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":"2025-04-23T09:57:31.541Z","search.uniqueid":"2-7889","search.resourcetype":2,"search.resourceid":7889,"handle":"123456789/8779","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","dc.abstract":["Annotation. This review presents an analysis of modern data on the role of oral microbiota in the etiology and pathogenesis of periodontitis as a widespread disease that negatively affects the quality of human life and is associated with the development of systemic pathology. The peculiarities of the oral cavity microbiota structure in healthy people and persons with periodontitis are characterised, the microorganisms etiologically significant in periodontitis are specified, species Porphyromonas gingivalis, Aggregatibacter actinomycetecomitans, Fusobacterium nucleatum and Tannerella forsythia, as well as Treponema denticola, Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros and the genus Spirochetes. The most significant role is attributed to Porphyromonas gingivalis, which is able to disrupt the balance of microbial communities and cause an infectious process. In addition, Porphyromonas gingivalis interacts with other microorganisms that colonise the periodontal pocket in the early stages of the disease, which contributes to the progression of periodontitis and irreversible changes in the supporting and retaining tissues of the tooth and alveolar bone, resulting in tooth loss. The aim of the study was to systematise the literature data on the study of the mechanisms of bacterial penetration into biofilm, oral tissues and further spread of the infectious process in the body to substantiate new possible strategies in the diagnosis, prevention and treatment of patients with periodontal diseases. © 2025 Clinical Dentistry LLC. All rights reserved."],"dc.abstract.en":["Annotation. This review presents an analysis of modern data on the role of oral microbiota in the etiology and pathogenesis of periodontitis as a widespread disease that negatively affects the quality of human life and is associated with the development of systemic pathology. The peculiarities of the oral cavity microbiota structure in healthy people and persons with periodontitis are characterised, the microorganisms etiologically significant in periodontitis are specified, species Porphyromonas gingivalis, Aggregatibacter actinomycetecomitans, Fusobacterium nucleatum and Tannerella forsythia, as well as Treponema denticola, Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros and the genus Spirochetes. The most significant role is attributed to Porphyromonas gingivalis, which is able to disrupt the balance of microbial communities and cause an infectious process. In addition, Porphyromonas gingivalis interacts with other microorganisms that colonise the periodontal pocket in the early stages of the disease, which contributes to the progression of periodontitis and irreversible changes in the supporting and retaining tissues of the tooth and alveolar bone, resulting in tooth loss. The aim of the study was to systematise the literature data on the study of the mechanisms of bacterial penetration into biofilm, oral tissues and further spread of the infectious process in the body to substantiate new possible strategies in the diagnosis, prevention and treatment of patients with periodontal diseases. © 2025 Clinical Dentistry LLC. All rights reserved."],"author":["Gimranova, I.A.","Gritsenko, V.A.","Rabinovich, I.M.","Akmalova, G.M.","Shvets, D.Yu.","Гимранова, И.А.","Гриценко, В.А.","Рабинович, И.М.","Акмалова, Г.М.","Швец, Д.Ю."],"author_keyword":["Gimranova, I.A.","Gritsenko, V.A.","Rabinovich, I.M.","Akmalova, G.M.","Shvets, D.Yu.","Гимранова, И.А.","Гриценко, В.А.","Рабинович, И.М.","Акмалова, Г.М.","Швец, Д.Ю."],"author_ac":["gimranova, i.a.\n|||\nGimranova, I.A.","gritsenko, v.a.\n|||\nGritsenko, V.A.","rabinovich, i.m.\n|||\nRabinovich, I.M.","akmalova, g.m.\n|||\nAkmalova, G.M.","shvets, d.yu.\n|||\nShvets, D.Yu.","гимранова, и.а.\n|||\nГимранова, И.А.","гриценко, в.а.\n|||\nГриценко, В.А.","рабинович, и.м.\n|||\nРабинович, И.М.","акмалова, г.м.\n|||\nАкмалова, Г.М.","швец, д.ю.\n|||\nШвец, Д.Ю."],"author_filter":["gimranova, i.a.