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1Academic Journal
Authors: O. A. Saburova, D. M. Sobchak, K. A. Otmakhova, О. А. Сабурова, Д. М. Собчак, К. А. Отмахова
Source: CHILDREN INFECTIONS; Том 21, № 1 (2022); 41-44 ; ДЕТСКИЕ ИНФЕКЦИИ; Том 21, № 1 (2022); 41-44 ; 2618-8139 ; 2072-8107 ; 10.22627/2072-8107-2022-21-1
Subject Terms: клеточный иммунитет, Pro-inflammatory mediators, interferons, cytokines, polymerase chain reaction, cellular immunity, провоспалительные медиаторы, интерфероны, интерлейкины
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Relation: https://detinf.elpub.ru/jour/article/view/678/547; Kashyap S., Shanker V. Zoster ophthalmicus with dissemination in a six year old immunocompetent child. Indian J Dermatol Venereol Leprol, 2014; 80: 382.; Papaloukas O., Giannouli G., Papaevangelou V. Successes and challenges in varicella vaccine. Ther Adv Vaccines, 2014; 2(2): 39—55.; Singh P., Karmacharya S., Rizyal A., Rijal A.P. HZO with retrobulbar neuritis. Nepal J Ophthalmol, 2016; 8(15): 78—81.; Okunuki Y., Sakai J., Kezuka T., Goto H. A case of herpes zoster uveitis with severe hyphemia. BMC Ophthalmology, 2014; 14: 74.; Wakim L.M., Woodward A., Bevan M.J. Mamory T-cell persisting within the brain after local infection show functional to their tissue of residence. Proc. Nat. Acad. Sci USA, 2010; 107: 17872—17879.; Kawai K., Gebremeskel B.G., Acosta C.J. Systematic review of incidence and complications of herpes zoster: towards a global perspective. BMJ Open, 2014; 4(6): e004833.; Paludan S.R., Horan K.A. Recognitin of herpesviruses by the innate immune system. Nat.Rev. Immunol, 2011; 11(2): 143—154.; Nielsen O.H., Ainsworth M.A. Tumor necrosis factor inhibitors for inflammatory bowel disease. New Engl. J. Med. 2013; 369: 754—762.; Grinde B. Herpesviruses: latency and reactivation — viral strategies and host response. J Microbiol, 2013; 5: 227—266.; Winsauer C., Kruglov A.A., Chashchina A.A., Drutskaya M.S., Nedospasov S.A. Cellular sources of pathogenic and protective TNF and experimental strategies based on utilization of TNF humanized mice. Cytokine Growth Factor Rev. 2014; 25: 115—123.; https://detinf.elpub.ru/jour/article/view/678
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2Academic Journal
Authors: Sevostianova, O. Iu., Chistyakova, G. N., Remizova, I. I., Sevostianova, N. E., Byzova, T. E., Севостьянова, О. Ю., Чистякова, Г. Н., Ремизова, И. И., Севостьянова, Н. Е., Бызова, Т. Е.
Subject Terms: UTERINE LEIOMYOMA, REPRODUCTIVE AGE, LYMPHOCYTE POPULATIONS, T-LYMPHOCYTE SUBPOPULATIONS, PROINFLAMMATORY MEDIATORS, ЛЕЙОМИОМА МАТКИ, РЕПРОДУКТИВНЫЙ ВОЗРАСТ, ПОПУЛЯЦИИ ЛИМФОЦИТОВ, СУБПОПУЛЯЦИИ Т-ЛИМФОЦИТОВ, ПРОВОСПАЛИТЕЛЬНЫЕ МЕДИАТОРЫ
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Relation: Scopus; http://elib.usma.ru/handle/usma/7192
Availability: http://elib.usma.ru/handle/usma/7192
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3Academic Journal
Authors: Pritulo, L. F.
Source: Клінічна анатомія та оперативна хірургія; Том 8, № 1 (2009); 48-53
Клиническая анатомия и оперативная хирургия; Том 8, № 1 (2009); 48-53
Clinical anatomy and operative surgery; Том 8, № 1 (2009); 48-53Subject Terms: peritonitis, proinflammatory mediators, cytokines of T-helpers of types 1, 2, children, перитоніт, прозапальні медіатори, цитокіни Т-хелперів 1, 2 типів, діти, перитонит, провоспалительные медиаторы, цитокины Т-хелперов 1, 2 типов, дети
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Access URL: http://kaos.bsmu.edu.ua/article/view/213747
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4Academic Journal
Authors: L. Litvinova S., N. Todosenko M., O. Khaziakhmatova G., I. Malinina P., K. Yurova A., Л. Литвинова С., Н. Тодосенко М., О. Хазиахматова Г., И. Малинина П., К. Юрова А.
