Background/Objectives: Drug repositioning has emerged as a promising strategy to address the innovation crisis in pharmaceutical development. While artificial intelligence enables efficient in silico hypothesis generation, clinical translation remains challenging. This study aims to evaluate the role of Real-World Evidence (RWE) in validating AI-generated drug-repositioning candidates. Methods: A comprehensive literature review was conducted in PubMed using a predefined search strategy integrating drug repositioning, artificial intelligence, and real-world data. After multi-stage screening, 22 original research articles were included for analysis. Results: Network-based algorithms and natural language processing dominated AI-driven hypothesis generation. Validation using Electronic Health Records and insurance databases enabled retrospective assessment of drug efficacy across large populations. Successful applications were identified in neurodegenerative, metabolic, infectious, autoimmune, and psychiatric diseases. Conclusions: The integration of AI-based analytics with RWE provides a promising framework for the preliminary verification of computational predictions, potentially informing the translational pathway toward clinical practice. However, the effectiveness of this approach remains dependent on data quality and the specific therapeutic context, requiring further standardization of clinical data.

Background/Objectives: The objective of this study was to map and synthesize the current evidence on hemostasis in chronic and acute liver disease within the framework of Patient Blood Management (PBM). Methods: Because research in this field is heterogeneous—spanning mechanistic studies, observational data, randomized controlled trials, guidelines, and expert reviews—a scoping review was selected to comprehensively map concepts. Findings were synthesized narratively to reflect the breadth and heterogeneity of available research. Results: Hemostasis in liver disease is characterized by a fragile state of rebalanced coagulation, where parallel reductions in pro- and anticoagulant factors coexist with variable fibrinolytic disturbances and thrombocytopenia. Conventional coagulation tests (CCTs) do not accurately reflect bleeding risk, whereas viscoelastic assays and thrombomodulin-modified thrombin generation testing provide a more physiologic assessment, though with limitations. Most bleeding events arise from portal hypertension rather than coagulopathy, and the routine prophylactic correction of abnormal results of CCTs is not supported by evidence. PBM-aligned strategies—such as restrictive transfusion, targeted fibrinogen replacement, and use of thrombopoietin receptor agonists (TPO-RAs)—reduce unnecessary blood product use. Thrombosis burden is increasingly recognized in this patient population. Anticoagulation is generally safe when individualized to liver function and clinical context, however significant variability persists in clinical practice, and high-quality data remain limited for advanced disease. Conclusions: Hemostasis in liver disease reflects a dynamic and unstable equilibrium rather than a simple bleeding tendency. Diagnostic and therapeutic strategies grounded in PBM principles improve safety by avoiding unnecessary transfusion and emphasize individualized care. Despite advances in understanding rebalanced hemostasis, major gaps remain in predicting thrombotic risk, standardizing advanced coagulation testing, and defining optimal management across disease stages.

Epithelial–mesenchymal plasticity encompasses a spectrum of epithelial and mesenchymal identity states that enable cells to adapt to changing biological contexts. While CD44 isoform usage and epithelial splicing regulators ESRP1/2 are well-characterized in cancer-associated epithelial–mesenchymal transition (EMT), their regulation across physiological, non-transformed identity states remains less well defined. Here, we employed a non-malignant human cellular system comprising primary dermal fibroblasts, induced pluripotent stem (iPS) cells, and iPS-derived mesenchymal stem cells (iPS-MSCs) to define discrete epithelial, intermediate epithelial/mesenchymal, and mesenchymal identity states positioned along an epithelial–mesenchymal identity axis. Morphological assessment, lineage marker profiling, and RT-qPCR analyses revealed reproducible population-level stratification of these states. CD44 expression and alternative splicing followed this hierarchy, with CD44s predominating in fibroblasts, broad variant exon inclusion in iPS cells, and intermediate patterns in iPS-MSCs. ESRP1 expression mirrored CD44 splicing architecture, and ESRP1 silencing in iPS cells induced a shift toward CD44s, confirming its functional contribution to epithelial-associated CD44 splicing. In contrast, Notch-related transcriptional readouts displayed distinct, context-dependent profiles across the examined identity states. Together, this study establishes a tractable non-transformed human model that captures selected molecular features associated with epithelial–mesenchymal plasticity beyond malignant contexts.

Background: The neutrophil-to-lymphocyte ratio (NLR) and monocyte-to-lymphocyte ratio (MLR) reflect the balance between innate and adaptive immunity and may indicate systemic inflammation. Objectives: To evaluate longitudinal changes in NLR and MLR in MS patients during relapse compared with relapse-free controls. Methods: In this retrospective single-center observational study, patients with MS were followed for 2 years. Individuals with at least one relapse and complete blood count data at predefined time points were included. Controls without relapse were selected in a 2:1 ratio and matched for age, sex, disease duration, EDSS score, and disease-modifying therapy category. NLR and MLR were assessed 3 months before relapse (or index date), during relapse, and 3 months after. Results: The study included 34 patients with relapse and 68 controls. During relapse, patients showed higher neutrophil and monocyte counts, lower lymphocyte counts, and elevated NLR and MLR compared with controls (all p < 0.001). NLR increased from 2.75 pre-relapse to 3.62 during relapse, then decreased to 2.67 (p = 0.0002). MLR rose from 0.45 to 0.54 and declined to 0.40 (p = 0.002). No significant changes were observed in controls. Conclusions: NLR and MLR demonstrated dynamic changes during MS relapse. These non-specific indices may serve as exploratory, complementary markers of relapse-associated inflammation, but require validation in larger prospective studies including MRI correlates.