10 research outputs found
The resocialization process of elderly and disabled through club activities in institutional care
The article presents the results of sociological research on the issues of the re-socialization of elderly and people with functional limitations and health problems through club activities, based on the example of five institutions (boarding houses for the elderly and disabled) located in Belgorod regio
ΠΠ΅Π½Π΅ΡΠΈΡΠ΅ΡΠΊΠ°Ρ ΠΌΠΎΠ΄Π΅Π»Ρ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π½Π΅ΠΉΡΠΎΠ½Π° Ρ ΠΌΡΡΠ΅ΠΉ Π»ΠΈΠ½ΠΈΠΈ B6SjL-tg: Π½ΠΎΠ²ΡΠ΅ Π΄Π°Π½Π½ΡΠ΅ ΠΎ Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠ΅ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΡΡ Π½Π°ΡΡΡΠ΅Π½ΠΈΠΉ ΠΈ ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΡ ΠΏΡΠΎΡΠ²Π»Π΅Π½ΠΈΠΉ Π½Π΅ΠΉΡΠΎΠ΄Π΅Π³Π΅Π½Π΅ΡΠ°ΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ°
Introduction. Over the past several decades, the study of mutations associated with motor neuron disease has led to the development of a number of transgenic animal models of motor neuron disease. One of the causes of the familial form of this disorder is mutations in the gene encoding Cu/Zn superoxide dismutase 1. The B6SJL-Tg (SOD1*G93A) mouse strain expresses a mutant form of human superoxide dismutase 1. Aim of study. To assess motor functions, dynamics of survival, and morphological changes in the spinal cord of transgenic B6SJL-Tg (SOD1*G93A) mice. Material and methods. In total, 31 animals have been studied. Starting from the age of 22 weeks, once every two weeks, the βopen fieldβ and βbeam walkingβ motor tests were performed. The morphological changes in the spinal cord were evaluated at intermediate (26β35 weeks) and late stages (40β45 weeks). Neuronal proteins NeuN and PGP9.5, gliofibrillar protein, cyclonucleotide phosphatase (a marker of oligodendroglia) and a marker protein of microglia IBA1 were detected by immunohistochemistry; antibodies MTC02 to the outer membrane protein were used to detect mitochondria. Results. Motor problems appeared at the age of 24β26 weeks and steadily progressed; one could see consistent paresis of the hindlimbs, then the forelimbs, which was accompanied by general hypotrophy of the animals. There was a greater variability in the timing of symptom onset and