Corrigendum: Integrative single-cell RNA sequencing and metabolomics decipher the imbalanced lipid-metabolism in maladaptive immune responses during sepsis.

[This corrects the article DOI: 10.3389/fimmu.2023.1181697.].

Biomonitoring urinary pesticide metabolites in preschool children by supported liquid extraction and ultra-high performance liquid chromatography-tandem mass spectrometry and their association with oxidative stress.

Investigating pesticide exposure and oxidative stress in preschool children is essential for elucidating the determinants of environmental health in early life, with human biomonitoring of urinary pesticide metabolites serving as a critical strategy for achieving this objective. This study demonstrated biomonitoring of 2 phenoxyacetic acid herbicides, 2 organophosphorus pesticide metabolites, and 4 pyrethroid pesticide metabolites in 159 preschool children and evaluated their association with oxidative stress biomarker 8-hydroxydeoxyguanosine. An enzymatic deconjugation process was used to release urinary pesticide metabolites, which were then extracted and enriched by supported liquid extraction, and quantified by ultra-high performance liquid chromatography-tandem mass spectrometry with internal standard calibration. Dichloromethane: methyl tert­butyl ether (1:1, v/v) was optimized as the solvent for supported liquid extraction, and we validated the method for linear range, recovery, matrix effect and method detection limit. Method detection limit of the pesticide metabolites ranged from 0.01 µg/L to 0.04 µg/L, with satisfactory recoveries ranging from 70.5 % to 95.5 %. 2,4,5-Trichlorophenoxyacetic acid was not detected, whereas the other seven pesticide metabolites were detected with frequencies ranging from 10.1 % to 100 %. The concentration of urinary pesticide metabolites did not significantly differ between boys and girls, with the median concentrations being 9.39 µg/L for boys and 4.90 µg/L for girls, respectively. Spearman correlation analysis indicated that significant positive correlations among urinary metabolites. Bayesian kernel machine regression revealed a significant positive association between urinary pesticide metabolites and 8-hydroxydeoxyguanosine. Para-nitrophenol was the pesticide metabolite that contributed significantly to the elevated level of oxidative stress.

The Ca2+-dependent phosphatase calcineurin dephosphorylates TBK1 to suppress antiviral innate immunity.

Tumor necrosis factor receptor-associated factor family member-associated NF-κB activator-binding kinase 1 (TBK1) plays a key role in the induction of the type 1 interferon (IFN-I) response, which is an important component of innate antiviral defense. Viruses target calcium (Ca2+) signaling networks, which participate in the regulation of the viral life cycle, as well as mediate the host antiviral response. Although many studies have focused on the role of Ca2+ signaling in the regulation of IFN-I, the relationship between Ca2+ and TBK1 in different infection models requires further elucidation. Here, we examined the effects of the Newcastle disease virus (NDV)-induced increase in intracellular Ca2+ levels on the suppression of host antiviral responses. We demonstrated that intracellular Ca2+ increased significantly during NDV infection, leading to impaired IFN-I production and antiviral immunity through the activation of calcineurin (CaN). Depletion of Ca²+ was found to lead to a significant increase in virus-induced IFN-I production resulting in the inhibition of viral replication. Mechanistically, the accumulation of Ca2+ in response to viral infection increases the phosphatase activity of CaN, which in turn dephosphorylates and inactivates TBK1 in a Ca2+-dependent manner. Furthermore, the inhibition of CaN on viral replication was counteracted in TBK1 knockout cells. Together, our data demonstrate that NDV hijacks Ca2+ signaling networks to negatively regulate innate immunity via the CaN-TBK1 signaling axis. Thus, our findings not only identify the mechanism by which viruses exploit Ca2+ signaling to evade the host antiviral response but also, more importantly, highlight the potential role of Ca2+ homeostasis in the viral innate immune response.IMPORTANCEViral infections disrupt intracellular Ca2+ homeostasis, which affects the regulation of various host processes to create conditions that are conducive for their own proliferation, including the host immune response. The mechanism by which viruses trigger TBK1 activation and IFN-I induction through viral pathogen-associated molecular patterns has been well defined. However, the effects of virus-mediated Ca2+ imbalance on the IFN-I pathway requires further elucidation, especially with respect to TBK1 activation. Herein, we report that NDV infection causes an increase in intracellular free Ca2+ that leads to activation of the serine/threonine phosphatase CaN, which subsequently dephosphorylates TBK1 and negatively regulates IFN-I production. Furthermore, depletion of Ca2+ or inhibition of CaN activity exerts antiviral effects by promoting the production of IFN-I and inhibiting viral replication. Thus, our results reveal the potential role of Ca2+ in the innate immune response to viruses and provide a theoretical reference for the treatment of viral infectious diseases.

