Introduction. Based on the common effector functions of polymorphonuclear neutrophils and macrophages as phagocytic cells, their role in the formation of an acute reaction of the respiratory tract to a cold stimulus in patients with asthma is of concern.

Aim. The study of the concentration of phagocytes, IL-17A and IFN-γ in the inflammatory pattern of the bronchi of asthma patients depending on the airway reaction to a cold stimulus.

Materials and methods. 129 patients with asthma were examined. The design of the study included questioning patients using a validated questionnaire Asthma Control Test (ACT, Quality Metric Inc., 2002), collection of induced and spontaneously produced sputum, exhaled breath condensate (EBC), bronchoprovocation test with a 3-minute isocapnic hyperventilation with cold (-20ºС) air (IHCA) with an assessment of the airway response (ΔFEV₁) by spirometry.

Results. Group 1 (n=55) included individuals with ΔFEV₁ -10% and below, group 2 (n=74) – with ΔFEV₁ above -10%: -15 (-21; -11) and -3.7 (-6.1; -0.38)%, respectively (p=0.0002). According to the level of ACT (17 [13; 21.5] and 19 [14; 22] points) and indicators of lung function (FEV1 [93.0±2.4 and 97.1±2.4%] and FEF25-75 [63.5±3.5 and 72.0±3.7%]), the patients had no significant intergroup differences. The pattern of bronchial inflammation in group 1 was mixed (neutrophils ≥40%), in group 2 – eosinophilic. In response to the IHCA test, the number of neutrophils significantly increased in the sputum of patients in group 1, the number of macrophages and the number of structurally intact epithelial cells decreased, in proportion to this, the level of IFN-γ and IFN-γ-inducible protein IP-10 (CXCL10) increased in the EBC in relation to patients of the 2nd group. A direct relationship was found between baseline concentrations of IP-10 and IFN-γ (Rs=0.7; p<0.01) in EBC.

Conclusion. The airway response to a cold stimulus of patients with asthma is accompanied by functional activation of phagocytic cells with an escalation of neutrophilic inflammation and a decrease in the number of macrophages infiltrating the bronchi associated with an increase in the concentration of IFN-γ, which stimulates the processes of respiratory burst and triggers cell destruction and cytolysis.

Introduction. The search for new highly effective methods for the treatment and control of bronchial asthma is an urgent task in pathophysiology and pharmacology. A promising substance for the regulation of systemic chronic inflammation is N-acylethanolamine (EPEA) of eicosapentaenoic acid, which exhibits immunoregulatory properties.

Aim. To study the dose-dependent effect of eicosapentaenoic acid ethanolamine on the synthesis and metabolism of oxylipins by blood cells in patients with asthma under in vitro conditions.

Materials and methods. The object of the study was the whole blood of 5 patients with controlled mild-to-moderate asthma and 6 healthy people. The in vitro experiment was carried out in lipopolysaccharide-stimulated blood after incubation for 30 minutes. Then the experimental substance N-acyl-ethanolamine of eicosapentaenoic acid (NAE 20:5) was added at concentrations of 1.0, 5.0 and 10.0 µM and incubated at 37ºC for 6 hours in gentle mixing mode. The level of oxylipins was studied by enzyme immunoassay.

Results. Experimental exposure to N-acylethanolamines of eicosapentenoic acid had the following effects. Under the influence of ethanolamine of eicosapentaenoic acid at a concentration of 1 µM, the level of PGE2 decreased by 51% (p<0.001) and the amount of 15-HEPE increased by 32% (p<0.05) in lipopolysaccharide-induced blood plasma relative to the values before exposure to ethanolamine. Also EPEA at this dosage showed a tendency to increase the level of 18HEPE. Exposure to EPEA at 5µM resulted in a significant decrease in LTB4 levels by 34% (p<0.001), PGE2 levels by 51% (p<0.001), as well as an increase in 12-HEPE levels by 33% (p<0.01), 15-HEPE by 36% (p<0.05) and 18-HEPE by 87% (p<0.01). Under the influence of EPEA at a dosage of 10 µM, a statistically significant effect on the entire spectrum of the studied oxylipins was revealed. Thus, the use of this dose of ethanolamide in LPS-induced blood showed a decrease in the concentration of LTB4 by 37% (p<0.001), LXA4 by 22% (p<0.05), PGE2 by 50% (p<0.001) and an increase in 5HEPE concentration by 25% (p<0.05), 12-HEPE by 76% (p<0.001), 15-HEPE by 75% (p<0.001), 18-HEPE by 155% (p<0.001) relative to pre-EPEA values.

Conclusion. Further study of NAE fatty acids opens up new perspectives in the study of targeted methods for correcting the inflammatory response in bronchial asthma.

Introduction. Mitochondria provide energy homeostasis of the cell by maintaining an optimal transmembrane electrochemical gradient (ΔΨm), which does not allow excessive formation of reactive oxygen species (ROS). However, under conditions of pathology, the normal functioning of mitochondria is disrupted, which can lead to ATP deficiency and/or increased production of ROS.

