Αποτελέσματα αναζήτησης - "ПРЕЖДЕВРЕМЕННОЕ СТАРЕНИЕ"

Συνεισφορές: The authors are grateful to the Multi-Access Center “Bioinformatics” for access to computing resources under Project FWNR2022-0020 and the Multi-Access Center “Conventional Animal Facility” for access to animals under Projects FWNR-2022-0019 and FWNR-2022-0015.

Πηγή: Vavilov Journal of Genetics and Breeding; Том 27, № 7 (2023); 794-806 ; Вавиловский журнал генетики и селекции; Том 27, № 7 (2023); 794-806 ; 2500-3259 ; 10.18699/VJGB-23-83

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Med. Sci. Monit. 2014;20:905-912. DOI 10.12659/MSM.890160; Taylor J.R., Morshed S.A., Parveen S., Mercadante M.T., Scahill L., Peterson B.S., King R.A., Leckman J.F., Lombroso P.J. An animal model of Tourette’s syndrome. Am. J. Psychiatry. 2002;159(4):657-660. DOI 10.1176/appi.ajp; Tharmalingam S., Khurana S., Murray A., Lamothe J., Tai T.C. Whole transcriptome analysis of adrenal glands from prenatal glucocorticoid programmed hypertensive rodents. Sci. Rep. 2020;10(1): 18755. DOI 10.1038/s41598-020-75652-y; Trent S., Dean R., Veit B., Cassano T., Bedse G., Ojarikre O.A., Humby T., Davies W. Biological mechanisms associated with increased perseveration and hyperactivity in a genetic mouse model of neurodevelopmental disorder. Psychoneuroendocrinology. 2013; 38(8):1370-1380. DOI 10.1016/j.psyneuen.2012.12.002; Wall V.L., Fischer E.K., Bland S.T. Isolation rearing attenuates social interaction-induced expression of immediate early gene protein products in the medial prefrontal cortex of male and female rats. Physiol. Behav. 2012;107(3):440-450. DOI 10.1016/j.physbeh.2012.09.002; Watanabe Y., Yoshida M., Yamanishi K., Yamamoto H., Okuzaki D., No jima H., Yasunaga T., Okamura H., Matsunaga H., Yamanishi H. Genetic analysis of genes causing hypertension and stroke in spontaneously hypertensive rats: gene expression profiles in the kidneys. Int. J. Mol. Med. 2015;36(3):712-724. DOI 10.3892/ijmm.2015. 2281; Wu H.M., Zhao C.C., Xie Q.M., Xu J., Fei G.H. TLR2-melatonin feedback loop regulates the activation of NLRP3 inflammasome in murine allergic airway inflammation. Front. Immunol. 2020;11:172.; Xiao G., Wang T., Zhuang W., Ye C., Luo L., Wang H., Lian G., Xie L. RNA sequencing analysis of monocrotaline-induced PAH reveals dysregulated chemokine and neuroactive ligand receptor pathways. Aging (Albany NY ). 2020;12(6):4953-4969. DOI 10.18632/aging.102922; Xie F., Wang L., Liu Y., Liu Z., Zhang Z., Pei J., Wu Z., Zhai M., Cao Y. ASMT regulates tumor metastasis through the circadian clock system in triplenegative breast cancer. Front. Oncol. 2020;10:537247. DOI 10.3389/fonc.2020.537247; Yang H., Zhang Z., Ding X., Jiang X., Tan L., Lin C., Xu L., Li G., Lu L., Qin Z., Feng X., Li M. RP58 knockdown contributes to hypoxia-ischemia-induced pineal dysfunction and circadian rhythm disruption in neonatal rats. J. Pineal Res. 2023;75(1):e12885. DOI 10.1111/jpi.12885; Ye J., Coulouris G., Zaretskaya I., Cutcutache I., Rozen S., Madden T.L. Primer-BLAST: a tool to design target-specific primers for polymerase chain reaction. BMC Bioinformatics. 2012;13:134. DOI 10.1186/1471-2105-13-134; Yoshida M., Watanabe Y., Yamanishi K., Yamashita A., Yamamoto H., Okuzaki D., Shimada K., Nojima H., Yasunaga T., Okamura H., Matsunaga H., Yamanishi H. 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Διαθεσιμότητα: https://vavilov.elpub.ru/jour/article/view/3979
https://doi.org/10.18699/VJGB-23-92

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10

Conference

Роль стресс-индуцированной патологии в преждевременном старении ветеранов боевых действий

Συγγραφείς: Torgashov, M. N., Myakotnykh, V. S., Ekusheva, E. V.

