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Full-process deformation monitoring and failure characteristics analysis of damaged coal under 3D laser scanning technology

Antibody responses to a highly conserved peptide in HCV E2 protein correlate with chronicity or spontaneous clearance of HCV infection

Hepatitis C virus (HCV) infection frequently progresses to chronicity rather than spontaneous clearance, resulting in severe liver diseases including cirrhosis and hepatocellular carcinoma. The molecular mechanisms governing infection outcomes remain poorly understood. We identified Peptide A, a highly conserved epitope (residues 442 to 451) within HCV glycoprotein E2, and demonstrated that differential antibody binding patterns to this region correlate with distinct infection outcomes. This immunogenic, nonneutralizing epitope localizes to a structurally exposed region that shares residue 442 as a boundary with the previously characterized Epitope II (residues 430 to 442) and is positioned adjacent to variable region 2 (VR2, residues 460 to 485). Antibodies requiring both F442 and F447 residues within Peptide A for binding emerged early following infection and demonstrated strong correlation with chronic HCV progression. In contrast, antibodies binding exclusively to F447 were associated with spontaneous viral clearance and consistently co-occurred with Epitope II antibodies during later phases of infection. By establishing the relationship between these distinct antibody binding patterns and divergent infection outcomes, our findings elucidate potential HCV immune evasion mechanisms and may facilitate the development of predictive tools for determining chronic versus clearance outcomes early in infection, as well as inform rational vaccine design strategies.

Decatungstate-photocatalyzed transfer hydrogenation of unsaturated compounds using alcohol as the hydrogen source

A rare 5’UTR variant in SEC24D reveals translational dysfunction in osteogenesis imperfecta: a roadmap for RNA therapeutic rescue

Gradient interfacial water dynamics for stable aqueous metal anodes

The deployment of renewable energy necessitates reliable grid-scale storage technologies. Aqueous metal battery systems are one of the promising candidates due to high safety, low cost, and high theoretical capacity of metal anodes, yet their long-term stability is hindered by dendritic growth and parasitic water-induced side reactions. In particular, in the case of aqueous zinc (Zn) batteries, high water reactivity at the metal anode results in hydrogen evolution and corrosion in conventional ZnSO 4 aqueous electrolytes. However, restrained water activity often leads to slow charge transport kinetics of solvated cations, limiting the high-rate operation capability of aqueous batteries. Here, we report a gradient composite hydrogel interlayer incorporating vermiculite (VMT) nanosheets within a polyacrylamide polymer matrix to synergistically regulate interfacial water dynamics and stabilize Zn anodes. Abundant hydroxyl groups and negatively charged silicate layers in VMT nanosheets strongly interact with adjacent water molecules, converting free water into bound water to suppress its activity. Charge transport behaviors of Zn ions in the hydrogel interlayer are further improved by rationally tuning the water activity along the depth of the interlayer, resulting in high ion diffusion kinetics close to the bulk electrolyte. Therefore, such a design enables Zn||Zn symmetric cells to stably cycle for over 2,000 h at 5 mA cm −2 and 5 mAh cm −2 , and sustain high current densities up to 40 mA cm −2 . This work brings critical scientific understanding on interfacial water dynamics and highlights its importance for durable metal anode during operation, advancing aqueous batteries toward practical grid-scale energy storage.

Field-effect passivation for minimized voltage loss in highly efficient antimony selenosulfide solar cells

Elevated neutrophil-to-lymphocyte ratio and the incidence of autoimmune diseases: evidence from a large prospective cohort study

