Search Results (117)

Background/Objectives: House dust mites (HDMs) are significant allergens that cause damage to nasal epithelial cells and have a role in the pathophysiology of allergic rhinitis. Lactobacillus johnsonii N5 supernatant (N5sup), a probiotic strain, exhibits possible protective properties; nevertheless, the molecular processes involved remain unclear. Methods: RPMI-2650 human nasal epithelial carcinoma cells were subjected to treatment with HDM, N5sup, or a combination of both. Results: The HDM stimulation induced a certain degree of transcriptional alterations. Compared with the control group, a total of 221 differentially expressed genes were identified in HDM-treated cells, which were mainly enriched in the IRE1–XBP1 branch of the unfolded protein response (UPR) pathway. Comprehensive investigation demonstrated that HDM increased the NR4A1–IRE1–XBP1 signaling pathway, characterized by elevated expression levels of NR4A1, ERN1 (IRE1), and XBP1. Both qRT-PCR and Western blotting verified that N5sup strongly inhibited the HDM-induced increase in NR4A1, IRE1, and XBP1. Analysis of the protein–protein interaction network further confirmed a central hub comprising NR4A1, IRE1, and XBP1. Conclusions: N5sup supernatant protects RPMI-2650 cells from HDM-induced injury, and this protective effect is associated with the NR4A1–IRE1–XBP1 pathway. These findings suggest that this signaling axis may serve as a potential therapeutic target for probiotic intervention in allergic airway diseases. Full article

Sweet corn is a globally important dual-purpose crop for both food and fresh vegetables. The plant architecture and ear-related traits directly determine its yield potential and field ecological adaptability. To elucidate the genetic architecture of these traits and identify superior alleles for breeding, we conducted a genome-wide association study (GWAS) on 11 agronomic traits using 30,597 high-quality SNP markers in a panel of 101 elite sweet corn inbred lines. Population genetic structure was analyzed using sparse non-negative matrix factorization (sNMF) and discriminant analysis of principal components (DAPC) algorithms, revealing three main clusters and six subpopulations. The clustering pattern was highly consistent with germplasm origin. Association mapping with the fixed and random Circulating Probability Unification (FarmCPU) model identified 16 significant marker–trait associations (MTAs), distributed across seven target agronomic traits. The phenotypic variance explained (PVE) by individual loci ranged from 8.0% to 16.0%. Among these, five stable MTAs across environments, a novel ERN locus (SNP25518) specific to sweet corn, and most association intervals overlapped with previously reported quantitative trait loci (QTLs). Within the ±0.15 Mb (defined by LD decay) flanking windows around the significant SNP loci, a total of 236 candidate genes were annotated, which are primarily involved in hormone signaling, carbon and nitrogen metabolism, cell division, and plant growth and development. In summary, this study dissected the genetic basis of key agronomic traits in sweet corn and provides a foundation for marker-assisted selection and functional validation. Full article

Background/Objectives: Obesity is associated with alterations in cognitive control processes that support performance monitoring and dietary self-regulation, but the neurocognitive markers most closely tied to body weight status in young adulthood remain unclear. Methods: Sixty-two young adults completed a modified Simon task while continuous electroencephalography (EEG) was recorded. Response-locked event-related potentials (ERPs) were quantified for error-related negativity (ERN) and error positivity (Pe). The association between body mass index (BMI) and ERP amplitudes was examined under three parameterizations: BMI as a continuous variable, BMI split into three categories (normal weight, overweight, obese), and BMI split into two median-matched categories. Results: Higher BMI was associated with reduced (less negative) ERN amplitude under continuous (r = 0.30, p = 0.016, and median-split, Cohen’s d = −0.69, p = 0.009) specifications, and at the level of a trend under the three-group classification F(2, 59) = 2.80, p = 0.069, η²p = 0.09. The association was most consistent for neutral trials, where it reached significance under the continuous (r = 0.32, p = 0.010) and three-group (F = 3.31, p = 0.043) specifications and approached significance under the median-split (d = −0.51, p = 0.051). The BMI-ERN association remained significant after adjustment for age, sex, cardiorespiratory fitness, physical activity, and trait impulsivity. In contrast, Pe amplitude did not differ as a function of BMI under any specification. In exploratory analyses that did not survive correction for multiple comparisons, Pe amplitude was positively associated with mindful eating disinhibition and negatively associated with UPPS-P Positive Urgency, independent of BMI. Conclusions: These cross-sectional findings indicate that elevated adiposity in young adulthood is associated with attenuated pre-conscious conflict and error monitoring (i.e., ERN), whereas conscious error awareness (i.e., Pe) is unrelated to body weight status. The exploratory Pe–trait associations are offered as hypotheses for future confirmatory work rather than as established effects. Full article

