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

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

2 ions correlated significantly with levels of tissue plasminogen activator.

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

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

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

6 revented plasma clot fibrinolysis induced by tissue plasminogen activator.

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

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

9 erine protease plasmin by staphylokinase and tissue plasminogen activator.

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

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

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

13 e thrombolytic and proteolytic properties of tissue plasminogen activator.

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

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

16 Between 2000 and 2001, 212 patients received tissue plasminogen activator.

17 e conformation to bind to the target enzyme, tissue plasminogen activator.

18 hin 100 s and retained significant levels of tissue plasminogen activator.

19 sidered marginal compared with urokinase and tissue plasminogen activator.

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

21 eers to investigate whether hypoxia releases tissue plasminogen activator.

22 cal sign of recanalization after intravenous tissue plasminogen activator.

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

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

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

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

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

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

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

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

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

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

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

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

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 roteases urokinase plasminogen activator and tissue plasminogen activator and down-regulation of the

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 utant may result in uncontrolled activity of tissue plasminogen activator, and so explain the epilept

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

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

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

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

60 ogen, fibrin D-dimer, von Willebrand factor, tissue plasminogen activator antigen, factor VII, prothr

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

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

63 Urokinase and recombinant tissue plasminogen activator are the currently available

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

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

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

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

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

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

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

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

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

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

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

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

76 A central tenet of fibrinolysis is that tissue plasminogen activator-dependent (t-PA- dependent)

77 2 to the cell surface dramatically increases tissue plasminogen activator-dependent plasminogen activ

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

79 Intravenous tissue plasminogen activator did not impact outcomes.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 orescently labelled neuropeptide Y (NPY) and tissue plasminogen activator from single granules.

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

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

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 Despite the barriers to the use of tissue plasminogen activator in the treatment of patient

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Tissue plasminogen activator levels were significantly i

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

123 Thrombolytic tissue plasminogen activator may be a useful adjunctive

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

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

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

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

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

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

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

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

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

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

134 n caused a dose-dependent increase in plasma tissue plasminogen activator (P<0.0001) that was suppres

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

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

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

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

139 defective in its inhibitory activity against tissue plasminogen activator relative to its wild-type c

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

141 anules in small fractions of a second, while tissue plasminogen activator remained in open granules f

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 fibrinolytic co-receptor for plasminogen and tissue plasminogen activator that stimulates activation

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

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

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

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

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

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

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

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

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

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

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

193 Two secretory proteins, tissue plasminogen activator (tPA) and brain-derived neu

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

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

196 was assayed by zymography, and expression of tissue plasminogen activator (tPA) and plasminogen activ

197 Plasma membrane receptors for tissue plasminogen activator (tPA) and plasminogen conce

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

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

200 ed the role of plasminogen activators (PAs) [tissue plasminogen activator (tPA) and urokinase plasmin

201 , we evaluated the relationships of elevated tissue plasminogen activator (tPA) antigen and D-dimer w

202 Although thrombolytic effects of tissue plasminogen activator (tPA) are beneficial, its n

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

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

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

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

209 Tissue plasminogen activator (tPA) for acute ischemic st

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

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

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

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

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

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

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

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

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

219 We have previously demonstrated that tissue plasminogen activator (tPA) in the amygdala promo

220 en activation, thereby predicting a role for tissue plasminogen activator (tPA) in this form of stres

221 I-1, a urokinase plasminogen activator (uPA)/tissue plasminogen activator (tPA) inhibitor.

222 Tissue plasminogen activator (tPA) is a secreted proteas

223 Tissue plasminogen activator (tPA) is a serine protease

224 Tissue Plasminogen Activator (tPA) is a serine protease

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

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

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

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

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

230 Although tissue plasminogen activator (tPA) is primarily responsi

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

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

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

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

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

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

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

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

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

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

241 1.5 to 4.5 hours) after standard intravenous tissue plasminogen activator (tPA) therapy.

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

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

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

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

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

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

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

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

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

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

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

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

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

255 252a (100 nm), and tPA STOP, an inhibitor of tissue plasminogen activator (tPA), an enzyme involved i

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

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

258 gen, low activated protein C ratio, D-dimer, tissue plasminogen activator (tPA), and plasminogen acti

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

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

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

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

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

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

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

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

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

268 re susceptibility is modulated by the enzyme tissue plasminogen activator (tPA), the normal physiolog

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

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

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

272 d transcriptional target of ELK-1, the human tissue plasminogen activator (tPA).

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

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

275 elivery system for site-specific delivery of 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 termined safety and efficacy of late APC and tissue-plasminogen activator (tPA) administrations in a

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

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

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

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

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

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

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

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

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

288 Outcomes after intravenous tissue plasminogen activator treatment via telemedicine

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

290 The folding of a variant of tissue plasminogen activator (v-tPA), a protein containi

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