Introduction. Chronic obstructive pulmonary disease (COPD) is a common condition of high social importance, in which the response of alveolar epithelium to cigarette smoke may play a critical role in disease pathogenesis.
Aim. To comprehensively characterize transcriptomic alterations in A549 cells in response to cigarette smoke extract (CSE), including differential gene expression and key signaling pathways, and to evaluate their potential contribution to pathological processes associated with COPD.
Materials and methods. A549 cells were cultured in DMEM until reaching 80% confluency, then incubated with 5% CSE or maintained under control conditions for 24 hours (n = 3 per group). Total RNA was extracted and enriched for mRNA. Sequencing was performed on the MGISEQ-200 platform in SE50 mode. Data analysis included read mapping (Salmon), differential gene expression analysis (DESeq2), and functional enrichment (Cytoscape).
Results. CSE exposure was associated with signs of actin cytoskeleton disorganization (Rho GTPase inhibition, ACTB downregulation) and endoplasmic reticulum stress, along with paradoxical activation of mTORC1 signaling amid suppression of transcription, proliferation, and apoptosis – a combination that may represent a state of metabolically active cellular stasis. Concomitantly, proteasomal degradation and antigen presentation of likely defective self-proteins were enhanced, possibly promoting immune surveillance. While proinflammatory signaling was generally attenuated, increased expression of IL1A, SPP1 and CSF3 may facilitate recruitment and activation of neutrophils, macrophages, and monocytes. Impaired efferocytosis (via upregulation of ANXA5) and defective apoptosis induction by cytotoxic T cells (due to disrupted granzyme endocytosis and inhibition of caspases) may lead to persistent inflammation with an autoimmune component.
Conclusion. Activation of mTORC1 signaling and autoantigen presentation under endoplasmic reticulum stress, as well as a potential reduction in the ability of cytotoxic T cells to induce apoptosis, may represent key pathogenic mechanisms of COPD, mediating alveolar epithelial injury induced by cigarette smoke.

Introduction. The pathogenesis of bronchial asthma largely depends on changes in the cells’ energy state, in which the mitochondrial membrane potential (MMP) plays a major role. A decrease in MMP is evident at the early stages of asthma development and may be one of the key pathological signs of the disease. The course and progression of asthma can be aggravated by various factors, including airborne particulate matter (PM). However, information on MMP changes in individual lymphocyte subpopulations under PM exposure is scarce.
Aim. To establish disturbances in the mitochondrial membrane potential of CD4+ cells in patients with mild asthma under the influence of ground-level atmospheric particulate matter.
Materials and methods. This in vitro study included 131 patients with asthma and 60 apparently healthy individuals. Model suspensions simulating the multicomponent pollution of Vladivostok air were used as a challenge. MMP levels (MMP-1 – MMP-5) were determined by flow cytometry, and the MMP coefficient (cMMP) was calculated.
Results. In asthma the main shifts occurred at MMP-1, MMP-2 and MMP-3 levels: the proportion of cells with high MMP decreased, whereas that of cells with moderately reduced MMP (MMP-2 and MMP-3) increased. PM exposure induced significant redistribution of MMP levels in asthma patients. Lower disease control was associated with more pronounced energy disturbances: in controlled versus partially controlled asthma, cMMP was 82.9% lower. Under PM exposure, cMMP fell by 27.2% and 16.3% in controlled and partially controlled asthma, respectively, compared with unexposed groups.
Conclusion. The study reveals features of CD4+-cell MMP impairment in mild bronchial asthma under atmospheric PM exposure, depending on disease-control level. Assessing MMP-level redistribution and the cMMP as an integral indicator of CD4+-cell energy status may facilitate early detection of energy-metabolism disorders in asthma and help optimise prevention of disease progression.

