Search Results (6,010)

In this article, we introduce and investigate a novel class of graphs that are called Power Congruence Graph PCGs, which are defined over the vertex set V$=\{0,1,2,\dots ,n-1\}$ where two vertices $a,b\in V$ are adjacent if $a^k\equiv b^k(modm)$ for some modulus $m\in M_p$, where $M_p=\{p,p^2,\dots ,p^t\mid p^t<n\}$. We thoroughly characterize the structural features of these graphs, establishing that each PCG decomposes into a union of $d+1$ complete components, where $d={\displaystyle \frac{p-1}{gcd(k,p-1)}}$. The component sizes are explicitly given for n, p, and k. This decomposition highlights symmetry patterns in the component arrangement, emphasizing connectedness and structural balance. We derive key graph-theoretic metrics such as degree distribution, size, chromatic number, clique number and domination number. We also compute the adjacency and Laplacian matrices, as well as their spectra and associated graph energies to better understand the structural similarities and differences among PCGs with different exponents and prime moduli. This paper offers a systematic framework for comprehending power congruence based graph constructs, integrating number theory with structural and spectral graph theory and illustrating the natural symmetry that underpins these combinatorial structures. Full article

Alzheimer’s (AD) and Parkinson’s disease (PD) are prominent neurodegenerative disorders characterized by early synaptic loss, which correlates more closely with clinical symptoms than neuronal death. This synaptic impairment is primarily driven by disruptions in synaptic vesicle (SV) trafficking, a critical process for maintaining synaptic integrity through a tightly regulated cycle involving clustering, docking-priming, Ca²⁺-triggered fusion, and endocytosis. In AD, amyloid-β (Aβ) oligomers interfere with SNARE-mediated fusion and endocytosis, while hyperphosphorylated tau obstructs vesicle mobility and docking, resulting in cumulative toxicity that aggravates SV defects. Conversely, in PD, α-synuclein (α-syn) aggregation alters vesicle clustering, membrane fusion, and recycling, and these effects are further influenced by Leucine-rich repeat kinase 2 (LRRK2)-Rab-related trafficking defects and the selective vulnerability of dopaminergic terminals. Different from previous reviews that address synaptic dysfunction in a broader manner, the present review is specifically organized around the SV trafficking cycle and compares both shared presynaptic endpoints and disease-specific upstream mechanisms in AD and PD. In addition, recent mechanism-oriented therapeutic strategies are summarized. This vesicle-cycle-centered perspective may provide a clearer framework for understanding presynaptic pathology and for guiding the development of earlier and more targeted interventions. Full article

Background/objectives: SARS-CoV-2 antibodies wane after natural infections and vaccinations. COVID-19 booster vaccination enhances the durability and functionality of antibodies against emerging SARS-CoV-2 variants. Data on booster-induced antibody durability in sub-Saharan Africa remain sparse. Comparative analysis of vaccine-induced responses between heterologous and homologous vaccination regimens remains limited. This study evaluated longitudinal RBD-specific IgG responses following homologous and heterologous COVID-19 booster vaccination in previously vaccinated adults. Methods: Adults with prior mRNA or adenoviral-vectored vaccination were boosted with either Pfizer (mRNA) or Janssen (adenoviral-vectored) vaccines. Plasma IgG binding to Wuhan, Delta, and Omicron RBDs was measured pre-booster and at 3, 6, and 9 months. A total of 181 participants were enrolled between November 2022 and October 2023. Results: More than 60% of participants had detectable pre-booster RBD- and N-antigen-specific IgG. Booster vaccination substantially increased Wuhan-specific RBD-IgG at three months, with limited boosting of Delta and Omicron responses. Antibody levels waned to pre-booster concentrations by month nine. Heterologous boosting with a viral-vectored prime followed by Pfizer mRNA significantly enhanced both peak RBD-IgG levels and durability. Conclusions: These longitudinal data provide rare real-world evidence on booster immunogenicity in African adults and demonstrate that heterologous regimens confer a short- to intermediate-term advantage in antibody magnitude compared to a homologous regimen. This benefit was most pronounced within the first six months post-boost. The findings support additional booster dosing to strengthen protection against emerging variants in sub-Saharan Africa. Full article

