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1 t of treatment delay on the effectiveness of antifibrinolytics.
2 use factor XI displays both procoagulant and antifibrinolytic activities, it has been postulated that
3                 Reverse zymography showed no antifibrinolytic activity in these zones.
4                   Indeed, for >40 years, the antifibrinolytic agent tranexamic acid has been administ
5 teric inhibition of plasmin could led to new antifibrinolytic agent(s) that may exhibit better effica
6 ared with the use of aminocaproic acid or no antifibrinolytic agent, aprotinin use was also associate
7  by the SERPINE1 gene), a u-PA inhibitor and antifibrinolytic agent, is often elevated in obesity and
8 d to delay clot lysis by enhancing a natural antifibrinolytic agent, thrombin-activatable fibrinolysi
9 ch are more potent than the most-widely used antifibrinolytic agent, tranexamic acid.
10 herefore, it has been proposed for use as an antifibrinolytic agent.
11 n those who received aminocaproic acid or no antifibrinolytic agent.
12 of thrombosis if empirically administered an antifibrinolytic agent.
13        Tranexamic acid (TXA) is an efficient antifibrinolytic agent; however, concerns remain about t
14                                Because the 2 antifibrinolytic agents appear to have similar efficacie
15                                              Antifibrinolytic agents are part of the treatment in som
16 inogen to aid infectivity has suggested that antifibrinolytic agents may have antiviral benefits.
17  and nonspecific support for hemostasis with antifibrinolytic agents or prothrombin complex concentra
18                                 The approved antifibrinolytic agents such as tranexamic acid, epsilon
19  or tranexamic acid, which have been used as antifibrinolytic agents to prevent blood loss during maj
20  from in vitro or animal studies, the use of antifibrinolytic agents to reduce bleeding in humans has
21                               The use of the antifibrinolytic agents urokinase and recombinant tissue
22                                          All antifibrinolytic agents were effective in reducing blood
23 ich are representative of a class of in vivo antifibrinolytic agents, have been determined at 2.1 ang
24 nephrotoxic insults are presented, including antifibrinolytic agents, obstructive jaundice, prostagla
25 olism (VTE) risk cautions against the use of antifibrinolytic agents.
26  surgery according to use of 2 lysine analog antifibrinolytics (aminocaproic acid and tranexamic acid
27 on, thereby preventing the generation of the antifibrinolytic and anti-inflammatory activities of TAF
28                                              Antifibrinolytics and heparinase partially reverse the a
29 ric clotting patterns, which was reversed by antifibrinolytics and heparinase.
30               Pharmacologic agents including antifibrinolytics and prohemostatic proteins are commonl
31 ilizing clots as tranexamic acid, a clinical antifibrinolytic, and in a pilot study of two dogs with
32 In addition, the use of medications, such as antifibrinolytics, and point of care testing, such as th
33                                              Antifibrinolytics appear safe in the population of older
34     However, recent studies suggest that the antifibrinolytic aprotinin is associated with increased
35 emic therapies including antiangiogenics and antifibrinolytics are now recommended as standard treatm
36                                              Antifibrinolytics are used to attenuate the coagulopathy
37                  Thus, the anticoagulant and antifibrinolytic cofactor activities of thrombomodulin h
38 ty is a hallmark of new thrombi and that the antifibrinolytic cross-linking effects of FXIIIa are ach
39      Further, we measured the ability of the antifibrinolytic drug TXA to inhibit this process.
40                       The most commonly used antifibrinolytic drug, tranexamic acid, is associated wi
41 addition of tranexamic acid (TXA) - a potent antifibrinolytic drug.
42                                              Antifibrinolytic drugs are routinely used worldwide to r
43                                              Antifibrinolytic drugs are used extensively for on-deman
44                                              Antifibrinolytic drugs are widely used to reduce blood l
45 e plasmin is a target for the development of antifibrinolytic drugs for use in cardiac surgery with c
46 l lead structures for the development of new antifibrinolytic drugs for use in cardiac surgery with c
47 rporeal circulation; however, the effects of antifibrinolytic drugs on proinflammatory and anti-infla
48                                              Antifibrinolytic drugs provide important pharmacological
49                                              Antifibrinolytic drugs such as aprotinin and epsilon-ami
50                                          The antifibrinolytic drugs tranexamic acid (TXA) and epsilon
51 suited for further development as injectable antifibrinolytic drugs.