Contributors: Работа выполнена в рамках программы повышения конкурентоспособности («дорожной кар- ты») и субсидии «Организация проведения научных исследований 20.4986.2017/ВУ» Балтийского федерального университета им. Иммануила Канта.
Source: Bulletin of Siberian Medicine; Том 16, № 4 (2017); 207-219 ; Бюллетень сибирской медицины; Том 16, № 4 (2017); 207-219 ; 1819-3684 ; 1682-0363 ; 10.20538/1682-0363-2017-16-4
Subject Terms: rheumatoid arthritis, activation molecules, proinflammatory mediators, dexamethasone, ревматоидный артрит, молекулы активации, провоспалительные медиаторы, дексаметазон
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Relation: https://bulletin.tomsk.ru/jour/article/view/1038/759; Matsuki F., Saegusa J., Miyamoto Y., Misaki K., Kumagai S., Morinobu A. CD45RA-Foxp3(high) activated/effector regulatory T cells in the CCR7+CD45RA-CD27+CD28+ central memory subset are decreased in peripheral blood from patients with rheumatoid arthritis // Biochem. Biophys Res. Commun. 2013; 438 (4): 778–783. DOI:10.1016/j.bbrc.2013.05.120.; Sava F., Toldi G., Treszl A., Hajdú J., Harmath Á., Tulassay T., Vásárhelyi B. Expression of lymphocyte activation markers of preterm neonates is associated with perinatal complications // BMC Immunol. 2016; 17 (1): 19. DOI:10.1186/s12865-016-0159-7.; Сохоневич Н.А. Роль цитокинов, имеющих общую γ-цепь рецепторов (IL-2, IL-7, IL-15), в регуляции функциональной активности Т-лимфоцитов: автореф. дис. … канд. мед. наук. Томск, 2015: 24. Sohonevich N.A. Rol’ citokinov, imeyushchih obshchuyu γ-cep’ receptorov (IL-2, IL-7, IL-15), v regulyacii funkcional’noj aktivnosti T-limfocitov [The role of cytokines, contains a common γ-chain of receptors (IL-2, IL-7, IL15), in the regulation of the functional activity of T-lymphocytes]: аvtoref. … dis. kand. med. nauk. Tomsk, 2015: 24 (in Russian).; Cho B.A., Sim J.H., Park J.A., Kim H.W., Yoo W.H., Lee S.H., Lee D.S., Kang J.S., Hwang Y.I., Lee W.J., Kang I., Lee E.B., Kim H.R. Characterization of effector memory CD8+ T cells in the synovial fluid of rheumatoid arthritis // J. Clin. Immunol. 2012; 32 (4): 709–720. DOI:10.1007/ s10875-012-9674-3.; Van Amelsfort J.M., Jacobs K.M., Bijlsma J.W., Lafeber F.P., Taams L.S. CD4(+)CD25(+) regulatory T-cells in rheumatoid arthritis: differences in the presence, phenotype, and function between peripheral blood and synovial fluid // Arthritis Rheum. 2004; 50 (9): 2775–2785. DOI:10.1002/art.20499.; Gattorno M., Prigione I., Morandi F., Gregorio A., Chiesa S., Ferlito F., Favre A., Uccelli A., Gambini C., Martini A., Pistoia V. Phenotypic and functional characterisation of CCR7+ and CCR7- CD4+ memory T cells homing to the joints in juvenile idiopathic arthritis // Arthritis. Res. Ther. 2005; 7 (2): R256–257. DOI:10.1186/ar1485.; Okada R., Kondo T., Matsuki F., Takata H., Takiguchi M. Phenotypic classification of human CD4+ T cell subsets and their differentiation // Int. Immunol. 2008; 20 (9): 1189–1199. DOI:10.1093/intimm/dxn075.; Baschant U., Tuckermann J. The role of the glucocorticoid receptor in inflammation and immunity // J. Steroid Biochem. Mol. Biol. 2010; 120 (2–3): 69–75. DOI:10.1016/j.jsbmb.2010.03.058.; Bischof F., Melms A. Glucocorticoids inhibit CD40 ligand expression of peripheral CD4+ lymphocytes // Cell Immunol. 