Introduction. Bitter taste receptors (TAS2Rs) can be expressed in airway epithelium and are of interest as therapeutic targets for asthma treatment. In a pilot study, we previously identified the most highly expressed TAS2Rs in the nasal epithelium of asthma patients and healthy individuals using NGS. Aim. To determine the relationship between TAS2Rs expression in the nasal epithelium and the disease control, inflammatory markers, airway patency and remodeling in patients with asthma. Materials and methods. The study included 173 patients with asthma (mean age: 46.0 ± 1.13 years; 60% females) of varying severity (56.4% – mild, 41.3% – moderate, 2.3% – severe asthma), predominantly with an uncontrolled disease course (71%). The patients underwent spirometric examination with obstruction reversibility testing and computed tomography (CT) based morphometric analysis of B1 and B10 segmental bronchi following bronchodilator administration. Serum concentrations of total IgE and cytokines (IL-2, IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, IFN-γ, TNF-α, IL-17A, IL-17F, and IL-22) were measured by ELISA and microparticle-based immunofluorescence assay (LEGENDplex), respectively. Expression of TAS2R4, TAS2R5, TAS2R14, TAS2R20, TAS2R31 and TAS2R38 genes was determined at mRNA level by quantitative reverse transcription PCR (qRT-PCR) in samples obtained from inferior turbinate brush biopsies. Results. Expression of all genes except TAS2R4 showed significant correlations. Decreased asthma control, as assessed by the ACT questionnaire, was associated with increased expression of TAS2R20 (β = -0.20, p = 0.03) and TAS2R38 (β = -0.20, p = 0.02) after adjustment for gender, age, body mass index, smoking index, FEV₁, and IgE level using multiple linear regression. No correlations were found between TAS2R gene expression and lung function parameters or bronchodilator response. Using PLS-SEM analysis, it was found that Th17-driven inflammation, primarily determined by IL-17A levels, is the main factor associated with both CT signs of bronchial remodeling (an inverse association with bronchial size (β = -0.57, p < 0.001) and a direct association with bronchial wall thickening (β = 0.34, p = 0.05)) as well as with increased TAS2R expression (most significantly with TAS2R5 (β = 0.40, p = 0.01) and TAS2R20 (β = 0.41, p = 0.01)). Bronchial remodeling itself was also associated with upregulation of TAS2Rs, particularly TAS2R5 (R² = 0.17, p = 0.002) and TAS2R20 (R² = 0.15, p = 0.006). However, a significant association with expression level was observed only for the latent variable reflecting bronchial size (β = -0.33, p < 0.001 for both TAS2R5 and TAS2R20). Conclusion. We found evidence of increased TAS2R genes expression with worsening asthma control, as well as in patients with more pronounced bronchial remodeling and elevated serum IL-17A. Given that TAS2R upregulation appears to be a secondary, compensatory response, TAS2R5 and TAS2R20 receptors emerge as the most promising targets for further investigation. 

Aim. To assess the functional status of the small airways by bodyplethysmography and to determine the degree of small-airway dysfunction (SAD) in patients with mild asthma.
Materials and methods. We examined 191 patients with mild asthma. The control group consisted of 36 healthy volunteers. Using bodyplethysmography, we evaluated functional residual capacity (FRC), residual volume (RV), total lung capacity (TLC) and the RV/TLC ratio. SAD was defined as RV > 140% predicted, RV/TLC > 125% predicted or FRC > 130% predicted. The severity of SAD was graded by percentage deviation from predicted values and z-scores.
Results. SAD was detected in 44 asthma patients. Cluster analysis based on RV, RV/TLC and FRC divided these patients into three clusters. Statistically significant differences between clusters were found for RV, RV/TLC and their z-scores. Cluster 1 was characterised by elevated RV and RV/TLC. In Cluster 2, compared with Cluster 1, high RV and RV/TLC were accompanied by an FRC increase in 50% of cases. Cluster 3 showed high RV, RV/TLC and FRC, along with a TLC increase in 55% of cases. Spirometry demonstrated a progressive decline in airway patency, reflected by reduced FEV1 and maximum expiratory flow rates (MEF); worsening obstruction resulted in reduced VC in Clusters 2 and 3. SAD was consistently accompanied by elevated RV and RV/TLC, indicating marked air-trapping.
Conclusion. SAD occurred in 23% of patients with mild asthma and was accompanied by a pronounced decrease in indices characteristic of bronchial-obstructive syndrome, including distal airways. RV, RV/TLC and their z-scores constitute the primary criteria for grading SAD in this patient population.

