ライフサイエンスコーパス: tissue plasminogen activator

1 eers to investigate whether hypoxia releases tissue plasminogen activator.

2 cal sign of recanalization after intravenous tissue plasminogen activator.

3 ds, high sensitivity C-reactive protein, and tissue plasminogen activator.

4 ed with elevated levels of tissue factor and tissue plasminogen activator.

5 ith delayed fibrin lysis via plasminogen and tissue plasminogen activator.

6 vely promotes clot lysis in combination with tissue plasminogen activator.

7 ted an intermediate phenotype in response to tissue plasminogen activator.

8 lar fraction of blood mediates resistance to tissue plasminogen activator.

9 revented plasma clot fibrinolysis induced by tissue plasminogen activator.

10 nexin A2, the coreceptor for plasminogen and tissue plasminogen activator.

11 s and the unexpected disulfide scrambling of tissue plasminogen activator.

12 such as thrombin, cathepsin B, tryptase, and tissue plasminogen activator.

13 that Plg-R(KT) also interacts directly with tissue plasminogen activator.

14 vator or EKOS ultrasound plus intra-arterial tissue plasminogen activator.

15 e plasminogen to plasmin that is mediated by tissue plasminogen activator.

16 owed by treatment with aspirin, heparin, and tissue plasminogen activator.

17 ions correlated significantly with levels of tissue plasminogen activator.

18 ta by secreting enzymatic factors, including tissue plasminogen activator.

19 erine protease plasmin by staphylokinase and tissue plasminogen activator.

20 e thrombolytic and proteolytic properties of tissue plasminogen activator.

21 sidered marginal compared with urokinase and tissue plasminogen activator.

22 in plasma treated with therapeutic levels of tissue plasminogen activator.

23 polipoprotein E2, E3, and E4 (1.3-1.8-fold), tissue plasminogen activator (2.7-fold), matrix metallop

24 to 6 hours after treatment with intravenous tissue plasminogen activator 3 to 6 hours after symptom

25 oids, antithrombins, or fibrinolytics (e.g., tissue plasminogen activator), 3) a control and/or sham

26 Thirty minutes of forearm-ischemia increased tissue plasminogen activator 31-fold (p<0.001).

27 y approved treatment for ischaemic stroke is tissue plasminogen activator, a clot-buster.

28 ulation selectively induced the secretion of tissue plasminogen activator, a key protease involved in

29 s of the brain accompanied by an increase in tissue plasminogen activator, a product of microglia imp

30 pin), a therapeutic monoclonal antibody, and tissue plasminogen activator (Activase).

31 - and basic fibroblast growth factor-induced tissue plasminogen activator activation, which is requir

32 In contrast, tissue plasminogen activator alone was not protective.

33 ared with intravenous alteplase (recombinant tissue plasminogen activator) alone for moderate or seve

34 assay for mouse plasma that is sensitive to tissue plasminogen activator, alpha2-antiplasmin, active

35 Intravenous recombinant tissue plasminogen activator (alteplase) was approved by

36 When coated with tissue plasminogen activator and administered intravenou

37 The crude odds ratio between tissue plasminogen activator and death was 3.35 (95% con

38 hown that the combination of an intrapleural tissue plasminogen activator and deoxyribonuclease thera

39 e measurement of nitric oxide, endothelin-1, tissue plasminogen activator and plasminogen activator i

40 tion), D-dimer, plasmin-antiplasmin complex, tissue plasminogen activator and plasminogen activator i

41 ellular proteolytic center by recruiting the tissue plasminogen activator and plasminogen and mediati

42 dicates that annexin A2 (A2), a receptor for tissue plasminogen activator and plasminogen, binds beta

43 F]wall, PPXbd enhanced fibrin sensitivity to tissue plasminogen activator and promoted clot retractio

44 lytic complex that assembles plasminogen and tissue plasminogen activator and promotes plasmin genera

45 n A2 functions in angiogenesis by binding to tissue plasminogen activator and regulating plasminogen