1998; 187 (1): 38–44. DOI:10.1006/ cimm.1998.1308.; Gutsol A.A., Sokhonevich N.A., Iurova K.A., Haziakhmatova O.G., Shupletsova V.V., Litvinova L.S. Dose-dependent effects of dexamethasone on functional activity of T-lymphocytes different grade of differentiation // Mol. Biol. (Mosk). 2015; 49 (1): 149–157.; Pandolfi J., Baz P., Fernández P., Discianni Lupi A., Payaslián F., Billordo L.A., Fainboim L., Arruvito L. Regulatory and effector T-cells are differentially modulated by dexamethasone // Clin. Immunol. 2013; 149 (3): 400–410. DOI:10.1016/j.clim.2013.09.008.; Ayroldi E., Macchiarulo A., Riccardi C. Targeting glucocorticoid side effects: selective glucocorticoid receptor modulator or glucocorticoid-induced leucine zipper? A perspective // Faseb. J. 2014; 28 (12): 5055–5070. DOI:10.1096/fj.14-254755.; Кремер Н.Ш. Теория вероятностей и математическая статистика. М.: ЮНИТИ-ДАНА, 2004: 573. Kremer N.Sh. Teoriya veroyatnostej i matematicheskaya statistika [Theory of Probability and Mathematical Statistics]. M.: YUNITI-DANA Publ., 2004: 573 (in Russian).; Reddy M., Eirikis E., Davis C., Davis H.M., Prabhakar U. Comparative analysis of lymphocyte activation marker expression and cytokine secretion profile in stimulated human peripheral blood mononuclear cell cultures: an in vitro model to monitor cellular immune function // J. Immunol. Methods. 2004; 293 (1–2): 127–142. DOI:10.1016/j.jim.2004.07.006.; Tang X., Yocum D.E., Dejonghe D., Nordensson K., Lake D.F., Richard J. Increased activation-induced cell death in peripheral lymphocytes of rheumatoid arthritis patients: the mechanism of action // Immunology. 2004; 112 (3): 496–505. DOI:10.1111/j.1365-2567.2004.01888.x.; Matsuki F., Saegusa J., Nishimura K., Miura Y., Kurosaka M., Kumagai S., Morinobu A. CD45RA-Foxp3(low) non-regulatory T cells in the CCR7-CD45RA-CD27+CD28+ effector memory subset are increased in synovial fluid from patients with rheumatoid arthritis // Cell Immunol. 2014; 290 (1): 96–101. DOI:10.1016/j.cellimm.2014.05.011.; Boumpas D.T., Anastassiou E.D., Older S.A., Tsokos G.C., Nelson D.L., Balow J.E. Dexamethasone inhibits human interleukin 2 but not interleukin 2 receptor gene expression in vitro at the level of nuclear transcription // J. Clin. Invest. 1991; 87 (5): 1739–1747. DOI:10.1172/ JCI115192.; Liberman A.C., Druker J., Perone M.J., Arzt E. Glucocorticoids in the regulation of transcription factors that control cytokine synthesis. Cytokine Growth // Factor Rev. 2007; 18 (1–2): 45–56. DOI:10.1016/j.cytogfr.2007.01.005.; Shipkova M., Wieland E. Surface markers of lymphocyte activation and markers of cell proliferation // Clin. Chim. Acta. 2012; 413 (17–18): 1338–1349. DOI:10.1016/j.cca.2011.11.006.; Paulsen M., Janssen O. Pro- and anti-apoptotic CD95 signaling in T-cells // Cell. Commun. Signal. 2011; 9: 7. DOI:10.1186/1478-811X-9-7.; Paulsen M., Valentin S., Mathew B., Adam-Klages S., Bertsch U., Lavrik I., Krammer P.H., Kabelitz D., Janssen O. Modulation of CD4+ T-cell activation by CD95 co-stimulation // Cell. Death. Differ. 2011; 18 (4): 619–631. DOI:10.1038/cdd.2010.134.; Liberman A.C., Refojo D., Antunica-Noguerol M., Holsboer F., Arzt E. Underlying mechanisms of cAMPand glucocorticoid-mediated inhibition of FasL expression in activation-induced cell death // Mol. Immunol. 2012; 50 (4): 220–235. DOI:10.1016/j.molimm.2012.01.008.; Baumann S., Dostert A., Novac N., Bauer A., Schmid W., Fas S.C., Krueger A., Heinzel T., Kirchhoff S., Schütz G., Krammer P.H. Glucocorticoids inhibit activation-induced cell death (AICD) via direct DNA-dependent repression of the CD95 ligand gene by a glucocorticoid receptor dimer // Blood. 