It is well established that ventricular arrhythmia (VA) is relatively common during pregnancy and carries different clinical significance depending on the presence or absence of structural heart disease (SHD). In women with SHD, VA more often reflects electrical and hemodynamic myocardial instability and is associated with an increased risk of heart failure, life-threatening tachyarrhythmias, hospitalization, and adverse obstetric and perinatal outcomes. In contrast, in women with a structurally normal heart, VA is predominantly idiopathic and has traditionally been considered benign. However, the physiological changes of pregnancy, including increased circulating blood volume, activation of neurohormonal mechanisms, and alterations in the electrophysiological properties of the myocardium, may modify the course of VA and its potential impact on both maternal and fetal outcomes. Quantitative assessment of arrhythmic burden is therefore of particular importance. VA burden is defined as the proportion of ventricular ectopic complexes relative to the total number of heartbeats during the monitoring period and is assessed primarily by Holter ECG monitoring. Recent studies in pregnant women without SHD suggest a possible association between a high VA burden and certain obstetric and fetal/neonatal complications; however, the threshold values associated with individual adverse outcomes vary considerably. Current pregnancy risk stratification models, including mWHO 2.0 and CARPREG II, do not incorporate ventricular ectopic burden as an independent parameter. This review compares data from studies including pregnant women with VA both with and without SHD, discusses potential mechanisms underlying adverse outcomes and the role of serial Holter ECG monitoring, and highlights the limitations of the current evidence base. Prospective studies with standardized assessment of arrhythmic burden, evaluation of VA dynamics across pregnancy trimesters, and long-term postpartum follow-up are needed to identify new risk predictors and improve individualized risk stratification
Cardiac sarcoidosis remains a diagnostic challenge and requires differential diagnosis to exclude other potential causes of pathological changes. Difficulties in diagnosis stem from the unknown aetiology of the disease, as well as the non-specific nature of its clinical manifestations. The aim of this review is to analyse data published over the last decade concerning the diagnosis of cardiac sarcoidosis. Materials and Methods . This article presents a narrative review of contemporary literature on the diagnosis of cardiac sarcoidosis. A search for publications was conducted across international and domestic electronic databases, including PubMed, Scopus, Web of Science, Google Scholar, and eLIBRARY.RU. The following keywords and their combinations were used in both English and Russian: cardiac sarcoidosis, heart transplantation for sarcoidosis, diagnosis of sarcoidosis. Results . The review predominantly includes publications from 2016–2026, alongside earlier fundamental studies and international clinical guidelines that are pivotal for understanding the issue. Selection criteria encompassed systematic reviews, meta-analyses, professional society clinical guidelines, prospective and retrospective cohort studies, and large patient registries dedicated to the diagnosis, management, and prognosis of cardiac sarcoidosis. Conclusion : This review focuses on modern diagnostic modalities and the management strategy for patients with cardiac sarcoidosis, which represents one of the most severe and prognostically unfavourable manifestations of systemic sarcoidosis. Diagnosis is frequently delayed due to non-specific symptoms and the patchy distribution of granulomatous inflammation within the myocardium. Presented case reports clearly demonstrate the capabilities of contemporary diagnostics and treatment strategies for patients with cardiac sarcoidosis.
Ionizing radiation has a pronounced nephrotoxic effect, initiating a cascade of pathophysiological processes leading to the development of radiation nephropathy (RN) and renal failure. This review is devoted to an analysis of the current state of research in the field of identifying metabolomic biomarkers that allow for early diagnosis and prediction of radiationinduced kidney damage under external irradiation. The paper systematizes literature data obtained using mass spectrometry (MS) and nuclear magnetic resonance (NMR) regarding changes in the profiles of lowmolecularweight metabolites in urine. The main focus is on profound disturbances in purine metabolism (primarily due to the accumulation of xanthine and hypoxanthine), critical shifts in the tricarboxylic acid cycle (TCA), reflecting mitochondrial dysfunction, as well as an imbalance in the lipid profile, including the accumulation of acylcarnitines. These metabolic alterations are key indicators of oxidative stress and proximal tubule dysfunction, and the degree of their severity directly correlates with clinical and dosimetric parameters. The review provides a detailed examination of critical dose thresholds: moderate functional changes manifest when the absorbed dose to the kidneys exceeds 4 Gy, while irreversible structural degradation and manifest RN develop when the threshold of 10 Gy is exceeded. The authors emphasize that the introduction of metabolomic profiling into clinical practice can radically improve the effectiveness of monitoring the condition of patients who have undergone radiation exposure. Unlike classical protein damage markers (NGAL, KIM1), which are sensitive only at late stages, dynamic patterns of acylcarnitines, TCA cycle intermediates, and purine metabolites make it possible to carry out early biodosimetry. This makes it possible not only to detect the fact of radiation damage but also to assess the received radiation dose in the very first hours after exposure, enabling timely nephroprotective therapy.
Primary cell cultures are an indispensable tool in fundamental research within modern cell biology. Their value lies in their close physiological resemblance to in vivo conditions, which significantly enhances the reliability and translational relevance of experimental data. However, the broad application of primary cells in vitro is constrained by their finite proliferative capacity, culminating in cellular senescence, which poses substantial challenges for long-term and highly reproducible studies. Cellular senescence represents a complex, multifaceted cellular response to diverse stimuli. Consequently, it is broadly classified into replicative senescence, oncogene-induced senescence (OIS), and stress-induced premature senescence. Each of these senescence modalities exhibits distinct molecular signatures, and elucidating these features is crucial for understanding how to bypass the cellular proliferative barrier through immortalization. Classical immortalization strategies, such as the ectopic expression of the telomerase catalytic subunit (TERT) or the introduction of viral oncogenes (e.g., SV40 Large T-antigen, HPV16 E6/E7) and proto-oncogenes, are highly effective but carry significant limitations. These include the inherent risk of oncogenic transformation and the alteration of the native cellular phenotype. Consequently, contemporary approaches such as conditional immortalization, non-integrating delivery systems, and combinatorial strategies are gaining prominence. These methods aim to sustain a high proliferative potential while preserving maximal phenotypic fidelity to the original primary cells. This review systematizes current knowledge regarding the distinct modalities of cellular senescence. It provides a comprehensive analysis of both primary and auxiliary immortalization techniques, critically evaluating their respective advantages and limitations. Furthermore, it characterizes contemporary immortalized cell lines with a specific focus on their phenotypic stability and translational potential in regenerative medicine, tissue engineering, 3D cell culture models, and preclinical pharmacology. The analysis presented herein is primarily based on data published within the last 15 years.
