Mutual regulation of microglia and astrocytes after Gas6 inhibits spinal cord injury.

JOURNAL/nrgr/04.03/01300535-202502000-00032/figure1/v/2024-05-28T214302Z/r/image-tiff Invasive inflammation and excessive scar formation are the main reasons for the difficulty in repairing nervous tissue after spinal cord injury. Microglia and astrocytes play key roles in the spinal cord injury micro-environment and share a close interaction. However, the mechanisms involved remain unclear. In this study, we found that after spinal cord injury, resting microglia (M0) were polarized into pro-inflammatory phenotypes (MG1 and MG3), while resting astrocytes were polarized into reactive and scar-forming phenotypes. The expression of growth arrest-specific 6 (Gas6) and its receptor Axl were significantly down-regulated in microglia and astrocytes after spinal cord injury. In vitro experiments showed that Gas6 had negative effects on the polarization of reactive astrocytes and pro-inflammatory microglia, and even inhibited the cross-regulation between them. We further demonstrated that Gas6 can inhibit the polarization of reactive astrocytes by suppressing the activation of the Yes-associated protein signaling pathway. This, in turn, inhibited the polarization of pro-inflammatory microglia by suppressing the activation of the nuclear factor-κB/p65 and Janus kinase/signal transducer and activator of transcription signaling pathways. In vivo experiments showed that Gas6 inhibited the polarization of pro-inflammatory microglia and reactive astrocytes in the injured spinal cord, thereby promoting tissue repair and motor function recovery. Overall, Gas6 may play a role in the treatment of spinal cord injury. It can inhibit the inflammatory pathway of microglia and polarization of astrocytes, attenuate the interaction between microglia and astrocytes in the inflammatory microenvironment, and thereby alleviate local inflammation and reduce scar formation in the spinal cord.

Stability of Li1.3Al0.3Ti1.7(PO4)3-Based Composite Electrolytes against Lithium Anodes Enhanced by Uniform Surface Coating of Two-Dimensional Graphene-like C3N4 on Particle Surfaces.

All-solid-state lithium (Li) batteries have attracted considerable interest due to their potential in high energy density as well as safety. However, the realization of a stable Li/solid-state electrolyte (SSE) interface remains challenging. Herein, two-dimensional graphene-like C3N4 (g-C3N4) as a coating layer on Li1.3Al0.3Ti1.7(PO4)3 (LATP) electrolyte (LATP@CN) has been applied to construct the stable Li/SSE interface. The g-C3N4 layer is uniformly coated on the LATP surface using the in situ calcination method, which not only enhances the dispersibility of LATP particles in poly(ethylene oxide) (PEO) through the interaction between surface functional groups but also suppresses the side reactions between Li and LATP. The coating layer can effectively improve the interfacial stability. As a result, the conductivity and stability of the obtained composite solid-state electrolytes (CSEs) against Li are enhanced. The Li∥CSEs∥Li symmetric cells stably cycle for 670 and 600 h at 0.1 and 0.2 mA cm-2, respectively. The Li∥CSEs∥LiFePO4 cells stably cycle more than 100 times at 0.1 and 0.2 C with a capacity retention rate of about 86% and 88%, respectively. This work inspires a new strategy to avoid the reactions between LATP and Li.

Unlocking Efficient Hydrogen Production: Nucleophilic Oxidation Reactions Coupled with Water Splitting.