\n|||\nGimranova, I.A.","gritsenko, v.a.\n|||\nGritsenko, V.A.","rabinovich, i.m.\n|||\nRabinovich, I.M.","akmalova, g.m.\n|||\nAkmalova, G.M.","shvets, d.yu.\n|||\nShvets, D.Yu.","гимранова, и.а.\n|||\nГимранова, И.А.","гриценко, в.а.\n|||\nГриценко, В.А.","рабинович, и.м.\n|||\nРабинович, И.М.","акмалова, г.м.\n|||\nАкмалова, Г.М.","швец, д.ю.\n|||\nШвец, Д.Ю."],"dc.contributor.author_hl":["Gimranova, I.A.","Gritsenko, V.A.","Rabinovich, I.M.","Akmalova, G.M.","Shvets, D.Yu.","Гимранова, И.А.","Гриценко, В.А.","Рабинович, И.М.","Акмалова, Г.М.","Швец, Д.Ю."],"dc.contributor.author_mlt":["Gimranova, I.A.","Gritsenko, V.A.","Rabinovich, I.M.","Akmalova, G.M.","Shvets, D.Yu.","Гимранова, И.А.","Гриценко, В.А.","Рабинович, И.М.","Акмалова, Г.М.","Швец, Д.Ю."],"dc.contributor.author":["Gimranova, I.A.","Gritsenko, V.A.","Rabinovich, I.M.","Akmalova, G.M.","Shvets, D.Yu.","Гимранова, И.А.","Гриценко, В.А.","Рабинович, И.М.","Акмалова, Г.М.","Швец, Д.Ю."],"dc.contributor.author_stored":["Gimranova, I.A.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Gritsenko, V.A.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Rabinovich, I.M.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Akmalova, G.M.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Shvets, D.Yu.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Гимранова, И.А.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Гриценко, В.А.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Рабинович, И.М.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Акмалова, Г.М.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Швец, Д.Ю.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.contributor.author.en":["Gimranova, I.A.","Gritsenko, V.A.","Rabinovich, I.M.","Akmalova, G.M.","Shvets, D.Yu."],"dc.contributor.author.ru_RU":["Гимранова, И.А.","Гриценко, В.А.","Рабинович, И.М.","Акмалова, Г.М.","Швец, Д.Ю."],"dc.date.accessioned_dt":"2025-04-23T09:55:31Z","dc.date.accessioned":["2025-04-23T09:55:31Z"],"dc.date.available":["2025-04-23T09:55:31Z"],"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":["В настоящем обзоре представлен анализ современных данных о роли оральной\nмикробиоты в этиологии и патогенезе пародонтита как широко распространенного заболевания, негативно влияющего на качество жизни человека и связанного с развитием системной патологии. Охарактеризованы особенности структуры микробиоты ротовой полости\nу здоровых людей и у лиц с пародонтитом, конкретизированы этиологически значимые при\nпародонтите микроорганизмы, относящиеся к видам Porphyromonas gingivalis, Aggregatibacter\nactinomycetecomitans, Fusobacterium nucleatum и Tannerella forsythia, также Treponema denticola, Filifactor alocis, Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros и роду\nSpirochetes. Обоснована роль Porphyromonas gingivalis как приоритетного возбудителя пародонтита, способного нарушать баланс в микробной экосистеме ротовой полости и вызвать\nинфекционный процесс. Обсужден вклад дисбиотических сдвигов оральной микробиоты\nв развитие локальных и системных патологических процессов. Систематизирована информация о механизмах проникновения бактерий в биопленку, ткани полости рта и дальнейшее\nраспространение инфекционного процесса в организме. Представленные данные важны для\nобоснования новых возможных стратегий в диагностике, профилактике и лечении пациентов\nс воспалительными заболеваниями пародонта."],"dc.description.abstract":["В настоящем обзоре представлен анализ современных данных о роли оральной\nмикробиоты в этиологии и патогенезе пародонтита как широко распространенного заболевания, негативно влияющего на качество жизни человека и связанного с развитием системной патологии. Охарактеризованы особенности структуры микробиоты ротовой полости\nу здоровых людей и у лиц с пародонтитом, конкретизированы этиологически значимые при\nпародонтите микроорганизмы, относящиеся к видам Porphyromonas gingivalis, Aggregatibacter\nactinomycetecomitans, Fusobacterium nucleatum и Tannerella forsythia, также Treponema denticola, Filifactor alocis, Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros и роду\nSpirochetes. Обоснована роль Porphyromonas gingivalis как приоритетного возбудителя пародонтита, способного нарушать баланс в микробной экосистеме