Introduction. Obstructive sleep apnea (OSA) is the most common sleep-disordered breathing condition. A significant number of OSA patients often present with cardiovascular comorbidities, particularly arterial hypertension. OSA is associated with changes in bioelectrical activity of the brain, such as slowing of electroencephalographic activity in the cortex and reduced interhemispheric synchronization. These changes can become pathophysiological markers of sleep-disordered breathing.
Aim. To investigate the effect of sleep-disordered breathing on a range of quantitative electroencephalogram (EEG) characteristics during nighttime sleep in patients with arterial hypertension and clinically significant OSA.
Materials and methods. The material for this retrospective study consisted of 84 polysomnographic records of patients predominantly diagnosed with arterial hypertension. Patients were divided into three groups based on the apneahypopnea index (AHI). Polysomnographic records were used to assess the synchronization measure of brain electrical activity between occipital EEG leads. The synchronization measure was evaluated using a method based on wavelet bicoherence calculation.
Results. Statistically significant differences were observed in the low-frequency ranges Δf1-Δf4: 0.2-1.0 Hz, 0.8-1.6 Hz, 1.0-2.0 Hz, 1.0-4.0 Hz. In these frequencies, the interhemispheric synchronization measure significantly decreased with increasing severity of apnea.
Conclusion. To determine the severity of obstructive sleep apnea, a parameter based on the synchronization measure evaluated from symmetrical occipital EEG signals in the frequency ranges 0.2-1.0 Hz, 0.8-1.6 Hz, 1.0-2.0 Hz, and 1.0-4.0 Hz can be considered. This may serve as the basis for developing and implementing new diagnostic tools for assessing the severity of sleep-disordered breathing in practice.

Aim. To study the clinical features of the course of acute coronary syndrome (ACS) in elderly patients with chronic obstructive pulmonary disease (COPD).
Materials and methods. The study included 78 patients with ACS: 43 patients with ACS and COPD (group 1) and 35 patients with ACS without COPD (group 2). All patients underwent comprehensive clinical, instrumental, and laboratory examinations.
Results. Among the risk factors for cardiovascular diseases (CVD), the most significant contributors to the development of ACS in patients with COPD were smoking, arterial hypertension, and elevated levels of C-reactive protein (CRP). Patients with ACS and COPD more frequently had non- ST-segment elevation myocardial infarction (NSTEMI). For patients with comorbid pathology, more pronounced changes in the coronary arteries were characteristic due to an increase in the total number of stenoses (p=0.02), hemodynamically significant stenosis (p=0.01), occlusions and critical stenoses (p=0.02), and extensive stenoses (p=0.04). Group 1 patients, compared to group 2, had hemodynamically significant stenosis located in the proximal (p=0.04) and distal (p=0.02) segments of the coronary arteries, as well as in second-order branches (p=0.02). No significant differences were found between the groups in the number of stenoses of the left main coronary artery and the middle segments of the major coronary arteries.
Conclusion. In elderly patients with COPD, ACS development was more often preceded by angina symptoms and atypical myocardial infarction presentations, with NSTEMI predominating in the myocardial infarction structure. The main CVD risk factors in COPD patients were smoking, arterial hypertension, and elevated CRP levels. Atherosclerotic coronary artery disease in ACS patients with COPD was characterized by multivessel disease, predominance of middle and distal coronary artery stenosis. A significant feature of coronary artery disease in comorbid elderly patients was the increased total number of stenoses and the number of extensive stenoses.