Background/Objectives: Obsessive–compulsive disorder (OCD) is associated not only with obsessions and compulsions, but also with cognitive dysfunction involving inhibitory control, cognitive flexibility, working memory, attention, decision-making, feedback learning, and performance monitoring. Electroencephalography (EEG), event-related potentials (ERPs), quantitative EEG, and time–frequency analyses provide temporally precise methods for examining how these cognitive abnormalities unfold during information processing. This review aimed to synthesise electrophysiological evidence on the neural correlates of cognitive dysfunction in OCD. Methods: A systematic literature search was conducted in PubMed/MEDLINE, Scopus, Web of Science Core Collection, Embase, PsycINFO, and Google Scholar from database inception to 30 May 2026. Eligible studies included patients with OCD and used EEG, qEEG, spectral EEG, EEG connectivity, or ERP methods in relation to cognitive performance, cognitive task demands, or cognitive dysfunction. Studies were grouped according to electrophysiological modality and ERP component. Because of methodological heterogeneity, findings were synthesised narratively and mechanistically rather than by meta-analysis. Methodological quality was assessed using ROBINS-I. Results: The search identified 1321 records, of which 42 studies met the inclusion criteria. Most studies used task-based ERP paradigms, while fewer examined resting-state EEG, qEEG, or oscillatory activity. The most consistent findings concerned altered performance monitoring and cognitive control, especially ERN, N2/N200, Pe, Pc, and P3/P300 abnormalities. ERN findings suggested excessive early error monitoring, whereas N2/N200 and P3/P300 findings indicated task-dependent abnormalities in inhibition, conflict processing, attentional allocation, stimulus evaluation, and context updating. Earlier components, including P50, N1/N100, P2/P200, and N450, suggested abnormalities in sensory gating, early attentional selection, stimulus evaluation, and interference control, particularly under emotionally salient or OCD-relevant conditions. FRN findings indicated altered feedback processing and reinforcement learning, while limited P600 evidence suggested inefficient working-memory preparation. Plain EEG and time–frequency studies further implicated abnormal theta, alpha, beta, and delta activity in monitoring, inhibition, arousal, and network efficiency. Conclusions: EEG-based evidence suggests that cognitive dysfunction in OCD reflects a dysregulated control system rather than a general reduction in cognitive ability. The disorder appears to involve excessive performance monitoring, abnormal sensory and attentional gating, inefficient inhibition, altered feedback evaluation, and reduced cognitive flexibility. However, the current evidence is limited by heterogeneity in samples, paradigms, EEG methodology, medication status, and statistical approaches. Future studies should use larger, well-characterised samples, standardised EEG/ERP paradigms, direct brain–behaviour analyses, and longitudinal designs to clarify whether electrophysiological abnormalities represent trait markers, state-dependent effects, compensatory mechanisms, or clinically useful predictors of cognitive dysfunction in OCD. Full article

