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1 lts from ordered breakdown of thrombi by the fibrinolytic system.
2 n between two proteins of the complement and fibrinolytic system.
3 ne protease plasmin, a central enzyme of the fibrinolytic system.
4 but subsequently generates inhibitors of the fibrinolytic system.
5 and the functioning of the plasminogen-based fibrinolytic system.
6  capable of inducing other components of the fibrinolytic system.
7 s, is considered a critical regulator of the fibrinolytic system.
8 PA suggested a decrease in inhibition of the fibrinolytic system.
9 bitor of coagulation, and dysfunction of the fibrinolytic system.
10 rliest targets attacked by plasmin following fibrinolytic system activation.
11 brinogen, were released in vivo early during fibrinolytic system activation.
12         In conclusion, troglitazone enhances fibrinolytic system activity in insulin-resistant type 2
13 d by approximately 20%, indicating augmented fibrinolytic system activity.
14 ne pathogens interact with components of the fibrinolytic system and co-opt its functions to facilita
15 I-1) is a major physiologic regulator of the fibrinolytic system and has recently gained recognition
16 ationships between protein components of the fibrinolytic system and infectivity by Mycobacterium avi
17 zed the effects of IL-1 on the expression of fibrinolytic system and matrix proteins in rat cardiac m
18      To examine the relationship between the fibrinolytic system and pulmonary fibrosis, lung inflamm
19    Additionally, the role of the coagulation/fibrinolytic systems and angiogenesis has also been exam
20 f endothelial activation, protein C pathway, fibrinolytic system, and complement.
21  coagulation and anticoagulant pathways, the fibrinolytic system, and platelets in the pathophysiolog
22 ment system, the blood clotting cascade, the fibrinolytic system, and the kallikrein-kinin system.
23 activation mechanisms of the coagulation and fibrinolytic systems, and therefore the prethrombotic st
24                  Haemodynamic forces and the fibrinolytic system are considered to be the principal m
25 tivating coagulation, yet its effects on the fibrinolytic system are not fully understood.
26             The complement, coagulation, and fibrinolytic systems are crucial for the maintenance of
27         These findings define the endogenous fibrinolytic system as an important regulator of clot re
28 ude components of complement and coagulation-fibrinolytic systems, as well as plasma lipoproteins.
29                                 Although the fibrinolytic system assembles at the site of pulmonary e
30 ion system is best known as an extracellular fibrinolytic system but was previously reported to also
31 d/or inhibition of natural anticoagulant and fibrinolytic systems by antiphospholipid antibodies.
32  These studies showed that the protein C and fibrinolytic systems can work in tandem to regulate even
33                          The coagulation and fibrinolytic systems contribute to malignancy by increas
34 Our findings indicate that disruption of p53-fibrinolytic system cross talk may serve as a novel inte
35                         Dysregulation of the fibrinolytic system developed during the course of infec
36  acids lower fibrinogen or interact with the fibrinolytic system directly.
37     Here, we present a basic overview of the fibrinolytic system, discuss fibrin as an innate immune
38       Absence of these two components of the fibrinolytic system, either urokinase or plasminogen, re
39 allenge to develop a selective and effective fibrinolytic system for thrombolysis with minimal undesi
40        To date, therapeutic targeting of the fibrinolytic system has been for 2 purposes: to promote
41                            Components of the fibrinolytic system have been implicated in cell migrato
42 lts of these studies indicate a role for the fibrinolytic system in acute lung injury and suggests th
43 plasma PAI-1 and relief of inhibition of the fibrinolytic system in elderly, obese subjects.
44 sults underscore the importance of the human fibrinolytic system in host-pathogen interactions in inv
45     Consistent with an important role of the fibrinolytic system in hypoxia-induced fibrin accumulati
46 ortant potential role of macrophages and the fibrinolytic system in ischemia-induced thrombosis.
