ライフサイエンスコーパス: nephritic

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 stic value of C3, soluble C5b-9 (sC5b-9), C3 nephritic factor, and rare disease-predicting variants i

15 also bound and inhibited C3 cleavage by the nephritic factor-stabilized convertase.

16 ) with normal C3 levels were positive for C3 nephritic factors by hemolytic assay.

17 k abnormal complement activity introduced by nephritic factors in the fluid phase.

18 tive-pathway (AP) hyperactivation induced by nephritic factors or complement gene mutations.

19 rtase and, in particular, those that involve nephritic factors, such as dense deposit disease.

20 C3 nephritic factors, that is, autoantibodies that stabiliz

21 autoantibodies to the C3 convertase, termed nephritic factors, which cause pathological stabilizatio

22 rved in humans with properdin-independent C3 nephritic factors.

23 ay C3 convertase, even in the presence of C3 nephritic factors.

24 Seven antinuclear antibody-positive, nephritic female (SWR x NZB)F(1) (SNF1) lupus mice were

25 kely to experience a flare, to have a severe nephritic flare, or to progress to ESRD.

26 sed to end-stage renal disease (ESRD); 9 had nephritic flares (all severe except for 1) and 2 had pro

27 Nephritic flares are common in patients with proliferati

28 bited proinflammatory cytokine production by nephritic glomeruli ex vivo and cultured bone marrow-der

29 nsferred into either normal rat glomeruli or nephritic glomeruli expressing active TGF-beta1.

30 Similarly, when isolated, nephritic glomeruli producing the active form of TGF-bet

31 XCL16 and its receptor CXCR6 were induced in nephritic glomeruli throughout the disease, and CXCL16 e

32 protein expression were markedly induced in nephritic glomeruli throughout the disease.

33 ines of macrophages purified from normal and nephritic glomeruli to ascertain whether macrophages act

34 otaxis of activated leukocytes isolated from nephritic glomeruli, significantly reduced leukocyte inf

35 unstimulated cells were transferred into the nephritic glomeruli, transgene expression was substantia

36 sed by enumeration of ED-1-positive cells in nephritic glomeruli.

37 iNOS and HO-1 were coinduced in nephritic glomeruli.

38 ese patients (45%) experienced renal flares (nephritic in 33, proteinuric in 8) after a mean followup

39 st induced autophagy and protected mice from nephritic kidney damage.

40 quire proinflammatory characteristics in the nephritic kidney.

41 lar and peritubular fibrin deposition in the nephritic kidney.

42 ory responses to inflammation in alpha7(-/-) nephritic kidneys did not compensate for the lack of alp

43 yed inflammatory chemokine protein levels in nephritic kidneys from lupus-prone MRL(lpr) mice.

44 Moreover, nephritic kidneys from mice with and without HLA-DR2 or

45 that mouse renal (MR) T cells isolated from nephritic kidneys of diseased recipients are host-derive

46 on B cells in active NPSLE and of CXCL12 in nephritic kidneys suggests that the CXCR4/CXCL12 axis mi

47 s induced on glomerular endothelial cells of nephritic kidneys, and TNFR2 expression on intrinsic cel

48 ls, as well as parenchymal cells, present in nephritic kidneys.

49 MR imaging signal and T2 relaxation time in nephritic kidneys.

50 XCL12, was significantly up-regulated in the nephritic kidneys.

51 Abs as well as Ig eluted from the kidneys of nephritic lupus mice cross-react with alpha-actinin.

52 c MRL/lpr lupus mice than the kidneys of non-nephritic lupus mice or healthy controls.

53 Renal deposition of circulating nephritic material is higher, and hence antibody- and en

54 n and caspase-1 activation in the kidneys of nephritic Mer-KO mice.

55 ven response occurring in the regional LN of nephritic mice during acute GN.

