コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 shock due to acute complement activation by cobra venom factor.
2 Sterne strain upon complement depletion with cobra venom factor.
3 en complement was depleted by treatment with cobra venom factor.
4 t participated in AP activation initiated by cobra venom factor.
5 Lewis rats, using intravenously administered cobra venom factor.
6 complement components via pretreatment with cobra venom factor.
10 health and disease; for instance, the use of cobra venom factor and depletion of C3 provided the init
11 was inhibited by complement depletion using cobra venom factor and did not develop in C3(-/-) mice.
12 llowing systemic activation of complement by cobra venom factor and in the L-selectin-, P-selectin-,
13 eukostasis in mice systemically infused with cobra venom factor and intrapulmonary transendothelial m
14 term after transient complement depletion by cobra venom factor and T cell immunosuppression by cyclo
15 ic activation by the alternative pathway and cobra venom factor C3 convertases; and 4) for susceptibi
18 epleting complement in chinchillas by use of cobra venom factor (CoVF) rendered two otherwise avirule
21 r first hamster hearts had been surviving in cobra venom factor (CVF) + CyA-treated rats for 10 days,
22 administered the complement-depleting agent cobra venom factor (CVF) 24 hr before HI lesioning and e
23 nografts, the inhibition of complement using cobra venom factor (CVF) accelerates pulmonary xenograft
24 the graft aorta in combination with systemic cobra venom factor (CVF) administration to deplete compl
25 prevented by brief complement inhibition by cobra venom factor (CVF) and sustained T-cell immunosupp
28 anted heterotopically into rats treated with cobra venom factor (CVF) develop disease over 72 hours.
29 me of primary immunization by treatment with cobra venom factor (CVF) diminished serum anti-PPS14 con
30 dy sought to (i) investigate the efficacy of cobra venom factor (CVF) in preventing hyperacute reject
32 activation of complement by i.v. infusion of cobra venom factor (CVF) is known to be P-selectin depen
33 in vivo, because complement depletion using cobra venom factor (CVF) markedly reduced the efficacy o
34 y after systemic activation of complement by cobra venom factor (CVF) or after intrapulmonary deposit
35 or inhibited by intraperitoneal injection of cobra venom factor (CVF) or complement receptor-related
37 depletion by treatment of athymic rats with cobra venom factor (CVF) partially reverses this effect.
40 on of complement C3 or its inactivation with Cobra Venom Factor (CVF) result in impaired muscle regen
42 ing pulmonary xenograft dysfunction by using cobra venom factor (CVF) to deplete recipient complement
44 xplored by intraperitoneal injection of 35 U cobra venom factor (CVF), 24 hours before antibody injec
46 A/2 as islet allograft recipients as well as cobra venom factor (CVF), a complement blocker, treatmen
47 l plasma, with or without heat inactivation, cobra venom factor (CVF), or lipopolysaccharide plus int
48 groups: no therapy, daily administration of cobra venom factor (CVF), or splenectomy plus daily CVF.
49 (MMF), anti-CD40L monoclonal antibody (mAb), cobra venom factor (CVF), pig hematopoietic growth facto
50 as generated in vivo by infusion of purified cobra venom factor (CVF), thymocyte apoptosis was signif
51 ction process was further investigated using cobra venom factor (CVF), which systemically depleted th
57 (GV) with the induction of lung injury using cobra venom factor (CVF); b) PLV-CVF group, animals rece
58 ion was significantly (p < 0.001) delayed by cobra venom factor (CVF; 11 +/- 8 h in four of five case
59 1 microg/mouse), we depleted complement with cobra venom factor (CVF; 7 U/mouse, intravenously [i.v.]
60 pressure (PEEP) before the administration of cobra venom factor; d) CVF-PLV group, animals received p
61 determined the C5-cleaving properties of the cobra venom factor-dependent C5 convertase (CVF, Bb) mad
62 This transient protection was abrogated by cobra venom factor depletion of complement from FcgammaR
63 C3(-/-) mice, and control mice injected with cobra venom factor developed pronounced corneal opacific
65 ls received partial liquid ventilation after cobra venom factor; e) CVF-PEEP group, animals received
66 Depletion of circulating complement with cobra venom factor eliminated, as expected, injury recor
67 after elastase perfusion, mice treated with cobra venom factor exhibited a mean aortic diameter of 9
68 CVF-PEEP group, animals received PEEP after cobra venom factor; f) PLV only group, animals received
69 t C3 in the periphery through treatment with cobra venom factor had a seizure rate comparable to that
74 e LPS injection, activation of complement by cobra venom factor led to significant elevation of serum
75 i-T-cell and natural killer cell antibodies, cobra venom factor, medronate-liposomes, and 4 Gy of who
77 swine kidney, maintenance therapy comprised cobra venom factor, mycophenolate mofetil, and an anti-C
78 T-cell depletion, complement depletion with cobra venom factor, mycophenolate mofetil, anti-CD154 mo
82 ated injury, either by the administration of cobra venom factor or soluble complement receptor I to t
83 diac transplants to survive long term (i.e., cobra venom factor plus cyclosporin A), inhibition of HO
87 scued in E8.5 Cmas-/- mice upon injection of cobra venom factor, resulting in exhaustion of the mater
88 hymocyte globulin, complement depletion with cobra venom factor, short courses of anti-CD154 mAb ther
89 epletion with ATG, complement depletion with cobra venom factor, short courses of cyclosporine, mycop
90 pig hearts transplanted into rats treated by cobra venom factor to avoid the hyperacute rejection.
94 rmal Lewis rats (complement-sufficient) with cobra venom factor-treated rats (complement-depleted).
95 rogenitor cells in marrow, were increased in cobra venom factor-treated recipients compared with simu
96 required for the protective effect of CRP as cobra venom factor treatment eliminated the effect of CR
97 ontributed to serum-induced dry eye disease, cobra venom factor was used to deplete complement activi
98 els, C3(-/-) mice and mice depleted of C3 by cobra venom factor were more susceptible to C. neoforman
99 howed that pretreatment of C57BL/6 mice with cobra venom factor, which depleted serum of complement a
100 is for the first clinical trial, except that cobra venom factor will be replaced by a clinically appr
101 globulin, an anti-CD20 mAb (Rituximab), and cobra venom factor, with maintenance therapy based on bl
102 ubstituted with the corresponding segment of cobra venom factor, Xenopus, or trout C3 (chimeric C3s)