Objectives: Insomnia is a highly prevalent sleep disorder involving complex neurochem-ical dysregulation; however, the spatial distribution of neurotransmitters and small-molecule metabolites across distinct brain microregions in the insomniac state re-mains poorly characterized. This study aimed to map region-specific metabolic perturba-tions in situ in a p-chlorophenylalanine (PCPA)-induced insomnia rat model using opti-mized matrix-assisted laser desorption/ionization mass spectrometry imaging (MAL-DI-MSI) integrated with targeted metabolomics validation. Methods: On-tissue chemical derivatization MALDI-MSI was optimized using α-cyano-4-hydroxycinnamic acid (CHCA) as the matrix on a Bruker tims TOF flex mass spectrometer. The rats received PCPA (400 mg/kg, intraperitoneal) for three days to establish the insomnia model. Metabolite identifi-cation was conducted using MetaboScape® software (2020b) and the Human Metabolome Database. Ultra-performance liquid chromatography–tandem mass spectrometry was em-ployed to quantify nine key neurotransmitters and metabolites across six brain microre-gions. Key synthetic enzyme expression was evaluated by immunofluorescence and West-ern blotting analyses. Results: TMP-TFB-derived brain slices clearly showed the distribu-tion of neurotransmitters in brain microregions. MALDI-MSI demonstrated that the spatial distribution and abundance of eight neurotransmitters were disturbed in brains of PCPA-induced insomniac rats. A total of 346 metabolites were characterized across six brain microregions (cerebellum, cortex, hippocampus, brainstem, hypothalamus, and stri-atum), with principal coordinate analysis revealing clear metabolic separation between control and insomniac rats. PCPA treatment markedly disrupted tryptophan and tyrosine metabolism, evidenced by decreased 5-HT, 5-HTP, and 5-HIAA, alongside region-specific alterations in DA, NE, HVA, and Ach. Additionally, GABA levels decreased in the hippo-campus, striatum, and hypothalamus, whereas glutamate increased throughout the brain. Targeted metabolomics validated the MSI findings, and Bland–Altman analysis confirmed good consistency between the two analytical platforms. PCPA further disturbed the meta-bolic enzymes MAOA, DDC, and TPH2 within the Trp-5-HTP-5-HT-5-HIAA metabolic pathway in the brainstem and TYH and DBA within the tyrosine-DA-NE metabolic pathway in the striatum. Conclusions: This study demonstrates that region-specific altera-tions in tryptophan and tyrosine metabolism pathways provide mechanistic insights into insomnia pathogenesis and potential therapeutic targets. Full article

Cancer cells are able to survive under conditions of high endoplasmic reticulum (ER) stress by activating the adaptive unfolded protein response (UPR), which is closely linked with autophagy. On the other hand, excessive and prolonged ER stress leads to apoptosis. However, the relationships between different UPR branches and apoptosis or autophagy vary in cancer cells of different origins and depend on the extent and nature of the stress signal. This study was designed to establish the role of ER stress sensors protein kinase RNA-like endoplasmic reticulum kinase (PERK) and inositol-requiring enzyme 1 (IRE1α) in apoptosis or autophagy signaling in T-lymphoblastic leukemia MOLT-3 cells via the RNA interference method. The cells were transfected with small interfering RNAs (si-PERK, si-IRE1α, or si-Cont) for 6 h and further cultured under normal conditions for 72 h to provide an insight into chronic effects of the gene silencing. The expression of apoptosis and autophagy effectors at the mRNA and protein levels was compared using RT-PCR and Western blot assays, respectively. Transfection of the cells with PERK siRNA led to a significant decrease in PERK protein and gene expression, and decreased phosphorylation of its downstream effector eukaryotic initiation factor 2α (eIF2α). PERK silencing was accompanied by activation of apoptosis-related genes and proteins—BCL2-associated X (Bax), caspase-3, C/EBP homologous protein (CHOP), while the levels of autophagy markers (Unc-51 like autophagy activating kinase 1 (ULK1), Beclin-1, and microtubule-associated proteins 1A/1B light chain 3 (LC3A/B)) remained stable. In contrast, treatment of the cells with si-IRE1α reduced the content of IRE1α, X-box-binding protein 1 (sXBP1), and glucose-regulated protein 78 (GRP78) proteins, but increased ERN1 gene expression. IRE1α RNA interference did not affect the levels of the pro-apoptotic marker Bax, but suppressed caspase-3, CHOP, c-Jun N-terminal kinase (JNK), and autophagy signaling molecules (ULK1, Beclin-1, LC3A/B) at both the transcriptional and translational levels. These results indicate that the PERK pathway is an important contributor to the survival of MOLT-3 cells under basal ER stress, while PERK depletion compromises the resistance of cells to UPR-mediated apoptosis. The IRE1α UPR branch is directly linked with autophagy-dependent signaling, although IRE1α knockdown exerted a more complicated influence on the cells, probably via activation of multiple pro-death and compensatory pro-survival regulatory mechanisms. Full article

