ライフサイエンスコーパス: thrombolytic

1 sure of thrombus to endogenous and exogenous thrombolytics.

2 use of the limited effectiveness of existing thrombolytics.

3 tracerebral haemorrhage after treatment with thrombolytics (2 [7%] telemedicine vs 2 [8%] telephone,

4 from baseline to the fifth year: intravenous thrombolytics (42.09% versus 72.84%), early antithrombot

5 the systemic circulation but regenerate its thrombolytic action upon contact with thrombin present o

6 s a multitarget small nitrone showing potent thrombolytic activity and free radicals scavenging power

7 min, showing considerably higher and quicker thrombolytic activity compared to the tPA-loaded liposom

8 Our objective was to assess endogenous thrombolytic activity in acute coronary syndrome (ACS) p

9 These data show for the first time a potent thrombolytic activity of ADAMTS13 in the setting of stro

10 hen evaluated in a rat thrombosis model, the thrombolytic activity of camouflaged tPA was similar to

11 ether ultrasonography can safely enhance the thrombolytic activity of t-PA.

12 ntration-dependent fashion the catalytic and thrombolytic activity of tissue plasminogen activator in

13 reactivity, allows assessment of endogenous thrombolytic activity to identify ACS patients who remai

14 besides the unquestionable benefit from its thrombolytic activity, tPA also has a deleterious effect

15 y patients at risk for thrombosis and inform thrombolytic administration for treating acute thrombosi

16 ystolic flow reversal (pulsatile flow) after thrombolytic administration on coronary angiography is a

17 would be related to long-term outcomes after thrombolytic administration.

18 ctive treatment option in conjunction with a thrombolytic agent for stroke patients.

19 uture directions for a safer use of tPA as a thrombolytic agent in the setting of acute ischemic stro

20 The effect of a thrombolytic agent on biochemical bond degradation was m

21 VWF) that blocks VWF binding to GPIb, of the thrombolytic agent recombinant tissue plasminogen activa

22 Finally, we show that the thrombolytic agent streptokinase has therapeutic value f

23 f important virulence factors, including the thrombolytic agent streptokinase, the protease inhibitor

24 urokinase-type plasminogen activator or the thrombolytic agent streptokinase.

25 ich regulates the expression of pili and the thrombolytic agent streptokinase.

26 lacing of the thrombus with a fibrin-binding thrombolytic agent such as alteplase is an alternative t

27 oup analyses to assess the effect of type of thrombolytic agent used and the strategy of emergent hos

28 up, and were independent of both the type of thrombolytic agent used, and whether or not the patient

29 minogen activator (TPA) with a direct-acting thrombolytic agent, plasmin, in an animal model of fibri

30 sue plasminogen activator, is an alternative thrombolytic agent.

31 ffinity obviates continuous infusion of this thrombolytic agent.

32 therapy and it is also used clinically as a thrombolytic agent.

33 , including intra-arterial administration of thrombolytic agents and mechanical interventions, show p

34 outcomes of patients with OTPHV treated with thrombolytic agents and with surgery since 1996.

35 h Gd-complexes (Gd-lip) co-encapsulated with thrombolytic agents can serve both for imaging and treat

36 TAFIa could enhance the efficacy of existing thrombolytic agents for the treatment of acute myocardia

37 as well as local intra-arterial delivery of thrombolytic agents in patients with acute stroke, are t

38 py may be a non-invasive safe alternative to thrombolytic agents in treating thrombotic CVC occlusion

39 Newer thrombolytic agents may have advantages, but are less we

40 Our findings indicate that thrombolytic agents may have therapeutic value in the tr

41 New devices, new thrombolytic agents, and new antithrombotic agents are c

42 learest indication for the administration of thrombolytic agents, but patients with acute pulmonary e

43 swered questions remain regarding the use of thrombolytic agents.

44 inogen activator are the currently available thrombolytic agents.

45 nimizes the duration of systemic exposure to thrombolytic agents.

46 tra-arterial thrombolysis, and trials of new thrombolytic agents.

47 tion, and the concomitant use of intravenous thrombolytics, among others.

