Background. Mortality associated with community-acquired pneumonia (CAP) continues to be a crucial health problem worldwide. Correct assessment of CAP severity and the level of care is pivotal in the disease outcome.

Aim. To evaluate the prognostic value of the CURB-65 and CRB-65 scores and their modifications in determining the risk of in-hospital mortality in patients with CAP.

Materials and methods. The retrospective study included 1,412 patients with CAP aged over 18 years. In a population of 1,020 patients, which was subsequently split into test (n = 676) and training (n = 344) samples in the ratio 2 : 1, we compared the predictive value of the CURB-65 (confusion, urea > 7 mmol / l, respiratory rate ≥ 30 / min, low blood pressure (BP), and age ≥ 65 years) and CRB-65 (confusion, respiratory rate ≥ 30 / min, low blood pressure (BP), and age ≥ 65 years) scores in identifying patients at high risk of in-hospital death. The specified scoring systems were modified by changing the cut-offs for each criterion to increase their accuracy. For comparison, we used the ROC analysis with the calculation of the area under the curve (AUC).

Results. The modified CURB-65 score with new cut-off values (age > 72 years, respiratory rate > 21 / min, urea level > 9.5 mmol / l, systolic blood pressure ≤ 105 mm Hg, and diastolic blood pressure ≤ 65 mm Hg) was more accurate than the original one in predicting death and was named CURB-72. The AUC for CURB-72 and CURB-65 was 0.946 (95% confidence interval (CI): 0.916–0.967) and 0.905 (95% CI: 0.869–0.934), respectively (p = 0.0034). The modified CRB-65 (CRB-72) score also outperformed the original model, but showed no statistically significant difference. While comparing the modified scoring systems, the new CURB-72 score surpassed the CRB-72 score and demonstrated maximum accuracy in identifying CAP patients at risk of in-hospital mortality (p = 0.0347).

Conclusion. The modified CURB-65 (CURB-72) and CRB-65 (CRB-72) scores demonstrated potential for assessing the prognosis of CAP and are superior to classical scoring systems. CURB-72 showed the highest sensitivity and specificity.

Aim. To conduct a comprehensive analysis of EEG recordings of schizophrenia patients receiving atypical antipsychotics as monotherapy.

Materials and methods. We examined 94 patients with schizophrenia aged 33 [28; 40] years with a disease duration of 10 [4; 15] years. The patients were divided into 5 groups depending on the antipsychotic drugs they took: 1) risperidone – 31 patients; 2) quetiapine – 20 patients; 3) aripiprazole – 11 patients; 4) olanzapine – 13 patients; 5) clozapine – 19 patients. EEG was recorded during wakefulness with closed eyes (background test), 3-minute hyperventilation, and rhythmic photostimulation in all patients. To describe and interpret the received recordings, the EEG classification according to J. Micoulaud – Franchi et al. was used.

Results. EEG modifications (score > 1A) were observed in 61.7% (n = 58) of patients. In the group of patients receiving risperidone, EEG modifications were found in 48.4% of cases, in patients taking quetiapine – in 70% of cases, aripiprazole – in 63.6% of cases, olanzapine – in 61.5% of cases, clozapine – in 73.7% of cases. The frequency of epileptiform patterns in patients receiving olanzapine was significantly higher than in those taking risperidone (p = 0.033) and clozapine (p = 0.032). Slowing in the EEG (score > 1) was more often observed in patients taking clozapine – 63.2% (n = 12), olanzapine – 61.5% (n = 8), and quetiapine – 60% (n = 12). Slower EEG waves were less common in patients receiving aripiprazole – 45.5% (n = 5) and risperidone – 45.2% (n = 14). In the group of patients with EEG slowing (score > 1), the dose of chlorpromazine equivalent was significantly greater compared to patients with normal EEG (p = 0.00046).

Conclusion. The data obtained demonstrate changes in EEG parameters during monotherapy with atypical antipsychotics and indicate their dose-dependent effect on the bioelectrical activity of the brain.