Introduction. Enterovirus infection (EVI) is globally distributed and manifests in a wide range of clinical forms. Herpangina is one of the most frequently recorded specific manifestations of EVI.
Aim. To evaluate the contribution of herpangina to the overall clinical spectrum of EVI in the Far Eastern Federal District (FEFD) and to identify the enterovirus types responsible for the disease.
Materials and methods. Morbidity data for herpangina were obtained from statistical reports of Rospotrebnadzor offices in the FEFD. Enterovirus typing was performed by sequencing a fragment of the VP1 capsid-protein gene. Phylogenetic analysis was conducted using partial nucleotide sequences of Coxsackievirus A2 (CV-A2).
Results. Analysis of EVI clinical forms in the FEFD from 2015 to 2024 revealed that herpangina was one of the leading manifestations, with an average proportion of 33.4%. Among 398 patients with herpangina, 92.5% were children under six years of age. Twenty-four enterovirus types were detected, predominantly CV-A10 (25.1%), CV-A6 (24.6%), CV-A5 (12.6%) and CV-A2 (7.5%). Dominant types varied by year: CV-A6 in 2015–2016, 2019 and 2023; CVA10 in 2017 and 2024; CV-A16 in 2018; CV-A5 in 2021. In several cases the virus was found in respiratory samples collected on days 5–12 of illness, indicating possible prolonged persistence of enteroviruses in the nasopharynx and contributing to the high transmissibility of herpangina. Phylogenetic analysis demonstrated genetic diversity within the CV-A2 population and concurrent circulation of lineages C and E in the FEFD during the same period.
Conclusion. Herpangina constitutes a significant proportion of all recorded EVI forms in the FEFD. In most cases the causative agents are enteroviruses of species Enterovirus alphacoxsackie. Strengthened preventive measures are essential to limit transmission and prevent outbreaks.

Introduction. Recurrent respiratory infections in children can present with a wide range of clinical manifestations and may lead to long-term consequences that require further investigation. Aim. To determine the clinical and functional characteristics of the post-infectious reactivity of the airways in children. Materials and methods. The study involved 103 children (38 girls and 65 boys) who had suffered from an acute respiratory infection. The average age of the children was 12.2 ± 0.34 years; height 144.3 ± 1.88 cm, weight 38.0 ± 1.63 kg. A comprehensive diagnostic assessment was conducted, including a questionnaire based on the expanded Asthma Predictive Index (API), collection of biological material from the oropharynx and nasopharynx to detect respiratory RNA and DNA viruses, and collection of peripheral blood to determine specific antibodies of classes M and G to atypical pathogens using enzyme-linked immunosorbent assay (ELISA). The following tests were performed: spirometry (FVC (forced vital capacity), FEV₁ (forced expiratory volume in the first second), FEV₁/FVC ratio, PEFR (peak expiratory flow rate), MEF₅₀ (maximum expiratory flow at the moment of exhaling the first 50% of FVC), MEF₇₅ (maximum expiratory flow at the moment of exhaling the first 75% of FVC), and MEF_25-75 (mean expiratory flow between 25% and 75% of FVC)) with an inhalation bronchodilator test using a short-acting β₂-agonist (salbutamol), as well as a bronchial provocation test with ultrasonic inhalation of distilled water (IDW). Results. The first group included 53 children with altered airway reactivity to the IDW test (ΔFEV_{1 IDW} -5.6 [-13.0; 6.5] %), while the second group consisted of 38 children who did not react to the IDW test (ΔFEV_{1 IDW} -2.9 [-6.0; 1.6] %). Children in the first group had lower spirometric parameters compared to the second group: FEV₁/FVC was 96.0 [92.0; 102.0] and 101.0 [94.0; 104.0] % (p=0.042); and MEF_25-75 was 68.0 [52.0; 88.0] and 80.0 [64.0; 95.0] % (p = 0.029), respectively. When analyzing respiratory pathogens, the first group showed a higher frequency of specific antibodies to M. pneumoniae at 42% compared to 18% in the second group (χ²=4.423; p<0.05). Additionally, in the first group, 28% of cases showed combined (mixed) infection with 2-4 pathogens simultaneously, compared to 8% in the second group (χ²=4.594; p<0.05). Correlation analysis indicated that a high level of IgM antibodies to M. pneumoniae corresponded to a more pronounced response of the small airways to bronchoprovocation with IDW (ΔMEF_{25-75 IDW}) (ρ = -0.63; p=0.01). Conclusion. The study confirms the significant impact of respiratory infections on airway reactivity in children, manifested by decreased spirometric parameters, an increased frequency of pathogen-specific antibodies, and their association with bronchial response to osmotic stimuli. The results of our study highlight the importance of early diagnosis of post-infectious airway reactivity in children.

