Auswahl der wissenschaftlichen Literatur zum Thema „Tubular-interstitial fibrosis“
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Zeitschriftenartikel zum Thema "Tubular-interstitial fibrosis"
Wyczanska, Maja, Jana Rohling, Ursula Keller, Marcus R. Benz, Carsten Kirschning und Bärbel Lange-Sperandio. „TLR2 mediates renal apoptosis in neonatal mice subjected experimentally to obstructive nephropathy“. PLOS ONE 18, Nr. 11 (28.11.2023): e0294142. http://dx.doi.org/10.1371/journal.pone.0294142.
Der volle Inhalt der QuelleChristensen, Erik I., und Pierre J. Verroust. „Interstitial fibrosis: tubular hypothesis versus glomerular hypothesis“. Kidney International 74, Nr. 10 (November 2008): 1233–36. http://dx.doi.org/10.1038/ki.2008.421.
Der volle Inhalt der QuelleRascio, Federica, Paola Pontrelli, Giuseppe Stefano Netti, Elisabetta Manno, Barbara Infante, Simona Simone, Giuseppe Castellano et al. „IgE-Mediated Immune Response and Antibody-Mediated Rejection“. Clinical Journal of the American Society of Nephrology 15, Nr. 10 (09.09.2020): 1474–83. http://dx.doi.org/10.2215/cjn.02870320.
Der volle Inhalt der QuelleEskild-Jensen, Anni, Lene Fogt Paulsen, Lise Wogensen, Ping Olesen, Lea Pedersen, Jørgen Frøkiær und Jens Randel Nyengaard. „AT1 receptor blockade prevents interstitial and glomerular apoptosis but not fibrosis in pigs with neonatal induced partial unilateral ureteral obstruction“. American Journal of Physiology-Renal Physiology 292, Nr. 6 (Juni 2007): F1771—F1781. http://dx.doi.org/10.1152/ajprenal.00479.2006.
Der volle Inhalt der QuelleWang, Shi-Nong, und Raimund Hirschberg. „Growth factor ultrafiltration in experimental diabetic nephropathy contributes to interstitial fibrosis“. American Journal of Physiology-Renal Physiology 278, Nr. 4 (01.04.2000): F554—F560. http://dx.doi.org/10.1152/ajprenal.2000.278.4.f554.
Der volle Inhalt der QuelleThomas, S. E., S. Anderson, K. L. Gordon, T. T. Oyama, S. J. Shankland und R. J. Johnson. „Tubulointerstitial disease in aging: evidence for underlying peritubular capillary damage, a potential role for renal ischemia.“ Journal of the American Society of Nephrology 9, Nr. 2 (Februar 1998): 231–42. http://dx.doi.org/10.1681/asn.v92231.
Der volle Inhalt der QuelleLeong, Khai Gene, Elyce Ozols, John Kanellis, David J. Nikolic-Paterson und Frank Y. Ma. „Cyclophilin A Promotes Inflammation in Acute Kidney Injury but Not in Renal Fibrosis“. International Journal of Molecular Sciences 21, Nr. 10 (22.05.2020): 3667. http://dx.doi.org/10.3390/ijms21103667.
Der volle Inhalt der QuelleWang, Shudan, Ming Wu, Luis Chiriboga, Chaim Putterman, Anna Broder und H. Michael Belmont. „4336 Renal Tubular Complement C9 Deposition is Associated with Renal Tubular Damage and Fibrosis in Lupus Nephritis“. Journal of Clinical and Translational Science 4, s1 (Juni 2020): 144. http://dx.doi.org/10.1017/cts.2020.424.
Der volle Inhalt der QuellePichler, R. H., N. Franceschini, B. A. Young, C. Hugo, T. F. Andoh, E. A. Burdmann, S. J. Shankland, C. E. Alpers, W. M. Bennett und W. G. Couser. „Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin.“ Journal of the American Society of Nephrology 6, Nr. 4 (Oktober 1995): 1186–96. http://dx.doi.org/10.1681/asn.v641186.
Der volle Inhalt der QuelleWang, Hao, Yujiao Deng, Limeng He, Yan Deng und Wei Zhang. „Renal Interstitial Fibrosis Detected on 18F-AlF-NOTA-FAPI-04 PET/CT in a Patient With Multiple Myeloma“. Clinical Nuclear Medicine 48, Nr. 10 (02.09.2023): 896–98. http://dx.doi.org/10.1097/rlu.0000000000004804.
Der volle Inhalt der QuelleDissertationen zum Thema "Tubular-interstitial fibrosis"
Bletsos, Vassili S. „The Role of CD40 Signaling in Chronic Renal Allograft Rejection in a Hypertensive Rat Model“. University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1532961455216765.
Der volle Inhalt der QuelleRoger, Elena. „Rôle de la Connexine 43 dans les maladies rénales tubulaires expérimentales“. Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS202.pdf.
