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. 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.identifier.uri":["http://hdl.handle.net/123456789/8932"],"dc.date.accessioned_dt":"2025-07-09T13:59:02Z","dc.date.accessioned":["2025-07-09T13:59:02Z"],"dc.date.available":["2025-07-09T13:59:02Z"],"publication_grp":["123456789/8932"],"bi_4_dis_filter":["madelung’s disease\n|||\nMadelung’s disease","lipectomy\n|||\nlipectomy","диффузный симметричный липоматоз\n|||\nдиффузный симметричный липоматоз","шеи новообразования\n|||\nшеи новообразования","липэктомия\n|||\nлипэктомия","diffuse symmetric lipomatosis\n|||\ndiffuse symmetric lipomatosis","adipose tissue proliferation\n|||\nadipose tissue proliferation","жировой ткани разрастание\n|||\nжировой ткани разрастание","болезнь маделунга\n|||\nболезнь Маделунга","neck neoplasms\n|||\nneck neoplasms"],"bi_4_dis_partial":["липэктомия","Madelung’s disease","diffuse symmetric lipomatosis","neck neoplasms","болезнь Маделунга","adipose tissue proliferation","шеи новообразования","lipectomy","диффузный симметричный липоматоз","жировой ткани разрастание"],"bi_4_dis_value_filter":["липэктомия","Madelung’s disease","diffuse symmetric lipomatosis","neck neoplasms","болезнь Маделунга","adipose tissue proliferation","шеи новообразования","lipectomy","диффузный симметричный липоматоз","жировой ткани разрастание"],"bi_sort_1_sort":"systemic benign lipomatosis (madelung’s disease): experience of surgical treatment. clinical case","bi_sort_3_sort":"2025-07-09T13:59:02Z","read":["g0"],"_version_":1837178072511545344},{"SolrIndexer.lastIndexed":"2025-05-06T09:42:15.105Z","search.uniqueid":"2-7931","search.resourcetype":2,"search.resourceid":7931,"handle":"123456789/8820","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","dc.abstract":["AIM: to assess features of pathomorphological changes in the intestinal wall in patients who had new coronavirus infection SARS-CoV-2. PATIENTS AND METHODS: the study included 8 patients who underwent surgery for complications of pseudomembranous colitis and had previously COVID-19. Six patients underwent colectomy, and two underwent subtotal colectomy with end ileostomy. Histology of the removed specimens was standard. RESULTS: in all specimens, in addition to the changes peculiar for pseudomembranous colitis, vascular lesions of the bowel wall were detected as vasculitis of small arteries and vessels of the microcirculatory network, phlebitis and thrombosis of venous vessels like in COVID-19. These pathological changes in blood vessels may reveal the intramural perfusion disorders of blood circulation, leading subsequently to ischemic changes. CONCLUSION: when treating patients with pseudomembranous colitis and postcovid syndrome, it is necessary to take into account the mutually aggravating effect of both diseases, when assessing risks, determining indications for surgery and conservative measures. © 2025, Association of Coloproctologists of Russia. All rights reserved."],"dc.abstract.en":["AIM: to assess features of pathomorphological changes in the intestinal wall in patients who had new coronavirus infection SARS-CoV-2. PATIENTS AND METHODS: the study included 8 patients who underwent surgery for complications of pseudomembranous colitis and had previously COVID-19. Six patients underwent colectomy, and two underwent subtotal colectomy with end ileostomy. Histology of the removed specimens was standard. RESULTS: in all specimens, in addition to the changes peculiar for pseudomembranous colitis, vascular lesions of the bowel wall were detected as vasculitis of small arteries and vessels of the microcirculatory network, phlebitis and thrombosis of venous vessels like in COVID-19. These pathological changes in blood vessels may reveal the intramural perfusion disorders of blood circulation, leading subsequently to ischemic changes. CONCLUSION: when treating patients with pseudomembranous colitis and postcovid syndrome, it is necessary to take into account the mutually aggravating effect of both diseases, when assessing risks, determining indications for surgery and conservative measures. © 2025, Association of Coloproctologists of Russia. All rights reserved."],"author":["Тимербулатов, В. М.","Мустафин, Т. И.","Тимербулатов, М. В.","Щекин, С. В.","Тимербулатов, Ш. В.","Гафарова, А. Р.","Гараев, Р. Р.","Timerbulatov, Vil’ M.","Mustafin, Tagir I.","Timerbulatov, Makhmud V.","Shchekin, Sergey V.","Timerbulatov, Shamil’ V.","Gafarova, Aigul R.","Garaev, Ruslan R."],"author_keyword":["Тимербулатов, В. М.","Мустафин, Т. И.","Тимербулатов, М. В.","Щекин, С. В.","Тимербулатов, Ш. В.","Гафарова, А. Р.","Гараев, Р. Р.","Timerbulatov, Vil’ M.","Mustafin, Tagir I.","Timerbulatov, Makhmud V.","Shchekin, Sergey V.","Timerbulatov, Shamil’ V.","Gafarova, Aigul R.","Garaev, Ruslan R."],"author_ac":["тимербулатов, в. м.\n|||\nТимербулатов, В. М.","мустафин, т. и.\n|||\nМустафин, Т. И.","тимербулатов, м. в.\n|||\nТимербулатов, М. В.","щекин, с. в.\n|||\nЩекин, С. В.","тимербулатов, ш. в.\n|||\nТимербулатов, Ш. В.","гафарова, а. р.\n|||\nГафарова, А. Р.","гараев, р. р.\n|||\nГараев, Р. Р.","timerbulatov, vil’ m.\n|||\nTimerbulatov, Vil’ M.","mustafin, tagir i.\n|||\nMustafin, Tagir I.","timerbulatov, makhmud v.\n|||\nTimerbulatov, Makhmud V.","shchekin, sergey v.\n|||\nShchekin, Sergey V.","timerbulatov, shamil’ v.\n|||\nTimerbulatov, Shamil’ V.","gafarova, aigul r.\n|||\nGafarova, Aigul R.","garaev, ruslan r.\n|||\nGaraev, Ruslan R."],"author_filter":["тимербулатов, в. м.\n|||\nТимербулатов, В. М.","мустафин, т. и.\n|||\nМустафин, Т. И.","тимербулатов, м. в.\n|||\nТимербулатов, М. В.","щекин, с. в.\n|||\nЩекин, С. В.","тимербулатов, ш. в.\n|||\nТимербулатов, Ш. В.","гафарова, а. р.\n|||\nГафарова, А. Р.","гараев, р. р.\n|||\nГараев, Р. Р.","timerbulatov, vil’ m.\n|||\nTimerbulatov, Vil’ M.","mustafin, tagir i.\n|||\nMustafin, Tagir I.","timerbulatov, makhmud v.\n|||\nTimerbulatov, Makhmud V.","shchekin, sergey v.\n|||\nShchekin, Sergey V.","timerbulatov, shamil’ v.\n|||\nTimerbulatov, Shamil’ V.","gafarova, aigul r.\n|||\nGafarova, Aigul R.","garaev, ruslan r.\n|||\nGaraev, Ruslan R."],"dc.contributor.author_hl":["Тимербулатов, В. М.","Мустафин, Т. И.","Тимербулатов, М. В.","Щекин, С. В.","Тимербулатов, Ш. В.","Гафарова, А. Р.","Гараев, Р. Р.","Timerbulatov, Vil’ M.","Mustafin, Tagir I.","Timerbulatov, Makhmud V.","Shchekin, Sergey V.","Timerbulatov, Shamil’ V.","Gafarova, Aigul R.","Garaev, Ruslan R."],"dc.contributor.author_mlt":["Тимербулатов, В. М.","Мустафин, Т. И.","Тимербулатов, М. В.","Щекин, С. В.","Тимербулатов, Ш. В.","Гафарова, А. Р.","Гараев, Р. Р.","Timerbulatov, Vil’ M.","Mustafin, Tagir I.","Timerbulatov, Makhmud V.","Shchekin, Sergey V.","Timerbulatov, Shamil’ V.","Gafarova, Aigul R.","Garaev, Ruslan R."],"dc.contributor.author":["Тимербулатов, В. М.","Мустафин, Т. И.","Тимербулатов, М. В.","Щекин, С. В.","Тимербулатов, Ш. В.","Гафарова, А. Р.","Гараев, Р. Р.","Timerbulatov, Vil’ M.","Mustafin, Tagir I.","Timerbulatov, Makhmud V.","Shchekin, Sergey V.","Timerbulatov, Shamil’ V.","Gafarova, Aigul R.","Garaev, Ruslan R."],"dc.contributor.author_stored":["Тимербулатов, В. М.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Мустафин, Т. И.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Тимербулатов, М. В.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Щекин, С. В.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Тимербулатов, Ш. В.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Гафарова, А. Р.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Гараев, Р. Р.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Timerbulatov, Vil’ M.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Mustafin, Tagir I.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Timerbulatov, Makhmud V.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Shchekin, Sergey V.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Timerbulatov, Shamil’ V.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Gafarova, Aigul R.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Garaev, Ruslan R.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.ru_RU":["Тимербулатов, В. М.","Мустафин, Т. И.","Тимербулатов, М. В.","Щекин, С. В.","Тимербулатов, Ш. В.","Гафарова, А. Р.","Гараев, Р. Р."],"dc.contributor.author.en":["Timerbulatov, Vil’ M.","Mustafin, Tagir I.","Timerbulatov, Makhmud V.","Shchekin, Sergey V.","Timerbulatov, Shamil’ V.","Gafarova, Aigul R.","Garaev, Ruslan R."],"dc.date.accessioned_dt":"2025-05-06T09:37:46Z","dc.date.accessioned":["2025-05-06T09:37:46Z"],"dc.date.available":["2025-05-06T09:37:46Z"],"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":["ЦЕЛЬ: изучить особенности патоморфологических изменений стенки кишечника у пациентов, перенесших новую коронавирусную инфекцию SARS-CoV-2.\nПАЦИЕНТЫ И МЕТОДЫ: в исследование включено 8 пациентов, оперированных по поводу осложнений псевдомембранозного колита, ранее перенесших COVID-19. Шести пациентам была выполнена колэктомия, а двум — субтотальная резекция ободочной кишки с концевой илеостомией. Гистологическое исследование удаленных препаратов проводилось по стандартной методике.\nРЕЗУЛЬТАТЫ: во всех препаратах, помимо изменений, характерных для псевдомембранозного колита, было выявлено поражение сосудов стенки в виде васкулита мелких артерий и сосудов микроциркуляторного русла, флебита и тромбоза венозных сосудов, характерных для COVID-19. Указанные патологические изменения сосудов могут являться свидетельством развития интрамуральных перфузионных расстройств кровообращения, приводящим в последующем к ишемическим изменениям.\nЗАКЛЮЧЕНИЕ: при лечении пациентов псевдомембранозным колитом и постковидным синдромом, необходимо принимать во внимание взаимно отягощающее действие обоих заболеваний, что должно учитываться при оценке рисков, определении показаний к операции и консервативных мероприятиях."],"dc.description.abstract":["ЦЕЛЬ: изучить особенности патоморфологических изменений стенки кишечника у пациентов, перенесших новую коронавирусную инфекцию SARS-CoV-2.\nПАЦИЕНТЫ И МЕТОДЫ: в исследование включено 8 пациентов, оперированных по поводу осложнений псевдомембранозного колита, ранее перенесших COVID-19. Шести пациентам была выполнена колэктомия, а двум — субтотальная резекция ободочной кишки с концевой илеостомией. Гистологическое исследование удаленных препаратов проводилось по стандартной методике.\nРЕЗУЛЬТАТЫ: во всех препаратах, помимо изменений, характерных для псевдомембранозного колита, было выявлено поражение сосудов стенки в виде васкулита мелких артерий и сосудов микроциркуляторного русла, флебита и тромбоза венозных сосудов, характерных для COVID-19. Указанные патологические изменения сосудов могут являться свидетельством развития интрамуральных перфузионных расстройств кровообращения, приводящим в последующем к ишемическим изменениям.