52 eutics that improve upon currently available antifibrinolytics, e.g., tranexamic acid (TXA, 1) and ap
53 se B (PCB) is an exopeptidase that exerts an antifibrinolytic effect by releasing C-terminal Lys and
54                                          The antifibrinolytic effect of HUVECs was abolished 66% by s
55                             In addition, the antifibrinolytic effect of TM was negated by monoclonal
56 y its content of oxidized phospholipids, and antifibrinolytic effects.
57 of Lp(a) within the blood vessel promotes an antifibrinolytic environment, foam cell formation, the g
58                                      Empiric antifibrinolytics for children should be questioned; thr
59 have demonstrated the safety and efficacy of antifibrinolytics for mild-to-moderate bleeding manifest
60  activated platelet membrane where it exerts antifibrinolytic function by cross-linking alpha2AP to f
61                       Our data show that the antifibrinolytic function of FXIII is independent of fib
62 operties of TFPI-2 or KD1 would diminish its antifibrinolytic function.
63 diated inhibition of TAFI activation and the antifibrinolytic functions of TAFIa.
64  of Mortality score, and plasma deficit, the antifibrinolytic group had decreased mortality at 6- and
65  demographic and physiologic parameters; the antifibrinolytic group had longer massive transfusion pr
66                                          The antifibrinolytic group was comparable with the nonantifi
67                                       In the antifibrinolytic group, there was significantly less 6-h
68 rders such as hemophilia A (HA), but current antifibrinolytics have unfavorable pharmacokinetic profi
69 cohort studies: Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage (CRASH-2) tr
70 e with more than 1000 patients that assessed antifibrinolytics in acute severe bleeding.
71      Consideration should be given to use of antifibrinolytics in pediatric patients with life-threat
72 y, epsilon-aminocaproic acid, an alternative antifibrinolytic, is considerably less expensive.
73 vealing a thrombomodulin- and TAFI-dependent antifibrinolytic mechanism.
74  Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the b
75 ildren were compared according to receipt of antifibrinolytic medication (tranexamic acid or aminocap
76                      Twelve percent received antifibrinolytic medication during the bleeding event (n
77                            Administration of antifibrinolytic medications during the life-threatening
78             Impact of cardiotomy suction and antifibrinolytics on markers of brain injury was assesse
79                                None received antifibrinolytics or blood products before TEG testing.
80 utics targeting major thrombin-generating or antifibrinolytic pathways may disrupt fibrin-mediated ho
81 a significant inhibition of procoagulant and antifibrinolytic pathways.
82                           In conclusion, the antifibrinolytic properties of Solulin are exhibited in
83 ave established important antithrombotic and antifibrinolytic properties of this serpin that have her
84 rough several mechanisms, including putative antifibrinolytic properties.
85  and monocyte chemotactic protein-1, and the antifibrinolytic protein plasminogen activator inhibitor
86 evels of fibrinogen, protein C activity, and antifibrinolytic proteins and deposition of fibrin in ti
87 ysis by irreversibly crosslinking fibrin and antifibrinolytic proteins.
88                                              Antifibrinolytics reduce death from bleeding in trauma a
89 e treatment options are presented, including antifibrinolytics, replacement products, and recombinant
90 omponents, giving rise to a procoagulant and antifibrinolytic state and eventual multiple organ failu
91               Crystal structures of the main antifibrinolytic targets, the lysine binding sites on pl
92                 Transexamic acid (TXA) is an antifibrinolytic that has been used successfully to prev
93                             Since the 1980s, antifibrinolytic therapies have assisted surgical teams
94 or the comparison with patients receiving no antifibrinolytic therapy (P=0.003) and 1.27 (95% CI, 1.1
95 ely, these data demonstrate that long-acting antifibrinolytic therapy can be achieved and that it pro
96 ine protease inhibitor, here we use the term antifibrinolytic therapy to include all three agents.) R
97 r ST-elevation myocardial infarction receive antifibrinolytic therapy to limit blood loss.
98 iven for modern evidence-based approaches to antifibrinolytic therapy, antiangiogenic therapy, and ir
99  acid, and 2029 patients (20.0%) received no antifibrinolytic therapy.
100  receiving aprotinin, tranexamic acid, or no antifibrinolytic treatment in the presence or absence of
101              To develop a recommendation for antifibrinolytic use in adult cardiac surgery, we perfor
102                                              Antifibrinolytic use was documented.
103            Here, we developed a long-lasting antifibrinolytic using small interfering RNA (siRNA) tar
104 analysis to determine the association of the antifibrinolytics with efficacy, safety and cost outcome

 
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