43 research outputs found

Cognitive modeling of informatization influence on socio-economic indicators of the region

Get PDF
The article discusses topical issues of the influence of informatization on the development of the country’s regions in the conditions of the modern unstable world. The nature of the development of a region can be reflected and understood on the basis of qualitative and quantitative information about its socio-economic indicators, about their relationship and trends in their changes under the influence of internal and external factors. At the same time, information can most often be incomplete, difficult to access, untimely, contradictory, etc. Therefore, in this paper, it is proposed to use a cognitive approach and cognitive modeling of complex systems to overcome the problems of information deficiency by imitating cognitive modeling of the structure and behavior of a complex regional system. The simulation was carried out using the author’s CMCS (Cognitive Modeling Complex System) software system. The results of multi-stage cognitive modeling, consisting in the development of cognitive maps β€œInfluence of ICT on the state of the region” and β€œDigitalization of the republic” (according to the socio-economic state of the Republic of Dagestan), analysis of structural properties and modeling scenarios for the development of situations on the model are presented. Scenarios make it possible to foresee the ways of possible development of the system under the influence of various factors, including the factor of informatization

Association of angiotensinogen and angiotensin II receptor type I polymorphisms with biomarkers of carbohydrate and lipid metabolism in Dagestan residents with type 2 diabetes and hypertension

Get PDF
Aim. To study the associations of angiotensinogen (AGT) (s4762(Π‘521Π’), rs699(Π’704C)) and angiotensin II receptor type I (AGTR1) (rs5186(A1166C)) genetic polymorphisms with serum levels of insulin, glucagon, C-peptide, leptin, as well as with dyslipidemia and glycemic levels in Dagestan residents with combination of type 2 diabetes (T2D) and hypertension (HTN), as well as with isolated T2D/HTN.Material and methods. We examined 16 patients with isolated T2D, 59 patients with T2D+HTN and 51 patients with isolated HTN from Dagestan. Genetic polymorphisms of the AGT and AGTR1 genes were studied. The levels of insulin, glucagon, C-peptide, and leptin were studied by enzyme-linked immunosorbent assay (ELISA), while lipid and carbohydrate metabolism β€” by biochemical methods.Results. In patients with T2D, the association of CC genotype of AGT gene rs4762(Π‘521Π’) polymorphism with a leptin decrease was determined, while its CT genotype was associated with an increase in serum level of triglycerides. The TC genotype of AGT gene rs699(Π’704C) polymorphism was associated with an increase in leptin, triglyceride and glucose levels. The AA genotype of AGTR1 gene rs5186(A1166C) polymorphism was associated with an increase in insulin and glucose levels, as well as a decrease in leptin level. In patients with a combination of T2D and HTN, CC and CT genotypes of AGT gene rs4762(Π‘521Π’) polymorphism was associated with a decrease in glucagon level. The TT genotype of AGT gene rs699(Π’704C) polymorphism was associated with an increase in insulin, triglyceride, glucose and body mass index (BMI) levels. In isolated HTN, the CC and CT genotypes of AGT gene rs4762(Π‘521Π’) polymorphism were associated ith a decrease in glucagon level. The TT genotype of AGT gene rs699(Π’704C) polymorphism was associated with increased levels of insulin, low density lipoproteins, and BMI.Conclusion. Associations of AGT (s4762(Π‘521Π’), rs699(Π’704C)) and AGTR1 (rs5186(A1166C)) genetic polymorphisms with carbohydrate and lipid metabolism changes are an important pathogenetic link of T2D and HTN, which allows developing an individual prognosis of these diseases in Dagestan residents

Accounting of motivators and demotivators under introduction of the brc system

Full text link
РассматриваСтся Π½Π΅ΠΎΠ±Ρ…ΠΎΠ΄ΠΈΠΌΠΎΡΡ‚ΡŒ ΡƒΡ‡Π΅Ρ‚Π° Π΄Π΅ΠΌΠΎΡ‚ΠΈΠ²Π°Ρ‚ΠΎΡ€ΠΎΠ² ΠΏΡ€ΠΈ Ρ€Π°Π±ΠΎΡ‚Π΅ с балльно-Ρ€Π΅ΠΉΡ‚ΠΈΠ½Π³ΠΎΠ²ΠΎΠΉ систСмой оцСниванияThe article considers the need to take into account demotivators when working with the BRS syste

