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1 protein that would produce full-blown active Heymann nephritis.
2 portions of gp330, devoid of RAP, to induce Heymann nephritis.
3 against this fusion protein produce passive Heymann nephritis.
4 role of iron in glomerular injury of passive Heymann nephritis.
5 mportant role in the pathogenesis of passive Heymann nephritis.
6 re, the iron status in the kidney in passive Heymann nephritis, a complement-dependent model of membr
7 in antibody-mediated pathogenesis of active Heymann nephritis, a model that should prove valuable fo
8 derable evidence that glomerular deposits in Heymann nephritis, a rat model of membranous nephritis,
9 dues 1 to 563 of megalin could induce active Heymann nephritis (AHN) as efficiently as the native pro
11 riuretic peptide; RNP) in vitro in rats with Heymann nephritis, an immunologically mediated model of
12 was upregulated in podocytes in the passive Heymann nephritis and puromycin aminonucleoside (PA) nep
13 4 to 1250) of the ectodomain, induces active Heymann nephritis and that heterologous antibodies again
16 ation used to immunize rats to induce active Heymann nephritis (HN), a model of membranous nephropath
18 target antigen involved in the induction of Heymann nephritis (HN), a rat model of human membranous
19 cytic receptor, is a major target antigen of Heymann nephritis (HN), an autoimmune disease in rats.
21 Identified as the pathogenic autoantigen of Heymann nephritis in rats, its functions have been studi
23 een reported that the immunogen that induces Heymann nephritis is a complex formed between gp330 and
26 mplement source; we also studied the passive Heymann nephritis model of experimental membranous nephr
29 experimental membranous nephropathy (passive Heymann nephritis (PHN)), complement C5b-9-induced prote
30 actin at the onset of proteinuria in passive Heymann nephritis (PHN), a rat model of human membranous
31 aining for MMP-9, while in rats with passive Heymann nephritis there was a major increase in MMP-9 pr
32 Immunization with megalin induces active Heymann nephritis, which reproduces features of human id
33 used to study changes that may occur during Heymann nephritis with respect to the plasminogen system
34 capable of inducing pathogenic antibodies of Heymann nephritis without a contributory role of RAP.
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