Search Results (2,995)

Single-molecular white circularly polarized luminescence emitters show promise for use in chiral displays and solid-state lighting, but their design remains challenging because broadband emission, exciton utilization, color balance, and chiroptical activity must be integrated within one molecule. Herein, we report a chiral single-molecular white emitter, DCz-PTZ, constructed through a π-interrupted strategy by combining a rigid spiro framework, an oxygen-bridged carbazole/cyanobenzene segment, and a phenothiazine donor. The interrupted conjugation suppresses excessive charge-transfer (CT) domination and enables dual emissive channels, including short-wavelength locally excited (LE) emission and long-wavelength CT emission. DCz-PTZ exhibits near-ideal white emission in dilute toluene solution with CIE coordinates of (0.33, 0.33), and maintains balanced dual emission in 5 wt% doped films with CIE coordinates of (0.32, 0.34). Photophysical studies support the assignment of the yellow emission to a thermally activated delayed fluorescence (TADF)-active CT state. The enantiomers show mirror-image circularly polarized signals with |g_lum| up to 2.9 × 10⁻³. Optimized white organic light-emitting diodes (WOLEDs) achieve color rendering index (CRI) up to 92 and a maximum external quantum efficiency (EQE_max) of 1.3%. This work demonstrates a π-interrupted molecular strategy for integrating dual emission, TADF exciton utilization, and circularly polarized electroluminescence (CPEL) in a single chiral emitter. Full article

Introduction: Aquatic chemical pollution is among the most worrying threats to ecosystem health. There is an ever-increasing variety of pollutant substances detected across the source-to-sea continuum, causing loss of biodiversity and ecological disequilibrium. Achieving cleaner and healthier systems relies on carrying out sustained, cost-effective, diagnosis and aquatic effects monitoring, within the adaptive management cycle. The available methods are, however, cumbersome, which creates a clear need for innovative expeditious approaches for low-cost surveillance monitoring. In the last decade, Raman Spectroscopy (RS) has gained wide recognition for application to biological questions, for its ability to uncover the complexity of molecules and their interactions. Various fields, from pharmacology to disease diagnosis and prognosis, have suffered an innovation revolution through the application of RS. In this technique inelastic light scattering of a small part of photons of an incident electromagnetic monochromatic light beam (ranging from near-infrared to visible or ultraviolet) is caused by the molecular vibration of chemical bonds. This results in shifts in energy, which indicate discrete vibrational modes of polarisable molecules, providing qualitative and quantitative assessments of the chemical composition and molecular structure of the sample. The technique shows high sensitivity, no need for sample preparation and the possibility of use in non-invasive and label-free analysis. Objective: The aim of this work is to present and discuss evidence about the application of Raman Spectroscopy (RS) to environmental diagnosis and aquatic effect monitoring of pollution. Methodology: The technique was applied to different biological models, i.e., diatoms, zebrafish embryos and larvae and freshwater snails. Quality assessments with diatoms were tested in environmental monitoring, while assessments with other models were done upon exposure to metals and organic contaminants. Results and conclusions: The Raman spectra obtained from the samples analysed comprised bands detected within the 800 to 2000 cm⁻¹ wavenumber range. These were related to bond vibrations of carbohydrates, DNA phosphate groups, proteins or CH, NH and OH stretching in lipids and proteins. Data analysis using chemometric methods clearly distinguished pollutant exposure from control sites or treatments, pointing out the potential for surveyance monitoring. The next steps include the comparison with other sensitive methods (e.g., locomotion and avoidance behaviours, omics methods) to assess efficiency and bring further mechanistic understanding. Full article

Abiotic stresses, including drought, salinity, alkalinity, temperature extremes, flooding, heavy metals, and emerging pollutants, challenge plant growth and productivity by disturbing water relations, ion balance, redox homeostasis, membrane stability, energy metabolism, and developmental progression. Although substantial progress has been made in the identification of stress-responsive hormones, second messengers, kinases, transcription factors, transporters, and metabolic regulators, plant stress adaptation cannot be fully explained by linear signaling cascades or single tolerance genes. A major unresolved question is how early molecular events are reorganized into coordinated physiological and developmental outputs that support survival, recovery, and productivity. In this review, we propose an intermolecular interaction-driven adaptive remodeling framework for plant abiotic stress responses. This framework emphasizes that stress tolerance emerges from dynamic changes in receptor–ligand recognition, protein–protein interactions, calcium decoding, redox-sensitive modification, phosphorylation networks, transcriptional regulation, chromatin-associated control, and metabolite-mediated feedback. We further emphasize ROS as integrative redox switches that connect stress sensing, defense activation, senescence-related transitions, and recovery, and chromatin-associated mechanisms as regulators that may stabilize primed or memory-like adaptive states. We discuss how these interaction networks converge on core signaling hubs, including abscisic acid, reactive oxygen species, Ca²⁺, and kinase/phosphatase systems, and how they remodel stomatal behavior, root architecture, ion and pH homeostasis, redox buffering, metabolism, development, and reproductive resilience. We further highlight how natural variation, multi-omics, genome editing, high-throughput phenotyping, and field validation can translate interaction-centered stress biology into crop resilience. This perspective provides a conceptual bridge between molecular stress perception, network behavior, physiological adaptation, and climate-resilient agriculture. Full article

