ライフサイエンスコーパス: streptokinase

1 sus 15.2 microm(-1) min(-1)) comparable with streptokinase.

2 plasminogen with an affinity comparable with streptokinase.

3 thrombolysis with fibrin-specific agents or streptokinase.

4 SUPA was at least 5-fold longer than that of streptokinase.

5 plasminogen activation through the action of streptokinase.

6 tokinase alone, or the combination of US and streptokinase.

7 and speB genes and reduced the secretion of streptokinase.

8 asminogen activator, but not by urokinase or streptokinase.

9 xpression of pili and the thrombolytic agent streptokinase.

10 d-dose tissue plasminogen activator (TPA) or streptokinase.

11 sue-type plasminogen activator (t-PA) versus streptokinase.

12 ies were exposed to ultrasound alone without streptokinase.

13 sminogen activator or the thrombolytic agent streptokinase.

14 nt underwent transhepatic portal infusion of streptokinase.

15 M protein (PAM), and the human Pg activator streptokinase.

16 tigenic stimulation with Candida albicans or streptokinase.

17 icantly attenuated by the fibrinolytic agent streptokinase.

18 esuscitation (c-ECPR), which did not receive streptokinase.

19 were all significantly reduced by the use of streptokinase.

20 resuscitation (t-ECPR) group, which received streptokinase 1 million units, and control extracorporea

21 arin (1000 IU/L); one group of pigs also had streptokinase (1.5 MIU/L) added.

22 tivated sonication combined with intravenous streptokinase, 10 of 17 iliofemoral arteries (59%) treat

23 Four trials compared angioplasty with streptokinase, 3 compared angioplasty with a 3- to 4-hou

24 TO III (4.2%) or by fibrinolytic assignment (streptokinase, 4.1%; alteplase, 4.3%; reteplase, 4.5%; c

25 reduced doses of alteplase (20 to 65 mg) or streptokinase (500 000 U to 1.5 MU).

26 n of kidneys transplanted through the use of streptokinase (63.6% with streptokinase vs. 42.6% with p

27 inactivation of genes encoding either PAM or streptokinase (a plasminogen activator) leads to loss of

28 ike staphylokinase, a single domain protein, streptokinase, a 3-domain (alpha, beta, and gamma) molec

29 Group A streptococci (GAS) secrete streptokinase, a specific activator of human plasminogen

30 in requirements indicated critical roles for streptokinase, activatable plasminogen, and fibrinogen.

31 the melting of these fragments with that of streptokinase allowed the first two transitions in the p

32 l groups: 1 of 17 arteries (6%) treated with streptokinase alone (P = .0012) and 1 of 14 arteries (7%

33 stered with either US alone at 0.75 W/cm(2), streptokinase alone, or the combination of US and strept

34 The precursor of streptokinase, an extracellular protein produced in path

35 ; alteplase, 4.3%; reteplase, 4.5%; combined streptokinase and alteplase, 4.4%; P=0.55).

36 ve been treated with the thrombolytic agents streptokinase and alteplase.

37 itored in real time during thrombolysis with streptokinase and heparin.

38 treatment with alteplase (2.0% vs 1.9% with streptokinase and intravenous heparin) was offset by a g

39 this counterion have been suggested: Ile1 of streptokinase and Lys698 of Plgn.

40 nteral anticoagulants as background therapy, streptokinase and non-accelerated infusion of alteplase

41 ase, and reteplase should be considered over streptokinase and non-accelerated infusion of alteplase.

42 en in a manner similar to that observed when streptokinase and plasminogen interact in the fluid phas

43 galactiae, has moderate sequence identity to streptokinase and staphylokinase, bacterial activators o

44 patients treated with accelerated TPA versus streptokinase and subcutaneous or intravenous heparin.

