ライフサイエンスコーパス: subendothelium

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1 y when spreading onto small sites of exposed subendothelium.

2 he A1 domain of von Willebrand factor in the subendothelium.

3 ory cells and favored their retention in the subendothelium.

4 tion of macrophages with lipoproteins in the subendothelium.

5 rand factor normally present in the vascular subendothelium.

6 ocess required for platelet spreading on the subendothelium.

7 as a binding site for vWF in human vascular subendothelium.

8 leading to platelet-rich microthrombi in the subendothelium.

9 that they will enter and be retained in the subendothelium.

10 ns of arteries and correlates with FN in the subendothelium.

11 complex mediates platelet attachment to both subendothelium and activated endothelium.

12 mers for multimeric binding to platelets and subendothelium and likely also increases affinity of the

13 bridge between constituents of the vascular subendothelium and platelet membrane receptors.

14 for recruitment of platelets to both exposed subendothelium and thrombi under arterial flow condition

15 -regulates both platelet adhesion to exposed subendothelium and thrombus formation in injured arterio

16 istently observed in glomerular endothelium, subendothelium, and mesangium in all kidneys removed due

17 te (ADP), in mediating thrombus formation on subendothelium at high shear rates.

18 complex, which mediates platelet adhesion to subendothelium at sites of injury.

19 flow and mediates their adhesion to damaged subendothelium at sites of vascular injury.

20 (vWF) mediates platelet adhesion to exposed subendothelium at sites of vascular injury.

21 n that mediates platelet adhesion to exposed subendothelium at sites of vascular injury.

22 ly with the type VI collagen microfibrils in subendothelium but not with fibrillin microfibrils or st

23 Mural thrombi form on exposed arterial subendothelium by a two-step process of platelet adhesio

24 VI collagen, and fibrillin in human vascular subendothelium by immunoelectron microscopy using single

25 Mononuclear cell migration into the vascular subendothelium constitutes an early event of the atherog

26 arly recruitment of mononuclear cells to the subendothelium in human atherosclerosis and that oxidize

27 Platelet spreading on the subendothelium in response to vascular injury is fundame

28 The vWF is present in subendothelium in the form of electron-dense aggregates

29 Monocyte recruitment into the subendothelium is a crucial step in atherosclerosis, and

30 chloride-injured veins platelet adhesion to subendothelium is decreased and thrombus growth is impai

31 uitment of blood monocytes into the arterial subendothelium is one of the earliest steps in atherogen

32 tion of iron-laden macrophages in the aortic subendothelium of apo E-deficient mice under basal condi

33 The adhesion of platelets to the subendothelium of blood vessels at sites of vascular inj

34 which mediates adhesion of platelets to the subendothelium of damaged blood vessels.

35 nd mediates the adhesion of platelets to the subendothelium of damaged blood vessels.

36 The endothelium and subendothelium of pig iliac arteries that were transduce

37 Laminin, a major component of the subendothelium, supports significant adhesion of sickle,

38 rombin and mediates platelet adhesion to the subendothelium under conditions of high shear stress.

39 y various soluble agonists or by adhesion to subendothelium under high shear, they release adenosine-

40 telets often combine, forming thrombi on the subendothelium, where collagen is exposed.

41 elevant binding site for vWF in the vascular subendothelium, where the type VI collagen-vWF complex m

42 in Fg(-/-) mice, but they detached from the subendothelium, which ultimately caused downstream occlu

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