55 research outputs found
Partial symmetry breaking and heteroclinic tangencies
We study some global aspects of the bifurcation of an equivariant family of
volume-contracting vector fields on the three-dimensional sphere. When part of
the symmetry is broken, the vector fields exhibit Bykov cycles. Close to the
symmetry, we investigate the mechanism of the emergence of heteroclinic
tangencies coexisting with transverse connections. We find persistent suspended
horseshoes accompanied by attracting periodic trajectories with long periods
On Global Bifurcations of Three-dimensional Diffeomorphisms Leading to Lorenz-like Attractors
We study dynamics and bifurcations of three-dimensional diffeomorphisms with nontransversal heteroclinic cycles. We show that bifurcations under consideration lead to the birth of Lorenz-like attractors. They can be viewed as attractors in the Poincare map for periodically perturbed classical Lorenz attractors and hence they can allow for the existence of homoclinic tangencies and wild hyperbolic sets
Πptimization approach to the synthesis of plasma stabilization system in tokamak ITER
Synthesis of the controller of ITER plasma stabilization system is considered. Stabilization system is based on
tokamak diagnostic measurements, defines the voltages in tokamak coils and has the filtering properties. Known
methods of synthesis of plasma regulators are advanced by the presented optimization approach. It makes possible
to meet the requirements for the dynamics of the stabilization process when considering a set of some arbitrary
plasma drops and disturbances. The proposed approach evaluates the ensemble of transient processes of the closed
object. Based on this estimations it is possible to use wide range of optimization techniques.Π ΠΎΠ·Π³Π»ΡΠ΄Π°ΡΡΡΡΡ ΡΠΈΠ½ΡΠ΅Π· ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠ° Π΄Π»Ρ ΡΠΈΡΡΠ΅ΠΌΠΈ ΡΡΠ°Π±ΡΠ»ΡΠ·Π°ΡΡΡ ΠΏΠ»Π°Π·ΠΌΠΈ Π² ΡΠΎΠΊΠ°ΠΌΠ°ΡΡ ΠΠ’ΠΠ . Π‘ΠΈΡΡΠ΅ΠΌΠ° ΡΡΠ°Π±ΡΠ»ΡΠ·Π°ΡΡΡ
Π·Π°ΡΠ½ΠΎΠ²Π°Π½Π° Π½Π° Π²ΠΈΠΌΡΡΠ°Ρ
Π΄ΡΠ°Π³Π½ΠΎΡΡΠΈΡΠ½ΠΎΡ ΡΠΈΡΡΠ΅ΠΌΠΈ ΡΠΎΠΊΠ°ΠΌΠ°ΠΊΠ°, Π²ΠΎΠ½Π° Π·Π°Π΄Π°Ρ Π½Π°ΠΏΡΡΠ³ΠΈ Π² ΠΊΠ΅ΡΡΡΡΠΈΡ
ΠΊΠΎΡΡΡΠΊΠ°Ρ
Ρ ΠΌΠ°Ρ Π²Π»Π°ΡΡΠΈΠ²ΠΎΡΡΡ ΡΡΠ»ΡΡΡΠ°ΡΡΡ. ΠΡΠ΄ΠΎΠΌΡ ΠΌΠ΅ΡΠΎΠ΄ΠΈ ΡΠΈΠ½ΡΠ΅Π·Ρ ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΡΠ² ΠΏΠ»Π°Π·ΠΌΠΈ Π²Π΄ΠΎΡΠΊΠΎΠ½Π°Π»Π΅Π½Ρ Π·Π°ΠΏΡΠΎΠΏΠΎΠ½ΠΎΠ²Π°Π½ΠΈΠΌ ΠΎΠΏΡΠΈΠΌΡΠ·Π°ΡΡΠΉΠ½ΠΈΠΌ
ΠΏΡΠ΄Ρ
ΠΎΠ΄ΠΎΠΌ. Π¦Π΅ Π΄Π°Ρ ΠΌΠΎΠΆΠ»ΠΈΠ²ΡΡΡΡ Π·Π°Π΄ΠΎΠ²ΠΎΠ»ΡΠ½ΠΈΡΠΈ Π²ΠΈΠΌΠΎΠ³ΠΈ Π΄ΠΎ ΡΠΊΠΎΡΡΡ Π΄ΠΈΠ½Π°ΠΌΡΠΊΠΈ ΠΏΡΠΎΡΠ΅ΡΡ ΡΡΠ°Π±ΡΠ»ΡΠ·Π°ΡΡΡ Π· ΡΡΠ°Ρ
ΡΠ²Π°Π½Π½ΡΠΌ
ΡΡΠ·Π½ΠΈΡ