The potential health hazards caused by microwave exposure have attracted increasing attention. Microwave radiation has been reported to induce oxidative stress in neural tissues, which is considered one of the primary mechanisms underlying its adverse effects on central nervous system function. The hippocampus is sensitive to microwave radiation, whereas underlying cellular and molecular mechanisms remain incompletely understood. In this study, microwave-exposed mice exhibited significantly impaired performance in the Go/No-go, Y-maze, and novel object recognition tests at 6 h and 7 days post-exposure, indicating deficits in hippocampus-dependent working memory. Single-cell RNA sequencing of hippocampal tissues from control and microwave-exposed mice yielded 94,088 high-quality cells across eight major cell types. Astrocyte sub-clustering identified five transcriptionally distinct subpopulations, with Astrocyte_S100a6 and Astrocyte_Son proportions increased and Astrocyte_Serpinf1 decreased in the radiation group. Analysis of astrocyte transcriptional state transitions showed microwave-exposed astrocytes were preferentially distributed toward terminal reactive states with depletion at early homeostatic nodes. Cell–cell communication analysis revealed increased total interactions and interaction strength following radiation. Astrocyte outgoing signaling was increased for pathways associated with vascular remodeling, phagocytic regulation, and neuroinflammation, while pathways related to trophic support were decreased. Incoming signaling showed increased activity in pathways linked to phagocytic recruitment and inflammatory mediation. Taken together, these findings indicate that microwave exposure is associated with hippocampus-dependent working memory deficits accompanied by transcriptional remodeling of astrocyte subpopulation composition, directional astrocyte state transitions toward reactive phenotypes, and broad alterations in astrocyte-centered intercellular communication, providing a cellular and molecular framework for understanding astrocyte involvement in microwave radiation-associated hippocampal dysfunction. Full article

Surface-enhanced Raman scattering (SERS) offers a powerful route for biomolecular detection because it combines molecular specificity with high sensitivity, rapid optical readout, and multiplexing capability. In real biological samples, however, analytical performance is rarely determined by signal enhancement alone. Biofluids such as serum, plasma, saliva, urine, and interstitial fluid contain complex biomolecular mixtures that interfere with target capture, spectral response, and data interpretation. A practical SERS biosensor must therefore localize targets, stabilize spectral responses, tolerate matrix-induced variation, and convert complex spectra into reliable analytical information. This review discusses recent progress in SERS biosensing from an integrated system perspective, with particular focus on artificial intelligence/machine learning (AI/ML)-assisted interpretation. Direct label-free SERS provides chemically transparent readouts but is limited by stochastic adsorption, hotspot heterogeneity, and spectral variation in complex samples. Bio-recognition interfaces improve target localization, while signal-transduction strategies based on nanotags, immunoassays, clustered regularly interspaced short palindromic repeats (CRISPR) systems, nanozymes, and lateral-flow formats decouple molecular recognition from spectral generation. Digital SERS further improves measurement robustness by converting fluctuating intensities into countable, event-based outputs. AI/ML-assisted analysis can support full-spectrum classification, calibration transfer, explainability, and patient-level decision-making. We frame AI/ML-assisted SERS biosensing as an integrated architecture connecting substrate design, interface engineering, signal transduction, digital measurement, and clinical validation. Future progress will depend as much on validation-ready workflows as on plasmonic enhancement itself, especially for systems intended to operate across different samples, instruments, and clinical settings. Full article

