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Polymer binders in battery electrodes may be either active or passive. This distinction depends on whether the polymer influences charge or mass transport in the electrode. Although it is desirable to understand how to tailor the macromolecular design of a polymer to play a passive or active role, design rules are still lacking, as is a framework to assess the divergence in such behaviors. Here, we reveal the molecular-level underpinnings that distinguish an active polyelectrolyte binder designed for lithium–sulfur batteries from a passive alternative. The binder, a cationic polyelectrolyte, is shown to both facilitate lithium-ion transport through its reconfigurable network of mobile anions and restrict polysulfide diffusion from mesoporous carbon hosts by anion metathesis, which we show is selective for higher oligomers. These attributes allow cells to be operated for >100 cycles with excellent rate capability using cathodes with areal sulfur loadings up to 8.1 mg cm –2 . Polymer binders in battery electrodes can affect their performance, however design rules are still lacking. Here, the authors reveal why polyelectrolyte binders outperform charge-neutral alternatives in lithium–sulfur batteries, showing how cationic polyelectrolytes can regulate ion transport selectively.

The spatiotemporal regulation of inflammasome activation remains unclear. To examine the mechanism underlying the assembly and regulation of the inflammasome response, here we perform an immunoprecipitation-mass spectrometry analysis of apoptosis-associated speck-like protein containing a CARD (ASC) and identify NCF4/1/2 as ASC-binding proteins. Reduced NCF4 expression is associated with colorectal cancer development and decreased five-year survival rate in patients with colorectal cancer. NCF4 cooperates with NCF1 and NCF2 to promote NLRP3 and AIM2 inflammasome activation. Mechanistically, NCF4 phosphorylation and puncta distribution switches from the NADPH complex to the perinuclear region, mediating ASC oligomerization, speck formation and inflammasome activation. NCF4 functions as a sensor of ROS levels, to establish a balance between ROS production and inflammasome activation. NCF4 deficiency causes severe colorectal cancer in mice, increases transit-amplifying and precancerous cells, reduces the frequency and activation of CD8 + T and NK cells, and impairs the inflammasome-IL-18-IFN-γ axis during the early phase of colorectal tumorigenesis. Our study implicates NCF4 in determining the spatial positioning of inflammasome assembly and contributing to inflammasome-mediated anti-tumor responses. The NADPH oxidase 2 (NOX2) complex is a main reactive oxygen species (ROS) source during inflammation. Here the authors report that NCF4, a subunit of the NOX2 complex, acts a sensor of ROS levels and regulates NLRP3 and AIM2 inflammasome activation, associated with attenuated colorectal cancer progression.

Parkinson’s disease (PD) is characterized by the degeneration of dopaminergic neurons and excessive microglial activation in the substantia nigra pars compacta (SNpc). In the present study, we aimed to demonstrate the therapeutic effectiveness of the potent sphingosine-1-phosphate receptor antagonist fingolimod (FTY720) in an animal model of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and to identify the potential mechanisms underlying these therapeutic effects. C57BL/6J mice were orally administered FTY720 before subcutaneous injection of MPTP. Open-field and rotarod tests were performed to determine the therapeutic effect of FTY720. The damage to dopaminergic neurons and the production of monoamine neurotransmitters were assessed using immunohistochemistry, high-performance liquid chromatography, and flow cytometry. Immunofluorescence (CD68- positive) and enzyme-linked immunosorbent assay were used to analyze the activation of microglia, and the levels of activated signaling molecules were measured using Western blotting. Our findings indicated that FTY720 significantly attenuated MPTP-induced behavioral deficits, reduced the loss of dopaminergic neurons, and increased dopamine release. FTY720 directly inhibited MPTP-induced microglial activation in the SNpc, suppressed the production of interleukin (IL)-6, IL-1β, and tumor necrosis factor-α in BV-2 microglial cells treated with 1-methyl-4-phenylpyridinium (MPP + ), and subsequently decreased apoptosis in SH-SY5Y neuroblastoma cells. Moreover, in MPP + -treated BV-2 cells and primary microglia, FTY720 treatment significantly attenuated the increases in the phosphorylation of PI3K/AKT/GSK-3β, reduced ROS generation and p65 activation, and also inhibited the activation of NLRP3 inflammasome and caspase-1. In conclusion, FTY720 may reduce PD progression by inhibiting NLRP3 inflammasome activation via its effects on ROS generation and p65 activation in microglia. These findings provide novel insights into the mechanisms underlying the therapeutic effects of FTY720, suggesting its potential as a novel therapeutic strategy against PD. Graphical Abstract FTY720 may reduce ROS production by inhibiting the PI3K/AKT/GSK-3β signaling pathway, while at the same time reducing p65 phosphorylation, thus decreasing NLRP3 inflammasome activation through these two pathways, ultimately reducing microglia activation-induced neuronal damage.