An advanced high-rate capability sodium-ion anode: Few-layered NbSe2 with a mechanism of parallel running intercalation and conversion.

The unique superconductivity and charge density wave transition characteristics of NbSe2 make it worthy of exploring its electrochemical performance and potential applications in the field of batteries. Herein, the bulk NbSe2 was successfully exfoliated into few-layered NbSe2 nanostructures by wet grinding exfoliation approach, which solved the issues of its long activation period and poor cycle stability. The strong Nb-Se bond in the plane and weak van der Waals force between the adjacent layers could render the fast Na+ diffusion, provide abundant reaction sites and multi-directional migration paths, thus accelerate the ionic conductivity. The theoretical calculations verified the high Na+ adsorption tendency between the NbSe2 interlayers stemming from the continuous region of charge accumulation. Thanks to the unique electronic and two-dimensional few-layered structures, the exfoliated NbSe2 exhibited a high cyclic stability with a capacity of 502 mA h g-1 over 2800 cycles at 10 A/g. In addition, the reaction mechanism was studied by in-situ X-ray diffraction and other tests, indicating a reaction mechanism containing of simultaneous intercalation (NbSe2↔NaxNbSe2↔NaNbSe2↔Na1+xNbSe2) and conversion processes in NbSe2. This parallelly running mechanism not only alleviates the volume change but also ensures a high specific capacity. Additionally, different lattice planes of the NaNbSe2 intermediate in the intercalation process experience varying degrees of contraction and expanding in d-spacing due to the influence of Coulombic force.

Association of phthalate exposure with type 2 diabetes and the mediating effect of oxidative stress: A case-control and computational toxicology study.

Phthalic acid esters (PAEs) are widely used as plasticizers and have been suggested to engender adverse effects on glucose metabolism. However, epidemiological data regarding the PAE mixture on type 2 diabetes (T2DM), as well as the mediating role of oxidative stress are scarce. This case-control study enrolled 206 T2DM cases and 206 matched controls in Guangdong Province, southern China. The concentrations of eleven phthalate metabolites (mPAEs) and the oxidative stress biomarker 8-hydroxy-2'-deoxyguanosine (8-OHdG) in urine were determined. Additionally, biomarkers of T2DM in paired serum were measured to assess glycemic status and levels of insulin resistance. Significantly positive associations were observed for mono-(2-ethylhexyl) phthalate (MEHP) and Mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) with T2DM (P < 0.001). Restricted cubic spline modeling revealed a non-linear dose-response relationship between MEHHP and T2DM (Pnon-linear = 0.001). The Bayesian kernel machine regression and quantile g-computation analyses demonstrated a significant positive joint effect of PAE exposure on T2DM risk, with MEHHP being the most significant contributor. The mediation analysis revealed marginal evidence that oxidative stress mediated the association between the mPAEs mixture and T2DM, while 8-OHdG respectively mediated 26.88 % and 12.24 % of MEHP and MEHHP on T2DM risk individually (Pmediation < 0.05). Di(2-ethylhexyl) phthalate (DEHP, the parent compound for MEHP and MEHHP) was used to further examine the potential molecular mechanisms by in silico analysis. Oxidative stress may be crucial in the link between DEHP and T2DM, particularly in the reactive oxygen species metabolic process and glucose import/metabolism. Molecular simulation docking experiments further demonstrated the core role of Peroxisome Proliferator Activated Receptor alpha (PPARα) among the DEHP-induced T2DM. These findings suggest that PAE exposure can alter oxidative stress via PPARα, thereby increasing T2DM risk.