Extracellular vesicles (EVs) are key mediators of intercellular communication across biological kingdoms, with central roles in immune regulation and disease processes. Despite shared structural features, EVs derived from bacteria, plants, and mammalian cells differ substantially in their biogenesis, molecular composition, and immunological functions. EV formation pathways generate vesicles with distinct cargo profiles, including pathogen-associated molecular patterns (PAMPs) in bacterial EVs, regulatory small RNAs in plant-derived vesicles, and cytokines, microRNAs, and antigen-presenting complexes in mammalian EVs. Differences in cargo result in divergent immune outcomes. Bacterial EVs predominantly activate innate immunity via pattern recognition receptors such as Toll-like receptors, whereas plant-derived EVs exhibit low immunogenicity and mediate cross-kingdom RNA interference. In contrast, mammalian EVs primarily regulate immune responses by modulating antigen presentation and cytokine signaling. These findings support a framework in which EV origin determines immunological function and therapeutic applicability. This perspective highlights the importance of selecting appropriate EV sources for vaccine development, regenerative medicine, and targeted delivery strategies, while addressing current challenges related to heterogeneity, standardization, and safety. Full article

Background/Objectives: Mosquitoes, including Culex quinquefasciatus and Aedes aegypti, are important vectors of dengue fever, Zika virus, West Nile virus, Japanese encephalitis virus, Eastern equine encephalitis virus, etc. Biological control has always been urgent in mosquito prevention due to resistance developing to synthetic insecticides and environmental toxicity by insecticides. Methods: The leaf essential oil of Mosla. chinensis was isolated, and major components were identified via GC-MS, followed by olfactory behavior assays to evaluate its repellent activity against C. quinquefasciatus. Additionally, the odorant-binding protein 1 and odorant-binding protein 2 (CquiOBP1-2) genes were prokaryotically expressed, and their fluorescence competitive binding activities with the active components of essential oils were examined. Results: The bioassays indicated this essential oil greatly repels C. quinquefasciatus, which will significantly protect people against vector-borne diseases. In the fluorescence competitive binding experiments, the CquiOBP1-2 proteins exhibit great binding capacities to volatile components, including Citronellal, Citronellol, Geraniol, Limonene and Isopulegol. Furthermore, the behavioral experimental results also indicate that the mixture of these five ligand compounds has an obvious repellent effect on mosquitoes, highlighting that they may be applied as potential mosquito repellent agents. Moreover, molecular docking and site-directed mutation analysis further confirm Phe123 and Gln77 are both key amino acid residues of CquiOBP1-2 proteins involved in the olfactory recognition of repellent ligand compounds from M. chinensis essential oil. Conclusions: The behavioral experimental verification and the exploration of olfactory molecular mechanisms are helpful to promote the biological control of plant essential oils in mosquito pests. Full article

Autism spectrum disorder is increasingly linked to altered microglial biology. However, current research models are limited by outdated descriptions of microglial “activation”. Here, we propose that microglial involvement in ASD is best understood as a problem of state mismatch, in which temporally programmed and regionally specialized microglial states fail to align with local developmental demands. We synthesize evidence across genetic models, human transcriptomics, and experimental systems to examine three axes of misalignment: developmental timing, circuit specificity, and functional phenotype. These mismatches produce divergent outcomes, including both excessive and insufficient synaptic pruning, and reflect a decoupling between microglial activation markers and effector capacity. We further evaluate molecular recognition systems governing microglia–synapse interactions, with emphasis on complement signaling and glycan-mediated pathways such as sialic acid–Siglec signaling and polysialylation. While glycosylation is not a universal driver of ASD pathology, it represents a plausible regulatory layer controlling synapse visibility and microglial engagement. This framework reconciles conflicting findings in the literature and positions microglia as dynamic developmental effectors whose misaligned state trajectories contribute to circuit-level dysfunction in ASD. Full article

Background: Ferrocene-containing compounds have gained attention in medicinal chemistry due to their unique redox and structural properties. This study investigates ferrocene-based analogues of imatinib and nilotinib to define their binding determinants within the ABL1 kinase domain using an integrated in silico approach, in relation to their previously reported cytotoxic activity. Methods: Ligand geometries were optimized at the B3LYP/def2-TZVP level with D3(BJ) dispersion and SMD solvation. Molecular docking against ABL1 (PDB ID: 2HYY) was performed using Glide SP, validated by re-docking and enrichment screening. Docked poses were refined using MM-GBSA (Prime, VSGB 2.1/OPLS4). The most active compounds (9 and 15a), together with the inactive control 15e, were subjected to three independent 500 ns molecular dynamics simulations (Desmond, OPLS4), followed by trajectory analysis including RMSD, RMSF, radius of gyration, SASA, and polar surface area. Results: Compounds 9 and 15a maintained stable binding within the ATP-binding pocket despite lacking the canonical hinge interaction with Met318, indicating hinge-independent binding. Their binding was mainly driven by interactions with Asp381 (DFG motif) and cation–π contacts with Lys271. In contrast, the compound 15e showed unstable binding, increased conformational flexibility, reduced pocket burial, and loss of key stabilizing interactions. Active compounds also preserved stable P-loop dynamics, with Tyr253 engagement suggesting a role in loop stabilization. Compound 9 exhibited the most constrained and reproducible binding mode among all analogues. Conclusions: Ferrocene-based analogues can sustain stable ABL1 binding via non-classical interaction networks independent of hinge recognition. The clear distinction between active compounds and the inactive analogue 15e supports the robustness of the proposed binding mode and provides a structural basis for their reported cytotoxic activity. These findings support further experimental evaluation of ferrocene-containing scaffolds as potential BCR-ABL1 inhibitors. Full article