Introduction. It is known that monocytes and derived macrophages play an important role in the development of chronic obstructive pulmonary disease (COPD). Previously, we found that cigarette smoke-sensitive TRPV1 channels have higher expression on monocytes and macrophages of COPD patients.
Aim. To investigate the effect of chronic TRPV1 activation on the differentiation of monocytes into macrophages in vitro.
Materials and methods. The study included 11 patients with COPD and 7 healthy non-smoking volunteers (control). Monocytes were obtained from peripheral blood mononuclear cells by plastic adhesion. Cells were cultured for 10 days in the presence of granulocytemacrophage colony-stimulating factor (GM-CSF) or GM-CSF and the TRPV1 agonist capsaicin. On the 11th day, the cells were stimulated with lipopolysaccharides (LPS). Expression of the genes encoding the transcription factors STAT1, STAT6, IRF3, JUN, MAF, RELA, cytokines IL1B, IL6, IL8, and three reference genes B2M, RACK1 and HPRT1 was assessed by quantitative PCR with reverse transcription.
Results. Initially, macrophages of COPD patients differentiated in the presence of GM-CSF had higher expression of STAT1 (2.98-fold, p=0.03) and JUN (1.6-fold, p=0.02). LPS stimulation was accompanied by upregulation of IRF3 (4.3-fold, p=0.04), RELA (1.3-fold, p=0.05) and interleukin genes. Under the action of LPS COPD macrophages had 3.2-fold higher expression of IRF3 as compared to the control (p=0.05). Capsaicin also caused upregulation of IRF3 in cells from COPD patients, thus the expression of this factor became 3.2-fold higher than in the control group (p=0.03). Differentiation with capsaicin sensitized macrophages to LPS. Under these conditions JUN expression increased both in COPD patients (1.8-fold, p=0.01) and in the control group (2.2-fold, p=0.02) as compared with cells differentiated with GM-CSF alone.
Conclusion. The obtained results indicate that in resting state macrophages from COPD patients are mostly characterized by a proinflammatory M1 polarization. LPS probably leads to an additional polarization towards M2b phenotype, when compared with the control, as indicated by an increase in the level of IRF3 transcripts. Capsaicin also promotes M2b polarization of COPD macrophages and may enhance the inflammatory response of cells to LPS.

Introduction. To analyze of the severity of respiratory symptoms in patients with chronic obstructive pulmonary disease (COPD), depending on the presence of an exacerbation or novel coronavirus infection (NCVI), taking into account the activity of acute phase blood parameters.
Materials and methods. The medical documentation of 162 patients with COPD was studied, which were divided into 3 groups: group 1 (n=61) ‒ COPD and NCVI, group 2 (n=53) – stable COPD, group 3 (n=48) ‒ COPD exacerbation. The severity of respiratory symptoms was assessed using points. To assess the activity of inflammation the following biochemical indicators were used ‒ C-reactive protein (CRP) and fibrinogen (g/L).
Results. According to the severity of cough and the intensity of dyspnea on the mMRC scale, the first, second and third groups did not differ statistically (p=0.07). Patients of the first group (82.5%) characterized by the absence of classical criteria for exacerbation of COPD. In terms of the severity of sputum production, the first, second and third groups are statistically different (p=0.0001). The first, second and third groups differ significantly in the level of serum CRP (p=0.0001) and fibrinogen (p=0.009). According to the results of the correlation analysis, some relationships found between respiratory symptoms and the level of CRP and fibrinogen.
Conclusion. The clinical feature of the associated course of stable COPD and NCVI is the presence of severe dyspnea and the absence of classic criteria for exacerbation of COPD. Systemic inflammation in NCVI and stable COPD are more pronounced than in isolated stable COPD or exacerbation and correlates with cough and dyspnea. Practitioners for the differential diagnosis of NCVI in stable COPD can use the data obtained.

Aim. To study the dynamics of respiratory system function in patients without a history of bronchopulmonary pathology after SARS-CoV-2 infection with virus-associated lung damage.
Materials and methods. A retrospective study was conducted on 29 patients (median age 46 [43-51] years) at two stages: visit 1 (1-4 months) and visit 2 (8-13 months) from the onset of COVID-19. Data from spirometry, bodyplethysmography, diffusion capacity test, impulse oscillometry (IOS), and chest computed tomography (CT) obtained during the acute phase of the disease (CTmax), as well as dyspnea assessed by the mMRC scale, were analyzed.
Results. The median CTmax was 75%, and 66% of patients received treatment in the intensive care unit. At visit 1, dyspnea was of mild or moderate severity. Medians of vital capacity (VC), total lung capacity (TLC), residual volume (RV), and diffusion capacity of the lungs (DLco) were reduced (<80% predicted). The median forced expiratory volume in the first second (FEV1) and IOS parameters were within normal ranges. However, increased reactance area (AX) and absolute frequency dependence of resistance (R5–R20) were found in 59% and 24% of cases, respectively. At visit 2, mild dyspnea persisted. Lung volumes were within normal limits, with statistically significant differences between visits. The median DLco was reduced at visit 1 but increased to normal at visit 2, with statistically significant differences between visits. The median IOS parameters remained within normal limits, with no statistically significant differences between visits. However, in visit 1 increased AX and (R5–R20) were observed in 59% and 24%, in visit 2 – 45% and 17% of cases, respectively, with no statistically significant differences between visits.
Conclusions. Among the long-term functional consequences of SARS-CoV-2 infection with virus-associated lung damage, decreased lung diffusion capacity (reduced DLco) and small airway dysfunction (increased AX and/or R5-R20) were noted in some patients. Impulse oscillometry should be included in the comprehensive functional assessment plan for patients after SARS-CoV-2 infection to diagnose small airway dysfunction.

