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The article provides an assessment of the energy efficiency of the use of downhole compensators in the reactors as part of the installation of electric centrifugal pumps. A scheme for replacing the electrotechnical complex of an oil production facility has been developed. The energy efficiency curves have been constructed characterizing the positive effect of the introduction of downhole compensators for different cross sections and lengths of supply cables.

The urgent nessesity of the democratization of the economic goverment is detected and justified for the mineral enterprises on the basis of strategic integrative interaction of stake-holders to make consistent decisions, preventing unfriendly take-over and raiding of economics objects. The complex of contr-raiding procedures has been characterized on the basis of successful Russian and world, i.d. Canadian, experience.

Chronic rhinosinusitis (CRS) is a disease caused by inflammation of the paranasal sinuses and its mucous membrane lasting for more than 4 weeks continuously. The aim of our study was to examine the main pathophysiological features of chronic IgE-mediated rhinosinusitis of bacterial etiology according to publications in the Russian Federation and in the world. A search was made through English- and Russian-language literature sources using the following databases: PubMed, MedLine, Web of Science, Russian Science Citation Index, Springer, Scopus, Scientific Research, Google Scholar, Crossref, eLibrary. The epidemiological features of CRS in the Russian Federation, bacterial pathogens and pathophysiological characteristics of CRS were analyzed. A 2-fold increase in the prevalence of CRS was registered over the past 20 years. Prevalence of the disease increases at longer age ranges. Chronic rhinosinusitis ranks first among all chronic diseases in the field of otorhinolaryngology. Allergic rhinitis, asthma, bronchiectasia, immunodeficiencies, cystic fibrosis, primary ciliary dyskinesia and autoimmune diseases are associated with CRS. The most common bacterial pathogens are S. aureus, Staphylococcus epidermidis and Propionibacterium acnes, Prevotella, Streptococcus and Veillonella, and some Gram-negative bacteria, e.g., Pseudomonas aeruginosa (P. aeruginosa), Proteus mirabilis and Klebsiella pneumoniae. Staphylococcus aureus (S. aureus) is involved in pathogenesis of nasal polyps. The colonizing bacteria may contribute to pathogenesis of CRS through the formation of biofilms. Alterations in the sino-nasal microbiome may also contribute to the development of CRS. An association of the CRS and CFTR gene mutations plays a significant role in the pathogenesis of chronic rhinosinusitis. An “immune barrier hypothesis” has been proposed as potential mechanism of CRS. Reduced expression of SPINK5, impaired STAT3 signaling, and T2R38 bitter taste receptor polymorphism have been identified in the pathogenesis of CRS. The T2R38 gene stimulates epithelial cells to produce nitrous oxide with a bactericidal effect, promotes mucociliary elimination of pathogens and prevention of upper respiratory tract infections, the polymorphism of this gene predisposes patients to gram-negative infectious diseases, and therefore is a risk factor for the development of CRS. In addition, antibody deficiency is the most common primary immunodeficiency associated with CRS.Hence, the pathogenesis of chronic IgE-mediated rhinosinusitis of bacterial etiology is associated with defects in innate immunity and mucociliary clearance, influence of the sinonasal microbiome, allergies, and genetic factors. A comprehensive assessment of these factors is necessary for the development of new preventive and therapeutic options for the correction of CRS.

When the body is infected with the bacterium Helicobacter pylori, a cytokine cascade is launched, which plays a key role in the progression of chronic inflammatory and destructive processes in the gastric mucosa. Thus, the secretion of a number of cytokines is stimulated, which in turn contribute to the attraction of immunocompetent cells and the development of inflammatory changes. However, hyperproduction of cytokines can lead to atrophic changes in the gastric mucosa and, as a result, degeneration into gastric cancer. Thus, the role of cytokines in precancerous conditions is ambiguous. On the one hand, they activate the immune response aimed at eliminating the pathogen. On the other hand, they themselves contribute to the progression of the disease.The complex clinical and laboratory study included patients: 60 with chronic gastritis (CG), 55 with chronic atrophic gastritis (CAG), 50 with gastric cancer (GC, stage I-II, morphological variant – adenocarcinoma) and 60 – control group. The diagnoses were verified according to international and Russian recommendations and confirmed by laboratory and instrumental studies. All patients were comparable in terms of gender and age characteristics (p > 0.05). All patients had specific IgG to H. pylori. The study was approved by the Local Ethics Committee of the FRC KSC SB RAS (protocol No. 11 dated November 11, 2013). All ethical requirements were observed, and the patients signed the informed consent form for participation. Patients and persons of the control group underwent a single blood sampling from the cubital vein upon admission to vacutainers with heparin.The levels of IL-2, IL-4, IL-8, TNFα, interferon-γ in the blood serum of patients and healthy individuals were determined using the enzyme immunoassay method using reagent kits manufactured by JSC “VectorBest”. Statistical data processing was carried out using the Statistica for Windows 8.0 application package.All patients with H. pylori-associated diseases (CG, CAG, GC) showed an increase in pro-inflammatory (IL-2, IL-8, IFNγ) with a significant increase in IL-8 in all patients and IFNγ in gastric cancer and antiinflammatory cytokine (IL-4) with a maximum value in gastric cancer. A combined Th1 and Th2 is found – a mediated immune response with a maximum violation of cytokine regulation in gastric cancer.

