Moderate/severe biatrial dilation predicts adverse events after ablation in atrial fibrillation with heart failure.

AIMS: To retrospectively compare the long-term outcomes following atrial fibrillation (AF) ablation between heart failure (HF) with preserved ejection fraction (EF) (HFpEF) and reduced/mildly reduced EF (HFr-mrEF) patients, and to identify novel predictors of adverse clinical events. METHODS: In total, 1402 AF patients with HF who underwent successful ablation were consecutively enrolled. Adverse clinical events including all-cause death, HF hospitalization, and stroke were followed up. Cox proportional hazards models were used to assess the associations between clinical factors and events. Kaplan-Meier analysis was performed to estimate the cumulative incidences of these events. A receiver operating characteristic curve was used to test the ability of these predictors. RESULTS: During a follow-up period of 42 ± 15 months, 265 (18.9%) patients experienced adverse clinical events after ablation. The cumulative incidence of adverse clinical events was significantly higher in HFr-mrEF than in HFpEF (25.4% vs. 15.7%, P < 0.001), the similar tendency was observed on all-cause death (10.5% vs. 6.5%, P = 0.011) and HF hospitalization (17.2% vs. 10.1%, P < 0.001). After multivariate adjustment, non-paroxysmal AF [hazard ratio (HR) 1.922, 95% confidence interval (CI) 1.130-3.268, P = 0.016], LAD ≥ 45 mm (HR 2.197, 95% CI 1.206-4.003, P < 0.001), LVEF (HR 0.959, 95% CI 0.946-0.981, P < 0.001), and RAD ≥ 45 mm (HR 2.044, 95% CI 1.362-3.238, P < 0.001) remained the independent predictors for developing adverse clinical events. A predictive model performed with non-paroxysmal AF, LAD ≥ 45 mm and RAD ≥ 45 mm yielded an area under curve of 0.728 (95% CI 0.696-0.760, P < 0.001). CONCLUSIONS: AF patients with HFpEF had better long-term outcomes than those with HFr-mrEF, and moderate/severe biatrial dilation could predict adverse clinical events following catheter ablation in AF and HF patients.

Evaluation of bidirectional causal association between cardiovascular diseases and pneumonia: A Mendelian randomization study.

AIMS: Observational evidence suggests a bidirectional relationship between cardiovascular diseases (CVDs) and pneumonia. However, the causality between CVDs and pneumonia remains undetermined. Thus, we aimed to investigate the bidirectional causality between CVDs and pneumonia using Mendelian randomization (MR) analysis. METHODS: Global genetic correlation analysis and bidirectional two-sample MR analysis were performed to infer the genetic correlation and causality between CVDs and pneumonia by using genome-wide association study (GWAS) summary data from GWAS meta-analysis study, FinnGen or UK Biobank consortium. Post-hoc power calculation was conducted to assess the power for detecting the causality. RESULTS: The linkage disequilibrium score regression analysis suggested a positive significant genetic correlation between CVDs and pneumonia. In the MR analysis, only genetically predicted ischemic stroke was causally associated with any pneumonia (odds ratio [OR]: 1.119, 95% confidence interval [CI]: 1.031-1.393), bacterial pneumonia (OR: 1.251, 95% CI: 1.032-1.516), and pneumococcal pneumonia (OR: 1.308, 95% CI: 1.093-1.565), but the causality was attenuated to non-significance after adjusting for deep venous thrombosis. However, the causal effects of pneumonia on CVDs were not detected. Post-hoc power calculations supported strong power (more than 80%) to detect the causality. CONCLUSIONS: Ischemic stroke is causally associated with an increased risk of pneumonia, but there is no evidence for the causal effect of pneumonia on CVDs. Our findings have important implications as they provide further support for the thrombosis risk screening as a strategy to reduce the incidence of pneumonia in patients with ischemic stroke.

This Mendelian randomization analysis aimed to investigate the bidirectional causality between cardiovascular diseases and pneumonia. Our findings support the causal association of ischemic stroke on pneumonia, but indicate no evidence for the causal effects of pneumonia on cardiovascular diseases. The causal association of ischemic stroke on pneumonia was revealed to rely on deep venous thrombosis, which provided further support for the thrombosis risk screening as a strategy to reduce the incidence of pneumonia in patients with ischemic stroke.