Colored rice is a type of functional cereal rich in bioactive substances such as anthocyanins. This article systematically reviews its molecular formation, nutritional quality, health effects, and industrial applications. At the molecular level, the biosynthesis of pigments such as anthocyanins is regulated by transcription factors including MYB and bHLH, and is influenced by environmental conditions such as light, temperature, and fertilization. Nutritional analysis shows that, compared to white rice, colored rice contains higher levels of resistant starch, high-quality protein, dietary fiber, minerals, and vitamins. In addition, it is rich in various phenolic compounds and gamma-aminobutyric acid (GABA). These bioactive components have functional food applications in chronic diseases such as diabetes, cardiovascular diseases, and cancer through multiple mechanisms. These mechanisms include antioxidant and anti-inflammatory activities, regulation of glucose and lipid metabolism, and modulation of the gut microbiota. Despite the advancements in molecular breeding and precision cultivation technologies that have driven variety improvement and diversified product development, the industry still faces challenges such as the contradiction between nutrient retention and processing palatability, as well as insufficient market recognition. In the future, it is necessary to integrate multidisciplinary technologies to promote the development of colored rice. This may contribute to modulating risk factors associated with chronic diseases based on precision nutrition evidence. Full article

The dopamine D₃ receptor (D₃R) has long been considered a secondary target in the treatment of Parkinson’s disease (PD), with therapeutic strategies primarily focused on D₂ receptor–mediated motor control. However, accumulating evidence now supports D₃R as a functionally distinct dopaminergic receptor subtype with specific relevance to non-motor symptom domains and dopaminergic signaling under hypodopaminergic conditions. Recent advances in high-resolution structural biology have elucidated the molecular basis of D₃R/D₂R discrimination, revealing how subtle residue-level and microstructural differences within a conserved G protein–coupled receptor framework shape ligand recognition and receptor activation. In parallel, the emergence of ligand-dependent biased signaling has refined current understanding of D₃R pharmacology. Selected ligands can preferentially engage Gα_i/o-mediated pathways while limiting β-arrestin recruitment and associated regulatory processes, providing a mechanistic rationale for more stable modulation of mesolimbic dopaminergic circuits involved in affective and motivational regulation. Beyond symptomatic modulation, preclinical studies suggest that D₃R signaling may influence neuronal resilience, synaptic plasticity, and adaptive responses to dopaminergic injury; however, such effects remain experimental and have not been demonstrated in clinical PD. This review integrates recent structural, signaling, and functional insights into D₃R biology, with particular emphasis on biased agonism and emerging therapeutic concepts. Although D₃R-targeted strategies do not currently represent disease-modifying interventions, they offer a rational framework for the development of next-generation dopaminergic therapies aimed at improving precision, tolerability, and long-term signaling stability in Parkinson’s disease. Full article

Multiple sclerosis (MS) is a chronic immune-mediated disease of the central nervous system characterized by demyelination, neuroinflammation, and progressive neurodegeneration. While there is a small component of genetic susceptibility to MS risk, environmental factors, including infectious exposures, are gaining increased recognition as playing a critical role in MS initiation and progression. Viral infections, especially by Epstein–Barr virus (EBV), have emerged as strong candidates and triggers of MS symptoms, through antibody-mediated molecular mimicry and B-cell dysregulation. In contrast, parasitic infections, including helminths and select protozoa, appear to exert neuroprotective effects by skewing immune responses toward regulation and tolerance. In this review, we examine antibody-driven mechanisms by which viral pathogens promote autoimmunity in MS and contrast these with parasite-induced immunoregulatory pathways that suppress pathogenic inflammation. We further discuss diagnostic and therapeutic implications, highlighting how insights from infectious immunology may inform novel strategies for MS treatment. Full article

