ライフサイエンスコーパス: tPA

1 tPA added extracellularly bound to the lumenal surface o

2 tPA also activated migratory signaling in vivo.

3 tPA Alu (I/D) (rs4646972) and PAI-1 (4G/5G) (rs1799889)

4 tPA independently induced transient IkappaBalpha phospho

5 tPA induced the phosphorylation of Erk1/2, p90 ribosomal

6 tPA is known to worsen neurovascular injury by amplifyin

7 tPA promoted the survival of both resting and lipopolysa

8 tPA was camouflaged with human serum albumin (HSA) via a

9 tPA(-/-), but not uPA(-/-), mice developed a systemic co

10 tPA-induced brain hemisphere reperfusion after photothro

11 tPA-Lynx1 may potentially be a new candidate mechanism f

12 rrier osteomyelitis patients had lower PAI-1/tPA complex levels compared to those with the D allele (

13 at annonacinone inhibited formation of PAI-1/tPA complex via enhancement of the substrate pathway.

14 Plasma PAI-1/tPA complex was assessed by enzyme-linked immuosorbent a

15 ereas PAI-1 expression (P = 0.022) and PAI-1/tPA complexes in plasma (P = 0.015) were lower after tra

16 The PAI-1/tPA complexes, D-dimers, and prothrombin fragment F1 + 2

17 Among the 58,353 tPA-treated patients, median age was 72 years, 50.3% wer

18 minogen and its tissue plasminogen activator tPA.

19 in 200 ms) and tissue plasminogen activator (tPA) (over many seconds) in adrenal chromaffin cells.

20 combinant tissue-type plasminogen activator (tPA) administration revealed that incomplete proteolysis

21 us intravenous tissue plasminogen activator (tPA) administration versus tPA administration alone and

22 times for tissue-type plasminogen activator (tPA) administration.

23 travenous (IV) tissue plasminogen activator (tPA) alone versus IV tPA + endovascular therapy (Solitai

24 ic parameters, tissue plasminogen activator (tPA) and its physiological inhibitor, plasminogen activa

25 ic activity of tissue plasminogen activator (tPA) becomes restricted in the adult brain if mice are r

26 ic activity of tissue plasminogen activator (tPA) becomes restricted in the adult brain in correlatio

27 ith the use of tissue plasminogen activator (tPA) flush during DCD procurements.

28 elease of tissue-type plasminogen activator (tPA) followed by delayed synthesis and release of urokin

29 on the use of tissue plasminogen activator (tPA) following cerebrovascular events demonstrates that

30 omplication of tissue plasminogen activator (tPA) for ischaemic stroke.

31 travenous tissue-type plasminogen activator (tPA) in acute ischemic stroke is time dependent.

32 therapy using tissue plasminogen activator (tPA) in acute stroke is associated with increased risks

33 travenous (IV) tissue plasminogen activator (tPA) in ischemic stroke patients treated with warfarin.

34 of intravenous tissue plasminogen activator (tPA) in patients with acute ischemic stroke (AIS) are ti

35 treatment with tissue plasminogen activator (tPA) in patients with acute ischemic stroke, guidelines

36 inolysis, tissue-type plasminogen activator (tPA) interacts with neurons and regulates multiple aspec

37 expression of tissue plasminogen activator (tPA) is increased in glial cells differentiated from neu

38 Intravenous tissue plasminogen activator (tPA) is known to improve outcomes in ischemic stroke; ho

39 Tissue-type plasminogen activator (tPA) is known to promote macrophage infiltration and ren

40 hereas labeled tissue plasminogen activator (tPA) is often discharged over many seconds.

41 Tissue-type plasminogen activator (tPA) is the major intravascular activator of fibrinolysi

42 Tissue plasminogen activator (tPA) is the only FDA-approved treatment for reperfusing

43 th recombinant tissue plasminogen activator (tPA) may exacerbate blood-brain barrier breakdown after

44 ed patients to tissue plasminogen activator (tPA) or placebo, and all DEFUSE patients received tPA.

45 travenous (IV) tissue plasminogen activator (tPA) therapy in acute ischemic stroke (AIS).

46 sociation with tissue plasminogen activator (tPA) thereby enhancing plasmin production, but whether C

47 on intravenous tissue plasminogen activator (tPA) use in Chicago, Illinois.

48 of intravenous tissue plasminogen activator (tPA) use in the United States.

