ライフサイエンスコーパス: tPA

1 tPA activity was reduced, and the tPA inhibitor plasmino

2 tPA added extracellularly bound to the lumenal surface o

3 tPA deficiency prevents NMDA receptors from triggering n

4 tPA independently induced transient IkappaBalpha phospho

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

6 tPA promoted the survival of both resting and lipopolysa

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

8 tPA-induced brain hemisphere reperfusion after photothro

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

10 the possibility that modulation of the PAI-1-tPA pathway may be beneficial in diseases associated wit

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

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

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

14 lmonary embolism randomly assigned to 1 of 4 tPA dosing regimens for ultrasound-facilitated, catheter

15 Accelerated tPA (tissue-type plasminogen activator) dosing regimens

16 The plasminogen activator tPA was lower in HA-NCI while neuroserpin, the CNS tPA i

17 lysis protease, tissue plasminogen activator tPA, without effects on hemostasis.

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

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

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

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

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

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

24 led release of tissue plasminogen activator (tPA) at the thrombus site.

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 a reduction in tissue plasminogen activator (tPA) caused by upregulation of its endogenous inhibitor

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

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

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

31 of intravenous tissue plasminogen activator (tPA) in acute ischemic stroke is associated with reduced

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

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

34 Tissue-type plasminogen activator (tPA) is a major mediator of fibrinolysis and, thereby, p

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

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

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

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

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

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

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

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

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

44 suggests that tissue plasminogen activator (tPA), currently the only FDA-approved medication for isc

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

46 ibrinolysis by tissue plasminogen activator (tPA), exacerbating the prothrombotic effect.

47 atio, D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1) and plat

48 time, D-dimer, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), and pla

49 Tissue plasminogen activator (tPA), which is reduced in Alzheimer's disease and in mou

50 enzyme such as tissue plasminogen activator (tPA).

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

52 of intravenous tissue plasminogen activator (tPA).

53 combinant tissue-type plasminogen activator (tPA).

54 ic delivery of tissue plasminogen activator (tPA).

55 avascular tissue-type plasminogen activator (tPA).

56 gment close to tissue plasminogen activator (tPA; residues gamma312-324) and plasminogen (alpha148-16

57 tissue and urokinase plasminogen activators (tPA and uPA).

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

59 Despite the potential risk of administering tPA to stroke mimics, opportunity remains for continued

60 tor) may increase the risk of administrating tPA to patients presenting with noncerebrovascular condi

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

62 ng intracranial hemorrhage is eliminated and tPA-S478A can be delivered intranasally hours after stro

63 rced unbinding via degradation of fibrin and tPA release.

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

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

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

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

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

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

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

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

72 tained elevation of MG53 in the bloodstream (tPA-MG53) have a healthier and longer life-span when com

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

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

75 ing and regulation of cytokine expression by tPA.

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

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

78 ce show increases in liver Plat, circulating tPA, fibrinolytic activity, bleeding time, and time to t

79 s lower in HA-NCI while neuroserpin, the CNS tPA inhibitor, was higher in AD and MCI cortical samples

80 and identify regulatory factors that control tPA expression by hepatocytes.

81 emented but not exceed 18% to 44% of current tPA payment.

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

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

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

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

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

87 he role and regulation of hepatocyte-derived tPA as a source of basal plasma tPA activity and as a co

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

89 Accelerated lower-dose tPA regimens for ultrasound-facilitated, catheter-direct

90 A dysfunctional tPA-plasmin system causes defective proteolytic degradat

91 EI-tPA emerges as a novel agent capable of improving the ef

92 EI-tPA-primed hiNPC grafted into lesion sites survived, dif

93 active tissue-type plasminogen activator (EI-tPA), prior to grafting into a T3 lesion site in a clini

94 Importantly, only SCI rats that received EI-tPA primed hiNPC demonstrated significantly improved mot

95 When hiNPC were treated with EI-tPA in culture, NMDA-R-dependent cell signaling was init

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

97 of proinflammatory cytokines and an elevated tPA level.

98 whereas passive release of the encapsulated tPA in pH 7.4 PBS buffer was 10% after 6 h.

