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The rapid advancement of generative artificial intelligence has introduced transformative opportunities and critical challenges for quality assurance in educational settings. This study aims to systematically map the scientific landscape on quality assurance in education mediated by generative artificial intelligence, identifying predominant methodological approaches, conceptual frameworks, and emerging research gaps. A bibliometric and scoping review was conducted following PRISMA-ScR guidance and integrating descriptive bibliometric analysis with qualitative thematic mapping. The analysis was based on 482 documents retrieved from Scopus and Web of Science, covering the period 2022-2026. The data were analyzed using a combined approach that integrates descriptive bibliometric analysis and qualitative content analysis of the abstracts. The results show a predominance of review studies, indicating a phase of conceptual consolidation in the field. There is also an increase in quantitative and experimental studies, reflecting a transition toward empirical validation of the use of generative artificial intelligence in education. From a conceptual perspective, the literature is primarily oriented toward quality assessment and ethical implications, particularly concerning biases, transparency, and responsible use of AI. In contrast, pedagogical frameworks and academic integrity show limited development. These findings highlight a structural tension between technological innovation and the need to ensure educational quality, ethical governance, and academic integrity. The need to develop integrative frameworks that articulate pedagogical, technological, and normative dimensions is emphasized. This study contributes to the understanding of an emerging field and provides relevant inputs for researchers, educators, and educational policymakers interested in the responsible implementation of generative artificial intelligence.

Sulfonamides remain important to medicinal and fine-chemical production but conventional aniline precursor routes like Pd-catalysed hydrogenation and Béchamp reductions carry sustainability, safety, and chemoselectivity challenges, especially for N-S bond integrity. This review assesses biocatalytic nitroreduction as a selective alternative for nitro-sulfonamides, focusing on p-aminobenzenesulfonamide (p-ABS). We summarise mechanistic and engineering advances in Type I (oxygen-insensitive) flavin-dependent nitroreductases (NTRs), highlight emerging roles and limits of Old Yellow Enzymes, and discuss auxiliary reductive platforms (H2-driven hydrogenases, photo-/electro-biocatalysis) for improved cofactor economy and endpoint selectivity. Process-intensification strategies, whole-cell vs. cell-free operation, immobilisation, packed-bed flow, on-line LC/IR PAT, and NAD(P)H regeneration via GDH/FDH or electroenzymatic modules are mapped to chemoselectivity risks (hydroxylamine accumulation, azo/azoxy formation) and mass-transfer constraints. We highlight development choices with green metrics (PMI, E-factor) and emphasise early LCA integration to avoid burden shifting from buffer salts or mediator residues. Evidence from continuous NTR reactors and immobilised formats supports scalable, aqueous, low-pressure operation; however, direct data on sulfonamide-linked nitroarenes is limited. This motivates a feasibility screen using an NTR panel (including engineered NfsB lineages), water-rich media with low co-solvent, and O2-tolerant settings. We conclude with a proposed flowsheet for p-ABS coupling immobilised NTR with FDH or electro-NAD(P)H supply, real-time analytics, and membrane-based product extraction. As direct data on sulfonamide-linked nitroarenes remain limited, this roadmap provides a practical and critical starting point for substrate-specific feasibility screening and future development.

The honeybee colony provides a remarkable example of aging plasticity emerging from collective biological organization. Through the reciprocal regulation of juvenile hormone (JH) and vitellogenin (Vg), honeybees demonstrate that aging is a dynamic and reversible process shaped by social and environmental conditions. The JH-Vg axis acts as a biological metronome that coordinates behavioral state, lifespan, and seasonal colony dynamics, synchronizing colony persistence with ecological and planetary rhythms. At the colony level, physiological states are continuously adjusted through interactions among endocrine regulation, pheromonal communication, and environmental cues. As a result, the colony maintains its organization not through static equilibrium, but through ongoing transitions between alternative physiological states that support either rapid growth or long-term survival. In this sense, the honeybee superorganism can be viewed as a self-organizing dissipative system-an open biological system that maintains order through the continuous exchange of energy, information, and resources with its environment. This perspective highlights how aging in eusocial insects emerges not solely from individual decline, but from multilevel regulatory interactions linking cells, organisms, colonies, and ecosystems.