Der volle Inhalt der QuelleChronic kidney disease (CKD) is a major public health problem, affecting millions of people worldwide. Although significant progress has been made, there is no specific treatment shown to arrest the progression of the disease. Therefore, the discovery of novel therapeutic targets is of crucial importance for an efficient treatment. Our main objective was to define the role of Connexin 43 (Cx43), a constitutive gap junction protein of, in the functional and structural adaptation of the kidney in response to chronic tubulointerstitial injury, using new genetic models of transgenic mice with temporal and tissue-specific control of this Cx expression. Our hypothesis, which is strongly supported by our previous studies, is that Cx43 can be abnormally expressed after aggression in adult tissue, leading to phenotypic changes that enable the aggressed tissue to adapt to the new pathological environment. We demonstrated that increased expression of Cx43 in renal tubules correlates positively with renal inflammation in two models of experimental renal tubular disease, by promoting the release of ATP into the extra-cellular environment and activation of the inflammasome. In addition, activation of the Hippo pathway, and more specifically Cx43-mediated nuclear translocation of YAP, is involved in tubulointerstitial fibrosis via activation of target genes. Specific inhibition of Cx43 in tubular cells had beneficial effects on the progression of renal tubulopathy, improving renal function and structure while limiting inflammation and tubulointerstitial fibrosis. Characterization of the molecular mechanisms involved in these two processes involving Cx43, has enriched our understanding of renal pathophysiology, confirming this protein as a new therapeutic target against the progression of CKD
Hwang, Kuo-Chan, und 黃國展. „Proteome analysis of the effect of (+)-Catechin toward tubular interstitial fibrosis by fluorogenic derivatization-liquid chromatography-tandem mass spectrometry method“. Thesis, 2012. http://ndltd.ncl.edu.tw/handle/18888450087904874418.
Der volle Inhalt der QuelleBücher zum Thema "Tubular-interstitial fibrosis"
Herrington, William G., Aron Chakera und Christopher A. O’Callaghan. Interstitial renal disease. Herausgegeben von Patrick Davey und David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0160.
Der volle Inhalt der QuelleSchiller, Adalbert, Adrian Covic und Liviu Segall. Chronic tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.
Der volle Inhalt der QuelleRadović, Milan, und Adalbert Schiller. Balkan endemic nephropathy. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.
Der volle Inhalt der QuelleHughes, Jeremy. Proteinuria as a direct cause of progression. Herausgegeben von David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
Der volle Inhalt der QuelleSegall, Liviu, und Adrian Covic. Immune-mediated tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
Der volle Inhalt der QuelleIzzedine, Hassan, und Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Herausgegeben von Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
Der volle Inhalt der QuelleBuchteile zum Thema "Tubular-interstitial fibrosis"
Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry et al. „Interstitial Fibrosis/Tubular Atrophy“. In Encyclopedia of Molecular Mechanisms of Disease, 1064. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7797.
Der volle Inhalt der Quelle„Tubular and interstitial disease“. In Oxford Desk Reference Nephrology, herausgegeben von Jonathan Barratt, Peter Topham, Sue Carr, Mustafa Arici und Adrian Liew, 140–84. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198777182.003.0005.
Der volle Inhalt der QuelleHarris, Kevin P. G. „Proteinuria: Implications for Progression and Management“. In Mechanisms and Clinical Management of Chronic Renal Failure, 146–72. Oxford University PressNew York, NY, 2000. http://dx.doi.org/10.1093/oso/9780192629333.003.0005.
Der volle Inhalt der QuelleDe Broe, Marc E., Channa Jayasumana, Patrick C. D’Haese, Monique M. Elseviers und Benjamin Vervaet. „Chronic tubulointerstitial nephritis“. In Oxford Textbook of Medicine, herausgegeben von John D. Firth, 4956–74. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0490.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Tubular-interstitial fibrosis"
Kammardi Shashiprakash, Avinash, Brendon Lutnick, Brandon Ginley, Darshana Govind, Nicholas Lucarelli, Kuang-Yu Jen, Avi Z. Rosenberg et al. „A distributed system improves inter-observer and AI concordance in annotating interstitial fibrosis and tubular atrophy“. In Digital and Computational Pathology, herausgegeben von John E. Tomaszewski und Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581789.
Der volle Inhalt der QuelleCABRAL, HIANNY RIBEIRO, ARTHUR LIRA ARAÚJO, PAULO ROBERTO SILVA JÚNIOR, JOSÉ GUSTAVO AGUIAR LOPES, DOUGLAS FIGUEIREDO SANTOS, NORIVAN SILVA LINHARES JÚNIOR, BÁRBARA ARAÚJO BATISTA und LUCAS GABRIEL CRUZ DE MENEZES CHAVES. „FOCAL TUBULAR ATROPHY AND INTERSTITIAL FIBROSIS RELATED TO THE USE OF LEFLUNOMIDE IN A PATIENT WITH RHEUMATOID ARTHRITIS: A CASE REPORT.“ In 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-104.
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