ライフサイエンスコーパス: stable plaque

コーパス検索結果 (１語後でソート)

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1 the 6th decade was due to sudden death with stable plaque).

2 cin was higher in asymptomatic patients with stable plaque.

3 with previous descriptions of lymphocytes in stable plaques.

4 erial hemorrhage, which might be due to less stable plaques.

5 ured and eroded unstable plaques, but not in stable plaques.

6 , CXCL9 and SCGF-beta compared to those with stable plaques.

7 ate plaques with a high risk of rupture from stable plaques.

8 l 147 [60 to 335]) compared to patients with stable plaque (16 [0 to 234] and 55 [36 to 157]; p < 0.0

9 R1 between the 3 and 12 weeks compared with stable plaque (50.80+/-7.2% versus 14.22+/-2.2%; P<0.001

10 ratio [OR] 21), glycoslyated hemoglobin with stable plaque and healed infarct (P = 0.03, OR 41), TC w

11 Women with stable plaque and healed infarct had elevated glycosylat

12 a significant association in blacks between stable plaque and left ventricular hypertrophy (risk rat

13 SLE patients with stable plaque and progressive plaque differed only in ba

14 e of thrombus (acute rupture, acute erosion, stable plaque), and heart weight.

15 icrog/mL in plaque erosion, 2.5 microg/mL in stable plaque, and 1.4 microg/mL in controls.

16 therothrombi, 71 sudden coronary deaths with stable plaque, and 158 control cases (unnatural sudden d

17 ing microparticles compared to patients with stable plaques, and may correlate with serum markers of

18 6 versus 0.47+/-0.02, P= 0.01) compared with stable plaque at 12 weeks.

19 otes repopulation of plaques with a SMC-rich stable plaque cell phenotype while reducing disease prog

20 ase 2, 3, 7, 9, 12, and 13 have more or less stable plaques, consistent with harmful or protective ef

21 t culprit unstable coronary plaques and four stable plaques from eight patients who had died suddenly

22 crimination of histologically vulnerable and stable plaques in this study suggests that NIR spectrosc

23 rosclerotic plaque without acute thrombosis (stable plaque) in 54.

24 The unstable plaque but not the stable plaque is invaded by clonally expanded T cells, s

25 l 78 [56 to 258] compared with patients with stable plaque (n = 14; 20 [0 to 251] and 55 [34 to 102];

26 n rupture (P<0.0001), erosion (P=0.005), and stable plaque (P=0.0003) versus controls.

27 ltivariate analysis, atherothrombi (P=0.02), stable plaque (P=0.003), and plaque burden (P=0.03) were

28 ompared with 22 (41 percent) of the men with stable plaques (P<0.001).

29 ssion is associated with histologically more stable plaques (P=0.011).

30 d atherosclerotic lesions and induced a more stable plaque phenotype, characterized by lower content

31 is, as well as reduced atherosclerosis and a stable plaque phenotype.

32 gen content was increased, indicating a more stable plaque phenotype.

33 oles, limiting plaque growth and promoting a stable plaque phenotype.

34 phage content in the plaque, indicative of a stable plaque phenotype.

35 lls and collagen, features consistent with a stable plaque phenotype.

36 compositional characteristics of a potential stable plaque phenotype.

37 tion and oxidative stress, indicating a more stable plaque phenotype.

38 feriority trial, adult patients with chronic stable plaque psoriasis (for >/=12 months) who were cand

39 ear stress (ESS) in the transition of early, stable plaques to high-risk atherosclerotic lesions.

40 eroded plaque with acute thrombus (n = 18), stable plaque with healed infarct (n = 18), and stable p

41 ture (P = 0.02, OR 7), and hypertension with stable plaque with healed infarct (P = 0.02, OR 15).

42 d plaques with acute thrombosis (n = 25) and stable plaques with and without healed myocardial infarc

43 ble plaque with healed infarct (n = 18), and stable plaque without infarction (n = 7).

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