Добірка наукової літератури з теми "Antifibrotics"
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Статті в журналах з теми "Antifibrotics"
Niitsu, Takayuki, Kiyoharu Fukushima, Sho Komukai, So Takata, Yuko Abe, Takuro Nii, Tomoki Kuge, et al. "Real-world impact of antifibrotics on prognosis in patients with progressive fibrosing interstitial lung disease." RMD Open 9, no. 1 (January 2023): e002667. http://dx.doi.org/10.1136/rmdopen-2022-002667.
Повний текст джерелаBos, Saskia, Laurens J. De Sadeleer, Arno Vanstapel, Hanne Beeckmans, Annelore Sacreas, Jonas Yserbyt, Wim A. Wuyts, and Robin Vos. "Antifibrotic drugs in lung transplantation and chronic lung allograft dysfunction: a review." European Respiratory Review 30, no. 160 (June 1, 2021): 210050. http://dx.doi.org/10.1183/16000617.0050-2021.
Повний текст джерелаSoskis, Alyssa, and Robert Hallowell. "Antifibrotic Therapy: Is There a Role in Myositis-Interstitial Lung Disease?" Respiration 100, no. 9 (2021): 923–32. http://dx.doi.org/10.1159/000515607.
Повний текст джерелаJegal, Yangjin, Jong Sun Park, Song Yee Kim, Hongseok Yoo, Sung Hwan Jeong, Jin Woo Song, Jae Ha Lee, et al. "Clinical Features, Diagnosis, Management, and Outcomes of Idiopathic Pulmonary Fibrosis in Korea: Analysis of the Korea IPF Cohort (KICO) Registry." Tuberculosis and Respiratory Diseases 85, no. 2 (April 1, 2022): 185–94. http://dx.doi.org/10.4046/trd.2021.0123.
Повний текст джерелаCaliskan, Canay, Benjamin Seeliger, Benedikt Jäger, Jan Fuge, Tobias Welte, Oliver Terwolbeck, Julia Freise, Coline H. M. van Moorsel, Yingze Zhang, and Antje Prasse. "Genetic Variation in CCL18 Gene Influences CCL18 Expression and Correlates with Survival in Idiopathic Pulmonary Fibrosis—Part B." Journal of Clinical Medicine 9, no. 6 (June 25, 2020): 1993. http://dx.doi.org/10.3390/jcm9061993.
Повний текст джерелаDhar, Raja. "Antifibrotics in India." Lung India 36, no. 5 (2019): 445. http://dx.doi.org/10.4103/lungindia.lungindia_379_19.
Повний текст джерелаAlbera, Carlo, Giulia Verri, Federico Sciarrone, Elena Sitia, Mauro Mangiapia, and Paolo Solidoro. "Progressive Fibrosing Interstitial Lung Diseases: A Current Perspective." Biomedicines 9, no. 9 (September 16, 2021): 1237. http://dx.doi.org/10.3390/biomedicines9091237.
Повний текст джерелаBoleto, Gonçalo, Jérôme Avouac, and Yannick Allanore. "The role of antifibrotic therapies in the treatment of systemic sclerosis–associated interstitial lung disease." Therapeutic Advances in Musculoskeletal Disease 14 (January 2022): 1759720X2110666. http://dx.doi.org/10.1177/1759720x211066686.
Повний текст джерелаCohen-Naftaly, Michal, and Scott L. Friedman. "Current status of novel antifibrotic therapies in patients with chronic liver disease." Therapeutic Advances in Gastroenterology 4, no. 6 (July 22, 2011): 391–417. http://dx.doi.org/10.1177/1756283x11413002.
Повний текст джерелаTzilas, Vasilios, Argyris Tzouvelekis, Evangelos Bouros, Theodoros Karampitsakos, Maria Ntassiou, Eleni Avdoula, Athena Trachalaki, Katerina Antoniou, Ganesh Raghu, and Demosthenes Bouros. "Clinical experience with antifibrotics in fibrotic hypersensitivity pneumonitis: a 3-year real-life observational study." ERJ Open Research 6, no. 4 (October 2020): 00152–2020. http://dx.doi.org/10.1183/23120541.00152-2020.
Повний текст джерелаДисертації з теми "Antifibrotics"
Venalis, Paulius. "The performance of antifibrotic agents in preclinical models of systemic sclerosis." Doctoral thesis, Lithuanian Academic Libraries Network (LABT), 2010. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2010~D_20101001_150819-57019.