Check of knowleadge using score-rating system and independent test control

Full text link
АнализируСтся ΠΏΡ€ΠΎΠ±Π»Π΅ΠΌΠ° дублирования балльно-Ρ€Π΅ΠΉΡ‚ΠΈΠ½Π³ΠΎΠ²ΠΎΠΉ систСмы оцСнивания ΠΈ нСзависимого тСстового контроля Π² систСмС ΠΏΠΎΠ΄Π³ΠΎΡ‚ΠΎΠ²ΠΊΠΈ спСциалистов. ΠŸΡ€Π΅Π΄Π»ΠΎΠΆΠ΅Π½Ρ‹ мСроприятия ΠΏΠΎ ΡƒΡΡ‚Ρ€Π°Π½Π΅Π½ΠΈΡŽ нСдостатковIn article it is told about duplication of score-rating system and independent test controlin training system of specialists. Actions for elimination of shortcomingsare offere

Twenty-year clinical progression of dysferlinopathy in patients from Dagestan

Get PDF
Β© 2017 Umakhanova, Bardakov, Mavlikeev, Chernova, Magomedova, Akhmedova, Yakovlev, Dalgatov, Fedotov, Isaev and Deev.To date, over 30 genes with mutations causing limb-girdle muscle dystrophy have been described. Dysferlinopathies are a form of limb-girdle muscle dystrophy type 2B with an incidence ranging from 1:1,300 to 1:200,000 in different populations. In 1996, Dr. S. N. Illarioshkin described a family from the Botlikhsky district of Dagestan, where limb-girdle muscle dystrophy type 2B and Miyoshi myopathy were diagnosed in 12 members from three generations of a large Avar family. In 2000, a previously undescribed mutation in the DYSF gene (c.TG573/574AT; p. Val67Asp) was detected in the affected members of this family. Twenty years later, in this work, we re-examine five known and seven newly affected family members previously diagnosed with dysferlinopathy. We observed disease progression in family members who were previously diagnosed and noted obvious clinical polymorphism of the disease. A typical clinical case is provided

Corrigendum: Twenty-year clinical progression of dysferlinopathy in patients from Dagestan [Front Neurol, 8, (2017) (77)] doi: 10.3389/fneur.2017.00077

Get PDF
The "Funding" section should be: This work was funded by Human Stem Cells Institute PJSC and Roman V. Deev. Theoretical part of this work was supported by Russian Scientific Foundation grant (14-15-00916). Ivan A. Yakovlev and Mikhail O. Mavlikeev were supported by the Russian Government Program of Competitive Growth of Kazan Federal University. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way

The clinical case of limb-girdle muscle dystrophy 2Q associated with myasthenic syndrome and lung damage

Get PDF
Limb-girdle muscle dystrophy 2Q is one of the rarest forms of plectinopathies and is represented by an isolated muscular dystrophic syndrome, according to two previously described literature reports. There are five forms of plectinopathies, including limb-girdle muscle dystrophy 2Q, are caused by mutations in the PLEC gene, the alternative splicing of which determines the synthesis of 9 isoforms of the plectin protein (1, 1a, 1b, 1c, 1d, 1e, 1f, 1g, 3) performing cytolinker function in the neuronal, epithelial and muscle tissue.The article describes the family observation of three sick siblings with the limb-girdle muscle dystrophy 2Q phenotype due to the presence of a new homozygous mutation (NM_201378.3:c.58G>T, NP_958780.1:p.Glu20Ter) in the isoform 1f PLEC revealed by whole-exome sequencing. Clinical, electromyography, visualization and histopathological features of limb-girdle muscle dystrophy 2Q were analyzed in detail. The onset of clinical manifestations in all the described siblings was observed in early childhood with moderate weakness mainly in the pelvic girdle muscles and proximal lower limbs with minimal involvement of the muscles of the shoulder girdle. A distinctive aspect is the stagnation of the myodystrophic process until 20β€”21 years, followed by the progression and development of episodes of respiratory failure, as well as the formation of rigidity of the cervical, thoracic spine and moderate contracture of the Achilles tendons. Typical features are marked atrophy of paravertebral muscles with the formation of pterygoid scapula and the presence of hypertrophy m. gastrocnemius, m. quadriceps femoris, m. deltoideus and m. triceps brachii. Histopathological examination m. vastus lateralis revealed myodystrophic process without inflammatory infiltration, muscle fiber cytoskeleton disorganization resulted from the plectin loss.Electrocardiography signs of the early repolarization syndrome, focal cardiosclerosis and sinus tachycardia are described. For the first time, involvement in the pathological process of pulmonary tissue in the form of noninfectious bronchiolitis, atelectasis, and the development of the myasthenic syndrome causing episodes of respiratory failure resulted in the death of two described siblings aged 29 and 31 years. Discussed pathogenetic role of PLEC 1f isoform in the development of described syndromes, expands understanding of rare nosology limb-girdle muscle dystrophy 2Q

