Selective Extraction of Critical Metals from Spent Lithium-Ion Batteries.

Selective and highly efficient extraction technologies for the recovery of critical metals including lithium, nickel, cobalt, and manganese from spent lithium-ion battery (LIB) cathode materials are essential in driving circularity. The tailored deep eutectic solvent (DES) choline chloride-formic acid (ChCl-FA) demonstrated a high selectivity and efficiency in extracting critical metals from mixed cathode materials (LiFePO4:Li(NiCoMn)1/3O2 mass ratio of 1:1) under mild conditions (80 °C, 120 min) with a solid-liquid mass ratio of 1:200. The leaching performance of critical metals could be further enhanced by mechanochemical processing because of particle size reduction, grain refinement, and internal energy storage. Furthermore, mechanochemical reactions effectively inhibited undesirable leaching of nontarget elements (iron and phosphorus), thus promoting the selectivity and leaching efficiency of critical metals. This was achieved through the preoxidation of Fe and the enhanced stability of iron phosphate framework, which significantly increased the separation factor of critical metals to nontarget elements from 56.9 to 1475. The proposed combination of ChCl-FA extraction and the mechanochemical reaction can achieve a highly selective extraction of critical metals from multisource spent LIBs under mild conditions.

Direct and Indirect Electron Transfer Routes of Chromium(VI) Reduction with Different Crystalline Ferric Oxyhydroxides in the Presence of Pyrogenic Carbon.

Electron transfer mediated by iron minerals is considered as a critical redox step for the dynamics of pollutants in soil. Herein, we explored the reduction process of Cr(VI) with different crystalline ferric oxyhydroxides in the presence of pyrogenic carbon (biochar). Both low- and high-crystallinity ferric oxyhydroxides induced Cr(VI) immobilization mainly via the sorption process, with a limited reduction process. However, the Cr(VI) reduction immobilization was inspired by the copresence of biochar. Low-crystallinity ferric oxyhydroxide had an intense chemical combination with biochar and strong sorption for Cr(VI) via inner-sphere complexation, leading to the indirect electron transfer route for Cr(VI) reduction, that is, the electron first transferred from biochar to iron mineral through C-O-Fe binding and then to Cr(VI) with Fe(III)/Fe(II) transformation on ferric oxyhydroxides. With increasing crystallinity of ferric oxyhydroxides, the direct electron transfer between biochar and Cr(VI) became the main electron transfer avenue for Cr(VI) reduction. The indirect electron transfer was suppressed in the high-crystallinity ferric oxyhydroxides due to less sorption of Cr(VI), limited combination with biochar, and higher iron stability. This study demonstrates that electron transfer mechanisms involving iron minerals change with the mineral crystallization process, which would affect the geochemical process of contaminants with pyrogenic carbon.

Critical Impact of Nitrogen Vacancies in Nonradical Carbocatalysis on Nitrogen-Doped Graphitic Biochar.

Nitrogen-doped graphitic biochar (NBC) has boosted the development of nonradical peroxymonosulfate (PMS) activation in environmental remediation. However, the specific role of nitrogen species played in NBC-based nonradical carbocatalysis remains vaguely interpreted. To pinpoint the critical nitrogen speciation, a sophisticated thermo-mechanochemical manipulation was exploited to prepare a series of NBCs with similar dimensional structures and oxygen levels but different nitrogen species (i.e., dopants and vacancies). Different from conventional perspectives, nonradical NBC-based carbocatalysis was found to be preferably determined by the nitrogen vacancies more than their parent nitrogen dopants. Raman depth analysis evidenced that a complete transformation of nitrogen dopants into nitrogen vacancies could be achieved at 800 °C, where an excellent nonradical abatement of 4-chlorophenol (4-CH, 90.9% removal) was found for the NBC800 with a low PMS consumption (1.24 mM). According to PMS adsorption experiments, nitrogen vacancies exhibited the highest affinity toward the PMS molecules compared to nitrogen dopants, which accounted for the superior carbocatalysis. Electron paramagnetic resonance and Raman spectroscopic analyses indicated that the original PMS molecules were bound to positively charged nitrogen vacancies, and a robust metastable complex (*HSO5-) evolved subsequently via hydrogen abstraction by adjacent persistent free radicals. In situ Raman techniques could be adopted to estimate the level of nitrogen vacancies associated with the polarization of electron distribution. The flexible feature and practical prospects of nitrogen vacancy-based carbocatalysis were also observed in the remediation of simulated phenolic industrial wastewater. Overall, this study unravels the dilemma in the current NBC-based nonradical carbocatalysis and advances our understanding of nitrogen doping technology for next-generation biochar design.

