ライフサイエンスコーパス: t-PA

1 t-PA also induced marked shape changes in both brain end

2 t-PA caused a concentration-dependent increase in permea

3 t-PA induces SK-N-SH cell proliferation via binding to G

4 t-PA inhibition markedly reduced contraction of the guin

5 r basal (P<0.02) and SP-stimulated (P=0.059) t-PA production but similar basal and stimulated PAI-1 p

6 ion suggested a risk model including IL-1ra, t-PA, and the Framingham Offspring Study T2D score, but

7 al score of multiple markers [interleukin-6, t-PA, intercellular adhesion molecule 1, and lipoprotein

8 endent anion channel (VDAC), which is also a t-PA-binding protein in these cells.

9 Binding of t-PA to VDAC occurs between a t-PA fibronectin type I finger domain located between am

10 milar inhibition, implying a role for both a t-PA receptor, most likely a low-density lipoprotein rec

11 ity is the result of a mechanism involving a t-PA lysine-dependent binding site in the GRP78 amino ac

12 thin two hours after the administration of a t-PA bolus occurred in 31 patients in the target group (

13 90 min TIMI 3 flow are use of an accelerated t-PA regimen (vs. streptokinase containing regimens) (ch

14 ndicate that ultrasound exposure accelerates t-PA binding, alters binding affinity, and increases max

15 D646E]Glu-Pg, by either tissue Pg activator (t-PA) or urokinase (u-PA) were compared when these Pg fo

16 A), as well as by added tissue Pg Activator (t-PA), suggesting that ADA and Pg bind simultaneously to

17 AR(-)(/-)), or tissue plasminogen activator (t-PA(-)(/-)), and in control wild-type (WT) mice.

18 th intravenous tissue plasminogen activator (t-PA) alone.

19 , intrapleural tissue plasminogen activator (t-PA) and DNase, t-PA and placebo, or DNase and placebo.

20 Plasma tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1)

21 Plasma tissue plasminogen activator (t-PA) and plasminogen-activator inhibitor 1 antigen and

22 doses of tissue-type plasminogen activator (t-PA) and recombinant tissue-type plasminogen activator

23 reactant, and tissue plasminogen activator (t-PA) antigen, a marker of endothelial dysfunction, even

24 of circulating tissue plasminogen activator (t-PA) antigen, D-dimer and von Willebrand factor (VWF) w

25 fragment 1+2, tissue plasminogen activator (t-PA) antigen, t-PA-plasminogen-activator inhibitor type

26 nolytic factor tissue plasminogen activator (t-PA) are unknown.

27 of why plasmin/tissue plasminogen activator (t-PA) can both activate and deactivate platelets prior t

28 Tissue-type plasminogen activator (t-PA) can modulate permeability of the neurovascular uni

29 2J2, increased tissue plasminogen activator (t-PA) expression by 2.5-fold without affecting plasminog

30 of intravenous tissue plasminogen activator (t-PA) for patients with moderate-to-severe acute ischemi

31 of plasmin by tissue plasminogen activator (t-PA) in the presence of APL cells that did or did not h

32 shown to store tissue plasminogen activator (t-PA) in vesicles.

33 lasminogen and tissue plasminogen activator (t-PA) independently at the cell surface, thereby enhanci

34 protease tissue-type plasminogen activator (t-PA) initiates the fibrinolytic protease cascade and pl

35 o release tissue-type plasminogen activator (t-PA) is critical for effective endogenous fibrinolysis.

36 ed, although a tissue plasminogen activator (t-PA) is recommended to restore patency to occluded cath

37 Currently, tissue plasminogen activator (t-PA) is the only approved thrombolytic drug for ischemi

38 sion levels of tissue plasminogen activator (t-PA) mRNA and protein were significantly decreased in N

39 DAC binds tissue-type plasminogen activator (t-PA) on human neuroblastoma SK-N-SH cells.

40 xes, with tissue-type plasminogen activator (t-PA) or urokinase (u-PA) resulted in rapid decreases of

41 leaved by tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA).

