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1 mes, and the idiotypically related family of nephritic Abs Id(LN)F(1), when compared with untreated S
3 i was significantly reduced in hemin-treated nephritic animals in which proteinuria was also attenuat
4 anscription-PCR of glomerular total RNA from nephritic animals or nephritic animals pretreated with h
8 res were classified as either proteinuric or nephritic based on changes in urinary protein and sedime
9 was increased in IMCD cell homogenates from nephritic compared with normal rats (388 +/- 32 versus 1
11 requently associated with the presence of C3 nephritic factor in child GP patients and with monoclona
13 oss of complement regulation is caused by C3 nephritic factor, an autoantibody directed against the C
16 autoantibodies to the C3 convertase, termed nephritic factors, which cause pathological stabilizatio
21 sed to end-stage renal disease (ESRD); 9 had nephritic flares (all severe except for 1) and 2 had pro
23 bited proinflammatory cytokine production by nephritic glomeruli ex vivo and cultured bone marrow-der
26 XCL16 and its receptor CXCR6 were induced in nephritic glomeruli throughout the disease, and CXCL16 e
28 ines of macrophages purified from normal and nephritic glomeruli to ascertain whether macrophages act
29 otaxis of activated leukocytes isolated from nephritic glomeruli, significantly reduced leukocyte inf
30 unstimulated cells were transferred into the nephritic glomeruli, transgene expression was substantia
33 ese patients (45%) experienced renal flares (nephritic in 33, proteinuric in 8) after a mean followup
36 ory responses to inflammation in alpha7(-/-) nephritic kidneys did not compensate for the lack of alp
39 that mouse renal (MR) T cells isolated from nephritic kidneys of diseased recipients are host-derive
40 on B cells in active NPSLE and of CXCL12 in nephritic kidneys suggests that the CXCR4/CXCL12 axis mi
41 s induced on glomerular endothelial cells of nephritic kidneys, and TNFR2 expression on intrinsic cel
44 Abs as well as Ig eluted from the kidneys of nephritic lupus mice cross-react with alpha-actinin.
51 expression of alpha8 integrin in normal and nephritic mice was confirmed by immunofluorescence and q
52 enal infiltrating neutrophils than wild-type nephritic mice, and neutrophil depletion did not affect
59 anel of seven glomerular-binding mAbs from a nephritic MRL-lpr mouse that bind to histones/nucleosome
60 s are significantly higher in the kidneys of nephritic MRL/lpr lupus mice than the kidneys of non-nep
62 ytes, and neutrophils, but not B cells, from nephritic NZB/W mice were more responsive to Ccr1 ligand
67 enal function was substantially decreased in nephritic p27-/- mice compared with control mice, and th
68 MP by isolated glomeruil and IMCD cells from nephritic rats after incubation with ANP and RNP was als
70 ment of hypertension in groups of normal non-nephritic rats and rats submitted to 16 wk of glomerulon
71 fusion of Zaprinast into one renal artery in nephritic rats normalized both the natriuretic response
73 interfere with PDGF-B signaling, we injected nephritic rats with PDGF-B neutralizing aptamers or the
74 reased to the same extent in both normal and nephritic rats, compared with their respective hydropeni
79 R-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag
81 these results show that treatment of older, nephritic SNF1 animals with long-term anti-CD40L immunot
83 disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the
87 ble circulating P-selectin were increased in nephritic wild-type mice and in chimeric mice with endot
88 cells progressively increased in kidneys of nephritic wild-type mice during the course of NTN, indic
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