48 a, a condition shown by itself to reduce the thrombolytic and proteolytic properties of tissue plasmi

49 Myxomavirus Serp-1 inhibits thrombolytic and thrombotic proteases, whereas mammalian

50 ed that ex vivo attachment of bioscavengers, thrombolytics, and nanoparticles (NPs) to glycophorin A

51 ilities, patients who received intracoronary thrombolytics, and those who received no medications wit

52 therefore also help in designing new, safer thrombolytic approaches.

53 ral arterial access site, >6-Fr sheath size, thrombolytics, arterial dissection, fluoroscopy time >30

54 lready arrested, the difficulty of obtaining thrombolytics at the bedside rapidly enough to administe

55 Furthermore, facilitated interventions with thrombolytic-based regimens should be avoided.

56 elevation myocardial infarction who receive thrombolytics, clopidogrel therapy confers broad benefit

57 bition in myocardial infarction treated with thromboLYtics (COMPLY) and COMplement inhibition in Myoc

58 ment elevation were eligible for IMR but had thrombolytic contraindications after excluding patients

59 inutes, from emergency department arrival to thrombolytic delivery.

60 as shortening ischemic times with the use of thrombolytic donor flush, may prevent IC after DCD LT.

61 a dose-dependent manner, even at 25% of the thrombolytic dose (1 mg/kg), manifest as rebleeding from

62 Bleeding occurred only at 8-fold the thrombolytic dose, on complete depletion of fibrinogen a

63 inogen activator (t-PA) is the only approved thrombolytic drug for ischemic stroke.

64 The newer thrombolytic drug tenecteplase has been investigated in

65 clots using a significantly lower amount of thrombolytic drug than is required when administered in

66 er, whether or not helium interacts with the thrombolytic drug tissue plasminogen activator, the only

67 ed alternative anticoagulants (11 patients), thrombolytic drugs (3 patients), inferior vena cava filt

68 The administration of thrombolytic drugs outside hospital by emergency physici

69 formed with a variety of neuroprotective and thrombolytic drugs provide many lessons that will help t

70 selection are investigating alteplase, other thrombolytic drugs, and novel endovascular devices, for

71 Despite the common use of thrombolytic drugs, especially in stroke treatment, ther

72 ally improve both the efficacy and safety of thrombolytic drugs, particularly in patients who are at

73 ate and thus minimizing the required dose of thrombolytic drugs.

74 nt mass loss/min in vitro without any use of thrombolytic drugs.

75 d diagnosis of pulmonary embolism and use of thrombolytics during cardiopulmonary resuscitation may n

76 the lack of good data supporting the use of thrombolytics during resuscitation, the belief that thro

77 We hypothesized that ADAMTS13 can exert a thrombolytic effect in VWF-containing thrombi in the set

78 oelastography and was able to potentiate the thrombolytic effect of tPA in vivo in a murine model.

79 erformed to study the molecular bases of NAC thrombolytic effect, including platelet aggregometry, pl

80 al actions on the CNS besides its well-known thrombolytic effect.

81 nce that the molecular target underlying the thrombolytic effects of NAC is principally the VWF that

82 Although thrombolytic effects of tissue plasminogen activator (tP

83 ic stroke outcome, suggesting that it exerts thrombolytic effects without significantly impairing nor

84 evelopment of adjuvant techniques to improve thrombolytic efficacy is important for advancing ischemi

85 ic GpIIb/IIIa inhibitor further improved its thrombolytic efficacy, essentially by accelerating throm

86 developed systems, and (iv) testing of their thrombolytic efficacy.

87 Thrombolytics (eg, tissue-type plasminogen activator [tP

88 rials, which together randomly assigned 7739 thrombolytic-eligible patients with ST-segment elevation

89 in blood, where its primary function is as a thrombolytic enzyme, and in the central nervous system w

90 Plasmin, the pivotal thrombolytic enzyme, is generated on the surface of many

91 n of plasminogen, the zymogen of the primary thrombolytic enzyme, plasmin, is markedly promoted when

92 sue-type plasminogen activator (tPA) is as a thrombolytic enzyme.

93 r inhibitor-1 (PAI-1) are causal factors for thrombolytic failure.

94 ient warm ischemia time (WIT) and the use of thrombolytic flush at the time of procurement to minimiz

95 Prophylaxis with thrombolytic flushes might prevent CVC infections and ca

96 To increase the effective use of thrombolytics for acute stroke, the expertise of vascula

97 Rapid clearance of thrombolytics from blood following intravenous injection

98 the fulfillment of the dual, hemostatic and thrombolytic, functions of thrombin.

