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1 as preceded by 2 hour of pulse-labeling with 5-bromodeoxyuridine.
2 ular proliferation, as assessed by uptake of 5-bromodeoxyuridine.
3 d cells and incorporated into genomic DNA as 5-bromodeoxyuridine.
4 S phase cells were labeled in vivo with 5-bromodeoxyuridine.
5 DNA in these glands with a different marker, 5-bromodeoxyuridine (5BrdU), resulted in the appearance
6 ivated cross-linking of a self-complementary 5-bromodeoxyuridine (5BrU)-substituted oligonucleotide w
7 elevations in numbers of cells incorporating 5'-bromodeoxyuridine, a marker of unscheduled DNA synthe
8 ife by using two cell cycle-specific labels: 5-bromodeoxyuridine, a thymidine analog that labels cell
9 i) hypersensitivity to the nucleoside analog 5-bromodeoxyuridine and (ii) retention of more uracil re
10 tion (types I and III) and incorporated more 5-bromodeoxyuridine and TUNEL staining compared with uns
11 l detection of a marker for DNA replication (5-bromodeoxyuridine) and several cell type-specific mark
12 rve-tracing techniques, birth-date labeling (5-bromodeoxyuridine), and electrophysiology were used to
13 naive CD4+ T cells were labeled ex vivo with 5-bromodeoxyuridine as well as stained directly for Ki67
14 nd and those that occur after treatment with 5-bromodeoxyuridine, as these mutations are also drastic
15 identification, RPE cells were labeled with 5-bromodeoxyuridine, before intraocular transplantation.
19 We have determined the in vivo effect of 5-bromodeoxyuridine (BrdU) administered to mice in the d
20 ilis chromosome with the nucleotide analogue 5-bromodeoxyuridine (BrdU) and for subcellular visualiza
22 quently we administered a cell cycle marker, 5-bromodeoxyuridine (BrdU) at early, middle or late peri
24 the pro-mitotic growth factors with that of 5-bromodeoxyuridine (BrdU) incorporation to determine if
28 beling (TUNEL) to detect the dying cells and 5-bromodeoxyuridine (BrdU) to label newly generated cell
30 48 h later by intraperitoneal injections of 5-bromodeoxyuridine (BrdU), a marker for cell proliferat
31 reased proliferative activity assessed using 5-bromodeoxyuridine (BrdU), Ki-67, and c-Myc relative to
34 n cortex, using markers for DNA replication (5-bromodeoxyuridine; BrdU) and progressive neuronal diff
35 s and compared with that found using in vivo 5-bromodeoxyuridine (BrdUrd) labeling in formalin-fixed
36 ine perchlorate (DiI)], birth date labeling (5-bromodeoxyuridine), confocal microscopy, and electroph
38 o myocardium induced DNA synthesis, shown by 5'-bromodeoxyuridine incorporation, and accumulation in
39 elevated proliferation rates as assessed by 5-bromodeoxyuridine incorporation and cell-cycle analysi
41 sustained in mitogen-restimulated myocytes, 5-bromodeoxyuridine incorporation experiments in serum-s
43 issociated cushion cells displayed increased 5-bromodeoxyuridine incorporation when infected with Q79
44 sing independent parameters of regeneration, 5-bromodeoxyuridine incorporation, proliferating cell nu
50 and ES cell-derived cardiomyocytes based on 5-bromodeoxyuridine labeling was similar, and immunocyto
52 ealed a 7-fold increase in the percentage of 5-bromodeoxyuridine-positive cells and a 20-40-fold incr
53 , mtDNA (labeled with the thymidine analogue 5-bromodeoxyuridine) remained distinctly localized to on
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