Abstract We prospectively assessed the association between neutrophil-to-lymphocyte ratio (NLR) and incident autoimmune disease risk using data from 430,347 UK Biobank participants recruited between 2006 and 2010. The NLR was calculated by dividing neutrophil counts by lymphocyte counts and categorized into quartiles. Cox regression models estimated hazard ratios (HRs) for per quartile increase of (1) a composite of 39 types of autoimmune diseases, (2) each specific autoimmune diseases, applying a 2-year lag-period and Bonferroni adjustments. Natural cubic spline analysis was performed to assess the threshold of NLR associated with autoimmune diseases. Among 430,347 participants (mean age: 56.4 years, 53.9% female), elevated NLR was significantly associated with any autoimmune diseases (27,571 events, HR per quartile increase: 1.09, 95% CI: 1.08–1.10; P-trend < 0.01). A non-linear association was observed, with risk significantly increasing above an NLR threshold of 2.51. Participants in the highest quartile (Q4) had a higher risk compared to Q1 (HR 1.30, 95% CI 1.26–1.35). Of 39 autoimmune diseases, 14 showed significant associations, most notably sarcoidosis (HR 1.52, 95% CI 1.38–1.67), antiphospholipid syndrome (1.46, 1.26–1.69), and autoimmune hepatitis (1.37, 1.20–1.56). These findings suggest elevated NLR as a potential pre-clinical indicator for identifying individuals at increased risk of autoimmune diseases.

Saccade-related LFP power transients in the primate amygdala and hippocampus linked to the perception of social status

A key aspect of healthy social functioning in both humans and nonhuman primates is the ability to extract status-related information from observing the social signals exchanged between individuals. Knowing the social status of others determines how long we look at them and how we engage with them in social interactions. While looking at faces and eyes requires a functionally intact amygdala, hippocampal memories guide the eyes toward socially relevant areas of a visual scene. We examined the local field potentials associated with socially meaningful eye movements in the amygdala and hippocampus of macaques as they watched videos of dominant–subordinate interactions among unfamiliar conspecifics. In both structures, the saccade-related potentials showed status-dependent amplitude modulation in specific frequency bands. In the amygdala, shifting gaze from lower- to higher-status individuals was associated with anticipatory power transients in the 20 to 25 Hz frequency band, whereas gaze shifts from higher- to lower-status individuals were marked by predominantly postsaccadic power transients. Following the gaze of the aggressive, dominant individual induced increased postsaccadic power in the gamma band in both the amygdala and hippocampus, with some variation in frequency depending on whether the saccade landed on the social partner or elsewhere. The timing, frequency, and status-specificity of these power transients reveal the contribution of the amygdala and hippocampus to the visual exploration of social scenes.

Little to no active faulting likely at Europa’s seafloor today

Developing a multidimensional scale of healing tourism experiences based on a mixed methods approach

Mechanical compression induces neuronal apoptosis, reduces synaptic activity, and promotes glial neuroinflammation in mice and humans

Mass effect, characterized by the compression and deformation of neural tissue from space-occupying lesions, can lead to debilitating neurological symptoms and poses a significant clinical challenge. In the primary brain tumor glioblastoma (GBM), we have shown previously that compressive solid stress originating from the growing tumor reduces cerebral blood flow, leading to neuronal loss, increased functional impairment, and poor clinical outcomes. However, the direct effects of compression on neurons and the underlying biophysical mechanisms are poorly understood. Here, using multiscale compression systems and physiologically relevant in vitro and in vivo models, we find that chronic mechanical compression induces neuronal apoptosis and loss of synaptic puncta, leading to disrupted neural network activity, as assessed by calcium imaging. This is accompanied by increased HIF-1 signaling and upregulation of downstream stress-adaptive genes in neurons. We further show that chronic compression triggers AP-1–driven gene expression in glial cells, promoting a neuroinflammatory response. Together, these findings reveal that solid stress directly contributes to neuronal dysfunction and inflammation caused by GBM by activating distinct pathways that can be targeted in future studies for neuroprotection.

Atypical β-strand insertion mediates the noncovalent cross-linking in amyloid aggregates

Adsorptive removal of reactive yellow S3R dye from aqueous solutions using green-synthesized copper nanoparticles