Plants are best understood as evolutionary holobionts, in which the host and its associated microbiomes operate as an integrated unit to influence growth, health, and stress resilience. This comprehensive review synthesizes the most current knowledge of plant-associated microbiomes across key ecological compartments, including the rhizosphere, endosphere, phyllosphere, and seeds, highlighting their assembly drivers, functional mechanisms, and translational potential. We dissect the molecular foundations of rhizobial and arbuscular mycorrhizal (AM) symbioses, the plant-AM fungus-bacterium continuum, alongside emerging concepts including the aerial root mucilagesphere, phyllosphere homeostasis, and the pathobiome. We further explore host genetic, metabolic, and environmental determinants of microbiome assembly, and present cutting-edge methodologies ranging from quantitative profiling to artificial intelligence-driven synthetic community design. Finally, we outline a strategic blueprint for harnessing standardized synthetic microbiomes and precision microbiome engineering to advance sustainable agriculture. This integrative framework bridges fundamental ecology with practical applications, delineating a path toward climate-resilient crop production.

Liquid biopsy now provides minimally invasive access to tumor-derived genomic and epigenetic information across the lung cancer continuum, and its clinical role continues to expand. This review examines that role across cancer detection (screening and diagnosis), treatment monitoring (advanced-disease genotyping, minimal residual disease (MRD) assessment, and resistance profiling at progression), and clinical outcome prediction. Plasma-based genotyping is now well established in advanced non-small cell lung cancer (NSCLC), while circulating tumor DNA (ctDNA)-based MRD detection in the curative-intent setting has accumulated a substantial evidence base over the past 5 years. Cell-free DNA (cfDNA) methylation, fragmentomics, and circulating tumor RNA (ctRNA) are emerging as complementary modalities, particularly when tumor shedding is low. We also consider concordance between liquid and tissue biopsies, the use of cerebrospinal fluid (CSF) ctDNA in central nervous system (CNS)-involved disease, and the practical issues of cost, reimbursement, and access that shape clinical adoption. The current state of the field can be framed across three tiers of evidence, with established applications, applications under prospective evaluation, and applications not yet ready for routine clinical use. No multi-cancer early detection (MCED) test has shown a mortality benefit to date, and ctDNA-guided treatment changes in metastatic disease still lack randomized overall-survival data.

Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease in which disease flares frequently recur at previously affected anatomical sites. This distinctive clinical pattern suggests the presence of residual inflammation and long-lasting local immune memory that persists beyond apparent clinical remission. To synthesize current evidence on the role of tissue-resident memory T (TRM) cells in the pathogenesis, chronicity, and relapse of AD, and to discuss how TRM biology may explain disease recurrence after treatment withdrawal and inform future therapeutic strategies. Narrative review of experimental, translational, and clinical studies addressing TRM differentiation, persistence, metabolic and epigenetic programming, clonal stability, microenvironmental crosstalk, and treatment-related modulation in AD and related chronic dermatoses. TRM are long-lived, non-circulating T cells retained in the skin through adhesion molecules, survival cytokines, metabolic adaptation, and stable epigenetic programs. In AD, both CD4+ and CD8+ TRM persist in lesional and clinically resolved skin and remain transcriptionally poised for rapid reactivation. Clinical studies consistently demonstrate disease relapse after discontinuation of biologics and JAK inhibitors, supporting the concept that current therapies suppress inflammatory pathways without eliminating pathogenic tissue memory. Emerging data suggest that selected interventions, including modulation of costimulatory pathways and survival signals, may partially influence immune memory and prolong disease control in subsets of patients. TRM constitute a central cellular substrate of residual disease memory in AD and provide a mechanistic explanation for site-specific relapse and treatment resistance. Therapeutic strategies that selectively modulate pathogenic TRM and their supporting microenvironment, while preserving protective barrier immunity, may be required to achieve durable remission.

