ライフサイエンスコーパス: fibrinoid

1 ndovascular trophoblasts (vEVTs) embedded in fibrinoid.

2 t also reemphasizes the relationship between fibrinoid and miliary aneurysm formation.

3 Rejection with fibrinoid arterial necrosis (4% of biopsies) did not res

4 Plasmin produced fibrinoid changes in the blood vessels at 24 h, coincidi

5 ive abnormalities such as lipohyalinosis and fibrinoid changes within penetrating artery branches vis

6 implied massive necrotizing vasculitis with fibrinoid degeneration compatible with immune complex-in

7 ocytic infiltrates, reactive macrophages and fibrinoid degeneration of vessel walls.

8 Associated damage included extensive fibrinoid deposits, fibrosis, avascular villi, and edema

9 eks, wild-type (WT) mice developed extensive fibrinoid hepatic venous thrombi and biochemical evidenc

10 uscle cells (VSMCs) are lost and replaced by fibrinoid, incorporating extravillous trophoblast (EVT)

11 stabilizing uteroplacental attachment at the fibrinoid layer found at the fetal-maternal junction.

12 marked reduction of glomerular proliferation/fibrinoid necrosis (by 71%), crescent formation (by 98%)

13 The dual stimulus (HG+Pg-LPS) increased fibrinoid necrosis (p < 0.05) and upregulated TLR-4 mRNA

14 trophy and became fibrotic; some also showed fibrinoid necrosis and a mixed inflammatory cell infiltr

15 ity of CAA-associated vasculopathic changes (fibrinoid necrosis and concentric splitting of the wall)

16 nucleated giant cells (MGCs), MGC death, and fibrinoid necrosis and fibrosis.

17 5% versus 9%; severe ATI, 75% versus 9%; and fibrinoid necrosis in glomeruli, 20% versus 0%, or arter

18 s versus 40% (2 of 5) for those who also had fibrinoid necrosis of arteries.

19 leads to increased vascular permeability and fibrinoid necrosis of blood vessel walls.

20 f leukocytoclastic vasculitis, consisting of fibrinoid necrosis of dermal vessels' walls and neutroph

21 (3) Type III: arterial fibrinoid necrosis or transmural inflammation with or wi

22 ograft, intimal edema, matrix deposition and fibrinoid necrosis were specifically presented in the xe

23 c capillary involvement) and AHR 2 (arterial fibrinoid necrosis).

24 us, specific arterial lesions (endarteritis, fibrinoid necrosis, activated endothelial cells, mononuc

25 nuated renal injury (albuminuria, glomerular fibrinoid necrosis, and crescent formation), but mAbs to

26 liferation, cellular crescents, neutrophils, fibrinoid necrosis, and tubulointerstitial inflammation

27 o endothelial cells, endothelial activation, fibrinoid necrosis, foam cells, and intimal fibrosis.

28 arcts, microhaemorrhage, larger haemorrhage, fibrinoid necrosis, microaneurysms, perivascular space d

29 within the wall of an arteriole at a site of fibrinoid necrosis.

30 ealed leukocytoclastic vasculitis with focal fibrinoid necrosis.

31 eritis, 28% with endarteritis, and 100% with fibrinoid necrosis.

32 A fibrinoid substance of unclear origin often covered the

33 Histopathology showed fibrinoid vascular necrosis, rare amastigote nests withi

34 Large fibrinoids with avascular villi, edema, and inflammation