life expectancy in males compared to females. The neurodegenerative process with damage to motor neurons was accompanied by the activation of micro- and astroglia. A sharp decrease in immunoreactivity to the mitochondrial marker MTC02 was found. Conclusion. The obtained results demonstrate new details of the development of a complex of motor and pathomorphological changes characteristic of motor neuron disease in B6SJL-Tg (SOD1*G93A) mice. Clarification of the fine dynamics of the neurodegenerative process in these animals is of great importance for monitoring the course of the disease during preclinical trials of new drugs and methods of gene therapy.ΠΠ²Π΅Π΄Π΅Π½ΠΈΠ΅. ΠΠ° ΠΏΠΎΡΠ»Π΅Π΄Π½ΠΈΠ΅ Π½Π΅ΡΠΊΠΎΠ»ΡΠΊΠΎ Π΄Π΅ΡΡΡΠΈΠ»Π΅ΡΠΈΠΉ ΠΈΠ·ΡΡΠ΅Π½ΠΈΠ΅ ΠΌΡΡΠ°ΡΠΈΠΉ, ΡΠ²ΡΠ·Π°Π½Π½ΡΡ
Ρ Π±ΠΎΠ»Π΅Π·Π½ΡΡ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π½Π΅ΠΉΡΠΎΠ½Π°, ΠΏΡΠΈΠ²Π΅Π»ΠΎ ΠΊ ΡΠ°Π·ΡΠ°Π±ΠΎΡΠΊΠ΅ ΡΡΠ΄Π° ΡΡΠ°Π½ΡΠ³Π΅Π½Π½ΡΡ
ΠΌΠΎΠ΄Π΅Π»Π΅ΠΉ ΡΡΠΎΠ³ΠΎ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡ Π½Π° ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
. ΠΠ΄Π½ΠΎΠΉ ΠΈΠ· ΠΈΠ·Π²Π΅ΡΡΠ½ΡΡ
ΠΏΡΠΈΡΠΈΠ½ ΡΠ΅ΠΌΠ΅ΠΉΠ½ΠΎΠΉ ΡΠΎΡΠΌΡ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π½Π΅ΠΉΡΠΎΠ½Π° ΡΠ²Π»ΡΡΡΡΡ ΠΌΡΡΠ°ΡΠΈΠΈ Π² Π³Π΅Π½Π΅, ΠΊΠΎΠ΄ΠΈΡΡΡΡΠ΅ΠΌ Cu / Zn-ΡΡΠΏΠ΅ΡΠΎΠΊΡΠΈΠ΄Π΄ΠΈΡΠΌΡΡΠ°Π·Ρ 1 (SOD1). ΠΠΈΠ½ΠΈΡ ΠΌΡΡΠ΅ΠΉ B6SJL-Tg (SOD1*G93A) ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡΡΠ΅Ρ ΠΌΡΡΠ°Π½ΡΠ½ΡΡ ΡΠΎΡΠΌΡ Π΄Π°Π½Π½ΠΎΠ³ΠΎ Π³Π΅Π½Π° ΠΈ ΠΌΠΎΠΆΠ΅Ρ ΡΠ°ΡΡΠΌΠ°ΡΡΠΈΠ²Π°ΡΡΡΡ ΠΊΠ°ΠΊ Π°Π½ΠΈΠΌΠ°Π»ΡΠ½Π°Ρ ΠΌΠΎΠ΄Π΅Π»Ρ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π½Π΅ΠΉΡΠΎΠ½Π°. Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ β ΠΎΡΠ΅Π½ΠΈΡΡ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΡΠ½ΠΊΡΠΈΠΈ, Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΡ Π²ΡΠΆΠΈΠ²Π°Π΅ΠΌΠΎΡΡΠΈ ΠΈ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ Π² ΡΠΏΠΈΠ½Π½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ ΡΡΠ°Π½ΡΠ³Π΅Π½Π½ΡΡ
ΠΌΡΡΠ΅ΠΉ B6SJL-Tg (SOD1*G93A). ΠΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. Π ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π±ΡΠ»ΠΎ Π²Π·ΡΡΠΎ 31 ΠΆΠΈΠ²ΠΎΡΠ½ΠΎΠ΅ Ρ ΡΠΊΠ°Π·Π°Π½Π½ΠΎΠΉ ΠΌΡΡΠ°ΡΠΈΠ΅ΠΉ, ΠΊΠΎΡΠΎΡΡΠΌ Π½Π°ΡΠΈΠ½Π°Ρ Ρ Π²ΠΎΠ·ΡΠ°ΡΡΠ° 22 Π½Π΅Π΄, ΡΠ°Π· Π² 2 Π½Π΅Π΄ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΠΈ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΡΠ΅ ΡΠ΅ΡΡΡ Β«ΠΎΡΠΊΡΡΡΠΎΠ΅ ΠΏΠΎΠ»Π΅Β» ΠΈ Β«ΡΡΠΆΠ°ΡΡΠ°ΡΡΡ Π΄ΠΎΡΠΎΠΆΠΊΠ°Β». ΠΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΡ Π² ΡΠΏΠΈΠ½Π½ΠΎΠΌ ΠΌΠΎΠ·Π³Π΅ ΠΎΡΠ΅Π½ΠΈΠ²Π°Π»ΠΈ Π½Π° ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΎΡΠ½ΡΡ
