Spodumene is an important lithium-bearing mineral which naturally exists as chemically inert alpha phase. Therefore, a calcination process at 1100 degrees C is traditionally employed for phase transformation to (3 phase, causing a large energy consumption. This work proposes an improved alkaline autoclave method using NaOH and NaAlO2 aiming to extract lithium directly from alpha-spodumene. Interestingly, the addition of NaAlO2 can significantly enhance the lithium extraction efficiency from 50.5 % (dissolution with NaOH only) to 94.7 %. Moreover, the investigation of dissolution behavior indicated that the added AlO2- can capture the dissolved Si, releasing more lithium into lixivium and achieving an efficient separation of Li from Si. The lithium-containing leachate was then directly evaporated to concentrate and prepare Li2CO3. Besides, the efficiency of lithium extraction still can remain at a relatively high level around 90 % with three cyclic dissolution steps by recycled alkaline liquor. This combined autoclave method shows potential as a promising way to extract lithium directly from alpha-spodumene without phase transformation at high temperature.

Precisely controlling the aluminum distribution and porosity in Beta zeolite is crucial for optimizing its catalytic performance. Herein, we report a facile but effective "bottom-up" method to achieve controllable regulation of the porosity and aluminum distribution of the final product by altering the feeding sequence of the silicon and aluminum sources. The aluminum-first route (Beta-Al) yielded similar to 20 nm nanocrystals with an Al-rich surface and abundant intercrystalline mesopores, whereas the silicon-first route (Beta-Si) generated similar to 400 nm large crystals with homogeneous Al distribution and intracrystalline mesopores. Mechanistic studies revealed that different feeding sequences led to distinct aluminosilicate precursors ([Si8Al]n vs [Si4Al]n) and governed two crystallization pathways: solid-solid rearrangement for Beta-Al and dissolution-rearrangement for Beta-Si. When evaluated in n-butane catalytic cracking, Beta-Al exhibited higher activity and ethylene selectivity, while Beta-Si showed superior stability and propylene selectivity. This work demonstrates that feeding sequence engineering serves as a practical and industrially promising approach to tune Beta zeolite for targeted catalytic cracking applications. This strategy is simple, requires no post-treatment, and offers practical advantages for industrial catalyst manufacturing, where synthesis simplicity and low cost are highly valued.

Liver fibrosis, a common outcome of chronic liver injury, is characterized by excessive inflammation and oxidative stress. Rutin, a bioactive flavonoid with known antioxidant and anti-inflammatory properties, has not been thoroughly investigated for its potential anti-fibrotic mechanisms. This study aimed to elucidate the role of Rutin in liver fibrosis and its underlying molecular pathways. A carbon tetrachloride (CCl₄)-induced murine liver fibrosis model was employed. Liver injury, fibrotic deposition, inflammatory response, and oxidative stress were evaluated through histopathological examination, Western blotting, quantitative real-time PCR, and RNA sequence. The involvement of immune-responsive gene 1 (IRG1) was investigated using IRG1-knockout mice, while molecular docking and cellular thermal shift assay (CETSA) were performed to assess Rutin-IRG1 binding. The results showed that Rutin treatment significantly attenuated CCl₄-induced hepatic injury and collagen accumulation, accompanied by reduced markers of fibrosis. Mechanistically, Rutin activated the IRG1-itaconate axis, leading to a notable decrease in reactive oxygen species and pro-inflammatory cytokine release by Nrf2 activation and NLRP3 inflammasome containment. Molecular analyses confirmed direct binding of Rutin to IRG1, stabilizing its structure and enhancing its functional activity. The protective effects of Rutin were abolished in IRG1-deficient mice, underscoring the essential role of IRG1 in its anti-fibrotic action. In conclusion, Rutin ameliorates liver fibrosis by mitigating oxidative stress and suppressing NLRP3 inflammasome activation through targeting the IRG1/itaconate pathway, revealing a novel immunometabolic mechanism for its hepatoprotective effect.