A large-scale survey of urinary parabens and triclocarban in the Chinese population as well as the influencing factors and health risks.

Parabens and triclocarban are widely applied as antimicrobial preservatives in foodstuffs, pharmaceuticals, cosmetics, and personal care products. However, few studies have been conducted on large-scale biomonitoring of parabens and triclocarban in the Chinese general population. In the present study, there were 1157 urine samples collected from 26 Chinese provincial capitals for parabens and triclocarban measurement to evaluate the exposure levels, spatial distribution, and influencing factors, as well as associated health risks in the Chinese population. The median concentrations of Σparabens and triclocarban were 14.0 and 0.03 µg/L, respectively. Methyl paraben was the predominant compound. Subjects in western China were more exposed to parabens, possibly due to climate differences resulting in higher consumption of personal care products. Subjects who were female, aged 18-44 years, or had a higher education level were found to have higher paraben concentrations. The frequency of drinking bottled water was positively associated with paraben exposure. The assessment of health risk based on urinary paraben concentrations indicated that 0.8 % of the subjects had a hazard index exceeding one unit, while Monte Carlo analysis suggested that 3.6 % of the Chinese population exposure to parabens had a potential non-carcinogenic risk. This large-scale biomonitoring study will help to understand the exposure levels of parabens and triclocarban in the Chinese general population and provide supporting information for government decision-making.

LRP1 induces anti-PD-1 resistance by modulating the DLL4-NOTCH2-CCL2 axis and redirecting M2-like macrophage polarisation in bladder cancer.

The tumour microenvironment (TME) drives bladder cancer (BLCA) progression. Targeting the TME has emerged as a promising strategy for BLCA treatment in recent years. Furthermore, checkpoint blockade therapies are only beneficial for a minority of patients with BLCA, and drug resistance is a barrier to achieving significant clinical effects of anti-programmed cell death protein-1 (PD-1)/programmed death protein ligand-1 (PD-L1) therapy. In this study, higher low-density lipoprotein receptor-related protein 1 (LRP1) levels were related to a poorer prognosis for patients with various cancers, including those with higher grades and later stages of BLCA. Enrichment analysis demonstrated that LRP1 plays a role in the epithelial-mesenchymal transition (EMT), NOTCH signalling pathway, and ubiquitination. LRP1 knockdown in BLCA cells delayed BLCA progression both in vivo and in vitro. Furthermore, LRP1 knockdown suppressed EMT, reduced DLL4-NOTCH2 signalling activity, and downregulated M2-like macrophage polarisation. Patients with BLCA and higher LRP1 levels responded weakly to anti-PD-1 therapy in the IMvigor210 cohort. Moreover, LRP1 knockdown enhanced the therapeutic effects of anti-PD-1 in mice. Taken together, our findings suggest that LRP1 is a potential target for improving the efficacy of anti-PD-1/PD-L1 therapy by preventing EMT and M2-like macrophage polarisation by blocking the DLL4-NOTCH2 axis.

Melt-quenched glass formation of a family of metal-carboxylate frameworks.

Metal-organic framework (MOF) glasses are an emerging class of glasses which complement traditional inorganic, organic and metallic counterparts due to their hybrid nature. Although a few zeolitic imidazolate frameworks have been made into glasses, how to melt and quench the largest subclass of MOFs, metal carboxylate frameworks, into glasses remains challenging. Here, we develop a strategy by grafting the zwitterions on the carboxylate ligands and incorporating organic acids in the framework channels to enable the glass formation. The charge delocalization of zwitterion-acid subsystem and the densely filled channels facilitate the coordination bonding mismatch and thus reduce the melting temperature. Following melt-quenching realizes the glass formation of a family of carboxylate MOFs (UiO-67, UiO-68 and DUT-5), which are usually believed to be un-meltable. Our work opens up an avenue for melt-quenching porous molecular solids into glasses.

