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1 d clotting time and, at higher doses, of the activated partial thromboplastin time.
2 r VIIc, antithrombin III, platelet count, or activated partial thromboplastin time.
3 nt activity and a marked prolongation of the activated partial thromboplastin time.
4 asma fibrinogen level, prothrombin time, and activated partial thromboplastin time.
5 ssay and had no effect on the TF-independent activated partial thromboplastin time.
6 ate levels, platelets, prothrombin time, and activated partial thromboplastin time.
7 (-1) IV argatroban, adjusted to maintain the activated partial thromboplastin time 1.5 to 3.0 times b
8 ban 2 microg x kg x min, adjusted to achieve activated partial thromboplastin times 1.5-3 times basel
10 one of two doses of heparin (n = 50) (target activated partial thromboplastin time, 65 to 90 seconds
11 ; thromobocytopenia (13% and 23%); prolonged activated partial thromboplastin time (8% and 18%); elev
12 ed by thrombin generation, prothrombin time, activated partial thromboplastin time, activated clottin
15 oagulation profiles (index normalized ratio, activated partial thromboplastin time) after reperfusion
17 fold, while eliminating more than 90% of its activated partial thromboplastin time and anti-factor Xa
18 of contact pathway components prolonged the activated partial thromboplastin time and decreased targ
19 p < 0.05) but was associated with prolonged activated partial thromboplastin time and extravascular
20 r correlation between the peak posttreatment activated partial thromboplastin time and post hoc weigh
23 ssure into the permissive range and returned activated partial thromboplastin time and prothrombin ti
27 rinogen levels and increased prothrombin and activated partial thromboplastin times and tissue factor
28 n common assays of thrombosis in vitro (e.g. activated partial thromboplastin time) and in vivo (e.g.
29 Platelets, fibrinogen, prothrombin index, activated partial thromboplastin time, and d-dimer as we
30 platelet count, bleeding, fibrinogen level, activated partial thromboplastin time, and somnolence.
31 mination of the activated clotting time, the activated partial thromboplastin time, and the cuticle b
32 anticoagulant effect as assessed by anti-Xa, activated partial thromboplastin time (aPTT) and activat
37 system and has relatively normal activity in activated partial thromboplastin time (aPTT) assays.
38 he tPA+heparin group without prolongation of activated partial thromboplastin time (aPTT) before and
39 screpant activity as measured by a one-stage activated partial thromboplastin time (aPTT) clotting as
40 t protein C mutants were characterized using activated partial thromboplastin time (APTT) clotting as
43 In response to infusion of thrombin, the activated partial thromboplastin time (APTT) increased b
46 ation of prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT) obtained be
47 f 2.39% with short prothrombin time (PT) and activated partial thromboplastin time (APTT) of 14.2 and
48 both antithrombins were titrated to a target activated partial thromboplastin time (aPTT) of 55 to 85
49 iter plates, frozen thawed washed platelets, activated partial thromboplastin time (aPTT) reagent and
52 ian international normalized ratio (INR) and activated partial thromboplastin time (aPTT) values were
54 mbin, prolong both the thrombin time and the activated partial thromboplastin time (aPTT) when added
55 lasma resulted in complete correction of the activated partial thromboplastin time (aPTT), and that i
56 mbin time (dTT), ecarin clotting time (ECT), activated partial thromboplastin time (aPTT), and thromb
58 in and celite activated clotting time (ACT), activated partial thromboplastin time (APTT), heparin co
59 ir corresponding CCTs [prothrombin time (PT)/activated partial thromboplastin time (aPTT), internatio
61 , with a significant 43% prolongation of the activated partial thromboplastin time (aPTT), over contr
63 d more potent than ATS-112 in prolonging the activated partial thromboplastin time (APTT), whereas AT
68 The APC resistance ratio values (ratio of activated partial thromboplastin time [APTT] clotting ti
69 e [WBCT], activated clotting time [ACT], and activated partial thromboplastin time [aPTT]) have remai
70 applied, while the acoustic assays namely ''activated Partial Thromboplastin Time'' (aPTT) and ''Pro