42 mbolysis using tissue-plasminogen activator (t-PA) reduced injury and improved motor deficits, but di

43 y release tissue-type plasminogen activator (t-PA) represents an important endogenous defence mechani

44 iates the tissue-type plasminogen activator (t-PA) response to exogenous bradykinin.

45 Stroke (NINDS) tissue plasminogen activator (t-PA) Stroke Trial to examine the relationship between a

46 in response to tissue plasminogen activator (t-PA) treatment in the acute phase of ischemic stroke.

47 Bowes melanoma tissue-plasminogen activator (t-PA) were found to possess Galbeta1-->4GlcNAcbeta1-->,

48 d reduced-dose tissue plasminogen activator (t-PA) will enhance infarct artery patency at 60 min in p

49 e treated with tissue plasminogen activator (t-PA) within three hours after the onset of symptoms of

50 nase (SK), and tissue plasminogen activator (t-PA)) in plasma samples are described.

51 clots such as tissue plasminogen activator (t-PA), connective tissue activation peptide III (CTAP II

52 Tissue-type plasminogen activator (t-PA), for example, possesses exquisitely stringent subs

53 n, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor n

54 ibrin D-dimer, tissue plasminogen activator (t-PA), leukocyte elastase, and lipoprotein(a) (all P<0.0

55 ence with tissue-type plasminogen activator (t-PA), which proved little better than streptokinase in

56 binds the tissue-type plasminogen activator (t-PA), which results in a decrease in K(m) and an increa

57 ze and release tissue plasminogen activator (t-PA).

58 ose thrombi to tissue plasminogen activator (t-PA).

59 celerated tissue-type plasminogen activator (t-PA).

60 tor (u-PA) and tissue plasminogen activator (t-PA).

61 c therapy with tissue plasminogen activator (t-PA).

62 cclusion, tissue-type plasminogen activator (t-PA; 1.42 mg/kg) was given intravenously over 90 minute

63 lg activator (u-PA) or tissue Plg activator (t-PA).

64 lytic factors (tissue plasminogen activator [t-PA] and plasminogen activator inhibitor-1 [PAI-1]) are

65 protein 4, and tissue plasminogen activator [t-PA]) as IR biomarkers.

66 -selectin, and tissue plasminogen activator [t-PA]) parameters.

67 th recombinant tissue plasminogen activator [t-PA], mechanical clot disruption or retrieval, or a com

68 including tissue-type plasminogen activator [t-PA], plasminogen activator inhibitor type 1 [PAI-I]),

69 dest reductions in bradykinin-induced active t-PA release (reduced by 37%, p = 0.03) and had a marked

70 (Group II); or 3) full-dose, weight-adjusted t-PA (Group III).

71 ified A2M serum levels at baseline and after t-PA infusion, but not mRNA expression or protein struct

72 fected FXII activity both prior to and after t-PA treatment.

73 ransformation (HT) and mortality rates after t-PA.

74 reduced inhibitory activity of PAI-1 against t-PA but not u-PA suggested that the mechanism of loop i

75 asmin inhibitor, antibodies directed against t-PA and u-PA, and epsilon-aminocaproic acid, a lysine a

76 ase tissue plasminogen activator (alteplase, t-PA), and have prolonged half-life features permitting

77 lysis of retrieved thrombi with DNase 1 and t-PA.

78 , for example GLUT-1, MT-1, CELF, MKP-1, and t-PA did not show any hypoxic regulation in either astro

79 azard ratio [HR] 1.28, 95% CI 1.03-1.59) and t-PA (HR 1.30, 1.02-1.65) were associated with incident

80 peak at 14:00 hours, CRP at 15:00 hours, and t-PA at 10:00 hours with diurnal variations of 10%, 34%,

81 ement by specific blood measures (lipids and t-PA).

82 The interactions between NSP and t-PA were distinct from those between plasmin and NSP, w

83 The r-PA and t-PA strategies yielded similar survival outcomes after

84 tial fibrosis in Pg(-)(/-), u-PA(-)(/-), and t-PA(-)(/-) mice relative to WT and u-PAR(-)(/-) mice.