Liver fibrosis is a common consequence of chronic liver injury, driven by persistent inflammation, oxidative stress, and excessive extracellular matrix deposition. The natural flavonoid rutin possesses antioxidant and anti-inflammatory properties and has shown hepatoprotective potential; however, its anti-fibrotic mechanism remains incompletely understood. This study aimed to investigate the protective effects of rutin and its underlying molecular mechanism in a carbon tetrachloride (CCl₄)-induced mouse model of liver fibrosis, with a particular focus on the role of immune-responsive gene 1 (IRG1). Liver fibrosis was induced in mice by CCl₄ administration. Hepatic injury, collagen deposition, inflammatory activation, and oxidative stress were evaluated using histological, biochemical, molecular, and transcriptomic approaches. The involvement of IRG1 was assessed by employing IRG1-deficient mice. Direct binding between rutin and IRG1 was examined through molecular docking, molecular dynamics simulations, and the cellular thermal shift assay (CETSA). Rutin treatment markedly alleviated CCl₄-induced hepatic injury, fibrotic deposition, inflammatory cytokine production, and reactive oxygen species accumulation. Mechanistically, rutin directly bound to and stabilized IRG1, which was associated with enhanced IRG1 enzymatic activity and increased endogenous itaconate production. This led to activation of Nrf2-mediated antioxidant signaling and suppression of NLRP3 inflammasome activation. Importantly, the protective effects of rutin were largely abolished in IRG1-deficient mice, confirming that IRG1 is essential for rutin-mediated hepatoprotection. These findings identify rutin as a potential anti-fibrotic agent that targets the IRG1/itaconate axis to coordinate antioxidant and anti-inflammatory responses during liver fibrosis.

With the rapid development of lithium-ion batteries, the recycling of spent batteries represents a major future challenge, particularly LiFePO4 batteries (LFP) due to their structural stability and high safety. This study proposes a simple and efficient pretreatment process, employing a combination of ultrasonic-assisted dilute alkali leaching and crushing-gas sorting to separate the cathode and anode material from spent LFP, respectively. The key parameters that affect the recovery efficiency of cathode materials from Al foil have been determined, including alkali concentration, liquid-solid ratio, ultrasonic frequency, and ultrasonic time. The separation efficiency between Al foil and cathode material can achieved 99.85%. The interface effect generated by the ultrasound cavitation promotes the separations of Al foil and cathode active materials. Meanwhile, the optimal crushing-gas sorting process parameters including particle size and gas flow rate was determined to recover Cu foil and graphite from the anode active material. A Cu recovery efficiency of 87.2% with a Cu grade of 84.6% was reached. Additionally, treatment with 3% HCl for 90 min was introduced to remove the residual Li in the recovered graphite. This method can provide a more efficient and sustainable way for the comprehensive separation and recovery of active materials from spent lithium-ion batteries.

Aiming to solve the disadvantage of significant energy consumption and excessive acid consumption in traditional sulfuric acid method to extract lithium from alpha-spodumene, a novel pyro-hydrometallurgical process was proposed by combining flash roasting for phase transformation with sulfuric acid pressure leaching. The effects of flash roasting parameters (temperature, time, particle size) on phase transformation and pressure leaching conditions (H2SO4 addition amount, liquid-solid ratio, temperature, time) on lithium extraction were systematically investigated. The optimal experiment results showed that the naturally existed alpha-spodumene can be transformed into beta phase at 1050 degrees C with 10 min by flash roasting. The encapsulated Li+ subsequently released with less sulfuric acid and underwent exchange with H+. High-efficiency leaching of Li with relatively low coleaching of Al and Si impurities was achieved by pressure leaching at 200 degrees C with much less sulfuric acid consumption. The leaching efficiency of Li, Al and Si were 94.7 %, 36.2 % and 0.14 %, respectively. Kinetic analysis indicated that the sulfuric acid pressure leaching process fitted well with the shrinking core model. An economic evaluation of this novel process was also conducted aiming to provide more guidance for its industrial application.

BACKGROUND:Liver fibrosis is a progressive disorder resulting from chronic liver injury, and its molecular mechanism remains incompletely elucidated. METHODS:The role of PROM2 was assessed by integrating transcriptomic datasets with in vivo liver fibrosis models. Functional analyses were performed using PROM2 knockdown or overexpression strategies, along with NLRP3 knockout models, to investigate its mechanistic involvement in epithelial-mesenchymal transition (EMT) and inflammasome activation. RESULTS:Transcriptomic analysis revealed that PROM2 expression was significantly upregulated in fibrotic livers and positively correlated with fibrosis- and EMT-related gene signatures. PROM2 knockdown significantly attenuated hepatic inflammation, inhibited EMT, and reduced fibrotic remodeling. In contrast, PROM2 overexpression aggravated these pathological features. Notably, in NLRP3-deficient mice, PROM2 overexpression failed to induce inflammation, EMT, or fibrosis, indicating that the pro-fibrotic effects of PROM2 are mediated through NLRP3 signaling. CONCLUSION:PROM2 contributes to liver fibrosis by promoting EMT and activating NLRP3-dependent inflammatory pathways, suggesting it as a potential therapeutic target for liver fibrosis.