49 of intravenous tissue plasminogen activator (tPA) within 3 hours of symptom onset to more recent guid

50 ic stroke with tissue plasminogen activator (tPA) within 4.5 hours of symptom onset, the most evidenc

51 sed cerebellar tissue plasminogen activator (tPA), a part of the tPA/plasmin proteolytic system, infl

52 Tissue-type plasminogen activator (tPA), a protease up-regulated in the kidneys with chroni

53 ike protein 2, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI)-1.

54 tin, myocilin, tissue plasminogen activator (tPA), and/or matrix metalloproteinase-2 (MMP2).

55 generation by tissue plasminogen activator (tPA), but not streptokinase, is slowed in fibrin clots c

56 centrations of tissue plasminogen activator (tPA), d-dimer, thrombin-antithrombin complex, and cytoki

57 activation by tissue plasminogen activator (tPA), reduced plasmin-mediated proteolysis of gamma'-Fn,

58 of intravenous tissue plasminogen activator (tPA).

59 combinant tissue-type plasminogen activator (tPA).

60 enzyme such as tissue plasminogen activator (tPA).

61 ic delivery of tissue plasminogen activator (tPA).

62 oding for tissue-type plasminogen activator (tPA).

63 SERPINE1) and tissue plasminogen activator (tPA, PLAT), such as PAI-1 (-675 4G/5G deletion/insertion

64 travenous [IV] tissue-plasminogen activator [tPA]; relative risk, 1.07 [99% confidence interval: 0.67

65 anying study, we suggest that, additionally, tPA itself stabilizes the fusion pore with dimensions th

66 ited by fears of inadvertently administering tPA in patients with intracerebral hemorrhage (ICH).

67 adoptive regulatory T cell transfer against tPA-induced haemorrhagic transformation.

68 In univariate analysis, tPA use increased over time, especially in those aged >8

69 regression models using VLCBV (p<0.001) and tPA (p=0.02) predicted PH independent of clinical factor

70 r 24 hrs were similar in saline controls and tPA-treated mice, whereas heparin-treated mice had 3-fol

71 rced unbinding via degradation of fibrin and tPA release.

72 as PAI-1 (-675 4G/5G deletion/insertion) and tPA (Alu insertion/deletion [I/D]), are associated with

73 lomerular mRNA expression of KLF2, KLF4, and tPA was lower and that of PAI-1 was higher in rTx-TMA th

74 g IGFBP3, IGFBP3-cleaving proteases (MMP and tPA), and protease modulators (TIMP1 and PAI-1).

75 s on the matrix degradation enzymes MMP2 and tPA differed significantly, suggesting that GW870086X fa

76 ase-9 activity in brain following stroke and tPA therapy.

77 Aortic wall PAI-1, uPA, and tPA concentrations were determined by western blot analy

78 tic occlusion of the middle cerebral artery, tPA administration increased brain hemorrhage transforma

79 Fibrinolytics such as tPA are already approved for other indications.

80 ICH, but rapidly assessing BBB damage before tPA administration is highly challenging.

81 marker for evaluating the risk of ICH before tPA administration.

82 Prestroke antiplatelet therapy before tPA administration for acute ischemic stroke.

83 In the second phase, ERK1/2 is activated by tPA independently of LRP1.

84 f clots to lysis by slowing Pg activation by tPA and provide another example of the intimate connecti

85 -S(481)A inhibited plasminogen activation by tPA and uPA, attenuated ICH, lowered plasma d-dimers, le

86 lag time for initiation of Pg activation by tPA was longer with gamma'-Fn than with gammaA-Fn.

87 ing and regulation of cytokine expression by tPA.

88 ICH expansion was also inhibited by tPA-S(481)A in WT mice anticoagulated with warfarin.

89 el, the thrombolytic activity of camouflaged tPA was similar to that of native tPA.

90 onfirmed the binding affinity of camouflaged tPA with the activated platelets.

91 The fractional bleaching of tPA-cerulean (tPA-cer) was greater when subsequently probed with TIR e

92 In contrast, tPA did not upregulate matrix metalloproteinases in our

93 gen was reduced by 2-fold with HSA-decorated tPA compared with that of native tPA, which is an indica

94 P = 0.01), with comparable uPA and decreased tPA levels (P = 0.02).

95 tingly, DEX and PRED significantly decreased tPA expression (P </= 0.01), while GW870086X had the opp

96 ously administered immediately after delayed tPA treatment in ischaemic mice, haemorrhagic transforma

97 ges were observed in the presence of delayed tPA after stroke, but were mitigated by regulatory T cel

98 of plasticity, unmasks experience-dependent tPA elevation in visual cortex of adult mice reared in s

99 e, our results indicate that myeloid-derived tPA promotes macrophage migration through a novel signal

100 ecruited by other LRP1 ligands, including EI-tPA and alpha2M*.