99 ng stroke recovery long after the window for thrombolytics has passed.

100 Clinically approved thrombolytics have significant drawbacks, including blee

101 m outcomes prediction on original Killip and thrombolytic in myocardial infarction scores.

102 rdiopulmonary arrest and discuss the role of thrombolytics in cardiopulmonary resuscitation.

103 ted heparin was administered in 33 (87%) and thrombolytics in four (11%).

104 hermore, combination treatment compared with thrombolytic monotherapy increased cerebral blood flow a

105 , the practicality of using alteplase as the thrombolytic of choice for this indication remained conj

106 assess their suitability for treatment with thrombolytics, on the basis of standard criteria.

107 dominant cause of disability worldwide, with thrombolytic or mechanical removal of the occlusion bein

108 enzyme elevation, some argue for the use of thrombolytics or catheter thrombectomy even for hemodyna

109 .7, 95% CI 1.3 to 5.5; p = 0.0092) with more thrombolytic (OR 4.7, 95% CI 2.3 to 9.7; p < 0.0001) and

110 as mammalian neuroserpin (NSP) inhibits only thrombolytic proteases.

111 diated sonothrombolysis device for improving thrombolytic rate and thus minimizing the required dose

112 Nine children who underwent the thrombolytic regimen and 13 who received standard antico

113 analyze our institutional experience with a thrombolytic regimen versus standard anticoagulation for

114 The thrombolytic regimen was associated with a markedly decr

115 UFH as adjunctive therapy in fibrin-specific thrombolytic regimens and improve coronary reperfusion r

116 ase is an alternative to continuous-infusion thrombolytic regimens and minimizes the duration of syst

117 sed the importance of presenting the risk of thrombolytic-related intracranial hemorrhage.

118 vere cerebral WMLs were associated with post-thrombolytic rPH but not with iPH within the ischemic ar

119 gment elevation AMI and contraindications to thrombolytics should be strongly considered.

120 ntial solution of this problem by developing thrombolytic sol-gel coatings which potentially could le

121 Assessment of endogenous thrombolytic status based on the lysis of platelet-rich

122 rombosis test (GTT) to assess thrombotic and thrombolytic status in 300 ACS patients receiving dual-a

123 Recent thrombolytic studies have suggested that simple measures

124 ed is an effective therapy with an excellent thrombolytic success rate for the treatment of prostheti

125 able by contact pathway inhibition, although thrombolytic susceptibility may benefit from polyP antag

126 rfusion induced by the administration of the thrombolytic Tenecteplase (TNK, 1.5 mg/kg, IV bolus) in

127 Thrombolytic therapies were permitted.

128 t from anticoagulation, and less frequently, thrombolytic therapies.

129 However, this model is not amenable to thrombolytic therapies.

130 nalyzed for standard ST-segment criteria for thrombolytic therapy (>1 mm in two or more contiguous le

131 th HF, P<0.0001), and more likely to receive thrombolytic therapy (14% versus 11%; P=0.0001).

132 -3.6% to -1.4%; P < .001) and greater use of thrombolytic therapy (4.8% vs 1.7%; adjusted difference,

133 Most patients who received thrombolytic therapy (76%, n=2939) received a fibrin-spe

134 nt elevation AMI to primary PTCA (n=3872) or thrombolytic therapy (n=3867).

135 erfusion therapy, mainly owing to "patented" thrombolytic therapy (odds ratio 1.15; p = 0.016).

136 that have impeded the more widespread use of thrombolytic therapy (tPA, tissue plasminogen activator)

137 t the bleeding complications associated with thrombolytic therapy after ischemic stroke might be coun

138 ies comprising 756 patients who had received thrombolytic therapy and 13 studies comprising 662 patie

139 With the advent of thrombolytic therapy and angioplasty, it has become poss

140 I, resulting in failure to meet criteria for thrombolytic therapy and as a consequence leading to ina

141 It is widely used as a fibrinolytic agent in thrombolytic therapy and it is also used clinically as a

142 The equivalency of thrombolytic therapy and surgery for the treatment of su

143 y group did not meet ST-segment criteria for thrombolytic therapy as compared with the control group

144 ly reperfusion has led to the development of thrombolytic therapy as the cornerstone of current manag

