Search Results (1,102)

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, characterized by pruritic and eczematous lesions. Skin barrier dysfunction and aberrant inflammatory responses are hallmark features of AD. Recent genome-wide association studies have implicated NLRP10, a unique member of the NOD-like receptors (NLRs) lacking a leucine-rich repeat (LRR) domain, in AD susceptibility. Unlike other NLRs, the physiological role of NLRP10 in skin remains incompletely understood. Emerging evidence shows that NLRP10 regulates keratinocyte survival and differentiation, acts as a molecular sensor for mitochondrial damage, enhances anti-microbial response and contributes to skin barrier function. This review summarizes current insights into NLRP10′s functions in skin homeostasis, its interplay with cell death pathways, and its role in maintaining skin barrier function. Furthermore, therapeutic opportunities to target NLRP10 as a novel strategy for modulating epidermal cell death and restoring barrier function in AD are highlighted. Full article

Rhizobia have been used for decades as biopreparations, successfully replacing synthetic nitrogen fertilizers in legume cultivation. They have a beneficial effect on the growth and yield of these plants when cultivated in soils that are deficient in both nitrogen and indigenous rhizobia. However, such preparations, containing strains that are characterized by high effectiveness in reducing atmospheric dinitrogen, are not universal. Their use is ineffective when plants are grown in soils that are already rich in strains with low effectiveness, because such inoculant strains are unable to effectively compete with native soil populations. This review discusses issues related to the rhizobia–legume symbiosis, with particular emphasis on inter-strain competition occurring in the soil and in the colonized plant tissues. The importance of Nod factors (NFs) in symbiosis and their broad impact on plant physiological and developmental processes are also discussed. Research results on the effects of NF-containing biopreparations on legume growth and yield are summarized. Moreover, this review explains how such preparations can support the growth and yield of legumes growing in soils containing numerous populations of low-effectiveness rhizobia. Finally, the potential for the application of this technology to non-legume plants is presented. Full article

Background and Objective: Cerebral cavernous malformation (CCM) is a vascular disorder causing seizures, neurological deficits, and hemorrhagic stroke. It can be sporadic or inherited via CCM1, CCM2, or CCM3 gene mutations. Inflammation is broadly recognized as a promoter of cerebral vascular malformations. This study explores inflammatory mechanisms and differences behind CCM-related hemorrhage and epilepsy. Material and Methods: The study group comprised 28 patients, ten patients with CCM-related epilepsy, and 18 patients who clinically presented with a cerebral hemorrhage at diagnosis. All patients underwent microsurgical resection of the CCMs. Formaldehyde-fixed, paraffin-embedded tissue samples were immunohistochemically stained using a monoclonal antibody against Cyclooxygenase 2 (COX-2) (Dako, Santa Clara, CA; Clone: CX-294) and NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) (ABCAM, Cambridge, MA, USA; ab214185). MRI and clinical data were correlated with immunohistochemical findings, and the analysis was conducted utilizing the Trainable Weka Segmentation algorithm. Results: Median CCM volume was 1.68 cm³ (IQR: 0.85–3.07 cm³). There were significantly more NLRP3-positive cells (32.56% to 91.98%; mean: 65.82%, median: 68.34%; SD: ±17.70%), compared to COX-2-positive cells (1.82% to 79.69%; mean: 45.87%, median: 49.06%; SD: ±22.56%). No correlation was shown between the volume of CCMs and a hemorrhage event (p = 0.13, 95% CI: 0.99–1.02). Symptomatic brain hemorrhage showed a significantly increased inflammatory enzyme upregulation from both COX-2 (p < 0.001) and NLRP3 (p = 0.009) versus patients with symptomatic CCM-related epilepsy at first diagnosis. Conclusions: Inflammatory processes in CCMs seem to be driven by broad and multiple pathways because both COX-2 and NLRP3-driven inflammatory pathways are consistently activated. As a novelty, this study showed that patients with symptomatic hemorrhage showed upregulated inflammatory enzyme activity compared to patients with CCM-related epilepsy. No direct links between NLRP3, COX-2 expression, and radiological, pathological, or preexisting patient conditions were found. Full article

