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1                                              rt-PA (recombinant tissue-type plasminogen activator) is
2 te consisted of either (1) plasma alone, (2) rt-PA, (3) OFP t-ELIP, (4) rt-PA and US, (5) OFP t-ELIP
3 re: 1) Ep (n = 6); 2) Ep + rt-PA (n = 6); 3) rt-PA (n = 6); and 4) placebo (n = 4).
4 plasma alone, (2) rt-PA, (3) OFP t-ELIP, (4) rt-PA and US, (5) OFP t-ELIP and US, (6) Definity and US
5 P t-ELIP and US, (6) Definity and US, or (7) rt-PA, Definity, and US (n = 16 clots per group).
6 y, and 220 kHz pulsed ultrasound accelerated rt-PA thrombolysis in a preclinical animal model of vasc
7 The recombinant tissue plasminogen activator rt-PA has been shown to significantly increase the numbe
8 combinant tissue-type plasminogen activator (rt-PA) (alpha half-life 4.5 min) or to placebo followed
9 us recombinant tissue plasminogen activator (rt-PA) after ischaemic stroke improves outcome.
10 us recombinant tissue plasminogen activator (rt-PA) are discussed.
11 ed recombinant tissue plasminogen activator (rt-PA) directly before reperfusion, and assessed neurolo
12 ombinant human tissue plasminogen activator (rt-PA) glycoprotein.
13 V) recombinant tissue plasminogen activator (rt-PA) has been demonstrated, endovascular therapy is an
14 combinant tissue-type plasminogen activator (rt-PA) improves outcomes for patients with acute ischemi
15 by recombinant tissue plasminogen activator (rt-PA) in laboratory and clinical studies.
16 ombined with low-dose plasminogen activator (rt-PA) inhibits platelet recruitment at sites of endothe
17    Recombinant tissue plasminogen activator (rt-PA) is a well-characterized glycoprotein with a great
18 ly recombinant tissue plasminogen activator (rt-PA), 1 mg per lumen, once per week, and twice-weekly
19 ng recombinant tissue plasminogen activator (rt-PA), 3) cannulating the retinal vein transvitreally,
20 e thrombolytic tissue plasminogen activator (rt-PA), is approved by the FDA for use in patients with
21 nd recombinant tissue plasminogen activator (rt-PA)-loaded echogenic liposomes (OFP t-ELIP) using dif
22 combinant tissue-type plasminogen activator (rt-PA, Activase) to methionine oxidation when treated wi
23    Recombinant tissue plasminogen activator (rt-PA, alteplase) improved functional outcome in patient
24 combinant tissue-type plasminogen activator [rt-PA]).
25 different between the two groups (6.2% after rt-PA and 5.6% after PTCA).
26 c-eligible patients not in shock: 5.4% after rt-PA and 5.2% after PTCA.
27 ence in the rate of reinfarction (2.9% after rt-PA and 2.5% after PTCA).
28 with increased risk of adverse outcome after rt-PA treatment.
29 tality was higher in patients in shock after rt-PA than after PTCA (52% vs. 32%, p < 0.0001).
30 nt difference in the mean overall cost of an rt-PA/heparin strategy as a locking solution for cathete
31 tic-eligible patients not in shock, PTCA and rt-PA are comparable alternative methods of reperfusion
32 threatening/serious systemic hemorrhage, any rt-PA complication, in-hospital mortality, and modified
33 aracterization of familiar proteins, such as rt-PA, using the new capabilities of modern analytical t
34 ) +/-LOX-1 (BI-0115) inhibitors given before rt-PA administration.
35 alence of EIC on baseline CT in the combined rt-PA and placebo groups was 31% (n = 194).
36         Short-term infusion Ep plus low-dose rt-PA acutely neutralizes the ability of damaged endothe
37                         Ep plus reduced-dose rt-PA has not previously been shown to render a recanali
38  with either Definity or OFP t-ELIP enhances rt-PA thrombolysis.
39 reatment groups were: 1) Ep (n = 6); 2) Ep + rt-PA (n = 6); 3) rt-PA (n = 6); and 4) placebo (n = 4).
40 hrombus and platelet aggregates only in Ep + rt-PA treated arteries.
41 re randomized to Ep alone (n = 5) or to Ep + rt-PA (n = 5).
42 telet aggregates with Ep alone and with Ep + rt-PA, but not with rt-PA alone.
43  ischaemic stroke patients meet criteria for rt-PA; therefore, alternative acute treatment strategies
44  all the evidence from randomised trials for rt-PA in acute ischaemic stroke in an updated systematic
45 TBHP, while three of the five methionines in rt-PA were found to be oxidizable.
46 tetrasaccharides, not previously observed in rt-PA.
47 we identified two novel glycan structures in rt-PA.
48 of the peptides and glycopeptide variants in rt-PA.
49 d-hole, multi-side-hole) were used to infuse rt-PA and Definity at the proximal edge or directly into
50                                  Intravenous rt-PA (recombinant tissue-type plasminogen activator) is
51 esults do not support the use of intravenous rt-PA for stroke treatment beyond 3 hours.
