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Impact of Indoor Environmental Quality on Student Behavior: A Case Study Using AI-Powered Computer Vision

Near-total Faraday rotation by the Hall effect in a 2D electron gas

Phenotypic and genotypic antimicrobial resistance profiles of gram-positive cocci and non-fermenting gram-negative rods

Shock-induced magnetic reconnection in the Venusian magnetotail

LncRNA TUG1 mitigates sepsis-induced acute lung injury via a ceRNA network regulating the CALM1/PRKG1/RYR3/AQP5 axis

Abstract Sepsis-induced acute lung injury (ALI) is a life-threatening condition associated with high mortality, yet the molecular mechanisms driving alveolar damage remain incompletely understood. Long non-coding RNA (lncRNA) TUG1 has been implicated in organ injury, but its specific role and regulatory network in septic ALI have not been fully elucidated.Using lipopolysaccharide (LPS)-treated mouse lung epithelial (MLE-12) cells and a murine model of ALI, we investigated the functional role of TUG1 through overexpression strategies. Gene expression, protein levels, inflammatory cytokines, and miRNA interactions were assessed via qPCR, Western blotting, ELISA, and dual-luciferase reporter assays. Bioinformatic analysis of public datasets (GSE241238, GSE48080) was performed to validate clinical relevance.TUG1 expression was significantly downregulated in LPS-induced ALI models. TUG1 overexpression mitigated inflammation and oxidative stress by acting as a competing endogenous RNA (ceRNA) for miR-222-3p, thereby derepressing CALM1. Activation of CALM1 subsequently engaged the PRKG1/RYR3 signaling cascade, leading to restoration of AQP5-mediated alveolar fluid clearance. Analysis of public datasets confirmed suppression of the TUG1/CALM1 axis in septic patients and revealed its association with adverse survival outcomes. While the preliminary sample sizes ( n  = 3 in vitro, n  = 5 in vivo) limit the statistical power (post-hoc 0.65), the robust trends support the TUG1 axis as a potential target, though larger cohort validation is needed.This study identifies TUG1 as a potential modulator of sepsis-induced ALI through the miR-222-3p/CALM1/PRKG1/RYR3/AQP5 axis. These findings underscore the therapeutic potential of targeting TUG1 to alleviate septic lung injury. These findings identify TUG1 as a protective lncRNA that acts via the miR-222-3p/CALM1 axis to regulate calcium signaling and alveolar fluid clearance. Targeting this pathway may offer a novel therapeutic strategy for sepsis-induced ALI.

Robust intensification of projected regional precipitation extremes over Africa

Abstract Extreme rainfall is increasing under climate warming, but its future patterns across Africa remain highly uncertain. Using Coupled Model Intercomparison Project Phase 6 (CMIP6) simulations, we assess projected changes in annual maximum one-day precipitation (Rx1day) and rare precipitation extremes across African subregions under both SSP2-4.5 and SSP5-8.5 scenarios. Our results show robust intensification of Rx1day by the late twenty-first century, with increases of ~5–10 mm day⁻¹ (15–23 mm day⁻¹) under SSP2-4.5 (SSP5-8.5), largest in convectively dominated equatorial regions such as West, Central, and Northeast Africa. Rare events that historically occurred once every 50 (100) years are projected to recur every ~5–10 ( ~ 6–14) years, with recurrence intervals as short as 2–3 years in equatorial regions under SSP5-8.5. This intensification is driven primarily by thermodynamic moistening associated with radiation-induced warming, while diabatic heating–driven dynamic changes modulate regional responses and account for much of the intermodel spread. A hierarchical emergent-constraint framework based on observed historical global mean surface temperature trends moderates mean Rx1day intensification by ~11–35% without altering its sign. Constrained and unconstrained projections indicate substantial continent-wide increases in population and gross domestic product exposure.