Epidemiologic Characteristics of SARS-CoV-2 Omicron BA.5.1.3 Variant and the Protection Provided By Inactivated Vaccination.

Omicron variants have become the dominant SARS-CoV-2 variants due to their increased transmissibility and immune-escape ability. An outbreak of the Omicron variant BA.5.1.3 occurred in August 2022 in Sanya, China. Studying Omicron variants can promote the understanding of them and further contribute to managing the SARS-CoV-2 prevalence. This retrospective study analyzed the data of 258 patients with asymptomatic or mild SARS-CoV-2 admitted to the First Cabin Hospital of Sanya, China, between August 14 and September 4, 2022. The 258 patients comprised 128 males and 130 females with a mean age of 36.6 years and mean length of medical observation (LMO) of 10.1 days. Multiple linear regression analysis indicated that LMO was positively and negatively associated with age (p = 0.036) and vaccination status (p = 0.004), respectively. A Cox proportional-hazards model revealed that age (hazard ratio [HR] = 0.99, p = 0.029) and vaccination (HR = 1.23, p = 0.023) were risk and protective factors for LMO, respectively. Causal mediation analysis indicated that vaccination suppressed the effect of prolonging LMO caused by increasing age. Recovery times became longer with increasing age, which could be counterbalanced by vaccination. The present results indicate that vaccination interventions, even those developed through inactivated approaches, can still provide protection against Omicron variants.

The Mechanisms of Resistin-Like Molecule-ß-Mediated Airway Inflammation in Chronic Obstructive Pulmonary Disease via Autophagy.

Background: The role of irreversible airway inflammatory damage in chronic obstructive pulmonary disease (COPD) progression is evident. Autophagy is an essential process in the cellular material metabolic cycle, and a family of resistant vegetative molecules may be involved in the COPD autophagic process. In this study, we investigated the mechanism of resistin-like molecule ß (RELMß) in COPD smoking-induced autophagy. Methods: Firstly, the expression differences of RELMß and autophagy markers between COPD and control groups were analyzed in the Gene Expression Omnibus (GEO) datasets and clinical specimens. Secondly, in vitro and in vivo experiments were conducted using immunoblotting, immunofluorescence, immunohistochemistry, and other methods to investigate the mechanism by which RELMß promotes airway inflammation through autophagy in a cigarette smoke extract-induced 16HBE cell inflammation model and a cigarette smoke-induced COPD-like mouse model. In addition, immunoprecipitation was used to analyze the binding of RELMß to the membrane protein TLR4. Results: The expression of RELMß and autophagy genes p62 and LC3B in lung tissue of COPD patients was significantly increased. RELMß can mediate the activation of autophagy in 16HBE cells, and through autophagy, it increases the expression of inflammatory cytokines in a cigarette smoke extract-induced 16HBE cell inflammation model. RELMß promotes cigarette smoke-induced COPD-like mouse airway inflammation through autophagy, and RELMß can mediate signal transduction through the cell membrane receptor TLR4. Conclusion: The RELMß binds to TLR4 to encourage signal transduction and that RELMß can promote inflammation in smoky COPD lungs through autophagy.

Echocardiographic Mitral Annular Calcification is Associated With Atrial Fibrillation Recurrence After Catheter Ablation.

There is a significant relation between mitral annular calcification (MAC) and the development of atrial fibrillation (AF) and major adverse cardiovascular events. However, the influence of MAC on the outcome of AF ablation remains unknown. The study cohort included 785 consecutive patients who underwent successful ablation. AF recurrence was monitored 3 months after ablation. Cox proportional hazards models were used to assess the association between MAC and AF recurrence. Kaplan-Meier analysis was performed to calculate the incidence of AF recurrence. Over a follow-up period of 16 ± 10 months, 190 patients (24.2%) experienced AF recurrence after ablation. MAC by echocardiography was identified in 42 patients (22%) with AF recurrence but only 60 without (10%, p <0.001). Patients with MAC were older (p <0.001), more often women (p <0.001), with a higher prevalence of hypertension (p <0.001) and diabetes mellitus (p<0.001), moderate/severe mitral regurgitation (p <0.001), larger left atrial dimension (p <0.001), and higher CHA2DS2-VASc score (p <0.001). Patients with MAC were more likely to develop AF recurrence than those without (36% vs 22%, respectively, p = 0.002). MAC was significantly associated with AF recurrence in the unadjusted analysis (hazard ratio 1.77, 95% confidence interval 1.26 to 2.58, p <0.001) and remained statistically significant after the multivariate adjustment (hazard ratio 1.48, 95% confidence interval 1.13 to 1.95, p = 0.001). In conclusion, echocardiographic MAC is significantly associated with an increased risk of AF recurrence after successful ablation, demonstrating an independent predictive value other than the established risk factors.