\nЗАКЛЮЧЕНИЕ: при лечении пациентов псевдомембранозным колитом и постковидным синдромом, необходимо принимать во внимание взаимно отягощающее действие обоих заболеваний, что должно учитываться при оценке рисков, определении показаний к операции и консервативных мероприятиях."],"dc.description.abstract.ru_RU":["ЦЕЛЬ: изучить особенности патоморфологических изменений стенки кишечника у пациентов, перенесших новую коронавирусную инфекцию SARS-CoV-2.\nПАЦИЕНТЫ И МЕТОДЫ: в исследование включено 8 пациентов, оперированных по поводу осложнений псевдомембранозного колита, ранее перенесших COVID-19. Шести пациентам была выполнена колэктомия, а двум — субтотальная резекция ободочной кишки с концевой илеостомией. Гистологическое исследование удаленных препаратов проводилось по стандартной методике.\nРЕЗУЛЬТАТЫ: во всех препаратах, помимо изменений, характерных для псевдомембранозного колита, было выявлено поражение сосудов стенки в виде васкулита мелких артерий и сосудов микроциркуляторного русла, флебита и тромбоза венозных сосудов, характерных для COVID-19. Указанные патологические изменения сосудов могут являться свидетельством развития интрамуральных перфузионных расстройств кровообращения, приводящим в последующем к ишемическим изменениям.\nЗАКЛЮЧЕНИЕ: при лечении пациентов псевдомембранозным колитом и постковидным синдромом, необходимо принимать во внимание взаимно отягощающее действие обоих заболеваний, что должно учитываться при оценке рисков, определении показаний к операции и консервативных мероприятиях."],"dc.doi":["10.33878/2073-7556-2025-24-1-38-45"],"dc.doi.en":["10.33878/2073-7556-2025-24-1-38-45"],"dc.identifier.issn":["2073-7556"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8820"],"dc.publisher":["Association of Coloproctologists of Russia"],"dc.publisher.en":["Association of Coloproctologists of Russia"],"dc.relation.ispartofseries":["Koloproktologia;т. 24 № 1"],"dc.relation.ispartofseries.en":["Koloproktologia;т. 24 № 1"],"subject":["псевдомембранозный колит","Clostridium difficile","COVID-19","васкулит","тромбоз мелких вен стенки кишки","Scopus","COVID-18","intestinal wall vein thrombosis","pseudomembranous colitis","vasculitis"],"subject_keyword":["псевдомембранозный колит","псевдомембранозный колит","Clostridium difficile","Clostridium difficile","COVID-19","COVID-19","васкулит","васкулит","тромбоз мелких вен стенки кишки","тромбоз мелких вен стенки кишки","Scopus","Scopus","COVID-18","COVID-18","intestinal wall vein thrombosis","intestinal wall vein thrombosis","pseudomembranous colitis","pseudomembranous colitis","vasculitis","vasculitis"],"subject_ac":["псевдомембранозный колит\n|||\nпсевдомембранозный колит","clostridium difficile\n|||\nClostridium difficile","covid-19\n|||\nCOVID-19","васкулит\n|||\nваскулит","тромбоз мелких вен стенки кишки\n|||\nтромбоз мелких вен стенки кишки","scopus\n|||\nScopus","covid-18\n|||\nCOVID-18","intestinal wall vein thrombosis\n|||\nintestinal wall vein thrombosis","pseudomembranous colitis\n|||\npseudomembranous colitis","vasculitis\n|||\nvasculitis"],"subject_tax_0_filter":["псевдомембранозный колит\n|||\nпсевдомембранозный колит","clostridium difficile\n|||\nClostridium difficile","covid-19\n|||\nCOVID-19","васкулит\n|||\nваскулит","тромбоз мелких вен стенки кишки\n|||\nтромбоз мелких вен стенки кишки","scopus\n|||\nScopus","covid-18\n|||\nCOVID-18","intestinal wall vein thrombosis\n|||\nintestinal wall vein thrombosis","pseudomembranous colitis\n|||\npseudomembranous colitis","vasculitis\n|||\nvasculitis"],"subject_filter":["псевдомембранозный колит\n|||\nпсевдомембранозный колит","clostridium difficile\n|||\nClostridium difficile","covid-19\n|||\nCOVID-19","васкулит\n|||\nваскулит","тромбоз мелких вен стенки кишки\n|||\nтромбоз мелких вен стенки кишки","scopus\n|||\nScopus","covid-18\n|||\nCOVID-18","intestinal wall vein thrombosis\n|||\nintestinal wall vein thrombosis","pseudomembranous colitis\n|||\npseudomembranous colitis","vasculitis\n|||\nvasculitis"],"dc.subject_mlt":["псевдомембранозный колит","Clostridium difficile","COVID-19","васкулит","тромбоз мелких вен стенки кишки","Scopus","COVID-18","intestinal wall vein thrombosis","pseudomembranous colitis","vasculitis"],"dc.subject":["псевдомембранозный колит","Clostridium difficile","COVID-19","васкулит","тромбоз мелких вен стенки кишки","Scopus","COVID-18","intestinal wall vein thrombosis","pseudomembranous colitis","vasculitis"],"dc.subject.ru_RU":["псевдомембранозный колит","COVID-19","васкулит","тромбоз мелких вен стенки кишки"],"dc.subject.en":["Clostridium difficile","Scopus","COVID-18","intestinal wall vein thrombosis","pseudomembranous colitis","vasculitis"],"title":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"title_keyword":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"title_ac":["pathohistological features of clostridium difficile-associated pseudomembranous colitis in post-covid-19 patients\n|||\nPathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","патогистологические особенности clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших covid-19\n|||\nПатогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"dc.title_sort":"Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","dc.title_hl":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"dc.title_mlt":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"dc.title":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients","Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"dc.title_stored":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.title.en":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients"],"dc.title.ru_RU":["Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"dc.title.alternative":["Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19","Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients"],"dc.title.alternative.ru_RU":["Патогистологические особенности Clostridium difficile-\nассоциированного псевдомембранозного колита\nу пациентов, перенесших COVID-19"],"dc.title.alternative.en":["Pathohistological features of Clostridium difficile-associated pseudomembranous colitis in post-COVID-19 patients"],"dc.type":["Article"],"dc.type.ru_RU":["Article"],"publication_grp":["123456789/8820"],"bi_2_dis_filter":["timerbulatov, makhmud v.\n|||\nTimerbulatov, Makhmud V.","тимербулатов, ш. в.\n|||\nТимербулатов, Ш. В.","timerbulatov, shamil’ v.\n|||\nTimerbulatov, Shamil’ V.","щекин, с. в.\n|||\nЩекин, С. В.","гафарова, а. р.\n|||\nГафарова, А. Р.","garaev, ruslan r.\n|||\nGaraev, Ruslan R.","тимербулатов, в. м.\n|||\nТимербулатов, В. М.","мустафин, т. и.\n|||\nМустафин, Т. И.","тимербулатов, м. в.\n|||\nТимербулатов, М. В.","timerbulatov, vil’ m.\n|||\nTimerbulatov, Vil’ M.","mustafin, tagir i.\n|||\nMustafin, Tagir I.","shchekin, sergey v.\n|||\nShchekin, Sergey V.","gafarova, aigul r.\n|||\nGafarova, Aigul R.","гараев, р. р.\n|||\nГараев, Р. Р."],"bi_2_dis_partial":["Timerbulatov, Vil’ M.","Timerbulatov, Makhmud V.","Garaev, Ruslan R.","Тимербулатов, Ш. В.","Тимербулатов, М. В.","Mustafin, Tagir I.","Gafarova, Aigul R.","Мустафин, Т. И.","Гараев, Р. Р.","Тимербулатов, В. М.","Timerbulatov, Shamil’ V.","Shchekin, Sergey V.","Щекин, С. В.","Гафарова, А. Р."],"bi_2_dis_value_filter":["Timerbulatov, Vil’ M.","Timerbulatov, Makhmud V.","Garaev, Ruslan R.","Тимербулатов, Ш. В.","Тимербулатов, М. В.","Mustafin, Tagir I.","Gafarova, Aigul R.","Мустафин, Т. И.","Гараев, Р. Р.","Тимербулатов, В. М.","Timerbulatov, Shamil’ V.","Shchekin, Sergey V.","Щекин, С. В.","Гафарова, А. Р."],"bi_4_dis_filter":["васкулит\n|||\nваскулит","тромбоз мелких вен стенки кишки\n|||\nтромбоз мелких вен стенки кишки","clostridium difficile\n|||\nClostridium difficile","vasculitis\n|||\nvasculitis","pseudomembranous colitis\n|||\npseudomembranous colitis","псевдомембранозный колит\n|||\nпсевдомембранозный колит","covid-19\n|||\nCOVID-19","intestinal wall vein thrombosis\n|||\nintestinal wall vein thrombosis","scopus\n|||\nScopus","covid-18\n|||\nCOVID-18"],"bi_4_dis_partial":["COVID-19","vasculitis","Scopus","Clostridium difficile","pseudomembranous colitis","васкулит","тромбоз мелких вен стенки кишки","intestinal wall vein thrombosis","псевдомембранозный колит","COVID-18"],"bi_4_dis_value_filter":["COVID-19","vasculitis","Scopus","Clostridium difficile","pseudomembranous colitis","васкулит","тромбоз мелких вен стенки кишки","intestinal wall vein thrombosis","псевдомембранозный колит","COVID-18"],"bi_sort_1_sort":"pathohistological features of clostridium difficile-associated pseudomembranous colitis in post-covid-19 patients","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-05-06T09:37:46Z","read":["g0"],"_version_":1831363710931697664},{"SolrIndexer.lastIndexed":"2025-05-07T11:03:28.304Z","search.uniqueid":"2-7943","search.resourcetype":2,"search.resourceid":7943,"handle":"123456789/8832","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","author":["Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Rakina, Militsa","Menyalo, Maxim","Enikeeva, Kadriia","Rafikova, Guzel","Sharifyanova, Yuliya","Pavlov, Valentin","Villert, Alisa","Kolomiets, Larisa","Kzhyshkowska, Julia"],"author_keyword":["Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Rakina, Militsa","Menyalo, Maxim","Enikeeva, Kadriia","Rafikova, Guzel","Sharifyanova, Yuliya","Pavlov, Valentin","Villert, Alisa","Kolomiets, Larisa","Kzhyshkowska, Julia"],"author_ac":["larionova, irina\n|||\nLarionova, Irina","iamshchikov, pavel\n|||\nIamshchikov, Pavel","kazakova, anna\n|||\nKazakova, Anna","rakina, militsa\n|||\nRakina, Militsa","menyalo, maxim\n|||\nMenyalo, Maxim","enikeeva, kadriia\n|||\nEnikeeva, Kadriia","rafikova, guzel\n|||\nRafikova, Guzel","sharifyanova, yuliya\n|||\nSharifyanova, Yuliya","pavlov, valentin\n|||\nPavlov, Valentin","villert, alisa\n|||\nVillert, Alisa","kolomiets, larisa\n|||\nKolomiets, Larisa","kzhyshkowska, julia\n|||\nKzhyshkowska, Julia"],"author_filter":["larionova, irina\n|||\nLarionova, Irina","iamshchikov, pavel\n|||\nIamshchikov, Pavel","kazakova, anna\n|||\nKazakova, Anna","rakina, militsa\n|||\nRakina, Militsa","menyalo, maxim\n|||\nMenyalo, Maxim","enikeeva, kadriia\n|||\nEnikeeva, Kadriia","rafikova, guzel\n|||\nRafikova, Guzel","sharifyanova, yuliya\n|||\nSharifyanova, Yuliya","pavlov, valentin\n|||\nPavlov, Valentin","villert, alisa\n|||\nVillert, Alisa","kolomiets, larisa\n|||\nKolomiets, Larisa","kzhyshkowska, julia\n|||\nKzhyshkowska, Julia"],"dc.contributor.author_hl":["Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