Food Biophysics
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2026
·Vol. 21
·期 1
·17
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IF 3.2
Zhang Xinyu,Li Yijie,Lin Hong,He Junbo,Feng Jiangtao,Cai Meng
To improve the lipophilicity and antioxidant potential of ferulic acid (FA), four novel 1- O -alkylglyceryl ferulates (C 8 Gly 1 F, C 12 Gly 1 F, C 16 Gly 1 F, and C 18:1 Gly 1 F) were synthesized via Novozym 435-catalyzed transesterification in n -hexane at 65 °C, achieving high conversion rates and good enzyme reusability. Crystallinity and thermal properties, analyzed by polarized light microscopy and DSC, revealed that C 12 Gly 1 F exhibited optimal crystallinity, while C 18:1 Gly 1 F, due to its unsaturated alkyl chain, was predominantly amorphous, suggesting enhanced solubility. Antioxidant assays (DPPH and ABTS) demonstrated higher radical scavenging activity compared to ethyl ferulate, with C 18:1 Gly 1 F showing the best performance. Density functional theory calculations revealed its high electron affinity, electrophilicity, and a delocalized HOMO–LUMO distribution, supporting its proposed antioxidant mechanism. These findings highlight the potential of 1- O -alkylglyceryl ferulates as effective lipophilic antioxidants for use in functional foods and lipid-based delivery systems.
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ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
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2026
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IF 0
Zhou Baochang,Li Guifang,Pan Zhangbin,Dong Bin,Du Zhenqi,Zhang Baiqiang,Li Mei,Wang Yonglei,Jia Ruibao
At present, the most commonly used advanced oxidation technology for drinking water treatment has the disadvantage of low utilization rate of oxidant. After research and comparison, the UV/H 2 O 2 /Fe(III) combined process selected in this study can effectively degrade sulfamethoxazole (SMX) in water and improve the utilization rate of hydrogen peroxide. The results showed that the removal rate of SMX by UV/H 2 O 2 /Fe(III) process was 96.7%, and the utilization rate of H 2 O 2 was increased by 25%; the UV/H 2 O 2 /Fe(III) combined process also had a good effect on the degradation of fluorescent components and other organic matter in water; the presence of nitrite ion and humic acid significantly reduced the degradation efficiency of SMX, under the condition of nitrite ion concentration of 5 mg/L or humic acid concentration of 10 mg/L, the removal rate of SMX by UV/H 2 O 2 /Fe(III) combined process decreased by 10.68% or 11.92%, respectively. In terms of mechanism research, the reactivity of SMX molecules was theoretically calculated by density functional theory (DFT), and the atoms with higher contribution rate were calculated, and the degradation products and four degradation pathways of SMX were identified and analyzed by mass spectrometry. Finally, the potential ecological toxicity of SMX and its degradation products was predicted by ECOSAR software and luminescent bacteria experiments; it was found that the toxicity of SMX and its degradation products was relatively high at 15 min.
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JOURNAL OF MATERIALS SCIENCE-MATERIALS IN ELECTRONICS
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2026
·Vol. 37
·期 3
·223
·
IF 2.8
Tang Zhe,Li Hongyu,Liu Zhen-guo,Zong Peng-an
Conductive silver pastes dominate electrode manufacturing in silicon heterojunction (SHJ) solar cells but suffer from high and volatile material costs. While silver-coated copper particles (Cu@Ag MPs) offer a promising low-cost alternative, conventional synthesis methods struggle to achieve uniform coatings, leading to poor oxidation stability and conductivity. Herein, we introduce a novel chloride-ion-assisted chemical reduction method to synthesize high-quality Cu@Ag MPs. The introduced Cl⁻ ions act as an electrostatic dispersant, effectively suppressing copper agglomeration and enabling the formation of a uniform and dense silver shell. The optimized Cu@Ag MPs (30 wt% Ag) exhibit excellent oxidation resistance below 300 °C and a low resistivity of 1.90 mΩ. When formulated into a low-temperature curing paste for SHJ solar cells, the composite ink achieves a volume resistivity of 8.22 × 10 –6 Ω·cm after curing at 210 °C. Remarkably, the paste demonstrates outstanding environmental stability, with only 1% resistivity degradation after 30 days of ambient exposure. This work presents a viable and cost-effective solution for photovoltaic metallization, reducing silver consumption by 70% while maintaining performance parity with commercial pastes, thereby paving the way for more sustainable solar cell manufacturing.