45 block enrolled in the Global Utilization of Streptokinase and t-PA [tissue-type plasminogen activato

46 rdial Infarction 9 and Global Utilization of Streptokinase and t-PA for Occluded Arteries 1 protocols

47 pared with t-PA in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

48 tients enrolled in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

49 In the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

50 41,021 patients in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

51 29,656 patients in the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

52 l safety end point was Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

53 eding according to the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

54 ed with the use of the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (G

55 ogy exists between the plasminogen activator streptokinase and the human voltage-dependent anion chan

56 We combined the Global Utilization of Streptokinase and Tissue plasminogen activator (alteplas

57 rovascular events, and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

58 diovascular events and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

59 Using data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

60 ad participated in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

61 Composite Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

62 ty endpoint was GUSTO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

63 Using data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

64 of both agents in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

65 olytic regimens in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

66 In the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

67 d 2200 patients in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

68 rolled in the GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

69 tients enrolled in the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

70 al Infarction), GUSTO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

71 ) and bleeding events (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

72 ce of recurrent MI and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

73 bleeding (according to Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

74 ding definition by the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

75 combined data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

76 Infarction (TIMI) and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

77 ombosis) and bleeding (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

78 reptokinase plus intravenous heparin and the streptokinase and tissue plasminogen activator plus intr

79 dial infarction in the Global Utilization of Streptokinase and Tissue-Plasminogen Activator for Occlu

80 enrolled in the GUSTO (Global Utilization of Streptokinase and Tissue-Type Plasminogen Activator for

81 U.S. patients enrolled in the Global Use of Streptokinase and TPA (alteplase) for Occluded Coronary

82 We pooled the datasets of the Global Use of Streptokinase and tPA for Occluded Arteries (GUSTO)-IIb,

83 ographic data from the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO-1) an

84 tients enrolled in the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GU

85 1 patients enrolled in Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries, a

86 activity of a secreted cysteine protease and streptokinase, and an altered immunoglobulin and fibrino

87 cellular products, including streptolysin O, streptokinase, and DNase, was not affected.

88 role for the secreted plasminogen activator, streptokinase, and identify the major surface fibrinogen

89 ve responses to Candida, tetanus toxoid, and streptokinase antigens was studied in peripheral blood m

90 ns and improve coronary reperfusion rates in streptokinase-based regimens.

91 high affinity binding to plasmin(ogen), the streptokinase beta-domain is required for nonproteolytic

92 ult of high affinity binding mediated by the streptokinase beta-domain.

93 O-I, in which mortality rate for t-PA versus streptokinase between 30 days and 1-year was 2.97% (hear

94 abciximab alone and 34% to 46% for doses of streptokinase between 500 000 U and 1.25 MU with abcixim

95 A streptokinase binding site for K5 is located between res

96 interactions with the plasminogen activator streptokinase but did not block complex formation.

97 w were seen when abciximab was combined with streptokinase, but there was an increased risk of bleedi

98 s were altered, including the genes encoding streptokinase, CAMP factor, streptolysin O, M protein (m

99 n complex based upon the known structures of streptokinase complexed with human plasmin supported the

100 The crystal structure of streptokinase complexed with the catalytic unit of human

101 When compared with streptokinase complexes, SKbetaswap-plasmin and SKbetasw

102 are use of an accelerated t-PA regimen (vs. streptokinase containing regimens) (chi2=39.1; p < or =

103 enes (nine different FCT-types), and (c) the streptokinase-encoding gene (ska) sequence (two differen

104 Streptokinase exhibited a complex endotherm whose shape

105 file of M3 GAS, as evident by a reduction in streptokinase expression and an enhancement of GRAB expr

106 ght to test whether FasX regulates pilus and streptokinase expression in a serotype-specific manner.

107 FasX enhanced streptokinase expression in each serotype, although the

108 was enhanced in strain AP53/covS(M), whereas streptokinase expression was only slightly affected by t

109 regulatory RNA FasX, which in turn enhanced streptokinase expression.

110 is susceptibility was dependent on bacterial streptokinase expression.

111 th kinetic parameters comparable to those of streptokinase for h-plasminogen.