Immunogenic cell death (ICD) links tumor cell demise to the activation of anti-tumor immunity, but its adoption has also generated inconsistent definitions and frequent overinterpretation of surrogate biomarkers. Here, we synthesize mechanistic and methodological evidence showing that danger-associated molecular patterns (DAMPs), cytokine release, and endoplasmic reticulum stress report immunogenic potential rather than ICD itself. We propose that ICD should be defined by its functional immunological endpoint, namely efficient antigen presentation and antigen-specific adaptive immunity, ideally culminating in protective immunological memory. To operationalize this principle, we introduce a hierarchy of experimental validation ranging from correlative hallmarks (Level 0) to innate immune integration (Level 1), antigen-specific T-cell priming (Level 2), definitive vaccination-rechallenge protection with immune-dependence testing (Level 3), and translational relevance supported by convergent human data (Level 4). We also discuss common pitfalls, equating inflammation, necrosis-associated DAMP release, or therapeutic benefit with ICD, and outline minimal immune-context controls (e.g., MHC-I, CD8⁺ T cells, Batf3-dependent dendritic cells, and innate sensing pathways) required to support robust claims. Finally, we highlight why ICD remains strongly context-dependent, shaped by dendritic-cell competence, innate licensing, purinergic metabolism, and microenvironmental constraints. Evidence-graded standards should improve reproducibility, strengthen peer review, and accelerate clinically meaningful ICD-based strategies. Full article

Viral infections with gastrointestinal involvement remain a significant global health burden with limited therapeutic options. While probiotics show antiviral potential, their impact on primary human intestinal epithelial defenses is poorly defined. This study utilized human intestinal organoid-derived monolayers (ODMs), generated from the non-inflamed mucosa of patients with inflammatory bowel disease, to examine how Bifidobacterium animalis ssp. lactis BB-12 (BB-12) and Lacticaseibacillus rhamnosus GG (LGG) modulate mucosal antiviral pathways. Unlike conventional Caco-2 cells, ODMs preserved physiological cellular diversity and intact innate signaling. Expression of viral receptors and interferon (IFN)-stimulated genes (ISGs) was quantified by RT-qPCR, while the effector 2′-5′-oligoadenylate synthetase 1 (OAS1) was also assessed by immunofluorescence and flow cytometry. Both probiotic strains modulated IFN-associated pathways; however, BB-12 induced a markedly stronger antiviral transcriptional response than LGG. Notably, OAS1 exhibited cell type-specific regulation; while goblet cells showed high basal levels, both probiotics enhanced OAS1 expression selectively in ileal enterocytes. Despite this shared effect, only BB-12 pretreatment significantly restricted Influenza A (H1N1) replication in ileal ODMs, whereas LGG did not significantly affect viral replication. These findings establish human ODMs as a superior platform for probiotic immunology, suggesting that BB-12 more effectively shapes epithelial antiviral “set-points” and highlighting OAS1 as a sensitive component of a broader antiviral program. Full article

Electromagnetic treatment (EMF) can stimulate seed germination and plant development, including mitigating the negative effects of stressors. One non-invasive approach to detecting the early effects of EMF exposure is the study of gas exchange dynamics during the seed imbibition stage. Gas chromatography was used to assess the effect of low-intensity non-thermal EMF on the concentration of H₂, O₂, CO₂, and NH₃ gases in the “soil–pea seed” system under optimal conditions and under salt stress. EMF treatment exhibited a variant-dependent effect. Under optimal conditions, it stimulated respiration (O₂ concentration decreased by 12%, CO₂ increased by 15%); under salinity, the concentration of both gases decreased by 8–10% relative to the control. H₂ emission proved to be a sensitive biochemical marker of the response to external factors. Under optimal conditions, EMF treatment nearly tripled H₂ emission and shifted its emission peak one day earlier, which may indicate accelerated mobilization of the seed’s defense systems under developing hypoxia. Salinity reduced H₂ levels by an order of magnitude, while EMF treatment stabilized the H₂ emission rate, reducing it by almost half. Thus, EMF should be regarded as a modifier of the seed’s metabolic response to imbibition conditions, rather than solely as a germination stimulant. Full article

