ライフサイエンスコーパス: CVF

1 CVF attenuated the development of AHR by O3.

2 CVF depleted both systemic and brain C3 by the time of s

3 CVF plus NK cell depletion further prolonged survival (>

4 CVF treatment, when given in the period immediately befo

5 CVF was given daily until rejection.

6 CVF was injected i.v., and neutrophil sequestration and

7 CVF was measured with a multistage treadmill test and wa

8 CVF-dependent C3 cleavage in the deficient serum require

9 2, p = .009); PEEP-CVF (24 +/- 1, p = .01); CVF-PLV (30 +/- 2, p = .03); and CVF-PEEP (37 +/- 1, p =

10 Platelet depletion did not affect CVF-induced up-regulation of lung vascular P-selectin, i

11 , p = .01); CVF-PLV (30 +/- 2, p = .03); and CVF-PEEP (37 +/- 1, p = .04).

12 TIMP-2 along with upregulation of MMP-2 and CVF-I in the atrium is associated with the development o

13 er, the combination of high-dose GPI 562 and CVF resulted in a significant decrease in intragraft pla

14 esis of xenograft rejection and that CyA and CVF suppress xenograft rejection by preventing exposure

15 Combination of CyA and CVF, which we have previously shown to overcome rejectio

16 investigated the effects of various sCR1 and CVF regimens, and combinations thereof, in the discordan

17 pha Gal) antibody, and a slower rise in anti-CVF antibody.

18 T=32 hr), although not to the same extent as CVF.

19 moderate PA, would be associated with better CVF and lower %BF.

20 Systemic complement depletion by CVF prevented the induction of anterior uveitis by anti-

21 These fevers were totally prevented by CVF (10 U/mouse, i.v.) pretreatment.

22 es of C3 and factor B activation in vitro by CVF demonstrated that in factor D-deficient serum the al

23 cobra venom factor-dependent C5 convertase (CVF, Bb) made with CVF purified from the venom of Naja n

24 By activating C3/C5 convertase, CVF depletes complement while additionally generating C5

25 Moreover, 30-35% of xenografts from CsA/CVF rats survived long term and accommodated in the seco

26 Xenografts from CsA/CVF-treated rats survived significantly longer upon retr

27 Long-term xenograft survival in CsA/CVF-treated recipients was associated with an ongoing Th

28 ly in the control group, whereas, in the CsA/CVF-treated group, IgG EXA were totally suppressed.

29 Thus, under CyA/CVF treatment, complement activation by hamster cells wa

30 the administration of cobra venom factor; d) CVF-PLV group, animals received partial liquid ventilati

31 enom factor (CVF), or splenectomy plus daily CVF.

32 uid ventilation after cobra venom factor; e) CVF-PEEP group, animals received PEEP after cobra venom

33 cantly decreased by administration of either CVF or Crry-Ig.

34 eturn, and when combined with blood exchange/CVF/CyA facilitated long-term survival of grafts.

35 ) or in combination with cobra venom factor (CVF) (DXR model).

36 ts had been surviving in cobra venom factor (CVF) + CyA-treated rats for 10 days, a time when the ant

37 mplement-depleting agent cobra venom factor (CVF) 24 hr before HI lesioning and evaluated both acute

38 tion of complement using cobra venom factor (CVF) accelerates pulmonary xenograft failure.

39 ombination with systemic cobra venom factor (CVF) administration to deplete complement when delayed x

40 complement inhibition by cobra venom factor (CVF) and sustained T-cell immunosuppression by cyclospor

41 rprisingly, injection of cobra venom factor (CVF) caused a profound and reproducible reduction in ser

42 Cobra venom factor (CVF) depletes complement and may therefore be of use in

43 y into rats treated with cobra venom factor (CVF) develop disease over 72 hours.

44 zation by treatment with cobra venom factor (CVF) diminished serum anti-PPS14 concentrations after pr

45 estigate the efficacy of cobra venom factor (CVF) in preventing hyperacute rejection (HAR) after pig-

46 Cobra venom factor (CVF) induces lung injury through oxidant- and neutrophil

47 ment by i.v. infusion of cobra venom factor (CVF) is known to be P-selectin dependent.

48 mplement depletion using cobra venom factor (CVF) markedly reduced the efficacy of rituximab and 1F5

49 ivation of complement by cobra venom factor (CVF) or after intrapulmonary deposition of IgG immune co

50 aperitoneal injection of cobra venom factor (CVF) or complement receptor-related gene y (Crry)-Ig, a

51 ed using either CsA plus cobra venom factor (CVF) or CsA plus rapamycin.

52 ent of athymic rats with cobra venom factor (CVF) partially reverses this effect.

53 mplement inhibition with cobra venom factor (CVF) plus daily and continuing cyclosporin A (CyA) preve

54 aperitoneal injection of cobra venom factor (CVF) reduced C3 levels in the cornea approximately 40%,

55 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regeneration following ca

56 it was preincubated with cobra venom factor (CVF) to deplete C3.