Osteoporosis is a systemic skeletal disorder characterized by reduced bone mass, deterioration of bone microarchitecture, and increased susceptibility to fragility fractures. Although conventional antiresorptive and anabolic drugs effectively reduce fracture risk in many patients, their clinical utility is restricted by poor tissue specificity, systemic adverse effects, adherence problems, discontinuation-related risks, and their limited capacity to regenerate osteoporotic bone defects after trauma or surgery. Biomaterial-based strategies provide complementary opportunities by combining local structural support, controlled therapeutic delivery, and microenvironmental regulation. In this review, we discuss biomaterial design from an osteoporosis-specific perspective, emphasizing how disease-associated abnormalities-impaired osteoblast function, excessive osteoclast activity, reduced angiogenesis, inflammatory dysregulation, compromised extracellular matrix quality, and weakened mechanical integrity-can be addressed by scaffolds, targeted drug delivery systems, and biologically derived platforms. Ceramic, polymeric, and composite scaffolds are compared with respect to osteoconduction, ion-mediated signaling, mechanical support, and manufacturability. Bone-targeted nanoparticles, injectable hydrogels, and stimuli-responsive carriers are evaluated as strategies for the localized delivery of antiresorptive agents, anabolic molecules, nucleic acids, and osteogenic cues. We further summarize platelet-rich plasma/platelet-rich fibrin, growth factor-loaded matrices, mesenchymal stem cell-laden scaffolds, extracellular vesicle-functionalized systems, and gene-activated matrices as emerging biological or cell-free regenerative platforms. Finally, key translational barriers, including long-term safety, reproducible manufacturing, standardized osteoporotic models, and regulatory pathways for combination products, are discussed. Overall, biomaterials should not be viewed as replacements for established pharmacotherapy but as disease-tailored local interventions that may improve osteoporotic fracture repair and bone regeneration when integrated with rational clinical management.

Attention-Deficit/Hyperactivity Disorder (ADHD) is a condition characterized by persistent patterns of inattention and/or hyperactivity-impulsivity. This case highlights the potential benefit of integrating Immersive Virtual Reality (IVR) with cognitive-behavioral therapy (CBT) in the rehabilitation of a child with ADHD. It contributes to emerging evidence by showing how a combined approach may simultaneously target executive, attentional, and motor domains within a single intervention. An 8-year-old child with deficits in sustained and selective attention, impaired executive functioning (including planning and working memory), impulsivity, and difficulties in motor regulation, as revealed during baseline assessments, impacting daily functioning. The patient was diagnosed with combined-type ADHD and underwent a 12-week CBT intervention, followed by integrated IVR-CBT intervention targeting executive functions and self-control, once a week for 12 weeks. The intervention was conducted using the CAREN (Computer Assisted Rehabilitation Environment), an immersive virtual reality platform integrating multisensory input and interactive tasks to promote cognitive and motor engagement. Post-intervention assessments showed improvements in sustained and selective attention, planning, working memory, and balance. There was also an increase in involvement and a reduction in impulsivity. The findings support the hypothesis that immersive, embodied interventions targeting both executive and sensorimotor processes may represent a promising novelty adjunctive rehabilitation approach. Further studies are needed to evaluate efficacy, generalizability, and to confirm these findings in larger samples. This case report was prepared in accordance with the CARE Guidelines.

Regenerative medicine is undergoing a paradigm shift from live-cell therapies to cell-free strategies. Within this evolving field, mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as a leading platform. These nanoscale vesicles deliver bioactive cargo that mediates critical therapeutic functions, including immunomodulation, angiogenesis, and anti-fibrosis. Furthermore, they offer improved safety, greater potential for standardization, and enhanced scalability compared to traditional live-cell therapies. However, clinical translation remains constrained by several challenges, such as inherent vesicle heterogeneity, limited targeting specificity, and bottlenecks in large-scale manufacturing. This review systematically examines the biogenesis of MSC-EVs, focusing specifically on exosomes, microvesicles, and apoptotic vesicles. We evaluate their functional performance across diverse regeneration contexts, encompassing orofacial, barrier, musculoskeletal, and visceral tissue regeneration. We further highlight innovative engineering strategies designed to enhance therapeutic efficacy, such as surface modification, cargo loading, and biomaterial-integrated delivery systems. In addition, we introduce an emerging approach utilizing engineered MSC aggregate-derived EVs inspired by organ morphogenesis. Finally, this article details the strategic framework required for clinical translation. The framework encompasses scalable production, rigorous quality control, comprehensive non-clinical studies, evolving regulatory pathways, and the current clinical trial landscape. Collectively, this work provides an integrated roadmap for advancing MSC-EVs as a next-generation precision platform for cell-free therapeutics.

