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1 romboglobulin (beta-TG), and thromboxane B2 (TXB2).
2 (>10 ng/mL) than in patients with low serum TXB2.
3 release of PF4 and beta-TG and generation of TXB2.
4 air pouch were PGE2, 6-keto PGF1 alpha, and TxB2.
5 ation of 8-epi-PGF2alpha, but not of PGE2 or TxB2.
6 for quantification of cyclooxygenase-derived TxB2.
7 ed multiple mass spectra similar to those of TxB2.
8 2, PGD2, PGF2alpha, and, to a lesser degree, TXB2.
10 etion of the major Tx metabolite, 11-dehydro TxB2 (-70 +/- 9.9% vs. -20.3 +/- 5.3%; P < 0.05) when co
13 crophages compared with controls resulted in TxB2 and 6-keto PGF1alpha becoming the two most abundant
14 ratio and reduced levels of the eicosanoids, TXB2 and 6-keto-PGF1alpha, in their plasma compared with
17 e (CR); urea nitrogen (BUN); thromboxane B2 (TXB2) and 6-keto prostaglandin F(1alpha) (6 kPGF(2alpha)
18 aspirin "resistance," serum thromboxane B2 (TXB2) and flow cytometric measures of arachidonic acid-i
19 L-6) and the lipid mediators thromboxane B2 (TxB2) and prostacyclin in hypothermic septic patients in
20 of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), and 8-epi-PGF2 alpha, but not of other F2-isopros
21 ed whole blood were prostaglandin E2 (PGE2), TxB2, and 6-keto PGF1 alpha; prostaglandins E1, D2, and
22 oheximide; and preventing synthesis of PGE2, TxB2, and 8-epi-PGF2 alpha with the specific PG G/H S-2
23 ess was defined as a level of residual serum TXB2 associated with elevated thrombotic risk (<99.0% in
25 ignificantly (peak pulmonary thromboxane B2 [TXB2] concentration = 668 pg/ml, p < 0.05) by meclofenam
26 gests that patients with high residual serum TXB2 concentrations were either noncompliant or underdos
28 vation to similar levels regardless of serum TXB2 concentrations, which suggests that patients with h
37 evated thrombotic risk (<99.0% inhibition or TXB2 >3.1 ng/ml) within 72 h after 3 daily aspirin doses
38 telet activation in patients with high serum TXB2 (>10 ng/mL) than in patients with low serum TXB2.
39 the following altered prostaglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the co
40 ide: prostaglandin E2 (PGE2)>thromboxane B2 (TxB2)>6-keto prostaglandin F1alpha (PGF1alpha), prostagl
43 56% of EC aspirin-treated subjects had serum TXB2 levels >3.1 ng/ml, compared with 18% and 11% of sub
46 ssary mediator of increased circulating PGI, TxB2, LTC4D4E4, TNF, and IL-6 levels in patients with se
48 d with in vivo platelet activation and serum TxB2 overproduction; aspirin 100 mg/day seems insufficie
49 1) and soluble P-selectin (p < 0.001), serum TxB2 (p = 0.030), mean platelet volume (p = 0.037), Pneu
51 significant reduction in urinary 11-dehydro-TxB2 production and suppression of 8-epi-PGF2 alpha and
55 M and 11beta-PGF2alpha as well as 11-dehydro-TXB2 showed a significant decrease in their urinary conc
56 dium and potassium, plasma concentrations of TXB2 (stable TXA2 metabolite) and PGF2alpha , soluble ce
57 e direct correlation between PCSK9 and 11-dh-TxB2 suggests PCSK9 as a mechanism potentially implicate
59 prostaglandin I2 (PGI2) and thromboxane B2 (TXB2), the stable metabolite of TXA2, via radioimmunoass
60 ction ranged from 0.5 pg for thromboxane B2 (TxB2) to 10 pg for 6-keto prostaglandin F1 alpha (6-keto
61 of major metabolites of both TxA2, 2,3-dinor TxB2 (Tx-M), and PGI2, 2,3-dinor 6-keto PGF(1alpha) (PGI
64 3 pmol/ mmol creatinine), whereas 11-dehydro TxB2 was significantly reduced (695 +/- 74 versus 95 +/-
67 latelet therapy, circulating PCSK9 and 11-dh-TxB2 were significantly correlated (Spearman's rho: 0.66
68 P-selectin and soluble CD40 ligand and serum TxB2 were significantly higher in patients who developed
71 stimulated production of the TXA2 metabolite TXB2, which was increased in eNOS(-/-) compared with WT
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