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In this report, morphological and molecular characteristics are provided for two members of the subfamily Microphalloidea distributed in the south of the Russian Far East. Some of trematode specimens found in larvae of mayflies, stoneflies, and caddisflies and then experimentally reared to the adult stage in hamsters, according to their morphological features, belong to the species Acanthatrium ovatum previously recorded from Japanese bats. Molecular data has confirmed their membership in the family Lecithodendriidae and similarity to trematodes identified as Lecithodendriidae sp. F from Japan. The other specimens, experimentally reared in chickens, according to their morphological characteristics, meet the diagnostic criteria of the genus Parabascus. However, this species is not clustered with representatives of this taxon in the phylogenetic reconstruction based on 28S rRNA gene data. A molecular analysis has shown that it forms a single cluster with Pachypsolus irroratus and is a member of the family Pachypsolidae. It is here placed in the new genus Pseudoparabascus n. g. under the name Pseudoparabascus khotenovskii comb. n. The phylogenetic reconstructions based on two other markers, the cox1 mtDNA gene and the ITS2 rDNA region, have confirmed the assignment of these specimens obtained in both experiments to the above-considered taxonomic groups.

Background/Objectives: To evaluate the Risk Factor-Weighted Clinical Likelihood (RF-CL) model for the diagnosis of chronic coronary syndrome (CCS) in men and women. Methods: The study included 222 patients (100 men and 122 women; mean age 64.76 &#xb1; 10.3 years) with suspected CCS. Diagnostic evaluation was performed in accordance with the 2024 clinical practice guidelines for stable coronary artery disease developed by the Russian Society of Cardiology. The clinical probability of obstructive coronary artery disease (CAD) was calculated for all patients using the RF-CL model. Results: Application of the RF-CL model demonstrated higher probabilities in men than in women (17% [11-27] vs. 6% [4,5,6,7,8,9,10], p < 0.001). Moderate CCS probability (RF-CL > 15-50%) was observed in 64% of men and 9.8% of women (p < 0.001); low probability (RF-CL > 5-15%) in 30% and 60.7% (p < 0.001); very low (RF-CL &#x2264; 5%) in 6% and 29.5% (p < 0.001). The prevalence of typical angina (21% vs. 17.2%, p = 0.47), atypical angina (31% vs. 26.2%, p = 0.43), and non-anginal chest pain (31% vs. 26.2%, p = 0.43) did not differ. Dyspnea was less frequent in men (44% vs. 59.8%, p = 0.02). Only 35 (15.8%) patients had indications for invasive coronary angiography (ICA), and significant stenosis (&#x2265;70%) was found in 17 patients. According to the ROC analysis, the cutoff value of RF-CL for predicting a positive stress test was 19.5% in men (AUC 0.723; p = 0.002), 6.5% in women (AUC 0.479; p = 0.852), and 15% in the overall cohort (AUC 0.737; p < 0.0001). Conclusions: Men with moderate and women with low probability of obstructive CAD are predominantly encountered in clinical practice when the RF-CL model is applied. Our observations have shown that ICA is indicated in relatively few patients and suggest potential overuse of exercise testing regardless of the clinicians' adherence to the traditional Diamond-Forrester model or the RF-CL algorithm in suspected CCS.

Bovine leukemia virus (BLV) is an oncogenic retrovirus and the etiological agent of enzootic bovine leukosis (EBL), which is spread worldwide. This study presents data on the genetic diversity of BLV in the Novosibirsk region of Russia. ELISA-positive samples were selected from six districts of the Novosibirsk region (Dovolnoye, Barabinsk, Tatarsk, Toguchin, Bolotnoye, and Kochenyovo districts). To assess the diversity of circulating BLV genotypes, samples were collected from settlements and districts that were geographically distant from each other and had no shared pasture lands. In total, 1410 bp fragments encoding the env gene region were obtained from 417 BLV-positive samples. Phylogenetic analysis classified 325 BLV strains (77.9%) as genotype 4 (G4) and 92 strains (22.1%) as genotype 7 (G7). A pairwise identity matrix was constructed for 268 amino acid residues. Pairwise identity of BLV amino acid sequences in the gp51 region ranged from 96.6% to 100% for G4 and from 97.4% to 100% for G7. Multiple alignment of the amino acid sequences identified 74 mutations found in the Russian BLV variants. Through the addition of 417 novel env BLV sequences to GenBank, this study significantly expands the foundational data and knowledge of BLV molecular epidemiology in Russia.

