Advanced Science
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2025
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IF 14.1
Zijian Zhao,Shujing Li,Han Ma,Zhou Zhou,Wentao Zhao,Zichen Wei,Yanbin Li,Qingguo Fei,Yueming Sun,Yunqian Dai
Ceramic nanofiber aerogels are emerging as promising thermal protection materials, yet their brittleness remains a critical challenge. This work designs a hierarchical fibrous aerogel consisting of streamlined dual-oxide nanofibers featuring a dense-sheath/porous-core architecture, simultaneously overcoming the intrinsic fragility while enabling thermal-protection. The obtained aerogel demonstrates ultra-low thermal conductivity and exceptional thermomechanical stability a high working temperatures. The aerogel structure, constructed from arbitrarily bendable nanofibers, reduces the overall density and effectively lowers thermal conductivity. The minimum density can reach as low as 8 mg·cm −3 . This unique structure enhances the mechanical stability of the entire aerogel in a wide working temperature (−196 to 1300 °C) upon 80% compression. The thermal conductivity achieves an extremely low value of 7 mW·m −1 ·K −1 . These attributes originate from the following mechanisms: depressing heat transfer by prolonging heat conduction pathways and offering interfacial insulation, while impeding phonon transport within nanopores. Upon simulated space-ground integrated experiments at ≈1200 °C, the ceramic nanofiber aerogel exhibits remarkable resistance to thermal vibration. The nanofiber aerogel can serve as an all-in-one platform to synergistically integrate noise absorption and catalytic conversion, thereby paving the way for future practical applications.
研究领域:
材料科学
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热工工程
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纳米技术
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航空航天工程
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能源材料
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Metallomics
·
2025
·Vol. 17
·期 12
·
IF 2.9
Yu Rui,Gan Ziye,Chen Ranran,Shen Yuhu,Deng Yunxia,Huang Zhiwei
The molecular mechanism of aluminum toxicity in biological systems remains poorly understood. In this study, the relationship between aluminum and intracellular calcium was investigated in Saccharomyces cerevisiae model cells. Genetic analysis demonstrated that deletion mutants of plasma membrane calcium transport cch1Δ and mid1Δ, as well as the Golgi calcium pump deletion mutant pmr1Δ, increased the sensitivity to aluminum, while their sensibility could be compensated by exogenous calcium. Strains of cch1Δ and mid1Δ treated by Ca2+ chelator EGTA was more sensitive to aluminum compared with BY4741 and pmc1Δ. Further ICP-AES analysis showed that calcium uptake through both CCH1 and MID1 did not detoxify by inhibiting aluminum absorption. Meanwhile, aluminum treatment did not change the intracellular calcium uptake in cch1Δ, and mid1Δ, although it increased the mRNA levels of CCH1 or MID1 in all tested strains. It suggests that the increase in intracellular calcium induced by aluminum is CCH1 and MID1-dependent. Subsequently, the intracellular calcineurin-CRZ1 pathway was activated under aluminum stress to promote the expression of CCH1, MID1 and PMR1. Notably, overexpression of PMR1 significantly reduced intracellular aluminum levels and enhanced aluminum tolerance in both wild-type and mutant strains (cch1Δ, cnb1Δ, and crz1Δ). Furthermore, another vesicle transport deletion mutant gos1Δ or the strains (WT and gos1Δ) treated by BFA (a vesicle transport inhibitor) showed enhanced sensitivity to aluminum stress. However, exogenous calcium and/or PMR1 overexpression could reverse this sensitivity. Altogether, increasing intracellular calcium serves as a protective response to aluminum stress. The calcium-related signaling, particularly PMR1-mediated vesicle transport, plays a crucial role in aluminum detoxification.