Background/Objectives: Assessing inhibitory function and error detection is crucial for the early detection of age-related cognitive decline. This study aimed to investigate the neural network dynamics underlying these functions in younger and older adults to better understand age-related changes in cognitive control. Methods: We recorded electroencephalograms (EEGs) during an inhibitory control task in 17 older and 15 younger healthy adults. Behavioral performance was assessed, and directional functional connectivity was analyzed using Low-Resolution Electromagnetic Tomography (LORETA), isolated effective coherence (iCoh), and Full Vector Field analysis across the theta, alpha, and beta frequency bands. Results: Older adults showed significantly fewer correct responses than younger adults. During incorrect responses, older adults exhibited strong beta-band directionality from the ventral anterior cingulate cortex (ACC) to the left frontal polar cortex (FPC), alongside strong intra-ACC connectivity. During correct responses, they demonstrated alpha- and beta-band directionality from the left dorsolateral prefrontal cortex (DLPFC) to the right FPC. Conversely, compared with older adults, younger adults demonstrated significantly stronger mutual directionality within the ACC and widespread robust connectivity among the ACC, bilateral DLPFC, and FPC during correct responses. Conclusions: Efficient inhibitory control in older adults appears to rely on higher-order error-monitoring and error detection networks. The altered network dynamics in older adults suggest an age-related decline in immediate cognitive control. Evaluating these neural networks via EEGs provides a potential non-invasive biomarker for early cognitive decline and highlights higher-order executive control as a promising target for preventive interventions. Full article

Legume–rhizobium symbiosis represents a crucial biological nitrogen fixation system. The AP2/ERF transcription factor ERN1 plays a vital role in nodulation of model legumes; however, its function in peanut (Arachis hypogaea), a typical crack-entry infection legume, remains unclear. To explore this, we performed transcriptome sequencing of peanut roots at 3 days post-inoculation (dpi) with rhizobium. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses showed that differentially expressed genes (DEGs) were mainly enriched in DNA-binding transcription factor activity, plant–pathogen interaction, and plant hormone signal transduction pathways. The most strongly up-regulated gene was AhERN1, which was highly expressed in peanut roots and nodules. Subcellular localization indicated that AhERN1 was a nuclear-localized protein, and yeast transcriptional activation assays confirmed that AhERN1 functions as a transcriptional activator relying on its C-terminal domain. Furthermore, hairy root overexpression of AhERN1 significantly increased the number of peanut nodules. Collectively, these results reveal that AhERN1 acts as a positive regulator to promote rhizobium-induced nodule development in peanut, providing new insights into the regulatory mechanism of nodulation in dalbergoid legumes. Full article

Classical swine fever (CSF), caused by the classical swine fever virus (CSFV), is an acute, febrile, and highly contagious disease that has led to significant economic losses in the global swine industry. Although the attenuated lapinized CSF vaccine (C-strain) has effectively controlled CSF outbreaks in China since the 1950s, it remains challenging to serologically differentiate infected from vaccinated animals (DIVA). Currently, the application of E2 subunit vaccines allows for DIVA by detecting antibodies against the E^rns protein. Therefore, this study aimed to develop a blocking ELISA for CSFV E^rns antibody detection using porcine monoclonal antibodies (mAbs) derived from single B cell technology. Peripheral blood mononuclear cells (PBMCs) were isolated from immunized pigs, and single CD21⁺IgM⁻E^rns-His tag⁺ B cells were sorted via flow cytometry. Using one-step PCR, full-length genes of porcine IgG heavy and light chains were amplified separately, yielding 11 porcine mAbs against the CSFV E^rns protein. Among these, three mAbs (E0S3, E0S5, and E0S10) exhibited broad reactivity, while two (E0S1, E0S4) showed no cross-reaction with bovine viral diarrhea virus (BVDV). Using mAb E0S4 as the blocking antibody, a blocking ELISA was established and optimized. The assay demonstrated a detection limit of 1:128, no cross-reactivity with other swine viruses or BVDV, and intra- and inter-assay coefficients of variation below 10%. ROC curve analysis determined an optimal cut-off value of 48.4%, with high sensitivity and specificity. In conclusion, the developed blocking ELISA provides a reliable tool for high-throughput serological surveillance, facilitating the DIVA strategy and contributing to CSF eradication programs. Full article