57 aft dysfunction by using cobra venom factor (CVF) to deplete recipient complement and transgenic swin

58 Administration of cobra venom factor (CVF), 1 day before and at the time of transplantation, r

59 toneal injection of 35 U cobra venom factor (CVF), 24 hours before antibody injection.

60 d to immobilized C3b and cobra venom factor (CVF), a C3b analogue.

61 ft recipients as well as cobra venom factor (CVF), a complement blocker, treatment.

62 thout heat inactivation, cobra venom factor (CVF), or lipopolysaccharide plus interferon-gamma treatm

63 daily administration of cobra venom factor (CVF), or splenectomy plus daily CVF.

64 noclonal antibody (mAb), cobra venom factor (CVF), pig hematopoietic growth factors (interleukin-3 (p

65 by infusion of purified cobra venom factor (CVF), thymocyte apoptosis was significantly increased.

66 rther investigated using cobra venom factor (CVF), which systemically depleted the rats of complement

67 susceptibilities to the cobra venom factor (CVF)-dependent convertase.

68 ft survival was 62 hr in cobra venom factor (CVF)-treated controls versus 108 hr (DSG), 129 hr (LEF),

69 us injection of purified cobra venom factor (CVF).

70 of complement (C) using cobra venom factor (CVF).

71 yclosporine (CsA) and/or cobra venom factor (CVF).

72 ion of lung injury using cobra venom factor (CVF); b) PLV-CVF group, animals received partial liquid

73 y (p < 0.001) delayed by cobra venom factor (CVF; 11 +/- 8 h in four of five cases) but was still mor

74 depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]).

75 are associated with cardiovascular fitness (CVF) and percentage of body fat (%BF) in adolescents.

76 e method, referred to as covariance fitting (CVF), couples Q-matrix calculations with a maximum likel

77 od HIV-1 DNA load, and cervicovaginal fluid (CVF) HIV-1 DNA load were determined using quantitative r

78 A higher index for CVF was associated with higher amounts of moderate and v

79 The cardiac collagen volume fraction (CVF) and cardiac myocyte apoptosis index in aFGF-NP+UTMD

80 in the LA, type I collagen volume fraction (CVF-I) increased significantly in the PmAF group followe

81 dilution as high as 1:32, while plasma from CVF-treated animals displays anti-HSV activity at lower

82 In the PsAF group, CVF-I/CVF-III ratio was significantly correlated with AF

83 3 for histologic neutrophil counting): a) GV-CVF group, animals received gas ventilation (GV) with th

84 d with the cobra venom factor only group (GV-CVF 47 +/- 2 neutrophils/high-power field), reductions i

85 4, p = .01) groups when compared with the GV-CVF group (0.62 +/- 0.07).

86 When compared with the GV-CVF group, a trend toward a reduction in myeloperoxidase

87 We conclude that (i) CVF prevents HAR, (ii) the addition of Spx + IS delays r

88 In the PsAF group, CVF-I/CVF-III ratio was significantly correlated with AF durat

89 Immunohistologic analysis in CVF-treated nude recipients with or without splenectomy

90 that the apparent role of these molecules in CVF-induced lung injury depends on the method used to bl

91 els of complement deposition were present in CVF-treated recipients.

92 to determine the degree to which variance in CVF and %BF was explained by PA, after control for age,

93 LA CVF-I significantly correlated with LA dimension and TIM

94 Analysis of lesioned, CVF-treated animals demonstrated minimal neuronal C3 dep

95 WBI, ATG, MMF, anti-CD40L mAb, CVF, pIL3, pSCF, and PGI2 had no effect on purified babo

96 diabetes group showed similar results (MCD, CVF and cardiac myocyte apoptosis index) to other aFGF t

97 ke conventional sum-of-squares minimization, CVF fits both the magnitude of the recorded current and

98 ated data generated using a consensus model, CVF leads to reasonable parameter estimates and accurate

99 H2 was found similarly to inhibit CP but not CVF convertase activation, and the effects of alanine su

100 vel, distal binding site for the CP, but not CVF convertase.

101 The concerted action of CVF and CPA significantly increases the life span of ath

102 However, administration of CVF abolishes the tolerance induction.

103 onatal rat brain, systemic administration of CVF does not eliminate complement deposition within inju

104 ystemic injection and topical application of CVF reduced local C3 levels >60%, which eliminated MAb-m

105 ever, whereas the core temperature (T(c)) of CVF vehicle-treated controls rose approximately 1 degree

106 e dose of CVF, or sCRI plus a single dose of CVF (MST=64 hr), had similar xenograft survival times.

