Search Results (825)

While state-of-the-art massive acoustic arrays typically rely on costly, specialized FPGA architectures or rigid proprietary hardware, there is a growing need for modular, high-density sensing in complex aeroacoustics environments. This paper presents the electronic and acoustic design of a multiplexed, modular, scalable, and low-cost massive acoustic array (MxArray) founded on an embedded Linux system. The AM3358 SoC microprocessor collects audio data through its multichannel audio peripheral, where it simultaneously receives four Time-Division Multiplexing streams of 16 microphones each. This multiplexed scheme enables the handling of 64 microphones per module, whose acquisition synchronization is set with the Precision Time Protocol and a pulse injection hardware. The combination of both BeagleBone Black and microphones based on Micro-Electro-Mechanical Systems yields a cost-effective solution with built-in Ethernet connectivity and accessible software development through an embedded Linux environment with audio libraries for hardware control. Sensors are arranged in an Underbrink Spiral pattern on a four-layer printed-circuit board. The perforated thin layout minimizes any airborne disturbance, exploiting a distribution that simultaneously achieves a low sidelobe level and a narrow main lobe when used with a beamforming algorithm. Measurement results for the developed module are presented, as well as an evaluation of a full-scale system comprising 16 modules (1024 microphones) arranged in a honeycomb pattern. The resulting instrument offers a practical and scalable solution for applications that require a large number of simultaneous microphone measurements, such as beamforming technology for aeroacoustics applications. Full article

Early-life nutrition is critical for the development and health of dairy calves, necessitating alternatives to in-feed antibiotics. This study investigated whether dietary glycerol monolaurate (GML) enhances growth performance, reduces diarrhea incidence, improves systemic antioxidant and immune status, and modulates hepatic immunometabolic function in calves. Twenty-four Holstein bull calves (7 ± 0.5 d of age) were randomly assigned by body weight and age to a control group or a GML-supplemented group, both fed milk replacer with starter feed provided throughout the 45-day trial. Calves in the GML group received GML at a dosage of 100 mg/kg of body weight, mixed into the milk replacer prior to feeding. Calves in the GML group had significantly greater final body weight, average daily gain, and starter intake during the latter period (d 23–45) compared with the control group. GML supplementation also significantly reduced the incidence of diarrhea and fever, alongside lower fecal scores and fewer antibiotic treatments. Plasma analysis revealed enhanced antioxidant capacity, as indicated by increased total antioxidant capacity and glutathione peroxidase, along with an improved immune profile characterized by elevated immunoglobulin G and reduced interleukin-2. Transcriptomic analysis of the liver showed that GML upregulated genes and pathways related to innate antiviral immunity, such as radical S-adenosyl methionine domain containing 2, interferon-stimulated gene 15, and MX dynamin like GTPase 1. Lipidomics further indicated that GML induced a targeted remodeling of hepatic lipids, including increased diacylglycerols and triacylglycerols and decreased specific phospholipids and sphingolipids, suggesting a metabolic shift supportive of immune activation and inflammatory control. In conclusion, dietary GML enhances growth and health in suckling calves, which is mediated through a coordinated immunometabolic reprogramming in the liver. GML represents a promising functional fat additive for sustainable calf rearing. Full article

This paper presents a modular FPGA-based Smart Multi-Functional Display (SMFD) architecture designed for low-power and real-time avionics applications. Conventional SMFD systems are typically based on tightly coupled monolithic architectures, which limit scalability, maintainability, and subsystem flexibility while increasing system complexity and power consumption. To address these limitations, the proposed architecture separates processing, display, and communication functions into independent hardware modules, enabling flexible system integration and subsystem-level optimization. It consists of four primary modules: an FPGA-based Programmable Logic Device (PLD) module for deterministic video processing and display timing control, an NXP i.MX8X CPU module for application-level management, a high-resolution LCD module, and a dedicated I/O module supporting avionics communication interfaces, including AFDX and RS422. The architecture combines FPGA-assisted real-time processing with power-aware task partitioning strategies to improve both timing predictability and energy efficiency. Experimental evaluation performed on the implemented hardware prototype demonstrates that the proposed architecture achieves approximately 40% reduction in power consumption compared to a conventional baseline configuration while maintaining real-time operational capability with an average processing latency of 12.7 ms. In addition, the FPGA-based implementation enables dynamic display reconfiguration with a measured switching time of approximately 235 ms. The results indicate that the proposed modular architecture provides an effective balance between power efficiency, real-time performance, scalability, and system flexibility for next-generation avionics display applications. Full article