The secondary contamination of nodularin disinfection by-products (NOD-DBPs) is a problem worthy of attention. In this study, prototypical NOD-R-DBPs were prepared, and their toxicity was assessed using conventional protein phosphatase (PPs) inhibition assay, confirming that structural changes in “Adda³” during chlorination are key factors leading to a significant reduction in NOD-R toxicity. However, some NOD-R-DBPs still exhibit certain levels of toxicity (2.8–81% of NOD-R). To elucidate the mechanism underlying the potential inhibitory effect of NOD-R-DBPs on protein phosphatase 2A (PP2A), molecular simulations were employed to establish interaction models between prototypical NOD-R-DBPs and PP2A using homology modeling strategies, and molecular docking was used to obtain candidate interaction parameters between prototypical NOD-R-DBPs and PP2A. Structural changes in “Adda³” weakened the hydrogen bonds “Adda³”Asn₁₁₇ and “Adda³”His₁₁₈. Subsequently, the disruption of “Adda³” altered key interactions between NOD-R-DBPs and PP2A (hydrogen bond Mdhb⁵ ← Arg₈₉, ionic bond Glu⁴-Arg₈₉, metal bond His₂₄₁-Mn₁²⁺, etc.). The changes in these interactions further altered the interactions between conserved amino acids and the catalytic center Mn²⁺ (ionic bond Asp₅₇-Mn₂²⁺), thereby increasing Mn²⁺ exposure. Meanwhile, the retained interactions promoted the binding of -PO₄ with the conserved amino acids His₁₁₈ and Arg₈₉. Prototypical NOD-R-DBPs retained the aforementioned key interactions and thus exhibit potential inhibitory effects on PP2A. The varying degrees of damage to the Adda³ structure led to significant differences in the inhibitory effects of different NOD-R-DBPs on PP2A. Full article

Background/Objectives: Global warming and concomitant extreme weather events have markedly increased the incidence of heat stroke. Heat stroke (HS) poses a substantial threat to cerebral health by triggering neuroinflammation and accelerating neurodegenerative processes. The activation of the Nod-like receptor protein 3 (NLRP3) inflammasome for interleukin-1β (IL-1β) secretion has been implicated as a critical mechanism underlying HS-related fatalities. However, the potential role of specific dietary factors to counteract heat stroke-induced neurotoxicity remains largely underexplored. We previously reported that eicosapentaenoic acid (EPA) and urolithin A (UroA), a gut metabolite of ellagic acid, effectively suppress NLRP3 inflammasome activation against metabolic or pathogenic insults. This study aimed to assess the impact of eicosapentaenoic acid (EPA), urolithin A (UroA), and their combination on mitigating heatstroke-mediated NLRP3 inflammasome activation in microglial cells. Methods: In vitro heatstroke conditions were replicated by subjecting murine BV2 microglial cells to a high temperature (41 °C) under hypoxic conditions. To achieve nutrient loading, BV2 cells were preincubated with either EPA (50 µM) or UroA (10 µM). NLRP3 inflammasome activation was evaluated by proinflammatory gene expression, caspase-1 cleavage in cells, and IL-1β secretion to the medium. The caspase-1 activation was determined using a luciferase-based inflammasome and protease activity reporter (iGLuc) assay. Results: Exposure to high temperatures under hypoxia successfully mimicked HS conditions and promoted NLRP3 inflammasome activation in BV2 cells. Both EPA and UroA substantially attenuated the heat stroke-induced priming of proinflammatory genes. More importantly, EPA and UroA demonstrated a synergistic effect in mitigating HS-induced active caspase-1 production, leading to a dramatic decrease in IL-1β secretion. This synergistic effect between EPA and UroA was further confirmed by the iGLuc reporter assay. Conclusions: Dietary enrichment with EPA and UroA precursors may constitute an efficacious strategy for mitigating heat stroke-mediated neuroinflammation and neurodegenerative diseases. Full article

The first film signed by Paolo Taviani without his brother Vittorio (who died in 2018) in more than 60 years, Leonora addio (2022) recapitulates and condenses an entire career by recounting the grotesque (real-life) journey of the burial, cremation, exhumation, transfer (from Rome to Sicily) and re-burial of Luigi Pirandello’s corpse over more than ten years, as well as by showing in the last thirty minutes an adaptation for the screen of “The Nail” (“Il chiodo”, the last novella by the renowned Sicilian writer). A quintessential testament film refracting the writer’s death in Vittorio’s (one of the film’s many Pirandello-esque mirror games) and alluding to the intellectual legacies of either, Leonora addio daringly thematizes the exploitation of cultural value as well as its political implications—particularly in the specific Italian context and, implicitly yet unmistakably, in the present day too. My paper will analyse Leonora addio paying particular attention to how this subtext intersects the film’s “testamentary” surface, to Deleuze’s “crystal images” (pervasively informing the structure of Leonora addio), to the film’s many nods to Kaos (a 1984 Pirandello adaptation for the screen by the Taviani, analysed mainly through the lens of Lacanian gaze theory) and to the role of death in both films. Full article

