Search Results (427)

Single-cell omics technologies have transformed the study of cellular heterogeneity, enabling high-resolution analysis of tissue development and complex traits. In sheep and goats, these approaches have been applied to skin, hair follicles, reproductive organs, metabolic tissues, and adipose tissue, revealing cell type-specific regulatory programs underlying traits such as wool quality, fertility, growth, and fat deposition. However, most studies rely on single-cell RNA sequencing (scRNA-seq) and are limited by incomplete genome annotation, insufficient coverage of production traits, and weak integration with population genetics, restricting their application in molecular breeding. This review summarizes advances in single-cell omics in sheep and goats, focusing on tissue development and trait formation. We further discuss emerging strategies that integrate single-cell multi-omics, spatial transcriptomics, and population genetics to resolve regulatory mechanisms in a cell type-specific and spatially informed context. Finally, we discuss CRISPR/Cas9-based validation to link genotype and phenotype, accelerating gene discovery and precision breeding in small ruminants. Full article

Pituitary apoplexy is an uncommon but clinically urgent complication that often involves intrasellar hemorrhage and tissue necrosis. The mechanisms linking acute tissue injury to the inflammatory tumor microenvironment remain incompletely defined. Here, we characterized the apoplexy-associated microenvironment and examined whether macrophage mechanosensitive signaling contributes to inflammatory amplification and tissue damage in pituitary neuroendocrine tumors (PitNETs). We combined single-cell RNA sequencing (scRNA-seq), histological validation, clinical stratification, and in vitro functional assays using apoplectic and non-apoplectic human PitNET specimens. Macrophage state transitions, intercellular communication, and transcriptional regulatory programs were analyzed, followed by an experimental assessment of the PIEZO1–Ca²⁺ axis and macrophage-conditioned medium-induced tumor cell death. Histological validation confirmed macrophage accumulation in apoplectic PitNETs, including a 1.67-fold increase in IBA-1-positive cells (p < 0.001). CellChat-inferred interaction metrics increased descriptively in apoplectic samples. Apoplectic tissues showed higher TNF-α expression (3.00-fold; p < 0.0001) and higher PIEZO1 fluorescence in IBA-1-positive regions (1.39-fold; p = 0.001). Yoda1 increased Calcium 520 fluorescence in macrophages (1.72-fold; p = 0.002), whereas Piezo1 knockdown reduced the Yoda1-associated response (p = 0.003). Conditioned medium from activated macrophages increased total Annexin V/PI-positive death in AtT-20 cells (0.53 ± 0.53% to 32.48 ± 1.14%; p < 0.001) and GH3 cells (0.82 ± 0.50% to 30.92 ± 1.11%; p < 0.001); Piezo1 knockdown or TNF-α neutralization attenuated this effect. Clinically, pathological necrosis was associated with higher symptom frequencies and a greater adjusted likelihood of two or more clinical symptoms. Together, these findings indicate that PIEZO1-related macrophage signaling may participate in TNF-α-associated tumor cell necroptosis in pituitary apoplexy. Pathological necrosis was linked to greater acute symptom burden and perioperative hormonal abnormalities, suggesting that it may identify a clinically severe apoplexy subtype. Full article

Introduction: Compassion is defined as the emotional response that arises when an individual perceives another’s suffering and is motivated to alleviate it. Purpose: To explore levels of self-compassion among nurses working in pediatric hospitals and examine their associations with nurses’ characteristics. Materials and Methods: This cross-sectional study included a convenience sample of 208 nurses from a public pediatric hospital. Data were collected through interviews using the Neff Self-Compassion Scale (SCS) which includes the following subscales: Self-Kindness, Common Humanity, Mindfulness, Self-Judgment, Isolation, and Over-Identification. The Greek-validated version of the instrument was used with acceptable internal consistency in the present sample (Cronbach’s alpha = 0.849). Data analysis included descriptive statistics and inferential tests (non-parametric comparisons and multiple linear regression), with statistical significance defined as p < 0.05. Results: The mean total Self-Compassion score was 83.24 ± 12.6 (range: 26–130). Regarding family-related factors, total Self-Compassion (p = 0.029), Common Humanity (p = 0.033), and Over-Identification (p = 0.041) were associated with the number of children. In relation to age, Self-Kindness (p = 0.033), Isolation (p = 0.005), and Over-Identification (p = 0.005) showed significant associations. Professional factors were also relevant, as Isolation was associated with total years of nursing experience (p = 0.032) and choice of nursing as a profession (p = 0.004), while Over-Identification was associated with years of experience in pediatric settings (p = 0.004) and choice of nursing as a profession (p = 0.049). Additionally, marital status was associated with Over-Identification (p = 0.045). Conclusions: Demographic and professional characteristics appear to influence the expression of Self-compassion. Healthcare organizations should implement targeted training programs to individualize professional development. Future research should explore work-related and personal factors influencing self-compassion to improve care quality and outcomes. Full article