Picosecond lasers are increasingly used for tattoo removal and selected pigmentary disorders, but treatment outcomes remain dependent on wavelength, pulse duration, spot size, fluence, pigment chemistry, lesion depth, treatment endpoint, and skin phototype. This narrative review evaluates 785 nm treatment as an emerging complementary option alongside established 532 nm and 1064 nm platforms. A reproducible targeted PubMed/MEDLINE search and structured descriptive evidence extraction were used to identify direct clinical 785 nm studies, mechanistic work, comparator studies, and device-specific regulatory documents. The literature demonstrates that wavelength, laser source, pulse duration, and platform architecture are related but non-interchangeable concepts. Direct 785 nm evidence is limited to small prospective studies, pilot studies, retrospective series, and case reports. The most consistent clinical signal concerns selected cool-colored tattoo pigments, while reports in ephelides, benign facial pigmentation, melasma, and brown dermal melanocytosis remain preliminary. Experimental melanosome-disruption data provide mechanistic plausibility but do not define clinical treatment or safety thresholds. Device terminology also requires caution because nominal 785 nm outputs may be described differently across publications and technical documents. Overall, 785 nm should be considered a target-specific adjunct rather than a universal replacement for 532 nm or 1064 nm treatment. Larger comparative studies with standardized parameters, objective outcomes, longer follow-up, and broader representation of darker skin phototypes are required.

The fat mass and obesity-associated protein (FTO), an RNA demethylase acting on both internal m6;A and cap-proximal m6;Am, functions in cancer as a context-dependent epitranscriptomic regulator whose net effect cannot be reduced to an oncogene-tumor-suppressor dichotomy. Its biological output is shaped by tumor lineage, subcellular localization, upstream signaling, and competing m6;A reader activities, predominantly YTHDF2-mediated decay and IGF2BP-mediated stabilization, although both reader families display additional non-canonical functions and are themselves modulated by post-translational modifications. Building on the now well-established context-dependence of FTO biology, which we do not claim as a novel observation, this review synthesizes current evidence on FTO's roles at the intersection of tumor immune contexture, immune checkpoint regulation, metabolic reprogramming, and therapeutic resistance. We examine how FTO may contribute to immune exclusion through metabolic competition, exosomal signaling, and stromal reprogramming; modulate PD-L1 expression through direct and indirect mechanisms; and influence response to chemotherapy, targeted therapy, radiotherapy, and CNS-directed treatment. Emerging FTO inhibitors, FTO-degraders, and combination strategies with immune checkpoint blockade, ferroptosis inducers, or glycolytic inhibitors are evaluated against their underlying preclinical evidence base. The contribution of this review lies less in proposing a new framework than in three forms of integration typically addressed in isolation: explicit calibration of mechanistic claims to evidence tier, systematic separation of tumor-intrinsic from immune-cell-intrinsic FTO functions across lymphoid and myeloid compartments, and translation of reader-network biology into biomarker-stratified trial design. Technical limitations of epitranscriptomic methods are addressed as constraints on inference. To our knowledge, no FTO-targeted strategy has yet entered Phase I oncology evaluation; current combination rationales therefore remain preclinically supported rather than clinically established.

Outcomes in squamous cell carcinomas (SCCa) of the head and neck, esophagus, and lungs are increasingly linked to the complex interplay between social determinants of health (SDoH) and biological pathways. The emerging field of social genomics provides mechanistic insight into how the environmental and socioeconomic conditions may influence tumor biology through stress-mediated pathways, epigenetic modifications, and altered gene expression. This review explores the role of adverse socioeconomic conditions such as neighborhood deprivation in shaping SCCa outcomes and the potential underlying mechanisms. In response to chronic stress, hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system become activated, leading to dysregulated immune signaling and proinflammatory gene expression pattern collectively known as the Conserved Transcriptional Response to Adversity (CTRA). We discuss epigenetic modifications including DNA methylation (DNAm), histone modification, and micro RNA (miRNA) dysregulation as potential mediators of these stress-related effects. Studies show that SCCa may have distinct race- and neighborhood-specific DNAm patterns including differential methylation of PAX5, HOXA7, and TFPI genes, and altered expression of xenobiotic metabolism genes regulated by Nrf2, a major stress response transcription factor. Therapeutic strategies targeting these biological mediators including β-adrenergic blockers, DNA methyltransferase inhibitors (e.g., azacytidine, decitabine), histone deacetylase inhibitors (e.g., vorinostat), and BET inhibitors have shown variable efficacy in preclinical and clinical SCCa models. Incorporating social context into tumor genomic analysis through geospatial modeling and neighborhood epigenomic profiling may offer a novel opportunity for identifying population-level cancer risk patterns and therapeutic targets. Social genomics provides a deeper understanding of the interaction of socio-environmental exposures with the epigenome and tumor biology influencing disparities in SCCa outcomes. Future research should integrate geospatial and multi-omics data to inform personalized cancer prevention and treatment strategies.

