The Siberian State Medical University, SibMed (Russian: «Сибирский государственный медицинский университет», СибГМУ) is a public medical school in Tomsk, Russia. It was founded in May, 1878 by the decree of the Emperor Alexander II. Today, Siberian State Medical University provides undergraduate, graduate, and postgraduate degrees in biochemistry, biophysics, general medicine, pediatrics, dentistry, pharmacy, and nursery fields. It is one of the few universities in Russia that has its own hospital that is not only providing medical care for citizens in Tomsk Region and other regions but, also, is a full-fledged training center for students and medical professionals. It has more than 6 500 students that come from 39 countries worldwide. In 2017, SibMed obtained the status of the only flagship medical university in Russia.
Recent advancements in oncology have markedly enhanced cancer survival rates; however, anticancer therapies, particularly anthracyclines, pose significant cardiovascular (CV) risks, collectively referred to as cancer therapy-related cardiovascular toxicity (CTR-CVT). This review consolidates evidence on strategies to mitigate CTR-CVT especially associated with anthracyclines. Neurohormonal blockers, including ACE inhibitors, ARBs, and β-blockers, constitute the foundation of prevention, although their efficacy varies: combinations such as ACEi/ARB with βB yield mixed outcomes, whereas carvedilol offers antioxidant benefits beyond β-blockade. Sacubitril/valsartan (ARNI) has demonstrated improvements in global longitudinal strain and LVEF preservation in the SARAH trial, albeit with associated hypotension risks. Aldosterone antagonists show potential, with spironolactone preserving LVEF and diastolic function, though eplerenone has not shown significant effects. Statins present conflicting data; the STOP-CA trial supports atorvastatin for LVEF preservation, while the PREVENT and SPARE-HF trials found no benefit. Emerging evidence suggests sodium-glucose cotransporter-2 inhibitors (SGLT2i), such as dapagliflozin and empagliflozin, as promising agents, with preclinical and early clinical data indicating cardioprotection through metabolic modulation, anti-inflammatory effects, and reduced oxidative stress. Gaps remain in understanding CTR-CVT pathophysiology, risk stratification, and the translation of preclinical findings. Future efforts should prioritize personalized approaches, dynamic risk assessment (e.g., HFA-ICOS tool), and a paradigm shift from oxidative stress to cardiometabolic dysfunction. Multidisciplinary collaboration is essential to optimize oncological outcomes while minimizing CV toxicity, with SGLT2i representing a key frontier for validation in ongoing trials.
Abstract The kidney–brain axis represents a bidirectional pathophysiological link between chronic kidney disease (CKD), acute kidney injury (AKI), and blood–brain barrier (BBB) dysfunction. CKD affects over 800 million individuals globally and is associated with accelerated cognitive decline, stroke, and neurodegenerative disorders. This review synthesizes evidence that uremic toxins, systemic inflammation, oxidative stress, hormonal dysregulation (erythropoietin deficiency, RAAS activation), and gut dysbiosis converge to impair BBB integrity via tight junction degradation, endothelial activation, and pericyte–astrocyte decoupling. These alterations facilitate neuroinflammation, neurotoxicity, and leukocyte infiltration, contributing to the pathogenesis of stroke, Alzheimer’s disease, Parkinson’s disease, epilepsy, and CKD-associated leukoencephalopathy. Hemodialysis-induced osmotic shifts and sleep fragmentation further exacerbate BBB and glymphatic dysfunction. Preserving BBB integrity through uremic toxin reduction, anti-inflammatory strategies, RAAS inhibition, and lifestyle interventions (e.g., exercise) emerges as a critical therapeutic goal. Future research must prioritize biomarker validation (claudin-5, S100B), neuroimaging correlations, and targeted BBB-protective therapies to mitigate neurological morbidity in renal disease.
Rationale. At the time of birth, the innervation of the rat heart is not complete: differentiation of neurons of the autonomic ganglia, growth of axons, and development of nerve fibers sheaths continue in the postnatal period of ontogenesis. Whether preterm birth affects the innervation of the heart has not been sufficiently studied. Aim: To perform immunohistochemical study of cardiac nerve fibers of preterm rats in the postnatal period of ontogenesis. Material and Methods . A morphological study of the development of intracardiac nerve fibers in the right and left ventricles, as well as the interventricular septum of the heart in full-term and 24-hour preterm Wistar rats on the 7th, 56th and 180th days of the postnatal period of ontogenesis was carried out. Immunohistochemical detection of PGP9.5 and tyrosine hydroxylase was carried out. The relative area of nerve fibers (PGP9.5-positive staining) and sympathetic postganglionic nerve fibers (tyrosine hydroxylase-positive staining) was determined dynamically, as well as the proportion of sympathetic nerve fibers from nerve fibers total number in the wall of the right and left ventricles, as well as the interventricular septum of the heart of full-term and 24-hour preterm rats. Results. It has been shown that on the 7th day of the postnatal period of ontogenesis in the right, left ventricle and interventricular septum of the heart in 24-hour preterm rats, the relative area of nerve fibers is reduced, compared with that in full-term animals, the differences are leveled out by the 56th day. The relative area of sympathetic postganglionic nerve fibers in the interventricular septum of 24-hour preterm rats on the 7th day of the postnatal period of ontogenesis remains lower, on the 56th day – is higher than in fullterm animals. The relative area of sympathetic postganglionic nerve fibers in the right ventricle of the heart of 24-hour preterm rats throughout the experiment remains lower, while in the left ventricle – does not differ from the parameters of full-term animals. Conclusion. There were revealed structural features of the development of intracardiac nerve fibers of the right and left ventricles of the heart, as well as the interventricular septum in 24-hour preterm rats in the postnatal period of ontogenesis, which may be the cause of a violation of the autonomic regulation of the heart.
Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction in which respiratory muscle involvement, particularly of the diaphragm, constitutes the principal risk factor for myasthenic crisis and respiratory failure. Objective structural evaluation of the diaphragm in MG remains incompletely standardized. This narrative review synthesizes published evidence on diaphragm thickness measurement in generalized MG, with attention to measurement reproducibility, normative reference values, structural-functional linkages, and potential clinical applications of computed tomography (CT). Studies were identified through a targeted search of peer-reviewed databases covering neuromuscular imaging, diaphragm physiology, and respiratory failure, with emphasis on MG. Studies reporting diaphragm measurements with explicit methodological details or clinical outcomes were prioritized, in both MG cohorts and mixed populations, with particular attention to CT. A small number of studies have used diaphragm ultrasound in MG to assess increased fatigability and predict extubation failure. Direct CT-ultrasound matching in myasthenic patients is lacking; however, in non-myasthenic populations, CT measurements at the L1 vertebral level and at the celiac trunk are reproducible and show consistent associations with ultrasound-derived functional indices of diaphragm dysfunction. Left-sided CT measurements correlate more strongly with multiple functional parameters, whereas right-sided measurements show moderate associations with selected indices. Interobserver agreement for CT is good in non-myasthenic cohorts. Because the available structural-functional evidence derives almost entirely from non-myasthenic, mixed neuromuscular, ICU, or diaphragmatic paralysis cohorts rather than MG-specific populations, these findings are hypothesis-generating: CT-based diaphragm assessment is a candidate structural surrogate for functional impairment in MG and a potential adjunct to risk stratification and therapeutic monitoring. The evidence base remains limited by small cohorts and reliance on mixed disease populations. CT is therefore currently best regarded as complementary rather than definitive, and prospective MG-specific studies, stratified by the Myasthenia Gravis Foundation of America (MGFA) class and antibody subtype (acetylcholine receptor, muscle-specific kinase, low-density lipoprotein receptor-related protein 4, seronegative) and integrated with diaphragmatic compound muscle action potential, diaphragm ultrasound, forced vital capacity, and negative inspiratory force trends, are needed before firm clinical thresholds can be established.
Chronic back pain (CBP) associated with intervertebral disc degeneration (IVDD) is a leading cause of medical consultations, decreased quality of life, and temporary and permanent disability. The mechanisms of CBP development and persistence in patients with IVDD have been studied for many years, but this issue remains far from resolved. The search for predictive biomarkers that could help identify patients with IVDD at high risk for CBP continues. In recent decades, research has shown increasing interest in identifying epigenetic biomarkers for this disorder. to summarize the results of preclinical and clinical studies on the role of microRNAs (miRs) as epigenetic biomarkers of the development and progression of CBP in patients with IVDD. English-language articles; original experimental (preclinical) studies; original clinical study; assessment of changes in systemic (in the blood) and/or local (in the intervertebral disk (IVD)) levels of miR expression in IVDD, either independently or in comparison with healthy controls; and studies that were completed and the results of which were published. PubMed, Springer, Google Scholar, Scopus, Oxford Press, Cochrane, and e-Library databases. Charting for this scoping review involved developing a data extraction form to summarize extracts and organize data from included studies. This was an iterative process where the charting tables and figures may be refined as the review progresses. 126 studies were analyzed in detail, focusing on their study designs and comparing changes in miR expression in animal models of IVDD and in patients with IVDD compared to healthy controls. During the preparation of this scoping review and upon subsequent detailed review of the original publications, it turned out that the results of one study were not justified by the authors due to identified technological problems (the article was withdrawn by the editorial board of the journal). Therefore, we excluded the results of this study from the subsequent analysis. As a result, this section summarizes the results of 60 preclinical and 65 clinical studies. Some miRs (e.g., miR-21 and miR-132) are associated with the regulation of inflammatory pathways that contribute to increased degradation of IVD extracellular matrix and enhanced nociceptive signaling through various mechanisms, contributing to the progression of CBP. Other miRs (e.g., miR-145 and miR-223) exert protective effects, enhance regenerative potential, and alleviate CBP. Despite the promising results of these studies, there are limitations in the use of miRs as perspective epigenetic biomarkers of CBP in patients with IVDD because the pattern of potentially predictive and protective miRs in relation to the mechanisms of CBP formation and progression in IVDD has not yet been sufficiently studied. The results of some preclinical and clinical studies are contradictory. Further research is needed to clarify the role of miR signatures in animal models and clinical trials on IVDD-specific CBP.