Facile green synthesis of selenium nanoparticles using olive (Olea europaea) leaf extract and their antimicrobial and antibiofilm properties

Abstract The spread of antibiotic-resistant microorganisms is increasing, posing a significant health threat to humans. The world is now using nanoparticles, particularly through green synthesis, as an effective alternative to traditional antimicrobials. Selenium nanoparticles (Se NPs) were produced from the Olea europaea plant extract and have been characterized using UV-Visible, FTIR, SEM, EDX, zeta potential, and HR-TEM. The antimicrobial effectiveness of Se NPs was evaluated against several microbial strains, including Staphylococcus aureus , Escherichia coli , Klebsiella pneumoniae , Citrobacter freundii , and Candida albicans , and its impact on their biofilm formation was tested. The UV-Vis spectrophotometer results displayed the highest absorption at 380 nm, indicating the synthesis of selenium nanoparticles. The biosynthesized Se NPs were uniform, well-dispersed, quasi-spherical in shape, and with particle sizes ranging from 2.60 to 4.75 nm. The antimicrobial activity analysis of Se NPs showed that C. albicans was mostly inhibited, recording an inhibition zone diameter of 35.98 ± 0.65 mm at 150 µg/mL. The antibiofilm assessment represented a 59.04% inhibition of C. albicans biofilm. In conclusion, Se NPs have proven to be economical, less toxic, and environmentally friendly antimicrobial agents for preventing and treating many bacterial and fungal infections.

GPCR kinases shape ACKR4 functions via differential C-terminal phosphorylation

Abstract Atypical chemokine receptor 4 (ACKR4) is a scavenger receptor that regulates the availability of chemokines, including CCL19, and consequently the responsiveness of their classical G protein coupled receptors (GPCRs). In contrast to classical chemokine receptors, ACKR4 is completely biased towards βarrestins and does not couple to G proteins. Here, we show that ACKR4 in its apo state constitutively pre-associates with βarrestins and cycles between the plasma membrane and endosomal compartments. We identify distinct serine and threonine residues in the tail region of ACKR4 involved in regulating steady-state receptor trafficking and chemokine uptake, and that a C-terminal serine/threonine cluster is key for both ligand-mediated βarrestin recruitment and efficient chemokine uptake. Moreover, different serine/threonine clusters in the tail region of ACKR4 account for steady-state and chemokine-driven association of the four non-visual GPCR kinases (GRKs), which differentially phosphorylate two serine and one threonine residues. We show that GRK5/6 primarily phosphorylate ACKR4 in the absence of chemokines, and that CCL19 stimulation recruits GRK2/3 to enhance ACKR4 phosphorylation. Notably, we found that apo ACKR4 forms a ternary complex with GRK2/3 and the G protein without activating it. Finally, we show that the C-terminal serine/threonine cluster of ACKR4 and GRK2 play leading roles in βarrestin recruitment and CCL19 internalisation.

Travel recommendation via diffusion-guided multiplex graph contrastive learning

Keratins coordinate tissue spreading by balancing spreading forces with tissue material properties

Abstract For tissues to spread, they must deform while staying intact. How spreading tissues balance flexibility with integrity is not yet well understood. Here, we show that keratin intermediate filaments adapt tissue mechanical resilience to the stresses arising in epithelial tissues during spreading. By analyzing the expansion of the enveloping cell layer (EVL) over the yolk cell in zebrafish embryos in vivo, we find that keratin network maturation in EVL cells is promoted by stresses building up within the spreading tissue. Through genetic interference and tissue rheology experiments, complemented by a vertex model with mechanochemical feedback, we demonstrate that stress-induced keratin network maturation in the EVL increases tissue viscosity, to prevent tissue rupture. Further, keratins are required in the yolk cell for mechanosensitive actomyosin network contraction and flow, the forces pulling the EVL. These dual mechanosensitive functions of keratins enable a balance between pulling force production and EVL mechanical resilience, ensuring uniform and robust tissue spreading.

Explainable multi-agent learning for adaptive terrorist network disruption

Abstract Disrupting terrorist networks remains a critical challenge for counter-crime units due to their adaptive, decentralized, and covert nature. Existing approaches provide valuable structural insights but often rely on static representations and do not capture the sequential and adversarial dynamics underlying real-world intervention processes. In this work, we propose an explainable, game-theoretic multi-agent reinforcement learning (MARL) framework for simulating and analyzing adaptive terrorist network disruption. We formulate the problem as a partially observable, sequential decision-making process between two agents: an attacker , representing a terrorist organization seeking to expand its operational or ideological influence, and a defender , modeling law enforcement entities tasked with disrupting influence and neutralizing key actors. The framework incorporates domain-informed reward functions that capture structural, behavioral, and resilience-related properties of networks, enabling both agents to learn policies through repeated interaction. A central contribution of this work is the integration of explainability into the learning framework, allowing the generation and quantitative evaluation of interpretable rationales for node-level intervention decisions. Rather than modeling the full complexity of radicalization processes, the proposed approach provides a stylized but tractable simulation environment for studying strategic interaction under uncertainty. Empirical evaluations on multiple real-world-inspired extremist network structures show that (i) disruption effectiveness improves with increasing intervention budget but exhibits non-monotonic and network-dependent behavior, (ii) outcomes are strongly shaped by attacker–defender strategy interactions rather than individual strategies alone, and (iii) learned policies produce consistent and structured explanation patterns that reveal underlying network vulnerabilities. These findings demonstrate that explainable MARL can provide actionable insights into adaptive intervention strategies and serve as a decision-support tool for intelligence-led policing in complex networked environments.

