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