Salt stress inhibits plant growth, requiring salt-tolerant genes for the development of resilient plants. A key tolerance mechanism is potassium/sodium homeostasis, governed by Shaker K⁺ channels. Given that Shaker K⁺ channels from salt-sensitive species have been extensively studied while their counterparts in salt-tolerant plants remain largely unexplored, this study investigates the evolution and function of these channels in salt-tolerant bermudagrass to address this knowledge gap. Genomic analysis identified 25 Shaker K⁺ channel genes, an expanded family relative to other species. Phylogenetics placed them into five groups (I–V), with groups I, II, III, and V expanded via segmental duplication. Salt stress response screening revealed that only CdKAT1.1 was rapidly upregulated. Functional assays in yeast demonstrated that both CdKAT1.1 and its closest homolog CdKAT1.2 improve potassium uptake and salt tolerance, but the enhancement from CdKAT1.1 was significantly greater. This work elucidates the expansion and functional divergence of Shaker K⁺ channels in bermudagrass. CdKAT1.1 emerges as a superior regulator of potassium efficiency and salt tolerance, making it a prime candidate for molecular breeding to improve plant resilience in saline-alkaline soils. Full article

Chronic alcohol consumption increases the risk of osteoporosis and fracture by disrupting bone remodeling, in part by enhancing osteoclastogenesis. However, the cellular mechanisms underlying this process remain incompletely defined. We analyzed scRNA-seq data from osteoclasts differentiated in vitro from bone marrow mononuclear cells obtained from macaques following 12 months of chronic ethanol or isocaloric control solution consumption. Module scoring, trajectory inference with generalized additive modeling (tradeSeq), and CellChat-based analyses of intercellular communication were applied to uncover ethanol-induced changes in metabolic reprogramming, lineage progression, and signaling network dynamics. Module scoring indicated metabolic reprogramming toward oxidative phosphorylation, with reduced glycolytic, migratory, and phagocytic activities. Pseudotime analysis revealed accelerated osteoclast lineage commitment, broader intermediate differentiation states, and stabilization of mature osteoclasts. CellChat analysis showed globally amplified intercellular signaling, with mature osteoclasts functioning as dominant communication hubs sustained by autocrine feedback. Together, chronic alcohol consumption rewired osteoclastogenesis through early fate priming, metabolic adaptation, and hierarchical remodeling of intercellular communication, promoting enhanced osteoclastogenesis. These findings provide mechanistic insight into alcohol-induced bone pathology and highlight potential targets for therapeutic intervention. Full article

Severe southern soybean crinkle leaf disease (SSCLD) reduces soybean seed yield by approximately 40%. Identifying the genes that control SSCLD is crucial for breeding resistant varieties and elucidating the molecular mechanisms underlying SSCLD infection. In this study, recombinant inbred lines (RILs, n = 236) derived from a cross between Nannong1138-2 (NN1138-2) and Zhengxiaodou (ZXD) were used as experimental materials. A field trial employing a randomized block design was conducted in four environments across two locations, Nanning (2019–2021) and Du’an (2020) in Guangxi, to identify the disease severity grades of SSCLD in the field. QTLs controlling SSCLD were detected via a genetic map constructed using 3255 SLAF (specific locus amplified fragment) markers from the recombinant inbred lines. RT–qPCR was used to analyze candidate gene expression at major effect loci. The results revealed that eight SSCLD-associated QTLs were identified on chromosomes 3, 6, 12, and 17. Notably, the qw12-1 locus on chromosome 12 was detected across three developmental stages in three of the four environments, explaining 10.18–58.20% of the phenotypic variation. RT–qPCR analysis of 12 disease resistance-related genes within the qw12-1 interval revealed that GLYMA_12G233000 and GLYMA_12G239200 presented significantly higher expression in crinkled leaf lines than in normal leaf lines during the V5 (fifth trifoliolate stage), R2 (full bloom stage), and R6 (full seed stage) stages. These genes were prioritized as potential prime candidates for SSCLD resistance genes. This research provides foundational data for the fine mapping of qw12-1 and cloning SSCLD-related genes, advancing our understanding of the molecular mechanisms underlying SSCLD. Full article