85 We demonstrate that both Pg and t-PA serve as a bridge between GRP78 and VDAC bringing t

86 Pg(-)(/-) and t-PA(-)(/-) mice demonstrated an enhanced increase in lu

87 exin II-mediated assembly of plasminogen and t-PA on monocyte/macrophages contributes to plasmin gene

88 xin II (Ann-II) as a co-receptor for Plg and t-PA that promotes and localizes plasmin generation near

89 sted odds of elevated C-reactive protein and t-PA (highest tertile versus lowest tertile) were 0.56 (

90 was Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) bleeding.

91 the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) criteria.

92 the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) definition.

93 the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO)-III Trial.

94 1.65) were associated with incident T2D, and t-PA predicted 5-year transition to hyperglycemia (odds

95 ivity and protein levels of tetranectin, and t-PA and its endogenous inhibitor PAI-1, were subsequent

96 (CRP), tissue plasminogen activator antigen (t-PA) and von Willebrand factor are associated with inci

97 ; the plasma concentrations of t-PA antigen, t-PA-PAI-1 complex, D-dimer, and plasmin-antiplasmin com

98 tissue plasminogen activator (t-PA) antigen, t-PA-plasminogen-activator inhibitor type 1 (PAI-1) comp

99 PT, PTT, Va, VIIIa, PC aPC t-PA, and D-dimer levels were assayed.

100 ke, continuous transcranial Doppler augments t-PA-induced arterial recanalization, with a nonsignific

101 Basal t-PA/PAI-1 molar ratio was significantly reduced in smok

102 y irreversible acyl-enzyme complexes between t-PA and PAI-1, suggesting that the physiologic effect o

103 The interactions between t-PA and NSP contrast with the formation of long-lived,

104 solute difference in mortality rates between t-PA and r-PA progressively narrowed over the predetermi

105 rinolysis in an in vitro system activated by t-PA, the results being used as measures of binding affi

106 tease catalytic triad.) Glu-Pg activation by t-PA was enhanced on HUVEC compared with the solution ph

107 es that were labile to selective cleavage by t-PA or u-PA when in the context of a peptide were intro

108 Lysis of intact fibrin is initiated by t-PA, and uPA activates the remaining plasminogens.

109 generated on the cell surface selectively by t-PA, modulates the astrocytic cytoskeleton, leading to

110 periodontal cases compared with non-cases), t-PA (11% higher), and LDL-C (11% higher).

111 activity of both single-chain and two-chain t-PA (sct-PA and tct-PA).

112 he catalytic efficiency of mature, two-chain t-PA toward plasminogen in the absence of a fibrin co-fa

113 Kinetic constants of Chromozym t-PA (MeSO(2)-D-Phe-Gly-Arg-pNA) hydrolysis at various p

114 ctor IX and amidolytic activity of Chromozym t-PA with IC50 values of 1.6 +/- 1.2, 3.5 +/- 0.3, and 8

115 al lysis of a fibrin-containing plasma clot, t-PA-dependent plasmin generation at the endothelial cel

116 Combined t-PA-DNase therapy was associated with a reduction in th

117 blood-sampled for fibrinogen, D-dimer, CRP, t-PA, and von Willebrand factor.

118 that tissue plasminogen activator-dependent (t-PA- dependent) conversion of plasminogen to active pla

119 ssue plasminogen activator (t-PA) and DNase, t-PA and placebo, or DNase and placebo.

120 in apart) with a 48-h infusion and half-dose t-PA (Group II) is associated with improved quality and

121 bound to the cell in the presence of either t-PA or u-PA, conversion to Lys-Pg was observed, but con

122 oke were randomly assigned to receive either t-PA or placebo.

123 , stepwise analyses identified only elevated t-PA and low HDL cholesterol levels as significant (P </

124 nhibition increases constitutive endothelial t-PA release through endogenous bradykinin.

125 is that ACE inhibition increases endothelial t-PA release through endogenous bradykinin.