Повний текст джерелаSisteminė sklerozė (SSc) – viena sunkiausių ir fatališkiausių autoimuninių sisteminių reumatinių ligų, o bazinių vaistų stygius, šiai ligai gydyti, itin didelis. Į onkologinę klinikinę praktiką įdiegtas tirozinkinazių inhibitorius – imatinibo mezilatas(IM). IM blokuoja TGF-β ir PDGF intraląstelinio signalo perdavimą ir taip sąlygoja fibrozės prevenciją SSc pelių modelyje. Mums buvo svarbu išsiaiškinti, ar imatinibas gali turėti įtakos ne tik prevencijai, bet ir susiformavusiai fibrozei. Be to TGF-β ir PDGF blokavimas angiogenezėje, galėtų riboti daug žadančio fibrozės inhibitoriaus IM naudojimą gydant SSc. Darbo tikslas: įvertinti imatinibo mezilato poveikį fibrozės procesui ir endoteliui sisteminės sklerozės eksperimentiniuose modeliuose ir ląstelių kultūrose. Darbo uždaviniai: įvertinti imatinibo efektyvumą neuždegiminiame SSc modelyje ir patikrinti imatinibo mezilato efektyvumą uždegiminiame suformuotos fibrozės modelyje; ištirti, ar terapinės imatinibo mezilato koncentracijos daro neigiamą poveikį gyvybinėms endotelio funkcijoms; įvertinti imatinibo mezilato poveikį angiogenezės etapams. Mūsų gauti duomenys rodo, kad: IM ne tik sustabdė bet ir paskatino jau egzistuojančios (bleomicino sukeltos) odos firbrozės regresiją; IM ryškiai sumažino poodžio ir odos storį, bei normalizavo miofibroblastų skaičių Tsk-1 pelėse; IM neturėjo poveikio endotelio ląstelių bazinėms funkcijoms; IM neturėjo neigiamo poveikio angiogenezės etapams.
Gerarduzzi, Casimiro. "The phosphoproteome network of the PGE2/EP axis: Extrapolation towards an Antifibrotic Machinery." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110368.
Повний текст джерелаLa fibrose est une maladie chronique complexe caractérisée par une réaction de réparation persistante. Sa pathogénie est mal comprise mais on la connaît pour exiger l'activité de TGFbeta et une tension extracellulaire de la matrice (ECM), qui dirige des fibroblastes dans une transition vers un phénotype de myofibroblast (FMT). Comme cellules effectrices de la réparation, les myofibroblasts migrent au site des dommages pour déposer des quantités excessives de collagène de type I aussi bien que d'autres protéines de matrice et pour stimuler de hauts niveaux de contraction. De telles actions sont essentielles pour la fermeture de blessure et le rétablissement de la structure normale du tissu cependant, laissé incontrôlé elle limite la réparation normale et le remodelage du tissu. Les mécanismes cellulaires et moléculaires réglant la fibrose ne sont pas bien définis mais les marqueurs du phénotype de myofibroblastes incluent des réarrangements cytosquelettiques importants, la formation des fibres de stress riches en alpha-actine du muscle lisses (alpha-sma), et des adhérences focales (FAs). Les voies importantes de signalisation qui soutiennent la différenciation myofibroblastique incluent une signalisation TGFbeta-dépendante, la Wnt/beta-catenin, la kinase de Ras/Raf/MAP et les voies dépendantes de la kinase Rho-Associée (ROCK). La résolution du phénotype de myofibroblast est essentielle pour empêcher la réparation continuelle de la blessure, autrement davantage de dépôt des protéines extracellulaire de la matrice explique la fibrose du tissu. Il est bien connu que la PGE2 empêche FMT humain par des mécanismes qui sont vaguement connus. Notre laboratoire a créé une stratégie pour mieux comprendre les voies de signalisation dans lesquelles la PGE2, un médiateur antifibrotique , empêche le développement de myofibroblast. Notre travail décrit un croquis complet du phosphoprotéome/GalphaS signalosome dépendante de la PGE2 dans les cellules avec le phénotype fibroblaste (par PhosphoScanTM, signalisation cellulaires), qui incluent des protéines liées à la différenciation cellulaire et à la structure cytosquelettique/adhérence. En outre, nous avons identifié la séquence des acides aminés spécifique de sites inédits de phosphorylation, une information indispensable vers le procédé de contrôle de l'activité d'une protéine. Des exemples de phosphoprotéines induites par la PGE2 liées aux activités myofibroblastic incluent le beta-cateninix(différenciation), le RIN1 (Ras-inhibiteur) (migration), le ROCK2 (contraction), aussi bien que les diverses protéines en amont et en aval de la ROCK. Donnant de la considération à notre stratégie, l'analyse mutationnelle du phosphosite ROCK2 a empêché l'inhibition de l'enzyme par la PGE2, inhibant potentiellement la contraction myofibroblastique. En outre, la mutation du phosphosite RIN1 a empêché l'inhibition de la PGE2 sur la migration induite par le TGFbeta, une autre caractéristique essentielle des myofibroblasts. D'autres observations inclus une inversion marquée de la phosphorylation des protéines du cytosquelette, la perte de formation de fibre de stress et des adhérences focales, la suppression de l'expression de l'alpha-actine du muscle lisses (alpha-sma), et le blocus du FMT par l'activation « de l'axe de biosynthèse des phospholipase/cyclooxygenase/mPGE synthase/prostaglandine E2» dans les fibroblastes humains. Finalement, les résultats encourageront la PGE2 en tant que cible thérapeutique potentielle pour le traitement de la fibrose.