Aim. To conduct a comparative assessment of the content of kisspeptin (KISS1) metastasis suppressor in the blood serum of apparently healthy individuals and patients with lung cancer (LC) and to analyze the associations between the KISS1 level and clinical and pathological characteristics of the disease.

Materials and methods. The study included 74 LC patients and 46 apparently healthy individuals. Stage I LC was diagnosed in 8 patients, stage II LC – in 7 patients, stage III LC – in 28 patients, and stage IV LC – in 31 patients. According to the histologic pattern, 32 tumors were characterized as adenocarcinoma, 29 – as squamous-cell carcinoma, 11 – as small-cell LC (SCLC), and 2 – as large-cell lung carcinoma. The pre-treatment KISS1 level in the blood serum was determined using the enzyme-linked immunosorbent assay kit (KISS1, CloudClone Corp., USA).

Results. The median serum KISS1 level in LC patients was 213 (range 7.8–716) pg / ml and was significantly higher than in the control group – 83.4 (0–180) pg / ml (p < 0.0001). The ROC analysis of the diagnostic value of serum KISS1 level demonstrated that the sensitivity of the test in relation to the healthy controls was 70% at a cutoff value of 152 pg / ml, and the specificity was 85% (AUC – 0.817; р < 0.0001). In stage I–II LC, the sensitivity did not exceed 50%. The level of KISS1 in the blood serum did not depend on the histologic type of the tumor. No significant differences in the serum KISS1 levels were observed both between non-small cell lung cancer (NSCLC) on the whole and neuroendocrine SCLC and between the main histologic types of NSCLC. The level of KISS1 increased with the disease stage (p < 0.05). However, none of the TNM staging system indices significantly influenced the level of the marker. No differences were found between serum KISS1 levels in patients with central or peripheral localization of the tumor.

Conclusion. The KISS1 level was elevated in LC patients compared to healthy controls and was a stage-dependent marker. It has high diagnostic specificity but insufficient sensitivity, especially at early stages of the disease. Based on the results of this study and literature data on the role of KISS1in NSCLC, we conclude that clinical implications of KISS1 in this disease require further research.

Aim. To study the features of transcriptional regulation of the activity and isoenzyme composition of lactate dehydrogenase in the kidneys of Rattus norvegicus L. in diabetic nephropathy.

Materials and methods. The study included 20 male laboratory rats (Rattus norvegicus L.) divided into two equal groups: “Norm” – intact rats injected with 0.9% NaCl intraperitoneally and “Diabetes” – animals with alloxaninduced diabetes (DM1 model). The activity, subcellular localization, and mobility of lactate dehydrogenase (LDH, EC 1.1.1.27) isoenzymes were studied using spectrophotometry and electrophoresis. LDHA and LDHB gene transcripts were analyzed by the polymerase chain reaction.

Results. Analysis of the LDH activity showed that this parameter increased by more than 6 times in the animals with diabetic nephropathy compared to the control group. Moreover, the increase in the rate of the LDH activity was a consequence of the enzyme activation in all the studied compartments of the cell and is consistent with the parameter in the homogenate. The increase in the LDH activity in diabetic nephropathy may result from redistribution of the activity rate between the available isoforms and may be associated with an increase in the transcription rate of genes encoding subunits A and B of this enzyme.

Conclusion. The increase in the LDH activity is likely associated with the activation of renal gluconeogenesis, the main substrate for which is lactic acid reabsorbed in the renal glomeruli. The revealed increase in the LDH activity in the kidneys of rats with diabetic nephropathy may be associated with adaptation of their metabolism to the pathological state.

Aim. To evaluate changes in the transcriptome of head and neck squamous cell carcinoma (HNSCC) tissue cells in patients after proton therapy.