Unveiling the emission mechanism in analog-doped carbazole-based organic afterglow materials

Enhancing spectral analysis of ghee adulteration via a deep learning-based multimodal attention mechanism

Interplay of oxygen vacancies and lanthanide emitters enables reversible upconversion switching

Integrated assessment of drinking water quality and child nitrate health risk using indices and Monte Carlo simulation

Protein-based pan-RAS inhibitor induces tumor regression in female mice via IFNγ and CD8+ T cell-dependent tumor necrosis

Abstract Mutations in K/H/N-RAS occur in approximately 30% of human cancers, yet most RAS mutants remain undruggable in clinical settings. Here, we describe a protein-based pan-RAS inhibitor, RRSP-RBD, that combines a RAS/Rap1A-specific endopeptidase (RRSP) with a RAS-binding domain (RBD). This engineered fusion protein localizes to RAS on the plasma membrane, where it cleaves RAS, disrupts RAS-effector interactions, and effectively inhibits downstream RAS signaling. To achieve intracellular delivery of RRSP-RBD in vivo, we engineer two cell-permeable variants. The diphtheria toxin-based version (RRSP-RBD-DTB) demonstrates femtomolar anti-tumor potency and induces tumor regression in a xenograft mouse model. The cell-permeable peptide-based version (RRSP-RBD-TAT) exhibits robust anti-tumor activity in syngeneic models without inducing irreversible toxicity in normal tissues. Interestingly, anti-tumor efficacy of RRSP-RBD-TAT critically depends on the tumor microenvironment, requiring infiltration by IFNγ +  CD8 +  T cells to mediate tumor regression. Pharmacokinetic and toxicity evaluations indicate that RRSP-RBD is tolerated under the conditions tested and support further investigation as a protein-based pan-RAS inhibitor (all mouse studies were performed in female mice).

Impact of hospital safety-net status on in-hospital and short-outcomes after hematopoietic stem cell transplantation

Deciphering electrochemomechanical interplay in rechargeable aqueous Zn||MnO2 batteries

The effect of narrative medicine-based education on academic performance and humanistic communication in residency training: a systematic review and meta-analysis

A phase II peri-operative study of pembrolizumab plus lenvatinib for mucosal melanoma

Abstract Mucosal melanoma is an aggressive malignancy with limited neoadjuvant options. We conducted a single arm, phase II study of neoadjuvant pembrolizumab plus lenvatinib followed by surgery and adjuvant pembrolizumab in resectable mucosal melanoma (NCT04622566) along with exploratory biomarker analysis. Primary objective was pathological complete response (pCR) rate; secondary endpoints included relapse-free survival (RFS), overall survival (OS), clinical response, surgical outcomes, and safety. Among 21 surgical patients, the pCR rate was 9.5%, major pathologic response (MPR) rate was 19.0%, and the pathologic response rate was 38.1%. Median RFS was 14.8 months (1-year rate: 61.9%); median OS was not reached. No grade 4–5 treatment-related toxicities or additional perioperative complications occcurred. Spatial profiling revealed a more immune-inflamed baseline microenvironment in responders, with activated CD4⁺/CD8⁺ T cell signatures associated with favorable outcomes. Treatment induced vascular normalization and increased T cell infiltration in non-responders, partially narrowing the immune gap. Responders exhibited higher prevalence of persistent TCR clonotypes and tighter spatial proximity between activated CD4⁺ and CD8⁺ T cells. Although the pre-specified primary endpoint was not met, our findings identify activated CD4 + /CD8 + T cell states and TCR persistence as key outcome-associated features, supporting immune-informed optimization of peri-operative therapy in mucosal melanoma.