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We next probed the effect of the induction of autophagy before Bin treatment.
Because drugs that inhibit tubulin polymerization also destabilize MTs [3], we next probed whether compound B destabilized metaphase spindles.
We next probed for glial cells in the optic nerve and nerve head of the guinea pig eye.
We next probed the role of gene expression noise in effecting the switch from the L to the H state.
We next probed whether the fast response times of Halo could support naturalistic sequences of hyperpolarization events, in response to trains of brief pulses of yellow light.
We next probed SDS-PAGE separated fractions for Ii and again found two peaks, in fractions 8 to 11 and 13 to15 (Fig. 3A).
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We next examined probe access resistance.
To eliminate those genes whose expression was even marginally affected by mefloquine exposure, we next removed probe sets that changed by 1.5 fold or more from control at any concentration, in any replicate of the mefloquine data, to generate a list of 94 probe sets differentially affected by OP exposure, but unaffected by mefloquine.
We next used Celltracker probe (Molecular Probes, Invitrogen Corporation, Carlsbad, CA, USA) to trace the long-term fluorescent image of CL1-5 cells i.v. injected into nude mice treated with or without CCN2 (1 mg/kg per day).
The nature of these two kinds of fuzzy controllers is next probed from the perspective of control engineering.
The role of nucleotide excision repair (NER) in the biocompatibility of click-linked DNA in mammalian cells was next probed.
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