Introduction: Luteolin inhibits platelet activation and thrombus formation, but the mechanisms are unclear. This study investigated the effects of luteolin on GPVI-mediated platelet activation in vitro and explored the effect of luteolin on thrombosis, coagulation, and platelet production in vivo . Methods: Washed human platelets were used for aggregation, membrane protein expression, ATP, Ca 2+ , and LDH release, platelet adhesion/spreading, and clot retraction experiments. Washed human platelets were used to detect collagen and convulxin-induced reactive oxygen species production and endogenous antioxidant effects. C57BL/6 male mice were used for ferric chloride-induced mesenteric thrombosis, collagen-epinephrine induced acute pulmonary embolism, tail bleeding, coagulation function, and luteolin toxicity experiments. The interaction between luteolin and GPVI was analyzed using solid phase binding assay and surface plasmon resonance (SPR). Results: Luteolin inhibited collagen- and convulxin-mediated platelet aggregation, adhesion, and release. Luteolin inhibited collagen- and convulxin-induced platelet ROS production and increased platelet endogenous antioxidant capacity. Luteolin reduced convulxin-induced activation of ITAM and MAPK signaling molecules. Molecular docking simulation showed that luteolin forms hydrogen bonds with GPVI. The solid phase binding assay showed that luteolin inhibited the interaction between collagen and GPVI. Surface plasmon resonance showed that luteolin bonded GPVI. Luteolin inhibited integrin αIIbβ3-mediated platelet activation. Luteolin inhibited mesenteric artery thrombosis and collagen- adrenergic-induced pulmonary thrombosis in mice. Luteolin decreased oxidative stress in vivo . Luteolin did not affect coagulation, hemostasis, or platelet production in mice. Discussion: Luteolin may be an effective and safe antiplatelet agent target for GPVI. A new mechanism (decreased oxidative stress) for the anti-platelet activity of luteolin has been identified.

Introduction: Pine wilt disease (PWD), caused by Bursaphelenchus xylophilus, has led to widespread logging interventions in subtropical China, especially clearcutting, yet the ecological consequences for insect communities remain poorly understood. Insects play critical roles in ecosystem functioning, making it essential to quantify how different logging strategies shape their diversity, community composition, and functional guilds.Methods: We established 48 stratified plots across four PWD-affected counties in Jiangxi Province to compare unlogged controls (UC), selection cutting (SC), and clearcutting (CC) treatments. Insect diversity was evaluated using Shannon and Simpson indices, while community structure was analyzed with PERMANOVA and NMDS ordinations. Indicator species were identified via IndVal analysis. Functional guild dynamics were measured across trophic groups, and structural equation modeling (SEM) was used to assess vegetation cover and litter thickness as mediators of diversity responses.Results: Clearcutting caused significant declines in insect diversity (Shannon index: UC 3.63 ± 0.02 vs. CC 3.14 ± 0.18; F = 19.17, p = 0.00057; Simpson index: UC 0.960 vs. CC 0.919). PERMANOVA attributed 60.7–89.5% of variation in insect community structure to logging treatment (p < 0.05), with NMDS ordinations showing distinct clustering: CC sites were dominated by disturbance-tolerant taxa (e.g., Cicindelidae, IndVal = 0.94), while UC sites harboured specialists (e.g., Libellulidae, IndVal = 0.95). Functional guild analysis revealed strong reductions in predators (−63.7%) and parasitoids (p < 0.001) under CC, whereas decomposers were relatively resilient. SEM demonstrated that vegetation cover (β = 0.69, p < 0.001) and litter thickness (β = 0.25, p = 0.041) acted as key mediators, with logging intensity indirectly depressing insect diversity via microhabitat degradation (model R2 = 0.81).Discussion and conclusion: Our findings show that intensive clearcutting exacerbates biodiversity loss and trophic collapse in insect communities of PWD-affected pine forests, largely through reductions in vegetation structure and litter. In contrast, lighter interventions such as selection cutting supported greater ecological resilience. To balance disease control with biodiversity conservation, retention forestry practices maintaining ≥30% canopy cover and 20–30 m3/ha deadwood are recommended to buffer microhabitats and sustain insect community functioning.

Xinmailong (XML), a bioactive composite extracted from , has been widely used to treat cardiovascular diseases such as congestive heart failure. However, it is unclear whether XML has antiplatelet and antithrombotic effects. The effects of XML on agonist-induced platelet aggregation, adhesion and spreading, granule secretion, integrin α II bβ3 activation, and thrombus formation were evaluated. Phosphorylation of Syk, PLCγ2, Akt, GSK3β, and MAPK signaling molecules was also studied on agonist-induced platelets. In addition, the antithrombotic effects of XML were observed using an acute pulmonary thrombosis mouse model. XML dose-dependently inhibited platelet aggregation and granule secretion induced by thrombin, collagen, and arachidonic acid (AA). XML also greatly reduced platelet adhesion and spreading on both collagen- and fibrinogen-coated surfaces. Biochemical analysis revealed that XML inhibited thrombin-, collagen-, and AA-induced phosphorylation of Syk, PLCγ2, Akt, GSK3β, and MAPK. Additionally, XML significantly inhibited thrombus formation in a collagen-epinephrine-induced acute pulmonary thrombosis mouse model. Here, we provide the first report showing that XML inhibits platelet function and that it possesses antithrombotic activity. This suggests that XML could be a potential therapeutic candidate to prevent or treat platelet-related cardiovascular diseases.