145 Primary PTCA was better than thrombolytic therapy at reducing overall short-term deat

146 rials is greatly needed to establish whether thrombolytic therapy can be considered standard of care

147 there is a low haemorrhagic threshold after thrombolytic therapy compared with that in wild-type mic

148 ry PTCA remained better than those seen with thrombolytic therapy during long-term follow-up, and wer

149 a patient who was successfully treated with thrombolytic therapy during pulmonary embolism-induced c

150 The benefit of intravenous thrombolytic therapy for acute ischemic stroke is time d

151 ity of Food and Drug Administration-approved thrombolytic therapy for acute ischemic stroke since 199

152 ave been introduced are discussed, including thrombolytic therapy for acute ischemic stroke, induced

153 erfusion success and clinical outcomes after thrombolytic therapy for acute myocardial infarction (AM

154 tracerebral haemorrhage is a complication of thrombolytic therapy for acute myocardial infarction, pu

155 ransluminal coronary angioplasty (PTCA) with thrombolytic therapy for acute ST-segment elevation myoc

156 th a poor prognosis in patients treated with thrombolytic therapy for AMI.

157 w is to provide an update on the progress of thrombolytic therapy for CRAO.

158 size and improve mortality in the setting of thrombolytic therapy for ST-elevation myocardial infarct

159 and safety and increase the time window for thrombolytic therapy for stroke with full- and half-dose

160 resent findings suggest that APC may improve thrombolytic therapy for stroke, in part, by reducing tP

161 unable to apply stockings, or they received thrombolytic therapy for the initial treatment of acute

162 Primary PTCA is more effective than thrombolytic therapy for the treatment of ST-segment ele

163 These data suggest that thrombolytic therapy for treatment of CNS ischemic disor

164 Recently, thrombolytic therapy has been suggested as a viable ther

165 Thrombolytic therapy has rarely been used in these patie

166 Thrombolytic therapy has yet to be validated as an effec

167 tly increasing the time window for effective thrombolytic therapy in acute ischemic stroke.

168 review is to offer an overview of the use of thrombolytic therapy in acute pulmonary embolism.

169 Registry, we examined the outcomes of use of thrombolytic therapy in patients with ischemic stroke wh

170 The use of thrombolytic therapy in pediatrics has increased over th

171 inical trials suggests a survival benefit of thrombolytic therapy in the elderly with STEMI, whereas

172 quate statistical power to determine whether thrombolytic therapy is associated with improved surviva

173 lytics during resuscitation, the belief that thrombolytic therapy is ineffective once a patient has a

174 However, administration of conventional thrombolytic therapy is limited by a low efficacy of pre

175 When this occurs, thrombolytic therapy is not routinely administered.

176 Current treatment of ischaemic stroke with thrombolytic therapy is restricted to 3-4.5 h after symp

177 Thrombolytic therapy is the cornerstone of treatment of

178 Case reports and case series suggest that thrombolytic therapy may be associated with lower risks

179 Thrombolytic therapy may be beneficial in the treatment

180 en for CRAO, emerging evidence suggests that thrombolytic therapy may be effective if administered pr

181 Intracoronary infusion of fibrin-specific thrombolytic therapy may provide a valuable and safe opt

182 Thrombolytic therapy may reduce the frequency of high in

183 the latest prospective study has shown that thrombolytic therapy not only has no beneficial effect b

184 Thrombolytic therapy of PVT has an unpredictable risk of

185 components of thrombotic development and of thrombolytic therapy of rtPA observed from human ischemi

186 re hemodynamically stable and do not require thrombolytic therapy or other interventions.

187 rin, beta-blockers, and reperfusion therapy (thrombolytic therapy or percutaneous coronary interventi

188 our of initial ECG, and overall reperfusion (thrombolytic therapy or PTCA).

189 morbidity and mortality, and the efficacy of thrombolytic therapy propelled the development and matur

190 best subsequent management of patients after thrombolytic therapy remains unclear.