101 Rapid ERK1/2 activation in response to EI-tPA and activated alpha2-macroglobulin (alpha2M*) requir

102 tion and ERK1/2 activation in response to EI-tPA.

103 at enzymatically active and inactive tPA (EI-tPA) activate ERK1/2 in a biphasic manner.

104 th LRP1 selectively in cells treated with EI-tPA or alpha2M*.

105 to retain the intrinsic capacity to elevate tPA in an experience-dependent manner but is effectively

106 of proinflammatory cytokines and an elevated tPA level.

107 n into cerebellum or prevented by endogenous tPA deletion in nr:tPA-knockout double mutants.

108 tPA, the plasma concentration of endogenous tPA increased 3-fold in response to LPS, to 116 +/- 15 p

109 loid cells are the main source of endogenous tPA that promotes macrophage migration.

110 ecifically binds to plasminogen and enhances tPA-mediated plasminogen activation.

111 The European tPA license precludes its use in anticoagulated patients

112 In sum, excess tPA/plasmin, through separate downstream molecular mecha

113 an be mimicked in wild-type PNs by exogenous tPA injection into cerebellum or prevented by endogenous

114 (i) Excess endogenous or exogenous tPA inhibits dendritic growth in vivo and in vitro by ac

115 In mice not treated with exogenous tPA, the plasma concentration of endogenous tPA increase

116 arriving </= 2 hours and fully eligible for tPA (P<0.001).

117 knock-out mice suggest an important role for tPA in the abnormal neuronal differentiation and plastic

118 Median DTN time for tPA administration declined from 77 minutes (interquarti

119 rovement initiative to improve DTN times for tPA administration in patients with AIS.

120 The DTN times for tPA administration of 60 minutes or less and in-hospital

121 The DTN times for tPA administration of 60 minutes or less increased from

122 e strategies to achieve faster DTN times for tPA administration, provided clinical decision support t

123 Despite improvements in DITs, DTN times for tPA treatment in patients with acute ischemic stroke rem

124 (ii) tPA/plasmin proteolysis impairs parallel fiber-PN synapt

125 dneys from WT mice was clearly attenuated in tPA knockout mice, which also displayed lower Rac-1 acti

126 gnificantly more apoptotic M1 macrophages in tPA-deficient mice than their wild-type counterparts, an

127 ted ICH expansion in uPA(-/-)mice but not in tPA(-/-) mice.

128 C3A binds to plasminogen and participates in tPA-mediated plasminogen activation.

129 that expansion of the initial fusion pore in tPA granules was delayed.

130 severe TBI, we found that ICH is reduced in tPA(-/-) and uPA(-/-) mice but increased in PAI-1(-/-) m

131 trate that enzymatically active and inactive tPA (EI-tPA) activate ERK1/2 in a biphasic manner.

132 Enzymatically active and inactive tPA demonstrated similar immune modulatory activity.

133 Catalytically inactive tPA-S(481)A inhibited plasminogen activation by tPA and

134 lar administration of enzymatically inactive tPA in mice blocked the toxicity of LPS.

135 70086X had the opposite effect and increased tPA expression in a concentration-dependent manner (P =

136 was independently associated with increased tPA use for patients with ischemic stroke presenting thr

137 In concordance, hantaviruses induced tPA but not PAI-1 in microvascular endothelial cells, an

138 confirmed that regulatory T cells inhibited tPA-induced endothelial expression of CCL2 and preserved

139 Intravenous tPA use </= 3 hours after onset increased from 4.0% to 7

140 Intravenous tPA use (measured as a fraction of patients with ischemi

141 Intravenous tPA-induced arterial recanalization within the first 24

142 tification and more than doubled intravenous tPA use at primary stroke centers.

143 Rates of intravenous tPA use were 3.8% and 10.1% (P < .001) and onset-to-trea

144 ith ischemic stroke who received intravenous tPA in 1545 registry hospitals from January 1, 2009, thr

145 with 59.3% of patients receiving intravenous tPA within 60 minutes and 30.4% within 45 minutes after

146 not support the assumption that intravenous tPA has a deleterious effect in acute ICH.