Rakina, Militsa","Menyalo, Maxim","Enikeeva, Kadriia","Rafikova, Guzel","Sharifyanova, Yuliya","Pavlov, Valentin","Villert, Alisa","Kolomiets, Larisa","Kzhyshkowska, Julia"],"dc.contributor.author_mlt":["Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Rakina, Militsa","Menyalo, Maxim","Enikeeva, Kadriia","Rafikova, Guzel","Sharifyanova, Yuliya","Pavlov, Valentin","Villert, Alisa","Kolomiets, Larisa","Kzhyshkowska, Julia"],"dc.contributor.author":["Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Rakina, Militsa","Menyalo, Maxim","Enikeeva, Kadriia","Rafikova, Guzel","Sharifyanova, Yuliya","Pavlov, Valentin","Villert, Alisa","Kolomiets, Larisa","Kzhyshkowska, Julia"],"dc.contributor.author_stored":["Larionova, Irina\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Iamshchikov, Pavel\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Kazakova, Anna\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Rakina, Militsa\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Menyalo, Maxim\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Enikeeva, Kadriia\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Rafikova, Guzel\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Sharifyanova, Yuliya\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Pavlov, Valentin\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Villert, Alisa\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Kolomiets, Larisa\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Kzhyshkowska, Julia\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.en":["Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Rakina, Militsa","Menyalo, Maxim","Enikeeva, Kadriia","Rafikova, Guzel","Sharifyanova, Yuliya","Pavlov, Valentin","Villert, Alisa","Kolomiets, Larisa","Kzhyshkowska, Julia"],"dc.date.accessioned_dt":"2025-05-07T11:01:55Z","dc.date.accessioned":["2025-05-07T11:01:55Z"],"dc.date.available":["2025-05-07T11:01:55Z"],"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":["Ovarian cancer (OC) is the most lethal gynecologic malignancy worldwide. The major clinical challenge includes the asymptomatic state of the disease, making diagnosis possible only at advanced stages. Another OC complication is the high relapse rate and poor prognosis following the standard first-line treatment with platinum-based chemotherapy. At present, numerous clinical trials are being conducted focusing on immunotherapy in OC; nevertheless, there are still no FDA-approved indications. Personalized decision regarding the immunotherapy, including immune checkpoint blockade and immune cell–based immunotherapies, can depend on the effective antigen presentation required for the cytotoxic immune response. The major aim of our study was to uncover tumor-specific transcriptional and epigenetic changes in peripheral blood monocytes in patients with high-grade serous ovarian cancer (HGSOC). Another key point was to elucidate how chemotherapy can reprogram monocytes and how that relates to changes in other immune subpopulations in the blood. To this end, we performed single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from patients with HGSOC who underwent neoadjuvant chemotherapeutic treatment (NACT) and in treatment-naïve patients. Monocyte cluster was significantly affected by tumor-derived factors as well as by chemotherapeutic treatment. Bioinformatical analysis revealed three distinct monocyte subpopulations within PBMCs based on feature gene expression – CD14.Mn.S100A8.9hi, CD14.Mn.MHC2hi and CD16.Mn subsets. The intriguing result was that NACT induced antigen presentation in monocytes by the transcriptional upregulation of MHC class II molecules, but not by epigenetic changes. Increased MHC class II gene expression was a feature observed across all three monocyte subpopulations after chemotherapy. Our data also demonstrated that chemotherapy inhibited interferon-dependent signaling pathways, but activated some TGFb-related genes. Our results can enable personalized decision regarding the necessity to systemically re-educate immune cells to prime ovarian cancer to respond to anti-cancer therapy or to improve personalized prescription of existing immunotherapy in either combination with chemotherapy or a monotherapy regimen. Copyright © 2024 Larionova, Iamshchikov, Kazakova, Rakina, Menyalo, Enikeeva, Rafikova, Sharifyanova, Pavlov, Villert, Kolomiets and Kzhyshkowska."],"dc.description.abstract":["Ovarian cancer (OC) is the most lethal gynecologic malignancy worldwide. The major clinical challenge includes the asymptomatic state of the disease, making diagnosis possible only at advanced stages. Another OC complication is the high relapse rate and poor prognosis following the standard first-line treatment with platinum-based chemotherapy. At present, numerous clinical trials are being conducted focusing on immunotherapy in OC; nevertheless, there are still no FDA-approved indications. Personalized decision regarding the immunotherapy, including immune checkpoint blockade and immune cell–based immunotherapies, can depend on the effective antigen presentation required for the cytotoxic immune response. The major aim of our study was to uncover tumor-specific transcriptional and epigenetic changes in peripheral blood monocytes in patients with high-grade serous ovarian cancer (HGSOC). Another key point was to elucidate how chemotherapy can reprogram monocytes and how that relates to changes in other immune subpopulations in the blood. To this end, we performed single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from patients with HGSOC who underwent neoadjuvant chemotherapeutic treatment (NACT) and in treatment-naïve patients. Monocyte cluster was significantly affected by tumor-derived factors as well as by chemotherapeutic treatment. Bioinformatical analysis revealed three distinct monocyte subpopulations within PBMCs based on feature gene expression – CD14.Mn.S100A8.9hi, CD14.Mn.MHC2hi and CD16.Mn subsets. The intriguing result was that NACT induced antigen presentation in monocytes by the transcriptional upregulation of MHC class II molecules, but not by epigenetic changes. Increased MHC class II gene expression was a feature observed across all three monocyte subpopulations after chemotherapy. Our data also demonstrated that chemotherapy inhibited interferon-dependent signaling pathways, but activated some TGFb-related genes. Our results can enable personalized decision regarding the necessity to systemically re-educate immune cells to prime ovarian cancer to respond to anti-cancer therapy or to improve personalized prescription of existing immunotherapy in either combination with chemotherapy or a monotherapy regimen. Copyright © 2024 Larionova, Iamshchikov, Kazakova, Rakina, Menyalo, Enikeeva, Rafikova, Sharifyanova, Pavlov, Villert, Kolomiets and Kzhyshkowska."],"dc.description.abstract.en":["Ovarian cancer (OC) is the most lethal gynecologic malignancy worldwide. The major clinical challenge includes the asymptomatic state of the disease, making diagnosis possible only at advanced stages. Another OC complication is the high relapse rate and poor prognosis following the standard first-line treatment with platinum-based chemotherapy. At present, numerous clinical trials are being conducted focusing on immunotherapy in OC; nevertheless, there are still no FDA-approved indications. Personalized decision regarding the immunotherapy, including immune checkpoint blockade and immune cell–based immunotherapies, can depend on the effective antigen presentation required for the cytotoxic immune response. The major aim of our study was to uncover tumor-specific transcriptional and epigenetic changes in peripheral blood monocytes in patients with high-grade serous ovarian cancer (HGSOC). Another key point was to elucidate how chemotherapy can reprogram monocytes and how that relates to changes in other immune subpopulations in the blood. To this end, we performed single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from patients with HGSOC who underwent neoadjuvant chemotherapeutic treatment (NACT) and in treatment-naïve patients. Monocyte cluster was significantly affected by tumor-derived factors as well as by chemotherapeutic treatment. Bioinformatical analysis revealed three distinct monocyte subpopulations within PBMCs based on feature gene expression – CD14.Mn.S100A8.9hi, CD14.Mn.MHC2hi and CD16.Mn subsets. The intriguing result was that NACT induced antigen presentation in monocytes by the transcriptional upregulation of MHC class II molecules, but not by epigenetic changes. Increased MHC class II gene expression was a feature observed across all three monocyte subpopulations after chemotherapy. Our data also demonstrated that chemotherapy inhibited interferon-dependent signaling pathways, but activated some TGFb-related genes. Our results can enable personalized decision regarding the necessity to systemically re-educate immune cells to prime ovarian cancer to respond to anti-cancer therapy or to improve personalized prescription of existing immunotherapy in either combination with chemotherapy or a monotherapy regimen. Copyright © 2024 Larionova, Iamshchikov, Kazakova, Rakina, Menyalo, Enikeeva, Rafikova, Sharifyanova, Pavlov, Villert, Kolomiets and Kzhyshkowska."],"dc.doi":["10.3389/fimmu.2024.1414716"],"dc.doi.en":["10.3389/fimmu.2024.1414716"],"dc.identifier.issn":["1664-3224"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8832"],"dc.language.iso":["en"],"dc.language.iso.en":["en"],"dc.publisher":["Frontiers Media SA"],"dc.publisher.en":["Frontiers Media SA"],"dc.relation.ispartofseries":["Frontiers in Immunology;v. 15"],"dc.relation.ispartofseries.en":["Frontiers in Immunology;v. 15"],"subject":["antigen presentation","chemotherapy","methylation","monocyte","ovarian cancer","single cell sequencing","transcriptome","Scopus"],"subject_keyword":["antigen presentation","antigen presentation","chemotherapy","chemotherapy","methylation","methylation","monocyte","monocyte","ovarian cancer","ovarian cancer","single cell sequencing","single cell sequencing","transcriptome","transcriptome","Scopus","Scopus"],"subject_ac":["antigen presentation\n|||\nantigen presentation","chemotherapy\n|||\nchemotherapy","methylation\n|||\nmethylation","monocyte\n|||\nmonocyte","ovarian cancer\n|||\novarian cancer","single cell sequencing\n|||\nsingle cell sequencing","transcriptome\n|||\ntranscriptome","scopus\n|||\nScopus"],"subject_tax_0_filter":["antigen presentation\n|||\nantigen presentation","chemotherapy\n|||\nchemotherapy","methylation\n|||\nmethylation","monocyte\n|||\nmonocyte","ovarian cancer\n|||\novarian cancer","single