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Cell Death & Disease
·
2026
·
IF 9.6
Yang Shizhou,Ma Yuejiang,Wu Tingting,Huang Xiufeng
Although hypoxia is a well-known key driver of metabolic reprogramming in endometrial cancer (EC), its role in lactate-mediated macrophage activation remains unclear. This study investigates whether hypoxia-mediated lactate metabolism reprogramming facilitated EC progression via macrophages. Our data demonstrated that hypoxia-inducible factor 1 subunit alpha (HIF1A) drives a lactate-regulated metabolic cascade, elevating glycolytic genes and monocarboxylate transporter 3 (MCT3) in EC cells to produce and export more lactate. This lactate is transported to macrophages by MCT1 to drive M2 macrophage polarization. Mechanistically, lactate induces lactylation of Histone 3 in the promoter of DNA methyltransferase 1 (DNMT1) gene and activates transcription in macrophages, leading to the silencing of NHE7 gene expression, a key regulator of intracellular pH. Critically, NHE7 downregulation drives M2 polarization and senescence through the mitogen-activated protein kinase (MAPK) pathway activation in macrophages, ultimately facilitating EC progression. In vivo, we successfully established a xenograft tumor model using Ishikawa cells, and the data further confirmed that NHE7-overexpressing macrophages effectively abrogate exogenous lactate-accelerated xenograft tumor growth, as well as its M2 polarization and senescence. These findings uncover that hypoxia-mediated lactate production and transmission promote tumor-macrophage crosstalk via the DNMT1-NHE7 axis and EC progression, which offers novel therapeutic targets for EC.
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BIOLOGICAL TRACE ELEMENT RESEARCH
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2026
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IF 3.6
An Hongmei,Zhang Lihong,Miao Jiale,Song Aiman,Zhang Jingzhuo,Maihemuti Wulike Baike,Cao Xianfeng,Wen Yongchang,Yan Ruiying,Ren Caijin,Bao Qianjiang,Wang Jiayu,Lei Yuhang
To investigate the protective effects of three antioxidants—lycopene (LP), proanthocyanidins (PC), and resveratrol (RES)—against Nano-TiO 2 -induced reproductive toxicity in male mice. A total of 110 healthy male ICR mice were randomly assigned to 11 experimental groups: the control group, the Nano-TiO 2 group, and combined treatment groups consisting of Nano-TiO 2 with low, medium, and high doses of LP, PC, and RES, respectively. Following 28 days of continuous intragastric administration, epididymal tissues were collected for assessment of semen quality, while testicular tissues were utilized to evaluate histopathological alterations, testicular functional enzyme activities, and markers of oxidative stress. Compared with the control group, after intragastric administration of Nano-TiO 2 , the testicular and epididymal coefficients of mice decreased, the sperm count, sperm progressive motility, and sperm motility rate significantly decreased ( P < 0.05), the sperm malformation rate significantly increased ( P < 0.05), the number of spermatogenic cells in the testicular spermatogenic tubules decreased, and the Johnsen score significantly decreased ( P < 0.05). The activities of acid phosphatase (ACP), alkaline phosphatase (AKP), lactate dehydrogenase (LDH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) decreased significantly ( P < 0.05). The level of malondialdehyde (MDA) was significantly increased ( P < 0.05). After the intervention with the three antioxidants, compared with the Nano-TiO 2 group, the testicular and epididymal coefficients increased. Compared with other doses, medium-dose LP, medium-high-dose PC, and all doses of RES significantly increased the forward motility and sperm motility of mice and significantly reduced the sperm deformity rate( P < 0.05). In addition, various doses of LP, medium - high- doses of PC, and low- doses RES significantly improved pathological damage caused by Nano-TiO 2 , such as testicular tissue structural disorder and decreased levels of spermatogenic cells and sperm. The activities of ACP, LDH, SOD, CAT, GSH, and GPx increased significantly ( P < 0.05), and the level of MDA in the testicular tissue decreased significantly. LP, PC, and RES had antagonistic effects on male reproductive toxicity induced by Nano-TiO 2 , the prominent effects of PC on the testicular organ coefficient and LP, especially 20 mg/kg LP, in improving semen quality and the expression of testicular functional enzymes in male mice need to be given due attention.