126 Net endothelial t-PA release was determined in vivo in response to intra

127 Net endothelial t-PA release was determined in vivo, in response to intr

128 Net endothelial t-PA release was significantly blunted with age in the s

129 cute oestrogen administration on endothelial t-PA release in postmenopausal women.

130 he acute effects of oestrogen on endothelial t-PA release, bradykinin and sodium nitroprusside dose-r

131 Regulated endothelial t-PA release declines with age in sedentary men.

132 smin generation in the presence of exogenous t-PA, and this activity was largely attributable to anne

133 with alterations in EC-derived fibrinolytic (t-PA) and antithrombotic (TFPI-1) factors.

134 nding odds ratios were 1.07 (0.99, 1.14) for t-PA antigen, 1.06 (1.00, 1.13) for D-dimer and 1.08 (1.

135 tor; 9% for D-dimer, 1% for CRP, and 16% for t-PA.

136 usted odds ratios were 1.13 (1.06, 1.21) for t-PA antigen (13 studies, 5494 cases), 1.23 (1.16, 1.32)

137 tes were 9.1% for SK with hirudin, 10.3% for t-PA with hirudin, 10.5% for t-PA with heparin and 14.9%

138 er baseline level were 1.25 (1.18, 1.33) for t-PA antigen, 1.01 (0.95, 1.07) for D-dimer and 1.11 (1.

139 udin, 10.3% for t-PA with hirudin, 10.5% for t-PA with heparin and 14.9% for SK with heparin (for tre

140 ocessing delay is particularly important for t-PA.

141 II peptide mimicking sequences necessary for t-PA binding blocked endothelial cell invasion of Matrig

142 than in GUSTO-I, in which mortality rate for t-PA versus streptokinase between 30 days and 1-year was

143 chemia-induced LRP, a signaling receptor for t-PA.

144 ystemic inflammation augmented local forearm t-PA release in men, which suggests that acute inflammat

145 Furthermore, vasa deferentia from t-PA-null mice were hyporesponsive to EFS (P<0.0001) but

146 Notably, hearts from t-PA-null mice released much less NE upon EFS than their

147 ke outcome at 3 months in patients not given t-PA.

148 lts in accelerated Pg activation when GRP78, t-PA, and Pg are bound together.

149 ncreased carotid and femoral IMTs and higher t-PA and PAI-I levels, indicating vascular damage and pe

150 However, t-PA does not always result in efficient thrombus dissol

151 hmias were significantly reduced (P<0.05) in t-PA-null hearts.

152 The increase in t-PA activity is the result of a mechanism involving a t

153 e highest dose of bradykinin the increase in t-PA antigen release was approximately 35 % less (P < 0.

154 This increase in t-PA expression correlated with a 4-fold induction in t-

155 gene transcription and a 3-fold increase in t-PA fibrinolytic activity and was blocked by the CYP in

156 ions, which was associated with increases in t-PA (29%; P=0.03) and decreases in PAI-1 (48%; P=0.01)

157 ession correlated with a 4-fold induction in t-PA gene transcription and a 3-fold increase in t-PA fi

158 pe (hemorrhage and fibrosis) was observed in t-PA(-)(/-) and Pg(+/-) mice.

159 to ischemia/reperfusion was much smaller in t-PA-null than in WT control mice (P<0.01).

160 An inactive t-PA variant inhibited the t-PA-mediated increase in per

161 in C supplementation significantly increased t-PA release in overweight/obese adults (from 0.2 +/- 0.

162 significantly potentiated bradykinin-induced t-PA release.

163 nd had a marked impairment of SFLLRN-induced t-PA antigen (p = 0.02) and activity (p = 0.006) release

164 Intrapleural t-PA-DNase therapy improved fluid drainage in patients w

165 ve endovascular therapy, and 181 intravenous t-PA.

166 with endovascular therapy after intravenous t-PA, as compared with intravenous t-PA alone.

167 in the endovascular-therapy and intravenous t-PA groups were similar for mortality at 90 days (19.1%

168 cular therapy and 2.75 hours for intravenous t-PA (P<0.001).