Introduction. Despite significant information on cardiovascular damage in older patients with COVID- 19, there is no clear understanding of the variability of cardiac diseases manifestations in young patients. Additionally, summarized data characterizing the severity of myocardial damage in these patients is lacking.
Aim. To compare laboratory and functional study data and identify predictors of cardiovascular damage in young patients with COVID-19.
Materials and methods. An analysis of 4,453 medical records from 2020 to 2022 was conducted. The focus was on patient age (18- 44 years), primary diagnosis, severity of COVID-19, comorbid conditions, timing of cardiovascular symptom onset, and laboratory and functional study data characterizing cardiovascular system damage. According to the inclusion and exclusion criteria, 132 medical records of patients aged 18 to 44 years with moderate COVID-19 were selected, including 49 with cardiovascular issues and 83 without cardiovascular pathology.
Results. Comparative analysis showed that cardiovascular system damage in young patients with moderate COVID-19, compared to those without cardiovascular pathology, was associated with elevated levels of C-reactive protein (CRP) (p=0.001), brain natriuretic peptide (NTproBNP) (p<0.0001), D-dimer (p<0.0001), and troponin I (p<0.0001). CRP levels in patients with pericarditis and acute myocardial infarction (AMI) were higher than in those with acute cerebrovascular accident (ACVA) (p=0.001). No differences in D-dimer levels were found between subgroups (p>0.05). Troponin I and NTproBNP levels in the AMI subgroup were higher than in the pericarditis (p<0.0001 and p=0.047, respectively) and ACVA (p=0.001 and p=0.043, respectively) subgroups. Patients with cardiovascular disorders had a reduced left ventricular ejection fraction (LVEF) (p=0.005) without significant changes in left ventricular end-systolic (p=0.200) and end-diastolic volumes (p=0.119). The lowest LVEF was found in the AMI and ACVA subgroups (p=0.001). Correlation-regression analysis revealed associations between cardiovascular complications and NTproBNP (r=0.673, p<0.001), troponin I (r=0.543, p<0.001), and D-dimer (r=0.363, p<0.001), as well as LVEF (r=-0.341, p<0.001). Significant stochastic relationships were also found between D-dimer and troponin I (r=0.532, p<0.001), NTproBNP (r=0.545, p<0.001); and between LVEF and troponin I (r=-0.420, p<0.001), NTproBNP (r=-0.314, p<0.001). Multivariate regression analysis showed that NTproBNP, with a sensitivity of 86.5% and specificity of 81.9%, is an independent predictor of cardiovascular complications in young patients with moderate COVID-19 (OR=1.175, p=0.001).
Conclusion. The results indicate that the severity of COVID-19, regardless of patient age and comorbidities, can be a factor in the development of cardiovascular complications. NTproBNP levels in the blood of COVID-19 patients can be an early marker of cardiovascular risk. However, further research is needed to confirm the pathogenetic role of cardiotropic protein in the development of pericarditis, AMI, and ACVA in these patients.