Aim. The aim of this study was to investigate the ΔΨm parameters and their relationship with the expression of TRP channels in peripheral blood leukocytes of patients with chronic obstructive pulmonary disease (COPD).

Materials and methods. The study included 23 patients with COPD of varying severity, 8 smokers without signs of bronchial obstruction and 9 healthy volunteers who had never smoked. All subjects underwent spirometry to assess the lung function. ΔΨm was determined by staining the cells with tetramethylrhodamine ethyl ester (TMRE) and measuring the fluorescent signal by flow cytometry, under basal conditions and pro-inflammatory stimulation with phorbol-12-myristate-13-acetate (PMA).

Results. We found that COPD patients were characterized by a significant increase in basal ΔΨm of monocytes (161.8 [153.8; 206.8] vs. 129.3 [75.5; 161.8], p=0.03) and lymphocytes (209,7 [184.7; 257.8] vs. 122.5 [67.9; 164.3], p=0.003) as compared with the control group. Stimulation of cells with PMA led to multidirectional changes in ΔΨm, while its increased level was still preserved in COPD. In monocytes of COPD patients, a decrease in ΔΨm in response to PMA stimulation was prevalent (75%), while in the majority (53.9%) of individuals in the control group ΔΨm, on the contrary, increased (p=0.08). In addition, among COPD patients, an increase in ΔΨm in monocytes was accompanied by an enhanced expression of TRPV4, while in the control group, among individuals with positive dynamics of ΔΨm, TRPV4 expression was, on the contrary, reduced.

Conclusion. The increased level of ΔΨm in the mononuclears of COPD patients is consistent with previously detected enhanced ROS production, but does not support the assumption about energy deficit in the cells. The revealed differences in the relationship between TRPV4 expression and ΔΨm dynamics may indicate the presence of pathological features in TRP signaling in COPD patients.

Introduction. It is known that the course of chronic obstructive pulmonary disease (COPD) may vary depending on the rate of bronchial obstruction progression. It has been shown that TRPV1 channels play an important role in the formation of some pathological syndromes typical for COPD.

Aim. To study the effect of single nucleotide polymorphisms (SNPs) of TRPV1 gene on the rate of bronchial obstruction progression in COPD patients.

Materials and methods. We examined 103 patients with COPD, including 47 with rapid progression of bronchial obstruction (decrease in FEV1≥50 ml/year). SNPs rs460716, rs222749, rs222747, and rs8065080 were genotyped by LATE-PCR.

Results. We established that rs460716 SNP had a significant effect on the development of progressive bronchial obstruction in COPD. The CC+TT genotypes were more common among patients with progressive disease (48.9% versus 23.2%), while the heterozygous genotype was protective (p=0.006). Differences remained significant after adjusting for sex, age, pack-year index and baseline FEV₁ (OR 3.2; 95%CI [1.32; 7.57], p=0.009).

Conclusion. The obtained results indicate a negative influence of the homozygous genotypes carriage for TRPV1 rs460716 SNP on the course of COPD. 

Aim. Assessment of the functional state of the diaphragm in patients with COPD who underwent COVID-19.

Materials and methods. The study included 35 patients with COPD complicated by compensated chronic cor pulmonale (CCP): group 1 included 15 patients with COPD who had COVID-19, group 2 included 20 patients with COPD. Patients were examined 3 months after suffering COVID-19. The functional state of the diaphragm was studied using the VIVID S70N ultrasound diagnostic system.

Results. The greatest decrease in the diaphragm dome height was detected in the 1st group (p=0.001). The excursion of the diaphragm during quiet breathing was increased in both groups, in the 2nd group the indicator was 11% more than in the 1st group. The diaphragm excursion during forced breathing was reduced in the 1st group (p=0.02). The rate of diaphragm excursion during inhalation and exhalation during quiet and forced breathing in both groups was significantly increased compared to the control group. However, in the 1st group, the rate of diaphragm excursion on expiration was 49% higher. These changes may indicate respiratory muscle fatigue in COPD patients who have had COVID-19. The thickness of the muscular part of the diaphragm during inhalation and exhalation during quiet breathing in both groups compared to the control group was significantly higher. These indicators in both groups did not significantly differ from each other. There was a decrease in the thickening fraction of the muscular part of the diaphragm during calm (p=0.01) and forced breathing (p=0.001) in both groups, which indicates the onset of fatigue of the muscles of the diaphragm in the 2nd group and the initial development of weakness of the diaphragm in the 1st group who had the greatest decrease in this indicator during forced breathing.

Conclusion. Ultrasonic diagnostic methods significantly expand the possibilities for assessing the functional state of the diaphragm. Patients with COPD who have undergone COVID-19 are characterized by a significant increase in the thickness of the diaphragm, limitation of its mobility, and a slowdown in the rate of relaxation of the muscular part of the diaphragm.