This article examines the 1910 philosophical dispute between Vladimir Ern and Semyon Frank in post-1905 Russia as a dispute over the criterion of philosophy itself. The controversy arose in a field where the meaning of “Russian philosophy,” the authority of neo-Kantian nauchnost’ [scientificity], the religious-ontological program of Put’, and the problem of culture had become closely interconnected. The article argues that the central issue concerned what makes a claim philosophical: participation in an antecedent order of being, or conceptual articulation, proof, and universally valid justification. Ern’s intervention is presented as an attempt to reconstitute philosophy through Logos. For Ern, modern rationalism separates the discursive-logical from the “fullness of reason,” producing ratio as an autonomous and ultimately meonic form of thought; Logos, by contrast, names the ontological principle through which thought remains inwardly bound to being. Frank’s response locates the issue in the concept of philosophy itself. While acknowledging intuition, ontologism, and the insufficiency of one-sided rationalism, he insists that every appeal to being becomes philosophical only when it enters the medium of concepts, reasons, and proof. The article argues that the controversy turns on two irreducible conditions internal to philosophy itself: thought must remain faithful to being, yet it must do so in a form through which its claims become philosophically valid. Read in this way, the Ern–Frank exchange discloses a constitutive tension between ontology and conceptual justification, and between historical embodiment and universal validity. Full article

Early detection of cancer biomarkers in blood is critical for improving patient outcomes; however, conventional immunoassays often rely on complex instrumentation and are not well suited for point-of-care testing or multiplexed analysis. Herein, we present a dual-mode colorimetric–surface-enhanced Raman scattering (SERS) lateral flow immunoassay (LFIA) platform for multiplexed detection of cancer biomarkers, employing elongated rod-shaped silver nanoshells (ERNSs) as SERS nanotags. The ERNS features a rough Ag shell with internally incorporated Raman labeling compounds (RLCs), enabling plasmonic extinction for visual readout and strong SERS signals for quantitative analysis while preserving the external metal surfaces for efficient antibody conjugation. Leveraging these advantages, a multiplex LFIA capable of simultaneously detecting prostate-specific antigen (PSA) and carbohydrate antigen 19-9 (CA19-9) on a single strip was successfully demonstrated. Visual inspection enabled rapid discrimination of samples at or near clinically relevant cut-off levels, while Raman analysis achieved limits of detection of 8.0 × 10⁻³ ng/mL for PSA and 5.4 × 10⁻² U/mL for CA19-9, corresponding to approximately 500-fold and 685-fold lower concentrations than their respective clinical thresholds. This ERNS-based colorimetric–SERS LFIA integrates rapid screening and highly sensitive quantification within a single platform and offers a versatile nanoprobe design strategy for multiplex biomarker detection and liquid biopsy-based diagnostic applications, with potential relevance to point-of-care settings. Full article

Pestiviruses, such as bovine viral diarrhea virus (BVDV) or classical swine fever virus (CSFV), are members of the family Flaviviridae and infect a broad range of species, causing significant economic losses in livestock. A unique feature of pestiviruses is the E^rns protein, which is part of the glycoprotein complex at the surface of the virion, but it is also secreted as an RNase that functions as an interferon (IFN) antagonist. This dual nature makes E^rns a particularly complex and multifunctional protein, highlighting its importance for understanding pestivirus biology. Bungowannah pestivirus (BuPV) was reported to exhibit high genetic plasticity, making it suitable for engineering recombinant tools. In this study, we generated a recombinant BuPV expressing green fluorescent protein (GFP) fused to the N-terminus of the E^rns protein from BVDV. The GFP-E^rns fusion was detected by fluorescence microscopy and remained stable across five serial passages. The recombinant virus infected all tested mammalian cell lines but replicated more slowly than the parental BuPV stock. RNase activity assays confirmed retention of enzymatic function. These results demonstrate stable expression, broad infectivity, and preserved activity of GFP-E^rns in the recombinant BuPV, indicating that this might be a useful tool for further investigations on pestivirus pathogenesis. Full article

