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1 t-PA also induced marked shape changes in both brain end
2 t-PA caused a concentration-dependent increase in permea
3 t-PA induces SK-N-SH cell proliferation via binding to G
4 t-PA inhibition markedly reduced contraction of the guin
5 r basal (P<0.02) and SP-stimulated (P=0.059) t-PA production but similar basal and stimulated PAI-1 p
6 ion suggested a risk model including IL-1ra, t-PA, and the Framingham Offspring Study T2D score, but
7 al score of multiple markers [interleukin-6, t-PA, intercellular adhesion molecule 1, and lipoprotein
10 milar inhibition, implying a role for both a t-PA receptor, most likely a low-density lipoprotein rec
11 ity is the result of a mechanism involving a t-PA lysine-dependent binding site in the GRP78 amino ac
12 thin two hours after the administration of a t-PA bolus occurred in 31 patients in the target group (
13 90 min TIMI 3 flow are use of an accelerated t-PA regimen (vs. streptokinase containing regimens) (ch
14 ndicate that ultrasound exposure accelerates t-PA binding, alters binding affinity, and increases max
15 D646E]Glu-Pg, by either tissue Pg activator (t-PA) or urokinase (u-PA) were compared when these Pg fo
16 A), as well as by added tissue Pg Activator (t-PA), suggesting that ADA and Pg bind simultaneously to
19 , intrapleural tissue plasminogen activator (t-PA) and DNase, t-PA and placebo, or DNase and placebo.
22 doses of tissue-type plasminogen activator (t-PA) and recombinant tissue-type plasminogen activator
23 reactant, and tissue plasminogen activator (t-PA) antigen, a marker of endothelial dysfunction, even
24 of circulating tissue plasminogen activator (t-PA) antigen, D-dimer and von Willebrand factor (VWF) w
25 fragment 1+2, tissue plasminogen activator (t-PA) antigen, t-PA-plasminogen-activator inhibitor type
27 of why plasmin/tissue plasminogen activator (t-PA) can both activate and deactivate platelets prior t
29 2J2, increased tissue plasminogen activator (t-PA) expression by 2.5-fold without affecting plasminog
30 of intravenous tissue plasminogen activator (t-PA) for patients with moderate-to-severe acute ischemi
31 of plasmin by tissue plasminogen activator (t-PA) in the presence of APL cells that did or did not h
33 lasminogen and tissue plasminogen activator (t-PA) independently at the cell surface, thereby enhanci
34 protease tissue-type plasminogen activator (t-PA) initiates the fibrinolytic protease cascade and pl
35 o release tissue-type plasminogen activator (t-PA) is critical for effective endogenous fibrinolysis.
36 ed, although a tissue plasminogen activator (t-PA) is recommended to restore patency to occluded cath
37 Currently, tissue plasminogen activator (t-PA) is the only approved thrombolytic drug for ischemi
38 sion levels of tissue plasminogen activator (t-PA) mRNA and protein were significantly decreased in N
40 xes, with tissue-type plasminogen activator (t-PA) or urokinase (u-PA) resulted in rapid decreases of
41 leaved by tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA).
42 y release tissue-type plasminogen activator (t-PA) represents an important endogenous defence mechani
44 Stroke (NINDS) tissue plasminogen activator (t-PA) Stroke Trial to examine the relationship between a
45 in response to tissue plasminogen activator (t-PA) treatment in the acute phase of ischemic stroke.