Multiple sclerosis (MS) is a chronic autoimmune disease characterized by sustained neuroinflammation and demyelination within the central nervous system (CNS). Vesatolimod (VES), a selective Toll-like receptor 7 (TLR7) agonist, has demonstrated both antiviral and immunomodulatory properties; however, its potential therapeutic value in neuroinflammatory contexts remains poorly understood. In this study, we evaluated the efficacy of VES in the experimental autoimmune encephalomyelitis (EAE) model of MS and elucidated its mechanisms of action. EAE was induced in mice by immunization with myelin oligodendrocyte glycoprotein (MOG_35–55). The therapeutic effects of VES were assessed through clinical scoring, body weight monitoring, histopathology, flow cytometry, quantitative proteomics, and Western blot analysis. Additionally, an in vitro model of lipopolysaccharide (LPS)-induced microglial activation was employed to investigate cell-autonomous mechanisms. Results showed that VES administration significantly ameliorated disease severity, reduced weight loss, and enhanced neurological function in EAE mice. Treatment with VES inhibited the differentiation of pro-inflammatory Th1 and Th17 cells while expanding regulatory T cell (Treg) populations. It also preserved blood–brain barrier (BBB) integrity, attenuated demyelination, and modulated microglial activation phenotypes within the CNS. At the molecular level, VES activated the Nrf2/HO-1 antioxidant pathway, thereby enhancing the expression of cytoprotective proteins. Proteomic profiling further revealed the downregulation of inflammation-related proteins, specifically those associated with TNF, IL-17, and NOD-like receptor signaling pathways. Collectively, these findings demonstrate that VES alleviates neuroinflammation in EAE through multimodal mechanisms—including peripheral and central immune regulation, BBB protection, and activation of endogenous antioxidant defenses—supporting its further development as a promising therapeutic candidate for MS. Full article

Bovine mastitis is one of the most prevalent and economically significant diseases affecting dairy cows worldwide, with Escherichia coli (E. coli) recognized as one of the principal pathogens causing acute mastitis. The innate immune system plays a crucial role in the defense of the bovine mammary gland, serving as the first line of defense against pathogen invasion. This study elucidated the pathological mechanisms and immune response-related molecular regulatory networks involved in E. coli-induced bovine mastitis. Histopathological and apoptosis analyses of mammary tissues were performed using hematoxylin-eosin (HE) staining and TUNEL staining, respectively, while RNA sequencing (RNA-seq) was conducted to identify differentially expressed genes (DEGs) and their associated signaling pathways. HE staining revealed typical inflammatory lesions in the mammary glands of mastitis cows. TUNEL staining further confirmed that the level of apoptosis in the mastitis group was significantly higher than in the healthy control group (p < 0.0001). RNA-seq analysis identified 2717 DEGs, with 2238 upregulated and 479 downregulated genes. The top 20 significantly upregulated genes (e.g., S100A12, IL1RN, IL1R2, CXCL8, SAA3, S100A8, S100A9, TREML2, TREM1, M-SAA3.2, PTX3, MMP9) were predominantly involved in inflammatory immune regulation, acute phase responses (e.g., HP, SAA3), and cellular signal transduction (e.g., PLEK, LPAR3). Gene Ontology (GO) enrichment analysis revealed that these DEGs were mainly associated with biological processes, such as signal transduction, immune response, inflammatory response, and transcriptional regulation. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that these DEGs were significantly enriched in key inflammatory and immune regulatory pathways, including the TNF signaling pathway, C-type lectin receptor signaling pathway, Chemokine signaling pathway, NOD-like receptor signaling pathway, NF-κ B signaling pathway, and IL-17 signaling pathway, suggesting that these pathways play central roles in the mammary immune defense against E. coli infection. In conclusion, this study demonstrated at the histopathological, cellular apoptosis, and transcriptomic levels that E. coli infection induces mammary tissue damage and apoptosis by activating immune and inflammation-related genes (S100A12, IL1RN, IL1R2, CXCL8, SAA3, S100A8, S100A9, TREML2, TREM1, M-SAA3.2, PTX3, MMP9) and key signaling pathways (TNF signaling pathway, C-type lectin receptor signaling pathway, Chemokine signaling pathway, NOD-like receptor signaling pathway, NF-κ B signaling pathway, IL-17 signaling pathway). The findings of this study provide a theoretical basis for probing into the pathogenesis of bovine mastitis and the development of targeted interventions. Full article