Hybrid ( laser- spark) a method of applying a reinforcement coating

Full text link
Hybrid spark -laser treatment shows a positive effect on the performance properties of coatings (roughness, thickness, continuity, adhesion).Гибридная элСктроискровая –лазСрная ΠΎΠ±Ρ€Π°Π±ΠΎΡ‚ΠΊΠ° ΠΏΠΎΠΊΠ°Π·Ρ‹Π²Π°Π΅Ρ‚ ΠΏΠΎΠ»ΠΎΠΆΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΠ΅ влияниС Π½Π° эксплуатационныС свойства ΠΏΠΎΠΊΡ€Ρ‹Ρ‚ΠΈΠΉ (ΡˆΠ΅Ρ€ΠΎΡ…ΠΎΠ²Π°Ρ‚ΠΎΡΡ‚ΡŒ, Ρ‚ΠΎΠ»Ρ‰ΠΈΠ½Ρƒ, ΡΠΏΠ»ΠΎΡˆΠ½ΠΎΡΡ‚ΡŒ, адгСзию)

ΠšΠ»ΠΈΠ½ΠΈΡ‡Π΅ΡΠΊΠΈΠΉ случай поясно-конСчностной ΠΌΡ‹ΡˆΠ΅Ρ‡Π½ΠΎΠΉ дистрофии 2Q, ассоциированной с миастСничСским синдромом ΠΈ ΠΏΠΎΡ€Π°ΠΆΠ΅Π½ΠΈΠ΅ΠΌ Π»Π΅Π³ΠΊΠΈΡ…