Electrocatalytic water splitting driven by sustainable energy is a clean and promising water-chemical fuel conversion technology for the production of high-purity green hydrogen. However, the sluggish kinetics of anodic oxygen evolution reaction (OER) pose challenges for large-scale hydrogen production, limiting its efficiency and safety. Recently, the anodic OER has been replaced by a nucleophilic oxidation reaction (NOR) with biomass as the substrate and coupled with a hydrogen evolution reaction (HER), which has attracted great interest. Anode NOR offers faster kinetics, generates high-value products, and reduces energy consumption. By coupling NOR with hydrogen evolution reaction, hydrogen production efficiency can be enhanced while yielding high-value oxidation products or degrading pollutants. Therefore, NOR-coupled HER hydrogen production is another new green electrolytic hydrogen production strategy after electrolytic water hydrogen production, which is of great significance for realizing sustainable energy development and global decarbonization. This review explores the potential of nucleophilic oxidation reactions as an alternative to OER and delves into NOR mechanisms, guiding future research in NOR-coupled hydrogen production. It assesses different NOR-coupled production methods, analyzing reaction pathways and catalyst effects. Furthermore, it evaluates the role of electrolyzers in industrialized NOR-coupled hydrogen production and discusses future prospects and challenges. This comprehensive review aims to advance efficient and economical large-scale hydrogen production.

Erratum: Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform.

This corrects the article 10.3791/66058.

Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform.

Gastric cancer is a common heterogeneous tumor. Most patients have advanced gastric cancer at the time of diagnosis and often need chemotherapy. Although 5-fluorouracil (5-FU) is widely used for treatment, its therapeutic sensitivity and drug tolerance still need to be determined, which emphasizes the importance of individualized administration. Pharmacogenetics can guide the clinical implementation of individualized treatment. Single nucleotide polymorphisms (SNPs), as a genetic marker, contribute to the selection of appropriate chemotherapy regimens and dosages. Some SNPs are associated with folate metabolism, the therapeutic target of 5-FU. Methylenetetrahydrofolate reductase (MTHFR) rs1801131 and rs1801133, dihydrofolate reductase (DHFR) rs1650697 and rs442767, methionine synthase (MTR) rs1805087, gamma-glutamyl hydrolase (GGH) rs11545078 and solute carrier family 19 member 1 (SLC19A1) rs1051298 have been investigated in different kinds of cancers and antifolate antitumor drugs, which have potential forecasting and guiding significance for application of 5-FU. The ion torrent next-generation semiconductor sequencing technology can rapidly detect gastric cancer-related SNPs. Each time a base is extended in a DNA chain, an H+ will be released, causing local pH changes. The ionic sensor detects pH changes and converts chemical signals into digital signals, achieving sequencing by synthesis. This technique has low sample requirement, simple operation, low cost, and fast sequencing speed, which is beneficial for guiding individualized chemotherapy by SNPs.

Efficacy and Safety of Interleukin-1 Inhibitors in the Management of Patients with Recurrent Pericarditis: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

BACKGROUND: The efficacy and safety of interleukin-1 (IL-1) inhibitors in patients with recurrent pericarditis (RP) remain to be determined. OBJECTIVE: We aimed to conduct a meta-analysis to investigate the impact of IL-1 inhibitors on patients suffering from RP. METHODS: The Cochrane Library, PubMed, EMBASE, ClinicalTrials.gov, and Web of Science databases were systematically searched to identify articles investigating the effects of IL-1 inhibitors in patients with RP up until January 2024. Relevant data on study characteristics and results were selected based on predefined criteria. The results were combined using a random effects model. RESULTS: The study included a total of 102 patients from three open-label randomized controlled trials. Overall, the use of IL-1 inhibitors, in comparison to placebo, demonstrated a significant reduction in the risk of pericarditis recurrence [risk ratio (RR) 0.13; 95% confident interval (CI) 0.05-0.30; p < 0.05; I2 = 0%]. However, the administration of IL-1 inhibitors may lead to certain adverse events (AEs), including infections and injection-site reactions. The risk of AEs is significantly higher with IL-1 inhibitors compared with placebo (RR 1.88; 95% CI 1.30-2.72; p < 0.05; I2 = 0%). Nevertheless, the occurrence of serious AEs among patients was relatively rare, and no fatalities were reported. CONCLUSION: This meta-analysis showed that IL-1 inhibitors can effectively reduce the risk of recurrence in patients with RP and are relatively safe. REGISTRATION: PROSPERO identifier number CRD42023492904.

