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1 ty-four (55%) of the 98 sinuses or bulbs had occlusive thrombosis.
2 involves a pathogenic pathway independent of occlusive thrombosis.
3 e hemostasis while preventing development of occlusive thrombosis.
4 tochemical carotid arterial injury to induce occlusive thrombosis.
5 ree of thrombus formation or even subsequent occlusive thrombosis.
6 n-occlusive thrombosis; and grade 3, central occlusive thrombosis.
7 ical carotid injury model was used to induce occlusive thrombosis.
8 nistration induces de-endothelialization and occlusive thrombosis.
9 pendently of their ability to participate in occlusive thrombosis.
10 ivo neoangiogenesis, plaque development, and occlusive thrombosis.
11 ccelerated in iron-loaded mice (mean time to occlusive thrombosis, 20.4+/-8.5 minutes; n=10) compared
12 ntages over fII(WT) animals: protection from occlusive thrombosis after arterial injury and markedly
13 d plaque tissue factor activity, the time to occlusive thrombosis after photochemical carotid plaque
14 sive age-dependent shortening of the time to occlusive thrombosis after vascular injury that correlat
16 rable to rupture, an event that precipitates occlusive thrombosis and clinically manifest disease (su
17 vs one [2%] of 42) such as reduced caliber, occlusive thrombosis, and lack of visibility; focal nodu
18 pheral thrombosis; grade 2, intermediate non-occlusive thrombosis; and grade 3, central occlusive thr
19 A) have emerged as a means of dissolution of occlusive thrombosis associated with acute myocardial in
20 ng injury; mice deficient in PAI-1 developed occlusive thrombosis at 127 +/- 15 minutes (P <.0001).
21 F interactions restores vessel patency after occlusive thrombosis by specifically disaggregating the
22 3 exhibited significantly prolonged times to occlusive thrombosis compared to WT mice indicating a pr
25 nogen activator (tPA), prolonged the time to occlusive thrombosis following photochemical injury to c
26 eptin receptor-deficient mice (n = 7) formed occlusive thrombosis in 75.2 (10.1) and 68.6 (10.3) minu
27 scular injury, wild-type mice (n = 8) formed occlusive thrombosis in a mean (SD) of 42.2 (4.6) minute
30 (mural thrombosis model) or embolic stroke (occlusive thrombosis model) followed by recombinant tiss
31 rothrombocytopenia but also protects against occlusive thrombosis or cerebral infarction,providing ne
32 hough the parent endothelial cells prevented occlusive thrombosis, perlecan-deficient cells were comp
33 , infusion of this HBDt.TFt results in rapid occlusive thrombosis selective only for tumor microvascu
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