G(8344) mutation as the only manifestation of disease in a carrier of myoclonus epilepsy and ragged-red fibers (MERRF) syndrome. Am J Hum Genet. 1993r;52(3):551–6. PMID: 8447321","Мазунин И.О., Володько Н.В., Стариковская Е.Б., Сукерник Р.И. Митохондриальный геном и митохондриальные заболевания человека. Молекулярная биология. 2010;44(5):755–72.","Celentano V., Esposito E., Perrotta S., Giglio M.C., Tarquini R., Luglio G., et al. Madelung disease: report of a case and review of the literature. Acta Chir Belg. 2014;114(6):417–20. PMID: 26021689","Lemaitre M., Chevalier B., Jannin A., Bourry J., Espiard S., Vantyghem M.C. Multiple symmetric and multiple familial lipomatosis. Presse Med. 2021;50(3):104077. DOI: 10.1016/j.lpm.2021.104077","Вецмадян Е.А., Труфанов Г.Е., Рязанов В.В., Мостовая О.Т., Новиков К.В., Карайванов Н.С. Ультразвуковая диагностика липом мягких тканей с использованием методик цветного допплеровского картирования и эластографии. Вестник Российской Военно-медицинской академии. 2012;2(38):43–50.","Богов А.А., Андреев П.С., Филиппов В.Л., Топыркин В.Г. Оперативное лечение болезни Маделунга. Практическая медицина. 2018;16(7-1):90–3.","Уракова Е.В., Нестеров О.В., Ильина Р.Ю., Лексин Р.В. Хирургическая тактика при рецидивирующем липоматозе (болезни Маделунга). Клинический случай. Практическая медицина. 2022;20(6):131–3.","Егай А.А., Тентимишев А.Э., Норматов Р.М., Тян А.С. Хирургическое лечение множественного симметричного липоматоза (болезнь Маделунга), осложненного сдавлением яремных вен с обеих сторон. Преимущества липэктомии перед липосакцией. Научное обозрение. Медицинские науки. 2022;1:5– 10. DOI: 10.17513/srms.1225","Тимербулатов М.В., Шорнина А.С., Лихтер Р.А., Каипов А.Э. Оценка липосакции в структуре абдоминопластики и сочетанной герниоабдоминопластики. Креативная хирургия и онкология. 2023;13(4):278–83. DOI: 10.24060/2076-3093-2023-13-4-278-283","Dang Y., Du X., Ou X., Zheng Q., Xie F. Advances in diagnosis and treatment of Madelung’s deformity. Am J Transl Res. 2023;15(7):4416–24.","Leti Acciaro A, Garagnani L, Lando M, Lana D, Sartini S, Adani R. Modified dome osteotomy and anterior locking plate fixation for distal radius variant of Madelung deformity: a retrospective study. J Plast Surg Hand Surg. 2022;56(2):121–6. DOI: 10.1080/2000656X.2021.1934845","Liu Q., Lyu H., Xu B., Lee J.H. Madelung disease epidemiology and clinical characteristics: a systemic review. Aesthetic Plast Surg. 2021;45(3):977–86. DOI: 10.1007/s00266-020-02083-5","Sia K.J., Tang I.P., Tan T.Y. Multiple symmetrical lipomatosis: case report and literature review. J Laryngol Otol. 2012;126(7):756–8. DOI: 10.1017/S0022215112000709","Kratz C., Lenard H.G., Ruzicka T., Gärtner J. Multiple symmetric lipomatosis: an unusual cause of childhood obesity and mental retardation. Eur J Paediatr Neurol. 2000;4(2):63–7. DOI: 10.1053/ejpn.2000.0264","Nounla J., Rolle U., Gräfe G., Kräling K. Benign symmetric lipomatosis with myelomeningocele in an adolescent: An uncommon association-case report. J Pediatr Surg. 2001;36(7):E13. DOI: 10.1053/jpsu.2001.24776","Madelung O.W. Über den Fetthals (diffuses Lipom des Halses). Arch Klin Chir. 1888;37:106-30.","Lanois P.E., Bensaude R. De ladeno-lipomatosesymetrique. Bull Mem Soc Med Hosp. 1898;1:298.","El Ouahabi H., Doubi S., Lahlou K., Boujraf S., Ajdi F. Launois-bensaude syndrome: A benign symmetric lipomatosis without alcohol association. Ann Afr Med. 2017;16(1):33–4. DOI: 10.4103/1596-3519.202082","Chen C.Y., Fang Q.Q., Wang X.F., Zhang M.X., Zhao W.Y., Shi B.H., et al. Madelung’s disease: lipectomy or liposuction? Biomed Res Int. 2018;3975974. DOI: 10.1155/2018/3975974","Coker J.E., Bryan J.A. Endocrine and metabolic disorders: Causes and pathogenesis of obesity. J. Fam. Pract. 2008;4:21–6.","González-García R., Rodríguez-Campo F.J., Sastre-Pérez J., Muñoz-Guerra M.F. Benign symmetric lipomatosis (Madelung’s disease): case reports and current management. Aesthetic Plast Surg. 2004;28(2):108– 12; discussion 113. DOI: 10.1007/s00266-004-3123-5","Holme E., Larsson N.G., Oldfors A., Tulinius M., Sahlin P., Stenman G. Multiple symmetric lipomas with high levels of mtDNA with the tRNA(Lys) A-->G(8344) mutation as the only manifestation of disease in a carrier of myoclonus epilepsy and ragged-red fibers (MERRF) syndrome. Am J Hum Genet. 1993r;52(3):551–6. PMID: 8447321","Мазунин И.О., Володько Н.В., Стариковская Е.Б., Сукерник Р.И. Митохондриальный геном и митохондриальные заболевания человека. Молекулярная биология. 2010;44(5):755–72.","Celentano V., Esposito E., Perrotta S., Giglio M.C., Tarquini R., Luglio G., et al. Madelung disease: report of a case and review of the literature. Acta Chir Belg. 2014;114(6):417–20. PMID: 26021689","Lemaitre M., Chevalier B., Jannin A., Bourry J., Espiard S., Vantyghem M.C. Multiple symmetric and multiple familial lipomatosis. Presse Med. 2021;50(3):104077. DOI: 10.1016/j.lpm.2021.104077","Вецмадян Е.А., Труфанов Г.Е., Рязанов В.В., Мостовая О.Т., Новиков К.В., Карайванов Н.С. Ультразвуковая диагностика липом мягких тканей с использованием методик цветного допплеровского картирования и эластографии. Вестник Российской Военно-медицинской академии. 2012;2(38):43–50.","Богов А.А., Андреев П.С., Филиппов В.Л., Топыркин В.Г. Оперативное лечение болезни Маделунга. Практическая медицина. 2018;16(7-1):90–3.","Уракова Е.В., Нестеров О.В., Ильина Р.Ю., Лексин Р.В. Хирургическая тактика при рецидивирующем липоматозе (болезни Маделунга). Клинический случай. Практическая медицина. 2022;20(6):131–3.","Егай А.А., Тентимишев А.Э., Норматов Р.М., Тян А.С. Хирургическое лечение множественного симметричного липоматоза (болезнь Маделунга), осложненного сдавлением яремных вен с обеих сторон. Преимущества липэктомии перед липосакцией. Научное обозрение. Медицинские науки. 2022;1:5– 10. DOI: 10.17513/srms.1225","Тимербулатов М.В., Шорнина А.С., Лихтер Р.А., Каипов А.Э. Оценка липосакции в структуре абдоминопластики и сочетанной герниоабдоминопластики. Креативная хирургия и онкология. 2023;13(4):278–83. DOI: 10.24060/2076-3093-2023-13-4-278-283","Dang Y., Du X., Ou X., Zheng Q., Xie F. Advances in diagnosis and treatment of Madelung’s deformity. Am J Transl Res. 2023;15(7):4416–24.","Leti Acciaro A, Garagnani L, Lando M, Lana D, Sartini S, Adani R. Modified dome osteotomy and anterior locking plate fixation for distal radius variant of Madelung deformity: a retrospective study. J Plast Surg Hand Surg. 2022;56(2):121–6. DOI: 10.1080/2000656X.2021.1934845"],"dc.citation.ru":["Liu Q., Lyu H., Xu B., Lee J.H. Madelung disease epidemiology and clinical characteristics: a systemic review. Aesthetic Plast Surg. 2021;45(3):977–86. DOI: 10.1007/s00266-020-02083-5","Sia K.J., Tang I.P., Tan T.Y. Multiple symmetrical lipomatosis: case report and literature review. J Laryngol Otol. 2012;126(7):756–8. DOI: 10.1017/S0022215112000709","Kratz C., Lenard H.G., Ruzicka T., Gärtner J. Multiple symmetric lipomatosis: an unusual cause of childhood obesity and mental retardation. Eur J Paediatr Neurol. 2000;4(2):63–7. DOI: 10.1053/ejpn.2000.0264","Nounla J., Rolle U., Gräfe G., Kräling K. Benign symmetric lipomatosis with myelomeningocele in an adolescent: An uncommon association-case report. J Pediatr Surg. 2001;36(7):E13. DOI: 10.1053/jpsu.2001.24776","Madelung O.W. Über den Fetthals (diffuses Lipom des Halses). Arch Klin Chir. 1888;37:106-30.","Lanois P.E., Bensaude R. De ladeno-lipomatosesymetrique. Bull Mem Soc Med Hosp. 1898;1:298.","El Ouahabi H., Doubi S., Lahlou K., Boujraf S., Ajdi F. Launois-bensaude syndrome: A benign symmetric lipomatosis without alcohol association. Ann Afr Med. 2017;16(1):33–4. DOI: 10.4103/1596-3519.202082","Chen C.Y., Fang Q.Q., Wang X.F., Zhang M.X., Zhao W.Y., Shi B.H., et al. Madelung’s disease: lipectomy or liposuction? Biomed Res Int. 2018;3975974. DOI: 10.1155/2018/3975974","Coker J.E., Bryan J.A. Endocrine and metabolic disorders: Causes and pathogenesis of obesity. J. Fam. Pract. 2008;4:21–6.","González-García R., Rodríguez-Campo F.J., Sastre-Pérez J., Muñoz-Guerra M.F. Benign symmetric lipomatosis (Madelung’s disease): case reports and current management. Aesthetic Plast Surg. 2004;28(2):108– 12; discussion 113. DOI: 10.1007/s00266-004-3123-5","Holme E., Larsson N.G., Oldfors A., Tulinius M., Sahlin P., Stenman G. Multiple symmetric lipomas with high levels of mtDNA with the tRNA(Lys) A-->G(8344) mutation as the only manifestation of disease in a carrier of myoclonus epilepsy and ragged-red fibers (MERRF) syndrome. Am J Hum Genet. 1993r;52(3):551–6. PMID: 8447321","Мазунин И.О., Володько Н.В., Стариковская Е.Б., Сукерник Р.И. Митохондриальный геном и митохондриальные заболевания человека. Молекулярная биология. 2010;44(5):755–72.","Celentano V., Esposito E., Perrotta S., Giglio M.C., Tarquini R., Luglio G., et al. Madelung disease: report of a case and review of the literature. Acta Chir Belg. 2014;114(6):417–20. PMID: 26021689","Lemaitre M., Chevalier B., Jannin A., Bourry J., Espiard S., Vantyghem M.C. Multiple symmetric and multiple familial lipomatosis. Presse Med. 2021;50(3):104077. DOI: 10.1016/j.lpm.2021.104077","Вецмадян Е.А., Труфанов Г.Е., Рязанов В.В., Мостовая О.Т., Новиков К.В., Карайванов Н.С. Ультразвуковая диагностика липом мягких тканей с использованием методик цветного допплеровского картирования и эластографии. Вестник Российской Военно-медицинской академии. 2012;2(38):43–50.","Богов А.А., Андреев П.С., Филиппов В.Л., Топыркин В.Г. Оперативное лечение болезни Маделунга. Практическая медицина. 2018;16(7-1):90–3.","Уракова Е.В., Нестеров О.В., Ильина Р.Ю., Лексин Р.В. Хирургическая тактика при рецидивирующем липоматозе (болезни Маделунга). Клинический случай. Практическая медицина. 2022;20(6):131–3.","Егай А.А., Тентимишев А.Э., Норматов Р.М., Тян А.С. Хирургическое лечение множественного симметричного липоматоза (болезнь Маделунга), осложненного сдавлением яремных вен с обеих сторон. Преимущества липэктомии перед липосакцией. Научное обозрение. Медицинские науки. 2022;1:5– 10. DOI: 10.17513/srms.1225","Тимербулатов М.В., Шорнина А.С., Лихтер Р.А., Каипов А.Э. Оценка липосакции в структуре абдоминопластики и сочетанной герниоабдоминопластики. Креативная хирургия и онкология. 2023;13(4):278–83. DOI: 10.24060/2076-3093-2023-13-4-278-283","Dang Y., Du X., Ou X., Zheng Q., Xie F. Advances in diagnosis and treatment of Madelung’s deformity. Am J Transl Res. 2023;15(7):4416–24.","Leti Acciaro A, Garagnani L, Lando M, Lana D, Sartini S, Adani R. Modified dome osteotomy and anterior locking plate fixation for distal radius variant of Madelung deformity: a retrospective study. J Plast Surg Hand Surg. 2022;56(2):121–6. DOI: 10.1080/2000656X.2021.1934845"],"dc.citation.en":["Liu Q., Lyu H., Xu B., Lee J.H. Madelung disease epidemiology and clinical characteristics: a systemic review. Aesthetic Plast Surg. 2021;45(3):977–86. DOI: 10.1007/s00266-020-02083-5","Sia K.J., Tang I.P., Tan T.Y. Multiple symmetrical lipomatosis: case report and literature review. J Laryngol Otol. 2012;126(7):756–8. DOI: 10.1017/S0022215112000709","Kratz C., Lenard H.G., Ruzicka T., Gärtner J. Multiple symmetric lipomatosis: an unusual cause of childhood obesity and mental retardation. Eur J Paediatr Neurol. 2000;4(2):63–7. DOI: 10.1053/ejpn.2000.0264","Nounla J., Rolle U., Gräfe G., Kräling K. Benign symmetric lipomatosis with myelomeningocele in an adolescent: An uncommon association-case report. J Pediatr Surg. 2001;36(7):E13. 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DOI: 10.1007/s00266-004-3123-5","Holme E., Larsson N.G., Oldfors A., Tulinius M., Sahlin P., Stenman G. Multiple symmetric lipomas with high levels of mtDNA with the tRNA(Lys) A-->G(8344) mutation as the only manifestation of disease in a carrier of myoclonus epilepsy and ragged-red fibers (MERRF) syndrome. Am J Hum Genet. 1993r;52(3):551–6. PMID: 8447321","Мазунин И.О., Володько Н.В., Стариковская Е.Б., Сукерник Р.И. Митохондриальный геном и митохондриальные заболевания человека. Молекулярная биология. 2010;44(5):755–72.","Celentano V., Esposito E., Perrotta S., Giglio M.C., Tarquini R., Luglio G., et al. Madelung disease: report of a case and review of the literature. Acta Chir Belg. 2014;114(6):417–20. PMID: 26021689","Lemaitre M., Chevalier B., Jannin A., Bourry J., Espiard S., Vantyghem M.C. Multiple symmetric and multiple familial lipomatosis. Presse Med. 2021;50(3):104077. DOI: 10.1016/j.lpm.2021.104077","Вецмадян Е.А., Труфанов Г.Е., Рязанов В.В., Мостовая О.Т., Новиков К.В., Карайванов Н.С. Ультразвуковая диагностика липом мягких тканей с использованием методик цветного допплеровского картирования и эластографии. Вестник Российской Военно-медицинской академии. 2012;2(38):43–50.","Богов А.А., Андреев П.С., Филиппов В.Л., Топыркин В.Г. Оперативное лечение болезни Маделунга. Практическая медицина. 2018;16(7-1):90–3.","Уракова Е.В., Нестеров О.В., Ильина Р.Ю., Лексин Р.В. Хирургическая тактика при рецидивирующем липоматозе (болезни Маделунга). Клинический случай. Практическая медицина. 2022;20(6):131–3.","Егай А.А., Тентимишев А.Э., Норматов Р.М., Тян А.С. Хирургическое лечение множественного симметричного липоматоза (болезнь Маделунга), осложненного сдавлением яремных вен с обеих сторон. Преимущества липэктомии перед липосакцией. Научное обозрение. Медицинские науки. 2022;1:5– 10. 