Introduction. COVID-19 infection alters the body’s immune tolerance, which can affect the course of systemic diseases caused by alterations in immune function. Patients with sarcoidosis, just like patients with systemic diseases, have impaired immune system function. They receive immunosuppressive therapy, so they are at risk of infectious diseases, including the viral ones.

Aim. To investigate the course of sarcoidosis in the period 2020-2022, the incidence of COVID-19 infection in patients treated by the pulmonologist of the sarcoidosis-polyclinic office of the Krasnoyarsk Regional Clinical Hospital and to evaluate the incidence of sarcoidosis after COVID-19.

Materials and methods. 301 outpatient charts of patients diagnosed with sarcoidosis were analyzed. Anamnestic data, information on vaccination against COVID-19, results of physical examination, multispiral computed tomography of thoracic organs in dynamics, data and methods of morphological verification, the volume of the received therapy for sarcoidosis were assessed.

Results. There was evidence that the combination of active sarcoidosis and COVID-19 did not contribute to a severe course of viral infection and progression in the course of granulomatosis. In patients with baseline moderate or severe pulmonary function impairment due to sarcoidosis and long-term use of systemic glucocorticosteroids, no increase in the incidence of adverse COVID-19 outcomes was noted. When analyzing fatal cases, it became known that in the first case, chronic recurrent sarcoidosis and prolonged use of systemic glucocorticosteroids were the factors determining the adverse prognosis in COVID- 19 In the second case, the combination of sarcoidosis with cardiovascular disease, diabetes mellitus, and obesity were adverse outcome factors. New cases of sarcoidosis after COVID-19 have been reported, this may be explained by the interaction between SARS-CoV-2 and human immune system, imbalance of proand anti-inflammatory cytokines, disruption of interferon production. However, this statement requires further research.

Introduction. Chryseobacterium indologenes bacteria are rarely detected, poorly studied opportunistic bacteria of the nonfermenting gram-negative bacilli group that are characterized by high intrinsic and acquired multidrug resistance and involvement in healthcare associated infections.

Aim. To analyze detection rate of C. indologenes strains from various biomaterials obtained from patients with pneumonia, as well as levels of pathogen drug resistance to antimicrobial drugs.

Materials and methods. The research included 1740 clinical samples obtained from patients with pneumonia hospitalized in in-patient facilities of the Khabarovsk city during the COVID-19 pandemic. Clinical samples included 1305 respiratory samples (744 sputum samples and 561 nasopharyngeal swabs), 435 samples of autopsy material (lung tissue) obtained from patients with a fatal outcome of the disease. The study was performed via classical bacteriological method. Pathogens were identified with Vitek 2 bacteriological analyzer and Vitek MS mass spectrometer. Sensitivity to antimicrobial drugs was determined by disk-diffusion method and in a bacteriological analyzer.

Results. A comparative analysis of detection of the entire nonfermenting gram-negative bacteria (NFGNB) group and C. indologenes from various clinical samples was carried out. Detection rate of NFGNB equaled 17.3%. NFGNB were isolated from autopsy material most often ‒ in 31.7% of cases, less often ‒ from sputum and nasopharyngeal smears (13.8% and 10.7%, respectively). C. indologenes was detected in 0.5% of the cases (8 isolates out of 1740 samples). Isolation of this pathogen was most frequent in nasopharyngeal smears – in 1.1% (6 cases out of 561 samples), least frequent ‒ from sputum, which totaled 0.3% (2 isolates from 744 samples). The detection rate of the pathogen in respiratory samples equaled 0.6% (8 isolates out of 1305 samples). This pathogen was not found in the autopsy material. Carbapenem-resistant variants of C. indologenes were isolated in 75% (6 cases out of 8) of the cases.

Conclusion. Further intensifying of diagnostic methods will result in more frequent detection of these unusual pathogens, clinical significance of which needs more justification.

Introduction. The constant increase in the prevalence of bronchial asthma in children and adolescents raises concerns about a parallel increase in obesity-related asthma and suggests that obesity alters asthma towards a phenotype that is more difficult to control. The development of multifactorial diseases (asthma and obesity) is based on complex intergenic interactions that must be taken into account when predicting the risk of developing an unfavorable course of the pathological process.

Aim. To study the contribution of polymorphic variants of the metabolism genes rs1042713 (Arg16Gly) and rs1042714 (Gln27Glu) of the β₂-adrenoceptor gene (ADRB2), rs4994 Trp64Arg of the β₃-adrenoceptor gene (ADRB3), rs1801282 of the PPARG gene, rs1799883 Ala54Thr of the FABP2 gene using Multifactor Dimensionality Reduction (MDR) in patients with asthma and obesity to identify significant intergenic interactions.

Materials and methods. 161 children withasthma were examined, including 59 patients with obesity of 1-3 degrees. The examination included general clinical, laboratory, and functional methods. The level of asthma control was determined according to the GINA criteria (2018). The study of gene polymorphisms was carried out by real-time polymerase chain reaction using sets of “Metabolism” (Research and Production Company “Litekh”, Moscow) on the CFX-96 Biorat device (USA).