This paper addresses a human resource allocation problem with spatial-temporal constraints (HRAP-SC) in the parallel assembly of complex products, such as satellites and aircraft. It involves coordinating a limited pool of multi-skilled workers across geographically distributed workstations, subject to rigorous constraints including team collaboration requirements, operation priorities, technological tail times (e.g., curing), and strict 8 h workdays. Existing exact approaches typically fail to converge due to the combinatorial explosion arising from the strong coupling of shared resources across workstations, while meta-heuristic methods often suffer from performance instability caused by hyper-parameter sensitivity. To overcome these limitations, we propose a pattern-based decomposition algorithm (PDA), a novel parameter-free exact solution framework. By exploiting the inherent symmetry of identical jobs and parallel workstations, PDA defines a set of canonical patterns to drastically reduce the search space. It employs an efficient traversal mechanism reinforced by rigorous mathematical bounds and pruning rules to eliminate unpromising solutions. Computational experiments demonstrate that PDA significantly outperforms state-of-the-art Mixed-Integer Programming (MIP) and Constraint Programming (CP) solvers. Unlike standard solvers, which frequently time out (3600 s), PDA strictly evaluates only a single pattern when proving optimality, and robustly scales to large industrial instances (e.g., six jobs comprising 78 operations) to provide high-quality schedules. By successfully solving complex scheduling problems that remain intractable for monolithic solvers, PDA provides a robust and automated decision-support tool for production management in complex manufacturing systems. Full article

Background/Objectives: Immune checkpoints are critical regulatory pathways that maintain peripheral tolerance and prevent autoimmunity. Among these, the programmed death-1/programmed death-ligand 1 (PD-1/PD-L1) axis serves as a major inhibitory pathway that terminates T cell responses. While protein-based checkpoint blockade (ICB) targeting this axis has revolutionized clinical cancer therapy, its clinical efficacy is frequently limited by low response rates, immune-related adverse events (irAEs), and the emergence of adaptive resistance. To break through these bottlenecks, genetic interruption has emerged as a high-precision alternative to modulate the PD-1/PD-L1 pathway at the nucleotide level. Methods: A comprehensive systematic review of literature was performed across major databases (PubMed, Web of Science), with a focus on high quality studies published up to 2026. Results: Direct genomic disruption via CRISPR/Cas9 and post-transcriptional silencing through RNA interference can effectively neutralize inhibitory signaling at its source. Recent advances demonstrate that targeting upstream regulatory nodes—including metabolic checkpoints (e.g., lactate metabolism) and biophysical mechanisms (e.g., liquid–liquid phase separation)—provides superior transcriptional control over PD-L1. Furthermore, engineering CAR-T cells with multiplex gene editing (e.g., TCR/B2M/PD-1 knockout) or localized scFv secretion significantly enhances antitumor potency while reducing systemic toxicity. Innovations in organ-targeted lipid nanoparticles and stimuli-responsive biomimetic carriers further address the delivery barriers in solid tumors. Conclusions: Gene therapy provides a high-precision platform for PD-1/PD-L1 modulation, offering a viable strategy to overcome adaptive resistance. Future clinical application depends on the refinement of safer editing tools, such as base editing, and the standardization of intelligent delivery systems to ensure controllable and scalable cancer immunotherapy. Full article