Kaolinite Enhances the Stability of the Dissolvable and Undissolvable Fractions of Biochar via Different Mechanisms.

Input of biomass-derived biochar into soil is recognized as a promising method of carbon sequestration. The long-term sequestration effect of biochar depends on the stability of both its dissolvable and undissolvable fractions in soil, which could be affected by their interactions with soil minerals. Here, walnut shell-derived biochar was divided into dissolvable and undissolvable fractions and then interacted with kaolinite. Stability of kaolinite-biochar associations was evaluated by chemical oxidation and biological degradation. At low dissolvable biochar concentrations, the association was mainly attributed to "Ca2+ bridging" and "ligand exchange", whereas "van der Waals attraction" was dominant at high concentrations. For the undissolvable biochar, kaolinite raised the activation energy of its surface by 22.1%, causing a reduction in biochar reactivity. By chemical oxidation, kaolinite reduced the C loss of total biochar by 42.5%, 33.1% resulting from undissolvable biochar and 9.4% from dissolvable biochar. Because of the presence of kaolinite, the loss of biodegradable C in total biochar was reduced by 49.4% and 48.2% from undissolvable fraction and 1.2% from dissolvable fraction. This study indicates that kaolinite can increase the stability of both dissolvable and undissolvable biochar, suggesting that kaolinite-rich soils could be a beneficial environment for biochar for long-term carbon sequestration.

Mineral-mediated stability of organic carbon in soil and relevant interaction mechanisms.

Soil, the largest terrestrial carbon reservoir, is central to climate change and relevant feedback to environmental health. Minerals are the essential components that contribute to over 60% of soil carbon storage. However, how the interactions between minerals and organic carbon shape the carbon transformation and stability remains poorly understood. Herein, we critically review the primary interactions between organic carbon and soil minerals and the relevant mechanisms, including sorption, redox reaction, co-precipitation, dissolution, polymerization, and catalytic reaction. These interactions, highly complex with the combination of multiple processes, greatly affect the stability of organic carbon through the following processes: (1) formation or deconstruction of the mineral-organic carbon association; (2) oxidative transformation of the organic carbon with minerals; (3) catalytic polymerization of organic carbon with minerals; and (4) varying association stability of organic carbon according to the mineral transformation. Several pieces of evidence related to the carbon turnover and stability during the interaction with soil minerals in the real eco-environment are then demonstrated. We also highlight the current research gaps and outline research priorities, which may map future directions for a deeper mechanisms-based understanding of the soil carbon storage capacity considering its interactions with minerals.

Enhanced adsorption of aromatic VOCs on hydrophobic porous biochar produced via microwave rapid pyrolysis.

To customize biochar suitable for efficient adsorption of benzene derivatives, this study presents programmed microwave pyrolysis to produce hydrophobic porous biochar with low-dose ferric chloride. Designated control of the ramping rates in the carbonization stage and the temperatures in the activation stage were conducive to enlarging the specific surface area. Iron species, including amorphous iron minerals, could create small-scale hotspots during microwave pyrolysis to promote microporous structure development. Compared with conventional pyrolysis, programmed microwave pyrolysis could increase the specific surface area from 288.6 m2 g-1 to 455.9 m2 g-1 with a short heating time (15 min vs. 2 h) under 650 °C. Engineered biochar exhibited higher adsorption capacity for benzene and toluene (136.6 and 94.6 mg g-1), and lower adsorption capacity for water vapour (6.2 mg g-1). These findings provide an innovative design of engineered biochar for the adsorption of volatile organic compounds in the environment.

Unlocking the solution-phase molecular transformation of biochar during intensive rainfall events: Implications for the long-term carbon cycle under climate change.

