High-percentage new energy distribution network line loss frequency division prediction based on wavelet transform and BIGRU-LSTM.

The access of new energy improves the flexibility of distribution network operation, but also leads to more complex mechanism of line loss. Therefore, starting from the nonlinear, fluctuating and multi-scale characteristics of line loss data, and based on the idea of decomposition prediction, this paper proposes a new method of line loss frequency division prediction based on wavelet transform and BIGRU-LSTM (Bidirectional Gated Recurrent Unit-Long Short Term Memory Network).Firstly, the grey relation analysis and the improved NARMA (Nonlinear Autoregressive Moving Average) correlation analysis method are used to extract the non-temporal and temporal influencing factors of line loss, and the corresponding feature data set is constructed. Then, the historical line loss data is decomposed into physical signals of different frequency bands by using wavelet transform, and the multi-dimensional input data of the prediction network is formed with the above characteristic data set. Finally, the BIGRU-LSTM prediction network is built to realize the probabilistic prediction of high-frequency and low-frequency components of line loss. The effectiveness and applicability of the method proposed in this paper were verified through numerical simulation. By dividing the line loss data into different frequency bands for frequency prediction, the mapping relationship between different line loss components and influencing factors was accurately matched, thereby improving the prediction accuracy.

Synergistic engineering of heterostructure and oxygen vacancy in cobalt hydroxide/aluminum oxyhydroxide as bifunctional electrocatalysts for urea-assisted hydrogen production.

Designing inexpensive, high-efficiency and durable bifunctional catalysts for urea oxidation reaction (UOR) and hydrogen evolution reaction (HER) is an encouraging tactic to produce hydrogen with reduced energy expenditure. Herein, oxygen vacancy-rich cobalt hydroxide/aluminum oxyhydroxide heterostructure on nickel foam (denoted as Co(OH)2/AlOOH/NF-100) has been fabricated using one step hydrothermal process. Theoretical calculation and experimental results indicate the electrons transfer from Co(OH)2 to highly active AlOOH results in the interfacial charge redistribution and optimization of electronic structure. Abundant oxygen vacancies in the heterostructure could improve the conductivity and simultaneously serve as the active sites for catalytic reaction. Consequently, the optimal Co(OH)2/AlOOH/NF-100 demonstrates excellent electrocatalytic performance for HER (62.9 mV@10 mA cm-2) and UOR (1.36 V@10 mA cm-2) due to the synergy between heterointerface and oxygen vacancies. Additionally, the in situ electrochemical impedance spectrum (EIS) for UOR suggests that the heterostructured catalyst exhibits rapid reaction kinetics, mass transfer and current response. Importantly, the urea-assisted electrolysis composed of the Co(OH)2/AlOOH/NF-100 manifests a low cell voltage (1.48 V @ 10 mA cm-2) in 1 M KOH containing 0.5 M urea. This work presents a promising avenue to the development of HER/UOR bifunctional electrocatalysts.

Bioactive daphnane diterpenes from the flower buds of Daphne genkwa (Thymelaeaceae).

Four diterpenes of the daphnane type were isolated from a methanol extract of the flower buds of Daphne genkwa, the two of them were new structures named genkwadanes J (1) and K (2). Their structures were determined based on analysis of their 1D- and 2D-NMR, HRESIMS and ECD calculations. Among the isolates, the cytotoxicity was assessed via the MTT method using the K562, MCF-7 and HeLa cancer cell lines, the positive control was taxol. Compounds 1 and 3 exhibited appreciable cytotoxic activity against the K562 cancer cell line with IC50 values between 6.58 and 5.33 µM. Compounds 2 and 4 showed noteworthy inhibitory effects against the MCF-7 cell line with IC50 values of 3.25 and 2.56 µM, respectively. All compounds showed weak cytotoxicities to the Hela cell line with IC50 values in the range of 20.19-55.23 µM.

Preserving mitochondrial homeostasis protects against drug-induced liver injury via inducing OPTN (optineurin)-dependent Mitophagy.