Humoral immunosuppression of exposure to polycyclic aromatic hydrocarbons and the roles of oxidative stress and inflammation.

Previous studies have indicated adverse health effects of exposure to polycyclic aromatic hydrocarbons (PAHs), but evidence on the association between PAH exposure and immunity is scarce and its underlying mechanism is largely unknown. This study assessed human exposure to PAHs by determining the concentrations of PAHs in serum and their metabolites in paired urine. The oxidative stress and inflammation levels were evaluated by urinary DNA damage biomarker 8-hydroxydeoxyguanosine, white blood cell counts and C-reaction protein. We investigated the relationship between PAH exposure and seven immunological components, and explored the indirect roles of oxidative stress and inflammation by mediation and moderation analysis. Multivariate regression analysis revealed that 1-hydroxynaphthalene and 2-hydroxyfluorene were negatively associated with immunoglobulin A, and 3-hydroxyphenanthrene was negatively correlated with complement component 3. Restricted cubic spline analysis demonstrated nonlinear relationships between some individual PAHs or their metabolites with immunological components. Bayesian kernel machine regression and quantile g-computation revealed significant associations of higher PAH exposure with decreased immunoglobulin G and kappa light chain levels. Phenanthrene was the compound that contributed the most to reduced immunoglobulin G. Mediation analysis demonstrated significant indirect effects of 8-hydroxydeoxyguanosine and white blood cell counts on the association between higher PAH exposure and decreased immunological components. Moderation analysis revealed that PAH exposure and decreased immunological components are significantly associated with higher levels of C-reaction protein and white blood cell counts. The results demonstrated significant immunosuppression of PAH exposure and highlighted the indirect roles of oxidative stress and inflammation. Interventions to reduce systemic inflammation may mitigate the adverse immune effects of PAH exposure.

Stabilizing Lattice Oxygen through Mn Doping in NiCo2O4-δ Spinel Electrocatalysts for Efficient and Durable Acid Oxygen Evolution.

Design the electrocatalysts without noble metal is still a challenge for oxygen evolution reaction (OER) in acid media. Herein, we reported the manganese (Mn) doping method to decrease the concentration of oxygen vacancy (VO) and form the Mn-O structure adjacent octahedral sites in spinel NiCo2O4-δ (NiMn1.5Co3O4-δ), which highly enhanced the activity and stability of spinel NiCo2O4-δ with a low overpotential (η) of 280 mV at j=10 mA cm-2 and long-term stability of 80 h in acid media. The isotopic labelling experiment based on differential electrochemical mass spectrometry (DEMS) clearly demonstrated the lattice oxygen in NiMn1.5Co3O4-δ is more stable due to strong Mn-O bond and shows synergetic adsorbate evolution mechanism (SAEM) for acid OER. Density functional theory (DFT) calculations reveal highly increased oxygen vacancy formation energy (EVO) of NiCo2O4-δ after Mn doping. More importantly, the highly hydrogen bonding between Mn-O and *OOH adsorbed on adjacent Co octahedral sites promote the formation of *OO from *OOH due to the greatly enhanced charge density of O in Mn substituted sites.

Newcastle disease virus infection remodels plasma phospholipid metabolism in chickens.

Newcastle disease is a global problem that causes huge economic losses and threatens the health and welfare of poultry. Despite the knowledge gained on the metabolic impact of NDV on cells, the extent to which infection modifies the plasma metabolic network in chickens remains unknown. Herein, we performed targeted metabolomic and lipidomic to create a plasma metabolic network map during NDV infection. Meanwhile, we used single-cell RNA sequencing to explore the heterogeneity of lung tissue cells in response to NDV infection in vivo. The results showed that NDV remodeled the plasma phospholipid metabolism network. NDV preferentially targets infected blood endothelial cells, antigen-presenting cells, fibroblasts, and neutrophils in lung tissue. Importantly, NDV may directly regulate ribosome protein transcription to facilitate efficient viral protein translation. In conclusion, NDV infection remodels the plasma phospholipid metabolism network in chickens. This work provides valuable insights to further understand the pathogenesis of NDV.