cell sequencing\n|||\nsingle cell sequencing","transcriptome\n|||\ntranscriptome","scopus\n|||\nScopus"],"subject_filter":["antigen presentation\n|||\nantigen presentation","chemotherapy\n|||\nchemotherapy","methylation\n|||\nmethylation","monocyte\n|||\nmonocyte","ovarian cancer\n|||\novarian cancer","single cell sequencing\n|||\nsingle cell sequencing","transcriptome\n|||\ntranscriptome","scopus\n|||\nScopus"],"dc.subject_mlt":["antigen presentation","chemotherapy","methylation","monocyte","ovarian cancer","single cell sequencing","transcriptome","Scopus"],"dc.subject":["antigen presentation","chemotherapy","methylation","monocyte","ovarian cancer","single cell sequencing","transcriptome","Scopus"],"dc.subject.en":["antigen presentation","chemotherapy","methylation","monocyte","ovarian cancer","single cell sequencing","transcriptome","Scopus"],"title":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"title_keyword":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"title_ac":["platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma\n|||\nPlatinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.title_sort":"Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma","dc.title_hl":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.title_mlt":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.title":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.title_stored":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.en":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.title.alternative":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.title.alternative.en":["Platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma"],"dc.type":["Article"],"dc.type.en":["Article"],"publication_grp":["123456789/8832"],"bi_2_dis_filter":["kazakova, anna\n|||\nKazakova, Anna","rakina, militsa\n|||\nRakina, Militsa","enikeeva, kadriia\n|||\nEnikeeva, Kadriia","larionova, irina\n|||\nLarionova, Irina","rafikova, guzel\n|||\nRafikova, Guzel","kzhyshkowska, julia\n|||\nKzhyshkowska, Julia","kolomiets, larisa\n|||\nKolomiets, Larisa","menyalo, maxim\n|||\nMenyalo, Maxim","sharifyanova, yuliya\n|||\nSharifyanova, Yuliya","pavlov, valentin\n|||\nPavlov, Valentin","villert, alisa\n|||\nVillert, Alisa","iamshchikov, pavel\n|||\nIamshchikov, Pavel"],"bi_2_dis_partial":["Menyalo, Maxim","Kolomiets, Larisa","Kzhyshkowska, Julia","Enikeeva, Kadriia","Rafikova, Guzel","Rakina, Militsa","Sharifyanova, Yuliya","Pavlov, Valentin","Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Villert, Alisa"],"bi_2_dis_value_filter":["Menyalo, Maxim","Kolomiets, Larisa","Kzhyshkowska, Julia","Enikeeva, Kadriia","Rafikova, Guzel","Rakina, Militsa","Sharifyanova, Yuliya","Pavlov, Valentin","Larionova, Irina","Iamshchikov, Pavel","Kazakova, Anna","Villert, Alisa"],"bi_4_dis_filter":["ovarian cancer\n|||\novarian cancer","transcriptome\n|||\ntranscriptome","chemotherapy\n|||\nchemotherapy","antigen presentation\n|||\nantigen presentation","methylation\n|||\nmethylation","single cell sequencing\n|||\nsingle cell sequencing","scopus\n|||\nScopus","monocyte\n|||\nmonocyte"],"bi_4_dis_partial":["antigen presentation","ovarian cancer","methylation","transcriptome","Scopus","monocyte","single cell sequencing","chemotherapy"],"bi_4_dis_value_filter":["antigen presentation","ovarian cancer","methylation","transcriptome","Scopus","monocyte","single cell sequencing","chemotherapy"],"bi_sort_1_sort":"platinum-based chemotherapy promotes antigen presenting potential in monocytes of patients with high-grade serous ovarian carcinoma","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-05-07T11:01:55Z","read":["g0"],"_version_":1831459417815515136},{"SolrIndexer.lastIndexed":"2025-04-28T10:11:22.7Z","search.uniqueid":"2-7893","search.resourcetype":2,"search.resourceid":7893,"handle":"123456789/8782","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","dc.abstract":["Обоснование. Точность определения давности наступления смерти человека имеет существенное юридическое зна-чение, поскольку от успешности решения этого вопроса во многом зависит исход расследования преступления против жизни и здоровья граждан . Особую актуальность вопрос определения давности наступления смерти приобретает в тех случаях, когда она наступила в условиях неочевидности, а мёртвое тело исследуют в позднем посмертном перио-де . При отсутствии убедительных доказательств ненасильственной смерти сотрудники следственных органов исходят из версии убийства неизвестными лицами, а точное время смерти помогает сузить круг расследования и подтвердит или опровергнуть эту версию . Однако гнилостная биотрансформация мёртвого тела затрудняет работу судебно-ме-дицинского эксперта, снижая точность ответов на вопросы следователя, что требует поиска новых объективных экс-пертных критериев .Цель исследования — изучить изменения удельной электропроводности синовиальной жидкости коленных суставов трупа при развитии его гнилостной трансформации с математическим описанием выявленных изменений на основе модели многослойного перцептрона для обоснования перспективности определения давности наступления смерти кондуктометрическим способом . Материалы и методы. Исследованы кондуктометрические свойства синовиальной жидкости коленных суставов 103 трупов лиц, умерших в возрасте 20–87 лет по различным причинам . Анализ проводили в позднем посмерт-ном периоде (до 10 сут) . Давность наступления смерти устанавливали комплексно с учётом медицинских, судебно- медицинских и следственных данных . Измерение электропроводности проводили с помощью портативного измерите-ля параметров «АКИП RLC 6109» с погрешностью 0,1% при частотах 100 Гц, 1 и 10 кГц . Результаты. Установлено, что удельная электропроводность синовиальной жидкости при частотах 100 Гц и 1 кГц достоверно зависит от давности смерти . Оптимальная математическая модель, описывающая данную взаимосвязь, — полином второй степени . Также предложена модель с архитектурой многослойного перцептрона 2-5-1, обеспечиваю-щая расчёт с погрешностью, не превышающей установленного в работе предела (достоверность >95%) . Заключение. Кондуктометрический анализ синовиальной жидкости коленных суставов трупа в позднем постморталь-ном периоде позволяет достоверно выявлять изменения её удельной электропроводности, обусловленные временем, прошедшим с момента смерти . Эти изменения могут служить основой для математической модели расчёта давности наступления смерти в позднем посмертном периоде . Наиболее точные предсказания обеспечивает модель No 2 с ар-хитектурой многослойного перцептрона 2-5-1, что делает её наиболее пригодной для решения данной задачи ."],"dc.abstract.ru_RU":["Обоснование. Точность определения давности наступления смерти человека имеет существенное юридическое зна-чение, поскольку от успешности решения этого вопроса во многом зависит исход расследования преступления против жизни и здоровья граждан . Особую актуальность вопрос определения давности наступления смерти приобретает в тех случаях, когда она наступила в условиях неочевидности, а мёртвое тело исследуют в позднем посмертном перио-де . При отсутствии убедительных доказательств ненасильственной смерти сотрудники следственных органов исходят из версии убийства неизвестными лицами, а точное время смерти помогает сузить круг расследования и подтвердит или опровергнуть эту версию . Однако гнилостная биотрансформация мёртвого тела затрудняет работу судебно-ме-дицинского эксперта, снижая точность ответов на вопросы следователя, что требует поиска новых объективных экс-пертных критериев .Цель исследования — изучить изменения удельной электропроводности синовиальной жидкости коленных суставов трупа при развитии его гнилостной трансформации с математическим описанием выявленных изменений на основе модели многослойного перцептрона для обоснования перспективности определения давности наступления смерти кондуктометрическим способом . Материалы и методы. Исследованы кондуктометрические свойства синовиальной жидкости коленных суставов 103 трупов лиц, умерших в возрасте 20–87 лет по различным причинам . Анализ проводили в позднем посмерт-ном периоде (до 10 сут) . Давность наступления смерти устанавливали комплексно с учётом медицинских, судебно- медицинских и следственных данных . Измерение электропроводности проводили с помощью портативного измерите-ля параметров «АКИП RLC 6109» с погрешностью 0,1% при частотах 100 Гц, 1 и 10 кГц . Результаты. Установлено, что удельная электропроводность синовиальной жидкости при частотах 100 Гц и 1 кГц достоверно зависит от давности смерти . Оптимальная математическая модель, описывающая данную взаимосвязь, — полином второй степени . Также предложена модель с архитектурой многослойного перцептрона 2-5-1, обеспечиваю-щая расчёт с погрешностью, не превышающей установленного в работе предела (достоверность >95%) . Заключение. Кондуктометрический анализ синовиальной жидкости коленных суставов трупа в позднем постморталь-ном периоде позволяет достоверно выявлять изменения её удельной электропроводности, обусловленные временем, прошедшим с момента смерти . Эти изменения могут служить основой для математической модели расчёта давности наступления смерти в позднем посмертном периоде . Наиболее точные предсказания обеспечивает модель No 2 с ар-хитектурой многослойного перцептрона 2-5-1, что делает её наиболее пригодной для решения данной задачи ."],"author":["Khalikov, Airat A.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Pozdeev, Alexey R.","Халиков, А .А .","Вавилов, А .Ю .","Агзамов, В .В .","Поздеев, А .Р ."],"author_keyword":["Khalikov, Airat A.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Pozdeev, Alexey R.","Халиков, А .А .","Вавилов, А .Ю .","Агзамов, В .В .","Поздеев, А .Р ."],"author_ac":["khalikov, airat a.\n|||\nKhalikov, Airat A.","vavilov, alexey yu.\n|||\nVavilov, Alexey Yu.","agzamov, vadim v.\n|||\nAgzamov, Vadim V.","pozdeev, alexey r.\n|||\nPozdeev, Alexey R.","халиков, а .а .\n|||\nХаликов, А .А .","вавилов, а .ю .\n|||\nВавилов, А .Ю .","агзамов, в .в .\n|||\nАгзамов, В .В .","поздеев, а .р .\n|||\nПоздеев, А .Р ."],"author_filter":["khalikov, airat a.\n|||\nKhalikov, Airat A.","vavilov, alexey yu.\n|||\nVavilov, Alexey Yu.","agzamov, vadim v.\n|||\nAgzamov, Vadim V.","pozdeev, alexey r.\n|||\nPozdeev, Alexey R.","халиков, а .а .\n|||\nХаликов, А .А .","вавилов, а .ю .\n|||\nВавилов, А .Ю .","агзамов, в .в .\n|||\nАгзамов, В .В .","поздеев, а .р .\n|||\nПоздеев, А .Р ."],"dc.contributor.author_hl":["Khalikov, Airat A.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Pozdeev, Alexey R.","Халиков, А .А .","Вавилов, А .Ю .","Агзамов, В .В .","Поздеев, А .Р ."],"dc.contributor.author_mlt":["Khalikov, Airat A.