ライフサイエンスコーパス: fibrinolysis

1 n liver by inhibiting degradation of fibrin (fibrinolysis).

2 brin formation, structure, and resistance to fibrinolysis.

3 at acidic pH and increased plasmin-mediated fibrinolysis.

4 able marker of activation of coagulation and fibrinolysis.

5 t aggregation and clot strength, and reduces fibrinolysis.

6 V/Va and regulates intrinsic coagulation and fibrinolysis.

7 intimate connections between coagulation and fibrinolysis.

8 M) in the context of influencing clotting or fibrinolysis.

9 ssue-type plasminogen activator-induced clot fibrinolysis.

10 es on the regulation of fibrin stability and fibrinolysis.

11 ion of tPA, resulting in inhibition of local fibrinolysis.

12 vere histopathological scores, and decreased fibrinolysis.

13 ontains covalently bound OxPL that influence fibrinolysis.

14 minutes after the MA is reached) documented fibrinolysis.

15 y RBC, plasma and platelet transfusions, and fibrinolysis.

16 es of the anticoagulant protein C system and fibrinolysis.

17 the complement system, clotting cascade and fibrinolysis.

18 minogen activator, an important regulator of fibrinolysis.

19 well as enhanced coagulation and suppressed fibrinolysis.

20 ion and tissue-plasminogen activator-induced fibrinolysis.

21 ess the effect of the OxPL on plasminogen on fibrinolysis.

22 access to reperfusion, mainly (53%) through fibrinolysis.

23 percutaneous coronary intervention (PPCI) or fibrinolysis.

24 tion and resulting in B. burgdorferi-induced fibrinolysis.

25 ontrol groups (p<.01), indicating suppressed fibrinolysis.

26 endothelial cell surface, thereby regulating fibrinolysis.

27 incorporated into a fibrin film also inhibit fibrinolysis.

28 lasmin with fibrin and decreases the rate of fibrinolysis.

29 ibitor, alpha(2)-antiplasmin (alpha(2)AP) on fibrinolysis.

30 clots from the vasculature, a process called fibrinolysis.

31 5%-0.8%) had an absolute contraindication to fibrinolysis.

32 s on the basis of modulation of perivascular fibrinolysis.

33 with putative roles in blood coagulation and fibrinolysis.

34 nced by thrombin generation, and tempered by fibrinolysis.

35 ogen) and its effect on fibrin structure and fibrinolysis.

36 ls mediate crosstalk between coagulation and fibrinolysis.

37 RBC-bound scFv/uPA-T caused thrombin-induced fibrinolysis.

38 o fibrin clots increases their resistance to fibrinolysis.

39 ced coarse networks that were susceptible to fibrinolysis.

40 rs, reflective of in vivo clot formation and fibrinolysis.

41 of interleukin-6 and to D-dimer products of fibrinolysis.

42 normally dense fibrin networks that resisted fibrinolysis.

43 cluding proinflammatory actions and impaired fibrinolysis.

44 t structure and increasing its resistance to fibrinolysis.

45 have a coagulation deficiency or a defect in fibrinolysis.

46 ental vascular beds that are associated with fibrinolysis.

47 r reperfusion strategy compared with on-site fibrinolysis.

48 o regulate cellular adhesion, migration, and fibrinolysis.

49 ses including coagulation, inflammation, and fibrinolysis.

50 on, coagulation activation and inhibition of fibrinolysis.

51 ls but also showed a TAFI-dependent delay in fibrinolysis.

52 any conflicting studies on factors affecting fibrinolysis.

53 e a stiffer clot, which is more resistant to fibrinolysis.

54 let dysfunction, endothelial activation, and fibrinolysis.

55 e uPA gene, but not the t-PA gene, inhibited fibrinolysis.

56 a paradigm that is relevant for therapeutic fibrinolysis.

57 lung function and alter systemic markers of fibrinolysis.

58 studies reporting outcomes of treatment with fibrinolysis.

59 ained for 147 patients treated with systemic fibrinolysis.

60 pact clots that resist internal and external fibrinolysis.

61 P inhibition may reduce bleeding by delaying fibrinolysis.

62 chanisms of Abeta(42) involvement in delayed fibrinolysis: (1) through the induction of a tighter fib

63 ith previous bypass surgery, or who received fibrinolysis, 2947 patients were included in the analysi

64 l </=12 hours from onset, 447 (30%) received fibrinolysis (66% prehospital; 97% with subsequent angio

65 pPCI) and in the population seen early (87% fibrinolysis, 85% pPCI beyond 90 minutes from call).

