戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ter the NH2-terminal cross-linking domain of alpha2 antiplasmin.
2 ry emboli, thrombus dissolution is halted by alpha2-antiplasmin.
3  human dermal fibroblasts in the presence of alpha2-antiplasmin.
4 de ligand derived from the amino terminus of alpha2-antiplasmin.
5 f Ile1 mutants and plasmin were resistant to alpha2-antiplasmin.
6 ble of protecting plasmin from inhibition by alpha2-antiplasmin.
7 uding uPA, tPA, PAI-1, protease nexin-1, and alpha2-antiplasmin.
8 o that of wild-type (WT) SK and resistant to alpha2-antiplasmin.
9 rand factor, thrombospondin, fibronectin and alpha2-antiplasmin.
10                                              alpha2-Antiplasmin (A2AP) is a major inhibitor of fibrin
11 tic pathway, including the plasmin inhibitor alpha2-antiplasmin (A2AP).
12 s sensitive to tissue plasminogen activator, alpha2-antiplasmin, active plasminogen activator inhibit
13 he tetramer did react slowly with the serpin alpha2-antiplasmin (alpha2-AP), suggesting a highly limi
14 ersibly inhibited by its principal inhibitor alpha2-antiplasmin (alpha2-AP).
15 asmin and inactivating the plasmin inhibitor alpha2-antiplasmin (alpha2-AP).
16                 During human blood clotting, alpha2-antiplasmin (alpha2AP) becomes covalently linked
17 hrombi against fibrinolysis by cross-linking alpha2-antiplasmin (alpha2AP) to fibrin.
18                                        Human alpha2-antiplasmin (alpha2AP), also known as alpha2-plas
19 a ligation in congenic mice with and without alpha2-antiplasmin (alpha2AP), the primary inhibitor of
20                                        Human alpha2-antiplasmin (alpha2AP, also called alpha2-plasmin
21 bound plasmin is shielded from inhibition by alpha2-antiplasmin and degrades amorphous protein aggreg
22                     Ex vivo, crosslinking of alpha2-antiplasmin and fibrin was impaired and fibrinoly
23  the resistance of the SK-plasmin complex to alpha2-antiplasmin, and controls fibrin-independent Pg a
24 ombin-activatable fibrinolysis inhibitor and alpha2-antiplasmin are counterbalanced by decreased plas
25  ETP (121% vs 99%, overall P < .01), plasmin-alpha2-antiplasmin complex (520 vs 409 mug/L, overall P
26 ETP], thrombin-antithrombin complex, plasmin-alpha2-antiplasmin complex, plasminogen activator inhibi
27                     Plasma levels of plasmin-alpha2-antiplasmin complexes increase with the extent of
28  plasminogen activator activity, and plasmin-alpha2-antiplasmin complexes), followed by inhibition (p
29 issue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes), whereas TNFR55:IgG did in
30 sed by tissue plasminogen activator, plasmin-alpha2-antiplasmin complexes, and plasminogen activator
31 issue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes; P <0.05), but did not infl
32 ) and had greater effects than inhibition of alpha2-antiplasmin cross-linking alone (group 4 versus 5
33      Factor XIIIa-mediated fibrin-fibrin and alpha2-antiplasmin-fibrin cross-linking both caused expe
34 selective inhibition of factor XIII-mediated alpha2-antiplasmin-fibrin cross-linking enhanced lysis (
35 IIa-mediated fibrin-fibrin cross-linking and alpha2-antiplasmin-fibrin cross-linking were measured in
36 tivity+TPA (76.0+/-11.9%); and (5) inhibited alpha2-antiplasmin-fibrin cross-linking+TPA (54.7+/-3.9%
37 m amyloid A, complement C3, pentraxin 3, and alpha2-antiplasmin in the liver, despite CNS neurodegene
38 al alpha2-antiplasmin levels treated with an alpha2-antiplasmin-inactivating antibody (P<0.0001).
39  than clinical-dose r-tPA alone (P<0.001) or alpha2-antiplasmin inactivation alone (P<0.001).
40           Dissolution of pulmonary emboli by alpha2-antiplasmin inactivation alone was comparable to
41        Despite greater thrombus dissolution, alpha2-antiplasmin inactivation alone, or in combination
42 ed the effects of plasminogen activation and alpha2-antiplasmin inactivation on experimental thrombus
43                     The effects of r-tPA and alpha2-antiplasmin inactivation on fibrinolysis and blee
44                                     However, alpha2-antiplasmin inactivation showed a unique pattern
45 ot dissolve emboli, but was synergistic with alpha2-antiplasmin inactivation, causing more embolus di
46 onsistent with this hypothesis, injection of alpha2-antiplasmin into cerebral ventricles markedly ame
47 e processes in the peripheral tissues, where alpha2-antiplasmin is more likely to be absent.
48 was markedly accelerated in mice with normal alpha2-antiplasmin levels treated with an alpha2-antipla
49 y regulator of the fibrinolytic system, like alpha2-antiplasmin, may have unique therapeutic value in
50 th essentially identical kinetics toward Met-alpha2-antiplasmin (Met-alpha2AP) and peptide substrates
51 as not due to altered levels of plasminogen, alpha2-antiplasmin, or fibrinogen.
52 9F magnetic resonance imaging, together with alpha2-antiplasmin peptide (alpha2AP)-targeted perfluoro
53 ndogenous fibrinolysis inhibitors, including alpha2-antiplasmin, plasminogen activator inhibitor-1, a
54           In the circulation, high levels of alpha2-antiplasmin rapidly and efficiently inhibit plasm
55 , glutamine-containing peptides derived from alpha2-antiplasmin, Staphylococcus aureus fibronectin bi
56 ere retained in clots from mice deficient in alpha2-antiplasmin, thrombin-activatable fibrinolysis in
57 incorporation of biotinamido-pentylamine and alpha2-antiplasmin to fibrin, and fibrin cross-linking,
58 lmonary emboli, assessed the contribution of alpha2-antiplasmin to fibrinolytic failure, and compared
59                              Inactivation of alpha2-antiplasmin was comparable to pharmacological r-t