147 ompared in patients treated with intravenous tPA alone or in combination with the Solitaire device (C

148 ent selection for treatment with intravenous tPA and or endovascular therapies versus nonreperfused c

149 ute ischemic stroke treated with intravenous tPA between January 2009 and December 2012.

150 troke patients were treated with intravenous tPA within 4.5 hours of symptom onset from 888 surveyed

151 ute ischemic stroke treated with intravenous tPA, those receiving antiplatelet therapy before the str

152 stroke patients with or without intravenous tPA treatment, compared to 115 age and gender-matched he

153 he first 7 days after stroke, post-ischaemic tPA treatment led to sustained suppression of regulatory

154 97 of 115] endovascular vs 56% [29 of 52] IV tPA; P < .001).

155 American guidelines accept IV tPA use with an international normalized ratio (INR) </=

156 cant differences between endovascular and IV tPA arms for primary outcome (44.7% [85 of 190] vs 38% [

157 The frequency of IV tPA use among all AIS patients, regardless of contraindi

158 rend favoring endovascular treatment over IV tPA alone for primary outcome (26% [12 of 46] vs 4% [one

159 238 patients with AIS, 240 (11%) received IV tPA.

160 plasminogen activator (tPA) alone versus IV tPA + endovascular therapy (Solitaire stent-retriever) u

161 ed data from 45,074 patients treated with IV tPA enrolled in the Safe Implementation of Thrombolysis

162 nctional outcome in patients treated with IV tPA for acute ischemic stroke.

163 Insights into the Lynx1-tPA plasticity mechanism may provide novel therapeutic t

164 In cultured macrophages, tPA inhibits the response to lipopolysaccharide (LPS) by

165 The expression of the fibrinolytic marker tPA was significantly higher (P = 0.009), whereas PAI-1

166 Moreover, ectopic FAK mimicked tPA and induced macrophage motility.

167 A-decorated tPA compared with that of native tPA, which is an indication of reduced risk of hemorrhag

168 amouflaged tPA was similar to that of native tPA.

169 n, was regenerated to ~90% of that of native tPA.

170 r prevented by endogenous tPA deletion in nr:tPA-knockout double mutants.

171 es) also improved, with approximately 65% of tPA-treated patients getting brain imaging </= 25 minute

172 Shielding with HSA suppressed 75% of tPA's activity which, upon contact with 25 nM thrombin,

173 The mechanism of action of tPA is affected by the number of molecules present with

174 rinciple study suggests that the activity of tPA can be suppressed by HSA and regenerated by thrombin

175 Delayed administration of tPA (10 mg/kg) resulted in haemorrhagic transformation i

176 Intravenous administration of tPA increased circulating PKal activity in mice.

177 The fractional bleaching of tPA-cerulean (tPA-cer) was greater when subsequently pro

178 In vivo, coadministration of tPA improved the anticancer efficacy of nanoparticle-enc

179 plasmin regulates the local concentration of tPA through forced unbinding via degradation of fibrin a

180 pact of regulatory T cells in the context of tPA-induced brain haemorrhage and investigated the under

181 riments indicated that subthreshold doses of tPA facilitated clot retraction through a plasmin-depend

182 ble to potentiate the thrombolytic effect of tPA in vivo in a murine model.

183 The cytoprotective effect of tPA required its receptor, LDL receptor-related protein-

184 NF-kappaB inhibitor abolished the effect of tPA.

185 Here, we assessed the effects of tPA in two models of ICH.

186 We investigated the effects of tPA on plasma prekallikrein (PPK) activation and the rol

187 These adverse effects of tPA were ameliorated in PPK (Klkb1)-deficient and FXII-d

188 py revealed that 71% of the fusion events of tPA-cer-containing granules maintained curvature for >10

189 Amperometry revealed that the expression of tPA-green fluorescent protein (GFP) prolonged the durati

190 oth genetic and adult specific inhibition of tPA activity can ablate the ocular dominance shift in Ly

191 anging from 5 to 189 min after initiation of tPA (median 65 min).

192 , premix of tPA ahead of time, initiation of tPA in brain imaging suite, and prompt data feedback to

193 ng angio-oedema within 24 h of initiation of tPA.

194 However, the low diffusive mobility of tPA cannot alone explain its slow postfusion release.

195 mined by the interplay between the number of tPA molecules in the system and clot structure.