Θεματικοί όροι: PREMATURE AGING, ПОСТТРАВМАТИЧЕСКОЕ СТРЕССОВОЕ РАССТРОЙСТВО, POST-TRAUMATIC STRESS DISORDER, ВЕТЕРАНЫ БОЕВЫХ ДЕЙСТВИЙ, ПРЕЖДЕВРЕМЕННОЕ СТАРЕНИЕ, CHRONIC PAIN, ХРОНИЧЕСКАЯ БОЛЬ, COMBAT VETERANS

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Σύνδεσμος πρόσβασης: http://elar.urfu.ru/handle/10995/109111

11

Academic Journal

Comparative characteristics of biological age and rate of aging of internally displaced and local students

Συγγραφείς: Zoryna Boiarska, Olga Dotsenko

Πηγή: ScienceRise: Biological Science; № 5-6(20-21) (2019); 24-29

Θεματικοί όροι: 0301 basic medicine, старение, биологический возраст, паспортный возраст, календарный возраст, темпы старения, преждевременное старение, статическая балансировка, самооценка, 0303 health sciences, 03 medical and health sciences, 4. Education, aging, biological age, passport age, calendar age, aging rate, premature aging, static balancing, self-esteem, старіння, біологічний вік, паспортний вік, календарний вік, темпи старіння, передчасне старіння, статичне балансування, самооцінка, 10. No inequality, UDС 159.922.63:57.017.6-057.73-057.87, 16. Peace & justice

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Σύνδεσμος πρόσβασης: http://journals.uran.ua/sr_bio/article/download/193789/194395
http://journals.uran.ua/sr_bio/article/view/193789
http://journals.uran.ua/sr_bio/article/download/193789/194395
http://journals.uran.ua/sr_bio/article/view/193789

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12

Academic Journal

Progeria (Hutchinson-Gilford Syndrome): Literature Review and Clinical Case ; Прогерия (синдром Хатчинсона – Гилфорда): обзор литературы и клинический случай

Συγγραφείς: Natalia V. Buchinskaya, Aida Zh. Akhenbekova, Aliya A. Bugybay, Mikhail M. Kostik, Н. В. Бучинская, А. Ж. Ахенбекова, А. А. Бугыбай, М. М. Костик

Συνεισφορές: The preparation of manuscript materials was carried out with the financial support of the Ministry of Science and Higher Education of Russian Federation (Agreement № 07515-2022-301, 20.04.2022), Подготовка материалов рукописи выполнена при финансовой поддержке Министерства науки и высшего образования Российской Федерации (Соглашение № 075-15-2022-301 от 20.04.2022)

Πηγή: Current Pediatrics; Том 21, № 3 (2022); 253-264 ; Вопросы современной педиатрии; Том 21, № 3 (2022); 253-264 ; 1682-5535 ; 1682-5527

Θεματικοί όροι: лечение, Hutchinson-Gilford Syndrome, premature aging, LMNA gene, congenital sclerodermia, treatment, синдром Хатчинсона – Гилфорда, преждевременное старение, ген LMNA, врожденная склеродермия

