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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 ation within the kidney by accelerated serum 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 ceptibility of the Wistar-Kyoto (WKY) rat to nephrotoxic nephritis, a rat model of Crgn.
8 ges isolated from the glomeruli of rats with nephrotoxic nephritis also induced apoptosis and suppres
9 t to ICAM-1, is not up-regulated by day 2 of nephrotoxic nephritis, and plays little part in early le
10 e complex disease induced in the accelerated nephrotoxic nephritis (ANTN) model.
11 ophages infiltrating glomeruli in telescoped nephrotoxic nephritis are programmed.
12 s, were significantly increased in mice with nephrotoxic nephritis as compared to control-injected mi
13 te the development of disease in accelerated nephrotoxic nephritis by influencing the development of
14 L in antibody-mediated nephritis, we induced nephrotoxic nephritis by passive antibody transfer to 12
15 trast, glomerular macrophages from rats with nephrotoxic nephritis did not express beta-glucuronidase
16                            In a rat model of nephrotoxic nephritis, glomerular expression of VCAM-1,
17 y 10, during the early inflammatory phase of nephrotoxic nephritis, had no effect on albuminuria or g
18 entic glomerulonephritis by inducing passive nephrotoxic nephritis in SPARC(+/+) and SPARC(-/-) mice.
19                                 Induction of nephrotoxic nephritis in the double-congenic rats (WKY.L
20  d (late treatment study) after induction of nephrotoxic nephritis in Wistar Kyoto rats.
21                                           In nephrotoxic nephritis in WKY rats, recombinant rat IFN-b
22 tive immune responses, we use the autologous nephrotoxic nephritis model with two disease induction p
23                    During the development of nephrotoxic nephritis (NTN) in the mouse, we find that a
24                                              Nephrotoxic nephritis (NTN) is characterized by acute ma
25  also unknown, we studied these cells in the nephrotoxic nephritis (NTN) model of acute crescentic GN
26 e effects have been observed for IL-6 in the nephrotoxic nephritis (NTN) model of acute crescentic GN
27 e studied the function of these cells in the nephrotoxic nephritis (NTN) model of cGN.
28     We studied the function of Treg17 in the nephrotoxic nephritis (NTN) model of crescentic GN.
29                              In the model of nephrotoxic nephritis (NTN) that is induced by a small d
30 acerbated disease following the induction of nephrotoxic nephritis (NTN).
31 ents and reverses proteinuria in accelerated nephrotoxic nephritis (NTN).
32   Inhibition of miR-193a in a mouse model of nephrotoxic nephritis resulted in reduced crescent forma
33                                    Injury in nephrotoxic nephritis was also decreased when assessed m
34                                              Nephrotoxic nephritis was induced in Wistar-Kyoto rats a
35  using a mouse model of acute crescentic GN (nephrotoxic nephritis), we identified CD4(+) T cells and
36                 By using the murine model of nephrotoxic nephritis, we investigated the role of S100A
37  decreased in the first week of experimental nephrotoxic nephritis, whereas reduction in glomerular n
38                                           In nephrotoxic nephritis, wild-type (WT) mice with glomerul

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