Schizophrenia is a complex mental disorder with multiple genetic and environmental factors contributing to its pathogenesis. Viral infections have been suggested to be one of the environmental factors associated with the development of this disorder. We comprehensively review all relevant published literature focusing on the relationship between schizophrenia and various viral infections, such as influenza virus, herpes virus 1 and 2 (HSV-1 and HSV-2), cytomegalovirus (CMV), Epstein-Barr virus (EBV), retrovirus, coronavirus, and Borna virus. These viruses may interfere with the normal maturation of the brain directly or through immune-induced mediators, such as cytokines, leading to the onset of schizophrenia. Changes in the expression of critical genes and elevated levels of inflammatory cytokines have been linked to virally-induced infections and relevant immune activities in schizophrenia. Future research is necessary to understand this relationship better and provide insight into the molecular mechanisms underlying the pathophysiology of schizophrenia.

Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by the destruction of insulin-producing pancreatic beta cells, resulting in lifelong insulin dependence. While genetic susceptibility—particularly human leukocyte antigen (HLA) class II alleles—is a major risk factor, accumulating evidence implicates viral infections as potential environmental triggers in disease onset and progression. This narrative review synthesizes current findings on the role of viral pathogens in T1DM pathogenesis. Enteroviruses, especially Coxsackie B strains, are the most extensively studied and show strong epidemiological and mechanistic associations with beta-cell autoimmunity. Large prospective studies—including Diabetes Virus Detection (DiViD), The environmental determinans of diabetes in the young (TEDDY), Miljøfaktorer i utvikling av type 1 diabetes (MIDIA), and Diabetes Autoimmunity Study in the Young (DAISY)—consistently demonstrate correlations between enteroviral presence and the initiation or acceleration of islet autoimmunity. Other viruses—such as mumps, rubella, rotavirus, influenza A (H1N1), and SARS-CoV-2—have been investigated for their potential involvement through direct cytotoxic effects, immune activation, or molecular mimicry. Interestingly, certain viruses like varicella-zoster virus (VZV) and cytomegalovirus (CMV) may exert modulatory or even protective influences on disease progression. Proposed mechanisms include direct beta-cell infection, molecular mimicry, bystander immune activation, and dysregulation of innate and adaptive immunity. Although definitive causality remains unconfirmed, the complex interplay between genetic predisposition, immune responses, and viral exposure underscores the need for further mechanistic research. Elucidating these pathways may inform future strategies for targeted prevention, early detection, and vaccine or antiviral development in at-risk populations.

Myocardial infarction is an emergency situation, and its early diagnosis is vital for patients and for the treatment which will be followed. Till now the diagnosis of myocardial infarction is based on the increased cardiac troponins I and T in the patient's serum, these biomarkers are the gold standard for the diagnosis of myocardial infarction but there are some limitations due to their slow release from the damaged myocytes. For this reason, new biomarkers are needed to be used for a faster diagnosis. New biomarkers should increase rapidly after acute myocardial infarction and should have cardiac selectivity. Myosin-binding protein C is a newly described candidate biomarker of cardiac injury and in small studies, it appears that its serum concentration decreases and increases faster than that of the troponin T and I. Cardiac troponins are released and cleared slowly after myocardial injury, complicating the diagnosis of an early and recurrent, acute myocardial infarction. Cardiac myosin-binding protein C is a similar cardiac protein that may have different release/clearance kinetics.

Obesity is a major global health problem and is closely associated with a broad range of metabolic disorders, including metabolic syndrome (MetS), dyslipidemia, hypertension, atherosclerosis, type 2 diabetes mellitus, and cardiovascular disease. The gut microbiota plays a central role in maintaining intestinal epithelial integrity, regulating glucose and lipid metabolism, and modulating immune function. Through the gut–brain axis, it also contributes to appetite regulation and energy homeostasis by influencing the release of anorexigenic hormones. Dysbiosis, including alterations in the relative abundance of major bacterial phyla such as Firmicutes and Bacteroidetes, has been associated with increased intestinal permeability, metabolic endotoxemia, and chronic low-grade inflammation, all of which may contribute to the development of obesity and insulin resistance. Diets rich in plant-derived fiber can beneficially shape gut microbiota composition. Bacterial fermentation of dietary fiber produces short-chain fatty acids (SCFAs), including butyrate, acetate, and propionate, which contribute to intestinal barrier integrity, inflammatory regulation, immune regulation, and metabolic homeostasis. Overall, the interaction between gut microbiota, diet, and host metabolic pathways represents a promising field for therapeutic and nutritional interventions aimed at preventing and managing MetS and metabolic diseases.

Sepsis is a life-threatening syndrome caused by dysregulated host response to infection and remains a major global health challenge with high healthcare burden. Early recognition is critical for improving outcomes, yet current diagnostic tools and conventional biomarkers such as C-reactive protein and procalcitonin have important limitations related to kinetics, specificity, and cost. This review examines Monocyte Distribution Width (MDW), a novel hematologic parameter derived from routine complete blood count analysis, as an emerging biomarker for early sepsis detection and prognostic assessment. MDW reflects monocyte morphological heterogeneity associated with innate immune activation and rises early in the inflammatory cascade, often at the time of initial clinical presentation. Evidence from emergency department and intensive care unit studies demonstrates that MDW provides high sensitivity and negative predictive value for early sepsis screening and performs comparably to or better than established biomarkers, particularly when integrated with clinical scoring systems and other laboratory indices. Beyond diagnosis, elevated MDW correlates with disease severity, organ dysfunction, and adverse outcomes, suggesting prognostic utility. Although promising, current evidence is limited by heterogeneity and the need for standardized cut-off values and multicenter validation. Overall, MDW represents a rapid, cost-effective adjunct that may enhance multimodal sepsis assessment and clinical decision-making.

Measurable residual disease (MRD) assessment has transformed response evaluation and prognostic stratification across hematologic malignancies. Advances in flow cytometry, polymerase chain reaction, next-generation sequencing, and circulating tumour DNA analysis have expanded the sensitivity and biological scope of residual disease detection. However, increasing analytical sensitivity does not necessarily translate into improved clinical utility. This narrative review critically examines contemporary MRD technologies, their analytical limitations, and their applications in acute myeloid leukaemia, acute lymphoblastic leukaemia, multiple myeloma, chronic lymphocytic leukaemia, lymphomas, and chronic myeloid leukaemia. Particular em-phasis is placed on MRD-guided treatment intensification, de-escalation, transplanta-tion decisions, treatment discontinuation, and pre-emptive intervention. Although MRD negativity is strongly associated with favourable outcomes, evidence demon-strating that MRD-guided treatment modification improves survival remains heterogeneous across diseases and therapeutic settings. The review also addresses preanalytical variables, assay validation, laboratory harmonization, standardized reporting, and the complementary role of molecular and immunophenotypic methodologies. Emerg-ing approaches involving artificial intelligence, single-cell profiling, spatial analysis, and multimodal predictive models are discussed. The proposed MRD 2.0 framework emphasizes the transition from increasingly sensitive detection toward integrated, longitudinal, biologically informed, and clinically actionable monitoring. Its successful implementation requires validated laboratory measurements and prospective evidence linking MRD-informed decisions to improved patient outcomes.