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Relation: https://vsp.spr-journal.ru/jour/article/view/2954/1195; Agarwal US, Sitaraman S, Mehta S, Panse G. HutchinsonGilford progeria syndrome. Indian J Dermatol Venereol Leprol. 2010;76(5):591. doi: https://doi.org/10.4103/0378-6323.69094; The Progeria Handbook. A guide for families and health providers of children with progeria. Gordon LB, ed. The Progeria Research Foundation; 2010. Available online: https://progeriaresearch.org/assets/files/PRFhandbook_0410.pdf. Accessed on July 01, 2022.; Hutchinson J. Case of congenital absence of hair, with atrophic condition of the skin and its appendages, in a boy whose motherhad been almost wholly bald from alopecia areata from the age of six. Lancet. 1886;1:923.; Gonzalo S, Kreienkamp R, Askjaer P. Hutchinson-Gilford progeria syndrome: a premature aging disease caused by LMNA gene mutations. Ageing Res Rev. 2017;33:18–29. doi: https://doi.org/10.1016/j.arr.2016.06.007; Gordon LB, Brown WT, Collins FS. Hutchinson-Gilford progeria syndrome. 2003 Dec 12 [Updated 2019 Jan 17]. In: GeneReviews [Internet]. Adam MP, Ardinger HH, Pafon RA, et al., eds. Seattle (WA): University of Washington, Seattle; 1993–2020.; Gonzalo S, Coll-Bonfill N, Genomic instability and innate immune responses to self-DNA in progeria. Geroscience. 2019;41(3):255– 266. doi: https://doi.org/10.1007/s11357-019-00082-2; Фофанова О.В. Синдром Гетчинсона-Гилфорда (прогерия) // Проблемы эндокринологии. — 1995. — Т. 41. — № 4. — С. 24–26. — doi: https://doi.org/10.14341/probl11459; Scaffidi P, Misteli T. Lamin A-dependent nuclear defects in human aging. Science. 2006;312(5776):1059–1063. doi: https://doi.org/10.1126/science.1127168; Burke B, Stewart CL. Functional architecture of the cell’s nucleus in development, aging, and disease. Curr Top Dev Biol. 2014;109:1– 52. doi: https://doi.org/10.1016/B978-0-12-397920-9.00006-8; Swift J, Ivanovska IL, Buxboim A, et al. Nuclear Lamin-A scales with tissue stiffness and enhances matrix-directed differentiation. Science. 2013;341(6149):1240104. doi: https://doi.org/10.1126/science.1240104; Martins F, Souca J, Pereira CD, et al. Nuclear envelope dysfunction and its contribution to the aging process. Aging Cell. 2020;19(5):e13143. doi: https://doi.org/10.1111/acel.13143; Vahabikashi A, Adam SA, Medalia O, Goldman RD. Nuclear lamins: Structure and function in mechanobiology. APL Bioeng. 2022;6(1):011503. doi: https://doi.org/10.1063/5.0082656; Gordon LB, Shapell H, Massaro J, et al. Association of Lonafarnib treatment vs no treatment with mortality rate in patients with Hutchinson-Gilford progeria syndrome. JAMA. 2018;319(16):1687– 1695. doi: https://doi.org/10.1001/jama.2018.3264; Goldman RD, Shumaker DK, Erdos MR, et al. Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome. Proc Natl Acad Sci U S A. 2004;101(24):8963–8968. doi: https://doi.org/10.1073/pnas.0402943101; Prokocimer M, Barkan R, Gruenbaum Y. Hutchinson-Gilford progeria syndrome through the lens of transcription. Aging Cell. 2013;12(4):533–543. doi: https://doi.org/10.1111/acel.12070; Hutchinson-gilford progeria syndrome; HGPS. In: OMIM® Online Mendelian Inheritance in Man® An Online Catalog of Human Genes and Genetic Disorders. Updated June 4, 2022. Available online: https://omim.org/entry/176670. Accessed on July 02, 2022.; Merideth MA, Gordon LB, Clauss S, et al. Phenotype and course of Hutchinson-Gilford progeria syndrome. N Engl J Med. 2008;358(6):592– 604. doi: https://doi.org/10.1056/NEJMoa0706898; Sevenants L, Wouters C, De Sandre-Giovannoli A, et al. Tight skin and limited joint movements as early presentation of HutchinsonGilford progeria in a 7-week-old infant. Eur J Pediatr. 2005;164(5):283– 286. doi: https://doi.org/10.1007/s00431-005-1635-x; Zhang J, Lian Q, Zhu G, et al. A human iPSC model of Hutchinson Gilford Progeria reveals vascular smooth muscle and mesenchymal stem cell defects. Cell Stem Cell. 2011;8(1):31–45. doi: https://doi.org/10.1016/j.stem.2010.12.002; Rork JF, Huang JT, Gordon LB, et al. Initial cutaneous manifestations of Hutchinson-Gilford progeria syndrome. Pediatr Dermatol. 2014;31(2):196–202. doi: https://doi.org/10.1111/pde.12284; Huang S, Liang Y, Wu W, et al. Analysis of a case with typical Hutchinson-Gilford progeria syndrome with scleroderma-like skin changes and review of literature. Zhonghua Er Ke Za Zhi. 2014;52(2):112–116.; Erdem N, Güneş AT, Avci O, Osma E. A case of HutchinsonGilford progeria syndrome mimicking scleroderma in early infancy. Dermatology. 1994;188(4):318–321. doi: https://doi.org/10.1159/000247175; Stevens AM, Torok KS, Li SC, et al. From immunopathogenesis of juvenile systemic sclerosis. Front Immunol. 2019;10:1352. doi: https://doi.org/10.3389/fimmu.2019.01352; Gordon CM, Gordon LB, Snyder BD, et al. Hutchinson-Gilford progeria is a skeletal dysplasia. J Bone Miner Res. 2011;26(7):1670– 1679. doi: https://doi.org/10.1002/jbmr.392; Ullrich NJ, Gordon LB. Chapter 18 — Hutchinson-Gilford progeria syndrome. Handb Clin Neurol. 2015;132:249–264. doi: https://doi.org/10.1016/B978-0-444-62702-5.00018-4; Domingo DL, Trujillo MI, Council SE, et al. Hutchinson-Gilford progeria syndrome: oral and craniofacial phenotype. Oral Dis. 2009;15(3):187– 195. doi: https://doi.org/10.1111/j.1601-0825.2009.01521.x; Guardiani E, Zalewski C, Brewer C, et al. Otologic and audiologic manifestations of Hutchinson-Gilford progeria syndrome. Laryngoscope. 