169 We conclude that the efficacy of intravenous t-PA in patients with acute ischemic stroke may be enhan

170 ditional endovascular therapy or intravenous t-PA alone, in a 2:1 ratio.

171 bination of these approaches) or intravenous t-PA.

172 my with the stent retriever plus intravenous t-PA reduced disability at 90 days over the entire range

173 o were receiving or had received intravenous t-PA to continue with t-PA alone (control group) or to u

174 igible patients who had received intravenous t-PA within 3 hours after symptom onset to receive addit

175 In patients receiving intravenous t-PA for acute ischemic stroke due to occlusions in the

176 approach is more effective than intravenous t-PA alone is uncertain.

177 rapy group (30.4%) and 63 in the intravenous t-PA group (34.8%) were alive without disability (odds r

178 endovascular therapy and 222 to intravenous t-PA alone).

179 hemorrhage, and the response to intravenous t-PA therapy.

180 stent retriever, in addition to intravenous t-PA, increases reperfusion rates and may improve long-t

181 travenous t-PA, as compared with intravenous t-PA alone.

182 the middle cerebral artery with intravenous t-PA within three hours after the onset of symptoms.

183 erior to standard treatment with intravenous t-PA.

184 ovascular therapy and 38.7% with intravenous t-PA; absolute adjusted difference, 1.5 percentage point

185 in the t-PA window who are ineligible for IV t-PA but have a large vascular occlusion.

186 ng a mouse model of ischemic stroke and late t-PA intervention, the neuroprotective activity of a mur

187 e alpha, MT-1, MKP-1, CELF, 12-lipoxygenase, t-PA, CAR-1, and an expressed sequence tag.

188 Marked, rapid local t-PA release occurred in response to isoproterenol, a be

189 d 1.33 microg/kg per min infusion with 50 mg t-PA (Group I); 2) 180/90 (10 min apart) and 2.0 g/kg pe

190 0 min apart) and 2.0 g/kg per min with 50 mg t-PA (Group II); or 3) full-dose, weight-adjusted t-PA (

191 33 microg/kg per min eptifibatide with 50 mg t-PA: 65% and 78% at 60 and 90 min, respectively.

192 o g/min) on forearm blood flow (FBF) and net t-PA release before and during intra-arterial infusion o

193 ponse, shifting the relationship between net t-PA release and FBF (P=0.005).

194 release, with a 96% reduction in overall net t-PA antigen release.

195 laprilat significantly increased resting net t-PA release (from 0.6+/-0.4 to 1.7+/-0.6 ng. min(-1) x

196 odermal cell line, the possibility of neural t-PA interacting with the L2/HNK-1-recognizing molecule,

197 s, and compatible with the release of neural t-PA into their walls.

198 After the incubation, basal NO, t-PA, PAI-1, TF, TFPI-1 production, and substance P (SP)

199 duction, and substance P (SP)-stimulated NO, t-PA, and PAI-1 production were determined.

200 lative arterial stasis and near abolition of t-PA release will strongly promote clot propagation and

201 safely enhance the thrombolytic activity of t-PA.

202 in addition to a significant augmentation of t-PA antigen (45 +/- 9 ng/100 ml/min at peak dose vs. 24

203 hese results indicate a sustained benefit of t-PA for such patients.

204 Binding of t-PA to VDAC induced a decrease in K(m) and an increase

205 Binding of t-PA to VDAC occurs between a t-PA fibronectin type I fi

206 The concentration of t-PA antigen correlated with that of the t-PA-PAI-1 comp

207 Concentrations of t-PA antigen, D-dimer and VWF may be more modestly assoc

208 oth increases); the plasma concentrations of t-PA antigen, t-PA-PAI-1 complex, D-dimer, and plasmin-a

209 itions, targeting the NE-releasing effect of t-PA may have valuable therapeutic potential.

