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1 in BCR/ABL-transformed cells is reduction of hypermotility.
2 ed expression of the fliA and fliC genes and hypermotility.
3 rlie withdrawal-induced hyperalgesia and gut hypermotility.
4 rocaine did not, however, produce subsequent hypermotility.
5 5-10 micrograms amphetamine into VP produced hypermotility.
6 re it binds Ena/VASP), and this mediates the hypermotility.
7 ing on control surfaces with TGFbeta induced hypermotility after a 1-day lag time and growth arrest b
9 d the lipopolysaccharide elicited apoptosis, hypermotility and impairment of filtration barrier funct
10 X. fastidiosa exhibited reduced cell length, hypermotility (and subsequent lack of biofilm formation)
13 nin 5 (LN5') immediately induced directional hypermotility at approximately 125 microm/hour, followed
14 ans infected with Giardia exhibit intestinal hypermotility, but the underlying mechanisms and functio
15 loss of GABA VTA neurons was associated with hypermotility, further supporting their important regula
16 ide over agar surfaces (referred to here as "hypermotility"), greater resistance to phage infection a
19 e models of giardiasis that small-intestinal hypermotility occurs in a delayed fashion relative to pe
22 n I triggered a TGFbetaRI kinase-independent hypermotility unaccompanied by smad translocation or gro
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