2005; 106(2): 617–625. DOI:10.1182/blood-2004-11-4390.; Banuelos J., Lu N.Z. A gradient of glucocorticoid sensitivity among helper T-cell cytokines // Cytokine Growth Factor Rev. 2016; 31: 27–35. DOI:10.1016/j.cytogfr.2016.05.002.; Spreafico R., Rossetti M., Whitaker J.W., Wang W., Lovell D.J., Albani S. Epi polymorphisms associated with the clinical outcome of autoimmune arthritis affect CD4+ T-cell activation pathways // Proc Natl Acad Sci USA. 2016; 113 (48): 13845–13850. DOI:10.1073/ pnas.1524056113.; Bertho N., Drénou B., Laupeze B., Berre C.L., Amiot L., Grosset J.M., Fardel O., Charron D., Mooney N., Fauchet R. HLA-DR-mediated apoptosis susceptibility discriminates differentiation stages of dendritic/monocytic APC // J. Immunol. 2000; 164 (5): 2379–2385.; Muehling L.M., Mai D.T., Kwok W.W., Heymann P.W., Pomés A., Woodfolk J.A. Circulating Memory CD4+ T-сells target conserved epitopes of rhinovirus capsid proteins and respond rapidly to experimental infection in humans //J. Immunol. 2016; 197 (8): 3214–3224. DOI:10.4049/jimmunol.1600663.; Spreafico R., Rossetti M., van Loosdregt J., Wallace C.A., Massa M., Magni-Manzoni S., Gattorno M., Martini A., Lovell D.J. Albani S. A circulating reservoir of pathogenic-like CD4+ T cells shares a genetic and phenotypic signature with the inflamed synovial micro-environment // Ann. Rheum. Dis. 2016; 75 (2): 459–465. DOI:10.1136/ annrheumdis-2014-206226.; Astry B, Harberts E, Moudgil KD. A cytokine-centric view of the pathogenesis and treatment of autoimmune arthritis // J. Interferon Cytokine Res. 2011; 31 (12): 927–940. DOI:10.1089/jir.2011.0094.; Konya C., Paz Z., Apostolidis S.A., Tsokos G.C. Update on the role of Interleukin 17 in rheumatologic autoimmune diseases // Cytokine. 2015; 75 (2): 207–215. DOI:10.1016/j.cyto.2015.01.003.; Elshabrawy H.A., Chen Z., Volin M.V., Ravella S., Virupannavar S., Shahrara S. The pathogenic role of angiogenesis in rheumatoid arthritis // Angiogenesis. 2015; 18 (4): 433–448. DOI:10.1007/s10456-015-9477-2.; Gharibi T., Majidi J., Kazemi T., Dehghanzadeh R., Motallebnezhad M., Babaloo Z. Biological effects of IL21 on different immune cells and its role in autoimmune diseases // Immunobiology. 2016; 221 (2): 357–367. DOI:10.1016/j.imbio.2015.09.021.; Koetz K., Bryl E., Spickschen K., O’Fallon W.M., Goronzy J.J., Weyand C.M. T-cell homeostasis in patients with rheumatoid arthritis // Proc. Natl. Acad. Sci. USA. 2000; 97 (16): 9203–9208.; Liberman A.C., Refojo D., Druker J., Toscano M., Rein T., Holsboer F., Arzt E. The activated glucocorticoid receptor inhibits the transcription factor T-bet by direct protein-protein interaction // Faseb. J. 2007; 21 (4): 1177– 1188. DOI:10.1096/fj.06-7452com.; Ratman D., Vanden Berghe W., Dejager L., Libert C., Tavernier J., Beck I.M., De Bosscher K. How glucocorticoid receptors modulate the activity of other transcription factors: a scope beyond tethering // Mol. Cell. Endocrinol. 2013; 380 (1–2): 41–54. DOI:10.1016/j.mce.2012.12.014.; Altonsy M.O., Sasse S.K., Phang T.L., Gerber A.N. Context-dependent cooperation between nuclear factor κB (NF-κB) and the glucocorticoid receptor at a TNFAIP3 intronic enhancer: a mechanism to maintain negative feedback control of inflammation // J. Biol. Chem. 2014; 289 (12): 8231–8239. DOI:10.1074/jbc.M113.545178.; Banuelos J., Cao Y., Shin S.C., Lu N.Z. Immunopathology alters Th17 cell glucocorticoid sensitivity // Allergy. 