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease, but effective therapeutic drugs are still lacking. Dihydrotanshinone I (DHTS), a natural product isolated from Salvia miltiorrhiza , has been shown to have ameliorative effects on NAFLD. The aim of this study was to investigate the hepatoprotective effect of DHTS on NAFLD and its mechanism. A model of NAFLD and DHTS treatment was established using a Western diet to observe the effect of DHTS on NAFLD, which were detected by immunohistochemical, immunofluorescence, and other experiments. The mechanism was further explored by constructing immune responsive gene 1 (IRG1) knockout mice, RNA sequence, and molecular docking. The results revealed that DHTS significantly improved diet-induced metabolic disorders in mice, notably alleviating liver inflammation, oxidative stress, and fibrosis. Further analysis revealed that the intervention of DHTS was associated with the activation of IRG1. Subsequent experiments confirmed that IRG1 gene deletion reversed the above protective effects of DHTS in NAFLD. Mechanistically, DHTS enhanced the antioxidant nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway through IRG1/itaconate and blocked the oxidative stress response in the liver. In addition, DHTS also inhibited the activation of NACHT-, leucine-rich repeat (LRR)-, and pyrin domain (PYD)-containing protein 3 (NLRP3) inflammasome via IRG1/itaconate, blocking the inflammatory amplification effect in the liver. The study suggests that DHTS may be a potential drug for the treatment of NAFLD, which exerts protective regulatory effects mainly through the IRG1/itaconate molecular pathway.

Micron-sized Si-based materials have attracted extensive attention for lithium-ion batteries due to their high theoretical capacity and low cost. However, its large volume expansion and low conductivity limit its further development. Here, a Si/ZnS anode material is prepared, in which ZnS nanoparticles are uniformly attached to the surface of micro-Si particles. The conversion reaction of ZnS generates metal Zn and Li2S, and the alloying reaction of Zn generates LixZn, the metal Zn and LixZn are used as conductive additives to improve the conductivity of the composites, while Li2S is used as an artificial solid electrolyte interfacial phase to promote the stability of the solid electrolyte interface of the composites, so that the prepared micron-sized Si-based anode exhibits excellent cycling stability. At a current density of 0.5 A g-1, the initial coulombic efficiency reaches 78.67 % and the discharge specific capacity is 1540.2 mAh g-1 after 200 cycles.

Background and Objectives: Non-alcoholic steatohepatitis (NASH) is a significant risk factor for hepatocellular carcinoma (HCC) development. Timely treatment during the NASH stage is essential to minimize the possibility of disease progression to HCC. Cuproptosis is a newly identified form of cellular death that could impact the progression of various diseases and cancers. Materials and Methods: Transcriptome and single-cell sequencing datasets were utilized to investigate the role of cuproptosis-related genes (CRGs) in NASH progression to HCC. FDX1, LIPT1, and PDHP were identified as CRGs in NASH patients, and FDX1, DBT, GCSH, SLC31A1, and DLAT were identified as CRGs in patients with NASH progressing to HCC. FDX1 was found to play a significant role in both NASH patients and patients with NASH progressing to HCC. This study constructed cuproptosis-related clusters (CRCs) using the Nonnegative Matrix Factorization algorithm, and they were linked to fatty acid metabolism and the PPAR signaling pathway in both NASH CRCs and HCC CRCs. The Weighted Correlation Network Analysis algorithm identified CRP, CRC, TAT, CXCL10, and ACTA1 as highly relevant genes in NASH CRCs and HCC CRCs. The expression of FDX1 was validated in both mouse models and human NASH samples. Results: The investigation highlights FDX1 as a pivotal CRG in both NASH and NASH progression to HCC. The comprehensive characterization of CRGs sheds light on their potential biofunctional importance in the context of NASH and HCC. Our experimental results show that FDX1 expression was significantly increased in NASH patients. Conclusions: The present study identified key CRGs, revealing their potential impact on NASH and HCC. Meanwhile, targeting FDX1 may prevent the progression of NASH to HCC.

