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1 mes, and the idiotypically related family of nephritic Abs Id(LN)F(1), when compared with untreated S
2 ctrum of reactivities was present equally in nephritic and non-nephritic sera.
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
5 omerular total RNA from nephritic animals or nephritic animals pretreated with hemin.
6                           Hemin treatment of nephritic animals resulted in upregulation of glomerular
7                Glomerular HO-1 expression in nephritic animals was upregulated by treatment with hemi
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
10 because blocking decay with properdin and C3 nephritic factor did not restore C3bBb formation.
11 requently associated with the presence of C3 nephritic factor in child GP patients and with monoclona
12                                  Although C3 nephritic factor was shown in family members with acquir
13 oss of complement regulation is caused by C3 nephritic factor, an autoantibody directed against the C
14  also bound and inhibited C3 cleavage by the nephritic factor-stabilized convertase.
15 rtase and, in particular, those that involve nephritic factors, such as dense deposit disease.
16  autoantibodies to the C3 convertase, termed nephritic factors, which cause pathological stabilizatio
17 rved in humans with properdin-independent C3 nephritic factors.
18 ay C3 convertase, even in the presence of C3 nephritic factors.
19         Seven antinuclear antibody-positive, nephritic female (SWR x NZB)F(1) (SNF1) lupus mice were
20 kely to experience a flare, to have a severe nephritic flare, or to progress to ESRD.
21 sed to end-stage renal disease (ESRD); 9 had nephritic flares (all severe except for 1) and 2 had pro
22                                              Nephritic flares are common in patients with proliferati
23 bited proinflammatory cytokine production by nephritic glomeruli ex vivo and cultured bone marrow-der
24 nsferred into either normal rat glomeruli or nephritic glomeruli expressing active TGF-beta1.
25                    Similarly, when isolated, nephritic glomeruli producing the active form of TGF-bet
26 XCL16 and its receptor CXCR6 were induced in nephritic glomeruli throughout the disease, and CXCL16 e
27  protein expression were markedly induced in nephritic glomeruli throughout the disease.
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
31 sed by enumeration of ED-1-positive cells in nephritic glomeruli.
32              iNOS and HO-1 were coinduced in nephritic glomeruli.
33 ese patients (45%) experienced renal flares (nephritic in 33, proteinuric in 8) after a mean followup
34 st induced autophagy and protected mice from nephritic kidney damage.
35 lar and peritubular fibrin deposition in the nephritic kidney.
36 ory responses to inflammation in alpha7(-/-) nephritic kidneys did not compensate for the lack of alp
37 yed inflammatory chemokine protein levels in nephritic kidneys from lupus-prone MRL(lpr) mice.
38                                    Moreover, nephritic kidneys from mice with and without HLA-DR2 or
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
42  MR imaging signal and T2 relaxation time in nephritic kidneys.
43 XCL12, was significantly up-regulated in the nephritic kidneys.
44 Abs as well as Ig eluted from the kidneys of nephritic lupus mice cross-react with alpha-actinin.
45 c MRL/lpr lupus mice than the kidneys of non-nephritic lupus mice or healthy controls.
46 n and caspase-1 activation in the kidneys of nephritic Mer-KO mice.
47 ven response occurring in the regional LN of nephritic mice during acute GN.
48                    Notably, IL-17F-deficient nephritic mice had fewer renal infiltrating neutrophils
49                  Kidney tissue from anti-GBM nephritic mice showed higher levels of integrin alpha(v)
50 pe in acute glomerulonephritis, we subjected nephritic mice to CD3-specific Ab treatment.
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
53 RL/lpr Fli1(+/-) compared with the Fli1(+/+) nephritic mice.
54 r Fli1(+/-) mice compared with the Fli1(+/+) nephritic mice.
55 d 800CW dye, were administered into anti-GBM nephritic mice.
56  was observed in the glomeruli of normal and nephritic mice.
57 ells after tail vein injection in normal and nephritic mice.
58 c TH17 immune response decreased markedly in nephritic miR-155(-/-) mice.
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
61      This study compared the gene profile of nephritic NZB/W kidney with nondiseased NZW controls.
62 ytes, and neutrophils, but not B cells, from nephritic NZB/W mice were more responsive to Ccr1 ligand
63                      Short-term treatment of nephritic NZB/W mice with the orally available Ccr1 anta
64                                           In nephritic NZB/W mice, renal F4/80(hi)/CD11c(int) macroph
65 ogression and increased survival of severely nephritic NZB/W mice.
66  of 22 patients without both antibodies were nephritic (OR 21.0, P < 10(-8)).
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
69 s increase, UcGMPV was significantly less in nephritic rats after the saline infusion.
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
72                        Systemic treatment of nephritic rats with IL-4 reduced NO generation by 40% bu
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
75 y in response to corticosteroid treatment in nephritic rats.
76 ssed by muscle electroporation in healthy or nephritic rats.
77 ntreated disease control, and PAI-1R-treated nephritic rats.
78 incidence of focal glomerulosclerosis in non-nephritic rats.
79 R-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag
80 ies was present equally in nephritic and non-nephritic sera.
81  these results show that treatment of older, nephritic SNF1 animals with long-term anti-CD40L immunot
82 M antinuclear antibodies from the kidneys of nephritic SNF1 lupus mice.
83  disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the
84                          Death was caused by nephritic syndrome, which progressed to renal failure as
85 are associated with Denys-Drash syndrome and nephritic syndrome.
86       Anti-MPO antibody transfer resulted in nephritic urine by dipstick and albuminuria by enzyme-li
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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