2011;121(10):2250–2255. doi: https://doi.org/10.1002/lary.22151; Gordon LB, Massaro J, D’Agostino RB Sr, et al. Impact of farnesylation inhibitors on survival in Hutchinson-Gilford progeria syndrome. Circulation. 2014;130(1):27–34. doi: https://doi.org/10.1161/CIRCULATIONAHA.113.008285; Cleveland RH, Gordon LB, Kleinman ME, et al. A prospective study of radiographic manifestations in Hutchinson-Gilford progeria syndrome. Pediatr Radiol. 2012;42(9):1089–1098. doi: https://doi.org/10.1007/s00247-012-2423-1; Gordon LB, Harten IA, Patti ME, Lichtenstein AH. Reduced adiponectin and HDL cholesterol without elevated C-reactive protein: clues to the biology of premature atherosclerosis in HutchinsonGilford progeria syndrome. J Pediatr. 2005;146(3):336–341. doi: https://doi.org/10.1016/j.jpeds.2004.10.064; Prakash A, Gordon LB, Kleinmann M, et al. Cardiac abnormalities in patients with Hutchinson-Gilford progeria syndrome. JAMA Cardiol. 2018;3(4):326–334. doi: https://doi.org/10.1001/jamacardio.2017.5235; Silvera VM, Gordon LB, Orbach DB, et al. Imaging characteristics of cerebrovascular arteriopathy and stroke in Hutchinson-Gilford progeria syndrome. Am J Neuroradiol. 2013;34(5):1091–1097. doi: https://doi.org/10.3174/ajnr.A3341; Jung HL, Coffinier C, Choe Y, et al. Regulation of prelamin A but not lamin C by miR-9, a brain-specific microRNA. Proc Natl Acad Sci USA. 2012;109(7):E423–E431. doi: https://doi.org/10.1073/pnas.1111780109; Gordon CM, Cleveland RH, Baltrusaitis K, et al. Extraskeletal Calcifications in Hutchinson-Gilford Progeria Syndrome. Bone. 2019;125:103–111. doi: https://doi.org/10.1016/j.bone.2019.05.008; Varela I, Pereira S, Ugalde AP, et al. Combined treatment with statins and aminobisphosphonates extends longevity in a mouse model of human premature aging. Nat Med. 2008;14(7):767–772. doi: https://doi.org/10.1038/nm1786; Gordon LB, Kleinman ME, Miller DT, et al. Clinical trial of a farnesyltransferase inhibitor in children with Hutchinson–Gilford progeria syndrome. Proc Natl Acad Sci U S A. 2012;109(41):16666– 16671. doi: https://doi.org/10.1073/pnas.1202529109; Study of Zoledronic Acid, Pravastatin, and Lonafarnib for Patients With Progeria. In: U.S. National Library of Medicine. ClinicalTrials.gov. Available online: https://clinicaltrials.gov/show/NCT00916747. Accessed on July 02, 2022.; Fong LG, Frost D, Meta M, et al. A protein farnesyltransferase inhibitor ameliorates disease in mouse model of progeria. Science. 2006;311(5767):1621–1623. doi: https://doi.org/10.1126/science.1124875; Yang SH, Meta M, Qiao X, et al. A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson–Gilford progeria syndrome mutation. J Clin Invest. 2006;116(8):2115– 2121. doi: https://doi.org/10.1172/JCI28968; Gordon LB, Kleinman ME, Massaro J, et al. Clinical trial of protein farnesylation inhibitors lonafarnib, pravastatin and zolendronic acid in children with Hutchinson-Gilford progeria syndrome. Circulation. 2016;134(2):114–125. doi: https://doi.org/10.1161/CIRCULATIONAHA.116.022188; Bikkul MU, Clements CS, Godwin LS, et al. Farnesyltransferase inhibitor and rapamycin correct aberrant genome organization and decrease DNA damage respectively in Hutchinson-Gilford progeria syndrome fibroblasts. Biogerontology. 2018;19(6):579–602. doi: https://doi.org/10.1007/s10522-018-9758-4; Cao K, Graziotto JJ, Blair CD, et al. Rapamycin reverses cellular phenotypes and enhances mutant protein clearance in HutchinsonGilford progeria syndrome cells. Sci Trancl Med. 2011;3(89):89ra58. doi: https://doi.org/10.1126/scitranslmed.3002346; Gabriel D, Roedl D, Gordon LB, Djabali K. Sulforaphane enhances progerin clearance in Hutchinson-Gilford progeria fibroblasts. Aging Cell. 2015;14(1):78–91. doi: https://doi.org/10.1111/acel.12300; Larrieu D, Britton S, Demir M, et al. Chemical inhibitor of NAT 10 corrects defects of laminopathic cells. Science. 2014;344(6183):527– 532. doi: https://doi.org/10.1126/science.1252651; Larrieu D, Vive E, Robson S, et al. Inhibition of the acetyltransferase NAT 10 normalizes progeric and aging cell by rebalancing the Transportin-1 nuclear import pathway. Sci Signal. 2018;11(537):eaar5401. doi: https://doi.org/10.1126/scisignal.aar5401; Pellegrini C, Columbaro M, Capanni C, et al. All-trans retinoic acid and rapamycin normalize Hutchinson Gilford progeria fibroblast phenotype. Oncotarget. 2015;6(30):29914–29928. doi: https://doi.org/10.18632/oncotarget.4939; Kubben N, Brimacombe KR, Donegan M, et al. A high-content imaging-based screening pipeline for the systematic identification of anti-progeroid compounds. Methods. 2016;96:46–58. doi: https://doi.org/10.1016/j.ymeth.2015.08.024; Kreienkamp R, Croke M, Neumann MA, et al. Vitamin D receptor signaling improves Hutchinson-Gilford progeria syndrome cellular phenotypes. Oncotarget. 2016;7(21):30018–30031. doi: https://doi.org/10.18632/oncotarget.9065; Liu C, Arnold R, Henriques G, Djabali K. 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Διαθεσιμότητα: https://vsp.spr-journal.ru/jour/article/view/2954
https://doi.org/10.15690/vsp.v21i3.2431