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irina\n|||\nRakhmatullina, Irina","bondarenko, igor\n|||\nBondarenko, Igor","colombo, nicoletta\n|||\nColombo, Nicoletta","svintsitskiy, valentyn\n|||\nSvintsitskiy, Valentyn","biela, luciano\n|||\nBiela, Luciano","nechaeva, marina\n|||\nNechaeva, Marina","lorusso, domenica\n|||\nLorusso, Domenica","scambia, giovanni\n|||\nScambia, Giovanni","cibula, david\n|||\nCibula, David","póka, róbert\n|||\nPóka, Róbert","oaknin, ana\n|||\nOaknin, Ana","safra, tamar\n|||\nSafra, Tamar","mackowiak-matejczyk, beata\n|||\nMackowiak-Matejczyk, Beata","ma, ling\n|||\nMa, Ling","thomas, daleen\n|||\nThomas, Daleen","lin, kevin k\n|||\nLin, Kevin K","mclachlan, karen\n|||\nMcLachlan, Karen","goble, sandra\n|||\nGoble, Sandra","kristeleit, rebecca\n|||\nKristeleit, Rebecca"],"author_filter":["oza, amit m\n|||\nOza, Amit M","lisyanskaya, alla\n|||\nLisyanskaya, Alla","fedenko, alexander\n|||\nFedenko, Alexander","de melo, andreia cristina\n|||\nde Melo, Andreia Cristina","shparyk, yaroslav\n|||\nShparyk, Yaroslav","rakhmatullina, irina\n|||\nRakhmatullina, Irina","bondarenko, igor\n|||\nBondarenko, Igor","colombo, nicoletta\n|||\nColombo, Nicoletta","svintsitskiy, valentyn\n|||\nSvintsitskiy, Valentyn","biela, luciano\n|||\nBiela, Luciano","nechaeva, marina\n|||\nNechaeva, Marina","lorusso, domenica\n|||\nLorusso, Domenica","scambia, giovanni\n|||\nScambia, Giovanni","cibula, david\n|||\nCibula, David","póka, róbert\n|||\nPóka, Róbert","oaknin, ana\n|||\nOaknin, Ana","safra, tamar\n|||\nSafra, Tamar","mackowiak-matejczyk, beata\n|||\nMackowiak-Matejczyk, Beata","ma, ling\n|||\nMa, Ling","thomas, daleen\n|||\nThomas, Daleen","lin, kevin k\n|||\nLin, Kevin K","mclachlan, karen\n|||\nMcLachlan, Karen","goble, sandra\n|||\nGoble, Sandra","kristeleit, rebecca\n|||\nKristeleit, Rebecca"],"dc.contributor.author_hl":["Oza, Amit M","Lisyanskaya, Alla","Fedenko, Alexander","de Melo, Andreia Cristina","Shparyk, Yaroslav","Rakhmatullina, Irina","Bondarenko, Igor","Colombo, Nicoletta","Svintsitskiy, Valentyn","Biela, Luciano","Nechaeva, Marina","Lorusso, Domenica","Scambia, Giovanni","Cibula, David","Póka, Róbert","Oaknin, Ana","Safra, Tamar","Mackowiak-Matejczyk, Beata","Ma, Ling","Thomas, Daleen","Lin, Kevin K","McLachlan, Karen","Goble, Sandra","Kristeleit, Rebecca"],"dc.contributor.author_mlt":["Oza, Amit M","Lisyanskaya, Alla","Fedenko, Alexander","de Melo, Andreia Cristina","Shparyk, Yaroslav","Rakhmatullina, Irina","Bondarenko, Igor","Colombo, Nicoletta","Svintsitskiy, Valentyn","Biela, Luciano","Nechaeva, Marina","Lorusso, Domenica","Scambia, Giovanni","Cibula, David","Póka, Róbert","Oaknin, Ana","Safra, Tamar","Mackowiak-Matejczyk, Beata","Ma, Ling","Thomas, Daleen","Lin, Kevin K","McLachlan, Karen","Goble, Sandra","Kristeleit, Rebecca"],"dc.contributor.author":["Oza, Amit M","Lisyanskaya, Alla","Fedenko, Alexander","de Melo, Andreia Cristina","Shparyk, Yaroslav","Rakhmatullina, Irina","Bondarenko, Igor","Colombo, Nicoletta","Svintsitskiy, Valentyn","Biela, Luciano","Nechaeva, Marina","Lorusso, Domenica","Scambia, Giovanni","Cibula, David","Póka, Róbert","Oaknin, Ana","Safra, Tamar","Mackowiak-Matejczyk, Beata","Ma, Ling","Thomas, Daleen","Lin, Kevin K","McLachlan, Karen","Goble, Sandra","Kristeleit, Rebecca"],"dc.contributor.author_stored":["Oza, Amit M\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Lisyanskaya, Alla\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Fedenko, Alexander\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","de Melo, Andreia Cristina\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Shparyk, Yaroslav\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Rakhmatullina, Irina\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Bondarenko, Igor\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Colombo, Nicoletta\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Svintsitskiy, Valentyn\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Biela, Luciano\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Nechaeva, Marina\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Lorusso, Domenica\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Scambia, Giovanni\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Cibula, David\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Póka, Róbert\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Oaknin, Ana\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Safra, Tamar\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Mackowiak-Matejczyk, Beata\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Ma, Ling\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Thomas, Daleen\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Lin, Kevin K\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","McLachlan, Karen\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Goble, Sandra\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Kristeleit, Rebecca\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.en":["Oza, Amit M","Lisyanskaya, Alla","Fedenko, Alexander","de Melo, Andreia Cristina","Shparyk, Yaroslav","Rakhmatullina, Irina","Bondarenko, Igor","Colombo, Nicoletta","Svintsitskiy, Valentyn","Biela, Luciano","Nechaeva, Marina","Lorusso, Domenica","Scambia, Giovanni","Cibula, David","Póka, Róbert","Oaknin, Ana","Safra, Tamar","Mackowiak-Matejczyk, Beata","Ma, Ling","Thomas, Daleen","Lin, Kevin K","McLachlan, Karen","Goble, Sandra","Kristeleit, Rebecca"],"dc.date.accessioned_dt":"2025-02-17T06:21:31Z","dc.date.accessioned":["2025-02-17T06:21:31Z"],"dc.date.available":["2025-02-17T06:21:31Z"],"dateIssued":["2025-01-01"],"dateIssued_keyword":["2025-01-01","2025"],"dateIssued_ac":["2025-01-01\n|||\n2025-01-01","2025"],"dateIssued.year":[2025],"dateIssued.year_sort":"2025","dc.date.issued_dt":"2025-01-01T00:00:00Z","dc.date.issued":["2025-01-01"],"dc.date.issued_stored":["2025-01-01\n|||\nnull\n|||\nnull\n|||\nnull\n|||\n"],"dc.description.abstract_hl":["Background: In the ARIEL4 trial of rucaparib versus standard-of-care chemotherapy in patients with relapsed BRCA-mutated ovarian carcinoma, the primary endpoint was met, showing improved investigator-assessed progression-free survival with rucaparib. Here, we present the final overall survival analysis of the trial and other post-progression outcomes. Methods: This open-label, randomised, controlled phase 3 trial was done at 64 hospitals and cancer centres in 12 countries, including Brazil, Canada, Czech Republic, Hungary, Israel, Italy, Poland, Russia, Spain, Ukraine, the UK, and the USA. Eligible patients were women aged 18 or older with BRCA1 or BRCA2-mutated ovarian carcinoma and had received at least two previous chemotherapy regimens. Patients had to have evaluable disease as per Response Evaluation Criteria in Solid Tumors (RECIST; version 1.1) criteria and an Eastern Cooperative Oncology Group performance status of 0 or 1. Patients were randomly assigned (2:1) using an interactive response technology and block randomisation (block size of six) and stratified by progression-free interval after the most recent platinum-containing therapy to receive oral rucaparib (600 mg twice daily administered in 28-day cycles) or chemotherapy on the basis of platinum-sensitivity status. In the chemotherapy group, patients with platinum-resistant disease (progression-free interval ≥1 to <6 months) or partially platinum-sensitive disease (progression-free interval ≥6 to <12 months) received weekly paclitaxel (starting dose 60–80 mg/m2 on days 1, 8, and 15). Patients with fully platinum-sensitive disease (progression-free interval ≥12 months) received the investigator's choice of platinum-based chemotherapy (single-agent cisplatin or carboplatin, or platinum-doublet chemotherapy), in 21-day or 28-day cycles. The primary endpoint (previously reported) was investigator-assessed progression-free survival, assessed in the efficacy population (all randomly assigned patients with deleterious BRCA1 or BRCA2 mutations without reversion mutations) and in the intention-to-treat population (all randomly assigned patients). Overall survival was a prespecified secondary endpoint and was analysed in the intention-to-treat population. Safety was assessed in all patients who received at least one dose of assigned study treatment. The cutoff date was April 10, 2022. This study is registered with ClinicalTrials.gov, NCT02855944; enrolment is complete and the study is closed. Findings: Between March 1, 2017, and Sept 24, 2020, 349 eligible patients were randomly assigned to receive rucaparib (n=233) or chemotherapy (n=116). 332 (95%) of 349 patients were white and 17 (5%) patients were other or of unknown race. In the chemotherapy group, 80 (69%) of 116 patients crossed over to receive rucaparib. Median follow-up was 41·2 months (IQR 37·8–44·6). At data cutoff for this final analysis (April 10, 2022), 244 (70%) of 349 patients had died: 167 (72%) of 233 in the rucaparib group and 77 (66%) of 116 in the rucaparib group. Median overall survival was 19·4 months (95% CI 15·2–23·6) in the rucaparib group versus 25·4 months (21·4–27·6) in the chemotherapy group (hazard ratio 1·3 [95% CI 1·0–1·7], p=0·047). No new safety signals were observed, including during crossover to rucaparib. The most common grade 3–4 adverse events across treatment groups included anaemia or decreased haemoglobin (reported in 59 [25%] of 232 patients in the rucaparib group and seven [6%] of 113 in the chemotherapy group), and neutropenia or decreased neutrophil count (in 26 [11%] of 232 in the rucaparib group and 16 [14%] of 113 patients in the chemotherapy group). Serious adverse events were reported in 66 (28%) of 232 patients in the rucaparib group and 14 (12%) of 113 patients in the chemotherapy group. Ten treatment-related deaths were reported in the rucaparib group, two of which were linked to judged to be related to rucaparib (cardiac disorder and myelodysplastic syndrome), and one death related to treatment was reported in the chemotherapy group, with no specific cause linked to the treatment. Interpretation: These data highlight the need for a better understanding of the most appropriate treatment for patients who have progressed on a poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, and the optimal sequencing of chemotherapy and PARP inhibitors in advanced ovarian cancer. Funding: Clovis Oncology. © 2025 Elsevier Ltd"],"dc.description.abstract":["Background: In the ARIEL4 trial of rucaparib versus standard-of-care chemotherapy in patients with relapsed BRCA-mutated ovarian carcinoma, the primary endpoint was met, showing improved investigator-assessed progression-free survival with rucaparib. Here, we present the final overall survival analysis of the trial and other post-progression outcomes. Methods: This open-label, randomised, controlled phase 3 trial was done at 64 hospitals and cancer centres in 12 countries, including Brazil, Canada, Czech Republic, Hungary, Israel, Italy, Poland, Russia, Spain, Ukraine, the UK, and the USA. Eligible patients were women aged 18 or older with BRCA1 or BRCA2-mutated ovarian carcinoma and had received at least two previous chemotherapy regimens. Patients had to have evaluable disease as per Response Evaluation Criteria in Solid Tumors (RECIST; version 1.1) criteria and an Eastern Cooperative Oncology Group performance status of 0 or 1. Patients were randomly assigned (2:1) using an interactive response technology and block randomisation (block size of six) and stratified by progression-free interval after the most recent platinum-containing therapy to receive oral rucaparib (600 mg twice daily administered in 28-day cycles) or chemotherapy on the basis of platinum-sensitivity status. In the chemotherapy group, patients with platinum-resistant disease (progression-free interval ≥1 to <6 months) or partially platinum-sensitive disease (progression-free interval ≥6 to <12 months) received weekly paclitaxel (starting dose 60–80 mg/m2 on days 1, 8, and 15). Patients with fully platinum-sensitive disease (progression-free interval ≥12 months) received the investigator's choice of platinum-based chemotherapy (single-agent cisplatin or carboplatin, or platinum-doublet chemotherapy), in 21-day or 28-day cycles. The primary endpoint (previously reported) was investigator-assessed progression-free survival, assessed in the efficacy population (all randomly assigned patients with deleterious BRCA1 or BRCA2 mutations without reversion mutations) and in the intention-to-treat population (all randomly assigned patients). Overall survival was a prespecified secondary endpoint and was analysed in the intention-to-treat population. Safety was assessed in all patients who received at least one dose of assigned study treatment. The cutoff date was April 10, 2022. This study is registered with ClinicalTrials.gov, NCT02855944; enrolment is complete and the study is closed. Findings: Between March 1, 2017, and Sept 24, 2020, 349 eligible patients were randomly assigned to receive rucaparib (n=233) or chemotherapy (n=116). 332 (95%) of 349 patients were white and 17 (5%) patients were other or of unknown race. In the chemotherapy group, 80 (69%) of 116 patients crossed over to receive rucaparib. Median follow-up was 41·2 months (IQR 37·8–44·6). At data cutoff for this final analysis (April 10, 2022), 244 (70%) of 349 patients had died: 167 (72%) of 233 in the rucaparib group and 77 (66%) of 116 in the rucaparib group. Median overall survival was 19·4 months (95% CI 15·2–23·6) in the rucaparib group versus 25·4 months (21·4–27·6) in the chemotherapy group (hazard ratio 1·3 [95% CI 1·0–1·7], p=0·047). No new safety signals were observed, including during crossover to rucaparib. The most common grade 3–4 adverse events across treatment groups included anaemia or decreased haemoglobin (reported in 59 [25%] of 232 patients in the rucaparib group and seven [6%] of 113 in the chemotherapy group), and neutropenia or decreased neutrophil count (in 26 [11%] of 232 in the rucaparib group and 16 [14%] of 113 patients in the chemotherapy group). Serious adverse events were reported in 66 (28%) of 232 patients in the rucaparib group and 14 (12%) of 113 patients in the chemotherapy group. Ten treatment-related deaths were reported in the rucaparib group, two of which were linked to judged to be related to rucaparib (cardiac disorder and myelodysplastic syndrome), and one death related to treatment was reported in the chemotherapy group, with no specific cause linked to the treatment. Interpretation: These data highlight the need for a better understanding of the most appropriate treatment for patients who have progressed on a poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, and the optimal sequencing of chemotherapy and PARP inhibitors in advanced ovarian cancer. Funding: Clovis Oncology. © 2025 Elsevier Ltd"],"dc.description.abstract.en":["Background: In the ARIEL4 trial of rucaparib versus standard-of-care chemotherapy in patients with relapsed BRCA-mutated ovarian carcinoma, the primary endpoint was met, showing improved investigator-assessed progression-free survival with rucaparib. Here, we present the final overall survival analysis of the trial and other post-progression outcomes. Methods: This open-label, randomised, controlled phase 3 trial was