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10.1002/art.39744 http://scihub22266oqcxt.onion/10.1002/art.39744 C5083145!5083145!27159593     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arthritis+Rheumatol 2016 ; 68 (11): 2740-51 Nephropedia Template TP {{tp|p=27159593|t=2016. BCL-2 as a Therapeutic Target in Human Tubulointerstitial Inflammation |pdf=|usr=}}{{27159593}} gab.com Text BCL-2 as a Therapeutic Target in Human Tubulointerstitial Inflammation JO: Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=27159593 #FOAvip Objective: In lupus nephritis (LuN), tubulointerstitial inflammation (TII) is associated with in situ adaptive immune cell networks that amplify local tissue damage. As patients with severe TII often fail conventional therapy and develop renal failure, understanding these in situ mechanisms might reveal new therapeutic targets. We hypothesized that in TII, dysregulated apoptotic regulators maintain local adaptive immunity and drive inflammation. Methods: We developed novel computational approaches that, when applied to multicolor confocal images, quantified apoptotic regulator protein expression in selected lymphocyte subsets. This approach was validated using laser capture microdissection (LCM) coupled to qPCR. Furthermore, we explored the consequences of dysregulated apoptotic mediator expression in a murine model of LuN. Results: Analyses of renal biopsies from LuN and mixed cellular allograft rejection patients revealed that BCL-2 was frequently expressed in infiltrating lymphocytes while expression of MCL-1 was low. In contrast, the reciprocal pattern of expression was observed in tonsil germinal centers. These results were consistent with RNA expression data obtained using LCM and qPCR. BCL-2 was also highly expressed in tubulointerstitial infiltrates of NZB/W F1 mice. Furthermore, treatment of NZB/W F1 mice with ABT-199, a selective oral inhibitor of BCL-2, prolonged survival and prevented proteinuria and development of TII in a prevention model. Interestingly, glomerular immune complexes were partially ameliorated by ABT-199 and serum anti-dsDNA antibody titers were unaffected. Conclusion: These data demonstrate BCL-2 as an attractive therapeutic target in LuN manifesting TII. Twit Text FOAVip BCL-2 as a Therapeutic Target in Human Tubulointerstitial Inflammation ????Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=27159593 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27159593 #FOAvip English Wikipedia <ref>{{Cite pmid|27159593}}</ref> BCL-2 as a Therapeutic Target in Human Tubulointerstitial Inflammation #MMPMID27159593 Ko K; Wang J; Perper S; Jiang Y; Yanez D; Kaverina N; Ai J; Liarski VM; Chang A; Peng Y; Lan L; Westmoreland S; Olson L; Giger ML; Wang LC; Clark MR Arthritis Rheumatol 2016[Nov]; 68 (11): 2740-51 PMID27159593show ga Objective: In lupus nephritis (LuN), tubulointerstitial inflammation (TII) is associated with in situ adaptive immune cell networks that amplify local tissue damage. As patients with severe TII often fail conventional therapy and develop renal failure, understanding these in situ mechanisms might reveal new therapeutic targets. We hypothesized that in TII, dysregulated apoptotic regulators maintain local adaptive immunity and drive inflammation. Methods: We developed novel computational approaches that, when applied to multicolor confocal images, quantified apoptotic regulator protein expression in selected lymphocyte subsets. This approach was validated using laser capture microdissection (LCM) coupled to qPCR. Furthermore, we explored the consequences of dysregulated apoptotic mediator expression in a murine model of LuN. Results: Analyses of renal biopsies from LuN and mixed cellular allograft rejection patients revealed that BCL-2 was frequently expressed in infiltrating lymphocytes while expression of MCL-1 was low. In contrast, the reciprocal pattern of expression was observed in tonsil germinal centers. These results were consistent with RNA expression data obtained using LCM and qPCR. BCL-2 was also highly expressed in tubulointerstitial infiltrates of NZB/W F1 mice. Furthermore, treatment of NZB/W F1 mice with ABT-199, a selective oral inhibitor of BCL-2, prolonged survival and prevented proteinuria and development of TII in a prevention model. Interestingly, glomerular immune complexes were partially ameliorated by ABT-199 and serum anti-dsDNA antibody titers were unaffected. Conclusion: These data demonstrate BCL-2 as an attractive therapeutic target in LuN manifesting TII. äBCL-2 as a Therapeutic Target in Human Tubulointerstitial Inflammation(epmc).pdf DeepDyve Pubget Overpricing