(26β35 Π½Π΅Π΄) ΠΈ ΠΏΠΎΠ·Π΄Π½ΠΈΡ
ΡΡΠ°Π΄ΠΈΡΡ
(40β45 Π½Π΅Π΄). ΠΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈ Π²ΡΡΠ²Π»ΡΠ»ΠΈ Π½Π΅ΠΉΡΠΎΠ½Π°Π»ΡΠ½ΡΠ΅ Π±Π΅Π»ΠΊΠΈ NeuN ΠΈ PGP9.5, Π³Π»ΠΈΠΎΡΠΈΠ±ΡΠΈΠ»Π»ΡΡΠ½ΡΠΉ Π±Π΅Π»ΠΎΠΊ, ΡΠΈΠΊΠ»ΠΎΠ½ΡΠΊΠ»Π΅ΠΎΡΠΈΠ΄ΡΠΎΡΡΠ°ΡΠ°Π·Ρ (ΠΌΠ°ΡΠΊΠ΅Ρ ΠΎΠ»ΠΈΠ³ΠΎΠ΄Π΅Π½Π΄ΡΠΎΠ³Π»ΠΈΠΈ) ΠΈ ΠΌΠ°ΡΠΊΠ΅ΡΠ½ΡΠΉ Π±Π΅Π»ΠΎΠΊ ΠΌΠΈΠΊΡΠΎΠ³Π»ΠΈΠΈ IBA1, Π΄Π»Ρ Π²ΡΡΠ²Π»Π΅Π½ΠΈΡ ΠΌΠΈΡΠΎΡ
ΠΎΠ½Π΄ΡΠΈΠΉ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π»ΠΈ Π°Π½ΡΠΈΡΠ΅Π»Π° MTC02 ΠΊ Π±Π΅Π»ΠΊΡ Π½Π°ΡΡΠΆΠ½ΠΎΠΉ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½Ρ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΠ²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΡΠ΅ Π½Π°ΡΡΡΠ΅Π½ΠΈΡ ΠΏΠΎΡΠ²Π»ΡΠ»ΠΈΡΡ Π² Π²ΠΎΠ·ΡΠ°ΡΡΠ΅ 24β26 Π½Π΅Π΄ ΠΈ Π½Π΅ΡΠΊΠ»ΠΎΠ½Π½ΠΎ ΠΏΡΠΎΠ³ΡΠ΅ΡΡΠΈΡΠΎΠ²Π°Π»ΠΈ, Π½Π°Π±Π»ΡΠ΄Π°Π»ΡΡ Π²ΠΎΡΡ
ΠΎΠ΄ΡΡΠΈΠΉ ΠΏΠ°ΡΠ΅Π· Π·Π°Π΄Π½ΠΈΡ
, Π·Π°ΡΠ΅ΠΌ ΠΏΠ΅ΡΠ΅Π΄Π½ΠΈΡ
ΠΊΠΎΠ½Π΅ΡΠ½ΠΎΡΡΠ΅ΠΉ, ΡΡΠΎ ΡΠΎΠΏΡΠΎΠ²ΠΎΠΆΠ΄Π°Π»ΠΎΡΡ ΠΎΠ±ΡΠ΅ΠΉ Π³ΠΈΠΏΠΎΡΡΠΎΡΠΈΠ΅ΠΉ ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
. ΠΡΠΌΠ΅ΡΠ΅Π½Π° Π±Γ³Π»ΡΡΠ°Ρ Π²Π°ΡΠΈΠ°Π±Π΅Π»ΡΠ½ΠΎΡΡΡ Π² ΡΡΠΎΠΊΠ°Ρ
ΠΏΠΎΡΠ²Π»Π΅Π½ΠΈΡ ΡΠΈΠΌΠΏΡΠΎΠΌΠΎΠ² ΠΈ ΠΏΡΠΎΠ΄ΠΎΠ»ΠΆΠΈΡΠ΅Π»ΡΠ½ΠΎΡΡΠΈ ΠΆΠΈΠ·Π½ΠΈ ΡΠ°ΠΌΡΠΎΠ² ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ ΡΠ°ΠΌΠΊΠ°ΠΌΠΈ. ΠΠ΅ΠΉΡΠΎΠ΄Π΅Π³Π΅Π½Π΅ΡΠ°ΡΠΈΠ²Π½ΡΠΉ ΠΏΡΠΎΡΠ΅ΡΡ Ρ ΠΏΠΎΡΠ°ΠΆΠ΅Π½ΠΈΠ΅ΠΌ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΡΡ
Π½Π΅ΠΉΡΠΎΠ½ΠΎΠ² ΡΠΎΠΏΡΠΎΠ²ΠΎΠΆΠ΄Π°Π»ΡΡ Π°ΠΊΡΠΈΠ²Π°ΡΠΈΠ΅ΠΉ ΠΌΠΈΠΊΡΠΎ- ΠΈ Π°ΡΡΡΠΎΠ³Π»ΠΈΠΈ. ΠΠ±Π½Π°ΡΡΠΆΠ΅Π½ΠΎ ΡΠ΅Π·ΠΊΠΎΠ΅ ΡΠ½ΠΈΠΆΠ΅Π½ΠΈΠ΅ ΠΈΠΌΠΌΡΠ½ΠΎΡΠ΅Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ ΠΊ ΠΌΠΈΡΠΎΡ
ΠΎΠ½Π΄ΡΠΈΠ°Π»ΡΠ½ΠΎΠΌΡ ΠΌΠ°ΡΠΊΠ΅ΡΡ MTC02. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΠΎΠ»ΡΡΠ΅Π½Π½ΡΠ΅ ΡΠ΅Π·ΡΠ»ΡΡΠ°ΡΡ Π΄Π΅ΠΌΠΎΠ½ΡΡΡΠΈΡΡΡΡ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΡ Ρ ΠΌΡΡΠ΅ΠΉ B6SJL-Tg (SOD1*G93A) ΠΊΠΎΠΌΠΏΠ»Π΅ΠΊΡΠ° Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΡΡ
ΠΈ ΠΏΠ°ΡΠΎΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈΠ·ΠΌΠ΅Π½Π΅Π½ΠΈΠΉ, Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠ½ΡΡ