Π½Π΅Π²ΠΈΠ·Π½Π°ΡΠ΅Π½ΠΎΡΡΠ΅ΠΉ Π² Π΄ΠΈΠ½Π°ΠΌΡΡΡ ΠΏΠ»Π°Π·ΠΌΠΈ, Π² ΡΠΎΠΌΡ ΡΠΈΡΠ»Ρ Π·Π±ΡΡΠ΅Π½Ρ ΠΏΠ»Π°Π·ΠΌΠΈ. ΠΠ°ΠΏΡΠΎΠΏΠΎΠ½ΠΎΠ²Π°Π½ΠΈΠΉ ΠΏΡΠ΄Ρ
ΡΠ΄ ΠΎΡΡΠ½ΡΡ Π°Π½ΡΠ°ΠΌΠ±Π»Ρ ΠΏΠ΅ΡΠ΅Ρ
ΡΠ΄Π½ΠΈΡ
ΠΏΡΠΎΡΠ΅ΡΡΠ² Π·Π°ΠΌΠΊΠ½ΡΡΠΎΠ³ΠΎ ΠΎΠ±'ΡΠΊΡΠ°. ΠΠ° ΠΎΡΠ½ΠΎΠ²Ρ Π·Π°ΠΏΡΠΎΠΏΠΎΠ½ΠΎΠ²Π°Π½ΠΈΡ
ΠΎΡΡΠ½ΠΎΠΊ ΠΌΠΎΠΆΠ½Π° Π²ΠΈΠΊΠΎΡΠΈΡΡΠΎΠ²ΡΠ²Π°ΡΠΈ
ΡΠΈΡΠΎΠΊΠΈΠΉ ΡΠΏΠ΅ΠΊΡΡ ΠΌΠ΅ΡΠΎΠ΄ΡΠ² ΠΎΠΏΡΠΈΠΌΡΠ·Π°ΡΡΡ.Π Π°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°Π΅ΡΡΡ ΡΠΈΠ½ΡΠ΅Π· ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠ° Π΄Π»Ρ ΡΠΈΡΡΠ΅ΠΌΡ ΡΡΠ°Π±ΠΈΠ»ΠΈΠ·Π°ΡΠΈΠΈ ΠΏΠ»Π°Π·ΠΌΡ Π² ΡΠΎΠΊΠ°ΠΌΠ°ΠΊΠ΅ ΠΠ’ΠΠ . Π‘ΠΈΡΡΠ΅ΠΌΠ° ΡΡΠ°Π±ΠΈΠ»ΠΈΠ·Π°ΡΠΈΠΈ ΠΎΡΠ½ΠΎΠ²Π°Π½Π° Π½Π° ΠΈΠ·ΠΌΠ΅ΡΠ΅Π½ΠΈΡΡ
Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ ΡΠΎΠΊΠ°ΠΌΠ°ΠΊΠ°, ΠΎΠ½Π° Π·Π°Π΄Π°ΡΡ Π½Π°ΠΏΡΡΠΆΠ΅Π½ΠΈΡ Π² ΡΠΏΡΠ°Π²Π»ΡΡΡΠΈΡ
ΠΊΠ°ΡΡΡΠΊΠ°Ρ
ΠΈ ΠΎΠ±Π»Π°Π΄Π°Π΅Ρ ΡΠ²ΠΎΠΉΡΡΠ²Π°ΠΌΠΈ ΡΠΈΠ»ΡΡΡΠ°ΡΠΈΠΈ. ΠΠ·Π²Π΅ΡΡΠ½ΡΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ ΡΠΈΠ½ΡΠ΅Π·Π° ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠΎΠ² ΠΏΠ»Π°Π·ΠΌΡ ΡΡΠΎΠ²Π΅ΡΡΠ΅Π½ΡΡΠ²ΠΎΠ²Π°Π½Ρ ΠΏΡΠ΅Π΄Π»Π°Π³Π°Π΅ΠΌΡΠΌ ΠΎΠΏΡΠΈΠΌΠΈΠ·Π°ΡΠΈΠΎΠ½Π½ΡΠΌ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ΠΎΠΌ. ΠΡΠΎ Π΄Π°Π΅Ρ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΠΎΡΡΡ ΡΠ΄ΠΎΠ²Π»Π΅ΡΠ²ΠΎΡΠΈΡΡ ΡΡΠ΅Π±ΠΎΠ²Π°Π½ΠΈΡ
ΠΊ ΠΊΠ°ΡΠ΅ΡΡΠ²Ρ Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠΈ ΠΏΡΠΎΡΠ΅ΡΡΠ° ΡΡΠ°Π±ΠΈΠ»ΠΈΠ·Π°ΡΠΈΠΈ Ρ ΡΡΡΡΠΎΠΌ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
Π½Π΅ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ½Π½ΠΎΡΡΠ΅ΠΉ Π² Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠ΅ ΠΏΠ»Π°Π·ΠΌΡ, Π²
ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ Π²ΠΎΠ·ΠΌΡΡΠ΅Π½ΠΈΠΉ ΠΏΠ»Π°Π·ΠΌΡ. ΠΡΠ΅Π΄Π»ΠΎΠΆΠ΅Π½Π½ΡΠΉ ΠΏΠΎΠ΄Ρ
ΠΎΠ΄ ΠΎΡΠ΅Π½ΠΈΠ²Π°Π΅Ρ Π°Π½ΡΠ°ΠΌΠ±Π»Ρ ΠΏΠ΅ΡΠ΅Ρ
ΠΎΠ΄Π½ΡΡ
ΠΏΡΠΎΡΠ΅ΡΡΠΎΠ² Π·Π°ΠΌΠΊΠ½ΡΡΠΎΠ³ΠΎ ΠΎΠ±ΡΠ΅ΠΊΡΠ°. ΠΠ° ΠΎΡΠ½ΠΎΠ²Π΅ ΠΏΡΠ΅Π΄Π»ΠΎΠΆΠ΅Π½Π½ΡΡ
ΠΎΡΠ΅Π½ΠΎΠΊ ΠΌΠΎΠΆΠ½ΠΎ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°ΡΡ ΡΠΈΡΠΎΠΊΠΈΠΉ ΡΠΏΠ΅ΠΊΡΡ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² ΠΎΠΏΡΠΈΠΌΠΈΠ·Π°ΡΠΈΠΈ
Microbiological oropharyngeal patterns in patients with different phenotypes of chronic obstructive pulmonary disease
Persistent bronchial inflammation in chronic obstructive pulmonary disease (COPD) is considered the cause of ventilation disorders and related contamination with conditionally pathogenic microorganisms; the latter can proceed and transform into a full infection, which can aggravate and exacerbate COPD. The aim of the study was to evaluate the relations between the oropharyngeal microbiota in patients with COPD and the clinical, functional, and prognostic parameters of the disease. Materials and Methods. 