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25 pages, 1534 KiB  
Review
Recent Advances in Micro- and Nano-Enhanced Intravascular Biosensors for Real-Time Monitoring, Early Disease Diagnosis, and Drug Therapy Monitoring
by Sonia Kudłacik-Kramarczyk, Weronika Kieres, Alicja Przybyłowicz, Celina Ziejewska, Joanna Marczyk and Marcel Krzan
Sensors 2025, 25(15), 4855; https://doi.org/10.3390/s25154855 (registering DOI) - 7 Aug 2025
Abstract
Intravascular biosensors have become a crucial and novel class of devices in healthcare, enabling the constant real-time monitoring of essential physiological parameters directly within the circulatory system. Recent developments in micro- and nanotechnology have relevantly improved the sensitivity, miniaturization, and biocompatibility of these [...] Read more.
Intravascular biosensors have become a crucial and novel class of devices in healthcare, enabling the constant real-time monitoring of essential physiological parameters directly within the circulatory system. Recent developments in micro- and nanotechnology have relevantly improved the sensitivity, miniaturization, and biocompatibility of these devices, thereby enabling their application in precision medicine. This review summarizes the latest advances in intravascular biosensor technologies, with a special focus on glucose and oxygen level monitoring, blood pressure and heart rate assessment, and early disease diagnostics, as well as modern approaches to drug therapy monitoring and delivery systems. Key challenges such as long-term biostability, signal accuracy, and regulatory approval processes are critical considerations. Innovative strategies, including biodegradable implants, nanomaterial-functionalized surfaces, and integration with artificial intelligence, are regarded as promising avenues to overcome current limitations. This review provides a comprehensive roadmap for upcoming research and the clinical translation of advanced intravascular biosensors with a strong emphasis on their transformative impact on personalized healthcare. Full article
(This article belongs to the Section Biosensors)
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25 pages, 1054 KiB  
Review
Gut Feeling: Biomarkers and Biosensors’ Potential in Revolutionizing Inflammatory Bowel Disease (IBD) Diagnosis and Prognosis—A Comprehensive Review
by Beatriz Teixeira, Helena M. R. Gonçalves and Paula Martins-Lopes
Biosensors 2025, 15(8), 513; https://doi.org/10.3390/bios15080513 (registering DOI) - 7 Aug 2025
Abstract
Inflammatory Bowel Diseases (IBDs) are complex, multifactorial disorders with no known cure, necessitating lifelong care and often leading to surgical interventions. This ongoing healthcare requirement, coupled with the increased use of biological drugs and rising disease prevalence, significantly increases the financial burden on [...] Read more.
Inflammatory Bowel Diseases (IBDs) are complex, multifactorial disorders with no known cure, necessitating lifelong care and often leading to surgical interventions. This ongoing healthcare requirement, coupled with the increased use of biological drugs and rising disease prevalence, significantly increases the financial burden on the healthcare systems. Thus, a number of novel technological approaches have emerged in order to face some of the pivotal questions still associated with IBD. In navigating the intricate landscape of IBD, biosensors act as indispensable allies, bridging the gap between traditional diagnostic methods and the evolving demands of precision medicine. Continuous progress in biosensor technology holds the key to transformative breakthroughs in IBD management, offering more effective and patient-centric healthcare solutions considering the One Health Approach. Here, we will delve into the landscape of biomarkers utilized in the diagnosis, monitoring, and management of IBD. From well-established serological and fecal markers to emerging genetic and epigenetic markers, we will explore the role of these biomarkers in aiding clinical decision-making and predicting treatment response. Additionally, we will discuss the potential of novel biomarkers currently under investigation to further refine disease stratification and personalized therapeutic approaches in IBD. By elucidating the utility of biosensors across the spectrum of IBD care, we aim to highlight their importance as valuable tools in optimizing patient outcomes and reducing healthcare costs. Full article
(This article belongs to the Special Issue Feature Papers of Biosensors)
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15 pages, 837 KiB  
Review
Resetting Time: The Role of Exercise Timing in Circadian Reprogramming for Metabolic Health
by Stuart J. Hesketh
Obesities 2025, 5(3), 59; https://doi.org/10.3390/obesities5030059 - 7 Aug 2025
Abstract
Circadian rhythms are intrinsic 24 h cycles that regulate metabolic processes across multiple tissues, with skeletal muscle emerging as a central node in this temporal network. Muscle clocks govern gene expression, fuel utilisation, mitochondrial function, and insulin sensitivity, thereby maintaining systemic energy homeostasis. [...] Read more.