Π΄Π»Ρ Π±ΠΎΠ»Π΅Π·Π½ΠΈ Π΄Π²ΠΈΠ³Π°ΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ Π½Π΅ΠΉΡΠΎΠ½Π°. Π£ΡΠΎΡΠ½Π΅Π½ΠΈΠ΅ ΡΠΎΠ½ΠΊΠΎΠΉ Π΄ΠΈΠ½Π°ΠΌΠΈΠΊΠΈ Π½Π΅ΠΉΡΠΎΠ΄Π΅Π³Π΅Π½Π΅ΡΠ°ΡΠΈΠ²Π½ΠΎΠ³ΠΎ ΠΏΡΠΎΡΠ΅ΡΡΠ° Ρ ΠΌΠΎΠ΄Π΅Π»ΡΠ½ΡΡ
ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
ΠΈΠΌΠ΅Π΅Ρ Π·Π½Π°ΡΠ΅Π½ΠΈΠ΅ Π΄Π»Ρ ΠΌΠΎΠ½ΠΈΡΠΎΡΠΈΠ½Π³Π° ΡΠ΅ΡΠ΅Π½ΠΈΡ Π±ΠΎΠ»Π΅Π·Π½ΠΈ ΠΏΡΠΈ ΠΏΡΠΎΠ²Π΅Π΄Π΅Π½ΠΈΠΈ Π΄ΠΎΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΈΡΠΏΡΡΠ°Π½ΠΈΠΉ Π½ΠΎΠ²ΡΡ
Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΡΡ
ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠΎΠ² ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ² Π³Π΅Π½Π½ΠΎΠΉ ΡΠ΅ΡΠ°ΠΏΠΈΠΈ
Genetic model of motor neuron disease in B6SJL-Tg mice: new data on the dynamics of motor symptoms and immunohistochemical manifestations of the neurodegenerative process
Introduction. Over the past several decades, the study of mutations associated with motor neuron disease has led to the development of a number of transgenic animal models of motor neuron disease. One of the causes of the familial form of this disorder is mutations in the gene encoding Cu/Zn superoxide dismutase 1. The B6SJL-Tg (SOD1*G93A) mouse strain expresses a mutant form of human superoxide dismutase 1. Aim of study. To assess motor functions, dynamics of survival, and morphological changes in the spinal cord of transgenic B6SJL-Tg (SOD1*G93A) mice. Material and methods. In total, 31 animals have been studied. Starting from the age of 22 weeks, once every two weeks, the βopen fieldβ and βbeam walkingβ motor tests were performed. The morphological changes in the spinal cord were evaluated at intermediate (26β35 weeks) and late stages (40β45 weeks). Neuronal proteins NeuN and PGP9.5, gliofibrillar protein, cyclonucleotide phosphatase (a marker of oligodendroglia) and a marker protein of microglia IBA1 were detected by immunohistochemistry; antibodies MTC02 to the outer membrane protein were used to detect mitochondria. Results. Motor problems appeared at the age of 24β26 weeks and steadily progressed; one could see consistent paresis of the hindlimbs, then the forelimbs, which was accompanied by general hypotrophy of the animals. There was a greater variability in the timing of symptom onset and life expectancy in males compared to females. The neurodegenerative