ライフサイエンスコーパス: cobra venom

1 act with CTX A3, a major component of Taiwan cobra venom, by use of affinity chromatography, circular

2 Naja sputatrix (Malayan spitting cobra) venom contains 15% secretory PLA2 of its dry weig

3 Rats given cobra venom factor (CoF) followed by a NTS shown to be c

4 epleting complement in chinchillas by use of cobra venom factor (CoVF) rendered two otherwise avirule

5 Cobra venom factor (CoVF) treatment, which depletes C3 a

6 562 alone (HAR model) or in combination with cobra venom factor (CVF) (DXR model).

7 r first hamster hearts had been surviving in cobra venom factor (CVF) + CyA-treated rats for 10 days,

8 administered the complement-depleting agent cobra venom factor (CVF) 24 hr before HI lesioning and e

9 nografts, the inhibition of complement using cobra venom factor (CVF) accelerates pulmonary xenograft

10 the graft aorta in combination with systemic cobra venom factor (CVF) administration to deplete compl

11 prevented by brief complement inhibition by cobra venom factor (CVF) and sustained T-cell immunosupp

12 Surprisingly, injection of cobra venom factor (CVF) caused a profound and reproduci

13 Cobra venom factor (CVF) depletes complement and may the

14 anted heterotopically into rats treated with cobra venom factor (CVF) develop disease over 72 hours.

15 me of primary immunization by treatment with cobra venom factor (CVF) diminished serum anti-PPS14 con

16 dy sought to (i) investigate the efficacy of cobra venom factor (CVF) in preventing hyperacute reject

17 Cobra venom factor (CVF) induces lung injury through oxi

18 activation of complement by i.v. infusion of cobra venom factor (CVF) is known to be P-selectin depen

19 in vivo, because complement depletion using cobra venom factor (CVF) markedly reduced the efficacy o

20 y after systemic activation of complement by cobra venom factor (CVF) or after intrapulmonary deposit

21 or inhibited by intraperitoneal injection of cobra venom factor (CVF) or complement receptor-related

22 enografts was achieved using either CsA plus cobra venom factor (CVF) or CsA plus rapamycin.

23 depletion by treatment of athymic rats with cobra venom factor (CVF) partially reverses this effect.

24 Transient complement inhibition with cobra venom factor (CVF) plus daily and continuing cyclo

25 Intraperitoneal injection of cobra venom factor (CVF) reduced C3 levels in the cornea

26 on of complement C3 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regen

27 ell activation when it was preincubated with cobra venom factor (CVF) to deplete C3.

28 ing pulmonary xenograft dysfunction by using cobra venom factor (CVF) to deplete recipient complement

29 Administration of cobra venom factor (CVF), 1 day before and at the time o

30 xplored by intraperitoneal injection of 35 U cobra venom factor (CVF), 24 hours before antibody injec

31 s B or D but did bind to immobilized C3b and cobra venom factor (CVF), a C3b analogue.

32 A/2 as islet allograft recipients as well as cobra venom factor (CVF), a complement blocker, treatmen

33 l plasma, with or without heat inactivation, cobra venom factor (CVF), or lipopolysaccharide plus int

34 groups: no therapy, daily administration of cobra venom factor (CVF), or splenectomy plus daily CVF.

35 (MMF), anti-CD40L monoclonal antibody (mAb), cobra venom factor (CVF), pig hematopoietic growth facto

36 as generated in vivo by infusion of purified cobra venom factor (CVF), thymocyte apoptosis was signif

37 ction process was further investigated using cobra venom factor (CVF), which systemically depleted th

38 ties, but had normal susceptibilities to the cobra venom factor (CVF)-dependent convertase.

39 Median graft survival was 62 hr in cobra venom factor (CVF)-treated controls versus 108 hr

40 respond to intravenous injection of purified cobra venom factor (CVF).

41 vation and depletion of complement (C) using cobra venom factor (CVF).

42 rats treated with cyclosporine (CsA) and/or cobra venom factor (CVF).

43 (GV) with the induction of lung injury using cobra venom factor (CVF); b) PLV-CVF group, animals rece

44 ion was significantly (p < 0.001) delayed by cobra venom factor (CVF; 11 +/- 8 h in four of five case

45 1 microg/mouse), we depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]

46 A convertase assembled with cobra venom factor and Bb was decayed by DAF, albeit far

47 was inhibited by complement depletion using cobra venom factor and did not develop in C3(-/-) mice.

48 llowing systemic activation of complement by cobra venom factor and in the L-selectin-, P-selectin-,

49 eukostasis in mice systemically infused with cobra venom factor and intrapulmonary transendothelial m

50 term after transient complement depletion by cobra venom factor and T cell immunosuppression by cyclo

51 ic activation by the alternative pathway and cobra venom factor C3 convertases; and 4) for susceptibi

52 Cobra venom factor completely inhibited complement activ

53 This transient protection was abrogated by cobra venom factor depletion of complement from FcgammaR

54 C3(-/-) mice, and control mice injected with cobra venom factor developed pronounced corneal opacific

55 Treatment with cobra venom factor did not affect survival, confirming t

56 Depletion of circulating complement with cobra venom factor eliminated, as expected, injury recor

57 after elastase perfusion, mice treated with cobra venom factor exhibited a mean aortic diameter of 9

58 t C3 in the periphery through treatment with cobra venom factor had a seizure rate comparable to that

59 Injecting cobra venom factor into wild-type mice activated the AP

60 e LPS injection, activation of complement by cobra venom factor led to significant elevation of serum

61 In the cobra venom factor model, sCR1sLex and sCR1[desLHR-A]sLe

62 In monkeys that received neither cobra venom factor nor dextran sulfate (group 1), there

63 The effect of complement depletion with cobra venom factor on porcine bone marrow cell (BMC) eng

64 When compared with the cobra venom factor only group (GV-CVF 47 +/- 2 neutrophi

65 ated injury, either by the administration of cobra venom factor or soluble complement receptor I to t

66 diac transplants to survive long term (i.e., cobra venom factor plus cyclosporin A), inhibition of HO

67 nt depletion in CD55(-/-)CD59(-/-) mice with cobra venom factor prevented these effects.

68 Decomplementation by cobra venom factor resulted in impaired entry of hepatoc

69 Injection of cobra venom factor resulted in prolongation of cardiac x

70 pig hearts transplanted into rats treated by cobra venom factor to avoid the hyperacute rejection.

71 Treatment of mice with cobra venom factor to deplete complement had insignifica

72 block C4 and C3 split product binding or by cobra venom factor to trigger C3 consumption.

73 required for the protective effect of CRP as cobra venom factor treatment eliminated the effect of CR

74 ontributed to serum-induced dry eye disease, cobra venom factor was used to deplete complement activi

75 els, C3(-/-) mice and mice depleted of C3 by cobra venom factor were more susceptible to C. neoforman

76 type mice cotreated with the TLR ligands and cobra venom factor, a potent complement activator.

77 y experiments using serum with added EDTA or cobra venom factor, a protein that depletes C3.

78 DAF did not bind cobra venom factor, implying that Bb decay is accelerate

79 i-T-cell and natural killer cell antibodies, cobra venom factor, medronate-liposomes, and 4 Gy of who

80 swine kidney, maintenance therapy comprised cobra venom factor, mycophenolate mofetil, and an anti-C

81 T-cell depletion, complement depletion with cobra venom factor, mycophenolate mofetil, anti-CD154 mo

82 hymocyte globulin, complement depletion with cobra venom factor, short courses of anti-CD154 mAb ther

83 epletion with ATG, complement depletion with cobra venom factor, short courses of cyclosporine, mycop

84 howed that pretreatment of C57BL/6 mice with cobra venom factor, which depleted serum of complement a

85 ubstituted with the corresponding segment of cobra venom factor, Xenopus, or trout C3 (chimeric C3s)

86 determined the C5-cleaving properties of the cobra venom factor-dependent C5 convertase (CVF, Bb) mad

87 In contrast, zymosan- and cobra venom factor-induced AP complement activation, and

88 In the present study, we used cobra venom factor-induced decomplementation to investig

89 gammaR(-/-) mice, but not in C3(-/-) mice or cobra venom factor-treated mice.

90 rmal Lewis rats (complement-sufficient) with cobra venom factor-treated rats (complement-depleted).

91 rogenitor cells in marrow, were increased in cobra venom factor-treated recipients compared with simu

92 shock due to acute complement activation by cobra venom factor.

93 Sterne strain upon complement depletion with cobra venom factor.

94 en complement was depleted by treatment with cobra venom factor.

95 t participated in AP activation initiated by cobra venom factor.

96 Lewis rats, using intravenously administered cobra venom factor.

97 complement components via pretreatment with cobra venom factor.

98 pressure (PEEP) before the administration of cobra venom factor; d) CVF-PLV group, animals received p

99 ls received partial liquid ventilation after cobra venom factor; e) CVF-PEEP group, animals received

100 CVF-PEEP group, animals received PEEP after cobra venom factor; f) PLV only group, animals received

101 to the GP Ib thrombin-binding site or by the cobra venom metalloproteinase, mocarhagin, that hydrolyz

102 n Ib-IX-V complex, we utilized mocarhagin, a cobra venom metalloproteinase, to generate a fragment (H

103 Cobra venom (Naja kaouthia) contains a toxin called alph

104 Phospholipase A2 from cobra venom (Naja naja atra) hydrolyzes carbonothioate p

105 xchange mass spectrometric evaluation of the cobra venom (Naja naja naja) group IA phospholipase A 2

106 Cardiotoxins (CTXs) from cobra venom show cytotoxicity toward several cell types.

107 In Naja kaouthia cobra venom, we have earlier discovered a covalent dimer

108 ants of the group IA phospholipase A(2) from cobra venom were constructed and expressed in the methyl