Materials and methods. Biopsy material obtained from 3 HNSCC patients before and after proton therapy at a total dose of 10 isoGy was homogenized, purified, and concentrated. Then total RNA was isolated with further purification and concentration with the RNA Clean & Concentrator kit (Zymo Research). Library quantitation was assessed using the Qubit 2.0 instrument (Invitrogen, Life Technologies). After isolation of 1 μg total RNA for sequencing, libraries were prepared on the Illumina platform using the TruSeq RNA Sample Prep Kit v2 with a 10-cycle enrichment step according to the manufacturer’s recommendations. The quality of RNA and the resulting libraries was checked using the Agilent 2100 Bioanalyzer system (Agilent Tec. Inc., USA). The RIN parameter for RNA was at least 7. The library concentration was assessed by real-time PCR on the CFX96 Touch Real-Time PCR Detection System (Bio-Rad, USA). Final libraries were pooled in equimolar ratios before sequencing on the Illumina HiSeq 2500 platform using 50 base-pair paired-end reads. The Q20 parameter for all samples was > 97%, and the number of reads averaged 60.2 million per sample. Raw reads were processed using the RTA 1.17.21.3 and Casava 1.8.2 (Illumina). The enrichment analysis was performed using the PANTHER 17.0 software.

Results. The transcriptome analysis of HNSCC after proton radiation therapy (5 x 2 isoGy) at a total dose of 10 isoGy revealed 1,414 significantly differentially expressed genes. The 10 most and least expressed genes and their associated signaling pathways were identified. A number of signaling pathways associated with the underexpressed genes were detected in HNSCC after proton therapy, such as: STAT5; PD-1 signaling pathway; marked MET-mediated activation of PTK2 signaling pathway, PDGF signaling; CD22-mediated regulation of BCR; and FCERI-mediated MAPK activation. In addition to the above signaling pathways, activation of collagen degradation, FCGR3A-mediated phagocytosis, and FCGR3A-mediated interleukin (IL)-10 synthesis are of interest. In the enrichment analysis among highly expressed genes, keratinization and biological oxidation processes were activated in HNSCC tissues after proton therapy.

Conclusion. Proton therapy in HNSCC leads to overexpression of genes involved in the regulation of keratinization and biological oxidation processes as well as to underexpression of genes associated with suppression of signaling pathways: STAT5, PD-1, MET-mediated activation of PTK2 signaling pathway, PDGF signaling; CD22-mediated regulation of BCR; FCERI-mediated MAPK activation, collagen degradation, FCGR3A-mediated phagocytosis activation, and FCGR3A-mediated IL-10 synthesis. All signaling pathways of underexpressed genes function in HNSCC cells if there is no negative influence on the tumor from outside (irradiation or delivery of antitumor drugs). The predominance of suppressed signaling pathways over activated ones most likely indicates a decrease in the functional potential of cells after proton therapy. The dose-dependence of PT effects necessitates further study of changes in cellular and molecular-genetic signatures of HNSCC after proton irradiation with different doses.

Aim. To study the effect of forced exercises on the content and parameters of oxidative phosphorylation in brown adipose tissue of mice with type II diabetes mellitus.

Materials and methods. To model the disease, we used a high-fat diet and physical exercises in the form of forced treadmill running for 4 weeks. The content of oxidative phosphorylation enzymes in brown adipose tissue was determined by Western blotting.

Results. Modeling diabetes in experimental animals was accompanied by expansion of adipose tissue. However, in brown adipose tissue, the content of all oxidative phosphorylation components decreases. Apparently, during type II diabetes mellitus modeling in mice, there is a decrease in the “energy efficiency” in brown adipose tissue, which is partially offset by an increase in its content in the body. Regular physical activity in mice with type II diabetes mellitus, in contrast to healthy animals, contributes to a decrease in the content of brown adipose tissue. At the same time, the content of most oxidative phosphorylation components in brown adipose tissue increases, in some casesб it even exceeds the baseline values. The latter is typical of a variable load mode – when the execution time of exercises periodically changes.

Conclusion. The obtained results suggest that metabolic rearrangements in brown adipose tissue may serve as some of the mechanisms of preventive and projective effects of physical activity in type 2 diabetes mellitus.

Background. Neutrophil extracellular traps (NETs) are net-like structures that have been investigated in inflammatory diseases. However, the presence of NETs in infected persons without clinical symptoms has not been yet studied.

Aim. To reveal NETs in healthy persons during and after the H1N1 influenza pandemic as well as to study the functional activity of NETs.