The emergence of multidrug-resistant pathogens has necessitated the search for novel therapeutic alternatives such as antimicrobial peptides (AMPs). Indolicidin (Ind) represents a highly promising candidate owing to its broad-spectrum activity and multimodal mechanisms; however, its clinical translation is limited by rapid proteolytic degradation and intrinsic host cytotoxicity. To overcome these pharmacological bottlenecks, this review places nanocarrier based delivery of Ind at its analytical center, rigorously evaluating the integration of Ind into nanoscale delivery systems as a transformative therapeutic strategy. We critically analyze how diverse organic and inorganic platforms fundamentally reconfigure Ind's mechanism of action, including the bidirectional relationship between nanoparticle-generated ROS and peptide-mediated membrane disruption. Furthermore, we discuss emerging bio-inspired approaches utilizing stimuli-responsive hydrogels, lipid cubic phases, and liposomes for programmed intracellular release. A critical assessment of long-term genotoxicological and ecotoxicological safety profiles is subsequently provided to address mandatory regulatory prerequisites. This integrated analysis establishes a comprehensive mechanistic and translational framework for the rational development of next-generation Ind-based antimicrobial nanomedicines, balancing structural tethering with supramolecular assembly to effectively combat antibiotic-resistant infections.

Secondary lymphedema (LE) can ensue after disruption of lymphatic vasculature, which may be caused by infection, surgery, or cancer treatment. Omics technologies can move the field beyond an anatomic description of lymphatic stasis by defining inflammatory, fibrotic, metabolic, lymphatic vascular, and genetic susceptibility programs that shape disease onset and progression. This review summarizes studies that use transcriptomic, proteomic, metabolomic, lipidomic, and emerging genomic or computational approaches in secondary LE. We synthesize how these datasets have identified candidate biomarkers, cell populations, signaling pathways, and therapeutic targets; highlight limitations of current platforms, samples, and bioinformatic pipelines; and propose future multi-omics strategies for diagnosis, risk stratification, and treatment development of secondary LE.

Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic erosive synovitis, progressive bone destruction, and marked inter-patient heterogeneity in disease course and treatment response. This review critically examines the mechanisms underlying RA immunological heterogeneity, including genetic susceptibility, epigenetic regulation, autoantibody diversification, synovial pathotypes, and gut-joint axis-related immune-metabolic interactions. We further discuss how peripheral blood multi-omics, synovial molecular pathology, and biopsy-driven clinical trial evidence may inform early stratification and prediction of primary non-response. Rather than proposing a deterministic precision-medicine model, this review emphasizes an evidence-weighted framework in which molecular and tissue-level biomarkers are integrated with clinical phenotype and longitudinal treatment response. Emerging approaches, including pharmacomicrobiomics, local drug delivery, nanomedicine, and cell-based therapies, are evaluated as investigational strategies that require further validation. Overall, this review highlights how a more critical understanding of RA heterogeneity may improve patient stratification and support more rational therapeutic selection.