Objectives Non-alcoholic steatohepatitis (NASH) is a chronic liver disease histologically characterized by liver steatosis, hepatocellular injury, inflammation and fibrosis, resulting in cirrhosis and hepatocellular carcinoma, but effective measures and obvious pathogenesis for NASH remain elusive. Chrysin (CH) has been reported to have anti-inflammatory effects but shows lower bioavailability.Methods In this study, a chrysin nanoliposome (CH-NL) was first prepared and characterized. Then, we used the methionine-choline-deficient (MCD) diet to induce a mouse model of NASH. Finally, the effects of CH and CH-NL on NASH were evaluated in the liver of NASH mice.Key findings The results showed that CH or CH-NL significantly reduced the accumulation of lipids in hepatocytes, alleviated liver injury, decreased the generation of radical oxygen species, and attenuated the accumulation of collagen fibre in the liver of NASH mice. In addition, CH and its nano-liposomes markedly inhibited the production of inflammatory cytokines and inflammatory cell infiltration in the liver of NASH mice. Further studies found that CH-NL and CH-NL downregulated the MCD diet-induced activation of Toll-like receptor 4 (TLR4) signalling pathway in the liver of mice.Conclusions CH and its nanoliposome alleviated MCD diet-induced NASH in mice, which might be through inhibiting TLR4 signalling pathway.

Background:Osteoarthritis (OA) is a common joint disease with long-term pain and dysfunction that negatively affects the quality of life of patients. Neutrophil extracellular traps (NETs), consisting of DNA, proteins and cytoplasm, are released by neutrophils and play an important role in a variety of diseases. However, the relationship between OA and NETs is unclear.Methods:In our study, we used bioinformatics to explore the relationship between OA and NETs and the potential biological markers. GSE55235, GSE55457, GSE117999 and GSE98918 were downloaded from the Gene Expression Omnibus (GEO) database for subsequent analysis.After differential analysis of OA expression matrices, intersection with NET-related genes (NRGs) was taken to identify Differentially expressed NRGs (DE-NRGs) in OA processes. Evaluation of immune cell infiltration by ssGSEA and CIBERSORT algorithm. The GSVA method was used to analyze the activity changes of Neutrophils pathway, Neutrophil degranulation and Neutrophil granule constituents pathway.Results:Based on RandomForest (RF), Least Absolute Shrinkage and Selection Operator (LASSO), and Support Vector Machine-Recursive Feature Elimination (SVM-RFE) learning algorithms, five core genes (CRISPLD2, IL1B, SLC25A37, MMP9, and TLR7) were identified to construct an OA-related nomogram model for predicting OA progression. ROC curve results for these genes validated the nomogram's reliability. Correlation analysis, functional enrichment, and drug predictions were performed for the core genes. TLR7 emerged as a key focus due to its high importance ranking in RF and SVM-RFE analyses. Gene Set Enrichment Analysis (GSEA) revealed a strong association between TLR7 and the Neutrophil extracellular trap pathway. Expression of core genes was demonstrated in mice OA models and human OA samples. TLR7 expression in ATDC5 cell line was significantly higher than control after TNFα induction, along with increased IL6 and MMP13.Conclusion:TLR7 may be related to NETs and affects OA.

Acetaminophen (APAP) overdose would lead to liver toxicity and even acute liver failure in severe cases by triggering an inflammatory response and oxidative stress. Sesamin has been reported to possess anti-inflammatory and antioxidant actions in several animal disease models. In the present study, the effects and mechanisms of sesamin on APAP-induced acute liver injury (ALI) were explored. The results showed that pretreatment with sesamin significantly alleviated APAP-induced ALI, as indicated by decreased serum aminotransferase activities, hepatic pathological damages, and hepatic cellular apoptosis. But sesamin has no significant effects on the expression of cytochrome P450 2E1 (CYP2E1), APAP-cysteine adducts (APAP-CYS) production, and glutathione content in the liver of APAP-administered mice. Moreover, APAP-induced liver oxidative stress and inflammatory response also were remarkedly attenuated by sesamin, including reducing hepatic reactive oxygen species levels, promoting antioxidant generation, and inhibiting the expression of TNF-α and IL-1β, as well as decreasing inflammatory cell recruitment. Notably, sesamin inhibited serum high-mobility group box 1 (HMGB1) releases and blocked hepatic activation of Toll-like receptor 4 (TLR4)-interleukin 1 receptor-associated kinase 3-nuclear factor kappa B (NF-κB) signaling pathway in APAP-administered mice. These findings indicated that sesamin could mitigate APAP-induced ALI through suppression of oxidative stress and inflammatory response, which might be mediated by the deactivation of HMGB1/TLR4/NF-κB signaling in mice.