112 he randomized Global Utilization of t-PA and Streptokinase for Occluded Coronary Arteries (GUSTO-I) t

113 rther show that cellular factors, as well as streptokinase from bacteria commonly coinfecting the res

114 Recombinant streptokinase gamma-domain bound to the b-plasminogen.SU

115 However, the streptokinase gamma-domain enhances the rates of active

116 ke mechanism was hypothesized to require the streptokinase gamma-domain, we examined the mechanism of

117 The streptokinase genes from S. equisimilis strains which ac

118 ated with the other regimens (7.3%, combined streptokinase groups).

119 Finally, we show that the thrombolytic agent streptokinase has therapeutic value for Adamts13(-/-) mi

120 ients were randomly assigned combinations of streptokinase, heparin, and accelerated tissue-plasminog

121 actor Xa, plasmin, protein Ca, uPA, tPA, and streptokinase); however, their selectivity for thrombin

122 mology to other streptococcal PAs, including streptokinase; however, PadA was found to align well wit

123 ator (t-PA), which proved little better than streptokinase in acute myocardial infarction.

124 qual effect as adjunctive therapy to TPA and streptokinase in preventing unsatisfactory outcome in pa

125 significantly augments lysis of thrombi with streptokinase in rabbit iliofemoral arteries.

126 The amino-terminal domain of streptokinase in the complex is hypothesized to enhance

127 ue damage occurred with the incorporation of streptokinase in the in situ flush medium.

128 The use of streptokinase in this porcine NHBD model conferred benef

129 his study confirmed not only the presence of streptokinases in nonhuman S. equisimilis isolates but a

130 tissue-type plasminogen activator (tPA), or streptokinase], in combination with one of a series of F

131 with immobilized (His)(6)-tagged recombinant streptokinases indicated that these recombinant streptok

132 eptokinases indicated that these recombinant streptokinases interacted with plasminogen in a manner s

133 Thus, streptokinase is a key pathogenicity factor and the prim

134 Streptokinase is a plasminogen activator widely used in

135 Streptokinase is highly specific for human plasminogen,

136 The beta domain of streptokinase is required for plasminogen activation and

137 tissue plasminogen activator (tPA), but not streptokinase, is slowed in fibrin clots containing Abet

138 -bound hPg is then activated by GAS-secreted streptokinase, leading to the generation of an invasive

139 de that a gamma-domain is not required for a streptokinase-like activation of b-plasminogen.

140 Because a streptokinase-like mechanism was hypothesized to require

141 Streptokinase may be less effective at saving lives in p

142 ed tissue-type plasminogen activator (t-PA), streptokinase or a combination of both agents in the Glo

143 Thrombolysis with streptokinase or alteplase further increased both parame

144 Treatment of aged plasma clots with either streptokinase or alteplase, at therapeutic levels, incre

145 nditions and after thrombolytic therapy with streptokinase or alteplase.

146 ts of clot age and thrombolysis, with either streptokinase or tissue-type plasminogen activator (tPA)

147 ys and can be lysed on addition of exogenous streptokinase or urokinase.

148 There were no direct comparisons of tPA with streptokinase or urokinase: much of the poor outcome in

149 lysis" OR "tissue plasminogen activator" OR "streptokinase" OR "urokinase." Search was not limited by

150 atistically indistinguishable from that with streptokinase (P = .47) but was marginally different fro

151 rlier treatment with accelerated t-PA versus streptokinase (p = 0.38).

152 min complex also was less resistant than the streptokinase-plasmin complex to inhibition by alpha(2)-

153 Analysis of the cleavage products of the streptokinase-plasminogen interaction indicated that hum

154 okinase-type plasminogen activator (UPA), or streptokinase/ plasminogen (37 U streptokinase plus 2 mu

155 UPA and streptokinase/plasminogen elicited decreases of 33 +/- 8

156 The critical contribution of the streptokinase-PLG interaction to GAS pathogenicity was r

157 r (UPA), or streptokinase/ plasminogen (37 U streptokinase plus 2 mumol/L plasminogen) for 24 hours,