Background/Objectives: Variants of MYPN, encoding a sarcomeric protein myopalladin, are associated with different types of cardiomyopathies and myopathies. However, the molecular mechanisms of MYPN-associated pathologies are still poorly understood. Methods: In this study, we generated induced pluripotent stem cells (iPSCs) from a hypertrophic cardiomyopathy patient carrying a novel p.N989I (c.2966A>T) variant of MYPN and used iPSC-derived cardiomyocytes to examine the impact of the variant on biophysical characteristics and transcriptomic profile. Results: No significant changes in parameters of calcium transients, sodium current and action potential were found in iPSC-derived cardiomyocytes with the p.N989I (c.2966A>T) variant of MYPN compared to non-isogenic cells from an unrelated healthy donor. At the transcriptomic level, MYPN-N989I cardiomyocytes demonstrated an upregulation of genes linked to cell cycle, mitotic spindle, microtubule cytoskeleton organization, and myogenic program genes. Downregulation of sarcomeric, Z-disc- and cell junction-associated genes, as well as genes involved in ATP synthesis, oxidative phosphorylation, and the SRF-signaling pathway, was also revealed. Conclusions: Our data suggest that the p.N989I (c.2966A>T) variant of MYPN plays a dual role in hypertrophic cardiomyopathy pathogenesis, disrupting not only sarcomeric and cytoskeletal organization but also the regulation of the muscle gene program.

Leading medical centers are currently considering pulsed electromagnetic therapy as a promising approach to prolong active life. The aim of this study was to investigate the effects of non-ionizing electromagnetic fields on mitochondrial activity and the state of the lipid peroxidation system, an antioxidant protection system in mice. The studies were carried out on 60 BALB/c mice in accordance with bioethical standards and general ethical principles of animal experimentation. The animals were divided into 5 groups. The groups were placed in different rooms, standing at a considerable distance from each other. Experimental animals were exposed to non-invasive electromagnetic therapy device "TOR". The mitochondrial activity of thymocytes and the total antioxidant potential of the blood plasma were analyzed in all animals. The study showed that weak non-ionizing non-thermal broadband pulsed electromagnetic fields (EMF) increased the antioxidant potential of mouse blood: at minimum exposure (1 min/h/10 nights) by almost 8% (p > 0.05), at maximum (5 min/h/10 nights) - by 20.6% (p< 0.05) - compared to the negative control group (young animals not exposed to EMF). The experiment confirms the dose-dependent stimulating effect of EMF on the mitochondria of thymocytes; at maximum exposure, the changes become statistically significant (increase in mitochondrial fluorescence by 29% compared to the negative control group, p< 0.05). The biological effects of non-ionizing electromagnetic fields are diverse. Due to their high penetrating power, they are able to affect deep-seated organs and tissues, thereby opening up new approaches in medicine and regenerative therapy that are cost-effective for patients and elicit cellular responses similar to physical exercise.

Objective: This umbrella review synthesizes and critically appraises the evidence on the efficacy and safety of tegoprazan-based versus proton pump inhibitor (PPI)-based regimens for Helicobacter pylori (H. pylori) eradication. Methods: This umbrella review was pre-registered in PROSPERO (CRD420251271120). Systematic reviews and meta-analyses published between 1 January 2018 and 10 December 2025 were identified through MEDLINE/PubMed, EMBASE, and the Cochrane Library. Reviews comparing tegoprazan-based and PPI-based eradication regimens in adult patients were included. Methodological quality was assessed using AMSTAR-2, risk of bias with ROBIS, and certainty of evidence with GRADE. Pooled relative risks (RRs) were calculated, with subgroup analyses by study design, treatment duration, and therapeutic regimen. Results: Eight systematic reviews and meta-analyses encompassing 17 primary studies and 12,714 participants were included. Tegoprazan-based regimens were associated with a statistically significant improvement in eradication efficacy compared with PPI-based therapies (RR = 1.019; 95% CI: 1.003-1.035; p = 0.021). In randomized controlled trials, the benefit was more pronounced (RR = 1.037; 95% CI: 1.015-1.061; p = 0.001), whereas no statistically significant benefit was observed in non-randomized studies (RR = 1.014; 95% CI: 0.991-1.037; p = 0.235). The efficacy advantage was mainly confined to quadruple therapy regimens (RR = 1.044; 95% CI: 1.002-1.088; p = 0.038). Tegoprazan-based regimens were associated with a lower incidence of overall adverse events compared with the PPI group (RR = 0.930; 95% CI: 0.885-0.976; p = 0.003). Conclusions: Tegoprazan-containing regimens were associated with a modest but statistically significant improvement in H. pylori eradication compared with PPI-containing regimens, particularly in randomized controlled trials and quadruple therapy regimens.