Oncolytic viruses (OVs) represent an emerging class of cancer immunotherapeutics. Arming OVs with immunomodulatory transgenes is a promising strategy to reshape the tumor microenvironment (TME) and enhance therapeutic efficacy. We developed the oncolytic Coxsackievirus B3 (CVB3) strain PD-H, which has previously shown antitumor activity in colorectal and pancreatic cancer models. Here, we evaluated the capacity of PD-H to express transgenes and investigated whether its antitumor efficacy in colorectal cancer can be enhanced by insertion of the interleukin-2 (IL-2) mimetic Neoleukin-2/15 (Neo-2/15). Transgene insertion was best tolerated at the VP1-2A junction of the PD-H polyprotein, with viral replication and cytotoxicity inversely correlating with insert size. Genetic stability depended on the host cell line, transgene sequence and transgene length, with inserts up to 350 bp remaining stable for at least 10 viral passages. PD-H-derived Neo-2/15 was biologically active and induced proliferation of human CD4+ and CD8+ T cells in vitro. In vivo, intratumoral administration of PD-Neo-2/15 reduced the growth of subcutaneous Colon-26 tumors more effectively than PD-H and was associated with modulation of the TME, including an increased proportion of CD8+ T cells. Taken together, we demonstrate that arming PD-H with Neo-2/15 is a promising strategy to further enhance its anticancer efficacy.

Cyanobacteria are increasingly positioned as photosynthetically powered, genetically tractable chassis for next-generation environmental remediation-operating as living filters that couple solar energy capture to active detoxification and resource recovery. This review synthesizes current advances in cyanobacteria-based remediation of heavy metals, micro- and nanoplastics, pathogens, and persistent organic pollutants, with particular emphasis on metabolic mechanisms, bioengineering strategies, and practical environmental applications. This review outlines a bioengineering roadmap for deploying cyanobacteria in wastewater and impacted aquatic systems to sequester and reclaim toxic heavy metals, trap nano/microplastics, attenuate pathogenic microorganisms, and chemically degrade recalcitrant organic pollutants. In the field of metal capture, recent advances in "living materials" have enabled the embedding of cyanobacteria in regenerable matrices for efficient removal and subsequent reclamation. Mechanistic insights into species such as Synechocystis have clarified adsorption behavior and stress-response determinants for cadmium and related metals, defining tunable targets including transporters, exporters, and chelation modules for strain improvement. Cobalt and uranium handling can now be rationally engineered by rewiring metal homeostasis systems or exploiting high-capacity biosorption using scalable biomass platforms like Spirulina. Beyond metals, cyanobacterial extracellular polymeric substances (EPS) are being leveraged as engineered bio-based flocculants to remove polystyrene micro- and nanoplastics, while consortia-based designs are emerging to facilitate polymer transformation. Collectively, these advances motivate the development of modular, field-ready cyanobacterial platforms immobilized, sensor-guided, and biocontained that integrate pollutant capture and circular recovery within sustainable photobioremediation pipelines. However, significant challenges remain, including field-scale validation, environmental variability, biosafety considerations, biomass management, economic feasibility, and regulatory constraints. Addressing these limitations will be essential for the practical implementation of cyanobacterial remediation technologies.

It remains controversial whether the lateral or the anterior approach is optimal for chest tube insertion in patients with traumatic pneumothorax (PTH). This study aimed to evaluate the incidence of functional malpositioning of chest tubes inserted via the lateral versus anterior approach in patients with traumatic pneumothorax (PTH) and/or hemopneumothorax (HPTH), with or without a preceding CT examination. We conducted a two-center, retrospective, observational study of consecutive patients treated with a chest tube for traumatic PTH/HPTH between August 2012 and September 2021. Patients were divided into two groups according to the presence or absence of CT examination before chest tube insertion: CT(+) or CT(-) group. In each group, the risk of functional malpositioning was compared between the lateral and anterior approaches. Among 388 patients, 271 patients were analyzed. The CT(+) group comprised 200 (74%) patients, while the CT(-) group comprised 71 (26%) patients. The adjusted odds ratio of functional malpositioning with the lateral approach was 1.38 (95% confidence interval 0.64-2.98, p&#x2009;=&#x2009;0.41) in the CT(+) group and 9.24 (95% confidence interval 1.49-57.50, p&#x2009;<&#x2009;0.01) in the CT(-) group. There was a trend suggesting that the risk of functional malposition of chest tubes associated with the lateral approach, compared with the anterior approach, was modified by the presence or absence of a preceding CT examination (p interaction&#x2009;=&#x2009;0.01). The occurrence of functional malpositioning of the chest tube in patients with traumatic PTH/HPTH was higher with the lateral approach in patients without a preceding CT examination.