158 5), 3% with abciximab alone (n=32), 10% with streptokinase plus abciximab (n=143), 7% with 50 mg of a

159 streptokinase with intravenous heparin; (3) streptokinase plus alteplase (tissue-type plasminogen ac

160 more bleeding was seen with the therapies of streptokinase plus intravenous heparin and the streptoki

161 (risk ratio [RR] 1.14 [95% CI 1.05-1.24] for streptokinase plus parenteral anticoagulants; RR 1.26 [1

162 This study using streptokinase preflush in the NHBD was found to improve

163 ble-blinded, randomised, controlled trial of streptokinase preflush or placebo for NHBD was performed

164 fusion requirements in the recipient whether streptokinase preflush or placebo was used.

165 he significance of these findings, series of streptokinase-producing Streptococcus equisimilis isolat

166 ectin/fibrinogen-binding/haemolytic-activity/streptokinase-regulator-X (FasX) sRNA, previously shown

167 ectin/fibrinogen-binding/haemolytic-activity/streptokinase-regulator-X (fasX) were identified in four

168 US or streptokinase resulted in minimal thrombolysis, but repe

169 lso increased transcription of ska (encoding streptokinase), sagA (streptolysin S), and speMF (mitoge

170 The streptokinase secreted by the equine isolate had little

171 The streptokinase secreted by the porcine isolate had limite

172 e isolate had little similarity to any known streptokinases secreted by either human or porcine isola

173 ed structural and functional similarities to streptokinases secreted by human isolates.

174 Streptokinases secreted by nonhuman isolates of group C

175 Streptokinase (SK) activates human fibrinolysis by induc

176 The bacterial protein streptokinase (SK) activates human plasminogen (Pg) into

177 Streptokinase (SK) activates plasminogen (Pg) by specifi

178 The role of the streptokinase (SK) alpha-domain in plasminogen (Pg) and

179 Streptokinase (SK) and staphylokinase form cofactor-enzy

180 Pathogenic bacteria have evolved PAs [e.g., streptokinase (SK) and staphylokinase] that exploit the

181 that hirudin might interact differently with streptokinase (SK) and tissue-type plasminogen activator

182 kinetics demonstrate a three-step pathway of streptokinase (SK) binding to plasminogen (Pg), the zymo

183 Streptokinase (SK) binds to plasminogen (Pg) to form a c

184 In contrast, streptokinase (SK) binds to Plgn to produce an initial i

185 However, streptokinase (SK) binds to Plgn, generating an active p

186 We previously demonstrated that streptokinase (SK) can be used to generate active site-l

187 Streptokinase (SK) circumvents this process and activate

188 Streptokinase (SK) conformationally activates the centra

189 the fibrinolytic proteinase plasmin (Pm) to streptokinase (SK) in a tight stoichiometric complex tra

190 ex, in contrast to a similar experiment with streptokinase (SK) in place of Sak, where substantial am

191 gh a unique but poorly understood mechanism, streptokinase (SK) interacts with human plasminogen to g

192 Streptokinase (SK) is a bacterial protein used for the t

193 The NH(2) terminus (residues 1-59) of streptokinase (SK) is a molecular switch that permits fi

194 Streptokinase (SK) is a robust Pg activator in physiolog

195 Though streptokinase (SK) is widely used to treat humans with t

196 Plasminogen (Pg) activators such as streptokinase (SK) save lives by generating plasmin to d

197 Binding of streptokinase (SK) to plasminogen (Pg) activates the zym

198 Binding of streptokinase (SK) to plasminogen (Pg) conformationally

199 Binding of streptokinase (SK) to plasminogen (Pg) induces conformat

200 ve site induced non-proteolytically in Pg by streptokinase (SK) was inactivated stoichiometrically wi

201 he pathway of plasminogen (Pg) activation by streptokinase (SK) was tested by the use of full time co

202 Compounds inhibiting gene expression of streptokinase (SK), a critical group A streptococcal (GA

203 Streptokinase (SK), a widely used thrombolytic agent, is

204 ogen activators (including urokinase (u-PA), streptokinase (SK), and tissue plasminogen activator (t-

205 Streptokinase (SK), secreted by Group A Streptococcus (G

206 eptococcus (GAS) strains secrete the protein streptokinase (SK), which functions by activating host h

207 vators but inhibits Pg activation induced by streptokinase (SK).