Background: Neoadjuvant partial breast irradiation using stereotactic body radiotherapy (SBRT) has emerged as a strategy to induce tumor and immune responses in early-stage, low-risk breast cancer. While prior studies have demonstrated encouraging response rates and evidence of immune modulation, the optimal radiotherapy regimen for immune priming remains unclear. SIGNAL 2.0 is a randomized phase II trial designed to compare the biological and immunological impact of a single-fraction versus three-fraction neoadjuvant SBRT. Materials and Methods: Sixty-one postmenopausal patients ≥ 50 years with unifocal, hormone positive, node-negative invasive ductal carcinoma < 3 cm were randomized 1:1 to receive either 21 Gy in one fraction or 30 Gy in three fractions, delivered to the tumor in the prone position. Core biopsies were collected pre-SBRT and 14–20 days post-SBRT at the time of surgery. Immune markers were assessed using tumor-infiltrating lymphocyte (TIL) scoring, NanoString nCounter PanCancer Immune Profiling, and NanoString GeoMx Digital Spatial Profiling (DSP). Results: Available tumor samples from 47 patients underwent paired tissue analysis. Three-fraction SBRT induced 200 differentially expressed genes, including enrichment of pathways related to adaptive immune activation, with significant increases in expression levels of macrophages, dendritic cells, neutrophils and CD8 T-cells. Proteomic profiling also identified a significant increase in the expression levels of neutrophils, Treg cells, macrophages, and NK cells in the tumor microenvironment of the samples from patients receiving the three-fraction regimen. Conclusions: Neoadjuvant SBRT induces measurable immune activation, with three-fraction regimens generating more extensive transcriptional, proteomic, and cellular immune changes than a single fraction. Three-fraction neoadjuvant SBRT may provide superior immune priming, providing a foundation for future trials integrating neoadjuvant radiotherapy with immunomodulatory therapies. Full article

Hantaviruses are emerging zoonotic pathogens responsible for two severe clinical syndromes: (i) haemorrhagic fever with renal syndrome (HFRS) and (ii) hantavirus cardiopulmonary syndrome (HCPS), collectively causing more than 200,000 human cases annually worldwide. Despite their public-health importance, the molecular mechanisms governing the host response and the population-level dynamics of rodent-to-human spillover remain incompletely characterised. The timeliness of this framework is underscored by the April–May 2026 outbreak of Andes orthohantavirus aboard the MV Hondius cruise ship, the first such cluster in a maritime setting, with three deaths reported across multiple countries. This event revealed critical gaps in existing models that treat humans solely as dead-end spillover hosts. Our coupled Susceptible-Exposed-Infectious-Recovered-Dead (SEIRD) model assumes no human-to-human transmission and is therefore designed for hantavirus strains where spillover does not lead to secondary human cases, specifically Hantaan virus (HTNV), Puumala virus (PUUV), Sin Nombre virus (SNV), and Dobrava-Belgrade virus (DOBV). The Andes virus (ANDV) outbreak aboard the MV Hondius is used as a real-world case study to assess the boundaries of our model and to motivate future extensions, not as a direct validation target for its quantitative predictions. Here, we present an integrated computational study combining three complementary analyses. First, we performed a preliminary phylogenetic analysis of the viral sequence, identifying Orthohantavirus andesense as the likely etiological agent responsible for the vessel-associated outbreak. Second, we carried out a downstream transcriptomic analysis of Hantaan virus (HTNV)-infected human umbilical vein endothelial cells (HUVECs), using publicly available RNA-seq data (GEO accession GSE133751, $n=3$ per group). This analysis identified 184 upregulated and 19 downregulated genes, highlighting a transcriptional response dominated by interferon-stimulated genes (ISGs), including CXCL10, CXCL11, MX2, DDX58, IRF7, STAT1, OASL, and CMPK2. We then constructed a protein–protein interaction (PPI) network using STRING, comprising 176 nodes and 3210 edges, and applied a composite network centrality score to rank putative regulatory hubs. This analysis identified ISG15, IRF1, CXCL10, STAT1, and DDX58 as the most central nodes. Pathway enrichment analysis confirmed a strong activation of interferon signalling (Reactome, $p=1.3\times {10}^{-63}$), antiviral defence mechanisms (Gene Ontology, $p=3.8\times {10}^{-58}$), and NF-$\kappa$B-related pathways, together with a concurrent suppression of ribosomal translation. Finally, we developed a coupled SEIRD epidemiological model that explicitly represents rodent-to-rodent and rodent-to-human transmission with logistic rodent population growth. Preliminary simulation analysis demonstrates that reducing human exposure to rodent excreta is substantially more effective than rodent population control alone for reducing human disease burden, and that rodent control in isolation can paradoxically increase human cases through a dilution-like effect. The integrated framework provides molecular and epidemiological insights relevant to hantavirus surveillance, therapeutic target identification, and public-health intervention design. Full article

