ライフサイエンスコーパス: cobra venom

1 targeted, modify cell responses to spitting cobra venoms.

2 Cobra venom affected the formation of myotubes and induc

3 affected by both Indian Russell's viper and cobra venoms and offers insights into the potential caus

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

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

6 rall, our systematic molecular dissection of cobra venom cytotoxicity provides insight into how we ca

7 While cobra venom decreased the viability, it did not largely

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

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

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

11 562 alone (HAR model) or in combination with cobra venom factor (CVF) (DXR model).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 1 microg/mouse), we depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]

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

52 health and disease; for instance, the use of cobra venom factor and depletion of C3 provided the init

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

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

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

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

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

58 Cobra venom factor completely inhibited complement activ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

82 is for the first clinical trial, except that cobra venom factor will be replaced by a clinically appr

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

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

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

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

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

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

89 scued in E8.5 Cmas-/- mice upon injection of cobra venom factor, resulting in exhaustion of the mater

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

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

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

93 globulin, an anti-CD20 mAb (Rituximab), and cobra venom factor, with maintenance therapy based on bl

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

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

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

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

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

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

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

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

102 Sterne strain upon complement depletion with cobra venom factor.

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

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

105 Lewis rats, using intravenously administered cobra venom factor.

106 complement components via pretreatment with cobra venom factor.

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

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

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

110 cal tissue damage caused by several spitting cobra venoms in murine models of envenoming.

111 Cobra venom-induced atrophy could not be reversed by sma

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

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

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

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

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

117 Beta-cardiotoxin (B-CTX) from the king cobra venom (Ophiophagus hannah) was previously proposed

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

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

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