Circadian rhythms are intrinsic 24 h cycles that regulate metabolic processes across multiple tissues, with skeletal muscle emerging as a central node in this temporal network. Muscle clocks govern gene expression, fuel utilisation, mitochondrial function, and insulin sensitivity, thereby maintaining systemic energy homeostasis. However, circadian misalignment, whether due to behavioural disruption, nutrient excess, or metabolic disease, impairs these rhythms and contributes to insulin resistance, and the development of obesity, and type 2 diabetes mellitus. Notably, the muscle clock remains responsive to non-photic cues, particularly exercise, which can reset and amplify circadian rhythms even in metabolically impaired states. This work synthesises multi-level evidence from rodent models, human trials, and in vitro studies to elucidate the role of skeletal muscle clocks in circadian metabolic health. It explores how exercise entrains the muscle clock via molecular pathways involving AMPK, SIRT1, and PGC-1α, and highlights the time-of-day dependency of these effects. Emerging data demonstrate that optimally timed exercise enhances glucose uptake, mitochondrial biogenesis, and circadian gene expression more effectively than time-agnostic training, especially in individuals with metabolic dysfunction. Finally, findings are integrated from multi-omic approaches that have uncovered dynamic, time-dependent molecular signatures that underpin circadian regulation and its disruption in obesity. These technologies are uncovering biomarkers and signalling nodes that may inform personalised, temporally targeted interventions. By combining mechanistic insights with translational implications, this review positions skeletal muscle clocks as both regulators and therapeutic targets in metabolic disease. It offers a conceptual framework for chrono-exercise strategies and highlights the promise of multi-omics in developing precision chrono-medicine approaches aimed at restoring circadian alignment and improving metabolic health outcomes. Full article
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11 pages, 365 KiB  
Review
Precision Oncology in Hodgkin’s Lymphoma: Immunotherapy and Emerging Therapeutic Frontiers
by Adit Singhal, David Mueller, Benjamin Ascherman, Pratik Shah, Wint Yan Aung, Edward Zhou and Maria J. Nieto
Lymphatics 2025, 3(3), 24; https://doi.org/10.3390/lymphatics3030024 - 6 Aug 2025
Abstract
Hodgkin’s Lymphoma (HL) affects approximately 8500 individuals annually in the United States. The 5-year relative survival rate has improved to 88.5%, driven by transformative advances in immunotherapy and precision oncology. The integration of Brentuximab vedotin (BV) and immune checkpoint inhibitors (ICIs) has redefined [...] Read more.