The El Niño–Southern Oscillation (ENSO) is the main driver of interannual climate variability, strongly influencing precipitation, temperature, and extreme events worldwide. In South America, its impacts are well documented. However, studies examining different ENSO types—Eastern Pacific (EP), Central Pacific (CP), and Mixed (MX), defined according to the location of sea surface temperature (SST) anomalies in the tropical Pacific—remain limited, particularly for the Brazilian subtropical climate. This study investigates rainfall variability in the Brazilian subtropical region associated with different ENSO types. Composite analyses of precipitation, wind, and SST anomalies were performed, and monthly rainfall data from 703 stations were used to identify homogeneous regions. The results show the intensity and spatial coherence of rainfall signals vary according to El Niño type, with EP events favoring widespread wet conditions and CP events producing more heterogeneous or locally negative anomalies. For La Niña, the intensity and seasonal distribution of negative rainfall anomalies vary by ENSO type: stronger impacts occur in summer (EP), spring (MX), and autumn (CP). These findings improve the understanding of ENSO-related rainfall variability in the Brazilian subtropical region and provide valuable insights for the management of climate-related risks in an area frequently affected by rainfall extremes. Full article

Fusarium root rot (caused by Fusarium verticillioides) is a destructive soilborne disease in maize, significantly reducing crop yields. The root symbiotic fungi Trichoderma species have been confirmed as effective biocontrol microbes for Fusarium root rot; however, the mechanistic role of Trichoderma-induced endophytes in suppressing Fusarium root rot in maize remains unclear. This study found that Trichoderma harzianum T30 significantly reduced the abundance of pathogens by 48.9% and increased the abundance of potentially antagonistic Bacillus strains (33%) in the root endophytic bacterial community. In addition, the hyd1 gene in T. harzianum T30 induced a 7.5-fold upregulation of ZmOPR7 in maize roots compared to the Δhyd1 mutant treatment, a gene related to the jasmonic acid (JA) pathway. Further, several endophytic Bacillus strains were specifically induced by a hyd1-overexpressing strain, including B. amyloliquefaciens MX66, B. velezensis C9, and B. velezensis GAGAN3. Three endophytes significantly (p < 0.05) reduced Fusarium root rot incidence in maize by 46.6–55.0% and upregulated the expression of jasmonic acid/ethylene (JA/ET) pathway-related genes (ZmOPR7, ZmOPR8 and ZmEIL1) by 5.4-, 1.5-, and 4.6-fold, respectively, compared to untreated controls. Meanwhile, the Bacillus strain also improved maize plant growth. This study examined how overexpression of the T. harzianum elicitor gene hyd1 (in the OE-hyd1 strain) affects the colonization dynamics of beneficial endophytic bacteria in maize roots. Additionally, it further suggested the contribution of selected endophytic Bacillus strains in suppressing Fusarium root rot in maize. Full article