ротовой полости и вызвать\nинфекционный процесс. Обсужден вклад дисбиотических сдвигов оральной микробиоты\nв развитие локальных и системных патологических процессов. Систематизирована информация о механизмах проникновения бактерий в биопленку, ткани полости рта и дальнейшее\nраспространение инфекционного процесса в организме. Представленные данные важны для\nобоснования новых возможных стратегий в диагностике, профилактике и лечении пациентов\nс воспалительными заболеваниями пародонта."],"dc.description.abstract.ru_RU":["В настоящем обзоре представлен анализ современных данных о роли оральной\nмикробиоты в этиологии и патогенезе пародонтита как широко распространенного заболевания, негативно влияющего на качество жизни человека и связанного с развитием системной патологии. Охарактеризованы особенности структуры микробиоты ротовой полости\nу здоровых людей и у лиц с пародонтитом, конкретизированы этиологически значимые при\nпародонтите микроорганизмы, относящиеся к видам Porphyromonas gingivalis, Aggregatibacter\nactinomycetecomitans, Fusobacterium nucleatum и Tannerella forsythia, также Treponema denticola, Filifactor alocis, Prevotella intermedia, Campylobacter rectus, Peptostreptococcus micros и роду\nSpirochetes. Обоснована роль Porphyromonas gingivalis как приоритетного возбудителя пародонтита, способного нарушать баланс в микробной экосистеме ротовой полости и вызвать\nинфекционный процесс. Обсужден вклад дисбиотических сдвигов оральной микробиоты\nв развитие локальных и системных патологических процессов. Систематизирована информация о механизмах проникновения бактерий в биопленку, ткани полости рта и дальнейшее\nраспространение инфекционного процесса в организме. Представленные данные важны для\nобоснования новых возможных стратегий в диагностике, профилактике и лечении пациентов\nс воспалительными заболеваниями пародонта."],"dc.doi":["10.37988/1811-153X_2025_1_179"],"dc.doi.en":["10.37988/1811-153X_2025_1_179"],"dc.identifier.issn":["1811-153X"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8779"],"dc.publisher":["Clinical Dentistry LLC"],"dc.publisher.en":["Clinical Dentistry LLC"],"dc.relation.ispartofseries":["Clinical Dentistry (Russia);т. 28 № 1"],"dc.relation.ispartofseries.en":["Clinical Dentistry (Russia);т. 28 № 1"],"subject":["микробиом полости рта","пародонтит","Porphyromonas gingivalis","Aggregatibacter actinomycetecomitans","Fusobacterium nucleatum","Tannerella forsythia","Scopus"],"subject_keyword":["микробиом полости рта","микробиом полости рта","пародонтит","пародонтит","Porphyromonas gingivalis","Porphyromonas gingivalis","Aggregatibacter actinomycetecomitans","Aggregatibacter actinomycetecomitans","Fusobacterium nucleatum","Fusobacterium nucleatum","Tannerella forsythia","Tannerella forsythia","Scopus","Scopus"],"subject_ac":["микробиом полости рта\n|||\nмикробиом полости рта","пародонтит\n|||\nпародонтит","porphyromonas gingivalis\n|||\nPorphyromonas gingivalis","aggregatibacter actinomycetecomitans\n|||\nAggregatibacter actinomycetecomitans","fusobacterium nucleatum\n|||\nFusobacterium nucleatum","tannerella forsythia\n|||\nTannerella forsythia","scopus\n|||\nScopus"],"subject_tax_0_filter":["микробиом полости рта\n|||\nмикробиом полости рта","пародонтит\n|||\nпародонтит","porphyromonas gingivalis\n|||\nPorphyromonas gingivalis","aggregatibacter actinomycetecomitans\n|||\nAggregatibacter actinomycetecomitans","fusobacterium nucleatum\n|||\nFusobacterium nucleatum","tannerella forsythia\n|||\nTannerella forsythia","scopus\n|||\nScopus"],"subject_filter":["микробиом полости рта\n|||\nмикробиом полости рта","пародонтит\n|||\nпародонтит","porphyromonas gingivalis\n|||\nPorphyromonas gingivalis","aggregatibacter actinomycetecomitans\n|||\nAggregatibacter actinomycetecomitans","fusobacterium nucleatum\n|||\nFusobacterium nucleatum","tannerella forsythia\n|||\nTannerella forsythia","scopus\n|||\nScopus"],"dc.subject_mlt":["микробиом полости рта","пародонтит","Porphyromonas gingivalis","Aggregatibacter actinomycetecomitans","Fusobacterium nucleatum","Tannerella forsythia","Scopus"],"dc.subject":["микробиом полости рта","пародонтит","Porphyromonas gingivalis","Aggregatibacter actinomycetecomitans","Fusobacterium nucleatum","Tannerella