66 Markers of fibrinolysis activation correlate significantly with mar

67 The value of fibrinolysis activity markers is very limited in aiding

68 rough percutaneous coronary intervention (or fibrinolysis), advances in antiplatelet agents and antic

69 To trend fibrinolysis after injury and determine the influence of

70 Real-time confocal analysis of fibrinolysis after recombinant tissue-type plasminogen a

71 tPA) is the major intravascular activator of fibrinolysis and a ligand for receptors involved in cell

72 ury while preserving its salutary effects on fibrinolysis and airway remodeling.

73 We also demonstrated that fibrinolysis and angiogenesis are severely impaired in A

74 -dose of NK administration appears enhancing fibrinolysis and anti-coagulation via several different

75 r-tPA and alpha2-antiplasmin inactivation on fibrinolysis and bleeding were examined in a humanized m

76 A link between excessive fibrinolysis and bradykinin generation that is estrogen

77 the molecular link between blood coagulation/fibrinolysis and CMKLR1-mediated immune responses.

78 ng the association between plasma markers of fibrinolysis and coronary artery disease, to establish t

79 plasmin, a general protease, which promotes fibrinolysis and degradation of extracellular matrix.

80 leukemia cells is associated with excessive fibrinolysis and hemorrhage, whereas anti-A2 autoantibod

81 chymal-transition (EMT), as well as enhanced fibrinolysis and impaired angiogenesis.

82 rk in diabetes is one mechanism for impaired fibrinolysis and increased thrombosis risk in this condi

83 Levels of endothelin-1 and markers of fibrinolysis and inflammation were also measured.

84 at stroke in the baboon without an effect on fibrinolysis and inflammation.

85 n gamma' modulates plasma clot structure and fibrinolysis and is also influenced by factors other tha

86 rs of inflammation and changes in markers of fibrinolysis and markers that affect autonomic control o

87 In contrast, OxPL on plasminogen facilitate fibrinolysis and may reduce atherothrombosis.

88 stabilizes clots and increases resistance to fibrinolysis and mechanical disruption.

89 high-risk patient to primary angioplasty or fibrinolysis and mortality.

90 bal assays that monitor fibrin formation and fibrinolysis and platelet aggregation in whole blood.

91 l rates were not significantly different for fibrinolysis and pPCI, both in the whole population (88%

92 ribute to regulation of the initial stage of fibrinolysis and provide proper orientation of the cross

93 rker profiles reflecting the balance between fibrinolysis and thrombosis and the intensity of inflamm

94 nally, phagocytic leukocytes are involved in fibrinolysis and thrombus resolution, and can regulate c

95 minogen activator-associated plasmin-induced fibrinolysis and/or a tissue-type plasminogen activator-

96 asminogen activator inhibitor-1 (markers for fibrinolysis) and alanine aminotransferase (ALT) (marker

97 n markers of oxidative stress, inflammation, fibrinolysis, and coagulation in nine hemodialysis patie

98 between thrombosis and fibrinolysis favoring fibrinolysis, and diminished intensity of the systemic i

99 factors including anticoagulants, dilution, fibrinolysis, and factor consumption.

100 uding preoperative anticoagulants, dilution, fibrinolysis, and factor consumption.

101 ion of the thrombin activatable inhibitor of fibrinolysis, and in a thrombin-independent, constitutiv

102 x damage, coagulation activation/inhibition, fibrinolysis, and inflammation in trauma patients at adm

103 involving proteases involved in coagulation, fibrinolysis, and inflammation.

104 lps coordinate coagulation, anticoagulation, fibrinolysis, and inflammation.

105 eolytic pathways, such as blood coagulation, fibrinolysis, and inflammation.

106 , exerts pleiotropic effects on coagulation, fibrinolysis, and inflammation.

107 by derivatizing A2, preventing perivascular fibrinolysis, and inhibiting directed endothelial cell m

108 tion, procoagulant or anticoagulant factors, fibrinolysis, and interactions between the coagulation s

109 domain of Fg, which regulates thrombosis and fibrinolysis, and may help explain the pulmonary haemorr

110 ity-driven chronic inflammation and impaired fibrinolysis appear to be major effector mechanisms of t

111 ressive MS motor cortex, where regulation of fibrinolysis appears perturbed.