Identification and validation of a novel apoptosis-related prognostic risk score model for lung adenocarcinoma.

The prognostic roles of apoptosis-related genes (ARGs) in lung adenocarcinoma (LUAD) have not been fully elucidated. In this study, differentially expressed genes (DEGs) associated with apoptosis and the hub genes were further identified. The prognostic values of the ARGs were evaluated using the LASSO Cox regression method. Prognostic values were determined using Kaplan-Meier (K-M) curves and receiver operating characteristic (ROC) curves in the TCGA and GEO datasets. The correlations, mutation data, and protein expression of the 10 ARGs predictive models were also analyzed. We identified 130 differentially expressed ARGs. DEGs were used to split LUAD cases into two subtypes whose overall survival (OS) were significantly different (P = 0.025). We developed a novel 10-gene signature using LASSO Cox regression. In both TCGA and GEO datasets, the results of the K-M curve and log-rank test showed significant difference in the survival rate of patients in the high-risk group and low-risk group (P < 0.0001). According to the GO and KEGG analyses, ARGs were enriched in cancer-related terms. In both cohorts, the immune status of the high-risk group was significantly lower than that of the low-risk group. Based on the differential expression of the ARGs, we established a new risk model to predict the prognosis of patients with LUAD.

The Role of Angiotensin II Receptor Blockers in the Management of Hypertrophic Cardiomyopathy: An Updated Meta-Analysis of Randomized Controlled Trials.

INTRODUCTION: The use of angiotensin II receptor blockers (ARBs) in the treatment of hypertrophic cardiomyopathy (HCM) remains a subject of controversy. METHODS: We conducted a comprehensive search of the Cochrane Library, PubMed, EMBASE, ClinicalTrials.gov, and Web of Science databases until October 2023 to identify articles investigating the effects of ARBs in patients diagnosed with HCM. Predefined criteria were utilized for selecting data on study characteristics and results. RESULTS: The study included a total of 387 patients from 6 randomized controlled trials, which were reported in 7 articles. The results of the meta-analysis revealed that the utilization of ARBs did not yield a reduction in left ventricular (LV) mass (p = 0.07) and maximum LV wall thickness (p = 0.25), nor did it demonstrate any improvement in LV fibrosis (p = 0.39). Furthermore, there was no significant impact observed on early diastolic mitral annular velocity (p = 0.19) and LV ejection fraction (p = 0.44). CONCLUSIONS: The administration of ARBs does not appear to yield improvements in cardiac structure, function, and myocardial fibrosis in patients with HCM.

Identification of genetic modifiers enhancing B7-H3-targeting CAR T cell therapy against glioblastoma through large-scale CRISPRi screening.

BACKGROUND: Glioblastoma multiforme (GBM) is a highly aggressive brain tumor with a poor prognosis. Current treatment options are limited and often ineffective. CAR T cell therapy has shown success in treating hematologic malignancies, and there is growing interest in its potential application in solid tumors, including GBM. However, current CAR T therapy lacks clinical efficacy against GBM due to tumor-related resistance mechanisms and CAR T cell deficiencies. Therefore, there is a need to improve CAR T cell therapy efficacy in GBM. METHODS: We conducted large-scale CRISPR interference (CRISPRi) screens in GBM cell line U87 MG cells co-cultured with B7-H3 targeting CAR T cells to identify genetic modifiers that can enhance CAR T cell-mediated tumor killing. Flow cytometry-based tumor killing assay and CAR T cell activation assay were performed to validate screening hits. Bioinformatic analyses on bulk and single-cell RNA sequencing data and the TCGA database were employed to elucidate the mechanism underlying enhanced CAR T efficacy upon knocking down the selected screening hits in U87 MG cells. RESULTS: We established B7-H3 as a targetable antigen for CAR T therapy in GBM. Through large-scale CRISPRi screening, we discovered genetic modifiers in GBM cells, including ARPC4, PI4KA, ATP6V1A, UBA1, and NDUFV1, that regulated the efficacy of CAR T cell-mediated tumor killing. Furthermore, we discovered that TNFSF15 was upregulated in both ARPC4 and NDUFV1 knockdown GBM cells and revealed an immunostimulatory role of TNFSF15 in modulating tumor-CAR T interaction to enhance CAR T cell efficacy. CONCLUSIONS: Our study highlights the power of CRISPR-based genetic screening in investigating tumor-CAR T interaction and identifies potential druggable targets in tumor cells that confer resistance to CAR T cell killing. Furthermore, we devised targeted strategies that synergize with CAR T therapy against GBM. These findings shed light on the development of novel combinatorial strategies for effective immunotherapy of GBM and other solid tumors.

