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1 ited the inactivation of plasmin by alpha(2)-antiplasmin.
2 otects plasmin from inactivation by alpha(2)-antiplasmin.
3 d by a neutralizing antibody versus alpha(2)-antiplasmin.
4  NH2-terminal cross-linking domain of alpha2 antiplasmin.
5 li, thrombus dissolution is halted by alpha2-antiplasmin.
6 rly as effective as that exerted by alpha(2)-antiplasmin.
7 logical inhibitor, the antiprotease alpha(2)-antiplasmin.
8 dermal fibroblasts in the presence of alpha2-antiplasmin.
9  protect plasmin from inhibition by alpha(2)-antiplasmin.
10 nd derived from the amino terminus of alpha2-antiplasmin.
11 lasmin that is readily inhibited by alpha(2)-antiplasmin.
12 mutants and plasmin were resistant to alpha2-antiplasmin.
13  resistance of the SK-Pm complex to alpha(2)-antiplasmin.
14 protecting plasmin from inhibition by alpha2-antiplasmin.
15 PA, tPA, PAI-1, protease nexin-1, and alpha2-antiplasmin.
16 of wild-type (WT) SK and resistant to alpha2-antiplasmin.
17 ctor, thrombospondin, fibronectin and alpha2-antiplasmin.
18  to inactivation of microplasmin by alpha(2)-antiplasmin.
19 tivators, or series inhibition of plasmin by antiplasmins.
20                                       alpha2-Antiplasmin (A2AP) is a major inhibitor of fibrinolysis
21 hway, including the plasmin inhibitor alpha2-antiplasmin (A2AP).
22                     The presence of alpha(2)-antiplasmin abolishes the potentiation of fibrinolysis b
23 smin immunization leads to production of IgG antiplasmin, aCL, and anti-beta(2)GPI in MRL/MpJ mice, b
24 tive to tissue plasminogen activator, alpha2-antiplasmin, active plasminogen activator inhibitor (PAI
25                                  The lack of antiplasmin activity and decreased antitrypsin activity
26 e-dependent effect on coagulation, depleting antiplasmin activity completely, then degrading fibrinog
27               In intact bacterial cells, the antiplasmin activity of miropin protects envelope protei
28 tor to examine the potential role of alpha 2-antiplasmin (alpha 2AP) in experimental pulmonary emboli
29 cross-linking) of plasmin inhibitor alpha(2)-antiplasmin (alpha(2)-AP) into fibrin clots increases th
30 III and the fibrinolytic inhibitor, alpha(2)-antiplasmin (alpha(2)AP) on fibrinolysis.
31 f heart explant cultures with either alpha(2)antiplasmin (alpha(2)AP), a major physiological plasmin
32 vity in clots was measured with (1) alpha(2)-antiplasmin (alpha(2)AP), a physiological glutamine subs
33   The primary inhibitor of plasmin, alpha(2)-antiplasmin (alpha(2)AP), is secreted by the liver into
34                               Human alpha(2)-antiplasmin (alpha(2)AP), the main inhibitor of plasmin-
35 amer did react slowly with the serpin alpha2-antiplasmin (alpha2-AP), suggesting a highly limited cat
36 nd inactivating the plasmin inhibitor alpha2-antiplasmin (alpha2-AP).
37  inhibited by its principal inhibitor alpha2-antiplasmin (alpha2-AP).
38          During human blood clotting, alpha2-antiplasmin (alpha2AP) becomes covalently linked to fibr
39 against fibrinolysis by cross-linking alpha2-antiplasmin (alpha2AP) to fibrin.
40                                      Alpha-2-antiplasmin (alpha2AP) undergoes both N- and C-terminal
41                                 Human alpha2-antiplasmin (alpha2AP), also known as alpha2-plasmin inh
42 ion in congenic mice with and without alpha2-antiplasmin (alpha2AP), the primary inhibitor of plasmin
43                                 Human alpha2-antiplasmin (alpha2AP, also called alpha2-plasmin inhibi
44 ct the reaction between plasmin and alpha(2)-antiplasmin and accelerate the inactivation of tPA and t
45         In S/D plasma, virtually 100% of the antiplasmin and approximately 50% of the antitrypsin are
46   However, even with complete consumption of antiplasmin and decreases in fibrinogen and factor VIII
47 lasmin is shielded from inhibition by alpha2-antiplasmin and degrades amorphous protein aggregates to
48              Ex vivo, crosslinking of alpha2-antiplasmin and fibrin was impaired and fibrinolysis was
49 PA and plasmin and the eventual depletion of antiplasmin and macroglobulin in an advancing (approxima
50 activator inhibitor-2, antithrombin, alpha 2-antiplasmin and protease nexin I.
