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1 on time-to-thrombolytic treatment with tPA (tissue-type plasminogen activator).
2 the provisional matrix and the protease tPA (tissue-type plasminogen activator).
3 okinase-type plasminogen activator (uPA) and tissue-type plasminogen activator.
4 minogen activator (uPA) and fibrinogen-bound tissue-type plasminogen activator.
5 a dose-dependent fashion in the presence of tissue-type plasminogen activator.
6 not evaluated as early after stroke onset as tissue-type plasminogen activator.
7 or of both urinary plasminogen activator and tissue-type plasminogen activator.
8 tatic interaction between these residues and tissue-type plasminogen activator.
9 activation of cell-associated plasminogen by tissue-type plasminogen activator.
10 tamate and specific protein ligands, such as tissue-type plasminogen activator.
11 cluding activated alpha(2)-macroglobulin and tissue-type plasminogen activator.
12 roteinase (MMP)-1 and -9, and urokinase- and tissue-type plasminogen activators.
13 accompanied by up-regulation of the neuronal tissue-type plasminogen activator, a serine protease kno
14 8-bromo-cAMP, causes a dramatic increase in tissue-type plasminogen activator activity secondary to
15 n was demonstrated by complete inhibition of tissue-type plasminogen activator activity with supernat
17 ith bleeding complications after intravenous tissue-type plasminogen activator administration to pati
18 thway inhibitor) and hyperfibrinolysis (high tissue-type plasminogen activator) (all p < .05 vs. youn
19 ioidosis have elevated circulating levels of tissue-type plasminogen activator, an important regulato
20 ndard of care: intravenous thrombolysis with tissue-type plasminogen activator and endovascular treat
21 vator inhibitor type 1 formed a complex with tissue-type plasminogen activator and inhibited its prot
22 significant reduction in expression both of tissue-type plasminogen activator and of urokinase-type
23 activation of fibrinolysis (plasma levels of tissue-type plasminogen activator and plasmin-alpha2-ant
24 sis was not influenced by TNFR55:IgG (plasma tissue-type plasminogen activator and plasmin-alpha2-ant
25 levels) and the fibrinolytic system (plasma tissue-type plasminogen activator and plasminogen activa
26 lso providing a common binding site for both tissue-type plasminogen activator and plasminogen via it
27 t amorphous protein aggregates interact with tissue-type plasminogen activator and plasminogen, via a
29 ntiation products, two well-known proteases: tissue-type plasminogen activator and urokinase, as well
30 nhibitor-1 (PAI-1), the primary inhibitor of tissue-type plasminogen activator and urokinase, is know
31 t inhibit several serine proteases including tissue-type plasminogen activator and urokinase-type pla
32 <60 minutes in >50% of patients treated with tissue-type plasminogen activator), and (5) face-to-face
33 angioplasty with a 3- to 4-hour infusion of tissue-type plasminogen activator, and 3 compared angiop
34 ligands, including matrix metalloprotease-9, tissue-type plasminogen activator, and alpha(2)-macroglo
35 ed protein, urokinase plasminogen activator, tissue-type plasminogen activator, and plasminogen activ
36 of the fibrinolytic system (plasma levels of tissue-type plasminogen activator, and plasminogen activ
37 ay containing purified thrombin, fibrinogen, tissue-type plasminogen activator, and plasminogen, clot
38 (intercellular adhesion molecule-1, ICAM-1), tissue-type plasminogen activator, and TM-inducible gluc
39 ulted in increased plasminogen activation by tissue-type plasminogen activator, and was dependent on
40 e to four weeks (p < 0.03) and a decrease in tissue-type plasminogen activator antigen from baseline
42 in cholesterol, homocysteine, triglycerides, tissue-type plasminogen-activator antigen, and C-relativ
43 ciated plasmin-induced fibrinolysis and/or a tissue-type plasminogen activator-associated decrease in
46 The LRP1 agonists, alpha2-macroglobulin and tissue-type plasminogen activator, attenuated expression
47 demonstrated that hepsin did not cleave pro-tissue-type plasminogen activator but efficiently conver
48 Canada are limited at present to intravenous tissue-type plasminogen activator, but bleeding complica
50 uding plasminogen activators (urokinase- and tissue-type plasminogen activators), coagulation enzymes
52 ng infection with Burkholderia pseudomallei, tissue-type plasminogen activator-deficient mice were pr
54 rs formed with decorin underwent accelerated tissue-type plasminogen activator-dependent fibrinolysis
55 conventional approaches such as recombinant tissue-type plasminogen activator, direct thrombin inhib
58 s study, we aimed to investigate the role of tissue-type plasminogen activator during melioidosis.
