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1 served mainly in tubular epithelial cells in CO-treated, but not air-exposed, kidney grafts at 3 hr a
2 rate that SFN reverses the effects of PMI in co-treated cells by reducing the accumulation of p62 in
3 s enhancer by nuclear proteins isolated from CO-treated cells, although HIF-1 protein levels were una
8 monstrate interesting activity profiles when co-treated in a panel of metal(II) cations in MIC assays
10 d upregulation of HIF-1alpha and VEGF in the CO-treated kidney grafts as early as 1 hr after reperfus
12 )types were different between TCDD alone and co-treated mice including important mediators of NAFLD p
16 s to beta-amyloid (Abeta) peptides, we first co-treated primary cultured microglia with a tyrosine ph
18 otably, 10, 1 and 0.1 microM 3Me-H TRH, when co-treated with 500 microM Glu, protected fetal neurons
19 10 cells were treated with an FA mixture and co-treated with 8-Br-cAMP to stimulate the steroidogenes
20 induction of hsp72 mRNA was blocked in cells co-treated with actinomycin D. hsp72 mRNA levels were af
22 ved GBM cells cultured in 3D microwells were co-treated with BAY 11-7082 and TMZ or BAY 11-7082 and T
23 g7 or Atg5 prolonged the survival of neurons co-treated with BDNF and rapamycin, suggesting that supp
25 a dramatic decrease in the survival of cells co-treated with Casodex and ATM inhibitor as compared wi
26 e in contrast to what we saw when cells were co-treated with cisplatin plus an EGFR tyrosine kinase i
29 so were studied in MG-63 cells that had been co-treated with either sterol and transforming growth fa
30 reactive oxygen species (ROS) scavenger, is co-treated with ETO, it inhibits an ETO-induced increase
32 17beta-estradiol (estrogen) for 1 h and then co-treated with glutamate, apoptotic death was significa
33 mitigates phosphorylation of STAT5 in cells co-treated with hGH, reducing intracellular STAT5 phosph
35 served when the GBM-derived U87MG cells were co-treated with LPS and Temozolomide (TMZ) in comparison
37 excitability is not present when animals are co-treated with NaBut suggesting gut derived mediators m
38 ment with recombinant MMP-9, either alone or co-treated with native TIMP-1, TIMP-3, or the engineered
40 ted in response to thapsigargin if they were co-treated with PMA, while adherent cells secreted in re
42 er 2 weeks and by 60% (P < 0.01) in dko mice co-treated with prednisolone over an 8 week treatment pe
44 deficient HL-60/MX2 cells and in HL-60 cells co-treated with the Top II catalytic inhibitor ICRF-193.