Materials and methods. The study included two groups of volunteers (n = 10 in each group) aged 20–25 years. The first group of volunteers was examined in the absence of acute diseases during one month before the study and in the absence of chronic diseases in the medical history. Volunteers of the second group were in contact with patients with influenza, but did not get sick. The comparative study also included patients with acute inflammation in the abdominal cavity (appendicitis, cholecystitis, abscess; 12 patients) and 9 patients with non-specific ulcerative colitis. Neutrophils were isolated from the blood by the traditional method of Ficoll density centrifugation. The number, morphology, and functional activity of NETs were determined (by capture of Klebsiella pneumoniae). SYBR Green I-based fluorescence microscopy was used to visualize and quantify NETs.

Results. In healthy volunteers who were not in contact with infected patients, spontaneous NETs formation did not occur. Neutrophils of persons who were in contact with infected patients spontaneously formed NETs. In this case the number of NETs reached 8.58 ± 0.51%, and the size of NETs amounted to 39.68 ± 3.52 µm. NETs effectively captured cells of the tested microorganism, which was accompanied by retraction of network fibers and transformation of the network structure into a cloud-like one, which retained 89.38 ± 5.86 microbial cells. For comparison, the NETs in patients with acute inflammation in the abdominal cavity captured and bound 20.2 ± 1 .67 microbial cells and with non-specific ulcerative colitis – 5.53 ± 0.34 cells.

Conclusion. High binding capacity of NETs is a factor contributing to effective defense of the body against the development of an infectious disease with manifested clinical symptoms.

Aim. To investigate the role of single nucleotide polymorphisms (SNPs) rs13041792, rs1801310, and rs6088660 in the GSS gene and environmental factors in the development of acute biliary pancreatitis (ABP) and its complications.

Materials and methods. The material for the study was blood samples obtained from 84 patients with ABP and 573 healthy individuals. Both groups were comparable in terms of gender and age. To diagnose ABP, we used the clinical guidelines recommended by the working group of the Russian Society of Surgeons. DNA was isolated by phenol / chloroform extraction. Multiplex genotyping of SNPs was performed by the iPLEX assay on the MALDITOF MassARRAY-4 genetic analyzer. Statistical data processing was performed using Statistica 10 and SNPStats software.

Results. We found that insufficient consumption of fresh vegetables and fruits increased the probability of ABP in carriers of genotypes G/A-A/A at rs1801310 in GSS (р = 0.02). The analysis revealed the association of the T allele at rs6088660 with the odds for developing acute pancreatitis (р = 0.007) and digestive fistulas (р = 0.02). A high probability of death was associated with rs1801310 (G/A genotype, р = 0.002) and rs6088660 (C/T genotype, р = 0.01) in the GSS gene.

Conclusion. SNPs rs6088660 and rs1801310 in the GSS gene can be used to predict the course of ABP.

Aim. To determine the role of 3D echocardiography parameters in the prognosis of long-term cardiovascular complications in patients with a first acute myocardial infarction (AMI).

Materials and methods. А prospective, single-center, observational study included 46 patients with a first AMI and successful PCI without a history of heart failure (HF) and shortness of breath upon admission. The examination of patients was performed in accordance with the Russian standards of medical care provision. Additionally, 3D echocardiography was performed, and N-terminal pro-brain natriuretic peptide (NT-proBNP) was determined. The main outcomes assessed were hospitalization with HF, sudden cardiac death, and combined endpoint. Median follow-up was 554 days (IQR 550–785).

Results. During the follow-up period, 9 hospitalizations with HF, 3 sudden cardiac deaths, and 12 combined endpoints were registered. The effect of 3D echocardiography parameters on the development of sudden cardiac death and combined endpoint has not been revealed. The effect of the studied parameters on the development of HF during the follow-up period that required hospitalization was evaluated. A statistically significant increase in the LV sphericity index was revealed in the group of patients with the registered outcome. We found significant direct correlations of left ventricular volume indices with prescription of diuretics in the post-discharge period; hospitalization with HF in the post-infarction period with the level of NT-pro-BNP, left atrial volume with the duration of index hospitalization, duration of eventless survival with ST elevation. We found a negative correlation of radial strain with prescription of diuretics in the post-discharge period. Predictors of hospitalization with HF in the post-infarction period were identified – parameters of radial strain, area strain, and circumferential strain, which were included in the model for calculating the risk of the outcome under study.