Disruption of mitochondrial function is observed in multiple drug-induced liver injuries (DILIs), a significant global health threat. However, how the mitochondrial dysfunction occurs and whether maintain mitochondrial homeostasis is beneficial for DILIs remains unclear. Here, we show that defective mitophagy by OPTN (optineurin) ablation causes disrupted mitochondrial homeostasis and aggravates hepatocytes necrosis in DILIs, while OPTN overexpression protects against DILI depending on its mitophagic function. Notably, mass spectrometry analysis identifies a new mitochondrial substrate, GCDH (glutaryl-CoA dehydrogenase), which can be selectively recruited by OPTN for mitophagic degradation, and a new cofactor, VCP (valosin containing protein) that interacts with OPTN to stabilize BECN1 during phagophore assembly, thus boosting OPTN-mediated mitophagy initiation to clear damaged mitochondria and preserve mitochondrial homeostasis in DILIs. Then, the accumulation of OPTN in different DILIs is further validated with a protective effect, and pyridoxine is screened and established to alleviate DILIs by inducing OPTN-mediated mitophagy. Collectively, our findings uncover a dual role of OPTN in mitophagy initiation and implicate the preservation of mitochondrial homeostasis via inducing OPTN-mediated mitophagy as a potential therapeutic approach for DILIs.Abbreviation: AILI: acetaminophen-induced liver injury; ALS: amyotrophic lateral sclerosis; APAP: acetaminophen; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; CHX: cycloheximide; Co-IP: co-immunoprecipitation; DILI: drug-induced liver injury; FL: full length; GCDH: glutaryl-CoA dehydrogenase; GOT1/AST: glutamic-oxaloacetic transaminase 1; GO: gene ontology; GSEA: gene set enrichment analysis; GPT/ALT: glutamic - pyruvic transaminase; INH: isoniazid; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MMP: mitochondrial membrane potential; MST: microscale thermophoresis; MT-CO2/COX-II: mitochondrially encoded cytochrome c oxidase II; OPTN: optineurin; PINK1: PTEN induced kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; TIMM23: translocase of inner mitochondrial membrane 23; TOMM20: translocase of outer mitochondrial membrane 20; TSN: toosendanin; VCP: valosin containing protein, WIPI2: WD repeat domain, phosphoinositide interacting 2.

Glyco-signatures in patients with advanced lung cancer during anti-PD-1/PD-L1 immunotherapy.

Immune checkpoint inhibitors (ICIs) targeting programmed cell death 1/programmed cell death ligand-1 (PD-1/PD-L1) have significantly prolonged the survival of advanced/metastatic patients with lung cancer. However, only a small proportion of patients can benefit from ICIs, and clinical management of the treatment process remains challenging. Glycosylation has added a new dimension to advance our understanding of tumor immunity and immunotherapy. To systematically characterize anti-PD-1/PD-L1 immunotherapy-related changes in serum glycoproteins, a series of serum samples from 12 patients with metastatic lung squamous cell carcinoma (SCC) and lung adenocarcinoma (ADC), collected before and during ICIs treatment, are firstly analyzed with mass-spectrometry-based label-free quantification method. Second, a stratification analysis is performed among anti-PD-1/PD-L1 responders and non-responders, with serum levels of glycopeptides correlated with treatment response. In addition, in an independent validation cohort, a large-scale site-specific profiling strategy based on chemical labeling is employed to confirm the unusual characteristics of IgG N-glycosylation associated with anti-PD-1/PD-L1 treatment. Unbiased label-free quantitative glycoproteomics reveals serum levels' alterations related to anti-PD-1/PD-L1 treatment in 27 out of 337 quantified glycopeptides. The intact glycopeptide EEQFN 177STYR (H3N4) corresponding to IgG4 is significantly increased during anti-PD-1/PD-L1 treatment (FC=2.65, P=0.0083) and has the highest increase in anti-PD-1/PD-L1 responders (FC=5.84, P=0.0190). Quantitative glycoproteomics based on protein purification and chemical labeling confirms this observation. Furthermore, obvious associations between the two intact glycopeptides (EEQFN 177STYR (H3N4) of IgG4, EEQYN 227STFR (H3N4F1) of IgG3) and response to treatment are observed, which may play a guiding role in cancer immunotherapy. Our findings could benefit future clinical disease management.