研究领域:
分子生物学
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环境毒理学
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细胞信号传导
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微生物生理学
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PubMed
高影响因子
Small
·
2026
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IF 11.8
Gaofeng Shu,Kai Li,Shiji Fang,Qianhui He,Jiayi Shi,Peiyao Liu,Fazong Wu,Min Xu,Weiqian Chen,Kai Yan,Jin Su,Jiansong Ji,Minjiang Chen
The therapeutic efficacy of transarterial chemoembolization (TACE) is strongly limited by the hypoxic and immunosuppressive tumor microenvironment (TME). Herein, monodisperse perfluorooctyl bromide (PFOB)-loaded fucoidan/gelatin microspheres (P@FGMS) with excellent oxygen-carrying capability were prepared for enhanced TACE treatment of hepatocellular carcinoma (HCC). It was found that the introduction of fucoidan endowed P@FGMS with excellent electrostatic affinity for positively charged doxorubicin (DOX) and metformin (MET), enabling their efficient co-loading and sustained release. The resulting drug-loaded microspheres (DMP@FGMS) largely enhanced chemotherapy sensitivity through an in-outside hypoxia remodeling strategy: the supplement of exogenous O 2 via PFOB and inhibition of intracellular oxygen consumption by MET. Notably, DMP@FGMS could not only modulate hypoxic TME, but also generate intracellular ROS and disrupt the redox homeostasis, thereby triggering cancer ferroptosis. Moreover, DMP@FGMS effectively remodeled the immunosuppressive TME by alleviating tumor hypoxia and inducing immunogenic cell death (ICD), thereby enhancing CD8 + T cell infiltration while reducing immunosuppressive cell populations. Consequently, DMP@FGMS could effectively suppress tumor growth in an orthotopic HCC rat model, with this effect further potentiated by combination with immune checkpoint blockade therapy. Therefore, this study demonstrates that DMP@FGMS is a potent embolic agent capable of remodeling the hypoxic/immunosuppressive TME, representing a promising strategy for TACE treatment of HCC.
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JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES
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2026
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IF 2.4
Meng-Yi Chi,Cong-Ying Zhang,Xiao-Yan Gao,Jia Yu,Chun-Ying Bai,Dan-Dan Hao
The chemotherapeutic agent cisplatin for solid tumors frequently induces cancer-associated cachexia characterized by weight loss and decreased skeletal muscle mass. These adverse cisplatin-related symptoms are dose‑limiting, and the ability to counteract drug-initiated muscle atrophy in cancer-associated cachexia remains a pharmacological challenge. The aim of this study was to determine the protective efficacy of lobetyolin, a natural compound derived from Codonopsis pilosula, known to exert antioxidant, anti‑inflammatory, and anti‑apoptotic activities, against cisplatin-induced skeletal muscle wasting and subsequently elucidate a potential underlying molecular mechanism of action using a mouse model. Mice were injected with cisplatin (4 mg/kg, i.p. every other day, 4 doses in total) with concurrent oral lobetyolin (20 or 40 mg/kg daily) for 8 days. Lobetyolin inhibited cisplatin-induced reductions in body weight and grip strength, ameliorated gastrocnemius muscle atrophy, and preserved myofiber cross‑sectional area. Mechanistically, lobetyolin restored superoxide dismutase (SOD) activity and glutathione (GSH) levels while diminishing malondialdehyde (MDA) content in gastrocnemius muscle. Lobetyolin was found to activate the AKT signaling axis as evidenced by enhanced phosphorylation of AKT (Ser473) and FoxO3α (Thr32), which suppressed FoxO3α nuclear translocation and downregulated the E3 ubiquitin ligase Fbx32, thereby diminishing proteasomal protein degradation. Concurrently, lobetyolin normalized the Bax/Bcl‑2 ratio to inhibit myocyte apoptosis. These findings demonstrated that lobetyolin may be considered as a multi‑targeted therapeutic candidate to counteract oxidative injury, protein catabolism, and myocyte apoptosis initiated by cisplatin. Data suggest that lobetyolin’s potential as a safe adjunctive agent against chemotherapy‑induced muscle wasting might involve AKT/FoxO3α pathway.
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Microbiology Spectrum
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2026
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IF 4.1
Jing Wu,Meimei Duan,Lin Cheng,Deyan Chen
The ongoing spread of the monkeypox outbreak underscores the urgent need for the development of effective therapeutics against the monkeypox virus (MPXV). Aminopterin is a classical antifolate agent known for its anti-tumor activity through the inhibition of folate metabolism. Here, aminopterin was identified as an effective anti-MPXV agent. It significantly inhibited MPXV replication, unlike other antifolate agents such as methotrexate, pemetrexed, and LSN3213218. In Vero E6 cells, the half-maximal inhibitory concentration (IC₅₀) was 36.10 nM, the half-cytotoxic concentration (CC₅₀) was 3,310 nM, and the selectivity index (SI) was 91.690. In human foreskin fibroblast cells, the IC50 was 32.73 nM, CC₅₀ exceeded 10 μM, and SI was greater than 305.530. In vivo, aminopterin not only inhibited MPXV infection but also mitigated high-dose viral infection-associated inflammation. Furthermore, the data indicated that aminopterin reduced viral load by interfering with viral attachment and replication. Together, these findings identify aminopterin as a promising candidate for anti-MPXV drug development.