Oncolytic Newcastle disease virus induced degradation of YAP through E3 ubiquitin ligase PRKN to exacerbate ferroptosis in tumor cells.

Ferroptosis, a form of programmed cell death characterized by iron-dependent lipid peroxidation, has recently gained considerable attention in the field of cancer therapy. There is significant crosstalk between ferroptosis and several classical signaling pathways, such as the Hippo pathway, which suppresses abnormal growth and is frequently aberrant in tumor tissues. Yes-associated protein 1 (YAP), the core effector molecule of the Hippo pathway, is abnormally expressed and activated in a variety of malignant tumor tissues. We previously proved that the oncolytic Newcastle disease virus (NDV) activated ferroptosis to kill tumor cells. NDV has been used in tumor therapy; however, its oncolytic mechanism is not completely understood. In this study, we demonstrated that NDV exacerbated ferroptosis in tumor cells by inducing ubiquitin-mediated degradation of YAP at Lys90 through E3 ubiquitin ligase parkin (PRKN). Blocking YAP degradation suppressed NDV-induced ferroptosis by suppressing the expression of Zrt/Irt-like protein 14 (ZIP14), a metal ion transporter that regulates iron uptake. These findings demonstrate that NDV exacerbated ferroptosis in tumor cells by inducing YAP degradation. Our study provides new insights into the mechanism of NDV-induced ferroptosis and highlights the critical role that oncolytic viruses play in the treatment of drug-resistant cancers.IMPORTANCEThe oncolytic Newcastle disease virus (NDV) is being developed for use in cancer treatment; however, its oncolytic mechanism is still not completely understood. The Hippo pathway, which is a tumor suppressor pathway, is frequently dysregulated in tumor tissues due to aberrant yes-associated protein 1 (YAP) activation. In this study, we have demonstrated that NDV degrades YAP to induce ferroptosis and promote virus replication in tumor cells. Notably, NDV was found to induce ubiquitin-mediated degradation of YAP at Lys90 through E3 ubiquitin ligase parkin (PRKN). Our study reveals a new mechanism by which NDV induces ferroptosis and provides new insights into NDV as an oncolytic agent for cancer treatment.

Evidence for non-Arrhenius behavior of EPDM rubber by combining Arrhenius and time-temperature superposition (TTS) extrapolations.

Studying the non-Arrhenius behavior of rubber is crucial to ensure appropriate lifetime prediction and reduce ineffective acceleration experiments. In this paper, accelerated thermal aging from 70 °C to 130 °C is conducted on an ethylene propylene diene monomer (EPDM) rubber and the tensile characteristics of the rubber are tested. Further, the popular Mooney-Rivlin equation is employed to analyze the influence of aging temperature and time on the effective crosslink densities. The enormous increase in the physical crosslinking density when the aging temperature reaches 115 °C demonstrates that the activation energy varied during the degradation process. By combining the Arrhenius extrapolation with the time-temperature superposition (TTS) extrapolation, a novel method to prove the non-Arrhenius behavior of EPDM rubber is provided. Based on the method proposed in this study, the activation energies for the high- and low-temperature processing of rubber can be determined.

Exosomes miRNA-499a-5p targeted CD38 to alleviate anthraquinone induced cardiotoxicity: experimental research.