Traditional dementia care training often falls short in equipping staff with the knowledge and skills needed to improve quality of life for people with dementia. Virtual Reality (VR)-based experiential learning has emerged as a promising approach, enhancing learning outcomes and training experience for individuals receiving education and training related to dementia care. This scoping review mapped VR education tools used in dementia care, the UX-related measurement methods employed, and the extent to which UX design has been integrated into these tools. Guided by Arksey and O’Malley’s framework, a systematic search was conducted across seven databases (Scopus, Web of Science, ProQuest, MEDLINE, CINAHL, IEEE Xplore, PubMed). PRISMA ScR guidelines were used to map gaps in UX design and engagement strategies within VR learning systems. Data were extracted using a comprehensive UX framework for immersive VR to synthesize user experience components. Twenty-four peer-reviewed publications were included, covering VR scenario development and UX. The findings suggest potential benefits of integrating UX principles into VR education tools to support training experience, learner satisfaction, and care quality. A key gap was identified: limited and inconsistent integration of UX design components and measurement methods within existing VR tools. Drawing on these insights, the review provides practical guidance for optimizing VR training programs in dementia care. Full article

Background/Aims: The increasing complexity of disasters requires effective integration of nurses into Civil Defense (CD) systems. Despite their crucial role, the competencies needed to operate within these multi-agency frameworks remain fragmented and insufficiently defined. The main aim of the study was to map nursing competencies for disaster response within the CD context, identifying essential skills, contextual variations, and barriers to application. Methods: A scoping review was conducted following the JBI methodology and reported according to PRISMA-ScR guidelines. Major databases (PubMed, CINAHL, Scopus, Embase) were searched without time limits, resulting in the inclusion of 27 studies published between 2011 and 2025. Results: 12 core competency domains were identified. Clinical care was the most cited competency (70% of studies), followed by communication (63%), leadership (60%), triage (48%), and psychosocial support (48%). The lack of specific training emerged as the primary individual barrier (44%), while the absence of standardized curricula was the leading systemic obstacle (41%). Competency requirements varied significantly based on the hazard type and organizational setting. Conclusions: Disaster nursing is emerging as an essential specialized field in response to the increasing frequency of climate-related events and global conflicts. There is an urgent need to move beyond purely clinical training to integrate “organizational literacy” and psychological resilience, harmonizing educational pathways with national CD policies and competency-based disaster preparedness programs. Full article

Renal-resident macrophages (RMs) are essential regulators of kidney homeostasis and repair, yet the mechanisms governing RM niche regeneration after acute depletion remain poorly defined. To overcome these limitations, we have developed an inducible human CD59- intermedilysin (hCD59-ILY) ablation system, enabling rapid, specific, and reversible depletion of targeted macrophage populations, and subsequent replenishment of RMs, followed by longitudinal scRNA-seq analysis of kidneys at baseline and days 1, 3, and 7 post-ablation. RM ablation triggered a rapid and sustained upregulation of Cx3cl1, predominantly in proximal tubular epithelial cells (PTC1/PTC2), establishing a persistent chemotactic niche signal that coincided with macrophage repopulation. Regenerating RMs transitioned from inflammatory/stress-associated states toward metabolically active and proliferative phenotypes enriched in glycolysis, oxidative phosphorylation, MYC, and cell-cycle programs, with attenuation of canonical inflammatory pathways. Cell–cell communication analysis revealed an early burst of intercellular signaling at day 1, followed by progressive normalization, with fibronectin (Fn1), osteopontin (Spp1), chemokine (Ccl), and amyloid precursor protein (App) axes emerging as key mediators of niche restoration. Transcriptional network analysis identified a conserved regulatory module (Tfe3, Mitf, Hif1a, Myc, Gabpa, Rcor1) coordinating macrophage differentiation and regenerative programming, linking metabolic adaptation to lineage reconstitution. Sub-clustering revealed five dynamically shifting RM subsets with distinct inflammatory, remodeling, proliferative, and surveillance states, reflecting a hierarchical regeneration process. Functional validation using clodronate-mediated depletion in Secreted Phosphoprotein 1 (Spp1) (Opn)-deficient mice demonstrated impaired macrophage repopulation, establishing osteopontin as a critical regulator of RM regeneration. Together, these data define a coordinated epithelial–immune circuit in which Cx3cl1-driven chemotaxis, Spp1-dependent signaling, and a core transcriptional network orchestrate macrophage niche reconstitution and kidney repair following acute immune cell ablation. Full article

