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10.1681/ASN.2014040407 http://scihub22266oqcxt.onion/10.1681/ASN.2014040407 C4552107!4552107!25762060     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2015 ; 26 (9): 2105-17 Nephropedia Template TP {{tp|p=25762060|t=2015. CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN |pdf=|usr=}}{{25762060}} gab.com Text CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25762060 #FOAvip ANCA-associated vasculitis is the most frequent cause of crescentic GN. To define new molecular and/or cellular biomarkers of this disease in the kidney, we performed microarray analyses of renal biopsy samples from patients with ANCA-associated crescentic GN. Expression profiles were correlated with clinical data in a prospective study of patients with renal ANCA disease. CC chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was identified as the most upregulated chemotactic cytokine in patients with newly diagnosed ANCA-associated crescentic GN. Macrophages and myeloid dendritic cells in the kidney were detected as CCL18-producing cells. The density of CCL18+ cells correlated with crescent formation, interstitial inflammation, and impairment of renal function. CCL18 protein levels were higher in sera of patients with renal ANCA disease compared with those in sera of patients with other forms of crescentic GN. CCL18 serum levels were higher in patients who suffered from ANCA-associated renal relapses compared with those in patients who remained in remission. Using a murine model of crescentic GN, we explored the effects of the CCL18 murine functional analog CCL8 and its receptor CCR8 on kidney function and morphology. Compared with wild-type mice, Ccr8?/? mice had significantly less infiltration of pathogenic mononuclear phagocytes. Furthermore, Ccr8?/? mice maintained renal function better and had reduced renal tissue injury. In summary, our data indicate that CCL18 drives renal inflammation through CCR8-expressing cells and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN. Twit Text FOAVip CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25762060 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25762060 #FOAvip English Wikipedia <ref>{{Cite pmid|25762060}}</ref> CC Chemokine Ligand 18 in ANCA-Associated Crescentic GN #MMPMID25762060 Brix SR; Stege G; Disteldorf E; Hoxha E; Krebs C; Krohn S; Otto B; Klätschke K; Herden E; Heymann F; Lira SA; Tacke F; Wolf G; Busch M; Jabs WJ; Özcan F; Keller F; Beige J; Wagner K; Helmchen U; Noriega M; Wiech T; Panzer U; Stahl RA J Am Soc Nephrol 2015[Sep]; 26 (9): 2105-17 PMID25762060show ga ANCA-associated vasculitis is the most frequent cause of crescentic GN. To define new molecular and/or cellular biomarkers of this disease in the kidney, we performed microarray analyses of renal biopsy samples from patients with ANCA-associated crescentic GN. Expression profiles were correlated with clinical data in a prospective study of patients with renal ANCA disease. CC chemokine ligand 18 (CCL18), acting through CC chemokine receptor 8 (CCR8) on mononuclear cells, was identified as the most upregulated chemotactic cytokine in patients with newly diagnosed ANCA-associated crescentic GN. Macrophages and myeloid dendritic cells in the kidney were detected as CCL18-producing cells. The density of CCL18+ cells correlated with crescent formation, interstitial inflammation, and impairment of renal function. CCL18 protein levels were higher in sera of patients with renal ANCA disease compared with those in sera of patients with other forms of crescentic GN. CCL18 serum levels were higher in patients who suffered from ANCA-associated renal relapses compared with those in patients who remained in remission. Using a murine model of crescentic GN, we explored the effects of the CCL18 murine functional analog CCL8 and its receptor CCR8 on kidney function and morphology. Compared with wild-type mice, Ccr8?/? mice had significantly less infiltration of pathogenic mononuclear phagocytes. Furthermore, Ccr8?/? mice maintained renal function better and had reduced renal tissue injury. In summary, our data indicate that CCL18 drives renal inflammation through CCR8-expressing cells and could serve as a biomarker for disease activity and renal relapse in ANCA-associated crescentic GN. äCC Chemokine Ligand 18 in ANCA-Associated Crescentic GN (epmc).pdf DeepDyve Pubget Overpricing