forsythia","Scopus"],"dc.subject.ru_RU":["микробиом полости рта","пародонтит"],"dc.subject.en":["Porphyromonas gingivalis","Aggregatibacter actinomycetecomitans","Fusobacterium nucleatum","Tannerella forsythia","Scopus"],"title":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"title_keyword":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"title_ac":["роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии\n|||\nРоль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","the role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology\n|||\nThe role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.title_sort":"Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","dc.title_hl":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.title_mlt":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.title":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.title_stored":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.ru_RU":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии"],"dc.title.en":["The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.title.alternative":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.title.alternative.ru_RU":["Роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии"],"dc.title.alternative.en":["The role of oral microbiota in the etiology, pathogenesis of periodontitis and systemic pathology"],"dc.type":["Article"],"dc.type.ru_RU":["Article"],"publication_grp":["123456789/8779"],"bi_2_dis_filter":["gimranova, i.a.\n|||\nGimranova, I.A.","rabinovich, i.m.\n|||\nRabinovich, I.M.","akmalova, g.m.\n|||\nAkmalova, G.M.","shvets, d.yu.\n|||\nShvets, D.Yu.","акмалова, г.м.\n|||\nАкмалова, Г.М.","рабинович, и.м.\n|||\nРабинович, И.М.","gritsenko, v.a.\n|||\nGritsenko, V.A.","гриценко, в.а.\n|||\nГриценко, В.А.","гимранова, и.а.\n|||\nГимранова, И.А.","швец, д.ю.\n|||\nШвец, Д.Ю."],"bi_2_dis_partial":["Рабинович, И.М.","Shvets, D.Yu.","Gimranova, I.A.","Швец, Д.Ю.","Rabinovich, I.M.","Гимранова, И.А.","Gritsenko, V.A.","Акмалова, Г.М.","Гриценко, В.А.","Akmalova, G.M."],"bi_2_dis_value_filter":["Рабинович, И.М.","Shvets, D.Yu.","Gimranova, I.A.","Швец, Д.Ю.","Rabinovich, I.M.","Гимранова, И.А.","Gritsenko, V.A.","Акмалова, Г.М.","Гриценко, В.А.","Akmalova, G.M."],"bi_4_dis_filter":["пародонтит\n|||\nпародонтит","fusobacterium nucleatum\n|||\nFusobacterium nucleatum","porphyromonas gingivalis\n|||\nPorphyromonas gingivalis","микробиом полости рта\n|||\nмикробиом полости рта","tannerella forsythia\n|||\nTannerella forsythia","aggregatibacter actinomycetecomitans\n|||\nAggregatibacter actinomycetecomitans","scopus\n|||\nScopus"],"bi_4_dis_partial":["Porphyromonas gingivalis","Tannerella forsythia","пародонтит","микробиом полости рта","Fusobacterium nucleatum","Scopus","Aggregatibacter actinomycetecomitans"],"bi_4_dis_value_filter":["Porphyromonas gingivalis","Tannerella forsythia","пародонтит","микробиом полости рта","Fusobacterium nucleatum","Scopus","Aggregatibacter actinomycetecomitans"],"bi_sort_1_sort":"роль оральной микробиоты в этиологии, патогенезе пародонтита и в системной патологии","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-04-23T09:55:31Z","read":["g0"],"_version_":1830186911319195648},{"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}]},"facet_counts":{"facet_queries":{},"facet_fields":{},"facet_dates":{},"facet_ranges":{},"facet_intervals":{}},"highlighting":{"2-7911":{"dc.abstract.en":[" of the experiment, the weight coefficients of their internal organs were recorded. Results and discussion. Chronic"],"dc.abstract":[" of the experiment, the weight coefficients of their internal organs were recorded. Results and discussion. Chronic"]},"2-7917":{"bi_4_dis_partial":["spinal diseases"],"dc.subject.en":["spinal diseases"],"dc.subject":["spinal diseases"],"dc.subject_mlt":["spinal diseases"],"dc.abstract.en":[" dysfunction 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"]},"2-7889":{"dc.abstract.en":[" in the etiology and pathogenesis of periodontitis as a widespread disease that negatively affects the quality"],"dc.abstract":[" in the etiology and pathogenesis of periodontitis as a widespread disease that negatively affects the quality"]},"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"]}}} -->