107 Grafts in rats treated with a single dose of CVF (MST=67 hr) or repetitive doses of CVF (MST=69 hr) s

108 ed that addition of sCR1 to a single dose of CVF resulted in decreased macrophage activation and redu

109 Animals treated with a single dose of CVF, or sCRI plus a single dose of CVF (MST=64 hr), had

110 se of CVF (MST=67 hr) or repetitive doses of CVF (MST=69 hr) survived significantly longer than those

111 re near normal, and the enhancing effects of CVF treatment on the secondary anti-PPS14 antibody respo

112 In the current studies, infusion of CVF caused the appearance in plasma of C5a (as revealed

113 in a time-dependent manner after infusion of CVF.

114 oons studied, the intramuscular injection of CVF (0.25 mg/kg) was followed by a marked reduction in s

115 and lung injury in response to injection of CVF occurs through alternative pathways in mice with gen

116 A second intramuscular injection of CVF on day 14 was ineffective in reducing C3, CH50, and

117 of extravascular albumin after injection of CVF when compared to wild-type mice.

118 The major oligosaccharide of CVF is known to contain alpha Gal residues, which we sug

119 o active enzyme conformational transition of CVF-bound factor B.

120 inetic models with up to 11 free parameters, CVF leads to reasonable parameter estimates.

121 r field): PLV-CVF (20 +/- 2, p = .009); PEEP-CVF (24 +/- 1, p = .01); CVF-PLV (30 +/- 2, p = .03); an

122 he PLV-CVF (0.29 +/- 0.08, p = .02) and PEEP-CVF (0.34 +/- 0.04, p = .01) groups when compared with t

123 before the induction of lung injury; c) PEEP-CVF group, animals received positive end-expiratory pres

124 The combination of CsA plus CVF, the latter given for either 2 days or 11 days, resu

125 njury using cobra venom factor (CVF); b) PLV-CVF group, animals received partial liquid ventilation b

126 l groups (neutrophils/high-power field): PLV-CVF (20 +/- 2, p = .009); PEEP-CVF (24 +/- 1, p = .01);

127 ntent was significantly decreased in the PLV-CVF (0.29 +/- 0.08, p = .02) and PEEP-CVF (0.34 +/- 0.04

128 In C6-deficient rats, CVF infusion caused the same level of lung injury (measu

129 Two received CVF+/-Spx, which extended survival to 5 and 6 days, resp

130 attendant toxicity associated with repeated CVF administration.

131 Twenty-seven CVF Sprague-Dawley rats were subjected to OPW exposures,

132 Six underwent Spx + CVF therapy + IS; graft survival was 3 hr (technical com

133 Both the basal and the CVF-inducible lung mRNA for inducible nitric oxide synth

134 the CVF-PLV (0.42 +/- 0.05, p = .07) and the CVF-PEEP (0.39 +/- 0.06, p = .07) groups.

135 In the CVF model, intravenous infusion (but not intratracheal i

136 ction in myeloperoxidase was observed in the CVF-PLV (0.42 +/- 0.05, p = .07) and the CVF-PEEP (0.39

137 we thus show that the addition of CPA to the CVF treatment results in a significant increase in viral

138 C1-INH prevented factor B from binding to CVF-coated beads and dissociated bound factor B from suc

139 1-INH showed cross competition in binding to CVF-coated beads.

140 aboon (n=3); group III, unmodified swine-to-(CVF treated) baboon (n=3); and group IV, hCD59/hDAF swin

141 (>7 days in four of five cases; p < 0.01 vs CVF only).

142 d 120 hr (DSG and LEF; all groups P<0.01 vs. CVF alone).

143 Similar results were found when CVF was injected in vivo during the early stages of CLP.

144 as 0.2 mug of antigen, and was maximal when CVF was administered within 2 days of immunization.

145 xenograft survival (2.2+/-0.4 days), whereas CVF alone led to minimal prolongation of survival (5.6+/

146 LEF or DSG along with CVF can result in the longest prolongation of xenograft

147 Blood exchange in combination with CVF/CyA treatment dramatically decreased the level of pr

148 When blood HIV-1 DNA load was combined with CVF HIV-1 DNA load, the association with transmission in

149 on, and leukocyte infiltration compared with CVF alone.

150 ith heat inactivation and was corrected with CVF treatment.

151 plus mAb and with a human C3 derivative with CVF-like functions (HC3-1496) plus mAb was both superior

152 -dependent C5 convertase (CVF, Bb) made with CVF purified from the venom of Naja naja (CVFn) and Naja

153 Pretreatment with CVF (group III) was ineffective in preventing xenograft

154 of the intragraft immune responses seen with CVF/sCR1 combination therapy may augment further therape

155 ompared with that in recipients treated with CVF alone.

156 at survive indefinitely in rats treated with CVF plus CyA express the anti-inflammatory gene heme oxy

157 f lymphoma-bearing mice after treatment with CVF plus mAb and with a human C3 derivative with CVF-lik

158 Without CVF, inhibition of cell infection by HSV is observed at