Background: Multiple sclerosis (MS) is a condition that requires long-term, multidisciplinary management. The growing digital transformation in healthcare has highlighted the central role of nurses in supporting key aspects such as patient self-management, continuity of (at home) care, and patient empowerment. However, evidence on nurse-led digital interventions in MS remains fragmented. Objective: To map the available literature on nurse-led digital interventions in MS, focusing on the role of nurses, clinical outcomes, and research gaps. Methods: The review was conducted using the methodological framework of the Joanna Briggs Institute (JBI) and the PRISMA-ScR checklist. A systematic search was performed in PubMed, Scopus, Web of Science, and CINAHL. Studies were included if they described digital or telehealth interventions led or coordinated by nurses in patients with MS. Results: A total of 12 studies published between 2015 and 2025 met the inclusion criteria. Four main thematic areas were identified: (1) telenursing and empowerment-based interventions; (2) mobile and web-based patient self-management programs; (3) digital systems for monitoring and integrated care pathways; and (4) digital interventions targeting symptom management and psychosocial outcomes. Across the studies, nurse-led digital interventions were associated with improvements in self-management, treatment adherence, self-efficacy, and health-promoting behaviors. Positive effects were also reported on clinical outcomes such as fatigue, sleep quality, and balance, as well as on psychosocial variables including quality of life, coping strategies, and emotional well-being. Furthermore, the identified systems, in general, contributed to enhanced continuity of care, patient engagement, and organizational efficiency. Conclusions: Nurse-led digital interventions represent a promising approach in the management of patients with multiple sclerosis, supporting both clinical and psychosocial outcomes while enhancing continuity of care. However, the current evidence base remains limited by small sample sizes, heterogeneity of interventions, and short follow-up periods. Future research should prioritize multicenter randomized studies with larger samples and long-term follow-up to strengthen the evidence. Additionally, the integration of digital interventions into routine clinical practice, along with targeted training for nurses, is essential to ensure sustainability, accessibility, and equitable implementation. Further studies should also explore cost-effectiveness and the impact on caregivers and long-term quality of life. Full article

Osteoarthritis (OA) and major depressive disorder (MDD) share inflammatory and oxidative stress pathways, but the role of programmed cell death (PCD) in their comorbidity remains unclear. This study used independent OA synovial and MDD peripheral blood transcriptomic datasets—not a unified comorbid discovery cohort—to identify candidate PCD-related molecular signatures commonly dysregulated in both conditions. Transcriptomic data from OA synovium and MDD brain tissues were obtained from GEO (six training [three OA synovial and three MDD peripheral-blood], seven validation, and two single-cell RNA-seq datasets). Differentially expressed genes (DEGs) were identified, and PCD-related DEGs were screened. Machine learning (LASSO, SVM-RFE, Random Forest) was used to identify hub PCD-DEGs from the OA training set. WGCNA identified MDD-associated modules for comorbidity-gene selection. Functional enrichment, immune infiltration, scRNA-seq localization, and clinical validation (qRT-PCR/WB) were performed. From the OA cohort, four hub PCD-DEGs (CDKN1A, CX3CR1, INHBB, RHOB) showed moderate diagnostic value for OA (nomogram AUC = 0.82). Eight candidate genes (VAMP8, PDK4, P2RX4, ITM2C, IL10RA, HSP90AA1, CTSO, CRIP1) were commonly dysregulated across both OA and MDD datasets. Immune infiltration revealed upregulated B memory cells, plasma cells, Tregs, and neutrophils in OA, and neutrophils in MDD. scRNA-seq localized CDKN1A/RHOB to OA synovial cells and HSP90AA1/ITM2C to MDD neurons. Enrichment analyses highlighted TNF signaling, apoptosis, and stress responses in both diseases. An independent OA–MDD clinical cohort confirmed differential expression of CDKN1A, RHOB, ITM2C, and HSP90AA1. This study identifies four PCD-related hub genes associated with OA and eight candidate comorbidity genes showing common dysregulation across OA and MDD datasets and in an independent clinical cohort. These findings generate hypotheses about shared inflammatory pathways linking OA and MDD. As these associations derive from independent disease-specific cohorts rather than a true comorbid discovery cohort, they represent candidate signatures requiring functional validation rather than established mechanisms. Full article