2016; 72 (3): 331–341. DOI:10.1111/all.13051.; Glass C.K., Saijo K. Nuclear receptor transrepression pathways that regulate inflammation in macrophages and T cells // Nat. Rev. Immunol. 2010; 10 (5): 365–376. DOI:10.1038/nri2748.; Hermann-Kleiter N., Baier G. NFAT pulls the strings during CD4+ T helper cell effector functions // Blood. 2010; 115 (15): 2989–2997. DOI:10.1182/blood-2009-10-233585.; Noack M., Ndongo-Thiam N., Miossec P. Evaluation of anti-inflammatory effects of steroids and arthritis-related biotherapies in an in vitro coculture model with immune cells and synoviocytes // Front Immunol. 2016; 7: 509. DOI:10.3389/fimmu.2016.00509.; Baschant U., Frappart L., Rauchhaus U., Bruns L., Reichardt H.M., Kamradt T., Bräuer R., Tuckermann J.P. Glucocorticoid therapy of antigen-induced arthritis depends on the dimerized glucocorticoid receptor in T-cells // Proc. Natl. Acad. Sci. USA. 2011; 108 (48): 19317– 19322. DOI:10.1073/pnas.1105857108.; https://bulletin.tomsk.ru/jour/article/view/1038
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5Academic Journal
Authors: E. S. Levitskaya, Е. С. Левицкая
Source: Medical Herald of the South of Russia; № 1 (2017); 21-27 ; Медицинский вестник Юга России; № 1 (2017); 21-27 ; 2618-7876 ; 2219-8075 ; 10.21886/2219-8075-2017-1
Subject Terms: провоспалительные медиаторы, small-diameter arteries, signaling pathways, proinflammatory mediators, фиброз почек, артерии малого диаметра, сигнальные пути
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Relation: https://www.medicalherald.ru/jour/article/view/487/385; https://www.medicalherald.ru/jour/article/downloadSuppFile/487/39; https://www.medicalherald.ru/jour/article/downloadSuppFile/487/40; Neovius M., Jacobson S.H., Eriksson J.K., Elinder C.G., Hylander B. Mortality in chronic kidney disease and renal replacement therapy: a population-based cohort study. // BMJ Open – 2014. – V.4. – P.e00425. doi:10.1136/bmjopen-2013-004251; Liu Y. Cellular and molecular mechanisms of renal fibrosis. // Nat Rev Nephrol. – 2011. – Vol.7(12). – P.684-696. doi:10.1038/nrneph.2011.149; Farris A.B., Colvin R.B. Renal Interstitial Fibrosis: Mechanisms and Evaluation In: Current Opinion in Nephrology and Hypertension. // CurrOpinNephrolHypertens. – 2012. – Vol.21(3). – P.289-300. doi:10.1097/MNH.0b013e3283521cfa; Zeisberg M., Neilson E.G. Mechanisms of tubulointerstitial fibrosis. // Journal of the American Society of Nephrology: JASN. – 2010. – Vol.21(11). – P.1819-1834. doi:10.1681/ASN.2010080793; Duffield J.S. Cellular and molecular mechanisms in kidney fibrosis. // J Clin Invest. – 2014. – Vol.124(6). – P.2299-2306. doi:10.1172/JCI72267; Genoves F., Manresa A.A., Leeming D.J., Karsdal M.A., Boor P. The extracellular matrix in the kidney: a source of novel noninvasive biomarkers of kidney fibrosis? // Fibrogenesis& Tissue Repair. – 2014. – Vol.7(1). – P.4. doi:10.1186/1755-1536-7-4; Савош В.В., Летковская Т.А., Черствый Е.Д., Сукало А.В. Клеточные механизмы формирования тубулоинтерстициальных изменений при первичных гломерулопатиях. // Медицинский журнал. – 2007. – №4. – С. 98-100.; Papasotiriou M., Genovese F., Klinkhammer B.M., Kunter U., Nielsen S.H., Karsdal M.A. et al. 