191 Thrombolytic therapy results in the accelerated lysis of

192 Thrombolytic therapy sessions were performed under trans

193 Thrombolytic therapy should be considered first-line the

194 Thrombolytic therapy use increased from 0.7% to 1.0% (p

195 Thrombolytic therapy using tissue plasminogen activator

196 es were randomized clinical trials comparing thrombolytic therapy vs anticoagulant therapy in pulmona

197 echocardiogram suggesting pulmonary embolus, thrombolytic therapy was administered during cardiopulmo

198 y stable with right ventricular dysfunction, thrombolytic therapy was associated with lower rates of

199 ystolic BP <100 mm Hg) who were eligible for thrombolytic therapy were randomized to either transfer

200 of ST-segment elevation and the frequency of thrombolytic therapy were significantly lower in the sul

201 Thrombolytic therapy with rtPA increases the risk of hem

202 mboembolism at baseline conditions and after thrombolytic therapy with streptokinase or alteplase.

203 on is, however, essential to improve current thrombolytic therapy with tissue plasminogen activator (

204 of patients receiving thrombolytic therapy, thrombolytic therapy within 1 hour of initial ECG, and o

205 d, including vascular pathologies, diabetes, thrombolytic therapy, and dysfibrinogenemia.

206 ss likely to receive aspirin, beta-blockers, thrombolytic therapy, angiography, and angioplasty durin

207 d discusses the current agents available for thrombolytic therapy, as well as indications for their u

208 there was no systematic worsening of time to thrombolytic therapy, balloon inflation, medication use

209 to reduce the complications associated with thrombolytic therapy, broaden the therapeutic window, an

210 t that cardiac rupture can be accelerated by thrombolytic therapy, but the relevance of this risk fac

211 as early enough to make it relevant to acute thrombolytic therapy, early BBB disruption as defined by

212 al data regarding the safety and efficacy of thrombolytic therapy, inferior vena cava filters, and em

213 Despite the benefit of thrombolytic therapy, on the basis of the results of cas

214 shed studies evaluating the effectiveness of thrombolytic therapy, primary percutaneous coronary inte

215 Patients with cardiac arrest, thrombolytic therapy, prior revascularization, or missin

216 includes aggressive wound care, debridement, thrombolytic therapy, restoration of tissue oxygenation,

217 t elevation myocardial infarction undergoing thrombolytic therapy, the degree of ST-segment resolutio

218 tion of patients most likely to benefit from thrombolytic therapy, the eligibility criteria were a pe

219 Percentages of patients receiving thrombolytic therapy, thrombolytic therapy within 1 hour

220 re 2 reperfusion strategies, primary PCI and thrombolytic therapy, which are both supported by clinic

221 ep venous system in 16 patients (80%) during thrombolytic therapy, with complete resolution of sympto

222 ed cerebral artery than systemic intravenous thrombolytic therapy.

223 rculating leukocytes prior to treatment with thrombolytic therapy.

224 rategies to shorten door-to-needle times for thrombolytic therapy.

225 es resulted in complete thrombus lysis after thrombolytic therapy.

226 ours of stroke onset prior to treatment with thrombolytic therapy.

227 Only a minority of stroke patients receive thrombolytic therapy.

228 hway may have beneficial consequences during thrombolytic therapy.

229 tly lower mortality and more frequent use of thrombolytic therapy.

230 mbosis and have significant implications for thrombolytic therapy.

231 e 8-24 h after onset, who are ineligible for thrombolytic therapy.

232 ulmonary embolism or serious bleeding during thrombolytic therapy.

233 ce of asymptomatic pulmonary embolism during thrombolytic therapy.

234 findings support efforts to shorten time to thrombolytic therapy.

235 ass grafting (CABG) is frequently used after thrombolytic therapy.

236 ical stroke and to extend the time window of thrombolytic therapy.

237 ome, other than an increased use of patented thrombolytic therapy.

238 tion MI treated with primary PCI rather than thrombolytic therapy.

239 nary artery bypass graft (CABG) surgery, and thrombolytic therapy.

240 vor with a PE index higher than 60% received thrombolytic therapy.

241 usion with percutaneous coronary stenting or thrombolytic therapy.

242 arly marker of long-term clinical benefit of thrombolytic therapy.

243 yme have potential use in antithrombotic and thrombolytic therapy.

244 ment elevation who have contraindications to thrombolytic therapy.

245 ul as a marker of microvascular injury after thrombolytic therapy.

246 better outcomes with primary PTCA than with thrombolytic therapy.

247 ential to optimize management and triage for thrombolytic therapy.

248 he safety, efficacy, and treatment window of thrombolytic therapy.

249 who are ineligible for standard intravenous thrombolytic therapy; however, its use is limited by the

250 the facilitated approach were mainly seen in thrombolytic-therapy-based regimens.