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MOLECULAR AND CELLULAR BIOCHEMISTRY
·
2026
·
IF 3.7
Wen Qiang,Yuan Yi,Liu Zhihua,Wang Lei,Pan Chunguo
Lung cancer (LC) is a leading cause of cancer-related mortality worldwide. While the chemokine CCL25 is implicated in the tumor microenvironment, its specific role in LC is not fully understood. Here, we identify CCL25 as a key promoter of tumor progression through a novel macrophage-mediated signaling axis. Bioinformatics and clinical analyses revealed that CCL25 is highly expressed in LC and correlates with M2 macrophage infiltration and poorer patient survival. In vitro, tumor-derived CCL25 drove M2 polarization of macrophages by upregulating its receptor CCR9. Functionally, these CCL25-CCR9-induced M2 macrophages secreted TGF-β1 and significantly enhanced the proliferation, migration, and invasion of LC cells. Mechanistically, this effect was mediated through the activation of the JAK/STAT signaling pathway and the subsequent upregulation of the downstream oncogene PIM2 in tumor cells. Both pharmacological inhibition of JAK/STAT and genetic knockdown of PIM2 reversed the tumor-promoting crosstalk. Single-cell transcriptomics confirmed the presence of a TGF-β1-expressing CCR9 + M2 macrophage subset in human tumors and revealed co-expression of CCR9 and PIM2 in tumor cells. In vivo, CCL25 overexpression accelerated tumor growth and M2 macrophage infiltration. Collectively, our findings define a complete CCL25-CCR9-TGF-β1-JAK/STAT-PIM2 signaling circuit wherein tumor cells educate macrophages to, in turn, fuel their own malignant progression, highlighting this axis as a potential therapeutic target in lung cancer.
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Science China-Earth Sciences
·
2026
·
IF 5.8
Zhao Xiaoyang,Yuan Guanghui,Cao Yingchang,Hao Fang,Liu Keyu,Jin Zihao,Fu Xiaohan,Shao Fulin
Clay minerals play a crucial role in catalyzing kerogen to form hydrocarbons, significantly influencing petroleum system evolution. Montmorillonite (MT) dehydrates upon heating; however, the catalytic mechanisms governing the thermal decomposition of organic matter at different dehydration levels remain unclear. Additionally, the mechanism by which external water suppresses MT’s catalytic efficiency remains debated. To resolve this issue, this study conducted pyrolysis simulation experiments (340 °C, 10 days) with various combinations of octadecanoic acid (OA), water, hydrochloric acid (HCl) solution, MT, dehydrated-MT, and illite. We integrated mineral/organic transformation analyses (XRD/FTIR/SSNMR/SEM), temperature-dependent characterization of solid acid sites (NH 3 -TPD/FTIR), and quantitative product measurements (GC/GC-MS) to elucidate how clay-bound water and external water differentially regulate organic-matter cracking pathways. The results suggest that clay-bound water controls reaction pathways by tuning both the type (Brønsted vs. Lewis) and density of solid acid sites. External water inhibits catalytic efficiency by reducing direct contact between organic matter and solid acid sites. Compared with untreated MT, 150 °C-dehydrated MT-OA system exhibited strong interlayer water polarization, which increased Brønsted acid site density and enhanced the carbonium-ion mechanism, thereby promoting isoalkane production. In contrast, 250 °C-dehydrated MT-OA system, where interlayer water was nearly eliminated, had fewer Brønsted acid sites but greater exposure of Lewis acid sites, facilitating decarboxylation and increasing CO 2 production. In hydrous systems, the addition of HCl solution did not enhance the carbonium-ion mechanism compared to the hydrous system with only water, indicating that only protons bound to solid acid sites, rather than liquid H + in water, can trigger the carbonium-ion reaction. This shows that the catalysis of organic-matter cracking by clay minerals such as MT is fundamentally an interfacial chemical process that requires direct mineral-organic contact; the presence of external water reduces catalytic efficiency primarily by physically separating OA from MT and hindering that contact. This study elucidates the controlling mechanisms of MT-catalyzed thermal cracking under different water conditions and deepens our understanding of hydrocarbon-generation pathways during kerogen maturation in sedimentary basins.