52 luate the safety and efficacy of intravenous rt-PA in patients with ischemic stroke who are taking NO
53 earched for randomised trials of intravenous rt-PA versus control given within 6 h of onset of acute
54 ION: The evidence indicates that intravenous rt-PA increased the proportion of patients who were aliv
55 effect of time to treatment with intravenous rt-PA (alteplase) on therapeutic benefit and clinical ri
56 ith ischemic stroke treated with intravenous rt-PA within 4.5 hours, 251 were taking NOACs (dabigatra
57 et population, 32% of the placebo and 34% of rt-PA patients had an excellent recovery at 90 days (P =
58            OFP t-ELIP preserved up to 76% of rt-PA activity in the presence of PAI-1, whereas only 24
59 teine) could shed light on the activation of rt-PA, upon stimulation by either oxidative or ischemic
60 0001) but were normalized by the addition of rt-PA.
61 lated bacteremia, and whether the benefit of rt-PA on catheter-related bacteremia was maintained in t
62                               The benefit of rt-PA was greatest in patients treated within 3 h (mRS 0
63                             Complications of rt-PA therapy, such as haemorrhagic transformation and a
64 remia partially offset the increased cost of rt-PA.
65 ion to the characterization of glycoforms of rt-PA.
66 el was utilized to investigate the impact of rt-PA delivered 4 hours poststroke onset as well as sele
67 dian time from presentation to initiation of rt-PA in the thrombolytic group was 42 min; the median t
68 symptom onset and prior to the initiation of rt-PA or placebo.
69               Administration of 0.9 mg/kg of rt-PA (n = 272) or placebo (n = 275) intravenously over
70 an structures based on existing knowledge of rt-PA glycans.
71                               The loading of rt-PA in OFP t-ELIP was assessed using spectrophotometry
72                 An approach to management of rt-PA complications is outlined.
73 e; however, there are few data on the use of rt-PA in patients who are receiving a non-vitamin K anta
74 on using decision analysis, assuming ongoing rt-PA effectiveness, the overall costs of the strategies
75 creased clot mass loss relative to saline or rt-PA alone in vitro, only when rt-PA was administered d
76                            Recombinant t-PA (rt-PA) induced exocytotic and carrier-mediated NE releas
77 INDINGS: In up to 12 trials (7012 patients), rt-PA given within 6 h of stroke significantly increased
78              Recombinant tissue plasminogen (rt-PA) with 35 cysteine residues has been completely ass
79 ng solution was higher in patients receiving rt-PA/heparin, but this was partially offset by lower co
80 her, it was tested whether the agent shields rt-PA against degradation by plasminogen activator inhib
81              This study found no significant rt-PA benefit on the 90-day efficacy end points in patie
82  twice-weekly heparin as a locking solution (rt-PA/heparin) resulted in lower risks of hemodialysis c
83                        Stroke and subsequent rt-PA treatment increased edema, hemorrhage, MMP-9 activ
84  these preliminary observations suggest that rt-PA appears to be reasonably well tolerated without pr
85 hanced lytic efficacy (p < 0.05) relative to rt-PA alone.
86 P can enhance the lytic activity relative to rt-PA or OFP t-ELIP alone, respectively.
87 g that EIC is unlikely to affect response to rt-PA treatment.
88 in anticoagulation increased HT secondary to rt-PA treatment as compared to nonanticoagulated control
89 4% activity was preserved for unencapsulated rt-PA.
90                 Although experience of using rt-PA in patients with ischemic stroke on a NOAC is limi
91 to saline or rt-PA alone in vitro, only when rt-PA was administered directly into clots via a multi-s
92 90 days was 6.9% with placebo and 11.0% with rt-PA (P = .09).
93     Patency on cath lab arrival was 61% with rt-PA (28% Thrombolysis in Myocardial Infarction trial [
94  9) +/- LOX-1 inhibitors in combination with rt-PA to improve stroke outcomes.
95   The risk of symptomatic ICH increased with rt-PA treatment.
96 h Ep alone and with Ep + rt-PA, but not with rt-PA alone.
97 on to treat otherwise eligible patients with rt-PA within 3 hours of stroke onset.
98 djusted mean cost for managing patients with rt-PA/heparin versus heparin alone was Can$323 (95% CI,
99 ability of early successful reperfusion with rt-PA.
100 ate negative aspects of ischemic stroke with rt-PA therapy, thus resulting in improved neurological f
101 hours was detected in the group treated with rt-PA (P>/=.22).
102                        Patients treated with rt-PA did better whether or not they had EICs, suggestin
103  up to 45 min faster than clots treated with rt-PA or saline.
104          In the first 10 days treatment with rt-PA significantly increased the rate of symptomatic in
105                      Combined treatment with rt-PA, Definity, and ultrasound in vivo increased the ra
106                           The use of US with rt-PA and Definity enhanced lytic efficacy (p < 0.05) re

 
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