ライフサイエンスコーパス: fibrinolysis

1 with putative roles in blood coagulation and fibrinolysis.

2 ses including coagulation, inflammation, and fibrinolysis.

3 on, coagulation activation and inhibition of fibrinolysis.

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

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

6 let dysfunction, endothelial activation, and fibrinolysis.

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

8 a paradigm that is relevant for therapeutic fibrinolysis.

9 lung function and alter systemic markers of fibrinolysis.

10 studies reporting outcomes of treatment with fibrinolysis.

11 ained for 147 patients treated with systemic fibrinolysis.

12 by enhanced fibrin formation and suppressed fibrinolysis.

13 pact clots that resist internal and external fibrinolysis.

14 P inhibition may reduce bleeding by delaying fibrinolysis.

15 brin formation, structure, and resistance to fibrinolysis.

16 at acidic pH and increased plasmin-mediated fibrinolysis.

17 t aggregation and clot strength, and reduces fibrinolysis.

18 roteins; and platelet-dependent, accelerated fibrinolysis.

19 V/Va and regulates intrinsic coagulation and fibrinolysis.

20 intimate connections between coagulation and fibrinolysis.

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

22 ssue-type plasminogen activator-induced clot fibrinolysis.

23 es on the regulation of fibrin stability and fibrinolysis.

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

25 affect primary hemostasis, coagulation, and fibrinolysis.

26 vere histopathological scores, and decreased fibrinolysis.

27 ontains covalently bound OxPL that influence fibrinolysis.

28 minutes after the MA is reached) documented fibrinolysis.

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

30 es of the anticoagulant protein C system and fibrinolysis.

31 the complement system, clotting cascade and fibrinolysis.

32 minogen activator, an important regulator of fibrinolysis.

33 well as enhanced coagulation and suppressed fibrinolysis.

34 ion and tissue-plasminogen activator-induced fibrinolysis.

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

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

37 percutaneous coronary intervention (PPCI) or fibrinolysis.

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

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

40 endothelial cell surface, thereby regulating fibrinolysis.

41 incorporated into a fibrin film also inhibit fibrinolysis.

42 lasmin with fibrin and decreases the rate of fibrinolysis.

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

44 ion defect in fibrinolysis, without systemic fibrinolysis.

45 normal fibrin formation kinetics but delayed fibrinolysis.

46 c perturbation of clot structure and delayed fibrinolysis.

47 flicting observations regarding the speed of fibrinolysis.

48 omarkers of inflammation, cardiac injury, or fibrinolysis.

49 fibrin clots protecting them from premature fibrinolysis.

50 tics, alters fibrin morphology, and inhibits fibrinolysis.

51 ents present with low levels of VHA-detected fibrinolysis.

52 ting 1 potential mechanism for modulation of fibrinolysis.

53 n (PCI) reduces mortality when compared with fibrinolysis.

54 any conflicting studies on factors affecting fibrinolysis.

55 able marker of activation of coagulation and fibrinolysis.

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

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

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

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

60 a few studies have compared coagulation and fibrinolysis across species.

61 Markers of fibrinolysis activation correlate significantly with mar

62 alyzed biomarkers of clotting, platelet, and fibrinolysis activation in human; furthermore in vitro s

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

64 To trend fibrinolysis after injury and determine the influence of

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

66 es to basal circulating levels of tPA and to fibrinolysis after vascular injury.

67 plasma tPA activity and as a contributor to fibrinolysis after vascular injury.

68 to stop blood loss and is later destroyed by fibrinolysis, an enzymatic cascade with feedback.

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

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

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

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

73 opment, describes novel therapies to enhance fibrinolysis and decrease inflammation in PE and DVT pat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 nogen activator (tPA) is a major mediator of fibrinolysis and, thereby, prevents excessive coagulatio

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

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

91 , such as pancreatic diseases, inflammation, fibrinolysis, and cancer.

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

93 1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury.