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Science China-Materials
·
2026
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IF 7.4
Yan Yuanzhi,Jing Xin,Wang Gangrong,Feng Peiyong,Mi Haoyang,Liu Yuejun,Geng Lihong
The development of hydrogels that simultaneously achieve high strength and good toughness remains a critical challenge in soft material science, particularly for applications in flexible electronics, soft robotics, and biomedical devices. Conventional approaches often suffer from a trade-off between mechanical robustness and functional performance. In this work, we present a novel solvent-driven dual-network entanglement strategy to fabricate a strong and tough poly (vinyl alcohol) (PVA)-based organo-hydrogel by synergistically combining isopropanol (IPA) solvent substitution to induce dense polymer chain entanglement and a sodium alginate (SA) ionic crosslinked network as a dynamic energy-dissipation phase. The resulting organo-hydrogel exhibits excellent mechanical performance with a tensile strength of 3.18 MPa and a toughness of 16.65 MJ/m 3 , representing increases of approximately 17 and 49 times that of conventional PVA hydrogels, respectively. Furthermore, the organo-hydrogel displays superior swelling resistance and long-term stability in aqueous environments, enabling reliable operation in challenging conditions such as underwater motion sensing and wearable strain detection. Morphological analyses reveal the critical role of solvent-mediated chain reorganization and dual-network interactions in achieving these properties. This work not only provides a versatile platform for designing robust gel materials but also offers fundamental insights into solvent-network interactions for advanced soft material engineering.
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METALLURGICAL AND MATERIALS TRANSACTIONS B-PROCESS METALLURGY AND MATERIALS PROCESSING SCIENCE
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2026
·
IF 3.1
Zhou Qican,Li Gang,Yuan Kai,Su Yiping,Shao Ningning,Bai Wensheng,Shen Xuehua,Zhang Zuotai
Alkali-activated slag mortars (AASM) face durability challenges, particularly the loss of mechanical strength under prolonged carbonation. This study investigated the mechanical, chemical, and pore structural evolution of AASM subjected to accelerated carbonation. Mortars were prepared by alkali-activating a mixture of blast furnace slag and steel slag, followed by exposure to pure CO 2 for different durations. Under 10 M NaOH activation, compressive strength initially increased, reaching 27.8 MPa after 6 hours of carbonation, but declined by 21 pct after 12 hours. TG/DSC analysis showed the maximum CaCO 3 content of 3.43 pct at 12 hours. The early strength gain was attributed to the formation of C–(A–)S–H gels and matrix densification, as confirmed by XRD, FT-IR, and BSE. However, the subsequent strength loss was not directly correlated with total porosity. Instead, MIP and micro-CT analyses revealed that pore size distribution—particularly the development of capillary pores (10 to 10,000 nm)—was critical in maintaining load-bearing capacity. These findings clarify the dual role of carbonation, showing how short-term exposure enhances strength while extended carbonation undermines it, and highlight pore size distribution control as a key strategy for improving AASM durability in sustainable construction. Graphical
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NEUROCHEMICAL RESEARCH
·
2026
·Vol. 51
·期 1
·50
·
IF 3.8
Zainab Syeda Rida,Khan Jehan Zeb,Batool Syeda Anaa,Nadeem Humaira,Tipu Muhammad Khalid,Fatima Humaira,Ahmad Nadeem,Ul-Haq Zaheer,Irshad Nadeem
1,3,4-Oxadiazole derivatives have attracted substantial attention as promising therapeutic agents for neurodegenerative disorders due to their anti-inflammatory and neuroprotective properties. This study specifically examined a 1,3,4-oxadiazole derivative, i.e.,-{[5-(3-bromophenyl)-1, 3, 4-oxadiazol-2-yl] sulfanyl} ethan-1-ol (abbreviated as OX-1), in the context of multiple sclerosis (MS). Currently, approximately 2.8 million individuals worldwide are living with MS. The study demonstrates the therapeutic potential of OX-1 using the experimental autoimmune encephalomyelitis (EAE) model of MS. Neurobehavioral assessments indicate significant improvements in clinical scoring, motor deficits, muscular strength, and locomotor activity in EAE subjects. Imaging test reveal notable improvements in spinal deformity, further supporting the efficacy of the compound. Comprehensive analyses, including antioxidant assays, RT-PCR, and comet assays, confirm that OX-1 effectively reduces oxidative stress, accompanied by a significant decrease in cytokine expression. Histological examinations reveal critical pathological changes in the hippocampus, cortex, eyes, spinal cord, and optic nerve. The data demonstrate that this compound exhibits neuroprotective effects by activating the Nrf2/HO-1 pathway, thereby reducing oxidative stress and enhancing the antioxidant defense system. Additionally, it suppresses the TLR4/NF-κB pathway, significantly lowering pro-inflammatory cytokine production and immune cell infiltration. Furthermore, molecular docking and simulation studies demonstrate the binding interactions and potential modulatory effects of OX-1 on HO-1 and NF-κB. These results emphasize the therapeutic promise of OX-1 in effectively alleviating the clinical signs and symptoms associated with EAE-induced MS. Graphical The graphical abstract of EAE model of MS.