Results. When comparing groups of children with asthma associated with obesity, a significant model of the interaction of the ADRB3 and FABP2 genes was determined. This two-locus model of intergenic interaction. According to this model, children with bronchial asthma with the following genotypes have an increased risk of obesity: Trp64Arg ADRΒ3 and Ala54Thr FABP2; Trp64Arg ADRΒ3 and Thr 54Thr FABP2; Trp64 Trp ADRΒ3 and Ala54Thr FABP2; Trp64 Trp ADRΒ3 and Thr 54Thr FABP2. In patients with AD associated with obesity and lack of disease control, we identified another statistically significant two-locus model of the interaction of the rs1042713 genes of the ADRB2 gene and PPARG. According to this model, children with the following genotypes have an increased risk of lack of disease control in patients with obesity-associated asthma: Arg16Gly ADRB2 and Pro12Ala PPARG; Arg16Gly ADRB2 and Ala12Ala PPARG; Gly16Gly ADRB2 and Pro12Ala PPARG; Gly16Gly ADRB2 and Ala12Ala PPARG.

Conclusion. The obtained results of the analysis of intergenic interactions indicate that a key role in the formation of predisposition to obesity in asthma patients belongs to the association of polymorphic variants of the ADRB3 (rs4994) and FABP2 (rs1799883) genes, and the risk of uncontrolled asthma in obese children are patients with a combination of polymorphisms rs1042713 of the ADRB2 gene and rs1801282 of the PPARG gene, as evidenced by revealed two-locus models of intergenic interactions that determine the predisposition to obesity in children with asthma and affect the course of the disease. Identification of genetic predictors of both asthma and obesity is important for identifying individuals with an increased risk of developing this disease, and requires further study in the search for probable cause-and-effect relationships and the creation of personalized programs depending on polymorphic gene variants.

Introduction. Currently, there is a separate phenotype “bronchial asthma – obesity”, manifested by a more severe course of the disease, low rates of achieving asthma control, resistance to basic therapy. Asthma, like obesity, is recognized as a classic example of multifactorial diseases, which are based on a rather complex gene network. The active search for genetic markers characterizing individual characteristics of human metabolism continues. Of particular interest are the genes involved in the regulation of fat and carbohydrate metabolism.

Aim. Analysis of associations of polymorphic loci Ala54Thr (G163A) of the FABP2 gene with bronchial asthma of varying severity and control of asthma in children.

Materials and methods. 161 children with bronchial asthma in remission were examined by a continuous sampling method, of which 59 patients with obesity of 1-3 degrees without concomitant endocrine pathology. The examination included general clinical, functional, and instrumental methods. The level of asthma control was determined according to the GINA criteria (2018). The biochemical study was carried out on an automatic analyzer SAPPHIRE 400 (Japan). The study of gene polymorphisms was carried out by real-time polymerase chain reaction using sets of “Metabolism” (Research and Production Company “Litekh”, Moscow) on the CFX-96 Biorat device (USA).

Results. We have not identified associations of the presence of polymorphic loci of the FABP2 gene with obesity. It was determined that in children with bronchial asthma, the frequency of carrying the homozygous genotype Thr/Thr and the minor allele Thr increased by 1.5 times compared to the control group (OR 9.043; 95%CI [2,093–39,073], p=0.0011 and OR 2.946; 95%CI [1,698‒5,111], p=0.001, respectively), and in children with bronchial asthma with and without asthma control, the carriage of the homozygous Thr/Thr genotype and the rare A allele increased the risk of uncontrolled bronchial asthma (OR 2.42; 95%CI [1.23‒4.79], p=0.03 and OR 1.75; 95%CI [1,119‒2,736], p=0.01), the frequency of the homozygous Ala/Ala genotype and the frequent Ala allele was detected 1.5 times more often in children with bronchial asthma associated with obesity (OR 2.176; 95%CI [1.001‒4.727], p=0.0008 and OR 2.378; 95%CI [1.495‒3.780], p=0.0002, respectively).

Conclusion. Although we have not identified associations of the presence of polymorphic loci of the FABP2 gene with obesity, it has been shown that children with Ala54Thr+Thr54Тhr genotypes have significantly higher glucose levels (4.9±0.06 mmol/L compared with carriers of the Ala54Ala genotype 4.0±0.06 mmol/L, p<0.001), cholesterol (4.8±0.4 mmol/L compared with carriers of the Ala54Ala genotype 3.93±0.1 mmol/L, p<0.05) and low density lipoproteins (2.55±0.09 mmol/L compared with carriers of the Ala54Ala genotype 2.26±0.1 mmol/L, p<0.05). There is an obvious need for further investigation of the effect of gene polymorphism on the indicators of carbohydrate and lipid metabolism, depending on the nature of diets. These issues require further study as part of the search for probable cause-and-effect relationships and the creation of personalized programs depending on polymorphic gene variants.