done at 64 hospitals and cancer centres in 12 countries, including Brazil, Canada, Czech Republic, Hungary, Israel, Italy, Poland, Russia, Spain, Ukraine, the UK, and the USA. Eligible patients were women aged 18 or older with BRCA1 or BRCA2-mutated ovarian carcinoma and had received at least two previous chemotherapy regimens. Patients had to have evaluable disease as per Response Evaluation Criteria in Solid Tumors (RECIST; version 1.1) criteria and an Eastern Cooperative Oncology Group performance status of 0 or 1. Patients were randomly assigned (2:1) using an interactive response technology and block randomisation (block size of six) and stratified by progression-free interval after the most recent platinum-containing therapy to receive oral rucaparib (600 mg twice daily administered in 28-day cycles) or chemotherapy on the basis of platinum-sensitivity status. In the chemotherapy group, patients with platinum-resistant disease (progression-free interval ≥1 to <6 months) or partially platinum-sensitive disease (progression-free interval ≥6 to <12 months) received weekly paclitaxel (starting dose 60–80 mg/m2 on days 1, 8, and 15). Patients with fully platinum-sensitive disease (progression-free interval ≥12 months) received the investigator's choice of platinum-based chemotherapy (single-agent cisplatin or carboplatin, or platinum-doublet chemotherapy), in 21-day or 28-day cycles. The primary endpoint (previously reported) was investigator-assessed progression-free survival, assessed in the efficacy population (all randomly assigned patients with deleterious BRCA1 or BRCA2 mutations without reversion mutations) and in the intention-to-treat population (all randomly assigned patients). Overall survival was a prespecified secondary endpoint and was analysed in the intention-to-treat population. Safety was assessed in all patients who received at least one dose of assigned study treatment. The cutoff date was April 10, 2022. This study is registered with ClinicalTrials.gov, NCT02855944; enrolment is complete and the study is closed. Findings: Between March 1, 2017, and Sept 24, 2020, 349 eligible patients were randomly assigned to receive rucaparib (n=233) or chemotherapy (n=116). 332 (95%) of 349 patients were white and 17 (5%) patients were other or of unknown race. In the chemotherapy group, 80 (69%) of 116 patients crossed over to receive rucaparib. Median follow-up was 41·2 months (IQR 37·8–44·6). At data cutoff for this final analysis (April 10, 2022), 244 (70%) of 349 patients had died: 167 (72%) of 233 in the rucaparib group and 77 (66%) of 116 in the rucaparib group. Median overall survival was 19·4 months (95% CI 15·2–23·6) in the rucaparib group versus 25·4 months (21·4–27·6) in the chemotherapy group (hazard ratio 1·3 [95% CI 1·0–1·7], p=0·047). No new safety signals were observed, including during crossover to rucaparib. The most common grade 3–4 adverse events across treatment groups included anaemia or decreased haemoglobin (reported in 59 [25%] of 232 patients in the rucaparib group and seven [6%] of 113 in the chemotherapy group), and neutropenia or decreased neutrophil count (in 26 [11%] of 232 in the rucaparib group and 16 [14%] of 113 patients in the chemotherapy group). Serious adverse events were reported in 66 (28%) of 232 patients in the rucaparib group and 14 (12%) of 113 patients in the chemotherapy group. Ten treatment-related deaths were reported in the rucaparib group, two of which were linked to judged to be related to rucaparib (cardiac disorder and myelodysplastic syndrome), and one death related to treatment was reported in the chemotherapy group, with no specific cause linked to the treatment. Interpretation: These data highlight the need for a better understanding of the most appropriate treatment for patients who have progressed on a poly(adenosine diphosphate-ribose) polymerase (PARP) inhibitor, and the optimal sequencing of chemotherapy and PARP inhibitors in advanced ovarian cancer. Funding: Clovis Oncology. © 2025 Elsevier Ltd"],"dc.doi":["10.1016/S1470-2045(24)00674-0"],"dc.doi.en":["10.1016/S1470-2045(24)00674-0"],"dc.identifier.issn":["1470-2045"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8680"],"dc.language.iso":["en"],"dc.language.iso.en":["en"],"dc.publisher":["Elsevier Ltd"],"dc.publisher.en":["Elsevier Ltd"],"dc.relation.ispartofseries":["The Lancet Oncology;т. 26 № 2"],"dc.relation.ispartofseries.en":["The Lancet Oncology;т. 26 № 2"],"subject":["Scopus"],"subject_keyword":["Scopus","Scopus"],"subject_ac":["scopus\n|||\nScopus"],"subject_tax_0_filter":["scopus\n|||\nScopus"],"subject_filter":["scopus\n|||\nScopus"],"dc.subject_mlt":["Scopus"],"dc.subject":["Scopus"],"dc.subject.en":["Scopus"],"title":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"title_keyword":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"title_ac":["rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious brca1 or brca2 mutation (ariel4): final results of an international, open-label, randomised, phase 3 trial\n|||\nRucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.title_sort":"Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial","dc.title_hl":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.title_mlt":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.title":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.title_stored":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.en":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.title.alternative":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.title.alternative.en":["Rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious BRCA1 or BRCA2 mutation (ARIEL4): final results of an international, open-label, randomised, phase 3 trial"],"dc.type":["Article"],"dc.type.en":["Article"],"publication_grp":["123456789/8680"],"bi_2_dis_filter":["biela, luciano\n|||\nBiela, Luciano","ma, ling\n|||\nMa, Ling","safra, tamar\n|||\nSafra, Tamar","mackowiak-matejczyk, beata\n|||\nMackowiak-Matejczyk, Beata","póka, róbert\n|||\nPóka, Róbert","bondarenko, igor\n|||\nBondarenko, Igor","colombo, nicoletta\n|||\nColombo, Nicoletta","nechaeva, marina\n|||\nNechaeva, Marina","oaknin, ana\n|||\nOaknin, Ana","thomas, daleen\n|||\nThomas, Daleen","mclachlan, karen\n|||\nMcLachlan, Karen","lorusso, domenica\n|||\nLorusso, Domenica","oza, amit m\n|||\nOza, Amit M","cibula, david\n|||\nCibula, David","fedenko, alexander\n|||\nFedenko, Alexander","de melo, andreia cristina\n|||\nde Melo, Andreia Cristina","lin, kevin k\n|||\nLin, Kevin K","rakhmatullina, irina\n|||\nRakhmatullina, Irina","shparyk, yaroslav\n|||\nShparyk, Yaroslav","lisyanskaya, alla\n|||\nLisyanskaya, Alla","kristeleit, rebecca\n|||\nKristeleit, Rebecca","goble, sandra\n|||\nGoble, Sandra","svintsitskiy, valentyn\n|||\nSvintsitskiy, Valentyn","scambia, giovanni\n|||\nScambia, Giovanni"],"bi_2_dis_partial":["Scambia, Giovanni","Póka, Róbert","Mackowiak-Matejczyk, Beata","Colombo, Nicoletta","Oaknin, Ana","Rakhmatullina, Irina","Fedenko, Alexander","Ma, Ling","Thomas, Daleen","McLachlan, Karen","Biela, Luciano","Lisyanskaya, Alla","Shparyk, Yaroslav","Oza, Amit M","Kristeleit, Rebecca","Goble, Sandra","Bondarenko, Igor","de Melo, Andreia Cristina","Svintsitskiy, Valentyn","Lin, Kevin K","Nechaeva, Marina","Cibula, David","Lorusso, Domenica","Safra, Tamar"],"bi_2_dis_value_filter":["Scambia, Giovanni","Póka, Róbert","Mackowiak-Matejczyk, Beata","Colombo, Nicoletta","Oaknin, Ana","Rakhmatullina, Irina","Fedenko, Alexander","Ma, Ling","Thomas, Daleen","McLachlan, Karen","Biela, Luciano","Lisyanskaya, Alla","Shparyk, Yaroslav","Oza, Amit M","Kristeleit, Rebecca","Goble, Sandra","Bondarenko, Igor","de Melo, Andreia Cristina","Svintsitskiy, Valentyn","Lin, Kevin K","Nechaeva, Marina","Cibula, David","Lorusso, Domenica","Safra, Tamar"],"bi_4_dis_filter":["scopus\n|||\nScopus"],"bi_4_dis_partial":["Scopus"],"bi_4_dis_value_filter":["Scopus"],"bi_sort_1_sort":"rucaparib versus chemotherapy for treatment of relapsed ovarian cancer with deleterious brca1 or brca2 mutation (ariel4): final results of an international, open-label, randomised, phase 3 trial","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-02-17T06:21:31Z","read":["g0"],"_version_":1824284598100557824},{"SolrIndexer.lastIndexed":"2025-05-06T07:40:26.772Z","search.uniqueid":"2-7926","search.resourcetype":2,"search.resourceid":7926,"handle":"123456789/8815","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","author":["Mustafin, R.N.","Khusnutdinova, E.K."],"author_keyword":["Mustafin, R.N.","Khusnutdinova, E.K."],"author_ac":["mustafin, r.n.\n|||\nMustafin, R.N.","khusnutdinova, e.k.\n|||\nKhusnutdinova, E.K."],"author_filter":["mustafin, r.n.\n|||\nMustafin, R.N.","khusnutdinova, e.k.\n|||\nKhusnutdinova, E.K."],"dc.contributor.author_hl":["Mustafin, R.N.","Khusnutdinova, E.K."],"dc.contributor.author_mlt":["Mustafin, R.N.","Khusnutdinova, E.K."],"dc.contributor.author":["Mustafin, R.N.","Khusnutdinova, E.K."],"dc.contributor.author_stored":["Mustafin, R.N.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Khusnutdinova, E.K.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.en":["Mustafin, R.N.","Khusnutdinova, E.K."],"dc.date.accessioned_dt":"2025-05-06T07:39:15Z","dc.date.accessioned":["2025-05-06T07:39:15Z"],"dc.date.available":["2025-05-06T07:39:15Z"],"dateIssued":["2025-01-01"],"dateIssued_keyword":["2025-01-01","2025"],"dateIssued_ac":["2025-01-01\n|||\n2025-01-01","2025"],"dateIssued.year":[2025],"dateIssued.year_sort":"2025","dc.date.issued_dt":"2025-01-01T00:00:00Z","dc.date.issued":["2025-01-01"],"dc.date.issued_stored":["2025-01-01\n|||\nnull\n|||\nnull\n|||\nnull\n|||\n"],"dc.description.abstract_hl":["Abstract: The conducted GWAS identified the association of osteoarthritis with more than 100 different SNPs, most of which are located in intronic and intergenic regions where genes encoding transposable elements and noncoding RNAs derived from them are located. A number of studies have also determined the activation of retroelements in joint tissues and in peripheral blood of patients with osteoarthritis. An assumption has been made that activated transposons, which cause aging and associated inflammation, influence the etiopathogenesis of osteoarthritis. To confirm this hypothesis, a search was conducted for data on changes in the expression of specific microRNAs derived from transposons during aging and osteoarthritis. As a result, 23 such microRNAs were found, the participation of which in the development of the disease is associated with an impact on genes and signaling pathways regulating cell proliferation and apoptosis, inflammatory and metabolic processes, and mechanisms of cartilage degradation. Changes in expression of these microRNAs indicate that the epigenetic mechanisms of aging are involved in osteoarthritis etiopathogenesis owing to pathological activation of transposable elements complementary to the sequences of noncoding RNAs derived from them in evolution. © Pleiades Publishing, Inc. 2025."],"dc.description.abstract":["Abstract: The conducted GWAS identified the association of osteoarthritis with more than 100 different SNPs, most of which are located in intronic and intergenic regions where genes encoding transposable elements and noncoding RNAs derived from them are located. A number of studies have also determined the activation of retroelements in joint tissues and in peripheral blood of patients with osteoarthritis. An assumption has been made that activated transposons, which cause aging and associated inflammation, influence the etiopathogenesis of osteoarthritis. To confirm this hypothesis, a search was conducted for data on changes in the expression of specific microRNAs derived from transposons during aging and osteoarthritis. As a result, 23 such microRNAs were found, the participation of which in the development of the disease is associated with an impact on genes and signaling pathways regulating cell proliferation and apoptosis, inflammatory and metabolic processes, and mechanisms of cartilage degradation. Changes in expression of these microRNAs indicate that the epigenetic mechanisms of aging are involved in osteoarthritis etiopathogenesis owing to pathological activation of transposable elements complementary to the sequences of noncoding RNAs derived from them in evolution. © Pleiades Publishing, Inc. 2025."],"dc.description.abstract.en":["Abstract: The conducted GWAS identified the association of osteoarthritis with more than 100 different SNPs, most of which are located in intronic and intergenic regions where genes encoding transposable elements and noncoding RNAs derived from them are located. A number of studies have also determined the activation of retroelements in joint tissues and in peripheral blood of patients with osteoarthritis. An assumption has been made that activated transposons, which cause aging and associated inflammation, influence the etiopathogenesis of osteoarthritis. To confirm this hypothesis, a search was conducted for data on changes in the expression of specific microRNAs derived from transposons during aging and osteoarthritis. As a result, 23 such microRNAs were found, the participation of which in the development of the disease is associated with an impact on genes and signaling pathways regulating cell proliferation and apoptosis, inflammatory and metabolic processes, and mechanisms of cartilage degradation. Changes in expression of these microRNAs indicate that the epigenetic mechanisms of aging are involved in osteoarthritis etiopathogenesis owing to pathological activation of transposable elements complementary to the sequences of noncoding RNAs derived from them in evolution. © Pleiades Publishing, Inc. 2025."],"dc.doi":["10.1134/S1022795424701357"],"dc.identifier.issn":["1022-7954"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8815"],"dc.language.iso":["en"],"dc.language.iso.en":["en"],"dc.publisher":["Pleiades Publishing"],"dc.publisher.en":["Pleiades Publishing"],"dc.relation.ispartofseries":["Russian Journal of Genetics;v. 61 № 1"],"dc.relation.ispartofseries.en":["Russian Journal of Genetics;v. 61 № 1"],"subject":["immune system","microRNA","osteoarthritis","retroelements","transposable elements","Scopus"],"subject_keyword":["immune system","immune system","microRNA","microRNA","osteoarthritis","osteoarthritis","retroelements","retroelements","transposable elements","transposable elements","Scopus","Scopus"],"subject_ac":["immune system\n|||\nimmune system","microrna\n|||\nmicroRNA","osteoarthritis\n|||\nosteoarthritis","retroelements\n|||\nretroelements","transposable elements\n|||\ntransposable elements","scopus\n|||\nScopus"],"subject_tax_0_filter":["immune system\n|||\nimmune system","microrna\n|||\nmicroRNA","osteoarthritis\n|||\nosteoarthritis","retroelements\n|||\nretroelements","transposable elements\n|||\ntransposable elements","scopus\n|||\nScopus"],"subject_filter":["immune system\n|||\nimmune system","microrna\n|||\nmicroRNA","osteoarthritis\n|||\nosteoarthritis","retroelements\n|||\nretroelements","transposable elements\n|||\ntransposable elements","scopus\n|||\nScopus"],"dc.subject_mlt":["immune system","microRNA","osteoarthritis","retroelements","transposable elements","Scopus"],"dc.subject":["immune system","microRNA","osteoarthritis","retroelements","transposable elements","Scopus"],"dc.subject.en":["immune system","microRNA","osteoarthritis","retroelements","transposable elements","Scopus"],"title":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"title_keyword":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"title_ac":["relationship of micrornas to transposons in osteoarthritis development\n|||\nRelationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.title_sort":"Relationship of MicroRNAs to Transposons in Osteoarthritis Development","dc.title_hl":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.title_mlt":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.title":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.title_stored":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.en":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.title.alternative":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.title.alternative.en":["Relationship of MicroRNAs to Transposons in Osteoarthritis Development"],"dc.type":["Article"],"dc.type.en":["Article"],"publication_grp":["123456789/8815"],"bi_2_dis_filter":["mustafin, r.n.