Conclusion. In patients with the first AMI in the absence of clinical signs of HF, to calculate the risk of hospitalization with HF within 550 days after MI, it is advisable to take into account the level of radial strain and use a prognostic model (1), including parameters of circumferential and area strain (according to 3D echocardiography data).

Aim. To study the parameters of the matrix metalloproteinase (MMP) / tissue inhibitors of metalloproteinase (TIMP) system in assessing the clinical course of pulmonary tuberculoma.

Materials and methods. We examined 87 patients (55 men and 32 women), average age 33 [28; 43] years, with a morphologically and bacteriologically confirmed diagnosis of tuberculoma, who received treatment at St. Petersburg Research Institute of Phthisiopulmonology. In all patients, computed tomography of the chest, fiberoptic bronchoscopy, and lung function tests were performed. In the blood serum, concentrations of MMP-1, -8, -9, and their tissue inhibitor TIMP-1 were determined using ELISA (R&D Systems, USA), and the activity of α2-macroglobulin (MG) was determined by the enzyme assays. For statistical data processing, Statistica 10.0 and R were used.

Results. In the study group, single and multiple tuberculomas were revealed in 37 and 63% of cases, respectively, necrotic areas – in 50% of patients, external respiration disorders – in 48% of cases, and catarrhal bronchitis (CB) – in 77% of cases. Tobacco smokers (TS) were identified in 69% of cases. Significant differences between MMP concentrations allowed us to distinguish four patterns from the characteristics adopted for the clinical and radiological assessment of disease intensity. It was shown that an increase in the levels of MMP-1 and MMP-9 can be a predictor of tuberculoma progression caused by a diffuse process with necrotic areas and bronchogenic dissemination (pattern 1, 2). Changes in the levels of MMP-8, TIMP-1 or MG (pattern 3, 4) were associated with permanent exposure to a non-specific component of inflammation (TS or CB).

Conclusion. Changes in the MMP / TIMP system parameters can be used as objective laboratory protein biomarkers to assess the clinical course of pulmonary tuberculoma.

Relevance. Objective comparison of biological markers and real clinical presentation is especially difficult in mental disorders, which are classified according to a large number of diagnostic criteria and a wide variety of symptoms. Therefore, the development of an effective system of biochemical markers and assessment of their relationship to optimize the diagnosis and treatment of schizophrenia are relevant.

The aim of the study was to develop a statistical model that combines known and tested biochemical markers for mental illnesses in patients with schizophrenia.

Materials and methods. The study included 47 women aged 18–50 years (median age – 22 years) with the diagnosis of schizophrenia (ICD-10, F20) and 25 healthy women of the same age. The model was based on the functional activity of complement, thrombodynamics parameters, markers of inflammation, glutamate and energy metabolism, and antioxidant defense, which were shown to be associated with the severity of schizophrenia. The listed markers were evaluated in plasma, platelets, and erythrocytes of sick and healthy individuals.

Results. Statistical software found pair correlations and features of the distribution of all markers as random variables in the examined groups and evaluated correlations between pairs of markers. Ten biomarkers were identified and united into a system that was adequately described by the logistic regression model. The model was evaluated using the Pearson’s test (χ2(11) = 57.6, p = 0.001) and calculation of correct predictions (91 and 80%) for samples of patients and healthy people, respectively.

Conclusion. Calculating the logistic equation resulted in the probability that the patient has schizophrenia involving the immune system, hemostasis, and oxidative stress. This model can be considered as a new formalized approach to the preclinical diagnosis of mental illnesses.

Aim. To study changes in the brachial – ankle pulse wave velocity (baPWV), ankle – brachial index (ABI), diastolic function, and global longitudinal strain of the left ventricle (LV) 3 and 12 months after COVID-19 pneumonia.