Lu, Changwu [Verfasser]. "Antifibrotic drugs: new candidates for the treatment of pulmonary arterial hypertension? / Changwu Lu." Gießen : Universitätsbibliothek, 2018. http://d-nb.info/1163533688/34.
Повний текст джерелаBrook, Nicholas Roger. "Nephrotoxicity of immunosuppressant drugs in salt-depletion and modification of effect by an antifibrotic agent." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29914.
Повний текст джерелаFinato, Angela Carolina. "Avaliação de terapias antifibróticas associadas aos antifúngicos itraconazol e cotrimoxazol em modelo murino de paracoccidioidomicose pulmonar." Botucatu, 2017. http://hdl.handle.net/11449/151468.
Повний текст джерелаResumo: Paracoccidioidomicose (PCM) é uma micose sistêmica causada por fungos do gênero Paracoccidioides; suas principais formas clínicas são aguda/subaguda, crônica e residual. A PCM é uma doença restrita a países da América Latina com maior incidência no Brasil, especialmente entre os trabalhadores rurais. A maioria dos pacientes com a forma crônica da doença, mesmo após tratamento eficaz, apresentam sequelas, incluindo fibrose pulmonar e adrenal. Os problemas sociais, econômicos e psicológicos desencadeados pela fibrose pulmonar são subestimados; além disso, a fibrose na PCM permanece negligenciada, uma vez que não há tratamento. Dessa forma, o estudo teve por objetivo investigar a influência de drogas com potencial antifibrótico (pentoxifilina - PTX, azitromicina - AZT e talidomida - Thal) associadas aos tratamentos antifúngicos com itraconazol - ITC e cotrimoxazol - CMX em modelo murino de PCM pulmonar. Para tanto, camundongos BALB/c machos foram inoculados com leveduras do isolado 326 de P. brasiliensis e após 8 semanas de infecção foi dado início aos esquemas terapêuticos: PTX/ITC, PTX/CMX, AZT/ITC, AZT/CMX, Thal/ITC e Thal/CMX. Após 8 semanas de tratamento, os animais foram eutanasiados a fim de se avaliar a deposição de fibras colágenas, produção de hidroxiprolina, recuperação de fungos viáveis e a porcentagem das áreas com lesão nos pulmões e peso corporal. Visando identificar os mecanismos envolvidos foi avaliada a produção de TGF-β1, CCL3, IFN-γ, TNF-α, IL-10, VEGF, IL-6,... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Paracoccidioidomycosis (PCM) is a systemic mycosis caused by fungi of Paracoccidioides genus; the main clinical forms are acute/subacute, chronic and residual. PCM is a disease restricted to Latin American countries with a higher incidence in Brazil, especially among rural workers. Most patients with the chronic form, even after effective treatment, present sequelae, including pulmonary and adrenal fibrosis. The social, economic and psychological problems triggered by pulmonary sequels are underestimated. In addition, fibrosis in PCM remains neglected, since there is no treatment. The aim of this study was to investigate the influence of antifibrotic drugs (pentoxifylline - PTX, azithromycin - AZT and thalidomide - Thal) associated with antifungal treatments with itraconazole - ITC and cotrimoxazole - CMX in a murine model of pulmonary PCM. Male BALB/c mice were inoculated with P. brasiliensis “isolated 326” and after 8 weeks of infection the treatment were started: PTX/ITC, PTX/CMX, AZT/ITC, AZT/CMX, Thal/ITC and Thal/CMX. After 8 weeks of treatment, the mice were euthanized in order to evaluate the deposition of collagen fibers, hydroxyproline production, recovery of viable fungi and the percentage of areas with injury in lung and body weight. In order to identify the mechanisms involved, the production of TGF-β1, CCL3, IFN-γ, TNF-α, IL-10, VEGF, IL-6, IL-1β, IL-17 and IL-2 in the lung homogenate was evaluated. Our findings revealed that infected mice treated with PTX/ITC s... (Complete abstract click electronic access below)
Mestre
Arias-Kuhn, Mónica S. "Antifibrotic therapy in the liver by adenovirus mediated expression of a TGF [beta]1 [beta 1] antisense mRNA /." Aachen : Shaker, 2004. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=013111065&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Повний текст джерелаArias-Kuhn, Mónica S. [Verfasser]. "Antifibrotic Therapy in the Liver by Adenovirus-mediated Expression of a TGF-beta1 Antisense mRNA / Mónica S Arias-Kuhn." Aachen : Shaker, 2004. http://d-nb.info/1181604060/34.