Stomach cancer is in the top ten in terms of prevalence and ranks 4th in terms of causes of death worldwide. The most common and most aggressive variant of gastric cancer is adenocarcinoma. The monocytic link of immunity provides the main line of the body's fight against malignant cells, while in patients with adenocarcinoma it is insufficiently studied. The purpose of the study was to evaluate the functional activity of monocytes in patients with gastric adenocarcinoma at different stages of the disease.Individuals (n = 164) were examined, among whom 85 were diagnosed with stage I-IV stomach adenocarcinoma. The study also involved 79 apparently healthy donors. The functional activity and oxygen-dependent phagocytosis of monocytes were assessed by the chemiluminescent method. Luminol was used as a chemiluminescence inducer. The respiratory burst was activated with opsonized zymosan.In patients with stomach adenocarcinoma, at rest (spontaneous chemiluminescence), an increase in the time the curve reached the maximum intensity of chemiluminescence (Tmax = 7957 s), the area under the chemiluminescence curve (Squr = 0.2 x 106), the activation index (1.89 c. u.) and a decrease in the maximum value of chemiluminescence intensity (Imax = 424 c. u.) relative to the control group (Tmax = 5533 s, Squr = 0.011 x 106, activation index = 0.88 c. u., Imax = 424 c. u., p < 0.05) were seen. When chemiluminescence is induced in patients with stomach adenocarcinoma, a statistically significant predominance of Squr is fixed (0.46 x 106, in the control group Squr = 0.031 x 106). Also, in the group of patients with stomach adenocarcinoma, monocytic phagocytosis was reduced by more than 2 times (29% vs 84% in the control group, p < 0.05). When analyzing the studied parameters, depending on the stage of the disease, it was found that the violation of the chemiluminescent reaction in patients with stomach adenocarcinoma is fixed already at an early stage. At the same time, in patients with stage IV stomach adenocarcinoma, the indicators of spontaneous and induced chemiluminescence are more than 2 times different from those in the control group and patients at stage I of the disease. The identified features indicate a decrease in the effectiveness of immune reactions of the monocytic link in stomach adenocarcinoma already in the early stages of the disease and can be used to detect early signs of immune disorders and optimize therapeutic approaches in this disease.

Conflicting data on the role of the metabolic syndrome (MS) in the development of hepatocellular carcinoma (HCC) require studies on the influence of molecular factors that are important in the development of HCC in MS, which was the goal of our review. Publications (scientific articles and reviews) over the past 10 years were studied and analyzed using the databases Web of Science, Scopus, PubMed, RSCI. The terms used for the search were “metabolic syndrome and non-alcoholic fatty liver disease”, “metabolic syndrome and non-alcoholic steatohepatitis”, “metabolic syndrome and hepatocellular carcinoma”. The total number of publications studied in all databases exceeded 570 units, while the review presents the most significant results at the present stage. Insulin resistance and obesity, through the development of a systemic chronic inflammatory state, lead to increased inflammation and fibrosis in the liver, which are prodromal signs of hepatocarcinogenesis, increase the production of insulin-like growth factor-1 and disrupt the regulation of the insulin-like growth factor pathway. People with HCC have been shown to overexpress IGF-2. IGF-binding proteins, due to the reduced bioavailability of free IGF-1 and IGF-2 in the circulation, are able to inhibit the growth of HCC. In MS, a pro-inflammatory state is detected, which is caused by the production of cytokines by adipocytes (IL-6, IL-8, IL-1β, tumor necrosis factor α (TNFα), VEGF and chemokine ligands 2 and 5), which recruit immune cells, promoting angiogenesis and enhancing chronic inflammation. Transcription factors (PPAR) are involved in hepatocarcinogenesis, the significance of different factors is not fully understood. Leptin has a positive prognostic value in HCC, improving overall survival, and visfatin has a negative effect on hepatocarcinogenesis. Activation of PAI-1 inhibits the progression of HCC through PPARγ stimulation. Adiponectin may be a prognostic marker in HCC, with a lower serum concentration positively correlated with worse prognosis.