Materials and methods. The dynamics of vascular age and LV global longitudinal strain was studied in 154 patients 3 and 12 months after COVID-19 pneumonia (51 ± 12 years, 48% were women). The control group consisted of 55 sexand age-matched individuals.

Results. During the follow-up, the average baPWV decreased (13.2 [11.8; 15.1] cm / sec vs. 13.0 [11.8; 14.1] cm/ s; p < 0.001), and the frequency of its elevated values declined (45.4 vs. 35.1%; p = 0.008). The average ABI increased (1.09 [1.04; 1.14] vs. 1.11 [1.06; 1.17]; p = 0.012), but remained within the normal range. LV global longitudinal strain (LV GLS) (–19.6 ± 2.2 and –19.7 ± 2.5%; p = 0.854) and the frequency of reduced LV GLS (21.4 and 26.6%; p = 0.268) did not change significantly and did not differ from values in the control group. Global longitudinal strain in the LV basal inferoseptal segment improved (–19.2 ± 3.6% vs. –20.1 ± 4.0%; p = 0.032). The early diastolic mitral annular velocity decreased (8.4 ± 3.0 cm / s vs. 8.0 ± 2.5 cm / s; p = 0.023). The LV isovolumic relaxation time was greater than in the control group (101.8 ± 22.3 ms at the 1st visit vs. 92.9 ± 21.5 ms; p = 0.012; 105.9 ± 21.9 ms vs. 92.9 ± 21.5 ms at the 2nd visit; p < 0.001). A positive correlation was found between baPWV (r = 0.209; p = 0.009) and ABI (r = 0.190; p = 0.021) and strain parameters of the LV basal segments 12 months after discharge.

Conclusion. Patients with optimal visualization on echocardiography at 12 months after COVID-19 pneumonia, compared to the results of the examination 3 months after the disease, had deteriorated parameters of LV diastolic function. LV GLS was within the grey zone and did not change significantly. An improvement in arterial stiffness was noted, associated with an improvement in the strain of basal LV segments.

Every year, the number of people diagnosed with Alzheimer’s disease is rapidly increasing. Despite numerous studies, it was not possible to select a therapy that would reliably slow down the course of the disease and result in its complete cure. In this case, any consideration of the issue related to the search for drugs to eliminate cognitive and psychoemotional disorders in Alzheimer’s disease is a pressing problem that deserves special attention.

We collected articles from the PubMed database published over the past 10 years. The aim of this review was to analyze the latest experimental data and results regarding the relationship between Alzheimer’s disease and the activity of neuropeptides, such as oxytocin, vasopressin, and neuropeptide S, and describing the effects that occur upon their administration. This will allow for a more complete understanding of the problem and update information on this issue. The ability of neuropeptides to restore impaired cognitive functions in an animal model of Alzheimer’s disease is examined in more detail.

Detailed information on the relationship and positive effect of the studied neuropeptides on Alzheimer’s disease allows to consider these neuropeptides as potential drugs for the treatment of this disease.

Multiple sclerosis remains the most common demyelinating disease of the central nervous system and ranks first among neurological diseases that lead to disability in young people. The most important diagnostic and prognostic marker, especially at an early stage of the disease, is magnetic resonance imaging (MRI), which currently remains the only method that allows to explore the entire central nervous system in vivo.

The review presents literature data on modern achievements in MRI-based diagnosis of multiple sclerosis. Key attention is paid to such promising methods as assessment of brain and spinal cord atrophy, brain perfusion MRI, and diffusion tensor imaging. Implementation of these approaches in MRI can help solve the problem of early diagnosis of multiple sclerosis and determine more reliable markers of a response to ongoing therapy.

The processes of proliferation and differentiation of progenitor and stem cells in the body are ensured by a specific microenvironment, the stem cell niche. Universal components have been identified for all niches: supporting cells, extracellular matrix, and soluble biological factors. A niche is a dynamic system whose activity depends on regeneration needs.

The review presents data on the structure of the hepatic stem cell niche and one of its main components – stellate cells and their role in pathology.

Aim. To review modern methods of diagnosis and treatment of vulvovaginal atrophy (VVA), which is one of the manifestations of genitourinary syndrome of menopause in periand postmenopausal women.