Secondary liver injury (SLI) is the most common complication in the development of inflammatory bowel disease (IBD), and it is susceptible to environmental factors, including diet patterns. As a food-brightening agent, titanium dioxide nanoparticles (TiO₂ NPs) are inevitably consumed by IBD patients. Currently, there are a few studies on TiO₂ NPs exposure to SLI in colitis mice. In this study, a SLI model was built using dextran sodium sulfate (DSS) free-drinking for 7 days after pre-exposure to TiO₂ NPs. The changes in the pathological results and liver function indicators suggested that high-dose TiO₂ NPs only exhibited a slight injury in the liver. With further analysis, we found that pre-exposure to high-dose TiO₂ NPs in mice with SLI led to an increase in intestinal permeability and hepatic LPS content, along with increased inflammatory cytokines and an anti-oxidative system imbalance. Subsequently, accumulated LPS and ROS overproduction activated the NOD-like receptor family pyrin-containing 3 (NLRP3) inflammasome, inducing hepatic cell pyroptosis. To provide compelling evidence, NLRP3 gene-deficient mice were used, and the results showed that the absence of NLRP3 improved liver function, alleviated hepatic inflammation, and reduced hepatic oxidative injury in SLI mice with TiO₂ NPs exposure. In summary, these results confirmed the critical role of the NLRP3 inflammasome in the TiO₂ NP-aggravated progression of SLI. Our study provided a comprehensive evaluation of foodborne nanoparticles on IBD complications, hoping that more studies can focus on IBD complications affected by environmental factors. Full article

Background/Objectives: Colorectal cancer (CRC) remains a major global health challenge and current therapies are not always effective. In addition, certain immune cell populations, such as myeloid-derived suppressor cells (MDSCs), pose a significant barrier to immune-based treatments. Some phytochemicals, particularly compounds derived from Allium spp. like Propyl-Propane Thiosulfonate (PTSO), have shown strong immunomodulatory potential in digestive disorders. This study aims to investigate the capacity of PTSO to modulate immune responses and affect tumor progression in CRC models, in vitro and in vivo, with a focus on the immune cell populations that comprise the tumor microenvironment. Methods: Human peripheral blood mononuclear cells (hPBMCs) were incubated with PTSO (25 μM for 48 h) and characterized by flow cytometry. These cells (1 × 10⁶) were then injected into NOD scid gamma (NSG) immunodeficient mice, which were simultaneously induced to develop a subcutaneous tumor by injection of HCT116 enriched cancer stem cells (CSCs) colonospheres (60,000 cells/mouse). Results: PTSO reduced MDSC populations, specifically, it significantly reduced monocytic (M-MDSCs, Control: 7.27 ± 0.53% vs. PTSO: 4.70 ± 2.39%; p = 0.0458) and polymorphonuclear (PMN-MDSCs, Control: 5.28 ± 0.99% vs. PTSO: 3.41 ± 1.58%; p = 0.0385) MDSCs. In parallel, PTSO increased T cell subpopulations, particularly interferon gamma (IFNG)-producing cytotoxic CD8⁺ T cells (Control: 9.52 ± 2.06% vs. PTSO: 15.04 ± 5.01%; p = 0.0685). In the humanized tumor xenograft mouse, the administration of PTSO-pretreated hPBMCs led to a significant reduction in tumor size (Control: 1.43 ± 0.82 cm³ vs. PTSO: 0.44 ± 0.35 cm³; p = 0.0068), accompanied by increased infiltration of CD4⁺ T lymphocytes and Natural Killer (NK) cells and downregulation of immunosuppressive genes. These effects resulted in a reduction in cancer cell proliferation and invasiveness. Conclusions: The dual effect of PTSO on immune cell populations, reducing immunosuppressive myeloid cells and enhancing effector T lymphocyte and NK cell responses, resulted in an anti-tumor effect, highlighting this bioactive compound as a promising adjuvant in CRC immunotherapy and opening avenues for future research combining immunotherapy with PTSO in alternative models to optimize dosing and enhance translational potential. Full article

