Search Results (30,677)

Listeria monocytogenes (L. monocytogenes) is a significant zoonotic pathogen responsible for listeriosis, a foodborne infection with high mortality. The inflammasome, an innate immune complex, plays a critical role in controlling pathogenic infections through its rapid inflammatory output. During L. monocytogenes infection, pore-forming toxins such as listeriolysin-O and flagellin are quickly recognized by pattern recognition receptors (PRRs), triggering inflammatory responses and activating the host’s anti-infection immunity. However, excessive or chronic inflammasome activation and subsequent interleukin-1β (IL-1β) release are implicated in the pathogenesis of L. monocytogenes. Although inflammasome activation is an effective defense against L. monocytogenes, the bacterium has evolved multiple mechanisms to inhibit this immune pathway. Hence, research on inflammasomes activation is crucial for better understanding the pathogenic mechanism of L. monocytogenes. In this review, we highlight recent advances in the understanding of the molecular mechanisms of inflammasome activation by L. monocytogenes infection. We then discuss advances in the role of the inflammasome pathway in the pathogenesis of L. monocytogenes, along with an overview of the applications of inflammasome inhibitors. Extensive studies into the mechanisms by which L. monocytogenes activates the inflammasome could lead to the discovery of novel therapeutic targets and strategies to fight L. monocytogenes infections. Full article

High-performance operation of permanent magnet synchronous motors (PMSMs) strongly depends on the reliable availability of rotor position and speed information. Although this information is commonly obtained using physical position sensors, such sensors increase system cost and structural complexity and may reduce long-term reliability, particularly in demanding operating environments. In this study, a model-based, discrete-time, nonlinear gradient observer is adapted for the sensorless estimation of rotor speed and position in PMSMs. The developed Runge–Kutta model-based gradient observer (RKGO) utilizes stator voltage inputs and measured stator currents within a mathematical motor model to estimate the system states. In contrast to conventional sensorless estimation approaches, the adopted observer framework exploits discretization-based gradient dynamics to enhance numerical robustness and convergence behavior under nonlinear operating conditions. The observer design specifically targets stable and accurate state estimation in discrete-time implementations, with a particular focus on low-speed operating conditions. The performance of the adapted method is experimentally evaluated under low-speed operating conditions, including transient and steady-state operation. Real-time implementation is carried out on a dSPACE DS1104 control platform, including loaded acceleration scenarios to assess practical robustness. In addition, a comparative analysis with the Extended Kalman Filter (EKF) and the Runge–Kutta Extended Kalman Filter (RKEKF) is conducted at 60 rad/s under identical experimental conditions. Experimental results show that the RKGO method achieves accurate steady-state speed and position estimation with acceptable transient performance. The findings demonstrate that RKGO can be considered a viable alternative for low-speed sensorless PMSM drive applications. Full article

The relationship between epilepsy, obesity, and metabolic syndrome (MetS) has emerged as a rapidly evolving area of neurobiology inquiry. Emerging evidence suggests that epilepsy extends beyond neuronal hyperexcitability, reframing it as a systemic condition characterized by significant metabolic dysregulation. Converging supports a bidirectional relationship while seizures, antiseizure medications (ASM), and neuroinflammation induce exacerbate potentiate epileptogenesis through shared molecular pathways. At the cellular level, chronic epileptic activity induces oxidative stress, mitochondrial dysfunction, and the activation of microglia and astrocytes. This, in turn, leads to the release of pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6. These mediators traverse the blood-brain barrier (BBB), subsequently modifying insulin signaling, and disrupting glucose homeostasis, which collectively fosters a pro-inflammatory and insulin-resistant environment. Furthermore, antiseizure medications such as valproate can exacerbate these effects by directly impairing insulin receptor signaling and altering adipokine production, ultimately contributing to weight gain and systemic metabolic dysregulation. Obesity and MetS induce neuroinflammatory and excitotoxic states that promote seizure onset via leptin resistance, reduced adiponectin levels, and compromised AMP-activated protein kinase (AMPK) signaling. Emerging evidence emphasizes the gut-brain axis as a crucial regulator in this reciprocal interaction. Dysbiosis, altered microbial metabolites (e.g., short-chain fatty acids), and heightened intestinal permeability facilitate systemic inflammation and BBB disruption, enhancing neuronal excitability. Insulin resistance in the brain disrupts synaptic transmission, impairs mitochondrial biogenesis, and compromises redox equilibrium, perpetuating a pathological cycle linking metabolic stress to epileptic activity. This review synthesizes the cellular, molecular, and systemic pathways connecting epilepsy, obesity, and MetS, and proposes that epilepsy be reconceptualized as a neuro-metabolic disorder. Insights into these convergent pathways provide a rationale for novel therapeutic strategies that simultaneously target seizure control and metabolic regulation, encompassing microbiota modulation, antioxidant therapy, and insulin-sensitizing interventions with the overarching aim of restoring neuro-metabolic homeostasis. Full article

