ライフサイエンスコーパス: TXB2

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.

9 t but significant inhibitory effect on serum TxB2 4 hr after dosing.

10 etion of the major Tx metabolite, 11-dehydro TxB2 (-70 +/- 9.9% vs. -20.3 +/- 5.3%; P < 0.05) when co

11 Ibuprofen reduced serum TxB2 (-95 +/- 2% vs. -6.9 +/- 4.2%; P < 0.001) and urina

12 and urinary 11-dehydro-thromboxane B2 (11-dh-TxB2), a marker of platelet activation.

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

15 ely stable threefold difference between Bapi-TXB2 and Bapi was observed for up to 6 days after inject

16 Nontolerant mice made high levels of TxB2 and heightened, early production of IL-2 and IL-4 d

17 kines TNF-alpha and IL-6 and lipid mediators TxB2 and prostacyclin.

18 e (CR); urea nitrogen (BUN); thromboxane B2 (TXB2) and 6-keto prostaglandin F(1alpha) (6 kPGF(2alpha)

19 aspirin "resistance," serum thromboxane B2 (TXB2) and flow cytometric measures of arachidonic acid-i

20 L-6) and the lipid mediators thromboxane B2 (TxB2) and prostacyclin in hypothermic septic patients in

21 of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), and 8-epi-PGF2 alpha, but not of other F2-isopros

22 ed whole blood were prostaglandin E2 (PGE2), TxB2, and 6-keto PGF1 alpha; prostaglandins E1, D2, and

23 oheximide; and preventing synthesis of PGE2, TxB2, and 8-epi-PGF2 alpha with the specific PG G/H S-2

24 ess was defined as a level of residual serum TXB2 associated with elevated thrombotic risk (<99.0% in

25 vealed more parenchymal distribution of Bapi-TXB2 compared with Bapi.

26 n-treated patients with MIs had higher serum TxB2 compared with those without MIs (p = 0.005).

27 ignificantly (peak pulmonary thromboxane B2 [TXB2] concentration = 668 pg/ml, p < 0.05) by meclofenam

28 gests that patients with high residual serum TXB2 concentrations were either noncompliant or underdos

29 In 680 of 682 evaluable patients, serum TXB2 concentrations were reduced compared with nonaspiri

30 vation to similar levels regardless of serum TXB2 concentrations, which suggests that patients with h

31 that FPI increases CSF 6-keto-PGF1alpha and TXB2 concentrations.

32 LTC4 , PGE2 , and 11-dehydro-TXB2 did not differ between the groups, but levels of LT

33 tive lipids, e.g. PGB1, PGE2, PGF2alpha, and TxB2, did not inhibit LKB1 activity (p > 0.05).

34 h improved CO, FMD, CFR, TAC, GLS, GWW, MDA, TxB2 (differences 10.42 ppm, 4.3%, 0.98, 1.8 mL/mmHg, 2.

35 In contrast, release of TXB2 from PVAT from females was greater than from males,

36 rin failed to achieve complete inhibition of TXB2 generation due to incomplete absorption.

37 C3a- and C5a-induced thromboxane (TXB2) generation and histamine release from HMC-1 cells

38 xtent of inhibition of serum thromboxane B2 (TXB2) generation.

39 e profile was PGF2alpha approximately PGE2 > TXB2 >> 6 keto-PGF1alpha.

40 evated thrombotic risk (<99.0% inhibition or TXB2 >3.1 ng/ml) within 72 h after 3 daily aspirin doses

41 telet activation in patients with high serum TXB2 (>10 ng/mL) than in patients with low serum TXB2.

42 the following altered prostaglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the co

43 ide: prostaglandin E2 (PGE2)>thromboxane B2 (TxB2)>6-keto prostaglandin F1alpha (PGF1alpha), prostagl

44 TXB2-hFc did not elicit any acute adverse reactions, bin

45 TXB2-hFc displayed 20-fold higher brain concentrations c

46 Likewise, IV dosing of TXB2-hFc fused with neurotensin (TXB2-hFc-NT) at 25 nmol

47 osing of TXB2 when fused to human Fc domain (TXB2-hFc) at 25 nmol/kg (1.875 mg/kg) in mice resulted i

48 V dosing of TXB2-hFc fused with neurotensin (TXB2-hFc-NT) at 25 nmol/kg resulted in a rapid and rever

49 ized upon treatment with PGD2 and 11-dehydro TXB2 in eosinophils of controls.

