Gotowa bibliografia na temat „Tubular-interstitial fibrosis”
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Artykuły w czasopismach na temat "Tubular-interstitial fibrosis"
Wyczanska, Maja, Jana Rohling, Ursula Keller, Marcus R. Benz, Carsten Kirschning i 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.
Pełny tekst źródłaChristensen, Erik I., i Pierre J. Verroust. "Interstitial fibrosis: tubular hypothesis versus glomerular hypothesis". Kidney International 74, nr 10 (listopad 2008): 1233–36. http://dx.doi.org/10.1038/ki.2008.421.
Pełny tekst źródłaRascio, Federica, Paola Pontrelli, Giuseppe Stefano Netti, Elisabetta Manno, Barbara Infante, Simona Simone, Giuseppe Castellano i in. "IgE-Mediated Immune Response and Antibody-Mediated Rejection". Clinical Journal of the American Society of Nephrology 15, nr 10 (9.09.2020): 1474–83. http://dx.doi.org/10.2215/cjn.02870320.
Pełny tekst źródłaEskild-Jensen, Anni, Lene Fogt Paulsen, Lise Wogensen, Ping Olesen, Lea Pedersen, Jørgen Frøkiær i 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 (czerwiec 2007): F1771—F1781. http://dx.doi.org/10.1152/ajprenal.00479.2006.
Pełny tekst źródłaWang, Shi-Nong, i Raimund Hirschberg. "Growth factor ultrafiltration in experimental diabetic nephropathy contributes to interstitial fibrosis". American Journal of Physiology-Renal Physiology 278, nr 4 (1.04.2000): F554—F560. http://dx.doi.org/10.1152/ajprenal.2000.278.4.f554.
Pełny tekst źródłaThomas, S. E., S. Anderson, K. L. Gordon, T. T. Oyama, S. J. Shankland i 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 (luty 1998): 231–42. http://dx.doi.org/10.1681/asn.v92231.
Pełny tekst źródłaLeong, Khai Gene, Elyce Ozols, John Kanellis, David J. Nikolic-Paterson i 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.
Pełny tekst źródłaWang, Shudan, Ming Wu, Luis Chiriboga, Chaim Putterman, Anna Broder i 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 (czerwiec 2020): 144. http://dx.doi.org/10.1017/cts.2020.424.
Pełny tekst źródłaPichler, R. H., N. Franceschini, B. A. Young, C. Hugo, T. F. Andoh, E. A. Burdmann, S. J. Shankland, C. E. Alpers, W. M. Bennett i W. G. Couser. "Pathogenesis of cyclosporine nephropathy: roles of angiotensin II and osteopontin." Journal of the American Society of Nephrology 6, nr 4 (październik 1995): 1186–96. http://dx.doi.org/10.1681/asn.v641186.
Pełny tekst źródłaWang, Hao, Yujiao Deng, Limeng He, Yan Deng i 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 (2.09.2023): 896–98. http://dx.doi.org/10.1097/rlu.0000000000004804.
Pełny tekst źródłaRozprawy doktorskie na temat "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.
Pełny tekst źródłaRoger, 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.
Pełny tekst źródłaChronic 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, i 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.
Pełny tekst źródłaKsiążki na temat "Tubular-interstitial fibrosis"
Herrington, William G., Aron Chakera i Christopher A. O’Callaghan. Interstitial renal disease. Redaktorzy Patrick Davey i David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0160.
Pełny tekst źródłaSchiller, Adalbert, Adrian Covic i Liviu Segall. Chronic tubulointerstitial nephritis. Redaktor Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0086_update_001.
Pełny tekst źródłaRadović, Milan, i Adalbert Schiller. Balkan endemic nephropathy. Redaktor Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0090_update_001.
Pełny tekst źródłaHughes, Jeremy. Proteinuria as a direct cause of progression. Redaktor David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0137.
Pełny tekst źródłaSegall, Liviu, i Adrian Covic. Immune-mediated tubulointerstitial nephritis. Redaktor Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
Pełny tekst źródłaIzzedine, Hassan, i Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Redaktor Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
Pełny tekst źródłaCzęści książek na temat "Tubular-interstitial fibrosis"
Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry i in. "Interstitial Fibrosis/Tubular Atrophy". W 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.
Pełny tekst źródła"Tubular and interstitial disease". W Oxford Desk Reference Nephrology, redaktorzy Jonathan Barratt, Peter Topham, Sue Carr, Mustafa Arici i Adrian Liew, 140–84. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198777182.003.0005.
Pełny tekst źródłaHarris, Kevin P. G. "Proteinuria: Implications for Progression and Management". W 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.
Pełny tekst źródłaDe Broe, Marc E., Channa Jayasumana, Patrick C. D’Haese, Monique M. Elseviers i Benjamin Vervaet. "Chronic tubulointerstitial nephritis". W Oxford Textbook of Medicine, redaktor John D. Firth, 4956–74. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0490.
Pełny tekst źródłaStreszczenia konferencji na temat "Tubular-interstitial fibrosis"
Kammardi Shashiprakash, Avinash, Brendon Lutnick, Brandon Ginley, Darshana Govind, Nicholas Lucarelli, Kuang-Yu Jen, Avi Z. Rosenberg i in. "A distributed system improves inter-observer and AI concordance in annotating interstitial fibrosis and tubular atrophy". W Digital and Computational Pathology, redaktorzy John E. Tomaszewski i Aaron D. Ward. SPIE, 2021. http://dx.doi.org/10.1117/12.2581789.
Pełny tekst źródłaCABRAL, HIANNY RIBEIRO, ARTHUR LIRA ARAÚJO, PAULO ROBERTO SILVA JÚNIOR, JOSÉ GUSTAVO AGUIAR LOPES, DOUGLAS FIGUEIREDO SANTOS, NORIVAN SILVA LINHARES JÚNIOR, BÁRBARA ARAÚJO BATISTA i 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." W 36º Congresso Brasileiro de Reumatologia. São Paulo: Editora Blucher, 2019. http://dx.doi.org/10.5151/sbr2019-104.
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