BACKGROUND: The purpose of this study was to investigate the effects of cardiac homing peptide (CHP) engineered bone marrow mesenchymal stem cells (BMMSc) derived exosomes (B-exo) loaded miRNA-499a-5p on doxorubicin (DOX) induced cardiotoxicity. METHODS: miRNA chip analysis was used to analyze the differences between DOX induced H9c2 cells and control group. CHP engineering was performed on BMMSc derived exosomes to obtain C-B-exo. miRNA-499a-5p mimic was introduced into C-B-exo by electroporation technology to obtain C-B-exo-miRNA-499a-5p. DOX was used to establish a model of cardiotoxicity to evaluate the effects of C-B-exo- miRNA-499a-5p in vivo and in vitro . Western blot, immunohistochemistry, immunofluorescence, and other molecular biology methods were used to evaluate the role and mechanism of C-B-exo-miRNA-499a-5p on DOX induced cardiotoxicity. RESULTS: miRNA chip analysis revealed that miRNA-499a-5p was one of the most differentially expressed miRNAs and significantly decreased in DOX induced H9c2 cells as compared to the control group. Exo-and B-exo have a double-layer membrane structure in the shape of a saucer. After engineering the CHP of B-exo, the results showed that the delivery of miRNA-499a-5p significantly increased and significantly reached the target organ (heart). The experimental results showed that C-B-exo-miRNA-499a-5p significantly improved electrocardiogram, decreased myocardial enzyme, serum and cardiac cytokines, improved cardiac pathological changes, inhibited CD38/MAPK/NF-κB signal pathway. CONCLUSIONS: In this study, C-B-exo-miRNA-499a-5p significantly improved DOX-induced cardiotoxicity via CD38/MAPK/NF-κB signal pathway, providing a new idea and method for the treatment of DOX induced cardiotoxicity.

Plasmonic coupling-boosted photothermal composite photocatalyst for achieving near-infrared photocatalytic hydrogen production.

The development of photocatalysts that effectively utilize low-energy photons for efficient photocatalysis still faces a number of challenges. Herein, an efficient NIR-driven system based on WO3-x/ZnIn2S4 (WO3-x/ZIS) prepared by a simple low-temperature water-bath method, and the optimal WO3-x/ZIS-3 composites can reach a hydrogen-production efficiency of 14.05 µmol g-1h-1 under NIR light irradiation. The localized surface plasmon (LSPR) resonance effect in WO3-x quantum dots (QDs) not only broadens the ZIS photo-response range, but also the photothermal effect of WO3-x can increase the local reaction temperature of WO3-x/ZIS composite system, thus enhancing the photothermal-assisted photocatalytic activity. In addition, density functional theory (DFT) calculations show that the difference in work function between WO3-x and ZIS can lead to the formation of interfacial electric field (IEF), which not only promotes the separation and migration efficiency of photogenerated carriers, but also facilitates the photocatalytic water splitting for hydrogen production. This study provides possible directions for the construction of NIR-driven photothermal-assisted photocatalytic hydrogen production system.

Simultaneously enhanced magnomechanical cooling and entanglement assisted by an auxiliary microwave cavity.

We propose a mechanism to simultaneously enhance quantum cooling and entanglement via coupling an auxiliary microwave cavity to a magnomechanical cavity. The auxiliary cavity acts as a dissipative cold reservoir that can efficiently cool multiple localized modes in the primary system via beam-splitter interactions, which enables us to obtain strong quantum cooling and entanglement. We analyze the stability of the system and determine the optimal parameter regime for cooling and entanglement under the auxiliary-microwave-cavity-assisted (AMCA) scheme. The maximum cooling enhancement rate of the magnon mode can reach 98.53%, which clearly reveals that the magnomechanical cooling is significantly improved in the presence of the AMCA. More importantly, the dual-mode entanglement of the system can also be significantly enhanced by AMCA in the full parameter region, where the initial magnon-phonon entanglement can be maximally enhanced by a factor of about 11. Another important result of the AMCA is that it also increases the robustness of the entanglement against temperature. Our approach provides a promising platform for the experimental realization of entanglement and quantum information processing based on cavity magnomechanics.

A Janus-ROS Healing System Promoting Infectious Bone Regeneration via Sono-Epigenetic Modulation.

