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1 ntic GN and a murine model of crescentic GN (nephrotoxic nephritis).
2 nd NGAL-knockout mice following induction of nephrotoxic nephritis.
3 fic T cell reactivity in the murine model of nephrotoxic nephritis.
4 d lipid A on the development of heterologous nephrotoxic nephritis.
5 unization on disease severity in accelerated nephrotoxic nephritis.
6 ctivated naturally in glomeruli of rats with nephrotoxic nephritis.
7 duced kidney injury during accelerated serum nephrotoxic nephritis.
8 ation within the kidney by accelerated serum nephrotoxic nephritis.
9 T cell-intrinsic IL-6R signaling, we induced nephrotoxic nephritis, a mouse model for crescentic GN,
10 ceptibility of the Wistar-Kyoto (WKY) rat to nephrotoxic nephritis, a rat model of Crgn.
11 ges isolated from the glomeruli of rats with nephrotoxic nephritis also induced apoptosis and suppres
12 t to ICAM-1, is not up-regulated by day 2 of nephrotoxic nephritis, and plays little part in early le
13 e complex disease induced in the accelerated nephrotoxic nephritis (ANTN) model.
14 ophages infiltrating glomeruli in telescoped nephrotoxic nephritis are programmed.
15 s, were significantly increased in mice with nephrotoxic nephritis as compared to control-injected mi
16               Similarly, in a mouse model of nephrotoxic nephritis, besides reducing inflammatory cyt
17 te the development of disease in accelerated nephrotoxic nephritis by influencing the development of
18 L in antibody-mediated nephritis, we induced nephrotoxic nephritis by passive antibody transfer to 12
19 trast, glomerular macrophages from rats with nephrotoxic nephritis did not express beta-glucuronidase
20                            In a rat model of nephrotoxic nephritis, glomerular expression of VCAM-1,
21 y 10, during the early inflammatory phase of nephrotoxic nephritis, had no effect on albuminuria or g
22 of crescentic nephritis, the authors induced nephrotoxic nephritis in BTLA-deficient mice and wild-ty
23 entic glomerulonephritis by inducing passive nephrotoxic nephritis in SPARC(+/+) and SPARC(-/-) mice.
24                                 Induction of nephrotoxic nephritis in the double-congenic rats (WKY.L
25  d (late treatment study) after induction of nephrotoxic nephritis in Wistar Kyoto rats.
26                                           In nephrotoxic nephritis in WKY rats, recombinant rat IFN-b
27                                          The nephrotoxic nephritis model of GN was studied in AREG(-/
28 tive immune responses, we use the autologous nephrotoxic nephritis model with two disease induction p
29 ntravascular monocyte subset behavior during nephrotoxic nephritis (NTN) in a novel WKY-hCD68-GFP mon
30                    During the development of nephrotoxic nephritis (NTN) in the mouse, we find that a
31                                              Nephrotoxic nephritis (NTN) is characterized by acute ma
32  also unknown, we studied these cells in the nephrotoxic nephritis (NTN) model of acute crescentic GN
33 e effects have been observed for IL-6 in the nephrotoxic nephritis (NTN) model of acute crescentic GN
34 e studied the function of these cells in the nephrotoxic nephritis (NTN) model of cGN.
35     We studied the function of Treg17 in the nephrotoxic nephritis (NTN) model of crescentic GN.
36                              In the model of nephrotoxic nephritis (NTN) that is induced by a small d
37                                   We induced nephrotoxic nephritis (NTN), a mouse model of crescentic
38 acerbated disease following the induction of nephrotoxic nephritis (NTN).
39 ents and reverses proteinuria in accelerated nephrotoxic nephritis (NTN).
40 lport model) and a glomerulonephritis model, nephrotoxic nephritis (NTN).
41 ted, then three disease models were induced: nephrotoxic nephritis (NTN, a model for crescentic GN),
42 pko)) mice, with a model of experimental GN (nephrotoxic nephritis, NTN).
43   Inhibition of miR-193a in a mouse model of nephrotoxic nephritis resulted in reduced crescent forma
44                                    Injury in nephrotoxic nephritis was also decreased when assessed m
45                                              Nephrotoxic nephritis was induced in Wistar-Kyoto rats a
46  using a mouse model of acute crescentic GN (nephrotoxic nephritis), we identified CD4(+) T cells and
47                 By using the murine model of nephrotoxic nephritis, we investigated the role of S100A
48  decreased in the first week of experimental nephrotoxic nephritis, whereas reduction in glomerular n
49                                           In nephrotoxic nephritis, wild-type (WT) mice with glomerul