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1 rimed neutrophils were present in arteriolar microthrombi.
2 crease portal pressure by promoting sinusoid microthrombi.
3 trophils and promoting formation of NETs and microthrombi.
4 , with five patients showing focal pulmonary microthrombi.
5 teria and recruited platelets into bacterial microthrombi.
6 nding to P- and L-selectin and mucin-induced microthrombi.
7 munostaining in leukocytes and platelet-rich microthrombi.
8 veolar inflammatory infiltrates and vascular microthrombi.
9 th the formation of fibrin-platelet multiple microthrombi.
10 and activation and the formation of multiple microthrombi.
11 n numerous areas, including those apart from microthrombi.
12 s are because of peribiliary vascular fibrin microthrombi.
13 ng microvasculature within fibrin-containing microthrombi.
14 ion biopsies, 4 showed widespread glomerular microthrombi.
15 n pathological cause of myocyte necrosis was microthrombi.
16 uPA, for localized plasminogen activation on microthrombi.
17 and congestion (70/70), often accompanied by microthrombi (27/70), superimposed acute bronchopneumoni
18  study demonstrates that platelet containing microthrombi accumulate in the retinal vasculature of th
19                                              Microthrombi and associated sites of BBB leakiness were
20 BMCs from the aCL-positive patient, we found microthrombi and infiltration of CD3+, CD8+, and CD19+ c
21 cytopenia coincided with sinusoidal platelet microthrombi and sinusoidal endothelial injury identifie
22  of these genes may promote the formation of microthrombi and thus contribute to the progression of l
23 including interstitial hemorrhages, platelet microthrombi, and edema, without leukocyte infiltration.
24 ding to a procoagulative state, formation of microthrombi, and tissue damage.
25 omeruli and interstitium rapidly progresses, microthrombi appear, and hematuria develops.
26                                     Platelet microthrombi are present in the diabetic retinal vascula
27  metastases by facilitating the formation of microthrombi around tumor cell emboli (TCE), thereby inh
28 4+/-17% of the surface areas were covered by microthrombi at 1 and 3 days, respectively.
29 d platelets by flow cytometry and in mucosal microthrombi by confocal microscopy.
30                                              Microthrombi, cardiomyocyte necrosis, and inflammatory i
31 ar injury (angiopoietin 2) and platelet-rich microthrombi (CD61) and induction of necrotic cell death
32 dings suggest that the formation of vascular microthrombi contributes to tumor necrosis, prompting in
33 oma mucins into mice generates platelet-rich microthrombi dependent on P- and L-selectin but not thro
34             Evidence for arterial and venous microthrombi, deposition of C5b-9 and MASP2 (representat
35 C) injury coupled to progression of platelet microthrombi facilitated by ADAMTS13 deficiency is chara
36 glomerulopathy with multiple platelet-fibrin microthrombi, focal interstitial hemorrhage, and acute c
37        The diminution of intragraft platelet microthrombi formation and leukocyte infiltration sugges
38 d organ injury due to endothelial damage and microthrombi formation in small vessels.
39 effectively augmented platelet adhesion, and microthrombi formation on fibrin(ogen), extracellular ma
40  an endotoxin or saline injection and tissue microthrombi formation was assessed by measuring the per
41 ular fibrin deposition, red cell congestion, microthrombi formation, and glomerular ultrastructural c
42 tin expression, neutrophil infiltration, and microthrombi formation.
43                          We compared cardiac microthrombi from COVID-19-positive autopsy cases to int
44                                              Microthrombi had significantly greater fibrin and termin
45                     Disseminated fibrin-rich microthrombi have been reported in patients who died fro
46 f blood-brain barrier (BBB) leakiness around microthrombi in a mouse model of traumatic brain injury.
47                    Mucins failed to generate microthrombi in cathepsin G-deficient mice.
48 rption and concentrated platelets and fibrin microthrombi in localized regions, a phenomenon less obs
49  found that carcinoma mucins do not generate microthrombi in mice lacking P-selectin glycoprotein lig
50 ia, schistocytosis, anemia, and VWF-positive microthrombi in multiple organs.
51  artery thrombi, whereas 9 of 14 (64.3%) had microthrombi in myocardial capillaries, arterioles, and
52 ry, heparin-sensitive but warfarin-resistant microthrombi in patients with occult, mucinous adenocarc
53                               Mucins induced microthrombi in radiation chimeras lacking endothelial P
54 irmed that LIBS-MPIOs bound significantly to microthrombi in reperfused myocardium.
55 findings indicate that cVWF is released from microthrombi in the context of microvascular occlusion.
56 motif, member 13), resulting in formation of microthrombi in the high sheer environment of the microv
57 sis and denudation, leading to platelet-rich microthrombi in the subendothelium.
58 trigger the rapid formation of platelet-rich microthrombi in vivo.
59 idney) against total injected radioactivity (microthrombi index, MI) 2.25 h after an endotoxin or sal
60 otein by endothelium and increased number of microthrombi inside capillaries.
61 gmented red blood cells, fibrin and platelet microthrombi, necrosis and detachment of endothelial cel
62 uring CAPS episodes were reviewed and showed microthrombi of dermal capillaries in 15 patients (94%).
63 o promoted firm platelet adhesion and stable microthrombi on VWF.
64 faces of vessels to mitogens associated with microthrombi over protracted intervals.
65 ic transcriptomic signatures of COVID-19 and microthrombi-positive COVID-19 hearts.
66 ual molar concentrations, Microlyse degrades microthrombi sevenfold more rapidly than blockade of pla
67          Experiment 2: multiple-system organ microthrombi study in which 125I-human fibrinogen was in
68 deficiency allows the unrestrained growth of microthrombi that are composed of von Willebrand factor
69 plained by defective clearance of intraorgan microthrombi that have been proposed to drive organ fail
70 injury, large-vessel thrombosis, and in situ microthrombi that may contribute to organ failure.
71  to both immobilized activated platelets and microthrombi under flow.
72                           Alveolar capillary microthrombi were 9 times as prevalent in patients with
73                                              Microthrombi were also observed in larvae after tmem242
74                                              Microthrombi were detected in 13 (87%) of 15 patients wi
75                                              Microthrombi were different in composition from intramyo
76                      Platelet aggregates and microthrombi were found adherent to the endothelial cell
77                                              Microthrombi were observed in 63% of cases in several or
78 ravenously injected into mice, platelet-rich microthrombi were rapidly generated.
79                                              Microthrombi, where observed, were scarce and endothelii
80 pulmonary autopsies confirmed NET-containing microthrombi with neutrophil-platelet infiltration.
81 ngiopathy characterized by extensive diffuse microthrombi within peripheral capillaries and arteriole
82                          Nonocclusive fibrin microthrombi (without ischemic injury) were identified i
83 OVID-19 cases frequently have cardiac fibrin microthrombi, without universal acute ischemic injury.