Повний текст джерелаÖcal, Sinan [Verfasser], Ulrich [Gutachter] Baumann, and Karsten [Gutachter] Niefind. "The HSP47 - Procollagen Interaction: Mechanism of pH-Dependent Client Release and Development of Antifibrotic Inhibitors / Sinan Öcal ; Gutachter: Ulrich Baumann, Karsten Niefind." Köln : Universitäts- und Stadtbibliothek Köln, 2017. http://d-nb.info/117241467X/34.
Повний текст джерелаKaps, Leonard [Verfasser]. "In vivo gene silencing in the liver with siRNA loaded non-biodegradable and biodegradable cationic nanohydrogel particles for antifibrotic therapy / Leonard Kaps." Mainz : Universitätsbibliothek Mainz, 2018. http://d-nb.info/1152103210/34.
Повний текст джерелаMatei, Alexandru-Emil [Verfasser], Jörg [Akademischer Betreuer] Distler, Jörg [Gutachter] Distler, and Georg [Gutachter] Schett. "Protein kinases G as downstream mediators of the antifibrotic effects of stimulators of soluble guanylate cyclase / Alexandru-Emil Matei ; Gutachter: Jörg Distler, Georg Schett ; Betreuer: Jörg Distler." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2019. http://d-nb.info/1202608485/34.
Повний текст джерелаКниги з теми "Antifibrotics"
Nanomedicine - Infectious Diseases, Immunotherapy, Diagnostics, Antifibrotics, Toxicology and Gene Medicine. Elsevier, 2012. http://dx.doi.org/10.1016/c2011-0-04217-5.
Повний текст джерелаNanomedicine: Infectious Diseases, Immunotherapy, Diagnostics, Antifibrotics, Toxicology and Gene Medicine. Elsevier Science & Technology Books, 2012.
Знайти повний текст джерелаDuzgunes, Nejat. Nanomedicine: Infectious Diseases, Immunotherapy, Diagnostics, Antifibrotics, Toxicology and Gene Medicine. Elsevier Science & Technology Books, 2012.
Знайти повний текст джерелаЧастини книг з теми "Antifibrotics"
Pinzani, Massimo. "Antifibrotic Drugs." In Portal Hypertension V, 211–17. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444393989.ch21.
Повний текст джерелаThuy, Le Thi Thanh, Hoang Hai, Vu Ngoc Hieu, Ninh Quoc Dat, Dinh Viet Hoang, and Norifumi Kawada. "Antifibrotic Therapy for Liver Cirrhosis." In The Evolving Landscape of Liver Cirrhosis Management, 167–89. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-7979-6_15.
Повний текст джерелаHanda, Tomohiro, and Arata Azuma. "Pharmacotherapy of IPF Using Antifibrotic Compounds." In Idiopathic Pulmonary Fibrosis, 147–59. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55582-7_9.
Повний текст джерелаZhang, Ying-Ying, Ying Yu, and Chen Yu. "Antifibrotic Roles of RAAS Blockers: Update." In Advances in Experimental Medicine and Biology, 671–91. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8871-2_33.
Повний текст джерелаEsmat, Gamal, and Maissa El Raziky. "Changing outcomes with antiviral or antifibrotic therapies." In Cirrhosis: A practical guide to management, 274–82. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118412640.ch24.