Spent lithium-ion battery electrolytes contain fluorine-, sulfur-, and phosphorus-bearing toxins, necessitating deep detoxification and directional conversion into C₁–C₆ light hydrocarbons. To elucidate the specific catalytic roles and sequential activation of cathode metals (Li, Ni, Co, Mn), this work systematically deconvolutes their mono- and multi-metallic migration mechanisms over a CaO-ZSM-5* catalyst during vacuum catalytic pyrolysis (530 °C, 100 Pa). Results reveal that Li⁺ and Ni²⁺ dominate C–O bond cleavage in carbonates and CaO-ZSM-5*-assisted decarboxylation and oxygen fixation, significantly increasing the relative hydrocarbon content. Conversely, Co^2/3+ and Mn⁴⁺ release reactive oxygen species, causing deep oxidation of hydrocarbons into CO₂ and antagonizing the targeted conversion. In multi-metallic systems, forming composite metal oxides (M_xN_yO_z) increases the energy barrier for releasing active catalytic ions, hindering carbonate cleavage and leaving unreacted carbonate feedstocks. For detoxification, F and P are effectively immobilized as CaF₂ and Ca₂P₂O₇. The relative content of detected gas-phase nitriles is minimized to <2% due to the strong antagonistic effect of Ni²⁺ on Li⁺-promoted hexanedinitrile cleavage, while sulfur species derived from 1,3-propane sultone are converted to SO₂ and ultimately mineralized as calcium and metal-sulfur salts. Mechanistically, product distributions and crystallographic properties suggest a hypothesized sequential activation model—Li⁺ → Ni²⁺ → Mn⁴⁺—governing reactivity, whereas Co^2/3+ does not participate in the synergistic detoxification and selective upgrading process. This migration–reaction coupling framework provides critical insights for cathode-assisted in situ catalytic pyrolysis and closed-loop electrolyte recycling. Full article

Biomolecular condensates in the cytoplasm and nucleus contribute to carcinogenesis through aberrant signaling by assorted transcription factors and fusion oncoproteins. Oral cancer, which is highly prevalent worldwide, frequently occurs in a U-shaped “high-risk” zone (floor of mouth, side of tongue, and anterior fauces) which forms the path of liquid transit through the mouth. We previously reported that environmental stresses of saliva-like hypotonicity and beverage-like temperature changes triggered cycles of disassembly/reassembly of biomolecular condensates of GFP-tagged human myxovirus resistance protein (MxA; alias Mx1) in oral cancer cells. In the present study, we identified some of the constituents of GFP-MxA cytoplasmic condensates in oral cells. These condensates were isolated from interferon (IFN)-λ1-treated GFP-MxA expressing OECM1 human oral cancer cells using magnetic bead-based immunoisolation. Unbiased peptide identification confirmed the presence of MxA/Mx1 peptides; however, the strongest intensity was for the BACH1 transcription factor family. Immunofluorescence analyses confirmed the association of BACH1 and the family member Nrf2 with cytoplasmic human GFP-MxA condensates. Moreover, GFP-BACH1 and GFP-Nrf2 colocalized with cytoplasmic human HA-MxA condensates in transiently transfected OECM1 cells. Western blot assays confirmed the presence of BACH1 and Nrf2 proteins in complexes isolated using anti-MxA pAb. As much as BACH1 and Nrf2 regulate oxidative stress response genes, it was remarkable that immunofluorescence assays revealed the presence of heme oxygenase 1 (HO1)—a downstream redox regulator—in GFP-MxA condensates. However, these condensates were devoid of p62, KEAP1 and Cul3. In terms of aberrant function, in live cells, the Nrf2 transcription factor underwent rapid disassembly and reassembly cycles driven by saliva-like hypotonicity, and was also disassembled by sulforaphane. The data highlight the unexpected intersections in oral cells between MxA condensates and BACH1, Nrf2 and HO1—proteins well known to be involved in pathways regulating cellular responses to environmental and oxidative stresses, antiviral defense, oral epithelial dysplasia, and cancer progression and metastases. Full article

