ライフサイエンスコーパス: microthrombi

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1 nding to P- and L-selectin and mucin-induced microthrombi.

2 munostaining in leukocytes and platelet-rich microthrombi.

3 th the formation of fibrin-platelet multiple microthrombi.

4 and activation and the formation of multiple microthrombi.

5 n numerous areas, including those apart from microthrombi.

6 teria and recruited platelets into bacterial microthrombi.

7 study demonstrates that platelet containing microthrombi accumulate in the retinal vasculature of th

8 BMCs from the aCL-positive patient, we found microthrombi and infiltration of CD3+, CD8+, and CD19+ c

9 of these genes may promote the formation of microthrombi and thus contribute to the progression of l

10 including interstitial hemorrhages, platelet microthrombi, and edema, without leukocyte infiltration.

11 ding to a procoagulative state, formation of microthrombi, and tissue damage.

12 Platelet microthrombi are present in the diabetic retinal vascula

13 metastases by facilitating the formation of microthrombi around tumor cell emboli (TCE), thereby inh

14 4+/-17% of the surface areas were covered by microthrombi at 1 and 3 days, respectively.

15 d platelets by flow cytometry and in mucosal microthrombi by confocal microscopy.

16 dings suggest that the formation of vascular microthrombi contributes to tumor necrosis, prompting in

17 oma mucins into mice generates platelet-rich microthrombi dependent on P- and L-selectin but not thro

18 C) injury coupled to progression of platelet microthrombi facilitated by ADAMTS13 deficiency is chara

19 glomerulopathy with multiple platelet-fibrin microthrombi, focal interstitial hemorrhage, and acute c

20 The diminution of intragraft platelet microthrombi formation and leukocyte infiltration sugges

21 effectively augmented platelet adhesion, and microthrombi formation on fibrin(ogen), extracellular ma

22 an endotoxin or saline injection and tissue microthrombi formation was assessed by measuring the per

23 ular fibrin deposition, red cell congestion, microthrombi formation, and glomerular ultrastructural c

24 tin expression, neutrophil infiltration, and microthrombi formation.

25 Mucins failed to generate microthrombi in cathepsin G-deficient mice.

26 found that carcinoma mucins do not generate microthrombi in mice lacking P-selectin glycoprotein lig

27 ia, schistocytosis, anemia, and VWF-positive microthrombi in multiple organs.

28 ry, heparin-sensitive but warfarin-resistant microthrombi in patients with occult, mucinous adenocarc

29 Mucins induced microthrombi in radiation chimeras lacking endothelial P

30 irmed that LIBS-MPIOs bound significantly to microthrombi in reperfused myocardium.

31 motif, member 13), resulting in formation of microthrombi in the high sheer environment of the microv

32 sis and denudation, leading to platelet-rich microthrombi in the subendothelium.

33 trigger the rapid formation of platelet-rich microthrombi in vivo.

34 idney) against total injected radioactivity (microthrombi index, MI) 2.25 h after an endotoxin or sal

35 otein by endothelium and increased number of microthrombi inside capillaries.

36 gmented red blood cells, fibrin and platelet microthrombi, necrosis and detachment of endothelial cel

37 o promoted firm platelet adhesion and stable microthrombi on VWF.

38 faces of vessels to mitogens associated with microthrombi over protracted intervals.

39 Experiment 2: multiple-system organ microthrombi study in which 125I-human fibrinogen was in

40 deficiency allows the unrestrained growth of microthrombi that are composed of von Willebrand factor

41 to both immobilized activated platelets and microthrombi under flow.

42 ravenously injected into mice, platelet-rich microthrombi were rapidly generated.

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