112 Reduced fibrinolysis appears to be a feature of ESRD, but its co

113 Coagulation and fibrinolysis are important in infections and systemic in

114 tivator inhibitor-1 (PAI-1), an inhibitor of fibrinolysis, are elevated in inflammatory conditions, i

115 k stratification and in identifying impaired fibrinolysis as a potential target for pharmacological m

116 his results in activation of coagulation and fibrinolysis, as may occur upon graft reperfusion in viv

117 ted derivatives have been tested in a plasma fibrinolysis assay and are more effective than the refer

118 c2-treated animals did not influence either fibrinolysis (assessed by tissue plasminogen activator,

119 inhibit thrombin generation and to stimulate fibrinolysis at submicromolar concentration.

120 Patterns of inflammatory, coagulation, and fibrinolysis biomarkers among men may explain reduced sh

121 schemic ex situ NMP results in activation of fibrinolysis, but not of coagulation.

122 ctor XIII (FXIII) stabilizes thrombi against fibrinolysis by cross-linking alpha2-antiplasmin (alpha2

123 of plasminogen in diabetes directly affects fibrinolysis by decreasing plasmin generation and reduci

124 2)-antiplasmin abolishes the potentiation of fibrinolysis by dsDNA.

125 lasmin but increases by 4-5-fold the rate of fibrinolysis by Glu-plasminogen/plasminogen activator.

126 Conversely, DNA could inhibit fibrinolysis by increasing the susceptibility of fibrino

127 tion in livers, mediated by an inhibition of fibrinolysis by PAI-1.

128 (0.1-1.0 mug/ml) does not affect the rate of fibrinolysis by plasmin but increases by 4-5-fold the ra

129 ism by which Abeta-fibrinogen binding delays fibrinolysis by plasmin.

130 ant implications regarding the regulation of fibrinolysis by platelet miRNA under diabetic mellitus.

131 formation, structure, and susceptibility to fibrinolysis by removing them from platelet-free plasma

132 physiological concentrations may potentiate fibrinolysis by stimulating fibrin-independent plasminog

133 2-Antiplasmin (A2AP) is a major inhibitor of fibrinolysis by virtue of its capacity to inhibit plasmi

134 ytopenia, fibrin polymerization defects, and fibrinolysis can be quickly assessed on thromboelastomet

135 pigs might also regulate the coagulation and fibrinolysis cascades and tested this in ex vivo human-t

136 Recently, we reported that impairment of fibrinolysis causes excessive fibrin deposition in NP an

137 y system and pericellular region to regulate fibrinolysis, cell adhesion, and migration.

138 ctivator and promoted clot retraction during fibrinolysis concomitant with an observed PPXbd-mediated

139 Activation of fibrinolysis correlated significantly with the degree of

140 It is not known whether prehospital fibrinolysis, coupled with timely coronary angiography,

141 the uPA-uPAR interaction in cell-associated fibrinolysis critical for suppression of fibrin accumula

142 s factor, interleukin [IL]-6, and IL-10) and fibrinolysis (d-dimer), and lower coagulation biomarkers

143 Willebrand factor, fibrinogen, factor XIII), fibrinolysis (D-dimer, tissue-type plasminogen activator

144 No studies examine fibrinolysis days after injury.

145 sential for fracture repair, but inefficient fibrinolysis decreases endochondral angiogenesis and oss

146 Thus, the regulation of fibrinolysis depends on the starting nature of fibrin fi

147 esponsible for digestion, blood coagulation, fibrinolysis, development, fertilization, apoptosis and

148 rkers of oxidative stress, inflammation, and fibrinolysis during hemodialysis, we conducted a randomi

149 ility to bacterial osteomyelitis, perhaps by fibrinolysis dysfunction.

150 ted with higher concentrations of markers of fibrinolysis, endothelial activation, matricellular prot

151 ation of procoagulation and anticoagulation, fibrinolysis, endothelial cell activation, matricellular

152 iage of stroke victims for intra intravenous fibrinolysis, even though emergency physicians are most

153 tion of the population capable of reaching a fibrinolysis facility </=60 minutes or a PPCI facility <

154 rgency coronary angiography was performed if fibrinolysis failed; otherwise, angiography was performe

155 ignificant pulmonary embolism, physiological fibrinolysis fails to dissolve thrombi acutely and r-tPA

156 e, an altered balance between thrombosis and fibrinolysis favoring fibrinolysis, and diminished inten

157 spitals with a mixed strategy of transfer or fibrinolysis fell from 195 to 138 minutes (P=0.002).