Megalurothrips usitatus (Bagnall) is a major pest of cowpeas that severely affects their yield and quality. Spinetoram (a semi-synthetic derivative of natural spinosyns, modified to improve potency, residual activity, and stability) is currently one of the primary insecticides used for its control; however, prolonged or repeated exposure to this insecticide may lead to sublethal effects and the development of resistance. This study aimed to clarify the transgenerational effects of sublethal spinetoram stress on the development, reproduction, and population parameters of M. usitatus, with F₄ offspring reared on untreated pods to assess maternal effects. The LC₂₅ of spinetoram against M. usitatus was determined using an improved leaf-tube residual film method, and the thrips were successively selected for three generations (F₁–F₃) at this concentration. An age-stage, two-sex life table was constructed to systematically analyze the developmental duration, adult longevity, fecundity, and population life table parameters of the F₄ generation. The results showed that after three consecutive generations of LC₂₅ stress, the resistance ratio of M. usitatus to spinetoram reached 2.7. Compared with the water control, the F₄ generation from the treated group exhibited significantly shortened 1st and 2nd instar nymphal durations, as well as the total egg-to-adult period, while the prepupal duration was significantly prolonged. Adult longevity in females decreased from 23.65 ± 1.05 days to 16.07 ± 1.40 days (32.1% reduction), and male longevity decreased from 18.78 ± 0.96 days to 15.40 ± 0.82 days (18.0% reduction). Mean fecundity per female decreased from 247.15 ± 30.47 to 34.53 ± 6.02 eggs (86.0% decrease). Regarding population parameters, the net reproductive rate (R₀) decreased from 98.80 ± 0.07 to 10.36 ± 0.01 (89.5% decrease), the intrinsic rate of increase (r) decreased from 0.2506 ± 0.0001 to 0.1452 ± 0.0001 (40.0% decrease), the finite rate of increase (λ) decreased from 1.2849 ± 0.0001 to 1.1564 ± 0.0001 (10.1% decrease), and the mean generation time (T) was shortened from 18.24 ± 0.001 days to 15.84 ± 0.001 days (13.2% reduction). Age-stage-specific life expectancy (e_xj) was significantly reduced across all developmental stages, indicating a shorter survival time. The peak age stage-specific reproductive value (v_xj) was significantly lower and occurred earlier. The peak values of the age-specific survival rate (l_x) and fecundity (f_x, m_x) curves were significantly lower in the treated group. These findings indicate that multigenerational sublethal exposure to spinetoram can induce low-level resistance in M. usitatus and suppress the population growth potential by shortening developmental duration, reducing life expectancy, and reproductive contribution, and significantly inhibiting fecundity and survival. These results reveal the transgenerational sublethal effects of spinetoram and provide a theoretical basis for the integrated pest management (IPM) and resistance control of M. usitatus. Full article

Background/Objectives: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a heterogeneous inflammatory disease in which eosinophilic subclassification is widely used for clinical stratification. However, it remains unclear how closely nominal histologic eosinophilic labels reflect the broader molecular organization of diseased tissue. Methods: We performed an inference-based integrative analysis of public datasets spanning discovery single-cell RNA sequencing (scRNA-seq), independent scRNA-seq validation, GeoMx digital spatial profiling, and bulk transcriptomic replication cohorts. A sample-level molecular burden framework was constructed using four dimensions: type 2 inflammation, epithelial injury/remodeling, extracellular-matrix remodeling, and barrier/defense impairment. Composite burden and component-level features were then examined across nominal eosinophilic categories, epithelial states, spatial compartments, and independent bulk cohorts. Results: Nominal eosinophilic labels were directionally informative but incompletely concordant with molecular burden. In the discovery cohort, eosinophilic CRSwNP samples were enriched toward the higher-burden end, whereas nominally non-eosinophilic CRSwNP samples extended across the intermediate-to-high burden range. Across discovery and validation scRNA-seq datasets, GeoMx spatial profiling, and independent bulk cohorts, the most reproducible burden-associated signals centered on epithelial injury/remodeling-like programs and related remodeling features. In the epithelial compartment, higher burden was associated with epithelial state reorganization, stronger wounding-associated activity, and trajectory-linked glandular/secretory remodeling. Independent validation and spatial analyses further supported epithelial wounding-, barrier-, and myeloid remodeling-related features, whereas type 2 context signals were directionally consistent but less uniform across platforms. In bulk replication, composite burden, epithelial wounding, and myeloid remodeling were more consistent across cohorts than type 2 context alone. Conclusions: Nominal eosinophilic labels in CRSwNP capture clinically relevant but incomplete information about underlying tissue biology. Epithelial injury/remodeling-like programs and remodeling-linked myeloid features emerged as the most stable organizational axes of molecular burden across public multimodal datasets. These findings support a graded, multidimensional view of CRSwNP and may complement, rather than replace, conventional pathology-based eosinophilic subclassification. Full article