Portable, affordable electroencephalography (EEG) amplifiers could enable neuroscience-scale data collection. The open-source OpenBCI Cyton shows promise in this regard, but remains undervalidated for cognitive neuroscience ERP experiments. We simultaneously recorded eight scalp electrodes with both Cyton and gold-standard Brain Products BrainAmp amplifiers across P3b-, ERN-, and N400-eliciting tasks. Five healthy volunteers completed visual oddball (P3b), flankers (ERN), and word association (N400) tasks. We quantified within-subject signal similarity using Pearson $r^2$, mean absolute error (MAE), mean arctangent absolute percentage error (MAAPE), and within-component window mean and standard deviation. Cyton signals showed $r^2$ = 97–100%, MAE ≈ 1 µV, and MAAPE ≈ 20% with BrainAmp signals at ERP sites of interest. No significant differences emerged in mean amplitudes within ERP component windows across amplifiers, though standard deviations differed significantly. These results demonstrate that the Cyton records highly similar but not identical scalp EEG as research-grade equipment. This first multi-subject, concurrent scalp EEG validation across multiple ERP components validates the Cyton for cognitive neuroscience and supports broader adoption of affordable open-source tools. Full article

Artificial intelligence (AI) and machine learning (ML) are reshaping cancer research and care. In pediatric oncology, early evidence—most robust in imaging—suggests value for diagnosis, risk stratification, and assessment of treatment response. Pediatric endocrine tumors are rare and heterogeneous, including intra- and extra-adrenal paraganglioma (PGL), adrenocortical tumors (ACT), differentiated and medullary thyroid carcinoma (DTC/MTC), and gastroenteropancreatic neuroendocrine neoplasms (GEP-NEN). Here, we provide a pediatric-first, entity-structured synthesis of AI/ML applications in endocrine tumors, paired with a methods-for-clinicians primer and a pediatric endocrine tumor guardrails checklist mapped to contemporary reporting/evaluation standards. We also outline a realistic EU-anchored roadmap for translation that leverages existing infrastructures (EXPeRT, ERN PaedCan). We find promising—yet preliminary—signals for early non-remission/recurrence modeling in pediatric DTC and interpretable survival prediction in pediatric ACT. For PGL and GEP-NEN, evidence remains adult-led (biochemical ML screening scores; CT/PET radiomics for metastatic risk or peptide receptor radionuclide therapy response) and serves primarily as methodological scaffolding for pediatrics. Cross-cutting insights include the centrality of calibration and validation hierarchy and the current limits of explainability (radiomics texture semantics; saliency ≠ mechanism). Translation is constrained by small datasets, domain shift across age groups and sites, limited external validation, and evolving regulatory expectations. We close with pragmatic, clinically anchored steps—benchmarks, multi-site pediatric validation, genotype-aware evaluation, and equity monitoring—to accelerate safe, equitable adoption in pediatric endocrine oncology. Full article

Test anxiety is considered to affect individuals’ cognitive control and task performance, particularly in error monitoring. While previous research has explored the relationship between anxiety and cognitive performance, this study aims to investigate the impact of test anxiety and cognitive stress on error processing, focusing on changes in error-related negativity (ERN). Participants were divided into high test anxiety (HTA) and low test anxiety (LTA) groups based on their scores on the Test Anxiety Scale (TAS). Cognitive stress was induced by administering the Raven’s Standard Progressive Matrices test, accompanied by instructions that emphasized score comparison with others. Participants completed the Subjective Test Anxiety Scale (STAS), the Short State Anxiety Inventory (SSAI), and a Flanker task before and after the stress manipulation. The effectiveness of the stress manipulation was confirmed by significant increases in STAS and SSAI scores and changes in behavioral performance. EEG data were recorded to analyze ERN, correct-response negativity (CRN), and ΔERN (ERN minus the CRN) amplitudes. HTA individuals exhibited a trend toward larger ERN amplitudes than LTA counterparts, indicating heightened sensitivity to errors. However, no significant changes in ERN amplitudes were observed between pre- and post-stress conditions. CRN and ΔERN amplitudes also showed no significant differences across anxiety groups or stress conditions. ERN changes appear to be more closely related to trait test anxiety than to transient stress. Full article