47 tion and expression of the components of the fibrinolytic system in patients with chronic rhinosinusi
48                 To determine the role of the fibrinolytic system in regulating the pathologies associ
49  this study emphasize the involvement of the fibrinolytic system in vascular repair processes after i
50                    Fibrin is degraded by the fibrinolytic system in which a plasminogen activator con
51 e known to express several components of the fibrinolytic system, including PAI-1.
52 ducing expression of other components of the fibrinolytic system, including uPAR.
53 nhibitor-1 (PAI-1) is a key regulator of the fibrinolytic system, inhibiting the serine proteases tis
54 ity of uPA to induce other components of the fibrinolytic system, involves posttranscriptional regula
55                                          The fibrinolytic system is a potential target to hamper Plas
56                                  Because the fibrinolytic system is active during repair processes th
57                            The status of the fibrinolytic system is controversial, as is the role of
58                                          The fibrinolytic system is known to play an important role i
59 nd urokinase-dependent pathways by which the fibrinolytic system is regulated in the lung.
60                                 Although the fibrinolytic system is strongly affected by infection, t
61     The canonical role of the hemostatic and fibrinolytic systems is to maintain vascular integrity.
62 fying the activity of a key regulator of the fibrinolytic system, like alpha2-antiplasmin, may have u
63                                    Thus, the fibrinolytic system linked by an activation cascade may
64             Because of the complexity of the fibrinolytic system, mathematical models closely tied wi
65  of disorders involving dysregulation of the fibrinolytic system may affect interactions between fibr
66 xaggerated activation of the coagulation and fibrinolytic systems may contribute to the clinically ob
67 effects of low ambient oxygen tension on the fibrinolytic system, mice were placed in a hypoxic envir
68 nsequently, modulation of the local cellular fibrinolytic system of catecholaminergic cells results i
69 ss the physiological impact of an imbalanced fibrinolytic system on both early and late stages of thi
70 assembly and activation of components of the fibrinolytic system on the abnormal fibrin, resulting in
71  suggesting that the plasma and cell surface fibrinolytic systems operate independently of one anothe
72 lderly, obese individuals, and its effect on fibrinolytic system peptides was measured.
73 in III complexes), nor the activation of the fibrinolytic system (plasma levels of tissue-type plasmi
74 hrombin III complexes, and activation of the fibrinolytic system (plasma levels of tissue-type plasmi
75 elium (plasma von Willebrand levels) and the fibrinolytic system (plasma tissue-type plasminogen acti
76                            Activation of the fibrinolytic system (plasminogen activator activity, tis
77 ionally activates the central zymogen of the fibrinolytic system, plasminogen (Pg).
78 sminogen axis provides cells with a powerful fibrinolytic system, plasminogen-deleted animals use alt
79 elial cells suggest that the coagulation and fibrinolytic systems play an important role in corneal w
80                                          The fibrinolytic system plays a key role in the regulation o
81   The results obtained suggest that the host fibrinolytic system plays an important role in tumor gro
82 ibitor-1 (PAI-1), a central regulator of the fibrinolytic system, plays an important role in determin
83      In addition, we observed altered airway fibrinolytic system protein balance consistent with prom
84            Despite abundant evidence for the fibrinolytic system regulating thrombosis, it has been o
85  cascades, such as the blood coagulation and fibrinolytic systems, required the evolution of protease
86 nd negative modulation of the local cellular fibrinolytic system resulted in substantial alterations
87 thesized that plasmin, the key enzyme of the fibrinolytic system, serves as a physiological backup en
88                                       In the fibrinolytic system, the serpin PAI-1 negatively regulat
89            However, if balanced by a healthy fibrinolytic system, thrombosis may not occur or cause l
90 hat experimental venous stasis activates the fibrinolytic system to block the development of venous t
91 e evolved mechanisms to hijack the mammalian fibrinolytic system to facilitate infection of the human
92 o link the renin-angiotensin system with the fibrinolytic system to regulate trophoblast invasion.
93 he interaction of malaria parasites with the fibrinolytic system using genetically engineered mosquit
94              No correlation was seen between fibrinolytic system variables and baseline concentration
95 gen and activity levels of components of the fibrinolytic system were measured by immunoassays, which