46 Bowes melanoma tissue-plasminogen activator (t-PA) were found to possess Galbeta1-->4GlcNAcbeta1-->,
47 d reduced-dose tissue plasminogen activator (t-PA) will enhance infarct artery patency at 60 min in p
48 e treated with tissue plasminogen activator (t-PA) within three hours after the onset of symptoms of
50 clots such as tissue plasminogen activator (t-PA), connective tissue activation peptide III (CTAP II
52 n, factor VII, tissue plasminogen activator (t-PA), LDL-C, von Willebrand factor, and soluble tumor n
53 ibrin D-dimer, tissue plasminogen activator (t-PA), leukocyte elastase, and lipoprotein(a) (all P<0.0
54 ence with tissue-type plasminogen activator (t-PA), which proved little better than streptokinase in
55 binds the tissue-type plasminogen activator (t-PA), which results in a decrease in K(m) and an increa
61 cclusion, tissue-type plasminogen activator (t-PA; 1.42 mg/kg) was given intravenously over 90 minute
63 lytic factors (tissue plasminogen activator [t-PA] and plasminogen activator inhibitor-1 [PAI-1]) are
66 th recombinant tissue plasminogen activator [t-PA], mechanical clot disruption or retrieval, or a com
67 including tissue-type plasminogen activator [t-PA], plasminogen activator inhibitor type 1 [PAI-I]),
68 dest reductions in bradykinin-induced active t-PA release (reduced by 37%, p = 0.03) and had a marked
70 ified A2M serum levels at baseline and after t-PA infusion, but not mRNA expression or protein struct
73 reduced inhibitory activity of PAI-1 against t-PA but not u-PA suggested that the mechanism of loop i
74 asmin inhibitor, antibodies directed against t-PA and u-PA, and epsilon-aminocaproic acid, a lysine a
75 ase tissue plasminogen activator (alteplase, t-PA), and have prolonged half-life features permitting
77 , for example GLUT-1, MT-1, CELF, MKP-1, and t-PA did not show any hypoxic regulation in either astro
78 azard ratio [HR] 1.28, 95% CI 1.03-1.59) and t-PA (HR 1.30, 1.02-1.65) were associated with incident
79 peak at 14:00 hours, CRP at 15:00 hours, and t-PA at 10:00 hours with diurnal variations of 10%, 34%,
83 tial fibrosis in Pg(-)(/-), u-PA(-)(/-), and t-PA(-)(/-) mice relative to WT and u-PAR(-)(/-) mice.
86 exin II-mediated assembly of plasminogen and t-PA on monocyte/macrophages contributes to plasmin gene
87 xin II (Ann-II) as a co-receptor for Plg and t-PA that promotes and localizes plasmin generation near
88 sted odds of elevated C-reactive protein and t-PA (highest tertile versus lowest tertile) were 0.56 (
89 was Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) bleeding.
90 the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) criteria.
91 the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) definition.
92 the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO)-III Trial.
93 1.65) were associated with incident T2D, and t-PA predicted 5-year transition to hyperglycemia (odds
94 ivity and protein levels of tetranectin, and t-PA and its endogenous inhibitor PAI-1, were subsequent
95 (CRP), tissue plasminogen activator antigen (t-PA) and von Willebrand factor are associated with inci
96 ; the plasma concentrations of t-PA antigen, t-PA-PAI-1 complex, D-dimer, and plasmin-antiplasmin com
97 tissue plasminogen activator (t-PA) antigen, t-PA-plasminogen-activator inhibitor type 1 (PAI-1) comp
99 ke, continuous transcranial Doppler augments t-PA-induced arterial recanalization, with a nonsignific
101 y irreversible acyl-enzyme complexes between t-PA and PAI-1, suggesting that the physiologic effect o
103 solute difference in mortality rates between t-PA and r-PA progressively narrowed over the predetermi
104 rinolysis in an in vitro system activated by t-PA, the results being used as measures of binding affi
105 tease catalytic triad.) Glu-Pg activation by t-PA was enhanced on HUVEC compared with the solution ph
106 es that were labile to selective cleavage by t-PA or u-PA when in the context of a peptide were intro
108 e of conversion of plasminogen to plasmin by t-PA was affected when platelets were added to the react
109 generated on the cell surface selectively by t-PA, modulates the astrocytic cytoskeleton, leading to
112 he catalytic efficiency of mature, two-chain t-PA toward plasminogen in the absence of a fibrin co-fa
114 ctor IX and amidolytic activity of Chromozym t-PA with IC50 values of 1.6 +/- 1.2, 3.5 +/- 0.3, and 8
115 al lysis of a fibrin-containing plasma clot, t-PA-dependent plasmin generation at the endothelial cel
118 that tissue plasminogen activator-dependent (t-PA- dependent) conversion of plasminogen to active pla
120 in apart) with a 48-h infusion and half-dose t-PA (Group II) is associated with improved quality and
121 bound to the cell in the presence of either t-PA or u-PA, conversion to Lys-Pg was observed, but con
123 , stepwise analyses identified only elevated t-PA and low HDL cholesterol levels as significant (P </
130 he acute effects of oestrogen on endothelial t-PA release, bradykinin and sodium nitroprusside dose-r
132 smin generation in the presence of exogenous t-PA, and this activity was largely attributable to anne
134 nding odds ratios were 1.07 (0.99, 1.14) for t-PA antigen, 1.06 (1.00, 1.13) for D-dimer and 1.08 (1.