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Graft inflammation and histologic indicators of kidney chronic allograft failure: low-expressing interleukin-10 genotypes cannot be ignored. // Transplantation. – 2010. – Vol.90(6). – P.630-638. doi:10.1097/TP.0b013e3181ea391e; Semedo P., Donizetti-Oliveira C., Burgos-Silva M., Cenedeze M.A., Avancini Costa Malheiros D.M., Pacheco-Silva A. et al. Bone marrow mononuclear cells attenuate fibrosis development after severe acute kidney injury. // Lab Invest. – 2010. – Vol.90(5). – P.685-95. doi:10.1038/labinvest.2010.45; Kitching A.R. Dendritic cells in progressive renal disease: some answers, many questions. // Nephrol Dial Transplant. – 2014. – Vol.29(12). – P.2185-2193. doi:10.1093/ndt/gfu076; Snelgrove S.L., Kausman J.Y., Lo C., Lo C., Ooi J.D., Coates P.T. et al. Renal dendritic cells adopt a pro-inflammatory phenotype in obstructive uropathy to activate T cells but do not directly contribute to fibrosis. // Am J Pathol. – 2012. – Vol.180(1). – P.91- 103. doi:10.1016/j.ajpath.2011.09.039; Baba A., Tachi M., Ejima Y., Endo Y. , Toyama H., Saito K. et al. Less contribution of mast cells to the progression of renal fibrosis in Rat kidneys with chronic renal failure. // NEPHROLOGY. – 2017. – Vol.22(2). – P.159-167. doi:10.1111/nep.12733; Zhao J., Wang L., Cao A., Jiang M., Chen X., Peng W. Renal Tubulointerstitial Fibrosis: A Review in Animal Models. // Journal of Integrative Nephrology &Andrology. – 2015. – Vol.2(3). – P.75-80. doi:10.4103/2225-1243.161428; López-Novoa J.M., Rodríguez-Peña A.B., Ortiz A., Martínez-Salgado C., López Hernández F.J. Etiopathology of chronic tubular, glomerular and renovascular nephropathies: Clinical implications. // Journal of Translational Medicine. – 2011. _ Vol.9. – P.13. doi:10.1186/1479-5876-9-13; López-Marín L., Chávez Y., García X.A., Flores W.M., García Y.M., Herrera R. et al. Histopathology of Chronic Kidney Disease of Unknown Etiology in Salvadoran Agricultural Communities. // MEDICCReview. – 2014. – Vol.16(2). – P.49-54.; Батюшин М.М. Сулодексид. Нефропротективные свойства и горизонты применения в нефрологии. // Медицинский совет. – 2015. – №7. – С. 68-71. doi:10.21518/2079-701X-2015-7-68-71; Tanaka Y., Kume S., Araki S., Isshiki K., Chin-Kanasaki M., Sakaguchi M. et al. Fenofibrate, a PPARα agonist, has renoprotective effects in mice by enhancing renal lipolysis. // Kidney Int. – 2011. – Vol.79(8). – P.871-82. doi:10.1038/ki.2010.530; Cho K.H., Kim H.J., Kamanna V.S., Vaziri N.D. Niacin improves renal lipid metabolism and slows progression in chronic kidney disease. // BiochimBiophysActa. – 2010. – Vol.1800(1). – P.6-15. doi:10.1016/j.bbagen.2009.10.009; Ortiz A., Ucero A.C., Egido J. Unravelling fibrosis: two newcomers and an old foe. // Nephrol Dial Transplant. – 2010. – Vol.25(11). – P.3492-5. doi:10.1093/ndt/gfq518; Wang Q., Usinger W., Nichols B., Gray J., Xu L., Seeley T.W. et al. Cooperative interaction of CTGF and TGF-β in animal models of fibrotic disease. // Fibrogenesis Tissue Repair. – 2011. – Vol.4(1). – P.4. doi:10.1186/1755-1536-4-4; Loeffler I., Wolf G. Transforming growth factor- and the progression of renal disease. // Nephrol. Dial. Transplant. – 2014. – Suppl.1. – P.i37-i45. doi:10.1093/ndt/gft267; Pohlers D., Brenmoehl J., Löffler I., Müller C.K., Leipner C., Schultze-Mosgau S. et al. TGF-beta and fibrosis in different organs – molecular pathway imprints. // BiochimBiophysActa. – 2009. – Vol.1792(8). – P.746-56. doi:10.1016/j.bbadis.2009.06.004; Lee H.S. Mechanisms and consequences of