A rare clinical condition associated with numerous diagnostic and treatment challenges, pregnancy-associated melanoma (PAM), is defined as melanoma diagnosed either during pregnancy or within the first year postpartum. The physiological changes in pregnancy (hormonal changes and immune modulation), along with the normal changes in the pregnant woman’s skin (skin color changes, etc.), may all hinder early detection of this disease and create concerns regarding the advancement of melanoma and the well-being of both the mother and her fetus. The purpose of this review article was to summarize the current literature on the incidence, biology, diagnostic methods and treatments of PAM, with an emphasis on comparison between the two forms of melanoma. More recent research indicates that pregnancy itself is not typically associated with decreased melanoma-specific survival rates. However, when worse results are reported, it appears that this may be more due to delays in initial diagnoses (diagnosis of cancer after delivery) or detection of cancer postpartum, as well as the increased number of stages of melanoma at which women were diagnosed at the time of their first evaluation compared to non-pregnant controls, rather than being a result of enhanced biologic aggressiveness in melanoma driven by pregnancy itself. The preclinical and translational models have suggested that pregnancy may influence melanoma biology through the mechanisms of hormonal signaling, immune system modulation and vascular remodeling; however, these mechanisms remain hypothesis-generating, and current clinical evidence does not indicate that changes in hormone levels during pregnancy negatively affect melanoma survival. Surgical excision is the mainstay of treatment and can be performed safely during pregnancy. In select patients, a sentinel lymph node biopsy may also be performed. Due to the risk of fetal harm, systemic therapy (targeted agents and/or immune checkpoint inhibitors) cannot be used for the treatment of PAM during pregnancy. Post-pregnancy treatment of PAM will follow standard melanoma treatment guidelines; however, the treatment options will need to take into consideration whether or not the patient is breastfeeding and if she desires to become pregnant again in the future. In summary, PAM will require a multidisciplinary, individualized approach to maximize oncologic outcomes while protecting the health of both the mother and her fetus. Awareness of this disease and timely diagnosis are critical to maximizing the prognosis. Full article

Melatonin, a well-known antioxidant, has been widely used in sperm cryopreservation of various animals, but its regulatory mechanism in fish remains unclear. This first study on teleosts suggests a potential molecular mechanism by which melatonin may improve post-thaw sperm quality of Epinephelus fuscoguttatus via targeting mitochondrial function. Compared with the melatonin group, the MT1 receptor-inhibited group showed slightly higher sperm motility (77.09 ± 3.41% vs. 76.50 ± 1.10%), significantly inhibited mitochondrial permeability transition pore (mPTP) opening (12.64 ± 1.05% vs. 18.29 ± 1.38%), and maintained higher mitochondrial membrane potential (MMP; 85.86 ± 0.18% vs. 81.81 ± 0.69%), with both groups performing better than the control. In contrast, the MT2-inhibited and MT1/2 dual-inhibited groups exhibited reduced sperm quality compared with the MT group, suggesting that MT2 may serve as the core receptor for melatonin to regulate mitochondrial homeostasis in teleosts. Mechanistically, melatonin-activated MT2 potentially inhibits mPTP opening via the PI3K/Akt/GSK-3β pathway, and this protective effect was abrogated by the PI3K and GSK-3β inhibitors. This receptor-mediated process synergized with melatonin’s direct antioxidant effect, as ROS levels in all melatonin-treated groups were significantly lower than the control. This study is the first to find pharmacological evidence for the melatonin–MT2/PI3K/GSK-3β axis in maintaining teleost sperm mitochondrial function; it also reveals potential mechanistic differences between teleosts and mammals and fills a critical knowledge gap regarding this signaling cascade in teleost reproductive biology. Full article