64 patients with COPD were included in the study; the participants were scheduled to visit our clinic on two occasions. In the first visit, their medical history was studied in detail and the major examination procedures were conducted. Those included an assessment of the respiratory function, the 6-minute walk test, the degree of dyspnea by the Medical Research Council scale, body plethysmography, the diffusion capacity of the lungs, and a chest CT scan. The second visit took place 12 months after the first one to assess the changes in the course of the disease. The result was considered negative if, in the second examination, the patientβs condition was found more severe. Oropharyngeal samples of all patients were sequenced to identify the V3βV4 variable sites of the 16S rRNA gene. Results. It is found that the microbiological oropharyngeal patterns in COPD patients depend on the source of micro-aspiration. In addition, the changes in the oropharyngeal microbiota correlate with the severity and prognosis of the disease, as well as the patient phenotype. Based on the data obtained by sequencing parts of the 16S rRNA gene, the role of oropharyngeal microbiota in determining the course and prognosis of COPD has been elucidated. Conclusion. The presented clinical and functional characteristics associated with oropharyngeal microbiota indicate that microaspirations from other body compartments not only affect the composition of oropharyngeal microbiota in patients with COPD but also have an important prognostic significance. Β© 2018, Nizhny Novgorod State Medical Academy. All rights reserved
Microbiological oropharyngeal patterns in patients with different phenotypes of chronic obstructive pulmonary disease
Persistent bronchial inflammation in chronic obstructive pulmonary disease (COPD) is considered the cause of ventilation disorders and related contamination with conditionally pathogenic microorganisms; the latter can proceed and transform into a full infection, which can aggravate and exacerbate COPD. The aim of the study was to evaluate the relations between the oropharyngeal microbiota in patients with COPD and the clinical, functional, and prognostic parameters of the disease. Materials and Methods. 