HFM-Tracker: a cell tracking algorithm based on hybrid feature matching.

Cell migration is known to be a fundamental biological process, playing an essential role in development, homeostasis, and diseases. This paper introduces a cell tracking algorithm named HFM-Tracker (Hybrid Feature Matching Tracker) that automatically identifies cell migration behaviours in consecutive images. It combines Contour Attention (CA) and Adaptive Confusion Matrix (ACM) modules to accurately capture cell contours in each image and track the dynamic behaviors of migrating cells in the field of view. Cells are firstly located and identified via the CA module-based cell detection network, and then associated and tracked via a cell tracking algorithm employing a hybrid feature-matching strategy. This proposed HFM-Tracker exhibits superiorities in cell detection and tracking, achieving 75% in MOTA (Multiple Object Tracking Accuracy) and 65% in IDF1 (ID F1 score). It provides quantitative analysis of the cell morphology and migration features, which could further help in understanding the complicated and diverse cell migration processes.

Decoding the tumour-modulatory roles of LIMK2.

LIM domains kinase 2 (LIMK2) is a 72 kDa protein that regulates actin and cytoskeleton reorganization. Once phosphorylated by its upstream activator (ROCK1), LIMK2 can phosphorylate cofilin to inactivate it. This relieves the levering stress on actin and allows polymerization to occur. Actin rearrangement is essential in regulating cell cycle progression, apoptosis, and migration. Dysregulation of the ROCK1/LIMK2/cofilin pathway has been reported to link to the development of various solid cancers such as breast, lung, and prostate cancer and liquid cancer like leukemia. This review aims to assess the findings from multiple reported in vitro, in vivo, and clinical studies on the potential tumour-regulatory role of LIMK2 in different human cancers. The findings of the selected literature unraveled that activated AKT, EGF, and TGF-ß pathways can upregulate the activities of the ROCK1/LIMK2/cofilin pathway. Besides cofilin, LIMK2 can modulate the cellular levels of other proteins, such as TPPP1, to promote microtubule polymerization. The tumour suppressor protein p53 can transactivate LIMK2b, a splice variant of LIMK2, to induce cell cycle arrest and allow DNA repair to occur before the cell enters the next phase of the cell cycle. Additionally, several non-coding RNAs, such as miR-135a and miR-939-5p, could also epigenetically regulate the expression of LIMK2. Since the expression of LIMK2 is dysregulated in several human cancers, measuring the tissue expression of LIMK2 could potentially help diagnose cancer and predict patient prognosis. As LIMK2 could play tumour-promoting and tumour-inhibiting roles in cancer development, more investigation should be conducted to carefully evaluate whether introducing a LIMK2 inhibitor in cancer patients could slow cancer progression without posing clinical harms.

Tumour-regulatory role of long non-coding RNA HOXA-AS3.

