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1 nce, and up to a 100-fold increase in plasma thromboxane B2.
2 GE2, PGF2 alpha, PGD2, 8-iso-PGF2 alpha, and thromboxane B2.
3 ionship between PCSK9 and urinary 11-dehydro-thromboxane B2 (11-dh-TxB2), a marker of platelet activa
4 creases in concentrations of prostaglandins, thromboxane B2, 15-HETE and 11-HETE in cerebellar sample
5 helial cell adhesion molecule-1, P-selectin, thromboxane B2, 6-ketoprostaglandin F1a, vascular cell a
6 nduced increases in plasma concentrations of thromboxane B2 (60 mins) and significantly (p < .05) pot
9 ls of leukotriene B4, leukotriene C4/D4, and thromboxane B2 above those of saline-treated rats with f
11 ines (TNF-alpha, IL-6, CXCL8), IL-12, CCL11, thromboxane B2 and immunoglobulin E at 24 h after local
12 and isofuranes, markers of oxidative stress, thromboxane B2 and immunoglobulin E were measured in bro
14 mporal correlation with elevations of plasma thromboxane B2 and were inhibited by an anti-C5a monoclo
15 yl leukotrienes, leukotriene B4 , 11-dehydro-thromboxane B2 , and prostaglandins E2 , D2 , and F2alph
16 onic acid-derived mediators, leukotriene B4, thromboxane B2, and prostaglandin E2 from stimulated alv
17 flammatory leukotriene B4 and procoagulating thromboxane B2, as well as lower specialized proresolvin
18 al side effects and did not inhibit platelet thromboxane B2 at plasma drug levels similar to those ob
20 increased (p < .05) plasma concentrations of thromboxane B2 by seven- to eight-fold at 30 to 120 mins
21 -PLC and the formation of prostaglandins and thromboxane B2 by the action of COX as compared to low d
22 factor-alpha, as well as leukotriene C4 and thromboxane B2, by human monocyte-derived macrophages.
23 lush grade=3 exhibited lower values of serum thromboxane B2 compared with those with myocardial blush
29 assay for the clopidogrel response and serum thromboxane B2 for the aspirin response) and aggregation
30 tivities, and eicosanoid (prostaglandins and thromboxane B2) formation from arachidonic acid via cycl
36 ffect of SC-58635 on platelet aggregation or thromboxane B2 levels, whereas aspirin caused significan
39 Although LTB4 levels were reduced, renal thromboxane B2 production and cytokine expression were n
41 staglandin E2, 6-ketoprostaglandin F1 alpha, thromboxane B2) production were measured at baseline, po
42 , M1 and M2 phenotypes were distinguished by thromboxane B2, prostaglandin (PG) E2, and PGD2 producti
43 lyzed for leukotriene B4, leukotriene C4/D4, thromboxane B2, prostaglandin E2, 6 keto-prostaglandin F
44 ons of leukotriene B4, prostaglandin E2, and thromboxane B2 released from A23187-stimulated alveolar
46 F=3.64; P=0.01334) and correlated with serum thromboxane B2 (rho=0.31; P=0.0413) in control but not i
47 erent eicosanoids, both prostaglandin E2 and thromboxane B2 significantly enhanced serum-induced germ
50 plasma creatinine (CR); urea nitrogen (BUN); thromboxane B2 (TXB2) and 6-keto prostaglandin F(1alpha)
51 etter understand aspirin "resistance," serum thromboxane B2 (TXB2) and flow cytometric measures of ar
52 interleukin 6 (IL-6) and the lipid mediators thromboxane B2 (TxB2) and prostacyclin in hypothermic se
54 Limits of detection ranged from 0.5 pg for thromboxane B2 (TxB2) to 10 pg for 6-keto prostaglandin
56 lipopolysaccharide: prostaglandin E2 (PGE2)>thromboxane B2 (TxB2)>6-keto prostaglandin F1alpha (PGF1
57 reased formation of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), and 8-epi-PGF2 alpha, but not of
59 le metabolite of prostaglandin I2 (PGI2) and thromboxane B2 (TXB2), the stable metabolite of TXA2, vi
62 se was blunted significantly (peak pulmonary thromboxane B2 [TXB2] concentration = 668 pg/ml, p < 0.0
63 din E2, 11-hydroxyeicosatetraenoic acid, and thromboxane B2 were identified as differentiating metabo
64 -VI,2,3-dinor-6-keto-PGF1alpha and 2,3-dinor-thromboxane B2 were increased in GhOEs, reflecting incre
66 ene C4/D4, 6-keto-prostaglandin F1alpha, and thromboxane B2 with corn oil were significantly increase
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