210 1, suggesting that the physiologic effect of t-PA-NSP interactions may be more complex than previousl

211 This efficacy is due to the effects of t-PA and urokinase plasminogen activator (uPA).

212 We examined the effects of t-PA using in vitro models of the blood-brain barrier.

213 rasound (1) greatly augments the efficacy of t-PA-mediated thrombolysis, (2) seems safe, and (3) has

214 Confocal images reveal the extension of t-PA axons to arterioles serving heart, brain, kidney, l

215 inolytic properties through the induction of t-PA and suggest that endothelial CYP2J2 may play an imp

216 romoter is cAMP-responsive, and induction of t-PA gene transcription by EETs correlated with increase

217 Infusion of t-PA did not dissolve these MCA occlusions.

218 morrhage within 30 hours after initiation of t-PA (6.2% and 5.9%, respectively; P=0.83).

219 amples were associated with higher levels of t-PA in particular.

220 min was sequentially added to 25 or 50 mg of t-PA.

221 In the clinic, a minibolus of t-PA followed by an infusion of uPA was administered to

222 is of this important biochemical property of t-PA remains obscure.

223 Net endothelial release rates of t-PA were calculated as the product of the arteriovenous

224 stochemistry demonstrated clear reduction of t-PA in NP, primarily in the epithelium and glands.

225 A Th2-mediated reduction of t-PA might lead to excessive fibrin deposition in the su

226 y epithelial cells showed down-regulation of t-PA, suggesting a potential Th2 mechanism in NP.

227 gular aerobic exercise on the net release of t-PA across the human forearm in vivo using both cross-s

228 an age-related decline in the net release of t-PA antigen.

229 Net endothelial release of t-PA was approximately 45 % higher (P < 0.01) after (fro

230 Net release of t-PA was approximately 95% higher (P < 0.01) after (from

231 Net endothelial release of t-PA was ~30 % higher (P < 0.01) in women taking ORT (fr

232 to the substrate or inhibitor specificity of t-PA in physiologically relevant reactions.

233 ghtings confirm the existence of a system of t-PA axons that is prominent in arterioles, and compatib

234 ed the kinetic properties of new variants of t-PA that contained point mutations at position 192.

235 uring 100 ng/min bradykinin, P=0.001) and on t-PA release 14-fold (from 21.2+/-7.9 to 317.4+/-118.9 n

236 indicated a positive causal effect of IR on t-PA concentrations.

237 arker and suggested a causal effect of IR on t-PA.

238 Treatment with DNase alone or t-PA alone was ineffective.

239 fect of enalaprilat or HOE 140 on the FBF or t-PA response to methacholine.

240 losartan but not of enalapril reduced plasma t-PA (11%; P=0.003) and PAI-1 (38%; P<0.001) antigen con

241 ation of vitamin C significantly potentiated t-PA release in overweight/obese adults.

242 ated a clinical-genetic model for predicting t-PA response.

243 Our validated LR-based score predicts t-PA safety in the Spanish population.

244 flow was present in 4 of 12 cases receiving t-PA alone compared with 10 of 12 cases receiving t-PA p

245 alone compared with 10 of 12 cases receiving t-PA plus ultrasound (P=0.003).

246 Recombinant t-PA (rt-PA) induced exocytotic and carrier-mediated NE

247 Rho kinase blocked these changes and reduced t-PA/plasminogen-mediated increase in permeability.

248 serpin (NSP) is a serpin thought to regulate t-PA enzymatic activity.

249 n the capacity of the endothelium to release t-PA in healthy postmenopausal women.

250 n the capacity of the endothelium to release t-PA in overweight and obese adults.

251 s the capacity of the endothelium to release t-PA in overweight/obese adults.

252 , the capacity of the endothelium to release t-PA increased approximately 55 % (P < 0.05) to levels s

253 e successful when adding DNase 1 to standard t-PA.