Non-alcoholic fatty liver disease currently affects more than 30% of the population. Recent studies highlight the role of genetic polymorphisms in genes associated with fat catabolism and anabolism in the manifestation of this condition and its progression. The work analyzes foreign publications on the molecular and biochemical aspects of these polymorphisms, as well as works studying their effect on the state of the liver and markers of its pathology over the past 10 years. Thus, polymorphisms of the PNPLA3, MBOAT7, and TM6SF2, affecting the functionality of the proteins they express, lead to a change in the metabolism of fatty acids in the liver, which in turn leads to the development of NAFLD and its progression. Despite the fact that the contribution of the rs738409 polymorphism of the PNPLA3 gene is well described both in foreign and Russian articles, polymorphisms of the MBOAT7 and TM6SF2 genes and their effect on NAFLD, as well as the molecular biochemical mechanisms underlying it, have been studied much worse in foreign studies and are little mentioned in Russian ones. In addition, the issue of the severity of the influence of the above polymorphisms on populations of different ethnic and age groups requires additional research. This work attempts to systematize the available data on these issues.

Obesity and metabolic syndrome are one of the major public health problems in the 21st century due to their prevalence. Nonalcoholic fatty liver disease, dyslipidemia, type 2 diabetes mellitus, arterial hypertension, chronic inflammation and anemia are non-communicable diseases accompanying obesity. With obesity, there is a violation of iron metabolism, iron deficiency, which further contributes to the development of metabolic disorders. Iron is the second most abundant metal on Earth, and its bioavailability is reduced due to the formation of insoluble oxides, while iron deficiency is the most common nutritional disorder. Iron metabolism in the body is associated with the formation of reactive oxygen species involved in lipid peroxidation processes. Iron metabolism in the human body is regulated at all levels; dysregulation of any stage of metabolism can lead to iron deficiency and the development of anemia associated with obesity. This review article summarizes data on molecular and cellular abnormalities in iron metabolism in obesity and metabolic syndrome. The aim of our study was to study, according to the literature, pathophysiological disorders in iron metabolism in the development of obesity and metabolic syndrome. In the future, more research is required to study iron metabolism in obesity with the aim of their preventive and therapeutic effects. The role of oxidative stress in impaired iron metabolism in obesity has not been fully studied, while iron deficiency enhances lipid peroxidation processes in antioxidant deficiency. Under these conditions, oxidative stress can damage cells and destroy red blood cells. The question arises whether the restoration of iron homeostasis in obesity can improve metabolic, inflammatory disorders and reduce the manifestation of oxidative stress, becoming a new innovative approach to the treatment of concomitant metabolic diseases associated with obesity.