Elimination of bacterial infections and simultaneously promoting osteogenic differentiation are highly required for infectious bone diseases. Massive reactive oxygen species (ROS) can damage cells, while low ROS concentrations as a molecular signal can regulate cellular fate. In this study, a Janus-ROS healing system is developed for infectious bone regeneration. An alendronate (ALN)-mediated defective metal-organic framework (MOF) sonosensitizer is prepared, which can effectively clear Methicillin-resistant Staphylococcus aureus (MRSA) infections and promote osteogenic differentiation under differential ultrasonic irradiation. In the presence of zirconium-phosphate coordination, the ALN-mediated porphyrin-based MOF (HN25) with a proper defect has great sonodynamic antibacterial efficiency (98.97%, 15 min) and bone-targeting ability. Notably, under low-power ultrasound irradiation, HN25 can increase the chromatin accessibility of ossification-related genes and FOXO1 to promote bone repair through low ROS concentrations. Animal models of paravertebral infection, fracture with infection, and osteomyelitis demonstrate that HN25 successfully realizes the targeted and potent repair of various infectious bone tissues through rapid MRSA elimination, inhibiting osteoclast activity and promoting bone regeneration. The results show that high catalytic efficiency and bioactive MOF can be constructed using pharmaceutical-mediated defect engineering. The Janus-ROS treatment is also a promising therapeutic mode for infectious tissue regeneration.

Synergy Between Surface Confinement and Heterointerfacial Regulations with Fast Electron/Ion Migration in InSe-PPy for Sodium-Ion Storage.

Layered indium selenide (InSe) is a new 2D semiconductor material with high carrier mobility, widely adjustable bandgap, and high ductility. However, its ion storage behavior and related electrochemical reaction mechanism are rarely reported. In this study, InSe nanoflakes encapsulated in conductive polypyrrole (InSe@PPy) are designed in consideration of restraining the severe volume change in the electrochemical reaction and increasing conductivity via in situ chemical oxidation polymerization. Density functional theory calculations demonstrate that the construction of heterostructure can generate an internal electric field to accelerate electron transfer via additional driving forces, offering synergistically enhanced structural stability, electrical conductivity, and Na+ diffusion process. The resulting InSe@PPy composite shows outstanding electrochemical performance in the sodium ion batteries system, achieving a high reversible capacity of 336.4 mA h g-1 after 500 cycles at 1 A g-1 and a long-term cyclic stability with capacity of 274.4 mA h g-1 after 2800 cycles at 5 A g-1 . In particular, the investigation of capacity fluctuation within the first cycling reveals the alternating significance of intercalation and conversion reactions and evanescent alloying reaction. The combined reaction mechanism of insertion, conversion, and alloying of InSe@PPy is revealed by in situ X-ray diffraction, ex situ electrochemical impedance spectroscopy, and transmission electron microscopy.

Association between polycyclic aromatic hydrocarbon exposure and liver function: The mediating roles of inflammation and oxidative stress.

Polycyclic aromatic hydrocarbon (PAH) exposure has been associated with adverse health effects, and accumulating evidence suggests that PAH exposure may impair liver function. However, the underlying mechanisms linking PAH exposure and liver function impairment remain unclear. This study aimed to explore the association between PAH exposure and liver function biomarkers, and the mediating effects of inflammation and oxidative stress. The cross-sectional study included 155 adults and their urinary PAH metabolites (OH-PAHs) were determined, and eight liver function biomarkers were measured in paired serum samples. A comprehensive statistical analysis investigated the linear, non-linear, individual, and joint effects of the association between urinary OH-PAHs and liver function biomarkers. The results indicated significant positive associations between urinary OH-PAH concentrations and liver function biomarker levels, suggesting that PAH exposure may adversely affect liver function. 2-hydroxyfluorene was identified as the individual metabolite contributing significantly to elevated gamma-glutamyl transferase levels. Further stratification by gender revealed that this association is more pronounced in males. Moreover, we observed significant mediation effects of the oxidative stress biomarker 8-hydroxy-2'-deoxyguanosine and the inflammatory biomarkers C-reactive protein and white blood cell count on this association. The physiological responses triggered by PAH exposure are mediated by inflammation, which serves as a link between oxidative stress, cellular injury, and elevated liver enzyme levels. The results demonstrated that increased inflammation and oxidative stress mediated the association between increased urinary OH-PAHs and elevated liver function biomarkers. The results contribute to a better understanding of the potential mechanisms underlying PAH exposure's hepatotoxic effects.