99 fibrin-agar plate model and the encapsulated tPA retained 97.4 +/- 1.7% of fibrinolytic activity as c

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

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

102 growth effects observed in vitro, exogenous tPA delivery increased poststroke axonal sprouting of co

103 unteracting the tPA reduction with exogenous tPA or with pharmacological inhibition or genetic deleti

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

105 mice, suggesting that endogenously expressed tPA promotes long-term neurological recovery after strok

106 For tPA payments in acute ischemic stroke, our model-based r

107 te with recovery scores after accounting for tPA (tissue-type plasminogen activator) treatment.

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

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

110 We show that hepatocyte tPA is downregulated by a pathway in which the corepress

111 In tPA knockout mice, intranasal administration of recombin

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

113 Although a slight decrease in tPA complication was observed among hospitals participat

114 pe tPA in rescuing neurological functions in tPA knockout stroke mice.

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

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

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

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

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

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

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

122 harmacological inhibition of PAI-1 increased tPA activity, prevented neurovascular uncoupling, and am

123 0-3-hour window) incentivized by increasing tPA payment by as much as 18% to 44% depending on willin

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

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

126 Door-to-needle times for intravenous tPA.

127 nes recommend against the use of intravenous tPA (tissue-type plasminogen activator; IV tPA) in acute

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

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

130 nt of acute ischemic stroke with intravenous tPA (tissue-type plasminogen activator) may increase the

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

132 d for acute ischemic stroke with intravenous tPA within 4.5 hours from the time they were last known

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

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

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

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

137 After permanent focal cerebral ischemia, tPA knockout mice developed more severe sensorimotor and

138 s tPA (tissue-type plasminogen activator; IV tPA) in acute ischemic stroke patients with prior ischem

139 ntinue to be vigilant about the safety of IV tPA in patients with prior stroke, particularly those wi

140 , there are limited data on the safety of IV tPA in this population.

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

142 inked to Medicare claims and treated with IV tPA at Get With The Guidelines-Stroke hospitals (Februar

143 We identified 293 patients treated with IV tPA who had a prior ischemic stroke within 3 months and

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

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

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

147 Notably, recombinant mutant tPA-S478A lacking protease activity (but retaining the E

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

149 amouflaged tPA was similar to that of native tPA.

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

151 tic activity as compared with that of native tPA.

152 valuation for Acute Ischemic Stroke network: tPA (tissue-type plasminogen activator) use, complicatio

153 Overall, 3.5% of tPA treatments were given to stroke mimics.

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

155 iles at 37 degrees C showed that over 90% of tPA was released through liposomal membrane destabilizat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 t contributes to basal circulating levels of tPA and to fibrinolysis after vascular injury.

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

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

176 d with a significant increase in the rate of tPA use, while it was significantly associated with a mo

177 selective delivery and effective release of tPA at the site of thrombus, thus achieving efficient cl

178 The release of tPA could be readily manipulated by changing the concent

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

180 Restoration of tPA activity could be of therapeutic value in diseases a

181 monstrate a previously unappreciated role of tPA in Abeta-related neurovascular dysfunction and in va

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

183 In this study, we investigated the role of tPA on primary neurons in culture and on brain recovery

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

185 arked enhancement of blood residence time of tPA from minutes to several days without any morphologic

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

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

188 We documented the use of tPA in stroke mimics, defined as patients who present wi

189 risk of bleeding associated with the use of tPA.

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

191 Studies on tPA regulation have focused on its acute local release b

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

193 cyte-derived tPA as a source of basal plasma tPA activity and as a contributor to fibrinolysis after

194 tes in determining the basal level of plasma tPA and identify regulatory factors that control tPA exp

195 unction of noninjury-induced systemic plasma tPA.

196 ctivity significantly associated with plasma tPA and PAI-1, suggesting endothelial cells as a potenti

197 ty were significantly associated with plasma tPA and PAI-1, suggesting that endothelial cells could b

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

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

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

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

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

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

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

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

206 e ischemic stroke (AIS) during intravenous r-tPA therapy and associated CA with response to therapy.