Obstructive jaundice caused by cholangiocarcinoma takes a special place among malignant disorders and surgical pathology in Russia. Involvement of nonspecific immunity and the role of neutrophils in carcinogenesis are ambiguously evaluated. The aim of this study was to study functional activity of peripheral blood neutrophilic granulocytes and their phenotype in obstructive jaundice caused by cholangiocarcinoma. The study included 56 patients with obstructive jaundice associated with cholangiocarcinoma at the T2- 3N0- 1M0 stage (clinical stages II-III), and 90 apparently healthy volunteers of similar age group. Neutrophilic granulocytes were isolated from peripheral blood by means of double-density Ficoll-Urografin gradient.Venous blood was collected in patients into vacutainers with heparin upon admission to the hospital, before the surgery was performed. Spontaneous cytokine production (IL-8, IFNá) was determined by enzyme-linked immunosorbent assay using Vector-Best diagnostic kits. To assess phagocytic activity of neutrophilic granulocytes, the phagocytic index (according to Hamburger), number of phagocytes (according to Wright) and the index of completed phagocytosis (according to Rudik, 2006) were calculated. Immunophenotyping of neutrophilic granulocytes was carried out using an FC500 flow cytometer (Beckman Coulter, USA) with monoclonal antibodies to CD11b+, CD16+, CD95+. The results were statistically analyzed using the Statistica v.12.0 software (StatSoft Inc., USA). To assess intergroup differences, the nonparametric Kruskal-Wallis tests (for three or more comparison groups) and Mann-Whitney tests (for pairwise comparison) were used. Comparison of groups for a qualitative binary trait was carried out using the two-sided Fisher’s exact test. Data are presented as Median (25 quartile-75 quartile).The study of the functional activity of peripheral blood neutrophiles in obstructive jaundice patients caused by cholangiocarcinoma revealed an increase in their relative and absolute number, increased phagocytic index and decreased phagocytic number of neutrophilic granulocytes, increased expression of CD11b+, CD16+, CD95+ immunological markers. The changes in neutrophil secretory activity were characterized by a decrease in cytokine production (IL-2, IFNá). An increase in functional activity of neutrophilic granulocytes, along with a decrease in their cytokine production suggests that, in obstructive jaundice observed in cholangiocarcinoma at clinical stage T2-3N0-1M0, an equilibrium stage is revealed between the cells of immune system and malignant tumor.

Background. The problem of gastric cancer remains unresolved throughout the world, while chronic atrophic gastritis (CAG) increases the likelihood of its development by 15 times. In the Russian Federation, the incidence of gastric cancer (GC) is among the highest, with it prevailing among males. One of the leading mechanisms in molecular pathology of membranes is lipid peroxidation (LPO). The severity of oxidative membrane damage depends on concomitant diseases, contributing to emergence and progression of pathological processes and development of cancer. Currently, the problem of LPO is unsolved in biological systems.The aim of this study was to investigate the state of LPO and antioxidant defense system in CAG and GC. Materials and methods. The parameters were studied in 45 patients with CAG and 50 patients with GC. The control group included 50 practically healthy volunteers without gastrointestinal complaints, who did not have changes in the gastric mucosa according to the fibroesophagogastroduodenoscopy (FEGDS) findings.Results. In patients with CAG, an increase in malondialdehyde, superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase was found in the blood plasma compared with the control group. In patients with CAG, lipid peroxidation was activated, and the malondialdehyde level increased by 3.5 times relative to normal values. At the same time, the body fought against oxidative stress by increasing the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase. All patients with GC showed pronounced oxidative stress in the blood plasma in the form of a 45-fold increase in malondialdehyde. The activity of the main antioxidant enzyme superoxide dismutase was reduced in GC. Catalase was activated, which indicated pronounced oxidative stress, significant damage to blood vessels, and massive cell death. Glutathione-related enzymes (glutathione S-transferase and glutathione peroxidase) and the antioxidant protein ceruloplasmin were activated, which also indicated significant oxidative stress and severe intoxication in patients with GC.Conclusion. Depending on the stage and type of cancer, an in-depth study of lipid peroxidation and factors of the antioxidant defense system can be used to correct therapy and prevent cancer and can serve as markers of progression and prognosis in gastric cancer.

The aim of our study was to evaluate the clinical-anamnestic, serological, immunological and biochemical tests used for early diagnostics of gastric cancer associated with Helicobacter pylori infection in the adult population of the Krasnoyarsk Territory. Materials and methods. The control group consisted of 104 apparently healthy blood donors, the comparison group – 97 patients with chronic atrophic gastritis as well as a group of patients with early gastric cancer comprising 98 subjects. Assessment of monocyte and neutrophil spontaneous and induced chemiluminescence (CL) was carried out on a 36-channel biochemiluminometer BLM-3607. Phagocytosis was measured by using a Beckman Coulter FC 500 flow cytometer. A Varian Cary Eclipse spectrofluorometer was used to study lipid peroxidation and factors of the antioxidant defense system. Results and discussion. While studying the phagocytic arm of immunity, it was found that all patients with early gastric cancer were reported to have parameters of the maximum intensity for neutrophil spontaneous CL from 17 831 c.u. and lower, whereas induced CL reached at least 30 000 c.u. Phagocytic activity of neutrophilic granulocytes in patients with early gastric cancer was 36% or less. While studying the indicators of monocytes, it was found that spontaneous and induced CL decreased from 454 c.u. and 1186 c.u., respectively, in the patients with early gastric cancer. Monocytic activity in early gastric cancer was 34% or less. In the study of lipid peroxidation, an antioxidant defense in patients with chronic atrophic gastritis and gastric cancer had increased malondialdehyde (MDA) level. Patients with gastric cancer had decreased activity of the enzyme catalase (CAT), whereas subjects with chronic atrophic gastritis had reduced glutathione peroxidase (GPO) level. In contrast, patients with early gastric cancer were featured with increased GPO activity. We have proposed coefficients for assessing the factors of the antioxydant defence system in patients: the ratio for superoxide dismutase to catalase activity (SOD/CAT) as well as the ratio for superoxide dismutase to glutathione peroxidase activity (SOD/GPO). Conclusion. During the study, threshold values of parameters were obtained for assigning groups at high risk of developing early gastric cancer, which can be used for screening in adult population.