\n|||\nMustafin, R.N.","khusnutdinova, e.k.\n|||\nKhusnutdinova, E.K."],"bi_2_dis_partial":["Khusnutdinova, E.K.","Mustafin, R.N."],"bi_2_dis_value_filter":["Khusnutdinova, E.K.","Mustafin, R.N."],"bi_4_dis_filter":["retroelements\n|||\nretroelements","osteoarthritis\n|||\nosteoarthritis","microrna\n|||\nmicroRNA","immune system\n|||\nimmune system","scopus\n|||\nScopus","transposable elements\n|||\ntransposable elements"],"bi_4_dis_partial":["retroelements","osteoarthritis","Scopus","immune system","microRNA","transposable elements"],"bi_4_dis_value_filter":["retroelements","osteoarthritis","Scopus","immune system","microRNA","transposable elements"],"bi_sort_1_sort":"relationship of micrornas to transposons in osteoarthritis development","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-05-06T07:39:15Z","read":["g0"],"_version_":1831356047587016704},{"SolrIndexer.lastIndexed":"2025-04-28T11:10:33.976Z","search.uniqueid":"2-7897","search.resourcetype":2,"search.resourceid":7897,"handle":"123456789/8786","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","dc.abstract":["Wegener’s granulomatosis (WG) or granulomatosis with polyangiitis is a primary systemic necrotizing vasculitis of small and medium-sized vessels with the development of foci of granulomatous inflammation. This is a severe, progressive, presumably autoimmune disease associated with antineutrophil cytoplasmic antibodies, which is detected mainly in people over 50 years of age. In the absence of timely treatment — immunosuppressive therapy (steroids and cytostatics to suppress disease activity, maintain remission and treat relapses), it can lead to the death of the patient. In the WG clinic, it begins with symptoms characteristic for respiratory infection, the lesions of the upper respiratory tract (rhinitis, nasopharyngitis, etc.), eyes, lungs (fibrosis, pleurisy, etc.) and kidneys (glomerulonephritis) prevail. One of the organs that are quite often (in about half of patients) affected by this disease, and, mainly, already in the early stages is the eye. With its defeat, in some cases, WG can even begin, but more and more often the eye is involved against the background of the development and long-term course of the inflammatory process of the upper respiratory tract and/or the first developed purulent inflammation of the middle ear in adult patients and nasal sinuses. In WG, any part of the eye can be affected, most often the anterior (most often scleritis, keratitis, less often — a corneal ulcer, etc.) and much less often — the posterior, and both in the form of a slight inflammation of the membranes of the eye to severe involvement of all its structures and orbit (pseudotumor) with the occurrence of low vision and even complete blindness. Difficulties in the diagnosis of WG usually arise due to the variety of forms and variants of the clinical course in the early stages of the disease, when ophthalmic changes are still of little specificity, and systemic ones are practically absent. Our clinical case of WG in a 62-year-old patient indicates that the diagnosis of this disease is far from simple and takes a very long period of time. Although the presence of episleritis/scleritis with a refractory course of the pathological process, especially if the patient had a history of bilateral purulent otitis media suffered by the patient and an infiltrate in the lungs, regarded, despite the biopsy during the first analysis, as a manifestation of atypical pneumonia, should already have alerted doctors to regarding the diagnosis of WG. Unfortunately, only severe dysphagia prompted the patient to be urgently hospitalized, to examine her as much as possible with a second revision of the previously taken lung biopsy material and to make the right decision in favor of the diagnosis of WG with the appointment of subsequent adequate treatment. © 2025, Real Time LLC. All rights reserved."],"dc.abstract.en":["Wegener’s granulomatosis (WG) or granulomatosis with polyangiitis is a primary systemic necrotizing vasculitis of small and medium-sized vessels with the development of foci of granulomatous inflammation. This is a severe, progressive, presumably autoimmune disease associated with antineutrophil cytoplasmic antibodies, which is detected mainly in people over 50 years of age. In the absence of timely treatment — immunosuppressive therapy (steroids and cytostatics to suppress disease activity, maintain remission and treat relapses), it can lead to the death of the patient. In the WG clinic, it begins with symptoms characteristic for respiratory infection, the lesions of the upper respiratory tract (rhinitis, nasopharyngitis, etc.), eyes, lungs (fibrosis, pleurisy, etc.) and kidneys (glomerulonephritis) prevail. One of the organs that are quite often (in about half of patients) affected by this disease, and, mainly, already in the early stages is the eye. With its defeat, in some cases, WG can even begin, but more and more often the eye is involved against the background of the development and long-term course of the inflammatory process of the upper respiratory tract and/or the first developed purulent inflammation of the middle ear in adult patients and nasal sinuses. In WG, any part of the eye can be affected, most often the anterior (most often scleritis, keratitis, less often — a corneal ulcer, etc.) and much less often — the posterior, and both in the form of a slight inflammation of the membranes of the eye to severe involvement of all its structures and orbit (pseudotumor) with the occurrence of low vision and even complete blindness. Difficulties in the diagnosis of WG usually arise due to the variety of forms and variants of the clinical course in the early stages of the disease, when ophthalmic changes are still of little specificity, and systemic ones are practically absent. Our clinical case of WG in a 62-year-old patient indicates that the diagnosis of this disease is far from simple and takes a very long period of time. Although the presence of episleritis/scleritis with a refractory course of the pathological process, especially if the patient had a history of bilateral purulent otitis media suffered by the patient and an infiltrate in the lungs, regarded, despite the biopsy during the first analysis, as a manifestation of atypical pneumonia, should already have alerted doctors to regarding the diagnosis of WG. Unfortunately, only severe dysphagia prompted the patient to be urgently hospitalized, to examine her as much as possible with a second revision of the previously taken lung biopsy material and to make the right decision in favor of the diagnosis of WG with the appointment of subsequent adequate treatment. © 2025, Real Time LLC. All rights reserved."],"author":["Bikbov, Mukharram M.","Babushkin, Alexander E.","Israfilova, Gulnara Z.","Бикбов, М.М.","Бабушкин, А.Э.","Исрафилова, Г.З."],"author_keyword":["Bikbov, Mukharram M.","Babushkin, Alexander E.","Israfilova, Gulnara Z.","Бикбов, М.М.","Бабушкин, А.Э.","Исрафилова, Г.З."],"author_ac":["bikbov, mukharram m.\n|||\nBikbov, Mukharram M.","babushkin, alexander e.\n|||\nBabushkin, Alexander E.","israfilova, gulnara z.\n|||\nIsrafilova, Gulnara Z.","бикбов, м.м.\n|||\nБикбов, М.М.","бабушкин, а.э.\n|||\nБабушкин, А.Э.","исрафилова, г.з.\n|||\nИсрафилова, Г.З."],"author_filter":["bikbov, mukharram m.\n|||\nBikbov, Mukharram M.","babushkin, alexander e.\n|||\nBabushkin, Alexander E.","israfilova, gulnara z.\n|||\nIsrafilova, Gulnara Z.","бикбов, м.м.\n|||\nБикбов, М.М.","бабушкин, а.э.\n|||\nБабушкин, А.Э.","исрафилова, г.з.\n|||\nИсрафилова, Г.З."],"dc.contributor.author_hl":["Bikbov, Mukharram M.","Babushkin, Alexander E.","Israfilova, Gulnara Z.","Бикбов, М.М.","Бабушкин, А.Э.","Исрафилова, Г.З."],"dc.contributor.author_mlt":["Bikbov, Mukharram M.","Babushkin, Alexander E.","Israfilova, Gulnara Z.","Бикбов, М.М.","Бабушкин, А.Э.","Исрафилова, Г.З."],"dc.contributor.author":["Bikbov, Mukharram M.","Babushkin, Alexander E.","Israfilova, Gulnara Z.","Бикбов, М.М.","Бабушкин, А.Э.","Исрафилова, Г.З."],"dc.contributor.author_stored":["Bikbov, Mukharram M.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Babushkin, Alexander E.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Israfilova, Gulnara Z.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Бикбов, М.М.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Бабушкин, А.Э.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Исрафилова, Г.З.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.contributor.author.en":["Bikbov, Mukharram M.","Babushkin, Alexander E.","Israfilova, Gulnara Z."],"dc.contributor.author.ru_RU":["Бикбов, М.М.","Бабушкин, А.Э.","Исрафилова, Г.З."],"dc.date.accessioned_dt":"2025-04-28T11:09:01Z","dc.date.accessioned":["2025-04-28T11:09:01Z"],"dc.date.available":["2025-04-28T11:09:01Z"],"dateIssued":["2025-01-01"],"dateIssued_keyword":["2025-01-01","2025"],"dateIssued_ac":["2025-01-01\n|||\n2025-01-01","2025"],"dateIssued.year":[2025],"dateIssued.year_sort":"2025","dc.date.issued_dt":"2025-01-01T00:00:00Z","dc.date.issued":["2025-01-01"],"dc.date.issued_stored":["2025-01-01\n|||\nnull\n|||\nnull\n|||\nnull\n|||\n"],"dc.description.abstract_hl":["ранулематоз Вегенера (ГВ), или гранулематоз с полиангиитом, представляет собой первичный системный некротизирующий\nваскулит сосудов мелкого и среднего калибра с развитием очагов гранулематозного воспаления. Это тяжелое, прогрессирующее,\nпредположительно аутоиммунное заболевание, ассоциированное с антинейтрофильными цитоплазматическими антителами,\nвыявляется в основном у людей старше 50 лет. При отсутствии своевременного лечения — иммуносупрессивной терапии (стеро-\nиды и цитостатики для подавления активности заболевания, поддержания ремиссии и лечения рецидивов) оно может привести\nк смерти пациента. В клинике ГВ начинается с симптомов, характерных для любой респираторной инфекции, превалирует\nпоражение верхних дыхательных путей (ринит, назофарингит и пр.), глаз, легких (фиброз, плеврит и т. д.) и почек (гломеруло-\nнефрит). Одним из органов, которые довольно часто (примерно у половины пациентов) поражаются при данном заболевании,\nпричем в основном уже на ранних стадиях, является глаз. С его поражения в ряде случаев может даже начинаться ГВ, но все же\nзначительно чаще орган зрения бывает задействован на фоне развития и длительного течения воспалительного процесса верхних\nдыхательных путей и/или впервые развившегося гнойного воспаления среднего уха у взрослых пациентов, носовых пазух. При ГВ\nможет поражаться любой отдел глаза, чаще всего передний (чаще всего склерит, кератит, реже — язва роговицы и пр.) и зна-\nчительно реже — задний, причем как в виде незначительного воспаления оболочек глаза, так и тяжелого вовлечения всех его\nструктур и орбиты (псевдотумор) с возникновением слабовидения и даже полной слепоты. Трудности в диагностике ГВ обычно\nвозникают из-за разнообразия форм и вариантов клинического течения на ранних стадиях заболевания, когда офтальмологиче-\nские изменения еще малоспецифичны, а системные практически отсутствуют. Приведенный клинический случай ГВ у 62-летней\nпациентки показывает, что диагностика данного заболевания происходит далеко не просто и занимает весьма длительный пе-\nриод времени. Хотя наличие эписклерита/склерита с рефрактерным течением патологического процесса, особенно при наличии в\nанамнезе двустороннего гнойного отита, перенесенного пациенткой, и инфильтрата в легких, расцененного, несмотря на биопсию\nпри первом анализе, как проявление нетипично протекающей пневмонии, уже должно было насторожить врачей в отношении\nдиагноза ГВ. К сожалению, только выраженная дисфагия побудила экстренно госпитализировать пациентку, максимально до-\nобследовать ее с повторным пересмотром ранее взятого биопсийного материала легких и принять правильное решение в пользу\nдиагноза ГВ с назначением последующего адекватного лечения."],"dc.description.abstract":["ранулематоз Вегенера (ГВ), или гранулематоз с полиангиитом, представляет собой первичный системный некротизирующий\nваскулит сосудов мелкого и среднего калибра с развитием очагов гранулематозного воспаления. Это тяжелое, прогрессирующее,\nпредположительно аутоиммунное