Human induced pluripotent stem cells (hiPSCs) hold great potential for patient-specific therapies. Transplantation of hiPSC-derived neural progenitor cells (NPCs) is a promising reparative strategy for spinal cord injury (SCI), but clinical translation requires efficient differentiation into desired neural lineages and purification before transplantation. Here, differentiated hiPSCs—reprogrammed from human skin fibroblasts using Sendai virus-mediated expression of OCT4, SOX2, KLF4, and C-MYC—into neural rosettes expressing SOX1 and PAX6, followed by neuronal precursors (β-tubulin III⁺/NESTIN⁺) and glial precursors (GFAP+/NESTIN+). Both neuronal and glial precursors expressed the A2B5 surface antigen. A2B5+ NPCs, purified by fluorescence-activated cell sorting (FACS), proliferated in vitro with mitogens, and differentiated into mature neurons and astrocytes under lineage-specific conditions. Then, NOD-SCID mice received a T9 contusion injury followed by transplantation of A2B5+ NPCs, human fibroblasts, or control medium at 8 days post-injury. At two months, grafted NPCs showed robust survival, progressive neuronal maturation (β-tubulin III⁺→doublecortin⁺→NeuN⁺), and astrocytic differentiation (GFAP+), particularly in spared white matter. Transplantation significantly increased spared white matter volume and improved hindlimb locomotor recovery, with no teratoma formation observed. These results demonstrate that hiPSC-derived, FACS-purified A2B5+ NPCs can survive, differentiate into neurons and astrocytes, and enhance functional recovery after SCI. This approach offers a safe and effective candidate cell source for treating SCI and potentially other neurological disorders. Full article

The utilization of saline–alkali water resources presents a promising approach for freshwater aquaculture. Red tilapia (Oreochromis spp.) exhibits moderate salinity tolerance, but its adaptation mechanism to alkaline conditions remains poorly understood. In the current study, five alkaline carbonate concentrations in a 60-day chronic stress experiment on red tilapia were evaluated. The experimental design included a control group (CA0, 0 mmol/L) and three treatment groups (CA10, 20 mmol/L; CA30, 30 mmol/L; and CA40 40 mmol/L). The results indicated that at alkaline carbonate concentrations exceeding 20 mmol/L, the gill filaments exhibited curling and deformation, the hepatocytes displayed migration, and tissue damage increased significantly. The gill’s antioxidant capacity initially decreased and then increased, with severe gill injury in the CA40 group, leading to significantly reduced levels of SOD, CAT, and GSH-PX compared to the CA40 group (p < 0.05). Conversely, the enzymatic activities related to energy metabolism showed an opposite trend under alkaline carbonate stress. The transcriptome analyses of gill tissues across five groups identified significant alterations in key pathways, including the metabolic process (endocytosis, focal adhesion, PI3K−Akt signaling pathway, MAPK signaling pathway, and Citrate cycle (TCA cycle)), and immune responses (mTOR signaling and NOD−like receptor signaling pathways). Additionally, we screened 13 differentially expressed genes (DEGs) as potential regulators of alkaline stress and validated their expression levels using quantitative real-time PCR (qPCR). This study preliminarily elucidated the molecular mechanism of red tilapia in the physiological regulation process under chronic alkaline stress, and offers a theoretical foundation for breeding programs aimed at developing alkali-tolerant strains for aquaculture in alkaline water environments. Full article