196 genetic resonance imaging scanner, premix of tPA ahead of time, initiation of tPA in brain imaging su

197 nges in patient characteristics and rates of tPA use over time among hospitalized acute ischemic stro

198 bleaching revealed a significant recovery of tPA-cer (but not NPY-cer) fluorescence within several hu

199 p-regulation of PAI-1 and down-regulation of tPA, resulting in inhibition of local fibrinolysis.

200 r confirmed the thrombin-mediated release of tPA from the camouflaged construct.

201 ere tPA-dependent because genetic removal of tPA in Lynx1 KO mice can block the monocular deprivation

202 We examined the role of tPA in macrophage motility in vivo by tracking fluoresce

203 We examined the role of tPA in macrophage survival, and found that tPA protected

204 crease in brain lesion size, whereas that of tPA (10 mg/kg) had a much smaller effect.

205 ion of KLF2 and KLF4 correlated with that of tPA and inversely with that of PAI-1 in rTx-TMA.

206 e was associated with improved timeliness of tPA administration following AIS on a national scale, an

207 We detected strong upregulation of tPA in the acute phase of illness and in PUUV-infected m

208 tions associated with the therapeutic use of tPA in stroke is not yet available.

209 But widespread use of tPA is still limited by fears of inadvertently administe

210 risk of bleeding associated with the use of tPA.

211 Using a set of deletion variants of tPA and pharmacological approaches, we demonstrated that

212 Delayed administration of diabody or tPA had no effect on lesion size, whereas the combined a

213 mbinant tissue-type plasminogen activator (r-tPA) in eligible patients with acute ischemic stroke to

214 ysis fails to dissolve thrombi acutely and r-tPA (recombinant tissue-type plasminogen activator) ther

215 port patients and providers in considering r-tPA for acute ischemic stroke.

216 rs, caregivers, and clinicians considering r-tPA treatment.

217 nd caused less bleeding than clinical-dose r-tPA (P<0.001).

218 ore embolus dissolution than clinical-dose r-tPA alone (P<0.001) or alpha2-antiplasmin inactivation a

219 Low-dose r-tPA alone did not dissolve emboli, but was synergistic w

220 ion alone, or in combination with low-dose r-tPA, did not lead to fibrinogen degradation, did not cau

221 activation alone was comparable to 3 mg/kg r-tPA.

222 Thrombolysis regimen (20 mg r-tPA over 15 hours) was identical in all patients.

223 The effects of r-tPA and alpha2-antiplasmin inactivation on fibrinolysis

224 s for describing the benefits and risks of r-tPA in a clinical setting.

225 ty in explaining the benefits and risks of r-tPA within the frenetic pace of emergency department car

226 iplasmin was comparable to pharmacological r-tPA for dissolving thrombi.

227 (framed positively) and risk of receiving r-tPA.

228 rn of thrombus specificity, because unlike r-tPA, it did not degrade fibrinogen or enhance experiment

229 odds that an eligible patient would receive tPA increased by 1.37-fold, adjusting for other covariat

230 All patients in era II received tPA flushed liver grafts.

231 or placebo, and all DEFUSE patients received tPA.

232 hip with other factors in patients receiving tPA at a UK centre.

233 ive patients (median age 70 years) receiving tPA treatment for confirmed ischaemic stroke were includ

234 of transcription 1 (STAT1), which regulated tPA gene expression via a STAT1-responsive enhancer elem

235 In a model of laser-induced vessel rupture, tPA also did not worsen hemorrhage volumes, while hepari

236 amouflaged construct is expected to suppress tPA's enzymatic activity in the systemic circulation but

237 e, and therefore had a greater mobility than tPA-cer.

238 ck-out mice, a mouse model for FXS, and that tPA is involved in the altered migration and differentia

239 Surprisingly, however, the assumption that tPA will worsen ICH has never been biologically tested.

240 Thus, it is clear that tPA promoted M1 macrophage survival through its receptor

241 These data demonstrate that tPA activates PPK in plasma and PKal inhibition reduces

242 cortex (V1) as a model, we demonstrate that tPA activity in V1 can be unmasked following 4 d of mono

243 ing cerebrovascular events demonstrates that tPA also plays important roles in the pathogenesis of st

244 We found that tPA and NPY are endogenously expressed in small and diff

245 f tPA in macrophage survival, and found that tPA protected macrophages from both staurosporine and H2

246 e marrow-derived macrophages, and found that tPA-deficient mice had markedly fewer infiltrating fluor

247 We hypothesized that tPA may be the endogenous factor that promotes macrophag

248 Altogether, the results indicate that tPA may prove to be an interesting potential target for

249 n than with epifluorescence, indicating that tPA-cer mobility was low.

