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1 d tumor necrosis factor-alpha, and pulmonary leukostasis).
2 role for these hormones in diabetic retinal leukostasis.
3 the major metabolic dysregulation promoting leukostasis.
4 cclusion by GFP(+) cells was used to measure leukostasis.
5 tion, but had no effect on Bax expression or leukostasis.
6 orneal inflammation and VEGF-induced retinal leukostasis.
7 creased generation of retinal superoxide and leukostasis.
8 dent transcription in retina, and subsequent leukostasis.
9 al NFAT isoforms in TNFalpha-induced retinal leukostasis.
10 increased retinal ICAM-1 levels (2.2-fold), leukostasis (1.9-fold), and BRB breakdown (2.1-fold, P <
11 human leukemia cells that may contribute to leukostasis, a complication associated with acute leukem
13 SAR 1118 eye drops significantly reduced leukostasis and blood-retinal barrier breakdown in a dos
15 lted in a significant suppression of retinal leukostasis and BRB breakdown in both early (72.4% and 8
16 hether endogenous VEGF(164) mediates retinal leukostasis and BRB breakdown in early and established d
23 bition (LY333531) prevented the increases in leukostasis and decreases in retinal blood flow in diabe
26 not only diminished fibrin accumulation and leukostasis and improved gas exchange and survival but a
28 subsequent graft ICAM-1 expression and graft leukostasis and markedly improved oxygenation, pulmonary
33 lockade with a mAb prevents diabetic retinal leukostasis and vascular leakage by 48.5% and 85.6%, res
34 hesion molecule-1 overexpression and reduced leukostasis and vascular leakage for at least 4 weeks af
35 ocyte adhesion to the capillary endothelium (leukostasis) and decreases in retinal blood flow may be
37 as intercellular adhesion molecule-1 levels, leukostasis, and blood-retinal barrier breakdown, in a r
39 enting diabetes-induced increases in ICAM-1, leukostasis, and breakdown of the blood-retinal barrier,
41 r NFAT-signaling in TNFalpha-induced retinal leukostasis, and identify NFATc2 and NFATc4 as potential
42 s of study to measure superoxide generation, leukostasis, and immunohistochemistry, and at 7 months t
43 inflammatory/angiogenic factors, attenuated leukostasis, and reduced retinal vascular leakage in bot
45 increases retinal vascular permeability and leukostasis, and these responses are mediated, in part,
46 ed retinal vascular permeability and retinal leukostasis, and these responses were ameliorated by PK
51 this study, we demonstrate that increases in leukostasis are observed in insulin-resistant states wit
53 d in streptozotocin-induced diabetic rats by leukostasis assay and Western blot analysis of intracell
56 wild-type mice and by 40% in APN-KO mice and leukostasis by 64% in wild-type mice and by 75% in APN-K
57 n the aqueous fluid by 21% (P<0.01), retinal leukostasis by 68% (P<0.01), and leukocyte accumulation
59 breakdown, even though it prevented retinal leukostasis, demonstrating that neither TNFalpha nor inf
60 icrovascular endothelial cell monolayers and leukostasis in an acute mouse model of retinal inflammat
64 es in vitro, and 4) inhibited both pulmonary leukostasis in mice systemically infused with cobra veno
66 tly ameliorated retinal vascular leakage and leukostasis in streptozotocin-induced diabetic rats and
67 lar endothelial growth factor (VEGF)-induced leukostasis in the choroid and retina was determined by
68 vivo, CD18 blockade significantly decreases leukostasis in the diabetic retinal microvasculature.
69 estigated the phenotype of cells involved in leukostasis in the early stages of streptozotocin-induce
71 f mice also caused a significant increase in leukostasis in the retina (AGE-Alb versus Alb, 6.89 vs.
74 ly associated with retinal leukocyte stasis (leukostasis) in the rat model of streptozotocin-induced
78 by blockade of VCAM-1 included increases in leukostasis, influx of bone marrow-derived cells, and ca
81 is characterized by increased permeability, leukostasis, microthrombosis, and apoptosis of capillary
83 for vascular permeability, vascular lesions, leukostasis, morphologic changes of micro- and macroglia
85 than in chronic leukemias, and particularly leukostasis occurs more often in acute myeloid leukemia
88 genase-deficient mice had significantly less leukostasis (P < 0.005) but not superoxide production or
89 re DR, as shown by retinal vascular leakage, leukostasis, pericyte loss, capillary degeneration, and
90 ncreases in inflammatory protein production, leukostasis, retinal damage, signs of anterior uveitis,
92 e-deficient mice also had significantly less leukostasis, superoxide production, and nuclear factor-k
94 itate an extensive retinal leukocyte stasis (leukostasis) that coincides with enhanced vascular perme
95 lood count itself, but complications such as leukostasis, tumor lysis syndrome, and disseminated intr
96 ect cytopathic effects may contribute to the leukostasis, vascular compromise, and capillary leak cha
98 sequence of PPAR-gamma activation, pulmonary leukostasis was decreased and oxygenation and overall su
101 s-induced increases in ICAM-1 expression and leukostasis were significantly inhibited by deletion of
102 ary bone marrow-derived cells, indicative of leukostasis, were only observed in diabetic animals rece
107 nd VEGF(164), for inducing leukocyte stasis (leukostasis) within the retinal vasculature and blood-re
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