critical role in lenvatinib resistance and may be novel specific targets and predictive markers for lenvatinib resistance in HCC.

Cu Atomic Chain Supported on Graphene Nanoribbon for Effective Conversion of CO2 to Ethanol.

The front cover artwork is provided by the group of Prof. Qiang Sun (Peking University, China). The image shows how Cu-decorated zigzag graphene nanoribbons can catalyze CO2 reduction to ethanol with a small energy barrier and tunable selectivity. Read the full text of the Article at 10.1002/cphc.202000476.

Cu Atomic Chain Supported on Graphene Nanoribbon for Effective Conversion of CO2 to Ethanol.

Cu catalysts are well-known for their good performance in CO2 conversion. Compared to CO and CH4 production, C2 products have higher volumetric energy densities and are more valuable in industrial applications. In this work, we screened the catalytic ability of C2 production on several 1D Cu atomic chain structures and find that Cu edge-decorated zigzag graphene nanoribbons (Cu-ZGNR) are capable of catalyzing CO2 conversion to ethanol, and CH3 CH2 OH is the main C2 product with a maximum free energy change of 0.60 eV. The planar tetracoordinate carbon structures in Cu-ZGNR provide unique chemical bonding features for catalytic reaction on the Cu atoms. Detailed mechanism analyses with transition states search show that CO* dimerization is favored against CHO* formation in the reaction. By adjusting the CO* coverage, the selectivity of the C2 product can be enhanced owing to less pronounced steric effects for COCHO*, which is feasible under experimental conditions. This study expands the catalyst family for C2 products from CO2 based on nano carbon structures with new features.

Metal-free Catalyst B2 S Sheet for Effective CO2 Electrochemical Reduction to CH3 OH.

Considering the problems of high costs, low catalytic activity and selectivity in the metal-based catalysts for CO2 electroreduction, we apply boron-containing metal-free B2 S sheet as an alternative to the traditional metal-based catalysts. Reaction energy calculations identify the preferred "Formate" pathway for CO2 conversion to CH3 OH on B2 S, in which the thermodynamic energy barrier obtained by using the Computational Hydrogen Electrode model is 0.57 eV, and the kinetic energy barrier obtained by searching the transition states is 1.18 eV. Another possible reaction pathway, "RWGS+CO-hydro", is suppressed and the hydrogen evolution reaction (HER) side reaction is nonspontaneous. Compared to Cu(211) with the highest catalytic activity among all transition metals, B2 S sheet exhibits a better catalytic activity with a lower overpotential for CO2 reduction and a better selectivity that suppresses the non-target reaction.

Antiperovskite Intermetallic Nanoparticles for Enhanced Oxygen Reduction.

Antiperovskite Co3 InC0.7 N0.3 nanomaterials with highly enhanced oxygen reduction reaction (ORR) performance were prepared by tuning nitrogen contents through a metal-organic framework (MOF)-derived strategy. The nanomaterial surpasses all reported noble-metal-free antiperovskites and even most perovskites in terms of onset potential (0.957 V at J=0.1 mA cm-2 ) and half-wave potential (0.854 V). The OER and zinc-air battery performance demonstrate its multifunctional oxygen catalytic activities. DFT calculation was performed and for the first time, a 4 e- dissociative ORR pathway on (200) facets of antiperovskite was revealed. Free energy studies showed that nitrogen substitution could strengthen the OH desorption as well as hydrogenation that accounts for the enhanced ORR performance. This work expands the scope for material design via tailoring the nitrogen contents for optimal reaction free energy and hence performance of the antiperovskite system.

Ambiguity Resolution for Passive 2-D Source Localization with a Uniform Circular Array.

This paper proposes two novel phase-based algorithms for the passive localization of a single source with a uniform circular array (UCA) under the case of measuring phase ambiguity based on two phase difference observation models, which are defined as the unambiguous-relative phase observation model (UARPOM) and the ambiguous-relative phase observation model (ARPOM). First, by analyzing the varying regularity of the phase differences between the adjacent array elements of a UCA, the corresponding relationship between the phase differences and the azimuth and elevation angle of the signal is derived. Based on the two phase observation models, two corresponding novel algorithms, namely, the phase integral accumulation and the randomized Hough transform (RHT), are addressed to resolve the phase ambiguity. Then, by using the unambiguous phase differences, the closed-form estimates of the azimuth and elevation angles are determined via a least squares (LS) algorithm. Compared with the existing phase-based methods, the proposed algorithms improve the estimation accuracy. Furthermore, our proposed algorithms are more flexible for the selection of an array radius. Such an advantage could be applied more broadly in practice than the previous methods of ambiguity resolution. Simulation results are presented to verify the effectiveness of the proposed algorithm.

Cu atomic chains supported on ß-borophene sheets for effective CO2 electroreduction.

The good performance of Cu displayed in CO2 conversion promotes the study on how to disperse Cu into 2D materials for better catalysis. Inspired by the recent studies on new 2D porous B sheets [Angew. Chem., Int. Ed., 2017, 56, 10093; Adv. Mater., 2018, 30, 1704025; Phys. Rev. Lett., 2017, 118, 096401], here for the first time we have explored the catalytic properties of Cu atomic chains on ß-borophene sheets, and have found that the Cu-B sheet can break the scaling relationship through providing secondary adsorption sites, thus leading to small overpotentials in the preferable reaction pathway CO2 → COOH* → CO* → CHO* → CH2O* → CH3O* → CH3OH. The Cu atomic chains also lower the energy barrier by forming assistant adsorptions of H*. Electronic structure analyses further show that the Cu atomic chain structure stabilizes the CHO* bonding through an enhanced σ bonding-π back-bonding mode. Our study not only sheds light on the design of new catalysts for effective CO2 conversion but also expands the applications of B sheets.