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1 g(C/-) splenocytes, which impeded lymphocyte egression.
2 ant airway MMP controlling inflammatory cell egression.
3 at a soluble factor(s) regulates the rate of egression.
4 NA2 coinciding with the first signs of viral egression.
5 n some instances, IFN-gamma induced parasite egression.
6 ses: (1) supramolecular exchanges (i.e., the egression and ingression of Pt complexes from and into C
10 t although inhibition of T-cell LFA-1 blocks egression by 75 +/- 5.6% (P<0.0001), inhibition of the L
12 ial epithelium, but we provide evidence that egression does not require epithelial injury, and can ta
17 ore, both colchicine and taxol prevented the egression of A. actinomycetemcomitans from host cells in
20 matrix metalloproteinase 2 (MMP2) for airway egression of lung eosinophils, a critical anti-inflammat
21 lishes the chemotactic gradient required for egression of lung inflammatory cells and prevention of l
22 omics approach to determine how MMPs promote egression of lung inflammatory cells through the airway.
23 emporally characterizing the CXCL12-mediated egression of MM cells from the BM stroma and its effects
27 rational stages appear important for surface egression or intracellular retention of empty HLA-DR.
29 he isomers is much faster than the entry and egression rates, and that the functional groups at the r
30 The initial phase of this increased rate of egression was inhibited by antibodies to inter- cellular