46 TFPI activity coincided with the release of tissue plasminogen activator and the peak of plasmin gen

47 chanism of action of intravenous recombinant tissue plasminogen activator and the rationale of variou

48 diated intrathrombus delivery of recombinant tissue plasminogen activator and thrombus aspiration or

49 e factor, as well as decreased production of tissue plasminogen activator and tissue factor pathway i

50 nts underwent MT with or without intravenous tissue plasminogen activator and were admitted to endova

51 n but also stimulates endothelial release of tissue-plasminogen activator and inhibits platelet aggre

52 d formulations of PAs such as streptokinase, tissue-plasminogen activator and urokinase have been dev

53 ctivator inhibitor type 1, reduced levels of tissue plasminogen activator, and lower d-dimer formatio

54 were chemorepulsive: alpha-2-macroglobulin, tissue plasminogen activator, and metallothionein III.

55 ibitor type 1 antigen and activity and lower tissue plasminogen activator antigen (known to track wit

56 llebrand factor antigen (p < or = 0.05), and tissue plasminogen activator antigen (p < 0.001 only in

57 n, fibrin D-dimer, C-reactive protein (CRP), tissue plasminogen activator antigen (t-PA) and von Will

58 ficant for von Willebrand factor antigen and tissue plasminogen activator antigen in women.

59 vator inhibitor type 1 antigen and activity, tissue plasminogen activator antigen, fibrinogen, D-dime

60 protein, von Willebrand factor antigen, and tissue plasminogen activator antigen.

61 Urokinase and recombinant tissue plasminogen activator are the currently available

62 bitor of urokinase plasminogen activator and tissue plasminogen activator, are implicated in the path

63 Furthermore, it reduced tissue plasminogen activator-associated hemorrhage in a

64 Patients treated with intravenous tissue plasminogen activator at Suburban Hospital, Bethe

65 NIHSS scores were determined before tissue plasminogen activator bolus and at 60 and 120 min

66 ion enhanced the effect of statins on TM and tissue plasminogen activator, but did not influence thro

67 The only therapy available is recombinant tissue plasminogen activator, but side effects limit its

68 intravenous and 5 intra-arterial recombinant tissue plasminogen activator cases.

69 3 and plasminogen, which after activation by tissue plasminogen activator cleaved the bound histone.

70 chanism of action of intravenous recombinant tissue plasminogen activator, clinical studies could inc

71 ormin had lower HbA1c, insulin, HOMA-IR, and tissue plasminogen activator compared with those taking

72 emotactic protein-1), and formation of PAI-1/tissue plasminogen activator complexes.

73 otactic protein-1 and the formation of PAI-1/tissue plasminogen activator complexes.

74 Treatment with tissue plasminogen activator, concomitant wound care, an

75 whereas injection of bradykinin, plasmin or tissue plasminogen activator did not elicit such a respo

76 Intravenous tissue plasminogen activator did not impact outcomes.

77 Combined delivery of plasminogen and tissue plasminogen activator during NMP lysed the plugs

78 IV recombinant tissue plasminogen activator, endovascular treatment, IV

79 On the contrary, recombinant tissue-plasminogen activator enhanced brain injury, whic

80 g IVF consisting of 1mg of recombinant human tissue plasminogen activator every 8 hours until clot cl

81 Patients were treated with IVT with tissue plasminogen activator followed by MT (IVT and MT

82 lation cardiac arrest and birth asphyxia and tissue plasminogen activator for ischemic stroke) have p

83 and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries (GUST

84 nts (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries [GUST

85 ing (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries moder

86 and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries moder

87 STO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Arteries) mode

88 STO (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

89 g to Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

90 the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

91 and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

92 the Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

93 and Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

94 site Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arter

95 loped a novel Ter119-polymeric NP containing tissue plasminogen activator for on-demand targeting of

96 K) liberates nitric oxide, prostacyclin, and tissue plasminogen activator from endothelial cells.

97 ransport and exocytosis of DCGs containing a tissue plasminogen activator-green fluorescent protein h

98 Patients treated with tissue plasminogen activator had approximately 30% great

99 Intravenous tissue plasminogen activator has been a cornerstone for

100 ted aspects of end-of-life treatment, use of tissue plasminogen activator, hospital spending, and len

101 of thrombolysis with intravenous recombinant tissue plasminogen activator in patients with acute isch

102 n the catalytic and thrombolytic activity of tissue plasminogen activator in vitro and ex vivo.