Background/Objectives: Diffuse large B-cell lymphoma (DLBCL) is molecularly heterogeneous, and approximately 30-50% of patients fail to achieve cure with standard R-CHOP. Genotype-directed first-line therapy may improve outcomes by targeting subtype-specific oncogenic pathways. This study evaluated the feasibility, efficacy, and safety of a molecularly adapted R-CHOP-X strategy with two-year follow-up. Methods: In this single-center, prospective, non-randomized study conducted between September 2023 and the data cut-off (16 September 2025), 43 adults with newly diagnosed DLBCL (excluding high-grade B-cell lymphoma, primary immune-privileged, and primary mediastinal large B-cell lymphomas) underwent tumor genotyping using the LymphGen classification after targeted sequencing: a 19-gene Sanger panel (Cohort 1, n = 35) or an expanded 60-gene panel (Cohort 2, n = 8; proof-of-concept). All patients received one initial cycle of R-CHOP as bridge therapy pending molecular profiling results, followed by five cycles of R-CHOP-X, with the additional agent (vorinostat, acalabrutinib, decitabine, or lenalidomide) selected according to molecular subtype. Response was assessed by PET/CT per Lugano criteria; adverse events were graded per NCI CTCAE v5.0. Results: The overall study population was predominantly high-risk: 72% had an IPI of 3-5, 58% had stage III-IV disease, and 67% exhibited a non-GCB immunophenotype. Expansion from the 19-gene to the 60-gene panel reduced unclassifiable (NOS) cases from 34% to 12%. The overall response rate was 100% (43/43); complete response among patients completing therapy was 100% (35/35). At two years, overall survival was 92% (95% CI 83-100%) and progression-free survival was 94% (95% CI 86-100%). Two early relapses occurred (NOS and N1 subtypes), both resulting in death. Grade 3-4 neutropenia, thrombocytopenia, and anemia occurred in 26%, 12%, and 7% of patients, respectively; no dose reductions or treatment discontinuations were recorded. Conclusions: Molecularly adapted R-CHOP-X is feasible and associated with high response rates and favorable two-year survival in newly diagnosed DLBCL, comparing favorably with historical R-CHOP outcomes in high-risk populations. Expanded genomic panels substantially improve molecular classifiability. These findings warrant validation in larger, multicenter, randomized clinical trials.

Pompe disease (PD) is a neuromuscular autosomal recessive disorder caused by mutation in the GAA gene, which encodes acid &#x3b1;-glucosidase (GAA), an enzyme responsible for hydrolyzing glycogen to glucose. Deficiency of this enzyme leads to pathological accumulation of glycogen in almost all tissues of the body, with the most pronounced effects in cardiac and skeletal muscle, as well as in the central nervous system. Two major clinical forms of PD are recognized: infantile-onset PD, characterized by almost complete absence of GAA activity and severe cardiomyopathy and neurological abnormalities, and late-onset PD, which primarily presents with impairment of respiratory and motor function. Since 2006, enzyme replacement therapy with recombinant GAA has been used to treat PD, improving survival and quality of life. However, this approach has several limitations: the need for lifelong infusions, the risk of immune responses, and the inability of the enzyme to cross the blood-brain barrier, which is particularly critical for infantile-onset PD. Consequently, alternative strategies are being developed, including gene therapy using adeno-associated virus vectors for GAA delivery to target tissues; these approaches are currently in phase I/II clinical trials. Transplantation of genetically modified hematopoietic stem cells also represents a promising therapeutic strategy, offering a single-intervention treatment with long-lasting effects. This review discusses the molecular mechanisms of PD, current and emerging disease models, and therapeutic approaches, which together open prospects for the development of potentially one-time curative treatments, despite persistent challenges such as immunogenicity and the need for long-term efficacy monitoring.