64 patients with COPD were included in the study; the participants were scheduled to visit our clinic on two occasions. In the first visit, their medical history was studied in detail and the major examination procedures were conducted. Those included an assessment of the respiratory function, the 6-minute walk test, the degree of dyspnea by the Medical Research Council scale, body plethysmography, the diffusion capacity of the lungs, and a chest CT scan. The second visit took place 12 months after the first one to assess the changes in the course of the disease. The result was considered negative if, in the second examination, the patientβs condition was found more severe. Oropharyngeal samples of all patients were sequenced to identify the V3βV4 variable sites of the 16S rRNA gene. Results. It is found that the microbiological oropharyngeal patterns in COPD patients depend on the source of micro-aspiration. In addition, the changes in the oropharyngeal microbiota correlate with the severity and prognosis of the disease, as well as the patient phenotype. Based on the data obtained by sequencing parts of the 16S rRNA gene, the role of oropharyngeal microbiota in determining the course and prognosis of COPD has been elucidated. Conclusion. The presented clinical and functional characteristics associated with oropharyngeal microbiota indicate that microaspirations from other body compartments not only affect the composition of oropharyngeal microbiota in patients with COPD but also have an important prognostic significance. Β© 2018, Nizhny Novgorod State Medical Academy. All rights reserved
Periostin as a biomarker of allergic inflammation in atopic bronchial asthma and allergic rhinitis (A pilot study)
Β© 2020, Privolzhsky Research Medical University. All rights reserved. The involvement of periostin in Th2-dependent allergic inflammation has been documented. However, the significance of periostin as a biomarker of local allergic inflammation in the nasal mucosa (NM) of patients with atopic bronchial asthma (BA) and allergic rhinitis (AR) is yet to be determined. The aim of the study was to determine the presence of periostin and evaluate its role as a non-invasive marker of allergic inflammation in the nasal secretions of children with atopic BA and AR. Materials and Methods. In 43 patients aged 4β17 years with atopic BA and AR, the NM was examined using nasal video-endoscopy and (if indicated) computed tomography; the amount of periostin in the nasal secretion was determined by the enzyme immunoassay. Results. Exacerbation of AR was accompanied by a statistically significant increase in the level of periostin in the nasal secretion: up to 0.84 [0.06; 48.79] ng/mg, whereas in remission, that was 0.13 [0.00; 0.36] ng/mg; p=0.04. This value