Sjögren’s disease (SjD) targets the salivary and lacrimal glands and is characterized by autoantibody production and glandular lymphocytic infiltrate with ectopic germinal centers (EGCs). The chemokine CCL25 recruits CCR9⁺ CD4⁺ T cells to the salivary glands to promote B cell activation. However, the therapeutic potential of targeting the CCL25–CCR9 axis to limit glandular inflammation and lymphoid neogenesis remains largely unexplored. Evaluate whether blocking the CCL25–CCR9⁺ T cell axis with a monoclonal antibody could reduce immune infiltration, ectopic germinal center (EGC) formation, and local autoantibody production in the NOD.H2(h4) mouse model of SjD. Female NOD.H2(h4) mice were administered anti-CCL25 antibody, isotype control, or PBS intraperitoneally for 12 weeks. Sera and saliva were collected to evaluate anti-Ro52 antibodies via ELISA across treatment groups. Salivary glands were harvested and processed for H&E staining to assess lymphocytic infiltration and focus scores. Treatment with α-CCL25 was well tolerated, with no significant differences in body weight or stimulated salivary flow between treatment groups. Histopathological evaluation revealed no reduction in lymphocytic infiltration, focus scores, or percentage of inflamed tissue in α-CCL25-treated mice compared to controls. Anti-Ro52 antibodies were undetectable in plasma or saliva across all groups and timepoints. Systemic CCL25 blockade did not significantly alter salivary gland inflammation, function, or autoantibody production in NOD.H2(h4) mice. These findings suggest that monotherapy targeting the CCL25–CCR9 axis may be insufficient to resolve glandular autoimmunity in this model and that additional or combinatorial strategies may be necessary for effective intervention. Full article

Heme enzymes that bind and reduce O₂ are susceptible to poisoning by NO. The high reactivity and affinity of NO for ferrous heme produces stable ferrous-NO complexes, which in theory should preclude O₂ binding and turnover. However, NO inhibition is often competitive with respect to O₂ and rapidly reversible, thus providing cellular and organismal survival advantages. This kinetic paradox has prompted a search for mechanisms for reversal and hence resistance. Here, I critically review proposed resistance mechanisms for NO dioxygenase (NOD) and cytochrome c oxidase (CcO), which substantiate reduction or oxidation of the tightly bound NO but nevertheless fail to provide kinetically viable solutions. A ferrous heme intermediate is clearly not available during rapid steady-state turnover. Reversible inhibition can be attributed to NO competing with O₂ in transient low-affinity interactions with either the ferric heme in NOD or the ferric heme-cupric center in CcO. Toward resolution, I review the underlying principles and evidence for kinetic control of ferric heme reduction via an O₂-triggered ferric heme spin crossover and an electronically-forced motion of the heme and structurally-linked protein side chains that elicit electron transfer and activate O₂ in the flavohemoglobin-type NOD. For CcO, kinetics, structures, and density functional theory point to the existence of an analogous O₂ and reduced oxygen intermediate-controlled electron-transfer gate with a linked proton pump function. A catalytic cycle and mechanism for CcO is finally at hand that links each of the four O₂-reducing electrons to each of the four pumped protons in time and space. A novel proton-conducting tunnel and channel, electron path, and pump mechanism, most notably first hypothesized by Mårten Wikström in 1977 and pursued since, are laid out for further scrutiny. In both models, low-energy spin-orbit couplings or ‘spintronic’ interactions with O₂ and NO or copper trigger the electronic motions within heme that activate electron transfer to O₂, and the exergonic reactions of transient reactive oxygen intermediates ultimately drive all enzyme, electron, and proton motions. Full article

The tribological behavior of ferritic ductile iron without ultrafine graphite nodules (FDI) and ferritic ductile iron with ultrafine graphite nodules (FDI-UG) was investigated in the present study. Ultrafine graphite nodules with a count of 3400 nod/mm² were introduced by annealing treatment of quenched ductile iron, which effectively reduced the friction coefficient of ferritic ductile iron from approximately 0.3 to 0.15. This improvement was attributed to the ultrafine graphite nodules, which, due to their small spacing, facilitated a more uniform distribution on the tribological surface. Additionally, the formation of ultrafine graphite nodules in ferritized ductile iron refined the grain size (15 μm) and enhanced the hardness of ferritic ductile iron (183 HV), thereby significantly reducing abrasive wear. The more uniform graphite lubrication on the tribosurface and high hardness of fine ferrite grains in FDI-UG further enhanced wear resistance between the frictional pairs, effectively suppressing adhesion wear at high loads (6 N). Consequently, the ferritic ductile iron containing ultrafine graphite nodules and fine ferrite grains exhibited a superior wear resistance (6.84 × 10⁻³ mm³ and 9.47 × 10⁻³ mm³) compared to its untreated counterpart (9.22 × 10⁻³ mm³ and 11.95 × 10⁻³ mm³). These findings suggest that the incorporation of ultrafine graphite nodules was an effective strategy to enhance the tribological properties of ductile iron. Full article