ライフサイエンスコーパス: atheromatous plaque

1 ole for secretory SMCs in the development of atheromatous plaque.

2 m (Lu-Tex) is a photosensitizer that targets atheromatous plaque.

3 ET-1 and its precursor, big ET-1, within the atheromatous plaque.

4 mutans has been found with high frequency in atheromatous plaques.

5 racterized by the presence of lesions called atheromatous plaques.

6 as reference segments and 1318 segments with atheromatous plaques.

7 , a pathogen also linked to endocarditis and atheromatous plaques.

8 abetes, aortic dimension, the presence of an atheromatous plaque and smoke in the left atrium.

9 overexpression of collagenolytic enzymes in atheromatous plaques and implicated MMPs in the destabil

10 e-related increase in the incidence of aorta atheromatous plaques and periaortic vascular channels in

11 ynthesis may influence both the stability of atheromatous plaques and the development of restenotic l

12 ent reductions in the inflammatory status of atheromatous plaque, and suggest that this effect may ha

13 ies have been detected in circulation and in atheromatous plaques, and immune complexes (ICs) formed

14 PA and vWF may correlate with instability of atheromatous plaques, and that their decrease after coro

15 s plaques < or = abdominal aortic aneurysm < atheromatous plaques; and correlate with macrophage cont

16 ity lipoprotein (OxHDL) within the intima of atheromatous plaques as well as in plasma; however, its

17 In our study, atheromatous plaques (ATH) and macroscopically intact ti

18 Pathological changes consisting of atheromatous plaques, atherosclerotic microaneurysms ext

19 We found that both the coronary atheromatous plaque burden and smoking habit are associa

20 que in the coronary arteries is a marker for atheromatous-plaque burden and is predictive of future r

21 Fibrous and atheromatous plaques but not normal arteries contained N

22 eriodontal pathogens have been detected from atheromatous plaque by amplification of the genetic mate

23 nical events but may evolve into complicated atheromatous plaques characterized by an accumulation of

24 Finally, atheromatous plaques contained higher levels of proinfla

25 The core of an atheromatous plaque contains lipids, macrophages, and ce

26 hought to play an important role in coronary atheromatous plaque destabilization.

27 Atheromatous plaque disruption often presents as complex

28 s have been developed that ablate or section atheromatous plaque during percutaneous coronary interve

29 tiation, progression, and destabilization of atheromatous plaques, eventually leading to the developm

30 h, composition, and rupture of intracoronary atheromatous plaque-factors that define the natural hist

31 Metformin attenuated Ang-II-induced atheromatous plaque formation and aortic aneurysm in Apo

32 regressing angiotensin II (Ang-II)-mediated atheromatous plaque formation in ApoE(-/-) mice.

33 Asynchronous movement of the carotid atheromatous plaque from B-mode ultrasound has been prev

34 have demonstrated a high incidence of CMV in atheromatous plaques from the coronary circulation.

35 sease, but the paucity of neutrophils in the atheromatous plaque has led to neglect of its potential

36 Improved understanding of the biology of atheromatous plaques has led to the concept of plaque vu

37 ynamic therapy (PDT) agent that localizes in atheromatous plaque in which it can be activated by far-

38 associated with irregularity and rupture of atheromatous plaques in both the carotid and coronary ar

39 al microbiota to the bloodstream and then to atheromatous plaques in carotid or other peripheral arte

40 t C pneumoniae can frequently be detected in atheromatous plaques in coronary arteries.

41 tic and asymptomatic patients would identify atheromatous plaques independently of stenosis.

42 showed that the enhanced glycolytic flux in atheromatous plaques of ApoE(-/-) mice was associated wi

43 lut1 connects the enhanced glucose uptake in atheromatous plaques of ApoE(-/-) mice with their myelop

44 o cause clinical manifestations (vulnerable, atheromatous plaques) or those less frequently associate

45 therosclerotic lesions (P < 0.004) and fewer atheromatous plaques (P < 0.008) when compared with ApoE

46 al plaque samples of all the four groups and atheromatous plaque samples of the C-S using reverse tra

47 Histological analysis of the atheromatous plaques showed no difference between lesion

48 al for atraumatic and effective debulking of atheromatous plaque through a biological mechanism, the

49 play a significant role in atherogenesis and atheromatous plaque vulnerability and may determine rapi

50 elet degranulation helps in the formation of atheromatous plaque, whereas the reciprocal interaction

51 abounded in the macrophage-rich shoulders of atheromatous plaques with histological features of vulne