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

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

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

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

98 We examined the relationship between stasis, fibrinolysis, and the development of experimental venous

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

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

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

102 Coagulation and fibrinolysis are important in infections and systemic in

103 This study identifies impaired fibrinolysis as a critical process in post-traumatic sec

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

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

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

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

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

109 A fibrinolysis-based strategy may be entertained at non-PC

110 macrophage requirement for plasmin-mediated fibrinolysis, both in vivo and in vitro, was negated by

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

112 Suppression of fibrinolysis by alpha2AP appears essential for stasis-in

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

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

115 a hemostatic enzyme essential for inhibiting fibrinolysis by irreversibly crosslinking fibrin and ant

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

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

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

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

120 Inhibition of fibrinolysis by the indirect plasmin inhibitor epsilon-a

121 s make the attached fibrin more resistant to fibrinolysis by tissue plasminogen activator (tPA), exac

122 2-Antiplasmin (A2AP) is a major inhibitor of fibrinolysis by virtue of its capacity to inhibit plasmi

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

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

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

126 e protease inhibitor (serpin) that regulates fibrinolysis, cell adhesion and cell motility via its in

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

128 Activation of fibrinolysis correlated significantly with the degree of

129 Tests of endogenous fibrinolysis could be used to identify patients with ACS

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

131 [ESR]), cardiac injury (troponin level), and fibrinolysis (D-dimer level).

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

133 No studies examine fibrinolysis days after injury.

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

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

136 ility to bacterial osteomyelitis, perhaps by fibrinolysis dysfunction.

137 that, in addition to its role in preventing fibrinolysis, elevated PAI-1 inhibits HGF's activation b

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

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

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

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

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

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

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

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

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

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

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

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

150 Therapeutic fibrinolysis has been dominated by the experience with t

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

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

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

154 or ultrasound-facilitated, catheter-directed fibrinolysis improve short-term computed tomographic-mea

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

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

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

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

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

160 The study identifies a critical role of fibrinolysis in macrophage migration, presumably through

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

162 er other serine proteases in blood, inhibits fibrinolysis in plasma more effectively than the gold-st

163 or ultrasound-facilitated, catheter-directed fibrinolysis in the OPTALYSE-PE trial (Optimum Duration

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

165 nt macrophages showed defective pericellular fibrinolysis in vitro.

166 porate into nascent fibrin clots, and impede fibrinolysis in vitro.

167 tumor growth and promoted vascular-directed fibrinolysis in vivo.

168 s of hemostasis (platelets, coagulation, and fibrinolysis) in patients with decompensated cirrhosis w

169 ed resistance of whole blood sickle clots to fibrinolysis, in part by decreasing platelet-derived PAI

170 As for fibrinolysis, increased tissue-type and urokinase-type p

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

172 ots from SCD patients, was more resistant to fibrinolysis, indicating that the cellular fraction of b

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

174 competitively inhibits thrombin-activatable fibrinolysis inhibitor (carboxypeptidase B2) activation

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

176 iting thrombomodulin or thrombin-activatable fibrinolysis inhibitor (TAFI) normalized PG, revealing a

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

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

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

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

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

182 ite cells with LAS, and thrombin-activatable fibrinolysis inhibitor activation peptide antigen with A

183 of VTE, attenuation of thrombin activatable fibrinolysis inhibitor activity is under investigation i

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

185 and decreased levels of thrombin-activatable fibrinolysis inhibitor and alpha2-antiplasmin are counte

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

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

188 om Tgfbr2iECKO mice failed to upregulate the fibrinolysis inhibitor plasminogen activator inhibitor 1

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

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

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

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

193 candidate for development of highly specific fibrinolysis inhibitors with reduced side effects.

194 ew generation of highly potent and selective fibrinolysis inhibitors.

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

196 Endogenous fibrinolysis is a powerful natural defense mechanism aga

197 Fibrinolysis is a valuable alternative for the treatment

198 Increased fibrinolysis is an important component of acute promyelo

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

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

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

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

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

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

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

206 Prehospital fibrinolysis markedly improved access to timely reperfus

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

208 In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and a

209 Endogenous fibrinolysis may provide a paradigm that is relevant for

210 Venous stasis activated fibrinolysis, measured by D-dimer levels, in alpha2AP(-/

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

212 s of stasis-induced deep vein thrombosis and fibrinolysis on thrombosis were examined by inferior ven

213 while being associated with little systemic fibrinolysis or bleeding.