process with damage to motor neurons was accompanied by the activation of micro- and astroglia. A sharp decrease in immunoreactivity to the mitochondrial marker MTC02 was found. Conclusion. The obtained results demonstrate new details of the development of a complex of motor and pathomorphological changes characteristic of motor neuron disease in B6SJL-Tg (SOD1*G93A) mice. Clarification of the fine dynamics of the neurodegenerative process in these animals is of great importance for monitoring the course of the disease during preclinical trials of new drugs and methods of gene therapy
EXPERIENCE OF USING LAKOSAMID IN VARIOUS FORMS OF EPILEPSY (The results of observational study in city outpatient health care chain of Moscow)
This paper presents experience of using Vimpat in outpatient health care chain of Moscow. In the observational study were attended 49 patients with difficult for treatment focal forms of epilepsy (cryptogenic and symptomatic forms). Vimpat used in complex therapy in the mean effective dose of 300-400 mg per day. As a result, the data on a cohort of Russian patients showed that Vimpat demonstrate a sufficiently high clinical efficacy (55%, p<0.01) and appropriate for use in patients with difficult for treatment forms of epilepsy in complex therapy when the previous treatment was ineffective
EXPERIENCE OF PROLONGED VALPROATE USE IN ADULT PATIENTS WITH FOCAL FORMS OF EPILEPSY (RESULTS OF OBSERVATION HELD IN OUT-PATIENT CLINICS OF MOSCOW)
Results of Depakine Chronosphere use in Moscow city out-patient clinics are demonstrated in the article. 48 patients with focal forms of epilepsy (cryptogenic and symptomatic) were examined: 32 men and 16 women in age of 16 - 59 years with different duration of disease and different types of seizures. Depakine Chronosphere was indicated to patients who were already taking antiepileptic drugs in monotherapy with efficacy of 50% and more, and also to patients with drug remission, but with side effects, requiring changes of current indications. Results of the observation demonstrated high efficacy of Depakine Chronosphere in adult patients with different forms of focal epilepsy in monotherapy and also its use possibility in case of noneffective or poor tolerability of other valproates and carbamazepine