254 In comparison with standard t-PA regimen, double-bolus eptifibatide (10 min apart) w

255 ell surface protein annexin II can stimulate t-PA-mediated plasminogen activation in the complete abs

256 Vitrectomy with subretinal t-PA injection and gas tamponade was found to be relativ

257 But the extension of such t-PA axons to arteries and arterioles throughout the org

258 Annexin II supported t-PA-dependent generation of cell surface plasmin and th

259 s stimulated the generation of cell-surface, t-PA-dependent plasmin twice as efficiently as the t(15;

260 The t-PA promoter is cAMP-responsive, and induction of t-PA

261 se, anti-annexin II IgG directed against the t-PA-binding tail domain inhibited plasminogen-dependent

262 erence in mortality at 12 months between the t-PA group and the placebo group (24 percent vs. 28 perc

263 found that the global statistic favored the t-PA group (odds ratio for a favorable outcome at 6 mont

264 At 1 year, the mortality rate for the t-PA-assigned group was 11.06%, and for r-PA it was 11.2

265 , mean TIMI grade flow was 0.75+/-1.4 in the t-PA alone group versus 2.58+/-0.9 in the t-PA plus ultr

266 90 minutes, the mean TIMI grade flow in the t-PA alone group was 0.92+/-1.4 compared with 2.42+/-1.9

267 he t-PA alone group versus 2.58+/-0.9 in the t-PA plus ultrasound group (P=0.001).

268 s 0.92+/-1.4 compared with 2.42+/-1.9 in the t-PA plus ultrasound group (P=0.006).

269 change in pleural opacity was greater in the t-PA-DNase group than in the placebo group (-29.5+/-23.3

270 rgical referral at 3 months was lower in the t-PA-DNase group than in the placebo group (2 of 48 pati

271 Enalaprilat increased the t-PA response to bradykinin to a greater extent than the

272 An inactive t-PA variant inhibited the t-PA-mediated increase in permeability, whereas blockade

273 Knockout of the uPA gene, but not the t-PA gene, inhibited fibrinolysis.

274 ity of the carbohydrate in the region of the t-PA active site.

275 us fibrinolysis, using one-thousandth of the t-PA concentration, is regularly lysing fibrin and induc

276 a transgenic mouse whose expressions of the t-PA promoter and enhanced green fluorescent protein are

277 of t-PA antigen correlated with that of the t-PA-PAI-1 complex in a linear regression model (squared

278 or acute ischemic stroke patients within the t-PA window who are ineligible for IV t-PA but have a la

279 r occlusion dose-dependently dissolved these t-PA-resistant thrombi resulting in fast restoration of

280 Thus, t-PA enhances NE release from sympathetic nerves and con

281 to a favorable 3 month outcome, response to t-PA, 3 month mortality, or risk of intracerebral hemorr

282 This effect was selective to t-PA and its close derivative tenecteplase.

283 The truncated t-PA variant reteplase had a minor effect on permeabilit

284 lted in accelerated Pg activation when VDAC, t-PA, and Pg were bound together.

285 y a second significant source of vessel wall t-PA.

286 We investigated whether t-PA modulates sympathetic activity.

287 ymorphisms were consistently associated with t-PA safety.

288 -like receptor and that its association with t-PA, Pg, and VDAC on the cell surface may be part of a

289 ved with angioplasty (n = 565) compared with t-PA (n = 573).

290 tivator, reteplase (r-PA), was compared with t-PA in the Global Utilization of Streptokinase and t-PA

291 otting, consistent with PAI-1 complexed with t-PA, as well as bands consistent with cleaved PAI-1, su

292 d received intravenous t-PA to continue with t-PA alone (control group) or to undergo endovascular th

293 to -2.4; P=0.005); the change observed with t-PA alone and with DNase alone (-17.2+/-24.3 and -14.7+

294 rrelated significantly (inversely) only with t-PA.

295 treatment window of reperfusion therapy with t-PA by limiting hemorrhagic transformation.

296 The patients treated with t-PA were at least 30 percent more likely to have minima

297 The 190 patients treated with t-PA who did not have an Apo E2 phenotype also had a gre

298 acute ischemic stroke who were treated with t-PA within three hours after the onset of symptoms were

299 th an Apo E2 phenotype who were treated with t-PA, the odds ratio (OR) of a favorable outcome at 3 mo

300 ncluded 1,172 patients who were treated with t-PA; 20.9% of them developed HT as evaluated by systema