51 se-plasmin complex to inhibition by alpha(2)-antiplasmin and was readily inhibited by soybean trypsin
52 sistance of the SK-plasmin complex to alpha2-antiplasmin, and controls fibrin-independent Pg activati
53 , plasminogen activator inhibitors, alpha(2)-antiplasmin, and inflammatory mediators.
54 inolytic inhibitors including PAI-1, alpha 2-antiplasmin, and TAFI were present in samples, which may
55 gulation (DIC) (fibrinogen, D-dimer, alpha-2-antiplasmin, antitrombin, prothrombin time, and platelet
56 ctivatable fibrinolysis inhibitor and alpha2-antiplasmin are counterbalanced by decreased plasminogen
57                                  Circulating antiplasmin-cleaving enzyme (APCE) has a role in fibrino
58                                  Circulating antiplasmin-cleaving enzyme (APCE), a prolyl-specific se
59 ng circulation, Met-alpha(2)AP is cleaved by antiplasmin-cleaving enzyme (APCE), yielding Asn-alpha(2
60 a2AP to yield Asn-alpha2AP and have named it antiplasmin-cleaving enzyme (APCE).
61  of alpha2AP is cleaved at the N terminus by antiplasmin-cleaving enzyme (or soluble fibroblast activ
62 o named fibroblast activation protein-alpha, antiplasmin-cleaving enzyme, and dipeptidyl prolyl pepti
63 21% vs 99%, overall P < .01), plasmin-alpha2-antiplasmin complex (520 vs 409 mug/L, overall P = .04),
64 en, t-PA-PAI-1 complex, D-dimer, and plasmin-antiplasmin complex also increased significantly.
65 hanges were present in AKI, a higher plasmin-antiplasmin complex indicated a hyperfibrinolytic state.
66                          D-dimer and plasmin-antiplasmin complex levels increased soon after start of
67 , intercellular adhesion molecule-1, plasmin-antiplasmin complex, and D-dimer levels were measured in
68 leukin-6, factor VIIc, factor VIIIc, plasmin-antiplasmin complex, and D-dimer were significantly grea
69  homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and inflammation and coagulation sc
70 tor, platelet activator inhibitor-1, plasmin-antiplasmin complex, D-dimer, thrombin activatable fibri
71 ed by shared variance in fibrinogen, plasmin-antiplasmin complex, factor VIII, D-dimer, and lipoprote
72 hrombin-antithrombin complex, plasmin-alpha2-antiplasmin complex, plasminogen activator inhibitor typ
73 of coagulation activation), D-dimer, plasmin-antiplasmin complex, tissue plasminogen activator and pl
74  plus thrombin-antithrombin complex, plasmin-antiplasmin complex, tissue plasminogen activator, plasm
75 nt included fibrinolytic factors and plasmin-antiplasmin complex.
76                 The concentration of plasmin/antiplasmin complexes (PAP complex) increased by approxi
77              Plasma levels of plasmin-alpha2-antiplasmin complexes increase with the extent of thromb
78 nogen activator activity, and plasmin-alpha2-antiplasmin complexes), followed by inhibition (plasma p
79 ype plasminogen activator and plasmin-alpha2-antiplasmin complexes), whereas TNFR55:IgG did inhibit t
80 ivator inhibitor type I, and plasmin/alpha 2-antiplasmin complexes).
81 tissue plasminogen activator, plasmin-alpha2-antiplasmin complexes, and plasminogen activator inhibit
82 lot or in the circulation by forming plasmin-antiplasmin complexes.
83 ype plasminogen activator and plasmin-alpha2-antiplasmin complexes; P <0.05), but did not influence i
84  and rscuPA, respectively; P < .05), alpha 2-antiplasmin consumption was less (P < .05), and D-dimer
85 ad greater effects than inhibition of alpha2-antiplasmin cross-linking alone (group 4 versus 5; P<0.0
86 ith KA, whereas a plasmin inhibitor, alpha-2-antiplasmin, failed to attenuate KA-induced retinal dama
87 rotect plasmin from inactivation by alpha(2)-antiplasmin, fibrin did protect human plasmin, which for
88 ctor XIIIa-mediated fibrin-fibrin and alpha2-antiplasmin-fibrin cross-linking both caused experimenta
89 ve inhibition of factor XIII-mediated alpha2-antiplasmin-fibrin cross-linking enhanced lysis (group 3
90 iated fibrin-fibrin cross-linking and alpha2-antiplasmin-fibrin cross-linking were measured in anesth
91 TPA (76.0+/-11.9%); and (5) inhibited alpha2-antiplasmin-fibrin cross-linking+TPA (54.7+/-3.9%).
92 use sera were analyzed for production of IgG antiplasmin, IgG aCL, and IgG anti-beta(2)-glycoprotein
93 zed MRL/MpJ mice produced high titers of IgG antiplasmin, IgG aCL, and IgG anti-beta(2)GPI.