Hodgkin’s Lymphoma (HL) affects approximately 8500 individuals annually in the United States. The 5-year relative survival rate has improved to 88.5%, driven by transformative advances in immunotherapy and precision oncology. The integration of Brentuximab vedotin (BV) and immune checkpoint inhibitors (ICIs) has redefined treatment paradigms. The phase III SWOG S1826 trial established nivolumab plus doxorubicin, vinblastine, and dacarbazine (N + AVD) as an emerging new standard for advanced-stage HL, achieving a 2-year progression-free survival (PFS) of 92% compared to 83% for BV plus AVD (HR 0.48, 95% CI: 0.33–0.70), with superior safety, particularly in patients over 60. In relapsed/refractory HL, pembrolizumab outperforms BV, with a median PFS of 13.2 versus 8.3 months (HR 0.65, 95% CI: 0.48–0.88), as demonstrated in the KEYNOTE-204 trial. Emerging strategies, including novel ICI combinations, minimal residual disease (MRD) monitoring via circulating tumor DNA (ctDNA), and artificial intelligence (AI)-driven diagnostics, promise to further personalize therapy. This review synthesizes HL’s epidemiology, pathogenesis, diagnostic innovations, and therapeutic advances, highlighting the role of precision medicine in addressing unmet needs and disparities in HL care. Full article
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34 pages, 1345 KiB  
Review
Unmasking Pediatric Asthma: Epigenetic Fingerprints and Markers of Respiratory Infections
by Alessandra Pandolfo, Rosalia Paola Gagliardo, Valentina Lazzara, Andrea Perri, Velia Malizia, Giuliana Ferrante, Amelia Licari, Stefania La Grutta and Giusy Daniela Albano
Int. J. Mol. Sci. 2025, 26(15), 7629; https://doi.org/10.3390/ijms26157629 - 6 Aug 2025
Abstract
Pediatric asthma is a multifactorial and heterogeneous disease determined by the dynamic interplay of genetic susceptibility, environmental exposures, and immune dysregulation. Recent advances have highlighted the pivotal role of epigenetic mechanisms, in particular, DNA methylation, histone modifications, and non-coding RNAs, in the regulation [...] Read more.
Pediatric asthma is a multifactorial and heterogeneous disease determined by the dynamic interplay of genetic susceptibility, environmental exposures, and immune dysregulation. Recent advances have highlighted the pivotal role of epigenetic mechanisms, in particular, DNA methylation, histone modifications, and non-coding RNAs, in the regulation of inflammatory pathways contributing to asthma phenotypes and endotypes. This review examines the role of respiratory viruses such as respiratory syncytial virus (RSV), rhinovirus (RV), and other bacterial and fungal infections that are mediators of infection-induced epithelial inflammation that drive epithelial homeostatic imbalance and induce persistent epigenetic alterations. These alterations lead to immune dysregulation, remodeling of the airways, and resistance to corticosteroids. A focused analysis of T2-high and T2-low asthma endotypes highlights unique epigenetic landscapes directing cytokines and cellular recruitment and thereby supports phenotype-specific aspects of disease pathogenesis. Additionally, this review also considers the role of miRNAs in the control of post-transcriptional networks that are pivotal in asthma exacerbation and the severity of the disease. We discuss novel and emerging epigenetic therapies, such as DNA methyltransferase inhibitors, histone deacetylase inhibitors, miRNA-based treatments, and immunomodulatory probiotics, that are in preclinical or early clinical development and may support precision medicine in asthma. Collectively, the current findings highlight the translational relevance of including pathogen-related biomarkers and epigenomic data for stratifying pediatric asthma patients and for the personalization of therapeutic regimens. Epigenetic dysregulation has emerged as a novel and potentially transformative approach for mitigating chronic inflammation and long-term morbidity in children with asthma. Full article
(This article belongs to the Special Issue Molecular Research in Airway Diseases)
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45 pages, 4319 KiB  
Review
Advancements in Radiomics-Based AI for Pancreatic Ductal Adenocarcinoma
by Georgios Lekkas, Eleni Vrochidou and George A. Papakostas
Bioengineering 2025, 12(8), 849; https://doi.org/10.3390/bioengineering12080849 (registering DOI) - 6 Aug 2025
Abstract
The advancement of artificial intelligence (AI), deep learning, and radiomics has introduced novel methodologies for the detection, classification, prognosis, and treatment evaluation of pancreatic ductal adenocarcinoma (PDAC). As the integration of AI into medical imaging continues to evolve, its potential to enhance early [...] Read more.
