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1 hemostasis but simultaneously contributes to thrombotic disease.
2 thms with proven safety for excluding venous thrombotic disease.
3 g promising new targets for the treatment of thrombotic disease.
4 new therapeutic strategies for treatment of thrombotic disease.
5 levels of procoagulant proteins and risk of thrombotic disease.
6 l importance to understanding hemostasis and thrombotic disease.
7 d is a promising clinical candidate to treat thrombotic disease.
8 a potential target for prevention of athero-thrombotic disease.
9 of the presence of multiple risk factors for thrombotic disease.
10 protein expression and familial and acquired thrombotic disease.
11 test candidate gene associations for athero-thrombotic disease.
12 point provides a unique mouse model of human thrombotic disease.
13 ch contribute to risk for and morbidity from thrombotic disease.
14 the blood clotting cascade in hemostasis and thrombotic disease.
15 new anticoagulant drugs for the treatment of thrombotic disease.
16 r endothelial cell TF in the pathogenesis of thrombotic disease.
17 n between postmenopausal use of hormones and thrombotic disease.
18 ping microbes, they promote inflammatory and thrombotic diseases.
19 processes are critical to the progression of thrombotic diseases.
20 approach for the treatment and prevention of thrombotic diseases.
21 lor is being evaluated in clinical trials of thrombotic diseases.
22 and soluble EPCR levels are associated with thrombotic diseases.
23 ADAMTS13, contributing to the development of thrombotic diseases.
24 or the development of therapeutic agents for thrombotic diseases.
25 of factor Xa inhibitors for the treatment of thrombotic diseases.
26 gulant activity associated with vascular and thrombotic diseases.
27 gender differences in platelet function and thrombotic diseases.
28 or impediment to the successful treatment of thrombotic diseases.
29 levels on the hemostatic balance in various thrombotic diseases.
30 e circulation is essential for prevention of thrombotic diseases.
32 seful therapeutic agents for gene therapy in thrombotic disease and postangioplasty or for transgenic
33 with nephrotic syndrome at highest risk for thrombotic disease and potentially target them for antic
34 normal hemostasis and likely plays roles in thrombotic diseases and also in host responses to pathog
35 s opportunity for understanding the basis of thrombotic diseases and bleeding disorders, with the pot
36 of utmost importance in the pathogenesis of thrombotic diseases and substances inhibiting TF synthes
37 , we review atherothrombotic disease, venous thrombotic disease, and atrial fibrillation in patients
38 h will enable elucidation of the genetics of thrombotic diseases, and serves as an example for the ge
41 cholestatic pruritus, lymphocyte homing, and thrombotic diseases by producing the lipid mediator lyso
42 ls maintaining a high index of suspicion for thrombotic disease, confirming diagnostic suspicions wit
43 herapeutic strategy and molecular target for thrombotic diseases, especially for thrombotic complicat
45 en venous thromboembolism (VTE) and arterial thrombotic diseases (ie, myocardial infarction and ische
48 more efficacious agents for the treatment of thrombotic disease involves the design and testing of in
53 mation by PAD4 inhibition in inflammatory or thrombotic diseases is not likely to increase host vulne
54 ase (SK) is widely used to treat humans with thrombotic disease, it is antigenic and anti-SK antibody
55 Although trichinellosis is known to cause thrombotic disease, serious thrombotic events are rare a
56 itical for hemostasis, but it also may cause thrombotic diseases, such as myocardial infarction or is
57 elial cell protein C receptor involvement in thrombotic disease suggests that the understanding of en
58 f coagulation, may better help manage venous thrombotic disease than a single DNA variant with a smal
60 y prove to be a useful adjunct in refractory thrombotic diseases that are not controlled with convent
61 add insights into the genetic regulation of thrombotic disease, we conducted a genome-wide associati
62 ociated with myocardial infarction and other thrombotic diseases whereas Glanzmann thrombasthenia, in
63 de a proof-of-concept approach for combating thrombotic diseases without increased bleeding risk, ind
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