Introduction. Pneumofibrosis (PF) is a morphological outcome of acute and chronic lung diseases, the progression of which leads to organ deficiency.

Aim. Development of a prognostic algorithm for assessing the risk of progression of post-inflammatory PF in children with chronic nonspecific lung diseases (CNSLD).

Materials and methods. The examination of 52 children with CNSLD with focal post-inflammatory PF was conducted, of which 26 children with progressive PF and 26 children with non-progressive PF. The children were selected according to the “case-control” scheme. The patients had a dynamic clinical and laboratory examination with multispiral computed tomography of the lungs. Determination of the “zero” genotypes of the detoxification genes GSTM1, GSTT1 was carried out by means of polymerase chain reaction. The odds ratio indicator was used to assess the relative risk.

Results. Based on the analysis of medico-social, clinical characteristics and genetic polymorphism, an individual prognostic algorithm for the risk of progression of post-inflammatory PF in children with CNSLD was developed. The algorithm includes the calculation of the total score (TS) of 7 medical and social indicators (living in an urban area; the presence of passive smoking; the duration of a pulmonological history of 4-9 years; the presence of congenital lung malformation; the number of acute respiratory infections (ARI) 4 or more times/year; the duration of ARI 11 days or more; taking antibiotics for more than 3 once/year) and the presence of deletions in the detoxification genes GSTM1 and GSTT1. With a value of TS 6.97 or more, a high risk of progression of PF is predicted, with TS 3.47-6.96 points, a moderate risk of progression of PF is diagnosed, with TS 3.46 or less points, a minimal risk of progression of PF.

Conclusion. The proposed algorithm allows predicting the risk of progression of post-inflammatory PF in children with CNSLD at the stage of early diagnosis and will prevent the spread of the process in the lungs with the help of preventive measures and preventive therapy, which will increase the duration and improve the quality of life of the patient.

Aim. Analysis of the structure of bronchopulmonary dysplasia (BPD) in children of the Amur region at the stage of medical care in outpatient and inpatient conditions of the Research Institute of MCP for the period from 20102021.

Materials and methods. The study used a retrospective analysis of outpatient records and medical histories of 146 patients with BPD aged from 1 month to 13 years.

Results. Among children with BPD, boys accounted for 56.6%, girls 44.3%. Preterm infants accounted for 84.9%, full-term babies – 15.1%. The classic form of the disease was diagnosed in 56% of children, the new form – in 44%. Since 2013, there has been a decrease in the frequency of occurrence of the classical form (in 2011 – 100%, in 2021 – 0%). The opposite pattern is typical for the new form (in 2010 – 14.3%, in 2021 − 100%). Since 2018, there has been a tendency for the new form to prevail over the classical form. Concomitant pathology of the respiratory system was diagnosed in 40.2% of patients (5.03% of them were malformations, stridor – 33.3%, their combination – 1.9%), and pathology of the cardiovascular system in 3.8% of cases.

Conclusion. The assessment and dynamics of the structure of BPD disease in the Amur region at the present stage is presented. We report the predominance of a new form of BPD over the classical one. The study noted the frequency of concomitant pathology on the part of the respiratory and circulatory systems in children with BPD. The identified features will be used to search for risk factors for the development and prognosis of this pathology.

Aim. To study the etiology of placental insufficiency in women in the second trimester of gestation during the influenza A(H3N2) epidemic and the A(H1N1)pdm pandemic.

Materials and methods. In 1865 patients in the second trimester of pregnancy, uncomplicated and complicated by exacerbation of chronic ENT pathology leading to the development of placental insufficiency, using laboratory methods in the blood, nasal epithelium and biological fluids, pathogens of monoand mixed infections (influenza A(H1N1)pdm), A(H3N2), influenza B, parainfluenza type 1-3, adenovirus, respiratory syncytial virus (RS), cytomegalovirus (CMV), herpes simplex virus type 1 and type 2 (HSV-1,2 type), candida infection (Candida albicans), chlamydia (Chlamydia trachomatis), mycoplasmosis (Mycoplasma hominis) and ureaplasmosis (Ureaplasma urealyticum) were detected. The first group consisted of 873 women with placental insufficiency diagnosed during the influenza A(H3N2) epidemic, the second group consisted of 890 patients with placental insufficiency diagnosed during circulation of the influenza A(H1N1)pdm in the population. The control group were 42 women without ENT diseases and placental insufficiency caused by monoand mixed viral infections during influenza A(H3N2) and 60 women with similar somatic, infectious and obstetric status, examined during pandemic influenza A(H1N1)pdm.

Results. With the development of placental insufficiency in women of the second group, compared with the first one, mono-influenza B and parainfluenza types 1-3 are diagnosed less frequently, as well as a combination of influenza A(H1N1) pdm and influenza B; influenza A(H1N1)pdm and parainfluenza types 1-3; influenza A(H1N1)pdm and RS virus; CMV and Chlamydia trachomatis; Mycoplasma hominis and Ureaplasma urealyticum; HSV-1,2 type, Candida albicans and Chlamydia trachomatis; as well as HSV-1,2 type, Candida albicans and Ureaplasma urealyticum. At the same time, exacerbations of mono-CMV, mono-HSV-1,2 type and Candida albicans are more common, as well as combinations of CMV+HSV-1,2 type; CMV+Candida albicans; CMV+Ureaplasma urealyticum; and CMV+Mycoplasma hominis; CMV+HSV-1,2 type+Candida albicans.