103 ety and efficacy of alteplase, a recombinant tissue plasminogen activator, in combination with minima

104 to obtain neuroprotection and inhibition of tissue plasminogen activator-induced brain hemorrhages.

105 ficient neuroprotective agent if given after tissue plasminogen activator-induced reperfusion.

106 hat intraischemic helium at 75 vol% inhibits tissue plasminogen activator-induced thrombolysis and su

107 ing or after ischemia, in order not to block tissue plasminogen activator-induced thrombolysis and to

108 due to the risk of inhibiting the benefit of tissue plasminogen activator-induced thrombolysis; and 2

109 which may in addition alleviate recombinant tissue-plasminogen activator-induced brain toxicity.

110 tissue factor-initiated fibrin formation and tissue-plasminogen activator-induced fibrinolysis.

111 nocyte chemotactic protein-1 (CCL2) (MCP-1), tissue plasminogen activator inhibitor (PAI-1), and regu

112 tably in the time intervals from intravenous tissue plasminogen activator initiation to groin punctur

113 at had received normal saline or recombinant tissue-plasminogen activator injections during early rep

114 ers and C-reactive protein, serum amyloid A, tissue plasminogen activator, interleukin-6, intercellul

115 After intravenous tissue plasminogen activator, intra-arterial mechanical

116 Tissue plasminogen activator is the only treatment optio

117 enecteplase, a genetically engineered mutant tissue plasminogen activator, is an alternative thrombol

118 r symptom onset with intravenous recombinant tissue plasminogen activator (IV rtPA) therapy.

119 We sought to determine if intravenous tissue plasminogen activator (IV tPA) use for acute isch

120 Although intravenous tissue plasminogen activator (IV-rtPA) was approved near

121 These patients have low tissue plasminogen activator levels and are not detectab

122 d a hyperfibrinolytic biomarker profile, low tissue plasminogen activator levels but high plasma leve

123 Tissue plasminogen activator levels were significantly i

124 ure of 20 mm Hg or greater after intravenous tissue plasminogen activator may be a clinical sign of r

125 Thrombolytic tissue plasminogen activator may be a useful adjunctive

126 Recent data indicating that lower doses of tissue plasminogen activator may be effective and safer

127 atients received daily low-dose infusions of tissue plasminogen activator (mean treatment duration, 1

128 lona data set received 0.9 mg/kg intravenous tissue plasminogen activator [mean age 69+/-12 versus 72

129 tent vascular occlusions despite intravenous tissue plasminogen activator, mechanical embolectomy app

130 n formation and plasminogen activation, with tissue plasminogen activator-mediated lysis being more e

131 ed five methods for evaluating the effect of tissue plasminogen activator on death among 6,269 ischem

132 of symptom onset followed by intra-arterial tissue plasminogen activator or EKOS ultrasound plus int

133 ia" AND "thrombolysis" OR "fibrinolysis" OR "tissue plasminogen activator" OR "streptokinase" OR "uro

134 vated protein C alone or in combination with tissue plasminogen activator, or both, 4 hours after emb

135 d an USAT regimen of 10 to 20 mg recombinant tissue plasminogen activator over 15 hours (n=30; USAT g

136 did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in t

137 t influence either fibrinolysis (assessed by tissue plasminogen activator, plasmin-alpha2-antiplasmin

138 rombin complex, plasmin-antiplasmin complex, tissue plasminogen activator, plasminogen activator inhi

139 racranial thrombus to alteplase (recombinant tissue plasminogen activator), potentially facilitating

140 Activating MMP gelatinases with tissue plasminogen activator potentiated cue-induced rei

141 ts (NMDA or glycine) and the serine protease tissue plasminogen activator, previously shown to potent

142 th and without ACE-I increased the amount of tissue plasminogen activator protein detected in mesangi

143 oagulation, partly caused by hypoxia induced tissue plasminogen activator release.

