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

3 plasminogen with an affinity comparable with streptokinase.

4 thrombolysis with fibrin-specific agents or streptokinase.

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

6 plasminogen activation through the action of streptokinase.

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

8 and speB genes and reduced the secretion of streptokinase.

9 asminogen activator, but not by urokinase or streptokinase.

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

11 xpression of pili and the thrombolytic agent streptokinase.

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

13 ies were exposed to ultrasound alone without streptokinase.

14 sminogen activator or the thrombolytic agent streptokinase.

15 nt underwent transhepatic portal infusion of streptokinase.

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

17 tigenic stimulation with Candida albicans or streptokinase.

18 icantly attenuated by the fibrinolytic agent 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 Using data from the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

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

63 ty endpoint was GUSTO (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 e criteria from GUSTO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

71 bleeding, according to Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occlu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 1 patients enrolled in Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries, a

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

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

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

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

92 g and mouse Pg, the activation properties of streptokinase are strictly attributed to the serine prot

93 half dose for patients 75 years or older (or streptokinase at full dose if cost is a consideration),

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

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

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

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

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

99 A streptokinase binding site for K5 is located between res

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

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

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

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

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

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

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

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

108 Streptokinase exhibited a complex endotherm whose shape

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

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

111 FasX enhanced streptokinase expression in each serotype, although the

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

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

114 is susceptibility was dependent on bacterial streptokinase expression.

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

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

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

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

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

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

121 The streptokinase genes from S. equisimilis strains which ac

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

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

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

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

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

127 Since the discovery of streptokinase in 1933, several additional fibrinolytic a

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

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

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

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

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

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

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

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

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

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

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

139 Streptokinase is a plasminogen activator widely used in

140 Streptokinase is highly specific for human plasminogen,

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

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

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

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

145 Because a streptokinase-like mechanism was hypothesized to require

146 Streptokinase may be less effective at saving lives in p

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

148 Thrombolysis with streptokinase or alteplase further increased both parame

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

150 nditions and after thrombolytic therapy with streptokinase or alteplase.

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

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

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

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

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

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

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

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

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

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

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

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

163 5), 3% with abciximab alone (n=32), 10% with streptokinase plus abciximab (n=143), 7% with 50 mg of a

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

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

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

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

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

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

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

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

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

173 US or streptokinase resulted in minimal thrombolysis, but repe

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

175 The streptokinase secreted by the equine isolate had little

176 The streptokinase secreted by the porcine isolate had limite

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

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

179 Streptokinases secreted by nonhuman isolates of group C

180 Streptokinase (SK) activates human fibrinolysis by induc

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

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

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

184 Streptokinase (SK) and staphylokinase form cofactor-enzy

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

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

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

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

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

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

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

192 Streptokinase (SK) circumvents this process and activate

193 Streptokinase (SK) conformationally activates the centra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 The coinherited Pattern D GAS-secreted streptokinase (SK2b) then accelerates cleavage of hPg at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 Streptokinase therapy for acute ischemic stroke has not

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

231 The unique abilities of streptokinase to nonproteolytically activate plasminogen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 Complexes of streptokinase with human plasminogen can hydrolytically

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

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

251 2 which, based on the sequence similarity of streptokinase with serine proteases, may be part of a su

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

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

254 combination of enzymatic solutions (based on streptokinase) with mechanical scrapping is used to remo