Aim: Disturbances in exhausted and classical memory B cells have been implicated in the pathogenesis of systemic lupus erythematosus (SLE) and lupus nephritis (LN), but the genetic regulation of their homeostasis remains poorly understood. Methods: We analyzed the single-cell RNA-seq data of peripheral blood mononuclear cells (PBMCs) from the NIH SLE dataset (GSE135779) and another published LN single-cell RNA-seq dataset (dbGAP database accession code phs001457.v1.p1). Overlapping differentially expressed genes (DEGs) in exhausted and classical memory B cells from SLE and LN patients were identified, and their altered expression was validated in B cells obtained from LN patients. GO and KEGG analyses were used to analyze associated pathways. The relationships between exhausted and classical memory B cells and cellular metabolic pathways were also assessed. Results: Three DEGs (IFI44L, XAF1, and MX1) were detected in both exhausted and classical memory B cells, and their increased expression was verified in classical and exhausted memory B cells obtained from LN patients during remission. The protein–protein interaction network of the DEGs suggested that STAT1 showed the highest eigenvector centrality for these DEGs. IFI44L, XAF1 and MX1 were involved in distinct biological processes and immune pathways (especially JAK-STAT). Classical memory B cells showed higher expression of genes involved in sulfur metabolism (SQRDL and TST), amino sugar metabolism (GFPT1 and UAP1), and butanoate metabolism (ACADS and ACAT1), while exhausted B cells exhibited inverse relationships with these metabolic pathways. Conclusions: Altered expression of IFI44L, XAF1 and MX1 is associated with distinct metabolic signatures and immune pathways in exhausted and classical memory B cells in SLE and LN. Full article

Background: The sensitivity of mammography screening is compromised in women with dense breast tissue. Supplemental ultrasound (S-US) can enhance cancer detection, but evidence regarding its feasibility, harms, and benefits within Western population-based screening programs remains limited. Methods: This pragmatic, prospective controlled trial was integrated into the German national mammography screening program across 16 sites. Breast density was assessed using automated AI software. Women with “critically dense” breasts (top 15–20%) were offered handheld supplemental S-US in addition to mammography (MXUS). The control group (MX-only) comprised women with comparable densities who did not receive S-US. Primary outcomes included cancer detection rate (CDR), recall rate, biopsy rate, and short-term follow-up recommendations. Results: From May 2020 to March 2024, 25,341 women underwent MXUS, while 38,529 received MX-only. The CDR was significantly higher in the MXUS group, at 10.7 per 1000 (95% CI: 9.4–12.0) compared to 7.2 per 1000 (95% CI: 6.4–8.1) in the MX-only group, yielding an incremental CDR of 3.5 per 1000 (95% CI: 1.9–5.0). However, MXUS led to higher rates of recall (6.6% vs. 5.4%), biopsies (3.2% vs. 1.5%), and short-term follow-up recommendations (0.9% vs. 0.5%). Conclusions: Implementing quality-assured S-US for women with critically dense breasts substantially increases the detection of invasive cancers, but also raises false positives. While these results support density-adapted screening, the high resource intensity suggests that future strategies should optimize risk stratification to target S-US more selectively. Long-term data are required to confirm clinical benefits. Full article