Aim. To assess the lung function in patients with bronchial asthma (BA) after new-onset coronavirus infection.
Materials and methods. Fifty-five patients who underwent COVID-19 participated in the study under conditions of voluntary informed consent. The main group consisted of 30 patients with mild BA, the comparison group – 25 patients without chronic respiratory diseases (CRD). According to chest computed tomography (CT) findings, the degree of lung parenchyma involvement was classified as follows: mild COVID-19 (CT 0 stage) in 14 patients; moderate COVID-19 (CT 1-2 stages) in 27 patients; and severe COVID-19 (CT 3-4 stages) in 14 patients. Lung function tests were conducted once, adhering to both Russian and international standards.
Results. In patients with BA, obstructive pulmonary function impairment was predominant at CT 1-2 stages (79%), CT 0 stage (67%), and CT 3-4 stages (43%). Lung diffusion capacity (LDC) was impaired predominantly in CT 3-4 stages in both BA patients and those without CRD, occurring in 57% of cases. Analysis of lung function showed that LDC reduction was detected in 17% of BA cases and 24% of non-CRD cases. There were no statistically significant changes in pulmonary ventilation among BA patients with impaired LDC compared to patients without CRD.
Conclusion. All patients with respiratory symptoms after COVID-19 should undergo comprehensive lung function assessment to identify bronchial obstruction, impaired lung diffusion capacity, and ensure timely intervention.

Introduction. Chronic rhinosinusitis with nasal polyps is a group of chronic recurrent inflammatory diseases of the nasal mucosa and paranasal sinuses with an incompletely understood etiopathogenesis. Despite various theories on the development of this disease and principles of pathogenetic therapy, some patients continue to suffer from the disease, which is resistant to both medical and surgical treatment.
The aim of this study was to identify the most significant risk factors for the development of polypoid rhinosinusitis in patients with chronic purulent rhinosinusitis using binary logistic regression.
Materials and methods. The study included patients diagnosed with chronic purulent rhinosinusitis (n=40) and chronic purulent-polypoid rhinosinusitis (n=40) who were treated at the otorhinolaryngology department of the Chita Clinical Hospital "RZD-Medicine" from 2016 to 2020. The control group consisted of 20 healthy volunteers, matched by sex and age with the study groups. All subjects underwent comprehensive clinical examinations, bacteriological analysis, endoscopic examination, and measurements of interleukin (IL)-1β, IL-2, IL-4, IL-6, IL-8, IL-10, defensins (HAD 1-3), heat shock protein 70 (HSP70), and autoantibodies to it in serum and nasal secretions, as well as the coagulation activity of nasal secretions. Binary logistic regression was used to analyze risk factors for the development of polypoid rhinosinusitis.
Results. We demonstrated that high predictive significance for the development of nasal mucosal polyps in patients with purulent rhinosinusitis is associated with concentrations of heat shock protein 70, IL-10, and HAD 1-3 in serum.
Conclusion. A test set that includes levels of HSP70, IL-10, and HAD 1-3 in serum can predict the development of chronic polypoid rhinosinusitis with 99% accuracy.

Introduction. COVID-19 causes direct and indirect placental damage through inflammatory monocytes/ macrophages, increasing the risk of infectious and inflammatory diseases in newborns.
Aim. To analyze the expression of CD68 by macrophages and structural changes in the placenta, and to assess the risks of obstetric and neonatal complications in cases of moderate COVID-19 during the third trimester of pregnancy.
Materials and methods. A histological examination was conducted on 33 placentas from women with moderate COVID-19 in the third trimester of pregnancy and 30 placentas from women not infected with SARS-CoV-2. Tissue sections were analyzed using an automated microscopy system for histological studies. CD68 expression on placental macrophages was studied using flow cytometry. Detection of SARS-CoV-2 RNA in placental tissue samples, as well as in nasopharyngeal swabs from newborns, was carried out by real-time reverse transcription polymerase chain reaction (RT-PCR).
Results. An increase in the number of CD68-positive macrophages was observed in the placentas from women with COVID-19 (80.8 (78.2; 83.5) %; p<0.0001) compared to samples from women not infected with SARS-CoV-2 (19.6 (17.2; 21.8) %). All placental samples and nasopharyngeal swabs from newborns of mothers with COVID-19 tested negative for SARS-CoV-2, indicating a low risk of vertical transmission. Histological analysis revealed signs of infectious involvement of both maternal and fetal placental parts, including focal deciduitis, villitis, and histiocytic intervillositis. Circulatory disorders were characterized by decidual vasculopathy, accelerated villous maturation, perivillous fibrin deposition, thrombosis, villous necrosis, and an increase in syncytial knots. A link was established between structural placental abnormalities and the development of chronic placental insufficiency (relative risk (RR)=2.33), preterm birth and premature rupture of membranes (RR=4.26), and fetal growth restriction. Newborns from mothers with COVID-19 exhibited complications such as cerebral ischemia and respiratory distress syndrome.
Conclusion. Moderate COVID-19 in the third trimester of pregnancy can induce structural changes in the placenta, reflecting both compensatory-adaptive responses and inflammation driven by CD68-expressing macrophages. These alterations are associated with a high risk of obstetric and neonatal complications.