increased progressively as the severity of AR increased from 0.16 [0.00; 0.36] ng/mg in the mild course to 0.20 [0.00; 9.03] ng/mg in AR of moderate severity, and to 10.70 [0.56; 769.20] ng/mg in most severe cases; p=0.048. Hypertrophy or polyposis of the nasal and/or paranasal mucosa was detected in 34.9% (15/43) of the examined patients. The concentration of periostin in the nasal secretion was lower in children without NM hypertrophy: 0.18 [0.001; 4.30] ng/mg vs 0.78 [0.13; 162.10] ng/mg in patients with NM hypertrophy; the differences were close to statistically significant: p=0.051. The level of nasal periostin depended on the clinical form of hypertrophy in the sinonasal mucosa, reaching 0.17 [0.00; 0.32] ng/mg in children with polyposis hyperplasia of NM and 21.6 [10.70; 1516.80] ng/mg β with hypertrophy of the NM in the medial surface of the concha; p=0.02. Conclusion. Exacerbation and increased severity of AR in patients with atopic BA are accompanied by an increased level of periostin in the nasal secretion. This allows us to consider the level of nasal periostin as a biomarker of local allergic inflammation in the NM of patients with atopic BA combined with AR. Hypertrophic changes in the sinonasal mucosa are generally accompanied by an increased level of nasal periostin; specifically, this level significantly depends on the clinical form of mucous membrane hypertrophy and requires additional studies
Periostin as a biomarker of allergic inflammation in atopic bronchial asthma and allergic rhinitis (A pilot study)
The involvement of periostin in Th2-dependent allergic inflammation has been documented. However, the significance of periostin as a biomarker of local allergic inflammation in the nasal mucosa (NM) of patients with atopic bronchial asthma (BA) and allergic rhinitis (AR) is yet to be determined. The aim of the study was to determine the presence of periostin and evaluate its role as a non-invasive marker of allergic inflammation in the nasal secretions of children with atopic BA and AR. Materials and Methods. In 43 patients aged 4β17 years with atopic BA and AR, the NM was examined using nasal video-endoscopy and (if indicated) computed tomography; the amount of periostin in the nasal secretion was determined by the enzyme immunoassay. Results. Exacerbation of AR was accompanied by a statistically significant increase in the level of periostin in the nasal secretion: up to 0.84 [0.06; 48.79] ng/mg, whereas in remission, that was 0.13 [0.00; 0.36] ng/mg; p=0.04. This value