The advancement of artificial intelligence (AI), deep learning, and radiomics has introduced novel methodologies for the detection, classification, prognosis, and treatment evaluation of pancreatic ductal adenocarcinoma (PDAC). As the integration of AI into medical imaging continues to evolve, its potential to enhance early detection, refine diagnostic precision, and optimize treatment strategies becomes increasingly evident. However, despite significant progress, various challenges remain, particularly in terms of clinical applicability, generalizability, interpretability, and integration into routine practice. Understanding the current state of research is crucial for identifying gaps in the literature and exploring opportunities for future advancements. This literature review aims to provide a comprehensive overview of the existing studies on AI applications in PDAC, with a focus on disease detection, classification, survival prediction, treatment response assessment, and radiogenomics. By analyzing the methodologies, findings, and limitations of these studies, we aim to highlight the strengths of AI-driven approaches while addressing critical gaps that hinder their clinical translation. Furthermore, this review aims to discuss future directions in the field, emphasizing the need for multi-institutional collaborations, explainable AI models, and the integration of multi-modal data to advance the role of AI in personalized medicine for PDAC. Full article
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13 pages, 286 KiB  
Review
Drug Repurposing and Artificial Intelligence in Multiple Sclerosis: Emerging Strategies for Precision Therapy
by Pedro Henrique Villar-Delfino, Paulo Pereira Christo and Caroline Maria Oliveira Volpe
Sclerosis 2025, 3(3), 28; https://doi.org/10.3390/sclerosis3030028 - 6 Aug 2025
Abstract
Multiple sclerosis (MS) is a chronic, immune-mediated disorder of the central nervous system (CNS) characterized by inflammation, demyelination, axonal degeneration, and gliosis. Its pathophysiology involves a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation, ultimately leading to progressive neurodegeneration and functional [...] Read more.
Multiple sclerosis (MS) is a chronic, immune-mediated disorder of the central nervous system (CNS) characterized by inflammation, demyelination, axonal degeneration, and gliosis. Its pathophysiology involves a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation, ultimately leading to progressive neurodegeneration and functional decline. Although significant advances have been made in disease-modifying therapies (DMTs), many patients continue to experience disease progression and unmet therapeutic needs. Drug repurposing—the identification of new indications for existing drugs—has emerged as a promising strategy in MS research, offering a cost-effective and time-efficient alternative to traditional drug development. Several compounds originally developed for other diseases, including immunomodulatory, anti-inflammatory, and neuroprotective agents, are currently under investigation for their efficacy in MS. Repurposed agents, such as selective sphingosine-1-phosphate (S1P) receptor modulators, kinase inhibitors, and metabolic regulators, have demonstrated potential in promoting neuroprotection, modulating immune responses, and supporting remyelination in both preclinical and clinical settings. Simultaneously, artificial intelligence (AI) is transforming drug discovery and precision medicine in MS. Machine learning and deep learning models are being employed to analyze high-dimensional biomedical data, predict drug–target interactions, streamline drug repurposing workflows, and enhance therapeutic candidate selection. By integrating multiomics and neuroimaging data, AI tools facilitate the identification of novel targets and support patient stratification for individualized treatment. This review highlights recent advances in drug repurposing and discovery for MS, with a particular emphasis on the emerging role of AI in accelerating therapeutic innovation and optimizing treatment strategies. Full article
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24 pages, 1028 KiB  
Review
Molecular Links Between Metabolism and Mental Health: Integrative Pathways from GDF15-Mediated Stress Signaling to Brain Energy Homeostasis
by Minju Seo, Seung Yeon Pyeon and Man S. Kim
Int. J. Mol. Sci. 2025, 26(15), 7611; https://doi.org/10.3390/ijms26157611 - 6 Aug 2025
Abstract
The relationship between metabolic dysfunction and mental health disorders is complex and has received increasing attention. This review integrates current research to explore how stress-related growth differentiation factor 15 (GDF15) signaling, ceramides derived from gut microbiota, and mitochondrial dysfunction in the brain interact [...] Read more.