Dexmedetomidine Mitigates Myocardial Ischemia/Reperfusion-Induced Mitochondrial Apoptosis through Targeting lncRNA HCP5.

Our study aimed to explore the function and mechanism of Dexmedetomidine (Dex) in regulating myocardial ischemia/reperfusion (I/R)-induced mitochondrial apoptosis through lncRNA HCP5. We demonstrated Dex suppressed I/R-induced myocardial infarction and mitochondrial apoptosis in vivo. Dex induced the expression of lncRNA HCP5 and MCL1, inhibited miR-29a expression and activated the JAK2/STAT3 signaling. Dex attenuated hypoxia/reoxygenation (H/R)-induced mitochondrial apoptosis by upregulating lncRNA HCP5 in cardiomyocytes. Overexpression of lncRNA HCP5 sponged miR-29a to suppress H/R-induced mitochondrial apoptosis. Knockdown of miR-29a also alleviated cardiomyocyte apoptosis by upregulating MCL1. Overexpression of lncRNA HCP5 activated the JAK2/STAT3 signaling through sponging miR-29a and enhancing MCL1 expression in cardiomyocytes. Dex mitigated myocardial I/R-induced mitochondrial apoptosis through the lncRNA HCP5/miR-29a/MCL1 axis and activation of the JAK2/STAT3 signaling.

Unravelling the origin of long-term stability for Cs+ and Sr2+ solidification inside sodalite.

Cesium (Cs+) and strontium (Sr2+) ions are the main fission byproducts in the reprocessing of spent nuclear fuels for nuclear power plants. Their long half-live period (30.17 years for 137Cs and 28.80 years for 90Sr) makes them very dangerous radionuclides. Hence the solidification of Cs+ and Sr2+ is of paramount importance for preventing them from entering the human food chain through water. Despite tremendous efforts for solidification, the long-term stability remains a great challenge due to the experimental limitation and lack of good evaluation indicators for such long half-life radionuclides. Using density functional theory (DFT), we investigate the origin of long-term stability for the solidification of Cs+ and Sr2+ inside sodalite and establish that the exchange energy and the diffusion barrier play an important role in gaining the long-term stability both thermodynamically and kinetically. The acidity/basicity, solvation, temperature, and diffusion effect are comprehensively studied. It is found that solidification of Cs+ and Sr2+ is mainly attributed to the solvation effect, zeolitic adsorption ability, and diffusion barriers. The present study provides theoretical evidence to use geopolymers to adsorb Cs+ and Sr2+ and convert the adsorbed geopolymers to zeolites to achieve solidification of Cs+ and Sr2+ with long-term stability.

A Water-Soluble Highly Oxidizing Cobalt Molecular Catalyst Designed for Bioinspired Water Oxidation.

Herein, we present a stable water-soluble cobalt complex supported by a dianionic 2,2'-([2,2'-bipyridine]-6,6'-diyl)bis(propan-2-ol) ligand scaffold, which is a rare example of a high-oxidation species, as demonstrated by structural, spectroscopic and theoretical data. Electron paramagnetic resonance (EPR) spectroscopy and magnetic susceptibility measurements revealed that the CoIV center of the mononuclear complex in the solid state resides in the high spin state (sextet, S=5/2). The complex can effectively catalyze water oxidation via a single-site water nucleophilic attack pathway with an overpotential of only 360 mV in a phosphate buffer with a pH of 6. The key intermediate toward water oxidation was speculated based on theoretical calculations and was identified by in situ spectroelectrochemical experiments. The results are important regarding the accessibility of high-oxidation state metal species in synthetic models for achieving robust and reactive oxidation catalysis.

Effect of microRNA-455-5p (miR-455-5p) on the Expression of the Cytokine Signaling-3 (SOCS3) Gene During Myocardial Infarction.