Alzheimer's disease (AD) remains an incurable neurodegenerative disorder. The concept of theranostics-combining diagnostic and therapeutic functions within a single nanoplatform-has been explored for over a decade. Despite a growing number of publications, no theranostic system has yet reached clinical application for AD. This critical review analyzes the fundamental conceptual contradictions that hinder the clinical translation of theranostic nanoplatforms for AD and identifies alternative strategies where nanotechnology may still be beneficial. The review presents key aspects essential for understanding theranostics challenges: AD molecular targets, analysis of existing nanoplatforms, identification of three inherent conceptual conflicts, and viable alternative approaches. Our analysis reveals three core conceptual conflicts: the pharmacokinetic conflict, where diagnostics demand rapid accumulation and clearance while therapy requires prolonged retention-exacerbated by minimal brain delivery (1-2% ID/g) and peripheral toxicity risks; the dose conflict, characterized by orders-of-magnitude disparities between diagnostic and therapeutic dosing, rarely quantified for identical particles; and the temporal conflict, pitting one-time diagnostics against chronic therapy needs, as long-persisting particles generate irremovable brain background signals. We further identify a pervasive methodological trap: predominant focus on mature &#x3b2;-amyloid (A&#x3b2;) fibrils overlooks soluble oligomers as the primary toxic species. We conclude by proposing viable alternatives: preclinical intervention for time-limited "hit-and-clear" applications; coordinated theranostic monitoring with separate diagnostics/therapy; theranostic pairs using ligand-matched, function-optimized particles; and external stimuli for temporal function separation. A practical roadmap guides the transition from conceptual demonstrations to clinical translation. Addressing these contradictions can transform theranostics from elegant chemical constructs into clinically meaningful AD tools.

Long non-coding RNAs (lncRNAs) interact with chromatin and recruit epigenetic complexes to specific genomic loci, yet their relationship with super-enhancers (SEs), key regulatory elements frequently reprogrammed in cancer, remains unexplored. We developed an integrative pipeline that combines RNA-chromatin contact data (RNA-Chrom), histone modification-lncRNA expression correlation profiles (HiMoRNA peaks), and super-enhancer annotations (SEdb 3.0) to map lncRNA-SE regulatory axes. Applying this framework to SNHG1 in HCT116 colorectal cancer cells, we identified 21 SNHG1-reactive super-enhancers (&#x3a8;-SEs) among 184 cancer-specific SEs, at which SNHG1 physical contacts co-occur with SNHG1-correlated histone modifications (HiMoRNA peaks), predominantly H3K4me1 (permutation p = 0.001, fold enrichment = 2.03). Comparison with 4145 lncRNAs demonstrated that epigenetic correlations alone do not distinguish SNHG1; instead, the addition of the contact layer is required to delineate the &#x3a8;-SE set. Differential expression (DESeq2) and co-expression analyses in 471 TCGA-COAD tumor samples identified 12 &#x3a8;-SE target genes (including CDC20, PDP1, and TOP1) consistently upregulated in both HCT116 cells and patient tumors and positively correlated with SNHG1, with the co-expression signal robust to tumor purity correction. The proposed &#x3a8;/&#x3a9; classification provides a generalizable framework for prioritizing super-enhancers at which lncRNA-chromatin interactions may shape the local epigenetic environment across cancer types.

Aquaculture is developing in many countries to meet the rising protein demand associated with a rapidly growing human population. However, intensification of production brings with it challenges such as deteriorating water quality and increasing disease outbreaks. These conditions lead to an increased risk of infectious diseases and led to higher mortality rates, which causes economic losses. Lactococcosis, particularly that caused by the Gram-positive bacterium Lactococcus garvieae, is one of the most common of these problems and can cause significant losses in various fish species. The intensive use of antibiotics for control purposes creates additional risks in terms of antimicrobial resistance, environmental pollution, and food safety. Therefore, natural feed additives have gained importance in recent years. Certain additives that support immune responses and increase disease resistance in fish have become prominent. Among these, phytobiotics, probiotics, prebiotics, and synbiotics are the most well-known and effective. Their widespread availability, lower cost, and environmental safety make these additives considered an alternative approach to aquaculture. Studies show that these additives strengthen both innate and adaptive immune responses, reduce infection severity, and reduce mortality associated with L. garvieae infections. However, there are still gaps in knowledge regarding how these substances regulate mechanisms such as the immune system, inflammatory processes, antioxidant defenses, and interactions with pathogens. This review aims to clarify these mechanisms by bringing together scientific data obtained in recent years. It also discusses how the information obtained can contribute to the development of safer feed additive strategies and the development of new vaccine approaches. This aims to support the establishment of a more sustainable production structure in the aquaculture sector.