Dysregulation of long non-coding RNA (lncRNA) HOXA-AS3 has been shown to contribute to the development of multiple cancer types. Several studies have presented the tumour-modulatory role or prognostic significance of this lncRNA in various kinds of cancer. Overall, HOXA-AS3 can act as a competing endogenous RNA (ceRNA) that inhibits the activity of seven microRNAs (miRNAs), including miR-29a-3p, miR-29 b-3p, miR-29c, miR-218-5p, miR-455-5p, miR-1286, and miR-4319. This relieves the downstream messenger RNA (mRNA) targets of these miRNAs from miRNA-mediated translational repression, allowing them to exert their effect in regulating cellular activities. Examples of the pathways regulated by lncRNA HOXA-AS3 and its associated downstream targets include the WNT/ß-catenin and epithelial-to-mesenchymal transition (EMT) activities. Besides, HOXA-AS3 can interact with other cellular proteins like homeobox HOXA3 and HOXA6, influencing the oncogenic signaling pathways associated with these proteins. Generally, HOXA-AS3 is overexpressed in most of the discussed human cancers, making this lncRNA a potential candidate to diagnose cancer or predict the clinical outcomes of cancer patients. Hence, targeting HOXA-AS3 could be a new therapeutic approach to slowing cancer progression or as a potential biomarker and therapeutic target. A drawback of using lncRNA HOXA-AS3 as a biomarker or therapeutic target is that most of the studies that have reported the tumour-regulatory roles of lncRNA HOXA-AS3 are single observational, in vitro, or in vivo studies. More in-depth mechanistic and large-scale clinical trials must be conducted to confirm the tumour-modulatory roles of lncRNA HOXA-AS3 further. Besides, no lncRNA HOXA-AS3 inhibitor has been tested preclinically and clinically, and designing such an inhibitor is crucial as it may potentially slow cancer progression.

Magnetic Nanoparticle-Based Microfluidic Platform for Automated Enrichment of High-Purity Extracellular Vesicles.

Extracellular vesicles (EVs) are available in various biological fluids and have highly heterogeneous sizes, origins, contents, and functions. Rapid enrichment of high-purity EVs remains crucial for enhancing research on EVs in tumors. In this work, we present a magnetic nanoparticle-based microfluidic platform (ExoCPR) for on-chip isolation, purification, and mild recovery of EVs from cell culture supernatant and plasma within 29 min. The ExoCPR chip integrates bubble-driven micromixers and immiscible filtration assisted by surface tension (IFAST) technology. The bubble-driven micromixer enhances the mixing between immunomagnetic beads and EVs, eliminating the need for manual pipetting or off-chip oscillatory incubation. The high-purity EVs were obtained after passing through the immiscible phase interface where hydrophilic or hydrophobic impurities nonspecifically bound to SIMI were removed. The ExoCPR chip had a capture efficiency of 75.8% and a release efficiency of 62.7% for model EVs. We also demonstrated the powerful performance of the ExoCPR in isolating EVs from biological samples (>90% purity). This chip was further employed in clinical plasma samples and showed that the number of GPC3-positive EVs isolated from hepatocellular carcinoma patients was significantly higher than that of healthy individuals. This ExoCPR chip may provide a promising tool for EV-based liquid biopsy and other fundamental research.

Discovery of novel SOS1 inhibitors using machine learning.

Overactivation of the rat sarcoma virus (RAS) signaling is responsible for 30% of all human malignancies. Son of sevenless 1 (SOS1), a crucial node in the RAS signaling pathway, could modulate RAS activation, offering a promising therapeutic strategy for RAS-driven cancers. Applying machine learning (ML)-based virtual screening (VS) on small-molecule databases, we selected a random forest (RF) regressor for its robustness and performance. Screening was performed with the L-series and EGFR-related datasets, and was extended to the Chinese National Compound Library (CNCL) with more than 1.4 million compounds. In addition to a series of documented SOS1-related molecules, we uncovered nine compounds that have an unexplored chemical framework and displayed inhibitory activity, with the most potent achieving more than 50% inhibition rate in the KRAS G12C/SOS1 PPI assay and an IC50 value in the proximity of 20 µg mL-1. Compared with the manner that known inhibitory agents bind to the target, hit compounds represented by CL01545365 occupy a unique pocket in molecular docking. An in silico drug-likeness assessment suggested that the compound has moderately favorable drug-like properties and pharmacokinetic characteristics. Altogether, our findings strongly support that, characterized by the distinctive binding modes, the recognition of novel skeletons from the carboxylic acid series could be candidates for developing promising SOS1 inhibitors.

