ライフサイエンスコーパス: factor V Leiden mutation

1 ratory abnormality of activated protein C or factor V Leiden mutation.

2 hemorrhagic stroke who are heterozygous for factor V Leiden mutation.

3 ic cerebral palsy, placental thrombosis, and factor V Leiden mutation.

4 Genotyping for the factor V Leiden mutation.

5 of thrombin formation was observed with the factor V(LEIDEN) mutation.

6 18.2%) as compared to those with an isolated factor V Leiden mutation (19.2%).

7 The discoveries of the factor V Leiden mutation and the prothrombin gene varian

8 d risk of thrombosis for women who carry the factor V Leiden mutation and use oral contraceptive pill

9 ithrombin III, to a translational product of factor V Leiden mutation, and to proteins C and S in chi

10 reports suggest that younger carriers of the factor V Leiden mutation are at greater risk for venous

11 of this study was to investigate whether the factor V Leiden mutation (Arg506Gln) is associated with

12 esented data support the hypothesis that the factor V(LEIDEN) mutation can increase thrombin formatio

13 proved survival of mice heterozygous for the factor V Leiden mutation complements results from the an

14 Prevalence of factor V Leiden mutation determined by a second-generati

15 confirm that carriers of this prothrombotic factor V Leiden mutation do not have an increased risk o

16 Factor V Leiden mutation does not seem to increase risks

17 that the system successfully identified the factor V Leiden mutations from human blood specimens.

18 with severe thrombophilia such as homozygous factor V Leiden mutation (FVL) depend on a positive fami

19 Among nonsmokers the factor V Leiden mutation had little effect (odds ratio 1

20 , we determined total homocysteine level and factor V Leiden mutation in baseline blood samples from

21 The high prevalence of the factor V Leiden mutation in certain populations has prom

22 ly relevant than genetic testing to detect a factor V Leiden mutation in identifying persons who are

23 ate to severe hemophilia A combined with the factor V(LEIDEN) mutation in vitro in a reconstituted mo

24 differences between men with and without the factor V Leiden mutation increased significantly with ag

25 thromboembolism in heterozygous carriers of factor V Leiden mutation increased with age at a rate si

26 Factor V Leiden mutation is associated with three- to si

27 different species strongly suggest that the factor V Leiden mutation is indeed a potent modifier of

28 The factor V Leiden mutation is not a significant risk facto

29 an Arg506Gln mutation in the factor V gene (factor V Leiden mutation) is the most common cause of fa

30 data are compatible with the hypothesis that factor V Leiden mutation may play a role in some cases o

31 For idiopathic VTE, in addition to the factor V (Leiden) mutation (odds ratio [OR], 5.13; 95% c

32 es of thromboembolic disease associated with factor V Leiden mutation or resistance to activated prot

33 rvival was significantly associated with the factor V Leiden mutation (p = .049).

34 The presence of factor V Leiden mutation predisposes patients to venous

35 The factor V Leiden mutation (R506Q), a prothrombotic gene p

36 IBD controls (4%) were heterozygotes for the factor V Leiden mutation (relative risk, 14.00; 95% conf

37 In patients with IBD, inheritance of the factor V Leiden mutation results in a significant increa

38 ymerase chain reaction was used to determine factor V Leiden mutation status in 156 study participant

39 k factors and indicate that determination of factor V Leiden mutation status should not be limited to

40 The presence of the factor V Leiden mutation was determined by coagulation a

41 The factor V Leiden mutation was found more often in women w

42 Prevalence of the factor V Leiden mutation was greater among case-patients

43 The factor V Leiden mutation was not associated with a signi

44 The factor V Leiden mutation was not significantly associate

45 A factor V Leiden mutation was present in 6 patients, prot

46 in III, and the translational product of the factor V Leiden mutation were isolated by recycling immu

47 severe hemophilia were heterozygous for the factor V(LEIDEN) mutation, which leads to the substituti

48 rioperative prophylaxis in patients with the factor V Leiden mutation who are undergoing hip or knee

49 were similar in men with and men without the factor V Leiden mutation who were younger than 50 years

50 he incidence and possible association of the factor V Leiden mutation with the development of thrombo

51 Thus, some 80% of all carriers of the factor V Leiden mutation would be detected if screening