The relationship between metabolic dysfunction and mental health disorders is complex and has received increasing attention. This review integrates current research to explore how stress-related growth differentiation factor 15 (GDF15) signaling, ceramides derived from gut microbiota, and mitochondrial dysfunction in the brain interact to influence both metabolic and psychiatric conditions. Evidence suggests that these pathways converge to regulate brain energy homeostasis through feedback mechanisms involving the autonomic nervous system and the hypothalamic–pituitary–adrenal axis. GDF15 emerges as a key stress-responsive biomarker that links peripheral metabolism with brainstem GDNF family receptor alpha-like (GFRAL)-mediated anxiety circuits. Meanwhile, ceramides impair hippocampal mitochondrial function via membrane incorporation and disruption of the respiratory chain. These disruptions may contribute to sustained pathological states such as depression, anxiety, and cognitive dysfunction. Although direct mechanistic data are limited, integrating these pathways provides a conceptual framework for understanding metabolic–psychiatric comorbidities. Furthermore, differences in age, sex, and genetics may influence these systems, highlighting the need for personalized interventions. Targeting mitochondrial function, GDF15-GFRAL signaling, and gut microbiota composition may offer new therapeutic strategies. This integrative perspective helps conceptualize how metabolic and psychiatric mechanisms interact for understanding the pathophysiology of metabolic and psychiatric comorbidities and highlights therapeutic targets for precision medicine. Full article
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38 pages, 1758 KiB  
Review
Beyond Blood Pressure: Emerging Pathways and Precision Approaches in Hypertension-Induced Kidney Damage
by Charlotte Delrue and Marijn M. Speeckaert
Int. J. Mol. Sci. 2025, 26(15), 7606; https://doi.org/10.3390/ijms26157606 - 6 Aug 2025
Abstract
Recent studies have demonstrated that the development and progression of hypertensive kidney injury comprise not only elevated systemic blood pressure but also a complex interplay of cellular, molecular, and genetic mechanisms. In this report, we outline the key emerging pathways—ranging from dysregulated renin–angiotensin [...] Read more.
Recent studies have demonstrated that the development and progression of hypertensive kidney injury comprise not only elevated systemic blood pressure but also a complex interplay of cellular, molecular, and genetic mechanisms. In this report, we outline the key emerging pathways—ranging from dysregulated renin–angiotensin system signaling, oxidative stress, immune-mediated inflammation, and metabolic abnormalities to epigenetic alterations and genetic susceptibilities—that contribute to kidney damage in hypertensive conditions. In addition, we also discuss precision medicine approaches like biomarker-directed therapies, pharmacologically targeted therapies, and device-based innovations for modulating these pathways. This integrative review emphasizes the application of omics technologies and genetically guided interventions to better stratify patients and offer personalized care for hypertensive kidney disease. Full article
(This article belongs to the Special Issue Recent Research on Hypertension and Related Complications)
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14 pages, 650 KiB  
Review
Not All Platelets Are Created Equal: A Review on Platelet Aging and Functional Quality in Regenerative Medicine
by Fábio Ramos Costa, Joseph Purita, Rubens Martins, Bruno Costa, Lucas Villasboas de Oliveira, Stephany Cares Huber, Gabriel Silva Santos, Luyddy Pires, Gabriel Azzini, André Kruel and José Fábio Lana
Cells 2025, 14(15), 1206; https://doi.org/10.3390/cells14151206 - 6 Aug 2025
Abstract
Platelet-rich plasma (PRP) is widely used in regenerative medicine, yet clinical outcomes remain inconsistent. While traditional strategies have focused on platelet concentration and activation methods, emerging evidence suggests that the biological age of platelets, especially platelet senescence, may be a critical but overlooked [...] Read more.