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Pozdeev, Alexey R.","Халиков, А .А .","Вавилов, А .Ю .","Агзамов, В .В .","Поздеев, А .Р ."],"dc.contributor.author":["Khalikov, Airat A.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Pozdeev, Alexey R.","Халиков, А .А .","Вавилов, А .Ю .","Агзамов, В .В .","Поздеев, А .Р ."],"dc.contributor.author_stored":["Khalikov, Airat A.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Vavilov, Alexey Yu.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Agzamov, Vadim V.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Pozdeev, Alexey R.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Халиков, А .А .\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Вавилов, А .Ю .\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Агзамов, В .В .\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Поздеев, А .Р .\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.contributor.author.en":["Khalikov, Airat A.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Pozdeev, Alexey R."],"dc.contributor.author.ru_RU":["Халиков, А .А .","Вавилов, А .Ю .","Агзамов, В .В .","Поздеев, А .Р ."],"dc.date.accessioned_dt":"2025-04-28T10:08:41Z","dc.date.accessioned":["2025-04-28T10:08:41Z"],"dc.date.available":["2025-04-28T10:08:41Z"],"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: The determination of time since death is of significant legal importance, because the findings of investigation of a crime against the life and health largely depends on the successful resolution of this issue. The determination of time since death becomes particularly significant in cases where the death circumstances are not evident and the cadaver is examined in the late postmortem period. Without conclusive evidence of a non-violent death, investigators assume homicide; the exact death time since death serves to narrow the options and confirm or refute this assumption. The putrefaction complicates the forensic examination, limiting the accuracy of answers to the investigator's questions and requiring the new objective expert criteria search. AIM: To assess changes in electrical conductivity of synovial fluid of knee joints at the stage putrefaction with mathematical description of the revealed changes on the basis of a multilayer perceptron to substantiate the prospects of determining the time since death by conductometric method. MATERIALS AND METHODS: Conductometric properties of synovial fluid of knee joints of 103 cadavers who died of various causes at the age of 20–87 years were studied. The study was performed in the late postmortem period (up to 10 days). The time since death was established comprehensively considering medical, forensic and investigative data. The electrical conductivity was measured using AKIP RLC 6109 measuring system, with an error of 0.1%, at frequencies of 0.1 kHz, 1 kHz, and 10 kHz. RESULTS: Electrical conductivity of synovial fluid at 100 Hz and 1 kHz was found to depend significantly on the time since death. The optimal mathematical model describing this correlation is a second degree polynomial. A model with a 2-5-1 multilayer perceptron architecture is also presented with an error that does not exceed the set limit (reliability >95%). CONCLUSIONS: Conductometric analysis of synovial fluid of cadavers’ knee joints in the late postmortem period allows to reliably detect changes in its electrical conductivity determined by the time since death. These changes can serve as a mathematical model basis for calculating the time since death in the late postmortem period. The most accurate predictions are provided by model No. 2 with a 2-5-1 multilayer perceptron architecture, making it the most suitable for this task. © 2025, Eco-Vector LLC. All rights reserved."],"dc.description.abstract":["BACKGROUND: The determination of time since death is of significant legal importance, because the findings of investigation of a crime against the life and health largely depends on the successful resolution of this issue. The determination of time since death becomes particularly significant in cases where the death circumstances are not evident and the cadaver is examined in the late postmortem period. Without conclusive evidence of a non-violent death, investigators assume homicide; the exact death time since death serves to narrow the options and confirm or refute this assumption. The putrefaction complicates the forensic examination, limiting the accuracy of answers to the investigator's questions and requiring the new objective expert criteria search. AIM: To assess changes in electrical conductivity of synovial fluid of knee joints at the stage putrefaction with mathematical description of the revealed changes on the basis of a multilayer perceptron to substantiate the prospects of determining the time since death by conductometric method. MATERIALS AND METHODS: Conductometric properties of synovial fluid of knee joints of 103 cadavers who died of various causes at the age of 20–87 years were studied. The study was performed in the late postmortem period (up to 10 days). The time since death was established comprehensively considering medical, forensic and investigative data. The electrical conductivity was measured using AKIP RLC 6109 measuring system, with an error of 0.1%, at frequencies of 0.1 kHz, 1 kHz, and 10 kHz. RESULTS: Electrical conductivity of synovial fluid at 100 Hz and 1 kHz was found to depend significantly on the time since death. The optimal mathematical model describing this correlation is a second degree polynomial. A model with a 2-5-1 multilayer perceptron architecture is also presented with an error that does not exceed the set limit (reliability >95%). CONCLUSIONS: Conductometric analysis of synovial fluid of cadavers’ knee joints in the late postmortem period allows to reliably detect changes in its electrical conductivity determined by the time since death. These changes can serve as a mathematical model basis for calculating the time since death in the late postmortem period. The most accurate predictions are provided by model No. 2 with a 2-5-1 multilayer perceptron architecture, making it the most suitable for this task. © 2025, Eco-Vector LLC. All rights reserved."],"dc.description.abstract.en":["BACKGROUND: The determination of time since death is of significant legal importance, because the findings of investigation of a crime against the life and health largely depends on the successful resolution of this issue. The determination of time since death becomes particularly significant in cases where the death circumstances are not evident and the cadaver is examined in the late postmortem period. Without conclusive evidence of a non-violent death, investigators assume homicide; the exact death time since death serves to narrow the options and confirm or refute this assumption. The putrefaction complicates the forensic examination, limiting the accuracy of answers to the investigator's questions and requiring the new objective expert criteria search. AIM: To assess changes in electrical conductivity of synovial fluid of knee joints at the stage putrefaction with mathematical description of the revealed changes on the basis of a multilayer perceptron to substantiate the prospects of determining the time since death by conductometric method. MATERIALS AND METHODS: Conductometric properties of synovial fluid of knee joints of 103 cadavers who died of various causes at the age of 20–87 years were studied. The study was performed in the late postmortem period (up to 10 days). The time since death was established comprehensively considering medical, forensic and investigative data. The electrical conductivity was measured using AKIP RLC 6109 measuring system, with an error of 0.1%, at frequencies of 0.1 kHz, 1 kHz, and 10 kHz. RESULTS: Electrical conductivity of synovial fluid at 100 Hz and 1 kHz was found to depend significantly on the time since death. The optimal mathematical model describing this correlation is a second degree polynomial. A model with a 2-5-1 multilayer perceptron architecture is also presented with an error that does not exceed the set limit (reliability >95%). CONCLUSIONS: Conductometric analysis of synovial fluid of cadavers’ knee joints in the late postmortem period allows to reliably detect changes in its electrical conductivity determined by the time since death. These changes can serve as a mathematical model basis for calculating the time since death in the late postmortem period. The most accurate predictions are provided by model No. 2 with a 2-5-1 multilayer perceptron architecture, making it the most suitable for this task. © 2025, Eco-Vector LLC. All rights reserved."],"dc.doi":["10.17816/fm16193"],"dc.doi.en":["10.17816/fm16193"],"dc.identifier.issn":["2411-8729"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8782"],"dc.publisher":["Eco-Vector LLC"],"dc.publisher.en":["Eco-Vector LLC"],"dc.relation.ispartofseries":["Russian Journal of Forensic Medicine;т. 11 № 1"],"dc.relation.ispartofseries.en":["Russian Journal of Forensic Medicine;т. 11 № 1"],"subject":["electrical conductivity","knee joint","late postmortem period","mathematical model","multilayer perceptron","synovial fluid","time since death","Scopus","электропроводность","синовиальная жидкость","коленный сустав","давность наступления смерти","поздний посмертный период","математическая модель","многослойный перцептрон"],"subject_keyword":["electrical conductivity","electrical conductivity","knee joint","knee joint","late postmortem period","late postmortem period","mathematical model","mathematical model","multilayer perceptron","multilayer perceptron","synovial fluid","synovial fluid","time since death","time since death","Scopus","Scopus","электропроводность","электропроводность","синовиальная жидкость","синовиальная жидкость","коленный сустав","коленный сустав","давность наступления смерти","давность наступления смерти","поздний посмертный период","поздний посмертный период","математическая модель","математическая модель","многослойный перцептрон","многослойный перцептрон"],"subject_ac":["electrical conductivity\n|||\nelectrical conductivity","knee joint\n|||\nknee joint","late postmortem period\n|||\nlate postmortem period","mathematical model\n|||\nmathematical model","multilayer perceptron\n|||\nmultilayer perceptron","synovial fluid\n|||\nsynovial fluid","time since death\n|||\ntime since death","scopus\n|||\nScopus","электропроводность\n|||\nэлектропроводность","синовиальная жидкость\n|||\nсиновиальная жидкость","коленный сустав\n|||\nколенный сустав","давность наступления смерти\n|||\nдавность наступления смерти","поздний посмертный период\n|||\nпоздний посмертный