144 Intravenous administration of recombinant tissue plasminogen activator remains the most beneficial

145 ly administration of intravenous recombinant tissue plasminogen activator (rt-PA) after ischaemic str

146 or thrombolysis with intravenous recombinant tissue plasminogen activator (rt-PA) are discussed.

147 lusion for 3 hours, administered recombinant tissue plasminogen activator (rt-PA) directly before rep

148 ar therapy over intravenous (IV) recombinant tissue plasminogen activator (rt-PA) has been demonstrat

149 Recombinant tissue plasminogen activator (rt-PA) is a well-character

150 recent randomized trial, weekly recombinant tissue plasminogen activator (rt-PA), 1 mg per lumen, on

151 cular level, only one drug, the thrombolytic tissue plasminogen activator (rt-PA), is approved by the

152 racterized octafluoropropane and recombinant tissue plasminogen activator (rt-PA)-loaded echogenic li

153 Recombinant tissue plasminogen activator (rt-PA, alteplase) improved

154 treatment with intravenous (IV) recombinant tissue plasminogen activator (rtPA) after mild stroke.

155 e not candidates for intravenous recombinant tissue plasminogen activator (rtPA) because their sympto

156 tent retrievers with intravenous recombinant tissue plasminogen activator (rtPA) compared with rtPA a

157 Clinical application of recombinant tissue plasminogen activator (rtPA) for stroke is limite

158 As thrombolysis with recombinant tissue plasminogen activator (rtPA) is a standard of car

159 d its potential interaction with recombinant tissue Plasminogen Activator (rtPA) makes it a candidate

160 ulation benefit of intravascular recombinant tissue plasminogen activator (rtPA) on functional outcom

161 atients treated with intravenous recombinant tissue plasminogen activator (rtPA) within 4(1/2) hours

162 GPIb, of the thrombolytic agent recombinant tissue plasminogen activator (rtPA), and of the GPIIb/II

163 acute ischemic stroke who were treated with tissue plasminogen activator, shorter door-to-needle tim

164 neligible for (or refractory to) intravenous tissue plasminogen activator should be treated with the

165 sue plasminogen activator start; intravenous tissue plasminogen activator start to randomization; ran

166 computed tomography (CT); CT to intravenous tissue plasminogen activator start; intravenous tissue p

167 l independence when treated with intravenous tissue plasminogen activator (t-PA) alone.

168 nts for 3 days: double placebo, intrapleural tissue plasminogen activator (t-PA) and DNase, t-PA and

169 Plasma tissue plasminogen activator (t-PA) and plasminogen-acti

170 active protein, an acute phase reactant, and tissue plasminogen activator (t-PA) antigen, a marker of

171 aimed to assess associations of circulating tissue plasminogen activator (t-PA) antigen, D-dimer and

172 used after the administration of intravenous tissue plasminogen activator (t-PA) for patients with mo

173 and vasa vasora were recently shown to store tissue plasminogen activator (t-PA) in vesicles.

174 eight heparin is not recommended, although a tissue plasminogen activator (t-PA) is recommended to re

175 Currently, tissue plasminogen activator (t-PA) is the only approved

176 Expression levels of tissue plasminogen activator (t-PA) mRNA and protein wer

177 individual variability exists in response to tissue plasminogen activator (t-PA) treatment in the acu

178 , interleukin-6, fibrinogen, fibrin D-dimer, tissue plasminogen activator (t-PA), leukocyte elastase,

179 Sympathetic neurons synthesize and release tissue plasminogen activator (t-PA).

180 to improve current thrombolytic therapy with tissue plasminogen activator (t-PA).