Impaired arginine/ornithine metabolism drives severe HFMD by promoting cytokine storm.

Introduction: The Hand, Foot and Mouth Disease (HFMD), caused by enterovirus 71 infection, is a global public health emergency. Severe HFMD poses a significant threat to the life and well-being of children. Numerous studies have indicated that the occurrence of severe HFMD is associated with cytokine storm. However, the precise molecular mechanism underlying cytokine storm development remains elusive, and there are currently no safe and effective treatments available for severe HFMD in children. Methods: In this study, we established a mouse model of severe HFMD to investigate the molecular mechanisms driving cytokine storm. We specifically analyzed metabolic disturbances, focusing on arginine/ornithine metabolism, and assessed the potential therapeutic effects of spermine, an ornithine metabolite. Results: Our results identified disturbances in arginine/ornithine metabolism as a pivotal factor driving cytokine storm onset in severe HFMD cases. Additionally, we discovered that spermine effectively mitigated the inflammatory injury phenotype observed in mice with severe HFMD. Discussion: In conclusion, our findings provide novel insights into the molecular mechanisms underlying severe HFMD from a metabolic perspective while offering a promising new strategy for its safe and effective treatment.

Relationship between four insulin resistance surrogates and regression to normoglycemia from prediabetes among Chinese adults: A longitudinal Cohort Study.

PURPOSE: We aimed to investigate the association of the triglyceride glucose-body mass index(TyG-BMI), metabolic score for insulin resistance (METS-IR) with regression to normoglycaemia, and further to compare the value of the four insulin resistance(IR) related indices(TyG-BMI, METS-IR, TyG and triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio) in identifying regressions to normoglycaemia from prediabetes. METHODS: A total of 15,025 patients with prediabetes from the DATA-DRYAD database were included. Cox proportional hazards regression models and restricted cubic spline functions were performed to explore the association and nonlinearity between the indices with the incidence rate of normoglycaemia. Sensitivity and subgroup analyses evaluated the robustness of our findings. RESULTS: Compared with the first quintile, TyG-BMI and METS-IR was negatively linked with the probability of regression to normoglycaemia from prediabetes, the adjusted effect size of the highest quintiles of METS-IR were the most obvious (HR:0.456,95% CI:0.4-0.519), followed by TG/HDL (HR:0.792, 95% CI:0.733-0.856), TyG-BMI (HR:0.816, 95% CI:0.73-0.911) and TyG (HR:0.841, 95% CI: 0.754-0.937) (all p for trend <0.001). A 1.0 SD increase in METS-IR induced a 43% decrease in the probability of regression to normoglycaemia, with 9.8% for TyG-BMI. There were nonlinear associations between TyG-BMI and METS-IR and outcomes, with the inflection point of the TyG-BMI being 218.2 and that of the METS-IR being 37. CONCLUSIONS: The METS-IR might be the most superior indicator among the four non-insulin indices in identifying regressions to normoglycaemia from prediabetes in clinical application. The inflection points of the METS-IR and TyG-BMI may be instructive therapeutic points for assessing the status of prediabetes in advance and making more appropriate management and health care decisions.

Self-enhanced localized alkalinity at the encapsulated Cu catalyst for superb electrocatalytic nitrate/nitrite reduction to NH3 in neutral electrolyte.

The electrocatalytic nitrate/nitrite reduction reaction (eNOx-RR) to ammonia (NH3) is thermodynamically more favorable than the eye-catching nitrogen (N2) electroreduction. To date, the high eNOx-RR-to-NH3 activity is limited to strong alkaline electrolytes but cannot be achieved in economic and sustainable neutral/near-neutral electrolytes. Here, we construct a copper (Cu) catalyst encapsulated inside the hydrophilic hierarchical nitrogen-doped carbon nanocages (Cu@hNCNC). During eNOx-RR, the hNCNC shell hinders the diffusion of generated OH- ions outward, thus creating a self-enhanced local high pH environment around the inside Cu nanoparticles. Consequently, the Cu@hNCNC catalyst exhibits an excellent eNOx-RR-to-NH3 activity in the neutral electrolyte, equivalent to the Cu catalyst immobilized on the outer surface of hNCNC (Cu/hNCNC) in strong alkaline electrolyte, with much better stability for the former. The optimal NH3 yield rate reaches 4.0 moles per hour per gram with a high Faradaic efficiency of 99.7%. The strong-alkalinity-free advantage facilitates the practicability of Cu@hNCNC catalyst as demonstrated in a coupled plasma-driven N2 oxidization with eNOx-RR-to-NH3.