The unclear turnover of soluble and solid phases of biochar during increasingly severe climate change (e.g., intensive rainfall) raised questions about the carbon stability of biochar in soil. Here, we present an in-depth analysis of the molecular-level transformations occurring in both the soluble and solid phases of biochar subjected to prolonged wet-dry cycles with simulated rainwater. Biochar properties, including surface functionality and carbon texture, greatly affected the transformation route and led to a distinct stability variation. The rich alkyl -CH3 on the low-temperature biochar (450 °C) was oxidized to hydroxymethyl -CH2OH or formyl -CHO, and the ester -COOC- or peptide -CONHC- bonds were fragmented in the meantime, causing the release of protein- or lipid-like organic carbon and the declined carbon stability (Æ, tested by H2O2 oxidation, from 60.1 % to 53.2 %). After a high-temperature (750 °C) pyrolysis process, only oxidation of the surface -OH with limited bond breaking occurred after rainwater elution, presenting a marginal composition difference with constant stability. However, the fragile carbon nature of biochar, caused by CO2 activation, led to enhanced fragmentation, oxidation, and hydration, resulting in the release of tannin-like organic carbon, which compromises the carbon storage (Æ decreased from 81.2 % to 73.0 %). Our findings evaluated the critical transformation of biochar during intensive rainfall, offering crucial insights for designing sustainable biochar and achieving carbon neutrality.

Macrophage ATG16L1 expression suppresses metabolic dysfunction-associated steatohepatitis progression by promoting lipophagy.

BACKGROUND/AIMS: Metabolic dysfunction-associated steatohepatitis (MASH) is an unmet clinical challenge due to the rapid increased occurrence but lacking approved drugs. Autophagy-related protein 16-like 1 (ATG16L1) plays an important role in the process of autophagy, which is indispensable for proper biogenesis of the autophagosome, but its role in modulating macrophage-related inflammation and metabolism during MASH has not been documented. Here, we aimed to elucidate the role of ATG16L1 in the progression of MASH. METHODS: Expression analysis was performed with liver samples from human and mice. MASH models were induced in myeloid-specific Atg16l1-deficient and myeloid-specific Atg16l1-overexpressed mice by high-fat and high-cholesterol diet or methionine- and choline-deficient diet to explore the function and mechanism of macrophage ATG16L1 in MASH. RESULTS: Macrophage-specific Atg16l1 knockout exacerbated MASH and inhibited energy expenditure, whereas macrophage-specific Atg16l1 transgenic overexpression attenuated MASH and promotes energy expenditure. Mechanistically, Atg16l1 knockout inhibited macrophage lipophagy, thereby suppressing macrophage ß-oxidation and decreasing the production of 4-hydroxynonenal, which further inhibited stimulator of interferon genes(STING) carbonylation. STING palmitoylation was enhanced, STING trafficking from the endoplasmic reticulum to the Golgi was promoted, and downstream STING signaling was activated, promoting proinflammatory and profibrotic cytokines secretion, resulting in hepatic steatosis and hepatic stellate cells activation. Moreover, Atg16l1-deficiency enhanced macrophage phagosome ability but inhibited lysosome formation, engulfing mtDNA released by pyroptotic hepatocytes. Increased mtDNA promoted cGAS/STING signaling activation. Moreover, pharmacological promotion of ATG16L1 substantially blocked MASH progression. CONCLUSION: ATG16L1 suppresses MASH progression by maintaining macrophage lipophagy, restraining liver inflammation, and may be a promising therapeutic target for MASH management.

MCC950 attenuates plasma cell mastitis in an MDSC-dependent manner.

Plasma cell mastitis (PCM) is a sterile inflammatory condition primarily characterized by periductal inflammation and ductal ectasia. Currently, there is a lack of non-invasive or minimally invasive treatment option other than surgical intervention. The NLRP3 inflammasome has been implicated in the pathogenesis and progression of various inflammatory diseases, however, its involvement in PCM has not yet been reported. In this study, we initially observed the pronounced upregulation of NLRP3 in both human and mouse PCM tissue and elucidated the mechanism underlying the attenuation of PCM through inhibition of NLRP3. We established the PCM murine model and collected samples on day 14, when inflammation reached its peak, for subsequent research purposes. MCC950, an NLRP3 inhibitor, was utilized to effectively ameliorate PCM by significantly reducing plasma cell infiltration in mammary tissue, as well as attenuate the expression of pro-inflammatory cytokines including IL-1ß, TNF-α, IL-2, and IL-6. Mechanistically, we observed that MCC950 augmented the function of myeloid-derived suppressor cells (MDSCs), which in turn inhibited the infiltration of plasma cells. Furthermore, it was noted that depleting MDSCs greatly compromised the therapeutic efficacy of MCC950. Collectively, our findings suggest that the administration of MCC950 has the potential to impede the progression of PCM by augmenting MDSCs both numerically and functionally, ultimately treating PCM effectively. This study provides valuable insights into the utilization of pharmacological agents for PCM treatment.