Aim. A study of the overlap syndrome of uninvestigated dyspepsia and heartburn at an industrial hub city of Eastern Siberia.Materials and methods. A total of 1,382 subjects (684 men and 698 women, mean age 40.6 years) were randomly selected and examined for the central district of Krasnoyarsk. The clinical check-up and interviewing results were registered with a standard questionnaire. Heartburn was diagnosed as per the Montreal Consensus. Since no endoscopic patient examination had been performed, dyspepsia was assumed uninvestigated. Dyspepsia was diagnosed as per the Rome IV criteria. The study conduction complied with ethical standards. Each participant signed an informed examination consent, in accordance to the regulations by the World Medical Association’s Declaration of Helsinki. The survey data were analysed with common statistical methods.Results. Heartburn, uninvestigated dyspepsia and their overlap syndrome had prevalence of 12.4, 21.1 and 5% in study population, respectively. Uninvestigated dyspepsia was registered in 40.4% patients with and 18.4% — without heartburn (p < 0.001). The risk factors of overlap syndrome were age >40 years (p = 0.002), obesity (p = 0.002), nonsteroidal anti-inflammatory drug and/or aspirin intake (p = 0.004) and tobacco smoking (p = 0.007). Among total patients with the heartburn/uninvestigated dyspepsia overlap syndrome, only 33.3% systemically had proton pump inhibitors, and only 17.4% had a prokinetic therapy.Conclusion. The heartburn/uninvestigated dyspepsia overlap syndrome is an actual issue in the Krasnoyarsk population. Attention is warranted to this problem to optimise treatment and prevention measures.

Aim. To study the content of cytokines in the blood serum of patients with obstructive jaundice of gallstone origin before and after surgical treatment, depending on the development of postoperative complications.Materials and methods. The treatment group consisted of 70 patients with the diagnosis of obstructive jaundice of gallstone origin, verified following a comprehensive clinical and instrumental examination. In 54 patients, the postoperative period was uncomplicated, and in 16 patients, various infectious complications in the postoperative period were revealed. The control group consisted of 125 healthy volunteers. The concentration of six cytokines (interleukin (IL)-2, IL-4, IL-18, IL-10, tumor necrosis factor alpha (TNFα), and interferon gamma (INF γ)) was determined using reagent kits manufactured by Vector-Best LLC (Novosibirsk, Russian Federation) by enzyme-linked immunosorbent assay on the Thermo Scientific analyzer (BioMerieux, France).Results. We identified significantly high concentrations of proinflammatory cytokines in the blood serum of patients with obstructive jaundice of gallstone origin upon admission, compared with the data obtained in the study of blood serum in the control group and in patients with obstructive jaundice after surgery. In the postoperative period in patients with obstructive jaundice without complications, the proinflammatory cytokines are significantly reduced and IL-4 is increased, whereas with the development of infectious complications, the level of proinflammatory cytokines is significantly elevated.Conclusion. In the pathogenesis of obstructive jaundice, a local inflammatory process plays an essential role. This is confirmed by statistically significant changes in the studied cytokines. The established increase in the concentration of IL-4, which has anti-inflammatory activity, indicates its importance in the mechanisms underlying the absence of infectious complications in the postoperative period of obstructive jaundice of gallstone origin. The revealed increase in the levels of IL-18, TNFα, and INFγ in the blood serum of patients suggests their role in the pathogenesis of infectious complications in the postoperative period of obstructive jaundice of gallstone origin.