Let­7f­5p Regulated by Hsa_circ_0000437 Ameliorates Bleomycin-Induced Skin Fibrosis.

The current treatment of skin fibrosis is limited in its effectiveness due to a lack of understanding of the underlying mechanisms. Previous research has shown a connection between microRNAs (miRNAs) and the development of skin fibrosis. Therefore, investigating miRNA for the treatment of skin fibrotic diseases is highly important and merits further exploration. In this study, we have discovered that let-7f-5p could suppress the proliferation, migration, and expression of collagen type I alpha 1 (COL1A1) in human dermal fibroblasts (HDFs). It was further determined that let-7f-5p could target thrombospondin-1 (THBS1), thereby inhibiting the TGF-ß2/Smad3 signaling pathway and exerting its biological effects. Additionally, let-7f-5p is regulated by Hsa_circ_0000437, which acts as a sponge molecule for let-7f-5p and consequently regulates the biological function of HDFs. Furthermore, our findings indicate that in vivo overexpression of let-7f-5p leads to a reduction in dermal thickness and COL1A1 expression, effectively inhibiting the progression of bleomycin (BLM)-induced skin fibrosis in mice. Hence, our research enhances the comprehension of the Hsa_circ_0000437/let-7f-5p/THBS1/TGF-ß2/Smad3 regulatory network, highlighting the potential of let-7f-5p as a therapeutic approach for the treatment of skin fibrosis.

Theoretical study on the H-atom abstraction reactions of pentanol + HȮ2, part I: five branched pentanol isomers.

The chemical kinetic studies of hydrogen atom (H-atom) abstraction reactions by hydroperoxyl (HȮ2) radicals from five branched pentanol isomers, including 3-methyl-1-butanol, 2-methyl-1-butanol, 1,1-dimethyl-1-propanol, 1,2-dimethyl-1-propanol, and 2,2-dimethyl-1-propanol were investigated systematically through high-level ab initio calculations. Geometry optimization, frequency analysis, and zero-point energy (ZPE) corrections were performed for six reactants, twenty-three transition states (TSs), and twenty-four products at the M06-2X/6-311++G(d,p) level of theory. The intrinsic reaction coordinate calculation was performed at the same level of theory to confirm the transition state connection. The one-dimensional hindered rotor treatment for low-frequency torsional modes was also treated at the M06-2X/6-311++G(d,p) level of theory. The QCISD(T)/CBS level of theory was used to calculate the single-point energies for the species whose T1 diagnostic value was lower than 0.035. At the same time, the CASPT2/CBS level of theory was used to calculate the single-point energies for the channel in which the T1 diagnostic value of transition states was greater than 0.035. Rate constants for the H-atom abstraction reactions from the five branched pentanol isomers by HȮ2 radicals were calculated by using conventional transition state theory with asymmetric Eckart tunneling corrections in the temperature range of 500-2000 K. Rate constants and branching ratios for the title reactions and the rate rules for ten different H-atom abstraction types were investigated. Temperature-dependent thermochemistry properties for all reactants and products were calculated by the composite methods of G3/G4/CBS-QB3/CBS-APNO, which were in good agreement with the data available in the literature. Rate constants for the H-atom abstraction reactions by HȮ2 radical from branched pentanol isomers were investigated in this work as part I, and those for linear pentanol isomers will be analyzed in part II. All the calculated kinetics and thermochemistry data can be utilized in the model development for branched pentanol isomers oxidation.

ABT­737 increases cisplatin sensitivity through the ROS­ASK1­JNK MAPK signaling axis in human ovarian cancer cisplatin­resistant A2780/DDP cells.