Prostaglandins (PGs), regulated by cyclooxygenase (COX) 2, play a significant role in the development of placental disorders in pathological pregnancy. A review of current literature reveals a lack of evidence demonstrating the involvement of PGs in the pathogenesis of early spontaneous miscarriages associated with cytomegalovirus (CMV) infection. The aim of this study was to investigate the levels of COX-2 and PG E2 in peripheral blood and determine their significance in predicting pregnancy loss during exacerbation of CMV infection at 7-8 weeks gestation.
Materials and methods. The study involved 70 patients experiencing an exacerbation of chronic CMV infection at 7-8 weeks of gestation, with 36 patients presenting with a threatened miscarriage (main group) and 34 patients without signs of threatened miscarriage (comparison group). CMV infection was diagnosed based on the presence of M and G class antibodies using enzyme-linked immunosorbent assay (ELISA), as well as CMV DNA detected by polymerase chain reaction. COX-2 levels in mononuclear cell lysates were determined using the "Assay Designs, COX-2" (USA) test systems, and PG E2 concentrations in blood serum were measured using "Cloud-Clone Corp." (USA) kits.
Results. Women with exacerbated CMV infection associated with spontaneous miscarriage at 7-8 weeks of gestation exhibited elevated concentrations of COX-2 (23.0±2.20 ng/mL) and PG E2 (850.10±35.0 pg/mL, p<0.001) compared to pregnant women without threatened miscarriage (12.75±1.35 ng/mL and 42.0±2.80 pg/mL, respectively).
Conclusion. The findings of this study underscore the significant role of elevated COX-2 and PG E2 concentrations in the pathogenesis of pregnancy loss during exacerbation of CMV infection at 7-8 weeks of gestation. The assessment of COX-2 and PG E2 levels should be considered as a predictive measure for the risk of pregnancy loss during exacerbation of CMV infection.

Introduction. Despite the known role of antenatal virus-associated brain damage in the neurological status impairment of newborns, there is a lack of studies addressing the clinical features of cytomegalovirus (CMV) infection. Aim. To provide a clinical and functional characterization of cerebral ischemia in newborns from mothers with exacerbation of CMV infection in the second trimester of pregnancy.
Materials and methods. Clinical and anamnestic data, Apgar scores, body weight, and resistance index in the anterior cerebral artery were studied in 30 newborns from mothers with uncomplicated pregnancies (control group) and 70 newborns from mothers who experienced an exacerbation of CMV infection in the second trimester of pregnancy (main group), including 38 with grade I cerebral ischemia (first subgroup) and 32 with grade II cerebral ischemia (second subgroup).
Results. Newborns in the first subgroup exhibited signs of intrauterine hypoxia, characterized by a lower Apgar score at 1 (p<0.001) and 5 minutes (p<0.001) compared to the control group. Average body weight values were also reduced (p<0.01). Changes in neuro-reflex status manifested as hyperexcitability and motor disorders. The resistance index in the anterior cerebral artery did not differ significantly (p>0.05). In the second subgroup, Apgar scores at 1 (p<0.001) and 5 minutes (p<0.001), as well as average weight indicators (p<0.01 and p<0.001), were lower than in the control group and the first subgroup. The clinical picture was dominated by hypertensive-hydrocephalic syndrome and suppression syndrome, with some cases showing signs of hyperexcitability and convulsive syndrome. Doppler imaging revealed an increase in the resistance index in the anterior cerebral artery (p<0.001).
Conclusion. Newborns from mothers with exacerbation of CMV infection in the second trimester of pregnancy exhibit hypertensive-hydrocephalic syndrome and suppression of neuro-reflex activity depending on the severity of cerebral ischemia, against a background of reduced blood flow in the anterior cerebral artery. Impaired cerebral hemodynamics in such newborns at birth may increase the risk of reduced adaptation in the postnatal developmental period.

