Vol 22, No 5 (2024)

Introduction. Many chemical compounds affect brain neurons differently than other cell populations. This is provided by the protective potential of the blood-brain barrier (BBB). One of the compounds capable of passing through the BBB is bacterial lipopolysaccharide (LPS). It can cause irreversible morphological changes in the neurons of the cerebral cortex.

The aim of the work is to study the mechanisms of neuronal damage and death.

Material and methods. More than 50 sources for 15 past years were analyzed at PubMed and Elibrary databases.

Results. Astrocytes recognize LPS due to toll-like receptors, and glial macrophages are also able to capture areas of the external bacterial membrane with LPS. However, variations in the dose of LPS, the method and frequency of its administration have different effects on the morphology of the cerebral cortex. In particular, it is relevant to study changes similar to those in aging and neurodegenerative processes.

Conclusion. The review examines the structural changes of neurons and glia in the use of LPS in adult animals. The authors conclude that repeated systemic administration of non-septic doses of LPS is most suitable for modeling aging-like changes, but it is necessary to develop a standardized model of such administration.

Introduction. Artificial intelligence (AI) technologies are becoming crucial in clinical diagnostics due to their ability to process and interpret large volumes of data. The implementation of AI for biomarker analysis opens new opportunities in personalized medicine, offering more accurate and individualized approaches to disease diagnosis and treatment. The relevance of this review stems from the need to systematize recent advances in AI application for biomarker analysis, which is critical for early diagnosis and prediction of chronic non-communicable diseases (NCDs).

Material and methods. The analysis of peer-reviewed scientific publications and reports from leading research centers over the past five years was conducted. Studies on the application of AI algorithms for analyzing genomic, proteomic, and metabolomic biomarkers were reviewed, including machine learning methods and deep neural networks. Special attention was paid to the integration of multi-marker panels for improving the accuracy of diagnosis and prediction of cardiovascular, digestive, respiratory, endocrine system diseases, as well as oncological and neurodegenerative pathologies.

Results. The application of AI has significantly increased the sensitivity and specificity of diagnostics, especially in complex cases requiring analysis of multiple disease parameters. The effectiveness of AI has been demonstrated in early diagnosis of lung, breast, and colorectal cancer, prediction of cardiovascular complications and NCDs progression, including diabetes mellitus and Alzheimer’s disease. AI’s significant contribution to the discovery of new biomarkers, optimization of personalized treatment, and improvement of therapeutic strategies has been noted.

Conclusion. The use of AI in biomarker analysis has become a significant breakthrough in medical diagnostics, particularly in oncology, cardiology, and neurodegenerative diseases. The technology allows integration of data about various biomarkers and contributes to creating more accurate models for disease diagnosis and prediction. Further development is associated with technology advancement and overcoming ethical and regulatory barriers, which will expand AI capabilities in clinical practice.

Introduction. Alcohol abuse is associated with telomere shortening. There is no convincing evidence of a “safe” level of alcohol consumption in this regard. Long-term studies in rodents are not feasible, and clinical trials with the administration of alcohol to healthy individuals is not ethically acceptable. An approach based on a relevant model of voluntary alcohol consumption in monkeys under controlled conditions is a significant alternative.

The aim of the study. To estimate the length of telomeres at long-term ethanol consumption by male rhesus macaques in under free choice with water

Methods. The study was performed on fourteen mature male Rhesus macaques of groups with low (median 0.62 g/kg/day) and high (median 2.71 g/kg/day) ethanol consumption as 4% (v./v.) solution with condition of all-day access and free choice with drinking water. The duration of consumption was 920 days. The relative length of telomeres was determined by quantitative PCR according to Cawthon (2002) in blood leukocytes.

Results. The relative average telomere length in the high-consumption group was 1.53±0.57 before the presentation of ethanol in the adaptation period (-32 day of the study), and at the consumption stage it was on 717 day 2.13±0.19 and on 917 day 4.61±0.7. In the low-consumption group, the average relative telomere length constituted 1.42±0.22, 1.55±0.15 and 3.3±0.47, respectively. The absolute count of leukocytes did not change significantly during the study. However, changes in the differential white cells count were revealed representing development of relative monocytosis by 917 day in both groups.

Conclusion. The data obtained do not confirm the association of long-term alcohol consumption in moderate doses with telomere length. The completed study has limitations related to the lack of control without consumption and evaluation in one sex.

Introduction. Ionizing radiation can lead to radiation damage to healthy pancreatic tissue, with the development of signs of post-radiation pancreatitis. Electron irradiation potentially has the most “sparing” effect on healthy tissue, but data on this are sparse. The search for means to protect healthy tissues from the effects of ionizing radiation remains relevant. Thus, the use of agents with antioxidant properties (N-acetylcysteine) can potentially slow down the development of post-radiation pancreatitis.

The aim of the study: assessment of the inflammatory response in the pancreas after administration of N-acetylcysteine in a radiation-induced pancreatitis model.

Methods. Wistar rats (n=120) were divided into four groups: I (n=30) – control; II (n=30) – irradiation with electrons in a total irradiation dose of 25 Gy; III (n=30) – pre-irradiation administration of N-acetylcysteine before electron irradiation; IV (n=30) – administration of N-acetylcysteine. Animals were removed from the experiment on the 7^th, 30^th and 90^th days. A morphological assessment of pancreatic fragments and an immunohistochemical study with antibodies to pro- (IL-1, IL-6) and anti-inflammatory (IL-10) cytokines, markers of T-lymphocytes (CD3) and macrophages (CD68) were carried out.

Results. At all stages of the experiment, high levels of expression of pro- and anti-inflammatory cytokines were observed in the electron irradiation group with a slight increase in the number of CD3⁺ T-lymphocytes and CD68⁺ macrophages. In the group of pre-radiation administration of N-acetylcysteine, increased levels of immunolabeling were also found when conducting reactions with antibodies to pro- and anti-inflammatory cytokines, however, by the third month of the experiment, practically no CD3⁺ and CD68⁺ immunocompetent cells were noted in this group.

Conclusion. Pancreatic local electron irradiation at a total dose of 25 Gy in the early stages leads to the development of a stromal-vascular inflammatory reaction with a capillary-parenchymal block with practically no cellular inflammatory infiltration. At the same time, pre-radiation administration of N-acetylcysteine partially prevents the development of post-radiation pancreatitis.