The tumor microenvironment of breast cancer presents high complexity and resistance to conventional therapies. Ferroptosis, a programed cell death that is dependent on iron and characterized by lipid peroxidation, arises as a promising therapeutic goal. This scoping review mapped evidence on the exogenous use of iron and selenium, in conventional or nano-particulated forms, in the modulation of ferroptosis as therapeutic strategy for breast cancer treatment, identifying knowledge gaps and opportunities for future research. We performed a scoping review and the methodology followed the guidelines of the Joanna Briggs Institute (JBI) and PRISMA-ScR. We made a systematic search in five data bases (Embase, Lilacs, PubMed (MEDLINE), Scopus, and Web of Science) between the years 2012 and 2025. Among 2.723 identified publications, we selected 48 studies. The results revealed predominance of nanoplatforms of iron (97.9%), focused on the Fenton reaction. The modulation of selenium for inactivation of GPX4 was shown to be effective, though still little-explored (n = 1). We evidenced that the induction of ferroptosis potentializes tumor immunogenicity and the effectiveness of combined therapies. We conclude that the field is under development; thus, the diversification of metabolic targets and trials of chronic toxicity are fundamental steps for future clinical research. Full article

Alzheimer’s Disease (AD), the most common form of dementia, is pathologically defined by extracellular beta-amyloid (Aβ) plaques and intraneuronal neurofibrillary tangles (NFTs), accompanied by chronic neuroinflammation. Recent advances in single-cell RNA sequencing (scRNA-seq/snRNA-seq) and spatial transcriptomics have provided unprecedented resolution for unraveling the cellular and molecular landscape of neuroinflammation in AD. While scRNA-seq enables high-throughput profiling of cellular heterogeneity across brain regions, spatial transcriptomics preserves tissue architecture to map cell-type-specific gene expression within its anatomical context. This review synthesizes the neuroinflammatory mechanisms of AD, outlines the technical evolution and comparative capabilities of single-cell and spatial omics platforms, including resolution, throughput, and compatibility with multiple sample types, and critically evaluates findings from studies in both animal models and human brain tissues. These approaches have revealed state-specific transitions in microglia and astrocytes, including shifts in transcriptional programs, metabolic reprogramming, and pro-inflammatory polarization across disease stages. Notably, spatial transcriptomic analyses demonstrate pronounced regional heterogeneity: periplaque microenvironments exhibit distinct immune-cell compositions and gene expression signatures. Collectively, these omics technologies are redefining the cellular basis of AD progression and hold the potential to impact the discovery of early diagnostic biomarkers and precision therapeutic targets. Full article

Oligodendrocytes (OLs) are specialized glial cells essential for the formation and maintenance of the myelin sheath within the central nervous system (CNS). Historically, OLs were considered a functionally homogeneous population. However, the advent and widespread application of single-cell and single-nucleus RNA sequencing (scRNA-seq/snRNA-seq) technologies since 2015 have revealed substantial transcriptional heterogeneity, varying according to developmental stage, anatomical region, and disease state. In this review, we synthesized current advances in the understanding of OL heterogeneity. Nine OL cell classes have been identified in the mouse somatosensory cortex and hippocampal CA1 region, later expanding to 13 distinct subpopulations across ten CNS regions. Furthermore, we characterized disease-associated oligodendrocytes (DAOs)/disease-associated oligodendrocyte lineages (DOLs), identified in various neurological diseases, including multiple sclerosis (MS), Alzheimer’s disease (AD), and spinal cord injury, focusing on their molecular markers, spatial distribution, and pathophysiological roles. We summarized key transcriptional regulatory networks underlying DAO induction, including the signal transducer and activator of transcription (STAT)/interferon regulatory factor (IRF) family, the Yin Yang 1 (YY1)/nuclear factor kappa B (NF-κB) axis, and the SOX9/SOX10 regulatory system. The utility of region-specific brain analyses using spatial transcriptomics (ST) in conjunction with these approaches was also discussed. Finally, we compiled the implications of patient stratification according to white matter glial response patterns derived from large-scale snRNA-seq analyses of patients with progressive MS. Our synthesis shows that oligodendrocytes consist of multiple distinct subtypes that vary across development, brain regions, and disease conditions. In pathological states, they adopt specific disease-associated programs that reflect context-dependent responses and may influence disease progression and repair. This work provides a framework for understanding how oligodendrocyte diversity contributes to neurological disease and may support the development of targeted remyelination therapies. Full article

