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1 Cell morphology was assessed by fluorescent staining.
2 debridement was monitored and visualized by fluorescent staining.
3 ty was assessed with confocal microscopy and fluorescent staining.
4 based on high and homogeneous expression on fluorescent staining.
11 with the use of 4,6-diamidino-2-phenylindole-fluorescent staining, and by decreases in the sensitivit
12 s assessed by electron microscopy, annexin V fluorescent staining, and flow-cytometric terminal deoxy
13 ll staining including cell permeabilization, fluorescent staining, and molecular delivery to viable c
14 ned by using confocal microscopy of multiple fluorescent stainings at the arterial level, and by usin
15 nt fluorophore labeling by the addition of a fluorescent staining dye to the sample proteins either d
20 sional electrophoresis (2-DE), visualized by fluorescent staining, imaged, and analyzed as a function
23 el sensitive approach which combines in situ fluorescent staining of accumulated decellularised ECM p
24 n enzyme-linked immunosorbent assay based on fluorescent staining of C. albicans with calcoflour.
26 found, using Yop beta-lactamase hybrids and fluorescent staining of live cells from plague-infected
28 gene was disrupted, based on phosphospecific fluorescent staining of proteins separated by 2-dimensio
33 ematically evaluated by in vitro and in situ fluorescent staining of the spinal cord and the brain, a
35 to examine differences in the proportion of fluorescent staining on the general surface membrane com
39 diverse suite of molecular tools and in situ fluorescent staining to target different levels of subce
40 in environmental samples, based on selective fluorescent staining using Nile Red (NR), followed by de
42 tary techniques such as Western blotting and fluorescent staining, we confirmed the differential expr
44 netic column-purified CD42(+) MK and 2-color fluorescent staining with antibodies directed against CD
46 of the FKBP12(F36V) fusion, and the level of fluorescent staining with FL-SLF' was proportional to th
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