251 stroke and total stroke rates were higher in thrombolytic-therapy-containing facilitated regimens tha

252 ular and molecular level, only one drug, the thrombolytic tissue plasminogen activator (rt-PA), is ap

253 Thrombolytic tissue plasminogen activator may be a usefu

254 In combination studies with the thrombolytic, tissue plasminogen activator (tPA) using a

255 The addition of thrombolytic to extracorporeal cardiopulmonary resuscita

256 tions associated with late administration of thrombolytic tPA.

257 lar hemorrhage volume (p=.001), but not with thrombolytic treatment (p=.05) or intracerebral hemorrha

258 of the incidence of CLABSI and intracatheter thrombolytic treatment (TT).

259 wever, sex disparities persist in the use of thrombolytic treatment (with alteplase) and lipid testin

260 t included patients who received intravenous thrombolytic treatment after perfusion CT were identifie

261 The paper reviews updates to the thrombolytic treatment as well as catheter-based treatme

262 Thrombolytic treatment did not affect long-term mortalit

263 therefore, encourage clinicians to: consider thrombolytic treatment for a wider variety of patients (

264 iaries aged >=65 years receiving intravenous thrombolytic treatment for acute ischemic stroke at 1490

265 apy strategies has reset a course to advance thrombolytic treatment for acute stroke and promises to

266 herapy to improve the efficacy and safety of thrombolytic treatment for ischaemic stroke.

267 e likelihood of severe disability/death with thrombolytic treatment for SPAN-100-positive (AOR, 0.46

268 orts to accelerate hospital presentation and thrombolytic treatment in patients with stroke.

269 las who were referred for pharmacomechanical thrombolytic treatment in the intervention unit of the R

270 ted with perfusion CT to receive intravenous thrombolytic treatment more than 3 hours after symptom o

271 Thrombolytic treatment of ischemic stroke with tissue pl

272 The long-term effect of thrombolytic treatment of pulmonary embolism (PE) is unk

273 with intermediate-risk PE and the effect of thrombolytic treatment on the persistence of symptoms or

274 uality initiative was associated with faster thrombolytic treatment times for acute ischemic stroke a

275 y representing US clinical practice, earlier thrombolytic treatment was associated with reduced morta

276 ome measure was whether the decision to give thrombolytic treatment was correct, as determined by cen

277 more than 185 mm Hg is a contraindication to thrombolytic treatment with intravenous alteplase in pat

278 Thrombolytic treatment with Plg activators significantly

279 Delayed thrombolytic treatment with recombinant tissue plasminog

280 of the diabody was compared to the standard thrombolytic treatment with recombinant tissue-type plas

281 Performance measurement was based on time-to-thrombolytic treatment with tPA (tissue-type plasminogen

282 s thrombotic occlusions usually resolve with thrombolytic treatment, such as alteplase.

283 To assist hospitals in providing faster thrombolytic treatment, the American Heart Association l

284 atory T cell adoptive transfer may alleviate thrombolytic treatment-induced haemorrhage in stroke vic

285 sured the incidence of ICH following REP and thrombolytic treatment.

286 vant treatment for stroke patients receiving thrombolytic treatment.

287 w findings have significant implications for thrombolytic treatment.

288 ents, and (3) delay in obtaining consent for thrombolytic treatment.

289 Effectiveness of longer duration US and MB thrombolytic treatments were studied (n = 4), which sugg

290 Mild strokes have been poorly represented in thrombolytic trials and only a few series have reported

291 Secondary outcomes were the rate of thrombolytic use, 90-day functional outcomes (Barthel in

292 Use of thrombolytics was associated with lower all-cause mortal

293 Intracatheter instillation of thrombolytics was more frequent in patients who received

294 Intravenous thrombolytics were used at an overall rate of 25% (31 [2

295 Thrombolytics were used at presentation in 19 (35%) pati

296 imaging and new clinical trials that combine thrombolytics with other pharmacological and interventio

297 Activation of the thrombolytic zymogens may therefore allow for both direc

298 Additionally, the thrombolytic zymogens plasminogen, urokinase, and plasma

299 Matriptase was also found to activate thrombolytic zymogens that have been shown to cleave and

300 e examined for their ability to activate the thrombolytic zymogens, and both resulted in activation o