158 curred in 116 of 939 patients (12.4%) in the fibrinolysis group and in 135 of 943 patients (14.3%) in

159 ore intracranial hemorrhages occurred in the fibrinolysis group than in the primary PCI group (1.0% v

160 the primary PCI group (relative risk in the fibrinolysis group, 0.86; 95% confidence interval, 0.68

161 phy was required in 36.3% of patients in the fibrinolysis group, whereas the remainder of patients un

162 Primary systemic fibrinolysis has an unfavorable risk-benefit ratio in in

163 Therapeutic fibrinolysis has been dominated by the experience with t

164 ng activation of the coagulation cascade and fibrinolysis, has been found to be increased during urti

165 research) shows that primary angioplasty and fibrinolysis have equivalent real-world survival.

166 s coronary intervention (PCI) is superior to fibrinolysis if performed in a timely manner but frequen

167 Because plasmin activity controls fibrinolysis in a variety of pathological conditions, in

168 nvincing evidence for the role of endogenous fibrinolysis in ACS, the prognostic value of plasma fibr

169 dissolution revealed abnormal thrombosis and fibrinolysis in AD mice.

170 However, the roles of fibrinogen and fibrinolysis in APAP-induced liver injury are not known.

171 We evaluate evidence for endogenous fibrinolysis in arterial thrombosis and review technique

172 im was to develop new strategies to modulate fibrinolysis in diabetes by interfering with fibrin-C3 i

173 omplex concentrate did not alter the delayed fibrinolysis in high-TM model blood.

174 timized lead compound, CM-352 (2), inhibited fibrinolysis in human whole blood functional assays and

175 impact of chronic inflammation and impaired fibrinolysis in mediating obesity-associated thrombosis

176 ated heparin (UFH) as adjunctive therapy for fibrinolysis in patients with ST-segment elevation myoca

177 rin instead of UFH as adjunctive therapy for fibrinolysis in patients with STEMI is cost effective ac

178 sed instead of UFH as adjunctive therapy for fibrinolysis in patients with STEMI.

179 arious reactants involved in coagulation and fibrinolysis in quiescent plasma.

180 ed to investigate plasminogen activation and fibrinolysis in the 2 types of fibrin, using wild-type t

181 The pivotal role of hypoactive endogenous fibrinolysis in the occurrence of thrombotic cardiovascu

182 asis on the early diagnosis and treatment of fibrinolysis in this cohort.

183 However, the effect of the high plasma TM on fibrinolysis in TM-AC is unknown.

184 om CTEPH patients is relatively resistant to fibrinolysis in vitro.

185 nt macrophages showed defective pericellular fibrinolysis in vitro.

186 CI or rescue PCI after full-dose intravenous fibrinolysis (in event of unanticipated transfer delays)

187 ibitor-1 (PAI-1), an endogenous inhibitor of fibrinolysis, increases APAP-induced liver injury in mic

188 data demonstrate that protracted endogenous fibrinolysis induced by TBI is primarily responsible for

189 finity and effectively prevented plasma clot fibrinolysis induced by tissue plasminogen activator.

190 Circulating thrombin-activatable fibrinolysis inhibitor (TAFI) and plasminogen activator

191 vation of protein C and thrombin-activatable fibrinolysis inhibitor (TAFI) and thereby helps coordina

192 ysis secondary to lower thrombin activatable fibrinolysis inhibitor (TAFI) production.

193 n depletion of PAI-1 or thrombin activatable fibrinolysis inhibitor (TAFI).

194 with TM also activates thrombin-activatable fibrinolysis inhibitor (TAFI).

195 Mature thrombin activatable fibrinolysis inhibitor (TAFIa) is a carboxypeptidase tha

196 plasma by an activated thrombin-activatable fibrinolysis inhibitor (TAFIa)-dependent mechanism.

197 c role for suppression of thrombin-activated fibrinolysis inhibitor activity.

198 activity levels of serum thrombin-activated fibrinolysis inhibitor and plasmin strongly correlated w

199 An alpha2-PI1-8-fused variant of the fibrinolysis inhibitor aprotinin was used to control the

200 ctivator inhibitor-1 or thrombin-activatable fibrinolysis inhibitor display modest phenotypes, but mi

201 tivator inhibitor-1 and thrombin-activatable fibrinolysis inhibitor succumb to yersiniosis with a phe

202 binding protein A, and thrombin-activatable fibrinolysis inhibitor were examined directly.