Conclusion. In the etiology of placental insufficiency in acute diseases of the ENT organs in women in the second trimester of gestation against the background of circulation of the A(H1N1)pdm influenza in the population, compared with placental dysfunction in pregnant women with a similar ENT pathology during the influenza A(H3N2) epidemic, there is an increase in the proportion of monocytomegalovirus, herpesvirus and candida infections, as well as mixed cytomegalovirus infection, the reactivation of which may be due to more pronounced virusinduced immunosuppression and hormonal status disorders, leading to local dysbiosis.

Aim. To study changes in the cytokine status in women with exacerbation of bronchial asthma caused by reactivation of cytomegalovirus infection (CMVI) in the second trimester of gestation.

Materials and methods. The concentration of pro-inflammatory cytokines (TNFα, IL-1β, IFNγ, IL-2) in blood serum was assessed in 112 women in the second trimester of pregnancy, uncomplicated and complicated by exacerbation of asthma caused by reactivation of CMVI. The first group included 30 women seronegative for CMVI with uncomplicated pregnancy. The second group consisted of 30 patients with exacerbation of mild asthma associated with CMVI, initiating the formation of chronic compensated placental insufficiency. The third group consisted of 27 patients with exacerbation of moderate asthma induced by CMVI reactivation leading to the development of chronic compensated placental insufficiency. The fourth group included 25 women with exacerbation of moderate asthma due to the acute phase of CMVI, which induces the development of chronic subcompensated placental insufficiency.

Results. It was found that in the blood serum of women of the first group, the concentration of TNFα was (Me) 21.5 (13.8–30.1) pg/mL, IL-1β – 18.2 (13.6–34.0) pg/mL, IFNγ – 137.4 (109.5‒174.2) pg/mL and IL-2 – 29.8 (21.0‒38.9) pg/mL. In patients of the second group, compared with the first one, there was an increase in the level of TNFα by 3.79 times (p=0.000001), IL-1β – by 4.8 times (p=0.000001), IFNγ – by 1.73 times (p=0.000001) and IL-2 by 2.91 times (p=0.000001). In the third group, unlike the second one, no significant differences were found between the concentrations of TNFα, IL-1β, IFNγ, and IL-2. In patients of the fourth group, in comparison with the third group, higher values of TNFα (1.35 times, p=0.00507), IL-1β (1.86 times, p=0.000001), IFNγ (1.31 times, p=0.000167), and IL-2 (1.5 times, p=0.0056) were registered.

Conclusion. During exacerbation of moderate asthma of cytomegalovirus etiology, leading to chronic subcompensated placental insufficiency, in comparison with exacerbation of moderate asthma caused by reactivation of CMVI, initiating the formation of chronic compensated placental insufficiency, activation of the systemic inflammatory response is most pronounced, leading to stimulation of the migration of monocytes, lymphocytes and neutrophils to the focus of inflammation at the level of small bronchi; also leading to disruption of intersystem relationships and to hemodynamic dysfunction of the placenta.

Aim. To evaluate changes in immunity in the second trimester of pregnancy in women with exacerbation of bronchial asthma associated with reactivation of cytomegalovirus infection (CMVI).

Materials and methods. The concentration of secretory immunoglobulin A (sIgA), immunoglobulin A (IgA), immunoglobulin G (IgG), immunoglobulin M (IgM) and circulating immune complexes (CIC) was studied in 112 women at 21-24 weeks of uncomplicated pregnancy and pregnancy complicated by exacerbation of mild-to-moderate asthma associated with CMVI. The first group included 30 women seronegative for CMV, with an uncomplicated pregnancy. The second group consisted of 30 patients with exacerbation of mild asthma, initiated by the acute phase of CMVI, which induces the development of chronic compensated placental insufficiency. The third group consisted of 27 patients with moderate asthma in the acute stage against the background of the acute phase of CMVI, leading to the formation of chronic compensated placental insufficiency. The fourth group included 25 patients with exacerbation of moderate asthma with CMV etiology, initiating the development of chronic subcompensated placental insufficiency.