To improve the fault location ability of the DC distribution network and ensure its power supply reliability, a fault location method based on the beetle swarm optimization algorithm is proposed. Firstly, the fault characteristics of the DC side after short-circuit fault are analyzed, and the mathematical model for fault location is established; then, the problem of fault location is transformed into the problem of parameter identification by discretization; finally, to verify the effectiveness of the method, a flexible DC distribution network model is built in MATLAB. The simulation results show that the proposed fault location method is accurate, not affected by the transition resistance, and has good robustness.

While extensive studies report that neonatal hypoxia-ischemia (HI) induces long-term cognitive impairment via inflammatory responses in the brain, little is known about the role of early peripheral inflammation response in HI injury. Here we used a neonatal hypoxia rodent model by subjecting postnatal day 0 (P0d) rat pups to systemic hypoxia (3.5 h), a condition that is commonly seen in clinic neonates, Then, an initial dose of minocycline (45 mg/kg) was injected intraperitoneally (i.p.) 2 h after the hypoxia exposure ended, followed by half dosage (22.5 mg/kg) minocycline treatment for next 6 consecutive days daily. Saline was injected as vehicle control. To examine how early peripheral inflammation responded to hypoxia and whether this peripheral inflammation response was associated to cognitive deficits. We found that neonatal hypoxia significantly increased leukocytes not only in blood, but also increased the monocytes in central nervous system (CNS), indicated by presence of C-C chemokine receptor type 2 (CCR2 )/CD11b CD45 positive cells and CCR2 protein expression level. The early onset of peripheral inflammation response was followed by a late onset of brain inflammation that was demonstrated by level of cytokine IL-1β and ionized calcium binding adapter molecule 1(Iba-1; activated microglial cell marker). Interrupted blood-brain barrier (BBB), hypomyelination and learning and memory deficits were seen after hypoxia. Interestingly, the cognitive function was highly correlated with hypoxia-induced leukocyte response. Notably, administration of minocycline even after the onset of hypoxia significantly suppressed leukocyte-mediated inflammation as well as brain inflammation, demonstrating neuroprotection in systemic hypoxia-induced brain damage. Our data provided new insights that systemic hypoxia induces cognitive dysfunction, which involves the leukocyte-mediated peripheral inflammation response.

A new Modified Iterative Fourier Technique (MIFT) is proposed for the design of interleaved linear antenna arrays which operate at different frequencies with no grating lobes, low-sidelobe levels, and wide bandwidths. In view of the Fourier transform mapping between the element excitations and array factor of uniform linear antenna array, the spectrum of the array factor is first acquired with FFT and its energy distributions are investigated thoroughly. The relationship between the carrier frequency and the element excitation is obtained by the density-weighting theory. In the following steps, the element excitations of interleaved subarrays are carefully selected in an alternate manner, which ensures that similar patterns can be achieved for interleaved subarrays. The Peak Sidelobe Levels (PSLs) of the interleaved subarrays are further reduced by the iterative Fourier transform algorithm. Numerical simulation results show that favorable design of the interleaved linear antenna arrays with different carrier frequencies can be obtained by the proposed method with favorable pattern similarity, low PSL, and wide bandwidths.

The mechanism by which inflammasome activation is modulated remains unclear. In this study, we identified an AIM2-interacting protein, the E3 ubiquitin ligase HUWE1, which was also found to interact with NLRP3 and NLRC4 through the HIN domain of AIM2 and the NACHT domains of NLRP3 and NLRC4. The BH3 domain of HUWE1 was important for its interaction with NLRP3, AIM2, and NLRC4. Caspase-1 maturation, IL-1β release, and pyroptosis were reduced in Huwe1-deficient bone marrow-derived macrophages (BMDMs) compared with WT BMDMs in response to stimuli to induce NLRP3, NLRC4, and AIM2 inflammasome activation. Furthermore, the activation of NLRP3, NLRC4, and AIM2 inflammasomes in both mouse and human cells was remarkably reduced by treatment with the HUWE1 inhibitor BI8622. HUWE1 mediated the K27-linked polyubiquitination of AIM2, NLRP3, and NLRC4, which led to inflammasome assembly, ASC speck formation, and sustained caspase-1 activation. Huwe1-deficient mice had an increased bacterial burden and decreased caspase-1 activation and IL-1β production upon Salmonella, Francisella, or Acinetobacter baumannii infection. Our study provides insights into the mechanisms of inflammasome activation as well as a potential therapeutic target against bacterial infection.