To explore the effect of microRNA-455-5p (miR-455-5p) and Cytokine Signaling-3 (SOCS3) expression, a model of the cell damage induced during myocardial infarction was established using H2O2. The cell counting Kit-8 (CCK-8) and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) assays were used to detect the cell viability and the expression of miR-455-5p and SOCS3 in cells cultured with different concentrations of H2O2. After the selection of the optimum culture concentration, a dual-luciferase reporter gene assay was used to detect the binding between and miR-455-5p and its potential target SOCS3. SOCS3 siRNA was transfected into cardiomyocytes using chitosan nanoparticles as a gene carrier, which led to the knockdown of SOCS3 expression, and the cells were transfected with miR-455-5p mimics and inhibitors. The expression of cardiac protective proteins was detected by western blotting, cell viability was detected by CCK8, and cell apoptosis was detected by flow cytometry. The aim of this study was to investigate the effect of miR-455-5p and SOCS3 expression on the activity and apoptosis of damaged cardiomyocytes, and to identify any protective effect on cardiomyocytes. Finally, after the simultaneous overexpression of SOCS3 and miR-455-5p, and the expression of cardiac protective proteins, cell activity, and apoptosis rate were detected. The results showed that the expression of miR-455-5p decreased in a concentration-dependent manner and that the expression of SOCS3 increased in a concentration-dependent manner when the cells were cultured in different concentrations of H2O2. The knockdown of SOCS3 expression promoted an increase in cell activity, an increase in cardiac protective proteins, and a decrease in apoptosis. The upregulation of miR-455-5p significantly inhibited the expression of SOCS3, increased cell activity, inhibited apoptosis, and exerted protective effects in myocardial cells. The overexpression of SOCS3 reversed the inhibition of SOCS3 by miR-455-5p and reduced the protective effect of miR-455-5p on myocardial cells. Therefore, this study showed that the upregulation of miR-455-5p significantly inhibited the expression of SOCS3 and resulted in the increased protection of cells damaged by H2O2, which was used as a model of myocardial infarction. These results indicate the potential of miR-455-5p in myocardial protection, suggesting that miRNA may be a resource for myocardial therapy.

Highly-stable cobalt metal organic framework with sheet-like structure for ultra-efficient water oxidation at high current density.

The development of efficient and robust non-precious electrocatalysts for water oxidation at a mild condition is extremely desirable for industrial water splitting. Herein we developed a facile solvothermal strategy to synthesize cobalt metal organic frameworks (Co-MOFs) with sheet-like structure, which showed highly promising performance for electrocatalytic oxygen evolution. The best Co-MOF sample afforded an ultra-high oxygen evolution current density of 63.4 mA cm-2 at 1.75 V in 1 M KOH with a catalyst loading of only 0.21 mg cm-2. Notably, its electrochemical performance remained unchanged after 10,000 cyclic voltammograms indicating very promising long-term stability. Detailed study of the mechanism of the oxygen evolution by density functional theory (DFT) indicated that the strong π-conjugation formed between the central cobalt ion and adjacent aromatic rings favored the high electrocatalytic performance. The solvothermally synthesized MOFs proposed in this paper are expected to inspire the rational design of high-performance electrocatalysts for water oxidation with atomic and molecular level structural control and the exploration of structure-performance relationships to understand the electrocatalytic origin.

The Inflammatory Response Induced by RELMß Upregulates IL-8 and IL-1ß Expression in Bronchial Epithelial Cells in COPD.

PURPOSE: Chronic obstructive pulmonary disease (COPD) is associated with a complex inflammatory regulatory network. Resistin-like molecule ß (RELMß) is highly expressed in the lungs of COPD patients. We aimed to investigate the proinflammatory effect of RELMß on airway epithelial cells in COPD. METHODS: First, a GEO dataset was used to analyze the expression of the RELMß gene in the COPD and control groups as well as the protein levels of RELMß in the sera of outpatients with COPD and normal control subjects in our hospital. We also stimulated 16HBE bronchial epithelial cells with recombinant RELMß protein and analyzed the expression of IL-8 and IL-1ß. We upregulated and downregulated the gene expression of RELMß in 16HBE cells and analyzed the expression of the inflammatory cytokines IL-8 and IL-1ß. In addition, we also examined the mechanism by which the p38 MAPK signaling pathway contributed to the regulation of IL-8 and IL-1ß expression by RELMß. RESULTS: RELMß expression was increased in COPD tissues in different data sets and in the serum of COPD patients in our hospital. IL-8 and IL-1ß expression was also increased in COPD tissues with high RELMß gene expression in different data sets. The RELMß gene was mainly related to inflammatory factors and inflammatory signaling pathways in the PPI regulatory network. Experiments at the cellular level showed that RELMß promoted the expression of the inflammatory cytokines IL-8 and IL-1ß, and this regulation was mediated by the p38 MAPK signaling pathway. CONCLUSION: RELMß can promote the expression of the inflammatory cytokines IL-8 and IL-1ß in bronchial epithelial cells of patients with COPD and exert inflammatory effects. RELMß may be a potential target for the treatment of COPD.

