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1 kade attenuated platelet-mediated NET-driven thrombogenicity.
2 lly the lowest indices of atherogenicity and thrombogenicity.
3 rome (ACS) to promote premature EC aging and thrombogenicity.
4 and platelet deposition, evidencing myosin's thrombogenicity.
5 all are critical factors in modulating stent thrombogenicity.
6 tissue factor is a key contributor to plaque thrombogenicity.
7  to modulate both platelet numbers and their thrombogenicity.
8 ween inflammation, plaque rupture, and blood thrombogenicity.
9 mong inflammation, plaque rupture, and blood thrombogenicity.
10 mmatory cell viability in determining plaque thrombogenicity.
11 rder to improve prosthetic graft patency and thrombogenicity.
12 significant predictor of a decrease in blood thrombogenicity.
13 tage heart failure, remain plagued by device thrombogenicity.
14 5%), showing a significant decrease in blood thrombogenicity.
15 role in both lesion stability and subsequent thrombogenicity.
16 ycemic improvement showed no change in blood thrombogenicity.
17 cules responsible for plaque instability and thrombogenicity.
18  is considered a major regulator of arterial thrombogenicity.
19 Tissue factor (TF) appears to mediate plaque thrombogenicity.
20       Polyester filling was added to enhance thrombogenicity.
21 pressed as essential amino acid (72.3-77.1), thrombogenicity (1.22-1.45), and atherogenicity indices
22              This is likely due to increased thrombogenicity and a foreign-body reaction.
23 ted/saturated FAs ratios, and the indices of thrombogenicity and atherogenicity depended on specific
24 re, our new coating exhibited both high anti-thrombogenicity and cell-adhesion properties, which fulf
25 s it efficiently attenuated inflammation and thrombogenicity and delayed hemodynamic changes.
26 able polymer and a metallic stent surface on thrombogenicity and endothelial cell coverage using diff
27 ctions particularly for proteins involved in thrombogenicity and enhanced platelet activity, but also
28          Our objectives were to quantify the thrombogenicity and extent of vascular injury created by
29 acodynamic effects of this approach on blood thrombogenicity and platelet reactivity remain unknown.
30 ting hemodynamic milieu and with the stent's thrombogenicity and pro-restenotic potential, thereby in
31 d comparative outcomes with respect to acute thrombogenicity and re-endothelialization among thin-str
32                                        Acute thrombogenicity and re-endothelialization represent clin
33 all the desired requirements, including anti-thrombogenicity and swift endothelialization, has not be
34 ese outcomes indicate differential trends in thrombogenicity and vascular healing among contemporary
35                                              Thrombogenicity and vascular healing differ among metall
36 ncluding barrier regulation of permeability, thrombogenicity, and leukocyte adherence, as well as pro
37 sed procoagulant mediators increase systemic thrombogenicity, and leukocytes are actively recruited t
38 ition of neointimal thickening, reduction in thrombogenicity, and restoration of endothelium-dependen
39 ts receptors, but the roles of the latter in thrombogenicity are less well-defined.
40 s suggest increased plaque TF expression and thrombogenicity as a novel mechanism for the increased r
41               Jcad-/- mice displayed reduced thrombogenicity as reflected by delayed time to carotid
42 determinant of both plaque vulnerability and thrombogenicity as they relate to plaque disruption.
43           This dynamic organ regulates blood thrombogenicity as well as contractile, secretory, and m
44 gy for controlling vascular inflammation and thrombogenicity associated with endothelial dysfunction.
45                        A comparison in acute thrombogenicity between the Magmaris sirolimus-eluting b
46 pothesized that the observed increased blood thrombogenicity (BT) observed in patients with type 2 di
47      Increased levels of uremic toxins cause thrombogenicity by increasing tissue factor (TF) express
48 mponents of atherosclerosis including plaque thrombogenicity, cellular migration, endothelial functio
49    EES demonstrated significantly less acute thrombogenicity compared with bioabsorbable EES and biol
50 IX-Padua exhibits similar immunogenicity and thrombogenicity compared with FIX wild type.
51 levels, TF expression in their arteries, and thrombogenicity compared with respective controls.
52 clot weights, a biological readout of venous thrombogenicity, compared with the control mice.
53 ittle is known of the effect of EI on vessel thrombogenicity due to delayed arterial healing.
54 have significant limitations with regards to thrombogenicity, durability, and inability to grow or re
55 ow capacity, low transvalvular gradient, low thrombogenicity, durability, easy availability, resistan
56 anced in silico and in vitro methods, Device Thrombogenicity Emulation (DTE) is a device design appro
57  support individualized therapy that targets thrombogenicity for better outcomes in patients with AMI
58 it of an ideal valve substitute, namely, low thrombogenicity, freedom from anticoagulation, durabilit
59 gn modifications successfully decreased pump thrombogenicity from initial designs.
60  stem cells, which resemble CDCs in size and thrombogenicity, have been associated with infarction af
61 n TF and TFPI and the regulation of vascular thrombogenicity in a model of vascular remodeling.
