ライフサイエンスコーパス: leukostasis

1 e number of PMo adherent to retinal vessels (leukostasis).

2 d tumor necrosis factor-alpha, and pulmonary leukostasis).

3 ermeability to labeled dextran and inhibited leukostasis.

4 other pathogenic behaviors in DR, including leukostasis.

5 ular adhesion molecule-1 overexpression, and leukostasis.

6 al NFAT isoforms in TNFalpha-induced retinal leukostasis.

7 role for these hormones in diabetic retinal leukostasis.

8 the major metabolic dysregulation promoting leukostasis.

9 tion, but had no effect on Bax expression or leukostasis.

10 orneal inflammation and VEGF-induced retinal leukostasis.

11 creased generation of retinal superoxide and leukostasis.

12 dent transcription in retina, and subsequent leukostasis.

13 cclusion by GFP(+) cells was used to measure leukostasis.

14 increased retinal ICAM-1 levels (2.2-fold), leukostasis (1.9-fold), and BRB breakdown (2.1-fold, P <

15 human leukemia cells that may contribute to leukostasis, a complication associated with acute leukem

16 However, leukostasis also requires diabetes-induced changes in th

17 SAR 1118 eye drops significantly reduced leukostasis and blood-retinal barrier breakdown in a dos

18 ed diabetic rat model by determining retinal leukostasis and blood-retinal barrier breakdown.

19 lted in a significant suppression of retinal leukostasis and BRB breakdown in both early (72.4% and 8

20 hether endogenous VEGF(164) mediates retinal leukostasis and BRB breakdown in early and established d

21 EGF(120) at inducing ICAM-1-mediated retinal leukostasis and BRB breakdown in vivo.

22 nth diabetic rats, and the effect on retinal leukostasis and BRB breakdown was quantified.

23 Retinal leukostasis and BRB breakdown were compared in nondiabet

24 Retinal leukostasis and BRB breakdown were simultaneously quanti

25 The inhibition of diabetic retinal leukostasis and BRB breakdown with EYE001 in early and e

26 and nitric oxide synthase (NOS2), developed leukostasis and capillary degeneration.

27 bition (LY333531) prevented the increases in leukostasis and decreases in retinal blood flow in diabe

28 Diabetes significantly increased both leukostasis and expression of ICAM-1, and PBM essentiall

29 est a role for superoxide in gut I/R-induced leukostasis and hypoxic stress in the liver.

30 not only diminished fibrin accumulation and leukostasis and improved gas exchange and survival but a

31 Retinal leukostasis and leakage increased with the duration of d

32 subsequent graft ICAM-1 expression and graft leukostasis and markedly improved oxygenation, pulmonary

33 effective in attenuating the gut I/R-induced leukostasis and NAD(P)H autofluorescence.

34 ch reduces KC function, attenuated the liver leukostasis and NPS elicited by gut I/R.

35 hs and in another model, blocks VEGF-induced leukostasis and retinal nonperfusion, which are associat

36 ession and 2) after 3 months of diabetes for leukostasis and retinal superoxide generation.

37 illaries and pericytes and increases in both leukostasis and superoxide production (P < 0.006).

38 lockade with a mAb prevents diabetic retinal leukostasis and vascular leakage by 48.5% and 85.6%, res

39 hesion molecule-1 overexpression and reduced leukostasis and vascular leakage for at least 4 weeks af

40 ocyte adhesion to the capillary endothelium (leukostasis) and decreases in retinal blood flow may be

41 on of the progressive BRB breakdown, retinal leukostasis, and apoptosis associated with DR.

42 of absence of PMo, there was no increase in leukostasis, and at 6 months of diabetes, the number of

43 as intercellular adhesion molecule-1 levels, leukostasis, and blood-retinal barrier breakdown, in a r

44 A expression, NFkappaB DNA-binding activity, leukostasis, and blood-retinal barrier breakdown.

45 enting diabetes-induced increases in ICAM-1, leukostasis, and breakdown of the blood-retinal barrier,

46 Optic nerves displayed hemorrhage, leukostasis, and foreign body crystallization.

47 r NFAT-signaling in TNFalpha-induced retinal leukostasis, and identify NFATc2 and NFATc4 as potential

48 s of study to measure superoxide generation, leukostasis, and immunohistochemistry, and at 7 months t

49 inflammatory/angiogenic factors, attenuated leukostasis, and reduced retinal vascular leakage in bot

50 d reduction of hyperglycemia-induced retinal leukostasis, and restoration of retinal blood-barrier fu

51 us PK induced retinal vascular permeability, leukostasis, and retinal hemorrhage.

52 increases retinal vascular permeability and leukostasis, and these responses are mediated, in part,

53 ed retinal vascular permeability and retinal leukostasis, and these responses were ameliorated by PK

54 -alpha-induced ICAM-1 and VCAM-1 expression, leukostasis, and vascular leakage in mouse retinas.

55 P1) in retinal adhesion molecule expression, leukostasis, and vascular leakage.

56 nduced increases in retinal VEGF expression, leukostasis, and vascular remodeling.

57 showed vessel wall endothelial cell changes, leukostasis, and vessel occlusion.

58 this study, we demonstrate that increases in leukostasis are observed in insulin-resistant states wit

59 Leukostasis, as well as increases in NPS and NAD(P)H aut

60 d in streptozotocin-induced diabetic rats by leukostasis assay and Western blot analysis of intracell

61 t alpha-lipoic acid normalized the amount of leukostasis but not retinal blood flow.