The effects of NCBP3 on METTL3-mediated m6A RNA methylation to enhance translation process in hypoxic cardiomyocytes.

Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. Our previous study has uncovered the global transcriptome and translatome profiles of cardiomyocytes in vitro and in vivo to response to hypoxia by RNA sequencing and ribosome profiling sequencing. We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of nuclear cap-binding subunit 3 (NCBP3) at 5' untranslation region of target genes. Although we observe that NCBP3 can facilitate translational process in myocardium under hypoxia stress, the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. In this study, we performed NCBP3 immunoprecipitation for mass spectrum and found that METTL3 and eIF4A2 particularly interacted with NCBP3 in hypoxic rat H9C2 cardiomyocytes. Furthermore, we observed that METTL3-mediated N6-methyladenosine (m6A) methylation was elevated in hypoxia, but compromised by NCBP3 or METTL3 knockdown. Finally, we also demonstrated that NCBP3/METTL3/eIF4A2 regulatory axis plays a specific role in cardiomyocytes undergoing hypoxic stress. Taken together, we unmasked NCBP3, a novel hypoxia-specific response protein functions as a scaffold to coordinate METTL3 and eIF4A2 for enhancing gene translation by m6A RNA methylation in cardiomyocytes upon hypoxic stress.

Toward Rational Understandings of α-C-H Functionalization: Energetic Studies of Representative Tertiary Amines.

Functionalization of α-C-H bonds of tertiary amines to build various α-C-X bonds has become a mainstream in synthetic chemistry nowadays. However, due to lack of fundamental knowledge on α-C-H bond strength as an energetic guideline, rational exploration of new synthetic methodologies remains a far-reaching anticipation. Herein, we report a unique hydricity-based approach to establish the first integrated energetic scale covering both the homolytic and heterolytic energies of α-C-H bonds for 45 representative tertiary amines and their radical cations. As showcased from the studies on tetrahydroisoquinolines (THIQs) by virtue of their thermodynamic criteria, the feasibility and mechanisms of THIQ oxidation were deduced, which, indeed, were found to correspond well with experimental observations. This integrated scale provides a good example to relate bond energetics with mechanisms and thermodynamic reactivity of amine α-C-H functionalization and hence, may be referenced for analyzing similar structure-property problems for various substrates.

Counterintuitive solvation effect of ionic-liquid/DMSO solvents on acidic C-H dissociation and insight into respective solvation.

How would acidic bond dissociation be affected by adding a small quantity of a weakly polar ionic liquid IL (the "apparent" or "measured" dielectric constant ε of the IL is around 10-15) into a strongly polar molecular solvent (e.g., ε of DMSO: 46.5), or vice versa? The answer is blurred, because no previous investigation was reported in this regard. Toward this, we, taking various IL/DMSO mixtures as representatives, have thoroughly investigated the effects of the respective solvent in ionic-molecular binary systems on self-dissociation of C-H acid phenylmalononitrile PhCH(CN)2 via pK a determination. As disclosed, in this category of binary media, (1) no linear correspondence exists between pK a and molar fractions of the respective solvent components; (2) only ∼1-2 mol% of weakly polar ILs in strongly polar DMSO make C-H bonds even more dissociative than in neat DMSO; (3) a small fraction of DMSO in ILs (<10 mol%) can dramatically ease acidic C-H-dissociation; and (4) while the DMSO fraction further increases, its acidifying effect becomes much attenuated. These findings, though maybe counterintuitive, have been rationalized on the basis of the precise pK a measurement of this work in relation to the respective roles of each solvent component in solvation.

Parity and carotid atherosclerosis in elderly Chinese women.