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PubMed
高影响因子
Small
·
2026
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IF 11.8
Zheng Wang,Yuhao Wu,Chunli Liu,Yi Zhang,Liguo Qin,Shan Lu,Yusen Luo,Sheng Li,Zhenjiang Cao,Ming Xu,Kai Xi,Peiping Yang,Guangneng Dong
MXene has emerged as a promising two-dimensional (2D) lubricant additive due to its layered structure, low interlayer shear strength, and tribochemical activity. However, their structural instability under oxygen-containing and high-temperature conditions often leads to oxidation and decomposition, which severely limits their practical use in lubrication systems. In this study, instead of suppressing this transformation, we harness the tribochemically induced in situ evolution of MXene to construct a self-adaptive lubricating interface for low friction and wear under oil lubrication. Comprehensive interfacial characterizations reveal that tribological loading drives the transformation of MXene into a highly graphitized carbon-rich tribofilm, while coordination interactions between oleic acid (OA) and MXene facilitate carbon reconstruction at the sliding interface. Reactive molecular dynamics (RMD) simulations further demonstrate that friction-induced shear promotes Ti–C bond dissociation and carbon graphitization, providing atomistic insights into the dynamic interfacial reconstruction process. The combined effects of tribochemical transformation and molecular coordination promote the formation and progressive reconstruction of a robust graphitized tribofilm, thereby sustaining low friction and enhancing wear resistance. This work provides new insights into the tribological behavior of MXene-based additives and highlights their potential for high-performance lubrication in advanced mechanical systems.
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MEASUREMENT
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2026
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IF 6.1
Yang Liu,Changyuan Xu,Yuqin Zhu,Jianxin He,Quanhua Xie,Yuanyuan He,Lei Wu,Dong Lai,Fei Fu,Qiongyao He,Bowen Jing,Guoqing Zhang,Nianbing Zhong
Moss-induced biocorrosion of stone heritage is a slow yet persistent deterioration process that alters the physicochemical conditions within porous stones, leading to structural damage and loss of cultural value. To conduct in-situ decoding of the pathogenic mechanism of mosses on sandstone, we developed a fiber Bragg grating (FBG)–based multi-parameter sensing system. The sensing system integrates three types of FBGs—temperature-sensing (T-FBG), strain-sensing (S-FBG), and polyacrylic acid–polyvinyl alcohol (PAA-PVA) coated pH-sensing FBG (H-FBG). The sensitivities and resolutions of T-FBG, S-FBG and H-FBG are 9.69 pm/℃ (0.01 ℃), 1.23 pm/με (0.1 με) and 38.63 pm/pH (0.02 pH units), respectively. A decoupling model based on a 3 × 3 sensitivity matrix was established to eliminate cross-sensitivity effects. During 60 days of Funaria hygrometrica colonization, the system captured dynamic variations including a maximal pH decrease of 0.5, a temperature fluctuation of 3.2 ℃, and an internal microstrain increase of 11.3 με. Microscopic and porosity analyses further confirmed the dual biochemical–mechanical degradation caused by metabolite secretion and rhizoid penetration. This work provides quantitative insights into moss-induced biocorrosion mechanisms and indicates the feasibility of optical fiber sensing as an early-warning strategy for preventive conservation of stone relics.
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CHEMICAL ENGINEERING JOURNAL
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2026
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IF 12.5
Yiwen Chen,Jun Guo,Penglong Li,Buming Chen,Hui Huang
A polarized crystalline/amorphous interface is constructed for OER catalysis. • Built-in electric fields regulate dynamic electrochemical reconstruction. • Efficient hydrogen production is achieved under harsh alkaline conditions. Efficient and durable oxygen evolution reaction electrocatalysts are essential for industrial-scale hydrogen production, yet regulating electrochemical reconstruction while maintaining structural stability remains challenging. Herein, a crystalline-weakly crystalline NiMoO 4 @FeOOH heterostructure is constructed to enable built-in electric field (BEF)-driven reconstruction regulation. The Fermi-level mismatch at the heterointerface induces charge redistribution and generates a polarized BEF, which directs the reconstruction pathway toward highly active NiFeOOH species while suppressing excessive structural degradation. The optimized catalyst achieves a low overpotential of 255 mV at 100 mA cm −2 , a Tafel slope of 52.1 mV dec −1 , and stable operation for 100 h in 30 wt% KOH at 80 °C, with an energy consumption of 4.84 kWh Nm −3 H 2 . Operando Raman, in situ electrochemical impedance spectroscopy, and XPS analyses reveal that the BEF accelerates Ni oxidation, promotes OH − adsorption, and facilitates interfacial charge transfer during reconstruction. Density functional theory calculations further confirm optimized oxygen intermediate adsorption and reduced reaction barriers. This work establishes a BEF-driven electrochemical reconstruction strategy for coupling interfacial electronic regulation with dynamic catalyst evolution toward high-performance OER electrocatalysts. Download: Download high-res image (154KB) Download: Download full-size image
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高影响因子
PLoS One
·
2026
·Vol. 21
·期 10
·e0359660