203 armacologic inhibition of thrombin-activated fibrinolysis inhibitor with UK-396082 could reduce renal

204 asmin complex, D-dimer, thrombin activatable fibrinolysis inhibitor, and lipoprotein(a) for major adv

205 in alpha2-antiplasmin, thrombin-activatable fibrinolysis inhibitor, or fibronectin, indicating RBC r

206 se B (CPB), also called thrombin-activatable fibrinolysis inhibitor, removes the C-terminal arginine

207 ) and B (CPB or activated thrombin-activable fibrinolysis inhibitor, TAFIa) enhanced the bioactivity

208 to 80% with inhibition of thrombin-activated fibrinolysis inhibitor.

209 uggest that plasminogen and plasmin-mediated fibrinolysis is a key modifier of the onset of neuroinfl

210 Fibrinolysis is a valuable alternative for the treatment

211 Increased fibrinolysis is an important component of acute promyelo

212 or capacity but its relative contribution to fibrinolysis is considered marginal compared with urokin

213 rged peptides, the turbidity is enhanced and fibrinolysis is delayed.

214 ons of such markers in reflecting endogenous fibrinolysis is discussed.

215 tasis and wound healing and help explain how fibrinolysis is greatly retarded as clots contract.

216 of S1A proteases involved in coagulation and fibrinolysis is summarized.

217 For acute ischemic stroke, fibrinolysis is the only treatment option with a very na

218 min induction, which may contribute to acute fibrinolysis, is a critical component of extravascular p

219 ctivator inhibitor-1 (PAI-1), which inhibits fibrinolysis, is a key circulating prothrombotic factor

220 IVH treatment by intraventricular fibrinolysis (IVF) was recently linked to reduced mortal

221 to-balloon [D2B] time </=90 min, and time to fibrinolysis </=30 min) with life expectancy and years o

222 tor inhibitor-1 (PAI-1) is known to modulate fibrinolysis, lung injury/fibrosis, and angiogenesis.

223 Prehospital fibrinolysis markedly improved access to timely reperfus

224 nostic role of impaired fibrinolysis, plasma fibrinolysis markers have been investigated in large pro

225 Activation of blood coagulation and fibrinolysis may be associated with increased risk of co

226 Endogenous fibrinolysis may provide a paradigm that is relevant for

227 t tests to assess spontaneous disintegration/fibrinolysis of platelet-rich thrombi under arterial flo

228 while being associated with little systemic fibrinolysis or bleeding.

229 rying a significant risk of causing systemic fibrinolysis or disrupting hemostatic clots.

230 nt-elevation myocardial infarction both with fibrinolysis or percutaneous coronary intervention minim

231 ding or without bleeding treated with either fibrinolysis or primary percutaneous coronary interventi

232 on myocardial infarction treated with either fibrinolysis or primary percutaneous coronary interventi

233 on myocardial infarction treated with either fibrinolysis or primary percutaneous coronary interventi

234 roke, although the thrombi were resistant to fibrinolysis or traditional antithrombotic agents.

235 OR "retinal ischemia" AND "thrombolysis" OR "fibrinolysis" OR "tissue plasminogen activator" OR "stre

236 improve timely access to reperfusion (PPCI, fibrinolysis, or both) were modeled and compared.

237 primary percutaneous coronary intervention, fibrinolysis, or no reperfusion.

238 CRS and control subjects, suggesting reduced fibrinolysis (P < 0.05).

239 We sought to compare coagulation and fibrinolysis parameters between healthy subjects and pat

240 ttokinase (NK) administration on coagulation/fibrinolysis parameters comprehensively in healthy male

241 g administration for analysis of coagulation/fibrinolysis parameters.

242 omocysteinemic by dietary means has impaired fibrinolysis, perivascular fibrin persistence, and atten

243 The existence of primary fibrinolysis (PF) and a defined mechanistic link to the

244 an adverse clinical course include systemic fibrinolysis, pharmacomechanical catheter-directed thera

245 e diagnostic and prognostic role of impaired fibrinolysis, plasma fibrinolysis markers have been inve

246 f coagulation (thrombin-antithrombin [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and complement

247 effects of in vivo plasminogen glycation on fibrinolysis, plasmin generation, protein proteolytic ac

248 r each exposure, ex vivo thrombus formation, fibrinolysis, platelet activation, and forearm blood flo

249 f haemostasis (coagulation, anticoagulation, fibrinolysis, platelets and endothelium).

250 We evaluated the clot retraction rate (CRR), fibrinolysis rate (FR), clot density (CD) (by confocal m

251 nfarction have increased bleeding risks with fibrinolysis relative to whites, yet these data were qui

252 favoring elevated coagulation and disrupted fibrinolysis responses.