период","математическая модель\n|||\nматематическая модель","многослойный перцептрон\n|||\nмногослойный перцептрон"],"subject_tax_0_filter":["electrical conductivity\n|||\nelectrical conductivity","knee joint\n|||\nknee joint","late postmortem period\n|||\nlate postmortem period","mathematical model\n|||\nmathematical model","multilayer perceptron\n|||\nmultilayer perceptron","synovial fluid\n|||\nsynovial fluid","time since death\n|||\ntime since death","scopus\n|||\nScopus","электропроводность\n|||\nэлектропроводность","синовиальная жидкость\n|||\nсиновиальная жидкость","коленный сустав\n|||\nколенный сустав","давность наступления смерти\n|||\nдавность наступления смерти","поздний посмертный период\n|||\nпоздний посмертный период","математическая модель\n|||\nматематическая модель","многослойный перцептрон\n|||\nмногослойный перцептрон"],"subject_filter":["electrical conductivity\n|||\nelectrical conductivity","knee joint\n|||\nknee joint","late postmortem period\n|||\nlate postmortem period","mathematical model\n|||\nmathematical model","multilayer perceptron\n|||\nmultilayer perceptron","synovial fluid\n|||\nsynovial fluid","time since death\n|||\ntime since death","scopus\n|||\nScopus","электропроводность\n|||\nэлектропроводность","синовиальная жидкость\n|||\nсиновиальная жидкость","коленный сустав\n|||\nколенный сустав","давность наступления смерти\n|||\nдавность наступления смерти","поздний посмертный период\n|||\nпоздний посмертный период","математическая модель\n|||\nматематическая модель","многослойный перцептрон\n|||\nмногослойный перцептрон"],"dc.subject_mlt":["electrical conductivity","knee joint","late postmortem period","mathematical model","multilayer perceptron","synovial fluid","time since death","Scopus","электропроводность","синовиальная жидкость","коленный сустав","давность наступления смерти","поздний посмертный период","математическая модель","многослойный перцептрон"],"dc.subject":["electrical conductivity","knee joint","late postmortem period","mathematical model","multilayer perceptron","synovial fluid","time since death","Scopus","электропроводность","синовиальная жидкость","коленный сустав","давность наступления смерти","поздний посмертный период","математическая модель","многослойный перцептрон"],"dc.subject.en":["electrical conductivity","knee joint","late postmortem period","mathematical model","multilayer perceptron","synovial fluid","time since death","Scopus"],"dc.subject.ru_RU":["электропроводность","синовиальная жидкость","коленный сустав","давность наступления смерти","поздний посмертный период","математическая модель","многослойный перцептрон"],"title":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"title_keyword":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"title_ac":["electrical conductivity of synovial fluid as a measure of death time in late postmortem examination\n|||\nElectrical conductivity of synovial fluid as a measure of death time in late postmortem examination","удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде\n|||\nУдельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.title_sort":"Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","dc.title_hl":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.title_mlt":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.title":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.title_stored":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU"],"dc.title.en":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination"],"dc.title.ru_RU":["Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.title.alternative":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.title.alternative.en":["Electrical conductivity of synovial fluid as a measure of death time in late postmortem examination"],"dc.title.alternative.ru_RU":["Удельная электропроводность синовиальной жидкости как критерий давности наступления смерти человека при исследовании трупа в позднем посмертном периоде"],"dc.type":["Article"],"dc.type.ru_RU":["Article"],"publication_grp":["123456789/8782"],"bi_2_dis_filter":["agzamov, vadim v.\n|||\nAgzamov, Vadim V.","халиков, а .а .\n|||\nХаликов, А .А .","vavilov, alexey yu.\n|||\nVavilov, Alexey Yu.","агзамов, в .в .\n|||\nАгзамов, В .В .","khalikov, airat a.\n|||\nKhalikov, Airat A.","поздеев, а .р .\n|||\nПоздеев, А .Р .","pozdeev, alexey r.\n|||\nPozdeev, Alexey R.","вавилов, а .ю .\n|||\nВавилов, А .Ю ."],"bi_2_dis_partial":["Pozdeev, Alexey R.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Халиков, А .А .","Поздеев, А .Р .","Агзамов, В .В .","Khalikov, Airat A.","Вавилов, А .Ю ."],"bi_2_dis_value_filter":["Pozdeev, Alexey R.","Vavilov, Alexey Yu.","Agzamov, Vadim V.","Халиков, А .А .","Поздеев, А .Р .","Агзамов, В .В .","Khalikov, Airat A.","Вавилов, А .Ю ."],"bi_4_dis_filter":["knee joint\n|||\nknee joint","синовиальная жидкость\n|||\nсиновиальная жидкость","давность наступления смерти\n|||\nдавность наступления смерти","scopus\n|||\nScopus","multilayer perceptron\n|||\nmultilayer perceptron","electrical conductivity\n|||\nelectrical conductivity","late postmortem period\n|||\nlate postmortem period","time since death\n|||\ntime since death","коленный сустав\n|||\nколенный сустав","поздний посмертный период\n|||\nпоздний посмертный период","математическая модель\n|||\nматематическая модель","mathematical model\n|||\nmathematical model","электропроводность\n|||\nэлектропроводность","synovial fluid\n|||\nsynovial fluid","многослойный перцептрон\n|||\nмногослойный перцептрон"],"bi_4_dis_partial":["электропроводность","синовиальная жидкость","Scopus","knee joint","давность наступления смерти","поздний посмертный период","математическая модель","synovial fluid","mathematical model","multilayer perceptron","многослойный перцептрон","коленный сустав","electrical conductivity","late postmortem period","time since death"],"bi_4_dis_value_filter":["электропроводность","синовиальная жидкость","Scopus","knee joint","давность наступления смерти","поздний посмертный период","математическая модель","synovial fluid","mathematical model","multilayer perceptron","многослойный перцептрон","коленный сустав","electrical conductivity","late postmortem period","time since death"],"bi_sort_1_sort":"electrical conductivity of synovial fluid as a measure of death time in late postmortem examination","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-04-28T10:08:41Z","read":["g0"],"_version_":1830640767699255296},{"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":"2025-05-06T09:11:51.005Z","search.uniqueid":"2-7928","search.resourcetype":2,"search.resourceid":7928,"handle":"123456789/8817","location":["m229","l684"],"location.comm":["229"],"location.coll":["684"],"withdrawn":"false","discoverable":"true","dc.abstract":["Background: Atherosclerosis is the leading cause of cardiovascular pathology in adults around the world. Association of the disease with age indicates the presence of common mechanisms for the development of aging and atherosclerosis. More data is emerging in the scientific literature on the role of non-coding RNAs and transposable elements in the mechanisms of aging and atherosclerosis. The search for the exact molecular mechanisms of atherosclerosis at the epigenetic levels will allow the development of new therapeutic methods. The aim of the study: To determine the role of transposable elements and non-coding RNAs in the etiopathogenesis of atherosclerosis and their relationship with each other. Materials and methods: We used the Scopus, WoS, PubMed databases to analyze the role of miRNAs, long non-coding RNAs, and retroelements in the development of aging ant atherosclerosis. Results: According to the analyzed literature, an important factor in the development of atherosclerosis is the pathological activation of transposable elements during aging, causing an interferon response and aseptic inflammation in the walls of blood vessels. The role of epigenetic factors in the etiopathogenesis of atherosclerosis has been determined, including microRNAs and long non-coding RNAs that change the expression of specific genes in macrophages, vascular smooth muscle cells and endothelial cells. Activation of transposable elements is reflected in changes in the expression of long non-coding RNAs and microRNAs that originate from them in evolution or are formed during the processing of their transcripts. An analysis of the scientific literature revealed 64 microRNAs derived from transposable elements, changes in the expression of which are specific to atherosclerosis. Of the 64 identified microRNAs, 34 are associated with aging, which indicates the role of activation transposable elements during aging in the initiation of the development of atherosclerosis. Conclusion: Since transposable elements are drivers of epigenetic regulation in ontogenesis, the results obtained for the first time in the scientific literature describe the most likely mechanisms of the influence of aging mechanisms on the development of atherosclerosis at the epigenetic level. This is due to the pathological activation of transposable elements during aging, which affects changes in the expression of non-coding RNAs derived from them due to the presence of complementary sequences and participation in general epigenetic networks regulating genome functioning. The data obtained on the role of microRNAs derived from transposable elements in the development of both atherosclerosis and aging confirm the proposed mechanisms of disease pathogenesis. © 2025 Belgorod State National Research University. All rights reserved."],"dc.abstract.en":["Background: Atherosclerosis is the leading cause of cardiovascular pathology in adults around the world. Association of the disease with age indicates the presence of common mechanisms for the development of aging and atherosclerosis. More data is emerging in the scientific literature on the role of non-coding RNAs and transposable elements in the mechanisms of aging and atherosclerosis. The search for the exact molecular mechanisms of atherosclerosis at the epigenetic levels will allow the development of new therapeutic methods. The aim of the study: To determine the role of transposable elements and non-coding RNAs in the etiopathogenesis of atherosclerosis and their relationship with each other. Materials and methods: We used the Scopus, WoS, PubMed databases to analyze the role of miRNAs, long non-coding RNAs, and retroelements in the development of aging ant atherosclerosis. Results: According to the analyzed literature, an important factor in the development of atherosclerosis is the pathological activation of transposable elements during aging, causing an interferon