заболевание, ассоциированное с антинейтрофильными цитоплазматическими антителами,\nвыявляется в основном у людей старше 50 лет. При отсутствии своевременного лечения — иммуносупрессивной терапии (стеро-\nиды и цитостатики для подавления активности заболевания, поддержания ремиссии и лечения рецидивов) оно может привести\nк смерти пациента. В клинике ГВ начинается с симптомов, характерных для любой респираторной инфекции, превалирует\nпоражение верхних дыхательных путей (ринит, назофарингит и пр.), глаз, легких (фиброз, плеврит и т. д.) и почек (гломеруло-\nнефрит). Одним из органов, которые довольно часто (примерно у половины пациентов) поражаются при данном заболевании,\nпричем в основном уже на ранних стадиях, является глаз. С его поражения в ряде случаев может даже начинаться ГВ, но все же\nзначительно чаще орган зрения бывает задействован на фоне развития и длительного течения воспалительного процесса верхних\nдыхательных путей и/или впервые развившегося гнойного воспаления среднего уха у взрослых пациентов, носовых пазух. При ГВ\nможет поражаться любой отдел глаза, чаще всего передний (чаще всего склерит, кератит, реже — язва роговицы и пр.) и зна-\nчительно реже — задний, причем как в виде незначительного воспаления оболочек глаза, так и тяжелого вовлечения всех его\nструктур и орбиты (псевдотумор) с возникновением слабовидения и даже полной слепоты. Трудности в диагностике ГВ обычно\nвозникают из-за разнообразия форм и вариантов клинического течения на ранних стадиях заболевания, когда офтальмологиче-\nские изменения еще малоспецифичны, а системные практически отсутствуют. Приведенный клинический случай ГВ у 62-летней\nпациентки показывает, что диагностика данного заболевания происходит далеко не просто и занимает весьма длительный пе-\nриод времени. Хотя наличие эписклерита/склерита с рефрактерным течением патологического процесса, особенно при наличии в\nанамнезе двустороннего гнойного отита, перенесенного пациенткой, и инфильтрата в легких, расцененного, несмотря на биопсию\nпри первом анализе, как проявление нетипично протекающей пневмонии, уже должно было насторожить врачей в отношении\nдиагноза ГВ. К сожалению, только выраженная дисфагия побудила экстренно госпитализировать пациентку, максимально до-\nобследовать ее с повторным пересмотром ранее взятого биопсийного материала легких и принять правильное решение в пользу\nдиагноза ГВ с назначением последующего адекватного лечения."],"dc.description.abstract.ru_RU":["ранулематоз Вегенера (ГВ), или гранулематоз с полиангиитом, представляет собой первичный системный некротизирующий\nваскулит сосудов мелкого и среднего калибра с развитием очагов гранулематозного воспаления. Это тяжелое, прогрессирующее,\nпредположительно аутоиммунное заболевание, ассоциированное с антинейтрофильными цитоплазматическими антителами,\nвыявляется в основном у людей старше 50 лет. При отсутствии своевременного лечения — иммуносупрессивной терапии (стеро-\nиды и цитостатики для подавления активности заболевания, поддержания ремиссии и лечения рецидивов) оно может привести\nк смерти пациента. В клинике ГВ начинается с симптомов, характерных для любой респираторной инфекции, превалирует\nпоражение верхних дыхательных путей (ринит, назофарингит и пр.), глаз, легких (фиброз, плеврит и т. д.) и почек (гломеруло-\nнефрит). Одним из органов, которые довольно часто (примерно у половины пациентов) поражаются при данном заболевании,\nпричем в основном уже на ранних стадиях, является глаз. С его поражения в ряде случаев может даже начинаться ГВ, но все же\nзначительно чаще орган зрения бывает задействован на фоне развития и длительного течения воспалительного процесса верхних\nдыхательных путей и/или впервые развившегося гнойного воспаления среднего уха у взрослых пациентов, носовых пазух. При ГВ\nможет поражаться любой отдел глаза, чаще всего передний (чаще всего склерит, кератит, реже — язва роговицы и пр.) и зна-\nчительно реже — задний, причем как в виде незначительного воспаления оболочек глаза, так и тяжелого вовлечения всех его\nструктур и орбиты (псевдотумор) с возникновением слабовидения и даже полной слепоты. Трудности в диагностике ГВ обычно\nвозникают из-за разнообразия форм и вариантов клинического течения на ранних стадиях заболевания, когда офтальмологиче-\nские изменения еще малоспецифичны, а системные практически отсутствуют. Приведенный клинический случай ГВ у 62-летней\nпациентки показывает, что диагностика данного заболевания происходит далеко не просто и занимает весьма длительный пе-\nриод времени. Хотя наличие эписклерита/склерита с рефрактерным течением патологического процесса, особенно при наличии в\nанамнезе двустороннего гнойного отита, перенесенного пациенткой, и инфильтрата в легких, расцененного, несмотря на биопсию\nпри первом анализе, как проявление нетипично протекающей пневмонии, уже должно было насторожить врачей в отношении\nдиагноза ГВ. К сожалению, только выраженная дисфагия побудила экстренно госпитализировать пациентку, максимально до-\nобследовать ее с повторным пересмотром ранее взятого биопсийного материала легких и принять правильное решение в пользу\nдиагноза ГВ с назначением последующего адекватного лечения."],"dc.doi":["10.21516/2072-0076-2025-18-1-114-120"],"dc.doi.en":["10.21516/2072-0076-2025-18-1-114-120"],"dc.identifier.issn":["2072-0076"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8786"],"dc.publisher":["Real Time LLC"],"dc.publisher.en":["Real Time LLC"],"dc.relation.ispartofseries":["Rossiiskii Oftal'mologicheskii Zhurnal;т. 18 № 1"],"dc.relation.ispartofseries.en":["Rossiiskii Oftal'mologicheskii Zhurnal;т. 18 № 1"],"subject":["гранулематоз Вегенера","гранулематоз с полиангиитом","некротизирующий васкулит","клинический случай","склерит","язва роговицы","clinical case","corneal ulcer","granulomatosis with polyangiitis","necrotizing vasculitis","scleritis","Wegener’s granulomatosis","Scopus"],"subject_keyword":["гранулематоз Вегенера","гранулематоз Вегенера","гранулематоз с полиангиитом","гранулематоз с полиангиитом","некротизирующий васкулит","некротизирующий васкулит","клинический случай","клинический случай","склерит","склерит","язва роговицы","язва роговицы","clinical case","clinical case","corneal ulcer","corneal ulcer","granulomatosis with polyangiitis","granulomatosis with polyangiitis","necrotizing vasculitis","necrotizing vasculitis","scleritis","scleritis","Wegener’s granulomatosis","Wegener’s granulomatosis","Scopus","Scopus"],"subject_ac":["гранулематоз вегенера\n|||\nгранулематоз Вегенера","гранулематоз с полиангиитом\n|||\nгранулематоз с полиангиитом","некротизирующий васкулит\n|||\nнекротизирующий васкулит","клинический случай\n|||\nклинический случай","склерит\n|||\nсклерит","язва роговицы\n|||\nязва роговицы","clinical case\n|||\nclinical case","corneal ulcer\n|||\ncorneal ulcer","granulomatosis with polyangiitis\n|||\ngranulomatosis with polyangiitis","necrotizing vasculitis\n|||\nnecrotizing vasculitis","scleritis\n|||\nscleritis","wegener’s granulomatosis\n|||\nWegener’s granulomatosis","scopus\n|||\nScopus"],"subject_tax_0_filter":["гранулематоз вегенера\n|||\nгранулематоз Вегенера","гранулематоз с полиангиитом\n|||\nгранулематоз с полиангиитом","некротизирующий васкулит\n|||\nнекротизирующий васкулит","клинический случай\n|||\nклинический случай","склерит\n|||\nсклерит","язва роговицы\n|||\nязва роговицы","clinical case\n|||\nclinical case","corneal ulcer\n|||\ncorneal ulcer","granulomatosis with polyangiitis\n|||\ngranulomatosis with polyangiitis","necrotizing vasculitis\n|||\nnecrotizing vasculitis","scleritis\n|||\nscleritis","wegener’s granulomatosis\n|||\nWegener’s granulomatosis","scopus\n|||\nScopus"],"subject_filter":["гранулематоз вегенера\n|||\nгранулематоз Вегенера","гранулематоз с полиангиитом\n|||\nгранулематоз с полиангиитом","некротизирующий васкулит\n|||\nнекротизирующий васкулит","клинический случай\n|||\nклинический случай","склерит\n|||\nсклерит","язва роговицы\n|||\nязва роговицы","clinical case\n|||\nclinical case","corneal ulcer\n|||\ncorneal ulcer","granulomatosis with polyangiitis\n|||\ngranulomatosis with polyangiitis","necrotizing vasculitis\n|||\nnecrotizing vasculitis","scleritis\n|||\nscleritis","wegener’s granulomatosis\n|||\nWegener’s granulomatosis","scopus\n|||\nScopus"],"dc.subject_mlt":["гранулематоз Вегенера","гранулематоз с полиангиитом","некротизирующий васкулит","клинический случай","склерит","язва роговицы","clinical case","corneal ulcer","granulomatosis with polyangiitis","necrotizing vasculitis","scleritis","Wegener’s granulomatosis","Scopus"],"dc.subject":["гранулематоз Вегенера","гранулематоз с полиангиитом","некротизирующий васкулит","клинический случай","склерит","язва роговицы","clinical case","corneal ulcer","granulomatosis with polyangiitis","necrotizing vasculitis","scleritis","Wegener’s granulomatosis","Scopus"],"dc.subject.ru_RU":["гранулематоз Вегенера","гранулематоз с полиангиитом","некротизирующий васкулит","клинический случай","склерит","язва роговицы"],"dc.subject.en":["clinical case","corneal ulcer","granulomatosis with polyangiitis","necrotizing vasculitis","scleritis","Wegener’s granulomatosis","Scopus"],"title":["Wegener’s granulomatosis in ophthalmic practice. Clinical case","Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"title_keyword":["Wegener’s granulomatosis in ophthalmic practice. Clinical case","Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"title_ac":["wegener’s granulomatosis in ophthalmic practice. clinical case\n|||\nWegener’s granulomatosis in ophthalmic practice. Clinical case","гранулематоз вегенера в офтальмологической практике. клинический случай\n|||\nГранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.title_sort":"Wegener’s granulomatosis in ophthalmic practice. Clinical case","dc.title_hl":["Wegener’s granulomatosis in ophthalmic practice. Clinical case","Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.title_mlt":["Wegener’s granulomatosis in ophthalmic practice. Clinical case","Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.title":["Wegener’s granulomatosis in ophthalmic practice. Clinical case","Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.title_stored":["Wegener’s granulomatosis in ophthalmic practice. Clinical case\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Гранулематоз Вегенера в офтальмологической практике. Клинический случай\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.title.en":["Wegener’s granulomatosis in ophthalmic practice. Clinical case"],"dc.title.ru_RU":["Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.title.alternative":["Wegener’s granulomatosis in ophthalmic practice. Clinical case","Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.title.alternative.en":["Wegener’s granulomatosis in ophthalmic practice. Clinical case"],"dc.title.alternative.ru_RU":["Гранулематоз Вегенера в офтальмологической практике. Клинический случай"],"dc.type":["Article"],"dc.type.ru_RU":["Article"],"publication_grp":["123456789/8786"],"bi_2_dis_filter":["исрафилова, г.з.\n|||\nИсрафилова, Г.З.","babushkin, alexander e.\n|||\nBabushkin, Alexander E.","bikbov, mukharram m.\n|||\nBikbov, Mukharram M.","israfilova, gulnara z.\n|||\nIsrafilova, Gulnara Z.","бикбов, м.м.\n|||\nБикбов, М.М.","бабушкин, а.э.\n|||\nБабушкин, А.Э."],"bi_2_dis_partial":["Бикбов, М.М.","Bikbov, Mukharram M.","Israfilova, Gulnara Z.","Бабушкин, А.Э.","Исрафилова, Г.З.","Babushkin, Alexander E."],"bi_2_dis_value_filter":["Бикбов, М.М.","Bikbov, Mukharram M.","Israfilova, Gulnara Z.","Бабушкин, А.Э.","Исрафилова, Г.З.","Babushkin, Alexander E."],"bi_4_dis_filter":["гранулематоз с полиангиитом\n|||\nгранулематоз с полиангиитом","granulomatosis with polyangiitis\n|||\ngranulomatosis with polyangiitis","clinical case\n|||\nclinical case","corneal ulcer\n|||\ncorneal ulcer","scopus\n|||\nScopus","scleritis\n|||\nscleritis","гранулематоз вегенера\n|||\nгранулематоз Вегенера","некротизирующий васкулит\n|||\nнекротизирующий васкулит","язва роговицы\n|||\nязва роговицы","necrotizing vasculitis\n|||\nnecrotizing vasculitis","wegener’s granulomatosis\n|||\nWegener’s granulomatosis","склерит\n|||\nсклерит","клинический случай\n|||\nклинический случай"],"bi_4_dis_partial":["язва роговицы","склерит","clinical case","Wegener’s granulomatosis","Scopus","corneal ulcer","гранулематоз Вегенера","granulomatosis with polyangiitis","некротизирующий васкулит","клинический случай","necrotizing vasculitis","гранулематоз с полиангиитом","scleritis"],"bi_4_dis_value_filter":["язва роговицы","склерит","clinical case","Wegener’s granulomatosis","Scopus","corneal ulcer","гранулематоз Вегенера","granulomatosis with polyangiitis","некротизирующий васкулит","клинический случай","necrotizing vasculitis","гранулематоз с полиангиитом","scleritis"],"bi_sort_1_sort":"wegener’s granulomatosis in ophthalmic practice. clinical case","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-04-28T11:09:01Z","read":["g0"],"_version_":1830644491467358208},{"SolrIndexer.lastIndexed":"2025-04-23T07:42:51.756Z","search.uniqueid":"2-7883","search.resourcetype":2,"search.resourceid":7883,"handle":"123456789/8773","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","author":["Mustafin, Rustam Nailevich"],"author_keyword":["Mustafin, Rustam Nailevich"],"author_ac":["mustafin, rustam nailevich\n|||\nMustafin, Rustam Nailevich"],"author_filter":["mustafin, rustam nailevich\n|||\nMustafin, Rustam Nailevich"],"dc.contributor.author_hl":["Mustafin, Rustam Nailevich"],"dc.contributor.author_mlt":["Mustafin, Rustam Nailevich"],"dc.contributor.author":["Mustafin, Rustam Nailevich"],"dc.contributor.author_stored":["Mustafin, Rustam Nailevich\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.en":["Mustafin, Rustam Nailevich"],"dc.date.accessioned_dt":"2025-04-23T07:41:34Z","dc.date.accessioned":["2025-04-23T07:41:34Z"],"dc.date.accessioned.en":["2025-04-23T07:41:34Z"],"dc.date.available":["2025-04-23T07:41:34Z"],"dateIssued":["2025-01-01"],"dateIssued_keyword":["2025-01-01","2025"],"dateIssued_ac":["2025-01-01\n|||\n2025-01-01","2025"],"dateIssued.year":[2025],"dateIssued.year_sort":"2025","dc.date.issued_dt":"2025-01-01T00:00:00Z","dc.date.issued":["2025-01-01"],"dc.date.issued_stored":["2025-01-01\n|||\nnull\n|||\nnull\n|||\nnull\n|||\n"],"dc.description.abstract_hl":["Frontotemporal dementia (FTD) develops in proteinopathies