71 blem, with fewer than 35% of patients having activated partial thromboplastin times (aPTTs) within a
73 me of human factor XI deficient plasma in an activated partial thromboplastin time assay, with a spec
76 sed for Western blots, prothrombin time, and activated partial thromboplastin time assays and fibrino
77 tivated protein C (APC) cofactor activity in activated partial thromboplastin time assays in PS-deple
79 nt was inactive in both prothrombin time and activated partial thromboplastin time assays; however, i
80 mboplastin time dose dependently; the median activated partial thromboplastin time at 10 minutes afte
81 ore than doubled activated clotting time and activated partial thromboplastin time at the higher dose
82 cosidase-treated FV was analyzed in an aPTT (activated partial thromboplastin time)-based APC sensiti
83 rotein S (r = 0.47, P = 0.035), but not with activated partial thromboplastin time-based APC resistan
85 ) or membrane bound TF, and has no effect on activated partial thromboplastin time, but is 70-fold le
87 lacked detectable anticoagulant activity in activated partial thromboplastin time clotting assays bu
89 n patients with impaired liver function, and activated partial thromboplastin time confounding may in
92 thin 4 hours by changes in prothrombin time, activated partial thromboplastin time, fibrinogen, fibri
94 sed lymphocyte count (five [12%]), prolonged activated partial thromboplastin time (four [10%]), and
95 troban-treated patients achieved therapeutic activated partial thromboplastin times generally within
97 n attempt to explain the prolongation of the activated partial thromboplastin time identified in pati
98 ted prolongation of the prothrombin time and activated partial thromboplastin time in affected indivi
100 ioate oligonucleotides (PS ODNs) prolong the activated partial thromboplastin time in human plasma by
102 a, decreased lymphocyte count, and prolonged activated partial thromboplastin time in the soft-tissue
103 vity and increases both prothrombin time and activated partial thromboplastin time in vitro or ex viv
104 eeding diathesis, prolonged prothrombin, and activated partial thromboplastin times, in whom no class
105 n, especially if the baseline (pretreatment) activated partial thromboplastin time is prolonged.
106 subtherapeutic bivalirudin anticoagulation (activated partial thromboplastin time less than twice th
107 parin at 100, 500, or 2500 units/kg produced activated partial thromboplastin time levels less than,
108 ontributes to sepsis, heparin titrated using activated partial thromboplastin times may be efficaciou
109 ern blot for alpha-2-macroglobulin (A2M) and activated partial thromboplastin time measurement for co
110 dose-pharmacodynamic response, reflected in activated partial thromboplastin time measurements, was
111 ls (701 patients) that compared therapeutic (activated partial thromboplastin time more than twice th
112 tive laboratory studies revealed a prolonged activated partial thromboplastin time of 49.2 seconds, a
115 500 units/kg with E. coli further increased activated partial thromboplastin time (p < .0001 vs. pla
117 t heparin (i.e., with placebo) increased the activated partial thromboplastin time (p = .002) close t
119 nd 4 hours (p < 0.05, respectively), and the activated partial thromboplastin time prolonged signific
122 l normalized ratio (r=0.72) but less so with activated partial thromboplastin time (r=0.56; all P<0.0
123 vity, plasminogen activator inhibitor 1, and activated partial thromboplastin time showed variability
125 APC levels and APC-dependent prolongation of activated partial thromboplastin times that were two- to
127 oss all dose levels) and sustained return of activated partial thromboplastin time to within the norm
128 < 10(9) /L, fibrinogen level <60 mg/dL, and activated partial thromboplastin time values >100 second
131 ity; a significant, dose-related increase in activated partial thromboplastin time was accompanied by
133 regation to gamma-thrombin was inhibited and activated partial thromboplastin time was increased afte
138 of streptococcal necrotizing fasciitis, the activated partial thromboplastin times were significantl
139 whole blood clotting times were normalized, activated partial thromboplastin times were substantiall
140 ncipient clot formation time, T(GP), and the activated partial thromboplastin time, whereas the assoc
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