56 Notably, IL-17F-deficient nephritic mice had fewer renal infiltrating neutrophils

57 By contrast, sEH inhibitor-treated nephritic mice had no survival benefit; however, histolo

58 Kidney tissue from anti-GBM nephritic mice showed higher levels of integrin alpha(v)

59 pe in acute glomerulonephritis, we subjected nephritic mice to CD3-specific Ab treatment.

60 expression of alpha8 integrin in normal and nephritic mice was confirmed by immunofluorescence and q

61 enal infiltrating neutrophils than wild-type nephritic mice, and neutrophil depletion did not affect

62 RL/lpr Fli1(+/-) compared with the Fli1(+/+) nephritic mice.

63 r Fli1(+/-) mice compared with the Fli1(+/+) nephritic mice.

64 d 800CW dye, were administered into anti-GBM nephritic mice.

65 was observed in the glomeruli of normal and nephritic mice.

66 ells after tail vein injection in normal and nephritic mice.

67 c TH17 immune response decreased markedly in nephritic miR-155(-/-) mice.

68 anel of seven glomerular-binding mAbs from a nephritic MRL-lpr mouse that bind to histones/nucleosome

69 s are significantly higher in the kidneys of nephritic MRL/lpr lupus mice than the kidneys of non-nep

70 This study compared the gene profile of nephritic NZB/W kidney with nondiseased NZW controls.

71 ytes, and neutrophils, but not B cells, from nephritic NZB/W mice were more responsive to Ccr1 ligand

72 Short-term treatment of nephritic NZB/W mice with the orally available Ccr1 anta

73 In nephritic NZB/W mice, renal F4/80(hi)/CD11c(int) macroph

74 ogression and increased survival of severely nephritic NZB/W mice.

75 of 22 patients without both antibodies were nephritic (OR 21.0, P < 10(-8)).

76 enal function was substantially decreased in nephritic p27-/- mice compared with control mice, and th

77 MP by isolated glomeruil and IMCD cells from nephritic rats after incubation with ANP and RNP was als

78 s increase, UcGMPV was significantly less in nephritic rats after the saline infusion.

79 ment of hypertension in groups of normal non-nephritic rats and rats submitted to 16 wk of glomerulon

80 fusion of Zaprinast into one renal artery in nephritic rats normalized both the natriuretic response

81 Systemic treatment of nephritic rats with IL-4 reduced NO generation by 40% bu

82 interfere with PDGF-B signaling, we injected nephritic rats with PDGF-B neutralizing aptamers or the

83 reased to the same extent in both normal and nephritic rats, compared with their respective hydropeni

84 ssed by muscle electroporation in healthy or nephritic rats.

85 ntreated disease control, and PAI-1R-treated nephritic rats.

86 y in response to corticosteroid treatment in nephritic rats.

87 incidence of focal glomerulosclerosis in non-nephritic rats.

88 R-155(-/-) and wild-type CD4(+) T cells into nephritic recombination activating gene 1-deficient (Rag

89 ies was present equally in nephritic and non-nephritic sera.

90 these results show that treatment of older, nephritic SNF1 animals with long-term anti-CD40L immunot

91 M antinuclear antibodies from the kidneys of nephritic SNF1 lupus mice.

92 of stellate cells and migration of renal and nephritic stem cells into the tubule.

93 disease gene associated with the congenital nephritic syndrome of the Finnish type, and Podocin, the

94 Acute presentation with full blown nephritic syndrome or rapidly progressive glomerulonephr

95 At onset of a nephritic syndrome with low C3 level, screening for anti

96 Death was caused by nephritic syndrome, which progressed to renal failure as

97 are associated with Denys-Drash syndrome and nephritic syndrome.

98 dian age was 61 years and 76% presented with nephritic syndrome.

99 Anti-MPO antibody transfer resulted in nephritic urine by dipstick and albuminuria by enzyme-li

100 ble circulating P-selectin were increased in nephritic wild-type mice and in chimeric mice with endot

101 cells progressively increased in kidneys of nephritic wild-type mice during the course of NTN, indic