BACKGROUND: The relationship between parity and atherosclerosis has been reported in some ethnic populations. However, results regarding Chinese women are still lacking. This study aimed to investigate the association of parity and carotid atherosclerosis, which has a predictive value of subsequent atherosclerotic events in elderly Chinese women. METHODS: A total of 2, 052 participants from the medical examination center of the Third Xiangya Hospital were enrolled in the study. A standardized, structured questionnaire was administered to collect information on subjects' demographic characteristics, socioeconomic status, and cardiovascular risk factors. High-resolution ultrasound was used to examine carotid plaques and carotid intima-media thickness (IMT). RESULTS: The mean age of participants was 66.1 ± 5.5 years. Women with more birth appeared to have a higher risk of carotid artery plaques. A multivariate-adjusted model yielded an odds ratio of 1.38 (95% CI: 12%-70%, P = 0.003) per birth. A positive association was observed between parity and common carotid IMT (ß ± SE: 0.029 ± 0.006, P < 0.001), and internal carotid IMT (ß ± SE: 0.011 ± 0.005, P = 0.03) in a univariate model; however, these associations became non-significant in multivariate-adjusted models. When common carotid IMT was classified into an IMT ≥ 1 mm group and an IMT < 1 mm group, higher parity was associated with more obvious thickening both in the unadjusted model (OR = 1.61, 95% CI: 1.29-2.00, P < 0.001) and in the fully adjusted model (OR = 1.43, 95% CI: 1.09-1.88, P = 0.01). CONCLUSIONS: There is a positive association between parity and risk of carotid plaques, as well as between parity and risk of obvious thickening for common carotid IMT in elderly Chinese women, indicating multiparous women might experience more atherosclerotic challenges.

The role of radical prostatectomy and definitive external beam radiotherapy in combined treatment for high-risk prostate cancer: a systematic review and meta-analysis.

The first-line treatment options for high-risk prostate cancer (PCa) are definitive external beam radiotherapy (EBRT) with or without androgen deprivation therapy (ADT) and radical prostatectomy (RP) with or without adjuvant therapies. However, few randomized trials have compared the survival outcomes of these two treatments. To systematically evaluate the survival outcomes of high-risk PCa patients treated with EBRT- or RP-based therapy, a comprehensive and up-to-date meta-analysis was performed. A systematic online search was conducted for randomized or observational studies that investigated biochemical relapse-free survival (bRFS), cancer-specific survival (CSS), and/or overall survival (OS), in relation to the use of RP or EBRT in patients with high-risk PCa. The summary hazard ratios (HRs) were estimated under the random effects models. We identified heterogeneity between studies using Q tests and measured it using I2 statistics. We evaluated publication bias using funnel plots and Egger's regression asymmetry tests. Seventeen studies (including one randomized controlled trial [RCT]) of low risk of bias were selected and up to 9504 patients were pooled. When comparing EBRT-based treatment with RP-based treatment, the pooled HRs for bRFS, CSS, and OS were 0.40 (95% confidence interval [CI]: 0.24-0.67), 1.36 (95% CI: 0.94-1.97), and 1.39 (95% CI: 1.18-1.62), respectively. Better OS for RP-based treatment and better bRFS for EBRT-based treatment have been identified, and there was no significant difference in CSS between the two treatments. RP-based treatment is recommended for high-risk PCa patients who value long-term survival, and EBRT-based treatment might be a promising alternative for elderly patients.

Hydroxo Iron(III) Sites in a Metal-Organic Framework: Proton-Coupled Electron Transfer and Catalytic Oxidation of Alcohol with Molecular Oxygen.

Metalloenzymes are powerful biocatalysts that can catalyze particular chemical reactions with high activity, selectivity, and specificity under mild conditions. Metal-organic frameworks (MOFs) composed of metal ions or metal clusters and organic ligands with defined cavities have the potential to impart enzyme-like catalytic activity and mimic metalloenzymes. Here, a new metal-organic framework implanted with hydroxo iron(III) sites with the structural and reactivity characteristics of iron-containing lipoxygenases is reported. Similar to lipoxygenases, the hydrogen atoms and electrons of the substrate can transfer to the hydroxo iron(III) sites, showing typical proton-coupled electron transfer behavior. In the reactivity mimicking biology system, similar to alcohol oxidase, the material also catalyses the oxidation of alcohol into aldehyde by using O2 with a high yield and 100% selectivity under mild conditions, without the use of a radical cocatalyst or photoexcitation. These results provide strong evidence for the high structural fidelity of enzymatically active sites in MOF materials, verifying that MOFs provide an ideal platform for designing biomimetic heterogeneous catalysts with high conversion efficiency and product selectivity.