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13

Academic Journal

CASE OF HETCHINSON-GILFORD SYNDROME ASSOCIATED WITH G608G MUTATION IN LMNA GENE AND METHYLENETRAGYDROPHOLATE REDUCTASE INSUFFICIENCY

Συγγραφείς: Molodan, L. V., Grechanina, O., Grechanina, Yu.

Πηγή: Neonatology, surgery and perinatal medicine; Том 8, № 1(27) (2018): NEONATOLOGY, SURGERY AND PERINATAL MEDICINE; 81-86
Неонатологія, хірургія та перинатальна медицина; Том 8, № 1(27) (2018): НЕОНАТОЛОГІЯ, ХІРУРГІЯ ТА ПЕРИНАТАЛЬНА МЕДИЦИНА; 81-86
Неонатология, хирургия и перинатальная медицина; Том 8, № 1(27) (2018): НЕОНАТОЛОГИЯ, ХИРУРГИЯ И ПЕРИНАТАЛЬНАЯ МЕДИЦИНА; 81-86

Θεματικοί όροι: синдром Гетчинсона-Гилфорда, преждевременное старение, мутация G608G в гене LMNA, недостаточность метилентетрагидрофолатредуктазы, феномен синтропии, эпигенетическая патология, синдром Гетчінсона-Гілфорда, передчасне старіння, мутація G608G в гені LMNA, недостатність метілентетрагідрофолатредуктази, феномен сінтропії, епігенетична патологія, Hutchinson-Gilford Syndrome, Premature Aging, G608G mutation in LMNA Gene, Methylene Tetrahydro-Reductase Deficiency, Synthropy Phenomenon, epigenetic pathology, 3. Good health