Seed aging is a major constraint for plant establishment in arid and semi-arid ecosystems, where poor seed vigor directly limits species persistence and restoration success. Desert species are particularly vulnerable to storage- and stress-induced deterioration, yet practical strategies to recover germination capacity in aged seeds remain limited. This study aimed to quantify aging-induced losses in germination performance and to evaluate whether exogenous gibberellic acid (GA₃) can partially restore seed vigor through physiological, biochemical, and hormonal regulation. Fresh seeds (FS), naturally aged (NA), and artificially aged (AA) seeds of four desert species (Salsola affinis C.A.Mey., Trigonella arcuata C.A.Mey., Ceratocarpus arenarius L., and Alyssum desertorum Stapf) were exposed to graded GA₃ concentrations (0–500 mg L⁻¹). Germination indices (GP, GR, GI, VI), antioxidant enzymes (SOD, POD, CAT), lipid peroxidation (MDA), phytohormones (IAA, ABA, cytokinins), and multivariate trait relationships were assessed. Without GA₃, NA reduced germination potential by 22.8–33.6%, while AA caused more severe losses of 42.4–67.8%, depending on species. Germination rate declined by 15.7–32.5% under NA and 36.4–65.2% under AA. GA₃ application improved all germination indices up to 200 mg L⁻¹ (GA200), which increased GP by 22.8–32.0% and vitality index by 17.0–28.5% compared with GA₀, whereas GA500 showed diminishing returns. Aging suppressed antioxidant enzymes by 15–20% (NA) and 30–45% (AA) and increased MDA by up to 50%, while GA200 enhanced SOD, POD, and CAT and reduced MDA by 8–18%. Aging also reduced IAA and cytokinins (~28–50%) and increased ABA (27.7–77.4%), with GA200 partially restoring hormonal balance. In conclusion, GA₃ at an optimal dose (200 mg L⁻¹) partially reverses aging-induced physiological and hormonal constraints, improving germination and vigor, although recovery remains limited under advanced deterioration. Full article

WRKY is a crucial transcription factor involved in plant growth, development, and responses to abiotic stress. In the present study, a total of 182 AaWRKY transcription factor members were identified across the Artemisia argyi genome and found to be distributed across 17 chromosomes. Evolutionary analysis revealed that segmental duplication served as the primary driver for family expansion, with the evolutionary trajectory shaped by strong purifying selection (Ka/Ks < 1.0). Phylogenetic classification categorized these members into seven highly conserved subgroups, while physicochemical analysis indicated that most AaWRKYs are unstable, hydrophilic proteins, consistent with the rapid turnover required for transcriptional switches. Transcriptomic profiling unveiled significant tissue-specific expression patterns, with over 50% of the members predominantly enriched in roots and specific genes, such as AaWRKY11, implicated in the regulation of leaf senescence. Protein–protein interaction (PPI) network analysis identified AaWRKY110 as a central regulatory hub linking the MAPK signaling pathway with the isoflavonoid biosynthetic machinery. Furthermore, comparative transcriptomic analysis between aphid-resistant (Ai20K) and susceptible (Ai72G) cultivars demonstrated that resistance is conferred by a priming mechanism involving high basal expression of key candidates, including AaWRKY82, 108, 128, and 71. In contrast, the susceptible genotype exhibited a delayed and ineffective hypersensitive-like response. Collectively, these findings elucidate the evolutionary dynamics of the AaWRKY family and provide critical genetic targets for the concurrent improvement of medicinal metabolite accumulation and biotic stress resilience in Artemisia argyi via molecular breeding. Full article