Ovarian cancer is a gynecological malignant tumor with the highest mortality rate, and chemotherapy resistance seriously affects patient therapeutic outcomes. It has been shown that the high expression of anti­apoptotic proteins Bcl­2 and Bcl­xL is closely related to ovarian cancer chemotherapy resistance. Therefore, reducing Bcl­2 and Bcl­xL expression levels may be essential for reversing drug resistance in ovarian cancer. ABT­737 is a BH3­only protein mimetic, which can effectively inhibit the expression of the anti­apoptotic proteins Bcl­xL and Bcl­2. Although it has been shown that ABT­737 can increase the sensitivity of ovarian cancer cells to cisplatin, the specific molecular mechanism remains unclear and requires further investigation. In the present study, the results revealed that ABT­737 can significantly increase the activation levels of JNK and ASK1 induced by cisplatin in A2780/DDP cells, which are cisplatin­resistant ovarian cancer cells. Inhibition of the JNK and ASK1 pathway could significantly reduce cisplatin cytotoxicity increased by ABT­737 in A2780/DDP cells, while inhibiting the ASK1 pathway could reduce JNK activation. In addition, it was further determined that ABT­737 could increase reactive oxygen species (ROS) levels in A2780/DDP cells induced by cisplatin. Furthermore, the inhibition of ROS could significantly reduce JNK and ASK1 activation and ABT­737­mediated increased cisplatin cytotoxicity in A2780/DDP cells. Overall, the current data identified that activation of the ROS­ASK1­JNK signaling axis plays an essential role in the ability of ABT­737 to increase cisplatin sensitivity in A2780/DDP cells. Therefore, upregulation the ROS­ASK1­JNK signaling axis is a potentially novel molecular mechanism by which ABT­737 can enhance cisplatin sensitivity of ovarian cancer cells. In addition, the present research can also provide new therapeutic strategies and new therapeutic targets for patients with cisplatin­resistant ovarian cancer with high Bcl­2/Bcl­xL expression patterns.

Scaling variation in the pinch-off of colloid-polymer mixtures.

HYPOTHESIS: The scaling laws of drop pinch-off are known to be affected by drop compositions including dissolved polymers and non-Brownian particles. When the size of the particles is comparable to the characteristic length scale of the polymer network, these particles may interact strongly with the polymer environment, leading to new types of scaling behaviors not reported before. EXPERIMENTS: Using high-speed imaging, we experimentally studied the time evolution of the neck diameter hmin of drops composed of silica nanoparticles dispersed in PEO solution when extruded from a nozzle. FINDINGS: After initial Newtonian necking with hmin âˆ¼ t2/3, the subsequent stage may exhibit scaling variation, characterized by either exponential or power-law decay, depending on the nanoparticle volume fraction ϕ. The exponential decay hmin âˆ¼ e-t/τ signifies the coil-stretch transition in typical viscoelastic suspensions. We conducted an analysis of the power-law scenario hmin âˆ¼ tα at high ϕ, categorizing the entire process into three distinct regimes based on the exponents α. The dependences of critical thicknesses at transition points and exponents on polymer concentration offer initial insights into the potential transition from heterogeneous to homogeneous thinning in the mixture. This novel scaling variation bears implications for accurately predicting and controlling droplet fragmentation in industrial applications.

Transcriptomic Hallmarks of Hypoxic-Ischemic Brain Injury: Insights from an in Vitro Model.