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IF 2.8
Pan Qu,Yongchao Gao,Xiaojie Li,Li Yang,Jie Tang,Manyun Chen,Yicheng Wang,Yilei Peng,Junyi Jiang,Weihua Huang,Wei Zhang,Yali Liu,Yali Ou
Ticagrelor, a commonly used antiplatelet medication, has been found to exhibit considerable inter-individual pharmacodynamic variability. Recent studies have revealed a close relationship between pharmacokinetics and pharmacodynamics, both of which can be influenced by gut microbiota. In this study, we explored whether the pharmacokinetics of ticagrelor is mediated by intestinal flora. We enrolled 22 healthy participants to assess the clinical pharmacokinetic profiles of ticagrelor and its metabolite AR-C124910XX after a single oral dose of ticagrelor. The fecal microbial compositions of individuals who exhibited distinct pharmacokinetic parameters were analyzed using 16S rRNA gene sequencing. Additionally, we conducted experiments involving the co-incubation of ticagrelor with fecal bacteria and a systematic exploration of the pharmacokinetics of ticagrelor in pseudo-germ-free (PGF) rats to illustrate the role of gut microbiota in ticagrelor metabolism, both in vitro and in vivo . Our findings revealed a three-fold difference in the bioavailability of ticagrelor among individuals. However, no difference was found in the composition of gut microbiota among individuals with different pharmacokinetic parameters. Quantitative analysis showed that gut microbiota cannot directly metabolize ticagrelor. Furthermore, there were no significant differences in AUC (0–48) , AUC (0-∞), and C max between ticagrelor and AR-C124910XX in PGF rats compared to normal control, either by single intragastric or intravenous administration. In conclusion, these findings suggest that gut microbiota has no impact on the pharmacokinetics of ticagrelor.
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高影响因子
JOURNAL OF HAZARDOUS MATERIALS
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2026
·
IF 10.6
Sulin Wang,Jian Xu,Fei Wang
Phase-resolved mass balances reveal aqueous PCE rebound during net PCE removal. • Rapid Fe(II) consumption weakens oxidation despite residual persulfate. • Fe-rich deposition and altered organic groups support changes in PCE retention. • Delayed PCE release outpaces effective oxidation, creating a kinetic mismatch. Ferrous iron-activated persulfate (Fe(II)/PDS) is widely used for in situ chemical oxidation (ISCO) of chlorinated solvents, yet aqueous rebound complicates treatment evaluation. Phase-resolved mass balances were combined with electron paramagnetic resonance (EPR) and surface characterization to examine tetrachloroethene (PCE) redistribution and removal. In homogeneous aqueous systems, PCE removal was rapid within 2 h, with rapid dissolved Fe(II) consumption. Among evaluated Fe(II):PDS ratios, 1:1 yielded the highest removal, with > 30% PDS persisting beyond the initial stage. Following Fe(II)/PDS addition to pre-equilibrated soil–water systems, aqueous PCE increased while soil-associated PCE decreased and total PCE mass declined monotonically. SEM–EDS, FTIR, and XRD indicated Fe-rich surface deposition and altered organic functional groups, supporting interfacial changes that weaken PCE retention. Soil addition attenuated EPR spin-adduct responses. In pre-equilibrated systems, the fitted sulfate-adduct response in soil extracts exhibited negligible variation between 10 and 120 min, consistent with continued soil-associated activation as intensive aqueous oxidation subsided. These observations support a kinetic mismatch between declining effective oxidative capacity and continued soil-to-water PCE release, allowing aqueous accumulation despite net removal. The findings provide a mechanistic basis for coordinating reagent transport and local activation with delayed contaminant release through alternating PDS and Fe(II) injection in groundwater circulation well (GCW) systems. Download: Download high-res image (273KB) Download: Download full-size image Mechanism of Radical‑pulse induced PCE rebound The aqueous PCE rebound observed in the investigated pre-equilibrated soil–water system is interpreted as the combined outcome of rapid initial oxidation, treatment-induced surface reconstruction, and delayed interphase mass transfer. Fe(II)/PDS activation generates an initial radical pulse involving SO 4 •− and ·OH, while dissolved Fe(II) is rapidly consumed. Reactive species can oxidize readily accessible PCE and competing soil constituents, including surface-associated organic moieties. Oxidative disturbance of SOM- and soft-carbon-associated sorption domains, together with the formation of Fe(III)-bearing surface deposits, may weaken PCE retention and reduce its immediate re-adsorption. Release from condensed SOM/hard-carbon domains and less-accessible intraparticle regions may persist as the initial aqueous oxidative activity declines. The pH evolution and relatively persistent sulfate-adduct response in soil extracts are consistent with continued soil-associated PDS activation, which may sustain slower oxidation within accessible domains. This activity, however, may not provide sufficient aqueous oxidative capacity to remove PCE at the rate of its release. Aqueous accumulation can therefore coexist with continued net PCE loss, as demonstrated by the phase-resolved mass measurements. The proposed mechanism links treatment-induced changes in contaminant retention to a kinetic mismatch between declining aqueous oxidative capacity and continued soil-to-water PCE release.
