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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.
12 he tetramer did react slowly with the serpin alpha2-antiplasmin (alpha2-AP), suggesting a highly limi
18 bound plasmin is shielded from inhibition by alpha2-antiplasmin and degrades amorphous protein aggreg
19 the resistance of the SK-plasmin complex to alpha2-antiplasmin, and controls fibrin-independent Pg a
20 ETP (121% vs 99%, overall P < .01), plasmin-alpha2-antiplasmin complex (520 vs 409 mug/L, overall P
21 ETP], thrombin-antithrombin complex, plasmin-alpha2-antiplasmin complex, plasminogen activator inhibi
23 plasminogen activator activity, and plasmin-alpha2-antiplasmin complexes), followed by inhibition (p
24 issue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes), whereas TNFR55:IgG did in
25 sed by tissue plasminogen activator, plasmin-alpha2-antiplasmin complexes, and plasminogen activator
26 issue-type plasminogen activator and plasmin-alpha2-antiplasmin complexes; P <0.05), but did not infl
27 ) and had greater effects than inhibition of alpha2-antiplasmin cross-linking alone (group 4 versus 5
29 selective inhibition of factor XIII-mediated alpha2-antiplasmin-fibrin cross-linking enhanced lysis (
30 IIa-mediated fibrin-fibrin cross-linking and alpha2-antiplasmin-fibrin cross-linking were measured in
31 tivity+TPA (76.0+/-11.9%); and (5) inhibited alpha2-antiplasmin-fibrin cross-linking+TPA (54.7+/-3.9%
32 m amyloid A, complement C3, pentraxin 3, and alpha2-antiplasmin in the liver, despite CNS neurodegene
33 al alpha2-antiplasmin levels treated with an alpha2-antiplasmin-inactivating antibody (P<0.0001).
37 ed the effects of plasminogen activation and alpha2-antiplasmin inactivation on experimental thrombus
40 ot dissolve emboli, but was synergistic with alpha2-antiplasmin inactivation, causing more embolus di
41 onsistent with this hypothesis, injection of alpha2-antiplasmin into cerebral ventricles markedly ame
42 was markedly accelerated in mice with normal alpha2-antiplasmin levels treated with an alpha2-antipla
43 y regulator of the fibrinolytic system, like alpha2-antiplasmin, may have unique therapeutic value in
44 th essentially identical kinetics toward Met-alpha2-antiplasmin (Met-alpha2AP) and peptide substrates
45 9F magnetic resonance imaging, together with alpha2-antiplasmin peptide (alpha2AP)-targeted perfluoro
46 , glutamine-containing peptides derived from alpha2-antiplasmin, Staphylococcus aureus fibronectin bi
47 ere retained in clots from mice deficient in alpha2-antiplasmin, thrombin-activatable fibrinolysis in
48 incorporation of biotinamido-pentylamine and alpha2-antiplasmin to fibrin, and fibrin cross-linking,
49 lmonary emboli, assessed the contribution of alpha2-antiplasmin to fibrinolytic failure, and compared
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