62 t thrombosis in animal models suggests stent thrombogenicity in human patients.
63 oth muscle cells, suggesting a cell-mediated thrombogenicity in patients with acute coronary syndrome
64 issue factor may be responsible for coronary thrombogenicity in patients with plaque rupture.
65 at plasmin is an endogenous regulator of VWF thrombogenicity, in particular when ADAMTS13 falls short
66 in malapposed or overlapping configurations, thrombogenicity increased compared with apposed, length-
67 , atherogenicity index (IA) (0.26-0.60), and thrombogenicity index (IT) (0.20-0.44).
68  22%, Atherogenicity Index (AI) 0.64 - 0.75, Thrombogenicity Index (TI) 0.77 - 1.44 and hypocholester
69    The atherogenicity index was 0.29 and the thrombogenicity index 0.47.
70 d fatty acids, the atherogenicity index, the thrombogenicity index, the hypo-cholesterolemic to hyper
71 tty acids, displaying low atherogenicity and thrombogenicity indexes (0.10 and 0.18; 0.23 and 0.70; 0
72                          The atherogenic and thrombogenicity indexes, as well as the hypocholesterole
73  direct prediction of the Atherogenicity and Thrombogenicity indexes, which are useful for the interp
74 nt, displaying the lowest atherogenicity and thrombogenicity indices (0.02 and 0.14; 0.12 and 0.34; 0
75 eous coronary intervention (PCI), those with thrombogenicity indices (n = 2705) were grouped accordin
76                  The present study evaluated thrombogenicity indices and their prognostic implication
77                                              Thrombogenicity indices were measured by thromboelastogr
78 lue, free fatty acid, and atherogenicity and thrombogenicity indices.
79 fic inhibition of TF activity reduced plaque thrombogenicity, inhibiting both platelet and fibrin(oge
80                      Whether increased blood thrombogenicity is associated with glycemic control has
81 tudy was designed to determine whether blood thrombogenicity is related to chronic glycemic control i
82 ality the indices of atherogenicity (IA) and thrombogenicity (IT) were calculated.
83 ered a major contributor to inflammation and thrombogenicity, little attention has been directed towa
84                                          The thrombogenicity of a disrupted atherosclerotic lesion is
85 the intrinsic pathway significantly enhances thrombogenicity of atherosclerotic lesions after removal
86                                     Although thrombogenicity of atherosclerotic plaques has been ascr
87 issue factor (TF) has been implicated in the thrombogenicity of atherosclerotic plaques.
88 ations for control of thrombus formation and thrombogenicity of biomaterials.
89 inflammatory mediators that can increase the thrombogenicity of blood.
90 dy examines the role of tissue factor in the thrombogenicity of different types of atherosclerotic pl
91        This study analyzes the role of TF on thrombogenicity of disrupted human atherosclerotic plaqu
92 t that it is an important determinant of the thrombogenicity of human atherosclerotic lesions after s
93                    This study assessed acute thrombogenicity of Magmaris compared with Absorb and the
94  are needed to determine whether the reduced thrombogenicity of Magmaris will result in reductions in
95  to the TF expression and hence to increased thrombogenicity of plaques during the inflammatory respo
96                                          The thrombogenicity of polymer-coated stents with thin strut
97                                          The thrombogenicity of the arterial specimens was assessed b
98 anticoagulant function, thereby reducing the thrombogenicity of the thrombus or injured vessel surfac
99      We previously reported on the different thrombogenicity of the various types of human atheroscle
100  not associated with serious adverse events, thrombogenicity, or virus transmission.
101  between improved glycemic control and blood thrombogenicity reduction.
102 atings uniformly reduce rather than increase thrombogenicity relative to matched bare metal counterpa
103 ss relations between dietary fatty acids and thrombogenicity reveals problems that need to be recogni
104 eutic agent in other conditions of increased thrombogenicity, such as acute coronary syndromes, and f
105 irmed, correlating with in vitro and in vivo thrombogenicity, supporting utility in guiding device de
106 durable, with low incidence of infection and thrombogenicity, their widespread application has been l
107 cence under atheroprone low shear stress and thrombogenicity through angiotensin II-induced redox-sen
108                 Prosenescent MPs promoted EC thrombogenicity through tissue factor upregulation, shed
109 endent pathway, linking the regulation of TF thrombogenicity to oxidative stress in the vasculature.
110 hysical prototypes in vitro by measuring VAD thrombogenicity using the modified prothrombinase assay.
111                                              Thrombogenicity was assessed by exposing all surfaces to
112                           Low probability of thrombogenicity was confirmed with a negative platelet a
113                                        Blood thrombogenicity was measured at baseline and after three
114  determine whether smoking influences plaque thrombogenicity, we examined the effect of cigarette smo
115            The indices of atherogenicity and thrombogenicity were also within the values considered t
116  addition, the indices of atherogenicity and thrombogenicity were significantly reduced in the low-ch
117 relor plus ASA with respect to ex vivo blood thrombogenicity, whereas markers sensitive to cyclo-oxyg

 
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