181 oke in male C57bl/6 mice, thrombolysis using tissue-plasminogen activator (t-PA) reduced injury and i

182 th factor, fatty acid-binding protein 4, and tissue plasminogen activator [t-PA]) as IR biomarkers.

183 ase) and novel (adiponectin, E-selectin, and tissue plasminogen activator [t-PA]) parameters.

184 (intraarterial thrombolysis with recombinant tissue plasminogen activator [t-PA], mechanical clot dis

185 I-1(-/-) mice, administration of recombinant tissue plasminogen activator (tenecteplase, 5 mg/kg) wor

186 helium interacts with the thrombolytic drug tissue plasminogen activator, the only approved therapy

187 not be administered before or together with tissue plasminogen activator therapy due to the risk of

188 safety tests, such as the d-dimer and/or the tissue plasminogen activator-to-plasminogen activator in

189 -treated mice, i.e. reduction of recombinant tissue-plasminogen activator toxicity through BSc2118 di

190 ory activities of the fibrinolysis protease, tissue plasminogen activator tPA, without effects on hem

191 and simultaneously binds plasminogen and its tissue plasminogen activator tPA.

192 ged neuropeptide-Y (NPY) (within 200 ms) and tissue plasminogen activator (tPA) (over many seconds) i

193 n or from the fibrin-enhanced stimulation of tissue plasminogen activator (tPA) activation of plasmin

194 We show that acute stress modulates tissue plasminogen activator (tPA) activity in the hippo

195 erwent endovascular therapy plus intravenous tissue plasminogen activator (tPA) administration versus

196 o randomized treatment with intravenous (IV) tissue plasminogen activator (tPA) alone versus IV tPA +

197 othelial cells by assembling plasminogen and tissue plasminogen activator (tPA) and accelerating the

198 the regulation of 2 fibrinolytic parameters, tissue plasminogen activator (tPA) and its physiological

199 nd tissue were collected at day 1 to measure tissue plasminogen activator (tPA) and plasminogen activ

200 Lysis by tissue plasminogen activator (tPA) and plasminogen or pl

201 s have indicated that elevated levels of the tissue plasminogen activator (tPA) and the urokinase pla

202 ified in nr cerebellum a 10-fold increase in tissue plasminogen activator (tPA) as a key component of

203 e of profibrinolytic enzymes, urokinase, and tissue plasminogen activator (TPA) as a source for plasm

204 targeted delivery and controlled release of tissue plasminogen activator (tPA) at the thrombus site.

205 experience-dependent proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in

206 Experience-dependent proteolytic activity of tissue plasminogen activator (tPA) becomes restricted in

207 by neural activation through a reduction in tissue plasminogen activator (tPA) caused by upregulatio

208 time and recipient WIT along with the use of tissue plasminogen activator (tPA) flush during DCD proc

209 A study on the use of tissue plasminogen activator (tPA) following cerebrovasc

210 Tissue plasminogen activator (tPA) for acute ischemic st

211 angio-oedema is a recognised complication of tissue plasminogen activator (tPA) for ischaemic stroke.

212 n (HT) is a major factor limiting the use of tissue plasminogen activator (tPA) for stroke patients.

213 rrhage is the primary factor limiting use of tissue plasminogen activator (tPA) for stroke.