Background: Intrahepatic cholangiocarcinoma (ICC) is an uncommon but increasingly recognized primary liver malignancy with a poor prognosis. Although surgical resection offers the only realistic opportunity for cure, recurrence is common and the optimal integration of surgery with systemic and liver-directed therapies continues to evolve. Summary: This review summarizes contemporary evidence on the diagnosis and multidisciplinary management of ICC with particular emphasis on surgical, systemic, locoregional, and transplant-based strategies. Cross-sectional imaging plays a central role in staging and assessing resectability including evaluation of vascular invasion and the future liver remnant. Upfront resection is appropriate for selected patients with resectable disease and preserved liver function, with margin-negative resection and lymphadenectomy remaining key oncologic goals. Systemic therapy continues to evolve with cytotoxic chemotherapy forming the backbone of treatment for advanced disease and immunotherapy and targeted agents demonstrating promise in biomarker-defined subgroups. Locoregional modalities such as hepatic arterial infusion therapy and radioembolization may provide disease control in liver-dominant ICC and are increasingly used within a multidisciplinary framework. Liver transplantation remains investigational but may offer favorable outcomes in highly selected early-stage disease. Full article

Background/Objectives: The mediating role of the diverse range of screen-based sedentary behaviors (SBs) remains understudied, particularly at younger ages. The present study examined the direct and indirect effects of parental BMI and education on ultra-processed food (UPF) consumption among preschoolers, testing the potential mediating role of screen time. Methods: The cross-sectional study sample comprised 919 kindergarten children (484 boys, 52.7%), with ages ranging from 2.2 to 6.8 years (mean: 4.7 ± 1.0 years). Screen-based sedentary behaviors (television viewing, smartphone use, tablet use, computer use, and playing electronic games) were measured by proxy-report fulfilled by parents, separately for weekdays and weekends. UPF consumption (drinks/yogurts, packaged/fast foods, and sweet/salty snacks) was assessed via 24 h recall scales. Path analysis mediation models tested direct effects of maternal/paternal BMI and education on UPF intake, and indirect effects through screen time, controlling for child age and sex. Results: Lower parental education and higher parental BMI were associated with increased mobile device use and UPF consumption (r = 0.10–0.28). Screen-based sedentary behaviors mediated the association between maternal BMI and UPF pathways (15–90% of total effects), particularly for sweet and salty snacks (50–90%). Parental education effects were also mediated by screen time (9–23% indirect effects), with paternal education showing stronger protection against packaged/fast foods. Conclusions: Mobile devices and watching television partially mediate intergenerational transmission of obesogenic dietary patterns from parental BMI/education to preschoolers’ UPF consumption. Findings of the current study support family-centered interventions targeting screen-time limits and UPF exposure, mainly at the weekends, to prevent early obesity trajectories. Full article

Welded joints in API 5L X70 pipeline steel represent critical locations for pipelines intended for hydrogen service because welding can create microstructural inhomogeneity, stress concentrations, and uneven mechanical properties that can promote hydrogen-assisted degradation. In hydrogen-containing environments, these effects may manifest as reduced ductility, loss of fracture resistance, and increased cracking susceptibility, particularly in the weld metal and heat-affected zone. Therefore, welding procedures for X70 intended for hydrogen applications must be evaluated using systematic mechanical testing and microstructural characterization under defined hydrogen exposure conditions. The study investigates the detrimental effects of hydrogen on the mechanical integrity of pipeline materials, focusing on welded joints of the API 5L X70 steel, a candidate material for use in hydrogen-containing environments. The weldability and structural performance of the X70 pipeline steel joints in hydrogen environments, produced using automated multi-pass metal active gas (MAG) welding, was experimentally studied. Welding was performed on a DN800 pipe with precise control over welding parameters. Comprehensive analyses were conducted on the welded joints, including microstructure examinations, hardness measurements, slow strain rate testing in high-pressure gaseous H₂ with a N₂ baseline and fracture toughness testing. In high-pressure hydrogen SSRT showed a moderate reduction in ductility relative to nitrogen, with reduction of area decreasing from 81.2% (N₂) to 69.1 and 71.5% (H₂), while time-to-failure remained comparable (475 min in N₂ vs. 497 and 496 min in H₂) Ultimate tensile strength was not reduced (579 MPa in N₂ vs. 609 and 597 MPa in H₂). Secondary surface cracks were observed only on specimens tested in hydrogen. Fracture mechanics testing after hydrogen exposure yielded K_IH values of 58–59 MPa√m in the weld metal and 57–61 MPa√m in the HAZ, exceeding the 55 MPa√m acceptance threshold applied in this study. The results highlight the necessity of optimized welding techniques and targeted material analyses to ensure the safety and durability of pipelines in hydrogen-rich environments, thereby contributing to the development of reliable infrastructure for sustainable energy systems. Full article