Integrated single-cell transcriptomics reveals the hypoxia-induced inflammation-cancer transformation in NASH-derived hepatocellular carcinoma.

Non-alcoholic fatty liver disease (NAFLD) has emerged as the primary risk factor for hepatocellular carcinoma (HCC), owing to improved vaccination rates of Hepatitis B and the increasing prevalence of metabolic syndrome related to obesity. Although the importance of innate and adaptive immune cells has been emphasized, the malignant transformation of hepatocytes and their intricate cellular network with the immune system remain unclear. The study incorporated four single-cell transcriptomic datasets of liver tissues covering healthy and NAFLD-related disease status. To identify the subsets and functions of hepatocytes and macrophages, we employed differential composition analysis, functional enrichment analysis, pseudotime analysis, and scenic analysis. Furthermore, an experimental mouse model for the transformation of nonalcoholic steatohepatitis into hepatocellular carcinoma was established for validation purposes. We defined CYP7A1+ hepatocytes enriched in precancerous lesions as 'Transitional Cells' in the progression from NAFLD to HCC. CYP7A1+ hepatocytes upregulated genes associated with stress response, inflammation and cancer-associated pathways and downregulated the normal hepatocyte signature. We observed that hypoxia activation accompanied the entire process of inflammation-cancer transformation. Hepatocyte-derived HIF1A was gradually activated during the progression of NAFLD disease to adapt to the hypoxic microenvironment and hepatocytes under hypoxic environment led to changes in the metabolism, proliferation and angiogenesis, promoting the occurrence of tumours. Meanwhile, hypoxia induced the polarization of RACK1+ macrophages that enriched in the liver tissues of NASH towards immunosuppressed TREM2+ macrophages. Moreover, immunosuppressive TREM2+ macrophages were recruited by tumour cells through the CCL15-CCR1 axis to enhance immunosuppressive microenvironment and promote NAFLD-related HCC progression. The study provides a deep understanding of the development mechanism of NAFLD-related HCC and offers theoretical support and experimental basis for biological targets, drug research, and clinical application.

Single-cell analysis reveals hypoxia-induced immunosuppressive microenvironment in intrahepatic cholangiocarcinoma.

The role of hypoxia in the tumor microenvironment of intrahepatic cholangiocarcinoma (iCCA) remains unclear. Here, we generated a comprehensive atlas of the entire tumor microenvironment and delineated the multifaceted cell-cell interactions to decipher hypoxia-induced pro-tumor immune suppression. We discovered hypoxia is significantly associated with iCCA progression via the activation of HIF1A expression. Moreover, hypoxia-dependent PPARγ-mediated fatty acid oxidation in APOE+ TAMs promoted M2 macrophage polarization by activating the HIF1A-PPARG-CD36 axis. These polarized APOE+ TAMs recruited Treg cell infiltration via the CCL3-CCR5 pair to form an immunosuppressive microenvironment. APOE+ TAMs tended to co-localize spatially with Treg cells in the malignant tissue based on spatial transcriptome data and immunofluorescence analysis results. We identified tumor-reactive CXCL13+ CD8-PreTex with specific high expression of ENTPD1 and ITGAE, which acted as precursors of CD8-Tex and had higher cytotoxicity, lower exhaustion, and more vigorous proliferation. Consequently, CXCL13+ CD8-PreTex functioned as a positive regulator of antitumor immunity by expressing the pro-inflammatory cytokines IFNG and TNF, associated with a better survival outcome. Our study reveals the mechanisms involved in hypoxia-induced immunosuppression and suggests that targeting precursor-exhausted CXCL13+CD8+ T cells might provide a pratical immunotherapeutic approach.

Integrated analysis of single-cell and bulk RNA sequencing data reveals a cellular senescence-related signature in hepatocellular carcinoma.

The mortality of hepatocellular carcinoma (HCC) is on the rise globally, particularly in the Western world, with etiology gradually shifting from virus-related liver diseases to metabolic disorders such as non-alcoholic fatty liver disease. Early detection of HCC is challenging, and effective prognostic indicators are currently lacking, urgently necessitating reliable markers to assist in treatment planning and clinical management. Here, we introduce hepatocellular carcinoma senescence genes (HSG) to assess cellular senescence in HCC and devise a hepatocellular carcinoma senescence score (HSS) for prognostic prediction. Higher HSS levels signify poorer prognosis and increased tumor proliferation activity. Additionally, we observe alterations in the tumor immune microenvironment with higher HSS levels, such as increased infiltration of Treg, potentially providing a basis for immunotherapy. Furthermore, we identify key genes, such as PTTG1, within the senescence gene set and demonstrate their regulatory roles in HCC cells and Treg through experimentation. In summary, we establish a scoring system based on hepatocellular carcinoma senescence genes for prognostic prediction in HCC, potentially offering guidance for clinical treatment planning.