Abstract Industrial dye pollution poses a significant environmental threat, particularly from azo dyes like Reactive Yellow S3R (RY S3R), which are resistant to conventional treatment methods. This study investigates the efficacy of green-synthesized copper nanoparticles (CuNPs), via Ficus Benjamina leaves, for removing RY S3R from aqueous solutions. The innovative adsorbent Ficus Benjamina nano zero-valent copper (Ficus-nZVCu) was described using SEM, EDAX, and FTIR. Batch adsorption studies assessed the impact of pH, contact time, adsorbent dosage, and starting concentration on elimination efficiency. Several adsorption models were tested, and the Langmuir isotherm (q max = 136.986 mg g − 1 , R 2  = 0.9992) revealed the best fit, suggesting monolayer adsorption. Chemisorption was indicated by the pseudo-second-order model (R 2  = 0.9993), which was validated by the kinetic analysis. Owing to its redox activity, the green Ficus-nZVCu adsorbent is a promising material for eliminating RYS3R in light of the data acquired and the fruitful research. The impact of major operational parameters was validated using artificial neural network models and response surface methods. According to this study, green-synthesized CuNPs can effectively and safely treat dye-contaminated wastewater.

CHAMP1 complex promotes heterochromatin assembly and reduces replication stress

Replication stress (RS) is a major driver of genomic instability and a hallmark of cancer cells. Although dynamic heterochromatin remodeling has been implicated in RS response, the precise mechanisms remain unclear. The CHAMP1 complex, composed of CHAMP1, POGZ, HP1α, and the H3K9 methyltransferase SETDB1, is known to regulate heterochromatin assembly at multiple genomic sites. Interestingly, upon RS, the CHAMP1 complex is transiently recruited to stalled replication forks, where it facilitates H3K9me3 deposition and establishes a repressive chromatin environment. The complex is required for stabilization of replication forks, and it shields forks from MRE11-mediated degradation. The complex also reduces RS at specific chromosomal sites, such as the heterochromatin-rich telomeric sites in tumor cells which use the ALT pathway of telomere maintenance. Loss of the CHAMP1 complex results in increased micronuclei formation and heightened sensitivity to RS. Loss of the complex also leads to a compensatory increase in other pathways which reduce RS, such as the FA pathway and the ATR/CHK1 pathway. Notably, CHAMP1 deficiency induces synthetic lethality with FANCM inhibition in ALT-positive tumor cells, and the CHAMP1 complex is essential for the survival of CCNE1-amplified ovarian cancers. These findings uncover a heterochromatin-based mechanism of replication fork stabilization and suggest that CHAMP1 may represent a candidate therapeutic vulnerability in cancers with elevated RS.

Sulfur-containing class of broad-spectrum antivirals improves influenza virus vaccine development

Abstract Enveloped viruses are significant zoonotic disease threats with the potential to cause global pandemics. We identified a class of small-molecule sulfur-containing antiviral compounds (XM series) that broadly inhibit enveloped viruses. Multidisciplinary approaches revealed that XM compounds alter the viral membrane lipid chemical composition, enhance membrane order within the hydrophobic bilayer, and increase membrane phase transition temperatures. This mechanism inhibits membrane fusion and viral entry, while leaving the viral glycoproteins and genomes largely unaffected. Leveraging these unique properties, we develop a proof-of-concept whole inactivated influenza virus (IIV) vaccine using XM-01 (XM-01-IIV). In a mouse model, XM-01-IIV elicit significantly enhanced neutralizing antibody responses against hemagglutinin and neuraminidase compared to traditional paraformaldehyde-inactivated vaccines. Further, XM-01-IIV reduces morbidity and mortality following influenza challenge, achieving protection comparable to live virus vaccination. This promising class of broadly acting antivirals can be highly impactful in the development of highly potent inactivated vaccines for enveloped viruses.

A hybrid CNN-transformer model with adaptive activation function for potato leaf disease classification

Abstract Potato plants are highly vulnerable to numerous diseases that can substantially affect both yield and quality. Conventional approaches for detecting these diseases are often labor-intensive, slow, and prone to inaccuracies, particularly under variable environmental conditions. This study presents a hybrid deep learning architecture, termed potato leaf diseases DenseNet (PLDNet) , which integrates a DenseNet-based convolutional neural network with a Transformer-based attention module to accurately classify potato leaf diseases. Furthermore, an adaptive parametric activation function, referred to as Adaptive Flatten p-Mish (AFpM) , is proposed to enhance the model’s learning flexibility and representational capacity. When evaluated on the PlantVillage and Mendeley datasets, PLDNet attains classification accuracies of 99.54% and 87.50%, respectively, surpassing contemporary state-of-the-art models and activation techniques. The proposed framework exhibits strong generalization performance and offers a scalable, efficient approach for automated plant disease identification. To highlight the novelty, the proposed AFpM activation function introduces a learnable parameter enabling adaptive nonlinearity, improving over Mish, Swish, and PFpM activation functions through dynamic gradient control. AFpM improves accuracy by 2.52% on Mendeley dataset, and 1.93% on PlantVillage dataset compared to PFpM, and by more than 3% compared to Swish and Mish.