Introduction. Coronavirus infection is accompanied by various neurological complications in which oxidative stress and inflammation play a role.
Aim. To clarify the relationship between previous coronavirus infection and the levels of oxidative-stress products and pro-inflammatory interleukins in patients with nervous-system diseases.
Materials and methods. The study involved 158 patients with nervous-system diseases; 47 had a history of COVID-19. The comparison group consisted of 26 participants without clinical signs of acute or chronic disease, matched for age and sex. The concentrations of oxidative-stress products in blood were determined using UV spectroscopy and colorimetric methods.
Results. Oxidative-stress products were elevated in patients with nervous-system diseases compared with healthy individuals, but no significant differences were found between patients with and without prior coronavirus infection. Only in the subgroup with central nervous-system diseases, post COVID-19 patients had diene conjugate levels 44% higher (p = 0.019) and conjugated diene and ketodiene levels 56% higher (p = 0.050) than patients without COVID-19. Lipid-oxidation products differed among subgroups with acute cerebrovascular accidents, central, and peripheral nervous-system diseases. In patients with acute cerebrovascular accidents and no history of COVID-19, levels of diene conjugates were 81% higher (p = 0.032), conjugated dienes and ketodienes 72% higher (p = 0.042), and lipid hydroperoxides 45% higher (p = 0.016) than in central nervous-system disease. Among post COVID patients, lipid-hydroperoxide levels in the acute cerebrovascular subgroup (80.0 ± 9.37 nmol mL⁻¹) were 37% (p = 0.03) and 32% (p = 0.03) higher than in the central and peripheral nervous-system subgroups (59.9 ± 7.07 and 62.2 ± 3.60 nmol mL⁻¹, respectively). Strong correlations between blood levels of pro-inflammatory interleukins and oxidatively modified lipids in post-COVID patients were most significant for IL-6 and IL-10.
Conclusion. Moderate oxidative-stress manifestations in patients with nervous-system diseases are largely attributable to the underlying disorders rather than to prior coronavirus infection. In the post COVID period, these patients retain an association between oxidative stress and inflammation.

Aim. To study the effect of dry carbon dioxide baths (DCB) and magnetotherapy (MT) on quality-oflife indicators, dyspnoea severity, psychological status and systemic inflammation in patients who had recovered from novel coronavirus infection (NCI).
Materials and methods. Patients with a history of NCI were divided into two groups. Group 1 (n = 20) received a course of DCB; Group 2 (n = 20) received a course of MT. A control group (n = 20) comprised relatively healthy individuals with no history of NCI (absence of anti-SARS-CoV-2 S-protein IgG at enrolment), matched by sex and age with the study groups. At baseline — all participants — and after treatment — patients in Groups 1 and 2 — completed questionnaires assessing quality of life, anxiety level and severity of respiratory symptoms (SF-36, HADS, mMRC, Borg scale). Blood plasma was collected to determine C-reactive protein (CRP) by ELISA (Cloud Clone Corp., Wuhan, Hubei, China).
Results. Post-COVID patients had lower quality-of-life scores and higher levels of anxiety, depression, dyspnoea and exercise intolerance than controls. Both DCB and MT improved quality-of-life scores and reduced anxiety, depression, dyspnoea and exercise-induced symptom burden in post-COVID patients compared with the control group. According to SF-36, mean total quality of life increased by 9.3% in Group 1 and by 4.55% in Group 2. On the HADS scale, anxiety fell by 16.3% and depression by 19.0% in Group 1; by 8.6% and 14.3%, respectively, in Group 2. In Group 1 the mMRC dyspnoea score decreased by 55%, and the Borg score by 50%; in Group 2 by 35% and 22.5%, respectively. DCB also significantly lowered CRP (p < 0.001) from 1.12 [0.42; 1.81] mg/mL before treatment to 0.91 [0.26; 1.57] mg/mL afterwards.
Conclusion. Dry carbon dioxide baths and magnetotherapy appear to be promising approaches for mitigating manifestations of post COVID syndrome, but their efficacy should be confirmed in larger studies.