60 nditioning hiNPC with enzymatically-inactive tissue-type plasminogen activator (EI-tPA), prior to gra
61 ide (LPS), including: enzymatically-inactive tissue-type plasminogen activator (EI-tPA); activated al
62 ligands, including alpha2-macroglobulin and tissue-type plasminogen activator, failed to cause LRP1
63 n (81%) were treated with intracoronary tPA (tissue-type plasminogen activator) followed by systemic
64 STO (Global Utilization of Streptokinase and Tissue-Type Plasminogen Activator for Occluded Coronary
65 low-dose (25 mg), slow infusion (6 hours) of tissue-type plasminogen activator for the treatment of p
66 lobal Utilization of Streptokinase and t-PA [tissue-type plasminogen activator] for Occluded Coronary
68 sed by Burkholderia pseudomallei, endogenous tissue-type plasminogen activator has harmful effects wi
70 nd more eligible patients to be treated with tissue-type plasminogen activator if onset is </=2 hours
71 dosis was associated with elevated levels of tissue-type plasminogen activator in lungs of infected w
74 1, 2010 and March 31, 2015 and who received tissue-type plasminogen activator in the emergency depar
75 10 patients with IS treated with intravenous tissue-type plasminogen activator in the Get With The Gu
76 ling proteins showed a higher abundance (eg, tissue-type plasminogen activator) in early compared wit
77 n plasma of pregnant women inhibits FXIa and tissue-type plasminogen activator-induced clot fibrinoly
79 formation but did not affect plasminogen and tissue-type plasminogen activator interactions with Fgal
80 ng patients with IS treated with intravenous tissue-type plasminogen activator is associated with hig
81 ents with acute ischemic stroke treated with tissue-type plasminogen activator is associated with imp
84 s known regarding outcomes after intravenous tissue-type plasminogen activator (IV tPA) therapy for a
85 ecommend against the use of intravenous tPA (tissue-type plasminogen activator; IV tPA) in acute isch
86 ulin G caused blisters to the same degree in tissue-type plasminogen activator knockout and control m
88 acute ischemic stroke with intravenous tPA (tissue-type plasminogen activator) may increase the risk
89 man plasminogen and facilitated the latter's tissue-type plasminogen activator-mediated activation to
90 -inducing activity of IGFBP3 is inhibited by tissue-type plasminogen activator-mediated proteolysis,
91 nase-type plasminogen activator mRNA but not tissue-type plasminogen activator mRNA correlated with f
93 n agreement, the influence of plasminogen or tissue-type plasminogen activator on binding of apo(a) t
95 ts function as an inhibitor of urokinase and tissue-type plasminogen activator (PA), PA inhibitor-1 (
97 ine proteases urinary plasminogen activator, tissue-type plasminogen activator, plasmin and thrombin
98 ytic system (plasminogen activator activity, tissue-type plasminogen activator, plasminogen activator
99 on of fibrinolysis (plasma concentrations of tissue-type plasminogen activator, plasminogen activator
100 of the fibrinolytic system (plasma levels of tissue-type plasminogen activator, plasminogen activator
102 inogen, factor XIII), fibrinolysis (D-dimer, tissue-type plasminogen activator, plasminogen activator
103 action of apo(a) with the ternary complex of tissue-type plasminogen activator, plasminogen and fibri
104 ronectin, vitronectin, laminin, single-chain tissue-type plasminogen activator, plasminogen, or any p
105 The predictive value of plasma levels of tissue-type plasminogen activator, platelet activator in
106 ms (MT1B/MT1A/MT-1F; from 2.9- to 3.2-fold), tissue-type plasminogen activator precursor (PLAT; 2.8-f
107 the isolated recombinant kringle 2 domain of tissue-type plasminogen activator (r-K2tPA), an amino ac
109 National guidelines endorse recombinant tissue-type plasminogen activator (r-tPA) in eligible pa