针对当前由粉煤灰制备氧化铝成本高、除杂难度大等问题,提出了以富铝粉煤灰为原料的硫酸加压浸取、钾明矾结晶净化、钾明矾热解生产氧化铝的新技术路线,并对关键环节进行了热力学分析和试验验证.结果表明:该技术路线可实现低物料消耗、低能耗浸出,高效地解决从复杂硫酸盐溶液中分离铝的问题,并实现了反应过程所需硫酸、硫酸钾以及过量硫酸的循环利用.通过与传统拜耳法生产氧化铝工艺对比,本文所述技术路线理论能耗和物料消耗更低、原料来源更广泛,展现了高硅富铝粉煤灰酸法生产氧化铝新工艺的广阔应用前景.

Objectives The role of Paeoniflorin on hepatic fibrosis and the specific mechanisms has not yet been elucidated. Therefore, we explored whether Paeoniflorin exerted protective effects on carbon tetrachloride (CCl4)-induced hepatic fibrosis and the underlying mechanisms. Methods A model of hepatic fibrosis was induced by intraperitoneally injecting with CCl4 (10% 5 mu l/g) twice a week for 7 weeks. To explore the effects of Paeoniflorin, mice were treated with Paeoniflorin (100 mg/kg) by gavage once a day at 1 week after modeling until they were sacrificed. Key findings Paeoniflorin remarkably improved liver function and histopathological changes of hepatic tissues in CCl4-induced liver injury. Besides, the serum MAO enzyme activity and hydroxyproline contents were notably decreased following the intervention of Paeoniflorin. The decreased expression of Vimentin, alpha -SMA, Col1a and Desmin manifested the inhibition of the hepatic stellate cells (HSCs) activation. Interestingly, Paeoniflorin intervention significantly upregulated the expression of heme oxygenase-1, and attenuated the inflammatory cytokines production as well as the CCl4-induced oxidative stress imbalance. Conclusions Paeoniflorin could effectively alleviate CCl4-induced hepatic fibrosis by upregulation of heme oxygenase-1, and it might be a new effective option for the comprehensive treatment of hepatic fibrosis.

An acidic mixture of sulfuric and fluosilicic acid (H2SO4+H2SiF6) was employed as lixiviant to enhance leaching of lithium from lepidolite. The H2SiF6 was obtained as a byproduct of anhydrous hydrofluoric acid production, aiming to provide HF molecules. It was found that the HF molecules were the main reaction component and played a key role in strengthening the dissolution of lepidolite. Different factors, including mass ratio of ore/H2SO4/H2SiF6, concentrations of H2SO4 and H2SiF6, leaching temperatures (40−80 °C) and time (15−75 min), were investigated. Moreover, an efficient tubular reactor was employed to improve this acid leaching system. Under the optimal conditions (ore/H2SO4/H2SiF6 mass ratio of 1:0.8:1.6, 80 wt.% H2SO4, 15 wt.% H2SiF6, 80 °C, 15 min), 97.9% of Li, 96.4% of K, 97.6% of Rb, 96.7% of Cs and 81.4% of Al (mass fraction) were leached. Additionally, a two-step thermal process was proposed to remove fluorine of leaching slurry. This acid treatment using an acidic mixture of H2SO4 and H2SiF6 in a continuous tubular reactor shows potential as an alternative process to extract lithium from lepidolite.

Coal fly ash, commonly produced from thermal power plants, is not only an industrial waste but an aluminum-rich resource that needs to be disposed of properly. This study aims to extract aluminum from coal fly ash using pressurized sulfuric acid (H2SO4) leaching and to investigate the dissolution mechanism during the leaching process. The effects of initial concentration of H2SO4, reaction temperature and time on the extraction of aluminum were investigated. Under optimized conditions (3 mol/l H2SO4, 220°C and 180 min), the extraction of aluminum reached 82.51%. It was found that mullite (3Al2O3·2SiO2) contained in coal fly ash was completely dissolved during the leaching, while the dissolution of silica-alumina glass beads was at a limited degree. The un-leached aluminum was found to be locked inside the glass beads which H2SO4 was unable to access.