94 pJ mice, but leads to production of only IgG antiplasmin in BALB/cJ mice.
95 id A, complement C3, pentraxin 3, and alpha2-antiplasmin in the liver, despite CNS neurodegeneration
96 lasma serpins-antithrombin, antitrypsin, and antiplasmin-in S/D plasma and FFP.
97 a2-antiplasmin levels treated with an alpha2-antiplasmin-inactivating antibody (P<0.0001).
98 linical-dose r-tPA alone (P<0.001) or alpha2-antiplasmin inactivation alone (P<0.001).
99    Dissolution of pulmonary emboli by alpha2-antiplasmin inactivation alone was comparable to 3 mg/kg
100 Despite greater thrombus dissolution, alpha2-antiplasmin inactivation alone, or in combination with l
101 effects of plasminogen activation and alpha2-antiplasmin inactivation on experimental thrombus dissol
102              The effects of r-tPA and alpha2-antiplasmin inactivation on fibrinolysis and bleeding we
103                              However, alpha2-antiplasmin inactivation showed a unique pattern of thro
104 olve emboli, but was synergistic with alpha2-antiplasmin inactivation, causing more embolus dissoluti
105 nt with this hypothesis, injection of alpha2-antiplasmin into cerebral ventricles markedly ameliorate
106 sses in the peripheral tissues, where alpha2-antiplasmin is more likely to be absent.
107 kedly accelerated in mice with normal alpha2-antiplasmin levels treated with an alpha2-antiplasmin-in
108 levels, greater than 5-fold elevated plasmin antiplasmin levels, and a complete absence of thrombelas
109 ator of the fibrinolytic system, like alpha2-antiplasmin, may have unique therapeutic value in pulmon
110                    Human precursive alpha(2)-antiplasmin (Met-alpha(2)AP), the only known physiologic
111 ntially identical kinetics toward Met-alpha2-antiplasmin (Met-alpha2AP) and peptide substrates.
112 zed BALB/cJ mice produced high titers of IgG antiplasmin only, while plasmin-immunized MRL/MpJ mice p
113 plus the specific plasmin inhibitor alpha(2)-antiplasmin or dermal fibroblasts isolated from plasmino
114  with the adjuvant alone did not develop IgG antiplasmin or IgG aCL.
115 es) and fibrin dissolution (D-dimer; plasmin-antiplasmin or PAP complexes) were also evaluated.
116 due to altered levels of plasminogen, alpha2-antiplasmin, or fibrinogen.
117  as markers of fibrinolysis: plasmin-alpha 2-antiplasmin (PAP) and D-dimer.
118 n-antithrombin [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and complement (C3b, C5a, C5b-9) in
119 etic resonance imaging, together with alpha2-antiplasmin peptide (alpha2AP)-targeted perfluorocarbon
120    There were no changes in vWF, and alpha-2-antiplasmin-plasmin complexes increased only in postthro
121 ator inhibitor-1 (PAI-1) Ag and Act, alpha-2-antiplasmin-plasmin complexes, and von Willebrand factor
122 us fibrinolysis inhibitors, including alpha2-antiplasmin, plasminogen activator inhibitor-1, and thro
123 ation process as aprotinin, but not alpha(2)-antiplasmin, prevented collagen dissolution.
124    In the circulation, high levels of alpha2-antiplasmin rapidly and efficiently inhibit plasmin acti
125 mine-containing peptides derived from alpha2-antiplasmin, Staphylococcus aureus fibronectin binding p
126 tb-bound plasmin from regulation by alpha(2)-antiplasmin, suggestive of an involvement of this enzyme
127 d serine protease activity; knockout of a(2)-antiplasmin, the physiological inhibitor of plasmin, enh
128 ained in clots from mice deficient in alpha2-antiplasmin, thrombin-activatable fibrinolysis inhibitor
129 ration of biotinamido-pentylamine and alpha2-antiplasmin to fibrin, and fibrin cross-linking, in cont
130  emboli, assessed the contribution of alpha2-antiplasmin to fibrinolytic failure, and compared the ef
131                       Inactivation of alpha2-antiplasmin was comparable to pharmacological r-tPA for
132                 Plm inactivation by alpha(2)-antiplasmin was significantly delayed when Plm was prein
133 othrombin fragment 1-2, D-dimer, and plasmin antiplasmin) were measured.

 
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