110 given to IL-10 (-/-) mice normalized the PAI/tissue-type plasminogen activator ratio, reduced pulmona
114 sttreatment of stroke with recombinant human tissue-type plasminogen activator (rht-PA) constrains th
115 e randomized to a 50-mg bolus of recombinant tissue-type plasminogen activator (rt-PA) (alpha half-li
117 amma (rIFN-gamma, Actimmune) and recombinant tissue-type plasminogen activator (rt-PA, Activase) to m
119 will maximally accelerate thrombolysis by r-tissue-type plasminogen activator (rTPA) and reduce resi
120 were exposed to 10 to 1000 ng/mL recombinant tissue-type plasminogen activator (RTPA), urokinase-type
124 the chymotrypsin family of serine proteases, tissue type plasminogen activator (t-PA) is not synthesi
125 s 120 times more efficiently by u-PA than by tissue type plasminogen activator (t-PA), an intimately
126 study compared the activities of recombinant tissue-type plasminogen activator (t-PA) and a plasminog
127 s is regulated in part by the interaction of tissue-type plasminogen activator (t-PA) and plasminogen
128 identified the currently available doses of tissue-type plasminogen activator (t-PA) and recombinant
129 for two intimately related serine proteases, tissue-type plasminogen activator (t-PA) and urokinase-t
132 ptide (TAP), after thrombolytic therapy with tissue-type plasminogen activator (t-PA) in a canine mod
137 the vascular endothelium locally to release tissue-type plasminogen activator (t-PA) is critical for
138 the chymotrypsin family of serine proteases, tissue-type plasminogen activator (t-PA) is not synthesi
139 n this study, we demonstrate that VDAC binds tissue-type plasminogen activator (t-PA) on human neurob
140 from all 358 patients with AMI randomized to tissue-type plasminogen activator (t-PA) or primary PTCA
141 ut not noncovalent Michaelis complexes, with tissue-type plasminogen activator (t-PA) or urokinase (u
142 t are efficiently and selectively cleaved by tissue-type plasminogen activator (t-PA) or urokinase-ty
144 y of vascular endothelium to locally release tissue-type plasminogen activator (t-PA) represents an i
145 ting enzyme (ACE) inhibition potentiates the tissue-type plasminogen activator (t-PA) response to exo
146 ve 30-day mortality benefit with accelerated tissue-type plasminogen activator (t-PA) versus streptok
149 1 patients randomized to receive accelerated tissue-type plasminogen activator (t-PA), streptokinase
150 ract differently with streptokinase (SK) and tissue-type plasminogen activator (t-PA), which could re
151 is has been dominated by the experience with tissue-type plasminogen activator (t-PA), which proved l
152 dy, we demonstrate that GRP78 also binds the tissue-type plasminogen activator (t-PA), which results
155 imultaneous decrease in the concentration of tissue-type plasminogen activator (t-PA)/PAI-1 complexes
157 and inflammatory marker proteins (including tissue-type plasminogen activator [t-PA], plasminogen ac
158 l evidence that maspin specifically inhibits tissue-type plasminogen activator that is associated wit
159 solve thrombi acutely and r-tPA (recombinant tissue-type plasminogen activator) therapy may be requir
160 333 patients (24%) who received recombinant tissue-type plasminogen activator, there was also no ben
164 urified protein is an efficient inhibitor of tissue type plasminogen activator (tPA), having an appar
166 e demonstrate that an increase in endogenous tissue-type plasminogen activator (tPA) activity in the
169 l analysis of fibrinolysis after recombinant tissue-type plasminogen activator (tPA) administration r
170 ing further reduction in treatment times for tissue-type plasminogen activator (tPA) administration.
174 t defensin inhibits fibrinolysis mediated by tissue-type plasminogen activator (tPA) and plasminogen.