50 tion and suppression of 8-epi-PGF2 alpha and TxB2 in serum.

51 In conclusion, TXB2 is a high affinity, species cross-reactive, and bra

52 56% of EC aspirin-treated subjects had serum TXB2 levels >3.1 ng/ml, compared with 18% and 11% of sub

53 The 24 hr TXB2 levels were significantly increased in group B (0 h

54 We now explore whether thromboxane B2 (TxB2)-like compounds, termed B2-isothromboxanes (B2-IsoT

55 ssary mediator of increased circulating PGI, TxB2, LTC4D4E4, TNF, and IL-6 levels in patients with se

56 At admission, plasma PCSK9 and urinary 11-dh-TxB2 (n = 852) were measured.

57 d with in vivo platelet activation and serum TxB2 overproduction; aspirin 100 mg/day seems insufficie

58 1) and soluble P-selectin (p < 0.001), serum TxB2 (p = 0.030), mean platelet volume (p = 0.037), Pneu

59 Plasma TxB2, PGI, LTC4D4E4, TNF, and IL-6, expressed as % basel

60 significant reduction in urinary 11-dehydro-TxB2 production and suppression of 8-epi-PGF2 alpha and

61 At study entry, urinary metabolites of TxB2, prostacyclin, and serum levels of TNF-alpha and IL

62 Plasma thromboxane B2 (TxB2), prostaglandin 6-keto-F1alpha (PGI), leukotriene B

63 In contrast, Met-induced TXB2 release was enhanced after FPI (340 +/- 20, 423 +/-

64 M and 11beta-PGF2alpha as well as 11-dehydro-TXB2 showed a significant decrease in their urinary conc

65 dium and potassium, plasma concentrations of TXB2 (stable TXA2 metabolite) and PGF2alpha , soluble ce

66 e direct correlation between PCSK9 and 11-dh-TxB2 suggests PCSK9 as a mechanism potentially implicate

67 Twelve patients had serum TXB2 that was lower than nonaspirinated healthy donors b

68 prostaglandin I2 (PGI2) and thromboxane B2 (TXB2), the stable metabolite of TXA2, via radioimmunoass

69 ction ranged from 0.5 pg for thromboxane B2 (TxB2) to 10 pg for 6-keto prostaglandin F1 alpha (6-keto

70 of major metabolites of both TxA2, 2,3-dinor TxB2 (Tx-M), and PGI2, 2,3-dinor 6-keto PGF(1alpha) (PGI

71 major enzymatic metabolite of TX (11-dehydro-TXB2 [TX-M]) were substantially increased.

72 Urinary 11-dehydro-TXB2 (U-TXM), a stable metabolite reflecting the whole-b

73 In conclusion, the TXB2 VNAR shuttle markedly increased brain uptake of pro

74 TXB2 VNAR was identified as a high affinity, species cro

75 TXB2 was fused to a human IgG1 Fc domain (hFc) or to the

76 Serum TxB2 was measured as an indicator of platelet COX-1 acti

77 3 pmol/ mmol creatinine), whereas 11-dehydro TxB2 was significantly reduced (695 +/- 74 versus 95 +/-

78 ame time point, brain concentrations of Bapi-TXB2 was threefold higher than Bapi.

79 When ATL and TXB2 were compared, levels changed in a statistically si

80 Levels of serum TxB2 were not different in smokers and nonsmokers and we

81 latelet therapy, circulating PCSK9 and 11-dh-TxB2 were significantly correlated (Spearman's rho: 0.66

82 P-selectin and soluble CD40 ligand and serum TxB2 were significantly higher in patients who developed

83 Levels of PGF2alpha and thromboxane B2 (TXB2 ) were quantified by ELISA, and PGF2alpha (FP) and

84 ), malondialdehyde (MDA) and thromboxane B2 (TxB2) were assessed in the acute and chronic study.

85 luble CD40 ligand, and serum thromboxane B2 (TxB2) were measured.

86 IV dosing of TXB2 when fused to human Fc domain (TXB2-hFc) at 25 nmol

87 stimulated production of the TXA2 metabolite TXB2, which was increased in eNOS(-/-) compared with WT

88 single domain shark antibody VNAR fragment (TXB2) with similar affinity to murine and human TfR1 was

89 ]) and 66% and 72% lower maximum decrease of TXB2, with marked interindividual variability.