involving TDP-43 (transactive response DNA-binding protein 43 kDa), tau, and FUS (fused in sarcoma) proteins, which possess antiviral properties and exert inhibitory effects on human transposable elements. Viruses and aging have been suggested to trigger FTD by activating specific retroelements. FTD is associated with multiple single nucleotide polymorphisms (SNPs), most located in intergenic and regulatory regions where many transposable element genes are found. Therefore, genetic predisposition to FTD may influence the interaction between retroelements and the TDP-43, tau, and FUS proteins, causing pathological conformation changes and aggregate formation. Subsequently, these aggregates lose their ability to inhibit retroelements, leading to the activation of transposable elements. This creates a harmful negative feedback loop in which TDP-43, tau, and FUS protein expressions are further enhanced by retroelement transcripts and proteins, resulting in protein aggregate accumulation and pathological disease progression. Hence, epigenetic inhibition of pathologically activated retroelements using micro-ribonucleic acids (microRNAs) derived from transposable elements has been proposed as a potential treatment for FTD. Finally, a review of the current scientific literature identified 13 appropriate microRNAs (miR-1246, -181c, -330, -345-5p, -361, -548a-3p, -548b-5p, -548c-5p, -571, -588, -659-3p, -708-3p, -887). © 2025 The Author(s)."],"dc.description.abstract":["Frontotemporal dementia (FTD) develops in proteinopathies involving TDP-43 (transactive response DNA-binding protein 43 kDa), tau, and FUS (fused in sarcoma) proteins, which possess antiviral properties and exert inhibitory effects on human transposable elements. Viruses and aging have been suggested to trigger FTD by activating specific retroelements. FTD is associated with multiple single nucleotide polymorphisms (SNPs), most located in intergenic and regulatory regions where many transposable element genes are found. Therefore, genetic predisposition to FTD may influence the interaction between retroelements and the TDP-43, tau, and FUS proteins, causing pathological conformation changes and aggregate formation. Subsequently, these aggregates lose their ability to inhibit retroelements, leading to the activation of transposable elements. This creates a harmful negative feedback loop in which TDP-43, tau, and FUS protein expressions are further enhanced by retroelement transcripts and proteins, resulting in protein aggregate accumulation and pathological disease progression. Hence, epigenetic inhibition of pathologically activated retroelements using micro-ribonucleic acids (microRNAs) derived from transposable elements has been proposed as a potential treatment for FTD. Finally, a review of the current scientific literature identified 13 appropriate microRNAs (miR-1246, -181c, -330, -345-5p, -361, -548a-3p, -548b-5p, -548c-5p, -571, -588, -659-3p, -708-3p, -887). © 2025 The Author(s)."],"dc.description.abstract.en":["Frontotemporal dementia (FTD) develops in proteinopathies involving TDP-43 (transactive response DNA-binding protein 43 kDa), tau, and FUS (fused in sarcoma) proteins, which possess antiviral properties and exert inhibitory effects on human transposable elements. Viruses and aging have been suggested to trigger FTD by activating specific retroelements. FTD is associated with multiple single nucleotide polymorphisms (SNPs), most located in intergenic and regulatory regions where many transposable element genes are found. Therefore, genetic predisposition to FTD may influence the interaction between retroelements and the TDP-43, tau, and FUS proteins, causing pathological conformation changes and aggregate formation. Subsequently, these aggregates lose their ability to inhibit retroelements, leading to the activation of transposable elements. This creates a harmful negative feedback loop in which TDP-43, tau, and FUS protein expressions are further enhanced by retroelement transcripts and proteins, resulting in protein aggregate accumulation and pathological disease progression. Hence, epigenetic inhibition of pathologically activated retroelements using micro-ribonucleic acids (microRNAs) derived from transposable elements has been proposed as a potential treatment for FTD. Finally, a review of the current scientific literature identified 13 appropriate microRNAs (miR-1246, -181c, -330, -345-5p, -361, -548a-3p, -548b-5p, -548c-5p, -571, -588, -659-3p, -708-3p, -887). © 2025 The Author(s)."],"dc.doi":["10.31083/FBS25922"],"dc.identifier.issn":["1945-0516"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8773"],"dc.language.iso":["en"],"dc.language.iso.en":["en"],"dc.publisher":["IMR Press Limited"],"dc.publisher.en":["IMR Press Limited"],"dc.relation.ispartofseries":["Frontiers in Bioscience - Scholar;v. 17 № 1"],"dc.relation.ispartofseries.en":["Frontiers in Bioscience - Scholar;v. 17 № 1"],"subject":["aging","antiviral proteins","frontotemporal dementia (FTD)","microRNA","retroelements","viruses","Scopus"],"subject_keyword":["aging","aging","antiviral proteins","antiviral proteins","frontotemporal dementia (FTD)","frontotemporal dementia (FTD)","microRNA","microRNA","retroelements","retroelements","viruses","viruses","Scopus","Scopus"],"subject_ac":["aging\n|||\naging","antiviral proteins\n|||\nantiviral proteins","frontotemporal dementia (ftd)\n|||\nfrontotemporal dementia (FTD)","microrna\n|||\nmicroRNA","retroelements\n|||\nretroelements","viruses\n|||\nviruses","scopus\n|||\nScopus"],"subject_tax_0_filter":["aging\n|||\naging","antiviral proteins\n|||\nantiviral proteins","frontotemporal dementia (ftd)\n|||\nfrontotemporal dementia (FTD)","microrna\n|||\nmicroRNA","retroelements\n|||\nretroelements","viruses\n|||\nviruses","scopus\n|||\nScopus"],"subject_filter":["aging\n|||\naging","antiviral proteins\n|||\nantiviral proteins","frontotemporal dementia (ftd)\n|||\nfrontotemporal dementia (FTD)","microrna\n|||\nmicroRNA","retroelements\n|||\nretroelements","viruses\n|||\nviruses","scopus\n|||\nScopus"],"dc.subject_mlt":["aging","antiviral proteins","frontotemporal dementia (FTD)","microRNA","retroelements","viruses","Scopus"],"dc.subject":["aging","antiviral proteins","frontotemporal dementia (FTD)","microRNA","retroelements","viruses","Scopus"],"dc.subject.en":["aging","antiviral proteins","frontotemporal dementia (FTD)","microRNA","retroelements","viruses","Scopus"],"title":["Role of Retroelements in Frontotemporal Dementia Development"],"title_keyword":["Role of Retroelements in Frontotemporal Dementia Development"],"title_ac":["role of retroelements in frontotemporal dementia development\n|||\nRole of Retroelements in Frontotemporal Dementia Development"],"dc.title_sort":"Role of Retroelements in Frontotemporal Dementia Development","dc.title_hl":["Role of Retroelements in Frontotemporal Dementia Development"],"dc.title_mlt":["Role of Retroelements in Frontotemporal Dementia Development"],"dc.title":["Role of Retroelements in Frontotemporal Dementia Development"],"dc.title_stored":["Role of Retroelements in Frontotemporal Dementia Development\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.en":["Role of Retroelements in Frontotemporal Dementia Development"],"dc.title.alternative":["Role of Retroelements in Frontotemporal Dementia Development"],"dc.title.alternative.en":["Role of Retroelements in Frontotemporal Dementia Development"],"dc.type":["Article"],"dc.type.en":["Article"],"publication_grp":["123456789/8773"],"bi_2_dis_filter":["mustafin, rustam nailevich\n|||\nMustafin, Rustam Nailevich"],"bi_2_dis_partial":["Mustafin, Rustam Nailevich"],"bi_2_dis_value_filter":["Mustafin, Rustam Nailevich"],"bi_4_dis_filter":["frontotemporal dementia (ftd)\n|||\nfrontotemporal dementia (FTD)","retroelements\n|||\nretroelements","antiviral proteins\n|||\nantiviral proteins","aging\n|||\naging","microrna\n|||\nmicroRNA","scopus\n|||\nScopus","viruses\n|||\nviruses"],"bi_4_dis_partial":["viruses","retroelements","Scopus","frontotemporal dementia (FTD)","microRNA","aging","antiviral proteins"],"bi_4_dis_value_filter":["viruses","retroelements","Scopus","frontotemporal dementia (FTD)","microRNA","aging","antiviral proteins"],"bi_sort_1_sort":"role of retroelements in frontotemporal dementia development","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-04-23T07:41:34Z","read":["g0"],"_version_":1830178439054753792},{"SolrIndexer.lastIndexed":"2025-05-06T07:35:41.842Z","search.uniqueid":"2-7925","search.resourcetype":2,"search.resourceid":7925,"handle":"123456789/8814","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","author":["Erdman, V.V.","Karimov, D.D.","Tuktarova, I.A.","Petintseva, A.A.","Timasheva, Y.R.","Nasibullin, T.R."],"author_keyword":["Erdman, V.V.","Karimov, D.D.","Tuktarova, I.A.","Petintseva, A.A.","Timasheva, Y.R.","Nasibullin, T.R."],"author_ac":["erdman, v.v.\n|||\nErdman, V.V.","karimov, d.d.\n|||\nKarimov, D.D.","tuktarova, i.a.\n|||\nTuktarova, I.A.","petintseva, a.a.\n|||\nPetintseva, A.A.","timasheva, y.r.\n|||\nTimasheva, Y.R.","nasibullin, t.r.\n|||\nNasibullin, T.R."],"author_filter":["erdman, v.v.\n|||\nErdman, V.V.","karimov, d.d.\n|||\nKarimov, D.D.","tuktarova, i.a.\n|||\nTuktarova, I.A.","petintseva, a.a.\n|||\nPetintseva, A.A.","timasheva, y.r.\n|||\nTimasheva, Y.R.","nasibullin, t.r.\n|||\nNasibullin, T.R."],"dc.contributor.author_hl":["Erdman, V.V.","Karimov, D.D.","Tuktarova, I.A.","Petintseva, A.A.","Timasheva, Y.R.","Nasibullin, T.R."],"dc.contributor.author_mlt":["Erdman, V.V.","Karimov, D.D.","Tuktarova, I.A.","Petintseva, A.A.","Timasheva, Y.R.","Nasibullin, T.R."],"dc.contributor.author":["Erdman, V.V.","Karimov, D.D.","Tuktarova, I.A.","Petintseva, A.A.","Timasheva, Y.R.","Nasibullin, T.R."],"dc.contributor.author_stored":["Erdman, V.V.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Karimov, D.D.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Tuktarova, I.A.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Petintseva, A.A.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Timasheva, Y.R.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Nasibullin, T.R.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.en":["Erdman, V.V.","Karimov, D.D.","Tuktarova, I.A.","Petintseva, A.A.","Timasheva, Y.R.","Nasibullin, T.R."],"dc.date.accessioned_dt":"2025-05-06T07:34:22Z","dc.date.accessioned":["2025-05-06T07:34:22Z"],"dc.date.available":["2025-05-06T07:34:22Z"],"dateIssued":["2025-01-01"],"dateIssued_keyword":["2025-01-01","2025"],"dateIssued_ac":["2025-01-01\n|||\n2025-01-01","2025"],"dateIssued.year":[2025],"dateIssued.year_sort":"2025","dc.date.issued_dt":"2025-01-01T00:00:00Z","dc.date.issued":["2025-01-01"],"dc.date.issued_stored":["2025-01-01\n|||\nnull\n|||\nnull\n|||\nnull\n|||\n"],"dc.description.abstract_hl":["Abstract—: To assess the contribution to survival of Alu insertions in the ACE, PLAT, COL13A1, LAMA2, CDH4, SEMA6A, PKHD1L1, STK38L, HECW1, and TEAD1 genes, which are candidates of aging and longevity, amid the senile physiological and pathological phenotype, an analysis of association with life expectancy was carried out. Survival and mortality data were obtained for 1382 elderly people who were selected from the sample of Tatars residing in the Republic of Bashkortostan (total 1790 people from 18 to 109 years). Mortality risk was higher among carriers of the STK38L Alu-insertion genotype (Ya5ac2145*II, HR = 2.07, P = 0.022). Alu insertion in the HECW1 and TEAD1 genes has demonstrated a survival protection effect (Ya5NBC182*II, HR = 0.71, P = 0.038 and Ya5ac2013*II, HR = 0.74, P = 0.035 respectively). The survival amid the persons with various clinical phenotypes was associated with the Alu polymorphism of the SEMA6A (Yb8NBC597*ID, HR = 0.54, P = 0.016 for the cerebrovascular diseases), TEAD1 (Ya5ac2013*II, HR = 0.57, P = 0.016 for the cardiovascular pathologies), and LAMA2 (Ya5-MLS19*ID, HR = 0.36, P = 0.03 for multimorbidity status) genes. Thus, the genes involved in the regulation of autophagy and apoptosis were associated with survival and longevity. © Pleiades Publishing, Inc. 2025."],"dc.description.abstract":["Abstract—: To assess the contribution to survival of Alu insertions in the ACE, PLAT, COL13A1, LAMA2, CDH4, SEMA6A, PKHD1L1, STK38L, HECW1, and TEAD1 genes, which are candidates of aging and longevity, amid the senile physiological and pathological phenotype, an analysis of association with life expectancy was carried out. Survival and mortality data were obtained for 1382 elderly people who were selected from the sample of Tatars residing in the Republic of Bashkortostan (total 1790 people from 18 to 109 years). Mortality risk was higher among carriers of the STK38L Alu-insertion genotype (Ya5ac2145*II, HR = 2.07, P = 0.022). Alu insertion in the HECW1 and TEAD1 genes has demonstrated a survival protection effect (Ya5NBC182*II, HR = 0.71, P = 0.038 and Ya5ac2013*II, HR = 0.74, P = 0.035 respectively). The survival amid the persons with various clinical phenotypes was associated with the Alu polymorphism of the SEMA6A (Yb8NBC597*ID, HR = 0.54, P = 0.016 for the cerebrovascular diseases), TEAD1 (Ya5ac2013*II, HR = 0.57, P = 0.016 for the cardiovascular pathologies), and LAMA2 (Ya5-MLS19*ID, HR = 0.36, P = 0.03 for multimorbidity status) genes. Thus, the genes involved in the regulation of autophagy and apoptosis were associated with survival and longevity. © Pleiades Publishing, Inc. 2025."],"dc.description.abstract.en":["Abstract—: To assess the contribution to survival of Alu insertions in the ACE, PLAT, COL13A1, LAMA2, CDH4, SEMA6A, PKHD1L1, STK38L, HECW1, and TEAD1 genes, which are candidates of aging and longevity, amid the senile physiological and pathological phenotype, an analysis of association with life expectancy was carried out. Survival and mortality data were obtained for 1382 elderly people who were selected from the sample of Tatars residing in the Republic of Bashkortostan (total 1790 people from 18 to 109 years). Mortality risk was higher among carriers of the STK38L Alu-insertion genotype (Ya5ac2145*II, HR = 2.07, P = 0.022). Alu insertion in the HECW1 and TEAD1 genes has demonstrated a survival protection effect (Ya5NBC182*II, HR = 0.71, P = 0.038 and Ya5ac2013*II, HR = 0.74, P = 0.035 respectively). The