Biomass combustion, as a key technology for achieving a low-carbon transformation of the energy system, faces multiple challenges in its efficient and clean utilization, including the high heterogeneity of fuels, the complex multi-scale coupling of the combustion process, and the attainment of ultra-low emissions. Traditional research methods have significant disconnections between microscopic mechanism understanding, macroscopic performance prediction of reactors, and end-of-pipe pollution control, which restricts the improvement of system performance. This review presents recent advances in advanced numerical simulation, pollutant control strategies, and bioenergy with carbon capture and storage (BECCS) pathways targeting ultra-low emissions in biomass combustion. This work synthesizes progress across three interconnected domains. First, methodologies are examined for integrating detailed chemical kinetics, particle-scale models, and reactor-scale simulations to develop high-fidelity predictive tools. Second, low-nitrogen combustion and synergistic pollutant control strategies for primary furnace types (e.g., grate, fluidized bed) are evaluated, alongside process optimization from fuel pretreatment to flue gas purification. Third, the potential for integrated design of biomass energy systems with carbon capture is assessed, emphasizing that system efficiency hinges on holistic “fuel-combustion-capture” chain optimization rather than isolated unit improvements. Future research directions are highlighted, including the development of physics-informed AI modeling paradigms, deeper co-design of multiple processes, and the establishment of robust life-cycle assessment frameworks. This review aims to provide a structured reference to inform both fundamental research and the practical development of next-generation clean biomass combustion technologies. Full article

To explore whether the causal chain of “Industry–University–Government Integrated Innovation Ecosystem → Novel Energy Storage Technology Innovation → Dual-Control Energy Targets” can be achieved, this study analyzes panel data from 30 provinces, municipalities, and autonomous regions in China (excluding Tibet, Hong Kong, Macao, and Taiwan) from 2010 to 2022. By employing a complex mediation effect model combining dynamic Qualitative Comparative Analysis (QCA) and the dynamic panel system Generalized Method of Moments (GMM) model, this study identifies five configuration pathways for driving innovation in novel energy storage technologies within an integrated innovation ecosystem. These include two industry digitalization–university innovation resource-dominant pathways: a government-light and digitally driven “university–industry” resource-sharing and knowledge-conversion synergy, and an industry leadership pathway embedded with university collaborative innovation under a digitalization framework. Two policy-driven hybrid and industry–leadership synergistic pathways are also extracted: a growth pathway for policy-supported hybrid organizations under insufficient industry digitalization and a policy-driven innovation substitution pathway compensating for the absence of university niche roles. Additionally, a multidimensional collaborative development pathway is identified, reflecting comprehensive collaboration. In the dynamic panel system GMM model, all five pathways collectively suppress total energy consumption and energy intensity, while also indirectly driving the achievement of dual-control energy targets through innovation in novel energy storage technologies. Pathways driven by government-light and digitally facilitated collaboration, industry leadership, and comprehensive collaboration show significant direct negative effects on energy consumption and intensity. However, the policy-driven innovation substitution pathway exhibits limited contribution due to the absence of university innovation components, thereby failing to significantly advance regional dual-control energy goals. Full article