175 trinsic tryptophan fluorescence of two-chain tissue-type plasminogen activator (tPA) and the proteina
177 ptide-blocked PAI-1 was a substrate for both tissue-type plasminogen activator (tPA) and trypsin and
179 tor-1 (PAI-1) to serine proteinases, such as tissue-type plasminogen activator (tPA) and urokinase-ty
180 teolysis, we explored the regulatory role of tissue-type plasminogen activator (tPA) and urokinase-ty
181 controls; in contrast, transcripts for both tissue-type plasminogen activator (tPA) and urokinase-ty
182 ivated into plasmin by two serine proteases: tissue-type plasminogen activator (tPA) and urokinase-ty
183 activator inhibitor 1 (PAI-1) that preserved tissue-type plasminogen activator (tPA) and urokinase-ty
184 opulmonary bypass (CPB) on PAI-1 antigen and tissue-type plasminogen activator (tPA) antigen and acti
185 ee measures of plasma fibrinolytic activity: tissue-type plasminogen activator (TPA) antigen, plasmin
186 (Fn) enhances plasminogen (Pg) activation by tissue-type plasminogen activator (tPA) by serving as a
190 e hypothesis, namely, that marked release of tissue-type plasminogen activator (tPA) followed by dela
192 cations of the thrombomodulin (TM) gene, the tissue-type plasminogen activator (tPA) gene, and the ur
193 w bolus fibrinolytics derived from the human tissue-type plasminogen activator (tPA) have emerged as
195 ates have been synthesized and evaluated for tissue-type plasminogen activator (tPA) hydrolysis in an
196 al trials suggest the benefit of intravenous tissue-type plasminogen activator (tPA) in acute ischemi
198 After stroke, the thrombolytic effect of tissue-type plasminogen activator (tPA) in the intravasc
201 functioning as an activator of fibrinolysis, tissue-type plasminogen activator (tPA) interacts with n
207 e best-known function of the serine protease tissue-type plasminogen activator (tPA) is as a thrombol
211 1 (PAI-1), a rapid inhibitor of both uPA and tissue-type plasminogen activator (tPA) is the major phy
214 estatic liver disease in mice suggested that tissue-type plasminogen activator (tPA) or urokinase pla
218 ranular colocalization of GH with endogenous tissue-type plasminogen activator (tPA) was also demonst
219 strated benefit to expanding the intravenous tissue-type plasminogen activator (tPA) window from 3 to
220 domized, blinded, dose-ranging comparison of tissue-type plasminogen activator (TPA) with a direct-ac
223 on of some early markers of differentiation, tissue-type plasminogen activator (tPA), AFP and keratin
224 urokinase-type plasminogen activator (uPA), tissue-type plasminogen activator (tPA), and plasma kall
225 activator (uPA), urokinase receptor (uPAR), tissue-type plasminogen activator (tPA), and plasminogen
226 L insertion for reactions with beta-trypsin, tissue-type plasminogen activator (tPA), and urokinase.
227 roserpin, a recently identified inhibitor of tissue-type plasminogen activator (tPA), is primarily lo
228 d thrombolysis, with either streptokinase or tissue-type plasminogen activator (tPA), on argatroban's
229 ll-free system, plasminogen activators [uPA, tissue-type plasminogen activator (tPA), or streptokinas
230 PAI-1, the primary physiologic regulator of tissue-type plasminogen activator (tPA), prolonged the t
231 n the luminal surface expressed the mRNA for tissue-type plasminogen activator (TPA), urokinase type
232 a showed a temporally enhanced expression of tissue-type plasminogen activator (tPA), urokinase-type
234 oxypeptidase activity in human plasma delays tissue-type plasminogen activator (TPA)-induced clot lys
245 hy confirmed clot dissolution in recombinant tissue-type plasminogen activator-treated animals, but e
246 here were 15 191 of 44 410 (34%) intravenous tissue-type plasminogen activator-treated IS patients wi
247 of the thrombus was detected in recombinant tissue-type plasminogen activator-treated rats but not i
248 ve thrombosis model) followed by recombinant tissue-type plasminogen activator treatment (10 mg/kg, I
250 red with prothrombin-deficient plasma delays tissue-type plasminogen activator-triggered lysis; this
252 not observed with proteases like trypsin and tissue-type plasminogen activator, unless the RGD sequen
253 mice individually deficient for plasminogen, tissue-type plasminogen activator, urokinase-type plasmi
254 tion for Acute Ischemic Stroke network: tPA (tissue-type plasminogen activator) use, complications re
261 modulates the interaction of plasminogen and tissue-type plasminogen activator with cultured human en
262 in(ogen) alphaC-domains bind plasminogen and tissue-type plasminogen activator with high affinity in
263 TEMI enrolled in the Enoxaparin Tenecteplase-Tissue-Type Plasminogen Activator With or Without Glycop
265 s heparin; (3) streptokinase plus alteplase (tissue-type plasminogen activator) with intravenous hepa
266 ement and supplement intravenous recombinant tissue-type plasminogen activator within the first 3 hou