Results. In women of the second group, the concentration of sIgA was 5.91±0.371 mg/L, IgA – 2.64±0.089 mg/mL, IgG – 15.4±0.791 mg/mL, IgM – 2.32±0.144 mg/mL, CIC – 0.176±0.004 optical density units (in the first group, respectively, 4.31±0.266 mg/L, p<0.001; 2.37±0.06 mg/mL, p<0.05; 13.3±0.293 mg/mL, p<0,05; 1.11±0.06 mg/mL, p<0.001; 0.092±0.005 optical density units, p<0.001). In patients of the third group, in contrast to the second one, no differences in immunity parameters were detected. In the fourth group, in comparison with the third one, lower parameters of sIgA (3.21±0.213 mg/L, p<0.001), IgA (1.43±0.081 mg/mL, p<0.001), as well as higher IgG values were detected (19.8±0.418 mg/mL, p<0.001), IgM (2.94±0.082 mg/mL, p<0.01) and CIC (0.198±0.005 optical density units, p<0.05).

Conclusion. In patients with moderate asthma with exacerbation against the background of CMVI reactivation, which initiates the formation of chronic subcompensated placental insufficiency, in contrast to women with moderate asthma in the stage of CMVI exacerbation in the second trimester of pregnancy, leading to chronic compensated placental insufficiency in the third trimester of gestation, a more pronounced imbalance of humoral immunity and autoimmune disorders are found, which are important in the development of chronic placental dysfunction.

Aim. To evaluate changes in blood flow in the uterine and umbilical arteries in the second trimester of gestation in women with exacerbation of bronchial asthma associated with reactivation of cytomegalovirus infection (CMVI).

Materials and methods. Using Doppler analysis, 115 patients were examined at 21-24 weeks of pregnancy, uncomplicated and complicated by exacerbation of mild to moderate asthma of cytomegalovirus etiology. The first group was represented by 30 seronegative women with uncomplicated pregnancy. The second group included 30 patients with mild asthma in the stage of exacerbation associated with CMVI, leading to chronic compensated placental insufficiency. The third group consisted of 30 patients with exacerbation of moderate asthma caused by CMVI reactivation, which initiated the development of chronic compensated placental insufficiency. The fourth group consisted of 25 women with moderate asthma in the acute stage against the background of the acute phase of CMVI, leading to the formation of chronic subcompensated placental insufficiency.

Results. In women in the second group, in comparison with the first group, the following changes were determined: in the right uterine artery, the systolic-diastolic ratio (SDR) was, respectively, 2.75±0.07 and 2.04±0.03 rel. units (р<0.001), pulsation index (PI) – 1.15±0.04 and 0.76±0.02 rel. units (p<0.001), resistance index (RI) – 0.63±0.01 and 0.51±0.01 rel. units (p<0.001); in the left uterine artery, SDR was, respectively, 2.84±0.09 and 1.98±0.05 rel. units (p<0.001), PI – 1.20±0.05 and 0.74±0.03 rel. units (p<0.001), RI – 0.64±0.01 and 0.49±0.01 rel. units (p<0.001); in the absence of statistically significant differences in the indicators of SDR in the umbilical artery – 3.62±0.09 and 3.41±0.06 rel. units, respectively (р>0.05), PI – 1.23±0.03 and 1.19±0.03 rel. units (p>0.05) and RI – 0.73±0.01 and 0.70±0.01 rel. units (p>0.05). In the third group, in comparison with the second one, vascular resistance did not differ significantly in the right, left uterine arteries and the umbilical cord artery. In patients of the fourth group, in contrast to the third one, higher values of resistance to blood flow were observed: in the right uterine artery – SDR (3.41±0.07 and 2.87±0.07 rel. units, p<0.001), PI (1.48±0.07 and 1.18±0.03 rel. units, p<0.001), RI (0.70±0.01 and 0.65±0.01 relative units, p<0.001); in the left uterine artery – SDR (3.33±0.11 and 2.88±0.09 rel. units, p<0.01), PI (1.45±0.05 and 1.19±0.05 rel. units, p<0.001), RI (0.70±0.01 and 0.68±0.01 rel. units, p<0.01); and also in the umbilical artery – SDR (4.39±0.13 and 3.65±0.12 rel. units, p<0.001), PI (1.45±0.04 and 1.24±0.03 rel. units, p<0.001), RI (0.79±0.01 and 0.72±0.01 rel. units, p<0.001).

Conclusion. In the pathogenesis of reduced blood flow in the basin of the uterine and umbilical arteries in women with exacerbation of moderately severe asthma of cytomegalovirus etiology, leading to the development of chronic subcompensated placental insufficiency, compared with uterine cord hemodynamics in asthma in the acute stage, caused by reactivation of CMVI in the second trimester of gestation, which initiates the formation of a chronic compensated form of placental dysfunction in the third trimester of pregnancy, an important role is played by viral stimulation of vasoconstrictor responses.

Aim. To study the composition of phospholipids in erythrocyte membranes of newborns from mothers who had viral pneumonia caused by SARS-CoV-2 in the third trimester of pregnancy.

Materials and methods. The study included newborns who were born to mothers diagnosed with COVID-19 and community-acquired pneumonia of viral etiology in the third trimester (main group). Of the total number of newborns (n=67), groups of children were formed from mothers with moderate pneumonia (group 1, n=34), and with severe pneumonia (group 2, n=33). The control group consisted of 35 newborns from practically healthy mothers. The quantitative composition of phospholipids in the membranes of erythrocytes of venous blood of the umbilical cord of newborns was determined by the method of two-dimensional thin-layer chromatography according to Kirchner.