Get PDF
Limb-girdle muscle dystrophy 2Q is one of the rarest forms of plectinopathies and is represented by an isolated muscular dystrophic syndrome, according to two previously described literature reports. There are five forms of plectinopathies, including limb-girdle muscle dystrophy 2Q, are caused by mutations in the PLEC gene, the alternative splicing of which determines the synthesis of 9 isoforms of the plectin protein (1, 1a, 1b, 1c, 1d, 1e, 1f, 1g, 3) performing cytolinker function in the neuronal, epithelial and muscle tissue.The article describes the family observation of three sick siblings with the limb-girdle muscle dystrophy 2Q phenotype due to the presence of a new homozygous mutation (NM_201378.3:c.58G>T, NP_958780.1:p.Glu20Ter) in the isoform 1f PLEC revealed by whole-exome sequencing. Clinical, electromyography, visualization and histopathological features of limb-girdle muscle dystrophy 2Q were analyzed in detail. The onset of clinical manifestations in all the described siblings was observed in early childhood with moderate weakness mainly in the pelvic girdle muscles and proximal lower limbs with minimal involvement of the muscles of the shoulder girdle. A distinctive aspect is the stagnation of the myodystrophic process until 20β€”21 years, followed by the progression and development of episodes of respiratory failure, as well as the formation of rigidity of the cervical, thoracic spine and moderate contracture of the Achilles tendons. Typical features are marked atrophy of paravertebral muscles with the formation of pterygoid scapula and the presence of hypertrophy m. gastrocnemius, m. quadriceps femoris, m. deltoideus and m. triceps brachii. Histopathological examination m. vastus lateralis revealed myodystrophic process without inflammatory infiltration, muscle fiber cytoskeleton disorganization resulted from the plectin loss.Electrocardiography signs of the early repolarization syndrome, focal cardiosclerosis and sinus tachycardia are described. For the first time, involvement in the pathological process of pulmonary tissue in