208 ch streptokinase was cleaved to form altered streptokinase (Sk*) was also determined.

209 y a subset of GAS strains, the gene encoding streptokinase (ska) is present in all GAS isolates.

210 sin O (slo), hyaluronic acid capsule (hasA), streptokinase (ska), and DNases (spd and spd3), which we

211 pression of the Csr-regulated hasABC operon, streptokinase (ska), and streptolysin S (sagA) during gr

212 Through the secreted plasminogen activator streptokinase (Ska), GAS activates human plasminogen int

213 expression of the secreted virulence factor streptokinase (SKA), negatively regulates the production

214 production of the secreted virulence factor streptokinase (SKA).

215 To examine this hypothesis, a chimeric streptokinase, SKbetaswap, was created by swapping the S

216 The amounts of streptokinase, streptolysin S, and capsule paralleled th

217 rulence factors (capsule, cysteine protease, streptokinase, streptolysin S, and streptodornase).

218 indication of reperfusion therapy in STEMI (streptokinase, tenecteplase, alteplase, and reteplase) w

219 is Pg activator (SUPA or PauA, SK uberis), a streptokinase that cannot activate human plasminogen.

220 ccal isolates from humans and horses secrete streptokinases that preferentially activate plasminogens

221 ce factors, including the thrombolytic agent streptokinase, the protease inhibitor-binding protein-G-

222 e evidence to suggest that tPA is safer than streptokinase; the apparent hazards and benefits may be

223 Streptokinase therapy for acute ischemic stroke has not

224 Liposome-based formulations of PAs such as streptokinase, tissue-plasminogen activator and urokinas

225 The unique abilities of streptokinase to nonproteolytically activate plasminogen

226 The addition of streptokinase to plasma resulted in the activation then

227 o investigate the effects of the addition of streptokinase to the in situ flush medium before transpl

228 Infarction phase 7 and Global Utilization of Streptokinase tPA for Occluded coronary arteries phase 1

229 The NHBD kidneys from the streptokinase-treated donors had a better appearance at

230 stance, and lower mean pressure index in the streptokinase-treated group of pigs.

231 r urokinase: much of the poor outcome in the streptokinase-treated patients might be explained by the

232 s for "clot busting" plasminogen activators (streptokinase, urokinase, and tissue plasminogen activat

233 through the use of streptokinase (63.6% with streptokinase vs. 42.6% with placebo), this did not achi

234 The site at which streptokinase was cleaved to form altered streptokinase

235 The structural organization of streptokinase was established through detailed study of

236 In 17 of 24 rabbits, 25000 units/kg streptokinase was then administered intravenously.

237 Streptokinase was used in eight trials (n=1837), and fib

238 Two proteolytic fragments of streptokinase were examined, a 37-kDa fragment beginning

239 lence factors (notably cysteine protease and streptokinase) were regulated in a biofilm-like manner.

240 reptococci, a common human pathogen, secrete streptokinase, which activates the host's blood clot-dis

241 The carboxyl-terminal domain of streptokinase, which binds near the activation loop of p

242 Complexes of streptokinase with human plasminogen can hydrolytically

243 h subcutaneous heparin (10.1%, P = .011) and streptokinase with intravenous heparin (10.1%, P = .009)

244 streptokinase with subcutaneous heparin; (2) streptokinase with intravenous heparin; (3) streptokinas

245 2 which, based on the sequence similarity of streptokinase with serine proteases, may be part of a su

246 ined in favor of accelerated TPA (9.1%) over streptokinase with subcutaneous heparin (10.1%, P = .011

247 One of four thrombolytic regimens: (1) streptokinase with subcutaneous heparin; (2) streptokina