214 Because tissue plasminogen activator (tPA) has been implicated i

215 Thrombolysis using tissue plasminogen activator (tPA) has been the key trea

216 Earlier administration of intravenous tissue plasminogen activator (tPA) in acute ischemic str

217 Thrombolytic therapy using tissue plasminogen activator (tPA) in acute stroke is as

218 diffusion-advection model of thrombolysis by tissue plasminogen activator (TPA) in an occluded vessel

219 rsy surrounds the safety of intravenous (IV) tissue plasminogen activator (tPA) in ischemic stroke pa

220 The benefits of intravenous tissue plasminogen activator (tPA) in patients with acut

221 ted time window available for treatment with tissue plasminogen activator (tPA) in patients with acut

222 Tissue plasminogen activator (tPA) is a serine protease

223 Tissue Plasminogen Activator (tPA) is a serine protease

224 Here, we show that the expression of tissue plasminogen activator (tPA) is increased in glial

225 Intravenous tissue plasminogen activator (tPA) is known to improve o

226 Intravenous tissue plasminogen activator (tPA) is known to improve o

227 rombolytic treatment of ischemic stroke with tissue plasminogen activator (tPA) is markedly limited o

228 within 200 ms after fusion, whereas labeled tissue plasminogen activator (tPA) is often discharged o

229 Although tissue plasminogen activator (tPA) is primarily responsi

230 Tissue plasminogen activator (tPA) is the only FDA-appro

231 ayed thrombolytic treatment with recombinant tissue plasminogen activator (tPA) may exacerbate blood-

232 Tissue plasminogen activator (tPA) modulates the NF-kapp

233 tide, Glu-Glu-Iso-Iso-Met-Asp (EEIIMD), with tissue plasminogen activator (tPA) on infarct volume and

234 n administered alone and in combination with tissue plasminogen activator (tPA) on measures of ischem

235 EPITHET randomized patients to tissue plasminogen activator (tPA) or placebo, and all D

236 , including Weibel-Palade bodies (WPBs), the tissue plasminogen activator (tPA) organelle, and the ty

237 the intracellular signaling events by which tissue plasminogen activator (tPA) promotes renal inters

238 rain hemorrhage is a serious complication of tissue plasminogen activator (tPA) therapy for ischemic

239 arteries remains the aim of intravenous (IV) tissue plasminogen activator (tPA) therapy in acute isch

240 lasminogen and enhances its association with tissue plasminogen activator (tPA) thereby enhancing pla

241 middle cerebral artery occlusion (MCAO) with tissue plasminogen activator (tPA) to assess inhibition

242 est primary stroke center had on intravenous tissue plasminogen activator (tPA) use in Chicago, Illin

243 t decade have increased rates of intravenous tissue plasminogen activator (tPA) use in the United Sta

244 The second aim showed that administration of tissue plasminogen activator (tPA) using a standard dose

245 n combination studies with the thrombolytic, tissue plasminogen activator (tPA) using a standard intr

246 etable, heparin-triggered release system for tissue plasminogen activator (tPA) was designed to preve

247 evolved from the initial use of intravenous tissue plasminogen activator (tPA) within 3 hours of sym

248 of patients with acute ischemic stroke with tissue plasminogen activator (tPA) within 4.5 hours of s

249 rotein concentration in the nr cerebellum of tissue plasminogen activator (tPA), a gene closely linke

250 mutant mouse's 10-fold-increased cerebellar tissue plasminogen activator (tPA), a part of the tPA/pl

251 Tissue plasminogen activator (tPA), a secreted serine pr

252 Here, we show that tissue plasminogen activator (tPA), a serine protease im

253 252a (100 nm), and tPA STOP, an inhibitor of tissue plasminogen activator (tPA), an enzyme involved i

254 PAI-1 inhibits the activity of tissue plasminogen activator (tPA), an enzyme that cleav

255 In this study, we show that tissue plasminogen activator (tPA), an extracellular pro

256 n, tissue factor, fibrinogen-like protein 2, tissue plasminogen activator (tPA), and plasminogen acti

257 erexpress annexin II (ANXII), a receptor for tissue plasminogen activator (tPA), and plasminogen, the

258 ysis by down-regulating the serine protease, tissue plasminogen activator (tPA), and up-regulating pl

259 Matrix metalloproteinase (MMP)-9, tissue plasminogen activator (tPA), and urokinase plasmi

260 sion and secretion of fibronectin, myocilin, tissue plasminogen activator (tPA), and/or matrix metall