Bovine viral diarrhea virus (BVDV), a globally persistent pathogen, causes bovine viral diarrhea-mucosal disease (BVD-MD), a contagious bovine disease posing significant pressures on both public health and economic development. Baicalin (BA), a flavonoid derived from Scutellaria baicalensis, exhibits broad antiviral activities but suffers from poor aqueous solubility and low bioavailability, limiting its therapeutic potential against BVDV. To address this limitation, we developed BA-loaded poly (ethylene gly-col)-poly (lactic-co-glycolic acid) (PEG-PLGA) nanoparticles (BA-PEG-PLGA NPs). While autophagy and NLRP3 inflammasome activation have been individually implicated in viral pathogenesis, their functional crosstalk during BVDV infection remains uncharacterized. Herein, we evaluated the antiviral efficacy of BA-PEG-PLGA NPs through integrated in vitro and in vivo experiments. We employed quantitative polymerase chain reaction (qPCR), transcriptome sequencing, Western blot analysis, immunofluorescence microscopy, flow cytometry, and enzyme-linked immunosorbent assay (ELISA) to investigate the mechanisms by which BA and BA-PEG-PLGA NPs combat bovine viral diarrhea virus (BVDV) infection. We found that both free BA and BA-PEG-PLGA NPs effectively attenuated BVDV replication in vitro and in vivo; notably, the nano-formulation exhibited superior efficacy. Mechanistically, BA and its nano-formulation restored autophagy homeostasis, suppressed ROS overproduction, and blocked NLRP3 inflammasome activation and pyroptotic cell death effects comparable to the specific NLRP3 inhibitor MCC950. These findings establish the autophagy–NLRP3/pyroptosis axis as a critical pathogenic mechanism in BVDV infection and reveal that nano-formulated baicalin represents an antiviral strategy by coordinately targeting this axis. This work not only provides a translatable nanomedicine approach for BVDV control but also expands the mechanistic understanding of flavonoid-based interventions in viral inflammatory diseases. Full article

This study investigated the molecular characteristics and genetic diversity of Fowl adenovirus (FAdV) strains circulating in commercial broiler and layer flocks in the Southern Marmara and Aegean regions of Türkiye between January and December 2025. Liver samples (n = 120) collected from twelve flocks with increased mortality and clinical signs compatible with adenoviral infection were analyzed. Detection was performed using circular amplification technology and PCR targeting the hexon L1 region, and positive samples were sequenced for molecular characterization. BLAST analysis showed that all isolates belonged to Aviadenovirus hepatitidis and were identified as serotype 8b. Pairwise comparisons showed high nucleotide identity among isolates (97.4–100%) and 98.1–100% similarity with the Turkish reference strain MK937075. Only three isolates displayed nucleotide substitutions, while most sequences were identical within the analyzed region. Amino acid similarity ranged from 95.2% to 100%. Phylogenetic analysis revealed that all isolates clustered within a single monophyletic group together with previously reported Turkish FAdV-8b strains. Necropsy findings included hepatomegaly, multifocal hepatic pallor, petechial hemorrhages, gizzard erosion, and serous pericardial involvement. The detection of genetically closely related isolates across multiple provinces suggests regional circulation of a common viral lineage. These findings demonstrate that FAdV-8b is currently the predominant serotype associated with inclusion body hepatitis outbreaks in this major poultry production area and highlight the importance of molecular surveillance and targeted control strategies, including breeder monitoring and region-specific vaccine development. Full article

Chryseobacterium indologenes MA9 is a causative agent of root rot disease in Panax notoginseng (P. notoginseng), with its high incidence being a major manifestation of continuous cropping barriers, severely hindering the sustainable development of the P. notoginseng industry. In this study, a novel lytic bacteriophage, MA9V-3, was isolated from wastewater, targeting C. indologenes MA9. The phage produced clear plaques, ranging from 1 to 3 mm in diameter, with a surrounding halo. Phage MA9V-3 achieved an adsorption rate of up to 80% after 30 min of contact with C. indologenes MA9, a latent period of approximately 40 min, and an average burst-size if 160 PFU/cell. Transmission electron microscopy revealed that phage MA9V-3 possesses an icosahedral head and a contractile tail, exhibiting a typical myovirus-like morphology. According to the latest ICTV taxonomy, MA9V-3 belongs to the class Caudoviricetes, and the phage’s biocontrol efficacy and inhibitory capacity were evaluated at different multiplicity of infection (MOI s). The results showed that the highest titer recorded at 1.6 × 10¹⁰ PFU/mL. Whole-genome sequencing revealed that MA9V-3 is a double-stranded circular DNA virus, with a genome length of 103,203 bp, GC content of 34.29%, and 150 open reading frames (ORFs), one of which is related to tRNA. Only 13 of these ORFs encode known functional sequences, likely due to the limited available gene data for such phages in the database, with additional details on hypothetical proteins yet to be uncovered. Comparative database analysis confirmed that the phage genome contains no antibiotic resistance or toxin-related genes. Phage therapy experiments were performed using MA9V-3 and two other phages screened in our laboratory. The experimental results showed that phage MA9V-3 may be a potential candidate for effectively controlling the infection of Panax notoginseng by C. indologenes MA9, and offering valuable insights into the potential application of phage therapy for managing bacterial plant diseases. Full article