Background: Emerging evidence suggests that metabolic, nutritional, and lifestyle-related factors may be associated with tinnitus occurrence and symptom burden. Nutritional status, obesity, and sedentary behavior have been hypothesized to be linked with auditory function, neural excitability, and tinnitus-related outcomes. This scoping review aimed to map and summarize the available evidence on associations between dietary factors, nutrient intake, body mass index (BMI), obesity, physical activity, and tinnitus occurrence, severity, and related clinical outcomes. Methods: A scoping review was conducted in accordance with the PRISMA-ScR reporting guidelines. A comprehensive search of PubMed, Web of Science, and Cochrane Library databases was performed. Eligible designs included randomized controlled trials, cohort studies, case–control studies, and cross-sectional studies. Data were extracted and synthesized narratively due to methodological heterogeneity. Results: Twenty-four studies met the inclusion criteria. Several observational studies reported associations between protein intake, lipid profile, micronutrient status, BMI, obesity, physical activity, and tinnitus-related outcomes. Evidence on antioxidant supplementation was heterogeneous, with some trials reporting favorable changes in tinnitus-related measures and others showing no significant benefit compared with placebo. Elevated BMI, obesity, and altered body composition were generally associated with tinnitus occurrence or greater symptom severity. Randomized trials suggested that structured lifestyle programs involving dietary modification, weight reduction, and physical activity may be associated with improvements in tinnitus severity and quality of life in selected patient groups. Conclusions: The available literature suggests potential associations between nutritional, metabolic, and lifestyle-related factors and tinnitus occurrence or symptom severity. However, the evidence is heterogeneous and largely observational, with inconsistent adjustment for hearing loss, psychological distress, and general health status. Further well-designed prospective studies and randomized controlled trials are needed before causal or clinical recommendations can be formulated. Full article

Background/Objectives: Immune-inflammatory activation is a central feature of aneurysmal subarachnoid hemorrhage (aSAH), yet the epitranscriptomic mechanisms underlying this response remain insufficiently understood. This study aimed to investigate RNA methylation-associated immune dysregulation in aSAH and to identify potential biomarkers and signaling pathways. Methods: Four Gene Expression Omnibus datasets were analyzed to characterize RNA methylation regulator-related immune alterations in aSAH. Single-sample gene set enrichment analysis (ssGSEA), weighted gene co-expression network analysis (WGCNA), and intersection with ImmPort immune genes were used to identify candidate genes. A total of 159 machine learning combinations were evaluated for model construction and external validation. Two-sample Mendelian randomization, single-cell RNA sequencing (scRNA-seq), and CellChat analyses were further performed. Peripheral blood samples from patients with aSAH (n = 12) and matched healthy controls (n = 12) were used for total m6A quantification and quantitative real-time PCR (qRT-PCR) validation, while Western blotting and immunofluorescence were used to validate the protein expression of LIFR, GP130, IGF2BP2, and RBM15B. Results: Eleven RNA methylation regulators were differentially expressed between aSAH and controls in GSE122897. The WGCNA module most strongly associated with RNA methylation regulator-related scores was enriched in immune response and myeloid activation pathways. Intersection analysis identified 25 candidate immune-inflammatory genes associated with RNA methylation regulator-related transcriptional patterns. Among 159 algorithms, an XGBoost-LASSO pipeline selected oncostatin M (OSM) as the key variable, and the resulting RNA methylation regulator-related immune-derived gene signature (RMRIGS) showed good discrimination between aSAH and controls across training and validation cohorts. Mendelian randomization supported a protective association of genetically predicted OSM expression with subarachnoid hemorrhage risk (IVW OR = 0.66, p = 0.014). Single-cell analysis showed that Osm was predominantly enriched in infiltrating Ccr2+ macrophages, whereas Lifr and Il6st were broadly expressed in activated microglial subpopulations, indicating the presence of an Osm − (Lifr + Il6st) communication axis after SAH. Clinically, total m6A levels were increased in peripheral blood samples from patients with aSAH, and OSM, together with several RNA methylation regulators, was upregulated and associated with m6A-related changes. In experimental models, the protein expression levels of LIFR, GP130, IGF2BP2, and RBM15B were all increased after SAH-related stimulation. Conclusions: RNA methylation programs may be involved in immune dysregulation in aSAH. The OSM-centered RMRIGS was associated with disease status and may provide insight into the interaction between peripheral immune activation and post-SAH neuroinflammation. The potential involvement of the OSM–LIFR/GP130 signaling axis and its association with RNA methylation regulator-related alterations warrant further investigation. Full article