increased progressively as the severity of AR increased from 0.16 [0.00; 0.36] ng/mg in the mild course to 0.20 [0.00; 9.03] ng/mg in AR of moderate severity, and to 10.70 [0.56; 769.20] ng/mg in most severe cases; p=0.048. Hypertrophy or polyposis of the nasal and/or paranasal mucosa was detected in 34.9% (15/43) of the examined patients. The concentration of periostin in the nasal secretion was lower in children without NM hypertrophy: 0.18 [0.001; 4.30] ng/mg vs 0.78 [0.13; 162.10] ng/mg in patients with NM hypertrophy; the differences were close to statistically significant: p=0.051. The level of nasal periostin depended on the clinical form of hypertrophy in the sinonasal mucosa, reaching 0.17 [0.00; 0.32] ng/mg in children with polyposis hyperplasia of NM and 21.6 [10.70; 1516.80] ng/mg β with hypertrophy of the NM in the medial surface of the concha; p=0.02. Conclusion. Exacerbation and increased severity of AR in patients with atopic BA are accompanied by an increased level of periostin in the nasal secretion. This allows us to consider the level of nasal periostin as a biomarker of local allergic inflammation in the NM of patients with atopic BA combined with AR. Hypertrophic changes in the sinonasal mucosa are generally accompanied by an increased level of nasal periostin; specifically, this level significantly depends on the clinical form of mucous membrane hypertrophy and requires additional studies. Β© 2020, Privolzhsky Research Medical University. All rights reserved
Extracellular matrix markers and methods for their study
The extracellular matrix (ECM) is a complex meshwork consisting mainly of proteins and carbohydrates; it is currently viewed as a key factor of tissue organization and homeostasis. In each organ, the composition of ECM is different: It includes a variety of fibrillar components, such as collagens, fibronectin, and elastin, as well as non-fibrillar molecules: Proteoglycans, hyaluronan, glycoproteins, and matrix proteins. ECM is an active tissue, where the de novo syntheses of structural components are constantly taking place. In parallel, ECM components undergo degradation catalyzed by a number of enzymes including matrix metalloproteinases. The synthesis and degradation of ECM components are controlled by mediators and cytokines, metabolic, epigenetic, and environmental factors. Currently, a large amount of evidence indicates that modifications (remodeling) of ECM play an important role in the pathogenesis of clinical conditions. This may explain the increasing interest in the markers of ECM remodeling both in health and disease. In recent years, many of the ECM markers were considered targets for diagnosing, predicting, and treating diseases. In this review, we discuss some of the currently known ECM markers and methods used for their determination. Β© 2019, Privolzhsky Research Medical University. All rights reserved