136 usted odds ratios were 1.13 (1.06, 1.21) for t-PA antigen (13 studies, 5494 cases), 1.23 (1.16, 1.32)
137 tes were 9.1% for SK with hirudin, 10.3% for t-PA with hirudin, 10.5% for t-PA with heparin and 14.9%
138 er baseline level were 1.25 (1.18, 1.33) for t-PA antigen, 1.01 (0.95, 1.07) for D-dimer and 1.11 (1.
139 udin, 10.3% for t-PA with hirudin, 10.5% for t-PA with heparin and 14.9% for SK with heparin (for tre
141 II peptide mimicking sequences necessary for t-PA binding blocked endothelial cell invasion of Matrig
142 than in GUSTO-I, in which mortality rate for t-PA versus streptokinase between 30 days and 1-year was
144 ystemic inflammation augmented local forearm t-PA release in men, which suggests that acute inflammat
149 ncreased carotid and femoral IMTs and higher t-PA and PAI-I levels, indicating vascular damage and pe
153 e highest dose of bradykinin the increase in t-PA antigen release was approximately 35 % less (P < 0.
155 gene transcription and a 3-fold increase in t-PA fibrinolytic activity and was blocked by the CYP in
156 ions, which was associated with increases in t-PA (29%; P=0.03) and decreases in PAI-1 (48%; P=0.01)
157 ession correlated with a 4-fold induction in t-PA gene transcription and a 3-fold increase in t-PA fi
161 in C supplementation significantly increased t-PA release in overweight/obese adults (from 0.2 +/- 0.
163 nd had a marked impairment of SFLLRN-induced t-PA antigen (p = 0.02) and activity (p = 0.006) release
167 in the endovascular-therapy and intravenous t-PA groups were similar for mortality at 90 days (19.1%
169 We conclude that the efficacy of intravenous t-PA in patients with acute ischemic stroke may be enhan
172 my with the stent retriever plus intravenous t-PA reduced disability at 90 days over the entire range
173 o were receiving or had received intravenous t-PA to continue with t-PA alone (control group) or to u
174 igible patients who had received intravenous t-PA within 3 hours after symptom onset to receive addit
177 rapy group (30.4%) and 63 in the intravenous t-PA group (34.8%) were alive without disability (odds r
180 stent retriever, in addition to intravenous t-PA, increases reperfusion rates and may improve long-t
182 the middle cerebral artery with intravenous t-PA within three hours after the onset of symptoms.
184 ovascular therapy and 38.7% with intravenous t-PA; absolute adjusted difference, 1.5 percentage point
186 ng a mouse model of ischemic stroke and late t-PA intervention, the neuroprotective activity of a mur
189 d 1.33 microg/kg per min infusion with 50 mg t-PA (Group I); 2) 180/90 (10 min apart) and 2.0 g/kg pe
190 0 min apart) and 2.0 g/kg per min with 50 mg t-PA (Group II); or 3) full-dose, weight-adjusted t-PA (
192 o g/min) on forearm blood flow (FBF) and net t-PA release before and during intra-arterial infusion o
195 laprilat significantly increased resting net t-PA release (from 0.6+/-0.4 to 1.7+/-0.6 ng. min(-1) x
196 odermal cell line, the possibility of neural t-PA interacting with the L2/HNK-1-recognizing molecule,
200 lative arterial stasis and near abolition of t-PA release will strongly promote clot propagation and
202 in addition to a significant augmentation of t-PA antigen (45 +/- 9 ng/100 ml/min at peak dose vs. 24
204 ized the effects of ultrasound on binding of t-PA to fibrin using a novel system in which radiolabele
209 oth increases); the plasma concentrations of t-PA antigen, t-PA-PAI-1 complex, D-dimer, and plasmin-a
211 1, suggesting that the physiologic effect of t-PA-NSP interactions may be more complex than previousl
214 rasound (1) greatly augments the efficacy of t-PA-mediated thrombolysis, (2) seems safe, and (3) has
215 Confocal images reveal the extension of t-PA axons to arterioles serving heart, brain, kidney, l
216 inolytic properties through the induction of t-PA and suggest that endothelial CYP2J2 may play an imp
217 romoter is cAMP-responsive, and induction of t-PA gene transcription by EETs correlated with increase
225 stochemistry demonstrated clear reduction of t-PA in NP, primarily in the epithelium and glands.