Dysregulation of a nucleotidyltransferase induces division and surface glycan defects in <i>Escherichia coli</i> by altering related metabolite levels

The cell surface of gram-negative Escherichia coli is rich in glycoconjugates, including O-antigen (O-Ag) and enterobacterial common antigen polysaccharides, which mediate interactions with the environment. Enzymes called nucleotidyltransferases produce nucleoside diphosphate sugars (NDP-sugars), the precursors to these and many other cellular glycans. Across bacteria, glucose-1-phosphate thymidylyltransferases (G1P-Ts) couple deoxythymidine triphosphate (dTTP) and glucose-1-phosphate to produce a key secondary metabolite, deoxythymidine diphosphate-glucose (dTDP-Glc). Flux through many glycan biosynthetic pathways is regulated through feedback inhibition at an allosteric site of the conserved bacterial G1P-T RmlA. Here, we sought to address the cellular consequences of G1P-T dysregulation on metabolic flux and E. coli physiology. Expression of a hyperactive RmlA variant in E. coli cells lacking native G1P-Ts abrogated growth, induced morphological defects, and increased sensitivity toward cell division inhibitors. These defects were suppressed through nucleotide supplementation, leading to the hypothesis that growth and division defects result from observed depletion of nucleotide pools required for DNA synthesis. Inspection of nucleotide metabolite compositions in E. coli lysates carrying mutant G1P-T, however, also indicated increased cellular concentrations of the primary metabolite uridine diphosphate glucose (UDP-Glc), which is known to block cell division. We found that high intracellular levels of UDP-Glc also unexpectedly halt the expression of O-Ag, which reveals that this metabolite is key for coordinating surface glycan biosynthesis and DNA precursor production prior to cell division. Overall, this work highlights the importance of G1P-T regulation and uncovers additional roles of UDP-Glc as a molecular sensor that mediates diverse bacterial biosynthetic processes.

Shape-morphing active particles with invertible effective polarizability for configurable locomotion and steering

Study on the combined influence mechanism of temperature, density and moisture content on the resistivity of loess

Structured electrolytes facilitate Grotthuss-type transport for enhanced proton-coupled electron transfer reactions

Concentrated hydrogen-bonded electrolytes (CoHBEs) are structured, electrochemically stable, less-volatile alternatives to aqueous and dilute nonaqueous electrolytes, however, with high viscosities that limit molecular diffusion. This work provides an understanding of the proton conduction mechanism in CoHBEs based on mixtures of acids and azoles and establishes a link between the structurally dictated transport properties and the proton-coupled electron transfer (PCET) reaction rates that can be leveraged for enhancing electrochemical reactions. Diffusion and relaxation NMR studies suggest a breaking of the viscosity–conductivity tradeoff, where at high azole concentrations (&gt;45 mol%), Grotthuss transport is more likely with lowered proton transfer energy barriers between the azole and the acid according to the machine learning (ML) accelerated ab initio path integral MD (AI-PIMD) simulations. Proton conduction pathways are found to be switchable between the hydrogen bonding networks of the acid and the azole, with imidazole chain forming structures better facilitating Grotthuss hopping. Supported by small-angle neutron scattering studies, the chains are found to have six member molecules on average with maximum of 3 to 4 imidazole/imidazoliums at 50 to 60 mol%. Despite their high viscosities, the measured PCET rates for quinones and phenazines measured in the protic CoHBEs present relatively high electron transfer rate constants (k 0 ~ 10 − 4 cm/s), validated by rotating disc electrode and scanning electrochemical microscopy measurements. The results demonstrate that strategic tuning of hydrogen-bond donor–acceptor interactions enables the decoupling of proton transport and viscosity, thereby impacting PCET reactions.