TGF-ß overexpression by podocytes in progressive podocyte disease. // Cell Tissue Res. – 2012. – Vol.347(1). – P.129-40. doi:10.1007/s00441-011-1169-7; Ronco C. Cardiorenal syndromes: definition and classification // ContribNephrol. – 2010. – Vol.164. – P.33-38. doi:10.1159/000313718; Leask A. Targeting the jagged/notch pathway: a new treatment for fibrosis? // J Cell Commun Signal. – 2010. – Vol.4(4). – P.197-8. doi:10.1007/s12079-010-0101-3; Sharma S., Sirin Y., Susztak K. The story of Notch and chronic kidney disease. // CurrOpinNephrolHypertens. – 2011. – Vol.20(1). – P.56-61. doi:10.1097/MNH.0b013e3283414c88; Maezawa Y., Takemoto M., Yokote K. Cell biology of diabetic nephropathy: Roles of endothelial cells, tubulointerstitial cells and podocytes. // J Diabetes Investig. – 2015. – Vol. 6(1). – P.3-15. doi:10.1111/jdi.12255; Sato C., Zhao G., Ilagan M.X. An Overview of Notch Signaling in Adult Tissue Renewal and Maintenance. // Curr Alzheimer Res. – 2012. – Vol.9(2). – P.227–240.; Ables J.L., Breunig J.J., Eisch A.J., Rakic P. Not(ch) just development: Notch signalling in the adult brain. // Nat Rev Neurosci. – 2011. – Vol.12(5). – P.269–283. doi:10.1038/nrn3024; Sirin Y., Susztak K. Notch in the kidney: development and disease. // J Pathol. – 2012. – Vol.226(2). – P.394-403. doi:10.1002/path.2967; Niranjan T., Bielesz B., Gruenwald A., Ponda M.P., Kopp J.B., Thomas D.B. et al. The Notch pathway in podocytes plays a role in the development of glomerular disease. // Nat Med. – 2008. – Vol.14(3). – P.290-8. doi:10.1038/nm1731; Xu Y., Xue S., Zhou J., Voorhees J.J., Fisher G.J. Notch and TGF-β pathways cooperatively regulate receptor protein tyrosine phosphatase-κ¯ (PTPRK) gene expression in human primary keratinocytes. // MolBiolCell. – 2015. - Vol26(6). – P.1199-1206. doi:10.1091/mbc.E14-12-1591; Батюшин М.М., Гадаборшева Х.З. Белок сосудистой адгезии-1 (VAP-1) и его роль в моделировании воспалительного процесса и фиброза. Нефрологический вектор. //Нефрология. - 2015. - №5. – С. 23-27.; Jen K.Y., Haragsim L., Laszik Z.G. Kidney microvasculature in health and disease. // ContribNephrol. – 2011. – Vol.169. – P.51- 72. doi:10.1159/000313945; Левицкая Е.С., Батюшин М.М., Пасечник Д.Г., Асрумян Э.Г. Ремоделирование почечных артерий – инициатор и мишень кардио-ренального континуума. // Кардиоваскулярная терапия и профилактика. - 2015. – Т. 4. - №1. – С. 90-96. doi:10.15829/1728-8800-2015-1-90-96; Левицкая Е.С., Батюшин М.М, Пасечник Д.Г., Антипова Н.В. Прогнозирование ремоделирования ткани почек с учетом структурных изменений почечных артерий малого диаметра. // Нефрология. - 2016. – Т. 20. - №5. – С. 55-61.; Tracy R.E. Renal Vasculature in Essential Hypertension: A Review of Some Contrarian Evidence. // ContribNephrol. – 2011. – Vol.169. – P.327-336. doi:10.1159/000314908; Hanamura K., Tojo A., Kinugasa S., Asaba K., Fujita T. The Resistive Index Is a Marker of Renal Function, Pathology, Prognosis, and Responsiveness to Steroid Therapy in Chronic Kidney Disease Patients. // International Journal of Nephrology. – 2012. – Vol.2012. – 9 p. doi:10.1155/2012/139565; Eirin A., Lerman L.O. Darkness at the End of the Tunnel: Poststenotic Kidney Injury. // Physiology (Bethesda). – 2013. – Vol.28(4). – P.245-253. doi:10.1152/physiol.00010.2013; https://www.medicalherald.ru/jour/article/view/487
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6Academic Journal
Authors: ЛЕВИЦКАЯ Е.С.