Evidence indicates that COVID-19 adversely affects the course of pregnancy; however, the mechanisms underlying the associated placental insufficiency and anaemia remain inadequately explored.
Aim. To assess the prognostic value of serum interleukin-6 (IL-6), hypoxia-inducible factor-1α (HIF-1α) and ferritin for the development of placental insufficiency in pregnant women with moderate COVID-19 and anaemia.
Materials and methods. Seventy-eight pregnant women were followed prospectively at predefined control points. Baseline (12–14 weeks’ gestation): all participants had experienced moderate COVID-19 (community-acquired pneumonia). Second control point (19–20 weeks): women were allocated to two groups according to the presence of anaemia: group 1 –COVID-19 with mild anaemia (n = 54); group 2 – COVID-19 without anaemia (n = 24). Third control point (30–32 weeks): group 1 was subdivided into subgroup 1A – placental insufficiency present (n = 34) and subgroup 1B –placental insufficiency absent (n = 20). COVID-19 was confirmed by SARS-CoV-2 RNA detection in oropharyngeal and nasopharyngeal swabs using polymerase chain reaction and, where indicated, by radiological criteria of viral lung injury. Serum IL-6 (pg/mL), HIF-1α (ng/mL) and ferritin (μg/L) were measured by solid-phase enzyme-linked immunosorbent assay with Vector-Best (Russia) and BCM Diagnostics (Austria) kits. Red-blood indices (haemoglobin, erythrocyte count) were obtained on a Medonic M haematology analyser (Switzerland).
Results. Women with COVID-19 and anaemia exhibited significantly higher IL-6 (p < 0.001), HIF-1α (p < 0.001) and ferritin (p < 0.001) concentrations than those without anaemia. Placental insufficiency was diagnosed in 63 % of the affected group. Strong positive correlations were found between placental insufficiency and HIF-1α (r = 0.76; p < 0.05), IL-6 (r = 0.82; p < 0.05) and ferritin (r = 0.72; p < 0.05). A prognostic index of placental insufficiency (PIPI) was derived: PIPI = –12.84 + 2.486 × HIF-1α – 0.921 × IL-6 + 0.380 × ferritin, where variables represent serum concentrations. The threshold value was 1.204: PIPI ≥ 1.204 indicated a high risk of placental insufficiency, whereas PIPI < 1.204 indicated no risk. Absolute PIPI values were directly proportional to risk magnitude.
Conclusion. Elevated serum IL-6, HIF-1α and ferritin are informative predictors of placental insufficiency in pregnant women with moderate COVID-19 and anaemia.