African swine fever virus (ASFV) is the causative agent of African swine fever (ASF), a fatal and highly contagious disease, resulting in enormous losses to the global swine industry. No licensed vaccines or effective therapeutics are currently available to control ASFV infection. Interferons (IFNs) serve as key mediators of host antiviral immunity by inducing interferon-stimulated genes (ISGs), but the specific mechanisms by which individual ISGs restrict ASFV replication remain unclear. Interferon-induced protein with tetratricopeptide repeats 3 (IFIT3, also called ISG60) has been shown to exhibit antiviral activity against various viruses, but its role in ASFV infection has not been previously studied. Here, we used porcine alveolar macrophages (PAMs), the primary target cells of ASFV, to investigate IFIT3’s function in ASFV replication. We found that overexpression of IFIT3 inhibited ASFV replication, while its knockdown enhanced viral propagation. Mechanistically, IFIT3 directly blocked ASFV adsorption to host cells, thereby suppressing all subsequent stages of the viral cycle. IFIT3 also specifically interacted with ASFV F334L, an early viral gene product that encodes the small subunit of ribonucleotide reductase, a key enzyme for viral DNA synthesis. Additionally, IFIT3 positively regulated the STAT1/TBK1/IRF3 signaling axis: its overexpression increased phosphorylation of TBK1 and IRF3, as well as the protein level of STAT1, while IFIT3 knockdown attenuated activation of these molecules. Transcriptomic analysis of IFIT3-knockout PAMs revealed significant suppression of innate immune pathways, including type I interferon, JAK-STAT, and RIG-I-like receptor pathways, along with downregulated expression of core antiviral molecules such as ISG15, MX1, and STAT1. Conversely, pathways related to viral adsorption, endocytosis, and cytoskeleton were activated, and pathways involved in protein translation initiation, endoplasmic reticulum stress, and autophagy were dysregulated, creating a favorable intracellular environment for ASFV replication. In conclusion, IFIT3 restricts ASFV replication possibly by inhibiting viral adsorption and promoting innate immune signaling, identifying it as a potential therapeutic target against ASFV. This study’s limitation is its in vitro PAM model; future work will validate IFIT3’s role in vivo and develop targeted inhibitors. Full article

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by immune dysregulation and multi-organ damage. Abnormal B cell activation and autoantibody production constitute the core pathological mechanism of SLE. However, the proportion, BCR pairing types, clonal evolution patterns, and transcriptomic features of dual BCR B cells in SLE remain incompletely elucidated. In this study, we employed single-cell RNA sequencing (scRNA-seq) combined with single-cell B cell receptor repertoire sequencing (scBCR-seq) to preliminarily analyze the proportion and characteristics of dual BCR B cells in SLE model mice (MRL/Lpr and SLE.Yaa) as well as in peripheral blood from SLE patients. The results showed: (1) Compared with control groups, the proportion of dual BCR B cells in SLE model mice and patients exhibited a decreasing trend, whereas the diversity of the CDR3 repertoire decreased and clonality increased. Increased clonal sharing was observed between single BCR B cells and dual BCR B cells. The main pairing types of dual BCR B cells were H + κ1 + κ2, H1 + H2 + κ, and H1 + H2 + κ + λ, with preferential utilization of autoimmunity-associated V gene families such as IGHV4-34, and high expression of IGHG subtypes. (2) Tracking analysis of B cell receptor clonality and effector molecule expression revealed that in SLE, dual BCR B cells tend to enrich in IFN-α/γ responses, TNF-NFκB inflammation, and complement pathways, and highly express interferon-related genes such as Ly6a, Isg15, MX1, and IFI6. (3) In both single BCR B and dual BCR B cells from SLE patients, the proportion of the naïve B cell subset decreased, whereas the proportions of plasma and Breg subsets increased and exhibited clonal expansion. SLE dual BCR Breg cells highly expressed IL10, HSPA1A, and others. This study is the first to reveal, at the high-throughput single-B-cell level, that the proportion, subset origin distribution, CDR3 repertoire composition, and effector molecule expression of dual BCR B cells display unique characteristics in SLE model mice and patients, providing baseline comparative data and novel research perspectives for further investigation into B cell effector functions and mechanisms in SLE patients. Full article