Non-alcoholic fatty liver disease (NAFLD) is the leading cause of liver disease in highly developed countries. The risk of developing NAFLD and associated complications varies greatly among people of different nationalities and is determined by environmental and genetic factors. Genome-wide studies have revealed strong and reproducible associations between gene variations such as PNPLA3, TM6SF2, MBOAT7, GCKR, HSD17B1, and NAFLD. In this article, we consider the influence of genes and environmental factors on the pathophysiological features of NAFLD. The use of a sufficient population sample with the analysis of SNP arrays and the use of sequencing methods (exome and genome as a whole) will lead to the discovery of additional genetic variants, will inevitably improve the understanding of the pathogenesis of NAFLD, and will allow the development of a technology for personalized risk in assessing the disease in a patient. The aim of our study was to study the genetic predictors of NAFLD based on literature data with the interpretation of the studies. There is now strong evidence that specific variants of genetic risk have a large effect on NAFLD, and their effect is comparable to that of major metabolic risk factors such as obesity and type 2 diabetes. The increased risk extends to the onset and progression of the entire spectrum of NAFLD manifestations, including overall mortality due to liver disease. Currently, individual genetic variants do not allow the creation of a personalized risk profile; therefore, the most expedient approach today is the development of polygenic risk assessments. The number of genetic loci associated with the prevalence and outcome of NAFLD remains limited. The use of a sufficient population sample with the analysis of SNP arrays and the use of sequencing methods (exome and genome as a whole) will lead to the discovery of additional genetic variants and will inevitably improve the understanding of the pathogenesis of NAFLD and will allow the development of a technology for personalized risk in the assessment of the disease.

Aim. A study of monocyte chemiluminescent activity at variant stages of gastric cancer.Materials and methods. The study enrolled 90 gastric cancer patients and 70 healthy donors. Spontaneous and induced chemiluminescence in monocytes was assessed for 90 min with a “BLM 3607” 36-channel chemiluminescence analyser (Russia). Opsonized zymosan-induced chemiluminescence enhancement was measured as a ratio of the areas under the induced vs. spontaneous chemiluminescence curves, the activation index. Statistical significance was estimated with the Mann—Whitney criterion (p < 0.05).Results. The maximal spontaneous monocyte chemiluminescence intensity significantly decreased in stage IV gastric cancer patients compared to the control cohort (p = 0.035). Time to maximum in spontaneous chemiluminescence increased in all gastric cancer patients vs. control (p = 0.001), and in stage IV gastric cancer vs. stage I patients (p = 0.043). The areas under a curve in spontaneous and induced monocyte chemiluminescence increased in all gastric cancer patients vs. control (p = 0.001), and in stage IV gastric cancer vs. stage I patients (p = 0.037). The activation index was higher in all gastric cancer cases compared to control (p = 0.001).Conclusion. All patients with gastric adenocarcinoma, irrespective of the stage, revealed changes in the monocyte chemiluminescence activity, i.e. a longer time to maximum in spontaneous chemiluminescence and larger area under the curve of spontaneous and induced chemiluminescence, the activation index. Maximal monocyte spontaneous chemiluminescence intensity diminished in stage IV gastric cancer compared to the control cohort. Immune activity reflected in monocyte chemiluminescence correlates with the stage of gastric adenocarcinoma.

One of the essential tasks of sustainable forest management is to maintain native biodiversity. Primary forest research is one of the ways to understand what this biodiversity is. Matherials and methods. The primary, as confirmed by their land-use history and structural peculiarities, mesic dark-conifer forests remain in Visim and Pechora–Ilych nature biosphere reserves (boreal and sub-boreal zones respectively, the Ural Mountains, Russian Federation). We compared the primary forests and post fire 100-year small-leaved deciduous forests by diversity of vascular flora and soil invertebrate macrofauna. Results and discussion. The diversity of some functional groups of species (low boreal herbs, earthworms) in post fire forests is lower than in primary forests, the research shows. These species largely depend on deadwood and other tree-related microhabitats common in the primary forests but not so in the 100-year post fire forests. Repeated fires at intervals of several decades, as is the case with the use of prescribed fires in forest management, will be expected to reduce the biodiversity quality of these specialist species. Additionally, we revealed that post fire forest flora is more synanthropic in the woodland of a small area (Visim reserve) than in the intact forest landscape (Pechora–Ilych reserve). It demonstrates that, within extensive woodlands, native forests are more resilient to sporadic stand-replacing disturbances than small woodlands. Conclusion. Strict conservation of intact forest landscapes is necessary as they serve as large buffer areas around the remaining primary forests to maintain native biodiversity.