Results. The study found a statistically significant decrease in the concentration of phosphatidylethanolamine and phosphatidylcholine in erythrocyte membranes in group 1 by 19 and 20%, respectively (p<0.001), in group 2 – by 31 and 29%, respectively (p<0.001); a significant increase in the concentration of lysophosphatidylcholine, sphingomyelin, phosphatidylserine and phosphatidylinositol in group 1 by 43, 8, 15 and 26%, respectively (p<0.001), in group 2 – by 67, 14, 23 and 35%, respectively (p<0.001), compared with their concentration in newborns of the control group.

Conclusion. Infection of the mother with SARS-CoV-2 during pregnancy is accompanied by structural disintegration of the erythrocyte membranes of their newborns, manifested by a change in the phospholipid profile in favor of an increase in the fractions of sphingo-, lyso-, inositoland serine phospholipids, which, ultimately, can disrupt the work of the oxygen transport system of the blood, contributing to the development of hypoxia.

Aim. Demonstration of a clinical case of a patient with small cell neuroendocrine cancer of the tracheal bifurcation zone, with metastases to the bone marrow, liver, spleen.

Materials and methods. A brief review of the literature on the diagnosis of neuroendocrine tumors of the lungs and bronchi is presented, and a clinical observation of small cell neuroendocrine cancer of the tracheal bifurcation zone with metastases to the bone marrow, liver and spleen from the personal practice of the authors is presented.

Results. The clinical picture of this patient was dominated by “hematological” manifestations: severe thrombocytopenia and hemorrhagic syndrome, anemia, due to which differential diagnosis with a systemic blood disease was initially carried out. There was no pain syndrome in the bones characteristic of metastatic lesions. Histological examination of the bronchial tumor biopsy and bone marrow trephine biopsy with immunohistochemical examination (IHC) helped in making the diagnosis. In both cases, IHC revealed tumor cells with the same phenotype.

Conclusion. Metastasis of tumors to the bone marrow can proceed without characteristic ossalgia and manifest itself only in hematological syndromes (changes in blood tests). Cytological and histological examination of the bone marrow, with IHC, helps in the diagnosis.

Introduction. Glycosphingolipids are compounds composed of hydrophilic sugar structures and hydrophobic ceramides. These molecules form lipid rafts or microdomains in the cell membrane together with cholesterol, sphingomyelin, glycosylphosphatidylinositol and molecules, which determines their properties.

Aim. To systematize data on the structure of lipid rafts, their involvement in the functioning of immunocompetent cells and the development of the immune response, and the mechanisms of SARS-CoV-2 viral invasion.

Materials and methods. From these positions, literary sources for 1981-2023 are analyzed. Literature search was carried out in information systems: PubMed and Google Scholar.

Results. There are separate works that reflect the role of lipid rafts as mediators of signal transduction in the development of innate and adaptive immune responses. Other studies describe their importance in pathogen-host interaction and avoidance of immune control. Recently, studies have appeared on the effect of lipid microdomains of the cell membrane on viral invasion, including that caused by SARS-CoV-2.

Conclusion. This review makes a significant contribution to understanding the role of lipid rafts in the functioning of the immune system and viral invasion, which determines the prospects for further research and the possibility of their use as therapeutic targets in the development of immunomodulatory drugs.

Introduction. Respiratory rate is known to be one of the most important indicators reflecting the vital functions of a person. An increase in respiratory rate can be found in many diseases and pathological conditions, for example, in chronic obstructive pulmonary disease, pneumonia, bronchial asthma, myocardial infarction, heart failure, anaemia, etc. Due to the active introduction of telemedicine monitoring into clinical practice, the measurement of the abovementioned indicator is particularly relevant for the purpose of early detection and prevention of complications of chronic non-infectious diseases, as well as dynamic monitoring of the condition of patients in both inpatient and outpatient settings.

Aim. To search and update information about existing and promising developments for the control of respiratory rate based on different physical principles.

Materials and methods. For this review we used databases PubMed, Scopus, MedLine and eLIBRARY. The following keywords were used for the search: “respiratory rate”, “contact”, “measurement”, “sensor”.

Results. Contact methods for measuring respiratory rate include a wide range of sensors based on various physical principles. All types of sensors have their own application, but also they have some drawbacks. In order to achieve maximum accuracy of respiratory rate monitoring, it is necessary to carefully assess the conditions in which the patient is located, selecting the most appropriate technological solutions for them. Probably, complex systems, including several different sensors, are able to overcome many shortcomings. In addition, the development of information analysis methods, machine learning and artificial intelligence technologies can increase the sensitivity and accuracy of methods of measuring respiratory rate, reducing the frequency of bias associated with various artefacts.

Conclusion. Thus, technological development opens up wide opportunities for long-term monitoring of vital functions, prevention and timely response to adverse events.