BACKGROUND: Hypoxic-ischemic injury of neurons is a pathological process observed in several neurological conditions, including ischemic stroke and neonatal hypoxic-ischemic brain injury (HIBI). An optimal treatment strategy for these conditions remains elusive. The present study delved deeper into the molecular alterations occurring during the injury process in order to identify potential therapeutic targets. METHODS: Oxygen-glucose deprivation/reperfusion (OGD/R) serves as an established in vitro model for the simulation of HIBI. This study utilized RNA sequencing to analyze rat primary hippocampal neurons that were subjected to either 0.5 or 2 h of OGD, followed by 0, 9, or 18 h of reperfusion. Differential expression analysis was conducted to identify genes dysregulated during OGD/R. Time-series analysis was used to identify genes exhibiting similar expression patterns over time. Additionally, functional enrichment analysis was conducted to explore their biological functions, and protein-protein interaction (PPI) network analyses were performed to identify hub genes. Quantitative real-time polymerase chain reaction (qRT-PCR) was used for validation of hub-gene expression. RESULTS: The study included a total of 24 samples. Analysis revealed distinct transcriptomic alterations after OGD/R processes, with significant dysregulation of genes such as Txnip, Btg2, Egr1 and Egr2. In the OGD process, 76 genes, in two identified clusters, showed a consistent increase in expression; functional analysis showed involvement of inflammatory responses and signaling pathways like tumor necrosis factor (TNF), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and interleukin 17 (IL-17). PPI network analysis suggested that Ccl2, Jun, Cxcl1, Ptprc, and Atf3 were potential hub genes. In the reperfusion process, 274 genes, in three clusters, showed initial upregulation followed by downregulation; functional analysis suggested association with apoptotic processes and neuronal death regulation. PPI network analysis identified Esr1, Igf-1, Edn1, Hmox1, Serpine1, and Spp1 as key hub genes. qRT-PCR validated these trends. CONCLUSIONS: The present study provides a comprehensive transcriptomic profile of an in vitro OGD/R process. Key hub genes and pathways were identified, offering potential targets for neuroprotection after hypoxic ischemia.

Neoadjuvant immunochemotherapy improves clinical outcomes of patients with esophageal cancer by mediating anti-tumor immunity of CD8+ T (Tc1) and CD16+ NK cells.

Background: Esophageal cancer (ESCA) is one of the most common tumors in the world, and treatment using neoadjuvant therapy (NT) based on radiotherapy and/or chemotherapy has still unsatisfactory results. Neoadjuvant immunochemotherapy (NICT) has also become an effective treatment strategy nowadays. However, its impact on the tumor microenvironment (TME) and regulatory mechanisms on T cells and NK cells needs to be further elucidated. Methods: A total of 279 cases of ESCA who underwent surgery alone [non-neoadjuvant therapy (NONE)], neoadjuvant chemotherapy (NCT), and NICT were collected, and their therapeutic effect and survival period were compared. Further, RNA sequencing combined with biological information was used to analyze the expression of immune-related genes. Immunohistochemistry, immunofluorescence, and quantitative real-time PCR (qRT-PCR) were used to verify the activation and infiltration status of CD8+ T and CD16+ NK cells, as well as the function and regulatory pathway of killing tumor cells. Results: Patients with ESCA in the NICT group showed better clinical response, median survival, and 2-year survival rates (p < 0.05) compared with the NCT group. Our RNA sequencing data revealed that NICT could promote the expression of immune-related genes. The infiltration and activation of immune cells centered with CD8+ T cells were significantly enhanced. CD8+ T cells activated by PD-1 inhibitors secreted more IFN-γ and cytotoxic effector factor cells through the transcription factor of EOMES and TBX21. At the same time, activated CD8+ T cells mediated the CD16+ NK cell activation and secreted more IFN-γ to kill ESCA cells. In addition, the immunofluorescence co-staining results showed that more CD276+ tumor cells and CD16+ NK cells were existed in pre-NCT and pre-NICT group. However, CD276+ tumor cells were reduced significantly in the post-NICT group, while they still appeared in the post-NCT group, which means that CD16+ NK cells can recognize and kill CD276+ tumor cells after immune checkpoint blocker (ICB) treatment. Conclusion: NICT can improve the therapeutic effect and survival period of resectable ESCA patients. NICT could promote the expression of immune-related genes and activate CD8+ T and CD16+ NK cells to secrete more IFN-γ to kill ESCA cells. It provides a theoretical basis and clinical evidence for its potential as an NT strategy in ESCA.

Phase Transformation on Multilayer 2M-WS2 for Improved Surface-enhanced Raman Scattering.