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

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

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

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

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

219 hen predicting the referral for intrapleural fibrinolysis or thoracic surgery (AUC 0.92 vs. 0.76).Con

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

221 studies have shown that impaired endogenous fibrinolysis (or hypofibrinolysis) can be detected in a

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

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

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

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

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

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

228 g administration for analysis of coagulation/fibrinolysis parameters.

229 eously or separately clotting, platelet, and fibrinolysis pathways giving special attention to the re

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

231 HA (rotation thromboelastometry [ROTEM]) and fibrinolysis plasma protein analysis including the fibri

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

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

234 inhibitor of the primary serine protease in fibrinolysis, plasmin.

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

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

237 like and anti-inflammatory activities of the fibrinolysis protease, tissue plasminogen activator tPA,

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

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

240 ith cirrhosis patients without AKI; however, fibrinolysis remained hyperactivated.

241 Whether and how these changes shift fibrinolysis remains to be determined.

242 favoring elevated coagulation and disrupted fibrinolysis responses.

243 or ultrasound-facilitated, catheter-directed fibrinolysis resulted in sustained recovery of RV-to-lef

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

245 TBI had significant increase in incidence of fibrinolysis SD beyond 1 hour after injury as compared t

246 Fibrinolysis SD is a reactive, compensatory mechanism th

247 ithin 1 hour of injury (51%); beyond 1 hour, fibrinolysis SD was the predominant phenotype (1-3 hours

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

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

250 definitions of hyperfibrinolysis (LY30 >=3), fibrinolysis shutdown (SD; LY30 <=0.8), and physiologic

251 Fibrinolysis shutdown is common postinjury and predicts

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

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

254 Pharmacological fibrinolysis stimulation is also used to destroy patholo

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

256 . pestis thwarts T cell defense by promoting fibrinolysis suggests novel therapeutic approaches to am

257 ies for reperfusion therapy include systemic fibrinolysis, surgical pulmonary embolectomy, and a grow

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

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

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

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

262 ormed within 120 minutes of STEMI diagnosis, fibrinolysis therapy should be administered to dissolve

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

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

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

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

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

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

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

270 election and optimization of coagulation and fibrinolysis translational research.

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

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

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

274 lation of fibrinolytic proteins that mediate fibrinolysis under flow.

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

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

277 cterized for their effects on clot structure/fibrinolysis, using turbidimetric and permeation analyse

278 .63 (95% confidence interval, 0.34-0.91) for fibrinolysis versus pPCI beyond 90 minutes of call in pa

279 .73 (95% confidence interval, 0.50-1.06) for fibrinolysis versus pPCI, 0.57 (95% confidence interval,

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

281 However, fibrinolysis was associated with a slightly increased ri

282 Physiologic fibrinolysis was associated with survival at all timepoi

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

284 Prolongation in fibrinolysis was consistent across plasma samples from h

285 Fibrinolysis was dependent upon flow and the balance bet

286 pha2-antiplasmin and fibrin was impaired and fibrinolysis was enhanced.

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

290 igation in PE patients to enhance endogenous fibrinolysis, whereas blockade of leukocyte interaction

291 terial biofilm can cause local inhibition of fibrinolysis, which could have possible deleterious effe

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

293 Catheter-directed fibrinolysis with or without mechanical thrombectomy is

294 Prehospital fibrinolysis with timely coronary angiography resulted i

295 In contrast, inhibition of fibrinolysis with tranexamic acid increased lesion volum

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

297 P2Y12 receptor antagonism with clopidogrel, fibrinolysis with urokinase, or DNA digestion with recom

298 ation is useful to assessing coagulation and fibrinolysis within the same sample.

299 atelet-dependent, gain-of-function defect in fibrinolysis, without systemic fibrinolysis.

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