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DESALINATION
·
2026
·
IF 9.9
Guohui Liu,Zhongsen Yan,Haiqing Chang,Kaiqin Xu,Dan Qu,Fangshu Qu
Aromaticity is associated with membrane wetting mitigation. • Humic acid (HA)––CaSO 4 interactions form larger-sized complexes. • Aromaticity strengthens HA–CaSO 4 affinity for PVDF and forms protective layers. • HA–CaSO 4 deposition redirects gypsum growth and reduces pore intrusion. Gypsum (CaSO 4 ∙2H 2 O) scaling is a critical issue that impedes the application of membrane distillation (MD) for treating hypersaline water and wastewater. However, the impact of ubiquitously present humic acid (HA) remains unclear. Herein, this study systematically investigates the effects of HA on both bulk and surface gypsum crystallization and elucidates the molecular-level mechanisms by which HA mitigates gypsum-scaling-induced membrane wetting. Bulk crystallization results indicated that HA retarded crystal growth and formed larger-sized HA–CaSO 4 complex, which was associated with membrane scaling behavior. Tailored HA pretreatments of a bench-scale MD system demonstrated that aromaticity showed a stronger positive correlation with membrane wetting control (R 2 = 0.920), compared with molecular weight and negative charge. Guided by this structure–performance relationship, membrane surface scaling behavior revealed that higher HA aromaticity enhanced hydrophobic interactions between HA–CaSO 4 complex and the polyvinylidene difluoride (PVDF) membrane. This interaction facilitated the deposition of larger-sized HA–CaSO 4 complex on the membrane surface and altered the growth orientation of gypsum, which suppressed crystal growth within membrane pores and consequently mitigated membrane wetting. While carboxyl groups are important for scaling mitigation by organic matter, the aromaticity of organic matter shapes scaling behavior in membrane processes treating saline water. Download: Download high-res image (124KB) Download: Download full-size image
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高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
·
2026
·
IF 5.2
Wenzhi Wu,Xiaohai Chen,Weiyi Zhang,Haoxin Fu,Jie Chen,Chenchen Qian,Saili Xie,Congcong Zeng
Sleep disorders, particularly insomnia, are highly prevalent worldwide, and melatonin is widely used therapeutically as a key regulator of the sleep-wake cycle. This study aimed to investigate the inhibitory effect of apatinib on melatonin metabolism and its underlying mechanism. We elucidated the effect of apatinib on the metabolism of melatonin using rat liver microsomes (RLM) and human liver microsomes (HLM) and recombinant human CYP1A2 (rCYP1A2), complemented by pharmacokinetics in rats and molecular docking. In vitro , apatinib showed non-competitive inhibition in RLM (IC 50 = 15.85 μΜ) and competitive inhibition in HLM (IC 50 = 5.10 μΜ) and rCYP1A2 (IC 50 = 3.60 μΜ). IC 50 shift analysis yielded a shift ratio of 1.26 in RLM, indicating that apatinib exhibited non-time-dependent inhibition on melatonin metabolism. In vivo , apatinib markedly increased melatonin exposure with AUC (area under the curve) increased by approximately 2.8-fold (P < 0.05) and decreased clearance by 70.39% (P < 0.05), while significantly reducing the exposure of 6-hydroxymelatonin (the main metabolite of melatonin). Furthermore, molecular docking simulations revealed that both melatonin and apatinib were bound to the active pocket of CYP1A2, sharing interactions with residues Thr124 and Leu497. Overall, apatinib inhibited CYP1A2-mediated metabolism of melatonin in vitro and increased melatonin exposure in vivo , suggesting a potential clinically relevant interaction that may warrant caution and individualized dosing/monitoring when co-administered. However, the findings are limited by the use of rat pharmacokinetics and in vitro systems, and require confirmation in human clinical studies.
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