In recent years, two-dimensional (2D) transition metal dichalcogenides (TMDCs) have been widely recognized as an ideal platform for surface-enhanced Raman scattering (SERS). Given their rich structural phases, phase transformation in 2D TMDCs is an efficient strategy to tailor their SERS performance. In this paper, we present the great SERS performance of multilayer 2M-WS2 and then investigate the effect of its phase transformation on SERS performance. It is observed that multilayer 2M-WS2 nanosheets undergo a thermally induced single-crystal phase transition from 2M-WS2 to 2H-WS2 upon thermal annealing or laser treatment. Distinguishing from the commercially available pure 2H-WS2 (P-2H-WS2), 2H-WS2 obtained by annealing and laser treatment still retain SERS properties comparable to those of 2M-WS2, among which the detection limits for CV molecules (10-8 M) are 3 orders of magnitude lower than that of P-2H-WS2 and the Raman intensity enhancements are ∼10-37 times higher. In contrast to the charge transfer (CT) mechanism governed by the Fermi level in metallic-phase 2M-WS2, 2H-WS2 obtained by phase transition exhibits accelerated CT facilitated by the bandgap reduction and reorganization resulting from the abundance of vacancies. This study introduces an interesting perspective and potential avenue for enhancing SERS through metal-to-semiconductor phase transitions in 2D TMDCs materials.

Atomic Confinement Empowered CoZn Dual-Single-Atom Nanotubes for H2O2 Production in Sequential Dual-Cathode Electro-Fenton Process.

Single-atom catalysts (SACs) are flourishing in various fields because of their 100% atomic utilization. However, their uncontrollable selectivity, poor stability and vulnerable inactivation remain critical challenges. According to theoretical predictions and experiments, a heteronuclear CoZn dual-single-atom confined in N/O-doped hollow carbon nanotube reactors (CoZnSA@CNTs) was synthesized via a spatial confinement growth strategy. CoZnSA@CNTs exhibited superior performance for H2O2 electrosynthesis over the entire pH range due to dual-confinement of the atomic sites and O2 molecule. CoZnSA@CNTs was favorable for H2O2 production mainly because the synergy of adjacent atomic sites, defect-rich feature and nanotube reactor promoted O2 enrichment and enhanced H2O2 reactivity/selectivity. The H2O2 selectivity reached nearly 100% in a range of 0.2 ∼ 0.65 V versus RHE and the yield achieved 7.50 M gcat -1 with CoZnSA@CNTs/carbon fiber felt, which exceeded most of the reported SACs in H-type cells. The obtained H2O2 was converted directly to sodium percarbonate and sodium perborate in a safe way for H2O2 storage/transportation. The sequential dual-cathode electron-Fenton process promoted the formation of reactive oxygen species (•OH, 1O2 and •O2 -) by activating the in-situ generated H2O2, enabling accelerated degradation of various pollutants and Cr(VI) detoxification in actual wastewater. This work proposes a promising confinement strategy for catalyst design and selectivity regulation of complex reactions. This article is protected by copyright. All rights reserved.

Easy-to-Lay Poly-N Heterocyclic Additives Enable Long-Term Stabilization of Zinc-Ion Capacitor Anodes under Deep Plating/Stripping.

Addition of organic compounds containing O/N heteroatoms to aqueous electrolytes such as ZnSO4 (ZS) solutions is one of the effective strategies to inhibit Zn anode dendrites and side reactions. However, addressing the stability of Zn plating/stripping at high current densities and areal capacities by this method is still a challenge, especially in capacitors known for high power and long life. Herein, an organic heterocyclic compound of 1, 4, 7, 10-tetraazacyclododecane (TC) containing four symmetrically distributed N atoms is employed as ZS additive, expanding the life of Zn anodes from ≈ 30 h to 1000 and 240 h at deep plating/stripping conditions of 10 and 20 mA cm-2/mAh cm-2, respectively; the cumulative capacity is as high as 5.0 Ah cm-2 with 99% Coulombic efficiency, far exceeding reported additives. TC with higher binding energies than H2O for Zn species tends to adsorb to Zn (002) in a lying manner and participate in the solvation shell of Zn2+, thus avoiding Zn dendrites and side-reaction damage, especially at high current densities. The TC-endowed Zn anode's stability under such extreme conditions is verified in Zn-ion capacitors (i.e., > 94.6% capacity retention after 28 000 cycles), providing new insights into the development of high-power Zn-based energy storage devices.