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JOURNAL OF HUMAN GENETICS
·
2025
·
IF 2.5
Yin Bin,Li Mu-Jia,Sun Jia-Lin,You Yue,Zhang Si-Di,Wan Qian-Xue,Yao Mei-Lin,Yang Cheng-Wei,Sun Hua-Qin,Lin Zi-Yuan,Shi Bing,Jia Zhong-Lin
The biological interactions between genetic and environmental modifiers play critical roles in the etiology of non-syndromic orofacial cleft (NSOC), but it is rarely studied. This study selected 47 environmental related genes from the metabolic pathways of smoking, drinking, hypoxia, and vitamins (including vitamin A, vitamin B9 (folic acid), vitamin C (ascorbic acid), vitamin D, and vitamin E), and test their associations with NSOC and its subtypes. We found that a novel gene SLC23A2 , the vitamin C transporter gene is significantly associated with non-syndromic cleft palate only (NSCPO) ( p = 3.25E-07, OR = 8.45, 95%CI:3.73–19.17). SLC23A2 is expressed in the craniofacial region of zebrafish (24hpf to 120hpf), obvious craniofacial abnormalities appeared in zebrafish (48hpf) when knock down the slc23a2 ( slc23a2 -MO). Knock down SLC23A2 in human embryonic palatal mesenchymal cell line (HEPM) induced decreased intracellular ascorbic acid (AA), increased reactive oxygen species (ROS), inhibited cell proliferation and triggered apoptosis, activated the PI3K-AKT-mTOR signaling pathway and inhibited autophagy; ROS levels and apoptosis ratio significantly decreased when we supplemented AA to HEPM cells with high ROS levels induced by Sin-1 (an exogenous ROS mimic). Knocked down SLC23A2 in HEPM cells or zebrafish, they became more sensitive to Sin-1, and AA supplementation was ineffective. In conclusion, we identified a novel susceptibility gene SLC23A2 for NSCPO, it may function by decreasing AA level, increasing the ROS levels, inducing apoptosis, and inhibiting autophagy through the activation of the PI3K-AKT-mTOR pathway in etiology of cleft palate.
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MOLECULAR PSYCHIATRY
·
2025
·
IF 10.1
Zhou Lingyan,Bao Feixiang,Zheng Jiajun,Ding Yingzhe,Xiao Jiahui,Zhang Jian,Qin Yongpeng,Yang Liang,Wu Yi,Meng Qi,Lu Manjiao,Long Qi,Hu Lingli,Li Chong,Wang Haitao,Huang Shijuan,Li Linpeng,Wang Junwei,Wang Wuming,Lu Gang,Chan Wai-Yee,Qin Dajiang,Chen Gong,Liu Xingguo
Mitochondrial DNA (mtDNA) mutations and/or depletion are implicated in epilepsy and many neurodegenerative diseases. However, systematic investigation into how mtDNA alterations relate to epilepsy and neural degeneration is needed. Here, we established a mouse model in which mtDNA depletion is induced by the Herpes Simplex Virus Type 1 (HSV-1) protein UL12.5 in the brain led to an epileptic phenotype characterized by abnormal electroencephalography (EEG) patterns and increased neural excitability in hippocampus. We also found that UL12.5 mediated mtDNA depletion in neurons in vitro (rho − ) causes epilepsy–like abnormal EEG. Caloric restriction (CR) or glucose restriction (GR) is a strategy proven to reduce epileptic activity, however GR mimetic 2-deoxy-D-glucose (2-DG), induced degeneration in mtDNA depleted neurons. Mechanistically, mtDNA depletion increased mitochondria-endoplasmic reticulum (ER) contacts, facilitating GR-induced mitochondrial calcium overload. Rho − neurons did not show changes in mitochondrial motility or membrane potential. Our study revealed an unexpected axis of mtDNA depletion, ER-mitochondrial contacts, and calcium overload in the rho − neuron model. Fasting-induced GR causes early motor dysfunction, accelerates epilepsy progression, and worsens neurodegeneration in UL12.5 mice. Importantly, the IP3R inhibitor 2-APB blocks the neurodegeneration induced by fasting. This is the first description of animal and neuronal models of mitochondrial epilepsy. Our findings with these models suggest that GR may not be a viable clinical intervention in patients with mtDNA depletion.
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