ライフサイエンスコーパス: arteriosclerotic

1 d aortic aneurysms was compared with that of arteriosclerotic aneurysms.

2 Disruption of CXCR3+ Th1 cell trafficking to arteriosclerotic arteries may contribute to the therapeu

3 and had lower ejection fraction and greater arteriosclerotic burden but less severe AS.

4 [95% CI, 3.2-22]) and variables representing arteriosclerotic burden.

5 sclerosis, diabetes, and uremia that promote arteriosclerotic calcification-elicit the ectopic vascul

6 obesity, hyperlipidemia, hyperglycemia, and arteriosclerotic calcification.

7 is an early key event in the development of arteriosclerotic cardiovascular disease (ASCVD), thus an

8 y-lowering B-vitamin intervention may reduce arteriosclerotic cardiovascular disease event rates in p

9 Arteriosclerotic cardiovascular disease is the leading c

10 ns reduced the rate of the primary composite arteriosclerotic cardiovascular disease outcome (myocard

11 w therapeutic strategy for the prevention of arteriosclerotic cardiovascular disease.

12 Several differences in arteriosclerotic changes in both the grey and white matt

13 mice, and we show that IFN-gamma can induce arteriosclerotic changes in the absence of detectable im

14 It was of interest that no arteriosclerotic changes were observed for the duration

15 cipients shows that IFN-gamma contributes to arteriosclerotic development following transplantation.

16 drome are affected by accelerated, premature arteriosclerotic disease that leads to heart attacks and

17 S activity as a result of ischemia or native arteriosclerotic disease, iNOS gene therapy may serve to

18 tonomous influence in experimental models of arteriosclerotic disease, which may have implications wi

19 littermate control WT mice developed robust arteriosclerotic disease.

20 es <50% narrowing, and controls were free of arteriosclerotic disease.

21 phenotypic response that promotes occlusive arteriosclerotic disease.

22 , a cytokine characteristically expressed in arteriosclerotic diseases, acts directly on vascular smo

23 edial immunoprivilege, are typically seen in arteriosclerotic diseases, such as atherosclerosis and t

24 lls that may contribute to the chronicity of arteriosclerotic diseases.

25 ies have identified increased mortality from arteriosclerotic heart disease among black men working i

26 T cells are essential in the early stages of arteriosclerotic lesion development after cardiac transp

27 ients underwent allograft biopsies to assess arteriosclerotic lesions and endothelial activation, end

28 ciated with cell growth and is active within arteriosclerotic lesions but is not known to be triggere

29 s of heme oxygenase action on heme, prevents arteriosclerotic lesions that occur following aorta tran

30 ions or cell death have been detected within arteriosclerotic lesions, and it is known that microbial

31 othelial dysfunction, systemic inflammation, arteriosclerotic lesions, and left ventricle remodeling,

32 ved myocardial architecture and were free of arteriosclerotic lesions.

33 ells may help prevent their proliferation in arteriosclerotic lesions.

34 A total of 492 total arteriosclerotic outcomes (primary outcome) and 317 CHF

35 he independent relationship between tHcy and arteriosclerotic outcomes and congestive heart failure (

36 nd may contribute to the excess incidence of arteriosclerotic outcomes experienced by both patient gr

37 No association between tHcy and arteriosclerotic outcomes was observed in a univariate m

38 rhomocysteinemia, a putative risk factor for arteriosclerotic outcomes, is seen in >85% of hemodialys

39 otal homocysteine levels are associated with arteriosclerotic outcomes.

40 ts provide a link between HCMV infection and arteriosclerotic plaque formation.

41 ll-surface molecules that cause the observed arteriosclerotic responses.

42 temic neutralization of IL-6R did not reduce arteriosclerotic thickening but reduced endothelial inte

43 ed the development of vascular rejection and arteriosclerotic thickening.

44 o the benefit of our patients afflicted with arteriosclerotic valvular and vascular diseases.

45 NO) bioavailability has been demonstrated in arteriosclerotic vascular disease, the integrity of this

46 e of the underlying disease and/or unrelated arteriosclerotic vascular events.

47 r smooth muscle cell PTH1R activity inhibits arteriosclerotic Wnt/beta-catenin signaling and reduces

48 of vascular PTH receptor (PTH1R) activity on arteriosclerotic Wnt/beta-catenin signaling in vitro and