Background/Objectives: Influenza, RSV, and SARS-CoV-2 co-circulate and evolve under immune and therapeutic pressures, complicating decision-making for both vaccine formulation and antiviral use. Fragmented, pathogen-specific sequencing approaches limit cross-virus comparability. Methods: We applied a standardized, multiplexed, amplicon-based next-generation sequencing (NGS) workflow to 34 diagnostic specimens (Ct < 35) positive for influenza A/B, RSV-A/B, or SARS-CoV-2. Sequencing libraries were generated and run on an Illumina MiSeq platform (2 × 250 bp). Although the wet-lab workflow is standardized across pathogens, consensus generation and annotation utilized two different analysis environments: Geneious Prime for influenza and MicrobioChek for RSV and SARS-CoV-2. Quality metrics included genome breadth and depth of coverage. Results: Near-complete genomes (mean coverage ≥98%) were recovered for all samples. Influenza A(H1N1)pdm09 sequences clustered in clade 6B.1A; A(H3N2) clustered in subclade 3C.2a1b.2a.2; and influenza B belonged to the Victoria lineage V1A.3a.2. RSV sequences were assigned to Nextclade clades A.D.5.1, A.D.1.10, A.D.2.1, and A.D.3 (RSV-A) and to B.D.4.1.3 and B.D.E.1 (RSV-B), consistent with the ON1 (RSV-A) and BA (RSV-B) genotypes prevalent in recent seasons. Clinically relevant mutations included changes in the influenza HA site and neuraminidase substitutions, RSV F-protein polymorphisms, and spike protein substitutions associated with recent Omicron sublineages (L455F/S, F456L) in SARS-CoV-2. Conclusions: A unified amplicon–NGS approach yields harmonized genomic data across respiratory viruses, enabling timely detection of antigenic drift and resistance markers while supporting integrated, cross-pathogen surveillance. Full article

Background: Herpes simplex virus (HSV), Epstein–Barr virus (EBV), and cytomegalovirus (CMV) establish lifelong latency in sensory neurons, lymphoid tissue, and myeloid–endothelial cells, respectively. A substantial proportion of adults worldwide are infected with all three viruses and may experience concurrent herpesvirus latency, yet they have largely been studied independently. This review examined whether latent and intermittently reactivating herpesviruses share overlapping inflammatory signatures and whether their combined presence contributes to chronic inflammatory burden. Methods: A narrative integrative review was conducted using MEDLINE, Embase, and Google Scholar (inception–October 2025). Evidence from thirty-one cohort studies and mechanistic investigations spanning virology, immunology, neurology, and clinical medicine was synthesized. Results: Herpesvirus reactivation rates ranged from 23% in general Intensive Care Unit (ICU) populations to 85% in severe COVID-19. Concurrent reactivation of multiple viruses occurred in 34–63% of critically ill patients and was associated with worse clinical outcomes. Notably, simultaneous CMV and EBV reactivation independently predicted mortality (adjusted hazard ratio, 3.17; 95% CI, 1.41–7.13). Across infections, overlapping inflammatory biomarkers, including IL-6, TNF-α, CRP, and PGE₂, were consistently elevated, reflecting convergent activation of IFN and NF-κB signaling pathways. Mechanistic studies suggest cross-compartment immune priming, where CMV-driven T-cell exhaustion facilitates EBV reactivation, and viral cytokine signaling enhances HSV-associated neuroinflammation. Conclusions: HSV, EBV, and CMV triple latency may represent an underrecognized contributor to chronic inflammation in immunocompetent hosts. Understanding this multi-virus inflammatory network may inform mechanistic research, biomarker-guided risk stratification, and therapeutic strategies targeting convergent inflammatory pathways. Prospective interventional studies incorporating concurrent multi-virus monitoring are needed to clarify causal relationships. Full article

Experiential learning through simulations offers a unique but often underutilized opportunity to bridge the gap between pedagogy and empirical research. This study addresses this gap by transforming the Pemberton’s Dilemma simulation from a classroom exercise into a quantitative, empirical research project to investigate the dynamics of trust, cooperation, and opportunistic behavior. To address questions related to such trust interactions, the simulation was modified to include variable payout stakes, restricted and permitted communication phases, and an additional surprise round to measure long-term trust reputation effects. From 2017 through 2025, data was gathered from a convenience sample of 611 students from a large public university in the Northwestern United States. Results indicate that non-trusting behavior has a significantly greater mirroring effect than trusting behavior and that higher financial stakes frequently prime groups toward opportunistic hedging. While opportunistic strategies yielded greater short-term gains, longitudinal analysis revealed a significant positive correlation between consistent trust and monetary outcomes. Furthermore, the surprise round data confirmed that prior trust violations severely diminished cooperation and earnings in the future unknown round. The study supports the benefits of integrating quantitative research into pedagogical experiential tools to advance scholarly understanding (in this case of trust dynamics and the vital role of transparent communication and sustainability-compatible strategies), enhance student learning, and to provide data-driven recommendations for organizations. Full article