The fabrication of semiconductor devices using submicron- and nanometer-scale silicon structures is based on lithography (patterning on a substrate) and etching (transferring a pattern onto the substrate) technologies. These processes typically require complex and expensive equipment, as well as extensive experimental optimization of etching parameters, especially for structures with an aspect ratio greater than 10. This work demonstrates a productive and relatively simple approach for fabricating an ordered array of vertically oriented monolithic silicon tubes with high-aspect-ratio internal cavities. The creation of these structures is based on Langmuir-Blodgett colloidal lithography, vacuum magnetron sputtering, and a continuous plasma etching process performed at "room" temperature of the substrate holder. To develop the fabrication process for high-aspect-ratio (>10) structures, we employed Bayesian optimization (a machine learning method), which proved highly efficient in reducing the number of experiments compared to a full factorial analysis. The resulting silicon tubes exhibited an average total reflectance of 3.7% over the 200-1600 nm wavelength range.

The central role of YB-1 in messenger ribonucleoprotein particle (mRNP) metabolism and stress-granule biology highlights the importance of defining the determinants of its self-assembly. YB-1 fibrillogenesis has been attributed primarily to the cold shock domain (CSD). Here, we show that the YB-1 fragment spanning residues 1-129 (AP-CSD) form amyloid fibrils under near-physiological ionic strength (0.12-0.15 M KCl). Fibrillization proceeds without a pronounced exponential growth phase and increases approximately linearly over 45-50 h. Far-UV circular dichroism (CD) and attenuated total reflection Fourier-transform infrared spectroscopy (ATR-FTIR) indicate no substantial change in overall secondary-structure content during aggregation. In parallel, 1H nuclear magnetic resonance (NMR) spectroscopy reveals the depletion of soluble species, and oriented fiber X-ray diffraction displays the hallmark cross-&#x3b2; reflections at approximately 4.7 &#xc5; and 10 &#xc5;. The prolonged formation time implies an activation barrier that is unlikely to require global refolding. Instead, it may reflect early association events such as dimerization or other local rearrangements required for primary nucleation, followed by consolidation into stable intermolecular contacts. Aggregation that preserves a largely native-like fold while establishing cross-&#x3b2; order may reduce recognition by cellular quality-control systems that preferentially target globally unfolded or strongly destabilized states. This provides a plausible framework for how YB-1 derived assemblies could persist under stress and during age-associated proteostasis decline.

Letter recognition is assumed to involve several levels of analysis, including coarse tuning for category and novelty and more fine tuning for specific features, related to letter orientation. We employed an oddball fast periodic visual stimulation (FPVS) paradigm with magnetoencephalography (Elekta VectorView, 306 sensors) to study neural discrimination responses in the source space. Using contrasts between native and foreign letters, digits, or inverted native letters, we aimed to isolate the neural responses to visual novelty, category, and orientation during character analysis. The study was conducted with a cohort of 25 adults. The response topography demonstrated bilateral organization, including language-related brain regions such as the ventral occipitotemporal cortex, inferior parietal cortex, and middle temporal areas. Comparing conditions, we revealed right lateralized parietal clusters, associated with novelty tuning, and left lateralized occipitotemporal clusters exhibiting higher activity for letters among digits discrimination, supporting the role of this area in letter processing. No distinct spatial patterns specific to orientation tuning were observed in comparison to novelty and category tuning. We propose that expertise-dependent orientation-specific tuning mechanisms may operate within an embedded neural framework that spatially overlaps with coarse tuning systems, but are characterized by specific spatiotemporal patterns.