Composition regulation of polyacrylonitrile-based polymer electrolytes enabling dual-interfacially stable solid-state lithium batteries.

The polyacrylonitrile (PAN) is an attractive matrix of polymer electrolytes owing to its wide electrochemical window and strong coordination with Li salts. However, the PAN-based electrolytes undergo severe interfacial problems from both cathode and anode sides, including uneven ionic transfer induced by high rigidity of dry PAN-based polymer, as well as inferior stability against Li-metal anode. Herein, the composition regulation of PAN-based electrolytes is proposed by introducing succinonitrile (SN) plastic crystal and LiNO3 salt for the construction of interfacially stable solid-state lithium batteries. The plastic nature of SN enables the rapid ionic transfer in electrolytes, along with the establishment of conformally interfacial contacts. Meanwhile, a stable solid-electrolyte-interface (SEI) layer consisting of Li3N and LiNO2 is in-situ formed at Li/electrolyte interface, contributing to the inhibition of uncontrol reactions between PAN and Li-metal. Consequently, the resultant Li symmetric cell delivers an extended critical current density of 1.7 mA cm-2 and an outstanding cycling lifespan of 700 h at 0.1 mA cm-2. Moreover, the corresponding solid-state LiNi0.6Co0.2Mn0.2O2/Li full cell shows an initial discharge capacity of 161 mAh/g followed by an outstanding capacity retention of 88.7 % after 100 cycles at 0.1C. This work paves the way for application of PAN-based electrolytes in the field of solid-state batteries by facile composition regulation.

Pharmacological suppression of the OTUD4/CD73 proteolytic axis revives antitumor immunity against immune-suppressive breast cancers.

Despite widespread utilization of immunotherapy, treating immune-cold tumors remains a challenge. Multiomic analyses and experimental validation identified the OTUD4/CD73 proteolytic axis as a promising target in treating immune-suppressive triple negative breast cancer (TNBC). Mechanistically, deubiquitylation of CD73 by OTUD4 counteracted its ubiquitylation by TRIM21, resulting in CD73 stabilization inhibiting tumor immune responses. We further demonstrated the importance of TGF-ß signaling for orchestrating the OTUD4/CD73 proteolytic axis within tumor cells. Spatial transcriptomics profiling discovered spatially resolved features of interacting malignant and immune cells pertaining to expression levels of OTUD4 and CD73. In addition, ST80, a newly developed inhibitor, specifically disrupted proteolytic interaction between CD73 and OTUD4, leading to reinvigoration of cytotoxic CD8+ T cell activities. In preclinical models of TNBC, ST80 treatment sensitized refractory tumors to anti-PD-L1 therapy. Collectively, our findings uncover what we believe to be a novel strategy for targeting the immunosuppressive OTUD4/CD73 proteolytic axis in treating immune-suppressive breast cancers with the inhibitor ST80.

m6A methyltransferase METTL14­mediated RP1­228H13.5 promotes the occurrence of liver cancer by targeting hsa­miR­205/ZIK1.

The aim of the present study was to explore the association between N6­methyladenosine (m6A) modification regulatory gene­related long noncoding (lnc)RNA RP1­228H13.5 and cancer prognosis through bioinformatics analysis, as well as the impact of RP1­228H13.5 on cell biology­related behaviors and specific molecular mechanisms. Bioinformatics analysis was used to construct a risk model consisting of nine genes. This model can reflect the survival time and differentiation degree of cancer. Subsequently, a competing endogenous RNA network consisting of 3 m6A­related lncRNAs, six microRNAs (miRs) and 201 mRNAs was constructed. A cell assay confirmed that RP1­228H13.5 is significantly upregulated in liver cancer cells, which can promote liver cancer cell proliferation, migration and invasion, and inhibit liver cancer cell apoptosis. The specific molecular mechanism may be the regulation of the expression of zinc finger protein interacting with K protein 1 (ZIK1) by targeting the downstream hsa­miR­205. Further experiments found that the m6A methyltransferase 14, N6­adenosine­methyltransferase subunit mediates the regulation of miR­205­5p expression by RP1­228H13.5. m6A methylation regulatory factor­related lncRNA has an important role in cancer. The targeting of hsa­miR­205 by RP1­228H13.5 to regulate ZIK1 may serve as a potential mechanism in the occurrence and development of liver cancer.