This article highlights the history of the development of the anatomy of the respiratory system. The preparation of this publication utilized articles from journals included in the Russian Science Citation Index (RSCI) and Pub- Med. The depth of the publication search spanned 20 years. The article summarizes knowledge about the development of ideas about the anatomy of the respiratory system. The first mentions of the respiratory organs—lungs, bronchi, trachea—date back to Ancient times. Scientists and physicians of that era attempted to determine the structure of the lungs. Not all medical schools associated breathing with the lungs. During the Renaissance, empirical knowledge in this field continued to accumulate. Autopsies allowed for more detailed descriptions of the chest structure, lungs, trachea, and bronchial system. The invention of the microscope in the 17th century enabled the study of lung structure down to the alveoli and capillaries. Various types of epithelial cells of the respiratory tract, nasal cavity sinuses, and more were described. In modern times, technologies have made it possible to obtain the first microphotographs showing the ultrastructure of the pulmonary capillary and the blood-gas barrier. The history of the development of the understanding of the anatomy of the respiratory system can be considered when studying specific topics within university courses such as "Human Anatomy," "History of Medicine," and "History of Biology."

Airway hyperresponsiveness (AHR) is a heterogeneous and complex disorder characterized by excessive narrowing of the airways in response to various exogenous and endogenous stimuli. This article presents information from the last five years, including 50 publications from PubMed and Google Scholar, on the most common viruses that provoke the development of airway hyperresponsiveness in children, including respiratory syncytial virus, rhinovirus, metapneumovirus, influenza and parainfluenza viruses, SARS-CoV-2 coronavirus, adenovirus, and bocavirus. It describes a number of pathophysiological mechanisms by which viruses damage the respiratory epithelium and lead to the formation of infectious and post-infectious bronchial hypersensitivity. The role of hyperexpression of cytokines and inflammatory mediators in the development of AHR, especially in early childhood, is emphasized. It is shown that the inflammatory process and a balanced immune response are crucial for mitigating the severity of the disease caused by viruses. Understanding the molecular mechanisms of inflammatory reactions and the immune response to acute respiratory viral infections can help develop more effective methods for the prevention and treatment of respiratory diseases in children.

Introduction. Asthma is a globally significant non-communicable disease with serious public health implications, affecting both children and adults. It includes high morbidity and mortality rates in severe cases. Understanding the reasons for decreased adherence to asthma therapy in adolescents remains a pressing issue for physicians across various specialties. It is important to analyze the challenges faced by young people that lead to ineffective asthma control.
Aim. To review the latest literature to understand the driving factors behind non-adherence to treatment regimens in adolescents with asthma, their consequences, and potential solutions to ensure better disease control.
Materials and methods. A systematic search was conducted in electronic databases including PubMed, Cochrane Library, Elsevier, Embase, Wiley, and CyberLeninka. The planned search depth was 2019-2024, using keywords: adherence to therapy in adolescents, asthma, therapy control.
Results. The literature review discusses the unique aspects of adherence to asthma therapy in adolescence, along with programs and methods successfully used to optimize medical care for adolescents with asthma.
Conclusion. The course of asthma during adolescence changes due to various factors: hormonal changes, the child's desire for separation from parents, fear of being different from peers, increased societal and school demands, stress, and psychological characteristics. Consequently, researchers from various countries are developing methods to improve therapy adherence and asthma control, such as educational programs in schools, the use of digital health technologies, and even financial incentives for adolescents. Implementing modern methods to enhance medical care for young people with asthma may help reduce mortality rates in this age group.

Gram-negative bacteria Stenotrophomonas maltophilia rank third among non-fermenting gram-negative bacteria in terms of detection frequency in various infectious pathologies. This review presents information on the various virulence factors, mechanisms used by S. maltophilia for colonization and infection of the human body, multiple drug resistance, clinical manifestations of the diseases caused, and methods of bacteriological diagnosis. The importance of early identification of this pathogen for practicing physicians is emphasized. The selection of treatment for infections caused by S. maltophilia is discussed, highlighting the challenges faced by both clinicians and microbiologists. To this end, current domestic and international scientific publications were reviewed using scientific electronic library search engines such as PubMed, Google Scholar, eLIBRARY.ru, and CyberLeninka.