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1 led to demonstrate a role for neutrophils in thrombogenesis.
2 o show that they may also mediate pathologic thrombogenesis.
3 ons in which NETs form and their relation to thrombogenesis.
4          Thus, we examined the role of L5 in thrombogenesis.
5  to Ang II and accelerated atherogenesis and thrombogenesis.
6  had significantly decreased FeCl(3)-induced thrombogenesis.
7 ition, inhibits MBL deposition, and prevents thrombogenesis.
8 istance may be an important factor in venous thrombogenesis.
9 e-response effects and shows improvements in thrombogenesis.
10 equired for normal hemostasis and pathologic thrombogenesis.
11 uration of AF, success of cardioversion, and thrombogenesis.
12 anical properties while reducing the risk of thrombogenesis.
13 their binding to monocytes are key events in thrombogenesis.
14 nown whether it can cleave plasma VWF during thrombogenesis.
15 ion, such as ischemia-reperfusion injury and thrombogenesis.
16         CD40-deficient mice exhibited normal thrombogenesis.
17 ndicated the importance of platelet DREAM in thrombogenesis.
18  part, related to enhanced platelet-mediated thrombogenesis.
19 ne the platelet adhesion pathways leading to thrombogenesis.
20 d in anucleate platelets and plays a role in thrombogenesis.
21 these different functions may be crucial for thrombogenesis.
22 ulation enzyme complexes present at sites of thrombogenesis and are potentially useful as antithrombo
23 of WBCs to the endothelial cells exacerbates thrombogenesis and contributes to the blockage of the bl
24 HS-2-derived PGI(2), was shown to accelerate thrombogenesis and elevate blood pressure in mice.
25 ogen axis as a central determinant in venous thrombogenesis and identify FXIII as a potential therape
26 ndividuals reveals intensified biomechanical thrombogenesis and multi-dimensional thrombus profile ab
27 eptor may also be relevant in intra-arterial thrombogenesis and myocardial ischemia-reperfusion injur
28 atients with AF have increased intravascular thrombogenesis and platelet activation compared with pat
29                          (300 mg) therapy on thrombogenesis and platelet activation in AF.
30  of atherosclerotic plaque or the balance of thrombogenesis and thrombolysis.
31 atic role in the regulation of vascular tone thrombogenesis and vascular remodeling.
32    Other causes of cerebral ischemia include thrombogenesis and vasculitis.
33 hanges in plasma fibrin D-dimer (an index of thrombogenesis) and beta-thromboglobulin (beta-TG, a mea
34 mbin generation (probably due to accelerated thrombogenesis) and inhibition of fibrinolysis precede r
35 ult in the fulfilment of Virchow's triad for thrombogenesis, and accord with a prothrombotic or hyper
36 ion accelerates atherosclerosis and promotes thrombogenesis, and inflammatory biomarkers have been co
37 tracellular matrix formation and remodeling, thrombogenesis, and those encoding cytokines/chemokines
38 s not only in the generation of thrombin and thrombogenesis, but also in vascular cell signaling.
39         mPges-1 depletion modestly increased thrombogenesis, but this response was markedly further a
40  is essential for preventing cell damage and thrombogenesis characteristic of aHUS.
41 iency conferred a >2-fold increase in venous thrombogenesis, characterized by increased leukocyte eng
42 ived PGI2 removes a protective constraint on thrombogenesis, hypertension, and atherogenesis in vivo.
43  and, unlike tirofiban, it suppresses venous thrombogenesis in a mouse model without increasing bleed
44 the established and purported mechanisms for thrombogenesis in atrial fibrillation.
45  ex vivo studies of the effects of myosin on thrombogenesis in fresh human blood were conducted.
46                       The pathophysiology of thrombogenesis in heart failure could well be explained
47 effect of atrial fibrillation (AF) on atrial thrombogenesis in humans by determining the impact of ra
48 nant human (rh) MBL restored FeCl(3)-induced thrombogenesis in MBL-null mice to levels comparable to
49 larly, IVIG lowered aPL levels and inhibited thrombogenesis in mice immunized with beta2GPI.
50 megakaryocytopoiesis, platelet function, and thrombogenesis in nonhuman primates.
51 udies have demonstrated increased markers of thrombogenesis in patients with atrial fibrillation (AF)
52 -function relationship in vWF properties for thrombogenesis in regions of high shear stress.
53 tor 1- and 2-deficient mice exhibited normal thrombogenesis in the presence of TNF-alpha.
54 d ferric chloride-induced occlusive arterial thrombogenesis in vivo.
55           The problem of thrombus formation (thrombogenesis) in heart failure may therefore be a much
56  of the coagulation protease cascade, drives thrombogenesis, inflammation, tumor cell metastasis, and
57 wever, the molecular mechanism of high UA on thrombogenesis is unknown.
58 ed for both normal hemostasis and pathologic thrombogenesis, it also participates in its own negative
59 remodeling is considered important in atrial thrombogenesis, its role never has been directly tested.
60 s via imaging and biomarkers associated with thrombogenesis may provide enhanced approaches to assess
61 ty, multiphysics models can be used to study thrombogenesis mechanisms in patient-specific anatomies,
62  awaited, measurement of suitable markers of thrombogenesis might prove to be valuable in identifying
63 portantly, mPGES-1 deletion affected neither thrombogenesis nor blood pressure.
64  vascular injury without a predisposition to thrombogenesis or hypertension.
65 ue for expedited detection and management of thrombogenesis phenomena in COVID-19 patients.
66 gical effects are relevant for microvascular thrombogenesis remains elusive.
67       The role of unsaturated fatty acids in thrombogenesis still remains controversial.
68 ls have been identified; and mouse models of thrombogenesis that permit experimental manipulation of
69               Blockade of MMP1-PAR1 curtails thrombogenesis under arterial flow conditions and inhibi
70 ty to evoked macrovascular and microvascular thrombogenesis was also unaltered.
71        The critical role for ADP in arterial thrombogenesis was established by the clinical success o
72                                              Thrombogenesis was initiated by electrolytic injury of t
73        The effect of perfused fibronectin on thrombogenesis was lost if fibronectin deposition was bl
74 ntribution from individual dietary lipids to thrombogenesis was reviewed in the preceding section of
75 ing myocardial schema/reperfusion injury and thrombogenesis when used at pharmacological doses in wil
76 rains atherogenesis, and fails to accelerate thrombogenesis, while suppressing prostaglandin E2 (PGE2
77 uates atherogenesis, and fails to accelerate thrombogenesis, while suppressing prostaglandin E2, but
78 echanism by which mPges-1 deletion restrains thrombogenesis, while suppression of PGE2 accounts for i
79 eatment resulted in intra-arterial occlusive thrombogenesis within 10 min in wild-type (WT) and C2/fa