Introduction. An exacerbation of mild asthma caused by reactivation of chronic cytomegalovirus (CMV) infection during pregnancy is frequently accompanied by cerebral and cardiac pathology in the offspring. Because perinatal brain injury adversely affects myocardial electrical stability, it is important to assess cardiac function in newborns with different severities of cerebral ischaemia whose mothers underwent a mild asthma exacerbation in the acute phase of chronic CMV infection during the second trimester.
Aim. To evaluate the cardiovascular system in newborns with cerebral ischaemia born to mothers who experienced a mild asthma exacerbation associated with chronic CMV reactivation during pregnancy.
Materials and methods. Apgar scores and electrocardiographic parameters were analysed in 41 newborns of mothers with uncomplicated pregnancies (control group) and in 61 newborns with cerebral ischaemia and an antenatal history complicated by a mild asthma exacerbation triggered by CMV reactivation in the mother during the second trimester (main group). The main group was divided into a first subgroup of 36 infants with grade I cerebral ischaemia and a second subgroup of 25 infants with grade II cerebral ischaemia.
Results. Compared with controls, infants in the first subgroup had lower Apgar scores at 1 min and 5 min (both p < 0.001) and lower birth weight (p < 0.01). They more often presented with skin pallor (χ2 = 6.95; p < 0.01), perioral cyanosis (χ2 = 6.77; p < 0.01), acrocyanosis (χ2 = 5.12; p < 0.05), muffled heart sounds (χ2 = 4.04; p < 0.05), systolic murmur (χ2 = 5.48; p < 0.05), tachycardia (χ2 = 7.60; p < 0.01), incomplete right bundle-branch block (χ2 = 9.50; p < 0.01), moderate (χ2 = 13.3; p < 0.001) and marked metabolic disturbances in the myocardium (χ2 = 5.99; p < 0.05). Compared with both the control group and the first subgroup, infants in the second subgroup had even lower Apgar scores at 1 min and 5 min (both p < 0.001) and lower birth weight (p < 0.01 and p < 0.001, respectively). Relative to the first subgroup, they more frequently exhibited skin pallor (χ2 = 4.31; p < 0.05), dyspnoea (χ2 = 4.21; p < 0.05), muffled heart sounds (χ2 = 5.07; p < 0.05), hepatomegaly (χ2 = 5.50; p < 0.05), bradycardia (χ2 = 4.21; p < 0.05), sinus arrhythmia (χ2 = 4.60; p < 0.05), marked metabolic myocardial disturbances (χ2 = 5.07; p < 0.05) and increased right-atrial load (χ2 = 10.9; p < 0.001).
Conclusion. In newborns whose mothers experienced a mild asthma exacerbation associated with chronic CMV reactivation during the second trimester, grade II cerebral ischaemia is accompanied by more frequent clinical and electrocardiographic abnormalities than grade I. These findings suggest that antenatal hypoxia adversely affects peripheral circulation, contributing to cardiovascular maladaptation in the early neonatal period.

Introduction. Providing the necessary assistance to palliative patients and their relatives is one of the urgent tasks of Russian healthcare, given the size of this group — the number of terminally ill patients potentially in need of palliative care was at least 1.7 million people in the Russian Federation in 2023. Malignancies — 60–80 % of which involve the respiratory system — account for most palliative-care cases. The shortage of staff in palliative-care services can be partly mitigated by involving volunteers. At the same time, the institution of palliative care itself is still in the process of formation, and it is important to record the motives of volunteers to improve the quality of care provided and manage this process.
Aim. To analyse the social portrait of palliative-care volunteers in the Sverdlovsk Region.
Materials and methods. During 2024, a survey of 107 students of the Sverdlovsk Regional Medical College was conducted.
Results. The overwhelming majority of those involved in volunteering were female students majoring in Nursing and General Medicine. According to respondents, volunteering ensures the development of communication skills, the ability to communicate and understand interlocutors, critical perception of professional mistakes, and also improves academic performance in practical training. The greatest influence on involvement in volunteer activities is provided by the opportunity to gain new experience, professional knowledge, skills and abilities, and an understanding of the benefits that volunteers bring to a sick person. The following contradictions in the perception of palliative volunteering are identified: a discrepancy between the development of communication skills and professional abilities of volunteers and the absence of significant personal changes in their lives; a contradiction between volunteers’ awareness of their usefulness and the acquisition of new experience, on the one hand, and a weak extrapolation of this experience to increased self-esteem and the ability to solve personal emotional problems, on the other; a discrepancy between gender stereotypes in society (care as a “women’s” job) and the need to attract volunteers of both sexes for palliative care.
Conclusion. The social portrait of a student volunteer in palliative care reflects a combination of professional orientation and value-emotional motives. Despite the difficulties, participation in volunteer activities contributes to the formation of competencies valued in medical practice and strengthens the social responsibility of young people. Systematic support from educational institutions, medical and public organizations is critical for the development of this practice. The data obtained provide an idea of the contradictions and prospects for the development of this group of volunteers in the context of developing relevant educational programs.