Platelet-rich plasma (PRP) is widely used in regenerative medicine, yet clinical outcomes remain inconsistent. While traditional strategies have focused on platelet concentration and activation methods, emerging evidence suggests that the biological age of platelets, especially platelet senescence, may be a critical but overlooked factor influencing therapeutic efficacy. Senescent platelets display reduced granule content, impaired responsiveness, and heightened pro-inflammatory behavior, all of which can compromise tissue repair and regeneration. This review explores the mechanisms underlying platelet aging, including oxidative stress, mitochondrial dysfunction, and systemic inflammation, and examines how these factors influence PRP performance across diverse clinical contexts. We discuss the functional consequences of platelet senescence, the impact of comorbidities and aging on PRP quality, and current tools to assess platelet functionality, such as HLA-I–based flow cytometry. In addition, we present strategies for pre-procedural optimization, advanced processing techniques, and adjunctive therapies aimed at enhancing platelet quality. Finally, we challenge the prevailing emphasis on high-volume blood collection, highlighting the limitations of quantity-focused protocols and advocating for a shift toward biologically precise, function-driven regenerative interventions. Recognizing and addressing platelet senescence is a key step toward unlocking the full therapeutic potential of PRP-based interventions. Full article
(This article belongs to the Section Cells of the Cardiovascular System)
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10 pages, 223 KiB  
Article
Lipoprotein(a) Levels in Heart Failure with Reduced and Preserved Ejection Fraction: A Retrospective Analysis
by Alaukika Agarwal, Rubab Sohail and Supreeti Behuria
Hearts 2025, 6(3), 20; https://doi.org/10.3390/hearts6030020 - 6 Aug 2025
Abstract
Background/Objectives: While elevated Lp(a) levels are associated with incident heart failure development, the role of Lp(a) in established heart failure with reduced ejection fraction (HFrEF) versus heart failure with preserved ejection fraction (HFpEF) remains unexplored. Methods: We conducted a retrospective analysis of 387 [...] Read more.
Background/Objectives: While elevated Lp(a) levels are associated with incident heart failure development, the role of Lp(a) in established heart failure with reduced ejection fraction (HFrEF) versus heart failure with preserved ejection fraction (HFpEF) remains unexplored. Methods: We conducted a retrospective analysis of 387 heart failure patients from our institutional database (January 2018–June 2024). Patients were categorized as HFrEF (n = 201) or HFpEF (n = 186) using ICD-10 codes. Categorical variables were compared between heart failure types using the Chi-square test or Fisher’s Exact test, and continuous variables were compared using the two-sample t-test or Wilcoxon rank-sum test, as appropriate. Logistic regression was utilized to assess heart failure type as a function of Lp(a) levels, adjusting for covariates. Spearman correlation assessed relationships between Lp(a) and pro-BNP levels. Results: Despite significant demographic and clinical differences between HFrEF and HFpEF patients, Lp(a) concentrations showed no significant variation between groups. Median Lp(a) levels were 60.9 nmol/dL (IQR: 21.9–136.7) in HFrEF versus 45.0 nmol/dL (IQR: 20.1–109.9) in HFpEF (p = 0.19). After adjusting for demographic and clinical covariates, Lp(a) showed no association with heart failure subtype (OR: 1.001, 95% CI: 0.99–1.004; p = 0.59). Conclusions: Lp(a) levels do not differ significantly between HFrEF and HFpEF phenotypes, suggesting possible shared pathophysiological mechanisms rather than phenotype-specific biomarker properties. These preliminary findings may support unified screening and treatment strategies for elevated Lp(a) across heart failure, pending confirmation in larger studies. Full article
15 pages, 2070 KiB  
Article
Machine Learning for Personalized Prediction of Electrocardiogram (EKG) Use in Emergency Care
by Hairong Wang and Xingyu Zhang
J. Pers. Med. 2025, 15(8), 358; https://doi.org/10.3390/jpm15080358 - 6 Aug 2025
Abstract
Background: Electrocardiograms (EKGs) are essential tools in emergency medicine, often used to evaluate chest pain, dyspnea, and other symptoms suggestive of cardiac dysfunction. Yet, EKGs are not universally administered to all emergency department (ED) patients. Understanding and predicting which patients receive an [...] Read more.