response and aseptic inflammation in the walls of blood vessels. The role of epigenetic factors in the etiopathogenesis of atherosclerosis has been determined, including microRNAs and long non-coding RNAs that change the expression of specific genes in macrophages, vascular smooth muscle cells and endothelial cells. Activation of transposable elements is reflected in changes in the expression of long non-coding RNAs and microRNAs that originate from them in evolution or are formed during the processing of their transcripts. An analysis of the scientific literature revealed 64 microRNAs derived from transposable elements, changes in the expression of which are specific to atherosclerosis. Of the 64 identified microRNAs, 34 are associated with aging, which indicates the role of activation transposable elements during aging in the initiation of the development of atherosclerosis. Conclusion: Since transposable elements are drivers of epigenetic regulation in ontogenesis, the results obtained for the first time in the scientific literature describe the most likely mechanisms of the influence of aging mechanisms on the development of atherosclerosis at the epigenetic level. This is due to the pathological activation of transposable elements during aging, which affects changes in the expression of non-coding RNAs derived from them due to the presence of complementary sequences and participation in general epigenetic networks regulating genome functioning. The data obtained on the role of microRNAs derived from transposable elements in the development of both atherosclerosis and aging confirm the proposed mechanisms of disease pathogenesis. © 2025 Belgorod State National Research University. All rights reserved."],"author":["Мустафин, Р.Н.","Хуснутдинова, Э.К.","Mustafin, Rustam N.","Khusnutdinova, Elza K."],"author_keyword":["Мустафин, Р.Н.","Хуснутдинова, Э.К.","Mustafin, Rustam N.","Khusnutdinova, Elza K."],"author_ac":["мустафин, р.н.\n|||\nМустафин, Р.Н.","хуснутдинова, э.к.\n|||\nХуснутдинова, Э.К.","mustafin, rustam n.\n|||\nMustafin, Rustam N.","khusnutdinova, elza k.\n|||\nKhusnutdinova, Elza K."],"author_filter":["мустафин, р.н.\n|||\nМустафин, Р.Н.","хуснутдинова, э.к.\n|||\nХуснутдинова, Э.К.","mustafin, rustam n.\n|||\nMustafin, Rustam N.","khusnutdinova, elza k.\n|||\nKhusnutdinova, Elza K."],"dc.contributor.author_hl":["Мустафин, Р.Н.","Хуснутдинова, Э.К.","Mustafin, Rustam N.","Khusnutdinova, Elza K."],"dc.contributor.author_mlt":["Мустафин, Р.Н.","Хуснутдинова, Э.К.","Mustafin, Rustam N.","Khusnutdinova, Elza K."],"dc.contributor.author":["Мустафин, Р.Н.","Хуснутдинова, Э.К.","Mustafin, Rustam N.","Khusnutdinova, Elza K."],"dc.contributor.author_stored":["Мустафин, Р.Н.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Хуснутдинова, Э.К.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Mustafin, Rustam N.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen","Khusnutdinova, Elza K.\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.contributor.author.ru_RU":["Мустафин, Р.Н.","Хуснутдинова, Э.К."],"dc.contributor.author.en":["Mustafin, Rustam N.","Khusnutdinova, Elza K."],"dc.date.accessioned_dt":"2025-05-06T09:10:32Z","dc.date.accessioned":["2025-05-06T09:10:32Z"],"dc.date.available":["2025-05-06T09:10:32Z"],"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":["Актуальность: Атеросклероз является ведущей причиной сердечно-сосудистой патологии\nвзрослого населения всего мира. Ассоциация болезни с возрастом свидетельствует о наличии\nобщих механизмов развития старения и атеросклероза. В научной литературе появляется все\nбольше данных о роли некодирующих РНК и мобильных генетических элементов в\nмеханизмах старения и атеросклероза. Поиск молекулярных механизмов болезни на\nэпигенетическом уровне позволит разрабатывать новые методы терапии. Цель исследования:\nОпределить роль транспозонов и некодирующих РНК в этиопатогенезе атеросклероза и их\nвзаимосвязь между собой в данных процессах. Материалы и методы: Использованы базы\nданных Scopus, WoS, PubMed для анализа роли микроРНК, длинных некодирующих РНК,\nтранспозонов в развитии старения и атеросклероза. Результаты: Согласно\nпроанализированной литературе, важным фактором развития атеросклероза является\nпатологическая активация транспозонов при старении, вызывающая интерфероновый ответ и\nасептическое воспаление в организме, в том числе в стенках сосудов. Определена роль\nэпигенетических факторов, в этиопатогенезе атеросклероза, включая микроРНК и длинные\nнекодирующие РНК, которые изменяют экспрессию специфических генов в макрофагах,\nгладкомышечных клетках сосудов и эндотелиоцитах. Активация транспозонов отражается в\nизменении экспрессии произошедших от них в эволюции или образующихся при процессинге\nих транскриптов длинных некодирующих РНК и микроРНК. Анализ научной литературы\nпозволил обнаружить 64 произошедших от транспозонов микроРНК, изменения экспрессии\nкоторых характерны для атеросклероза. Из 64 выявленных микроРНК 34 ассоциированы со\nстарением, что свидетельствует о роли патологически активированных при старении\nтранспозонов в инициации развития атеросклероза. Заключение: Поскольку транспозоны\nявляются драйверами эпигенетической регуляции в онтогенезе, полученные результаты\nвпервые в научной литературе описывают наиболее вероятные механизмы влияния механизмов старения на развитие атеросклероза на эпигенетическом уровне. Это обусловлено\nпатологической активацией транспозонов с возрастом, что оказывает влияние на изменение\nэкспрессии произошедших от них некодирующих РНК за счет наличия комплементарных\nпоследовательностей и участия в общих эпигенетических сетях регуляции функционирования\nгенома. Полученные данные о роли произошедших от транспозонов микроРНК в развитии как\nатеросклероза, так и старения, подтверждают предложенные механизмы патогенеза болезни."],"dc.description.abstract":["Актуальность: Атеросклероз является ведущей причиной сердечно-сосудистой патологии\nвзрослого населения всего мира. Ассоциация болезни с возрастом свидетельствует о наличии\nобщих механизмов развития старения и атеросклероза. В научной литературе появляется все\nбольше данных о роли некодирующих РНК и мобильных генетических элементов в\nмеханизмах старения и атеросклероза. Поиск молекулярных механизмов болезни на\nэпигенетическом уровне позволит разрабатывать новые методы терапии. Цель исследования:\nОпределить роль транспозонов и некодирующих РНК в этиопатогенезе атеросклероза и их\nвзаимосвязь между собой в данных процессах. Материалы и методы: Использованы базы\nданных Scopus, WoS, PubMed для анализа роли микроРНК, длинных некодирующих РНК,\nтранспозонов в развитии старения и атеросклероза. Результаты: Согласно\nпроанализированной литературе, важным фактором развития атеросклероза является\nпатологическая активация транспозонов при старении, вызывающая интерфероновый ответ и\nасептическое воспаление в организме, в том числе в стенках сосудов. Определена роль\nэпигенетических факторов, в этиопатогенезе атеросклероза, включая микроРНК и длинные\nнекодирующие РНК, которые изменяют экспрессию специфических генов в макрофагах,\nгладкомышечных клетках сосудов и эндотелиоцитах. Активация транспозонов отражается в\nизменении экспрессии произошедших от них в эволюции или образующихся при процессинге\nих транскриптов длинных некодирующих РНК и микроРНК. Анализ научной литературы\nпозволил обнаружить 64 произошедших от транспозонов микроРНК, изменения экспрессии\nкоторых характерны для атеросклероза. Из 64 выявленных микроРНК 34 ассоциированы со\nстарением, что свидетельствует о роли патологически активированных при старении\nтранспозонов в инициации развития атеросклероза. Заключение: Поскольку транспозоны\nявляются драйверами эпигенетической регуляции в онтогенезе, полученные результаты\nвпервые в научной литературе описывают наиболее вероятные механизмы влияния механизмов старения на развитие атеросклероза на эпигенетическом уровне. Это обусловлено\nпатологической активацией транспозонов с возрастом, что оказывает влияние на изменение\nэкспрессии произошедших от них некодирующих РНК за счет наличия комплементарных\nпоследовательностей и участия в общих эпигенетических сетях регуляции функционирования\nгенома. Полученные данные о роли произошедших от транспозонов микроРНК в развитии как\nатеросклероза, так и старения, подтверждают предложенные механизмы патогенеза болезни."],"dc.description.abstract.ru_RU":["Актуальность: Атеросклероз является ведущей причиной сердечно-сосудистой патологии\nвзрослого населения всего мира. Ассоциация болезни с возрастом свидетельствует о наличии\nобщих механизмов развития старения и атеросклероза. В научной литературе появляется все\nбольше данных о роли некодирующих РНК и мобильных генетических элементов в\nмеханизмах старения и атеросклероза. Поиск молекулярных механизмов болезни на\nэпигенетическом уровне позволит разрабатывать новые методы терапии. Цель исследования:\nОпределить роль транспозонов и некодирующих РНК в этиопатогенезе атеросклероза и их\nвзаимосвязь между собой в данных процессах. Материалы и методы: Использованы базы\nданных Scopus, WoS, PubMed для анализа роли микроРНК, длинных некодирующих РНК,\nтранспозонов в развитии старения и атеросклероза. Результаты: Согласно\nпроанализированной литературе, важным фактором развития атеросклероза является\nпатологическая активация транспозонов при старении, вызывающая интерфероновый ответ и\nасептическое воспаление в организме, в том числе в стенках сосудов. Определена роль\nэпигенетических факторов, в этиопатогенезе атеросклероза, включая микроРНК и длинные\nнекодирующие РНК, которые изменяют экспрессию специфических генов в макрофагах,\nгладкомышечных клетках сосудов и эндотелиоцитах. Активация транспозонов отражается в\nизменении экспрессии произошедших от них в эволюции или образующихся при процессинге\nих транскриптов длинных некодирующих РНК и микроРНК. Анализ научной литературы\nпозволил обнаружить 64 произошедших от транспозонов микроРНК, изменения экспрессии\nкоторых характерны для атеросклероза. Из 64 выявленных микроРНК 34 ассоциированы со\nстарением, что свидетельствует о роли патологически активированных при старении\nтранспозонов в инициации развития атеросклероза. Заключение: Поскольку транспозоны\nявляются драйверами эпигенетической регуляции в онтогенезе, полученные результаты\nвпервые в научной литературе описывают наиболее вероятные механизмы влияния механизмов старения на развитие атеросклероза на эпигенетическом уровне. Это обусловлено\nпатологической активацией транспозонов с возрастом, что оказывает влияние на изменение\nэкспрессии произошедших от них некодирующих РНК за счет наличия комплементарных\nпоследовательностей