survival amid the persons with various clinical phenotypes was associated with the Alu polymorphism of the SEMA6A (Yb8NBC597*ID, HR = 0.54, P = 0.016 for the cerebrovascular diseases), TEAD1 (Ya5ac2013*II, HR = 0.57, P = 0.016 for the cardiovascular pathologies), and LAMA2 (Ya5-MLS19*ID, HR = 0.36, P = 0.03 for multimorbidity status) genes. Thus, the genes involved in the regulation of autophagy and apoptosis were associated with survival and longevity. © Pleiades Publishing, Inc. 2025."],"dc.doi":["10.1134/S1022795424701448"],"dc.identifier.issn":["1022-7954"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8814"],"dc.language.iso":["en"],"dc.language.iso.en":["en"],"dc.publisher":["Pleiades Publishing"],"dc.publisher.en":["Pleiades Publishing"],"dc.relation.ispartofseries":["Russian Journal of Genetics;v. 61 № 1"],"dc.relation.ispartofseries.en":["Russian Journal of Genetics;v. 61 № 1"],"subject":["aging","Alu polymorphism","HECW1","LAMA2","longevity","SEMA6A genes","STK38L","survival analysis","TEAD1","Scopus"],"subject_keyword":["aging","aging","Alu polymorphism","Alu polymorphism","HECW1","HECW1","LAMA2","LAMA2","longevity","longevity","SEMA6A genes","SEMA6A genes","STK38L","STK38L","survival analysis","survival analysis","TEAD1","TEAD1","Scopus","Scopus"],"subject_ac":["aging\n|||\naging","alu polymorphism\n|||\nAlu polymorphism","hecw1\n|||\nHECW1","lama2\n|||\nLAMA2","longevity\n|||\nlongevity","sema6a genes\n|||\nSEMA6A genes","stk38l\n|||\nSTK38L","survival analysis\n|||\nsurvival analysis","tead1\n|||\nTEAD1","scopus\n|||\nScopus"],"subject_tax_0_filter":["aging\n|||\naging","alu polymorphism\n|||\nAlu polymorphism","hecw1\n|||\nHECW1","lama2\n|||\nLAMA2","longevity\n|||\nlongevity","sema6a genes\n|||\nSEMA6A genes","stk38l\n|||\nSTK38L","survival analysis\n|||\nsurvival analysis","tead1\n|||\nTEAD1","scopus\n|||\nScopus"],"subject_filter":["aging\n|||\naging","alu polymorphism\n|||\nAlu polymorphism","hecw1\n|||\nHECW1","lama2\n|||\nLAMA2","longevity\n|||\nlongevity","sema6a genes\n|||\nSEMA6A genes","stk38l\n|||\nSTK38L","survival analysis\n|||\nsurvival analysis","tead1\n|||\nTEAD1","scopus\n|||\nScopus"],"dc.subject_mlt":["aging","Alu polymorphism","HECW1","LAMA2","longevity","SEMA6A genes","STK38L","survival analysis","TEAD1","Scopus"],"dc.subject":["aging","Alu polymorphism","HECW1","LAMA2","longevity","SEMA6A genes","STK38L","survival analysis","TEAD1","Scopus"],"dc.subject.en":["aging","Alu polymorphism","HECW1","LAMA2","longevity","SEMA6A genes","STK38L","survival analysis","TEAD1","Scopus"],"title":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"title_keyword":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"title_ac":["alu polymorphisms of autophagy and apoptosis regulatory genes as human lifespan factors\n|||\nAlu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.title_sort":"Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors","dc.title_hl":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.title_mlt":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.title":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.title_stored":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.en":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.title.alternative":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.title.alternative.en":["Alu Polymorphisms of Autophagy and Apoptosis Regulatory Genes as Human Lifespan Factors"],"dc.type":["Article"],"dc.type.en":["Article"],"publication_grp":["123456789/8814"],"bi_2_dis_filter":["petintseva, a.a.\n|||\nPetintseva, A.A.","nasibullin, t.r.\n|||\nNasibullin, T.R.","erdman, v.v.\n|||\nErdman, V.V.","karimov, d.d.\n|||\nKarimov, D.D.","timasheva, y.r.\n|||\nTimasheva, Y.R.","tuktarova, i.a.\n|||\nTuktarova, I.A."],"bi_2_dis_partial":["Nasibullin, T.R.","Karimov, D.D.","Erdman, V.V.","Tuktarova, I.A.","Timasheva, Y.R.","Petintseva, A.A."],"bi_2_dis_value_filter":["Nasibullin, T.R.","Karimov, D.D.","Erdman, V.V.","Tuktarova, I.A.","Timasheva, Y.R.","Petintseva, A.A."],"bi_4_dis_filter":["longevity\n|||\nlongevity","survival analysis\n|||\nsurvival analysis","hecw1\n|||\nHECW1","aging\n|||\naging","alu polymorphism\n|||\nAlu polymorphism","sema6a genes\n|||\nSEMA6A genes","tead1\n|||\nTEAD1","stk38l\n|||\nSTK38L","scopus\n|||\nScopus","lama2\n|||\nLAMA2"],"bi_4_dis_partial":["SEMA6A genes","LAMA2","survival analysis","Scopus","HECW1","Alu polymorphism","longevity","STK38L","aging","TEAD1"],"bi_4_dis_value_filter":["SEMA6A genes","LAMA2","survival analysis","Scopus","HECW1","Alu polymorphism","longevity","STK38L","aging","TEAD1"],"bi_sort_1_sort":"alu polymorphisms of autophagy and apoptosis regulatory genes as human lifespan factors","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-05-06T07:34:22Z","read":["g0"],"_version_":1831355748817305600},{"SolrIndexer.lastIndexed":"2025-04-30T09:30:35.678Z","search.uniqueid":"2-7908","search.resourcetype":2,"search.resourceid":7908,"handle":"123456789/8797","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","dc.abstract":["Treatment of patients with aggressive multiple sclerosis (MS) characterized by severe progression of disability within a short period of time is a complex task as there are no uniform criteria for determining such disease progression type and, accordingly, no optimal strategies for prescribing medication. Standardised criteria are also needed to assess prevalence in the general patient population and to plan medical and social care. Objective: to analyse clinical and demographic characteristics of patients with aggressive MS in the Republic of Bashkortostan (RB). Material and methods. The study included 2670 patients registered in the Multiple Sclerosis Centre of the Republic of Bashkortostan. To determine the types of MS progression, criteria of the 2022 clinical guidelines for MS were used. When analysing the data on disability, the data from the control group, which consisted of MS patients without limitations in working capacity and disability, were also used. Results. Rapidly progressive MS (RPMS) and highly active MS (HAMS) were diagnosed in 8.9% of the total number of patients. Women predominated in both groups. In the group of patients with aggressive MS, the progression rate was significantly higher than in the HAMS group. Six percent of patients included in the registry became disabled (group II or I) within 5 years of the disease, and 10% within 10 years. These groups are characterized by a high rate of disease progression. Conclusion. In the RB, RPMS and HAMS were diagnosed in 8.9% of patients, with a predominance of women. © 2025 Ima-Press Publishing House. All rights reserved."],"dc.abstract.en":["Treatment of patients with aggressive multiple sclerosis (MS) characterized by severe progression of disability within a short period of time is a complex task as there are no uniform criteria for determining such disease progression type and, accordingly, no optimal strategies for prescribing medication. Standardised criteria are also needed to assess prevalence in the general patient population and to plan medical and social care. Objective: to analyse clinical and demographic characteristics of patients with aggressive MS in the Republic of Bashkortostan (RB). Material and methods. The study included 2670 patients registered in the Multiple Sclerosis Centre of the Republic of Bashkortostan. To determine the types of MS progression, criteria of the 2022 clinical guidelines for MS were used. When analysing the data on disability, the data from the control group, which consisted of MS patients without limitations in working capacity and disability, were also used. Results. Rapidly progressive MS (RPMS) and highly active MS (HAMS) were diagnosed in 8.9% of the total number of patients. Women predominated in both groups. In the group of patients with aggressive MS, the progression rate was significantly higher than in the HAMS group. Six percent of patients included in the registry became disabled (group II or I) within 5 years of the disease, and 10% within 10 years. These groups are characterized by a high rate of disease progression. Conclusion. In the RB, RPMS and HAMS were diagnosed in 8.9% of patients, with a predominance of women. © 2025 Ima-Press Publishing House. All rights reserved."],"author":["Bakhtiyarova, K.Z.","Kuzmina, U.Sh.","Lyutov, O.V.","Talipova, I.D.","Akhmetgaleeva, N.F.","Galiullin, T.R.","Kutlubaev, M.A.","Бахтиярова, К.З.","Кузьмина, У.Ш.","Лютов, О.В.","Талипова, И.Д.","Ахметгалеева, Н.Ф.","Галиуллин, Т.Р.","Кутлубаев, М.А."],"author_keyword":["Bakhtiyarova, K.Z.","Kuzmina, U.Sh.","Lyutov, O.V.","Talipova, I.D.","Akhmetgaleeva, N.F.","Galiullin, T.R.","Kutlubaev, M.A.","Бахтиярова, К.З.","Кузьмина, У.Ш.","Лютов, О.В.","Талипова, И.Д.","Ахметгалеева, Н.Ф.","Галиуллин, Т.Р.","Кутлубаев, М.А."],"author_ac":["bakhtiyarova, k.z.\n|||\nBakhtiyarova, K.Z.","kuzmina, u.sh.\n|||\nKuzmina, U.Sh.","lyutov, o.v.\n|||\nLyutov, O.V.","talipova, i.d.\n|||\nTalipova, I.D.","akhmetgaleeva, n.f.\n|||\nAkhmetgaleeva, N.F.","galiullin, t.r.\n|||\nGaliullin, T.R.","kutlubaev, m.a.\n|||\nKutlubaev, M.A.","бахтиярова, к.з.\n|||\nБахтиярова, К.З.","кузьмина, у.ш.\n|||\nКузьмина, У.Ш.","лютов, о.в.\n|||\nЛютов, О.В.","талипова, и.д.\n|||\nТалипова, И.Д.","ахметгалеева, н.ф.\n|||\nАхметгалеева, Н.Ф.","галиуллин, т.р.\n|||\nГалиуллин, Т.Р.","кутлубаев, м.а.\n|||\nКутлубаев, М.А."],"author_filter":["bakhtiyarova, k.z.\n|||\nBakhtiyarova, K.Z.","kuzmina, u.sh.\n|||\nKuzmina, U.Sh.","lyutov, o.v.\n|||\nLyutov, O.V.","talipova, i.d.\n|||\nTalipova, I.D.","akhmetgaleeva, n.f.\n|||\nAkhmetgaleeva, N.F.","galiullin, t.r.\n|||\nGaliullin, T.R.","kutlubaev, m.a.\n|||\nKutlubaev, M.A.","бахтиярова, к.з.\n|||\nБахтиярова, К.З.","кузьмина, у.ш.\n|||\nКузьмина, У.Ш.","лютов, о.в.\n|||\nЛютов, О.В.","талипова, и.д.\n|||\nТалипова, И.Д.","ахметгалеева, н.ф.\n|||\nАхметгалеева, Н.Ф.","галиуллин, т.р.\n|||\nГалиуллин, Т.Р.","кутлубаев, м.а.\n|||\nКутлубаев, М.А."],"dc.contributor.author_hl":["Bakhtiyarova, K.Z.","Kuzmina, U.Sh.","Lyutov, O.V.","Talipova, I.D.","Akhmetgaleeva, N.F.","Galiullin, T.R.","Kutlubaev, M.A.","Бахтиярова, К.З.","Кузьмина, У.Ш.","Лютов, О.В.","Талипова, И.Д.","Ахметгалеева, Н.Ф.","Галиуллин, Т.Р.","Кутлубаев, М.А."],"dc.contributor.author_mlt":["Bakhtiyarova, K.Z.","Kuzmina, U.Sh.","Lyutov, O.V.","Talipova, I.D.","Akhmetgaleeva, N.F.","Galiullin, T.R.","Kutlubaev, M.A.","Бахтиярова, К.З.","Кузьмина, У.Ш.","Лютов, О.В.","Талипова, И.Д.","Ахметгалеева, Н.Ф.","Галиуллин, Т.Р.","Кутлубаев, М.А."],"dc.contributor.author":["Bakhtiyarova, K.Z.","Kuzmina, U.Sh.","Lyutov, O.V.","Talipova, I.D.","Akhmetgaleeva, N.F.","Galiullin, T.R.","Kutlubaev, M.A.","Бахтиярова, К.З.","Кузьмина, У.Ш.","Лютов, О.В.","Талипова, И.Д.","Ахметгалеева, Н.Ф.","Галиуллин, Т.Р.","Кутлубаев, М.А."],"dc.contributor.author_stored":["Bakhtiyarova, K.Z.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Kuzmina, U.Sh.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Lyutov, O.V.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Talipova, I.D.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Akhmetgaleeva, N.F.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Galiullin, T.R.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Kutlubaev, M.A.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Бахтиярова, К.З.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Кузьмина, У.Ш.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Лютов, О.В.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Талипова, И.Д.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Ахметгалеева, Н.Ф.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Галиуллин, Т.Р.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Кутлубаев, М.А.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.contributor.author.en":["Bakhtiyarova, K.Z.","Kuzmina, U.Sh.","Lyutov, O.V.","Talipova, I.D.","Akhmetgaleeva, N.F.","Galiullin, T.R.","Kutlubaev, M.A."],"dc.contributor.author.ru_RU":["Бахтиярова, К.З.","Кузьмина, У.Ш.","Лютов, О.В.","Талипова, И.Д.","Ахметгалеева, Н.Ф.","Галиуллин, Т.Р.","Кутлубаев, М.А."],"dc.date.accessioned_dt":"2025-04-30T09:28:59Z","dc.date.accessioned":["2025-04-30T09:28:59Z"],"dc.date.available":["2025-04-30T09:28:59Z"],"dateIssued":["2025-01-01"],"dateIssued_keyword":["2025-01-01","2025"],"dateIssued_ac":["2025-01-01\n|||\n2025-01-01","2025"],"dateIssued.year":[2025],"dateIssued.year_sort":"2025","dc.date.issued_dt":"2025-01-01T00:00:00Z","dc.date.issued":["2025-01-01"],"dc.date.issued_stored":["2025-01-01\n|||\nnull\n|||\nnull\n|||\nnull\n|||\n"],"dc.description.abstract_hl":["Лечение больных с агрессивным рассеянным склерозом (РС), характеризующимся резким прогрессированием инвалидности в течение короткого периода времени, представляется сложной задачей в связи с отсутствием единых критериев для установления данного типа течения заболевания и, соответственно, оптимальных стратегий для назначения препаратов. Единые критерии требуются также для оценки его распространенности в общей популяции больных и планирования медико-социальной помощи.\nЦель исследования – анализ клинико-демографических характеристик пациентов с агрессивным РС в Республике Башкортостан (РБ).\nМатериал и методы. В исследование было включено 2670 больных, состоящих на учете в Центре рассеянного склероза РБ. Для определения типов течения РС использовали критерии из Клинических рекомендаций по РС за 2022 г. При анализе данных о нетрудоспособности использовали также данные контрольной группы, которую составили пациенты с РС, не имеющие ограничений трудоспособности и группы инвалидности.\nРезультаты. Быстропрогрессирующий РС (БПРС) и высокоактивный РС (ВАРС) диагностирован у 8,9% от общего числа пациентов. В обеих группах преобладают женщины. В группе больных с агрессивным РС скорость прогрессирования значимо выше, чем\nв группе ВАРС. Инвалидами II или I группы за 5 лет заболевания стали 6% пациентов, включенных в регистр, а за 10 лет – 10%.\nДля данных групп характерна большая скорость прогрессирования заболевания.\nЗаключение. В РБ БПРС и ВАРС диагностированы у 8,9% пациентов с преобладанием у женщин."],"dc.description.abstract":["Лечение больных с агрессивным рассеянным склерозом (РС), характеризующимся резким прогрессированием инвалидности в течение короткого периода времени, представляется сложной задачей в связи с отсутствием единых критериев для установления данного типа течения заболевания и, соответственно, оптимальных стратегий для назначения препаратов. Единые критерии требуются также для оценки его распространенности в общей популяции больных и планирования медико-социальной помощи.