Повний текст джерелаMenke, A., R. Vogelmann, M. Bachem, and G. Adler. "Mechanisms of Fibrosis and Potential Antifibrotic Agents." In Pancreatic Disease, 132–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60068-5_13.
Повний текст джерелаCordeiro, M. Francesca, Annelie Maass, Clive Migdal та Li Guo. "TGF-β-Related Antifibrotic Strategies in the Eye". У Transforming Growth Factor-β in Cancer Therapy, Volume I, 663–73. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-292-2_42.
Повний текст джерелаSchuppan, Detlef, Jae Jin Cho, Masahiko Koda, and Eckhart G. Hahn. "Lecture - Antifibrotic Therapy: Future Cure for Portal Hypertension?" In Portal Hypertension III: Proceedings of the Third Baverno International Consensus Workshop on Definitions, Methodology and Therapeutic Strategies, 112–26. Oxford, UK: Blackwell Science Ltd, 2008. http://dx.doi.org/10.1002/9780470760154.ch8.
Повний текст джерелаLupher Jr., Mark L., and W. Scott Willett. "Serum amyloid P: A novel antifibrotic agent with therapeutic potential." In New Drugs and Targets for Asthma and COPD, 261–66. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320829.
Повний текст джерелаMathew, Anna, Robyn Cunard, and Kumar Sharma. "Antifibrotic Treatment and Other New Strategies for Improving Renal Outcomes." In Contributions to Nephrology, 217–27. Basel: KARGER, 2011. http://dx.doi.org/10.1159/000325671.
Повний текст джерелаТези доповідей конференцій з теми "Antifibrotics"
Muñoz Burgos, M., M. Mejias Trueba, and T. Desongles Corrales. "4CPS-123 Antifibrotics in idiopathic pulmonary fibrosis management: pirfenidone and nintedanib." In 24th EAHP Congress, 27th–29th March 2019, Barcelona, Spain. British Medical Journal Publishing Group, 2019. http://dx.doi.org/10.1136/ejhpharm-2019-eahpconf.272.
Повний текст джерелаSand, Jannie, Natasja Gudmann, Sarah Rønnow, Sarah Brockbank, Simon Cruwys, Morten Karsdal, and Diana Leeming. "Scar-in-a-Jar, an in vitro screening tool for antifibrotics." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa597.
Повний текст джерелаPorse, Simon, Nils Hoyer, Thomas Skovhus Prior, Elisabeth Bendstrup, and Saher B. Shaker. "Prognostic significance of dose reduction of antifibrotics in patients with IPF." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.oa1204.
Повний текст джерелаLlanos-González, Ana Belén, Sara García Gil, Juan Alfonso Bonilla Arjona, Sonia García Hernández, Verónica S. Hernández García, Paula Pérez De Armas, Nelson Mesa León, and Orlando Acosta Fernández. "Experience with antifibrotics treatment in progressive interstitial lung diseases non-IPF." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2375.
Повний текст джерелаHuong, YK, V. Dhunnoo, C. Leonard, R. Venkateswaran, and N. Chaudhuri. "M24 Do antifibrotics impact on lung transplantation outcomes in idiopathic pulmonary fibrosis?" In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.446.
Повний текст джерелаBhomra, PS, GA Burge, AM Turner, PS Burge, and GI Walters. "P158 Which factors predict early discontinuation of antifibrotics in idiopathic pulmonary fibrosis?" In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.316.
Повний текст джерелаRyan, J., K. Malcolm, E. D. Farrand, N. A. Kolaitis, B. J. Ley, J. K. Brown, and J. R. Greenland. "Medication Discontinuation and Survival in Elderly Veterans on Antifibrotics for Idiopathic Pulmonary Fibrosis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4761.
Повний текст джерелаNaqvi, M., and A. West. "P138 Review of patient longevity when managed with antifibrotics for idiopathic pulmonary fibrosis." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.283.
Повний текст джерелаTzilas, Vasilios, Argyrios Tzouvelekis, Evangelos Bouros, Theodoros Karampitsakos, Maria Ntassiou, Eleni Avdoula, Athina Trachalaki, Katerina Antoniou, and Demosthenes Bouros. "Efficacy of antifibrotics in chronic hypersensitivity pneumonitis. A 3 year real-life observational study." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.737.
Повний текст джерелаAdams, C., S. Shapera, C. J. Ryerson, P. Wilcox, T. M. To, M. Sadatsafavi, J. Morisset, et al. "'Real World' Therapeutic Approach and Associations with FVC Decline in IPF Patients Treated with Antifibrotics." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1504.
Повний текст джерела