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7Academic Journal
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8Academic Journal
Source: Медицинский вестник Юга России.
Subject Terms: RENAL FIBROSIS,SMALL-DIAMETER ARTERIES,SIGNALING PATHWAYS,PROINFLAMMATORY MEDIATORS,ОБЗОР,ФИБРОЗ ПОЧЕК,АРТЕРИИ МАЛОГО ДИАМЕТРА,СИГНАЛЬНЫЕ ПУТИ,ПРОВОСПАЛИТЕЛЬНЫЕ МЕДИАТОРЫ, 3. Good health
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9Academic Journal
Authors: Pascale de Lonlay, Asmaa Mamoune, Yamina Hamel, Michel Bahuau, Sabrina Vergnaud, Moniqu Piraud, Lætitia Lallemand, Marie-Ange Nguyen More, Mai Thao Vio, Norma Beatriz Romero, Monique Piraud, Marie-Ange Ngu Nguyen Morel, Mai Thao Viou
Source: Neuromuscular Diseases; Том 5, № 1 (2015); 10-18 ; Нервно-мышечные болезни; Том 5, № 1 (2015); 10-18 ; 2413-0443 ; 2222-8721 ; 10.17650/2222-8721-2015-5-1
Subject Terms: статины, fever, temperature-dependent rhabdomyolysis, inherited rhabdomyolysis, environment, thermolability, aldolase A, myopathy, myoglobinuria, pro-inflammatory mediators, hemolytic anemia, myositis, ATP, statins, lipid droplets, лихорадка, термочувствительный рабдомиолиз, наследственный рабдомиолиз, окружающая среда, термолабильность, альдолаза А, миопатия, миоглобинурия, провоспалительные медиаторы, гемолитическая анемия, миозит, аденозинтрифосфат
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10Academic Journal
Source: Наука и здравоохранение.
Subject Terms: морфофункциональные изменения, pro–inflammatory mediators, легочная патология, lung fibrоsis, 3. Good health, провоспалительные медиаторы, фиброз легких, morphofunctional сhаngеs, өкпе фиброзы, иондаушы сәулелер, өкпе патологиясы, морфофункционалды бұзылыстар, ионизирующее излучение, pulmonary pathology, iоnizing rаdiаtiоn, қабыну медиаторлары
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11Academic Journal
Authors: Притуло, Л., Бисюк, Ю., Притула, В., Филоненко, Т., Спахи, О., Шаевский, Д., Ионичева, Е.
Subject Terms: ПРОВОСПАЛИТЕЛЬНЫЕ МЕДИАТОРЫ, ЦИТОКИНЫ Т-ХЕЛПЕРОВ 1, 2 ТИПОВ, ГНОЙНО-СЕПТИЧЕСКИЕ ЗАБОЛЕВАНИЯ, ДЕТИ, ПРОЗАПАЛЬНі МЕДіАТОРИ, ЦИТОКіНИ Т-ХЕЛПЕРИ 1, 2 ТИПіВ, ГНіЙНО-СЕПТИЧНі ЗАХВОРЮВАННЯ, ДіТИ
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12Academic Journal
Authors: Pritulo, L. F., Bisyuk, Yu. A., Pritula, V. P.
Source: Патологія; № 1 (2012)
Pathologia; № 1 (2012)
Патология; № 1 (2012)Subject Terms: провоспалительные медиаторы, цитокины Т-хелперов 1, 2 типов, гнойно-септические заболевания, дети, proinflammatory mediators, citokines of 1, 2 types T-helperS, purulent-septic diseases, children, прозапальні медіатори, цитокіни Т-хелпери 1, 2 типів, гнійно-септичні захворювання, діти, 3. Good health
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Access URL: http://pat.zsmu.edu.ua/article/view/15849