\nЦель исследования – анализ клинико-демографических характеристик пациентов с агрессивным РС в Республике Башкортостан (РБ).\nМатериал и методы. В исследование было включено 2670 больных, состоящих на учете в Центре рассеянного склероза РБ. Для определения типов течения РС использовали критерии из Клинических рекомендаций по РС за 2022 г. При анализе данных о нетрудоспособности использовали также данные контрольной группы, которую составили пациенты с РС, не имеющие ограничений трудоспособности и группы инвалидности.\nРезультаты. Быстропрогрессирующий РС (БПРС) и высокоактивный РС (ВАРС) диагностирован у 8,9% от общего числа пациентов. В обеих группах преобладают женщины. В группе больных с агрессивным РС скорость прогрессирования значимо выше, чем\nв группе ВАРС. Инвалидами II или I группы за 5 лет заболевания стали 6% пациентов, включенных в регистр, а за 10 лет – 10%.\nДля данных групп характерна большая скорость прогрессирования заболевания.\nЗаключение. В РБ БПРС и ВАРС диагностированы у 8,9% пациентов с преобладанием у женщин."],"dc.description.abstract.ru_RU":["Лечение больных с агрессивным рассеянным склерозом (РС), характеризующимся резким прогрессированием инвалидности в течение короткого периода времени, представляется сложной задачей в связи с отсутствием единых критериев для установления данного типа течения заболевания и, соответственно, оптимальных стратегий для назначения препаратов. Единые критерии требуются также для оценки его распространенности в общей популяции больных и планирования медико-социальной помощи.\nЦель исследования – анализ клинико-демографических характеристик пациентов с агрессивным РС в Республике Башкортостан (РБ).\nМатериал и методы. В исследование было включено 2670 больных, состоящих на учете в Центре рассеянного склероза РБ. Для определения типов течения РС использовали критерии из Клинических рекомендаций по РС за 2022 г. При анализе данных о нетрудоспособности использовали также данные контрольной группы, которую составили пациенты с РС, не имеющие ограничений трудоспособности и группы инвалидности.\nРезультаты. Быстропрогрессирующий РС (БПРС) и высокоактивный РС (ВАРС) диагностирован у 8,9% от общего числа пациентов. В обеих группах преобладают женщины. В группе больных с агрессивным РС скорость прогрессирования значимо выше, чем\nв группе ВАРС. Инвалидами II или I группы за 5 лет заболевания стали 6% пациентов, включенных в регистр, а за 10 лет – 10%.\nДля данных групп характерна большая скорость прогрессирования заболевания.\nЗаключение. В РБ БПРС и ВАРС диагностированы у 8,9% пациентов с преобладанием у женщин."],"dc.doi":["10.14412/2074-2711-2025-1-10-15"],"dc.doi.en":["10.14412/2074-2711-2025-1-10-15"],"dc.identifier.issn":["1995-4484"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8797"],"dc.publisher":["Ima-Press Publishing House"],"dc.publisher.en":["Ima-Press Publishing House"],"dc.relation.ispartofseries":["Nauchno-Prakticheskaya Revmatologiya;т. 17 № 1"],"dc.relation.ispartofseries.en":["Nauchno-Prakticheskaya Revmatologiya;т. 17 № 1"],"subject":["рассеянный склероз","агрессивный рассеянный склероз","высокоактивный рассеянный склероз","инвалидность","Scopus","aggressive multiple sclerosis","disability","highly active multiple sclerosis","multiple sclerosis"],"subject_keyword":["рассеянный склероз","рассеянный склероз","агрессивный рассеянный склероз","агрессивный рассеянный склероз","высокоактивный рассеянный склероз","высокоактивный рассеянный склероз","инвалидность","инвалидность","Scopus","Scopus","aggressive multiple sclerosis","aggressive multiple sclerosis","disability","disability","highly active multiple sclerosis","highly active multiple sclerosis","multiple sclerosis","multiple sclerosis"],"subject_ac":["рассеянный склероз\n|||\nрассеянный склероз","агрессивный рассеянный склероз\n|||\nагрессивный рассеянный склероз","высокоактивный рассеянный склероз\n|||\nвысокоактивный рассеянный склероз","инвалидность\n|||\nинвалидность","scopus\n|||\nScopus","aggressive multiple sclerosis\n|||\naggressive multiple sclerosis","disability\n|||\ndisability","highly active multiple sclerosis\n|||\nhighly active multiple sclerosis","multiple sclerosis\n|||\nmultiple sclerosis"],"subject_tax_0_filter":["рассеянный склероз\n|||\nрассеянный склероз","агрессивный рассеянный склероз\n|||\nагрессивный рассеянный склероз","высокоактивный рассеянный склероз\n|||\nвысокоактивный рассеянный склероз","инвалидность\n|||\nинвалидность","scopus\n|||\nScopus","aggressive multiple sclerosis\n|||\naggressive multiple sclerosis","disability\n|||\ndisability","highly active multiple sclerosis\n|||\nhighly active multiple sclerosis","multiple sclerosis\n|||\nmultiple sclerosis"],"subject_filter":["рассеянный склероз\n|||\nрассеянный склероз","агрессивный рассеянный склероз\n|||\nагрессивный рассеянный склероз","высокоактивный рассеянный склероз\n|||\nвысокоактивный рассеянный склероз","инвалидность\n|||\nинвалидность","scopus\n|||\nScopus","aggressive multiple sclerosis\n|||\naggressive multiple sclerosis","disability\n|||\ndisability","highly active multiple sclerosis\n|||\nhighly active multiple sclerosis","multiple sclerosis\n|||\nmultiple sclerosis"],"dc.subject_mlt":["рассеянный склероз","агрессивный рассеянный склероз","высокоактивный рассеянный склероз","инвалидность","Scopus","aggressive multiple sclerosis","disability","highly active multiple sclerosis","multiple sclerosis"],"dc.subject":["рассеянный склероз","агрессивный рассеянный склероз","высокоактивный рассеянный склероз","инвалидность","Scopus","aggressive multiple sclerosis","disability","highly active multiple sclerosis","multiple sclerosis"],"dc.subject.ru_RU":["рассеянный склероз","агрессивный рассеянный склероз","высокоактивный рассеянный склероз","инвалидность"],"dc.subject.en":["Scopus","aggressive multiple sclerosis","disability","highly active multiple sclerosis","multiple sclerosis"],"title":["Aggressive multiple sclerosis in the Republic of Bashkortostan","Агрессивный рассеянный склероз в Республике Башкортостан"],"title_keyword":["Aggressive multiple sclerosis in the Republic of Bashkortostan","Агрессивный рассеянный склероз в Республике Башкортостан"],"title_ac":["aggressive multiple sclerosis in the republic of bashkortostan\n|||\nAggressive multiple sclerosis in the Republic of Bashkortostan","агрессивный рассеянный склероз в республике башкортостан\n|||\nАгрессивный рассеянный склероз в Республике Башкортостан"],"dc.title_sort":"Aggressive multiple sclerosis in the Republic of Bashkortostan","dc.title_hl":["Aggressive multiple sclerosis in the Republic of Bashkortostan","Агрессивный рассеянный склероз в Республике Башкортостан"],"dc.title_mlt":["Aggressive multiple sclerosis in the Republic of Bashkortostan","Агрессивный рассеянный склероз в Республике Башкортостан"],"dc.title":["Aggressive multiple sclerosis in the Republic of Bashkortostan","Агрессивный рассеянный склероз в Республике Башкортостан"],"dc.title_stored":["Aggressive multiple sclerosis in the Republic of Bashkortostan\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Агрессивный рассеянный склероз в Республике Башкортостан\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.title.en":["Aggressive multiple sclerosis in the Republic of Bashkortostan"],"dc.title.ru_RU":["Агрессивный рассеянный склероз в Республике Башкортостан"],"dc.title.alternative":["Aggressive multiple sclerosis in the Republic of Bashkortostan","Агрессивный рассеянный склероз в Республике Башкортостан"],"dc.title.alternative.en":["Aggressive multiple sclerosis in the Republic of Bashkortostan"],"dc.title.alternative.ru_RU":["Агрессивный рассеянный склероз в Республике Башкортостан"],"dc.type":["Article"],"dc.type.ru_RU":["Article"],"publication_grp":["123456789/8797"],"bi_2_dis_filter":["lyutov, o.v.\n|||\nLyutov, O.V.","akhmetgaleeva, n.f.\n|||\nAkhmetgaleeva, N.F.","talipova, i.d.\n|||\nTalipova, I.D.","galiullin, t.r.\n|||\nGaliullin, T.R.","кузьмина, у.ш.\n|||\nКузьмина, У.Ш.","ахметгалеева, н.ф.\n|||\nАхметгалеева, Н.Ф.","бахтиярова, к.з.\n|||\nБахтиярова, К.З.","кутлубаев, м.а.\n|||\nКутлубаев, М.А.","kuzmina, u.sh.\n|||\nKuzmina, U.Sh.","kutlubaev, m.a.\n|||\nKutlubaev, M.A.","bakhtiyarova, k.z.\n|||\nBakhtiyarova, K.Z.","галиуллин, т.р.\n|||\nГалиуллин, Т.Р.","лютов, о.в.\n|||\nЛютов, О.В.","талипова, и.д.\n|||\nТалипова, И.Д."],"bi_2_dis_partial":["Kuzmina, U.Sh.","Galiullin, T.R.","Галиуллин, Т.Р.","Кутлубаев, М.А.","Ахметгалеева, Н.Ф.","Лютов, О.В.","Кузьмина, У.Ш.","Талипова, И.Д.","Talipova, I.D.","Бахтиярова, К.З.","Akhmetgaleeva, N.F.","Lyutov, O.V.","Kutlubaev, M.A.","Bakhtiyarova, K.Z."],"bi_2_dis_value_filter":["Kuzmina, U.Sh.","Galiullin, T.R.","Галиуллин, Т.Р.","Кутлубаев, М.А.","Ахметгалеева, Н.Ф.","Лютов, О.В.","Кузьмина, У.Ш.","Талипова, И.Д.","Talipova, I.D.","Бахтиярова, К.З.","Akhmetgaleeva, N.F.","Lyutov, O.V.","Kutlubaev, M.A.","Bakhtiyarova, K.Z."],"bi_4_dis_filter":["aggressive multiple sclerosis\n|||\naggressive multiple sclerosis","агрессивный рассеянный склероз\n|||\nагрессивный рассеянный склероз","highly active multiple sclerosis\n|||\nhighly active multiple sclerosis","multiple sclerosis\n|||\nmultiple sclerosis","рассеянный склероз\n|||\nрассеянный склероз","инвалидность\n|||\nинвалидность","disability\n|||\ndisability","scopus\n|||\nScopus","высокоактивный рассеянный склероз\n|||\nвысокоактивный рассеянный 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syndrome, allowing early diagnosis and differential diagnosis of the disease. © Eco-Vector, 2025."],"subject":["spinal diseases"],"dc.abstract":[" dysfunction syndrome, allowing early diagnosis and differential diagnosis of the disease. © Eco-Vector, 2025."]},"2-7785":{"dc.description.abstract":["Asthma is a common complex disease with susceptibility defined through an interplay of genetic"],"dc.description.abstract.en":["Asthma is a common complex disease with susceptibility defined through an interplay of genetic"],"dc.description.abstract_hl":["Asthma is a common complex disease with susceptibility defined through an interplay of genetic"]},"2-7805":{"dc.description.abstract":[", there are a number of factors that influence the course of the disease, the contribution of which is poorly"],"dc.description.abstract.en":[", there are a number of factors that influence the course of the disease, the contribution of which is poorly"],"dc.description.abstract_hl":[", there are a number of factors that influence the course of the disease, the contribution of which is poorly"]},"2-8043":{"dc.title.en":["Systemic Benign Lipomatosis (Madelung’s Disease): Experience of Surgical Treatment. Clinical Case"],"dc.title":["Systemic Benign Lipomatosis (Madelung’s Disease): Experience of Surgical Treatment. Clinical Case"],"dc.title_hl":["Systemic Benign Lipomatosis (Madelung’s Disease): Experience of Surgical Treatment. Clinical Case"],"dc.title_mlt":["Systemic Benign Lipomatosis (Madelung’s Disease): Experience of Surgical Treatment. Clinical Case"],"bi_4_dis_partial":["Madelung’s disease"],"dc.subject.en":["Madelung’s disease"],"title":["Systemic Benign Lipomatosis (Madelung’s Disease): Experience of Surgical Treatment. Clinical Case"],"dc.citation.en":["Liu Q., Lyu H., Xu B., Lee J.H. Madelung disease epidemiology and clinical characteristics: a"],"dc.subject":["Madelung’s disease"],"dc.citation.ru":["Liu Q., Lyu H., Xu B., Lee J.H. Madelung disease epidemiology and clinical characteristics: a"],"dc.subject_mlt":["Madelung’s disease"],"dc.abstract.en":["

Introduction. Diffuse symmetric lipomatosis (Madelung’s disease) is a rare"],"dc.citation":["Liu Q., Lyu H., Xu B., Lee J.H. Madelung disease epidemiology and clinical characteristics: a"],"subject":["Madelung’s disease"],"dc.abstract":["

Introduction. Diffuse symmetric lipomatosis (Madelung’s disease) is a rare"]},"2-7793":{"dc.description.abstract":[" regimens. Patients had to have evaluable disease as per Response Evaluation Criteria in Solid Tumors"],"dc.description.abstract.en":[" regimens. Patients had to have evaluable disease as per Response Evaluation Criteria in Solid Tumors"],"dc.description.abstract_hl":[" regimens. Patients had to have evaluable disease as per Response Evaluation Criteria in Solid Tumors"]},"2-7926":{"dc.description.abstract":[" of the disease is associated with an impact on genes and signaling pathways regulating cell proliferation"],"dc.description.abstract.en":[" of the disease is associated with an impact on genes and signaling pathways regulating cell proliferation"],"dc.description.abstract_hl":[" of the disease is associated with an impact on genes and signaling pathways regulating cell proliferation"]},"2-7897":{"dc.abstract.en":[". This is a severe, progressive, presumably autoimmune disease associated with antineutrophil cytoplasmic"],"dc.abstract":[". This is a severe, progressive, presumably autoimmune disease associated with antineutrophil cytoplasmic"]},"2-7883":{"dc.description.abstract":[" accumulation and pathological disease progression. Hence, epigenetic inhibition of pathologically activated"],"dc.description.abstract.en":[" accumulation and pathological disease progression. Hence, epigenetic inhibition of pathologically activated"],"dc.description.abstract_hl":[" accumulation and pathological disease progression. Hence, epigenetic inhibition of pathologically activated"]},"2-7925":{"dc.description.abstract":[" of the SEMA6A (Yb8NBC597*ID, HR = 0.54, P = 0.016 for the cerebrovascular diseases), TEAD1 (Ya5ac2013*II, HR"],"dc.description.abstract.en":[" of the SEMA6A (Yb8NBC597*ID, HR = 0.54, P = 0.016 for the cerebrovascular diseases), TEAD1 (Ya5ac2013*II, HR"],"dc.description.abstract_hl":[" of the SEMA6A (Yb8NBC597*ID, HR = 0.54, P = 0.016 for the cerebrovascular diseases), TEAD1 (Ya5ac2013*II, HR"]},"2-7908":{"dc.abstract.en":[" such disease progression type and, accordingly, no optimal strategies for prescribing medication. Standardised"],"dc.abstract":[" such disease progression type and, accordingly, no optimal strategies for prescribing medication. Standardised"]}}} -->