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1 nts with functional connections to a complex thrombotic disease.
2 hemostasis but simultaneously contributes to thrombotic disease.
3 g promising new targets for the treatment of thrombotic disease.
4 thms with proven safety for excluding venous thrombotic disease.
5 new therapeutic strategies for treatment of thrombotic disease.
6 levels of procoagulant proteins and risk of thrombotic disease.
7 l importance to understanding hemostasis and thrombotic disease.
8 yndrome (APS), a life-threatening autoimmune thrombotic disease.
9 d is a promising clinical candidate to treat thrombotic disease.
10 a potential target for prevention of athero-thrombotic disease.
11 of the presence of multiple risk factors for thrombotic disease.
12 protein expression and familial and acquired thrombotic disease.
13 VID-19) is thought to predispose patients to thrombotic disease.
14 test candidate gene associations for athero-thrombotic disease.
15 point provides a unique mouse model of human thrombotic disease.
16 ch contribute to risk for and morbidity from thrombotic disease.
17 the blood clotting cascade in hemostasis and thrombotic disease.
18 new anticoagulant drugs for the treatment of thrombotic disease.
19 r endothelial cell TF in the pathogenesis of thrombotic disease.
20 n between postmenopausal use of hormones and thrombotic disease.
21 ategy to treat or prevent cardiovascular and thrombotic disease.
22 ght hold value for other forms of VWF-driven thrombotic disease.
23 e circulation is essential for prevention of thrombotic diseases.
24 ping microbes, they promote inflammatory and thrombotic diseases.
25 processes are critical to the progression of thrombotic diseases.
26 Genetic factors contribute to the risk of thrombotic diseases.
27 approach for the treatment and prevention of thrombotic diseases.
28 lor is being evaluated in clinical trials of thrombotic diseases.
29 and soluble EPCR levels are associated with thrombotic diseases.
30 ADAMTS13, contributing to the development of thrombotic diseases.
31 or the development of therapeutic agents for thrombotic diseases.
32 of factor Xa inhibitors for the treatment of thrombotic diseases.
33 gulant activity associated with vascular and thrombotic diseases.
34 gender differences in platelet function and thrombotic diseases.
35 or impediment to the successful treatment of thrombotic diseases.
36 levels on the hemostatic balance in various thrombotic diseases.
37 ogy and the pathogenesis of inflammatory and thrombotic diseases.
38 sed as an anticoagulant to prevent and treat thrombotic diseases.
39 has been associated with immune-mediated and thrombotic diseases.
40 rs with a broad range of atherosclerotic and thrombotic diseases.
41 in organelles implicated in inflammatory and thrombotic diseases.
43 ional therapeutic targets for the control of thrombotic disease and is highly relevant to other secre
44 seful therapeutic agents for gene therapy in thrombotic disease and postangioplasty or for transgenic
45 with nephrotic syndrome at highest risk for thrombotic disease and potentially target them for antic
46 normal hemostasis and likely plays roles in thrombotic diseases and also in host responses to pathog
47 s opportunity for understanding the basis of thrombotic diseases and bleeding disorders, with the pot
48 of utmost importance in the pathogenesis of thrombotic diseases and substances inhibiting TF synthes
49 , we review atherothrombotic disease, venous thrombotic disease, and atrial fibrillation in patients
50 e roles in infection, sepsis, wound healing, thrombotic disease, and cancer propagation, all of which
51 h will enable elucidation of the genetics of thrombotic diseases, and serves as an example for the ge
54 cholestatic pruritus, lymphocyte homing, and thrombotic diseases by producing the lipid mediator lyso
55 ls maintaining a high index of suspicion for thrombotic disease, confirming diagnostic suspicions wit
56 S-CoV-2 infection may predispose patients to thrombotic disease due to excessive inflammation, platel
57 herapeutic strategy and molecular target for thrombotic diseases, especially for thrombotic complicat
59 en venous thromboembolism (VTE) and arterial thrombotic diseases (ie, myocardial infarction and ische
63 ty and mortality for patients afflicted with thrombotic diseases, including stroke and myocardial inf
64 more efficacious agents for the treatment of thrombotic disease involves the design and testing of in
69 mation by PAD4 inhibition in inflammatory or thrombotic diseases is not likely to increase host vulne
70 ase (SK) is widely used to treat humans with thrombotic disease, it is antigenic and anti-SK antibody
71 or challenge given the serious nature of the thrombotic disease observed, which has become refractory
72 sk factors, biomarkers of coagulation, other thrombotic diseases, or plasma levels of a broad array o
73 Although trichinellosis is known to cause thrombotic disease, serious thrombotic events are rare a
74 itical for hemostasis, but it also may cause thrombotic diseases, such as myocardial infarction or is
75 in its circulating levels may contribute to thrombotic diseases, such as venous thromboembolism (VTE
76 elial cell protein C receptor involvement in thrombotic disease suggests that the understanding of en
77 f coagulation, may better help manage venous thrombotic disease than a single DNA variant with a smal
79 y prove to be a useful adjunct in refractory thrombotic diseases that are not controlled with convent
80 add insights into the genetic regulation of thrombotic disease, we conducted a genome-wide associati
81 ociated with myocardial infarction and other thrombotic diseases whereas Glanzmann thrombasthenia, in
82 tors XIIa and XIa, 2 factors contributing to thrombotic disease while playing a limited role in hemos
83 de a proof-of-concept approach for combating thrombotic diseases without increased bleeding risk, ind
84 a new validated target for the treatment of thrombotic diseases without the risk of bleeding or off-