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1 ents beginning treatment with warfarin for a thrombotic disorder.
2 bition by NO in two brothers with a cerebral thrombotic disorder.
3 type to phenotype in families with a complex thrombotic disorder.
4 tions for the understanding and treatment of thrombotic disorders.
5 in acquired TTP and potentially other immune thrombotic disorders.
6 as therapeutic targets for inflammatory and thrombotic disorders.
7 herapeutic avenues for treating bleeding and thrombotic disorders.
8 ed in plasma and was shown to associate with thrombotic disorders.
9 efforts to develop PAR antagonists to treat thrombotic disorders.
10 oG in platelets are particularly relevant to thrombotic disorders.
11 cterized by naturally occurring bleeding and thrombotic disorders.
12 and treatment strategies to prevent or limit thrombotic disorders.
13 fened clots are associated with bleeding and thrombotic disorders.
14 therefore may play a role in the etiology of thrombotic disorders.
15 s and increase risk for negative outcomes in thrombotic disorders.
16 ed glycans that are clinically used to treat thrombotic disorders.
17 se, and development of therapeutics to treat thrombotic disorders.
18 therefore may play a role in the etiology of thrombotic disorders.
19 lity that HDACi might be a novel therapy for thrombotic disorders.
20 tic strategies to combat atherosclerosis and thrombotic disorders.
21 ys are targets for molecular intervention in thrombotic disorders.
22 ssible genotypes for three genes involved in thrombotic disorders.
23 eful therapeutic agents for the treatment of thrombotic disorders.
24 for the prevention and treatment of arterial thrombotic disorders.
25 critical role in normal haemostasis, and in thrombotic disorders.
26 nose 601 patients with inherited bleeding or thrombotic disorders.
27 ike cancer, sepsis, sickle cell disease, and thrombotic disorders.
28 ortant role in prevention of bleeding and in thrombotic disorders.
29 widely used anticoagulant medicine to treat thrombotic disorders.
30 les of complement in immune complex-mediated thrombotic disorders.
31 d to improved therapies to prevent and treat thrombotic disorders.
32 ential involvement of anti-PF4 antibodies in thrombotic disorders.
33 and might suggest novel approaches to these thrombotic disorders.
34 ociation would be a new approach to treating thrombotic disorders.
35 ischaemic heart disease [0.78 (0.76-0.80)], thrombotic disorders [0.78 (0.74-0.83)], and dysrhythmia
36 s with high titers of ACA but no evidence of thrombotic disorders, 37 received kidney transplants.
37 at risk of coronary-artery disease and other thrombotic disorders--a condition defined as the prethro
38 rd a therapeutic for patients suffering from thrombotic disorders and a diagnostic tool for monitorin
39 ls of soluble P-selectin are associated with thrombotic disorders and may predict future cardiovascul
40 ctions and also relevant to the pathology of thrombotic disorders and vasoocclusive events in sickle
41 to more clearly define the role of Lp(a) in thrombotic disorders, and to determine the extent to whi
42 een applied to the diagnosis of bleeding and thrombotic disorders, as well as to dosing and monitorin
43 hrombocytopenia (HIT) is a life-threatening, thrombotic disorder associated with development of anti-
44 ibility of their therapeutic use in treating thrombotic disorders associated with aberrant expression
45 uced thrombocytopenia (HIT) is an autoimmune thrombotic disorder caused by immune complexes containin
46 ombocytopenic purpura (TTP) is a devastating thrombotic disorder caused by widespread microvascular t
47 clear indication that the course of a severe thrombotic disorder could be manipulated by blocking the
48 morbidity and the mortality associated with thrombotic disorders, defining the mechanisms underlying
50 en, factor XIII, and cardiovascular or other thrombotic disorders have focused much attention on thes
51 on therapy is a mainstay of the treatment of thrombotic disorders; however, conventional anticoagulan
54 tion cascade, is known to be responsible for thrombotic disorders in many diseases including bacteria
55 proaches to the prevention and management of thrombotic disorders in obese and overweight patients ar
57 be explored as a novel treatment of arterial thrombotic disorders, including hereditary and acquired
58 t activation may contribute to various human thrombotic disorders involving both the micro- and macro
59 n, the clinical utility of targeting them in thrombotic disorders is already being explored in clinic
61 iolipin antibodies (ACA) in association with thrombotic disorders of arterial and/or venus systems, s
62 icoagulant drugs for use among patients with thrombotic disorders of the venous and arterial circulat
63 this issue of Blood, An et al(1) report that thrombotic disorders such as factor V Leiden are often t
64 thrombi and restore vessel patency in acute thrombotic disorders such as ischemic stroke, acute coro
65 ad documented evidence of one or more of the thrombotic disorders such as lupus, frequent abortions,
66 allow Slit2 to effectively prevent and treat thrombotic disorders such as myocardial infarction and s
67 iving increased morbidity and mortality from thrombotic disorders such as myocardial infarction, stro
68 Prevailing approaches to manage autoimmune thrombotic disorders, such as heparin-induced thrombocyt
69 openia (HIT) is a life- and limb-threatening thrombotic disorder that develops after exposure to hepa
71 tance in the pathogenesis and progression of thrombotic disorders that are exacerbated by leukocyte-p
72 limit thrombosis in this and possibly other thrombotic disorders that occur in the setting of inflam
73 e utility of ATAs in the management of acute thrombotic disorders through rapid, transient, and targe
74 AR4 as possible targets for the treatment of thrombotic disorders, we compared the efficacy of protea
75 ibody syndrome (APS) is a complex autoimmune thrombotic disorder with defined clinical phenotypes.
76 se of cardiovascular mortality, is a complex thrombotic disorder with environmental and genetic deter