261 Indeed, plasmin generation by tissue plasminogen activator (tPA), but not streptokinas

262 Emerging evidence suggests that tissue plasminogen activator (tPA), currently the only F

263 ay 7, and peritoneal fluid concentrations of tissue plasminogen activator (tPA), d-dimer, thrombin-an

264 hed fibrin more resistant to fibrinolysis by tissue plasminogen activator (tPA), exacerbating the pro

265 ime international normalized ratio, D-dimer, tissue plasminogen activator (tPA), plasminogen activato

266 activated partial prothrombin time, D-dimer, tissue plasminogen activator (tPA), plasminogen activato

267 e measure of platelet activation) and plasma tissue plasminogen activator (tPA), plasminogen-activato

268 lasminogen (Pg) binding and/or activation by tissue plasminogen activator (tPA), reduced plasmin-medi

269 Tissue plasminogen activator (tPA), which is reduced in

270 Constructs of herstatin and modified tissue plasminogen activator (tPA)-herstatin were expres

271 KA1 levels in tissue plasminogen activator (tPA)-KO mice were also unc

272 elivery system for site-specific delivery of tissue plasminogen activator (tPA).

273 CTI, and fibrinolysis was induced by adding tissue plasminogen activator (tPA).

274 ugh the use of a fibrinolytic enzyme such as tissue plasminogen activator (tPA).

275 care, which includes the use of intravenous tissue plasminogen activator (tPA).

276 hat the clearance of the core protein by the tissue plasminogen activator (tPA)/plasmin proteolytic s

277 activator inhibitor-1 (PAI-1, SERPINE1) and tissue plasminogen activator (tPA, PLAT), such as PAI-1

278 icted to bind fibrinogen D fragment close to tissue plasminogen activator (tPA; residues gamma312-324

279 termined safety and efficacy of late APC and tissue-plasminogen activator (tPA) administrations in a

280 The benefits of intravenous tissue-plasminogen activator (tPA) in acute ischemic str

281 Here we show that tissue-plasminogen activator (tPA), a protease implicate

282 f atherothrombosis (fibrin, antithrombin and tissue plasminogen activator [tPA]) and endothelial acti

283 ovascular vs 38% [27 of 70] intravenous [IV] tissue-plasminogen activator [tPA]; relative risk, 1.07

284 ere more frequent in placebo vs. recombinant tissue plasminogen activator-treated groups (p=.03 and p

285 in 13.6% of placebo and 6.4% of recombinant tissue plasminogen activator-treated patients (p=.37).

286 reatment with BSc2118 and YC1 in recombinant tissue-plasminogen activator-treated animals was in the

287 increased in saline-treated and recombinant tissue-plasminogen activator-treated mice after BSc2118

288 ] years) and had higher rates of intravenous tissue plasminogen activator treatment (174 [74.4%] vs 1

289 Outcomes after intravenous tissue plasminogen activator treatment via telemedicine

290 ted Tomographic Score (ASPECTS), intravenous tissue plasminogen activator treatment, and time from LK

291 ment has made it from bench to bedside since tissue plasminogen activator was introduced in 1996.

292 plasmin or a combination of plasminogen and tissue plasminogen activators were included in clotting

293 ccharides released from recombinant TNK-tPA (tissue plasminogen activator) were derivatized with 5-am

294 oglobin, serum amyloid P, procalcitonin, and tissue plasminogen activator) were significantly higher

295 HSF1 reduced statin-induced upregulation of tissue plasminogen activator, whereas downregulation of

296 okinase-type plasminogen activator (uPA) and tissue plasminogen activator, which binds tightly to the

297 nal revascularization success using low-dose tissue plasminogen activator within 3 h of symptom onset

298 Six patients (4%) received intravenous tissue plasminogen activator without complications.

299 nsferred patients suggested that intravenous tissue plasminogen activator would be delayed by 12 minu

300 20-mile radius from onset, then intravenous tissue plasminogen activator would be delayed by 7 minut