CD8+ T cells sustain antitumor response by mediating crosstalk between adenosine A2A receptor and glutathione/GPX4.

Antitumor responses of CD8+ T cells are tightly regulated by distinct metabolic fitness. High levels of glutathione (GSH) are observed in the majority of tumors, contributing to cancer progression and treatment resistance in part by preventing glutathione peroxidase 4-dependent (GPX4-dependent) ferroptosis. Here, we show the necessity of adenosine A2A receptor (A2AR) signaling and the GSH/GPX4 axis in orchestrating metabolic fitness and survival of functionally competent CD8+ T cells. Activated CD8+ T cells treated ex vivo with simultaneous inhibition of A2AR and lipid peroxidation acquire a superior capacity to proliferate and persist in vivo, demonstrating a translatable means to prevent ferroptosis in adoptive cell therapy. Additionally, we identify a particular cluster of intratumoral CD8+ T cells expressing a putative gene signature of GSH metabolism (GMGS) in association with clinical response and survival across several human cancers. Our study addresses a key role of GSH/GPX4 and adenosinergic pathways in fine-tuning the metabolic fitness of antitumor CD8+ T cells.

Galvanic stabilization of Zn metals for long-life aqueous batteries.

Rechargeable aqueous Zn-ion batteries have received extensive attention due to their environmental friendliness, high safety, and low cost. However, the Zn dendrite growth during plating/stripping cycles, which deteriorates coulombic efficiency and shortens the cycle life, dramatically hinders the application of Zn anodes in batteries. Herein, we propose to grow an In layer on Zn foils through spontaneous Galvanic reaction to address the challenging Zn dendrites.In-situoptical observations show that this strategy effectively suppresses the dendrite growth, thereby leading to a robust and stable Zn metal anode with low voltage hysteresis (30 mV at 0.4 mA·cm-2) and long cycle life of over 1200 h in symmetric cells. Meanwhile, the full cell assembled with the modified Zn anode and MnO2cathode exhibits excellent cycling performance over 2000 cycles and a high discharge capacity of 89.1 mAh·g-1. This work provides an efficient pathway for interfacial engineering towards stable Zn anodes.

Synergistic effect of organic matter-floc size-bound water and multifactorial quantitative model of optimal reagent demand in sewage sludge conditioning process prior to dewatering.

The high amount of densely hydrated organic substance present in sewage sludge impedes its filterability, thus restricting sludge disposal. Although chemical conditioning can facilitate filtration, the diverse sludge properties complicate the quantitative control of conditioning process. Investigating how to accurately quantify the optimal reagent demand (ORD) based on the critical physicochemical properties of the target sludge is an effective way to address the current issue. This study focused on the sewage and stockpiled sludge with varying properties, and their ORD under different chemical conditioning. The results showed that organic content, floc size, and bound water synergistically influenced conditioning process. The quantitative models were established between their coupling indicators and ORD, with coupling indicators including the ratio of organic content to floc size, the ratio of flow viscosity to floc size, and the ratio of the product of organic content and bound water to floc size. The linear correlation of the coupling indicator with ORD was higher than that of the traditional single-factor indicator. Furthermore, the inherent filterability of the sludge was somewhat separate from the adjustability of its filtration. A "dual-system" impact model was proposed to characterized the conditioning and filtration processes. These results provide theoretical guidance for the quantitative regulation of conditioning and filtration processes of sludge with complex characteristics.