250 We propose that tPA within the granule lumen controls its own discharge.

251 We show that tPA increases PKal activity in vitro in both murine and

252 In vitro studies showed that tPA promoted macrophage motility through its CD11b-media

253 These results suggest that tPA may be a general factor in the immunological respons

254 The tPA signaling response was distinguished from the signat

255 The tPA-mediated macrophage survival was eliminated by PD980

256 regulatory T cells completely abolished the tPA-induced elevation of MMP9 and CCL2 after stroke.

257 to our knowledge an association between the tPA Alu (I/D) polymorphism and susceptibility to bacteri

258 In time-lapse imaging, blocking the tPA function promotes early glial differentiation and re

259 d I allele carriers (56.3% vs 46.3%) for the tPA Alu (I/D) polymorphism were significantly more frequ

260 and in PUUV-infected macaques and found the tPA level to positively correlate with disease severity.

261 regulatory T cell-afforded protection in the tPA-treated stroke model is mediated by two inhibitory m

262 By mediating the tPA response in macrophages, the NMDA-R provides a pathw

263 Alterations of the tPA expression in the embryonic, postnatal, and adult br

264 e plasminogen activator (tPA), a part of the tPA/plasmin proteolytic system, influences several diffe

265 P1-dependent phase varied inversely with the tPA concentration.

266 sium are prevented by the treatment with the tPA-neutralizing antibody in FMRP-deficient cells during

267 ted trypsin-like serine proteases (thrombin, tPA, FXa, plasmin, plasma kallikrein, trypsin, FVIIa).

268 more common contributor to delays in timely tPA therapy for acute ischemic stroke.

269 In contrast to tPA, the diabody did not increase accumulative bleeding.

270 , Rac-1, and NF-kappaB were indispensable to tPA-induced macrophage migration as either infection of

271 ce pretreated with a PKal inhibitor prior to tPA.

272 me (median 24 versus 20 minutes) and door-to-tPA time (median 81 versus 72 minutes) also improved, wi

273 pe I and II interferons directly upregulated tPA through signal transducer and activator of transcrip

274 inogen activator (tPA) administration versus tPA administration alone and to investigate variables th

275 These structural and functional changes were tPA-dependent because genetic removal of tPA in Lynx1 KO

276 When tPA function is blocked with an antibody, enhanced migra

277 When tPA is introduced at the clot or thrombus edge, lysis pr

278 reshold is readily achieved in patients when tPA is administered therapeutically for stroke.

279 is study, we examined the mechanism by which tPA initiates cell signaling in PC12 and N2a neuron-like

280 Herein, we show that the mechanism by which tPA neutralizes LPS involves rapid reversal of IkappaBal

281 duces cerebral complications associated with tPA-mediated thrombolysis in stroke.

282 l thrombectomy vs standard medical care with tPA was associated with improved functional outcomes and

283 1110 who received standard medical care with tPA.

284 improved significantly by coincubation with tPA.

285 uorophores in a granule, are consistent with tPA-cer being 100% mobile, with a diffusion coefficient

286 Cotreatment with tPA resulted in greater intratumoral penetration of a mo

287 the combined administration of diabody with tPA caused a 1.7-fold decrease in lesion size.

288 from gammaA-Fg when lysis was initiated with tPA/Pg when FPA and FPB were both released, but not when

289 those arriving </= 2 hours and treated with tPA </= 3 hours after onset (n=50 798) from 2003 to 2011

290 cluded 71,169 patients with AIS treated with tPA (27,319 during the preintervention period from April

291 were severe (1% of all patients treated with tPA), requiring urgent advanced airway management.

292 murine thrombotic stroke model treated with tPA.

293 ncreased risk for bleeding when treated with tPA.

294 95 to present reviewing early treatment with tPA and prehospital stroke evaluation and treatment.

295 Treatment with tPA has expanded to include more patients with mild defi

296 Furthermore, treatment with tPA led to decompression of blood vessels and improved t

297 toward earlier evaluation and treatment with tPA, particularly into the first hour after symptom onse

298 (ICH) is the primary reason for withholding tPA therapy from patients with ischemic stroke.

299 Although stroke patients without tPA treatment gradually repopulated the numbers of circu

300 enia, and improved neurologic outcome in WT, tPA(-/-), and uPA(-/-) mice.