Leucomisine is a major component of renewable plant raw material Artemisia leucodes Schrenk, a sesquiterpene &#x3b3;-lactone exhibiting antioxidant, hypoglycemic, antiparasitic, and hepatoprotective activities. However, the use of leucomisine in pharmaceuticals is limited by its insufficient bioavailability associated with low aqueous solubility. Therefore, the effect of solid-state synthesis based on leucomisine using the methods of "solvent removal", "simple mixing", and "mixture heating", with disodium glycyrrhizinate as a carrier, on the aqueous solubility of leucomisine was investigated. It was established that the synthesized solid dispersions exhibit increased solubility (7-19-fold) and dissolution rate (36-100-fold) of leucomisine released from the carrier. The most pronounced stimulation of the dissolution process was observed for samples obtained using the "simple mixing" method. Based on physicochemical studies (visible-range spectrophotometry, microcrystalloscopy, investigation of optical properties of solutions, and X-Ray phase analysis), it was determined that the enhancement of solubility is attributed to the loss of crystalline state, micronization, and the solubilization process of leucomisine by the carrier, as well as to the formation of a colloidal solution of leucomisine stabilized by disodium glycyrrhizinate.

Sepsis remains a major global health challenge due to its complex pathophysiology and limited therapeutic options. Nanomedicine offers innovative strategies to address these limitations by enabling diverse nanoparticle designs and mechanisms that modulate the septic response. This review examines the dynamic interactions between nanoparticles and the immune system, with a focus on how protein corona formation shapes nanoparticle behavior, biodistribution, and therapeutic efficacy. Disease-specific protein corona profiles can serve as pathology "fingerprints" for diagnosis and targeted delivery, and their controlled formation is now emerging as a therapeutic tool rather than only a diagnostic readout. While the protein corona is a spontaneous biomolecular layer, its composition can be rationally steered to support defined therapeutic goals. In this context, decoy nanoparticles are engineered to sequester pathogens or inflammatory mediators, such as cytokines, histones, and neutrophil extracellular traps, thereby mitigating inflammation and tissue damage. This review discusses how protein corona engineering can potentiate decoy strategies in sepsis diagnosis and therapy, highlighting key platforms including macrophage&#x2011;like nanoparticles that neutralize endotoxins and cytokines, histone&#x2011;binding hydrogels, and mesoporous silica nanoparticles that scavenge cell&#x2011;free DNA and inhibit Toll&#x2011;like receptor activation. We also address how Artificial Intelligence can improve prediction of protein corona dynamics and identification of disease&#x2011;specific protein signatures, enabling more personalized nanodecoy design. Given the highly dynamic and heterogeneous nature of sepsis, characterized by evolving circulating mediators and protein profiles, integrating protein corona control with decoy mechanisms offers a multifaceted route to limit immune dysregulation, enhance drug delivery, and reduce organ damage, paving the way toward precision nanomedicine in sepsis.

Background/Objectives: Glioblastoma multiforme (GBM) is the most infiltrative, treatment-resistant, and deadly brain tumor in adults. Given the extremely malignant phenotype of the GBM cells, the high intratumoral heterogeneity, and the limited efficacy of the vast majority of chemotherapeutics due to the restrictive nature of the blood-brain barrier, GBM remains largely incurable. Methods: Utilizing the U87, U251, and T98G GBM cell lines, diverse in vitro approaches (Western blotting, quantitative real-time PCR, flow cytometry, immunofluorescence, Luc-reporter analysis, microscopic examination, and scanning electron microscopy), and pharmacological inhibition, we investigated for the first time the cell death decisions in the GBM cells in response to the LCS1269 treatment. Results: We showed that LCS1269 collapsed the mitochondrial potential and triggered both intrinsic and extrinsic apoptosis. Importantly, our findings demonstrated that LCS1269-mediated apoptosis was paralleled by an induction of both MLKL-dependent necroptosis and caspase-3/GSDME-dependent pyroptosis. Using a combination of specific inhibitors, we further demonstrated that apoptosis, necroptosis, and pyroptosis provoked by LCS1269 occur simultaneously and orchestrate a peculiar form of programmed cell death, which is known as PANoptosis. We subsequently found that LCS1269-induced PANoptosis may be initiated either through the RIPK1-PANoptosome alone or through the integrated ZBP1-, AIM2-, and RIPK1-PANoptosomes. Additionally, we revealed that LCS1269-mediated PANoptosis may be closely related to micronuclei formation. Conclusions: Taken together, our results confirm that LCS1269 is a promising anti-glioblastoma agent that is capable of effectively promoting GBM cell death via PANoptosis.

[This corrects the article DOI: 10.1007/s12195-026-00888-z.].