Background/Objectives: Alzheimer’s disease (AD) disproportionately affects women, who account for nearly two-thirds of affected individuals worldwide. This sex imbalance cannot be explained by longevity alone and likely reflects complex interactions among biological sex, endocrine aging, genetic susceptibility, and brain-specific mechanisms of vulnerability. Neuroimaging has played a pivotal role in characterizing these sex-related differences in vivo, enabling the assessment of amyloid-β deposition, tau propagation, neurodegeneration, cerebral glucose metabolism, and network reorganization. This invited review examines AD through a rigorously sex-specific neuroimaging perspective, with particular emphasis on implications for women’s brain health. Methods: We integrated evidence from structural MRI, FDG-PET, amyloid-PET, tau-PET, estrogen receptor PET, diffusion MRI, and fluid biomarkers, together with epidemiological, molecular, genetic, and endocrine studies. The review focuses on female-specific trajectories of AD initiation and progression, highlighting the contribution of neuroendocrine aging, menopause, metabolic dysfunction, and sex-modulated genetic risk factors. Results: Available evidence indicates that women exhibit distinct biological and neuroimaging signatures across the AD continuum. Menopause emerges as a critical neuroendocrine transition associated with metabolic decline, altered brain connectivity, increased amyloid and tau vulnerability, and progressive neurodegeneration. Female-specific patterns of tau propagation and sex-dependent interactions with genetic risk factors further contribute to differential disease trajectories. Advanced multimodal neuroimaging approaches have substantially improved the characterization of these mechanisms and their relationship with cognitive decline and clinical progression. Conclusions: A sex-specific neuroimaging framework is essential to improve understanding of AD pathophysiology and to advance precision medicine approaches tailored to women’s brain health. Recognition of endocrine aging and female-specific biological vulnerability may inform earlier identification of at-risk individuals and the development of targeted prevention and treatment strategies. Future research should prioritize sex-aware longitudinal studies and multimodal biomarker integration to optimize personalized interventions in AD. Full article

The iminosugar N-butyldeoxynojirimycin (Miglustat) is clinically used for the inhibition of ceramide glucosyltransferase for treating Type 1 Gaucher and Niemann–Pick type C diseases. This drug also inhibits glycogen debranching enzyme (GDE), the enzyme responsible for terminal glycogen catabolism via coordinated glucotransferase and amylo-α-1,6-glucosidase (GC) activities, although the structural basis for inhibition has been undefined. Here, we report the crystal structure of Candida glabrata GDE in complex with Miglustat, revealing inhibitor engagement at the conserved GC domain in an area that was previously hypothesized to accommodate the α-1,6-linked glucose moiety of glycogen. Structure-guided mutagenesis demonstrates that alanine substitution of residues at the GC site abolishes Miglustat binding, functionally validating the pocket and defining the interaction hot spots. To assess the possible relevance of these observations to the human enzyme, in silico docking predicts that Miglustat binds to the human enzyme in a pose close, albeit not identical, to our structure. These findings provide an opportunity to determine the molecular basis of GDE–inhibitor recognition, rationalize reported off-target effects of Miglustat, and provide a template for designing iminosugar therapies with reduced off-target binding. Full article

Background: Reverse transcription is a key step in emerging RNA diagnostics, but reverse transcriptase (RT) enzymes often fail in the presence of inhibitors carried over from clinical samples or introduced during RNA extraction. Here, we dissect the molecular basis of inhibitor resistance in five engineered variants (V1 to V5) of Moloney Murine Leukemia Virus RT, originally optimized for thermostability and catalytic activity. Methods: Using a systematic framework that integrates structural analysis, thermal profiling, and diagnostic benchmarking, we evaluated cDNA synthesis from 40 to 70 °C under a panel of 11 clinically relevant inhibitors. Results: Across 30 mutations assessed, a recurrent set of substitutions (E69K, E302K/R, W313F, and N454K), present in RT V1 and V4, was associated with enhanced robustness, consistent with strengthened enzyme–nucleic acid engagement, while L435G likely contributes by modulating conformational flexibility. Notably, inhibitor tolerance was maximal at moderate reaction temperatures (≈40 °C), where productive enzyme–substrate interactions best offset inhibitory stress, while the wild-type enzyme was effectively inactivated by several inhibitors under the conditions tested. Although the engineered RTs remained catalytically competent at higher temperatures, increased thermal stress may destabilize productive enzyme–nucleic acid complexes, reducing resistance under inhibitory conditions. Conclusions: Together, these findings support substrate engagement as an important determinant of RT robustness and provide practical guidance for engineering inhibitor-resistant RTs for high-sensitivity RT-qPCR. Full article