62 F(ab')2 fragments decreased diabetic retinal leukostasis by 62% (n = 5, P = 0.001).

63 wild-type mice and by 40% in APN-KO mice and leukostasis by 64% in wild-type mice and by 75% in APN-K

64 n the aqueous fluid by 21% (P<0.01), retinal leukostasis by 68% (P<0.01), and leukocyte accumulation

65 en to the peripheral blood with death due to leukostasis by day 15.

66 breakdown, even though it prevented retinal leukostasis, demonstrating that neither TNFalpha nor inf

67 icrovascular endothelial cell monolayers and leukostasis in an acute mouse model of retinal inflammat

68 The attenuation in pulmonary leukostasis in animals treated with PLV is equivalent to

69 einterpretation of the functional meaning of leukostasis in diabetes and document within the natural

70 uced increases in ICAM-1 may promote retinal leukostasis in diabetic eyes.

71 microvascular endothelial cells and retinal leukostasis in diabetic mice, presumably by inhibiting n

72 We conclude that leukostasis in early diabetic retinopathy involves activ

73 es in vitro, and 4) inhibited both pulmonary leukostasis in mice systemically infused with cobra veno

74 Retinal leukostasis in mice was assessed after perfusion with FI

75 eliorated retinal NV, hyperpermeability, and leukostasis in Pparalpha(-/-) mice with OIR.

76 tly ameliorated retinal vascular leakage and leukostasis in streptozotocin-induced diabetic rats and

77 lar endothelial growth factor (VEGF)-induced leukostasis in the choroid and retina was determined by

78 vivo, CD18 blockade significantly decreases leukostasis in the diabetic retinal microvasculature.

79 estigated the phenotype of cells involved in leukostasis in the early stages of streptozotocin-induce

80 icantly reduced retinal vascular leakage and leukostasis in the OIR model.

81 f mice also caused a significant increase in leukostasis in the retina (AGE-Alb versus Alb, 6.89 vs.

82 Leukostasis in vivo and ex vivo in retinal capillaries w

83 was shown to reduce TNFalpha-induced retinal leukostasis in vivo.

84 ly associated with retinal leukocyte stasis (leukostasis) in the rat model of streptozotocin-induced

85 izing antibody prevents the permeability and leukostasis increases by 79% and 54%, respectively.

86 Retinal leukostasis increases within days of developing diabetes

87 Post-transplant graft leukostasis, inflammation, and thrombosis are consequent

88 by blockade of VCAM-1 included increases in leukostasis, influx of bone marrow-derived cells, and ca

89 The leukostasis is accompanied by the up-regulation of inter

90 These findings suggest that leukostasis is associated with endothelial dysfunction,

91 is characterized by increased permeability, leukostasis, microthrombosis, and apoptosis of capillary

92 Increases in leukostasis/monocyte adhesion to the capillary endotheli

93 for vascular permeability, vascular lesions, leukostasis, morphologic changes of micro- and macroglia

94 Maximum leukostasis occurred when both donor and recipient were

95 than in chronic leukemias, and particularly leukostasis occurs more often in acute myeloid leukemia

96 ndothelium, because statin therapy prevented leukostasis only when recipient mice were treated.

97 D had little or no effect on gut I/R-induced leukostasis or capillary no-reflow in the liver.

98 genase-deficient mice had significantly less leukostasis (P < 0.005) but not superoxide production or

99 re DR, as shown by retinal vascular leakage, leukostasis, pericyte loss, capillary degeneration, and

100 ncreases in inflammatory protein production, leukostasis, retinal damage, signs of anterior uveitis,

101 Inflammation-mediated leukostasis, retinal ischemia, and neovascularization an

102 e-deficient mice also had significantly less leukostasis, superoxide production, and nuclear factor-k

103 ificantly more effective in reducing retinal leukostasis than was P-selectin blockade.

104 itate an extensive retinal leukocyte stasis (leukostasis) that coincides with enhanced vascular perme

105 lood count itself, but complications such as leukostasis, tumor lysis syndrome, and disseminated intr

106 ect cytopathic effects may contribute to the leukostasis, vascular compromise, and capillary leak cha

107 Leukostasis was assessed using FITC-conjugated ConA to l

108 sequence of PPAR-gamma activation, pulmonary leukostasis was decreased and oxygenation and overall su

109 Leukostasis was measured by fluorescein isothiocyanate-c

110 Leukostasis was measured with a static adhesion assay ex

111 s-induced increases in ICAM-1 expression and leukostasis were significantly inhibited by deletion of

112 ary bone marrow-derived cells, indicative of leukostasis, were only observed in diabetic animals rece

113 Rosuvastatin treatment prevented leukostasis when both recipient and donor were treated b

114 ust traverse the microvasculature to prevent leukostasis, which is the entrapment of monocytes within

115 We found leukostasis with retinal arteriole occlusion in all trea

116 tric oxide (NO), cyclooxygenase (COX)-2, and leukostasis within retinal microvessels.

117 F), nitric oxide (NO), cyclooxygenase-2, and leukostasis within retinal microvessels.

118 nd VEGF(164), for inducing leukocyte stasis (leukostasis) within the retinal vasculature and blood-re