MCC950 promotes diabetic wound healing through modulating macrophage polarization in an MDSC-dependent manner.

Diabetic foot ulcers (DFUs) are serious skin injuries whereby the wound healing process is frequently stalled in the inflammatory phase. Currently, there is a lack of effective therapeutic strategies. MCC950, a highly selective nod-like receptor family pyrin domain containing 3 (NLRP3) inhibitor, has been reported to show strong anti-inflammation effects in many diseases. In this study, we unveiled the role of MCC950 in DFU mice model and its underlying molecular mechanisms. MCC950 could significantly accelerate diabetic wound healing, as shown by shortened healing time and better healing quality. Moreover, increased M2 phenotype macrophages and decreased pro-inflammatory genes were observed in MCC950-treated DFU mice. Additionally, myeloid-derived suppressor cells (MDSCs) were significantly increased in blood, spleen and wound tissues at different time courses. Specifically, MCC950 could recruit more MDSCs in an early phase in DFU mice, exerting an anti-inflammation effect. We identified the cell crosstalk between macrophages and MDSCs with MCC950 treatment process. Depleting MDSCs in vivo could eliminate the therapeutic effect of MCC950 on diabetic wound healing through inhibiting M2 macrophage polarization. Besides, MDSCs isolated from the wounds of MCC950 or saline treated mice were cocultured with bone marrow derived macrophage (BMDM) in a transwell system. Results confirmed that MDSCs sorted from MCC950 treated mice caused a significant increased percentage of M2 macrophages. Collectively, our findings suggest that the administration of MCC950 has the potential to accelerate diabetic wound healing by promoting M2 macrophage polarization in an MDSC-dependent manner. This study provides valuable insights into the utilization of pharmacological agents for DFU treatment.

Contribution of Insulin Resistance and ß Cell Dysfunction to Gestational Diabetes Stratified for Pre-pregnant Body Mass Index.

The objective of the study was to evaluate the contribution of insulin resistance and ß cell dysfunction to gestational diabetes mellitus (GDM) in Chinese women stratified by pre-pregnant body mass index (BMI). A total of 847 pregnant women were enrolled. They were divided into low BMI and high BMI groups according to the median of pre-pregnancy BMI. The homeostasis model assessment of insulin resistance (HOMA-IR) and ß cell function (HOMA-ß), Matsuda index, and 60-min insulinogenic index (IGI60) were used to evaluate insulin resistance and ß cell function. In all the participants, 150 (17.71%) were diagnosed with GDM. ROC analyses showed that in the low BMI group, the association of ß cell dysfunction (IGI60 or HOMA-ß) with GDM was stronger than that of insulin resistance (Matsuda index or HOMA-IR), while in the high BMI group, the association of ß cell dysfunction with GDM was weaker than that of insulin resistance (all P < 0.05). Among all GDM patients, 47.33% demonstrated predominant insulin resistance (Matsuda index < 25th percentile), and 46% had predominant ß cell defect (IGI60 < 25th percentile). In the low BMI group, 15.09% of GDM patients demonstrated predominant insulin resistance, and 62.26% of GDM patients had predominant ß cell defect, whereas in the high BMI group, 64.95% of GDM patients demonstrated mainly insulin resistance and 36.08% of GDM patients had mainly ß cell defect. In women with low BMI, ß cell dysfunction is the major etiologic factor, whereas, in women with high BMI, insulin resistance is the predominant etiologic factor in the development of GDM.

Lactate supports Treg function and immune balance via MGAT1 effects on N-glycosylation in the mitochondria.