Background: Electrocardiograms (EKGs) are essential tools in emergency medicine, often used to evaluate chest pain, dyspnea, and other symptoms suggestive of cardiac dysfunction. Yet, EKGs are not universally administered to all emergency department (ED) patients. Understanding and predicting which patients receive an EKG may offer insights into clinical decision making, resource allocation, and potential disparities in care. This study examines whether integrating structured clinical data with free-text patient narratives can improve prediction of EKG utilization in the ED. Methods: We conducted a retrospective observational study to predict electrocardiogram (EKG) utilization using data from 13,115 adult emergency department (ED) visits in the nationally representative 2021 National Hospital Ambulatory Medical Care Survey–Emergency Department (NHAMCS-ED), leveraging both structured features—demographics, vital signs, comorbidities, arrival mode, and triage acuity, with the most influential selected via Lasso regression—and unstructured patient narratives transformed into numerical embeddings using Clinical-BERT. Four supervised learning models—Logistic Regression (LR), Support Vector Machine (SVM), Random Forest (RF) and Extreme Gradient Boosting (XGB)—were trained on three inputs (structured data only, text embeddings only, and a late-fusion combined model); hyperparameters were optimized by grid search with 5-fold cross-validation; performance was evaluated via AUROC, accuracy, sensitivity, specificity and precision; and interpretability was assessed using SHAP values and Permutation Feature Importance. Results: EKGs were administered in 30.6% of adult ED visits. Patients who received EKGs were more likely to be older, White, Medicare-insured, and to present with abnormal vital signs or higher triage severity. Across all models, the combined data approach yielded superior predictive performance. The SVM and LR achieved the highest area under the ROC curve (AUC = 0.860 and 0.861) when using both structured and unstructured data, compared to 0.772 with structured data alone and 0.823 and 0.822 with unstructured data alone. Similar improvements were observed in accuracy, sensitivity, and specificity. Conclusions: Integrating structured clinical data with patient narratives significantly enhances the ability to predict EKG utilization in the emergency department. These findings support a personalized medicine framework by demonstrating how multimodal data integration can enable individualized, real-time decision support in the ED. Full article
(This article belongs to the Special Issue Machine Learning in Epidemiology)
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20 pages, 941 KiB  
Article
Bioanalytical Method Validations of Three Alpha1-Antitrypsin Measurement Methods Required for Clinical Sample Analysis
by Andrea Engelmaier, Martin Zimmermann, Harald A. Butterweck and Alfred Weber
Pharmaceuticals 2025, 18(8), 1165; https://doi.org/10.3390/ph18081165 - 6 Aug 2025
Abstract
Background/Objectives: The quality of clinical studies is largely determined by the bioanalytical methods used for testing study samples. Rigorous assay validation following defined criteria, for example, the European Medicines Agency guideline for bioanalytical method validation, is a prerequisite for such assays. Alpha1-antitrypsin [...] Read more.
Background/Objectives: The quality of clinical studies is largely determined by the bioanalytical methods used for testing study samples. Rigorous assay validation following defined criteria, for example, the European Medicines Agency guideline for bioanalytical method validation, is a prerequisite for such assays. Alpha1-antitrypsin (AAT) measurement, i.e., the specific measurement of AAT protein and its associated elastase-inhibitory activity, is an integral part of assay panels for clinical studies addressing AAT deficiency. Specifically, AAT must be measured in the matrix of citrated human plasma as well as in diluted solutions with high salt concentrations obtained through bronchoalveolar lavage (BAL). Sensitive and selective measurement methods are required, as BAL has a low level of AAT. Methods: We present the validation data obtained for three AAT measurement methods. Two of them, nephelometry and the enzyme-linked immunosorbent assay, which clearly differ in their sensitivity, provide AAT protein concentrations. The third is the highly sensitive, newly developed elastase complex formation immunosorbent assay that specifically measures the inhibitory activity of AAT against its pivotal target, protease neutrophil elastase. Using samples with relevant AAT concentrations, we addressed the assays’ characteristics: accuracy, precision, linearity, selectivity, specificity, limit of quantification and short-term analyte stability Results: Overall, the three methods demonstrated low total errors, a combined measure reflecting accuracy and precision, even at low analyte concentrations of less than 0.5 µg/mL; adequate linearity over the required assay range; and acceptable selectivity and specificity. Furthermore, the short-time stability of the analyte was also demonstrated. Conclusions: All three AAT measurement methods met the acceptance criteria defined by the guidelines on bioanalytical assay validation, qualifying these methods for clinical sample analysis. Full article
(This article belongs to the Section Biopharmaceuticals)
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27 pages, 1619 KiB  
Review
Epigenetic Mechanisms Governing Nrf2 Expression and Its Role in Ferroptosis
by Linbo Li, Xinjun Liu, Zizhen Si and Xidi Wang
Biomedicines 2025, 13(8), 1913; https://doi.org/10.3390/biomedicines13081913 - 5 Aug 2025
Abstract
Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation participating in various diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a central regulator of cellular redox homeostasis and a key determinant of ferroptosis resistance. Nrf2 activates [...] Read more.
Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation participating in various diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a central regulator of cellular redox homeostasis and a key determinant of ferroptosis resistance. Nrf2 activates the expression of downstream antioxidant genes to protect cells from oxidative stress and ferroptosis. Consequently, precise regulation of Nrf2 expression is crucial. Recent studies have revealed that complex epigenetic mechanisms involving DNA methylation, histone modifications, and non-coding RNA networks regulate Nrf2 expression. DNA methylation usually suppresses while histone acetylation promotes Nrf2 expression. The influences of histone methylation on NFE2L2 are site- and methylation degree-dependent. m6A modification stabilizes NFE2L2 mRNA to promote Nrf2 expression and thereby inhibit ferroptosis. This article summarizes current understanding of the epigenetic mechanisms controlling Nrf2 expression and Nrf2-mediated ferroptosis pathways and their implications in disease models. The challenges associated with the epigenetic regulation of Nrf2 and future research directions are also discussed. A comprehensive understanding of this regulatory interplay could open new avenues for intervention in ferroptosis-related diseases by fine-tuning cellular redox balance through the epigenetic modulation of Nrf2. Full article
(This article belongs to the Special Issue Oxidative Stress in Health and Disease)
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39 pages, 1914 KiB  
Review
Mechanistic Insights into the Pathogenesis of Polycystic Kidney Disease
by Qasim Al-orjani, Lubna A. Alshriem, Gillian Gallagher, Raghad Buqaileh, Neela Azizi and Wissam AbouAlaiwi
Cells 2025, 14(15), 1203; https://doi.org/10.3390/cells14151203 - 5 Aug 2025
Abstract
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a systemic ciliopathy resulting from loss-of-function mutations in the PKD1 and PKD2 genes, which encode polycystin-1 (PC1) and polycystin-2 (PC2), respectively. PC1 and PC2 regulate mechanosensation, calcium signaling, and key pathways controlling tubular epithelial structure and [...] Read more.
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a systemic ciliopathy resulting from loss-of-function mutations in the PKD1 and PKD2 genes, which encode polycystin-1 (PC1) and polycystin-2 (PC2), respectively. PC1 and PC2 regulate mechanosensation, calcium signaling, and key pathways controlling tubular epithelial structure and function. Loss of PC1/PC2 disrupts calcium homeostasis, elevates cAMP, and activates proliferative cascades such as PKA–B-Raf–MEK–ERK, mTOR, and Wnt, driving cystogenesis via epithelial proliferation, impaired apoptosis, fluid secretion, and fibrosis. Recent evidence also implicates novel signaling axes in ADPKD progression including, the Hippo pathway, where dysregulated YAP/TAZ activity enhances c-Myc-mediated proliferation; the stimulator of interferon genes (STING) pathway, which is activated by mitochondrial DNA release and linked to NF-κB-driven inflammation and fibrosis; and the TWEAK/Fn14 pathway, which mediates pro-inflammatory and pro-apoptotic responses via ERK and NF-κB activation in tubular cells. Mitochondrial dysfunction, oxidative stress, and maladaptive extracellular matrix remodeling further exacerbate disease progression. A refined understanding of ADPKD’s complex signaling networks provides a foundation for precision medicine and next-generation therapeutics. This review gathers recent molecular insights and highlights both established and emerging targets to guide targeted treatment strategies in ADPKD. Full article
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