The enzyme-like catalytic hydrogen abstraction reaction mechanisms of cyclic hydrocarbons with magnesium-diluted Fe-MOF-74.

Enzymatic heme and non-heme Fe(iv)-O species usually play an important role in hydrogen abstraction of biocatalytic reactions, yet duplicating the reactivity in biomimicry remains a great challenge. Based on Xiao et al.'s experimental work [Nat. Chem., 2014, 6(7), 590], we theoretically found that in the presence of the oxidant N2O, the enzyme-like metal organic framework, i.e., magnesium-diluted Fe-MOF-74 [Fe/(Mg)-MOF-74] can activate the C-H bonds of 1,4-cyclohexadiene (CHD) into benzene with a two-step hydrogen abstraction mechanism based on the density functional theory (DFT) level. It is shown that the first transition state about the cleavage of the N-O bond of N2O to form the Fe(iv)-O species is the rate-determining step with activation enthalpy of 19.4 kcal mol-1 and the complete reaction is exothermic by 62.8 kcal mol-1 on quintet rather than on triplet PES. In addition, we proposed a rebound mechanism of cyclic cyclohexane (CHA) hydroxylation to cyclohexanol which has not been studied experimentally. Note that the activation enthalpies on the first hydrogen abstraction for both cyclic CHD and cyclohexane are just 8.1 and 3.5 kcal mol-1, respectively, which are less than that of 13.9 kcal mol-1 for chained ethane. Most importantly, for the hydrogen abstraction of methane catalyzed by M/(Mg)-MOF-74 (M = Cu, Ni, Fe, and Co), we found that the activation enthalpies versus the C-H bond length of methane of TSs, NPA charge of the reacting oxyl atom have linear relationships with different slopes, i.e., shorter C-H bond and less absolute value of NPA charge of oxyl atom are associated with lower activation enthalpy; while for the activation of methane, ethane, propane and CHD catalyzed by Fe/(Mg)-MOF-74, there also exists positive correlations between activation enthalpies, bond dissociation energies (BDEs) and C-H bond lengths in TSs, respectively. We hope the present theoretical study may provide the guideline to predict the performance of MOFs in C-H bond activation reactions.

Effect of Small Molecule Additives in the Prenucleation Stage of Semiconductor CdSe Quantum Dots.

For the addition of small molecules in the prenucleation stage of colloidal CdSe conventional quantum dots (QDs), there is insufficient knowledge regarding what are advantageous circumstances. Here, we present a study about such addition. When CH3COOH or Zn(OOCCH3)2 is added in the prenucleation stage (at 120 °C) of a reaction consisting of cadmium myristate (Cd(OOC(CH2)12CH3)2, Cd(MA)2 made from CdO) and Se powder in 1-octadecene (ODE), CdSe magic-size clusters (MSCs) exhibiting a single sharp absorption doublet at 433/460 nm are synthesized in a single-ensemble form (around 220 °C). We demonstrate that such small molecule addition suppresses the nucleation and growth of QDs and thus directs a competitive process to the formation of MSCs. The present study provides insight into the individual but linked pathways to forming CdSe QDs and MSCs and introduces new avenues to improve the production of MSCs through the addition of small molecules in the prenucleation stage.

Ventral tegmental area activation promotes firing precision and strength through circuit inhibition in the primary auditory cortex.

The activation of the ventral tegmental area (VTA) can rebuild the tonotopic representation in the primary auditory cortex (A1), but the cellular mechanisms remain largely unknown. Here, we investigated the firing patterns and membrane potential dynamics of neurons in A1 under the influence of VTA activation using in vivo intracellular recording. We found that VTA activation can significantly reduce the variability of sound evoked responses and promote the firing precision and strength of A1 neurons. Furthermore, the compressed response window was caused by an early hyperpolarization as a result of enhanced circuit inhibition. Our study suggested a possible mechanism of how the reward system affects information processing in sensory cortex: VTA activation strengthens cortical inhibition, which shortens the response window of post-synaptic cortical neurons and further promotes the precision and strength of neuronal activity.