228 gular aerobic exercise on the net release of t-PA across the human forearm in vivo using both cross-s
234 ghtings confirm the existence of a system of t-PA axons that is prominent in arterioles, and compatib
235 ed the kinetic properties of new variants of t-PA that contained point mutations at position 192.
236 uring 100 ng/min bradykinin, P=0.001) and on t-PA release 14-fold (from 21.2+/-7.9 to 317.4+/-118.9 n
241 losartan but not of enalapril reduced plasma t-PA (11%; P=0.003) and PAI-1 (38%; P<0.001) antigen con
245 flow was present in 4 of 12 cases receiving t-PA alone compared with 10 of 12 cases receiving t-PA p
248 Rho kinase blocked these changes and reduced t-PA/plasminogen-mediated increase in permeability.
253 , the capacity of the endothelium to release t-PA increased approximately 55 % (P < 0.05) to levels s
256 ell surface protein annexin II can stimulate t-PA-mediated plasminogen activation in the complete abs
260 s stimulated the generation of cell-surface, t-PA-dependent plasmin twice as efficiently as the t(15;
262 se, anti-annexin II IgG directed against the t-PA-binding tail domain inhibited plasminogen-dependent
263 erence in mortality at 12 months between the t-PA group and the placebo group (24 percent vs. 28 perc
264 found that the global statistic favored the t-PA group (odds ratio for a favorable outcome at 6 mont
266 , mean TIMI grade flow was 0.75+/-1.4 in the t-PA alone group versus 2.58+/-0.9 in the t-PA plus ultr
267 90 minutes, the mean TIMI grade flow in the t-PA alone group was 0.92+/-1.4 compared with 2.42+/-1.9
270 change in pleural opacity was greater in the t-PA-DNase group than in the placebo group (-29.5+/-23.3
271 rgical referral at 3 months was lower in the t-PA-DNase group than in the placebo group (2 of 48 pati
276 us fibrinolysis, using one-thousandth of the t-PA concentration, is regularly lysing fibrin and induc
277 a transgenic mouse whose expressions of the t-PA promoter and enhanced green fluorescent protein are
278 of t-PA antigen correlated with that of the t-PA-PAI-1 complex in a linear regression model (squared
279 or acute ischemic stroke patients within the t-PA window who are ineligible for IV t-PA but have a la
280 r occlusion dose-dependently dissolved these t-PA-resistant thrombi resulting in fast restoration of
282 to a favorable 3 month outcome, response to t-PA, 3 month mortality, or risk of intracerebral hemorr
289 -like receptor and that its association with t-PA, Pg, and VDAC on the cell surface may be part of a
291 tivator, reteplase (r-PA), was compared with t-PA in the Global Utilization of Streptokinase and t-PA
292 otting, consistent with PAI-1 complexed with t-PA, as well as bands consistent with cleaved PAI-1, su
293 d received intravenous t-PA to continue with t-PA alone (control group) or to undergo endovascular th
294 to -2.4; P=0.005); the change observed with t-PA alone and with DNase alone (-17.2+/-24.3 and -14.7+
298 acute ischemic stroke who were treated with t-PA within three hours after the onset of symptoms were
299 th an Apo E2 phenotype who were treated with t-PA, the odds ratio (OR) of a favorable outcome at 3 mo
300 ncluded 1,172 patients who were treated with t-PA; 20.9% of them developed HT as evaluated by systema
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