Materials and methods. A review of domestic and foreign literature on the prevalence and modern methods of diagnosis and treatment of VVA was carried out.

Results. Unlike vasomotor symptoms, VVA progresses with age, causing a significant impairment in women’s quality of life. Symptoms usually begin to bother perimenopausal patients, but their frequency and severity increase significantly in postmenopausal women. Diagnosis of VVA can present some difficulties, as many women perceive their condition as a natural manifestation of aging and do not seek medical care. Currently, drug and non-drug therapies for VVA have been proposed, each of which has its own characteristics, indications, and contraindications. However, the safety and effectiveness of some of them have not been fully proven.

Conclusion. VVA is common in periand postmenopausal women. Modern aspects of the diagnosis and treatment of this pathology can significantly improve the quality of life of patients with VVA symptoms. However, further research is needed to confirm safety of the proposed treatment methods, and search for new techniques is required.

In the interests of practical healthcare, routine classifications should be modified as rarely as possible. At the same time changes should be discarded only on sufficient grounds, for example, when there are no obvious advantages of a new classification over the existing ones or they can no longer be modified by introducing fundamental changes and amendments. In this regard, the evolution of approaches to the classification of chronic heart failure (CHF) is prominent. It becomes particularly relevant due to the fact that currently experts of the Russian Society of Cardiology (RSC) are actively discussing a new draft classification of CHF. The authors of the lecture gave a brief historical insight and reviewed the main classifications of CHF used in North America, Europe, and Russia. The new classification of CHF proposed by RSC experts, which is actually a modified classification of North American colleagues, does not have obvious advantages over the currently used CHF classification in Russia (since 2002). The latter is based on the classification by Vasilenko – Strazhesko which is familiar to domestic internists, since it has become an indispensable part of their clinical practice and has stood the test of time. In addition, its underlying principles provide the potential for its flexible modification.

The aim of the present study was to summarize the data on the spectrum of genetic diseases and their phenotypic manifestations in case of structural and functional defects in 75 genes, pathogenic variants of which are associated with the formation of different types of cardiomyopathy (CMP). The search for scientific publications was carried out in foreign (PubMed) and Russian (eLibrary) digital libraries. The data analysis was performed using the Simple ClinVar, An Online Catalog of Human Genes and Genetic Disorders, and STRING databases.

It was shown that the vast majority of CMP genes are pleiotropic. Monogenic diseases caused by mutations in CMP genes are characterized by a wide range of pathological manifestations in various organs and systems (cardiovascular, nervous, endocrine, musculoskeletal systems, connective tissue, skin and appendages, organs of vision and hearing, kidneys) as well as by metabolic and immune disorders. Therefore, if a patient (regardless of the primary diagnosis) has pathogenic / likely pathogenic variants or variants of uncertain significance in the CMP genes, we recommend a detailed and comprehensive clinical examination. This is important for clarifying the effects of rare genetic variants, identifying significant clinical and prognostic features for CMP and monogenic diseases associated with CMP genes, and identifying risk groups and controllable triggers that contribute to the manifestation of pathogenic genetic variants.

Normal lung microbiota is a small number of transient microbes; however, respiratory pathology may be associated with persistent microbial colonization of the lungs. It remains a poorly understood and mysterious part of the pathogenesis of tuberculosis infection.

The review considers the general pathogenetic mechanisms of the effect of lung microbiota in respiratory pathology and presents the main methodological difficulties in the study of the lung microbiome. This review is aimed at analyzing the results of the available studies on diverse microbial composition of human lungs in tuberculosis using metagenomic sequencing methods. Despite high variability of the presented data, we can conclude that dysbiosis in tuberculosis is more often characterized by a decrease in bacterial diversity and enrichment of lung microbiota with anaerobic bacteria. Acinetobacter, Campylobacter, Moraxella, Pseudomonas, Staphylococcus, and Streptococcus, as well as some other microorganisms are indicated as important pathogenetic factors of dysbiosis in pulmonary tuberculosis, the role of which is yet to be elucidated.