207 AIS patients eligible for intravenous r-tPA therapy were recruited.

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

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

210 The total dose of r-tPA (recombinant tissue-type plasminogen activator) was

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

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

213 YSE-PE trial (Optimum Duration and Dose of r-tPA With the Acoustic Pulse Thrombolysis Procedure for I

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

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

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

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

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

219 th tPA, relatively few patients who received tPA for presumed stroke were ultimately not diagnosed wi

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

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

222 treatment with the protease-dead recombinant tPA-S478A holds particular promise as a neurorestorative

223 ce, intranasal administration of recombinant tPA protein 6 hours poststroke and 7 more times at 2 d i

224 Treatment with recombinant tPA stimulated axonal growth in culture, an effect indep

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

226 PAI-1 inhibition restores tPA activity, rescues neurovascular coupling, reduces am

227 ared with tPA-treated true ischemic strokes, tPA-treated mimics were younger (median 54 versus 71 yea

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

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

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

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

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

233 These findings demonstrate that tPA improves long-term functional outcomes in a clinical

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

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

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

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

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

239 The tPA deficit attenuated functional hyperemia by suppressi

240 The tPA signaling response was distinguished from the signat

241 The tPA-loaded liposomes were PEGylated to improve their sta

242 The tPA-mediated macrophage survival was eliminated by PD980

243 The tPA-MG53 mice show normal glucose handling and insulin s

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

245 tPA activity was reduced, and the tPA inhibitor plasminogen inhibitor-1 (PAI-1) was increa

246 Counteracting the tPA reduction with exogenous tPA or with pharmacological

247 presence of activated platelets enabled the tPA-loaded, cRGD-coated, PEGylated liposomes to induce e

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

249 More importantly, the tPA-MG53 mice display remarkable dermal wound healing ca

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

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

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

253 1 represses ATF6, which is an inducer of the tPA gene Plat Hepatocyte-DACH1-knockout mice show increa

254 The data unveil a selective role of the tPA in the suppression of functional hyperemia induced b

255 uicker thrombolytic activity compared to the tPA-loaded liposomes without cRGD labelling.

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

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

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

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

260 ce pretreated with a PKal inhibitor prior to tPA.

261 line in the rate of complications related to tPA (-5.9%; 95% CI, -9.2% to -2.6%).

262 gen activator) use, complications related to tPA use, door-to-needle time, ambulation at discharge, d

263 F-like domain) was as effective as wild-type tPA in rescuing neurological functions in tPA knockout s

264 of plasmin via two activators: tissue-type (tPA) and urokinase-type (uPA).

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

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

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

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

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

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

271 Therefore, we investigated whether tPA is involved in the neurovascular dysfunction of Abet

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

273 le to modulate the interaction of PAI-1 with tPA and uPA in a way not previously described for a huma

274 The complication rates associated with tPA in stroke mimics were low.

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

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

277 1110 who received standard medical care with tPA.

278 improved significantly by coincubation with tPA.

279 Crry treatment, alone or in combination with tPA, limited perilesional complement deposition, reduced

280 Compared with tPA-treated true ischemic strokes, tPA-treated mimics we

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

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

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

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

285 48-160) binding sites, thus interfering with tPA-plasminogen interaction and representing 1 potential

286 8 666 patients (79.2%) who were treated with tPA and had door-to-needle times of longer than 45 minut

287 4 367 patients (55.9%) who were treated with tPA and had door-to-needle times of longer than 60 minut

288 with suspected ischemic stroke treated with tPA from 485 US hospitals between January 2010 and Decem

289 Among the 61 426 patients treated with tPA within 4.5 hours, the median age was 80 years and 43

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

291 n this large cohort of patients treated with tPA, relatively few patients who received tPA for presum

292 murine thrombotic stroke model treated with tPA.

293 ncreased risk for bleeding when treated with tPA.

294 based on time-to-thrombolytic treatment with tPA (tissue-type plasminogen activator).

295 95 to present reviewing early treatment with tPA and prehospital stroke evaluation and treatment.

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.