ΠΠ°ΡΠΊΠ΅ΡΡ ΡΠΎΡΡΠΎΡΠ½ΠΈΡ ΡΠΊΡΡΡΠ°ΡΠ΅Π»Π»ΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ ΠΌΠ°ΡΡΠΈΠΊΡΠ° ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΈΡ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ (ΠΎΠ±Π·ΠΎΡ)
The extracellular matrix (ECM) is a complex meshwork consisting mainly of proteins and carbohydrates; it is currently viewed as a key factor of tissue organization and homeostasis. In each organ, the composition of ECM is different: it includes a variety of fibrillar components, such as collagens, fibronectin, and elastin, as well as non-fibrillar molecules: proteoglycans, hyaluronan, glycoproteins, and matrix proteins. ECM is an active tissue, where the de novo syntheses of structural components are constantly taking place. In parallel, ECM components undergo degradation catalyzed by a number of enzymes including matrix metalloproteinases. The synthesis and degradation of ECM components are controlled by mediators and cytokines, metabolic, epigenetic, and environmental factors. Currently, a large amount of evidence indicates that modifications (remodeling) of ECM play an important role in the pathogenesis of clinical conditions. This may explain the increasing interest in the markers of ECM remodeling both in health and disease. In recent years, many of the ECM markers were considered targets for diagnosing, predicting, and treating diseases. In this review, we discuss some of the currently known ECM markers and methods used for their determination.ΠΠΊΡΡΡΠ°ΡΠ΅Π»Π»ΡΠ»ΡΡΠ½ΡΠΉ (Π²Π½Π΅ΠΊΠ»Π΅ΡΠΎΡΠ½ΡΠΉ) ΠΌΠ°ΡΡΠΈΠΊΡ (ΠΠ¦Π) ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»ΡΠ΅Ρ ΡΠΎΠ±ΠΎΠΉ ΡΠ»ΠΎΠΆΠ½ΡΡ ΡΠ΅ΡΡΠ°ΡΡΡ ΡΡΡΡΠΊΡΡΡΡ, ΡΠΎΡΡΠΎΡΡΡΡ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎ ΠΈΠ· Π±Π΅Π»ΠΊΠΎΠ² ΠΈ ΡΠ³Π»Π΅Π²ΠΎΠ΄ΠΎΠ², ΠΈ ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°Π΅ΡΡΡ Π² Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ ΠΊΠ°ΠΊ ΠΊΠ»ΡΡΠ΅Π²ΠΎΠΉ ΡΠ΅Π³ΡΠ»ΡΡΠΎΡ ΠΎΡΠ³Π°Π½ΠΈΠ·Π°ΡΠΈΠΈ ΡΠΊΠ°Π½Π΅ΠΉ ΠΈ Π³ΠΎΠΌΠ΅ΠΎΡΡΠ°Π·Π°. Π ΠΊΠ°ΠΆΠ΄ΠΎΠΌ ΠΎΡΠ³Π°Π½Π΅ ΡΠΎΡΡΠ°Π² ΠΠ¦Π ΡΠ°Π·Π»ΠΈΡΠ΅Π½, Π²ΠΊΠ»ΡΡΠ°Π΅Ρ ΡΠ°Π·Π½ΠΎΠΎΠ±ΡΠ°Π·Π½ΡΠ΅ ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠ½ΡΠ΅ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΡ, ΡΠ°ΠΊΠΈΠ΅ ΠΊΠ°ΠΊ ΠΊΠΎΠ»Π»Π°Π³Π΅Π½Ρ, ΡΠΈΠ±ΡΠΎΠ½Π΅ΠΊΡΠΈΠ½ ΠΈ ΡΠ»Π°ΡΡΠΈΠ½, ΠΈ Π½Π΅ΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠ½ΡΠ΅ ΠΌΠΎΠ»Π΅ΠΊΡΠ»Ρ - ΠΏΡΠΎΡΠ΅ΠΎΠ³Π»ΠΈΠΊΠ°Π½Ρ, Π³ΠΈΠ°Π»ΡΡΠΎΠ½Π°Π½ ΠΈ Π³Π»ΠΈΠΊΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½Ρ, ΠΌΠ°ΡΡΠΈΠΊΡΠ½ΡΠ΅ Π±Π΅Π»ΠΊΠΈ. ΠΠ¦Π ΡΠ²Π»ΡΠ΅ΡΡΡ Π°ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΡΡΡΡΠΊΡΡΡΠΎΠΉ, Π² ΠΊΠΎΡΠΎΡΠΎΠΉ ΠΏΠΎΡΡΠΎΡΠ½Π½ΠΎ ΠΏΡΠΎΠΈΡΡ
ΠΎΠ΄ΡΡ ΠΏΡΠΎΡΠ΅ΡΡΡ ΡΠΈΠ½ΡΠ΅Π·Π° de novo ΡΡΡΡΠΊΡΡΡΠ½ΡΡ
ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΠΎΠ² ΠΈ ΠΏΠ°ΡΠ°Π»Π»Π΅Π»ΡΠ½ΠΎ - ΠΈΡ
Π΄Π΅Π³ΡΠ°Π΄Π°ΡΠΈΠΈ, ΠΎΡΡΡΠ΅ΡΡΠ²Π»ΡΠ΅ΠΌΠΎΠΉ ΠΏΡΠ΅ΠΈΠΌΡΡΠ΅ΡΡΠ²Π΅Π½Π½ΠΎ Ρ ΡΡΠ°ΡΡΠΈΠ΅ΠΌ ΡΠ΅ΡΠΌΠ΅Π½ΡΠΎΠ², Π² ΡΠΎΠΌ ΡΠΈΡΠ»Π΅ ΠΌΠ°ΡΡΠΈΠΊΡΠ½ΡΡ
ΠΌΠ΅ΡΠ°Π»Π»ΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½Π°Π·. Π‘ΠΈΠ½ΡΠ΅Π· ΠΈ Π΄Π΅Π³ΡΠ°Π΄Π°ΡΠΈΡ ΠΊΠΎΠΌΠΏΠΎΠ½Π΅Π½ΡΠΎΠ² ΠΌΠ°ΡΡΠΈΠΊΡΠ° Π½Π°Ρ
ΠΎΠ΄ΡΡΡΡ ΠΏΠΎΠ΄ ΡΠ»ΠΎΠΆΠ½ΡΠΌ ΡΠ΅Π³ΡΠ»ΡΡΠΎΡΠ½ΡΠΌ Π²Π»ΠΈΡΠ½ΠΈΠ΅ΠΌ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΠΌΠ΅Π΄ΠΈΠ°ΡΠΎΡΠΎΠ² ΠΈ ΡΠΈΡΠΎΠΊΠΈΠ½ΠΎΠ², ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΡΠ΅ΡΠΊΠΈΡ
, ΡΠΏΠΈΠ³Π΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈ ΡΡΠ΅Π΄ΠΎΠ²ΡΡ
Π²ΠΎΠ·Π΄Π΅ΠΉΡΡΠ²ΠΈΠΉ. Π Π½Π°ΡΡΠΎΡΡΠ΅Π΅ Π²ΡΠ΅ΠΌΡ Π½Π°ΠΊΠΎΠΏΠ»Π΅Π½ΠΎ Π±ΠΎΠ»ΡΡΠΎΠ΅ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ Π΄ΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΡΡΡΠ², ΡΡΠΎ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ ΠΠ¦Π ΠΈΠ³ΡΠ°ΡΡ Π²Π°ΠΆΠ½ΡΡ ΡΠΎΠ»Ρ ΠΏΡΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΠΎΡΡΠΎΡΠ½ΠΈΡΡ
. ΠΡΠΈΠΌ ΠΎΠ±ΡΡΠ»ΠΎΠ²Π»Π΅Π½ ΠΈΠ½ΡΠ΅ΡΠ΅Ρ ΠΊ ΠΏΠΎΠΈΡΠΊΡ ΠΌΠ°ΡΠΊΠ΅ΡΠΎΠ², ΠΎΡΡΠ°ΠΆΠ°ΡΡΠΈΡ
ΡΠΎΡΡΠΎΡΠ½ΠΈΠ΅ ΠΠ¦Π Π² ΡΠ°Π·Π½ΡΡ
ΠΎΡΠ³Π°Π½Π°Ρ
ΠΈ ΡΠΊΠ°Π½ΡΡ
ΠΊΠ°ΠΊ Π² ΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΡΡΠ»ΠΎΠ²ΠΈΡΡ
, ΡΠ°ΠΊ ΠΈ ΠΏΡΠΈ ΡΠ°Π·Π»ΠΈΡΠ½ΡΡ
Π²Π°ΡΠΈΠ°Π½ΡΠ°Ρ
ΠΏΠ°ΡΠΎΠ»ΠΎΠ³ΠΈΠΈ. Π ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΠ΅ Π³ΠΎΠ΄Ρ ΠΌΠ½ΠΎΠ³ΠΈΠ΅ ΠΈΠ· ΠΌΠΎΠ»Π΅ΠΊΡΠ» ΠΠ¦Π ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°ΡΡΡΡ Π² ΠΊΠ°ΡΠ΅ΡΡΠ²Π΅ ΠΌΠΈΡΠ΅Π½Π΅ΠΉ Π΄Π»Ρ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ, ΠΏΡΠΎΠ³Π½ΠΎΠ·ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΈ Π»Π΅ΡΠ΅Π½ΠΈΡ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ. Π Π΄Π°Π½Π½ΠΎΠΌ ΠΎΠ±Π·ΠΎΡΠ΅ ΠΌΡ ΡΠΈΡΡΠ΅ΠΌΠ°ΡΠΈΠ·ΠΈΡΠΎΠ²Π°Π»ΠΈ ΠΎΡΠ½ΠΎΠ²Π½ΡΠ΅ ΠΎΠΏΠΈΡΠ°Π½Π½ΡΠ΅ Π² Π½Π°ΡΡΠΎΡΡΠΈΠΉ ΠΌΠΎΠΌΠ΅Π½Ρ ΠΌΠ°ΡΠΊΠ΅ΡΡ ΡΠΎΡΡΠΎΡΠ½ΠΈΡ ΠΠ¦Π ΠΈ ΠΈΡΠΏΠΎΠ»ΡΠ·ΡΠ΅ΠΌΡΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΈΡ
ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ
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