Current research reports that lactate affects Treg metabolism, although the precise mechanism has only been partially elucidated. In this study, we presented evidence demonstrating that elevated lactate levels enhanced cell proliferation, suppressive capabilities, and oxidative phosphorylation (OXPHOS) in human Tregs. The expression levels of Monocarboxylate Transporters 1/2/4 (MCT1/2/4) regulate intracellular lactate concentration, thereby influencing the varying responses observed in naive Tregs and memory Tregs. Through mitochondrial isolation, sequencing, and analysis of human Tregs, we determined that Alpha-1,3-Mannosyl-Glycoprotein 2-Beta-N-Acetylglucosaminyltransferase (MGAT1) served as the pivotal driver initiating downstream N-glycosylation events involving progranulin (GRN) and hypoxia-upregulated 1 (HYOU1), consequently enhancing Treg OXPHOS. The mechanism by which MGAT1 was upregulated in mitochondria depended on elevated intracellular lactate that promoted the activation of XBP1s, which, in turn, supported MGAT1 transcription as well as the interaction of lactate with the translocase of the mitochondrial outer membrane 70 (TOM70) import receptor, facilitating MGAT1 translocation into mitochondria. Pre-treatment of Tregs with lactate reduced mortality in a xenogeneic graft-versus-host disease (GvHD) model. Together, these findings underscored the active regulatory role of lactate in human Treg metabolism through the upregulation of MGAT1 transcription and its facilitated translocation into the mitochondria.

Tumor-resident microbiota contributes to colorectal cancer liver metastasis by lactylation and immune modulation.

The role of tumor-resident microbiota in modulating tumor immunity remains unclear. Here, we discovered an abundance of intra-tumoral bacteria, such us E.coli, residing and resulting in Colorectal cancer liver metastasis (CRLM). E.coli enhanced lactate production, which mediated M2 macrophage polarization by suppressing nuclear factor-κB -gene binding (NF-κB) signaling through retinoic acid-inducible gene 1 (RIG-I) lactylation. Lactylation of RIG-I suppressed recruitment of NF-κB to the Nlrp3 promoter in macrophages, thereby reducing its transcription. This loss of Nlrp3 affected the immunosuppressive activities of regulatory T cells (Tregs) and the antitumor activities of and CD8+ T cells. Small-molecule compound screening identified a RIG-I lactylation inhibitor that suppressed M2 polarization and sensitized CRLM to 5-fluorouracil (5-FU). Our findings suggest that tumor-resident microbiota may be a potential target for preventing and treating CRLM.

Mechanochemical synthesis of calcium-biochar for decontamination of arsenic-containing acid mine drainage.

Ca-biochar is an efficient material for As(III)-containing acid mine drainage (AMD) decontamination, while it is challenging to fabricate Ca-biochar with oyster shell waste as the Ca source due to its complex structure. Herein, a mechanochemical method was proposed to activate oyster shell waste and wood waste for Ca-biochar design and production, and its efficacy and relevant mechanisms for AMD detoxification were evaluated. The smaller size Ca-biochar produced by the medium-speed ball milling showed a higher As(III) removal (74.0 %) compared to high-speed ball milling (60.9 %), attributed to the formation of finer Ca(OH)2 while avoiding particle aggregation, which could release more Ca (89.0 mg/g) and alkalinity for the co-precipitation of As. Meanwhile, wood-based biochar substrate served as a platform for co-precipitation, and its surface functionality supported the oxidative immobilization of As. This study presents a promising route for upcycling food and wood waste to produce Ca-biochar for AMD decontamination.

A perspective on the recovery mechanisms of spent lithium iron phosphate cathode materials in different oxidation environments.

Oxidative extraction has become an economically viable option for recycling lithium (Li) from spent lithium iron phosphate (LiFePO4) batteries. In this study, the releases behaviour of Li from spent LiFePO4 batteries under different oxidizing conditions was investigated with sodium hypochlorite (NaClO) as the solid oxidant. We revealed that, due to the intervention of graphitic carbon, the generated species of Li in mechanochemical oxidation (NaClO:LiFePO4 at a molar ratio of 2:1, 5 min, and 600 rpm) was lithium carbonate (Li2CO3). The graphite layer provided a channel for the conversion of Li species released by mechanochemical oxidation. While in hydrometallurgical oxidation (NaClO:LiFePO4 at a molar ratio of 2:1 and 12.5 min), the presence of hydrogen species led to the formation of lithium chloride (LiCl). Moreover, life cycle assessment (LCA) demonstrated that for recycling 1.0 kg of spent LiFePO4 batteries, mechanochemical and hydrometallurgical oxidation could reduce carbon footprints by 2.81 kg CO2 eq and 2.88 kg CO2 eq, respectively. Our results indicate that the oxidative environment determines the release pathway of Li from the spent LiFePO4 cathode material, thereby regulating the product forms of Li and environmental impacts. This study can provide key technical guidance for Li recycling from spent LiFePO4 batteries.