и участия в общих эпигенетических сетях регуляции функционирования\nгенома. Полученные данные о роли произошедших от транспозонов микроРНК в развитии как\nатеросклероза, так и старения, подтверждают предложенные механизмы патогенеза болезни."],"dc.doi":["10.18413/2658-6533-2025-11-1-0-2"],"dc.doi.en":["10.18413/2658-6533-2025-11-1-0-2"],"dc.identifier.issn":["2658-6533"],"dc.identifier.uri":["http://hdl.handle.net/123456789/8817"],"dc.publisher":["Belgorod State National Research University"],"dc.publisher.en":["Belgorod State National Research University"],"dc.relation.ispartofseries":["Research Results in Biomedicine;т. 11 № 1"],"dc.relation.ispartofseries.en":["Research Results in Biomedicine;т. 11 № 1"],"subject":["атеросклероз","воспаление","длинные некодирующие РНК","микроРНК","старение","транспозоны","Scopus","aging","atherosclerosis","inflammation","long non-coding RNA","microRNA","transposable elements"],"subject_keyword":["атеросклероз","атеросклероз","воспаление","воспаление","длинные некодирующие РНК","длинные некодирующие РНК","микроРНК","микроРНК","старение","старение","транспозоны","транспозоны","Scopus","Scopus","aging","aging","atherosclerosis","atherosclerosis","inflammation","inflammation","long non-coding RNA","long non-coding RNA","microRNA","microRNA","transposable elements","transposable elements"],"subject_ac":["атеросклероз\n|||\nатеросклероз","воспаление\n|||\nвоспаление","длинные некодирующие рнк\n|||\nдлинные некодирующие РНК","микрорнк\n|||\nмикроРНК","старение\n|||\nстарение","транспозоны\n|||\nтранспозоны","scopus\n|||\nScopus","aging\n|||\naging","atherosclerosis\n|||\natherosclerosis","inflammation\n|||\ninflammation","long non-coding rna\n|||\nlong non-coding RNA","microrna\n|||\nmicroRNA","transposable elements\n|||\ntransposable elements"],"subject_tax_0_filter":["атеросклероз\n|||\nатеросклероз","воспаление\n|||\nвоспаление","длинные некодирующие рнк\n|||\nдлинные некодирующие РНК","микрорнк\n|||\nмикроРНК","старение\n|||\nстарение","транспозоны\n|||\nтранспозоны","scopus\n|||\nScopus","aging\n|||\naging","atherosclerosis\n|||\natherosclerosis","inflammation\n|||\ninflammation","long non-coding rna\n|||\nlong non-coding RNA","microrna\n|||\nmicroRNA","transposable elements\n|||\ntransposable elements"],"subject_filter":["атеросклероз\n|||\nатеросклероз","воспаление\n|||\nвоспаление","длинные некодирующие рнк\n|||\nдлинные некодирующие РНК","микрорнк\n|||\nмикроРНК","старение\n|||\nстарение","транспозоны\n|||\nтранспозоны","scopus\n|||\nScopus","aging\n|||\naging","atherosclerosis\n|||\natherosclerosis","inflammation\n|||\ninflammation","long non-coding rna\n|||\nlong non-coding RNA","microrna\n|||\nmicroRNA","transposable elements\n|||\ntransposable elements"],"dc.subject_mlt":["атеросклероз","воспаление","длинные некодирующие РНК","микроРНК","старение","транспозоны","Scopus","aging","atherosclerosis","inflammation","long non-coding RNA","microRNA","transposable elements"],"dc.subject":["атеросклероз","воспаление","длинные некодирующие РНК","микроРНК","старение","транспозоны","Scopus","aging","atherosclerosis","inflammation","long non-coding RNA","microRNA","transposable elements"],"dc.subject.ru_RU":["атеросклероз","воспаление","длинные некодирующие РНК","микроРНК","старение","транспозоны"],"dc.subject.en":["Scopus","aging","atherosclerosis","inflammation","long non-coding RNA","microRNA","transposable elements"],"title":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"title_keyword":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"title_ac":["взаимосвязь мобильных генетических элементов с некодирующими рнк в развитии атеросклероза (обзор)\n|||\nВзаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","relationship of transposable elements with non-coding rnas in the development of atherosclerosis (review)\n|||\nRelationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.title_sort":"Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","dc.title_hl":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.title_mlt":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.title":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.title_stored":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nru_RU","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)\n|||\nnull\n|||\nnull\n|||\nnull\n|||\nen"],"dc.title.ru_RU":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)"],"dc.title.en":["Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.title.alternative":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)","Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.title.alternative.ru_RU":["Взаимосвязь мобильных генетических элементов с некодирующими РНК в развитии атеросклероза (обзор)"],"dc.title.alternative.en":["Relationship of transposable elements with non-coding RNAs in the development of atherosclerosis (review)"],"dc.type":["Article"],"dc.type.ru_RU":["Article"],"publication_grp":["123456789/8817"],"bi_2_dis_filter":["хуснутдинова, э.к.\n|||\nХуснутдинова, Э.К.","mustafin, rustam n.\n|||\nMustafin, Rustam N.","мустафин, р.н.\n|||\nМустафин, Р.Н.","khusnutdinova, elza k.\n|||\nKhusnutdinova, Elza K."],"bi_2_dis_partial":["Хуснутдинова, Э.К.","Mustafin, Rustam N.","Мустафин, Р.Н.","Khusnutdinova, Elza K."],"bi_2_dis_value_filter":["Хуснутдинова, Э.К.","Mustafin, Rustam N.","Мустафин, Р.Н.","Khusnutdinova, Elza K."],"bi_4_dis_filter":["inflammation\n|||\ninflammation","старение\n|||\nстарение","aging\n|||\naging","длинные некодирующие рнк\n|||\nдлинные некодирующие РНК","microrna\n|||\nmicroRNA","воспаление\n|||\nвоспаление","scopus\n|||\nScopus","atherosclerosis\n|||\natherosclerosis","транспозоны\n|||\nтранспозоны","атеросклероз\n|||\nатеросклероз","long non-coding rna\n|||\nlong non-coding RNA","микрорнк\n|||\nмикроРНК","transposable elements\n|||\ntransposable elements"],"bi_4_dis_partial":["микроРНК","atherosclerosis","атеросклероз","Scopus","старение","длинные некодирующие РНК","inflammation","воспаление","microRNA","long non-coding RNA","aging","транспозоны","transposable elements"],"bi_4_dis_value_filter":["микроРНК","atherosclerosis","атеросклероз","Scopus","старение","длинные некодирующие РНК","inflammation","воспаление","microRNA","long non-coding RNA","aging","транспозоны","transposable elements"],"bi_sort_1_sort":"взаимосвязь мобильных генетических элементов с некодирующими рнк в развитии атеросклероза (обзор)","bi_sort_2_sort":"2025","bi_sort_3_sort":"2025-05-06T09:10:32Z","read":["g0"],"_version_":1831361798225264640}]},"facet_counts":{"facet_queries":{},"facet_fields":{},"facet_dates":{},"facet_ranges":{},"facet_intervals":{}},"highlighting":{"2-7778":{"dc.description.abstract":[" the position of the posterior BM by lifting the posterior BM pole, i.e., induces changes in the subfoveal"],"dc.description.abstract.en":[" the position of the posterior BM by lifting the posterior BM pole, i.e., induces changes in the subfoveal"],"dc.description.abstract_hl":[" the position of the posterior BM by lifting the posterior BM pole, i.e., induces changes in the subfoveal"]},"2-7807":{"dc.description.abstract":[" in PBMCs from IPF patients compared to healthy controls, including lncRNAs MALAT1 (Fold Change = 3.809, P"],"dc.description.abstract.en":[" in PBMCs from IPF patients compared to healthy controls, including lncRNAs MALAT1 (Fold Change = 3.809, P"],"dc.description.abstract_hl":[" in PBMCs from IPF patients compared to healthy controls, including lncRNAs MALAT1 (Fold Change = 3.809, P"]},"2-8042":{"dc.citation.en":[", and factors affecting therapeutic outcome. Endocrine Rev. 2012;33:920–80. DOI: 10.1210/er.2012-1030"],"dc.citation.ru":[", and factors affecting therapeutic outcome. Endocrine Rev. 2012;33:920–80. DOI: 10.1210/er.2012-1030"],"dc.abstract.en":[". Conclusion. The study highlights the potential of interventional endocrine surgery as a"],"dc.citation":[", and factors affecting therapeutic outcome. Endocrine Rev. 2012;33:920–80. DOI: 10.1210/er.2012-1030"],"dc.abstract":[". Conclusion. The study highlights the potential of interventional endocrine surgery as a"]},"2-7926":{"dc.description.abstract":[" was conducted for data on changes in the expression of specific microRNAs derived from transposons during aging"],"dc.description.abstract.en":[" was conducted for data on changes in the expression of specific microRNAs derived from transposons during aging"],"dc.description.abstract_hl":[" was conducted for data on changes in the expression of specific microRNAs derived from transposons during aging"]},"2-8043":{"dc.citation.en":["Coker J.E., Bryan J.A. Endocrine and metabolic disorders: Causes and pathogenesis of obesity. J"],"dc.citation.ru":["Coker J.E., Bryan J.A. Endocrine and metabolic disorders: Causes and pathogenesis of obesity. J"],"dc.citation":["Coker J.E., Bryan J.A. Endocrine and metabolic disorders: Causes and pathogenesis of obesity. J"]},"2-7931":{"dc.abstract.en":["AIM: to assess features of pathomorphological changes in the intestinal wall in patients who had"],"dc.abstract":["AIM: to assess features of pathomorphological changes in the intestinal wall in patients who had"]},"2-7943":{"dc.description.abstract":[". The major aim of our study was to uncover tumor-specific transcriptional and epigenetic changes"],"dc.description.abstract.en":[". The major aim of our study was to uncover tumor-specific transcriptional and epigenetic changes"],"dc.description.abstract_hl":[". The major aim of our study was to uncover tumor-specific transcriptional and epigenetic changes"]},"2-7893":{"dc.description.abstract":[" and requiring the new objective expert criteria search. AIM: To assess changes in electrical conductivity"],"dc.description.abstract.en":[" and requiring the new objective expert criteria search. AIM: To assess changes in electrical conductivity"],"dc.description.abstract_hl":[" and requiring the new objective expert criteria search. AIM: To assess changes in electrical conductivity"]},"2-7883":{"dc.description.abstract":[" and the TDP-43, tau, and FUS proteins, causing pathological conformation changes and aggregate formation"],"dc.description.abstract.en":[" and the TDP-43, tau, and FUS proteins, causing pathological conformation changes and aggregate formation"],"dc.description.abstract_hl":[" and the TDP-43, tau, and FUS proteins, causing pathological conformation changes and aggregate formation"]},"2-7928":{"dc.abstract.en":[" in the etiopathogenesis of atherosclerosis has been determined, including microRNAs and long non-coding RNAs that change"],"dc.abstract":[" in the etiopathogenesis of atherosclerosis has been determined, including microRNAs and long non-coding RNAs that change"]}}} -->