Introduction. Primary ciliary dyskinesia (PCD) is a rare hereditary disease from the group of ciliopathies, characterized by involvement of all parts of the respiratory tract with the development of a chronic inflammatory process and bronchiectasis.
Aim. To describe the observation of a patient with PCD in order to familiarize physicians with the clinical features of the disease and current diagnostic capabilities.
Materials and methods. A clinical case of PCD detected in a child followed at the Khabarovsk Branch of the Far Eastern Scientific Center of Physiology and Pathology of Respiration — Research Institute for the Protection of Motherhood and Childhood — is presented.
Results. Based on anamnestic (pulmonological history since six months of age, repeated protracted bronchitis, pneumonias), clinical (frequent rhinitis, otitis, wet cough), and instrumental (spiral computed tomography, bronchoscopy) data, PCD was suspected in the child. High-speed video microscopy revealed a marked decrease in ciliated epithelium function due to a reduction in the percentage of cells with motile cilia, decreased ciliary beat frequency, and an altered beat pattern. Whole-genome testing detected a compound heterozygote in the DNAH9 gene associated with the disease: primary ciliary dyskinesia, type 40. The patient was diagnosed with: congenital malformation of the bronchi: primary ciliary dyskinesia Q32.4.
Conclusion. The difficulties and possibilities of diagnosing PCD are demonstrated, facilitating the prescription of adequate systemic therapy — a key condition for an optimistic prognosis in children with this nosology.

This review summarises current data on the role of ectopic bitter-taste receptors (TAS2R) in the pathogenesis of asthma within a personalised-therapy framework. TAS2R expressed in airway epithelium, airway smoothmuscle cells and immunocompetent cells participate in key inflammatory pathways and regulate bronchial tone. Receptor activation induces airway smooth-muscle relaxation through signalling cascades that are independent of β2-adrenergic receptors and cAMP, maintaining efficacy when β2-agonist sensitivity is reduced. In the T2-high endotype, TAS2R suppress IL-4, IL-5 and IL-13, thereby attenuating eosinophilic inflammation and mast-cell degranulation. In non-T2 asthma, TAS2R inhibit pro-inflammatory mediators (IL-17, IL-8/CXCL8, TNF-α) and curb neutrophil and macrophage activity. Consequently, TAS2R are viewed as promising pharmacological targets, particularly for difficult-to-control asthma resistant to inhaled glucocorticosteroids. The literature already cites compounds with TAS2R-agonist activity, and the search for novel endogenous agonists is ongoing. The evidence underscores the need for further studies to clarify TAS2R molecular mechanisms, evaluate TAS2R-oriented therapy across asthma endotypes, and assess the clinical efficacy and safety of agents designed to personalise treatment based on the genetic and functional characteristics of these receptors.

High prevalence of herpes-virus infection among women of reproductive age and the possibility of latent persistence with subsequent reactivation highlight the importance of studying the morphological changes in the placenta that arise when infected with herpes simplex viruses (HSV) types 1 and 2. This article provides a morphological characterisation of placental alterations in herpesvirus infection and their association with the development of perinatal pathology in the fetus. Microscopic features that allow suspicion of herpetic placental involvement are described: chronic villitis, intervillositis, vasculitis, focal villous necrosis, trophoblast destruction, damage to Kachchenko–Hofbauer cells, and formation of giant multinucleated cells with viral inclusions (Cowdry type B HSV cells). Differences between HSV-1 and HSV-2 are analysed with respect to the severity of inflammatory-destructive and vascular changes, as well as the clinical consequences of intra-uterine infection. A greater neurotropism and propensity for generalised infection of HSV-2 compared with HSV-1 is noted. The review was prepared using publications indexed in international and Russian scientific databases, including PubMed, eLibrary and Google Scholar. Search terms included: herpetic placentitis, intervillositis, funiculitis, placental pathomorphology, fetoplacental insufficiency, association with perinatal pathology and their combinations in Russian and English.

Acinetobacter baumannii is one of the most frequently detected infectious agents worldwide, the important features of which are a high mutation rate, leading to the rapid development of antibiotic resistance, and resistance to disinfection. This review presents information on the significance of this pathogen in infectious pathology, the mechanisms underlying diseases associated with A. baumannii, virulence factors, multiple drug resistance of the pathogen, its resistance to aggressive environmental factors, the methods used by the pathogen to colonize and infect the human body, risk factors for infection, and clinical forms of the diseases it causes. The choice of drugs for the treatment of infections caused by A. baumannii is discussed. A search and analysis of scientific publications was carried out using electronic library search systems – eLIBRARY.ru, PubMed, Google Scholar, CyberLeninka