253 These findings suggest a role for impaired fibrinolysis resulting in worse gas exchange and decreas

254 hagic complications due in part to excessive fibrinolysis, resulting from the excessive generation of

255 ing reduced thrombin production and enhanced fibrinolysis secondary to lower thrombin activatable fib

256 itions of hyperfibrinolysis (HF; LY30 >/=3), fibrinolysis shutdown (SD; LY30 </=0.8), and normal (LY3

257 Fibrinolysis shutdown is common postinjury and predicts

258 They are complementary in fibrinolysis so that in combination, their effect is syn

259 rain injury (TBI) and massive transfusion on fibrinolysis status.

260 markers associated with vasoconstriction and fibrinolysis, suggesting that OO supplementation may be

261 Abnormal activation of the coagulation and fibrinolysis system is one of the hallmarks of DHF/DSS.

262 , the NMDA-R provides a pathway by which the fibrinolysis system may regulate innate immunity.

263 immunoassays, which replaced earlier global fibrinolysis tests.

264 We developed a multiscale model of fibrinolysis that includes the main chemical reactions:

265 grees C resulted in a decrease in markers of fibrinolysis the next day.

266 nfluences fibrin architecture and attenuates fibrinolysis through reduced binding of fibrinolytic pro

267 role in the generation of plasmin leading to fibrinolysis, thus providing a link to the clinical hemo

268 n addition to functioning as an activator of fibrinolysis, tissue-type plasminogen activator (tPA) in

269 enzymatic processes that mediate endogenous fibrinolysis to physiologically maintain vessel patency.

270 to identify kinetic conditions necessary for fibrinolysis to proceed as a front.

271 se-type plasminogen activator (uPA)-mediated fibrinolysis to the pericellular micro-environment but a

272 rity of the population and improve access to fibrinolysis to those living in regional and remote area

273 platelet thrombi and/or enhanced endogenous fibrinolysis, to reduce infarct size.

274 py) and a series of more than 5 patients for fibrinolysis treatment or more than 20 cases when untrea

275 termine which intervention-catheter-directed fibrinolysis, ultrasound-assisted thrombolysis, percutan

276 r localization during thrombus formation and fibrinolysis under flow are not defined.

277 lation of fibrinolytic proteins that mediate fibrinolysis under flow.

278 These findings support a fibrinolysis-unrelated role for Plg in modulating cell p

279 formed under flow, we examine dose-dependent fibrinolysis using fluorescence microscopy.

280 In contrast, endogenous fibrinolysis, using one-thousandth of the t-PA concentra

281 .63 (95% confidence interval, 0.34-0.91) for fibrinolysis versus pPCI beyond 90 minutes of call in pa

282 .73 (95% confidence interval, 0.50-1.06) for fibrinolysis versus pPCI, 0.57 (95% confidence interval,

283 fidence interval, 0.36-0.88) for prehospital fibrinolysis versus pPCI, and 0.63 (95% confidence inter

284 However, fibrinolysis was associated with a slightly increased ri

285 We found that fibrinolysis was beneficial at 4.5 hours or earlier afte

286 Fibrinolysis was dependent upon flow and the balance bet

287 ood with 5 pM Tf in the presence of CTI, and fibrinolysis was induced by adding tissue plasminogen ac

288 Delayed fibrinolysis was reproduced in high-TM model plasma and

289 65 STEMI-confirmed patients (87.7%), whereas fibrinolysis was required in 16 patients (8.5%), with 56

290 ause of enhanced clot turbidity and delay in fibrinolysis was revealed by a crystal structure of the

291 these NS1-induced Plg cross-reactive Abs on fibrinolysis, we isolated several Plg cross-reactive ant

292 ht to exert its effect through inhibition of fibrinolysis, we undertook exploratory analyses of its e

293 fibrinolytic therapy, especially prehospital fibrinolysis, when primary percutaneous coronary interve

294 ation of dense fibrin networks that resisted fibrinolysis, whereas unstimulated intravascular (endoth

295 tion of the balance between fibrogenesis and fibrinolysis, which results in accumulation of excessive

296 The emerging novel global assays of fibrinolysis will require large-scale clinical trials be

297 factors V and VIII and a derepression of the fibrinolysis with high plasma levels of plasminogen acti

298 Prehospital fibrinolysis with timely coronary angiography resulted i

299 Similarly, inhibiting endogenous fibrinolysis with tranexamic acid reduced retraction of

300 dentified plasminogen, a protein involved in fibrinolysis, wound healing, and tissue remodeling, as a