Electron donation of Fe-Mn biochar for chromium(VI) immobilization: Key roles of embedded zero-valent iron clusters within iron-manganese oxide.

The dense surface passivation layer on zero-valent iron (ZVI) restricts its efficiency for water decontamination, causing a poor economy and waste of resources. Herein, we found that the ZVI on Fe-Mn biochar could afford a high electron-donating efficiency for the Cr(VI) reduction and immobilization. Over 78.0% of Fe in the Fe-Mn biochar was used for the Cr(VI) reduction and immobilization, i.e., 56.2 - 161.7 times higher than the commercial ZVI (0.5%) and modified ZVI (0.9 -1.3%), indicating that the unique ZVI species in Fe-Mn biochar offered an outstanding Fe utilization efficiency. We proposed that oxygen atoms in the FeO in the FeMnO2 precursor were removed during pyrolysis with biochar while the MnO skeleton was preserved, forming the embedded ZVI clusters within Fe-Mn oxide. The unique structure inhibited the formation of the Fe-Cr complex on Fe(0), which would facilitate the electron transfer between core Fe(0) and Cr(VI). Moreover, the surface FeMnO2 inhibited the diffusion of Fe and facilitated its affinity with pollutants, thus supporting higher efficiency for pollutant immobilization. The preserved performance of Fe-Mn biochar was proved in industrial wastewater and after long-term oxidation process, and the economic benefit was evaluated. This work provides a new approach for developing active ZVI-based materials with high Fe utilization efficiency and economics for water pollution control.

TAK1 deficiency promotes liver injury and tumorigenesis via ferroptosis and macrophage cGAS-STING signalling.

Background & Aims: Oxidative stress-mediated ferroptosis and macrophage-related inflammation play an important role in various liver diseases. Here, we explored if and how hepatocyte ferroptosis regulates macrophage stimulator of interferon genes (STING) activation in the development of spontaneous liver damage, fibrosis, and tumorigenesis. Methods: We used a transforming growth factor-beta-activated kinase 1 (TAK1) deficiency-induced model of spontaneous liver damage, fibrosis, and tumorigenesis to investigate hepatocyte ferroptosis and its impact on macrophage STING signalling. Primary hepatocytes and macrophages were used for in vitro experiments. Results: Significant liver injury and increased numbers of intrahepatic M1 macrophages were found in hepatocyte-specific TAK1-deficient (TAK1ΔHEP) mice, peaking at 4 weeks and gradually decreasing at 8 and 12 weeks. Meanwhile, activation of STING signalling was observed in livers from TAK1ΔHEP mice at 4 weeks and had decreased at 8 and 12 weeks. Treatment with a STING inhibitor promoted macrophage M2 polarisation and alleviated liver injury, fibrosis, and tumour burden. TAK1 deficiency exacerbated liver iron metabolism in mice with a high-iron diet. Moreover, consistent with the results from single-cell RNA-Seq dataset, TAK1ΔHEP mice demonstrated an increased oxidative response and hepatocellular ferroptosis, which could be inhibited by reactive oxygen species scavenging. Suppression of ferroptosis by ferrostatin-1 inhibited the activation of macrophage STING signalling, leading to attenuated liver injury and fibrosis and a reduced tumour burden. Mechanistically, increased intrahepatic and serum levels of 8-hydroxydeoxyguanosine were detected in TAK1ΔHEP mice, which was suppressed by ferroptosis inhibition. Treatment with 8-hydroxydeoxyguanosine antibody inhibited macrophage STING activation in TAK1ΔHEP mice. Conclusions: Hepatocellular ferroptosis-derived oxidative DNA damage promotes macrophage STING activation to facilitate the development of liver injury, fibrosis, and tumorigenesis. Inhibition of macrophage STING may represent a novel therapeutic approach for the prevention of chronic liver disease. Impact and implications: The precise mechanism by which hepatocyte ferroptosis regulates macrophage STING activation in the progression of liver damage, fibrosis, and tumorigenesis remains unclear. Herein, we show that deletion of TAK1 in hepatocytes caused oxidative stress-mediated ferroptosis and macrophage-related inflammation in the development of spontaneous liver injury, fibrosis, and hepatocellular carcinoma.