the form of noninfectious bronchiolitis, atelectasis, and the development of the myasthenic syndrome causing episodes of respiratory failure resulted in the death of two described siblings aged 29 and 31 years. Discussed pathogenetic role of PLEC 1f isoform in the development of described syndromes, expands understanding of rare nosology limb-girdle muscle dystrophy 2Q.Поясно-конСчностная ΠΌΡ‹ΡˆΠ΅Ρ‡Π½Π°Ρ дистрофия 2Q являСтся ΠΎΠ΄Π½ΠΎΠΉ ΠΈΠ· Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ Ρ€Π΅Π΄ΠΊΠΈΡ… Ρ„ΠΎΡ€ΠΌ ΠΏΠ»Π΅ΠΊΡ‚ΠΈΠ½ΠΎΠΏΠ°Ρ‚ΠΈΠΉ ΠΈ проявляСтся ΠΈΠ·ΠΎΠ»ΠΈΡ€ΠΎΠ²Π°Π½Π½Ρ‹ΠΌ ΠΌΡ‹ΡˆΠ΅Ρ‡Π½Ρ‹ΠΌ дистрофичСским синдромом согласно Π΄Π²ΡƒΠΌ Ρ€Π°Π½Π΅Π΅ прСдставлСнным Π² Π»ΠΈΡ‚Π΅Ρ€Π°Ρ‚ΡƒΡ€Π΅ описаниям. ΠŸΡΡ‚ΡŒ ΡΡƒΡ‰Π΅ΡΡ‚Π²ΡƒΡŽΡ‰ΠΈΡ… Ρ„ΠΎΡ€ΠΌ ΠΏΠ»Π΅ΠΊΡ‚ΠΈΠ½ΠΎΠΏΠ°Ρ‚ΠΈΠΉ, Π² Ρ‚ΠΎΠΌ числС поясно-конСчностная ΠΌΡ‹ΡˆΠ΅Ρ‡Π½Π°Ρ дистрофия 2Q, обусловлСны мутациями Π² Π³Π΅Π½Π΅ PLEC, Π°Π»ΡŒΡ‚Π΅Ρ€Π½Π°Ρ‚ΠΈΠ²Π½Ρ‹ΠΉ сплайсинг ΠΊΠΎΡ‚ΠΎΡ€ΠΎΠ³ΠΎ опрСдСляСт синтСз 9 ΠΈΠ·ΠΎΡ„ΠΎΡ€ΠΌ Π±Π΅Π»ΠΊΠ° ΠΏΠ»Π΅ΠΊΡ‚ΠΈΠ½Π° (1, 1Π°, 1b, 1c, 1d, 1Π΅, 1f,1g, 3), Π²Ρ‹ΠΏΠΎΠ»Π½ΡΡŽΡ‰ΠΈΡ… Ρ†ΠΈΡ‚ΠΎΠ»ΠΈΠ½ΠΊΠ΅Ρ€Π½ΡƒΡŽ Ρ„ΡƒΠ½ΠΊΡ†ΠΈΡŽ Π² Π½Π΅ΠΉΡ€ΠΎΠ½Π°Π»ΡŒΠ½ΠΎΠΉ, ΡΠΏΠΈΡ‚Π΅Π»ΠΈΠ°Π»ΡŒΠ½ΠΎΠΉ ΠΈ ΠΌΡ‹ΡˆΠ΅Ρ‡Π½ΠΎΠΉ тканях.Π’ ΡΡ‚Π°Ρ‚ΡŒΠ΅ прСдставлСно описаниС сСмСйного наблюдСния 3 Π±ΠΎΠ»ΡŒΠ½Ρ‹Ρ… сибсов с поясно-конСчностной ΠΌΡ‹ΡˆΠ΅Ρ‡Π½ΠΎΠΉ дистрофиСй 2Q, обусловлСнного Π½Π°Π»ΠΈΡ‡ΠΈΠ΅ΠΌ Π½ΠΎΠ²ΠΎΠΉ Π³ΠΎΠΌΠΎΠ·ΠΈΠ³ΠΎΡ‚Π½ΠΎΠΉ ΠΌΡƒΡ‚Π°Ρ†ΠΈΠΈ (NM_201378.3:c.58G>T, NP_958780.1:p.Glu20Ter) Π² ΠΈΠ·ΠΎΡ„ΠΎΡ€ΠΌΠ΅ 1f Π³Π΅Π½Π° PLEC, выявлСнной с ΠΏΠΎΠΌΠΎΡ‰ΡŒΡŽ полноэкзомного сСквСнирования. Π”Π΅Ρ‚Π°Π»ΡŒΠ½ΠΎ ΠΏΡ€ΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡ€ΠΎΠ²Π°Π½Ρ‹ клиничСскиС, элСктронСйромиографичСскиС, Π²ΠΈΠ·ΡƒΠ°Π»ΠΈΠ·Π°Ρ†ΠΈΠΎΠ½Π½Ρ‹Π΅ ΠΈ патогистологичСскиС особСнности поясно-конСчностной ΠΌΡ‹ΡˆΠ΅Ρ‡Π½ΠΎΠΉ дистрофии 2Q. Π”Π΅Π±ΡŽΡ‚ клиничСских проявлСний Ρƒ всСх описанных Ρ‡Π»Π΅Π½ΠΎΠ² сСмьи наблюдался Π² Ρ€Π°Π½Π½Π΅ΠΌ дСтском возрастС Π² Π²ΠΈΠ΄Π΅ ΡƒΠΌΠ΅Ρ€Π΅Π½Π½ΠΎΠΉ слабости прСимущСствСнно ΠΌΡ‹ΡˆΡ† Ρ‚Π°Π·ΠΎΠ²ΠΎΠ³ΠΎ пояса ΠΈ ΠΏΡ€ΠΎΠΊΡΠΈΠΌΠ°Π»ΡŒΠ½Ρ‹Ρ… ΠΎΡ‚Π΄Π΅Π»ΠΎΠ² Π½ΠΎΠ³ с ΠΌΠΈΠ½ΠΈΠΌΠ°Π»ΡŒΠ½Ρ‹ΠΌ Π²ΠΎΠ²Π»Π΅Ρ‡Π΅Π½ΠΈΠ΅ΠΌ ΠΌΡ‹ΡˆΡ† ΠΏΠ»Π΅Ρ‡Π΅Π²ΠΎΠ³ΠΎ пояса. ΠžΡ‚Π»ΠΈΡ‡ΠΈΡ‚Π΅Π»ΡŒΠ½Ρ‹ΠΌ аспСктом являСтся стагнация миодистрофичСского процСсса Π΄ΠΎ 20β€”21 Π³ΠΎΠ΄Π° с ΠΏΠΎΡΠ»Π΅Π΄ΡƒΡŽΡ‰ΠΈΠΌ прогрСссированиСм ΠΈ Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΠ΅ΠΌ эпизодов Π΄Ρ‹Ρ…Π°Ρ‚Π΅Π»ΡŒΠ½ΠΎΠΉ нСдостаточности, Π° Ρ‚Π°ΠΊΠΆΠ΅ Ρ„ΠΎΡ€ΠΌΠΈΡ€ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ригидности шСйного, Π³Ρ€ΡƒΠ΄Π½ΠΎΠ³ΠΎ ΠΎΡ‚Π΄Π΅Π»Π° ΠΏΠΎΠ·Π²ΠΎΠ½ΠΎΡ‡Π½ΠΈΠΊΠ° ΠΈ ΡƒΠΌΠ΅Ρ€Π΅Π½Π½ΠΎΠΉ ΠΊΠΎΠ½Ρ‚Ρ€Π°ΠΊΡ‚ΡƒΡ€Ρ‹ Π°Ρ…ΠΈΠ»Π»ΠΎΠ²Ρ‹Ρ… сухоТилий. Π₯Π°Ρ€Π°ΠΊΡ‚Π΅Ρ€Π½Ρ‹ΠΌΠΈ ΡΠ²Π»ΡΡŽΡ‚ΡΡ выраТСнная атрофия mm. paravertebralis с Ρ„ΠΎΡ€ΠΌΠΈΡ€ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΊΡ€Ρ‹Π»ΠΎΠ²ΠΈΠ΄Π½Ρ‹Ρ… Π»ΠΎΠΏΠ°Ρ‚ΠΎΠΊ ΠΈ Π½Π°Π»ΠΈΡ‡ΠΈΠ΅ Π³ΠΈΠΏΠ΅Ρ€Ρ‚Ρ€ΠΎΡ„ΠΈΠΈ m. gastrocnemius, m. quadriceps femoris, m. deltoideus ΠΈ m. triceps brachii. ΠŸΠ°Ρ‚ΠΎΠ³ΠΈΡΡ‚ΠΎΠ»ΠΎΠ³ΠΈΡ‡Π΅ΡΠΊΠΎΠ΅ исслСдованиС m. vastus lateralis ΠΎΡ‚Ρ€Π°ΠΆΠ°Π΅Ρ‚ Π½Π°Π»ΠΈΡ‡ΠΈΠ΅ миодистрофичСского процСсса Π±Π΅Π· Π²ΠΎΡΠΏΠ°Π»ΠΈΡ‚Π΅Π»ΡŒΠ½ΠΎΠΉ ΠΈΠ½Ρ„ΠΈΠ»ΡŒΡ‚Ρ€Π°Ρ†ΠΈΠΈ, Π΄Π΅Π·ΠΎΡ€Π³Π°Π½ΠΈΠ·Π°Ρ†ΠΈΡŽ цитоскСлСта ΠΌΡ‹ΡˆΠ΅Ρ‡Π½Ρ‹Ρ… Π²ΠΎΠ»ΠΎΠΊΠΎΠ½ ΠΈ ΡƒΡ‚Ρ€Π°Ρ‚Ρƒ ΠΏΠ»Π΅ΠΊΡ‚ΠΈΠ½Π°. ΠžΠΏΠΈΡΠ°Π½Ρ‹ элСктрокардиографичСскиС ΠΏΡ€ΠΈΠ·Π½Π°ΠΊΠΈ синдрома Ρ€Π°Π½Π½Π΅ΠΉ рСполяризации, ΠΎΡ‡Π°Π³ΠΎΠ²ΠΎΠ³ΠΎ кардиосклСроза ΠΈ синусовой Ρ‚Π°Ρ…ΠΈΠΊΠ°Ρ€Π΄ΠΈΠΈ. Π’ΠΏΠ΅Ρ€Π²Ρ‹Π΅ Π² Π»ΠΈΡ‚Π΅Ρ€Π°Ρ‚ΡƒΡ€Π΅ прСдставлСно сочСтаниС пояс-Π½ΠΎ-конСчностной ΠΌΡ‹ΡˆΠ΅Ρ‡Π½ΠΎΠΉ дистрофии 2Q с ΠΏΠΎΡ€Π°ΠΆΠ΅Π½ΠΈΠ΅ΠΌ Π»Π΅Π³ΠΊΠΈΡ… Π² Π²ΠΈΠ΄Π΅ Π½Π΅ΠΈΠ½Ρ„Π΅ΠΊΡ†ΠΈΠΎΠ½Π½ΠΎΠ³ΠΎ Π±Ρ€ΠΎΠ½Ρ…ΠΈΠΎΠ»ΠΈΡ‚Π°, Π°Ρ‚Π΅Π»Π΅ΠΊΡ‚Π°Π·ΠΎΠ² ΠΈ Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΠ΅ΠΌ миастСничСского синдрома, ΠΎΠ±ΡƒΡΠ»ΠΎΠ²Π»ΠΈΠ²Π°ΡŽΡ‰ΠΈΠΌΠΈ эпизоды Π΄Ρ‹Ρ…Π°Ρ‚Π΅Π»ΡŒΠ½ΠΎΠΉ нСдостаточности ΠΈ повлСкшиС ΡΠΌΠ΅Ρ€Ρ‚ΡŒ 2 описываСмых сибсов Π² возрастС 29 ΠΈ 31 Π³ΠΎΠ΄Π°. ΠžΠ±ΡΡƒΠΆΠ΄Π°Π΅ΠΌΠΎΠ΅ патогСнСтичСскоС Π·Π½Π°Ρ‡Π΅Π½ΠΈΠ΅ 1f-ΠΈΠ·ΠΎΡ„ΠΎΡ€ΠΌΡ‹ ΠΏΠ»Π΅ΠΊΡ‚ΠΈΠ½Π° Π² Ρ€Π°Π·Π²ΠΈΡ‚ΠΈΠΈ описанных синдромов позволяСт Ρ€Π°ΡΡˆΠΈΡ€ΠΈΡ‚ΡŒ прСдставлСниС ΠΎ Ρ€Π΅Π΄ΠΊΠΎΠΉ Π½ΠΎΠ·ΠΎΠ»ΠΎΠ³ΠΈΠΈ β€” поясно-конСчностной ΠΌΡ‹ΡˆΠ΅Ρ‡Π½ΠΎΠΉ дистрофии 2Q
corecore

We use cookies to improve our website.

Learn more