Background: Tirzepatide, a dual GIP/GLP-1 receptor agonist, demonstrates substantial glycemic and weight benefits versus GLP-1 receptor agonists in indirect comparisons, but direct comparative safety evidence versus dulaglutide remains limited. We evaluated comparative safety (primary outcome: overall adverse events) and efficacy. Methods: Following PRISMA 2020 (prospectively registered: PROSPERO CRD420251276594), we searched MEDLINE, Embase, Scopus, and CENTRAL (inception–31 December 2025) for randomized controlled trials (≥26 weeks) comparing once-weekly tirzepatide with dulaglutide in adults with type 2 diabetes. Three trials (N = 13,590 participants) were included. Dichotomous outcomes were pooled using random-effects models (risk ratios [RRs], 95% confidence intervals [CIs]). GRADE assessed certainty of evidence. Results: Overall adverse event incidence did not differ significantly (RR 1.04 [0.98–1.10]; I² = 36%; moderate-certainty evidence). Discontinuation due to adverse events was consistently higher with tirzepatide (RR 1.32 [1.20–1.45]; I² = 0%; high-certainty evidence), representing a 32% increased risk across all populations. Categorical HbA1c target achievement was analyzed in two trials; the third trial reported HbA1c as a continuous outcome only. At the primary threshold (HbA1c < 7.0%), tirzepatide was consistently superior with no heterogeneity (RR 1.48 [1.33–1.64]; I² = 0%; p < 0.00001). Across all thresholds combined, heterogeneity was extreme (I² = 92%), limiting confidence in any pooled summary estimate; the greatest instability occurred at the strictest threshold (HbA1c < 5.7%; I² = 98%; p = 0.40). Tirzepatide showed greater HbA1c target attainment in treatment-naive patients receiving dulaglutide 0.75 mg, whereas the glycemic advantage was smaller in patients with established cardiovascular disease receiving dulaglutide 1.5 mg. Categorical weight-loss outcomes were analyzed in two trials; tirzepatide was associated with greater weight-loss threshold achievement (RR 8.80 [4.04–19.17]; very low-certainty evidence), although interpretation is limited by substantial heterogeneity and restricted generalizability. Serious adverse events were not significantly different (RR 0.82 [0.47–1.43]; I² = 42%). Conclusions: Overall adverse events were similar between treatments, but tirzepatide consistently increased discontinuation risk, indicating a clinically important tolerability-persistence trade-off. Glycemic efficacy was highly population-dependent: benefits were consistent at the primary HbA1c target (<7.0%; I² = 0%) in early-stage disease, whereas the advantage was smaller in long-standing disease with established cardiovascular disease. Tirzepatide may be favored when glycemic or weight efficacy is prioritized in earlier-stage disease, provided tolerability is proactively managed. Dulaglutide remains appropriate when persistence is threatened by tolerability concerns or cardiovascular risk reduction is the primary goal. Full article

The rapid expansion of cardiac imaging has substantially increased patient and occupational exposure to low-dose ionizing radiation. Evidence suggests that cumulative exposures below 100 mSv may contribute to long-term risks of cancer and non-cancer diseases, including cardiovascular disease. However, establishing causality at these dose levels is challenging, as epidemiological studies are limited by heterogeneous endpoints, uncertainties in dose reconstruction, and incomplete control of confounding factors. Molecular biomarkers offer a promising strategy to bridge the gap between radiation exposure and clinically manifest disease, enabling more precise individualized risk assessment and targeted preventive strategies. This review summarizes current evidence on genetic and epigenetic biomarkers for evaluating the biological effects of radiation in cardiac imaging and interventional cardiology and examines their potential role in risk stratification and occupational surveillance. Genetic markers—including γ-H2AX foci, micronucleus assays, and telomere length alterations—alongside epigenetic modifications such as DNA methylation changes and microRNA expression profiles provide sensitive indicators of radiation-induced cellular damage. Integrating biomarker profiling with individualized dosimetry and longitudinal follow-up may improve risk prediction, enhance occupational protection, and support safer, more sustainable imaging practices in contemporary cardiovascular care. Full article